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CHOLESTEROL

The average person’s body owns about 1/3 of a pound (150 grams or 5 ounces) of cholesterol. Most of this is found in membranes, and about 7 grams in carried in our blood. The daily turnover of cholesterol is about 1 gram. Cholesterol is unique in that our body can make it but, once made, cannot break it down. The removal of cholesterol is increased by dietary fiber. If fiber is absent, up to 94% of the cholesterol and bile acids are reabsorbed and recycled.

We have to remember the following:
Humans cannot metabolize large amounts of dietary cholesterol effectively. The mechanism which regulates our body’s cholesterol levels does not compensate well for dietary cholesterol. High meat diets contain too little cholesterol-removing fiber.

LDLs are often called “bad cholesterol” and HDLs are called “good cholesterol”. Ideal cholesterol levels should be from 140 to 165 mg/dl, with LDL from 30 to 50 mg/dl, and HDL from 80 to 90 mg/dl. Over 244 is an ideal heart attack victim, 210 is the average American level. Ideal triglyceride levels should be around 170 to 200 mg/dl. Ideal is below 140. Every 1% increase in blood cholesterol translates into a 2% increase in heart disease. Triglycerides are sugar related fats that usually appear in your thighs and hips. If your triglyceride level is above 250 your heart attack risk is twice as high.

Nutritional therapy plan:
· Saturated fat is the real culprit as well as overeating. Focus your diet on plant foods like red yeast rice.
  Reducing bad fats, adding a high fiber diet is still the key to reducing cholesterol. Reduce sugar by the
  “Glycemic Diet” to lower triglycerides.
· Certain foods like soy foods, olive oil, walnuts, avocados, yams, whole grains like oats, high fiber fruits
  and vegetables, beans, yogurt and cultured foods help in cholesterol reduction.
· Substantially reduce or avoid animal fats, red meats, fried foods, and fatty dairy foods, salty or sugary foods.
· Eat smaller meals especially late at night. A little wine with dinner reduces stress and raises HDLs.
· Supplements: Alfalfa, Omega 3 flax oil, CoQ10, Grapeseed Extract, Niacin B3, Vitamin C, the minerals calcium,
  copper, zinc, and chromium are also helpful. (It is never recommended to take one mineral at a time; it should
  be taken as a combination).
· Reduce your body weight. If you are 10 pounds overweight, your body produces an extra 100mg of cholesterol
  every day. Exercise!!!!!!
· Eliminate tobacco use of all kinds, nicotine raises cholesterol levels.
· Lecithin and vitamin E, these nutrients function efficiently in cleaning the arteries when taken in whole food.
  Lecithin is found in most legumes, especially soybeans.
· Apples, bananas, carrots, cold-water fish, garlic, grapefruit are just additional recommendations.
· Water soluble dietary fiber is very important in reducing serum cholesterol. It is found in barley, beans,
  brown rice, fruits, glucomannan, guar gum, and oats. Oat bran and brown rice are proven cholesterol
  reducing foods.
· Drink fresh juices daily especially carrot, celery, and beet juices. Carrot juices help flush out fat from bile in
  the liver and this helps cholesterol.
· Do a monthly spirulina fast, with carrot and celery juice, and lemon and steam distilled water.
· Other than walnuts, stay away from nuts. Walnuts should only be eaten when they are raw.
· Avoid gas forming foods like Brussels sprouts, cabbage, cauliflower, and sweet pickles.
· Learn stress management techniques.

Considerations:
· No margarine or vegetable shortening, these products contain compounds called cis- and trans-fatty acids that
  become oxidized when exposed to heat and can clog arteries. The New England Journal of Medicine,
  observation of 15000 coffee drinkers revealed that as the intake of coffee rises, the amount of
  cholesterol in the blood goes up.
· Cream substitutes (nondairy coffee creamers) are actually poor alternatives to dairy products. Many contain
  coconut oil, which is highly saturated fat. Soymilk or almond milk is better.
· Kombucha tea and Milk Thistle tea (Green Teas) are helpful.
· Certain drugs raise cholesterol levels. Steroids, oral contraceptives, Lasix, and other diuretics, Dopar,
  Larodopa, Sinement, Beta-blockers etc.

Below is a recent Harvard School of Public Health Study:
Fats and Cholesterol - The Good, The Bad, and The Healthy Diet "Eat a low-fat, low-cholesterol diet." Most of us have heard this simple recommendation so often over the past two decades that we can recite it in our sleep. Touted as a way to lose weight and prevent cancer and heart disease, it's no wonder much of the nation - and food producers - hopped on board.

Unfortunately, this simple message is now largely out of date. Detailed research -much of it done at Harvard - shows that the total amount of fat in the diet, whether high or low, isn't really linked with disease. What really matters is the type of fat in the diet. New results from the large and long Women's Health Initiative Dietary Modification Trial showed that eating a low-fat diet for 8 years did not prevent heart disease, breast cancer, or colon cancer, and didn't do much for weight loss, either.(1-4)

What is becoming clearer and clearer is that bad fats, meaning saturated and trans fats, increase the risk for certain diseases while good fats, meaning monounsaturated and polyunsaturated fats, lower the risk. The key is to substitute good fats for bad fats.

And cholesterol in food? Although it is still important to limit the amount of cholesterol you eat, especially if you have diabetes, dietary cholesterol isn't nearly the villain it's been portrayed to be. Cholesterol in the bloodstream is what's most important. High blood cholesterol levels greatly increase the risk for heart disease. But the average person makes about 75% of blood cholesterol in his or her liver, while only about 25% is absorbed from food. The biggest influence on blood cholesterol level is the mix of fats in the diet.


DIETARY FATS

Type Of Fat

Main Source

State At Room Temperature


Effect on Cholesterol Levels

MonounsaturatedOlives; olive oil, canola oil, peanut oil; cashews, almonds, peanuts, and most other nuts; avocadosLiquidLowers LDL; raises HDL
PolyunsaturatedCorn, soybean, safflower, and cottonseed oils; fishLiquidLowers LDL; raises HDL
SaturatedWhole milk, butter, cheese, and ice cream; red meat; chocolate; coconuts, coconut milk, and coconut oilSolidRaises both LDL and HDL
TransMost margarines; vegetable shortening; partially hydrogenated vegetable oil; deep-fried chips; many fast foods; most commercial baked goodsSolid or semi-solidRaises LDL; lowers HDL

The Cholesterol--Heart Disease Connection

Cholesterol is a wax-like substance. The liver makes it and links it to carrier proteins called lipoproteins that let it dissolve in blood and be transported to all parts of the body. Why? Cholesterol plays essential roles in the formation of cell membranes, some hormones, and vitamin D.

Too much cholesterol in the blood, though, can lead to problems. In the 1960s and 70s, scientists established a link between high blood cholesterol levels and heart disease. Deposits of cholesterol can build up inside arteries. These deposits, called plaque, can narrow an artery enough to slow or block blood flow. This narrowing process, called atherosclerosis, commonly occurs in arteries that nourish the heart (the coronary arteries). When one or more sections of heart muscle fail to get enough blood, and thus the oxygen and nutrients they need, the result may be the chest pain known as angina. In addition, plaque can rupture, causing blood clots that may lead to heart attack, stroke, or sudden death. Fortunately, the buildup of cholesterol can be slowed, stopped, and even reversed.

Cholesterol-carrying lipoproteins play central roles in the development of atherosclerotic plaque and cardiovascular disease. The two main types of lipoproteins basically work in opposite directions.

Low-density lipoproteins (LDL) carry cholesterol from the liver to the rest of the body. When there is too much LDL cholesterol in the blood, it can be deposited on the walls of the coronary arteries. Because of this, LDL cholesterol is often referred to as the "bad" cholesterol.

High-density lipoproteins (HDL) carry cholesterol from the blood back to the liver, which processes the cholesterol for elimination from the body. HDL makes it less likely that excess cholesterol in the blood will be deposited in the coronary arteries, which is why HDL cholesterol is often referred to as the "good" cholesterol.

In general, the higher your LDL and the lower your HDL, the greater your risk for atherosclerosis and heart disease.

For adults age 20 years or over, the latest guidelines from the National Cholesterol Education Program recommend the following optimal levels:
· Total cholesterol less than 200 milligrams per deciliter (mg/dl)
· HDL cholesterol levels greater than 40 mg/dl
· LDL cholesterol levels less than 100 mg/dl

Dietary Fat, Dietary Cholesterol, and Blood Cholesterol Levels
One of the most important determinants of blood cholesterol level is fat in the diet - not total fat, as mentioned already, but specific types of fat. Some types of fat are clearly good for cholesterol levels and others are clearly bad for them.

Cholesterol in food
While it is well known that high blood cholesterol levels are associated with an increased risk for heart disease, scientific studies have shown that there is only a weak relationship between the amount of cholesterol a person consumes and their blood cholesterol levels or risk for heart disease. For some people with high cholesterol, reducing the amount of cholesterol in the diet has a small but helpful impact on blood cholesterol levels. For others, the amount of cholesterol eaten has little impact on the amount of cholesterol circulating in the blood.

In a study of over 80,000 female nurses, Harvard researchers actually found that increasing cholesterol intake by 200 mg for every 1000 calories in the diet (about an egg a day) did not appreciably increase the risk for heart disease.(5)

Eggs
Long vilified by well-meaning doctors and scientists for their high cholesterol co ntent, eggs are now making a bit of a comeback. Recent research by Harvard investigators has shown that moderate egg consumption--up to one a day--does not increase heart disease risk in healthy individuals.(5) While it's true that egg yolks have a lot of cholesterol--and, therefore may slightly affect blood cholesterol levels--eggs also contain nutrients that may help lower the risk for heart disease, including protein, vitamins B12 and D, riboflavin, and folate.

So, when eaten in moderation, eggs can be part of a healthy diet. People with diabetes, though, should probably limit themselves to no more than two or three eggs a week, as the Nurses' Health Study found that for such individuals, an egg a day might increase the risk for heart disease. Similarly, people who have difficulty controlling their blood cholesterol may also want to be cautious about eating egg yolks and choose foods made with egg whites instead.

Dietary Fats - The Bad Fats
Some fats are bad because they tend to worsen blood cholesterol levels.

Saturated Fats
Saturated fats are mainly animal fats. They are found in meat, seafood, whole-milk dairy products (cheese, milk, and ice cream), poultry skin, and egg yolks. Some plant foods are also high in saturated fats, including coconut and coconut oil, palm oil, and palm kernel oil. Saturated fats raise total blood cholesterol levels more than dietary cholesterol because they tend to boost both good HDL and bad LDL cholesterol. The net effect is negative, meaning it's important to limit saturated fats.

Trans Fats
Trans fatty acids are fats produced by heating liquid vegetable oils in the presence of hydrogen. This process is known as hydrogenation. The more hydrogenated an oil is, the harder it will be at room temperature. For example, a spreadable tub margarine is less hydrogenated and so has fewer trans fats than a stick margarine.

Most of the trans fats in the American diet are found in commercially prepared baked goods, margarines, snack foods, and processed foods. Commercially prepared fried foods, like French fries and onion rings, also contain a good deal of trans fat.

Trans fats are even worse for cholesterol levels than saturated fats because they raise bad LDL and lower good HDL. They also fire inflammation,(6) an overactivity of the immune system that has been implicated in heart disease, stroke, diabetes, and other chronic conditions. While you should limit your intake of saturated fats, it is important to eliminate trans fats from partially hydrogenated oils from your diet. (Manufacturers must now list trans fats on the food label, right beneath saturated fats.)

The Good Fats Some fats are good because they can improve blood cholesterol levels.

Unsaturated Fats--Polyunsaturated and Monounsaturated
Unsaturated fats are found in products derived from plant sources, such as vegetable oils, nuts, and seeds. There are two main categories: polyunsaturated fats (which are found in high concentrations in sunflower, corn, and soybean oils) and monounsaturated fats (which are found in high concentrations in canola, peanut, and olive oils). In studies in which polyunsaturated and monounsaturated fats were eaten in place of carbohydrates, these good fats decreased LDL levels and increased HDL levels.
PERCENTAGE OF SPECIFIC TYPES OF FAT IN COMMON OILS AND FATS*

Oils

Saturated

Mono-Unsaturated


Poly-Unsaturated


Trans

Canola758290
Safflower912740
Corn1324600
Olive137280
Soybean1644370
Peanut1749320
Palm5037100
Coconut87620
Cooking Fats
Shortening22292918
Lard3944111
Buter602655
Margarine / Spreads
70% Soybean Oil, Stick1822923
67% Corn & Soybean Oil Spread, Tub16274411
48% Soybean Oil, Tub1724498
60% Sunflower, Soybean Oil, andCanola Oil Spread, Tub1822545
*Values expressed as percent of total fat; data are from analyses at Harvard School of Public Health Lipid Laboratory and U.S.D.A. publications.

Dietary Fats and Heart Disease: Beyond the "30%" Recommendation
For years, a low-fat diet was hailed as the centerpiece of a heart-healthy lifestyle, even though there was little evidence that this eating strategy prevented heart disease. The American Heart Association and others urged everyone to limit fat intake to 30% or less of daily calories. One problem with a generic low-fat diet is that it throws out fats that are good for the heart with those that are bad for it. Another problem is that many people who switch to a low-fat diet replace fats with pasta, white rice, bread, and other foods chock full of easily digested carbohydrates.

Several reports over the years have questioned the wisdom of recommending a low-fat diet for preventing or retarding heart disease. Perhaps the biggest nail in the coffin came from the Women's Health Initiative Dietary Modification Trial, published in the February 8, 2006, Journal of the American Medical Association.(3) This eight-year trial, which included almost 49,000 women, found virtually identical rates of heart attacks, strokes, and other forms of cardiovascular disease in women who followed a low-fat diet and women who didn't.

The relation of fat intake to health is one of the areas that Harvard researchers have examined in detail over the last 20 years in two large studies. The Nurses' Health Study and the Health Professionals Follow-up Study have found no link between the overall percentage of calories from fat and any important health outcome, including cancer, heart disease, and weight gain.

What was important in these studies was the type of fat in the diet.(7) There are clear links between the different types of dietary fats and heart disease. Logically, most of the influence that fat intake has on heart disease is due to its effect on blood cholesterol levels.

Ounce for ounce, trans fats are far worse than saturated fats when it comes to heart disease. The Nurses' Health Study found that replacing only 30 calories (7 grams) of carbohydrates every day with 30 calories (4 grams) of trans fats nearly doubled the risk for heart disease.(8) Saturated fats increased risk as well, but not nearly as much.

For the good fats, there is consistent evidence that high intake of either monounsaturated or polyunsaturated fat lowers the risk for heart disease. In the Nurses' Health Study, replacing 80 calories of carbohydrates with 80 calories of either polyunsaturated or monounsaturated fats lowered the risk for heart disease by about 30 to 40 percent.(7)

Fish, an important source of the polyunsaturated fat known as omega-3 fatty acid, has received much attention for its potential to lower heart disease risk. There is strong evidence that fish and fish oil consumption reduces the risk of heart disease deaths and so-called "sudden deaths." A combined analysis of multiple studies suggests that eating just 6 oz per week of fatty (dark meat) fish, such as salmon, herring, mackerel, anchovies, or sardines, may be enough to reduce the risk of dying from heart disease by 36 percent.(9) Higher intakes may be beneficial for people who already have heart disease: One large trial found that by getting 1 gram per day of omega-3 fatty acids over a 3.5 year period, people who had survived a heart attack could lower their risk of dying from heart disease by 25 percent.(10) The study participants got their omega-3s from a capsule; getting a gram a day from fish would mean eating two to three 6-oz servings per week of fatty fish.

