Before you can treat patients suffering from this interlinked combination of disorders, you have to understand the underlying causes.
METABOLIC SYNDROME (AKA SYNDROME X, OR METSYN), with its four hallmark symptoms of obesity, hypertension, dyslipidemia, and hyperglycemia, is an increasing health risk for the U.S. population.
In March 2005, the National Institutes of Health and the New England Journal of Medicine published a paper stating that because of this epidemic, the current generation is projected to have a shorter life expectancy then the previous one — for the first time in recorded history. Since then, things have gotten worse.1
The crisis continues despite changes in the USDA food pyramid, the emergence of new pharmaceutical agents (especially for pre-diabetes and type II diabetes), the removal of soda vending machines from schools, and even first lady Michelle Obama’s crusade against obesity. MetSyn, with its comorbidities (cardiovascular disease, stroke, blindness, amputations, etc.), accounts for the majority of healthcare dollars being spent.
Defining metabolic syndrome
In 1987, Gerald Reaven, MD, professor of medicine at Stanford University’s College of Medicine, first demonstrated that the four hallmark symptoms shared a common factor: hyper-insulinemia coupled with insulin resistance. He coined the term “Syndrome X” to illustrate the point: the four legs of the X represent the symptoms (hypertension, central obesity, hyperglycemia, and dyslipidemia), and the nexus of the X represents the cells no longer responding to normal amounts of insulin. This is the standard medical model of the disease.
The failure of current treatments
People are being ravaged by MetSyn because healthcare providers have ignored the model. Instead of focusing attention on the root cause of MetSyn, practitioners have been treating each of the symptoms as separate, unrelated diseases.
Thus there are new dietary recommendations and trendy diets as well as a plethora of exercise regimens
prescribed for obesity. Then there are “diet pills” and the myriad prescription drugs to control the other three symptoms.
A focus on controlling symptoms admits by default that nothing can be done for the causative factors. This attitude of acceptance is bad enough and unaffordable in the long run, but if you understand the pathophysiology of MetSyn, you can see why many of these treatments actually make the other symptoms worse.
Hyper-insulinemia causes a patient’s pancreas to secrete an exaggerated amount of insulin in response to rises in blood glucose. This can be confirmed by doing a fasting insulin level or the standard glucose challenge test and ordering insulin levels along with glucose levels at time zero, and at one-hour and
two-hour intervals post-challenge.
But most practitioners, instead of looking for hyper-insulinemia, focus on glucose level or hemoglobin A1c (the symptoms) and prescribe drugs such as sulfonylureas (e.g., glyburide, glipizide, and glimperide), which cause the pancreas to secrete even more insulin, or they prescribe insulin in an attempt to control the symptoms. If the model is correct, then this therapy should make the effects of MetSyn worse — and it does.
The importance of homeostasis
If insulin only mediated glucose uptake by the cells and did nothing else, MetSyn probably would not occur. This is not the case, however, as when the amount of insulin remains consistently elevated it causes other problems.
Consider the concept of homeostasis: The body strives to maintain a stable internal environment in the face of constantly changing, often hostile external factors. To maintain health, the body’s blood pressure, blood glucose, body temperature, pH balance, etc., must remain within a relatively narrow range.
The body achieves homeostasis by means of the action-reaction principle, with mechanisms that exert contrasting effects to achieve balance.
For example: Vasodilation versus vasoconstriction, oxidation versus reduction, anabolism versus catabolism, etc. These systems are carefully regulated by the nervous and endocrine systems.
Glucose homeostasis is essential for life because specific cells in the body can only use glucose as an energy source (e.g., certain brain cells, the adrenal medulla, and red blood cells). Whether in time of feast or famine, blood glucose must remain in a certain range and insulin and glucagon are the master hormones that control this process. The body needs both of these hormones, which have opposite physiological functions, to maintain balance. If an imbalance occurs, dysfunction or disease will arise.
The physiological effects of insulin
Insulin’s primary function is to mediate glucose uptake to muscle cells, and in this way it helps regulate blood glucose homeostasis. Insulin binds to other receptors in the body, however, and affects many physiological parameters.
If insulin receptors on the muscle cells become resistant to insulin’s effect and no longer uptake glucose effectively, the pancreas will produce more insulin to ensure glucose uptake. But if insulin levels are increased, it also affects other receptors that modulate other bodily functions.
