AUTHOR: Biomed Mom TITLE: US Sugar Tariffs Led to Ubiquitous Use of High Fructose Corn Syrup DATE: 4/06/2010 06:20:00 AM ----- BODY:
The Great Sugar Shaft
by James Bovard, April 1998
The U.S. government has devotedly jacked up American sugar prices far above world market prices since the close of the War of 1812. The sugar industry is one of America's oldest infant industries — yet it dodders with the same uncompetitiveness that it showed during the second term of James Madison. Few cases better illustrate how trade policy can be completely immune to economic sense.

The U.S. imposed high tariffs on sugar in 1816 in order to placate the growers in the newly acquired Louisiana territory. In the 1820s, sugar plantation owners complained that growing sugar in the United States was "warring with nature" because the U.S. climate was unsuited to sugar production. Naturally, the plantation owners believed that all Americans should be conscripted into the "war." Protectionists warned that if sugar tariffs were lifted, then the value of slaves working on the sugar plantations would collapse — thus causing a general fall in slave values throughout the South.

In 1934, the U.S. government imposed sugar import quotas to complement high sugar tariffs and direct government subsidies to sugar growers. By the 1950s, the U.S. sugar program was renown for its byzantine, impenetrable regulations. Like most arcane systems, the sugar program vested vast power in the few people who understood and controlled the system. As author Douglas Cater observed in 1964, "In reviewing the sugar quotas, House Agriculture Committee Chairman Cooley has had the habit of receiving the [foreign representatives interested in acquiring sugar quotas] one by one to make their presentations, then summoning each afterward to announce his verdict. By all accounts, he has a zest for this princely power and enjoys the frequent meetings with foreign ambassadors to confer on matters of sugar and state."

Sugar quotas have also provided a safety net for former congressmen, many of whom have been hired as lobbyists for foreign sugar producers.

Since 1980, the sugar program has cost consumers and taxpayers the equivalent of more than $3 million for each American sugar grower. Some people win the lottery; other people grow sugar. Congressmen justify the sugar program as protecting Americans from the "roller-coaster of international sugar prices," as Rep. Byron Dorgan (D.-N.D.) declared. Unfortunately, Congress protects consumers from the roller-coaster by pegging American sugar prices on a level with the Goodyear blimp floating far above the amusement park. U.S. sugar prices have been as high as or higher than world prices for 44 of the last 45 years.

Sugar sold for 21 cents a pound in the United States when the world sugar price was less than 3 cents a pound. Each 1-cent increase in the price of sugar adds between $250 million and $300 million to consumers' food bills. A Commerce Department study estimated that the sugar program was costing American consumers more than $3 billion a year.

Congress, in a moment of economic sobriety, abolished sugar quotas in June 1974. But, on May 5, 1982, President Reagan reimposed import quotas. The quotas sought to create an artificial shortage of sugar that would drive up U.S. prices and force consumers to unknowingly support American sugar growers. And by keeping the subsidies covert and off-budget, quotas did not interfere with Reagan's bragging about how he was cutting wasteful government spending.

Between May 1982 and November 1984, the U.S. government reduced the sugar import quotas six times as the USDA desperately tried to balance foreign and domestic sugar supplies with domestic demand.

While USDA bureaucrats worked overtime to minutely regulate the quantity of sugar allowed into the United States, a bomb went off that destroyed their best-laid plans. On November 6, 1984, both Coca Cola and Pepsi announced plans to stop using sugar in soft drinks, replacing it with high-fructose corn syrup. At the drop of two press releases, U.S. sugar consumption decreased by more than 500,000 tons a year — equal to the entire quotas of 25 of the 42 nations allowed to sell sugar to the United States. The quota program drove sugar prices so high that it wrecked the market for sugar — and thereby destroyed the government's ability to control sugar supply and demand. On January 16, 1985, Agriculture Secretary John Block announced an effective 20 percent cut in the quota for all exporting countries.

Sugar quotas made it very profitable to import products with high amounts of sugar. As a USDA report noted, "The incentive to circumvent restrictions had led to creation of new products which had never been traded in the United States and which were designed specifically for the U.S. market." On June 28, 1983, Reagan declared an embargo on imports of certain blends and mixtures of sugar and other ingredients in bulk containers. Naturally, businesses began importing some of the same products in smaller containers. The Economic Report of the President noted, "Entrepreneurs were importing high-sugar content products, such as iced-tea mix, and then sifting their sugar content from them and selling the sugar at the high domestic price." On November 7, 1984, the Customs Service announced new restrictions on sugar- and sweetener-blend imports.

Federal restrictions made sugar smuggling immensely profitable. The Justice Department caught 30 companies in a major sting operation named Operation Bittersweet. Federal prosecutors were proud that the crackdown netted $16 million in fines for the government — less than one-tenth of 1 percent of what the sugar program cost American consumers during the 1980s. The Justice Department was more worried about businessmen's bringing in cheap foreign sugar than about the sugar lobby's bribing of congressmen to extort billions of dollars from consumers. (Public Voice for Food and Health Policy, a Washington, D.C., consumer lobby, reported that the sugar lobby donated more than $3 million to congressmen between 1984 and 1989.)

A few thousand sugar growers became the tail that wagged the dog of American foreign policy. Early in 1982, Reagan announced the Caribbean Basin Initiative (CBI) to aid Caribbean nations by giving them expanded access to the U.S. market. In his May 5, 1982, announcement, Reagan promised, "The interests of foreign suppliers are also protected, since this system provides such suppliers reasonable access to a stable, higher-priced U.S. market. In arriving at this decision, we have taken fully into account the CBI." But between 1981 and 1988, USDA slashed the amount of sugar that Caribbean nations could ship to the United States by 74 percent. The State Department estimated that the reductions in sugar-import quotas cost Third World nations $800 million a year. The sugar program has indirectly become a full-employment program for the U.S. Drug Enforcement Agency, as many poor Third World farmers who previously grew sugar cane are now harvesting marijuana.

The Reagan administration responded to sugar-import cutbacks by creating a new foreign-aid program — the Quota Offset Program — to give free food to countries hurt by reductions. In 1986, the United States. dumped almost $200 million of free food on Caribbean nations and the Philippines. As the Wall Street Journal reported, "By flooding local markets and driving commodity prices down, the U.S. is making it more difficult for local farmers to replace sugar with other crops." Richard Holwill, deputy assistant secretary of state, observed, "It makes us look like damn fools when we go down there and preach free enterprise."

The U.S. government's generosity to sugar farmers victimizes other American businesses. Brazil retaliated against the United States for cutting its sugar quota by reducing its purchases of American grain. In the Dominican Republic, former sugar growers are now producing wheat and corn, thereby providing more competition for American farmers. American candy producers are at a disadvantage because foreign companies can buy their sugar at much lower prices. Since 1982, dextrose and confectionery coating imports have risen tenfold and chocolate imports are up fivefold.

The sugar program has also decreased soybean exports. In the Red River valley of Minnesota, heavily subsidized sugar growers have bid up the rents on farmland by more than 50 percent. As a result, relatively unsubsidized soybean farmers can no longer find sufficient land to grow soybeans, America's premier export crop. This illustrates how restrictions on imports become restrictions on exports.

The sugar program is corporate welfare in its most overt form. The General Accounting Office estimated that only 17 of the nation's largest sugar cane farmers received more than half of all the benefits provided by the sugar cane subsidies. GAO also estimated that the 28 largest Florida sugar cane producers received almost 90 percent of all the benefits enjoyed by Florida sugar producers from federal programs.

The number of American jobs destroyed by sugar quotas since 1980 exceeds the total number of sugar farmers in the United States. The Commerce Department estimates that the high price of sugar has destroyed almost 9,000 U.S. jobs in food manufacturing since 1981. In early 1990, the Brach Candy Company announced plans to close its Chicago candy factory and relocate 3,000 jobs to Canada because of the high cost of sugar in the United States. Thanks to the cutback in sugar imports, 10 sugar refineries have closed in recent years and 7,000 refinery jobs have been lost. The United States has only 13,000 sugar farmers.

Many observers expected that, with the Republican Revolution in Congress, the sugar program would be abolished when the new farm bill was written in 1996. Instead, the sugar program's survival became one of the starkest symbols of that revolution's collapse. Two-hundred and twenty-three House members cosponsored a bill to get rid of the sugar program; but, when push came to shove, the sugar lobby persuaded several sponsors of the bill (including freshman conservative stalwarts Rep. Steve Stockman [R.-Tex.] and Rep. Sue Myrick [R.-N.C.]) to switch sides. The House voted 217-208 to continue the program.

Environmentalists were anxious about the adverse effects of Florida sugar cane production on the Everglades. Congress did not choose the obvious solution — ending subsides that irrationally encourage sugar production in a fragile area — but instead voted $200 million to clean up the Everglades by buying some of the sugar cane fields from farmers.

There is no reason why the United States must produce its own sugar cane. Sugar is cheaper in Canada primarily because Canada has almost no sugar growers — and thus no trade restrictions or government support programs. Paying lavish subsidies to produce sugar in Florida makes as much sense as creating a federal subsidy program to grow bananas in Massachusetts. The only thing that could make American sugar cane farmers world-class competitive would be massive global warming.

Mr. Bovard is the author of Lost Rights: The Destruction of American Liberty (St. Martin's Press, 1994) and Shakedown (Viking-Penguin Press, 1995).

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----- -------- AUTHOR: Biomed Mom TITLE: Gut healing, Intestinal Permeability, Biofilm DATE: 4/05/2010 05:21:00 PM ----- BODY:
Beyond Probiotics
Hidden Causes of GI Dysfunction
By Chris D. Meletis, ND
Often, in the absence of overt disease, the extent of an individual’s colon-supporting supplement regimen consists exclusively of consuming a good probiotic. Yet, in order for the good bacteria found in probiotics to flourish in the colonic environment, there are other steps we need to take to ensure our gut is hospitable to the friendly bacteria our bodies need to thrive—regardless of whether an individual is healthy or whether that individual suffers from irritable bowel syndrome or another gastrointestinal disease. The colon is essentially our body’s compost pile, used to nurture our garden of friendly flora.

There are two often-overlooked aspects of gut health that are essential to keeping our colon healthy and to ensure it remains a hospitable environment where good bacteria can thrive. First, gut health is linked to a substance called butyrate. If the intestine isn’t working at its optimal best, levels of butyrate can undergo a decline, putting individuals at risk for colon cancer. Butyrate levels are closely tied to the health of the intestine and to levels of friendly flora found in the gut.

A second aspect of gut health is known as intestinal permeability. This can be a huge factor, even in seemingly healthy individuals. Intestinal permeability refers to the potential for nutrients and bacteria to escape through a weakened intestinal wall. When intestinal permeability is increased, food and nutrient absorption is impaired. Dysfunction in intestinal permeability can result in leaky gut syndrome, where larger molecules in the intestines pass through into the blood. This can trigger immediate damage and immune system reactions since these large molecules are perceived as foreign. Progressive damage occurs to the intestinal lining, eventually allowing disease-causing bacteria, undigested food particles, and toxins to pass directly into the bloodstream.

Dysfunctions in intestinal permeability are associated not only with intestinal diseases such as ulcerative colitis, irritable bowel syndrome and Crohn’s disease, but also with chronic fatigue syndrome, psoriasis, food allergies, autoimmune disease and arthritis. Impaired intestinal permeability also occurs in patients undergoing chemotherapy and in heart disease patients.

I briefly discussed intestinal permeability in my last article on GI health. In this article, I will go into further detail about this damaging aspect of intestinal health and explain how increasing butyrate can be a powerful tool in not only restoring ideal colon function but also improving energy levels and the overall health of the body.

Building Butyrate for Colonic Health

Butyrate, a major short-chain fatty acid produced in the human gut by bacterial fermentation of dietary fiber, exhibits strong tumor suppressing activity. Butyrate is an important energy source for cells lining the intestine and plays a role in the maintenance of colonic balance. Butyrate exerts potent effects on a variety of colonic mucosal functions such as inhibition of inflammation and carcinogenesis. Butyrate also reinforces various components that play a role in the colonic defense barrier and decrease oxidative stress. In addition, butyrate may promote satiety.1

Low levels of butyrate are linked to increased risk of colon cancer. A loss of balance in the colon caused by either genetic mutations or environmental factors such as dietary habits can increase the risk for the formation of aberrant crypt foci (the earliest identifiable cancerous lesions in the colon) and ultimately the development of colon cancer. Evidence exists that butyrate reduces the number and the size of aberrant crypt foci in the colon.2

Butyrate’s inhibition of colon cancer is thought to arise from its ability to act as a natural histone deacetylase inhibitor, which results in activation of certain genes known to induce apoptosis (cell death) in cancer cells.2

Low butyrate levels occur in healthy humans prior to the onset of disease, often in response to a poor diet high in sugar and low in fiber. Low butyrate levels also are found in disease states such as ulcerative colitis and Crohn’s disease, especially in patients with moderate to severe mucosal inflammation.3 The monocarboxylate transporter helps colon cells uptake butyrate and during inflammatory bowel disease the monocarboxylate transporter is impaired, preventing the butyrate from getting to the cells.4

The Colonic Barrier and Overall Health

Abnormal intestinal permeability, like low butyrate levels, is another concern that can serve as a hidden reason why we might not be feeling our optimal best. A dysfunction can present in intestinal permeability when an individual is consuming a less than optimal diet or due to other factors such as psychological stress.5

Intestinal permeability, in fact, may be the main cause behind why the body becomes sensitive to a particular type of food. One group of researchers evaluated the intestinal permeability in subjects with adverse reactions to food. Twenty-one subjects with a food allergy and 20 with food hypersensitivity who were on allergen-free diets were enrolled and divided into four groups according to the seriousness of their referred clinical symptoms. The study authors found statistically significant differences in intestinal permeability in subjects with food allergy or hypersensitivity compared to control patients. The worse the intestinal permeability, the more serious the clinical symptoms in patients with food allergy and hypersensitivity.6

According to the researchers, “The present data demonstrate that impaired intestinal permeability, measured in our conditions, is present in all subjects with adverse reactions to food. In addition, for the first time, we report a statistically significant association between the severity of referred clinical symptoms and the increasing of Intestinal Permeability Index. These data reveal that intestinal permeability is not strictly dependent on IgE-mediated processes but could better be related to other mechanisms involved in early food sensitization, as breast-feeding, or microbial environment that influence the development of oral tolerance in early infancy.”

Impaired intestinal permeability is often linked with GI diseases such as ulcerative colitis and Crohn’s. However, new research is unearthing a surprising link between malfunctions in the colonic barrier and a number of non-gastrointestinal conditions such as heart disease.

In a recent study, scientists evaluated the function of the gut in 22 patients with chronic heart failure (CHF) and 22 control subjects. Chronic heart failure patients, compared with control patients, had a 35 percent increase of small intestinal permeability and a 210 percent increase of large intestinal permeability. Additionally, higher concentrations of adherent bacteria were found within mucus of CHF patients compared to control subjects.7

The researchers determined, “Chronic heart failure is a multisystem disorder in which intestinal morphology, permeability, and absorption are modified. Increased intestinal permeability and an augmented bacterial biofilm may contribute to the origin of both chronic inflammation and malnutrition.”

Strengthening the Colon

Raising butyrate levels and reducing the permeability of the intestinal barrier can have far reaching consequences for our health that extend beyond the gastrointestinal tract. Consequently, nutritional support is key.

Increasing fiber intake through consumption of a fiber supplement is one of the easiest ways to increase butyrate levels in the body. Fiber is well known for its ability to protect against colon cancer and its ability to raise butyrate levels is thought to be one of the main ways in which it protects the colon. The benefits of dietary fiber on inflammatory bowel disease may also be related to the production of butyrate that occurs when fiber is fermented in the colon. Butyrate appears to decrease the inflammatory response.8

Combining fiber and a good probiotic with specific botanicals, amino acids and fatty acids known to reduce intestinal permeability can provide additional support for the colon. Phosphatidylcholine, for example, can enhance butyrate’s ability to inhibit colon cancer cells, and therefore works well with fiber to strengthen the intestinal environment.9

The amino acid glutamine is one of the most powerful tools for reducing intestinal permeability, thereby protecting the body against the negative consequences of a leaky gut. In a recent review, researchers studied the medical literature to determine if glutamine was effective in reducing intestinal permeability in critically ill patients. In this group of patients, intestinal permeability can have particularly lethal consequences, causing bacteremia, sepsis, and multiple organ failure syndrome. After studying the medical literature, the scientists concluded that glutamine administration by the intravenous or oral route has a protective effect that prevents or reduces the intensity of the increase in intestinal permeability. Glutamine also reduces the frequency of systemic infections.10

Another group of researchers drew a similar conclusion after studying chemotherapy patients with gastrointestinal cancer. In this group of subjects, oral glutamine decreased intestinal permeability and maintained the intestinal barrier.11

Berberine is another substance that can help reduce intestinal permeability and stop beneficial nutrients from escaping through the intestinal wall.12 Berberine also is highly effective at inhibiting the growth of pathogens that invade the colon.

In my clinical practice, I have found that the best way to improve butyrate levels and reduce intestinal permeability is to combine a good fiber supplement with a supplement that contains phosphatidylcholine, L-glutamine, berberine, deglycyrrhizinated licorice (DGL), N-acetyl glucosamine, marshmallow (Althaea officinalis) root, cabbage powder, slippery elm (Ulmus rubra) bark, and gamma oryzanol. This often results in an increased level of friendly flora in the gut and maximizes the effectiveness of any probiotic supplement consumed. After undertaking this approach, patients often report improvement in their gastrointestinal tract and increased overall health and energy.

Conclusion

The gut uses a disproportionate amount of energy (about 25 percent of total oxygen consumption) for the size of the tissue (about 6 percent of body weight).13 Consequently, it’s especially important to provide this part of the body with as much support as possible. Fiber, probiotics, the amino acid L-glutamine, the fatty acid phosphatidylcholine, N-acetyl glucosamine, deglycyrrhizinated licorice and select botanicals such as marshmallow, berberine, cabbage powder and slippery elm can help raise levels of butyrate and reduce intestinal permeability. This approach can result in a healthier colon, improved energy and enhanced overall health.

References


1. Hamer HM, Jonkers D, Venema K, Vanhoutvin S, Troost FJ, Brummer RJ. Review article: the role of butyrate on colonic function. Aliment Pharmacol Ther. 2008 Jan 15;27(2):104-19.
2. Kim YS, Milner JA. Dietary modulation of colon cancer risk. J Nutr. 2007 Nov;137(11 Suppl):2576S-2579S.
3. Duffy MM, Regan MC, Ravichandran P, O’Keane C, Harrington MG, Fitzpatrick JM, O’Connell PR. Mucosal metabolism in ulcerative colitis and Crohn’s disease. Dis Colon Rectum. 1998 Nov;41(11):1399-405.
4. Thibault R, De Coppet P, Daly K, Bourreille A, Cuff M, Bonnet C, Mosnier JF, Galmiche JP, Shirazi-Beechey S, Segain JP. Down-regulation of the monocarboxylate transporter 1 is involved in butyrate deficiency during intestinal inflammation. Gastroenterology. 2007 Dec;133(6):1916-27.
5. Zareie M, Johnson-Henry K, Jury J, Yang PC, Ngan BY, McKay DM, Soderholm JD, Perdue MH, Sherman PM. Probiotics prevent bacterial translocation and improve intestinal barrier function in rats following chronic psychological stress. Gut. 2006 Nov;55(11):1553-60. Epub 2006 Apr 25.
6. Ventura MT, Polimeno L, Amoruso AC, Gatti F, Annoscia E, Marinaro M, Di Leo E, Matino MG, Buquicchio R, Bonini S, Tursi A, Francavilla A. Intestinal permeability in patients with adverse reactions to food. Dig Liver Dis. 2006 Oct;38(10):732-6.
7. Sandek A, Bauditz J, Swidsinski A, Buhner S, Weber-Eibel J, von Haehling S, Schroedl W, Karhausen T, Doehner W, Rauchhaus M, Poole-Wilson P, Volk HD, Lochs H, Anker SD. Altered intestinal function in patients with chronic heart failure. J Am Coll Cardiol. 2007 Oct 16;50(16):1561-9.
8. Rose DJ, DeMeo MT, Keshavarzian A, Hamaker BR. Influence of dietary fiber on inflammatory bowel disease and colon cancer: importance of fermentation pattern. Nutr Rev. 2007 Feb;65(2):51-62.
9. Hossain Z, Konishi M, Hosokawa M, Takahashi K. Effect of polyunsaturated fatty acid-enriched phosphatidylcholine and phosphatidylserine on butyrate-induced growth inhibition, differentiation and apoptosis in Caco-2 cells. Cell Biochem Funct. 2006 Mar-Apr;24(2):159-65.
10. De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of glutamine. Crit Care Med. 2005 May;33(5):1175-8.
11. Zhonghua Wei Chang Wai Ke Za Zhi. 2006 Jan;9(1):59-61. [Protective effect of glutamine on intestinal barrier function in patients receiving chemotherapy] [Article in Chinese]. Jiang HP, Liu CA.
12. Taylor CT, Winter DC, Skelly MM, O’Donoghue DP, O’Sullivan GC, Harvey BJ, Baird AW. Berberine inhibits ion transport in human colonic epithelia. Eur J Pharmacol. 1999 Feb 26;368(1):111-8.
13. Britton R, Krehbiel C. Nutrient metabolism by gut tissues. J Dairy Sci. 1993 Jul;76(7):2125-31.

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----- -------- AUTHOR: Biomed Mom TITLE: Homeopathic Treatment for Adoption Trauma DATE: 4/05/2010 04:35:00 PM ----- BODY:
Remedies

Anacardium - Adoption is a split, both emotionally and genetically. The child is split from the original family and identity and graphed onto a new family and identity. The Anacardium child has a divided will, not sure if they are a devil or an angel. The Anacardium state can be caused by isolation and separation at birth, or after, leading to an extreme lack of confidence and a feeling of powerlessness. To compensate for this feeling, the person becomes aggressive and cruel. A keynote of the Anacardium state is a cold, hardhearted stare, which can be quite disconcerting to parents. The child's behavior may appear very normal except in their drawings, which may have violent themes, and they may be attracted to playing with matches. The child's dreams may also be violent, but they will rarely share their dreams with others.

Gallic acid - The Gallic acid state can be caused by the shock of a sudden separation from a primary caretaker. From that time onward, the child does everything possible to prevent being left alone. This child feels abandoned and reacts with manipulation and even violence in seeking protection from further abandonment. The child insists on being watched constantly and wakes up frequently at night to check that the parents are still nearby. This child won't stay alone for even a minute and is rude and abusive to those around them, even to friends. The child can be extremely jealous and threatening to siblings. Gallic acid children are often hyperactive and cannot focus on their tasks, or schoolwork.

Hura - Hura treats the condition of feeling unwanted and abandoned by one's nearest relatives, or friends. The child will feel that she doesn't belong, doesn't fit in. In addition, Hura children feel that they are disgusting as though they have leprosy and are, therefore, outcasts. Some Hura children will compensate for the feeling of being despised by showing contempt for others. The child will often have a skin disorder, such as eczema, or joint problems such as juvenile rheumatoid arthritis.

Lac humanum - Lac humanum is a remedy made from human breast milk. The child who needs it will feel completely alone, as if nobody is there for them. This is the experience of many adopted children who never receive bonding from the birthmother and who were never breastfed. The child feels a sense of isolation, even a sense of not inhabiting her own body. Others easily take advantage of her because she tends to their needs before her own.

Magnesium carbonicum - J. T. Kent wrote in his Lectures on Homeopathic Materia Medica: “I once had in charge an orphanage, where we had sixty to one hundred babies on hand all the time. The puzzle of my life was to find remedies for the cases that were going into marasmus (wasting away). A large number of them were clandestine babies. It was sort of Sheltering Arms for these little ones. The whole year elapsed, and we were losing babies every week from this gradual decline, until I saw the image of these babies in Magnesia carbonicum and after that many of them were cured.” Because of Kent's work, this is usually the first remedy thought of for adoptive children, or orphans.

Magnesium muriaticum - The Magnesium muriaticum child is a peacemaker. It's a good remedy for children whose parents are arguing or divorcing, or whose family members are engaged in conflict. The Magnesium muriaticum child wants everyone to be happy and harmonious. An adopted child who needs Magnesium muriaticum will be frightened whenever her parents argue, fearing that they will break-up and she will be abandoned, just as her birthmother had abandoned her.

Natrum muriaticum - Like the Anacardium state, the Natrum muriaticum state can be caused by isolation and separation at birth. It is a well-known remedy for babies who have been taken from their mothers and placed in an incubator at birth. The Natrum muriaticum child is easily hurt and protects herself with emotional reserve. There is an inner grief due to being left alone without adequate nurturing. These children are so closed it's hard to get to know them. They say little and reveal nothing about what is really going on in their lives. They are easily offended, and remember any insult for a long time - sometimes forever.

Pulsatilla - The Pulsatilla state can be caused by rejection of the child by the mother, or separation from the mother at an early age. The child feels unloved and unwanted. In her struggle to get enough love, the child will be clingy, weepy and manipulative. She has an insatiable desire for attention and reassurance, often asking, “Do you love me?”

Saccharum officianale - A remedy for those who did not receive enough love, or nurturing, in their early life. The child will usually have an extreme craving for sweets and may have a sugar imbalance problem such as hypoglycemia. She may also have extreme thirst. The child will compensate for lack of nurturing with two types of behaviors: firstly, she may constantly seek closeness with the parents, especially the mother, always wanting cuddles and wanting to sleep in the parent's bed. And secondly, the child may have behavior problems such as kicking and hitting other children, sibling jealousy, defiant behavior, or hyperactivity. Some children will compensate for a lack of nurturing by refusing any form of affection. These children have the same desperate need for love, but will refuse contact with the parents.

Not every adopted child will need one of these remedies. We always recommend remedies based on the totality of the whole person, not just one factor such as adoption. Any troubled child, whether adopted or not, will benefit from professional homeopathic care. The homeopath may consider the wounds of adoption as a possible etiology, and will determine if any of these remedies fit the picture.

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----- -------- AUTHOR: Biomed Mom TITLE: D3 amounts needed to achieve optimal levels. DATE: 2/20/2010 06:38:00 AM ----- BODY:
Dosage of Vitamin D Needed To Achieve 35 to 40 ng/ml (90-100 nmol/L)

Historically, 400 IU (10 ug) of vitamin D was recommended for better health because it closely approximated the amount of vitamin D in a teaspoonful of cod liver oil. However, 800 to 1,000 IU is the dose that may have a better chance of giving a patient a normal vitamin D level. In some countries, vitamin D is listed in micrograms, and the relationship is as follows:

2.5 mcg (micrograms) = 100 IU.
5 mcg = 200 IU.
10 mcg = 400 IU.
15 mcg = 600 IU.
20 mcg = 800 IU.
It is much easier to access the patient’s need after a vitamin D blood test. Few individuals would allow their clinician to simply guess an individual’s cholesterol level before placing him/her on some type of medication. Clinicians have access to an accurate lipid test that provides guidance. The same is true for vitamin D levels. Clinicians should not suggest high intakes of vitamin D (5,000 IU for example) before recommending the 25-OH vitamin D test.

Health care professionals need to keep in mind that in general, 100 IU (2.5 mcg) of vitamin D per day can raise the vitamin D blood test only 1 ng/ml or just 2.5 nmol/L after 2 to 3 months. How much vitamin D is needed per day to obtain a normal vitamin D blood level? The following examples include:

100 IU (2.5 mcg) per day increases vitamin D blood levels 1 ng/ml (2.5 nmol/L).
200 IU (5 mcg) per day increases vitamin D blood levels 2 ng/ml (5 nmol/L).
400 IU (10 mcg) per day increases vitamin D blood levels 4 ng/ml (10 nmol/L).
500 IU (12.5 mcg) per day increases vitamin D blood levels 5 ng/ml (12.5 nmol/L).
800 IU (20 mcg) per day increases vitamin D blood levels 8 ng/ml (20 nmol/L).
1000 IU (25 mcg) per day increases vitamin D blood levels 10 ng/ml (25 nmol/L).
2000 IU (50 mcg) per day increases vitamin D blood levels 20 ng/ml (50 nmol/L).
If the vitamin D blood test was 30 ng/ml (75 nmol/L) and a 40 ng/ml (100 nmol/L) level was desired, 1,000 IU (25 mcg) of vitamin D per day over several months should be taken to achieve a normal blood level or 40 ng/ml (100 nmol/L). Upon reaching the goal, most individuals need to supplement with 800 to 1,000 IU per day to maintain this level. Only working closely with a clinician over time can provide the most accurate answer. However, issues of insurance and health care access suggest that 800 to 1,000 IU is ample for many individuals who are not able to have their blood tested.

