OHM Meeting on Metabolic Syndrome
Orthomolecular Health Medicine (OHM) is a close-knit group, based in San Francisco, advocating nutrition and megavitamin therapy. The group is one of several orthomolecular groups that champion ideas subscribed to by biochemist Roger Williams, PhD, and Nobel laureate Linus Pauling. Williams is best remembered for his nutritional work establishing the basis for biochemical individuality: individuals' needing different levels of nutrients based on biochemical and genetic needs. Pauling's broad-based recommending of megadose levels of vitamin C has played a key role in its use for treating cancer, atherosclerosis, and other degenerative diseases. For the past three decades, Richard Kunin, MD, and Iga Mosbauer, MS, have organized the San Francisco annual event. It is a little gem of a meeting offering excellent talks which has been underappreciated by the larger nutrition and naturopathic community. This year's meeting, which focused on metabolic syndrome, was no exception.
Gerald Reaven, MD, professor of medicine at Stanford University, was a much anticipated speaker. His research in metabolic syndrome has been documented with many papers he has authored. Reaven is greatly concerned that the ravaging effects of Syndrome X, another name for metabolic syndrome, frequently go undiagnosed. Even today after years of clinical research, metabolic syndrome's CPT code is not well accepted. Yet the disorder plays a pivotal role in fostering hypertension, lipid dysfunctioning, coronary and cerebral cardiovascular disease, adult onset diabetes, polycystic ovarian syndrome, and inflammatory disorders. Reaven cautions that 50% of patients do not have obesity, expanded waistlines, or increased BMIs. At his clinic nearly all patients with metabolic syndrome have elevated insulin levels on glucose tolerance test testing. Reaven recommends routine fasting insulin testing. At his lab, levels of 8% are considered normal; levels of 15% are abnormal, suggesting metabolic syndrome. From Reaven's perspective, aggressive treatment of metabolic syndrome with diet, exercise, and behavior modification is well justified in preventing complicating disorders.
Elson Haas, MD
Dr. Haas is a well-recognized Bay Area orthomolecular MD, author, and, as he prefers to think of himself, nutrition educator. He thinks that leading a support group and counseling 20 patients on dieting, exercise, and detoxification is a vital role for the physician. Haas's teaching focuses on the basics because most patients with metabolic syndrome do not follow a nutritive diet, engage in exercise, or undertake any detoxifying. Physicians cannot just hand out a prescription for metformin and tell a patient to watch one's diet and exercise. Despite the books, TV shows, and Internet, most patients with metabolic syndrome need "the doctor's prescription" to eat a Mediterranean-based diet, drink more water, eat lighter, know about glycemic foods, detoxify by alkalinizing and using the sauna, actively move and exercise, destress, and routinely use a prudent supplement regimen appropriate for one's metabolic state.
Haas recommends periodic use of the "Master Cleanse." The cleansing drink is consumed 8 times per day. To 8 ounces of water one adds 2 tbsp. of lemon juice, 1 tbsp. pure maple syrup, and 1/10 tsp. cayenne pepper. Mix well. Haas advises to rinse the mouth after each use.
I would recommend an additional cleanse that may be easier on the system and doesn't require a full fast. This cleanse is also suitable for treating yeast syndrome. One practitioner has labeled this the Acutrol protocol. The ingredients include bentonite, psyllium, capryllic oil, and a probiotic. Usually the drink is prepared on arising or anytime 2 hours after eating. Take 1 to 2 tbsp. of bentonite, add 1 to 3 tsp. of capryllic oil, 1/2 tsp. of a probiotic in 8 ounces of water, adding last 1 to 2 tbsp. of psyllium. The psyllium will thicken up the mixture quickly so it should be mixed and drunk immediately. Once or more daily is a good cleanse over several weeks or longer.
Robert Lustig, MD
Perhaps the most controversial lecture at the OHM meeting was presented by Dr. Lustig, professor of pediatrics at the University of California-San Francisco. His topic was titled "Childhood Obesity: How to Fix It." Lustig's first slide was a photo of a sculpture dated from 22,000 BC: the Venus von Willendorf, seen at the Vienna Museum of Natural History. It is clearly an obese female; obesity has been a human condition as long as there have been humans. Yet the per capita incidence of obesity has taken a sharp upswing in the US over the past two decades. With obesity, metabolic syndrome has also increased in incidence. Lustig points out that obesity is increasing in all age groups, especially in children – even infants. And the epidemic of obesity is not limited to the US; it is being seen in developed and developing nations. Are we all just on a wild eating craze? From a caloric point of view, the answer would appear to be "yes."