Eating fish may help prevent heart disease in several ways. It may replace red meat or other less-healthy sources of protein. More importantly, the omega-3 fats in fish appear to protect the heart against the development of erratic and potentially deadly cardiac rhythm disturbances. The American Heart Association currently recommends that people eat at least two servings of fish a week.(11)

Although there has been some recent concern about contaminants in fish such as mercury and PCBs, the evidence suggests that the proven health benefit of fish consumption is much greater than the potential for harm among individuals who consume fish one to two times per week. So for most people, the best advice is simply to eat a variety of different seafood twice a week, without worrying about mercury or PCBs. The main exception to this advice is for women who are or might become pregnant, nursing mothers, and young children: These groups should include fish in their diets, since omega-3 fats promote normal brain development in children and are important for the health of the mother. But these groups should avoid eating four specific fish species that are higher in mercury - swordfish, tilefish/golden bass, shark, and king mackerel - and should limit albacore tuna to no more than 6 ounces per week. Instead, they should eat two servings per week of a variety of other fish and shellfish, such as salmon, shrimp, chunk light tuna, and scallops. (For more information, see the FDA/EPA dietary advice statement on mercury in fish and shellfish).

If you eat a lot of fish - five or more servings a week - be sure to vary the types of fish you eat and limit consumption of the four species that are higher in mercury (swordfish, tilefish/golden bass, shark, and king mackerel). And one final piece of advice on fish: Levels of PCBs and dioxins in fish are very low, similar to levels in meats, dairy and eggs, so this should not influence your decision about which fish to eat. But if you eat a lot of freshwater fish - more than one serving a day - or eat locally-caught sports fish from inland waters, it makes sense to consult local advisories. (The EPA website has links to state fish advisories.)

Dietary Fats and Cancer
Heart disease is not the only condition that has been linked with fat intake. Researchers once suspected an association between dietary fat and certain cancers. Here again, the type of fat - and not the total amount - seemed to be most important.

Breast Cancer
By the early 1980s, most nutrition experts believed that dietary fat was a major cause of breast cancer.(12,13) This thinking was largely based on international comparisons showing higher breast cancer rates in countries with higher per capita fat intake. But such comparisons are very broad in nature. As more detailed studies were performed over the next couple of decades, the apparent link between total fat intake and breast cancer has faded.(14) The Women's Health Initiative Dietary Modification Trial, which was specifically designed to examine the effect of a low-fat diet on the development of breast cancer, showed similar rates of breast cancer in women eating a low-fat diet and in those eating a "regular" diet.(4)

Other studies - including those by Harvard researchers - of different types of fat have failed to find a link with breast cancer. However, some European studies have reported suggestive findings of lower breast cancer risk among women with a high intake of monounsaturated fats (mainly in the form of olive oil).(15,16)

Colon Cancer
As with breast cancer, international comparisons initially suggested an association between total dietary fat intake and colon cancer risk. But later studies contradicted these earlier findings and revealed instead an association that was weak at best. As was the case with breast cancer, women in the Women's Health Initiative Dietary Modification Trial who ate a low-fat diet developed colon cancer at the same rate as women who didn't.(1) Although fat intake doesn't seem to increase colon cancer risk, high consumption of red meat still does appear to do so.(17)

Prostate Cancer
Although the exact connection between dietary fat and prostate cancer is far from clear, there is some evidence that diets high in animal fat and saturated fat increase prostate cancer risk. However, some studies have also shown no association, while others have implicated unsaturated fats. Clearly much more research is needed to clear up the exact links between dietary fat and prostate cancer.

Other Cancers
Preliminary research has also linked the intake of certain kinds fat with other cancers, though much more research is needed to confirm these results. In the Nurses' Health Study, Harvard researchers found that a high intake of trans fats increased the risk for non-Hodgkin's lymphoma and that a high saturated fat intake increased the risk for endometrial cancer.

Dietary Fat and Obesity
It is a common belief that the more fat you eat, the more body fat you put on, and the more weight you gain. This belief has been bolstered by much of the nutrition advice given to people over the past decade, which has focused on lowering total fat intake while increasing carbohydrate intake. But it isn't completely true, and the advice has been misguided. For example, while Americans have gradually decreased the proportion of calories they get from fat over the last decade, rates of obesity have increased steeply.

Over the short term, following a low-fat diet does lead to weight loss. But so does following a high-fat, low-carbohydrate diet. Actually, almost any diet that helps you take in fewer calories works over the short term. In other words, low-fat diets appear to offer no apparent advantages over diets with fat levels close to the national average. This was demonstrated in the Women's Health Initiative Dietary Modification Trial. Women in this trial who were assigned to a low-fat diet did not lose, or gain, any more weight than women eating a "usual" diet.(2)

Although more research is needed, a prudent recommendation for losing weight or maintaining a healthy weight is to be mindful of the amount of food you eat in relation to the amount of calories you burn in a day. Exercising regularly is especially beneficial.

The Bottom Line: Recommendations for Fat Intake
Although the different types of fat have a varied - and admittedly confusing - effect on health and disease, the basic message is simple: chuck out the bad fats and replace them with good fats. Try to limit saturated fats in your diet, and try to eliminate trans fats from partially hydrogenated oils (a report from the Institute of Medicine has concluded that there is no safe level of trans fats in the diet)).(18) Replace saturated and trans fats with polyunsaturated and monounsaturated fats.

As of January 1, 2006, trans fat must be listed on food labels. More and more "trans-fat" free products are becoming available (there's even a trans fat-free Crisco on the market). Keep in mind, though, that according to the FDA, a product claiming to have zero trans fat can actually contain up to a half gram. (Canada set a different standard of zero as under 0.2 grams.) So you may still want to scan the ingredient list for "partially hydrogenated vegetable oil" and "vegetable shortening," and look for an alternative product without those words, especially if it's something you eat regularly.

Tips for lowering trans fat intake:
· Choose liquid vegetable oils, or a choose a soft tub margarine that contains little or no trans fats.
· Reduce intake of commercially prepared baked goods, snack foods, and processed foods, including fast foods. To be on the safe side, assume that all such products contain trans fats unless they are labeled otherwise.
· When foods containing partially hydrogenated oils can't be avoided, choose products that list the partially hydrogenated oils near the end of the ingredient list.
· To avoid trans fats in restaurants, one strategy is to avoid deep-fried foods, since many restaurants continue to use partially hydrogenated oils in their fryers. You may be able to help change this cooking practice by asking your server, the chef, or manager if the establishment uses trans-free oils.

References
1. Beresford SA, Johnson KC, Ritenbaugh C, et al. Low-fat dietary pattern and risk of colorectal cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006; 295:643-54.
2. Howard BV, Manson JE, Stefanick ML, et al. Low-fat dietary pattern and weight change over 7 years: the Women's Health Initiative Dietary Modification Trial. JAMA 2006; 295:39-49.
3. Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006; 295:655-66.
4. Prentice RL, Caan B, Chlebowski RT, et al. Low-fat dietary pattern and risk of invasive breast cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006; 295:629-42.
5. Hu FB, Stampfer MJ, Rimm EB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999; 281:1387-94.
6. Mozaffarian D, Pischon T, Hankinson SE, et al. Dietary intake of trans fatty acids and systemic inflammation in women. American Journal of Clinical Nutrition 2004; 79:606-12.
7. Hu FB, Manson JE, Willett WC. Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr 2001; 20:5-19.
8. Willett WC, Stampfer MJ, Manson JE, et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 1993; 341:581-5.
9. Mozaffarian D, Rimm EB. Fish intake, contaminants, and human health: evaluating the risks and the benefits. JAMA 2006; 296:1885-1899.
10. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico. Lancet 1999; 354:447-55.
11. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation 2002; 106:2747-57.
12. Willett WC, MacMahon B. Diet and cancer--an overview. N Engl J Med 1984; 310:633-8.
13. Willett WC, MacMahon B. Diet and cancer--an overview (second of two parts). N Engl J Med 1984; 310:697-703.
14. Smith-Warner SA, Spiegelman D, Adami HO, et al. Types of dietary fat and breast cancer: a pooled analysis of cohort studies. Int J Cancer 2001; 92:767-74.
15. Sieri S, Krogh V, Pala V, et al. Dietary patterns and risk of breast cancer in the ORDET cohort. Cancer Epidemiol Biomarkers Prev 2004; 13:567-72.
16. Kushi L, Giovannucci E. Dietary fat and cancer. Am J Med 2002; 113 Suppl 9B:63S-70S. 17. Giovannucci E, Goldin B. The role of fat, fatty acids, and total energy intake in the etiology of human colon cancer. Am J Clin Nutr 1997; 66:1564S-1571S.
18. Institute of Medicine. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids. Washington, DC: National Academies Press, 2002.


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DYSBIOSIS - What Is It?


Signs of Dysbiosis:
1. Chronic unexplained fatigue
2. Frequent constipation
3. Faulty digestion, acid reflux
4. Poor sleeping habits, including nightmares
5. Allergies and chronic food sensitivities
6. Peptic ulcers
7. Difficulty losing weight
8. Joint pain/inflammation
9. Bad breath and gum disease
10. Frequent colds, flu and infections
11. Chronic yeast problems & Candida albican overgrowth
12. Acne, eczema, skin & foot problems
13. Extreme menstrual or menopausal symptoms

The Royal Academy of Medicine in Great Britain states that 80% of all degenerative disease is due to an imbalance of micro-flora in the digestive tract, which produces a compromised immune system. 60% of the immune system receptor cells are located in the colon with another 15% located in the lower part of the small intestine GI tract, especially the colon. By maintaining proper micro ecology and pH environment, the immune system will not be compromised.

"All diseases start in the bowel" - Dr. Bernard Jensen, DC, Ph.D.

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PROBIOTICS - What Do They Do?


Probiotics - The Friendly Flora:
1. Beneficial bacteria that reside in the body
2. Essential for human life and good health
3. A well balanced and well researched probiotic product is no longer a luxury... it is a necessity
4. Approximately four pounds in the human body, most in the GI tract, also found in oral cavity, throat and vagina
5. We need 85% good bacteria and 15% bad bacteria for optimal health, research is showing that 15% good
    and 85% bad today
6. Levels of friendly bacteria are decreasing with rising global toxicity
7. Optimal health traditionally required 100 billion to 1000 billion beneficial bacteria per ml.
    Researchers predict the 21st century high tech body might need 100 trillion beneficial flora colonies
    to preserve good health
8. They used to come in foods like fermented milk or yogurt
9. Fact: During America's Civil War, when sauerkraut was a part of the prisoner's diet, from 90% to 5%
    death rate (small pox)
10. Probiotics help to: digest foods, provide enzymes necessary to metabolize cholesterol and bile acids,
    synthesis of vitamin K.
11. Synthesis of B6 and Thiamine, extracts calories from the food we eat and stores those calories in
    fat cells for later use.
12. Transports nutrients, produce lactase, enhances mineral absorption, prevents diarrhea.
13. Decreases asthma and anemia, curtail thrush, manufactures essential fatty acids and short chain fats.
14. Breakdown and rebuilds hormones, promotes healthy metabolism, breaks down bile acids,
    brakes down toxins.
15. Increases energy, aid in weight management

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ADD & ADHD



ADD & ADHD are diagnosed now more than ever before. Increased awareness about these conditions may contribute in part to the rise of documented cases. Other reasons may include, changes to our diets, lack of essential nutrients, greater exposure to indoor and outdoor pollution, and increased exposure to biologically active agents in our foods(additives/chemicals/excitotoxins) and water. The symptoms of ADD/ADHD are manifestations of a dysfunction of the central nervous system.

What makes this condition difficult are the patterns of imbalances observed in these disorders in the fact that they vary from person to person in an individualized, person-specific way. This is why stabilizing this condition requires a very individualistic case study.

People with ADD/ADHD may be fine the one minute but “off the wall” the next. This apparent random behavior may not be random at all. It may be caused by food or environmental reactions. It could be caused by:

1. Mineral Imbalances (Enzyme and vitamin deficiency)
2. Amino Acid deficiency
3. Fatty Acid deficiency
4. Toxic metals at a cellular level
5. Excitotoxins

It is presently estimated that from 18 million to 22 million children may be placed on activity-modifying drugs such as Ritalin by 2006. Of this group 40% - 50% will NOT be helped by this approach. Drugs should be the last choice of defense – especially when the drugs come with such a long line of side effects. Alternative forms of therapy should certainly be considered before such steps are taken.

In an astonishing article entitled Why are Kids Killing Kids. Dr. Gerald Olarsch, discusses the consequences of mineral deficiency as it relates to kids in the USA. He tells us about a behavior known as pica, a severe and obsessive craving for foods due to mineral deficiencies. Dr. Olarsch feels it is because our body temporarily translates sugar and salt consumption as a fulfillment of the cravings for nutritional minerals. Another ramification of long-term mineral deficiency is that the body will latch on to heavy metals in an attempt to satisfy itself. If the body has no minerals to latch on to it will latch on to and store excess lead, aluminum, copper etc.

The Standard American Diet (SAD) is just that SAD! It is high in refined sugars, additives, preservatives. Hyperactive behavior may result when blood sugar rise rapidly after the intake of these foods. When the blood sugar levels are high, the body releases insulin, this radically lowers the blood sugar – this drop in blood sugar then forces the body to produce adrenaline. The result is hyperkinetic behavior, mental confusion, irritability, anxiety, nervousness and violence – wow that sounds like ADHD?

Laurence B. Procani, RN and Orthomolecular Consultant at Bio-Spectrum Analysis Inc., points out that there is a biochemical difference between ADD and ADHD. The difference is the hyperactive part, and she is able to see this difference, consistently on a cellular level. She believes that ADHD people are fast oxidizers who are often high strung or emotional. The slow oxidizer on other hand is the person with ADD without the hyperactivity. This person’s body does not metabolize available glucose fast enough as opposed to a sudden rise in blood sugar of the fast oxidizer. This person is prone to confusion, nervousness, irritability and panic.

However even if we eat the healthiest diet, we have to have healthy insides to gain the benefits of that food and nutrients. Thus the nutritional value of any food depends upon its absorption in the intestinal tract. So I guess we are NOT what we eat – rather we are what we ABSORB.

We get used to living in a certain way and it is hard to change. Even so, it is important for family members to support one another. Research shows that attempts to modify diet and lifestyle of children with ADD or ADHD are rarely successful unless the parents are willing to change also. Change is difficult but in serious conditions the results will well be worth the effort.

People with ADD/ADHD lack supplies of neurotransmitters, especially serotonin. Serotonin is manufactured in the brain in the presence of B6 and tryptophan. Tryptophan is an essential amino acid. If that and B6 is short the body cannot make serotonin. Calcium/magnesium ratio is a key factor as well – insufficient magnesium can result in high insulin levels which reduces serotonin. Therefore it is necessary to ensure an adequate supply of magnesium in addition to B6 and amino acids.

ADD/ADHD are not mysterious diseases of unknown origin. Children and adults are being successfully treated through natural means. However it is important to realize the uniqueness of this condition. Every case needs to be studied and evaluated through a process of elimination in order to understand the origin of each case. We can do this through individual analysis.

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PSYCHODIETETICS & ORTHOMOLECULAR NUTRITION


"Ortho means 'right'- the right molecules in the right amounts. Orthomolecular medicine leads to the best health and the greatest decrease in disease. It is the most effective prevention in the treatment of disease."
Dr. Linus Pauling

Two times Nobel Prize winner,
founder of Orthomolecular Medicine


A group of progressive minded physicians helped pioneer a new way of treating mental disorders. In 1968, Nobel Prize winner Linus Pauling, Ph.D. originated the term "orthomolecular" to describe an approach to medicine that uses naturally occurring substances normally present in the body. "Ortho" means correct or normal, and orthomolecular physicians recognize that, in many cases of physiological disorders, health can be reestablished by properly correcting, or normalizing, the balance of vitamins, minerals, amino acids, fatty acids and other substances in the body.