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----- -------- AUTHOR: Biomed Mom TITLE: Natural Approaches to ADHD DATE: 2/04/2009 09:51:00 AM ----- BODY:
Nutritional Breakthroughs for ADHD by Angela Stengler, ND Could food allergies be causing your child's ADHD? After a child has been diagnosed with attention deficit disorder, many parents come to me with questions and concerns regarding their child's diagnosis and possible treatments. No one is really sure what causes hyperactivy in children, although there are plenty of culprits people point to--sugar sensitivities, environmental toxins, food allergies--but no one thing has been identified as the specific cause. Unfortunately, when a diagnosis is made, quite often the only solution provided to parents is a prescription for stimulants like Ritalin. However, drugs are not your only choice and there are natural therapies available to you that can safely and effectively treat ADHD in your child--and without any of the negative side effects caused by some drug therapies. I have outlined several below. Read them, and then consult with your pediatrician or naturopath to see which treatment would be best suited for your child. POSSIBLE CAUSES OF ADHD Food additives Over 5,000 food additives are present in the food supply, and according to Benjamin Feingold, MD, 40 to 50 percent of all hyperactive children have some sort of sensitivity to the artificial colorings, flavorings and preservatives used in many processed foods. Feingold bases his claims on 1,200 cases of learning and behavior disorders observed in childern that were linked directly to food additives. This seems to suggest that there is a direct correlation between diets high in processed foods and hyperactivity in children. How Villainous is Sugar? For some kids, sugar is a major factor in mood, behavior and attention patterns. It has been demonstrated that destructive, aggressive and restless behavior correlates directly with the amount of sugar consumed on a daily basis. Once again, diet is both the problem and the solution. Food Allergies/Sensitivities The most common food sensitivities in children are to the following foods: •sugar •cow's milk •wheat •chocolate •soy •citrus fruit •corn •peanuts Double-blind studies have shown that when children with ADHD follow a hypoallergenic diet, substantial improvement in their symptoms are demonstrated. It should be noted that food sensitivities and food allergies are not the same thing. Food allergies are present when a child exhibits severe reactions to allergens--like peanuts or albumen from eggs--present in foods. Symptoms can include, shortness of breath, breaking out in hives, vomiting or anaphylaxis, a life-threatening condition which is characterized by the swelling of the throat and tongue. Food sensitivities are exhibited when a child is given food--like dairy products in the lactose intolerant child--which he is unable to digest properly. Commonly, he will experience indigestion, gas or irritable bowels as a result of eating these foods. If you suspect a food allergy in your child, make an appointment to get him tested. Dietary Steps You Can Take 1. Add more whole foods to the diet (whole grains, legumes, vegetables, fish) while eliminating (or at least decreasing) processed foods that contain white flour, processed sugars and hydrogenated oils (i.e, chips, cookies and sodas). 2. It goes without saying that you should make it your business to read the ingredient labels on all food products you buy for your children. Many parents don't realize that much of the pre-packaged food--including supermarket multi-vitamins and the so-called "fruit" drinks--they give to their children is loaded with artificial sweeteners, preservatives, dyes and other harmful additives that could be triggering specific behavioral and health problems in their children. If the chemical ingredients outnumber organic ingredients--or if they are the first few ingredients listed--on a food label, you may want to consider buying something else. Check labels on milk, meat and eggs too because many farmers feed hormones and antibiotics to their livestock. 3. Shop for organic fruits, vegetables and meats. These are foods that have been grown according to specific agricultural practices (typcially without using chemical pesticides or fertilizers). Hit the health food store for whole grain breads and healthy snacks to give to your kids in place of the processed ones they've been eating. Not only do these foods taste great, but they are much better for your kids overall health (many are lower in fats and sugars). 4. Natural sugars like those found in fruit and fruit juices, or natural sweeteners like honey, blackstrap molasses and rice bran syrup, should replace all processed sugars in your child's diet (this includes raw or brown sugars). If your child drinks a lot of soda make the switch to 100 percent fruit juices and dilute them 50 percent with water. Instead of those sugary breakfast cerals, try feeding your kids oatmeal topped with honey and fresh fruit, or give them naturally sweetened granola or muesli. They'll have more energy between breakfast and lunch, and their teachers will love you for it. 5. Eliminate all the foods listed under Food Allergies/Sensitivies from your child's diet for four weeks and see if their behavior improves. Wheat alternatives, such as oat, kamut and spelt, are available at most health food stores as are milk alternatives like calcium-enriched rice or oat milk. Both taste great and come in flavors like chocolate and vanilla. Yogurt made from goat's milk should be substituted for products made from cow's milk (the same is true for cheeses, too). Other Potential Factors Could food allergies be causing your child's ADHD? NUTRITIONAL DEFICIENCIES & ADHD Nutritional deficiencies are a widespread cause of learning and behavior problems in children. Studies have shown increased intelligence in children who added multivitamin supplements to their daily diets. Thiamin, niacin, vitamins B6 and B12, copper, iodine, iron, magnesium, manganese, potassium and zinc are nutrients that play a vital role in proper brain and nervous system function. Many ADHD children can benefit from an extra 500 to 1,000 milligrams of calcium and magnesium in their diet. Food sources are the best means for incorporating these important nutrients into your child's diet (especially as laid out in the previous dietary steps), but if your child can't drink milk or doesn't like to eat his green leafy veggies, vitamin supplements are the next best answer. American Kids Iron Deficient Surprisingly, the most common nutrient deficiency in American children is iron deficiency (again, a direct result of a nutrionally deficient diet). Studies have linked iron deficiency with decreased attentiveness, a narrow attention span and decreased voluntary activity. These symptoms are usually reversed after supplementation. A severe deficiency in iron can lead to anemia, which in turn can lead to listlessness, tiredness and low energy levels in children--symptoms which make it difficult for children to pay attention in school. If you suspect that your child is anemic have him tested by your physician. Always have your child tested for iron deficiency before administering iron supplements. Legumes, green leafy vegetables, blackstrap molasses and lean red meats are the best sources for iron. Look for liquid iron supplements, which are easier for kids to take, and are less likely to cause constipation or stomach upset--two of the occasional side effects of iron supplementation in children. What Are Smart Fats? Current research shows a link between learning and behavioral difficulties and deficiencies in essential fatty acids (EFAs) like docosahexanoic acid (DHA), one of the most important essential fatty acids. EFAs are commonly referred to as Omega 3 and Omega 6 fats. Oils, like evening primrose oil, flaxseed oil and borage oil, are high in EFAs. DHA plays a pivotal role in brain and retina development in babies, and the richest sources of it are a mother's breast milk and fish oils. Researchers at Purdue University looked at the levels of essential fatty acids in children, especially DHA, and found that kids with ADHD tended to have significantly lower levels of essential fatty acids in their blood. Children with ADHD should be given vitamin supplements that contain a combination of essential fatty acids that includes DHA. Nursing your children for as long as possible, and--when they are older--getting them to eat deep water fish like salmon, halibut and tuna are ways to ensure they get enough essential fatty acids into their diet during the crucial developmental years (when the body is still growing and in need of quality nutrients). Phosphatidylserine Phosphatidylserine (known as PS) is a specific brain nutrient that can be supplemented to help promote proper brain and neurological function. It works to balance the cell-to-cell communication that occurs in the brain. I recommend giving PS by itself to children with ADHD or in combination with DHA or the herb ginkgo biloba (which has excellent research supporting its benefit on memory and concentration). PS appears to help improve concentration and have a calming effect on hyperactive kids. Most PS supplements are soy-based. Typical dosage for a 12-year-old would be 200 to 400 milligrams daily. Consult your naturopathic physician or nutritionist for specific dosage requirements for your child based on his age, size and weight. ENVIRONMENTAL TOXINS Heavy Metals Finally, numerous studies have found a strong relationship between childhood learning disabilities and body storage of heavy metals (lead, mercury, cadmium, copper and manganese). Heavy metals are stored in the bones and fatty tissues of the body, like the liver and the kidneys, and high levels in very young children can hinder proper development of the brain and central nervous system. Lead is the primary culprit of heavy metal toxicity in young children, especially among toddlers living in old houses where they eat the lead paint that chips off of walls and windowsills. A child who is suffering from mild lead or heavy metal poisoning may not exhibit any specific symptoms, so a hair analysis is the best screening test for heavy metal toxicity and mineral imbalances. What Can You Do? Adding calcium and magnesium supplements to your child's diet is one way to counter potential lead poisoning (in the body, lead competes with calcium. A child exposed to high levels of lead paint dust will absorb the lead and excrete the calicium). January 1999 Dr. Angela Stengler is a certified naturopathic physician based in Oceanside, California. Women's and children's health are the focus of the practice run by her and her husband, Dr. Mark Stengler. In addition to maintaining her medical practice, Dr. Stengler hosts a weekly radio show on natural medicine, and she is the author of several books on the benefits of alternative medicine, which you can find at her Web site, The Natural Physician.

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----- -------- AUTHOR: Biomed Mom TITLE: Serotonin for ADHD DATE: 1/15/2009 07:37:00 AM ----- BODY:
Serotonin May Be Better Target For ADHD Treatment Researchers at the Howard Hughes Medical Institute (HHMI) at Duke University have discovered that Ritalin and other stimulants exert their paradoxical calming effects by boosting serotonin levels in the brain. Elevating serotonin appears to restore the delicate balance between the brain chemicals dopamine and serotonin and calms hyperactivity, says HHMI investigator Marc Caron at Duke University Medical Center. Caron is an author of the study published in the January 15 issue of the journal Science. Attention deficit hyperactivity disorder (ADHD) affects three to six per cent of school-aged children. Symptoms include restlessness, impulsiveness, and difficulty concentrating. Stimulants commonly used to treat ADHD are so effective that "researchers haven't really taken the time to investigate how they work," says Caron. Previous dogma, says Caron, held that the calming action of Ritalin works through the neurotransmitter dopamine. Specifically, researchers believed that Ritalin and other stimulants interact with the dopamine transporter protein (DAT), a housekeeper of sorts for nerve pathways. After a nerve impulse moves from one neuron to another, DAT removes residual dopamine from the synaptic cleft-the space between two neurons-and repackages it for future use. Caron's team suspected that dopamine wasn't the only key to understanding ADHD, so they turned to mice in which they had "knocked out" the gene that codes for DAT. Since there is no DAT to "mop up" dopamine from the synaptic cleft, the brains of the mice are flooded with dopamine. The excess dopamine causes restlessness and hyperactivity, behaviors that are strikingly similar to those exhibited by children with ADHD. When placed in a maze that normal mice negotiate in less than three minutes, the knockout mice became distracted-performing extraneous activities such as sniffing and rearing - and they failed to finish in less than five minutes. The knockout mice also seemed unable to suppress inappropriate impulses - another hallmark of ADHD. Surprisingly, the knockout mice were still calmed by Ritalin, Dexedrine and other stimulants even though they lacked the protein target on which Ritalin and Dexedrine were thought to act. "That caused us to look for other systems that these stimulants might affect," says Caron. To test whether the stimulants interact with dopamine through another mechanism, the researchers administered Ritalin to the normal and knockout mice and monitored their brain levels of dopamine. Ritalin boosted dopamine levels in the normal mice, but it did not alter dopamine levels in knockout mice. That result implied that "Ritalin could not be acting on dopamine," says Caron. They then studied whether the stimulants altered levels of the neurotransmitter serotonin. The scientists administered Prozac - a well-known inhibitor of serotonin reuptake - to the knockout mice. After ingesting Prozac, the knockout mice showed dramatic declines in hyperactivity. "This suggests that rather than acting directly on dopamine, the stimulants create a calming effect by increase serotonin levels," Caron says. "Our experiments imply that proper balance between dopamine and serotonin are key," says Raul Gainetdinov, a member of Caron's research team. "Hyperactivity may develop when the relationship between dopamine and serotonin is thrown off balance." The brain has 15 types of receptors that bind to serotonin, and Gainetdinov is now trying to determine which specific serotonin receptors mediate the effects of Ritalin. The hope, says Caron, "is that we can replace Ritalin with a very specific compound that targets a single subset of receptors." While Prozac calmed hyperactivity in the knockout mice, Gainetdinov says that "Prozac isn't the best, because it isn't very selective." Caron and Gainetdinov are optimistic that a new generation of compounds that interact more specifically with the serotonin system will prove to be safer and more effective for treatments for ADHD.

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----- -------- AUTHOR: Biomed Mom TITLE: Serotonin's effects on multiple body systems DATE: 1/15/2009 07:15:00 AM ----- BODY:
One Dangerous Deficiency Links IBS, Migraines, and More Health News By VRP Staff When you think of serotonin deficiency, the first consequence that might spring to mind is depression. And if so, you’d be right. But there’s more to this neurotransmitter than meets the eye—a lot more. Migraines, irritable bowel syndrome, fibromyalgia, obesity, even asthma… believe it or not, all of these serious conditions can be traced back to depleted serotonin levels. And the effects on your body can be as damaging as they are diverse. Serotonin is one of your brain’s most crucial messengers. It’s released by your neurons to send signals to other neurons, after which it’s returned to its original parent neuron to be reused. But if your levels are low, serotonin’s time on your synapse is cut short. It’s recaptured before it can finish its job—at a very high cost to your health, mentally and physically. In addition to depression, low levels of serotonin–and its precursor tryptophan–have been linked to binge eating, carbohydrate cravings, and weight gain.1 Studies show that obese and overweight diabetic patients have levels that are well below normal–and in clinical trials, increased brain serotonin led to both reduced caloric intake and resulting weight loss.2–4 But it’s not just your waistline that benefits from this critical neurotransmitter. Studies have shown that increasing serotonin levels can fight insomnia by improving sleep continuity.5 Research also shows that increased serotonin relieves migraines as effectively as standard drug therapy and aids in relief of chronic tension headaches.6–7 This same ability has made it a unique target in the treatment of fibromyalgia, with serotonin deficiency implicated for lower pain thresholds and higher clinical measures of perceived pain in patients.8–10 In an even more surprising connection, serotonin has also been identified as a major player in gut motility.11–12 Special serotonin–releasing cells can be found throughout your digestive system, responsible for stimulating peristaltic motion and pushing waste through your digestive tract.13 Even the development and severity of asthma has been linked to depression, anxiety, and low–serotonin related disorders—revealing yet another function under this neurotransmitter’s powerful influence.14 Proper levels of serotonin are essential for your health—and one way to ensure higher levels of this neurotransmitter is by boosting your intake of tryptophan, an essential amino acid found in high–protein foods that is responsible for serotonin synthesis in your brain. Research has shown that supplementing with tryptophan (and its metabolite 5–hydroxytryptophan, or 5–HTP) can replenish serotonin naturally and effectively—easing depression, anxiety, migraines, insomnia, and fibromyalgia symptoms in several clinical studies.15–17 References: 1. Gendall KA, Joyce PR. Meal–induced changes in tryptophan:LNAA ratio: effects on craving and binge eating. Eat Behav. 2000 Sep;1(1):53–62. 2. Breum L, Rasmussen MH, Hilsted J, Fernstrom JD. Twenty–four–hour plasma tryptophan concentrations and ratios are below normal in obese subjects and are not normalized by substantial weight reduction. Am J Clin Nutr. 2003 May;77(5):1112–1118. 3. Ceci F, Cangiano C, Cairella M, et al. The effects of oral 5–hydroxytryptophan administration on feeding behavior in obese adult female subjects. J Neural Transm 1989;76(2):109–117. 4. Cangiano C, Ceci F, Cascino A, et al. Eating behavior and adherence to dietary prescriptions in obese adult subjects treated with 5–hydroxytryptophan. Am J Clin Nutr 1992 Nov;56(5):863–867. 5. Riemann D, Vorderholzer U. Treatment of depression and sleep disorders. Significance of serotonin and L–tryptophan in pathophysiology and therapy. Fortschr Med. 1998 Nov;116(32):40–42. 6. Titus F, Dávalos A, Alom J, Codina A. 5–Hydroxytryptophan versus methysergide in the prophylaxis of migraine. Randomized clinical trial. Eur Neurol. 1986;25(5):327–329. 7. Ribeiro CA. L–5–Hydroxytryptophan in the prophylaxis of chronic tension–type headache: a double–blind, randomized, placebo–controlled study. For the Portuguese Head Society. Headache. 2000 Jun;40(6):451–456. 8. Birdsall TC. 5–Hydroxytryptophan: a clinically–effective serotonin precursor. Altern Med Rev. 1998 Aug;3(4):271–280. 9. Hrycaj P, Stratz T, Muller W. Platelet 3Himipramine uptake receptor density and serum serotonin levels in patients with fibromyalgia/fibrositis syndrome. J Rheumatol. 1993;20:1986–1988. [letter] 10. Russell IJ, Michalek JE, Vipraio GA, et al. Platelet 3H–imipramine uptake receptor density and serum serotonin levels in patients with fibromyalgia/fibrositis syndrome. J Rheumatol 1992;19:104–109. 11. Fayyaz M, Lackner JM. Serotonin receptor modulators in the treatment of irritable bowel syndrome. Ther Clin Risk Manag. 2008 Feb;4(1):41–48. 12. Gershon MD. The enteric nervous system: a second brain. Hosp Pract (Minneap). 1999 Jul 15;34(7):31–32,35–38,41–42. 13. Grider JR. Desensitization of the peristaltic reflex induced by mucosal stimulation with the selective 5–HT4 agonist tegaserod. Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G319–G327. 14. Goodwin RD, Sourander A, Duarte CS, et al. Do mental health problems in childhood predict chronic physical conditions among males in early adulthood? Evidence from a community–based prospective study. Psychol Med. 2008 May 28:1–11. 15. Poldinger W, Calanchini B, Schwarz W. A functional approach to depression: serotonin deficiency as a target syndrome in a comparison of 5–hydroxytryptophan and fluvoxamine. Psychopathology. 1991;24:53–81. 16. Kahn RS, Westenberg HG. L–5–hydroxytryptophan in the treatment of anxiety disorders. J Affect Disord. 1985 Mar–Apr;8(2):197–200. 17. Puttini PS, Caruso I. Primary fibromyalgia and 5–hydroxy–L–tryptophan: a 90 day open study. J Int Med Res. 1992;20:182–189.

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----- -------- AUTHOR: Biomed Mom TITLE: EFAs and ADHD DATE: 12/30/2008 12:41:00 PM ----- BODY:
Behavioural disorders, impulsivity and violent behaviour Attention deficit hyperactivity disorder (ADHD) is characterised by inattentive, impulsive and hyperactive behaviour occurring in children but some aspects of the condition may persist into adulthood (Richardson and Puri 2000, Richardson and Ross 2000, Arnold 2001). ADHD is a significant and increasing problem. It is estimated that it affects about 2% of school-aged children in the UK and 4% of school-aged children in the USA (Richardson and Puri 2000) and the use of medication to treat ADHD has increased dramatically in the last 10 years. Results of one study suggest that fish consumption may be associated with violent and impulsive behaviour (Hibbeln 2001). This cross-national survey of seafood consumption in 26 countries found that those with higher rates of seafood consumption tended to have lower rates of mortality due to homicide. The authors point out, however, there were many potentially confounding factors in this study and the hypothesis that fish consumption may help to reduce impulsive and violent behaviour should be tested in double-blind, placebo-controlled trials. Boys aged 6-12 years with ADHD were found to have significantly lower plasma levels of AA, EPA and DHA compared to normal controls (Stevens, Zentall, Deck et al 1995). In a further study of boys of the same age, significantly greater scores indicating behaviour problems, temper tantrums and sleep problems were reported in subjects with lower plasma total n-3 fatty acid concentrations (Stevens, Zentall, Abate et al 1995). However, a double-blind placebo controlled trial of DHA supplementation (345 mg/day for 4 months) in children with ADHD found that DHA treatment did not decrease ADHD symptoms compared with placebo (Voigt, Llorente, Jensen et al 2001). The authors pointed out however, that lack of response to DHA supplementation did not necessarily mean that a low brain content of DHA is not involved in the aetiology of ADHD. It is possible that in the population studied, a benefit of DHA was not produced because other essential nutrients were also lacking. It was suggested in recent reviews that ADHD may be linked to some other behavioural and neurological disorders, namely dyslexia, dyspraxia and autism, by an involvement of fatty acid metabolism (Richardson and Ross 2000; Bell, Sargent, Tocher et al 2000) and some studies of violent, impulsive and antisocial behaviour have also made this connection. Such behaviour has been linked to tissue deficiencies of n-3 fatty acids (Corrigan, Gray, Strathdee et al 1994; Stevens, Zentall , Deck et al 1995; Stevens, Zentall, Abate et al 1995; Hibbeln, Umhau, Linnoila et al 1998; Burgess, Stevens, Zhang et al 2000) and other nutrients including vitamins and minerals (Schoenthaler, Amos, Doraz et al 1997, Walsh, Isaacson, Rehman et al 1997). Virkkunen, Horrobin, Jenkins et al (1986) found that in a group of violent and impulsive offenders, plasma DHA was significantly lower than controls while n6 fatty acids were significantly elevated. In a double-blind, placebo-controlled trial on young adult male prisoners, dietary supplementation with vitamins and minerals, as well as fish oil (80 mg per day EPA and 44 mg per day DHA) and evening primrose oil, resulted in 26% fewer disciplinary offences in the supplemented group compared to placebo and 35% fewer disciplinary offences in the supplemented group compared to the baseline frequency (Gesch, Hammond, Hampson et al 2002). A recent double-blind placebo-controlled trial investigated the effects of dietary supplementation for 12 weeks with tuna oil (186 mg per day EPA, 480 mg per day DHA) and evening primrose oil in children with specific learning difficulties such as dyslexia (Richardson and Puri 2002). It was found that supplementation produced significant benefits. It has also been suggested that DHA in particular might be useful in treatment of dyslexia and dyspraxia as well as ADHD (Stordy 1995, 1997, 2000). Dyspraxia is a condition involving reduced motor skills manifesting as excessive clumsiness and there is a close link between dyspraxia and dyslexia (Stordy 1997). Stordy (1995) reported that, in a preliminary study, supplementation for one month with 480 mg per day DHA significantly improved an aspect of vision called dark adaptation in five dyslexic children. In a later open study of 15 children with dyspraxia, supplementation with the same dose of tuna oil and evening primrose oil as used in the study by Richardson and Puri (2002), produced significant improvements in scores for manual dexterity, ball skills and static and dynamic balance. The studies described above, of impulsive and violent behaviour amongst prisoners and its possible association with PUFA status (Virkkunen, Horrobin, Jenkins et al 1986, Gesch, Hammond, Hampson et al 2002) may be compared to a series of studies of aggression in Japanese students. Hamazaki, Sawazaki, Itomura et al (1996) conducted a double-blind, placebo-controlled trial of fish oil supplementation (1.5-1.8 g DHA per day) and after three months of treatment, aggression scores were significantly lower in the DHA group compared to placebo. However, the reason for the difference was that aggression scores in the placebo group had increased while those in the DHA group did not change significantly. The difference was accounted for by the fact that the final assessment in the trial occurred just before academic examinations, which it was suggested had caused psychological stress. A similar trial was conducted on different students who did not face such stress and no significant change in hostility was recorded in the DHA or placebo group (Hamazaki, Sawazaki, Nagao et al 1998). The authors concluded that DHA administration could help to control aggression only at times of psychological stress (Hamazaki, Sawazaki, Itomura et al 2001). Hibbeln, Umhau, George et al (1997) pointed out that an apparent prevention of increased aggression is surprising because baseline intake of n-3 PUFA in the study population was relatively high. In a third double-blind, placebo- controlled trial on students. Plasma catecholamines were measured during a two-month period of continuous psychological stress due to university examinations (Sawazaki, Hamazaki, Yazawa et al 1999). In the DHA group, who took 1.5g DHA per day during the examination period, noradrenaline levels were significantly reduced. The authors interpreted this change as indicating that subjects in the DHA group adapted to stress more favourably than controls and that DHA may help to reduce the risk of stress-related diseases in individuals under long-lasting psychological stress (Hamazaki, Sawazaki, Nagasawa et al 1999, Hamazaki, Itomura, Sawazaki et al 2000). In another study by the same group, Thai subjects aged 50-60 years, from a university and surrounding villages, were studied in a double-blind placebo-controlled trial in which the treatment was the same DHA supplement as used in the previous trials (Hamazaki, Thienprasert, Kheovichai et al 2002). DHA administration reduced aggression scores amongst university employees but not amongst village-dwellers. The authors speculated that the difference was caused by a larger placebo effect amongst villagers or a lower sensitivity amongst villagers to the psychological stressor (a video of stressful events) used in the study. Conclusion The epidemiological evidence that DHA-deficiency is a cause of violent and impulsive behaviour is supportive but not conclusive. Also, the few available studies of plasma fatty acids demonstrate lower DHA levels in individuals with ADHD. Data from supplementation studies are inconsistent but there are sufficient positive results to strengthen the view that DHA deficiency may be associated with adverse behavioural consequences.