The situation becomes more complicated as these receptors become insulin resistant at different times. So, in a typical case, a MetSyn patient will present to the doctor with some central obesity, elevated blood pressure, elevated blood glucose, and a less- than-stellar lipid panel.
The patient may be told to lose weight by eating more fruits and vegetables, to cut down on fats and cholesterol, and do some light exercise. This standard first-line therapy of lifestyle changes sounds reasonable.
The compliant patient makes these changes and returns in two months. Imagine his shock and disappointment in learning his symptoms have worsened.
Now he is given a low dose ACE inhibitor, a diuretic for his hyper- tension, and placed on metformin and glyburide to help control hyperglycemia. The glyburide tells the pancreas to secrete more insulin and the patient gains more weight.
Insulin also ramps up the enzyme HMG-CoA reductase, which tells the body to produce more cholesterol. Excess insulin also drives the kidneys to retain sodium and waste magnesium, which is an essential element for insulin receptor sensitivity. The result is that hypertension and insulin resistance worsen.
Usually, at this point (if not sooner), a statin is added along with niacin and another oral hypoglycemic,
and the patient starts the march toward insulin therapy. This is why many such patients find themselves on six to nine prescription drugs, which is the current “standard of care” for MetSyn.
Food as medication
Now suppose that the above patient visited a chiropractor first. This particular doctor is skilled in the use of a muscle-sparing protein diet, not a hyper-protein diet like Atkins. The diet will be low in fat — particularly saturated fat — and restrict carbohydrates to about 40 grams daily, mainly from fibrous vegetables.
The doctor may explain the medical model of MetSyn and how the overproduction of insulin can contribute to all the observed symptoms. Correcting hyper-insulinemia is straightforward: all carbo- hydrates (with the exception of fiber) will eventually be turned into glucose, either quickly or slowly. As glucose is absorbed, the pancreas begins to secrete (in this case, too much) insulin. By restricting carbohydrates, the production of insulin can be reduced quickly.
Patients who are hypo-glycemic may be afraid of such a restrictive protocol. They need to understand that hypoglycemia is usually the consequence of an overproduction of insulin, not a lack of carbohydrates.
During the first three days of the protocol, the patient may feel a little tired or weak, but once the glycogen is gone and his body switches over to muscle and fat, he will have plenty of energy and his hypoglycemic episodes will be a thing of the past.
Under the influence of glucagon
Six weeks later the patient returns. He is 30 pounds lighter and his MD has told him his blood work is fantastic. This is because the patient has reset his pancreas, which no longer is pumping out too much insulin, so he can now start to put fruits, grains, and dairy back into his diet.
After this patient’s glycogen reserves were depleted and carbohydrates continued to be restricted, his body had to maintain proper blood glucose levels. Under these conditions, the pancreas produces more glucagon (which raises blood sugar) and less insulin (which lowers blood sugar).
But there is more to glucagon than this primary function. Glucagon also stimulates two adipocyte (fat cell) enzymes (HSL and ATGL) and inhibits a third (lipoprotein lipase). The result is the release of trigylcerides from fat cells (to be used as fuel) as opposed to insulin’s effect, which is to store fat.
Glucagon enhances the entry of free fatty acids across the mitochondrial membranes so they can be used as fuel (insulin inhibits this). Glucagon also greatly inhibits the action of HMG- CoA reductase (along with the other enzymes necessary for cholesterol synthesis) and forces cells to pull cholesterol from the bloodstream via the stimulation of low-density lipoprotein receptors.
This is why the patient’s lipid panel came back stellar. Finally, in the kidneys, the retention of sodium caused by excess insulin has now been corrected and the hypertension has resolved.
The pathophysiology of MetSyn is predictable. The reversal of the syndrome is also predictable and repeatable. In fact, this exact method is being employed by more than 700 practices in the U.S. and Canada as well as in many medical practices. Tens of thousands of patients have experienced the same benefits described above.
Thanks to your training and philosophy, you too can become a leading force in helping to reverse the terrible effects of MetSyn. Consider this your call to action.
1Mozumdar A, Liguori G. Persistent Increase of Prevalence of Metabolic Syndrome Among US Adults: NHANES III to NHANES 1999-2006. Diabetes Care. 2011;(34)216-9.