Causes of Eating Disorders

Causes of Eating Disorders - Eating disorders are an increasing public health problem among young women: they may give rise to serious physical problems such as hypothermia, hypotension, electrolyte imbalance, endocrine disorders and kidney failure.

Women with eating disorders are also at risk of long-term psychological and social problems, including depression, anxiety, substance abuse and suicide. The costs in terms of quality of life, loss of productivity, serious medical problems and mortality are high.

Clinical eating disorders include anorexia nervosa and bulimia nervosa.

Anorexia is characterized by a severely calorie-restricted diet, resulting in a body weight that is at least 85% below that expected for age and height.

Bulimia is identified by frequent fluctuations in weight and recurrent episodes of compulsive bingeing followed by self-induced vomiting, purging, fasting, laxative use and/or excessive exercise in attempts to avoid weight gain.

Eating disorders not otherwise specified include behaviours such as chronic dieting, purging and binge-eating, which do not meet the full criteria for a specific eating disorder, they are two to five times as common as the clinical eating disorders.

In addition to eating disorders, preoccupation with weight and body image, and self-concept disturbances, are more prevalent among women than men. Personal, behavioural and socio-environmental factors, such as negative body image, low self-esteem, fear of becoming fat, chronic dieting and social pressures to be thin, are identified risk factors.

Body Image

Body image concerns and preoccupation with body weight and shape increase as girls become older and more aware of the idealized societal preference for a thin body shape. The images of women in the media and popular culture place pressure on vulnerable young girls and women to live up to these expectations, regardless of their natural body shape.

In British Columbia, it was found that by age 18, 80% of girls at all weights reported that they would like to weigh less. A school-based population study involving 1,739 adolescent women aged 12 to 18 years in Toronto, Hamilton and Ottawa found that current dieting to lose weight was reported by 23% of participants, binge-eating by 15%, self-induced vomiting by 8.2% and the use of diet pills by 2.4%.

Body shape dissatisfaction and preoccupation with weight are not limited to adolescents but also occur in children.

A recent Canadian school-based study concluded that 34% of prepubescent girls, 36% of early pubescent girls and 76% of post-pubescent girls were dissatisfied with their body shape.

In a survey of eating and smoking behaviours among boys and girls in grades 4 to 8 in south western Ontario and Charlottetown, more than 25% from each grade reported not eating breakfast every day, and there was a sharp increase among girls beginning in grade 7.

Unhealthy eating patterns in childhood can adversely affect health, contribute to chronic disease in later life, and often persist into adolescence and adulthood, since change is difficult once eating patterns are established.

The starvation associated with anorexia and the chronic vomiting frequently associated with bulimia can cause serious medical problems, such as hypothermia, hypotension, anemia, osteoporosis, endocrine abnormalities, dehydration, kidney stones, metabolic alkalosis and dental caries.

Girls and women with eating disorders are also at increased risk of menstrual irregularities such as amenorrhea, infertility, miscarriages and fetal complications such as prematurity, low birth weight, malformations and low Apgar scores (a recording of the physical health of a newborn infant, determined after examination of the adequacy of respiration, heart action, muscle tone, skin colour and reflexes).

Mothers who have or have had an eating disorder may also create abnormal behavioural patterns when feeding their children, such as irregular feeding schedules, detached non-interactive mealtimes, and use of food for non-nutritive purposes, which may lead to second-generation eating problems.

In addition to depression, anxiety and obsessive-compulsive disorders, eating disorders are also associated with diminished libido, altered sleeping patterns, irritability and suicide attempts.

Ontario women with bulimia have higher levels of anxiety, depression and alcohol abuse than those without bulimia. Smoking and substance abuse are much more prominent among teenaged girls with eating disorders than among those with healthy eating habits.

In an analysis of the 1997 Ontario Student Drug Use Survey, adolescent females who perceived themselves as overweight were almost 50% more likely to smoke than those who considered themselves of average weight or too thin, whereas weight perceptions were not associated with smoking among males.

Several studies have suggested an association between a traumatic experience (sexual or physical abuse) and later self-injury. A recent study found that among patients with eating disorders there is a more than 30% lifetime risk of self-injurious behaviour.

The rate of death from anorexia is higher than from bulimia because of the complications of starvation and electrolyte imbalances, or suicide.

A recent review reported a mortality rate of 0.6% for anorexia as compared with 0.3% for bulimia. A longitudinal U.S. study (21-year follow-up) of 84 women with anorexia reported that 14 women (16.7%) had died, and 12 of the 14 had died of causes directly related to anorexia; the observed death rate was 9.8 times greater than expected.

Cultural beliefs and attitudes are identified as significant contributing factors in the development of eating disorders. A few studies propose that cultural beliefs may actually protect ethnic groups against eating disorders, but their effect may be eroded as adolescents face pressures of adopting the behavior patterns of the surrounding culture.

A recent study of Mexican-American women across generations reported that second-generation women displayed the most disordered eating patterns and the highest degree of adopting the behavior patterns of mainstream U.S. culture. Experiences of cultural change (such as those of immigrants, for example) may also increase vulnerability to eating disorders.

Adapted from: Enza Gucciardi, Nalan Celasun, Farah Ahmad and Donna E Stewart. Eating Disorders. BMC Women's Health 2004, 4(Suppl 1):S21. doi:10.1186/1472-6874-4-S1-S21.© 2004 Gucciardi et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).

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Should Creatine Supplements be Banned? - Part 5 of 5

Should Creatine Supplements be Banned? Opponents of creatine supplementation have claimed that it is not safe for children and adolescents. While fewer investigations have been conducted in using younger participants, no study has shown creatine monohydrate to have adverse effects in children.

In fact, long-term creatine monohydrate supplementation (e.g., 4 – 8 grams/day for up to 3 years) has been used as an adjunctive therapy for a number of creatine synthesis deficiencies and neuromuscular disorders in children. Clinical trials are also being conducted in children with Duschenne muscular dystrophy.

However, as less is known about the effects of supplemental creatine on children and adolescents, it is the view of the International Society of Sports Nutrition (ISSN) that younger athletes should consider a creatine supplement only if the following conditions are met:

1. The athlete is past puberty and is involved in serious/competitive training that may benefit from creatine supplementation;

2. The athlete is eating a well-balanced, performance-enhancing diet;

3. The athlete and his/her parents understand the truth concerning the effects of creatine supplementation;

4. The athlete's parents approve that their child takes supplemental creatine;

5. Creatine supplementation can be supervised by the athlete’s parents, trainers, coaches, and/or physician;

6. Quality supplements are used; and,

7. The athlete does not exceed recommended dosages.

If these conditions are met, then it would seem reasonable that high school athletes should be able to take a creatine supplement. Doing so may actually provide a safe nutritional alternative to illegal anabolic steroids or other potentially harmful drugs.

Conversely, if the above conditions are not met, then creatine supplementation may not be appropriate. It appears that this is no different than teaching young athletes' proper training and dietary strategies to optimize performance.

Creatine is not a panacea or short cut to athletic success. It can, however, offer some benefits to optimize training of athletes involved in intense exercise in a similar manner that ingesting a high-carbohydrate diet, sports drinks, and/or carbohydrate loading can optimize performance of an endurance athlete.