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----- -------- AUTHOR: Biomed Mom TITLE: Pine Bark and ADHD DATE: 12/04/2008 10:42:00 AM ----- BODY:
Pine Bark Extract Helps Calm ADHD in Jack but Not Jill By Neil Osterweil, Senior Associate Editor, MedPage Today Published: June 16, 2006 Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine. BRATISLAVA, Slovakia, June 16 — Pine bark extract, a substance known as Pycnogenol, seems to calm boys with attention-deficit hyperactivity disorder (ADHD), according to researchers here. Girls were not helped.Action Points -------------------------------------------------------------------------------- Explain to interested parents and children that this study appears to show that Pycnogenol, a standardized extract of pine bark, is effective at treating some symptoms of ADHD. Caution that this was a small, short duration study and was not sufficiently powered to detect a possible effect of gender. In addition some of the improvements noted did not reach statistical significance. The boys with ADHD given Pycnogenol, from the bark of the French maritime pine, had modest but significant reductions of hyperactivity and inattention, according to Jana Trebaticka, M.D., and colleagues, of the Child University Hospital at Comenius University, and the University of Münster in Germany. "These findings are especially notable for parents who are concerned about overmedicating children diagnosed with ADHD," said Peter Rohdewald of Münster, a co-author. "Many families are seeking natural options to avoid the potentially dangerous side effects of prescription drugs," he added. Unlike Ritalin (methylphenidate), the mechanism of action of Pycnogenol in ADHD is unclear, but it may involve alteration of the response to the catecholamines dopamine and norepinephrine, the authors wrote in the June 17 issue of European Child & Adolescent Psychiatry. In open-label studies and case reports, the extract has been reported to improve symptoms of ADHD, the authors said, prompting them to start a randomized, double-blind, placebo-controlled trial. The study was funded by Horphag Research Limited, UK, the maker or Pycnogenol. The investigators enrolled 61 children (50 boys and 11 girls), mean age 9.5 years (range six to 14) with diagnoses of ADHD. The children were randomized on a 2.5:1 ratio to either placebo or Pycnogenol at 1 mg/kg/day orally for four weeks. At baseline, after one month of treatment and at two months of follow-up the children were tested for ADHD symptoms with standard questionnaires, including the Child Attention Problems (teacher-rated) instrument, Conner's Teacher and Parent Rating scales, and a modified Wechsler Intelligence Scale. Analysis was by intention-to-treat. The investigators found that in the boys but not girls who received four weeks of therapy with the active drug. there were significant improvements over baseline and compared with placebo for teacher ratings on hyperactivity (P=0.008 over baseline) and inattention (P=0.00014 over baseline). At one month after the end of the trial, the apparent drug benefit had disappeared and ADHD symptom scores returned to baseline levels. On the Conner Teacher Rating Scale teachers noted following one month of treatment with Pycnogenol reduction of inattention which was not statistically significant (P=0.07) compared with start and marginally significant compared with placebo (P=0.049). "Hyperactivity was also lower compared with the start as well as with placebo following Pycnogenol treatment; however, the decrease failed to reach significance (P=0.45 and P=0.28)," they wrote. Parental ratings of inattention not differ significantly from baseline to study end, however, the authors noted. "Following one month of treatment with Pycnogenol, the lower score for hyperactivity compared to placebo was not stastiscally significant (P=0.065)," they wrote. "The tests for visual-motoric coordination and concentration-Weight scores-were also different for placebo and Pycnogenol group at start." No serious side effects were reported, although observers noted "a rise in slowness" in one patient, and moderate gastric discomfort in another. There were no changes over baseline in either the Pycnogenol or placebo groups in basic biochemical parameters such as bilirubin, glucose, liver enzymes, uric acid, or lipids after one month. "Our results point to an option to use Pycnogenol as a natural supplement to relieve ADHD symptoms of children," the authors wrote. Because there were only six girls in the Pycnogenol group and five in the placebo group, the study was insufficiently powered to detect a possible effect of gender, the authors acknowledged. They also pointed out that their data are limited by the small number of participants and the by the short duration of the study. Primary source: European Child & Adolescent Psychiatry Source reference: Trebaticka J et al. "Treatment of ADHD with French maritime pine bark extract, Pycnogenol"Eur Child Adolesc Psychiatry DOI 10.1007/s00787-006-0538-3 Additional ADHD/ADD Coverage Find this article at: http://www.medpagetoday.com/Psychiatry/ADHD-ADD/3563

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----- -------- AUTHOR: Biomed Mom TITLE: Non-medical solutions for ADHD DATE: 11/14/2008 06:28:00 AM ----- BODY:
http://www.wisechoiceeducationalservices.com/articles/article10.html By Suzanne Day Parents of children with learning or attention problems will often react negatively to the use of medications, which are recommended by the medical profession. However, what parents really need and want is guidance in their search for solutions. This article attempts only to guide parents to a better understanding of the different aspects of the biochemical components of learning difficulties and attention behavioural problems. I do not pretend to be an expert in the nutrition but an expert on the brain, which is fuelled by nutrition. Parents and professionals dealing with attention deficits in children observe the food-mood connection, which is more evident in some children than others. Behaviours are based on thoughts and memories processed in the brain. The neurons (brain cells) transmit information as electrical signals with the use of neurotransmitters. These transmissions constitute the biochemical basis for changes in behaviours. The brain, one of the most vital organs of the body, receives its nutrition directly from the blood stream. Therefore, balanced nutrients will enhance the biochemical and electrical functions of the brain, which in turn affect learning. Imbalance of nutrients, especially through a diet of junk food, snack and fast food, will have an adverse effect, aggravating or intensifing learning and behavioural problems. The efficient functioning of the brain requires at least the essential amino acids, essential fatty acids, essential monosaccharides (glyconutirents), vitamins, minerals, and water. Essential Amino Acids Proteins provide the needed amino acids to build healthy nerve cells. These nerve cells then provide new connections to increase retrieval (memory). Most children with learning and attention difficulties need to consume more proteins, rather than starch and sugar. However, Dr. Amen in his book Healing ADD, has found that children with obsessive-compulsive behaviours require a balanced diet of protein and starch. He also explains that these children may also benefit from additional specific amino acids which are precursors of the neurotransmitters that help with the neurotransmission of the electric influx into the brain. For example, tyrosine is a building block for dopamine (control of movements, pleasure centers, and motivation). Tyrosine is a non-essential amino acid which is abundant in brown rice, leafy vegetables, and milk. Tyrosine is considered a “spark protein”. This amino acid as a supplement is known as L-tyrosine, and should be taken on an empty stomach. Tryptophan and 5-HTP are essential amino acids and are building blocks for the neurotransmitter serotonin, which controls our emotions and our sleeping patterns. Tryptophan is considered a “sedative-protein”. Most vegetables and nuts contain tryptophan. GABA, still another essential neurotransmitter, is an anti-anxiety agent. GABA is formed in the body by glutamic acid that can be synthesized from other amino acids. Phenylalanine is an amino acid precursor of norepinephrine (arousal and attention) coming in the form of DLAP as a nutritional supplement. Proteins are essential because they contain the necessary amino acids to build healthy nerve cells. Whether supplemented or taken in the diet, amino acids must be present for children to be able to overcome with learning difficulties or those with behavioural issues. Essential Fatty Acids Dr. Michael Lyon has done extensive research to better understand some of the main nutritional root causes of attention difficulties. The essential fatty acids, omega-3 and omega-6, are required by every cell in the human body and especially in the brain which is 60% fat. These essential fatty acids seems to be greatly involved in the ability to stay focused and complete tasks. The most commonly available omega-3 fatty acids is known as alpha linolenic acid (ALA) and can be found in large quantity in flax seed oil. The omega-6 fatty acid is known as linoleic acid (LA) and can be found in pumkin , sunflower, or sesame seeds. We recommend that you use a coffee grinder and grind your seeds as you need them because they start loosing the value as soon as the seed is broken. Only if the right enzymes are present in the body, will these acids be converted to incorporate them in the brain and the immune system. However, too often the body is inefficient in converting them. The best sources of essential fatty acids are the fish oils: tuna, salmon, and cod. Hydrogenation and Trans-fatty Acids Dr Lyon as well as many other experts on this topic, warns about the use of hydrogenated fats and trans-fatty acids ( the margarine, shortening, and cooking oils) which contain almost no essential fatty acids. Hydrogenation, the most common way of drastically changing natural oils, heats oils at high temperatures. The heat alters the molecule structure, which in turn interferes with the biochemical processes, “clogging” our physiological systems, our brains included. Udo Erasmus explains that “the molecule has its “head on backwards.” Not only does the heated oil looses its nutrients, but a catalyst (heavy metals like aluminium) is added, leaving remnants in these oils that are eaten by people. Udo Erasmus concludes “The 60 grams (2 ounces) of margarine and shortening we consume each day contain more than twice as many “food additives” than are found in the other 2640 grams of food that men consume each day (1740grams by women).” “Leaky Gut” and Debris in the Blood Dr. Lyon states, "Optimal digestion, good nutrient absorption and a leak proof gut are essential for good health." Based on his experience, brain health and gut health are vitally linked. In his book, Is Your Child's Brain Starving, he explains that most children with attention deficit and hyperactivity present a “leaky gut”. As well, they lack friendly bacteria in the gut, and have different types of intestinal parasites. Let’s explain briefly the term “leaky gut”. Normally the lining of the small intestine protects us from undigested food getting into the blood stream. Unfortunately, due to different factors including the excessive consumption of starchy or sugary foods, which ADD children crave, the tight junctions between cells of the intestinal lining detach and gaps form between the cells. This leaky gut allows molecular debris to circulate throughout the entire body, interfering with organ functions. The brain is one of our vital organs and these irritants adversely affect it. Milk and its Molecule Modification One of the most common types of molecular debris is milk protein. Milk has always been recognized as an essential nutrient for building healthy bodies. However, new research has shown that milk can create allergies and seems to be the cause of many ear infections. What is happening? The problem is not the milk, but what happens when milk is homogenized and radiated. Homogenizing milk breaks down the fat molecules into minute particles, which can cross the gut barrier and be absorbed into the blood stream. This causes many problems including allergic reactions and ear infections. These “foreign” protein molecules weaken the immune system because the body recognizes the milk protein as an enemy. Organs, like the brain, are often attacked. Although, soya milk is often used to replace cows’ milk, it appears to be difficult to digest for some children, who lack the necessary enzymes. See the article “Why you should avoid Soy”, by Sally Fallon (www.mercola.com/article/soy/avoid_soy.) Healing the “Leaky Gut” Research has confirmed what Dr. Lyon found with ADD: behaviour problems, including attention problems, autism, and schizophrenia, are often linked to intestinal problems. Elaine Gottschall has brought relief to thousands with her research and her diet. In her book, Breaking the Vicious Cycle, she explains the importance of a healthy intestinal tract. According to her, inefficiency in digesting double sugars, disaccharides like table sugar and polysaccharides, leads to mal-absorption and inflammatory bowel disease. Her diet, the ‘Specific Carbohydrate Diet’, is based on a monosaccharide diet (one molecule of sugar) like glucose. Interestingly, neurobiologists have discovered that more than 90% of all the serotonin (a neurotransmitter) made and then stored, is in the gut. The lack of serotonin is blamed for depression, anxiety, and insomnia. Poor digestion, absorption and elimination may lead to mental, emotional and physical sickness. White Sugar and Hypoglycemia In my work with children with learning and attention problems, I regularly witness the fact that these children often crave sugar and starch (starch becomes sugar after it is metabolized.) Parents and educators often observe, that these children are hyperactive for a short period and then a few hours later, they become lethargic. A high sugar food made with white sugar like a chocolate bar, a soda pop, or candies, stimulate the pancreas to secrete insulin which triggers cells throughout the body to pull the excess glucose out of the bloodstream and store it for later use. Soon, the glucose available to the brain has dropped. Neurons, unable to store glucose, experience an energy crisis. The ability to focus and think suffers. This glucose deficiency is called hypoglycemia, and it can even lead to unconsciousness. The Very “Bad” Sugar: Aspartame Much research has been done on Aspartame, an artificial sweetener, used in such brands as Equal and Nutrasweet. It is about 200 times sweeter than the refined sugar. Dr. Mercola reports that “Aspartame complaints represent 80-85% of food complaints registered with the FDA. In 1991, the National Institutes of Health listed 167 symptoms and reasons to avoid the use of aspartame, but today it remains a multi-million dollar business. Known to erode intelligence and affect short-term memory, the components of this toxic sweetener may lead to a wide variety of ailments…” (the list is included in his article from his web site). He recommends an helpful documentary on this subject Sweet Misery: A Poisoned World. The “Good Sugars”: the Glyconutrients A team from the University of Arkansas, directed by Dr. Dykman has conducted special studies evaluating the effects of different types of sugars (glyconutrients) upon brain function. The term glyconutrient refers to sugars that are absolutely essential for proper cellular survival and function, especially for the immune system cells. Most people know about glucose (from sucrose or white sugar) and galactose (from milk). However, little is known about the other six essential sugars, which are not readily available through a regular diet and need to be metabolized. Abundant research studies have identified the eight essential sugars (monosaccharides) needed for cells to communicate. This fact is noted in the latest Harper Biochemistry Dictionary, a medical desk reference. Dr. Dykman‘s study, found that certain single-cell sugars or monosaccharides enhanced brainwave frequencies associated with attention and alertness, increased reaction time, and concentration. Studies clearly show the important benefits children receive from ingesting these eight essential sugars as a nutritional supplement. “Breakfast Eaters” have Better Attention Span than “Breakfast Skippers” There are many components in a child’s diet, which will have a direct affect on brain function, behaviour and academic performance. William Sears, M.D. and Lynda Thompson, PhD in their A.D.D. Book, consecrated one chapter to the subject of feeding a child's brain. According to them, "it is not only the type of food but when and how you eat it that affects brain function." Their studies show that breakfast eaters, especially those that eat a breakfast rich in protein and calcium, generally have higher grades. Breakfast skippers, on the other hand, are more likely to be sluggish and overeat throughout the rest of the day. This is observed in the change of the brain waves patterns of children training with neurofeedback at our office. We frequently observe an increase in the theta wave (the slow waves (corresponding to a tune-out mental set) after a child has eaten sugary cereals or worst after eating pancakes with maple syrup for breakfast! Neurofeedback uses a quantitative electroencephalogram (QEEG) (see article on neurofeedback training for attention span). Obviously, if a child has an increase in slow brain waves, he/she will be sluggish at school and this will have an adverse impact on behaviour and grades. The Need of Supplements in our Diet It is well recognized even by the American Medical Association that we now need to add to our diets vitamin and mineral supplements because of our depleted soils. Adding to the pesticides and other chemicals polluting added to our food chain, fruits and vegetables are lacking the essential nutrients, called “phytonutrients” because they are often picked before they ripen. These “phytonutrients” strengthen our immune systems and work like enzymes aiding digestion and absorption. Supplementing the diet with enzymes will often help people with learning and attention difficulties because the lack of digestion and absorption is often one of their physiological weaknesses. Heavy Metals and Brain Function Unfortunately, heavy metals like mercury, lead, and aluminum found in our drinking water, water pipes, some vaccines, some junk food, and the air we breathe (are just some of the source of heavy metals ingestion) interfere with the absorption of necessary minerals, like zinc. Research has shown that high intercellular copper levels and low zinc levels cause many children to be hyperactive. Antioxidants are essentials in neutralizing free radicals oxidative stress (like rust produced on metal ) that heavy metals create. Chelation can be used to remove heavy metals from the body, preventing any interference in vitamin and mineral absorption and allowing the body to replenish the cells with the healthy metals. Water and the brain health Drinking several glasses of water per day is essential, but few do it. Dr. F. Batmanghelidj's book, Your Body's Many Cries for Water (you are not sick, you are thirsty) will motivate its readers to drink water. Here is an excerpt from his book: "The human body is composed of 25% solid matter and 75% water. Brain tissue is said to consist of 85% water. Every function of the body is monitored and pegged to the efficient flow of water. “Water distribution” is the only way of making sure that not only an adequate amount of water, but its transported elements (hormones, chemical messengers, and nutrients) first reach the more vital organs.” With the use of the QEEG , I have regularly observed children, gaining more control over their slow brain waves, after drinking a glass of water. Water is necessary for the body, but not all water is equal. Chlorine, which is present in city tap water, will prevent the absorption of tyrosine, an important amino acid. Our water can also be contaminated with heavy metals. City tap water needs to be purified. Osmosis water filtering systems and distilled water filtering systems are not the best filtration methods for long-term consumption. Water from these types of filtration systems not only remove essential minerals, but this water will leach the body of its minerals. It is also interesting to know that the osmosis water has a “low pH” which means that the water is acidic and may interfere with the alkaline state of the body. Efficient water filtration systems are available and are able to remove harmful substances and yet retain the important minerals. Therefore, before children start consuming more water to transport nutrients to the body organs, attention needs to be paid to the type of water these children are ingesting. Genetically Engineered Food Our children’s health in the form of undiagnosed food allergies or intolerance to food (such as celiac disease) may be linked to genetically engineered food It is since 1997 that we have had a wide variety of unlabelled genetically-engineered foods enter our supermarket shelves. Genetic engineering has to do with implanting conglomerations of genes from viruses, bacteria, insects, and animals onto our fruits, grains, nuts, and vegetables. Would it be possible that one explanation of these allergies to nuts, unheard few years ago, could be linked with the modified structure of the nuts? For example, in tests conducted at the University of Nebraska and reported in the New England Journal of Medicine, researchers found that soybeans modified with genes from Brazil nuts produced proteins that resulted in extreme, potentially deadly allergic reactions in people sensitive to the nuts. The human body is amazingly designed. Scientist consider that we have approximately 70 trillions of cells in our body. These cells continually multiply and die resulting in having a brand new body every seven or eight years. The health of the body depends on the health of the cells which produce energy. This article enumerate some facts about the reasons why our brain can be weakened. The good news is that if we limit the ingestion of the “bad stuff” and feed the body with the nutrients it needs to function efficiently, the body can regenerate itself. To summarize, children and adults with behavioural, learning and attention problems Firstly, they should AVOID (as much as possible): * JUNK FOOD, snack food, and fast food * the genetically modified organisms * trans-fatty acids (hydrogenated oil), * food containing pesticides (www.ewg.org) * white sugar (pop, cereal, candy…) * white flour (pasta, pizza…) * food dyes (especially the red and yellow ones) * Aspartame (sugar substitute in candy and gum) and MSG (flavor enhancer) * caffeine and chocolate * homogenized milk and be careful with soya milk which is often difficult to digest * preservatives * carbonated drinks Secondly, they NEED: * vitamins (fruits, vegetables, whole grains) * minerals * phytochemical supplements * proteins (amino acids) * essential fatty acids * glyconutrients, eight essential monosaccharides (sugars) * drink daily more purified water (one quart of water for every fifty pounds of weight.) * probiotics, which are the good bacteria needed in the intestines * get rid of toxins through exercise and antioxidants (Vitamin C is excellent) * get rid of parasites * sleep well The intention of this article is to not create more problems, but to summarize the main nutritional issues related to learning and attention behaviours in order better understand some of the physical root problems of learning and attention behaviours. Pursue your research, and pray for wisdom that you may glean what you need to help your children and yourselves. Make the changes step by step. Ask God for wisdom to know what you cannot change and wisdom to know what you can and need to do. A professional assessment of your child’s balance of nutrients in relation to his/her learning and attention inefficiencies may helpful. If you need help in assessing the learning and attention inefficiencies of your child I would love to help you. Do not hesitate to contact us if you have any further questions or needs. “Behold, the eye of the Lord is upon them that fear him, upon them that hope in his mercy: to deliver their soul from death, and to keep them alive in famine. Our soul waiteth for the Lord: he is our help and our shield.” Psalm 33: 18-19 Resources To know more about glyconutrients (the good sugars): (phone David: 705-726-5971 or www.mannapages.com/davidday (the Canadian one)) Books Is Your Child's Brain Starving? Michael R. Lyon, M.D. Healing the Hyper Active Brain, Michael R. Lyon, M.D. (www.functionalmedecine.ca) Your Body's Many Cries for Water, F.Batmanghelidj, M.D. (www.watercure.com) The ADD Book, by William Sears, M.D. and Lynda Thompson, Ph.D. Breaking the Vicious Cycle, by . Elaine Gottschall (www.breakingtheviciouscycle.info) and (www.pecanbread.com) Fat that Heal, Fats that Kill, Udo Erasmus Miracle Sugars, Rita Elkins, M.H. The Second Brain, Your gut has a mind of its own, Michael D. Gershon, M.D. Healing ADD, Daniel G. Amen, M.D. (www.amenclinic.com) How to Survive on a Toxic Planet, Dr. Steve Nugent The Safe Shopper’s Bible. By Dr. Samuel Epstein, MD & David Steinman Nutrition and Mental Illness, by Carl C. Pfeiffer,Ph.D,M.D. Web sites: Dr Joseph Mercola (www.mercola.com) (look for the article "Why you should avoid Soy" by Sally Fallon and for the DVD "Sweet Misery: A Poisoned World") Environmental Causes of Learning Disabilities (www.chem-tox.com/pregnancy/learning_disabilities.htm) The Truth about Soy (www.soyonlineservice.co.nz) To know more about glyconutrients (the good sugars): (phone David: 705-726-5971 or www.mannapages.com/davidday (the Canadian one)) Copyright 2005 Suzanne Day, Neuropsychologist member of l’Ordre des psychologues du Québec

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----- -------- AUTHOR: Biomed Mom TITLE: Orthomolecular treatment of mental health DATE: 6/15/2008 03:17:00 PM ----- BODY:
FOR IMMEDIATE RELEASE Orthomolecular Medicine News Service, October 7, 2005 Mental Health Treatment That Works (OMNS) Doctors report that mental health problems including depression, bipolar disorder, schizophrenia, ADHD, anti-social and learning disorders, and obsessive-compulsive disorders often have a common cause: insufficient nutrients in the brain. Nutritionally-oriented physicians assert that the cure for these problems is to give the body the extra nutrients it needs, especially when under abnormal stress. Orthomolecular medical researchers say the future of psychiatry is in nutrition because nutrition has such a long, safe and effective history of correcting many mental problems. Nutrients such as the B-vitamins are most successful when taken regularly, taken in relatively high doses, and taken in conjunction with vitamin C, the essential fatty acids (EFA’s), and the minerals magnesium and selenium. A summary of what has worked for many people follows below. The safety of vitamins and minerals is extraordinary, and the expense of trying them is much less than the cost of hazardous pharmaceutical drugs. These nutrients can be purchased in a discount or heath store. Taking 1,000 mg of vitamin B-3 three times a day often cures mild to moderate depression. Dramatic results are often achieved within one week of beginning this nutritional program, especially in alcoholics. (1) Sometimes a simple deficiency of vitamin D causes depression. 3,000 I.U./day from all sources can alleviate the problem. (2) 3,000 mg/day or more of niacin (vitamin B-3), along with the same quantity of vitamin C, taken in divided doses throughout the day can successfully treat both schizophrenia and bipolar disorder. (3) Vitamins B-3, B-6, C and the minerals magnesium and zinc frequently produce a good response in ADHD and autistic children. (4) Vitamins B-6, folate, and B-12 taken together lower elevated homocysteine levels in the elderly while improving mental function. (5) As pointed out by chemistry professor and vitamin discoverer Roger J. Williams, PhD (6), each individual has different nutritional needs and responds differently to nutrients. Are you tired of being depressed, suffering from anxiety, paying huge prescription drug bills for unsafe prescriptions that don’t solve the problem or produce undesirable side effects? Are you tired of the piece-meal trial and error approach to finding a solution to your mental or emotional problems? If so, adults should consider the following nutritional protocol, which will bathe your brain and nerves in natural nutrients and may well produce dramatic results. The cost of trying the program below is less than the cost of a typical doctor’s office visit. It is safe and convenient. All of these nutrients can be purchased at large discount stores. After the morning meal take: * A multivitamin tablet * 1,000 mg of vitamin B-3 (as niacinamide or inositol hexanicotinate) * One B-complex tablet * 100 mg of vitamin B-6 * 1,200 mcg of vitamin B-9 (folate or folic acid) * 1,000-2,000 IU of vitamin D (the lower number if you get sunshine, the higher number if you don't) * 1,000 mg of vitamin C * 200 mg of magnesium * 50 mg of zinc * 200 micrograms (mcg) of selenium * 30 grams of soy protein powder and one tablespoon of lecithin granules mixed into a small glass of juice or milk A supplement of omega-3 fatty acids [eicosapentaenoic acid (EPA), docosahexanoic acid (DHA) and alpha-linolenic acid (ALA)] After the midday meal: * 1,000 mg of vitamin B-3 * 1,200 mcg of vitamin folate * 100 mg of vitamin B-6 * One B-complex tablet * 1,000 mg of vitamin C * 200 mg of magnesium After the evening meal: * A multivitamin tablet * 1,000 mg of vitamin B-3 * 1,000 mg of vitamin C * One B-complex tablet * 100 mg of vitamin B-6 All of the above supplements are safe in the recommended amounts, as well as inexpensive and convenient. There is not even one death per year from vitamins. Pharmaceutical drugs, properly prescribed and taken as directed, kill over 100,000 Americans annually. Hospital errors kill still more. Restoring health must be done nutritionally, not pharmacologically. All cells in all persons are made exclusively from what we drink and eat. Not one cell is made out of drugs. The most common mistake made by people who take vitamins is they fail to take enough vitamins. The reason one nutrient can cure so many different illnesses is because a deficiency of one nutrient can cause many different illnesses. What is Orthomolecular Medicine? Linus Pauling defined orthomolecular medicine as "the treatment of disease by the provision of the optimum molecular environment, especially the optimum concentrations of substances normally present in the human body." Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org Take the Orthomolecular Quiz at http://www.orthomolecular.org/quiz/index.shtml The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource. Editorial Review Board: Abram Hoffer, M.D., Ph.D. Harold D. Foster, Ph.D. Bradford Weeks, M.D. Carolyn Dean, M.D. N.D. Erik Paterson, M.D. Thomas Levy, M.D., J.D. Andrew W. Saul, contact person. email: omns@orthomolecular.org To UNSUBSCRIBE: http://www.orthomolecular.org/unsubscribe.html To subscribe at no charge: http://www.orthomolecular.org/subscribe.html References for further reading: 1. Hoffer A. Vitamin B-3: Niacin and its amide. http://www.doctoryourself.com/hoffer_niacin.html Also: Cheraskin E, Ringsdorf WM and Brecher A. Psychodietetics. Bantam Books, 1974. 2. Vieth R, Kimball S, Hu A, Walfish PG. Randomized comparison of the effects of the vitamin D3 adequate intake versus 100 mcg (4000 IU) per day on biochemical responses and the wellbeing of patients. Nutr J. 2004 Jul 19;3:8. 3. Hoffer A. Healing schizophrenia: Complementary vitamin & drug treatments. Toronto: CCNM Press, 2004. Also: Hawkins D and Pauling L. Orthomolecular psychiatry, San Francisco: Freeman, 1973. Also: Hoffer A. Niacin therapy in psychiatry, Charles C. Thomas, 1962. 4. Hoffer A. Healing children's attention and behavior disorders: Complementary nutritional & psychological treatments. Toronto: CCNM Press, 2004. Also: Hoffer A. Dr. Hoffer's ABC of natural nutrition for children. Kingston, Ontario: Quarry Press, 1999. 5. Selhub J, Jacques PF, Wilson PWF, Rush D, Rosenberg IH. Vitamin status and intake as primary determinants of homocysteinemia in an elderly population. JAMA 1993. 270:2693-2698. Also: Verhoef P, Meleady R, Daly LE, Graham IM, Robinson K, Boers GHJ, et al. Homocysteine, vitamin status and risk of vascular disease. European Heart Journal 1999. 20:1234-1244. 6. http://neon.cm.utexas.edu/williams/ (end)
----- -------- AUTHOR: Biomed Mom TITLE: PTSD and neurobiology DATE: 4/29/2008 05:05:00 PM ----- BODY:
The Body Keeps The Score:
Memory & the Evolving Psychobiology of Post Traumatic Stress
by Bessel van der Kolk


Bessel A. van der Kolk, MD.
Harvard Medical School
HRI Trauma Center
227 Babcock Street
Boston, MA 02146

This is a version of an article first published in the Harvard Review of Psychiatry, 1994, 1(5), 253-265. Note that this online version may have minor differences from the published version.
The author wishes to thank Rita Fisler, Ed.M. for her editorial assistance.
Background

For more than a century, ever since people's responses to overwhelming experiences were first systematically explored, it has been noted that the psychological effects of trauma are expressed as changes in the biological stress response. In 1889, Pierre Janet (1), postulated that intense emotional reactions make events traumatic by interfering with the integration of the experience into existing memory schemes. Intense emotions, Janet thought, cause memories of particular events to be dissociated from consciousness, and to be stored, instead, as visceral sensations (anxiety and panic), or as visual images (nightmares and flashbacks). Janet also observed that traumatized patients seemed to react to reminders of the trauma with emergency responses that had been relevant to the original threat, but that had no bearing on current experience. He noted that victims had trouble learning from experience: unable to put the trauma behind them, their energies were absorbed by keeping their emotions under control at the expense of paying attention to current exigencies. They became fixated upon the past, in some cases by being obsessed with the trauma, but more often by behaving and feeling like they were traumatized over and over again without being able to locate the origins of these feelings (2,3).

Freud also considered the tendency to stay fixated on the trauma to be biologically based: "After severe shock.. the dream life continually takes the patient back to the situation of his disaster from which he awakens with renewed terror.. the patient has undergone a physical fixation to the trauma"(4). Pavlov's investigations continued the tradition of explaining the effects of trauma as the result of lasting physiological alterations. He, and others employing his paradigm, coined the term "defensive reaction" for a cluster of innate reflexive responses to environmental threat (5). Many studies have shown how the response to potent environmental stimuli (unconditional stimuli-US) becomes a conditioned reaction. After repeated aversive stimulation, intrinsically non-threatening cues associated with the trauma (conditional stimuli-CS) become capable of eliciting the defensive reaction by themselves (conditional response-CR). A rape victim may respond to conditioned stimuli, such as the approach by an unknown man, as if she were about to be raped again, and experience panic. Pavlov also pointed out that individual differences in temperament accounted for the diversity of long term adaptations to trauma.

Abraham Kardiner(6), who first systematically defined posttraumatic stress for American audiences, noted that sufferers from "traumatic neuroses" develop an enduring vigilance for and sensitivity to environmental threat, and stated that "the nucleus of the neurosis is a physioneurosis. This is present on the battlefield and during the entire process of organization; it outlives every intermediary accommodative device, and persists in the chronic forms. The traumatic syndrome is ever present and unchanged". In "Men under Stress", Grinker and Spiegel (7) catalogue the physical symptoms of soldiers in acute posttraumatic states: flexor changes in posture, hyperkinesis, "violently propulsive gait", tremor at rest, masklike facies, cogwheel rigidity, gastric distress, urinary incontinence, mutism, and a violent startle reflex. They noted the similarity between many of these symptoms and those of diseases of the extrapyramidal motor system. Today we can understand them as the result of stimulation of biological systems, particularly of ascending amine projections. Contemporary research on the biology of PTSD, generally uninformed by this earlier research, confirms that there are persistent and profound alterations in stress hormones secretion and memory processing in people with PTSD.
The Symptomatology of PTSD

Starting with Kardiner(6), and closely followed by Lindemann (8), a vast literature on combat trauma, crimes, rape, kidnapping, natural disasters, accidents and imprisonment have shown that the trauma response is bimodal: hypermnesia, hyper-reactivity to stimuli and traumatic reexperiencing coexist with psychic numbing, avoidance, amnesia and anhedonia (9,10,11,12). These responses to extreme experiences are so consistent across traumatic stimuli that this biphasic reaction appears to be the normative response to any overwhelming and uncontrollable experience. In many people who have undergone severe stress, the post-traumatic response fades over time, while it persists in others. Much work remains to be done to spell out issues of resilience and vulnerability, but magnitude of exposure, prior trauma, and social support appear to be the three most significant predictors for developing chronic PTSD (13,14).