Like their more conventional colleagues orthomolecular physicians acknowledge that mental disorders originate from a faulty brain chemistry. However they rely less on prescription medication. They acknowledge the importance of amino acids and how they play a role in creating and regulating neurotransmitters.

Perhaps the greatest contributions made by orthomolecular medicine involves psychiatirc disorders. Abraham Hoffer, MD, and Humphrey Osmond, MD began using large doses of niacin, along with other medicines to successfully treat schizophrenics. Their studies showed that niacin, along with standard medical therapy doubled the number of recoveries in a one year period.

Even today physicians grossly neglect the importance of diet and nutrition. This draconian thinking flies in the face of the research showing up in our own medical journals. The SAD (Standard American Diet) is deficient. Complicating this matter is the reliance on the RDA (Rcommended Daily Allowance) for proper vitamin and mineral doses not to mention the food pyramid. The RDA originated in 1940 and has done very little to adjust the numbers even though our society, food sources and toxic levels are off the charts.

The concept of biochemical individuality is based on the work of Roger J. Williams, Ph.D. Orthomolecular physicians believe RDA levels are not even close to being optimal. In 1987 Richard Kunin, MD summarized the principles of orthomolecular medicine.

1. Nutrition comes first in medical diagnosis and treatment, and nutrient related disorders are
    usually curable once the nutritional balance is achieved.
2. Biochemical individuality is the norm in medical practice; therefore RDA values are unreliable nutrient
    guidelines. Many people require an intake of certain nutrients far beyond the RDA suggested range,
    due to their genetic disposition and environment.
3. Drug treatment is used only for specific indications and always mindful of the potential dangers and
    adverse effects.
4. Environmental pollution and food adulteration are inescapable facts of modern life and are a medical priority.
5. Blood tests do not always reflect the tissue levels of a nutrient.
6. Hope is the indispensable ally of the physician and the absolute right of the patient.


THE MAIN CAUSES OF DEPRESSION, MENTAL FATIGUE AND MENTAL CONFUSION INCLUDE THE FOLLOWING:

Poor Sleep:
Poor sleep depletes mood-controlling neurotransmitters including the happy hormone serotonin. Decreased serotonin leads to depression, mental fatigue, lower pain threshold, and sugar cravings. The amino acid Tryptophan is converted into serotonin. Low-protein diets, malabsorption disorders, and nutritional deficiencies can contribute to serotonin deficiencies.

Protien Deficiencies:
Low protein diets, poor digestion, and malabsorption syndromes contribute to amino acid deficiencies. Remember, amino acids along with certain vitamins and minerals are co-factors to create neurotransmitters.

Nutritional Deficiencies:
Nutritional deficiencies are quite common in USA. In one study up to 50% of patients admitted for hospital care had nutritional deficiencies. (Roubenhouff R, et al, 1987).

A chromium deficiency, which is especially common among those taking cholesterol lowering drugs, can cause hypoglycemia and mood disorders. (Anderson, R.A., 1984)

A deficiency in any B-vitamin can lead to depression, brain fog, and mental fatigue. Magnesium and vitamin B6 are co-factors in the production of dopamine, GABA and serotonin. Birth control pills and Premarin can deplete B6. (Russ C, Hendricks T, Chrisley B, et al, 1983)

Vitamin C helps produce dopamine, norepinenepehrine and serotonin. It plays a major role in the production of the adrenal hormone adrenaline (fight or flight). A deficiency in adrenal function can contribute to fatigue, depression, and confusion. A deficiency of any of the essential nutrients can create a chain reaction leading to all sorts of mood disorders, anxiety, depression and panic disorders.

Allergic Disorders:
Food and chemical sensitivities can cause all sorts of symptoms. Allergic inflammation of the mucous membrane of the intestinal tract causes irritable bowel. Allergic inflammation of the nasal membranes creates sinusitis. Allergic reactions to the respiratory tissue create bronchial spasms (asthma). Allergic reactions can also occur within the brain, creating mental confusion, depression, anxiety and other mood disorders.


AMINO ACIDS AND ORTHOMOLECULAR MEDICINE

Most people who consult their medical doctor for mood disorders will be placed on prescription medication. Many of these are in the form of “selective serotonin reuptake inhibitors” (SSRI). These drugs like Lexapro, Prozac, Paxil, Celexa and Zoloft are supposed to help the brain be more efficient at using the serotonin it produces. However what if the body isn’t producing it – then these drugs will not be as effective?

Where do neurotransmitters come from?
Neurotransmitters are brain chemicals that help relay electrical messages from one nerve cell to another. Neurotransmitters are produced from the amino acids in the foods we eat. Amino acids join together in a certain pattern to create a protein. Eating a protein rich diet allows us to replenish our ongoing demand for the “essential amino acids”. Half the amino acids are essential, this means our bodies can’t manufacture them and we must get them from the proteins we eat. Certain amino acids with vitamins (B6, B3 and C) and minerals (magnesium) produce neurotransmitters. The amino acid Tryptophan turns into serotonin, the amino acid phenylalanine turns into epinenephrine. Thus amino acids are raw nutrients needed to manufacture the neurotransmitters which regulate our moods.

What do neurotransmitters do?
They help regulate pain, reduce anxiety, promote happiness, initiate sleep, boost energy, and mental clarity. The neurotransmitters that cause excitatory reactions are known as catecholamines, they epinephrine and norepinephrin (adrenaline), are derived from the amino acid phenylalanine. Inhibitory or relaxing neurotransmitters include serotonin, and gamma-amino butyric acid (GABA) coming from glutamine.

Correcting the cause of the mood disorders:
No one is born with a Prozac deficiency. However people can develop a serotonin deficiency. Using a SSRI doesn’t correct the cause, if someone is out of gas (serotonin), why should you use a gasoline additive (SSRI)?Why not fill the tank (brain) with gas (serotonin) instead. – Dr. Roger Murphree, DC, CNS. www.DrRodger.com

Depression and mood disorders affect over 17 million Americans. Prozac was cleared by the FDA in 1988. By 1994, it had become the fastest growing prescription drug in America with sales over $1.2 billion. Prozac has had some positive effects on people with depression, however 1734 suicide deaths and over 28 000 adverse reactions have come from the drug.

Prescription anti-depressants may cause depression, addiction, suicide, tardive dyskinesia, sexual dysfunction and tardive dementia. These side effects are due to poor liver function and drug induced nutritional deficiencies.

The June issue in 1990 of "Health Letter", estimated that muscle tremours affect a whopping 15%-25% of all Prozac patients. Medical science show us now that how feel is largerly related by the foods we eat. Serotonin elevates mood, reduces food cravings, increases pain threshold, promotes deep sleep, relieves tension and calms the systems of the body.

GABA is a tripetide made from three amino acids. It is an inhibitory hormone and has a calming effect on the brain. Nardil and Marplan are MOA (monoamine oxide inhibitors). MOA inhibitors and some tranquilizers (Xanax) work by increasing the effectiveness of the neurotransmitter GABA. Dopamine and norepinephrine increase mental clarity and alertness, reduce fatigue and elevate moods - they are synthesized from the amino acid phenylalanine.

  Psychodietetic Profile Download

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ONCOLOGY NUTRITION



Immune system attacking cancer cell

Science-based Approach
AICR's expert report Food, Nutrition and the Prevention of Cancer: a global perspective established the relationship between a predominantly plant-based diet and reduced cancer risk. The report suggests that eating more vegetables, fruits, whole grains and beans coupled with increased physical activity can reduce cancer risk by 30 to 40 percent. Foods That Fight Cancer summarizes current research on some specific foods.

Cancer Prevention and Weight Management
The same predominantly plant-based diet coupled with increased physical activity can play a major role in weight loss as well.

Popular high-protein and low-carb diets have confused some people about weight-loss strategies. But research shows that vegetables and fruits are a powerful tool in weight management, too. The fiber and water in plant foods make you feel satisfied without filling you up with calories.

The three strategies for both cancer prevention and weight loss are very similar.


Strategies for Cancer Prevention
1. Eat a greater proportion of plant foods
2. Keep physically active
3. Maintain a healthy weight
Strategies for Weight Loss
1. Eat a greater proportion of plant foods
2. Keep physically active
3. Reduce your portion size



cancer cell development


tumor growth

breast cancer tumor


brain cancer tumor


Related Articles


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  Microwave Dangers
  Must read on CANCER
  Cancer survivor lifestyle changes
  Red meat and breast cancer
  Vitamine C and cancer
  Margarine and cancer
  Weight loss resistance and cancer

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IMMUNE SYSTEM - Your Main Defense


Introduction
The human immune system is a truly amazing constellation of responses to attacks from outside the body. It has many facets, a number of which can change to optimize the response to these unwanted intrusions. The system is remarkably effective, most of the time. This note will give you a brief outline of some of the processes involved. An antigen is any substance that elicits an immune response, from a virus to a sliver. The immune system has a series of dual natures, the most important of which is self/non-self recognition. The others are: general/specific, natural/adaptive = innate/acquired, cell-mediated/humoral, active/passive, primary/secondary. Parts of the immune system are antigen-specific (they recognize and act against particular antigens), systemic (not confined to the initial infection site, but work throughout the body), and have memory (recognize and mount an even stronger attack to the same antigen the next time). Self/non-self recognition is achieved by having every cell display a marker based on the major histocompatibility complex (MHC). Any cell not displaying this marker is treated as non-self and attacked. The process is so effective that undigested proteins are treated as antigens. Sometimes the process breaks down and the immune system attacks self-cells. This is the case of autoimmune diseases like multiple sclerosis, systemic lupus erythematosus, and some forms of arthritis and diabetes. There are cases where the immune response to innocuous substances is inappropriate. This is the case of allergies and the simple substance that elicits the response is called an allergen.

Fluid Systems of the Body
There are two main fluid systems in the body: blood and lymph. The blood and lymph systems are intertwined throughout the body and they are responsible for transporting the agents of the immune system.

The Blood System
The 5 liters of blood of a 70 kg (154 lb) person constitute about 7% of the body's total weight. The blood flows from the heart into arteries, then to capillaries, and returns to the heart through veins.Blood is composed of 52–62% liquid plasma and 38–48% cells. The plasma is mostly water (91.5%) and acts as a solvent for transporting other materials (7% protein [consisting of albumins (54%), globulins (38%), fibrinogen (7%), and assorted other stuff (1%)] and 1.5% other stuff). Blood is slightly alkaline (pH = 7.40 ± .05) and a tad heavier than water (density = 1.057 ± .009).All blood cells are manufactured by stem cells, which live mainly in the bone marrow, via a process called hematopoiesis. The stem cells produce hemocytoblasts that differentiate into the precursors for all the different types of blood cells. Hemocytoblasts mature into three types of blood cells: erythrocytes (red blood cells or RBCs), leukocytes (white blood cells or WBCs), and thrombocytes (platelets).The leukocytes are further subdivided into granulocytes (containing large granules in the cytoplasm) and agranulocytes (without granules). The granulocytes consist of neutrophils (55–70%), eosinophils (1–3%), and basophils (0.5–1.0%). The agranulocytes are lymphocytes (consisting of B cells and T cells) and monocytes. Lymphocytes circulate in the blood and lymph systems, and make their home in the lymphoid organs. All of the major cells in the blood system are illustrated below.

There are 5000–10,000 WBCs per mm3 and they live 5-9 days. About 2,400,000 RBCs are produced each second and each lives for about 120 days (They migrate to the spleen to die. Once there, that organ scavenges usable proteins from their carcasses). A healthy male has about 5 million RBCs per mm3, whereas females have a bit fewer than 5 million.

Normal Adult Blood Cell Counts

Red Blood Cells

5.0*106/mm3
Platelets
2.5*105/mm3
Leukocytes
7.3*103/mm3
Neutrophil
50-70%
Lymphocyte
20-40%
Monocyte
1-6%
Eosinophil
1-3%
Basophil
< 1%
The goo on RBCs is responsible for the usual ABO blood grouping, among other things. The grouping is characterized by the presence or absence of A and/or B antigens on the surface of the RBCs. Blood type AB means both antigens are present and type O means both antigens are absent. Type A blood has A antigens and type B blood has B antigens.Some of the blood, but not red blood cells (RBCs), is pushed through the capillaries into the interstitial fluid.

The Lymph System
Lymph is an alkaline (pH > 7.0) fluid that is usually clear, transparent, and colorless. It flows in the lymphatic vessels and bathes tissues and organs in its protective covering. There are no RBCs in lymph and it has a lower protein content than blood. Like blood, it is slightly heavier than water (density = 1.019 ± .003). The lymph flows from the interstitial fluid through lymphatic vessels up to either the thoracic duct or right lymph duct, which terminate in the subclavian veins, where lymph is mixed into the blood. (The right lymph duct drains the right sides of the thorax, neck, and head, whereas the thoracic duct drains the rest of the body.) Lymph carries lipids and lipid-soluble vitamins absorbed from the gastrointestinal (GI) tract. Since there is no active pump in the lymph system, there is no back-pressure produced. The lymphatic vessels, like veins, have one-way valves that prevent backflow. Additionally, along these vessels there are small bean-shaped lymph nodes that serve as filters of the lymphatic fluid. It is in the lymph nodes where antigen is usually presented to the immune system. The human lymphoid system has the following:· primary organs: bone marrow (in the hollow center of bones) and the thymus gland (located behind the breastbone above the heart), and · secondary organs at or near possible portals of entry for pathogens: adenoids, tonsils, spleen (located at the upper left of the abdomen), lymph nodes (along the lymphatic vessels with concentrations in the neck, armpits, abdomen, and groin), Peyer's patches (within the intestines), and the appendix.

Innate Immunity
The innate immunity system is what we are born with and it is nonspecific; all antigens are attacked pretty much equally. It is genetically based and we pass it on to our offspring.Surface Barriers or Mucosal Immunity

1. The first and, arguably, most important barrier is the skin. The skin cannot be penetrated by most organisms unless it already has an opening, such as a nick, scratch, or cut.

2. Mechanically, pathogens are expelled from the lungs by ciliary action as the tiny hairs move in an upward motion; coughing and sneezing abruptly eject both living and nonliving things from the respiratory system; the flushing action of tears, saliva, and urine also force out pathogens, as does the sloughing off of skin.

3. Sticky mucus in respiratory and gastrointestinal tracts traps many microorganisms.

4. Acid pH (< 7.0) of skin secretions inhibits bacterial growth. Hair follicles secrete sebum that contains lactic acid and fatty acids both of which inhibit the growth of some pathogenic bacteria and fungi. Areas of the skin not covered with hair, such as the palms and soles of the feet, are most susceptible to fungal infections. Think athlete's foot.

5. Saliva, tears, nasal secretions, and perspiration contain lysozyme, an enzyme that destroys Gram positive bacterial cell walls causing cell lysis. Vaginal secretions are also slightly acidic (after the onset of menses). Spermine and zinc in semen destroy some pathogens. Lactoperoxidase is a powerful enzyme found in mother's milk.

6. The stomach is a formidable obstacle insofar as its mucosa secrete hydrochloric acid (0.9 < pH < 3.0, very acidic) and protein-digesting enzymes that kill many pathogens. The stomach can even destroy drugs and other chemicals.