The Ethics of Creatine

Several athletic governing bodies and special interest groups have questioned whether it is ethical for athletes to take creatine supplements as a method of enhancing performance. Since research indicates that creatine monohydrate can improve performance, and it would be difficult to ingest enough creatine from food in the diet, they rationalize that it is unethical to do so.

In this age of steroid suspicion in sports, some argue that if you allow athletes to take creatine, they may be more predisposed to try other dangerous supplements and/or drugs. Still others have attempted to directly lump creatine in with anabolic steroids and/or banned stimulants and have called for a ban on the use of creatine monohydrate and other supplements among athletes.

Finally, fresh off of the ban of dietary supplements containing ephedra, some have called for a ban on the sale of creatine monohydrate citing safety concerns.

Creatine supplementation is not currently banned by any athletic organization although the NCAA does not allow institutions to provide creatine monohydrate or other "muscle building" supplements to their athletes (e.g., protein, amino acids, HMB, etc). In this case, athletes must purchase creatine containing supplements on their own.

The International Olympic Committee considered these arguments and ruled that there was no need to ban creatine supplements since creatine is readily found in meat and fish and there is no valid test to determine whether athletes are taking it.

In light of the research that has been conducted with creatine monohydrate, it appears that those who call for a ban on it are merely familiar with the anecdotal myths surrounding the supplement, and not the actual facts.

We see no difference between creatine supplementation and ethical methods of gaining athletic advantage such as using advanced training techniques and proper nutritional methods.

Carbohydrate loading is a nutritional technique used to enhance performance by enhancing glycogen stores. We see no difference between such a practice and supplementing with creatine to enhance skeletal muscle creatine and phosphocreatine stores.

If anything, it could be argued that banning the use of creatine would be unethical as it has been reported to decrease the incidence of musculoskeletal injuries, heat stress, provide neuroprotective effects, and expedite rehabilitation from injury.

Conclusion

It is the position of the International Society of Sports Nutrition that the use of creatine as a nutritional supplement within established guidelines is safe, effective, and ethical. Despite lingering myths concerning creatine supplementation in conjunction with exercise, creatine monohydrate remains one of the most extensively studied, as well as effective, nutritional aids available to athletes.

Hundreds of studies have shown the effectiveness of creatine monohydrate supplementation in improving anaerobic capacity, strength, and lean body mass in conjunction with training. In addition, creatine monohydrate has repeatedly been reported to be safe, as well as possibly beneficial in preventing injury.

Finally, the future of creatine research looks bright in regard to the areas of transport mechanisms, improved muscle retention, as well as treatment of numerous clinical maladies via supplementation.

Reproduced with minor omissions, including references for ease of reading, from: Buford TW, Kreider RB, Stout JR, Greenwood M, Campbell B, Spano M, Ziegenfuss T, Lopez H, Landis J, Antonio J. International Society of Sports Nutrition position stand: creatine supplementation and exercise. Journal of the International Society of Sports Nutrition 2007, 4:6 (30 August 2007). doi:10.1186/1550-2783-4-6. © 2007 Buford et al; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).


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Blueberry Skins Lower Cholesterol Naturally

Research shows that blueberry skins lower cholesterol naturally. Levels of LDL (or "bad" cholesterol) were 19 percent lower in blueberry-supplemented hamsters.

According to a Agricultural Research Service (ARS) study announced at the American Chemical Society's (ACS) national meeting in Chicago, blueberry skins could be a key to controlling cholesterol.

ARS chemist Agnes Rimando and collaborators found that feeding hamsters a diet extremely high in cholesterol, but supplemented with freeze-dried skins of rabbiteye blueberries, produced plasma total cholesterol levels 37 percent lower than those of hamsters fed a control diet.

Levels of LDL - or "bad" - cholesterol were 19 percent lower in the blueberry-supplemented hamsters.

In addition, Rimando, in the ARS Natural Products Utilization Research Unit at Oxford, Miss., found that hamsters eating the blueberry-enhanced food fared better than hamsters fed the high-cholesterol diet augmented instead with the lipid-lowering drug ciprofibrate. Animals in that group exhibited 17 percent less total cholesterol—and two percent less LDL cholesterol—than the control group.

The results may be linked to constituents in blueberry skins that can activate a protein involved in the breakdown and import of fats, according to Rimando.

Among these constituents are resveratrol and pterostilbene, which have been cited for their antioxidant properties.

Her main collaborator in the study was chemist Wallace H. Yokoyama of the ARS Processed Foods Research Unit in Albany, Calif.

The researchers used 10 hamsters per treatment group, as well as a control diet containing the high amounts of cholesterol, but no supplements.

Supplemented diets consisted of either 7.6 percent blueberry skins or 25 milligrams of ciprofibrate per kilogram of diet.

Rimando collaborated in another study, also described at Sunday's meeting, which demonstrated pterostilbene's potential to fight colon cancer.

In that research, led by Rutgers University scientist Bandaru S. Reddy, nine rats fed a diet supplemented with 40 parts per million of pterostilbene showed 57 percent fewer induced colon lesions than nine other rats fed an unsupplemented diet.

Source: Luis Pons, Agricultural Research Service, the U.S. Department of Agriculture's chief scientific research agency. Photo courtesy ARS, USDA.

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Children and Television - Helping Your Child Lose Weight

Children and Television - Helping Your Child Lose Weight: According to US researchers who followed 550 children aged 11 to 13 over a period of 20 months, for each hour they spent watching television, their food intake was found at the end of the period to have increased by 167 calories a day. The study was published in the Archives of Paediatric and Adolescent Medicine.

Help Your Child Lose Weight - K-State Nutrition Expert Offers Advice to Parents.

Greasy burgers and French fries, video games and lack of exercise are just a few reasons for the increasing number of overweight children. Recent studies show that children are more overweight today than children 20 years ago.

A Kansas State University expert on child nutrition says that children have poor eating habits, watch more television and are less physically active.

"Children are exercising a lot less," says Paula Peters. "They are less active in school with less physical education being offered, plus when they come home from school they may be sitting down in front of the television.

"We know that kids are watching more television than they used to, or playing video games rather than going outside to play, which could be the result of a lot of things," Peters added.

Many kids are at home alone after school, and many parents don't want their kids outside playing for safety reasons, so they sit in front of the TV instead, said Peters. It's society in general that is causing a lot of problems with our exercise, as well as our eating habits.

"If you look at data from 20 years ago, a lot of us are eating a little bit better than we did 20 years ago, even children," said Peters. "The amount of fat in our diets has gone down in the last 20 years, and the number of calories we're eating is probably not too much different than it was 20 years ago.

"But yet on the whole, we are becoming more and more overweight," Peters added. So we have to really think about what we might be doing that is causing us to be heavier."

According to Peters, parents influence what children eat, and they will eat what the parents eat even though a lot of parents think that the children don't pay attention to what they do and what they tell them to do.

Peters encourages healthy eating habits for the entire family, but she offers advice to parents who are concerned about their children being overweight:

* Parents should check with the family physician to make sure that their child really is overweight because people sometimes forget that humans come in all shapes and sizes, and we can look at a child and what looks overweight to us, may not be.

* We really don't want to put children on weight loss diets. Kids are growing very rapidly and if we limit the amount of energy, the amount of calories they take in, we could be limiting the amount of nutrients that they can get. And they need the nutrients to grow properly.