In an apparent attempt to compensate for chronic hyperarousal, traumatized people seem to shut down: on a behavioral level, by avoiding stimuli reminiscent of the trauma; on a psychobiological level, by emotional numbing, which extends to both trauma-related, and everyday experience (15). Thus, people with chronic PTSD tend to suffer from numbing of responsiveness to the environment, punctuated by intermittent hyperarousal in response to conditional traumatic stimuli. However, as Pitman has pointed out (16), in PTSD, the stimuli that precipitate emergency responses may not be conditional enough: many triggers not directly related to the traumatic experience may precipitate extreme reactions. Thus, people with PTSD suffer both from generalized hyperarousal and from physiological emergency reactions to specific reminders(9,10) The loss of affective modulation that is so central in PTSD mayhelp explain the observation that traumatized people lose the capacity to utilize affect states as signals (18). Instead of using feelings as cues to attend to incoming information, in people with PTSD arousal is likely to precipitate flight or fight reactions (19). Thus, they are prone to go immediately from stimulus to response without making the necessary psychological assessment of the meaning of what is going on. This makes them prone to freeze, or, alternatively, to overreact and intimidate others in response to minor provocations (12,20).
Psychophysiology

Abnormal psychophysiological responses in PTSD have been demonstrated on two different levels: 1) in response to specific reminders of the trauma and 2) in response to intense, but neutral stimuli, such as acoustic startle. The first paradigm implies heightened physiological arousal to sounds, images, and thoughts related to specific traumatic incidents. A large number of studies have confirmed that traumatized individuals respond to such stimuli with significant conditioned autonomic reactions, such as heart rate, skin conductance and blood pressure (20,21,22,23, 24,25). The highly elevated physiological responses that accompany the recall of traumatic experiences that happened years, and sometimes decades before, illustrate the intensity and timelessness with which traumatic memories continue to affect current experience (3,16). This phenomenon has generally been understood in the light of Peter Lang's work (26) which shows that emotionally laden imagery correlates with measurable autonomic responses. Lang has proposed that emotional memories are stored as "associative networks", that are activated when a person is confronted with situations that stimulate a sufficient number of elements that make up these networks. One significant measure of treatment outcome that has become widely accepted in recent years is a decrease in physiological arousal in response to imagery related to the trauma (27). However, Shalev et al (28) have shown that desensitization to specific trauma-related mental images does not necessarily generalize to recollections of other traumatic events, as well.

Kolb (29) was the first to propose that excessive stimulation of the CNS at the time of the trauma may result in permanent neuronal changes that have a negative effect on learning, habituation, and stimulus discrimination. These neuronal changes would not depend on actual exposure to reminders of the trauma for expression. The abnormal startle response characteristic of PTSD (10) exemplifies such neuronal changes.

Despite the fact that an abnormal acoustic startle response (ASR) has been seen as a cardinal feature of the trauma response for over half a century, systematic explorations of the ASR in PTSD have just begun. The ASR consists of a characteristic sequence of muscular and autonomic responses elicited by sudden and intense stimuli (30,31). The neuronal pathways involved consist of only a small number of mediating synapses between the receptor and effector and a large projection to brain areas responsible for CNS activation and stimulus evaluation (31). The ASR is mediated by excitatory amino acids such as glutamate and aspartate and is modulated by a variety of neurotransmitters and second messengers at both the spinal and supraspinal level (32). Habituation of the ASR in normals occurs after 3 to 5 presentations (30).

Several studies have demonstrated abnormalities in habituation to the ASR in PTSD (33,34,35,36). Shalev et al (33) found a failure to habituate both to CNS and ANS-mediated responses to ASR in 93% of the PTSD group, compared with 22% of the control subjects. Interestingly, people who previously met criteria for PTSD, but no longer do so now, continue to show failure of habituation of the ASR (van der Kolk et al, unpublished data; Pitman et al, unpublished data), which raises the question whether abnormal habituation to acoustic startle is a marker of, or a vulnerability factor for developing PTSD.

The failure to habituate to acoustic startle suggests that traumatized people have difficulty evaluating sensory stimuli, and mobilizing appropriate levels of physiological arousal(30). Thus, the inability of people with PTSD to properly integrate memories of the trauma and, instead, to get mired in a continuous reliving of the past, is mirrored physiologically in the misinterpretation of innocuous stimuli, such as the ASR, as potential threats.
The Hormonal Stress Response & the Psychobiology of PTSD

Post Traumatic Stress Disorder develops following exposure to events that are intensely distressing. Intense stress is accompanied by the release of endogenous, stress-responsive neurohormones, such as cortisol, epinephrine and norepinephrine (NE), vasopressin, oxytocin and endogenous opioids. These stress hormones help the organism mobilize the required energy to deal with the stress, ranging from increased glucose release to enhanced immune function. In a well-functioning organism, stress produces rapid and pronounced hormonal responses. However, chronic and persistent stress inhibits the effectiveness of the stress response and induces desensitization (37).

Much still remains to be learned about the specific roles of the different neurohormones in the stress response. NE is secreted by the Locus Coeruleus(LC) and distributed through much of the CNS, particularly the neocortex and the limbic system, where it plays a role in memory consolidation and helps initiate fight/ flight behaviors. Adrenocorticotropin (ACTH) is released from the anterior pituitary, and activates a cascade of reactions, eventuating in release of glucocorticoids from the adrenals. The precise interrelation between Hypothalamic-Pituitary-Adrenal (HPA) Axis hormones and the catecholamines in the stress response is not entirely clear, but it is known that stressors that activate NE neurons also increase CRF concentrations in the LC (38), while intracerebral ventricular infusion of CRF increases NE in the forebrain (39). Glucocorticoids and catecholamines may modulate each other's effects: in acute stress, cortisol helps regulate stress hormone release via a negative feedback loop to the hippocampus, hypothalamus and pituitary (40) and there is evidence that corticosteroids normalize catecholamine-induced arousal in limbic midbrain structures in response to stress (41). Thus, the simultaneous activation of corticosteroids and catecholamines could stimulate active coping behaviors, while increased arousal in the presence of low glucocorticoid levels may promote undifferentiated fight or flight reactions (42).

While acute stress activates the HPA axis and increases glucocorticoid levels, organisms adapt to chronic stress by activating a negative feedback loop that results in 1) decreased resting glucocorticoid levels in chronically stressed organisms, (43), 2) decreased glucocorticoid secretion in response to subsequent stress (42), and 3) increased concentration of glucocorticoid receptors in the hippocampus (44). Yehuda has suggested that increased concentration of glucocorticoid receptors could facilitate a stronger glucocorticoid negative feedback, resulting in a more sensitive HPA axis and a faster recovery from acute stress (45).

Chronic exposure to stress affects both acute and chronic adaptation: it permanently alters how an organism deals with its environment on a day-to-day basis, and it interferes with how it copes with subsequent acute stress (45).
Neuroendocrine Abnormalities in PTSD

Since there is an extensive animal literature on the effects of inescapable stress on the biological stress response of other species, such as monkeys and rats, much of the biological research on people with PTSD has focussed on testing the applicability of those research findings to people with PTSD (46,47). People with PTSD, like chronically and inescapbly shocked animals, seem to suffer from a persistent activation of the biological stress response upon exposure to stimuli reminiscent of the trauma.

1) Catecholamines. Neuroendocrine studies of Vietnam veterans with PTSD have found good evidence for chronically increased sympathetic nervous system activity in PTSD. One study (48) found elevated 24h excretions of urinary NE and epinephrine in PTSD combat veterans compared with patients with other psychiatric diagnoses. While Pitman & Orr (49) did not replicate these findings in 20 veterans and 15 combat controls, the mean urinary NE excretion values in their combat controls (58.0 ug/day) were substantially higher than those previously reported in normal populations. The expected compensatory downregulation of adrenergic receptors in response to increased levels of norepinephrine was confirmed by a study that found decreased platelet alpha-2 adrenergic receptors in combat veterans with PTSD, compared with normal controls (50). Another study also found an abnormally low alpha-2 adrenergic receptor-mediated adenylate cyclase signal transduction (51). In a recent study Southwick et al (52) used yohimbine injections (0.4 mg/kg), which activate noradrenergic neurons by blocking the alpha-2 auto- receptor, to study noradrenergic neuronal dysregulation in Vietnam veterans with PTSD. Yohimbine precipitated panic attacks in 70% of subjects and flashbacks in 40%. Subjects responded with larger increases in plasma MHPG than controls. Yohimbine precipitated significant increases in all PTSD symptoms.

2) Corticosteroids. Two studies have shown that veterans with PTSD have low urinary cortisol excretion, even when they have comorbid major depressive disorder (42,53). One study failed to replicate this finding (49). In a series of studies, Yehuda et al (42,54) found increased numbers of lymphocyte glucocorticoid receptors in Vietnam veterans with PTSD. Interestingly, the number of glucocorticoid receptors was proportional to the severity of PTSD symptoms. Yehuda (54) also has reported the results of an unpublished study by Heidi Resnick, in which acute cortisol response to trauma was studied from blood samples from 20 acute rape victims. Three months later, a prior trauma history was taken, and the subjects were evaluated for the presence of PTSD. Victims with a prior history of sexual abuse were significantly more likely to have developed PTSD three months following the rape than rape victims who did not develop PTSD. Cortisol levels shortly after the rape were correlated with histories of prior assaults: the mean initial cortisol level of individuals with a prior assault history was 15 ug/dl compared to 30 ug/dl in individuals without. These findings can be interpreted to mean either that prior exposure to traumatic events result in a blunted cortisol response to subsequent trauma, or in a quicker return of cortisol to baseline following stress. The fact that Yehuda et al (45) also found subjects with PTSD to be hyperresponsive to low doses of dexamethasone argues for an enhanced sensitivity of the HPA feedback in traumatized patients.

3) Serotonin. While the role of serotonin in PTSD has not been systematically investigated, both the fact that inescapably shocked animals develop decreased CNS serotonin levels (55), and that serotonin re-uptake blockers are effective pharmacological agents in the treatment of PTSD, justify a brief consideration of the potential role of this neurotransmitter in PTSD. Decreased serotonin in humans has repeatedly been correlated with impulsivity and aggression (56,57,58). The literature tends to readily assume that these relationships are based on genetic traits. However, studies of impulsive, aggressive and suicidal patients seem to find at least as robust an association between those behaviors and histories of childhood trauma (e.g. 59,60,61). It is likely that both temperament and experience affect relative CNS serotonin levels (12).

Low serotonin in animals is also related to an inability to modulate arousal, as exemplified by an exaggerated startle (62,63), and increased arousal in response to novel stimuli, handling, or pain (63). The behavioral effects of serotonin depletion on animals is characterized by hyperirritability, hyperexitability, and hypersensitivity, and an "...exaggerated emotional arousal and/or aggressive display, to relatively mild stimuli" (63). These behaviors bear a striking resemblance to the phenomenology of PTSD in humans. Furthermore, serotonin re-uptake inhibitors have been found to be the most effective pharmacological treatment of both obsessive thinking in people with OCD (64), and of involuntary preoccupation with traumatic memories in people with PTSD (65,66). It is likely that serotonin plays a role in the capacity to monitor the environment flexibly and to respond with behaviors that are situation-appropriate, rather than reacting to internal stimuli that are irrelevant to current demands.

4). Endogenous opioids. Stress induced analgesia (SIA) has been described in experimental animals following a variety of inescapable stressors such as electric shock, fighting, starvation and cold water swim (67). In severely stressed animals, opiate withdrawal symptoms can be produced both by termination of the stressful stimulus or by naloxone injections. Stimulated by the findings that fear activates the secretion of endogenous opioid peptides, and that SIA can become conditioned to subsequent stressors and to previously neutral events associated with the noxious stimulus, we tested the hypothesis that in people with PTSD, re-exposure to a stimulus resembling the original trauma will cause an endogenous opioid response that can be indirectly measured as naloxone reversible analgesia (68,69). We found that two decades after the original trauma, people with PTSD developed opioid-mediated analgesia in response to a stimulus resembling the traumatic stressor, which we correlated with a secretion of endogenous opioids equivalent to 8 mg of morphine. Self-reports of emotional responses suggested that endogenous opioids were responsible for a relative blunting of the emotional response to the traumatic stimulus.
Endogenous Opiates & Stress Induced Analgesia: Possible Implications for Affective Function

When young animals are isolated, and older ones attacked, they respond initially with aggression (hyperarousal- fight- protest), and, if that does not produce the required results, with withdrawal (numbing-flight-despair). Fear-induced attack or protest patterns in the young serve to attract protection, and in mature animals to prevent or counteract the predator's activity. During external attacks pain-inhibition is a useful defensive capacity, because attention to pain would interfere with effective defense: grooming or licking wounds may attract opponents and stimulate further attack (70). Thus defensive and pain-motivated behaviors are mutually inhibitory. Stress-induced analgesia protects organisms against feeling pain while engaged in defensive activities. As early as 1946, Beecher (71), after observing that 75% of severely wounded soldiers on the Italian front did not request morphine, speculated that "strong emotions can block pain". Today, we can reasonably assume that this is due to the release of endogenous opioids(68,69).

Endogenous opioids, which inhibit pain and reduce panic, are secreted after prolonged exposure to severe stress. Siegfried et al (70) have observed that memory is impaired in animals when they can no longer actively influence the outcome of a threatening situation. They showed that both the freeze response and panic interfere with effective memory processing: excessive endogenous opioids and NE both interfere with the storage of experience in explicit memory. Freeze/numbing responses may serve the function of allowing organisms to not "consciously experience" or not to remember situations of overwhelming stress (and which thus will also keep them from learning from experience). We have proposed that the dissociative reactions in people in response to trauma may be analogous to this complex of behaviors that occur in animals after prolonged exposure to severe uncontrollable stress (68).
Developmental Level Affects the Psychobiological Effects of Trauma

While most studies on PTSD have been done on adults, particularly on war veterans, in recent years a small prospective literature is emerging that documents the differential effects of trauma at various age levels. Anxiety disorders, chronic hyperarousal, and behavioral disturbances have been regularly described in traumatized children (e.g.72,73,74). In addition to the reactions to discrete, one time, traumatic incidents documented in these studies, intrafamilial abuse is increasingly recognized to produce complex post-traumatic syndromes (75), which involve chronic affect dysregulation, destructive behavior against self and others, learning disablities, dissociative problems, somatization, and distortions in concepts about self and others (76,77). The Field Trials for DSM IV showed that these this conglomeration of symptoms tended to occur together and that the severity of this syndrome was proportional to the age of onset of the trauma and its duration (78).

While current research on traumatized children is outside the scope of this review, it is important to recognize that a range of neurobiological abnormalities are beginning to be identified in this population. Frank Putnam's prospective, but as yet unpublished, studies (personal communications, 1991,1992,1993) are showing major neuroendocrine disturbances in sexually abused girls compared with normals. Research on the psychobiology of childhood trauma can be profitably informed by the vast literature on the psychobiological effects of trauma and deprivation in non-human primates (12,79).
Trauma & Memory: The Flexibility of Memory & the Engraving of Trauma

One hundred years ago, Pierre Janet (1) suggested that the most fundamental of mental activities is the storage and categorization of incoming sensations into memory, and the retrieval of those memories under appropriate circumstances. He, like contemporary memory researchers, understood that what is now called semantic, or declarative, memory is an active and constructive process and that remembering depends on existing mental schemata (3,80): once an event or a particular bit of information is integrated into existing mental schemes, it will no longer be accessible as a separate, immutable entity, but be distorted both by prior experience, and by the emotional state at the time of recall(3). PTSD, by definition, is accompanied by memory disturbances, consisting of both hypermnesias and amnesias (9,10). Research into the nature of traumatic memories (3) indicates that trauma interferes with delarative memory, i.e. conscious recall of experience, but does not inhibit implicit, or non-declarative memory, the memory system that controls conditioned emotional responses, skills and habits, and sensorimotor sensations related to experience. There now is enough information available about the biology of memory storage and retrieval to start building coherent hypotheses regarding the underlying psychobiological processes involved in these memory disturbances (3,16,17,25).

In the beginning of this century Janet already noted that: "certain happenings ... leave indelible and distressing memories-- memories to which the sufferer continually returns, and by which he is tormented by day and by night" (81). Clinicians and researchers dealing with traumatized patients have repeatedly made the observation that the sensory experiences and visual images related to the trauma seem not to fade over time, and appear to be less subject to distortion than ordinary experiences (1,49,82). When people are traumatized, they are said to experience "speechless terror": the emotional impact of the event may interfere with the capacity to capture the experience in words or symbols. Piaget (83) thought that under such circumstances, failure of semantic memory leads to the organization of memory on a somatosensory or iconic level (such as somatic sensations, behavioral enactments, nightmares and flashbacks). He pointed out: "It is precisely because there is no immediate accommodation that there is complete dissociation of the inner activity from the external world. As the external world is solely represented by images, it is assimilated without resistance (i.e. unattached to other memories) to the unconscious ego".
Traumatic memories are state dependent.

Research has shown that, under ordinary conditions, many traumatized people, including rape victims (84), battered women (85) and abused children (86) have a fairly good psychosocial adjustment. However, they do not respond to stress the way other people do. Under pressure, they may feel, or act as if they were traumatized all over again. Thus, high states of arousal seem to selectively promote retrieval of traumatic memories, sensory information, or behaviors associated with prior traumatic experiences (9,10). The tendency of traumatized organisms to revert to irrelevant emergency behaviors in response to minor stress has been well documented in animals, as well. Studies at the Wisconsin primate laboratory have shown that rhesus monkeys with histories of severe early maternal deprivation display marked withdrawal or aggression in response to emotional or physical stimuli (such as exposure to loud noises, or the administration of amphetamines), even after a long period of good social adjustment (87). In experiments with mice, Mitchell and his colleagues (88) found that the relative degree of arousal interacts with prior exposure to high stress to determine how an animal will react to novel stimuli. In a state of low arousal, animals tend to be curious and seek novelty. During high arousal, they are frightened, avoid novelty, and perseverate in familiar behavior, regardless of the outcome. Under ordinary circumstances, an animal will choose the most pleasant of two alternatives. When hyperaroused, it will seek whatever is familiar, regardless of the intrinsic rewards. Thus, animals who have been locked in a box in which they were exposed to electric shocks and then released return to those boxes when they are subsequently stressed. Mitchell concluded that this perseveration is nonassociative, i.e. uncoupled from the usual reward systems.

In people, analogous phenomena have been documented: memories (somatic or symbolic) related to the trauma are elicited by heightened arousal (89). Information acquired in an aroused, or otherwise altered state of mind is retrieved more readily when people are brought back to that particular state of mind (90,91). State dependent memory retrieval may also be involved in dissociative phenomena in which traumatized persons may be wholly or partially amnestic for memories or behaviors enacted while in altered states of mind (2,3,92).

Contemporary biological researchers have shown that medications that stimulate autonomic arousal may precipitate visual images and affect states associated with prior traumatic experiences in people with PTSD, but not in controls. In patients with PTSD the injection of drugs such as lactate (93) and yohimbine (52) tends to precipitate panic attacks, flashbacks (exact reliving experiences) of earlier trauma, or both. In our own laboratory, approximately 20% of PTSD subjects responded with a flashback of a traumatic experience when they were presented with acoustic startle stimuli.
Trauma, neurohormones and memory consolidation.

When people are under severe stress, they secrete endogenous stress hormones that affect the strength of memory consolidation. Based on animal models it has been widely assumed (3,46,94) that massive secretion of neurohormones at the time of the trauma plays a role in the long term potentiation (LTP) (and thus, the over- consolidation) of traumatic memories. Mammals seem equipped with memory storage mechanisms that ordinarily modulate the strength of memory consolidation according to the strength of the accompanying hormonal stimulation (95,96). This capacity helps the organism evaluate the importance of subsequent sensory input according to the relative strength of associated memory traces. This phenomenon appears to be largely mediated by NE input to the amygdala (97,98, figure 2). In traumatized organisms, the capacity to access relevant memories appears to have gone awry: they become overconditioned to access memory traces of the trauma and to "remember" the trauma whenever aroused. While norepinephrine (NE) seems to be the principal hormone involved in producing LTP, other neurohormones secreted under particular stressful circumstances, such as endorphins and oxytocin, actually inhibit memory consolidation (99).

The role of NE in memory consolidation has been shown to have an inverted U-shaped function (95,96): both very low and very high levels of CNS NE activity interfere with memory storage. Excessive NE release at the time of the trauma, as well as the release of other neurohormones, such as endogenous opioids, oxytocin and vasopressin, are likely to play a role in creating the hypermnesias and the amnesias that are a quintessential part of PTSD (9,10). It is of interest that childbirth, which can be extraordinarily stressful, almost never seems to result in post traumatic problems (100). Oxytocin may play a protective role that prevents the overconsolidation of memories surrounding childbirth.

Physiological arousal in general can trigger trauma-related memories, while, conversely, trauma-related memories precipitate generalized physiological arousal. It is likely that the frequent re-living of a traumatic event in flashbacks or nightmares cause a re-release of stress hormones which further kindle the strength of the memory trace (46). Such a positive feedback loop could cause subclinical PTSD to escalate into clinical PTSD (16), in which the strength of the memories appear so deeply engraved that Pitman and Orr (17) have called it "the Black Hole" in the mental life of the PTSD patient, that attracts all associations to it, and saps current life of its significance.
Memory, Trauma & the Limbic System

The limbic system is thought to be the part of the CNS that maintains and guides the emotions and behavior necessary for self-preservation and survival of the species (101), and that is critically involved in the storage and retrieval of memory. During both waking and sleeping states signals from the sensory organs continuously travel to the thalamus whence they are distributed to the cortex (setting up a "stream of thought"), to the basal ganglia (setting up a "stream of movement") and to the limbic system where they set up a "stream of emotions"(102), that determine the emotional significance of the sensory input. It appears that most processing of sensory input occurs outside of conscious awareness, and only novel, significant or threatening information is selectively passed on to the neocortex for further attention. Since people with PTSD appear to over-interpret sensory input as a recurrence of past trauma and since recent studies have suggested limbic system abnormalities in brain imaging studies of traumatized patients (103,104), a review of the psychobiology of trauma would be incomplete without considering the role of the limbic system in PTSD (also see 105). Two particular areas of the limbic system have been implicated in the processing of emotionally charged memories: the amygdala and the hippocampus (Table 2).

The amygdala. Of all areas in the CNS, the amygdala is most clearly implicated in the evaluation of the emotional meaning of incoming stimuli (106). Several investigators have proposed that the amygdala assigns free-floating feelings of significance to sensory input, which the neocortex then further elaborates and imbues with personal meaning (101,106,107,108). Moreover, it is thought to integrate internal representations of the external world in the form of memory images with emotional experiences associated with those memories (80). After assigning meaning to sensory information, the amygdala guides emotional behavior by projections to the hypothalamus, hippocampus and basal forebrain (106,107,109).

The septo-hippocampal system, which anatomically is adjacent to the amygdala, is thought to record in memory the spatial and temporal dimensions of experience and to play an important role in the categorization and storage of incoming stimuli in memory. Proper functioning of the hippocampus is necessary for explicit or declarative memory (109). The hippocampus is thought to be involved in the evaluation of spatially and temporally unrelated events, comparing them with previously stored information and determining whether and how they are associated with each other, with reward, punishment, novelty or non-reward (107,110). The hippocampus is also implicated in playing a role in the inhibition of exploratory behavior and in obsessional thinking, while hippocampal damage is associated with hyper-responsiveness to environmental stimuli (111,112).

The slow maturation of the hippocampus, which is not fully myelinated till after the third or fourth year of life, is seen as the cause of infantile amnesia (113,114). In contrast, it is thought that the memory system that subserves the affective quality of experience (roughly speaking procedural, or "taxon" memory) matures earlier and is less subject to disruption by stress (112).

As the CNS matures, memory storage shifts from primarily sensorimotor (motoric action) and perceptual representations (iconic), to symbolic and linguistic modes of organization of mental experience (83). With maturation, there is an increasing ability to categorize experience, and link it with existing mental schemes. However, even as the organism matures, this capacity, and with it, the hippocampal localization system, remains vulnerable to disruption (45,107,110,115,116). A variety of external and internal stimuli, such as stress induced corticosterone production (117), decreases hippocampal activity. However, even when stress interferes with hippocampally mediated memory storage and categorization, it is likely that some mental representation of the experience is laid down by means of a system that records affective experience, but that has no capacity for symbolic processing and placement in space and time (figure 2).

Decreased hippocampal functioning causes behavioral disinhibition, possibly by stimulating incoming stimuli to be interpreted in the direction of "emergency" (fight/flight) responses. The neurotransmitter serotonin plays a crucial role in the capacity of the septo-hippocampal system to activate inhibitory pathways that prevent the initiation of emergency responses until it is clear that they will be of use (110). This observation made us very interested in a possible role for serotonergic agents in the treatment of PTSD.
"Emotional memories are forever"

In animals, high level stimulation of the amygdala interferes with hippocampal functioning (107, 109). This implies that intense affect may inhibit proper evaluation and categorization of experience. In mature animals one-time intense stimulation of the amygdala will produce lasting changes in neuronal excitability and enduring behavioral changes in the direction of either fight or flight (118). In kindling experiments with animals, Adamec et al (119) have shown that, following growth in amplitude of amygdala and hippocampal seizure activity, permanent changes in limbic physiology cause a lasting changes in defensiveness and in predatory aggression. Pre-existing "personality" played a significant role in the behavioral effects of amygdala stimulation in cats: animals that are temperamentally insensitive to threat and prone to attack tend become more aggressive, while in highly defensive animals different pathways were activated, increasing behavioral inhibition (119).

In a series of experiments, LeDoux has utilized repeated electrical stimulation of the amygdala to produce conditioned fear responses. He found that cortical lesions prevent their extinction. This led him to conclude that, once formed, the subcortical traces of the conditioned fear response are indelible, and that "emotional memory may be forever" (118). In 1987, Lawrence Kolb (29) postulated that patients with PTSD suffer from impaired cortical control over subcortical areas responsible for learning, habituation, and stimulus discrimination. The concept of indelible subcortical emotional responses, held in check to varying degrees by cortical and septo-hippocampal activity, has led to the speculation that delayed onset PTSD may be the expression of subcortically mediated emotional responses that escape cortical, and possibly hippocampal, inhibitory control (3,16,94,120,121).

Decreased inhibitory control may occur under a variety of circumstances: under the influence of drugs and alcohol, during sleep (as nightmares), with aging, and after exposure to strong reminders of the traumatic past. It is conceivable that traumatic memories then could emerge, not in the distorted fashion of ordinary recall, but as affect states, somatic sensations or as visual images (nightmares [81] or flashbacks [52]) that are timeless and unmodified by further experience.
Psychopharmacological Treatment

The goal of treatment of PTSD is to help people live in the present, without feeling or behaving according to irrelevant demands belonging to the past. Psychologically, this means that traumatic experiences need to be located in time and place and distinguished from current reality. However, hyperarousal, intrusive reliving, numbing and dissociation get in the way of separating current reality from past trauma. Hence, medications that affect these PTSD symptoms are often essential for patients to begin to achieve a sense of safety and perspective from which to approach their tasks. While numerous articles have been written about the drug treatment of PTSD, to date, only 134 people with PTSD have been enrolledin published double blind studies. Most of these have been Vietnamcombat veterans. Unfortunately, up until recently, only medications which seem to be of limited therapeutic usefulness have beenthesubject of adequate scientific scrutiny. While the only published double blind studies of medications in the treatment of PTSDhave been tricyclic antidepressants and MAO Inhibitors (122,123,124), it is sometimes assumed that they therefore also are themosteffective. Three double-blind trials of tricyclic antidepressants have been published (122,124,125), two of which demonstrated modest improvement in PTSD symptoms. While positive resultshave been claimed for numerous other medications in case reportsand open studies, at the present time there are no data aboutwhich patient and which PTSD symptom will predictably respond toanyof them. Success has been claimed for just about every class ofpsychoactive medication, including benzodiazepines (127), tricyclic antidepressants (122,125), monamine oxidase inhibitors (122,129) lithium carbonate (127), beta adrenergic blockers and clonidine (130), carbamezapine (131) and antipsychotic agents. The accumulated clinical experience seems to indicate that understanding thebasic neurobiology of arousal and appraisal is the most useful guideinselecting medications for people with PTSD (124,125). Autonomic arousal can be reduced at different levels in the CNS: throughinhibition of locus coeruleus noradrenergic activity with clonidine and the beta adrenergic blockers (130,132), or by increasing the inhibitory effect of the gaba-ergic system with gaba- ergicagonists (the benzodiazepines). During the past two years a numberof case reports and open clinical trials of fluoxetine were followedby our double blind study of 64 PTSD subjects with fluoxetine (65). Unlike the tricyclic antidepressants, which were effective on either the intrusive (imipramine) or numbing (amitryptiline) symptoms of PTSD, fluoxetine proved to be effective forthewhole spectrum of PTSD symptoms. It also acted more rapidly thanthetricyclics. The fact that fluoxetine has proven to be such aneffective treatment for PTSD supports a larger role of the serotonergic system in PTSD (66). Rorschach tests adminstered by blindscorers revealed that subjects on fluoxetine became able to takedistance from the emotional impact of incoming stimuli and to becomeable to utilize cognition to harness the emotional responses tounstructured visual stimuli (van der Kolk et al, unpublished).