Normal flora are the microbes, mostly bacteria, that live in and on the body with, usually, no harmful effects to us. We have about 1013 cells in our bodies and 1014 bacteria, most of which live in the large intestine. There are 103–104 microbes per cm2 on the skin (Staphylococcus aureus, Staph. epidermidis, diphtheroids, streptococci, Candida, etc.). Various bacteria live in the nose and mouth. Lactobacilli live in the stomach and small intestine. The upper intestine has about 104 bacteria per gram; the large bowel has 1011 per gram, of which 95–99% are anaerobes (An anaerobe is a microorganism that can live without oxygen, while an aerobe requires oxygen.) or bacteroides. The urogenitary tract is lightly colonized by various bacteria and diphtheroids. After puberty, the vagina is colonized by Lactobacillus aerophilus that ferment glycogen to maintain an acid pH.Normal flora fill almost all of the available ecological niches in the body and produce bacteriocidins, defensins, cationic proteins, and lactoferrin all of which work to destroy other bacteria that compete for their niche in the body. The resident bacteria can become problematic when they invade spaces in which they were not meant to be. As examples: (a) staphylococcus living on the skin can gain entry to the body through small cuts/nicks. (b) Some antibiotics, in particular clindamycin, kill some of the bacteria in our intestinal tract. This causes an overgrowth of Clostridium difficile, which results in pseudomembranous colitis, a rather painful condition wherein the inner lining of the intestine cracks and bleeds.A phagocyte is a cell that attracts (by chemotaxis), adheres to, engulfs, and ingests foreign bodies. Promonocytes are made in the bone marrow, after which they are released into the blood and called circulating monocytes, which eventually mature into macrophages (meaning "big eaters", see below).

Some macrophages are concentrated in the lungs, liver (Kupffer cells), lining of the lymph nodes and spleen, brain microglia, kidney mesoangial cells, synovial A cells, and osteoclasts. They are long-lived, depend on mitochondria for energy, and are best at attacking dead cells and pathogens capable of living within cells. Once a macrophage phagocytizes a cell, it places some of its proteins, called epitopes, on its surface—much like a fighter plane displaying its hits. These surface markers serve as an alarm to other immune cells that then infer the form of the invader. All cells that do this are called antigen presenting cells (APCs).

The non-fixed or wandering macrophages roam the blood vessels and can even leave them to go to an infection site where they destroy dead tissue and pathogens. Emigration by squeezing through the capillary walls to the tissue is called diapedesis or extravasation. The presence of histamines at the infection site attract the cells to their source.

Natural killer cells move in the blood and lymph to lyse (cause to burst) cancer cells and virus-infected body cells. They are large granular lymphocytes that attach to the glycoproteins on the surfaces of infected cells and kill them.Polymorphonuclear neutrophils, also called polys for short, are phagocytes that have no mitochondria and get their energy from stored glycogen. They are nondividing, short-lived (half-life of 6–8 hours, 1–4 day lifespan), and have a segmented nucleus. [The picture below shows the neutrophil phagocytizing bacteria, in yellow.] They constitute 50–75% of all leukocytes. The neutrophils provide the major defense against pyogenic (pus-forming) bacteria and are the first on the scene to fight infection. They are followed by the wandering macrophages about three to four hours later.

The complement system is a major triggered enzyme plasma system. It coats microbes with molecules that make them more susceptible to engulfment by phagocytes. Vascular permeability mediators increase the permeability of the capillaries to allow more plasma and complement fluid to flow to the site of infection. They also encourage polys to adhere to the walls of capillaries (margination) from which they can squeeze through in a matter of minutes to arrive at a damaged area. Once phagocytes do their job, they die and their "corpses," pockets of damaged tissue, and fluid form pus. Eosinophils are attracted to cells coated with complement C3B, where they release major basic protein (MBP), cationic protein, perforins, and oxygen metabolites, all of which work together to burn holes in cells and helminths (worms). About 13% of the WBCs are eosinophils. Their lifespan is about 8–12 days. Neutrophils, eosinophils, and macrophages are all phagocytes.Dendritic cells are covered with a maze of membranous processes that look like nerve cell dendrites. Most of them are highly efficient antigen presenting cells. There are four basic types: Langerhans cells, interstitial dendritic cells, interdigitating dendritic cells, and circulating dendritic cells. Our major concern will be Langerhans cells, which are found in the epidermis and mucous membranes, especially in the anal, vaginal, and oral cavities. These cells make a point of attracting antigen and efficiently presenting it to T helper cells for their activation. [This accounts, in part, for the transmission of HIV via sexual contact.]

Each of the cells in the innate immune system bind to antigen using pattern-recognition receptors. These receptors are encoded in the germ line of each person. This immunity is passed from generation to generation. Over the course of human development these receptors for pathogen-associated molecular patterns have evolved via natural selection to be specific to certain characteristics of broad classes of infectious organisms. There are several hundred of these receptors and they recognize patterns of bacterial lipopolysaccharide, peptidoglycan, bacterial DNA, dsRNA, and other substances. Clearly, they are set to target both Gram-negative and Gram-positive bacteria.

Adaptive or Acquired Immunity
Lymphocytes come in two major types: B cells and T cells. The peripheral blood contains 20–50% of circulating lymphocytes; the rest move in the lymph system. Roughly 80% of them are T cells, 15% B cells and remainder are null or undifferentiated cells. Lymphocytes constitute 20–40% of the body's WBCs. Their total mass is about the same as that of the brain or liver. (Heavy stuff!)B cells are produced in the stem cells of the bone marrow; they produce antibody and oversee humoral immunity. T cells are nonantibody-producing lymphocytes which are also produced in the bone marrow but sensitized in the thymus and constitute the basis of cell-mediated immunity. The production of these cells is diagrammed below.Parts of the immune system are changeable and can adapt to better attack the invading antigen. There are two fundamental adaptive mechanisms: cell-mediated immunity and humoral immunity.

Cell-mediated immunity
Macrophages engulf antigens, process them internally, then display parts of them on their surface together with some of their own proteins. This sensitizes the T cells to recognize these antigens. All cells are coated with various substances. CD stands for cluster of differentiation and there are more than one hundred and sixty clusters, each of which is a different chemical molecule that coats the surface. CD8+ is read "CD8 positive." Every T and B cell has about 105 = 100,000 molecules on its surface. B cells are coated with CD21, CD35, CD40, and CD45 in addition to other non-CD molecules. T cells have CD2, CD3, CD4, CD28, CD45R, and other non-CD molecules on their surfaces. The large number of molecules on the surfaces of lymphocytes allows huge variability in the forms of the receptors. They are produced with random configurations on their surfaces. There are some 1018 different structurally different receptors. Essentially, an antigen may find a near-perfect fit with a very small number of lymphocytes, perhaps as few as one.T cells are primed in the thymus, where they undergo two selection processes. The first positive selection process weeds out only those T cells with the correct set of receptors that can recognize the MHC molecules responsible for self-recognition. Then a negative selection process begins whereby T cells that can recognize MHC molecules complexed with foreign peptides are allowed to pass out of the thymus.Cytotoxic or killer T cells (CD8+) do their work by releasing lymphotoxins, which cause cell lysis. Helper T cells (CD4+) serve as managers, directing the immune response. They secrete chemicals called lymphokines that stimulate cytotoxic T cells and B cells to grow and divide, attract neutrophils, and enhance the ability of macrophages to engulf and destroy microbes. Suppressor T cells inhibit the production of cytotoxic T cells once they are unneeded, lest they cause more damage than necessary. Memory T cells are programmed to recognize and respond to a pathogen once it has invaded and been repelled.

Humoral immunity
An immunocompetent but as yet immature B-lymphocyte is stimulated to maturity when an antigen binds to its surface receptors and there is a T helper cell nearby (to release a cytokine). This sensitizes or primes the B cell and it undergoes clonal selection, which means it reproduces asexually by mitosis. Most of the family of clones become plasma cells. These cells, after an initial lag, produce highly specific antibodies at a rate of as many as 2000 molecules per second for four to five days. The other B cells become long-lived memory cells. Antibodies, also called immunoglobulins or Igs [with molecular weights of 150–900 Md], constitute the gamma globulin part of the blood proteins. They are soluble proteins secreted by the plasma offspring (clones) of primed B cells. The antibodies inactivate antigens by, (a) complement fixation (proteins attach to antigen surface and cause holes to form, i.e., cell lysis), (b) neutralization (binding to specific sites to prevent attachment—this is the same as taking their parking space), (c) agglutination (clumping), (d) precipitation (forcing insolubility and settling out of solution), and other more arcane methods. Constituents of gamma globulin are: IgG-76%, IgA-15%, IgM-8%, IgD-1%, and IgE-0.002% (responsible for autoimmune responses, such as allergies and diseases like arthritis, multiple sclerosis, and systemic lupus erythematosus). IgG is the only antibody that can cross the placental barrier to the fetus and it is responsible for the 3 to 6 month immune protection of newborns that is conferred by the mother.



IgM is the dominant antibody produced in primary immune responses, while IgG dominates in secondary immune responses. IgM is physically much larger than the other immunoglobulins.

Notice the many degrees of flexibility of the antibody molecule. This freedom of movement allows it to more easily conform to the nooks and crannies on an antigen. The upper part or Fab (antigen binding) portion of the antibody molecule (physically and not necessarily chemically) attaches to specific proteins [called epitopes] on the antigen. Thus antibody recognizes the epitope and not the entire antigen. The Fc region is crystallizable and is responsible for effector functions, i.e., the end to which immune cells can attach.Lest you think that these are the only forms of antibody produced, you should realize that the B cells can produce as many as 1014 conformationally different forms.The process by which T cells and B cells interact with antigens is summarized in the diagram below.

In the ABO blood typing system, when an A antigen is present (in a person of blood type A), the body produces an anti-B antibody, and similarly for a B antigen. The blood of someone of type AB, has both antigens, hence has neither antibody. Thus that person can be transfused with any type of blood, since there is no antibody to attack foreign blood antigens. A person of blood type O has neither antigen but both antibodies and cannot receive AB, A, or B type blood, but they can donate blood for use by anybody. If someone with blood type A received blood of type B, the body's anti-B antibodies would attack the new blood cells and death would be imminent.All of these of these mechanisms hinge on the attachment of antigen and cell receptors. Since there are many, many receptor shapes available, WBCs seek to optimize the degree of confluence between the two receptors. The number of these "best fit" receptors may be quite small, even as few as a single cell. This attests to the specificity of the interaction. Nevertheless, cells can bind to receptors whose fit is less than optimal when required. This is referred to as cross-reactivity. Cross-reactivity has its limits. There are many receptors to which virions cannot possibly bind. Very few viruses can bind to skin cells. The design of immunizing vaccines hinges on the specificity and cross-reactivity of these bonds. The more specific the bond, the more effective and long-lived the vaccine. The smallpox vaccine, which is made from the vaccinia virus that causes cowpox, is a very good match for the smallpox receptors. Hence, that vaccine is 100% effective and provides immunity for about 20 years. Vaccines for cholera have a relatively poor fit so they do not protect against all forms of the disease and protect for less than a year.The goal of all vaccines is promote a primary immune reaction so that when the organism is again exposed to the antigen, a much stronger secondary immune response will be elicited. Any subsequent immune response to an antigen is called a secondary response and it has
1. a shorter lag time,
2. more rapid buildup,
3. a higher overall level of response,
4. a more specific or better "fit" to the invading antigen,
5. utilizes IgG instead of the large multipurpose antibody IgM.

Summary
Immunity can be either natural or artificial, innate or acquired=adaptive, and either active or passive.

· Active natural (contact with infection): develops slowly, is long term, and antigen specific.

· Active artificial (immunization): develops slowly, lasts for several years, and is specific to the antigen
  for which the immunization was given.

· Passive natural (transplacental = mother to child): develops immediately, is temporary, and affects
  all antigens to which the mother has immunity.

· Passive artificial (injection of gamma globulin): develops immediately, is temporary, and affects
  all antigens to which the donor has immunity.

Objectives
Know: antigen, overall properties of the immune system, allergen; major fluid systems of the body; hematopoiesis occurs in stem cells of the bone; erythrocytes, leukocytes, and thrombocytes; types of white blood cells; lymphoid system and lymph nodes; mucosal immunity and types of surface barriers to infection; normal flora; phagocytes, macrophages, antigen presenting cells, neutrophils, B cells and T cells are produced in the bone marrow and T cells are primed in the thymus, CD4+ and CD8+ cells, helper cells, memory cells, cytotoxic cells, suppressor cells; priming and clonal selection; antibody and Igs; differences between identifying self and non-self, innate and acquired immunity, primary and secondary immunity, active and passive immunity; specificity and cross-reactivity.


    


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SPORTS DYSTONIAS & YIPS


Basic information on Yips!
We give the "Yips" a neurological name by calling it focal dystonia. However the problem has a real basic yet complicated explanation. I have devoted the last five years of my life to these phenomena as I personally developed the yips with the driver in golf.

Very little cognitive psychology, hypnotherapy or any psycho-pump up positivism, will make an imprint on this issue. Once you have the yips you have them, however you can teach and re-associate your brain to stay ahead of them. No positive thinking or positive affirmations will make you overcome this problem. However being positive is a lot better than being negative.

However most of my answers were found in neurology and brain learning patterns for this phenomena.

The problem with the yips stem from a part of the brain that is actually trying to help you, believe it or not. So when you are yipping; your body and brain are actually trying to help you through the fight or flight response. The actual problem starts in the SYMPATHETIC NERVOUS SYSTEM: The division of the autonomic nervous system that acts as a sort of red alert system that goes into action when one is faced with an emergency situation. If the sympathetic nervous system is stimulated, the heart beats faster and the blood pressure rises, exactly what happens when you yip it. The blood that is near the skin or in the stomach area rushes to the muscle tissues, thus preparing the individual for evasive or defensive action, fight or flight. The sympathetic nervous system was designed to help one cope with infrequent, emergency situations. However the tension of modern living and how we stress ourselves out (golf course), forces this system to work overtime, thus resulting in blocking motor cortex behaviors.

The part of the body that assists in all this is the HPA (Hypothalamic-pituitary-adrenal-cortical-axis). I am not trying to give you a lesson in medicine; I am just trying to explain to you the yips are a natural biological response to excessive "non-conscious" anxieties.

So in basic terms, it is your "primal brain" that causes you to yip it. This part of the brain does not understand anything about golf; it only understands how to keep you alive. Thus this means your primal brain only understands fear and anxiety. So any kind of excessive anxiety over a long period of time is going to spring this part of the brain into action. So it sees no difference between you being chased by a lion or you being scared of missing a short putt, hitting it out of bounds, chipping it. Fear is fear, and when your brain sees that white ball, associates that to a chip shot, associates that to a golf course, now you have a group of associations that the primal brain is scared off. So to protect you from having a heart attach, because the primal brain feels how your body is reacting to this associative anxiety, it is going to put a BLOCK on this behavior, THUS a total YIP.

ANXIETY, STRESS, FEAR, PANIC, PHOBIAS AND FOCAL DYSTONIAS "THE YIPS"

Distinguishing between them
The definitions of fear and anxiety are often confounded, the words being used interchangeably for the same general concept, even though there are obvious advantages to using two distinct words to designate separate though related phenomena.

The word fear comes from the Old English word faer (Oxford English Dictionary, 1933), which meant "sudden calamity or danger". It is currently defined as "an agitated foreboding often of some real or specific peril" (Webster’s Third International Dictionary, 1981) and as "the possibility that something dreaded or unwanted may occur" (Standard College Dictionary, 1963). These definitions underscore several connotations to the word fear; it points to the possible occurrence of an "unwanted" or calamitous event; the event has not yet occurred (that is, it is in the future); the individual is concerned (agitated foreboding) about the event. Fear, then refers to the appraisal that there is actual or potential danger in a given situation. It is a cognitive process as opposed to an emotional reaction.