In the past three decades, men have been eating at least 150 calories more, women at least 200 calories more per day. We could blame fast food, more fatty and sugary food, less activity, and greater stress. Lustig reminded us that in the 1980s, lipid research suggested that excess fat was our problem. At that time, Atkins's theories on eating fatty foods were considered wrong. So the fat in our diet was replaced with carbohydrates, generally sugar. Heart disease risk didn't change much with diet, and waistlines actually increased.
One of the observations made about nutritional habits in the past two decades is the dramatic increase in fruity drink consumption. A large part of the increased calories was the greater consumption of fructose. Fructose has been available as high-fructose corn syrup (HFCS) since 1976. HCFS has replaced cane sugar in many foods and beverages. Lustig theorizes that HCFS may be responsible for the obesity epidemic and increasing metabolic syndrome. A review of the biochemistry of glucose metabolism is dramatically different from fructose metabolism. Although glucose excess leads to a decrease in insulin sensitivity and more fatty acid deposition, fructose is metabolized by very different pathways, leading to highly decreased insulin sensitivity and abnormal lipid deposition. Additionally, fructose metabolism tends to create inflammatory byproducts which accelerate the inflammation process. Indeed, fructose biochemistry looks very similar to the metabolism of ethyl alcohol, whose byproducts insult the liver, disrupt insulin sensitivity, alter skeletal muscle and adipose cell metabolism, and disrupt the immune system through inflammatory mechanisms.
Lustig hypothesizes that obesity is not a behavioral disorder or lack of exercise. He thinks that it is HCFS permeating all parts if the diet which is the culprit. Fructose, like alcohol, encourages chronic use just as with any dependency. It is not enough to be told to go a diet and to exercise. Avoidance of HCFS is a major factor in addressing the obesity epidemic and metabolic syndrome.
Dr. Jeffrey Bland, chief science officer of Metagenics, is well known for his outstanding work in functional medicine. At the institute that he presides over in Gig Harbor, Washington, Dr. Bland oversees research and clinical studies in functional medicine. He appreciates the opportunity that he has had to direct the clinical research of over 30 scientists and health professionals working in Gig Harbor. Dr. Bland lectures widely on functional medicine and updates subscribers monthly with his "audio" review, available now for more than 25 years.
Bland's article in this issue of the Townsend Letter is "Making Clinical Sense of the Inflammation/Chronic Disease Story." The section "Case History of Alzheimer's Disease and Anti-Inflammatories" addresses the difficulty in understanding inflammation's role in causing and treating chronic disease. In the early 1990s, clinical research suggested that patients with early-stage Alzheimer's disease would have less impairment if they used an anti-inflammatory drug. Indeed, indomethacin appeared to slow cognitive impairment in mild to moderate Alzheimer's patients. Further, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) among twins appeared to prevent the onset of Alzheimer's process. Other reports in the mid-1990s appeared to confirm similar results, with ibuprofen slowing the rate of cognitive decline.
However, more recent reports suggest that NSAIDs may actually contribute to deterioration in the Alzheimer's disease process. One report in 2010 found that regular use of NSAIDs increased the development of abnormal neurologic plaque thought to be responsible for increased cognitive decline in Alzheimer's. Another study involving a much larger number of Alzheimer's patients found that routine use of NSAIDs worsened rather than improved cognitive functioning. Bland explains that while the earlier results suggest that anti-inflammatory strategies might appear to lessen disease activity, excess anti-inflammatory activity might prevent certain cells to express "helpful inflammation" which would slow the neurodegenerative process. Indeed, another Alzheimer's study suggested that NSAIDs may help slow the early stages of the disease, but then encourage progressive cognitive deterioration in the latter stages. It would appear that anti-inflammatory therapies do offer help but may also aggravate disease. This would also argue that drug therapies pose significant risks and must always be weighed pro and con when considering ongoing treatment.