While the subjects improved clinically, their startle habituation got worse (van der Kolk et al, unpublished). The 5-HT1a agonist buspirone shows some promise in facilitating habituation (133) and thus may play a useful adjunctive role in the pharmaco- therapy of PTSD. Even newer research has suggested abnormalities of the N-methyl-D-aspartate (NMDA) receptor and of glutamate in PTSD (134), opening up potential new avenues for the psychopharmacological treatment of PTSD.

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Adopt Biomed

This blog gathers information about biomedical interventions for children with adoption trauma and Reactive Attachment Disorder. Posts are gathered from multiple websites in one place. Most posts contain unedited text relating to biomedical treatment, dietary changes, vitamins, homeopathy, herbs, etc. Where possible, the link to the original information is included.

Tuesday, April 6, 2010

US Sugar Tariffs Led to Ubiquitous Use of High Fructose Corn Syrup

The Great Sugar Shaft
by James Bovard, April 1998
The U.S. government has devotedly jacked up American sugar prices far above world market prices since the close of the War of 1812. The sugar industry is one of America's oldest infant industries — yet it dodders with the same uncompetitiveness that it showed during the second term of James Madison. Few cases better illustrate how trade policy can be completely immune to economic sense.

The U.S. imposed high tariffs on sugar in 1816 in order to placate the growers in the newly acquired Louisiana territory. In the 1820s, sugar plantation owners complained that growing sugar in the United States was "warring with nature" because the U.S. climate was unsuited to sugar production. Naturally, the plantation owners believed that all Americans should be conscripted into the "war." Protectionists warned that if sugar tariffs were lifted, then the value of slaves working on the sugar plantations would collapse — thus causing a general fall in slave values throughout the South.

In 1934, the U.S. government imposed sugar import quotas to complement high sugar tariffs and direct government subsidies to sugar growers. By the 1950s, the U.S. sugar program was renown for its byzantine, impenetrable regulations. Like most arcane systems, the sugar program vested vast power in the few people who understood and controlled the system. As author Douglas Cater observed in 1964, "In reviewing the sugar quotas, House Agriculture Committee Chairman Cooley has had the habit of receiving the [foreign representatives interested in acquiring sugar quotas] one by one to make their presentations, then summoning each afterward to announce his verdict. By all accounts, he has a zest for this princely power and enjoys the frequent meetings with foreign ambassadors to confer on matters of sugar and state."

Sugar quotas have also provided a safety net for former congressmen, many of whom have been hired as lobbyists for foreign sugar producers.

Since 1980, the sugar program has cost consumers and taxpayers the equivalent of more than $3 million for each American sugar grower. Some people win the lottery; other people grow sugar. Congressmen justify the sugar program as protecting Americans from the "roller-coaster of international sugar prices," as Rep. Byron Dorgan (D.-N.D.) declared. Unfortunately, Congress protects consumers from the roller-coaster by pegging American sugar prices on a level with the Goodyear blimp floating far above the amusement park. U.S. sugar prices have been as high as or higher than world prices for 44 of the last 45 years.

Sugar sold for 21 cents a pound in the United States when the world sugar price was less than 3 cents a pound. Each 1-cent increase in the price of sugar adds between $250 million and $300 million to consumers' food bills. A Commerce Department study estimated that the sugar program was costing American consumers more than $3 billion a year.

Congress, in a moment of economic sobriety, abolished sugar quotas in June 1974. But, on May 5, 1982, President Reagan reimposed import quotas. The quotas sought to create an artificial shortage of sugar that would drive up U.S. prices and force consumers to unknowingly support American sugar growers. And by keeping the subsidies covert and off-budget, quotas did not interfere with Reagan's bragging about how he was cutting wasteful government spending.

Between May 1982 and November 1984, the U.S. government reduced the sugar import quotas six times as the USDA desperately tried to balance foreign and domestic sugar supplies with domestic demand.

While USDA bureaucrats worked overtime to minutely regulate the quantity of sugar allowed into the United States, a bomb went off that destroyed their best-laid plans. On November 6, 1984, both Coca Cola and Pepsi announced plans to stop using sugar in soft drinks, replacing it with high-fructose corn syrup. At the drop of two press releases, U.S. sugar consumption decreased by more than 500,000 tons a year — equal to the entire quotas of 25 of the 42 nations allowed to sell sugar to the United States. The quota program drove sugar prices so high that it wrecked the market for sugar — and thereby destroyed the government's ability to control sugar supply and demand. On January 16, 1985, Agriculture Secretary John Block announced an effective 20 percent cut in the quota for all exporting countries.

Sugar quotas made it very profitable to import products with high amounts of sugar. As a USDA report noted, "The incentive to circumvent restrictions had led to creation of new products which had never been traded in the United States and which were designed specifically for the U.S. market." On June 28, 1983, Reagan declared an embargo on imports of certain blends and mixtures of sugar and other ingredients in bulk containers. Naturally, businesses began importing some of the same products in smaller containers. The Economic Report of the President noted, "Entrepreneurs were importing high-sugar content products, such as iced-tea mix, and then sifting their sugar content from them and selling the sugar at the high domestic price." On November 7, 1984, the Customs Service announced new restrictions on sugar- and sweetener-blend imports.

Federal restrictions made sugar smuggling immensely profitable. The Justice Department caught 30 companies in a major sting operation named Operation Bittersweet. Federal prosecutors were proud that the crackdown netted $16 million in fines for the government — less than one-tenth of 1 percent of what the sugar program cost American consumers during the 1980s. The Justice Department was more worried about businessmen's bringing in cheap foreign sugar than about the sugar lobby's bribing of congressmen to extort billions of dollars from consumers. (Public Voice for Food and Health Policy, a Washington, D.C., consumer lobby, reported that the sugar lobby donated more than $3 million to congressmen between 1984 and 1989.)

A few thousand sugar growers became the tail that wagged the dog of American foreign policy. Early in 1982, Reagan announced the Caribbean Basin Initiative (CBI) to aid Caribbean nations by giving them expanded access to the U.S. market. In his May 5, 1982, announcement, Reagan promised, "The interests of foreign suppliers are also protected, since this system provides such suppliers reasonable access to a stable, higher-priced U.S. market. In arriving at this decision, we have taken fully into account the CBI." But between 1981 and 1988, USDA slashed the amount of sugar that Caribbean nations could ship to the United States by 74 percent. The State Department estimated that the reductions in sugar-import quotas cost Third World nations $800 million a year. The sugar program has indirectly become a full-employment program for the U.S. Drug Enforcement Agency, as many poor Third World farmers who previously grew sugar cane are now harvesting marijuana.

The Reagan administration responded to sugar-import cutbacks by creating a new foreign-aid program — the Quota Offset Program — to give free food to countries hurt by reductions. In 1986, the United States. dumped almost $200 million of free food on Caribbean nations and the Philippines. As the Wall Street Journal reported, "By flooding local markets and driving commodity prices down, the U.S. is making it more difficult for local farmers to replace sugar with other crops." Richard Holwill, deputy assistant secretary of state, observed, "It makes us look like damn fools when we go down there and preach free enterprise."

The U.S. government's generosity to sugar farmers victimizes other American businesses. Brazil retaliated against the United States for cutting its sugar quota by reducing its purchases of American grain. In the Dominican Republic, former sugar growers are now producing wheat and corn, thereby providing more competition for American farmers. American candy producers are at a disadvantage because foreign companies can buy their sugar at much lower prices. Since 1982, dextrose and confectionery coating imports have risen tenfold and chocolate imports are up fivefold.

The sugar program has also decreased soybean exports. In the Red River valley of Minnesota, heavily subsidized sugar growers have bid up the rents on farmland by more than 50 percent. As a result, relatively unsubsidized soybean farmers can no longer find sufficient land to grow soybeans, America's premier export crop. This illustrates how restrictions on imports become restrictions on exports.

The sugar program is corporate welfare in its most overt form. The General Accounting Office estimated that only 17 of the nation's largest sugar cane farmers received more than half of all the benefits provided by the sugar cane subsidies. GAO also estimated that the 28 largest Florida sugar cane producers received almost 90 percent of all the benefits enjoyed by Florida sugar producers from federal programs.

The number of American jobs destroyed by sugar quotas since 1980 exceeds the total number of sugar farmers in the United States. The Commerce Department estimates that the high price of sugar has destroyed almost 9,000 U.S. jobs in food manufacturing since 1981. In early 1990, the Brach Candy Company announced plans to close its Chicago candy factory and relocate 3,000 jobs to Canada because of the high cost of sugar in the United States. Thanks to the cutback in sugar imports, 10 sugar refineries have closed in recent years and 7,000 refinery jobs have been lost. The United States has only 13,000 sugar farmers.

Many observers expected that, with the Republican Revolution in Congress, the sugar program would be abolished when the new farm bill was written in 1996. Instead, the sugar program's survival became one of the starkest symbols of that revolution's collapse. Two-hundred and twenty-three House members cosponsored a bill to get rid of the sugar program; but, when push came to shove, the sugar lobby persuaded several sponsors of the bill (including freshman conservative stalwarts Rep. Steve Stockman [R.-Tex.] and Rep. Sue Myrick [R.-N.C.]) to switch sides. The House voted 217-208 to continue the program.

Environmentalists were anxious about the adverse effects of Florida sugar cane production on the Everglades. Congress did not choose the obvious solution — ending subsides that irrationally encourage sugar production in a fragile area — but instead voted $200 million to clean up the Everglades by buying some of the sugar cane fields from farmers.

There is no reason why the United States must produce its own sugar cane. Sugar is cheaper in Canada primarily because Canada has almost no sugar growers — and thus no trade restrictions or government support programs. Paying lavish subsidies to produce sugar in Florida makes as much sense as creating a federal subsidy program to grow bananas in Massachusetts. The only thing that could make American sugar cane farmers world-class competitive would be massive global warming.

Mr. Bovard is the author of Lost Rights: The Destruction of American Liberty (St. Martin's Press, 1994) and Shakedown (Viking-Penguin Press, 1995).

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Monday, April 5, 2010

Gut healing, Intestinal Permeability, Biofilm

Beyond Probiotics
Hidden Causes of GI Dysfunction
By Chris D. Meletis, ND
Often, in the absence of overt disease, the extent of an individual’s colon-supporting supplement regimen consists exclusively of consuming a good probiotic. Yet, in order for the good bacteria found in probiotics to flourish in the colonic environment, there are other steps we need to take to ensure our gut is hospitable to the friendly bacteria our bodies need to thrive—regardless of whether an individual is healthy or whether that individual suffers from irritable bowel syndrome or another gastrointestinal disease. The colon is essentially our body’s compost pile, used to nurture our garden of friendly flora.

There are two often-overlooked aspects of gut health that are essential to keeping our colon healthy and to ensure it remains a hospitable environment where good bacteria can thrive. First, gut health is linked to a substance called butyrate. If the intestine isn’t working at its optimal best, levels of butyrate can undergo a decline, putting individuals at risk for colon cancer. Butyrate levels are closely tied to the health of the intestine and to levels of friendly flora found in the gut.

A second aspect of gut health is known as intestinal permeability. This can be a huge factor, even in seemingly healthy individuals. Intestinal permeability refers to the potential for nutrients and bacteria to escape through a weakened intestinal wall. When intestinal permeability is increased, food and nutrient absorption is impaired. Dysfunction in intestinal permeability can result in leaky gut syndrome, where larger molecules in the intestines pass through into the blood. This can trigger immediate damage and immune system reactions since these large molecules are perceived as foreign. Progressive damage occurs to the intestinal lining, eventually allowing disease-causing bacteria, undigested food particles, and toxins to pass directly into the bloodstream.

Dysfunctions in intestinal permeability are associated not only with intestinal diseases such as ulcerative colitis, irritable bowel syndrome and Crohn’s disease, but also with chronic fatigue syndrome, psoriasis, food allergies, autoimmune disease and arthritis. Impaired intestinal permeability also occurs in patients undergoing chemotherapy and in heart disease patients.

I briefly discussed intestinal permeability in my last article on GI health. In this article, I will go into further detail about this damaging aspect of intestinal health and explain how increasing butyrate can be a powerful tool in not only restoring ideal colon function but also improving energy levels and the overall health of the body.

Building Butyrate for Colonic Health

Butyrate, a major short-chain fatty acid produced in the human gut by bacterial fermentation of dietary fiber, exhibits strong tumor suppressing activity. Butyrate is an important energy source for cells lining the intestine and plays a role in the maintenance of colonic balance. Butyrate exerts potent effects on a variety of colonic mucosal functions such as inhibition of inflammation and carcinogenesis. Butyrate also reinforces various components that play a role in the colonic defense barrier and decrease oxidative stress. In addition, butyrate may promote satiety.1

Low levels of butyrate are linked to increased risk of colon cancer. A loss of balance in the colon caused by either genetic mutations or environmental factors such as dietary habits can increase the risk for the formation of aberrant crypt foci (the earliest identifiable cancerous lesions in the colon) and ultimately the development of colon cancer. Evidence exists that butyrate reduces the number and the size of aberrant crypt foci in the colon.2

Butyrate’s inhibition of colon cancer is thought to arise from its ability to act as a natural histone deacetylase inhibitor, which results in activation of certain genes known to induce apoptosis (cell death) in cancer cells.2

Low butyrate levels occur in healthy humans prior to the onset of disease, often in response to a poor diet high in sugar and low in fiber. Low butyrate levels also are found in disease states such as ulcerative colitis and Crohn’s disease, especially in patients with moderate to severe mucosal inflammation.3 The monocarboxylate transporter helps colon cells uptake butyrate and during inflammatory bowel disease the monocarboxylate transporter is impaired, preventing the butyrate from getting to the cells.4

The Colonic Barrier and Overall Health

Abnormal intestinal permeability, like low butyrate levels, is another concern that can serve as a hidden reason why we might not be feeling our optimal best. A dysfunction can present in intestinal permeability when an individual is consuming a less than optimal diet or due to other factors such as psychological stress.5

Intestinal permeability, in fact, may be the main cause behind why the body becomes sensitive to a particular type of food. One group of researchers evaluated the intestinal permeability in subjects with adverse reactions to food. Twenty-one subjects with a food allergy and 20 with food hypersensitivity who were on allergen-free diets were enrolled and divided into four groups according to the seriousness of their referred clinical symptoms. The study authors found statistically significant differences in intestinal permeability in subjects with food allergy or hypersensitivity compared to control patients. The worse the intestinal permeability, the more serious the clinical symptoms in patients with food allergy and hypersensitivity.6

According to the researchers, “The present data demonstrate that impaired intestinal permeability, measured in our conditions, is present in all subjects with adverse reactions to food. In addition, for the first time, we report a statistically significant association between the severity of referred clinical symptoms and the increasing of Intestinal Permeability Index. These data reveal that intestinal permeability is not strictly dependent on IgE-mediated processes but could better be related to other mechanisms involved in early food sensitization, as breast-feeding, or microbial environment that influence the development of oral tolerance in early infancy.”

Impaired intestinal permeability is often linked with GI diseases such as ulcerative colitis and Crohn’s. However, new research is unearthing a surprising link between malfunctions in the colonic barrier and a number of non-gastrointestinal conditions such as heart disease.

In a recent study, scientists evaluated the function of the gut in 22 patients with chronic heart failure (CHF) and 22 control subjects. Chronic heart failure patients, compared with control patients, had a 35 percent increase of small intestinal permeability and a 210 percent increase of large intestinal permeability. Additionally, higher concentrations of adherent bacteria were found within mucus of CHF patients compared to control subjects.7

The researchers determined, “Chronic heart failure is a multisystem disorder in which intestinal morphology, permeability, and absorption are modified. Increased intestinal permeability and an augmented bacterial biofilm may contribute to the origin of both chronic inflammation and malnutrition.”

Strengthening the Colon

Raising butyrate levels and reducing the permeability of the intestinal barrier can have far reaching consequences for our health that extend beyond the gastrointestinal tract. Consequently, nutritional support is key.

Increasing fiber intake through consumption of a fiber supplement is one of the easiest ways to increase butyrate levels in the body. Fiber is well known for its ability to protect against colon cancer and its ability to raise butyrate levels is thought to be one of the main ways in which it protects the colon. The benefits of dietary fiber on inflammatory bowel disease may also be related to the production of butyrate that occurs when fiber is fermented in the colon. Butyrate appears to decrease the inflammatory response.8

Combining fiber and a good probiotic with specific botanicals, amino acids and fatty acids known to reduce intestinal permeability can provide additional support for the colon. Phosphatidylcholine, for example, can enhance butyrate’s ability to inhibit colon cancer cells, and therefore works well with fiber to strengthen the intestinal environment.9

The amino acid glutamine is one of the most powerful tools for reducing intestinal permeability, thereby protecting the body against the negative consequences of a leaky gut. In a recent review, researchers studied the medical literature to determine if glutamine was effective in reducing intestinal permeability in critically ill patients. In this group of patients, intestinal permeability can have particularly lethal consequences, causing bacteremia, sepsis, and multiple organ failure syndrome. After studying the medical literature, the scientists concluded that glutamine administration by the intravenous or oral route has a protective effect that prevents or reduces the intensity of the increase in intestinal permeability. Glutamine also reduces the frequency of systemic infections.10

Another group of researchers drew a similar conclusion after studying chemotherapy patients with gastrointestinal cancer. In this group of subjects, oral glutamine decreased intestinal permeability and maintained the intestinal barrier.11

Berberine is another substance that can help reduce intestinal permeability and stop beneficial nutrients from escaping through the intestinal wall.12 Berberine also is highly effective at inhibiting the growth of pathogens that invade the colon.

In my clinical practice, I have found that the best way to improve butyrate levels and reduce intestinal permeability is to combine a good fiber supplement with a supplement that contains phosphatidylcholine, L-glutamine, berberine, deglycyrrhizinated licorice (DGL), N-acetyl glucosamine, marshmallow (Althaea officinalis) root, cabbage powder, slippery elm (Ulmus rubra) bark, and gamma oryzanol. This often results in an increased level of friendly flora in the gut and maximizes the effectiveness of any probiotic supplement consumed. After undertaking this approach, patients often report improvement in their gastrointestinal tract and increased overall health and energy.

Conclusion

The gut uses a disproportionate amount of energy (about 25 percent of total oxygen consumption) for the size of the tissue (about 6 percent of body weight).13 Consequently, it’s especially important to provide this part of the body with as much support as possible. Fiber, probiotics, the amino acid L-glutamine, the fatty acid phosphatidylcholine, N-acetyl glucosamine, deglycyrrhizinated licorice and select botanicals such as marshmallow, berberine, cabbage powder and slippery elm can help raise levels of butyrate and reduce intestinal permeability. This approach can result in a healthier colon, improved energy and enhanced overall health.

References


1. Hamer HM, Jonkers D, Venema K, Vanhoutvin S, Troost FJ, Brummer RJ. Review article: the role of butyrate on colonic function. Aliment Pharmacol Ther. 2008 Jan 15;27(2):104-19.
2. Kim YS, Milner JA. Dietary modulation of colon cancer risk. J Nutr. 2007 Nov;137(11 Suppl):2576S-2579S.
3. Duffy MM, Regan MC, Ravichandran P, O’Keane C, Harrington MG, Fitzpatrick JM, O’Connell PR. Mucosal metabolism in ulcerative colitis and Crohn’s disease. Dis Colon Rectum. 1998 Nov;41(11):1399-405.
4. Thibault R, De Coppet P, Daly K, Bourreille A, Cuff M, Bonnet C, Mosnier JF, Galmiche JP, Shirazi-Beechey S, Segain JP. Down-regulation of the monocarboxylate transporter 1 is involved in butyrate deficiency during intestinal inflammation. Gastroenterology. 2007 Dec;133(6):1916-27.
5. Zareie M, Johnson-Henry K, Jury J, Yang PC, Ngan BY, McKay DM, Soderholm JD, Perdue MH, Sherman PM. Probiotics prevent bacterial translocation and improve intestinal barrier function in rats following chronic psychological stress. Gut. 2006 Nov;55(11):1553-60. Epub 2006 Apr 25.
6. Ventura MT, Polimeno L, Amoruso AC, Gatti F, Annoscia E, Marinaro M, Di Leo E, Matino MG, Buquicchio R, Bonini S, Tursi A, Francavilla A. Intestinal permeability in patients with adverse reactions to food. Dig Liver Dis. 2006 Oct;38(10):732-6.
7. Sandek A, Bauditz J, Swidsinski A, Buhner S, Weber-Eibel J, von Haehling S, Schroedl W, Karhausen T, Doehner W, Rauchhaus M, Poole-Wilson P, Volk HD, Lochs H, Anker SD. Altered intestinal function in patients with chronic heart failure. J Am Coll Cardiol. 2007 Oct 16;50(16):1561-9.
8. Rose DJ, DeMeo MT, Keshavarzian A, Hamaker BR. Influence of dietary fiber on inflammatory bowel disease and colon cancer: importance of fermentation pattern. Nutr Rev. 2007 Feb;65(2):51-62.
9. Hossain Z, Konishi M, Hosokawa M, Takahashi K. Effect of polyunsaturated fatty acid-enriched phosphatidylcholine and phosphatidylserine on butyrate-induced growth inhibition, differentiation and apoptosis in Caco-2 cells. Cell Biochem Funct. 2006 Mar-Apr;24(2):159-65.
10. De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of glutamine. Crit Care Med. 2005 May;33(5):1175-8.
11. Zhonghua Wei Chang Wai Ke Za Zhi. 2006 Jan;9(1):59-61. [Protective effect of glutamine on intestinal barrier function in patients receiving chemotherapy] [Article in Chinese]. Jiang HP, Liu CA.
12. Taylor CT, Winter DC, Skelly MM, O’Donoghue DP, O’Sullivan GC, Harvey BJ, Baird AW. Berberine inhibits ion transport in human colonic epithelia. Eur J Pharmacol. 1999 Feb 26;368(1):111-8.
13. Britton R, Krehbiel C. Nutrient metabolism by gut tissues. J Dairy Sci. 1993 Jul;76(7):2125-31.

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Homeopathic Treatment for Adoption Trauma

Remedies

Anacardium - Adoption is a split, both emotionally and genetically. The child is split from the original family and identity and graphed onto a new family and identity. The Anacardium child has a divided will, not sure if they are a devil or an angel. The Anacardium state can be caused by isolation and separation at birth, or after, leading to an extreme lack of confidence and a feeling of powerlessness. To compensate for this feeling, the person becomes aggressive and cruel. A keynote of the Anacardium state is a cold, hardhearted stare, which can be quite disconcerting to parents. The child's behavior may appear very normal except in their drawings, which may have violent themes, and they may be attracted to playing with matches. The child's dreams may also be violent, but they will rarely share their dreams with others.

Gallic acid - The Gallic acid state can be caused by the shock of a sudden separation from a primary caretaker. From that time onward, the child does everything possible to prevent being left alone. This child feels abandoned and reacts with manipulation and even violence in seeking protection from further abandonment. The child insists on being watched constantly and wakes up frequently at night to check that the parents are still nearby. This child won't stay alone for even a minute and is rude and abusive to those around them, even to friends. The child can be extremely jealous and threatening to siblings. Gallic acid children are often hyperactive and cannot focus on their tasks, or schoolwork.

Hura - Hura treats the condition of feeling unwanted and abandoned by one's nearest relatives, or friends. The child will feel that she doesn't belong, doesn't fit in. In addition, Hura children feel that they are disgusting as though they have leprosy and are, therefore, outcasts. Some Hura children will compensate for the feeling of being despised by showing contempt for others. The child will often have a skin disorder, such as eczema, or joint problems such as juvenile rheumatoid arthritis.

Lac humanum - Lac humanum is a remedy made from human breast milk. The child who needs it will feel completely alone, as if nobody is there for them. This is the experience of many adopted children who never receive bonding from the birthmother and who were never breastfed. The child feels a sense of isolation, even a sense of not inhabiting her own body. Others easily take advantage of her because she tends to their needs before her own.

Magnesium carbonicum - J. T. Kent wrote in his Lectures on Homeopathic Materia Medica: “I once had in charge an orphanage, where we had sixty to one hundred babies on hand all the time. The puzzle of my life was to find remedies for the cases that were going into marasmus (wasting away). A large number of them were clandestine babies. It was sort of Sheltering Arms for these little ones. The whole year elapsed, and we were losing babies every week from this gradual decline, until I saw the image of these babies in Magnesia carbonicum and after that many of them were cured.” Because of Kent's work, this is usually the first remedy thought of for adoptive children, or orphans.

Magnesium muriaticum - The Magnesium muriaticum child is a peacemaker. It's a good remedy for children whose parents are arguing or divorcing, or whose family members are engaged in conflict. The Magnesium muriaticum child wants everyone to be happy and harmonious. An adopted child who needs Magnesium muriaticum will be frightened whenever her parents argue, fearing that they will break-up and she will be abandoned, just as her birthmother had abandoned her.

Natrum muriaticum - Like the Anacardium state, the Natrum muriaticum state can be caused by isolation and separation at birth. It is a well-known remedy for babies who have been taken from their mothers and placed in an incubator at birth. The Natrum muriaticum child is easily hurt and protects herself with emotional reserve. There is an inner grief due to being left alone without adequate nurturing. These children are so closed it's hard to get to know them. They say little and reveal nothing about what is really going on in their lives. They are easily offended, and remember any insult for a long time - sometimes forever.

Pulsatilla - The Pulsatilla state can be caused by rejection of the child by the mother, or separation from the mother at an early age. The child feels unloved and unwanted. In her struggle to get enough love, the child will be clingy, weepy and manipulative. She has an insatiable desire for attention and reassurance, often asking, “Do you love me?”

Saccharum officianale - A remedy for those who did not receive enough love, or nurturing, in their early life. The child will usually have an extreme craving for sweets and may have a sugar imbalance problem such as hypoglycemia. She may also have extreme thirst. The child will compensate for lack of nurturing with two types of behaviors: firstly, she may constantly seek closeness with the parents, especially the mother, always wanting cuddles and wanting to sleep in the parent's bed. And secondly, the child may have behavior problems such as kicking and hitting other children, sibling jealousy, defiant behavior, or hyperactivity. Some children will compensate for a lack of nurturing by refusing any form of affection. These children have the same desperate need for love, but will refuse contact with the parents.

Not every adopted child will need one of these remedies. We always recommend remedies based on the totality of the whole person, not just one factor such as adoption. Any troubled child, whether adopted or not, will benefit from professional homeopathic care. The homeopath may consider the wounds of adoption as a possible etiology, and will determine if any of these remedies fit the picture.

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Saturday, February 20, 2010

D3 amounts needed to achieve optimal levels.

Dosage of Vitamin D Needed To Achieve 35 to 40 ng/ml (90-100 nmol/L)

Historically, 400 IU (10 ug) of vitamin D was recommended for better health because it closely approximated the amount of vitamin D in a teaspoonful of cod liver oil. However, 800 to 1,000 IU is the dose that may have a better chance of giving a patient a normal vitamin D level. In some countries, vitamin D is listed in micrograms, and the relationship is as follows:

2.5 mcg (micrograms) = 100 IU.
5 mcg = 200 IU.
10 mcg = 400 IU.
15 mcg = 600 IU.
20 mcg = 800 IU.
It is much easier to access the patient’s need after a vitamin D blood test. Few individuals would allow their clinician to simply guess an individual’s cholesterol level before placing him/her on some type of medication. Clinicians have access to an accurate lipid test that provides guidance. The same is true for vitamin D levels. Clinicians should not suggest high intakes of vitamin D (5,000 IU for example) before recommending the 25-OH vitamin D test.

Health care professionals need to keep in mind that in general, 100 IU (2.5 mcg) of vitamin D per day can raise the vitamin D blood test only 1 ng/ml or just 2.5 nmol/L after 2 to 3 months. How much vitamin D is needed per day to obtain a normal vitamin D blood level? The following examples include:

100 IU (2.5 mcg) per day increases vitamin D blood levels 1 ng/ml (2.5 nmol/L).
200 IU (5 mcg) per day increases vitamin D blood levels 2 ng/ml (5 nmol/L).
400 IU (10 mcg) per day increases vitamin D blood levels 4 ng/ml (10 nmol/L).
500 IU (12.5 mcg) per day increases vitamin D blood levels 5 ng/ml (12.5 nmol/L).
800 IU (20 mcg) per day increases vitamin D blood levels 8 ng/ml (20 nmol/L).
1000 IU (25 mcg) per day increases vitamin D blood levels 10 ng/ml (25 nmol/L).
2000 IU (50 mcg) per day increases vitamin D blood levels 20 ng/ml (50 nmol/L).
If the vitamin D blood test was 30 ng/ml (75 nmol/L) and a 40 ng/ml (100 nmol/L) level was desired, 1,000 IU (25 mcg) of vitamin D per day over several months should be taken to achieve a normal blood level or 40 ng/ml (100 nmol/L). Upon reaching the goal, most individuals need to supplement with 800 to 1,000 IU per day to maintain this level. Only working closely with a clinician over time can provide the most accurate answer. However, issues of insurance and health care access suggest that 800 to 1,000 IU is ample for many individuals who are not able to have their blood tested.