Anxiety, on the other hand is defined as a "tense emotional state" (Funk & Wagnalls, 1963) and is often marked by such physical symptoms as tension, tremor, sweating, palpitation and increased pulse rate. The term anxiety comes from the Latin word anxius, and its usage dates back to as early as 1525. The Latin term was defined as a condition of agitation and distress. The stem of anxius - anx – comes from another Latin word, angere, which means to "choke" or to "strangle". The word anxius, probably referred to choking frequently experienced by anxious individuals (Lewis, 1970). We here this term used a lot in golf. This has a direct relation to stress and the HPA.

Phobia refers to a specific kind of fear and is defined as an "exaggerated and often disabling fear" (Webster’s Third International Dictionary, 1981). A phobia is also characterized by an intense desire to avoid the feared situation, and evokes anxiety when one is exposed to this situation. The word is derived from the Greek word phobos for "flight".

Panic is defined as a "sudden overpowering fright…accompanied by increasing or frantic attempts to secure safety" (Webster’s Third International Dictionary, 1981). The word, which was in use as early as 1603, derives from the name of the Greek deity Panikos, the god of woods and shepherds, who was regarded as the cause of panic among the Persians at marathon and, by the Greeks, as the cause of any sudden, groundless fear.

The professional athletes struggling with a Focal Dystonia will experience two or more of these physical and emotional experiences at the same time thus making top athletic performance impossible.

Anxiety may be distinguished from fear in that the former is an emotional process while fear is a cognitive one. Fear involves the intellectual appraisal of a threatening stimulus; anxiety involves the emotional response to that appraisal. When a person has anxiety he experiences a subjectively unpleasant emotional state characterized by unpleasant subjective feelings such as tension or nervousness, and by physiological symptoms like heart palpitations, tremor, nausea and dizziness. A fear is activated when a person is exposed, either physically or psychologically, to the stimulus situation he considers threatening. When the fear becomes activated, he experiences anxiety. Fear then is the appraisal of danger, anxiety is the unpleasant feeling state evoked when fear is stimulated. In addition to anxiety a variety of symptoms referable to the autonomic and the somatic nervous systems may be provoked concurrently. In a putting "yipping" case the fear would be the "possibility of missing the short putt" because the stroke might fall apart (physical), to go with the embarrassment of missing a short one (psychological), then this will activate anxiety that will in effect cause all the fears to become reality.

A phobia refers to a specific object of fear. Initially a person is afraid of missing the short putt. When in the situation, he is acutely afraid of consequences (other people’s thoughts, embarrassment, inability to perform etc.). When phobia or fear is activated, the individual’s reaction may range from mild anxiety to panic. The objects of phobias can range from small to large – the main quality of a phobia is that it involves the appraisal of a high degree of risk in a situation that is relatively safe. So the same person with the fear of missing a short putt will perceive this shot as "dangerous". However, he does not experience anxiety until he finds himself in that situation. A player might say: "I might stand over a short putt and not be able to take the putter back; this will embarrass me because I am a professional golfer, and I am not supposed to do this". The person who perceives this threat as overwhelming may have a panic attack.

The concept of danger arises from the possible consequences. Before he sets foot on the course this fear is latent, once in the presence of the association, the fear become activated, and all the unpleasant affective and physiological symptoms associated with panic attacks are aroused. Thus panic is an intense, acute state of anxiety associated with the other dramatic physiological, motor, and cognitive symptoms. The physiological correlates of panic are an intensified version of those of anxiety – that is rapid pulse, dizziness, cold and profuse sweating and tremor. In addition, one has a sense of impending catastrophe, pervasive inhibitions, and an overwhelming desire to flee or get help. This is what is called the stage of the full blown yip!

Anxiety is often looked at as a performance inhibitor, however very few experts have actually gone out to research and understand its influence from a psychological and physiological perspective in golf. Anxiety is related to a certain level of stress that either makes us perform well, inconsistent or "choke".

In people with anxiety-related disorders, fear comes to organize and control the person’s life to the extent of severe functional impairment. High levels of anxiety inhibit and distort rational cognitive processing. Cognitive interventions with these people often include educating them about the physiological symptoms of anxiety such as the racing heart, shortness of breath, and sweaty palms. These people are taught that feelings of dread are secondary to autonomic symptoms and should not be taken as seriously as they feel. A focus on understanding normal biological processes usually redirects the client away from catastrophic attributions of serious illness.

The boost of cortical processing from psycho-education is combined with exposure and response prevention. Exposure and response prevention means that the client faces the feared stimulus, without being allowed to retreat back to the "safety" environment. Exposure is usually systematic, gradual, and paired with relaxation training used to aid in the down regulation of effective arousal. This process combines increased cortical processing (thought) with the result of exposure (affect), allowing fear circuitry to integrate with cortical circuitry in order to permit inhibition, habituation, and increased conscious control (Cozolino, 2002).

How does this translate into what is going on in the brain during sports intervention? Research has demonstrated that disorders of anxiety and depression correlate with changes in metabolic balance within the brain. For example, symptoms of depression correlate with changes in activation in the frontal cortex – lower levels of activation in the left and higher levels in the right (Baxter et al., 1985; Field, Healy, Goldstein, Perry, & Bendell, 1988) have found. Alternately, the imbalance in functioning may be due to dysregulation among different regions within the frontal cortex (Brody et al., 2001).

Symptoms of obsessive-compulsive disorder correlate with heightened activation in the medial portions of the frontal cortex and a subcortical structure called the caudate nucleus (Rauch et al., 1994). Posttraumatic flashbacks and states of high arousal correlate with higher levels of activation in right-sided limbic and medial frontal structures. Importantly, high arousal also correlates with decreased metabolism in the expressive language centers of the left hemisphere (Rauch et al., 1996).

There is an increasing awareness that neural networks throughout the brain are stimulated to grow and organize by interaction with the social environment. Early relationship becomes neurally encoded in networks of sensory, motor, and emotional learning to form what dynamic therapists call inner objects. These inner objects have the power to soothe or dysregulate, depending on the quality of our attachment experiences with significant others. These unconscious memories organize our inner worlds both when we are alone and when we are in the proximity of others. Given the essential social organization of the brain, at some level we always experience ourselves in context of others.

In line with this, differentiation needs to be understood. Differentiation is the development of autonomy – a balance between the recognition of the needs of self and others. Anxiety is the enemy of differentiation that is the more frightened people are, the more dependent and primitive they become in their interaction with others and their environment (Bowen, 1978).

When individuals become anxious and this processing regression occurs, family members try – unconsciously and consciously – to shape the family in a manner so as to reduce their own anxiety. The primal responses to anxiety is quite common in sport, this is part of what people perceive as "choking".

The Amygdala and Anxiety
The amygdala is a central neural hub of emotional experience, suggesting that it may be involved with some of the more unusual human experiences. Electrical stimulation of the amygdala results in a wide variety of bodily sensations (Halgren, Walter, Cherlow, & Crandall, 1978). Feelings of anxiety, déjà vu, and memory like hallucinations have also been reported with the stimulation of the amygdala (Chapman, Walter, Markham, Rand, & Crandall, 1967; Penfield & Perot, 1963; Weingarten, Cherlow, & Holmgren, 1977). Because of its low threshold, subtle seizure activity may trigger the amygdala to activate normally inhibited sensory and emotional memories that then break into conscious awareness (Sarter & Markowitsch, 1985). The primitive memories may also become activated in states of stress and posttraumatic arousal (Van der Kolk & Greenberg, 1987). Individuals under stress may become particularly vulnerable to the intrusion of powerful memories of early childhood (Cozolino, 1997).

The amygdala is located within the limbic system and beneath the temporal lobes on each side of the brain. It is well developed at birth and has a significant role in the networks involved with emotional learning (Brodal, 1992). Portions of the amygdala (the basolateral areas) have evolved in tandem with the expansion of the cerebral cortex in humans (Stephan & Andy, 1977). The amygdala’s neural connectivity supports its participation in the integration of the different senses with a special emphasis on vision (van Hoesen, 1981). The amygdala functions as an organ of appraisal for danger, safety, and familiarity in approach-avoidance situations (Sarter & Markowitsch, 1985).

The amygdala’s direct neural connectivity with the hypothalamus (Amaral, Veazy & Cowan, 1982) and limbic-motor circuits allows it to trigger rapid action. The power of phobias and flashbacks is greatly enhanced by the involvement of immediate and intense somatic activation provided by this direct connectivity. Thus, the amygdala is one of the key components of affective memory, not just in infancy but also throughout life (Ross, Homan, & Buck, 1994). In the fully developed brain, the amygdala enhances hippocampal processing of emotional memory by stimulating the release of norepinephrine and glucocorticoids via other brain structures (McGaugh, 1996; McGaugh et al., 1993). Through these chemical messages, the hippocampus is put on notice that what is being experienced is important to remember.

The hippocampus is noted for its late maturation, with the myelination of cortical-hippocampal circuits continuing into late adolescence (Benes, 1989). Research suggests that sustained stress results in excessive exposure of the hippocampus to glucocorticoids, released in the response to acute stress (Sapolsky, 1987). Prolonged high levels of glucocorticoids can result in dendritic degeneration, increased vulnerability to future neurological insult, inhibited hippocampal functioning, and cell death (Wantanabe, Gould, & McEwen, 1992). Given that chronic stress correlates with decreased hippocampal volume, and that so many of us suffer from it, it might be a good time to look at this from a nutritional protective standpoint.

The amygdala has a central role in the emotional and somatic organization of experience, whereas the hippocampus is vital for conscious, logical, and cooperative social functioning. The amygdala and the hippocampus play opposite roles in an attention-directing process. By accentuating small differences among inputs, the amygdala heightens awareness of specific aspects of the environment (attention) whereas the hippocampus inhibits responses, attention, and stimulus input habitation (Douglas, 1967; Kimble, 1968; Marr, 1971). The amygdala is involved with generalization, the hippocampus with discrimination (Sherry & Schacter, 1987). The amygdala will make us jump at the sight of a spider, whereas the hippocampus will allow us to remember that this particular spider is not poisonous, so we shouldn’t worry. Flashbacks from traumatic experiences likely reside in amygdaloid memory networks. Focal Dystonia ("Yips" victims in golf), describe these "freeze modes" as powerful, multisensory, often triggered by associative stress, and experienced as if they were occurring in the present. These flashbacks also have the characteristic of being stereotyped and repetitive, suggesting that they are not subject to the assimilating and contextualizing properties of hippocampal memory networks (Jacobs & Nadel, 1985).

The behavior of all organisms is based on approaching what is life sustaining and avoiding what is dangerous. The proper integration and balance between right and left hemisphere functioning allows us to experience a healthy mixture of positive and negative emotional experiences, as well as to regulate and manage anxiety. The left hemisphere is bias toward anxiety, suspiciousness, and negativity keeps the body alert to danger. Right hemisphere biased neural processing, measured in a variety of ways, and has been shown to correlate with low self-esteem (Persinger & Makarec, 1991). The same phenomena holds true for anxiety. Primates with extreme left frontal activity are more fearful and defensive, and have higher levels of stress hormones, than do those with activity biased toward the right hemisphere (Kalin, Larson, Shelton, & Davidson, 1998). The neural circuitry involved in fear and anxiety, although biased toward the left hemisphere, involves both hemispheres and all levels of the triune brain. The most primitive subcortical fight or flight circuitry, shared with our reptilian ancestors, interacts with the most highly evolved association areas of the cerebral cortex (Cozolino, 2002). This might explain in golf dystonias like "yipping", why an experienced golfer misses short putts that beginner golfers will never miss. The connection between every kind of anxiety and the core biological mechanisms of physical survival supports the philosophical notion that all anxiety, at its core may be the fear of death (Tillich, 1974). This explains why accumulative associatively learned and developed anxiety through all the senses of the nervous system might lead to competitive meltdown, because like the proper positive things are learned through the associative process, so is the negativity and thus anxiety.

Some anxieties appear to be hard wired, specific to primates, and linked to both our present and past survival needs. We know now that the amygdala plays a central role in the expression and regulation of anxiety and fear. Anxiety and fear are the conscious emotional aspects of the body’s ongoing appraisal of what is dangerous and life threatening. Anxiety can be triggered by countless conscious or unconscious cues and has the power to shape our behaviors, thoughts, and feelings. At its most adaptive, anxiety encourages us to step back from the edge of a cliff, check the road twice before crossing it.

How is this relevant to golf?
The Mayo Clinic is undertaking a study of the "yips" in golf – the mysterious affliction in putting manifested by freezing over the putt, shaky hands, and a stabbing stroke. Previous researchers have classified yips as an occupational focal hand dystonia, a type of movement disorder apparently caused by degeneration of neural circuitry following decades of the same hand movement.

In order to fully understand this phenomenon we need to look at the physiological and psychological associations that lead to this problem. It also needs to be understood that this problem has a very strong physiological base and the body needs to be replenished by nutrients to get back to optimal performance. However before the explanation is given to replenish the abused organs, lets continue to look at the processes that cause this depletion.

Neuroscience of Occupational Focal Hand Dystonia
These earlier putting studies are in line with modern neuroscience, in which occupational focal hand dystonia is only imperfectly understood (Hochberg et al., 1990; Wake Forest Neurosurgery, 2001), but is no longer considered to be psychological in origin (e.g., Abbruzzesse et al., 2001; Adler, 2000; Hallet, 1998; Hochberg et al., 1990; Sheehy and Marsden, 1982). Classed as a movement disorder along with Parkison’s Disease, cortico-basal degeneration (CBD), and various forms of spasticity (Dystonia Medical Research Foundation, 2001; We Move, 2001), focal hand dystonia has been linked with:
Sensorimotor degradation of hand-finger neurons in the sensory cortex (blurring of the fine sensory discrimination of finger and hand proprioception underlying movement control) (Abbruzzesse et al., 2001; Byl et al., 2000).

Basal ganglia dysfunction in the release of prepotent motor programs by inhibition of inhibition (Ibanez et al., 1999; Reilly at al., 1992; Tinazzi et al., 1999; Toro et al., 2000).

Imbalanced forearm muscle inhibition patterns (Nakashima et al. 1989).

Furthermore, occupational focal dystonias are not restricted to the hands (e.g., "auctioneer’s jaw", "writers cramp": Scolding et al., 1995).

The emerging picture is of a complex loop of brain centers integrating perception, emotion, and movement that is subject to disruption at varying points with resulting movement deficits that can be quite similar. For example, vestibular dysfunction contributes to spasmodic torticollis ( a related dystonia; Munchau et al., 2001); cervical spinal lesions can produce dystonia like deficits in hand movements without involvement of cerebral circuits (Uncini et al., 1994); and cerebellar degeneration results in excess cortical activation in motor control (Liepert et al., 2000). Focal hand dystonia is considered mostly intractable, but limited relief can be gained from periodic injections of the hand muscles with botulinum toxin A. In addition brain surgery with thalamotomies (lesions of basal-cortico motor control loop at a point in the thalamus) has been effective

(Kelly, 2001; Mempel et al., 1986). However not many golfers want to take up this option for their affliction in missing crucial putts under pressure.