* Children need to trust their own body signals of hunger. When a parent limits food and a child is made to go hungry, they may become preoccupied with food. When food is available, they may overeat out of fear of going hungry again. Encourage children to eat until satisfied and then stop.

* If the child is overweight, teach them healthy eating habits. Rather than restricting the amount of calories they take in, or restricting a food group or a favorite food, it's better to help them develop some sound eating habits with a balanced diet.

* Families don't eat together often and they tend to snack constantly. We don't need to cut out snacks completely but have scheduled times when the snacks will be available, and then have some healthy foods for the children to choose from at those times. Parents should establish regular meals and snacks for the whole family.

* Exercise is also very important. Try spending more time playing with your child. This could include bike riding, walking, jumping rope or participating in an organized sport.

* It's really important to be careful what we say to children with regard to weight. Children can interpret a negative comment from a parent to mean the parent doesn't really love them, or doesn't accept them for how they look. It is important for their self-esteem to feel loved and accepted for who they are, not how they look.

"By following these guidelines and explaining to children that people are different and not everyone will be thin, we will promote healthy eating and exercise habits," said Peters. "This will go a long way toward decreasing the risk for overweight."

For questions, contact Paula Peters at 785-532-1666.
Source: K-State Media Relations, K-State's news service. Used with permission.

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Bean Consumption Lowers Cholesterol

Adding beans to your diet may help lower cholesterol. Study shows that cooked dry pinto beans added to a regular daily diet lowers cholesterol.

Researchers tested 80 volunteers aged 18 to 55 years. Half were healthy, while half had at least two symptoms that lead to metabolic syndrome, a combination of conditions that signal a risk for cardiovascular disease.

Those with "pre-metabolic-syndrome" had abdominal obesity and either high triglyceride levels, low HDL "good" cholesterol, high blood sugar, or high blood pressure.

For 12 weeks, half of the group was randomly selected to eat one-half cup of cooked dry pinto beans daily along with their regular daily diet. The others ate a replacement serving of chicken soup instead of the pinto beans.

The findings show that, compared to measures taken prior to the 12-week test phase, all the volunteers—the healthy ones as well as those with symptoms—who ate pinto beans saw a reduction in their cholesterol levels.

Experts consider a lipid profile, which provides a complete cholesterol count based on blood tests, to be a valid biomarker for the risk of cardiovascular disease. Because cardiovascular disease is a lifestyle-related disease, interventions that improve cholesterol profiles are considered beneficial to health. Positive changes in physical activity and diet may result in substantial improvements.

While the findings confirm earlier studies by other researchers showing that eating beans lowers cholesterol levels, the mechanisms that underlie the effect require further study.

These results, published in the November issue of the Journal of Nutrition by the ARS scientists and their colleagues, add to a growing—and convincing—body of evidence that beans are a heart healthy food choice.

The lead authors, chemist Philip Reeves and nutritionist John Finley (no longer with ARS), conducted the study at the agency's Grand Forks Human Nutrition Research Center in Grand Forks, N.D. ARS is the U.S. Department of Agriculture's chief scientific research agency.

Source: Rosalie Marion Bliss, USDA, Agricultural Research Service - ARS is the U.S. Department of Agriculture's chief scientific research agency. November 28, 2007. Used with permission.

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Diabetes Risk and High Blood Pressure Medications

Diabetes Risk and High Blood Pressure Medications: A greater diabetes risk in patients taking high blood pressure medications.

In a long-term study of older adults with high blood pressure from the National Heart, Lung, and Blood Institute of the National Institutes of Health, participants without diabetes who were taking high blood pressure medications experienced increased average fasting glucose levels.

This was true regardless of which class of medication was used: diuretic, ACE inhibitor, or calcium channel blocker.

During a 4 year period, the glucose changes led to new diagnoses of diabetes in approximately 1 in 10 participants (diuretic 11.0 percent, ACE inhibitor 7.8 percent and calcium channel blocker 9.3 percent .)

However, the results of this Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) analysis showed no significant evidence that the new onset diabetes increased the risk of stroke, heart failure, or death from any cause, but it did increase the risk of heart attack.

In those taking a diuretic, the relationship between new diabetes and coronary disease was actually less than in those taking the other drugs and not significant for the diuretic.

According to the authors, this suggests that the glucose changes induced by diuretics do not lead to heart disease in the same way as diabetes caused by overweight, inactivity, and genetic predisposition.

This finding is strongly supported by previous findings in a 14-year follow-up of the Systolic Hypertension in the Elderly Program (SHEP).

“Fasting Glucose and Incident Diabetes Mellitus in Older Non-diabetic Adults Randomized to Receive Three Different Classes of Antihypertensive Treatment,” is published in the November 13, 2006 issue of Archives of Internal Medicine.

Reference: NHLBI National Heart, Lung, and Blood Institute

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Strong Abdominal Muscles Don’t Require Exercise Machines

Strong Abdominal Muscles Don’t Require Exercise Machines - MANHATTAN - If all you want for Christmas is a great set of abs, then a recent study of ab machine effectiveness is just for you.

Exercise scientists at Kansas State University found that the unassisted crunch or sit-up is as good a workout for the abdominal muscles as any you'd get using typical abdominal exercise equipment on the market now.

Consumer appetite for abdominal exercise machines has gone biggie-size in recent years: in 1998, according to the Sports Business Research Network, Americans spent $115 million on ab machines alone, with sales rising. In fact, says K-State biomechanics professor Larry Noble, ab machine sales have been one of the few components of the overall sports equipment market that's still growing.

What drives this market? It's about equal parts health concern and vanity. Lower back injuries, for example, are largely the result of weak abdominal musculature, and it's a costly health issue. In any given year, half the U.S. population experiences lower back pain. Direct medical costs for low back pain exceeded $24 billion in 1990.

Beyond that, the crunch is on, so to speak, to have a flat stomach. There's been no scientific evaluation of various claims of equipment effectiveness, say the K-State researchers. Infomercials have been the sole source of product information.

Noble and graduate student Kasee Hildenbrand, also a certified athletic trainer, conducted the research. Hildenbrand measured electrical activity in the belly of the abdominal muscles of each participant during exercise. She detected no significant differences in muscle electrical activity.

The group of very fit K-State students performed repetitions of unassisted crunches as well as abdominal exercises on the Abroller, Abslide and Fit-ball -- devices that represent the broad categories of abdominal exercise equipment on the market now.

"We're confident in saying you can do a crunch without equipment and get the same benefit as if you purchase any of these categories of equipment," Hildenbrand said. Some people are more motivated to exercise when they use equipment, she noted. The choice to equip or not to equip is personal.

"Our results suggest that doing abdominal strengthening exercises with equipment does not elicit any greater muscle activity of the targeted rectus abdominus muscle than if you perform traditional abdominal crunches," she and Noble said.

The researchers looked at another muscle group, the rectus femoris, a hip flexor muscle and not technically an abdominal muscle. They included it because it is one of the most powerful muscles used in bending, and in the typical American population the rectus femoris is more powerful than the rectus abdominus.