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Wednesday, February 4, 2009

Natural Approaches to ADHD

Nutritional Breakthroughs for ADHD by Angela Stengler, ND Could food allergies be causing your child's ADHD? After a child has been diagnosed with attention deficit disorder, many parents come to me with questions and concerns regarding their child's diagnosis and possible treatments. No one is really sure what causes hyperactivy in children, although there are plenty of culprits people point to--sugar sensitivities, environmental toxins, food allergies--but no one thing has been identified as the specific cause. Unfortunately, when a diagnosis is made, quite often the only solution provided to parents is a prescription for stimulants like Ritalin. However, drugs are not your only choice and there are natural therapies available to you that can safely and effectively treat ADHD in your child--and without any of the negative side effects caused by some drug therapies. I have outlined several below. Read them, and then consult with your pediatrician or naturopath to see which treatment would be best suited for your child. POSSIBLE CAUSES OF ADHD Food additives Over 5,000 food additives are present in the food supply, and according to Benjamin Feingold, MD, 40 to 50 percent of all hyperactive children have some sort of sensitivity to the artificial colorings, flavorings and preservatives used in many processed foods. Feingold bases his claims on 1,200 cases of learning and behavior disorders observed in childern that were linked directly to food additives. This seems to suggest that there is a direct correlation between diets high in processed foods and hyperactivity in children. How Villainous is Sugar? For some kids, sugar is a major factor in mood, behavior and attention patterns. It has been demonstrated that destructive, aggressive and restless behavior correlates directly with the amount of sugar consumed on a daily basis. Once again, diet is both the problem and the solution. Food Allergies/Sensitivities The most common food sensitivities in children are to the following foods: •sugar •cow's milk •wheat •chocolate •soy •citrus fruit •corn •peanuts Double-blind studies have shown that when children with ADHD follow a hypoallergenic diet, substantial improvement in their symptoms are demonstrated. It should be noted that food sensitivities and food allergies are not the same thing. Food allergies are present when a child exhibits severe reactions to allergens--like peanuts or albumen from eggs--present in foods. Symptoms can include, shortness of breath, breaking out in hives, vomiting or anaphylaxis, a life-threatening condition which is characterized by the swelling of the throat and tongue. Food sensitivities are exhibited when a child is given food--like dairy products in the lactose intolerant child--which he is unable to digest properly. Commonly, he will experience indigestion, gas or irritable bowels as a result of eating these foods. If you suspect a food allergy in your child, make an appointment to get him tested. Dietary Steps You Can Take 1. Add more whole foods to the diet (whole grains, legumes, vegetables, fish) while eliminating (or at least decreasing) processed foods that contain white flour, processed sugars and hydrogenated oils (i.e, chips, cookies and sodas). 2. It goes without saying that you should make it your business to read the ingredient labels on all food products you buy for your children. Many parents don't realize that much of the pre-packaged food--including supermarket multi-vitamins and the so-called "fruit" drinks--they give to their children is loaded with artificial sweeteners, preservatives, dyes and other harmful additives that could be triggering specific behavioral and health problems in their children. If the chemical ingredients outnumber organic ingredients--or if they are the first few ingredients listed--on a food label, you may want to consider buying something else. Check labels on milk, meat and eggs too because many farmers feed hormones and antibiotics to their livestock. 3. Shop for organic fruits, vegetables and meats. These are foods that have been grown according to specific agricultural practices (typcially without using chemical pesticides or fertilizers). Hit the health food store for whole grain breads and healthy snacks to give to your kids in place of the processed ones they've been eating. Not only do these foods taste great, but they are much better for your kids overall health (many are lower in fats and sugars). 4. Natural sugars like those found in fruit and fruit juices, or natural sweeteners like honey, blackstrap molasses and rice bran syrup, should replace all processed sugars in your child's diet (this includes raw or brown sugars). If your child drinks a lot of soda make the switch to 100 percent fruit juices and dilute them 50 percent with water. Instead of those sugary breakfast cerals, try feeding your kids oatmeal topped with honey and fresh fruit, or give them naturally sweetened granola or muesli. They'll have more energy between breakfast and lunch, and their teachers will love you for it. 5. Eliminate all the foods listed under Food Allergies/Sensitivies from your child's diet for four weeks and see if their behavior improves. Wheat alternatives, such as oat, kamut and spelt, are available at most health food stores as are milk alternatives like calcium-enriched rice or oat milk. Both taste great and come in flavors like chocolate and vanilla. Yogurt made from goat's milk should be substituted for products made from cow's milk (the same is true for cheeses, too). Other Potential Factors Could food allergies be causing your child's ADHD? NUTRITIONAL DEFICIENCIES & ADHD Nutritional deficiencies are a widespread cause of learning and behavior problems in children. Studies have shown increased intelligence in children who added multivitamin supplements to their daily diets. Thiamin, niacin, vitamins B6 and B12, copper, iodine, iron, magnesium, manganese, potassium and zinc are nutrients that play a vital role in proper brain and nervous system function. Many ADHD children can benefit from an extra 500 to 1,000 milligrams of calcium and magnesium in their diet. Food sources are the best means for incorporating these important nutrients into your child's diet (especially as laid out in the previous dietary steps), but if your child can't drink milk or doesn't like to eat his green leafy veggies, vitamin supplements are the next best answer. American Kids Iron Deficient Surprisingly, the most common nutrient deficiency in American children is iron deficiency (again, a direct result of a nutrionally deficient diet). Studies have linked iron deficiency with decreased attentiveness, a narrow attention span and decreased voluntary activity. These symptoms are usually reversed after supplementation. A severe deficiency in iron can lead to anemia, which in turn can lead to listlessness, tiredness and low energy levels in children--symptoms which make it difficult for children to pay attention in school. If you suspect that your child is anemic have him tested by your physician. Always have your child tested for iron deficiency before administering iron supplements. Legumes, green leafy vegetables, blackstrap molasses and lean red meats are the best sources for iron. Look for liquid iron supplements, which are easier for kids to take, and are less likely to cause constipation or stomach upset--two of the occasional side effects of iron supplementation in children. What Are Smart Fats? Current research shows a link between learning and behavioral difficulties and deficiencies in essential fatty acids (EFAs) like docosahexanoic acid (DHA), one of the most important essential fatty acids. EFAs are commonly referred to as Omega 3 and Omega 6 fats. Oils, like evening primrose oil, flaxseed oil and borage oil, are high in EFAs. DHA plays a pivotal role in brain and retina development in babies, and the richest sources of it are a mother's breast milk and fish oils. Researchers at Purdue University looked at the levels of essential fatty acids in children, especially DHA, and found that kids with ADHD tended to have significantly lower levels of essential fatty acids in their blood. Children with ADHD should be given vitamin supplements that contain a combination of essential fatty acids that includes DHA. Nursing your children for as long as possible, and--when they are older--getting them to eat deep water fish like salmon, halibut and tuna are ways to ensure they get enough essential fatty acids into their diet during the crucial developmental years (when the body is still growing and in need of quality nutrients). Phosphatidylserine Phosphatidylserine (known as PS) is a specific brain nutrient that can be supplemented to help promote proper brain and neurological function. It works to balance the cell-to-cell communication that occurs in the brain. I recommend giving PS by itself to children with ADHD or in combination with DHA or the herb ginkgo biloba (which has excellent research supporting its benefit on memory and concentration). PS appears to help improve concentration and have a calming effect on hyperactive kids. Most PS supplements are soy-based. Typical dosage for a 12-year-old would be 200 to 400 milligrams daily. Consult your naturopathic physician or nutritionist for specific dosage requirements for your child based on his age, size and weight. ENVIRONMENTAL TOXINS Heavy Metals Finally, numerous studies have found a strong relationship between childhood learning disabilities and body storage of heavy metals (lead, mercury, cadmium, copper and manganese). Heavy metals are stored in the bones and fatty tissues of the body, like the liver and the kidneys, and high levels in very young children can hinder proper development of the brain and central nervous system. Lead is the primary culprit of heavy metal toxicity in young children, especially among toddlers living in old houses where they eat the lead paint that chips off of walls and windowsills. A child who is suffering from mild lead or heavy metal poisoning may not exhibit any specific symptoms, so a hair analysis is the best screening test for heavy metal toxicity and mineral imbalances. What Can You Do? Adding calcium and magnesium supplements to your child's diet is one way to counter potential lead poisoning (in the body, lead competes with calcium. A child exposed to high levels of lead paint dust will absorb the lead and excrete the calicium). January 1999 Dr. Angela Stengler is a certified naturopathic physician based in Oceanside, California. Women's and children's health are the focus of the practice run by her and her husband, Dr. Mark Stengler. In addition to maintaining her medical practice, Dr. Stengler hosts a weekly radio show on natural medicine, and she is the author of several books on the benefits of alternative medicine, which you can find at her Web site, The Natural Physician.

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Thursday, January 15, 2009

Serotonin for ADHD

Serotonin May Be Better Target For ADHD Treatment Researchers at the Howard Hughes Medical Institute (HHMI) at Duke University have discovered that Ritalin and other stimulants exert their paradoxical calming effects by boosting serotonin levels in the brain. Elevating serotonin appears to restore the delicate balance between the brain chemicals dopamine and serotonin and calms hyperactivity, says HHMI investigator Marc Caron at Duke University Medical Center. Caron is an author of the study published in the January 15 issue of the journal Science. Attention deficit hyperactivity disorder (ADHD) affects three to six per cent of school-aged children. Symptoms include restlessness, impulsiveness, and difficulty concentrating. Stimulants commonly used to treat ADHD are so effective that "researchers haven't really taken the time to investigate how they work," says Caron. Previous dogma, says Caron, held that the calming action of Ritalin works through the neurotransmitter dopamine. Specifically, researchers believed that Ritalin and other stimulants interact with the dopamine transporter protein (DAT), a housekeeper of sorts for nerve pathways. After a nerve impulse moves from one neuron to another, DAT removes residual dopamine from the synaptic cleft-the space between two neurons-and repackages it for future use. Caron's team suspected that dopamine wasn't the only key to understanding ADHD, so they turned to mice in which they had "knocked out" the gene that codes for DAT. Since there is no DAT to "mop up" dopamine from the synaptic cleft, the brains of the mice are flooded with dopamine. The excess dopamine causes restlessness and hyperactivity, behaviors that are strikingly similar to those exhibited by children with ADHD. When placed in a maze that normal mice negotiate in less than three minutes, the knockout mice became distracted-performing extraneous activities such as sniffing and rearing - and they failed to finish in less than five minutes. The knockout mice also seemed unable to suppress inappropriate impulses - another hallmark of ADHD. Surprisingly, the knockout mice were still calmed by Ritalin, Dexedrine and other stimulants even though they lacked the protein target on which Ritalin and Dexedrine were thought to act. "That caused us to look for other systems that these stimulants might affect," says Caron. To test whether the stimulants interact with dopamine through another mechanism, the researchers administered Ritalin to the normal and knockout mice and monitored their brain levels of dopamine. Ritalin boosted dopamine levels in the normal mice, but it did not alter dopamine levels in knockout mice. That result implied that "Ritalin could not be acting on dopamine," says Caron. They then studied whether the stimulants altered levels of the neurotransmitter serotonin. The scientists administered Prozac - a well-known inhibitor of serotonin reuptake - to the knockout mice. After ingesting Prozac, the knockout mice showed dramatic declines in hyperactivity. "This suggests that rather than acting directly on dopamine, the stimulants create a calming effect by increase serotonin levels," Caron says. "Our experiments imply that proper balance between dopamine and serotonin are key," says Raul Gainetdinov, a member of Caron's research team. "Hyperactivity may develop when the relationship between dopamine and serotonin is thrown off balance." The brain has 15 types of receptors that bind to serotonin, and Gainetdinov is now trying to determine which specific serotonin receptors mediate the effects of Ritalin. The hope, says Caron, "is that we can replace Ritalin with a very specific compound that targets a single subset of receptors." While Prozac calmed hyperactivity in the knockout mice, Gainetdinov says that "Prozac isn't the best, because it isn't very selective." Caron and Gainetdinov are optimistic that a new generation of compounds that interact more specifically with the serotonin system will prove to be safer and more effective for treatments for ADHD.

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Serotonin's effects on multiple body systems

One Dangerous Deficiency Links IBS, Migraines, and More Health News By VRP Staff When you think of serotonin deficiency, the first consequence that might spring to mind is depression. And if so, you’d be right. But there’s more to this neurotransmitter than meets the eye—a lot more. Migraines, irritable bowel syndrome, fibromyalgia, obesity, even asthma… believe it or not, all of these serious conditions can be traced back to depleted serotonin levels. And the effects on your body can be as damaging as they are diverse. Serotonin is one of your brain’s most crucial messengers. It’s released by your neurons to send signals to other neurons, after which it’s returned to its original parent neuron to be reused. But if your levels are low, serotonin’s time on your synapse is cut short. It’s recaptured before it can finish its job—at a very high cost to your health, mentally and physically. In addition to depression, low levels of serotonin–and its precursor tryptophan–have been linked to binge eating, carbohydrate cravings, and weight gain.1 Studies show that obese and overweight diabetic patients have levels that are well below normal–and in clinical trials, increased brain serotonin led to both reduced caloric intake and resulting weight loss.2–4 But it’s not just your waistline that benefits from this critical neurotransmitter. Studies have shown that increasing serotonin levels can fight insomnia by improving sleep continuity.5 Research also shows that increased serotonin relieves migraines as effectively as standard drug therapy and aids in relief of chronic tension headaches.6–7 This same ability has made it a unique target in the treatment of fibromyalgia, with serotonin deficiency implicated for lower pain thresholds and higher clinical measures of perceived pain in patients.8–10 In an even more surprising connection, serotonin has also been identified as a major player in gut motility.11–12 Special serotonin–releasing cells can be found throughout your digestive system, responsible for stimulating peristaltic motion and pushing waste through your digestive tract.13 Even the development and severity of asthma has been linked to depression, anxiety, and low–serotonin related disorders—revealing yet another function under this neurotransmitter’s powerful influence.14 Proper levels of serotonin are essential for your health—and one way to ensure higher levels of this neurotransmitter is by boosting your intake of tryptophan, an essential amino acid found in high–protein foods that is responsible for serotonin synthesis in your brain. Research has shown that supplementing with tryptophan (and its metabolite 5–hydroxytryptophan, or 5–HTP) can replenish serotonin naturally and effectively—easing depression, anxiety, migraines, insomnia, and fibromyalgia symptoms in several clinical studies.15–17 References: 1. Gendall KA, Joyce PR. Meal–induced changes in tryptophan:LNAA ratio: effects on craving and binge eating. Eat Behav. 2000 Sep;1(1):53–62. 2. Breum L, Rasmussen MH, Hilsted J, Fernstrom JD. Twenty–four–hour plasma tryptophan concentrations and ratios are below normal in obese subjects and are not normalized by substantial weight reduction. Am J Clin Nutr. 2003 May;77(5):1112–1118. 3. Ceci F, Cangiano C, Cairella M, et al. The effects of oral 5–hydroxytryptophan administration on feeding behavior in obese adult female subjects. J Neural Transm 1989;76(2):109–117. 4. Cangiano C, Ceci F, Cascino A, et al. Eating behavior and adherence to dietary prescriptions in obese adult subjects treated with 5–hydroxytryptophan. Am J Clin Nutr 1992 Nov;56(5):863–867. 5. Riemann D, Vorderholzer U. Treatment of depression and sleep disorders. Significance of serotonin and L–tryptophan in pathophysiology and therapy. Fortschr Med. 1998 Nov;116(32):40–42. 6. Titus F, Dávalos A, Alom J, Codina A. 5–Hydroxytryptophan versus methysergide in the prophylaxis of migraine. Randomized clinical trial. Eur Neurol. 1986;25(5):327–329. 7. Ribeiro CA. L–5–Hydroxytryptophan in the prophylaxis of chronic tension–type headache: a double–blind, randomized, placebo–controlled study. For the Portuguese Head Society. Headache. 2000 Jun;40(6):451–456. 8. Birdsall TC. 5–Hydroxytryptophan: a clinically–effective serotonin precursor. Altern Med Rev. 1998 Aug;3(4):271–280. 9. Hrycaj P, Stratz T, Muller W. Platelet 3Himipramine uptake receptor density and serum serotonin levels in patients with fibromyalgia/fibrositis syndrome. J Rheumatol. 1993;20:1986–1988. [letter] 10. Russell IJ, Michalek JE, Vipraio GA, et al. Platelet 3H–imipramine uptake receptor density and serum serotonin levels in patients with fibromyalgia/fibrositis syndrome. J Rheumatol 1992;19:104–109. 11. Fayyaz M, Lackner JM. Serotonin receptor modulators in the treatment of irritable bowel syndrome. Ther Clin Risk Manag. 2008 Feb;4(1):41–48. 12. Gershon MD. The enteric nervous system: a second brain. Hosp Pract (Minneap). 1999 Jul 15;34(7):31–32,35–38,41–42. 13. Grider JR. Desensitization of the peristaltic reflex induced by mucosal stimulation with the selective 5–HT4 agonist tegaserod. Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G319–G327. 14. Goodwin RD, Sourander A, Duarte CS, et al. Do mental health problems in childhood predict chronic physical conditions among males in early adulthood? Evidence from a community–based prospective study. Psychol Med. 2008 May 28:1–11. 15. Poldinger W, Calanchini B, Schwarz W. A functional approach to depression: serotonin deficiency as a target syndrome in a comparison of 5–hydroxytryptophan and fluvoxamine. Psychopathology. 1991;24:53–81. 16. Kahn RS, Westenberg HG. L–5–hydroxytryptophan in the treatment of anxiety disorders. J Affect Disord. 1985 Mar–Apr;8(2):197–200. 17. Puttini PS, Caruso I. Primary fibromyalgia and 5–hydroxy–L–tryptophan: a 90 day open study. J Int Med Res. 1992;20:182–189.

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Tuesday, December 30, 2008

EFAs and ADHD

Behavioural disorders, impulsivity and violent behaviour Attention deficit hyperactivity disorder (ADHD) is characterised by inattentive, impulsive and hyperactive behaviour occurring in children but some aspects of the condition may persist into adulthood (Richardson and Puri 2000, Richardson and Ross 2000, Arnold 2001). ADHD is a significant and increasing problem. It is estimated that it affects about 2% of school-aged children in the UK and 4% of school-aged children in the USA (Richardson and Puri 2000) and the use of medication to treat ADHD has increased dramatically in the last 10 years. Results of one study suggest that fish consumption may be associated with violent and impulsive behaviour (Hibbeln 2001). This cross-national survey of seafood consumption in 26 countries found that those with higher rates of seafood consumption tended to have lower rates of mortality due to homicide. The authors point out, however, there were many potentially confounding factors in this study and the hypothesis that fish consumption may help to reduce impulsive and violent behaviour should be tested in double-blind, placebo-controlled trials. Boys aged 6-12 years with ADHD were found to have significantly lower plasma levels of AA, EPA and DHA compared to normal controls (Stevens, Zentall, Deck et al 1995). In a further study of boys of the same age, significantly greater scores indicating behaviour problems, temper tantrums and sleep problems were reported in subjects with lower plasma total n-3 fatty acid concentrations (Stevens, Zentall, Abate et al 1995). However, a double-blind placebo controlled trial of DHA supplementation (345 mg/day for 4 months) in children with ADHD found that DHA treatment did not decrease ADHD symptoms compared with placebo (Voigt, Llorente, Jensen et al 2001). The authors pointed out however, that lack of response to DHA supplementation did not necessarily mean that a low brain content of DHA is not involved in the aetiology of ADHD. It is possible that in the population studied, a benefit of DHA was not produced because other essential nutrients were also lacking. It was suggested in recent reviews that ADHD may be linked to some other behavioural and neurological disorders, namely dyslexia, dyspraxia and autism, by an involvement of fatty acid metabolism (Richardson and Ross 2000; Bell, Sargent, Tocher et al 2000) and some studies of violent, impulsive and antisocial behaviour have also made this connection. Such behaviour has been linked to tissue deficiencies of n-3 fatty acids (Corrigan, Gray, Strathdee et al 1994; Stevens, Zentall , Deck et al 1995; Stevens, Zentall, Abate et al 1995; Hibbeln, Umhau, Linnoila et al 1998; Burgess, Stevens, Zhang et al 2000) and other nutrients including vitamins and minerals (Schoenthaler, Amos, Doraz et al 1997, Walsh, Isaacson, Rehman et al 1997). Virkkunen, Horrobin, Jenkins et al (1986) found that in a group of violent and impulsive offenders, plasma DHA was significantly lower than controls while n6 fatty acids were significantly elevated. In a double-blind, placebo-controlled trial on young adult male prisoners, dietary supplementation with vitamins and minerals, as well as fish oil (80 mg per day EPA and 44 mg per day DHA) and evening primrose oil, resulted in 26% fewer disciplinary offences in the supplemented group compared to placebo and 35% fewer disciplinary offences in the supplemented group compared to the baseline frequency (Gesch, Hammond, Hampson et al 2002). A recent double-blind placebo-controlled trial investigated the effects of dietary supplementation for 12 weeks with tuna oil (186 mg per day EPA, 480 mg per day DHA) and evening primrose oil in children with specific learning difficulties such as dyslexia (Richardson and Puri 2002). It was found that supplementation produced significant benefits. It has also been suggested that DHA in particular might be useful in treatment of dyslexia and dyspraxia as well as ADHD (Stordy 1995, 1997, 2000). Dyspraxia is a condition involving reduced motor skills manifesting as excessive clumsiness and there is a close link between dyspraxia and dyslexia (Stordy 1997). Stordy (1995) reported that, in a preliminary study, supplementation for one month with 480 mg per day DHA significantly improved an aspect of vision called dark adaptation in five dyslexic children. In a later open study of 15 children with dyspraxia, supplementation with the same dose of tuna oil and evening primrose oil as used in the study by Richardson and Puri (2002), produced significant improvements in scores for manual dexterity, ball skills and static and dynamic balance. The studies described above, of impulsive and violent behaviour amongst prisoners and its possible association with PUFA status (Virkkunen, Horrobin, Jenkins et al 1986, Gesch, Hammond, Hampson et al 2002) may be compared to a series of studies of aggression in Japanese students. Hamazaki, Sawazaki, Itomura et al (1996) conducted a double-blind, placebo-controlled trial of fish oil supplementation (1.5-1.8 g DHA per day) and after three months of treatment, aggression scores were significantly lower in the DHA group compared to placebo. However, the reason for the difference was that aggression scores in the placebo group had increased while those in the DHA group did not change significantly. The difference was accounted for by the fact that the final assessment in the trial occurred just before academic examinations, which it was suggested had caused psychological stress. A similar trial was conducted on different students who did not face such stress and no significant change in hostility was recorded in the DHA or placebo group (Hamazaki, Sawazaki, Nagao et al 1998). The authors concluded that DHA administration could help to control aggression only at times of psychological stress (Hamazaki, Sawazaki, Itomura et al 2001). Hibbeln, Umhau, George et al (1997) pointed out that an apparent prevention of increased aggression is surprising because baseline intake of n-3 PUFA in the study population was relatively high. In a third double-blind, placebo- controlled trial on students. Plasma catecholamines were measured during a two-month period of continuous psychological stress due to university examinations (Sawazaki, Hamazaki, Yazawa et al 1999). In the DHA group, who took 1.5g DHA per day during the examination period, noradrenaline levels were significantly reduced. The authors interpreted this change as indicating that subjects in the DHA group adapted to stress more favourably than controls and that DHA may help to reduce the risk of stress-related diseases in individuals under long-lasting psychological stress (Hamazaki, Sawazaki, Nagasawa et al 1999, Hamazaki, Itomura, Sawazaki et al 2000). In another study by the same group, Thai subjects aged 50-60 years, from a university and surrounding villages, were studied in a double-blind placebo-controlled trial in which the treatment was the same DHA supplement as used in the previous trials (Hamazaki, Thienprasert, Kheovichai et al 2002). DHA administration reduced aggression scores amongst university employees but not amongst village-dwellers. The authors speculated that the difference was caused by a larger placebo effect amongst villagers or a lower sensitivity amongst villagers to the psychological stressor (a video of stressful events) used in the study. Conclusion The epidemiological evidence that DHA-deficiency is a cause of violent and impulsive behaviour is supportive but not conclusive. Also, the few available studies of plasma fatty acids demonstrate lower DHA levels in individuals with ADHD. Data from supplementation studies are inconsistent but there are sufficient positive results to strengthen the view that DHA deficiency may be associated with adverse behavioural consequences.