The Mayo Clinic team includes Dr. Crews from the department of Exercise Science at Arizona State University (Crews, 2001). The Mayo Clinic position on the yips apparently builds upon other studies by Dr. Crews on "choking" under pressure in golf and on attentional patterns in putting (Crews and Landers, 1993). Choking is generally understood to refer to anxiety-sponsored increases in arousal level that lead to performance deficit, typically associated with failure in intense situations or in high pressure competition. The 1996 experience of Greg Norman at the Masters in losing a final round six-shot lead to Nick Faldo prompted NBC program Dateline to bankroll a study of choking in golf by Dr. Crews and others. This research consisted of an EEG study of ten amateur golfers with an average golfing experience of five years, and handicaps ranging from 11.5 to 26. The task was a trial of 20 five foot putts for baseline, followed by a second trial of putts on condition that the golfers who improved won $300 while the golfers who performed worse than baseline would have to pay $100. Five did better and five did worse (Linder et al.; 1998; Abrahams, 2001).

Basing her analysis of choking upon EEG patterns, Dr. Crews concluded that successful golfers had increased cortical activity just like unsuccessful golfers, but the activation was spread evenly over both hemispheres of the brain, whereas activation for unsuccessful golfers concentrated in the left (dominant) hemisphere (Abrahams, 2001).

Dr. Crews interpreted the increased left-brain EEG activity as anxiety-related and employment of right-brain processes. In keeping with this analysis of handling pressure, Dr. Crews teaches "right brain" golf by encouraging golfers to use imagery, relaxation techniques, and target focus as ways to promote right-brain activation and therefore hemispheric balance. This research was awarded the First Annual Golf Science award from the Golf Magazine and the World Scientific Congress on Golf.

The concept of anxiety and physiological research methodology followed in the Mayo Clinic study is closely similar to that utilized by Dr. Crews in her "choking" studies (Smith et al., 2000). And the behavioral aspects of anxiety are also similarly identified (heart rate increase and higher level of cortical excitation associated with anxiety).

The Question of Therapy or Cure
The Mayo Clinic study does not attempt analysis of treatment or cure for its description of yips behaviors. Instead, the team lists possible interventions for future study including:
Compensatory golf techniques (long putters, fat grips, grip style or position change, grip pressure adjustment, "sidesaddle" putting, reliance upon non-dominant hand, reliance upon shoulders rather than hands for
stroke, etc.)

Neuromuscular re-educated (New swings and postures)

Sport Psychology cognitive therapies

Biofeedback

Relaxation therapy

Mental imagery Thought-control (e.g., meditation, mindfulness, positive self-talk, self hypnosis, neurolinguistic programming)

Anxiolytic pharmacology (beta-blockers and tranquilizers)

The Mayo Clinic study affords a detailed look at the current understanding of the yips among golfers and golf scientists. However, the phenomena under examination must be observed separately by well-crafted experimental protocols for a deeper understanding of the controlling neurophysiolocigal processes. Without this deeper understanding, effective therapy will likely remain elusive.

The unfortunate problem with a lot of this research and investigation is that the experts in each field do not combine the sciences to understand the whole problem. Psychologists want to handle the problem with behavior modification and positive affirmation modalities. They want to include the techniques of relaxation that are effective in certain other pressure situations but not in cases of focal dystonia (yips). At this point you need to make physiological, neurological and psychological changes to stay ahead of the problem. The body at this point (yipping stage) is in "fight or flight mode" and is completely depleted from a lot of nutrients because of the physiological drain and strain it has been put under. Because of this "fight or flight" issue the brain is in primal mode and no consciously manipulated thought process (like positive thinking) will make a difference.

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MORE ABOUT STRESS


Stress, in specific distress and eustress in the professional world of golf are the underlying bases for the development of "Focal Dystonia". This disorder has a neuropsychological basis and forces golfers not to be able to control their motor behaviors under severe pressure, as discussed in-depth.

Today, stress refers to the undue pressures of living in a fast-paced society. Hans Selye, who began his research in the 1930’s, was the first to describe biological stress and explain its effects on health. In his classic book The Stress of Life, originally published in 1955 and revised and reprinted in 1978, he defines stress as the "nonspecific response of the body to any demand." Nonspecific in this case, refers to any event or stimulus, whether it is external (such as a touch or a noise) or internal (such as emotion). Fundamentally stress is the wear and tear of living. Some people are prepared through genetic favor to handle it better.

The modern expression "stressed out", although overused and vague, refers to a state of anxiety, worry, or exhaustion that has resulted from difficult or challenging experiences. The term implies the existence or potential rise of unpleasant symptoms.

Stress, by itself, saps energy. When we are to deal with life’s challenges calmly and efficiently, we expend energy at a lower rate than if we were dealing with the challenges and experiencing stress. Under stress we become exhausted much quicker than we do otherwise, and recover energy a lot slower. Certain stress creates symptoms such as digestive upset, insomnia, fatigue and muscle tension. These symptoms reflect the disruption of energy and consequent disruptions of body systems.

Ancestral vital energy is supplemented by food, water, air, and perhaps other natural sources, such as stress and Mother Earth herself. Vital foods impart this energy as well. Some wild foods or super foods, such as nettles, dandelion, yellow dock greens, and green foods like spirulina and wheat grass juice is especially rich in energy.

Maintaining strong digestion ensures that we receive vital energy from food. Dr Bernard Jensen was a big believer in the health of the bowel; he felt all diseases start in the bowel (Jensen, 1981).

What stress is not
Since the term stress is often used quite loosely, many confusing and contradictory definitions of it have been formulated; hence, it will be useful to add a few remarks stating clearly what it is not (Selye, 1984):
Stress is not merely nervous tension. This fact must be especially emphasized, since most laymen and even many scientists tend to identify biological stress with nervous exhaustion or intense emotional arousal. In man, with his highly developed nervous system, emotional stimuli are in fact the most common stressors.

Stress is not always the nonspecific result of damage. It is immaterial whether a stressor is pleasant or unpleasant; its stressor effect depends merely on the intensity of the demand made upon the adaptive capacity of the body. A round of golf or a golf shot that creates great pleasure can produce considerable stress without causing harmful effects.

Stress is not something to be avoided. No matter what you do or what happens to you, there arises a demand for necessary energy required to maintain life, to resist aggression and to adapt to constantly changing external influences. Even while you are sleeping or fully relaxed, you are under some stress.

Complete freedom from stress is death. Contrary to public opinion we must not – and indeed cannot – avoid stress, we can meet it efficiently and enjoy it by learning more about its mechanism and adjusting our philosophy of life accordingly.

Stress is not an emergency discharge of hormones from the adrenal medulla. An adrenaline discharge is often seen in acute stress affecting the whole body, but it plays no conspicuous role in generalized inflammatory diseases like arthritis and tuberculosis, although they can produce considerable stress.

Stress is not everything that causes a secretion by the adrenal cortex of its hormones, the corticoids. ACTH, the adrenal-stimulating pituitary hormone, can discharge corticoids without producing any evidence of stress.

Stress is not the same as deviation from homeostasis, the steady state of the body. Any specific biological function eventually causes marked deviations from the normal resting state in the active organ.

Stress is not anything that causes alarm reaction or the G.A.S. as a whole. These reactions are characterized by certain measurable organ chances which are caused by stress and hence could not themselves be stress.

Stress is not a specific reaction. The stress response is, by definition, not specific, since it can produce virtually any agent.

Stress is not always a bad thing. Certain stress can be beneficial.

Stress cannot and should not be avoided. Even while we are asleep our heart must continue to beat, our lungs breath, and our brains dream.

Whatever the problem, it can only be met through one of two basic reaction forms: actively – through fight, or passively – through flight. The stress-producing factors, technically called stressors are different, yet they all elicit essentially the same biological stress response. Stress is the nonspecific response of the body to any demand made upon it (Selye, 1974). From the point of view of its stress producing or stressor activity, it is immaterial whether the agent or situation we face is pleasant or unpleasant; all that counts is the intensity of the demand for readjustment or adaptation.

The process of stress on a physiological level is as follows: The adrenals are endocrine glands situated just above each kidney. They consist of two parts, the outer layer (or cortex) and the inner core (or medulla). The cortex produces hormones that are called corticoids, whereas the medulla secretes adrenalin and related hormones, all of which play important roles in the response to stress. The thymus (a large lymphatic organ in the chest) and the lymph nodes (such as can be felt in the groins and armpits) form a single system usually referred to as the thymicolymphatic apparatus, which is mainly involved in immune defense reactions (Selye, 1976).

It has become evident through all types of research that the same set of organ changes caused by the glandular extracts were also produced by cold, heat, infection, trauma, hemorrhage, nervous irritation, and many other stimuli. Thus in all forms of stress the body basically reacts in the same way. This reaction was first described in 1936 as a "syndrome produced by various nocuous agents, and subsequently became know as general adaptation syndrome (G.A.S.) also known as biological stress syndrome (Selye, 1974). Its three stages – the alarm reaction (1), the stage of resistance (2), and the stage of exhaustion (3). After the initial alarm reaction, the body becomes adapted and begins to resist, the length of the resistance period depending upon the body’s innate adaptability and the intensity of the stressor. Lastly exhaustion will ensue.

The focal dystonia problem area in golf makes this behavior a very visible one in "yip" cases. First the golfer starts feeling trepidation about a short putt, then with extensive, associative exposure to the same anxiety this resistance will result in the body to fight "decelerating the stroke" (body doesn’t want to allow the stroke to happen, wants to put a block on the behavior or fight it) or flight "accelerating the stroke" (body wants the action to be dealt with as quickly as possible to get rid of anxiety by rapid flight.) At this point no conscious manipulation (mechanical thoughts about the stroke) will be helpful, the brain has gone "instinctive" and your logical mind means nothing. "Fear is fear at this point, whether it is a short putt or something more life threatening, the body sees them as the same. When the body’s self-preservation kicks in, you know the stress is at its fullest destructive potential. Finally you have the stage of exhaustion, following the long-continued exposure to the same stressor, to which the body had become adjusted, but now they are irreversible, just like the "yips" in golf. Once you have them, you have them! Your system is drained by this associative anxiety and needs to be recharged with the proper neurological disassociations (mechanical postures) and the proper nutrients to recharge the body and the organs. The process of adaptation should now start.

Our reserves of adaptation energy could be compared to an inherited fortune, from which we can make withdrawals, but there is no proof that we can make deposits in this case. Complete restoration is completely impossible, because every biologic activity leaves some irreversible "chemical scar". It is now generally recognized that the emergency discharge of adrenalin represents only one aspect of the acute phase of the initial alarm reaction. At least equally important in the maintenance of homeostasis is the hypothalamus-pituitary-adrenal-cortical axis.

This axis is a coordinated system consisting of the hypothalamus (a brain region at the base of skull) that is connected with the pituitary gland (hypophysis), which regulates adrenocortical activity (Crick, 1994). The stressor excites the hypothalamus through pathways not yet fully identified, to produce a substance that stimulates the pituitary to discharge the hormone ACTH (for adrenocorticotrophic) hormone in the blood. ACTH in turn induces the external, cortical portion of the adrenal to secrete corticoids. These elicit thymus shrinkage, simultaneously with any other changes, such as atrophy of the lymph nodes, inhibition of inflammatory reactions, and production of sugar (a readily available source of energy) (Selye, 1976).

Walter Cannon designated in 1932 the "emergency adrenalin secretion" in response to fear or rage. In his classic book, The Wisdom of the Body, he summarized his lifework on the distinct mechanisms which maintain the normalcy of sugar, protein, fat, calcium, oxygen, and temperature of the blood, as well as many other individual specific adaptive mechanisms. These are all the things of vital essence in sports performance enhancement as well.

As we can see, a certain amount of stress is needed to tune you up for sports action, to perform at your top level in golf or any sport. This is especially true for eustress, which is enjoyable in itself and actually gives purpose to life. On the other hand we need to learn the limits of our endurance before we exceed them dangerously.

The physiological benefits of exercise and playing sports are well documented. Public interest has centered on the role endorphin plays in mood-state changes (Hopson, 1988) and lately there is some scientific evidence to support such a link. Perhaps the reason we pump up our endorphin with exercise is because it makes us feel calm – an inner reward for being fit. This was previously called the "runners high", but we should like rename it "athletic calm". This supports the concept that a healthy body houses a healthy mind. However, endorphins may act similarly to the exogenous opioids; the obligatory athlete may have learned to self-titrate his or her endorphins, and thus mood states, and that discontinuing pulsatile activity could lead to an endogenous dysphoric withdrawal state that could only be alleviated by the hedonistic pleasures of exercised induced endorphin (Begel & Burton, 2000). Thus in short we might get addicted to feeling competitive and the stress levels will wear and tear at the body pretty dramatically. Endorphins have been an important of human evolution – the human species functioned best when physically fit – a state that endorphin may have helped facilitate. There are many neurochemicals that affect moods and human performance; it just so happens that endorphin is one of the few for which such information is known.

Stress and the HPA
Earlier the HPA was mentioned; let’s look at it a little more closely to understand exactly what it does and how it is effected by stress. The hypothalamic-pituitary-adrenal axis also can be called "stress axis" is the classic example of the stimulatory system, with it myriad actions, reactions, and feedback loops (Herman, Prewitt & Cullinan, 1996). It is also an example of a system that can be over activated with maladaptive outcomes. Normally, the HPA axis functions as a pulsatile system for management of stress and control of energy production. Glucocorticoids (cortisol) are the end result, which have widespread multifunction catabolic stimulatory effects, including the release of glucose from the liver for energy availability.

The physiology of the HPA stress response is the outcome of sequential and parallel processing of relevant stimulus attributes on both positive and negative effect, which upon researching a certain threshold at the hypothalamic paraventricular nucleus (PVN), then activates the HPA system (Begel & Burton, 2000). There would appear to be two overall approaches to activating this system. The primary "systematic" high-priority system demands immediate response via unimpeded input to the PVN region – such as from major blood loss or serious respiratory distress. When this happens, all stops are pulled, and the body instantly goes into a profound stress-response mode (Herman et al., 1996).

The second "processive or neurogenic" stress response system requires a series of active processing by the brain to determine if the stress has enough relevance to cause activation of the PVN. This requires indirect routing of the stimulatory message, such as pain or stress, via the cortex, prefrontal cortex, hippocampus, amygdala, and septum.

The locus coeruleus can release massive amounts catecholamines, mostly noradrenaline, which can give the effect of a full blown panic-phobic reaction and subsequently indirectly activate the PVN. Stressor stimulation mediated through the dorsal raphe nucleus (serotonin) is a modest excitator to the PVA-HPA (Morgan, 1986). In addition various fluid and electrolyte shifts and blood-pressure changes can cause a sudden release of various peptides, one being angiotensin II, which has indirect effects on the PVN-HPA. This multisystem modulation of stress-filtering is a variable requirement prior to activating the PVN. There may be an additional final screening within the limbic system before final loading of the PVN. But once loaded, the PVN activates the HPA, and the systematic stress response is irrevocably on its way (Herman et al., 1996).

The HPA system is but one aspect of the limbic system’s role in stress integration. Limbic outflow goes to many regions of the brain, the PVN to HPA system being but one. The final relays insure proper control of the degree of the HPA response, and in part is prone to habituation by repeated exposures – cellular learning. Athletes, by their repeated training are exposing their PVA-HPA to stress management learning, even at a cellular level. The closer the training can simulate the true stress of competition, the more optimum the adaptation would be to stress. Normally cortisol levels fluctuate over a 24 hour period, part of the cardiac rhythms, reaching a 40-fold peak up to 150 ng/mL in the morning, and dropping to near zero by late afternoon. Under severe stressful circumstances cortisol levels may rise to 400 ng/mL (Morgan, 1985). Therefore depending on the time of the stressor, the effect may be more or less magnified. However due to the fact the stress response levels are so much greater than normal fluctuations, the stressor-outcomes are probably not much blunted by the time of day. If enough stress is placed on a person time of day is irrelevant.