When abdominal exercises are done incorrectly, it's the rectus femoris that gets the workout instead of rectus abdominus. To perform a proper crunch that works the rectus abdominus, athletic trainer Hildenbrand instructs: lie on your back, knees bent, feet unanchored, arms behind your head resting on the neck. Crunch forward till your shoulder blades are off the mat or floor.

"Our guts are a real problem," Hildenbrand said. "As Americans become a more obese and sedentary population, we're getting ab messages about lower back health and from the popular culture that says a thin belly is in."

She hopes people pay attention to those lower back health concerns. Research has found over and over that the abdominal musculature is key in preventing or correcting problems associated with lower back pain.

"If the abs are strong and doing their job, they tip the pelvis backward, which straightens the lower back so a person is in correct alignment," she said. Strong abs counteract the strong hip flexors. The whole point of strong abs is to keep the pelvis in alignment so it supports the spine in correct alignment.

"Even if a person is overweight or has a fat belly, it's still very important to have strong abdominal muscles, she adds. Getting rid of a fat belly will take more than abdominal exercises, however. That takes a change of diet and an exercise program that includes functional exercises like walking, running, swinging a racket, or swimming, exercises that move, twist and flex the muscles that wrap around the body's core.

"In other words, don't bank your entire abdominal strength on doing crunches," Hildenbrand says. "Crunches are a very important part of the picture, but you also will need to twist the body functionally to keep it strong."

Hildenbrand presented the poster, "Abdominal Muscle Activity While Performing Trunk Flexion Exercises Using the Abroller, Abslide, Fit-ball and Conventionally Performed Trunk Curls," in June 2002 at the National Athletic Trainers Conference in Dallas. The poster had won second prize in October 2001 at the regional conference of the American College of Sports Medicine.

Hometown Connection

Kasee Hildenbrand is a 1994 graduate of Cheney (Wash.) High School. She is the daughter of Daniel and Pamela Melchior, Stoughton Road, Cheney, Wash.. She earned her undergraduate degree in sports medicine and physical education in 1998 from Whitworth College, Spokane, Wash.

Sources: Kasee Hildenbrand at 785-532-3211 or [email protected] and professor Larry Noble at 785-532-6979 or [email protected]. News release prepared by: Kay Garrett

Kansas State University is a comprehensive, research, land-grant institution first serving students and the people of Kansas, and also the nation and the world.
Used with premission.

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Medical Safety of Creatine Supplementation - Part 4 of 5

Medical Safety of Creatine Supplementation: While the only clinically significant side effect reported in the research literature is that of weight gain, many anecdotal claims of side effects including dehydration, cramping, kidney and liver damage, musculoskeletal injury, gastrointestinal distress, and anterior (leg) compartment syndrome still exist in the media and popular literature.

While athletes who are taking creatine monohydrate may experience these symptoms, the scientific literature suggests that these athletes have no greater, and a possibly lower, risk of these symptoms than those not supplementing with creatine monohydrate.

Many of these fears have been generated by the media and data taken from case studies (n = 1). Poortmans and Francaux reported that the claims of deleterious effects of creatine supplements on renal function began in 1998.

These claims followed a report that creatine supplementation was detrimental to renal glomerular filtration rate (GFR) in a 25-year-old man who had previously presented with kidney disease (glomerulosclerosis and corticosteroid-responsive nephritic syndrome).

Three days later, a French sports newspaper, L'Equipe, reported that supplemental creatine is dangerous for the kidneys in any condition. Several European newspapers then picked up the "news" and reported the same. Since that time, other individual case studies have been published posing that creatine monohydrate supplementation caused deleterious effects on renal function.

Much of the concern about creatine monohydrate supplementation and renal function has centered around concerns over increased serum creatinine levels. While creatinine does make up a portion of GFR and must be excreted by the kidneys, there is no evidence to support the notion that normal creatine intakes(less than 25 g/d) in healthy adults cause renal dysfunction.

In fact, Poortmans et al. have shown no detrimental effects of short- (5 days), medium- (14 days), or long-term (10 months to 5 years) creatine monohydrate supplementation on renal function.

Interestingly, Kreider et al. observed no significant difference in creatinine levels between creatine monohydrate users and controls, yet most athletes (regardless of whether taking creatine monohydrate or not) had elevated creatinine levels along with proper clearance during intense training. The authors noted that if serum creatinine was examined as the sole measure of renal function, it would appear that nearly all of the athletes (regardless of creatine monohydrate usage) were experiencing renal distress.

Although case studies have reported problems, these large-scale, controlled studies have shown no evidence indicating that creatine monohydrate supplementation in healthy individuals is a detriment to kidney functioning.

Another anecdotal complaint about supplemental creatine is that the long-term effects are not known.

Widespread use of creatine monohydrate began in the 1990's. Over the last few years a number of researchers have begun to release results of long-term safety trials. So far, no long-term side effects have been observed in athletes (up to 5 years), infants with creatine synthesis deficiency (up to 3 years), or in clinical patient populations (up to 5 years).

One cohort of patients taking 1.5 – 3 grams/day of creatine monohydrate has been monitored since 1981 with no significant side effects.

In addition, research has demonstrated a number of potentially helpful clinical uses of creatine monohydrate in heart patients, infants and patients with creatine synthesis deficiency, patients suffering orthopaedic injury, and patients with various neuromuscular diseases.

Potential medical uses of supplemental creatine have been investigated since the mid 1970s. Initially, research focused on the role of creatine monohydrate and/or creatine phosphate in reducing heart arrhythmias and/or improving heart function during ischemic events.

Interest in medical uses of creatine supplements has expanded to include those with creatine deficiencies, brain and/or spinal cord injuries, muscular dystrophy, diabetes, high cholesterol/triglyceride levels, and pulmonary disease among others.

Although more research is needed to determine the extent of the clinical utility, some promising results have been reported in a number of studies suggesting that creatine supplements may have therapeutic benefit in certain patient populations.

In conjunction with short- and long-term studies in healthy populations, this evidence suggests that creatine supplementation appears to be safe when taken within recommended usage guidelines.

Reproduced with minor omissions, including references for ease of reading, from: Buford TW, Kreider RB, Stout JR, Greenwood M, Campbell B, Spano M, Ziegenfuss T, Lopez H, Landis J, Antonio J. International Society of Sports Nutrition position stand: creatine supplementation and exercise. Journal of the International Society of Sports Nutrition 2007, 4:6 (30 August 2007). doi:10.1186/1550-2783-4-6. © 2007 Buford et al; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).

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Causes of Cognitive Losses in the Brain

What causes the cognitive part of the brain to stop working?

Cognition can be defined as the mental process of knowing, including aspects such as awareness, perception, reasoning, and judgment and the ability to use simple-to-complex information to meet the challenges of daily living.

The brain’s billions of neurons “talk” to one another through chemical neurotransmitters that convey signals through neural pathways. These chemical transporters which include norepinephrine, serotonin, and dopamine are key to signal movement. Dopamine has many functions within the brain. In particular, it can affect the way the brain controls movements.

Neurons that can’t get their messages through signalling pathways are like cell (mobile) phones that can’t get their signals through to other cell phones. As the brain matures, cell division becomes largely restricted to specific regions of the brain, and brain cells tend to become more vulnerable to two partners in crime: oxidative stress and inflammation.