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Thursday, December 4, 2008

Pine Bark and ADHD

Pine Bark Extract Helps Calm ADHD in Jack but Not Jill By Neil Osterweil, Senior Associate Editor, MedPage Today Published: June 16, 2006 Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine. BRATISLAVA, Slovakia, June 16 — Pine bark extract, a substance known as Pycnogenol, seems to calm boys with attention-deficit hyperactivity disorder (ADHD), according to researchers here. Girls were not helped.Action Points -------------------------------------------------------------------------------- Explain to interested parents and children that this study appears to show that Pycnogenol, a standardized extract of pine bark, is effective at treating some symptoms of ADHD. Caution that this was a small, short duration study and was not sufficiently powered to detect a possible effect of gender. In addition some of the improvements noted did not reach statistical significance. The boys with ADHD given Pycnogenol, from the bark of the French maritime pine, had modest but significant reductions of hyperactivity and inattention, according to Jana Trebaticka, M.D., and colleagues, of the Child University Hospital at Comenius University, and the University of Münster in Germany. "These findings are especially notable for parents who are concerned about overmedicating children diagnosed with ADHD," said Peter Rohdewald of Münster, a co-author. "Many families are seeking natural options to avoid the potentially dangerous side effects of prescription drugs," he added. Unlike Ritalin (methylphenidate), the mechanism of action of Pycnogenol in ADHD is unclear, but it may involve alteration of the response to the catecholamines dopamine and norepinephrine, the authors wrote in the June 17 issue of European Child & Adolescent Psychiatry. In open-label studies and case reports, the extract has been reported to improve symptoms of ADHD, the authors said, prompting them to start a randomized, double-blind, placebo-controlled trial. The study was funded by Horphag Research Limited, UK, the maker or Pycnogenol. The investigators enrolled 61 children (50 boys and 11 girls), mean age 9.5 years (range six to 14) with diagnoses of ADHD. The children were randomized on a 2.5:1 ratio to either placebo or Pycnogenol at 1 mg/kg/day orally for four weeks. At baseline, after one month of treatment and at two months of follow-up the children were tested for ADHD symptoms with standard questionnaires, including the Child Attention Problems (teacher-rated) instrument, Conner's Teacher and Parent Rating scales, and a modified Wechsler Intelligence Scale. Analysis was by intention-to-treat. The investigators found that in the boys but not girls who received four weeks of therapy with the active drug. there were significant improvements over baseline and compared with placebo for teacher ratings on hyperactivity (P=0.008 over baseline) and inattention (P=0.00014 over baseline). At one month after the end of the trial, the apparent drug benefit had disappeared and ADHD symptom scores returned to baseline levels. On the Conner Teacher Rating Scale teachers noted following one month of treatment with Pycnogenol reduction of inattention which was not statistically significant (P=0.07) compared with start and marginally significant compared with placebo (P=0.049). "Hyperactivity was also lower compared with the start as well as with placebo following Pycnogenol treatment; however, the decrease failed to reach significance (P=0.45 and P=0.28)," they wrote. Parental ratings of inattention not differ significantly from baseline to study end, however, the authors noted. "Following one month of treatment with Pycnogenol, the lower score for hyperactivity compared to placebo was not stastiscally significant (P=0.065)," they wrote. "The tests for visual-motoric coordination and concentration-Weight scores-were also different for placebo and Pycnogenol group at start." No serious side effects were reported, although observers noted "a rise in slowness" in one patient, and moderate gastric discomfort in another. There were no changes over baseline in either the Pycnogenol or placebo groups in basic biochemical parameters such as bilirubin, glucose, liver enzymes, uric acid, or lipids after one month. "Our results point to an option to use Pycnogenol as a natural supplement to relieve ADHD symptoms of children," the authors wrote. Because there were only six girls in the Pycnogenol group and five in the placebo group, the study was insufficiently powered to detect a possible effect of gender, the authors acknowledged. They also pointed out that their data are limited by the small number of participants and the by the short duration of the study. Primary source: European Child & Adolescent Psychiatry Source reference: Trebaticka J et al. "Treatment of ADHD with French maritime pine bark extract, Pycnogenol"Eur Child Adolesc Psychiatry DOI 10.1007/s00787-006-0538-3 Additional ADHD/ADD Coverage Find this article at: http://www.medpagetoday.com/Psychiatry/ADHD-ADD/3563

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Friday, November 14, 2008

Non-medical solutions for ADHD

http://www.wisechoiceeducationalservices.com/articles/article10.html By Suzanne Day Parents of children with learning or attention problems will often react negatively to the use of medications, which are recommended by the medical profession. However, what parents really need and want is guidance in their search for solutions. This article attempts only to guide parents to a better understanding of the different aspects of the biochemical components of learning difficulties and attention behavioural problems. I do not pretend to be an expert in the nutrition but an expert on the brain, which is fuelled by nutrition. Parents and professionals dealing with attention deficits in children observe the food-mood connection, which is more evident in some children than others. Behaviours are based on thoughts and memories processed in the brain. The neurons (brain cells) transmit information as electrical signals with the use of neurotransmitters. These transmissions constitute the biochemical basis for changes in behaviours. The brain, one of the most vital organs of the body, receives its nutrition directly from the blood stream. Therefore, balanced nutrients will enhance the biochemical and electrical functions of the brain, which in turn affect learning. Imbalance of nutrients, especially through a diet of junk food, snack and fast food, will have an adverse effect, aggravating or intensifing learning and behavioural problems. The efficient functioning of the brain requires at least the essential amino acids, essential fatty acids, essential monosaccharides (glyconutirents), vitamins, minerals, and water. Essential Amino Acids Proteins provide the needed amino acids to build healthy nerve cells. These nerve cells then provide new connections to increase retrieval (memory). Most children with learning and attention difficulties need to consume more proteins, rather than starch and sugar. However, Dr. Amen in his book Healing ADD, has found that children with obsessive-compulsive behaviours require a balanced diet of protein and starch. He also explains that these children may also benefit from additional specific amino acids which are precursors of the neurotransmitters that help with the neurotransmission of the electric influx into the brain. For example, tyrosine is a building block for dopamine (control of movements, pleasure centers, and motivation). Tyrosine is a non-essential amino acid which is abundant in brown rice, leafy vegetables, and milk. Tyrosine is considered a “spark protein”. This amino acid as a supplement is known as L-tyrosine, and should be taken on an empty stomach. Tryptophan and 5-HTP are essential amino acids and are building blocks for the neurotransmitter serotonin, which controls our emotions and our sleeping patterns. Tryptophan is considered a “sedative-protein”. Most vegetables and nuts contain tryptophan. GABA, still another essential neurotransmitter, is an anti-anxiety agent. GABA is formed in the body by glutamic acid that can be synthesized from other amino acids. Phenylalanine is an amino acid precursor of norepinephrine (arousal and attention) coming in the form of DLAP as a nutritional supplement. Proteins are essential because they contain the necessary amino acids to build healthy nerve cells. Whether supplemented or taken in the diet, amino acids must be present for children to be able to overcome with learning difficulties or those with behavioural issues. Essential Fatty Acids Dr. Michael Lyon has done extensive research to better understand some of the main nutritional root causes of attention difficulties. The essential fatty acids, omega-3 and omega-6, are required by every cell in the human body and especially in the brain which is 60% fat. These essential fatty acids seems to be greatly involved in the ability to stay focused and complete tasks. The most commonly available omega-3 fatty acids is known as alpha linolenic acid (ALA) and can be found in large quantity in flax seed oil. The omega-6 fatty acid is known as linoleic acid (LA) and can be found in pumkin , sunflower, or sesame seeds. We recommend that you use a coffee grinder and grind your seeds as you need them because they start loosing the value as soon as the seed is broken. Only if the right enzymes are present in the body, will these acids be converted to incorporate them in the brain and the immune system. However, too often the body is inefficient in converting them. The best sources of essential fatty acids are the fish oils: tuna, salmon, and cod. Hydrogenation and Trans-fatty Acids Dr Lyon as well as many other experts on this topic, warns about the use of hydrogenated fats and trans-fatty acids ( the margarine, shortening, and cooking oils) which contain almost no essential fatty acids. Hydrogenation, the most common way of drastically changing natural oils, heats oils at high temperatures. The heat alters the molecule structure, which in turn interferes with the biochemical processes, “clogging” our physiological systems, our brains included. Udo Erasmus explains that “the molecule has its “head on backwards.” Not only does the heated oil looses its nutrients, but a catalyst (heavy metals like aluminium) is added, leaving remnants in these oils that are eaten by people. Udo Erasmus concludes “The 60 grams (2 ounces) of margarine and shortening we consume each day contain more than twice as many “food additives” than are found in the other 2640 grams of food that men consume each day (1740grams by women).” “Leaky Gut” and Debris in the Blood Dr. Lyon states, "Optimal digestion, good nutrient absorption and a leak proof gut are essential for good health." Based on his experience, brain health and gut health are vitally linked. In his book, Is Your Child's Brain Starving, he explains that most children with attention deficit and hyperactivity present a “leaky gut”. As well, they lack friendly bacteria in the gut, and have different types of intestinal parasites. Let’s explain briefly the term “leaky gut”. Normally the lining of the small intestine protects us from undigested food getting into the blood stream. Unfortunately, due to different factors including the excessive consumption of starchy or sugary foods, which ADD children crave, the tight junctions between cells of the intestinal lining detach and gaps form between the cells. This leaky gut allows molecular debris to circulate throughout the entire body, interfering with organ functions. The brain is one of our vital organs and these irritants adversely affect it. Milk and its Molecule Modification One of the most common types of molecular debris is milk protein. Milk has always been recognized as an essential nutrient for building healthy bodies. However, new research has shown that milk can create allergies and seems to be the cause of many ear infections. What is happening? The problem is not the milk, but what happens when milk is homogenized and radiated. Homogenizing milk breaks down the fat molecules into minute particles, which can cross the gut barrier and be absorbed into the blood stream. This causes many problems including allergic reactions and ear infections. These “foreign” protein molecules weaken the immune system because the body recognizes the milk protein as an enemy. Organs, like the brain, are often attacked. Although, soya milk is often used to replace cows’ milk, it appears to be difficult to digest for some children, who lack the necessary enzymes. See the article “Why you should avoid Soy”, by Sally Fallon (www.mercola.com/article/soy/avoid_soy.) Healing the “Leaky Gut” Research has confirmed what Dr. Lyon found with ADD: behaviour problems, including attention problems, autism, and schizophrenia, are often linked to intestinal problems. Elaine Gottschall has brought relief to thousands with her research and her diet. In her book, Breaking the Vicious Cycle, she explains the importance of a healthy intestinal tract. According to her, inefficiency in digesting double sugars, disaccharides like table sugar and polysaccharides, leads to mal-absorption and inflammatory bowel disease. Her diet, the ‘Specific Carbohydrate Diet’, is based on a monosaccharide diet (one molecule of sugar) like glucose. Interestingly, neurobiologists have discovered that more than 90% of all the serotonin (a neurotransmitter) made and then stored, is in the gut. The lack of serotonin is blamed for depression, anxiety, and insomnia. Poor digestion, absorption and elimination may lead to mental, emotional and physical sickness. White Sugar and Hypoglycemia In my work with children with learning and attention problems, I regularly witness the fact that these children often crave sugar and starch (starch becomes sugar after it is metabolized.) Parents and educators often observe, that these children are hyperactive for a short period and then a few hours later, they become lethargic. A high sugar food made with white sugar like a chocolate bar, a soda pop, or candies, stimulate the pancreas to secrete insulin which triggers cells throughout the body to pull the excess glucose out of the bloodstream and store it for later use. Soon, the glucose available to the brain has dropped. Neurons, unable to store glucose, experience an energy crisis. The ability to focus and think suffers. This glucose deficiency is called hypoglycemia, and it can even lead to unconsciousness. The Very “Bad” Sugar: Aspartame Much research has been done on Aspartame, an artificial sweetener, used in such brands as Equal and Nutrasweet. It is about 200 times sweeter than the refined sugar. Dr. Mercola reports that “Aspartame complaints represent 80-85% of food complaints registered with the FDA. In 1991, the National Institutes of Health listed 167 symptoms and reasons to avoid the use of aspartame, but today it remains a multi-million dollar business. Known to erode intelligence and affect short-term memory, the components of this toxic sweetener may lead to a wide variety of ailments…” (the list is included in his article from his web site). He recommends an helpful documentary on this subject Sweet Misery: A Poisoned World. The “Good Sugars”: the Glyconutrients A team from the University of Arkansas, directed by Dr. Dykman has conducted special studies evaluating the effects of different types of sugars (glyconutrients) upon brain function. The term glyconutrient refers to sugars that are absolutely essential for proper cellular survival and function, especially for the immune system cells. Most people know about glucose (from sucrose or white sugar) and galactose (from milk). However, little is known about the other six essential sugars, which are not readily available through a regular diet and need to be metabolized. Abundant research studies have identified the eight essential sugars (monosaccharides) needed for cells to communicate. This fact is noted in the latest Harper Biochemistry Dictionary, a medical desk reference. Dr. Dykman‘s study, found that certain single-cell sugars or monosaccharides enhanced brainwave frequencies associated with attention and alertness, increased reaction time, and concentration. Studies clearly show the important benefits children receive from ingesting these eight essential sugars as a nutritional supplement. “Breakfast Eaters” have Better Attention Span than “Breakfast Skippers” There are many components in a child’s diet, which will have a direct affect on brain function, behaviour and academic performance. William Sears, M.D. and Lynda Thompson, PhD in their A.D.D. Book, consecrated one chapter to the subject of feeding a child's brain. According to them, "it is not only the type of food but when and how you eat it that affects brain function." Their studies show that breakfast eaters, especially those that eat a breakfast rich in protein and calcium, generally have higher grades. Breakfast skippers, on the other hand, are more likely to be sluggish and overeat throughout the rest of the day. This is observed in the change of the brain waves patterns of children training with neurofeedback at our office. We frequently observe an increase in the theta wave (the slow waves (corresponding to a tune-out mental set) after a child has eaten sugary cereals or worst after eating pancakes with maple syrup for breakfast! Neurofeedback uses a quantitative electroencephalogram (QEEG) (see article on neurofeedback training for attention span). Obviously, if a child has an increase in slow brain waves, he/she will be sluggish at school and this will have an adverse impact on behaviour and grades. The Need of Supplements in our Diet It is well recognized even by the American Medical Association that we now need to add to our diets vitamin and mineral supplements because of our depleted soils. Adding to the pesticides and other chemicals polluting added to our food chain, fruits and vegetables are lacking the essential nutrients, called “phytonutrients” because they are often picked before they ripen. These “phytonutrients” strengthen our immune systems and work like enzymes aiding digestion and absorption. Supplementing the diet with enzymes will often help people with learning and attention difficulties because the lack of digestion and absorption is often one of their physiological weaknesses. Heavy Metals and Brain Function Unfortunately, heavy metals like mercury, lead, and aluminum found in our drinking water, water pipes, some vaccines, some junk food, and the air we breathe (are just some of the source of heavy metals ingestion) interfere with the absorption of necessary minerals, like zinc. Research has shown that high intercellular copper levels and low zinc levels cause many children to be hyperactive. Antioxidants are essentials in neutralizing free radicals oxidative stress (like rust produced on metal ) that heavy metals create. Chelation can be used to remove heavy metals from the body, preventing any interference in vitamin and mineral absorption and allowing the body to replenish the cells with the healthy metals. Water and the brain health Drinking several glasses of water per day is essential, but few do it. Dr. F. Batmanghelidj's book, Your Body's Many Cries for Water (you are not sick, you are thirsty) will motivate its readers to drink water. Here is an excerpt from his book: "The human body is composed of 25% solid matter and 75% water. Brain tissue is said to consist of 85% water. Every function of the body is monitored and pegged to the efficient flow of water. “Water distribution” is the only way of making sure that not only an adequate amount of water, but its transported elements (hormones, chemical messengers, and nutrients) first reach the more vital organs.” With the use of the QEEG , I have regularly observed children, gaining more control over their slow brain waves, after drinking a glass of water. Water is necessary for the body, but not all water is equal. Chlorine, which is present in city tap water, will prevent the absorption of tyrosine, an important amino acid. Our water can also be contaminated with heavy metals. City tap water needs to be purified. Osmosis water filtering systems and distilled water filtering systems are not the best filtration methods for long-term consumption. Water from these types of filtration systems not only remove essential minerals, but this water will leach the body of its minerals. It is also interesting to know that the osmosis water has a “low pH” which means that the water is acidic and may interfere with the alkaline state of the body. Efficient water filtration systems are available and are able to remove harmful substances and yet retain the important minerals. Therefore, before children start consuming more water to transport nutrients to the body organs, attention needs to be paid to the type of water these children are ingesting. Genetically Engineered Food Our children’s health in the form of undiagnosed food allergies or intolerance to food (such as celiac disease) may be linked to genetically engineered food It is since 1997 that we have had a wide variety of unlabelled genetically-engineered foods enter our supermarket shelves. Genetic engineering has to do with implanting conglomerations of genes from viruses, bacteria, insects, and animals onto our fruits, grains, nuts, and vegetables. Would it be possible that one explanation of these allergies to nuts, unheard few years ago, could be linked with the modified structure of the nuts? For example, in tests conducted at the University of Nebraska and reported in the New England Journal of Medicine, researchers found that soybeans modified with genes from Brazil nuts produced proteins that resulted in extreme, potentially deadly allergic reactions in people sensitive to the nuts. The human body is amazingly designed. Scientist consider that we have approximately 70 trillions of cells in our body. These cells continually multiply and die resulting in having a brand new body every seven or eight years. The health of the body depends on the health of the cells which produce energy. This article enumerate some facts about the reasons why our brain can be weakened. The good news is that if we limit the ingestion of the “bad stuff” and feed the body with the nutrients it needs to function efficiently, the body can regenerate itself. To summarize, children and adults with behavioural, learning and attention problems Firstly, they should AVOID (as much as possible): * JUNK FOOD, snack food, and fast food * the genetically modified organisms * trans-fatty acids (hydrogenated oil), * food containing pesticides (www.ewg.org) * white sugar (pop, cereal, candy…) * white flour (pasta, pizza…) * food dyes (especially the red and yellow ones) * Aspartame (sugar substitute in candy and gum) and MSG (flavor enhancer) * caffeine and chocolate * homogenized milk and be careful with soya milk which is often difficult to digest * preservatives * carbonated drinks Secondly, they NEED: * vitamins (fruits, vegetables, whole grains) * minerals * phytochemical supplements * proteins (amino acids) * essential fatty acids * glyconutrients, eight essential monosaccharides (sugars) * drink daily more purified water (one quart of water for every fifty pounds of weight.) * probiotics, which are the good bacteria needed in the intestines * get rid of toxins through exercise and antioxidants (Vitamin C is excellent) * get rid of parasites * sleep well The intention of this article is to not create more problems, but to summarize the main nutritional issues related to learning and attention behaviours in order better understand some of the physical root problems of learning and attention behaviours. Pursue your research, and pray for wisdom that you may glean what you need to help your children and yourselves. Make the changes step by step. Ask God for wisdom to know what you cannot change and wisdom to know what you can and need to do. A professional assessment of your child’s balance of nutrients in relation to his/her learning and attention inefficiencies may helpful. If you need help in assessing the learning and attention inefficiencies of your child I would love to help you. Do not hesitate to contact us if you have any further questions or needs. “Behold, the eye of the Lord is upon them that fear him, upon them that hope in his mercy: to deliver their soul from death, and to keep them alive in famine. Our soul waiteth for the Lord: he is our help and our shield.” Psalm 33: 18-19 Resources To know more about glyconutrients (the good sugars): (phone David: 705-726-5971 or www.mannapages.com/davidday (the Canadian one)) Books Is Your Child's Brain Starving? Michael R. Lyon, M.D. Healing the Hyper Active Brain, Michael R. Lyon, M.D. (www.functionalmedecine.ca) Your Body's Many Cries for Water, F.Batmanghelidj, M.D. (www.watercure.com) The ADD Book, by William Sears, M.D. and Lynda Thompson, Ph.D. Breaking the Vicious Cycle, by . Elaine Gottschall (www.breakingtheviciouscycle.info) and (www.pecanbread.com) Fat that Heal, Fats that Kill, Udo Erasmus Miracle Sugars, Rita Elkins, M.H. The Second Brain, Your gut has a mind of its own, Michael D. Gershon, M.D. Healing ADD, Daniel G. Amen, M.D. (www.amenclinic.com) How to Survive on a Toxic Planet, Dr. Steve Nugent The Safe Shopper’s Bible. By Dr. Samuel Epstein, MD & David Steinman Nutrition and Mental Illness, by Carl C. Pfeiffer,Ph.D,M.D. Web sites: Dr Joseph Mercola (www.mercola.com) (look for the article "Why you should avoid Soy" by Sally Fallon and for the DVD "Sweet Misery: A Poisoned World") Environmental Causes of Learning Disabilities (www.chem-tox.com/pregnancy/learning_disabilities.htm) The Truth about Soy (www.soyonlineservice.co.nz) To know more about glyconutrients (the good sugars): (phone David: 705-726-5971 or www.mannapages.com/davidday (the Canadian one)) Copyright 2005 Suzanne Day, Neuropsychologist member of l’Ordre des psychologues du Québec

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Sunday, June 15, 2008

Orthomolecular treatment of mental health

FOR IMMEDIATE RELEASE Orthomolecular Medicine News Service, October 7, 2005 Mental Health Treatment That Works (OMNS) Doctors report that mental health problems including depression, bipolar disorder, schizophrenia, ADHD, anti-social and learning disorders, and obsessive-compulsive disorders often have a common cause: insufficient nutrients in the brain. Nutritionally-oriented physicians assert that the cure for these problems is to give the body the extra nutrients it needs, especially when under abnormal stress. Orthomolecular medical researchers say the future of psychiatry is in nutrition because nutrition has such a long, safe and effective history of correcting many mental problems. Nutrients such as the B-vitamins are most successful when taken regularly, taken in relatively high doses, and taken in conjunction with vitamin C, the essential fatty acids (EFA’s), and the minerals magnesium and selenium. A summary of what has worked for many people follows below. The safety of vitamins and minerals is extraordinary, and the expense of trying them is much less than the cost of hazardous pharmaceutical drugs. These nutrients can be purchased in a discount or heath store. Taking 1,000 mg of vitamin B-3 three times a day often cures mild to moderate depression. Dramatic results are often achieved within one week of beginning this nutritional program, especially in alcoholics. (1) Sometimes a simple deficiency of vitamin D causes depression. 3,000 I.U./day from all sources can alleviate the problem. (2) 3,000 mg/day or more of niacin (vitamin B-3), along with the same quantity of vitamin C, taken in divided doses throughout the day can successfully treat both schizophrenia and bipolar disorder. (3) Vitamins B-3, B-6, C and the minerals magnesium and zinc frequently produce a good response in ADHD and autistic children. (4) Vitamins B-6, folate, and B-12 taken together lower elevated homocysteine levels in the elderly while improving mental function. (5) As pointed out by chemistry professor and vitamin discoverer Roger J. Williams, PhD (6), each individual has different nutritional needs and responds differently to nutrients. Are you tired of being depressed, suffering from anxiety, paying huge prescription drug bills for unsafe prescriptions that don’t solve the problem or produce undesirable side effects? Are you tired of the piece-meal trial and error approach to finding a solution to your mental or emotional problems? If so, adults should consider the following nutritional protocol, which will bathe your brain and nerves in natural nutrients and may well produce dramatic results. The cost of trying the program below is less than the cost of a typical doctor’s office visit. It is safe and convenient. All of these nutrients can be purchased at large discount stores. After the morning meal take: * A multivitamin tablet * 1,000 mg of vitamin B-3 (as niacinamide or inositol hexanicotinate) * One B-complex tablet * 100 mg of vitamin B-6 * 1,200 mcg of vitamin B-9 (folate or folic acid) * 1,000-2,000 IU of vitamin D (the lower number if you get sunshine, the higher number if you don't) * 1,000 mg of vitamin C * 200 mg of magnesium * 50 mg of zinc * 200 micrograms (mcg) of selenium * 30 grams of soy protein powder and one tablespoon of lecithin granules mixed into a small glass of juice or milk A supplement of omega-3 fatty acids [eicosapentaenoic acid (EPA), docosahexanoic acid (DHA) and alpha-linolenic acid (ALA)] After the midday meal: * 1,000 mg of vitamin B-3 * 1,200 mcg of vitamin folate * 100 mg of vitamin B-6 * One B-complex tablet * 1,000 mg of vitamin C * 200 mg of magnesium After the evening meal: * A multivitamin tablet * 1,000 mg of vitamin B-3 * 1,000 mg of vitamin C * One B-complex tablet * 100 mg of vitamin B-6 All of the above supplements are safe in the recommended amounts, as well as inexpensive and convenient. There is not even one death per year from vitamins. Pharmaceutical drugs, properly prescribed and taken as directed, kill over 100,000 Americans annually. Hospital errors kill still more. Restoring health must be done nutritionally, not pharmacologically. All cells in all persons are made exclusively from what we drink and eat. Not one cell is made out of drugs. The most common mistake made by people who take vitamins is they fail to take enough vitamins. The reason one nutrient can cure so many different illnesses is because a deficiency of one nutrient can cause many different illnesses. What is Orthomolecular Medicine? Linus Pauling defined orthomolecular medicine as "the treatment of disease by the provision of the optimum molecular environment, especially the optimum concentrations of substances normally present in the human body." Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org Take the Orthomolecular Quiz at http://www.orthomolecular.org/quiz/index.shtml The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource. Editorial Review Board: Abram Hoffer, M.D., Ph.D. Harold D. Foster, Ph.D. Bradford Weeks, M.D. Carolyn Dean, M.D. N.D. Erik Paterson, M.D. Thomas Levy, M.D., J.D. Andrew W. Saul, contact person. email: omns@orthomolecular.org To UNSUBSCRIBE: http://www.orthomolecular.org/unsubscribe.html To subscribe at no charge: http://www.orthomolecular.org/subscribe.html References for further reading: 1. Hoffer A. Vitamin B-3: Niacin and its amide. http://www.doctoryourself.com/hoffer_niacin.html Also: Cheraskin E, Ringsdorf WM and Brecher A. Psychodietetics. Bantam Books, 1974. 2. Vieth R, Kimball S, Hu A, Walfish PG. Randomized comparison of the effects of the vitamin D3 adequate intake versus 100 mcg (4000 IU) per day on biochemical responses and the wellbeing of patients. Nutr J. 2004 Jul 19;3:8. 3. Hoffer A. Healing schizophrenia: Complementary vitamin & drug treatments. Toronto: CCNM Press, 2004. Also: Hawkins D and Pauling L. Orthomolecular psychiatry, San Francisco: Freeman, 1973. Also: Hoffer A. Niacin therapy in psychiatry, Charles C. Thomas, 1962. 4. Hoffer A. Healing children's attention and behavior disorders: Complementary nutritional & psychological treatments. Toronto: CCNM Press, 2004. Also: Hoffer A. Dr. Hoffer's ABC of natural nutrition for children. Kingston, Ontario: Quarry Press, 1999. 5. Selhub J, Jacques PF, Wilson PWF, Rush D, Rosenberg IH. Vitamin status and intake as primary determinants of homocysteinemia in an elderly population. JAMA 1993. 270:2693-2698. Also: Verhoef P, Meleady R, Daly LE, Graham IM, Robinson K, Boers GHJ, et al. Homocysteine, vitamin status and risk of vascular disease. European Heart Journal 1999. 20:1234-1244. 6. http://neon.cm.utexas.edu/williams/ (end)

Tuesday, April 29, 2008

PTSD and neurobiology

The Body Keeps The Score:
Memory & the Evolving Psychobiology of Post Traumatic Stress
by Bessel van der Kolk


Bessel A. van der Kolk, MD.
Harvard Medical School
HRI Trauma Center
227 Babcock Street
Boston, MA 02146

This is a version of an article first published in the Harvard Review of Psychiatry, 1994, 1(5), 253-265. Note that this online version may have minor differences from the published version.
The author wishes to thank Rita Fisler, Ed.M. for her editorial assistance.
Background

For more than a century, ever since people's responses to overwhelming experiences were first systematically explored, it has been noted that the psychological effects of trauma are expressed as changes in the biological stress response. In 1889, Pierre Janet (1), postulated that intense emotional reactions make events traumatic by interfering with the integration of the experience into existing memory schemes. Intense emotions, Janet thought, cause memories of particular events to be dissociated from consciousness, and to be stored, instead, as visceral sensations (anxiety and panic), or as visual images (nightmares and flashbacks). Janet also observed that traumatized patients seemed to react to reminders of the trauma with emergency responses that had been relevant to the original threat, but that had no bearing on current experience. He noted that victims had trouble learning from experience: unable to put the trauma behind them, their energies were absorbed by keeping their emotions under control at the expense of paying attention to current exigencies. They became fixated upon the past, in some cases by being obsessed with the trauma, but more often by behaving and feeling like they were traumatized over and over again without being able to locate the origins of these feelings (2,3).

Freud also considered the tendency to stay fixated on the trauma to be biologically based: "After severe shock.. the dream life continually takes the patient back to the situation of his disaster from which he awakens with renewed terror.. the patient has undergone a physical fixation to the trauma"(4). Pavlov's investigations continued the tradition of explaining the effects of trauma as the result of lasting physiological alterations. He, and others employing his paradigm, coined the term "defensive reaction" for a cluster of innate reflexive responses to environmental threat (5). Many studies have shown how the response to potent environmental stimuli (unconditional stimuli-US) becomes a conditioned reaction. After repeated aversive stimulation, intrinsically non-threatening cues associated with the trauma (conditional stimuli-CS) become capable of eliciting the defensive reaction by themselves (conditional response-CR). A rape victim may respond to conditioned stimuli, such as the approach by an unknown man, as if she were about to be raped again, and experience panic. Pavlov also pointed out that individual differences in temperament accounted for the diversity of long term adaptations to trauma.

Abraham Kardiner(6), who first systematically defined posttraumatic stress for American audiences, noted that sufferers from "traumatic neuroses" develop an enduring vigilance for and sensitivity to environmental threat, and stated that "the nucleus of the neurosis is a physioneurosis. This is present on the battlefield and during the entire process of organization; it outlives every intermediary accommodative device, and persists in the chronic forms. The traumatic syndrome is ever present and unchanged". In "Men under Stress", Grinker and Spiegel (7) catalogue the physical symptoms of soldiers in acute posttraumatic states: flexor changes in posture, hyperkinesis, "violently propulsive gait", tremor at rest, masklike facies, cogwheel rigidity, gastric distress, urinary incontinence, mutism, and a violent startle reflex. They noted the similarity between many of these symptoms and those of diseases of the extrapyramidal motor system. Today we can understand them as the result of stimulation of biological systems, particularly of ascending amine projections. Contemporary research on the biology of PTSD, generally uninformed by this earlier research, confirms that there are persistent and profound alterations in stress hormones secretion and memory processing in people with PTSD.
The Symptomatology of PTSD

Starting with Kardiner(6), and closely followed by Lindemann (8), a vast literature on combat trauma, crimes, rape, kidnapping, natural disasters, accidents and imprisonment have shown that the trauma response is bimodal: hypermnesia, hyper-reactivity to stimuli and traumatic reexperiencing coexist with psychic numbing, avoidance, amnesia and anhedonia (9,10,11,12). These responses to extreme experiences are so consistent across traumatic stimuli that this biphasic reaction appears to be the normative response to any overwhelming and uncontrollable experience. In many people who have undergone severe stress, the post-traumatic response fades over time, while it persists in others. Much work remains to be done to spell out issues of resilience and vulnerability, but magnitude of exposure, prior trauma, and social support appear to be the three most significant predictors for developing chronic PTSD (13,14).