However after a major stressor event, the body tries to return to a normal baseline. Initially, part of the stressor signal will cause a somewhat delayed response of B-endorphin (Begel & Burton, 2000). This in effect has an inhibitory effect on the HPA-axis. The athlete with robust (cellular training) release of endorphin probably has an advantage in managing his stressor-modulating counter-response. This is something found in the top athletes of each sport, like Nicklaus, Woods, Jones, Hogan and Watson in golf. Secondly the very presence of elevated cortisol will have negative feedback effect upon further activation with the hypothalamus. Thus, the body is stressed, it responds, and then it calms itself down.

This nicely designed stimulatory system starts to maladapt if the stress is continuous. Prolonged activation of the hypothalamus will in time lead to a failure of the negative feedback such that the HPA axis becomes tonically stimulated, resulting in continuous high levels of glucocorticoids. This in turn can lead into multiple end-organ and muscular disorders like focal dystonia in golf. Thus a golfer being exposed to the same fear on a golf course every time he plays will activate the HPA through the PVA, and with extensive associative exposure the body learns this stressor (short putt, out of bounce fence, chip shots, driving, long irons etc.). This stressor then becomes a fear, then, phobia with enough exposure, however the entire problem stems from the HPA. It is ironic that the part of the body that is there to "help" you cope better under pressure is also the one that hurts you with excessive use.

For the athlete controlling PVN and HPA responses is tricky. Insufficient stressor activation might lead to poor competitive response. Yet an over activity of the pressure response system may also lead to poor performance or worse, like "yipping or focal dystonia". Unfortunately there are no simple tests that can be used to titrate on-line the stressor responses, nor are there any guidelines as to what response levels are optimums. In addition, some athletic activities, such as golf require a calm mental-physical state, however the demands on the body are almost as great as weight lifting if you weigh up how much more time you are exposed to fears and anxieties on a golf course. Many golfers have unwittingly learned how to gauge their stress levels in order to facilitate their personal best performance. This usually takes many practice sessions and various levels of competitive play in order to know how hard to push and when to back off and foster a calmer mood.

Recent studies have suggested that a host of other neurochemicals, such as serotonin and gamma-amino-butyric-acid (GABA), are felt to have a profound influence on moods, and thus presumably on athletic behavior. However, the details are currently unknown. All these neurochemicals affect each other; action on the part of one will affect another. It would appear that the neuro-psycho-biological-soup that influences our behavior is somewhat like a child’s mobile, a ripple at one end can send repercussions rattling all through the system. To compound the confusion, it is likely that we are currently only looking at a very small portion of what we should. This is why we need to nourish the brain and body properly for optimal sports performance.

The Signs of Danger

Medical Symptoms

Among the most generally used and reliable measures of stress are the blood levels of adrenalines, corticoids, ACTH and a drop in blood eosinophils.

Self-observable Signs
General irritability
Pounding of the heart, as an indication of high blood pressure (often due to stress)
Dryness of throat and mouth
Impulsive behavior, emotional instability
The overpowering urge to cry or run and hide
Inability to concentrate
Feelings of unreality, weakness and dizziness
Fatigue and loss of energy
"Floating anxiety" not sure what we are afraid of
"Keyed up" feeling, emotional alertness
Trembling and nervous ticks
Easily startled by sounds, hate noise
High pitched, nervous laughter
Stuttering and other speech difficulties
Grinding of teeth
Insomnia
Hypermotility or hyperkinesia, the inability to sit still, always moving parts of the body
Sweating
The frequent need to urinate
Diarrhea, indigestion, queasiness in the stomach, even vomiting
Migraine headaches
Premenstrual tension
Pain in the neck or lower back
Loss of appetite
Increased smoking
Increased used of legally and illegal drugs
Nightmares
Neurotic behavior
Psychoses
Accident prone

NUTRITIONAL APPROACH TO STRESS RELIEF

Stress is stress as discussed before, thus in order to look at the proper nutritional approach to help combat it; we need to look at the proper nutritional approach as a whole, not just focusing on the sports nutrition. Reiteration of this statement is vital.

Because diet is likely to be closely linked with stressful events, what we eat has a huge impact on body chemistry and ultimately on health. Under stress, we tend to choose foods that are not the best for us; with care and consideration, however we can learn to use food in support of healing and good health. We know that a number of important neurotransmitters, which affect mood and mechanisms for coping with stress, are built from amino acid molecules found in protein foods. An example is serotonin, made by the body from the amino acid L-tryptophan, found in soy, dairy products and meats. This neurotransmitter is essential in coping with anxiety, depression and insomnia.

All cells, organs, and systems of the body are governed by the principle that continual overuse or use in one direction to the exclusion of others will break down the body’s normal, self-regulated state of health. Experimenting with foods as sources of amino acids as a part of a normal, healthy diet is an excellent way to work toward overcoming the effects of stress. In natural food stores, many amino acids are available in pure form as a supplement.

The amino acid GABA, is not found in food, it is known to calm the brain and can help issues of anxiety, depression and hypertension. Glycine is found in turkey, wheat germ, carrot, cottage cheese, celery and almonds. It is a sedative to the brain and can help in depression disorders. Leucine is found in wheat germ, milk, avocado, yogurt, chicken, almonds, walnuts and cheese. It promotes protein synthesis and slows the effects of stress; it is great to help low energy levels resulting from severe stress. L-Tryptophan can be found in soy, pinto, mung beans, tempeh, tofu and lentils. It influences serotonin concentration in the brain; it is good for pain, insomnia and depression (Hobbs, 1944).

In the classic herbalism of the early twentieth century, any herb that affected the nervous system in any way was called a nervine. Nervines can be divided into six subcategories.

Sedative nervines. The calmatives, they reduce anxiety and have a calming effect on the central nervous system. These herbs are frequently used in formulas for nervousness, sleeplessness, and mild anxiety. Examples are valerian, hops, kava-kava and lavender.

Analgesic nervines. They help to reduce nerve or muscle pain, although they can be useful for any kind of pain. Typically, these herbs will not work so well or so quickly as aspirin, but a well designed formula containing some of these herbs can be helpful in reducing pain and promoting healing with few side effects. Examples include valerian, St. John’s wort and Jamaican Dogwood. Stimulating nervines. These stimulate and raise the tone of the sympathetic nervous system and also raise the sympathetic tone. Small amounts of these herbs combined in a formula can enhance mental and physical performance and reduce fatigue. Examples are rosemary, kola nut, ephedra, coffee and tea. Tonic nervines. Nourish the nervous system and should be taken for extended periods of time – at least three months – in order to help nourish and support the function of the nervous system. Examples include wild oats, passion flower, celery, and sea vegetables such as nori and wakame.

Psychotropic nervines. It enhances intuition and could aid in understanding about the meaning of unconscious images. Examples are Kava-kava and mugwort.

Soporific nervines. Is a great aid in all the sleeping processes. Examples St. John’s wort and California poppy.

Stress and malnutrition
Severe physical and emotional stress greatly increases loss of vitamin C and zinc both water soluble nutrients. Most likely there is a similar increased demand for all nutrients when one is under stress, for stress may induce a state of malnutrition just as that which follows faulty diet. When both stress and malnutrition is combined the effect is grossly magnified. When you are eating a tremendous amount of junk food before or during sporting events you are also malnourished. Your body and mind with the pressure it is under cannot function optimally.

Over the past two decades, it has become clear that the pituitary and hypothalamic hormones are involved in brain activity and have an effect on behavior (Hoffer & Walker, 1994). Nutrients and the right kinds of foods for the mind are vital. A neurotransmitter is the chemical language sent between cells in the human brain. These neurotransmitters allow the brain cells to talk to each other. Deficiency in neurotransmitter function results in depression, lifelessness, moods, irritability, sleeplessness, anxiety, brain fog, cravings and addictions. Depleted supplies of these "feel good" neurotransmitters make it difficult for you to feel happy, on track, focused and motivated. Neurotransmitter deficiencies can be caused through genetics, stress, and diets low in amino acids and through alcohol and drug abuse.

Two key amino acids are necessary to make the other neurotransmitters. Phenylalanine is an essential amino acid that makes you feel happy and motivated. Glutamine is a conditionally essential amino acid that can keep you calm, focused and in control. Both are very important in optimum sports performance. The body cannot convert Phenylalanine form other nutrients, it must depend on outside sources and specific supplements to acquire sufficient amounts. Since amino acids from meat, eggs, and dairy sources cannot readily be utilized by the brain, it is necessary to take supplements which also contain co-factors that help them across the blood brain barrier. The Rhodiola rosea extract has been shown to influence learning and memory, by supporting the neurotransmitters and affecting the brain chemistry. Tests using Rhodiola showed the quality of the task performed was dependent on fatigue levels. When Rhodiola was administered, it effectively increased a person’s resistance to fatigue, enhanced back muscle strength, hand strength and improved coordination. All of which are vital for sports performance enhancement in golf.

Neurotransmitter support is necessary for the brain function at top performance. Memory loss may be nothing more than amino acid deficiency, causing a short circuit. When athletes compete, they maximize their brain activity to keep focused. Poor diets and low amino acid levels will prevent this. No matter what we do, our thinking process determines the outcome of our actions. With good neurotransmitter support we can make choices that can keep us at peak performance.

Effects of stress on trace minerals
According to a study out of University of Health Sciences in Bethesda, the University of Michigan Medical School in Ann Arbor, and the USDA Human Nutrition Research Center in Beltsville, Maryland, trace mineral levels are altered by stress.

Plasma levels of zinc, iron, copper, selenium, and selected blood proteins such as ferritin were monitored and dietary intakes were measured in 66 men before, during, and after a five day period of physical and psychological stress called "Hell Week". Physical stress included simulated combat exercises, and an obstacle course, aerobic workouts; psychological stresses included performance anxiety, verbal confrontations, and no-win situations.

The results of this study showed dietary intake of minerals during the stressful period greater than the Recommended Dietary Allowance (RDA), Zinc intake averaged 23.6 mg (RDA = 15 mg), iron intake averaged 35.4 mg (RDA = 10 mg), copper intake averaged 3.0 mg (RDA = 70 mcg). Despite adequate dietary intake, plasma levels of minerals decreased by 33%, 44%, 12%, and 9%, respectively. In addition, mineral carrying proteins increased as much as 59%, suggesting increased removal of trace minerals from tissue stores. Although the trace mineral alterations were transient, they required seven days without further stress plus adequate dietary intake to return to their former levels. The results of this study show that the physical and psychological stress in healthy adults produces alterations in trace mineral status characteristic of an acute-phase response (deficiency) despite otherwise adequate dietary intake.

Recent discoveries have proven beyond a doubt that our brain and immune systems are interlinked. Our thoughts affect our cellular level. The field of "Psychoneuroimmuneology" is a blossoming discipline which studies the mind-body connection. We experience stress on three levels: physical, environmental, and mental/emotional (Lipski, 1996). Stress plays a major role in many digestive problems. Like any professional or competitive golfer will tell you that they all have had diarrhea from "nerves" before a big event. The ‘butterflies" that people feel in their stomach when they are nervous happen to all of us. Continued stress in our body, mind or meanings affects the whole body’s ability to heal and perform. If the body is using most of its energy to put out fires, it has less time for maintenance and repair. Because the digestive tract repairs and replaces itself every few days, it is one of the first places where our bodies alert us that all is not well. Athletes with digestive-related problems can benefit from stress management tools. Mental stress is one of the greatest challenges to our immune systems, putting pressure on nearly every organ and system in the body. Let’s look at the "Quick Ideas" for stress management (Lipski, 1996):
Eat healthy foods
Develop better communication skills
Exercise regularly
Spend time outdoors
Each day should have pleasure and relaxation
Meditate
Realize that you are not perfect
Think creatively
Go at your own pace
Think of solutions, not problems
Prioritize
Keep journals
Live one day at a time
Play and laugh
Spend time with family and friends
Be flexible
View problems as opportunities to grow
Plan for chaos
Set priorities
Breathe deeply
Plan ahead
Learn to say "No"
Unplug your phone
Make lists
Take long showers or baths
Drive 10 mph slower
Take on day per week to relax
Be loving and caring and trust people have good intensions

It is an unfortunate fact that 80% of illnesses can be traced back to stress (Ramazanov & Suarez, 1999). The Academy for Family Physicians reports about two-thirds of all office visits are prompted by stress. Stress is a silent killer, with little resistance mounted against it. Unlike bacteria, viruses and even cancer, which our immune system can counteract and destroy, stress suppresses immunity and destroys our resistance to other forms of attack. A study conducted in 1991 and published in Psychological Science, showed that certain detrimental effects on stress (such as increasing the number of suppressor T-cells) are only seen in people who are overly sensitive to stress. For thousand of years, people all around the world have been using adaptogens (things that help the body deal with stress).

Rhodiola rosea is probably the least-known adaptogen in the West and yet maybe the most impressive of all. It has been shown to normalize the immune system and glucocorticoid hormone levels in a positive way, bringing them into balance. The main targets of Rhodiola rosea are stress related molecules called neurotransmitters. These include serotonin, dopamine, epinephrine, norepinephrine as well as other active molecules in the brain. Serotonin is one of the most actively investigated chemicals in the body, specifically as it relates to its role in brain function.

The brain however is only a small part of serotonin’s arena of effect. This ubiquitous chemical participates in many processes throughout the body, including smooth muscle contraction, temperature regulation, appetite, pain perception, behavior, blood pressure and respiration. Although the amount of serotonin in the brain is relatively small, when compared to other parts of the body, its importance in brain function cannot be underestimated. Serotonin is clearly implicated in the etiology of treatment of many disorders, particularly those of the central nervous system, including anxiety, depression, obsessive compulsive disorder, schizophrenia, stroke, obesity, pain, hypertension, vascular disorders, migraine and nausea. Serotonin cannot cross the blood brain barrier; therefore the biosynthesis of brain serotonin that takes place in the brain is due to its precursor amino acid, called tryptophan. This is actively transported in the brain through the foods we eat. Scientists have found the Rhodiola rosea enhances the level of serotonin in the brain. Additionally, research points to Rhodiola as playing an important role in the biosynthesis and preservation of serotonin and neurotransmitters. Rhodiola’s ability to help the body adapt to stress may lie in its ability to enhance serotonin levels (Ramazanov & Suarez, 1999).

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THE NEUROBIOLOGY AND NUTRITION OF ATHLETIC TRAINING


It is very important to understand the functions of the brain and its neuro-chemical activity. Once again the brain absorbs 25% of the glucose that we take in. This is why it is important to fully investigate the function of the brain and then set out to give it the best possible nutrients through the proper diet. This will enhance performance, concentration and focus, not to mention the tremendous health benefits.

Athletes are often looking for that special nutrient or magical program that will somehow help them to configure their minds and bodies into some purpose-fulfilling mold. While some of these so-called "juices" may be externally derived, there now appears to be an abundance of complex intertwining neuro-hormonal substrates that both influence athletic behavior and, in turn, are influenced by that same behavior.

The catecholamines were perhaps the first recognized endogenous agents that might be part of athletic psychobiology – an adrenergic driver of performance. The early work on the stressor effects of the hypothalamic-pituitary-adrenal axis (HPA) and the general adaptation syndrome was an important first link with the body’s endogenous chemicals and emotional status. In 1975 the endorphins were discovered, and were intuitively considered to influence mood – first thought of as "runner’s high". This was not confirmed until 1987 (Allen & Coen). Although the endogenous morphines have been found to activate a calm neuroinhibitory mood state, it has also been noted that certain moods could independently influence endorphin’s mood-state effect, a sort of feedback loop between moods and chemicals. The example modeled by the endorphins is probably mimicked by countless other neural-acting substrates, the actions of which have yet to be uncovered.