In the body, free radicals - weakened atoms formed during activities of daily living - are missing an electron and want to bond with neighbouring biomolecules to stabilize. The problem is that unless neutralized, free radicals cause cellular damage known as “oxidative stress.”

Cellular antioxidant defence systems counterbalance these rogue molecules, but they’re not completely effective - particularly as the body and brain mature. The brain is thought to be especially vulnerable to oxidative stress.

Although people naturally lose brain cells throughout their lives, the process of neuronal death does not necessarily accelerate with aging. “There is a lot of individual difference,” says Agricultural Research Service neuroscientist James Joseph. “Loss of mental agility may be less due to loss of brain cells than to the cells’ failure to communicate effectively.”

Eight years ago, Joseph and colleagues began publishing a series of studies, done in rodents, that shed light on the relationship between various diets and the mechanisms behind cognitive losses in specific neighbourhoods of the aging brain.

Many in the series are groundbreaking in that they challenge the long-accepted belief that the central nervous system, which includes the brain, is not capable of regenerating itself. Other published studies in the series reiterate similar findings based on primate and human brain research at the Salk Institute for Biological Studies, San Diego, California.

Scientists there, using new technologies, disputed the notion that the brain does not make new neurons - a process called “neurogenesis” - into old age. The brain doesn't remain fixed after early development with damage being irreparable, but continues to change throughout a person's life, with damaged cells being repaired and new ones made but at a much slower rate as we age.

“Weighing just 3 pounds, the brain accounts for only 2 percent of the body’s total mass, yet it uses up to half of the body’s total oxygen consumed during mental activity,” says Agricultural Research Service neuroscientist James Joseph. “Phytochemicals, together with essential nutrients in foods, provide a health-benefits cocktail of sorts. It is feasible that continued research in this area will point to dietary regimens that are effective in boosting neuronal function.”

Although the exact cause of Alzheimer’s is not completely understood, experts have recently identified one mechanism involving the insufficient breakdown and recycling of amyloid protein in the brain.

The mechanism is both genetic and physiological. In those individuals, normally harmless amyloid protein turns into fragments of amyloid beta, which build up as plaque in the brain rather than being escorted into cellular recycling. That action leads to cell death and weakened neuronal communication.

A rat study at the USDA Human Nutrition Research Center on Aging looked at the aged brain’s ability to change physiologically - a condition scientists refer to as “neuronal plasticity.” In addition to cell division and differentiation, or “mission assignment,” brain tissue undergoes many other changes throughout aging.

For example, a newborn sprouts billions of nerve cells while soaking up information from the environment. But lower levels of synapse growth continue in waves throughout the lifespan. Little-used synapses are eliminated, while others are strengthened in a neuronal pruning process, of sorts.

While seeking to protect and repair tissue, microglia cells produce and send out molecular stress signals, some by way of defensive cytokines, as a call to other cells. Those signals begin a cascade of reactions, including the activation of genes that express proteins and other stress chemicals to help clear away cellular debris.

Microglia cells are a part of the neuroglia, which in turn is part of the delicate connective tissue framework which supports the nervous matter and blood vessels of the brain and spinal cord.

Microglial activation by amyloid beta (mentioned above) is thought to be a key event in the progression of Alzheimer’s disease. “When microglia are stuck in an always-on loop in response to plaque build-up in the brain, they become problematic in and of themselves,” says Joseph.

Microglial activation is considered the hallmark of inflammation in the central nervous system.

Future studies at Human Nutrition Research Center on Aging (HNRCA) will ideally include use of new diagnostic tools as well as human clinical trials. Neuroimaging equipment, for example, could be used to monitor the influence of various dietary factors on development of plaque within the human brain. Such studies aim to find the best dietary regimens to help adults preserve their mental capabilities while aging.

The link between nutrition and cognitive function is an area that has been largely overlooked in the past. But recent studies looking at the potential protective role of foods such as berries, green tea, and fish against cognitive impairment shows that this is slowly changing.

Adapted and modified from: “Nutrition and Brain Function” published in the August 2007 issue of Agricultural Research magazine. Rosalie Marion Bliss, Agricultural Research Service Information Staff. Photo courtesy of USDA, ARS. Used with permission.

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Dementia Treatment – Lower Homocysteine Levels

An elevated blood level of homocysteine is a risk factor for cognitive impairment and dementia.

This article relates to 7 case reports regarding the administration of the antioxidant N-acetylcysteine together with folate (folic acid) and vitamin B to cognitively impaired patients with elevated levels of homocysteine.

A link between high blood folate (folic acid) levels and relatively lower homocysteine levels has long been known. Scientists have also long known that being seriously deficient in vitamin B12 leads to impaired cognitive function due to neurological complications.

Therefore, homocysteine can be lowered by folate (folic acid) and/or vitamin B12 supplementation. (See Cognitive Function - Folic Acid and Vitamin B12 Deficiency and Homocysteine )

Andrew McCaddon, an Honorary Research Fellow of the Wales College of Medicine in the UK, presented clinical and radiological findings from administering the antioxidant N-acetylcysteine together with B vitamins to cognitively impaired patients with elevated levels of homocysteine.

Note: N-acetylcysteine was used in conjunction with folate (folic acid) and vitamin B12 as antioxidants might also be required for optimal reduction of homocysteine in both nerves and blood vessel tissue.

N-acetylcysteine increases urinary excretion of homocysteine, leading Ventura and colleagues to suggest that this approach may be an important associative or alternative therapy for elevated levels of homocysteine. (Pharmacology 2003, 68:105-114).

Case presentations

Case 1

A 78 year old lady presented with fatigue, anxiety and depression. She had angular cheilosis (inflammation and cracking of the lips which may occur secondary to a vitamin C or B-complex or mineral deficiency) but was not anaemic, despite a profound vitamin B12 deficiency with normal blood and red cell folate. She had parietal cell antibodies but a normal Schilling test. She “...felt better” after monthly injections of B12 (1,000 micrograms) were commenced, but nevertheless remained anxious.

A year later she developed memory impairment, with difficulty remembering names. She scored 21/30 on Mini-mental state examination. It was felt that she had a dementia, perhaps with associated depression, and she was commenced on an antidepressant (a selective serotonin reuptake inhibitor). Her depression slowly resolved but her cognitive decline continued.

A year later she scored 18/30 on Mini-mental state examination and 28/70 on the Alzheimer's disease assessment scale. In view of her persistent dementia despite regular B12 injections, she was commenced on oral N-acetylcysteine (NAC) (600 mg) daily.

Two weeks later her husband reported a noticeable improvement in her memory. She now remembered names and faces she previously would have struggled to recall. Her Mini-mental state examination improved to 21/30 and Alzheimer's disease assessment scale to 20/70. The areas of improvement were in scores of orientation, copying skills, word-recall, naming and commands.

Case 2

An 84 year old lady presented with a three year history of short-term memory impairment and early Parkinsonism for which she took L-dopa. She was otherwise well. She scored 12/28 on the 6 Item Cognitive Impairment Test. Investigations revealed an above normal total blood homocysteine level, but normal serum vitamin B12, folate and red cell folate. She was not anaemic, but had borderline hypothyroidism.

In view of her elevated total homocysteine, and despite 'normal' serum B vitamin levels, she was commenced on daily oral B12 (1000 mg), folic acid (5 mg) and N-acetylcysteine (NAC) (600 mg). Within one month her total homocysteine fell to 7.5 μmol/L.