In an apparent attempt to compensate for chronic hyperarousal, traumatized people seem to shut down: on a behavioral level, by avoiding stimuli reminiscent of the trauma; on a psychobiological level, by emotional numbing, which extends to both trauma-related, and everyday experience (15). Thus, people with chronic PTSD tend to suffer from numbing of responsiveness to the environment, punctuated by intermittent hyperarousal in response to conditional traumatic stimuli. However, as Pitman has pointed out (16), in PTSD, the stimuli that precipitate emergency responses may not be conditional enough: many triggers not directly related to the traumatic experience may precipitate extreme reactions. Thus, people with PTSD suffer both from generalized hyperarousal and from physiological emergency reactions to specific reminders(9,10) The loss of affective modulation that is so central in PTSD mayhelp explain the observation that traumatized people lose the capacity to utilize affect states as signals (18). Instead of using feelings as cues to attend to incoming information, in people with PTSD arousal is likely to precipitate flight or fight reactions (19). Thus, they are prone to go immediately from stimulus to response without making the necessary psychological assessment of the meaning of what is going on. This makes them prone to freeze, or, alternatively, to overreact and intimidate others in response to minor provocations (12,20).
Psychophysiology

Abnormal psychophysiological responses in PTSD have been demonstrated on two different levels: 1) in response to specific reminders of the trauma and 2) in response to intense, but neutral stimuli, such as acoustic startle. The first paradigm implies heightened physiological arousal to sounds, images, and thoughts related to specific traumatic incidents. A large number of studies have confirmed that traumatized individuals respond to such stimuli with significant conditioned autonomic reactions, such as heart rate, skin conductance and blood pressure (20,21,22,23, 24,25). The highly elevated physiological responses that accompany the recall of traumatic experiences that happened years, and sometimes decades before, illustrate the intensity and timelessness with which traumatic memories continue to affect current experience (3,16). This phenomenon has generally been understood in the light of Peter Lang's work (26) which shows that emotionally laden imagery correlates with measurable autonomic responses. Lang has proposed that emotional memories are stored as "associative networks", that are activated when a person is confronted with situations that stimulate a sufficient number of elements that make up these networks. One significant measure of treatment outcome that has become widely accepted in recent years is a decrease in physiological arousal in response to imagery related to the trauma (27). However, Shalev et al (28) have shown that desensitization to specific trauma-related mental images does not necessarily generalize to recollections of other traumatic events, as well.

Kolb (29) was the first to propose that excessive stimulation of the CNS at the time of the trauma may result in permanent neuronal changes that have a negative effect on learning, habituation, and stimulus discrimination. These neuronal changes would not depend on actual exposure to reminders of the trauma for expression. The abnormal startle response characteristic of PTSD (10) exemplifies such neuronal changes.

Despite the fact that an abnormal acoustic startle response (ASR) has been seen as a cardinal feature of the trauma response for over half a century, systematic explorations of the ASR in PTSD have just begun. The ASR consists of a characteristic sequence of muscular and autonomic responses elicited by sudden and intense stimuli (30,31). The neuronal pathways involved consist of only a small number of mediating synapses between the receptor and effector and a large projection to brain areas responsible for CNS activation and stimulus evaluation (31). The ASR is mediated by excitatory amino acids such as glutamate and aspartate and is modulated by a variety of neurotransmitters and second messengers at both the spinal and supraspinal level (32). Habituation of the ASR in normals occurs after 3 to 5 presentations (30).

Several studies have demonstrated abnormalities in habituation to the ASR in PTSD (33,34,35,36). Shalev et al (33) found a failure to habituate both to CNS and ANS-mediated responses to ASR in 93% of the PTSD group, compared with 22% of the control subjects. Interestingly, people who previously met criteria for PTSD, but no longer do so now, continue to show failure of habituation of the ASR (van der Kolk et al, unpublished data; Pitman et al, unpublished data), which raises the question whether abnormal habituation to acoustic startle is a marker of, or a vulnerability factor for developing PTSD.

The failure to habituate to acoustic startle suggests that traumatized people have difficulty evaluating sensory stimuli, and mobilizing appropriate levels of physiological arousal(30). Thus, the inability of people with PTSD to properly integrate memories of the trauma and, instead, to get mired in a continuous reliving of the past, is mirrored physiologically in the misinterpretation of innocuous stimuli, such as the ASR, as potential threats.
The Hormonal Stress Response & the Psychobiology of PTSD

Post Traumatic Stress Disorder develops following exposure to events that are intensely distressing. Intense stress is accompanied by the release of endogenous, stress-responsive neurohormones, such as cortisol, epinephrine and norepinephrine (NE), vasopressin, oxytocin and endogenous opioids. These stress hormones help the organism mobilize the required energy to deal with the stress, ranging from increased glucose release to enhanced immune function. In a well-functioning organism, stress produces rapid and pronounced hormonal responses. However, chronic and persistent stress inhibits the effectiveness of the stress response and induces desensitization (37).

Much still remains to be learned about the specific roles of the different neurohormones in the stress response. NE is secreted by the Locus Coeruleus(LC) and distributed through much of the CNS, particularly the neocortex and the limbic system, where it plays a role in memory consolidation and helps initiate fight/ flight behaviors. Adrenocorticotropin (ACTH) is released from the anterior pituitary, and activates a cascade of reactions, eventuating in release of glucocorticoids from the adrenals. The precise interrelation between Hypothalamic-Pituitary-Adrenal (HPA) Axis hormones and the catecholamines in the stress response is not entirely clear, but it is known that stressors that activate NE neurons also increase CRF concentrations in the LC (38), while intracerebral ventricular infusion of CRF increases NE in the forebrain (39). Glucocorticoids and catecholamines may modulate each other's effects: in acute stress, cortisol helps regulate stress hormone release via a negative feedback loop to the hippocampus, hypothalamus and pituitary (40) and there is evidence that corticosteroids normalize catecholamine-induced arousal in limbic midbrain structures in response to stress (41). Thus, the simultaneous activation of corticosteroids and catecholamines could stimulate active coping behaviors, while increased arousal in the presence of low glucocorticoid levels may promote undifferentiated fight or flight reactions (42).

While acute stress activates the HPA axis and increases glucocorticoid levels, organisms adapt to chronic stress by activating a negative feedback loop that results in 1) decreased resting glucocorticoid levels in chronically stressed organisms, (43), 2) decreased glucocorticoid secretion in response to subsequent stress (42), and 3) increased concentration of glucocorticoid receptors in the hippocampus (44). Yehuda has suggested that increased concentration of glucocorticoid receptors could facilitate a stronger glucocorticoid negative feedback, resulting in a more sensitive HPA axis and a faster recovery from acute stress (45).

Chronic exposure to stress affects both acute and chronic adaptation: it permanently alters how an organism deals with its environment on a day-to-day basis, and it interferes with how it copes with subsequent acute stress (45).
Neuroendocrine Abnormalities in PTSD

Since there is an extensive animal literature on the effects of inescapable stress on the biological stress response of other species, such as monkeys and rats, much of the biological research on people with PTSD has focussed on testing the applicability of those research findings to people with PTSD (46,47). People with PTSD, like chronically and inescapbly shocked animals, seem to suffer from a persistent activation of the biological stress response upon exposure to stimuli reminiscent of the trauma.

1) Catecholamines. Neuroendocrine studies of Vietnam veterans with PTSD have found good evidence for chronically increased sympathetic nervous system activity in PTSD. One study (48) found elevated 24h excretions of urinary NE and epinephrine in PTSD combat veterans compared with patients with other psychiatric diagnoses. While Pitman & Orr (49) did not replicate these findings in 20 veterans and 15 combat controls, the mean urinary NE excretion values in their combat controls (58.0 ug/day) were substantially higher than those previously reported in normal populations. The expected compensatory downregulation of adrenergic receptors in response to increased levels of norepinephrine was confirmed by a study that found decreased platelet alpha-2 adrenergic receptors in combat veterans with PTSD, compared with normal controls (50). Another study also found an abnormally low alpha-2 adrenergic receptor-mediated adenylate cyclase signal transduction (51). In a recent study Southwick et al (52) used yohimbine injections (0.4 mg/kg), which activate noradrenergic neurons by blocking the alpha-2 auto- receptor, to study noradrenergic neuronal dysregulation in Vietnam veterans with PTSD. Yohimbine precipitated panic attacks in 70% of subjects and flashbacks in 40%. Subjects responded with larger increases in plasma MHPG than controls. Yohimbine precipitated significant increases in all PTSD symptoms.

2) Corticosteroids. Two studies have shown that veterans with PTSD have low urinary cortisol excretion, even when they have comorbid major depressive disorder (42,53). One study failed to replicate this finding (49). In a series of studies, Yehuda et al (42,54) found increased numbers of lymphocyte glucocorticoid receptors in Vietnam veterans with PTSD. Interestingly, the number of glucocorticoid receptors was proportional to the severity of PTSD symptoms. Yehuda (54) also has reported the results of an unpublished study by Heidi Resnick, in which acute cortisol response to trauma was studied from blood samples from 20 acute rape victims. Three months later, a prior trauma history was taken, and the subjects were evaluated for the presence of PTSD. Victims with a prior history of sexual abuse were significantly more likely to have developed PTSD three months following the rape than rape victims who did not develop PTSD. Cortisol levels shortly after the rape were correlated with histories of prior assaults: the mean initial cortisol level of individuals with a prior assault history was 15 ug/dl compared to 30 ug/dl in individuals without. These findings can be interpreted to mean either that prior exposure to traumatic events result in a blunted cortisol response to subsequent trauma, or in a quicker return of cortisol to baseline following stress. The fact that Yehuda et al (45) also found subjects with PTSD to be hyperresponsive to low doses of dexamethasone argues for an enhanced sensitivity of the HPA feedback in traumatized patients.

3) Serotonin. While the role of serotonin in PTSD has not been systematically investigated, both the fact that inescapably shocked animals develop decreased CNS serotonin levels (55), and that serotonin re-uptake blockers are effective pharmacological agents in the treatment of PTSD, justify a brief consideration of the potential role of this neurotransmitter in PTSD. Decreased serotonin in humans has repeatedly been correlated with impulsivity and aggression (56,57,58). The literature tends to readily assume that these relationships are based on genetic traits. However, studies of impulsive, aggressive and suicidal patients seem to find at least as robust an association between those behaviors and histories of childhood trauma (e.g. 59,60,61). It is likely that both temperament and experience affect relative CNS serotonin levels (12).

Low serotonin in animals is also related to an inability to modulate arousal, as exemplified by an exaggerated startle (62,63), and increased arousal in response to novel stimuli, handling, or pain (63). The behavioral effects of serotonin depletion on animals is characterized by hyperirritability, hyperexitability, and hypersensitivity, and an "...exaggerated emotional arousal and/or aggressive display, to relatively mild stimuli" (63). These behaviors bear a striking resemblance to the phenomenology of PTSD in humans. Furthermore, serotonin re-uptake inhibitors have been found to be the most effective pharmacological treatment of both obsessive thinking in people with OCD (64), and of involuntary preoccupation with traumatic memories in people with PTSD (65,66). It is likely that serotonin plays a role in the capacity to monitor the environment flexibly and to respond with behaviors that are situation-appropriate, rather than reacting to internal stimuli that are irrelevant to current demands.

4). Endogenous opioids. Stress induced analgesia (SIA) has been described in experimental animals following a variety of inescapable stressors such as electric shock, fighting, starvation and cold water swim (67). In severely stressed animals, opiate withdrawal symptoms can be produced both by termination of the stressful stimulus or by naloxone injections. Stimulated by the findings that fear activates the secretion of endogenous opioid peptides, and that SIA can become conditioned to subsequent stressors and to previously neutral events associated with the noxious stimulus, we tested the hypothesis that in people with PTSD, re-exposure to a stimulus resembling the original trauma will cause an endogenous opioid response that can be indirectly measured as naloxone reversible analgesia (68,69). We found that two decades after the original trauma, people with PTSD developed opioid-mediated analgesia in response to a stimulus resembling the traumatic stressor, which we correlated with a secretion of endogenous opioids equivalent to 8 mg of morphine. Self-reports of emotional responses suggested that endogenous opioids were responsible for a relative blunting of the emotional response to the traumatic stimulus.
Endogenous Opiates & Stress Induced Analgesia: Possible Implications for Affective Function

When young animals are isolated, and older ones attacked, they respond initially with aggression (hyperarousal- fight- protest), and, if that does not produce the required results, with withdrawal (numbing-flight-despair). Fear-induced attack or protest patterns in the young serve to attract protection, and in mature animals to prevent or counteract the predator's activity. During external attacks pain-inhibition is a useful defensive capacity, because attention to pain would interfere with effective defense: grooming or licking wounds may attract opponents and stimulate further attack (70). Thus defensive and pain-motivated behaviors are mutually inhibitory. Stress-induced analgesia protects organisms against feeling pain while engaged in defensive activities. As early as 1946, Beecher (71), after observing that 75% of severely wounded soldiers on the Italian front did not request morphine, speculated that "strong emotions can block pain". Today, we can reasonably assume that this is due to the release of endogenous opioids(68,69).

Endogenous opioids, which inhibit pain and reduce panic, are secreted after prolonged exposure to severe stress. Siegfried et al (70) have observed that memory is impaired in animals when they can no longer actively influence the outcome of a threatening situation. They showed that both the freeze response and panic interfere with effective memory processing: excessive endogenous opioids and NE both interfere with the storage of experience in explicit memory. Freeze/numbing responses may serve the function of allowing organisms to not "consciously experience" or not to remember situations of overwhelming stress (and which thus will also keep them from learning from experience). We have proposed that the dissociative reactions in people in response to trauma may be analogous to this complex of behaviors that occur in animals after prolonged exposure to severe uncontrollable stress (68).
Developmental Level Affects the Psychobiological Effects of Trauma

While most studies on PTSD have been done on adults, particularly on war veterans, in recent years a small prospective literature is emerging that documents the differential effects of trauma at various age levels. Anxiety disorders, chronic hyperarousal, and behavioral disturbances have been regularly described in traumatized children (e.g.72,73,74). In addition to the reactions to discrete, one time, traumatic incidents documented in these studies, intrafamilial abuse is increasingly recognized to produce complex post-traumatic syndromes (75), which involve chronic affect dysregulation, destructive behavior against self and others, learning disablities, dissociative problems, somatization, and distortions in concepts about self and others (76,77). The Field Trials for DSM IV showed that these this conglomeration of symptoms tended to occur together and that the severity of this syndrome was proportional to the age of onset of the trauma and its duration (78).

While current research on traumatized children is outside the scope of this review, it is important to recognize that a range of neurobiological abnormalities are beginning to be identified in this population. Frank Putnam's prospective, but as yet unpublished, studies (personal communications, 1991,1992,1993) are showing major neuroendocrine disturbances in sexually abused girls compared with normals. Research on the psychobiology of childhood trauma can be profitably informed by the vast literature on the psychobiological effects of trauma and deprivation in non-human primates (12,79).
Trauma & Memory: The Flexibility of Memory & the Engraving of Trauma

One hundred years ago, Pierre Janet (1) suggested that the most fundamental of mental activities is the storage and categorization of incoming sensations into memory, and the retrieval of those memories under appropriate circumstances. He, like contemporary memory researchers, understood that what is now called semantic, or declarative, memory is an active and constructive process and that remembering depends on existing mental schemata (3,80): once an event or a particular bit of information is integrated into existing mental schemes, it will no longer be accessible as a separate, immutable entity, but be distorted both by prior experience, and by the emotional state at the time of recall(3). PTSD, by definition, is accompanied by memory disturbances, consisting of both hypermnesias and amnesias (9,10). Research into the nature of traumatic memories (3) indicates that trauma interferes with delarative memory, i.e. conscious recall of experience, but does not inhibit implicit, or non-declarative memory, the memory system that controls conditioned emotional responses, skills and habits, and sensorimotor sensations related to experience. There now is enough information available about the biology of memory storage and retrieval to start building coherent hypotheses regarding the underlying psychobiological processes involved in these memory disturbances (3,16,17,25).

In the beginning of this century Janet already noted that: "certain happenings ... leave indelible and distressing memories-- memories to which the sufferer continually returns, and by which he is tormented by day and by night" (81). Clinicians and researchers dealing with traumatized patients have repeatedly made the observation that the sensory experiences and visual images related to the trauma seem not to fade over time, and appear to be less subject to distortion than ordinary experiences (1,49,82). When people are traumatized, they are said to experience "speechless terror": the emotional impact of the event may interfere with the capacity to capture the experience in words or symbols. Piaget (83) thought that under such circumstances, failure of semantic memory leads to the organization of memory on a somatosensory or iconic level (such as somatic sensations, behavioral enactments, nightmares and flashbacks). He pointed out: "It is precisely because there is no immediate accommodation that there is complete dissociation of the inner activity from the external world. As the external world is solely represented by images, it is assimilated without resistance (i.e. unattached to other memories) to the unconscious ego".
Traumatic memories are state dependent.

Research has shown that, under ordinary conditions, many traumatized people, including rape victims (84), battered women (85) and abused children (86) have a fairly good psychosocial adjustment. However, they do not respond to stress the way other people do. Under pressure, they may feel, or act as if they were traumatized all over again. Thus, high states of arousal seem to selectively promote retrieval of traumatic memories, sensory information, or behaviors associated with prior traumatic experiences (9,10). The tendency of traumatized organisms to revert to irrelevant emergency behaviors in response to minor stress has been well documented in animals, as well. Studies at the Wisconsin primate laboratory have shown that rhesus monkeys with histories of severe early maternal deprivation display marked withdrawal or aggression in response to emotional or physical stimuli (such as exposure to loud noises, or the administration of amphetamines), even after a long period of good social adjustment (87). In experiments with mice, Mitchell and his colleagues (88) found that the relative degree of arousal interacts with prior exposure to high stress to determine how an animal will react to novel stimuli. In a state of low arousal, animals tend to be curious and seek novelty. During high arousal, they are frightened, avoid novelty, and perseverate in familiar behavior, regardless of the outcome. Under ordinary circumstances, an animal will choose the most pleasant of two alternatives. When hyperaroused, it will seek whatever is familiar, regardless of the intrinsic rewards. Thus, animals who have been locked in a box in which they were exposed to electric shocks and then released return to those boxes when they are subsequently stressed. Mitchell concluded that this perseveration is nonassociative, i.e. uncoupled from the usual reward systems.

In people, analogous phenomena have been documented: memories (somatic or symbolic) related to the trauma are elicited by heightened arousal (89). Information acquired in an aroused, or otherwise altered state of mind is retrieved more readily when people are brought back to that particular state of mind (90,91). State dependent memory retrieval may also be involved in dissociative phenomena in which traumatized persons may be wholly or partially amnestic for memories or behaviors enacted while in altered states of mind (2,3,92).

Contemporary biological researchers have shown that medications that stimulate autonomic arousal may precipitate visual images and affect states associated with prior traumatic experiences in people with PTSD, but not in controls. In patients with PTSD the injection of drugs such as lactate (93) and yohimbine (52) tends to precipitate panic attacks, flashbacks (exact reliving experiences) of earlier trauma, or both. In our own laboratory, approximately 20% of PTSD subjects responded with a flashback of a traumatic experience when they were presented with acoustic startle stimuli.
Trauma, neurohormones and memory consolidation.

When people are under severe stress, they secrete endogenous stress hormones that affect the strength of memory consolidation. Based on animal models it has been widely assumed (3,46,94) that massive secretion of neurohormones at the time of the trauma plays a role in the long term potentiation (LTP) (and thus, the over- consolidation) of traumatic memories. Mammals seem equipped with memory storage mechanisms that ordinarily modulate the strength of memory consolidation according to the strength of the accompanying hormonal stimulation (95,96). This capacity helps the organism evaluate the importance of subsequent sensory input according to the relative strength of associated memory traces. This phenomenon appears to be largely mediated by NE input to the amygdala (97,98, figure 2). In traumatized organisms, the capacity to access relevant memories appears to have gone awry: they become overconditioned to access memory traces of the trauma and to "remember" the trauma whenever aroused. While norepinephrine (NE) seems to be the principal hormone involved in producing LTP, other neurohormones secreted under particular stressful circumstances, such as endorphins and oxytocin, actually inhibit memory consolidation (99).

The role of NE in memory consolidation has been shown to have an inverted U-shaped function (95,96): both very low and very high levels of CNS NE activity interfere with memory storage. Excessive NE release at the time of the trauma, as well as the release of other neurohormones, such as endogenous opioids, oxytocin and vasopressin, are likely to play a role in creating the hypermnesias and the amnesias that are a quintessential part of PTSD (9,10). It is of interest that childbirth, which can be extraordinarily stressful, almost never seems to result in post traumatic problems (100). Oxytocin may play a protective role that prevents the overconsolidation of memories surrounding childbirth.

Physiological arousal in general can trigger trauma-related memories, while, conversely, trauma-related memories precipitate generalized physiological arousal. It is likely that the frequent re-living of a traumatic event in flashbacks or nightmares cause a re-release of stress hormones which further kindle the strength of the memory trace (46). Such a positive feedback loop could cause subclinical PTSD to escalate into clinical PTSD (16), in which the strength of the memories appear so deeply engraved that Pitman and Orr (17) have called it "the Black Hole" in the mental life of the PTSD patient, that attracts all associations to it, and saps current life of its significance.
Memory, Trauma & the Limbic System

The limbic system is thought to be the part of the CNS that maintains and guides the emotions and behavior necessary for self-preservation and survival of the species (101), and that is critically involved in the storage and retrieval of memory. During both waking and sleeping states signals from the sensory organs continuously travel to the thalamus whence they are distributed to the cortex (setting up a "stream of thought"), to the basal ganglia (setting up a "stream of movement") and to the limbic system where they set up a "stream of emotions"(102), that determine the emotional significance of the sensory input. It appears that most processing of sensory input occurs outside of conscious awareness, and only novel, significant or threatening information is selectively passed on to the neocortex for further attention. Since people with PTSD appear to over-interpret sensory input as a recurrence of past trauma and since recent studies have suggested limbic system abnormalities in brain imaging studies of traumatized patients (103,104), a review of the psychobiology of trauma would be incomplete without considering the role of the limbic system in PTSD (also see 105). Two particular areas of the limbic system have been implicated in the processing of emotionally charged memories: the amygdala and the hippocampus (Table 2).

The amygdala. Of all areas in the CNS, the amygdala is most clearly implicated in the evaluation of the emotional meaning of incoming stimuli (106). Several investigators have proposed that the amygdala assigns free-floating feelings of significance to sensory input, which the neocortex then further elaborates and imbues with personal meaning (101,106,107,108). Moreover, it is thought to integrate internal representations of the external world in the form of memory images with emotional experiences associated with those memories (80). After assigning meaning to sensory information, the amygdala guides emotional behavior by projections to the hypothalamus, hippocampus and basal forebrain (106,107,109).

The septo-hippocampal system, which anatomically is adjacent to the amygdala, is thought to record in memory the spatial and temporal dimensions of experience and to play an important role in the categorization and storage of incoming stimuli in memory. Proper functioning of the hippocampus is necessary for explicit or declarative memory (109). The hippocampus is thought to be involved in the evaluation of spatially and temporally unrelated events, comparing them with previously stored information and determining whether and how they are associated with each other, with reward, punishment, novelty or non-reward (107,110). The hippocampus is also implicated in playing a role in the inhibition of exploratory behavior and in obsessional thinking, while hippocampal damage is associated with hyper-responsiveness to environmental stimuli (111,112).

The slow maturation of the hippocampus, which is not fully myelinated till after the third or fourth year of life, is seen as the cause of infantile amnesia (113,114). In contrast, it is thought that the memory system that subserves the affective quality of experience (roughly speaking procedural, or "taxon" memory) matures earlier and is less subject to disruption by stress (112).

As the CNS matures, memory storage shifts from primarily sensorimotor (motoric action) and perceptual representations (iconic), to symbolic and linguistic modes of organization of mental experience (83). With maturation, there is an increasing ability to categorize experience, and link it with existing mental schemes. However, even as the organism matures, this capacity, and with it, the hippocampal localization system, remains vulnerable to disruption (45,107,110,115,116). A variety of external and internal stimuli, such as stress induced corticosterone production (117), decreases hippocampal activity. However, even when stress interferes with hippocampally mediated memory storage and categorization, it is likely that some mental representation of the experience is laid down by means of a system that records affective experience, but that has no capacity for symbolic processing and placement in space and time (figure 2).

Decreased hippocampal functioning causes behavioral disinhibition, possibly by stimulating incoming stimuli to be interpreted in the direction of "emergency" (fight/flight) responses. The neurotransmitter serotonin plays a crucial role in the capacity of the septo-hippocampal system to activate inhibitory pathways that prevent the initiation of emergency responses until it is clear that they will be of use (110). This observation made us very interested in a possible role for serotonergic agents in the treatment of PTSD.
"Emotional memories are forever"

In animals, high level stimulation of the amygdala interferes with hippocampal functioning (107, 109). This implies that intense affect may inhibit proper evaluation and categorization of experience. In mature animals one-time intense stimulation of the amygdala will produce lasting changes in neuronal excitability and enduring behavioral changes in the direction of either fight or flight (118). In kindling experiments with animals, Adamec et al (119) have shown that, following growth in amplitude of amygdala and hippocampal seizure activity, permanent changes in limbic physiology cause a lasting changes in defensiveness and in predatory aggression. Pre-existing "personality" played a significant role in the behavioral effects of amygdala stimulation in cats: animals that are temperamentally insensitive to threat and prone to attack tend become more aggressive, while in highly defensive animals different pathways were activated, increasing behavioral inhibition (119).

In a series of experiments, LeDoux has utilized repeated electrical stimulation of the amygdala to produce conditioned fear responses. He found that cortical lesions prevent their extinction. This led him to conclude that, once formed, the subcortical traces of the conditioned fear response are indelible, and that "emotional memory may be forever" (118). In 1987, Lawrence Kolb (29) postulated that patients with PTSD suffer from impaired cortical control over subcortical areas responsible for learning, habituation, and stimulus discrimination. The concept of indelible subcortical emotional responses, held in check to varying degrees by cortical and septo-hippocampal activity, has led to the speculation that delayed onset PTSD may be the expression of subcortically mediated emotional responses that escape cortical, and possibly hippocampal, inhibitory control (3,16,94,120,121).

Decreased inhibitory control may occur under a variety of circumstances: under the influence of drugs and alcohol, during sleep (as nightmares), with aging, and after exposure to strong reminders of the traumatic past. It is conceivable that traumatic memories then could emerge, not in the distorted fashion of ordinary recall, but as affect states, somatic sensations or as visual images (nightmares [81] or flashbacks [52]) that are timeless and unmodified by further experience.
Psychopharmacological Treatment

The goal of treatment of PTSD is to help people live in the present, without feeling or behaving according to irrelevant demands belonging to the past. Psychologically, this means that traumatic experiences need to be located in time and place and distinguished from current reality. However, hyperarousal, intrusive reliving, numbing and dissociation get in the way of separating current reality from past trauma. Hence, medications that affect these PTSD symptoms are often essential for patients to begin to achieve a sense of safety and perspective from which to approach their tasks. While numerous articles have been written about the drug treatment of PTSD, to date, only 134 people with PTSD have been enrolledin published double blind studies. Most of these have been Vietnamcombat veterans. Unfortunately, up until recently, only medications which seem to be of limited therapeutic usefulness have beenthesubject of adequate scientific scrutiny. While the only published double blind studies of medications in the treatment of PTSDhave been tricyclic antidepressants and MAO Inhibitors (122,123,124), it is sometimes assumed that they therefore also are themosteffective. Three double-blind trials of tricyclic antidepressants have been published (122,124,125), two of which demonstrated modest improvement in PTSD symptoms. While positive resultshave been claimed for numerous other medications in case reportsand open studies, at the present time there are no data aboutwhich patient and which PTSD symptom will predictably respond toanyof them. Success has been claimed for just about every class ofpsychoactive medication, including benzodiazepines (127), tricyclic antidepressants (122,125), monamine oxidase inhibitors (122,129) lithium carbonate (127), beta adrenergic blockers and clonidine (130), carbamezapine (131) and antipsychotic agents. The accumulated clinical experience seems to indicate that understanding thebasic neurobiology of arousal and appraisal is the most useful guideinselecting medications for people with PTSD (124,125). Autonomic arousal can be reduced at different levels in the CNS: throughinhibition of locus coeruleus noradrenergic activity with clonidine and the beta adrenergic blockers (130,132), or by increasing the inhibitory effect of the gaba-ergic system with gaba- ergicagonists (the benzodiazepines). During the past two years a numberof case reports and open clinical trials of fluoxetine were followedby our double blind study of 64 PTSD subjects with fluoxetine (65). Unlike the tricyclic antidepressants, which were effective on either the intrusive (imipramine) or numbing (amitryptiline) symptoms of PTSD, fluoxetine proved to be effective forthewhole spectrum of PTSD symptoms. It also acted more rapidly thanthetricyclics. The fact that fluoxetine has proven to be such aneffective treatment for PTSD supports a larger role of the serotonergic system in PTSD (66). Rorschach tests adminstered by blindscorers revealed that subjects on fluoxetine became able to takedistance from the emotional impact of incoming stimuli and to becomeable to utilize cognition to harness the emotional responses tounstructured visual stimuli (van der Kolk et al, unpublished).

While the subjects improved clinically, their startle habituation got worse (van der Kolk et al, unpublished). The 5-HT1a agonist buspirone shows some promise in facilitating habituation (133) and thus may play a useful adjunctive role in the pharmaco- therapy of PTSD. Even newer research has suggested abnormalities of the N-methyl-D-aspartate (NMDA) receptor and of glutamate in PTSD (134), opening up potential new avenues for the psychopharmacological treatment of PTSD.

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