What is the source of these potential mood-modifying neuropsychology markers? A simple overview starts with 26 chromosomes, which contain about 80 000 genes, which in turn are composed of about 3 billion chemical bases within the DNA chains. DNA sits a paired RNA helix within the cell nucleus, dictating what that particular cell will do and when it will do it. With endless permutations and combinations, it is utterly amazing that anything works at all. Yet it does – but not without flaws. Some are obvious like cystic fibrosis or schizophrenia; others are not, like excessive serotonin reuptake. The development of our chemical basis was probably predicated upon a background of natural selection that favored those genes that governed the most favorable combination of physical and mood states.

Among some cellular duties are the productions of neurochemicals, or some response to the perception of neurochemicals at receptors. Neurochemicals are usually secondary or tertiary messengers, either to activate or suppress something. The primary messenger within a particular neurochemical sequence is usually some external cue. For example, darkness is a primary messenger that sets the biological clock, which then sets in motion a whole series of fluctuations within the hormonal systems. These rhythms within the neurochemical brew sets forth a background hippus, or ebb and flow, of chemical levels that peak at specific times, then subside to their baseline levels, which in some cases is near or at zero. Cortisol levels, for example, reach their highest just prior to the morning wake. The clinical effects of these chemicals can generally be felt on both sides of the peak. When thyroid hormone rises, we feel energized; when it drops we feel lethargic (Begel and Burton, 1999).

In many circumstances, if we know the effect of an elevated neurochemical, then we can roughly predict the effect of its low level – the abstinence or opposite. For the stimulator chemicals like cortisol or thyroxin, abstinence becomes an excitatory type function. This excitation or inhibition is primarily measured at cellular level, but as the affect influences several million cells, the effect is felt macroscopically, that is, at the human behavior level. The malfunction scenario for each neurochemical may be expressed as either excessive or deficient amounts. Each neurochemical has a unique functional life span, which for the most part is determined by the speed and amount of its formation, its degradation and the level of opposing chemicals. When the body lacks certain circulating nutrients, we call it "hunger". It has a predictable onset lag of about 4 to 6 hours from the last dosage; reaches a withdrawal peak over 12 to 24 hours, then the abstinence feeling subside, even if not satisfied. An example: Nicotine withdrawal is felt in 30 minutes, peaks by 60, and lingers for up to 2 weeks. It was once thought that nicotine directly caused people to be agitated; however, the agitation does not come from nicotine, but from its abstinence – the withdrawal. It would thus appear that for some agents, the so-called clinically interesting phase might not come from its action, but from inaction (Prior, 1982).

Neurochemistry of Learning and Memory
It is very important in working with athletes and especially professional golfers to have an in-depth knowledge on memory and learning especially on a motor-neuron level. This is why we will take an extensive look at it, and then look at the best nutritional approach to best feed the brain to perform at top level.

Several neurochemical processes have been implicated in learning and memory, some of which are described below. One neurochemical process modifies the number of neuron sites available on postsynaptic membranes. Lynch and Bauldry (1984) and Siman et al. (1985) noted increases in the number of receptors following stimulation of a postsynaptic membrane. Therefore, even if the amount of transmitter released per action potential were unchanged, having more receptors on the postsynaptic membrane would increase the magnitude of the neurotransmitter’s effect. Lynch and Bauldry argue that the receptors were there all along, but were occluded on the inside by a network of fodrin, a protein. Fodrin is decomposed by an enzyme that is activated by calcium ions. Calcium enters the postsynaptic membrane through channels activated by the neurotransmitter. Many action potentials in rapid sequence are required for enough calcium to activate this enzymatic process. Fodrin acts as a sort of internal skeleton for the membrane, and as fodrin is removed, the dendritic spines swell. The amount of neurotransmitter released with each action potential can change with experience as has been extensively studied in the marine mollusk, Aplysia (Kandel, 1979; Kandel & Schwartz, 1982). Once again we see the importance of calcium in so many facets of nutrition and health.

The brain is neither predetermined nor unchanging, but rather is an organ of continuous adaptation. Thus the brain is always going to adjust and develop as we want it to. This is why it is so difficult to "go back to your old golf swing" once you have made very radical changes. The brain stores new memories and thus it gets confused to what is old and what is new, it is just progressively adapting to new motor behaviors. The brain and nervous system are built and sculpted neuron by neuron, through the interaction of our genetic programming and environmental influences (Changeux & Danchin, 1976) in what is now called use-dependent development. The architectural sculpting of our brain determines the shape of all our experiences. Neuroscience helps us to understand the process of how the brain is built and shaped by early interpersonal experiences, and how associative learning creates an interpersonal matrix capable of rebuilding it (Schore, 1994; Siegel, 1999).

In Golf we should not overlook the basic methods that the brain learns from, and has learned from for thousands of years. The strongest form of learning is through the processes of association. Practically all the things that we learn we learn through this method. Thus the best way to enhance golf swing changes is to enhance them through associative learning.

The process of memory has four main components (Mark & Mark, 1989):
The first focuses on attention and concentration.
The second is a process called encoding, which is the way the brain converts a perception into an engram - a physical memory representation in the brain.
Once the engrams are formed in the brain, they are stored in so-called memory banks.
The fourth process is known as retrieval, which is the ability to stored memories.

The growth and connectivity of neurons is the basic mechanism of all learning, memory and adaptation. Learning can be reflected in neural changes in a number of ways, including the growth of new neurons, the expansion of existing neurons and the changes in the connectivity between existing neurons (Cozolino, 2002). All of these changes are expressions of plasticity, or the ability of the nervous system to change. There is some proof that in certain primates there is neurogenesis; this is the birth of new neurons, especially in the regions of the ongoing learning areas like the hippocampus, the amygdala, and the frontal and temporal lobes (Eriksson et al., 1998; Gould, Reeves, Graziano, & Gross, 1999; Gould, Tanapat, Hastings, & Shors, 1999; Gross, 2000). Existing neurons grow through the expansion and branching of the dendrites they project to their neurons. There is sufficient evidence that neurons demonstrate growth changes in reaction to new experiences and learning (Purves & Voyvodic, 1987). Neurons interconnect to form neural networks, and neural networks in turn, integrate with one another to perform increasingly complex tasks. For example, networks that participate in language, emotion, and memory need to become integrated in order for us to recall and tell an emotionally meaningful story with the proper affect, correct details and appropriate words. Association areas within the brain serve the roles of bridging, coordinating, and directing multiple neural circuits to which they are connected. Although the actual mechanisms of this integration are not yet known, they are likely to include some combination of communication within and between neurons, the relationships among local neuronal circuits, and the interactions between functional brain systems (Trojan & Pokorny, 1999).

A number of researchers have discovered from experimental investigations that a person’s memory can be increased manifold when items to be remembered are associated with images or other known information. These associations are also called mnemonics.

Another overlooked fact about memory is that it is always easier to remember something if it’s part of a song or a verse. There is, in fact, a very good anatomical reason for this. Versification and melody are generated chiefly in the nondominant or right hemisphere. When words (which originate in the left hemisphere in most right-handed people) are put together with verse or song, the whole brain and its memory power are focused for optimal retrieval (Mark & Mark, 1989). This is why we can remember the words of certain songs once the melody is playing, even if we haven’t heard the song in many years. However if you try to say the words without the melody in the background, similar memory retrieval is almost impossible. This form of training memory doesn’t work only on a verbal level but also on a neurophysiological level.

4 + 4 x 4 = 32 x 32 = 1024 (Associative Golf Memory Development):
If you really want to store memory more permanently you need to associate all the learning processes for optimal memory recall. Short term memory which is stored in the hippocampus will develop into long term memories stored in the cortex, if this exposure is done with almost 1000 exact repetitions or more. The memory storage will be enhanced greatly by this, however the memory is even more enhanced if associative learning through verse or rhyme is included (Crick, 1994). If we use this information and develop an associative learning method for golf swings it will look something like this.

Take 32 golf balls; divide them up into 8 groups of 4. Hit four golf balls thinking about all the mechanical aspects that you want to work on, such as plane, grip, stance, take-away, posture etc. Then, hit the next four singing a song in your head, it is important to use the same verse, rhyme or song with every repetition. Repeat this until the 32 balls have been hit. Do this 32 ball drill no more than twice a day. It is known that short term memories are stored in the brain for up to six months (Crick, 1994) so we do not need to rush this process. Also if done properly it will take about a half an hour per session (32 ball drill). The brain is kept fresh when learning sessions are kept short and sweet. Repeat this 32 ball drill, 32 times over a good period of time. Doing this will not only enhance the memory, but instead of thinking mechanically about your swing under pressure, you will actually be able to have memory recall of mechanics by just singing the song while swinging. This is the best form of anxiety control under pressure and one of the best ways to play golf non-mechanically which has been proven time and time again not be effective. When we try to manipulate muscle by conscious mechanical thoughts, we will never be able to swing freely. We repeat this drill 32 times to get above the 1000 mark; this will ensure cortex memory storage as mentioned previously by Dr. Crick.

Nutrition and the brain
Now that we have taken an extensive look at the brain and some neurological processes in learning we need to make sure as athletes that we feed it the proper nutrients.

A neurotransmitter is the chemical language sent between cells in the human brain. These neurotransmitters allow the brain cells to talk to each other. Deficiencies in neurotransmitter function result in depression, lifelessness, moods, irritability, sleeplessness, anxiety, brain fog, cravings and addictions. Depleted supplies of neurotransmitters make it difficult for you to feel happy, on track and motivated.

Neurotransmitter deficiencies can be caused through genetics, stress, diets low in amino acids, and through alcohol or drug abuse. Two key amino acids are necessary to make the other neurotransmitters. Phenylalanine is an essential amino acid that makes you feel happy and motivated. Glutamine is a conditionally essential amino acid that can keep you calm, focused and in control. In order to function properly, the body must have the essential amino acid, Phenylalanine. Since the body cannot convert this from other nutrients, it must depend on outside sources and specific supplements to acquire sufficient amounts. Since amino acids from meat, eggs, and dairy sources cannot readily be utilized by the brain, it is necessary to take supplements which also contain co-factors that help them cross the blood brain barrier.

The Rhodiola rosea extract has been shown to influence learning and memory, by supporting neurotransmitters and affecting the brain’s chemistry. Tests using Rhodiola showed the quality of the task performed was dependant on fatigue levels. When Rhodiola was administered, it effectively increased a person’s resistance to fatigue, enhanced back muscle strength, hand-strength endurance and improved coordination, all vital in golf.

Neurotransmitter support is necessary for the brain to function at high level sports performance. Memory loss may be nothing more than an amino acid deficiency, causing a short circuit. When athletes compete, they adequate brain activity to keep focused. Poor diets and low amino acid levels will prevent this. No matter what we do, our thinking process determines the outcome of our actions. With good neurotransmitter support we can make choices that can keep us at peak performance.

Three other neurotransmitters in the brain affect activity and aggression, the perception of sensation, sleep, mood, and performance. The three are norepinephrine, dopamine, and serotonin. Their concentration in the brain can be affected by the intake of certain amino acids, including tryptophan and tyrosine, which are contained in food. It is increasingly clear from research that brain messages passed from cell to cell by neurotransmitters can be enhanced by the food we eat. The neurotransmitter dopamine for example, which is deficient in the brains of people with Parkinson’s disease, and the neurotransmitter norepinephrine are considered to be alertness chemicals. Increased levels of these neurotransmitters produce distinct changes in mood and behavior, including the tendency to think more quickly and rapidly. Thus it comes as no surprise that when people eat foods containing large amounts of certain amino acids, their moods and behaviors will be affected. The effects that Wurtmans (1977) and other brain researchers have observed about various dietary substances are real. They have reported on research that shows that high-protein, low fat foods increase alertness and concentration, while a meal high in carbohydrates is associated with relaxation.

Certain principles are applied to all diets, whether diets are for weight loss or brain power. One general principle, for example, is not to take excessive salt because in some people it tends to produce a chronic increase in blood pressure and increases the risk of strokes. The same is true for ingesting hard or saturated fats. Brain power diets are not for weight loss, it is to give your brain the best nutrients. The brain is everything in life, without it you simply are nothing!

The "Brain Power Diet" is based on getting the correct amounts of electrolytes, vitamins, minerals, and amino acids in your daily diet. The key nutrients associated with brain function are the electrolytes: calcium, magnesium, sodium, and chloride; and the vitamins: B1 (thiamine), B3 (niacin), B6 (pyridoxine), B9 (folate), B12, and C; as well as minerals: iron, copper, and zinc (Mark & Mark, 1989). Essential brain nutrients also include choline, which is an important metabolite. Essential amino acids, especially tyrosine and tryptophan (mentioned before), which contain chemical building blocks of neurotransmitters. The most extensive 14-Day Brain Power Diet can be found in the brilliant book, Brain Power, written by Vernon Mark and Jeffrey Mark. It is well worth the time in investigating it.

Numerous books have been written on the mental aspect of golf. Hitting the "perfect" golf shots depend on the close relation between mind and muscle. If the mind is shooting erroneous signals due to a chemical breakdown, you may lose control of the muscle in your arm. This will result in the golf shot not going where you want it to go. The chemical breakdown in the brain will then cause you to throw your club out of anger and frustration. Anxiety, anger and tension can be increased by certain foods that we eat other foods can help us calm down. Analyzing behavior anomalies without addressing the chemical breakdowns in the brain that is caused by nutritional deficiencies, is putting the cart before the horse. The messages creating emotions are transmitted between cells in the human brain by neurotransmitters as mentioned before.

Temper outbursts can happen; you may feel depressed, lethargic, moody, irritable, and anxious, experience sleeplessness, food cravings and addictions if your brain is "starved". Depleted supplies of endorphins make it difficult for you to feel happy, on track and motivated. Muscle control and accuracy can also be affected by deficiencies in specific amino acids. Supplementing your diet with flaxseed and lecithin can support the operation nerve fibers in the brain. Lecithin, used as an emulsifier in many foods, is necessary for the smooth flow of messages through the nervous system, thereby preventing disruption of muscle coordination. The essential fatty acids (EFAs) in flax, aid the transmission of nerve impulses that are needed for normal brain functioning.

Brain enhancing herbs are also finding their way into power-bars and sports drinks. Gingko biloba is purported to increase mental alertness; kava kava and ginger work together to act as a relaxant to control temper; Maca, a Peruvian herb, promotes mental clarity and Camu-camu is used to control anxiety (Anderson & Peiper, 1999). Rosemary, which can be added to your bath, can help relieve bouts of depression, mental fatigue, lethargy or apathy after a poor round. Sage has a natural ability to feed nerves, so it is useful after temper outbursts. It also supplies oxygen to the cortex of the brain, which acts to revitalize it and bring thoughts into better focus.

According to Dr. Graham and Jon Stabler who wrote, The Eight Traits of a Champion Golfer, say: "Everyone’s body chemistry is different, and has a direct impact on the way we experience emotions. If you work hard to change your thoughts and attitudes, but cannot seem to accomplish it, you need to look more closely for biological reasons. A change in diet, increasing exercise levels, using certain supplements, and possibly an anti-depressant medication, may help you gain increased control over your emotions when your biology is a contributor to mental stress."

Some of the effects of the brain may actually come from the body. Golfers put their body’s through some rather extraordinary trauma. Repeated swings to one side, constant bending and twisting and playing without stretching first, can lock up your muscles, restricting nerve impulses to the brain resulting in tension, anxiety, restlessness and irritability. Supplements or brain-supporting foods may help, but to affect long term benefits, focus should be given to correcting the underlying problem.

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