She was assessed by a Psychogeriatrician three months after her initial presentation. She now showed no significant cognitive deficits; she scored 28/30 on Mini-mental state examination.

The psychogeriatrician was “...particularly impressed that she could provide the Christian names of all her five children and twelve grandchildren without any problems” and it was felt that she now had no obvious diagnosis of a dementia.

Case 3

A 77 year old lady presented with a six month history of confusion and memory loss. An aunt had early-onset Alzheimer’s Disease. On examination she was disorientated to time and had demonstrable memory impairment. She was vitamin B12 deficient but with normal serum and red cell folate.

She commenced monthly intramuscular B12 injections (1,000 mg) but continued to deteriorate.

She became fatigued and developed visual hallucinations and persecutory ideas. She had naming difficulties, her repetition was poor, and she had constructional dyspraxia.

It was felt she had probable Alzheimer’s Disease. She was admitted for care, scoring only 13/30 on Mini-mental state examination. She was commenced on an acetylcholinesterase inhibitor with slight initial improvement (15/30). Nevertheless her condition continued to deteriorate. She developed dysphagia (a condition in which swallowing is difficult or painful) and weight loss due to a grade III oesophagitis (inflammation of the esophagus).

Oral N-acetylcysteine (NAC) (600 mg daily) was added to her treatment and her family and carers noticed a significant improvement. She became more alert and recognised her close family; a formal cognitive assessment was not performed in view of the severity of her dementia and associated physical condition. Sadly she died from a bronchopneumonia several weeks later.

Case 4

An 87 year old retired school headmistress presented with a three year history of gradually deteriorating short-term memory and general 'confusion'; she frequently mislaid things and often wandered, forgetting her way home. She had a past medical history of diverticular disease (a herniation through the muscular wall of a tubular organ, especially the colon) and an osteoarthritic hip, but was otherwise well.

On examination it was felt she was suffering from a senile dementia of moderate severity although no formal cognitive scores were recorded. Routine investigations were normal other than a highly elevated total homocysteine.

She was commenced on folic acid 5 mg daily and oral hydroxo-B12 1,000 mcg daily, together with N-acetylcysteine (NAC) 600 mg daily. Her total homocysteine fell to 6.6 μmol/L six-months later, at which time she felt generally well although she remained mildly confused.

Her daughter commented on a marked improvement in her general behaviour, although she remained forgetful at times. Three years later she remains very well and continues to be cared for at home with no major difficulties.

Case 5

An 84 year old lady presented with a two year history of increasing forgetfulness and confusion and no significant previous illnesses. She was cared for at home by her daughter. On formal examination she was disorientated in time and place with demonstrable short-term memory impairment.

It was felt she had a moderate dementia; she scored 55 out of 70 on an Alzheimer's disease assessment scale. Blood investigations were normal other than an elevated total homocysteine and low red cell folate (157mg/l). She was not anaemic.

She was commenced on daily oral cyano-B12 (150 mg daily) folic acid (5 mg) and NAC (600 mg) daily. One month later she had gained ten points on Alzheimer's disease assessment scale score. Her daughter also reported that she was “...generally more settled and content, and less likely to wander.”

Case 6

A 71 year old retired engineer presented with a ten year history of gradually progressive short-term memory impairment. His wife had become concerned because he had recently lost his way driving to a regular address. He complained of losing objects and forgetting people's names.

His father had died of senile dementia aged 74, with symptoms developing at aged 60 years. The patient himself had a past medical history of hypertension controlled by beta-blocker. On cognitive examination he scored poorly on 6 Item Cognitive Impairment Test (12/28). Routine blood investigations revealed elevated total homocysteine with normal serum vitamin B12, folate and red cell folate.

He was commenced on daily oral cyano-B12 (1,000 mg) folate (5 mg) and NAC (600 mg). His wife reported a "...definite and immediate improvement" within two weeks of commencing treatment.

His total homocysteine fell to 9.6 μmol/L. He was seen by a Psychogeriatrician one month later. He now scored 28/30 on Mini-mental state examination with a CAMCOG of 115/125, indicating only a mild cognitive deficit.

A diagnosis of "age-related cognitive impairment" was made. He has continued on this treatment for the last two years and continues to score well on cognitive assessments. He scored 27/30 on his most recent assessment and has now commenced an acetylcholinesterase inhibitor in addition to B vitamins and NAC supplementation.

Case 7

A 75 year old retired College Lecturer presented with a four year history of increasing forgetfulness. In particular he frequently mislaid things, and had occasional difficulty remembering people's names. His wife had become concerned about his ability to drive. He had a past medical history of prostatic carcinoma treated with radiotherapy, anxiety/depression, and gastro-oesophageal reflux, but was generally well in himself.

On cognitive examination he was disorientated in time and had demonstrable short term memory impairment. He scored 8/28 on 6 Item Cognitive Impairment Test and 16/39 on TICS-m. An MRI scan showed several foci consistent with small vessel disease. Blood investigations revealed raised total homocysteine of 14.6 μmol/L, borderline low serum B12, but normal folate and red cell folate.

He was commenced on daily oral cyano-B12 (1000 mg), folic acid (5 mg) and NAC (600 mg). After one month he had gained five points on TICS-m (21/39). His total homocysteine
fell to 8.3 μmol/L.

He was personally delighted with the treatment. His wife commented that "...he was becoming very forgetful, quite retiring, quiet, sleepy all the time, not interested in his food or in life. Now, there's a marked improvement. We can discuss the news without any problem. He's reading again. He's interested in life once more."

One year later, he remains well and has successfully regained his driving license following a formal assessment. A repeat MRI scan showed no significant progression in the extent or size of the focal areas of abnormality in the deep white matter, and no change in ventricular configuration.

Andrew McCaddon concluded: These reports demonstrate the apparent clinical efficacy of the addition of N-acetylcysteine (NAC) to B vitamin regimes in elevated homocysteine level patients with cognitive impairment. NAC was well-tolerated in all patients; there were no reported side-effects.

There is now strong evidence that elevated blood levels of homocysteine are associated with dementia in general, including both vascular dementia and Alzheimer’s Disease. However, the mechanism underlying this association remains unclear. The clinical responses to N-acetylcysteine (NAC) in these cases suggest that homocysteine might also be a surrogate marker for the effects of oxidative stress on neurovascular tissues (both nerves and blood vessel tissues).

The radiological findings in Case 7 are notable. Elevated homocysteine levels are associated with brain atrophy and white matter lesions. The annual estimate of progression of white matter lesions in cognitively intact elderly individuals is approximately 0.6 mL/year.

Though not formally quantified, the apparent halting of disease progression in Case 7 is of significance. Follow-up scans were not performed in the earlier cases.

A notable feature in all cases was the complete absence of anaemia. Indeed, despite the clear association between metabolic evidence of B12 and/or folate deficiency and dementia, anaemia and macrocytosis are invariably absent in these patients.

Elevated homocysteine levels in these patients potentially arises from oxidative depletion of vitamin B12 and folate. Such depletion is, of course, subtly different from our current concepts of classical deficiency due to malnutrition or malabsorption.

