Dr. Janet Abshire on The Metabolic Syndrome

Dr. Abshire has years of experience in weight loss medicine and offers individualized therapeutic lifestyle change programs that help reverse the metabolic syndrome and the need for medication. While in college studying nutrition she was involved in research relating to the metabolic consequences of a high fructose corn syrup diet rats in Dr. Richard Freedland's Lab. Later, while working at the county, because of her patient advocacy, she was asked to serve as acting Medical Director over 9 county primary care clinics for Sacramento County, Department of Health and Human Services. While there she helped write a grant, and headed a committee of a successful program that taught nutrition, cooking, and exercise classes in 5 languages around the area for the indigent poor to promote positive lifestyle change. She is currently involved with the CMA’s, California Medical Associations Obesity Prevention Project.

Many problems can be caused downstream from one malfunction. Therefore correcting the root source of the malfunction may correct many conditions. A great example of this is the Metabolic Syndrome and its relation to diabetes, hypertension, hyperlipidemia, osteoporosis, cancer, dementia, etc. The metabolic syndrome like all disease states is related to an individuals genetic predisposition combined with environmental factors. As always it is multifactorial and personalized in the causation and expression. A diet high in processed carbohydrates and saturated fat is known to be related to obesity, insulin resistance and the metabolic syndrome.

It is notable that some morbidly obese individuals do not have metabolic syndrome, which means there are genetic differences, or other mechanisms causing the syndrome, such as co-triggers and co-mediators.

When studied, the healthy obese seem to have happy fat cells. Unhappy fat cells are one cause of metabolic syndrome. It is as if they get too full and ask for help from other cells to help eat up the excess triglycerides, which is the form of fat that is processed for storage. It is easy to see how a high fat diet can cause too many triglycerides, but what is also true is a high processed carb meal can generate even a higher level of triglycerides in the blood than a high fat meal. Very early bio-markers of metabolic malfunction are found in studies of lipids leading to the insulin resistant state. Abdominal fat known as VAT functions as an endocrine organ in orchestrating these malfunctions. Interestingly, certain pollutants in the bloodstream have been found in one study to be more correlated to early insulin resistance than obesity. And, emerging research is also pointing to the importance of microflora in the gut as playing a role in insulin resistance. Therefore, it is best to have a holistic approach to this chronic disease problem.

It appears that a large percentage of the human population are influenced by high amounts of sugar in the blood, such as produced by processed foods. High Fructose Corn Syrup, HFCS, is a special culprit as fructose bypasses a key controlling enzyme to create a runaway amount of even larger amounts of triglycerides than usual. This happens because fructose comes in the side door, below where a normal feedback message would cause the production to slow down.

HFCS really needs to be taxed, along with trans fats. I helped with research experiments on rats in college. Rats on the high fructose purina rat chow diet, with an equal number of calories to the regular purina rat chow diet were lethargic, dumpy, had sarcopecic obesity, little muscle and lots of fat, and a very yellow fatty liver. The sudden, large rise of blood sugar and resulting runaway triglycerides produced creates a metabolic state that effectively talks to our genes and changes the expression of our genes to make metabolic syndrome and the associated diseases. When the diet is reversed, the changes do not reverse right away. The new metabolism can get a foothold and be difficult to correct.

An epigenetic effect is where the DNA, genotype, does not change, but the expression of the genes, the phenotype, does. The normal and natural response of our DNA for many of us to the standard American Diet is Metabolic syndrome. It hit me when I read What Darwin didn't Know in National Geographic earlier this year. That offspring of the adults on the Standard American Diet, the SAD diet, may have epigenetic changes passed down to them as an adaptation to their dietary environment. In the National Geographic article, birds with the same DNA living on different sides of the island responding to the available local food, worms vs nuts, will grow to be different in size and color and shape. They will have a different a shape of their beaks, one to best get worms and the other to best crack nuts. And they will no longer interbreed with the parent species within just a few generations.

Some individuals are genetically more susceptible to getting diabetes. I believe that parents that do not even have diabetes yet but eat a diet high in processed foods may inadvertently pass on a tendency of diabetes to their children, causing a greater proportion of the population to be more epigenetically susceptible to getting diabetes. This may be one more factor contributing to our blossoming childhood epidemic of obesity and diabetes, along with the childrens' diets of processed foods, the increased portion sizes, the decrease in exercise, the decreased consumption of fresh vegetables and fruits, the possible endocrine and metabolic disruption from pollutants, and the high saturated fat/high sugar diet putting too many triglycerides in the blood and changing the gut flora for the worse. It seems we are developing a new human race of obese diabetics.