The epidemiological evidence (the branch of medical science dealing with the transmission and control of disease) is now of sufficient strength that elevated levels of homocysteine should be considered a potential risk factor for dementia in elderly patients. At the very least, clinicians should determine the folate and vitamin B12 status of these patients, irrespective of whether or not there is a macrocytic anaemia.

Derived and adapted from: Andrew McCaddon. Homocysteine and cognitive impairment; a case series in a General Practice setting. Nutrition Journal 2006, 5:6 (15 February 2006) doi:10.1186/1475-2891-5-6.
© 2006 McCaddon; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)

Photo courtesy of USDA, ARS

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The Best Creatine? Creatine Monohydrate Effectiveness - Part 3 of 5

The Best Creatine? Creatine Monohydrate Effectiveness: Many forms of creatine exist in the marketplace, and these choices can be very confusing for the consumer. Most of these forms of creatine have been reported to be no better than traditional creatine monohydrate in terms of increasing strength or performance.

The addition of nutrients that increase insulin levels and/or improve insulin sensitivity has been a major source of interest in the last few years by scientists looking to optimize the ergogenic effects of creatine.

The addition of certain macronutrients appears to significantly augment muscle retention of creatine. Green et al. reported that adding 93 g of carbohydrate to 5 g of creatine monohydrate increased total muscle creatine by 60%. Likewise, Steenge et al. reported that adding 47 g of carbohydrate and 50 g of protein to creatine monohydrate was as effective at promoting muscle retention of creatine as adding 96 g of carbohydrate.

Additional investigations by Greenwood and colleagues have reported increased creatine retention from the addition of dextrose or low levels of D-pinitol (a plant extract with insulin-like properties). While the addition of these nutrients has proved to increase muscle retention, several recent investigations have reported these combinations to be no more effective at improving muscle strength and endurance or athletic performance.

Other recent studies, however, have indicated a potential benefit on anaerobic power, muscle hypertrophy, and 1 RM muscle strength when combining protein with creatine. It appears that combining creatine monohydrate with carbohydrate or carbohydrate and protein produces optimal results. Studies suggest that increasing skeletal muscle creatine uptake may enhance the benefits of training.

Creatine monohydrate appears to be the most effective nutritional supplement currently available in terms of improving lean body mass and anaerobic capacity.
To date, several hundred peer-reviewed research studies have been conducted to evaluate the efficacy of creatine monohydrate supplementation in improving exercise performance. Nearly 70% of these studies have reported a significant improvement in exercise capacity, while the others have generally reported non-significant gains in performance.

No studies have reported an ergolytic effect on performance although some have suggested that weight gain associated with creatine monohydrate supplementation could be detrimental in sports such as running or swimming.

The average gain in performance from these studies typically ranges between 10 to 15% depending on the variable of interest. For example, short-term creatine monohydrate supplementation has been reported to improve maximal power/strength (5–15%), work performed during sets of maximal effort muscle contractions (5–15%), single-effort sprint performance (1–5%), and work performed during repetitive sprint performance (5–15%).

Long-term creatine monohydrate supplementation appears to enhance the overall quality of training, leading to 5 to 15% greater gains in strength and performance. Nearly all studies indicate that "proper" creatine monohydrate supplementation increases body mass by about 1 to 2 kg in the first week of loading.

The vast expanse of literature confirming the effectiveness of creatine monohydrate supplementation is far beyond the scope of this review. Briefly, short-term adaptations reported from creatine monohydrate supplementation include increased cycling power, total work performed on the bench press and jump squat, as well as improved sport performance in sprinting, swimming, and soccer.

Long-term adaptations when combining creatine monohydrate supplementation with training include increased muscle creatine and phosphocreatine content, lean body mass, strength, sprint performance, power, rate of force development, and muscle diameter. In long-term studies, subjects taking creatine monohydrate typically gain about twice as much body mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to 12 weeks of training) than subjects taking a placebo.

The tremendous numbers of investigations conducted with positive results from creatine monohydrate supplementation lead us to conclude that it is the most effective nutritional supplement available today for increasing high-intensity exercise capacity and building lean mass.

Reproduced with minor omissions, including references for ease of reading, from: Buford TW, Kreider RB, Stout JR, Greenwood M, Campbell B, Spano M, Ziegenfuss T, Lopez H, Landis J, Antonio J. International Society of Sports Nutrition position stand: creatine supplementation and exercise. Journal of the International Society of Sports Nutrition 2007, 4:6 (30 August 2007). doi:10.1186/1550-2783-4-6. © 2007 Buford et al; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).

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Is Vitamin D an Autism Treatment?

Is Vitamin D an Autism Treatment? …it has now been suggested that autism may be caused by insufficient vitamin D during pregnancy and/or early years. Autistic children have difficulty in forming relationships, but they also tend to have larger heads, changes similar to those found in baby rats that are bred with insufficient vitamin D. (The Telegraph, Why is Vitamin D So Vital?).

Extracted from a periodic newsletter from the Vitamin D Council by John Cannell, MD

The following is Dr. Cannell’s reply to one of a number of questions sent to him regarding vitamin D and autism.

Dear Dr. Cannell:

Who are you to write an article on autism? You didn't even publish it in a medical journal. You are not with a university. You have not published very much. You have no expertise on autism. No autism experts support your theory. There is no evidence to support the theory. Shouldn't you leave this to experts before you give parents more false hopes?

Mary, Trenton, New Jersey.

Dear Mary:

You are right, I am a nobody; just ask my ex-wife. In the Toronto Globe, I explained why I have not yet submitted the paper. As far as giving false hopes, I've thought about that charge. Right now, regardless of what advocacy groups say, autism is rather hopeless. That is, no treatment, including vitamin D, has been shown to materially affect the clinical course of autism. As a psychiatrist, my observation is that people would rather live with a false hope than with no hope.

Furthermore, if autistic children began taking vitamin D, the worse that can happen is that a period of false hope will followed by dashed hopes and then parents will be back to hopelessness. In the meantime, they will have made their child vitamin D sufficient. Vitamin D deficiency is a serious problem in childhood. (Postgrad Med J. 2007 Apr;83(978):230-5).

As far as the theory having no support from experts, Dr. Richard Mills, research director of the National Autistic Society in England, was quoted in the Telegraph article on the autism/vitamin D theory: "There has been speculation in the past about autism being more common in high-latitude countries that get less sunlight and a tie-up with rickets has been suggested - observations which support the theory."

Finally, you said there is no evidence to support the theory. I assume you meant there is no proof. The first statement is absolutely false, the second absolutely true. As I detailed in my paper, there is a lot of evidence to support the theory. In fact, if anyone can come up with an autism fact, that the theory cannot explain, I'd like to know about it.

Even the announcement of a link between television viewing and autism supports the theory. Furthermore, the TV/autism link is actually evidence of a treatment effect. That is, if autistic children who play outside in the sunshine more - watching less TV - have less severe illness, it may be due to the Sun-God, who bestows her precious gift of calcitriol (natural vitamin D) into the brains of children playing outside in her sunlight but not into the brains of children watching TV inside in the darkness. (Natl Bur Econ Res Bull Aging Health. 2007 Winter;(18):2-3).

As far as proof the theory is true, there is, of course, none. In medicine, proof means randomized controlled human trials, the gold standard for proof. However, proof is the last step, not the first. First comes evidence, then comes a theory, then comes researchers disproving those theories. It works that way. Sometimes we never get to the last step, proof. For example, please point me to a single randomized controlled human trial proving cigarette smoking is dangerous? Instead, the convincing evidence of smoking's dangerousness lies in epidemiological (population) studies, not randomized controlled trials.

Proof, or disproof, of the autism vitamin D theory will take years, years during which young autistic brains will continue to suffer irreparable damage. Perhaps vitamin D' powerful anti-inflammatory actions will help prevent that damage, perhaps not.

It's something of a Pascal's wager, betting on vitamin D instead of the existence of God, risking your child's brain instead of eternal damnation. "If you believe vitamin D helps autism and turn out to be incorrect, you have lost nothing - but if you don't believe in vitamin D and turn out to be incorrect, your child will suffer irreparable brain damage."

John Cannell, MD
The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422
Used with permission.

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Disclaimer: The information contained in this article is presented for information purposes only and is in no way intended to replace professional medical care or attention by a qualified practitioner. It cannot and should not be used as a basis for diagnosis or choice of treatment.

Fish Reduces Risk of Dementia and Alzheimer’s

Fish and Omega-3 Fats Reduce Risk of Dementia and Alzheimer’s

Fish consumption has been associated with lower risk of dementia and alzheimer’s. Fish is the best source of omega-3 fatty acids, which have been shown to be essential for neurocognitive development and normal brain functioning.

Several studies have demonstrated that consumption of one omega-3 fatty acid in particular, docosahexaenoic acid (DHA), is important for memory performance.

According to a WorldNetDaily.com article by reporter Mollie Martin, over 1,200 patients participated in an epidemiological (population) study showing that people with high DHA levels were 45 percent less likely to develop dementia than people with low DHA levels.

This suggests that proper DHA intake may reduce the risk of developing Alzheimer's disease.

DHA is the most abundant omega-3 fatty acid in most tissues, and it is present in large amounts in the brain and retina. When an omega-3 fatty acid deficiency exists, the body compensates by replacing it with the corresponding omega-6 fatty acids.

Our ancestor’s diet comprised of equal proportions of omega-3 fatty acids and omega-6 fats. In the past 100 years, Western diets have lowered the ratio of omega-3 to omega-6 to about 1:25.

The following is a November 14, 2006 news release from the United States Department Of Agriculture (USDA), Agricultural Research Service (ARS) by Rosalie Marion Bliss (last modified on 14/8/2007).

People who ate the most fish on a weekly basis - putting them in the top quarter of a study population - were nearly 50 percent less likely to develop the mental deterioration known as dementia over time than participants in any of the other three quarters.

The observational study was led by Ernst J. Schaefer, an Agricultural Research Service-funded scientist. ARS is the U.S. Department of Agriculture's chief scientific research agency. Schaefer is a physician specializing in nutrition and health with the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston, Mass.

He and co-authors were looking for a relationship between blood levels of the fatty acid DHA and the risk of developing dementia.

DHA is short for docosahexaenoic acid, a so-called "heart-healthy" omega-3 fatty acid. Several different studies have linked either low DHA, or low fish intake levels, with the incidence of dementia.

The study was published in the November 13 issue of the Archives of Neurology. Schaefer and colleagues analyzed available dietary questionnaires and blood levels of DHA of nearly 900 men and women, aged 55 to 88, who participated in the longitudinal Framingham (Mass.) Heart Study.

At the beginning of a nine-year period, all of the participants were found to be free of dementia.

Using proportional regression analysis, the researchers determined the relative impact not only of blood levels of DHA, but also of potential "confounding" variables such as age, gender, homocysteine and apolipoprotein-E levels, genotype and education.

They found that the participants who reported consuming an average of about three servings of oily fish a week - equivalent to blood levels of DHA at 180 milligrams daily - were associated with a significantly reduced risk of developing dementia of all types, including Alzheimer's disease.

No other fatty acid blood level was independently linked to the risk of dementia. The study suggests that relatively higher fish consumption over time correlates with a lower incidence of dementia in the over-55 set.

Part of this Article and photo courtesy of the USDA, Agricultural Research Service
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Heart Disease - Red Wine Reduces Risk

Heart Disease - Red Wine Reduces Risk: Red wine contains a rich source of a large number of antioxidants, namely the phenolic acids and polyphenols, which provide it with its protective oxidation reduction potential thereby reducing heart disease risk..

Epidemiological (population) studies have shown that despite the high intake of saturated fatty acids within the diets of some populations, a reduced mortality rate from cardiovascular (heart) disease is attributed to the high consumption of red wine, independent of its alcohol content, the 'French Paradox'. (Lancet 1992, ):1523-6).

Studies also indicate that sub-populations already at a high risk of coronary heart disease (CHD) (i.e. elderly) may potentially experience a greater beneficial effect from moderate wine consumption. (J Intern Med 2001, 250(4):291-308).

Moderate consumption of red wine has also been shown to retard or slow the blood clearance of high density lipoproteins (HDL cholesterol), a positive factor in lowering the risk of development of cardiovascular disease. It is also indicated that red wine inhibits LDL cholesterol oxidation more efficiently than white wine and at much lower concentrations. (J Am Coll Nutr 1999, 18(2):137-43).

Australian researchers from the University of Newcastle, Victoria University and Deakin University carried out a study with 40 volunteers to measure the effects of moderate red wine consumption on antioxidant status and oxidative stress in the circulation. Oxidative stress is the consequence of an imbalance of oxidants and antioxidants.

Twenty young (18-30 yrs) and 20 older (greater or equal to 50 yrs) volunteers were recruited. Each age group was randomly divided into treatment subjects who consumed 400 mL/day of red wine for two weeks, or control subjects who abstained from alcohol for two weeks, after which they crossed over into the other group. Blood samples were collected before and after red wine consumption and were used for analysis of blood total antioxidant status.

In the current study total antioxidant status in the blood increased after red wine consumption.

These results strongly suggest that in the presence of red wine consumption, total antioxidant status has the ability to increase significantly.

This increase was slightly more prominent in older individuals who increased their total antioxidant status 16% after consuming the red wine for two weeks compared to the younger individuals who increased 7%, despite the fact that young individuals had higher resting concentrations of total antioxidant status.

Our results are also shared in a study by Fernandez-Pachon and colleagues, who eluded that antioxidant values determined before wine intake were statistically different from those measured 30 minutes after consumption. (J Agric Food Chem 2005, 53(12):5024-9).

Our study however, extends beyond Fernandez-Pachon's by advocating that the consistent consumption of wine may offer the ability to significantly enhance total antioxidant status over a longer period.

This sustained elevation of total antioxidant status further confirms that the lower incidence of cardiovascular disease in populations who consume red wine on a regular basis is due to an increase in circulating oxidative protection.

In addition it also suggests that a lifetime of red wine consumption is not needed to achieve a sustained increase in circulating oxidative protection, two weeks is long enough to boost total antioxidant status.

Derived and adapted from: Michelle Micallef, Louise Lexis and Paul Lewandowski. Red wine consumption increases antioxidant status and decreases oxidative stress in the circulation of both young and old humans. Nutrition Journal 2007, 6:27doi:10.1186/.
© 2007 Micallef et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)

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