Metabolic Syndrome

It has been observed for a number of years that conditions such as adult onset diabetes, hypertension, elevated blood levels of cholesterol, elevated serum levels of low-density lipoproteins, obesity, and coronary heart disease are common disorders that often occur in one patient. Cardiologists originally described a condition, termed syndrome X, that identified patients with angina pectoris and positive stress-test ECG but with no evidence of stenoses of the coronary arteries. Further study revealed that these patients often have a decreased insulin-stimulated glucose uptake. In 1988 medical researcher Gerald Reaven postulated that these metabolic and cardiovascular disorders are a multifaceted syndrome characterized by insulin resistance with compensatory increased insulin secretion of the pancreas leading to elevated levels of insulin in the blood, or hyperinsulinemia.

Subsequent studies have shown that increased insulin concentrations in the blood, as a marker of decreased insulin sensitivity, can be correlated with an increased risk of hypertension, hyperlipidemia and non-insulin dependent diabetes (NIDDM). These studies support Reaven’s hypothesis, coined metabolic syndrome X (syndrome X, or metabolic syndrome, MetS), that insulin resistance and hyperinsulinemia may increase the risk of developing cardiovascular disease, as well as other disease such as cancer. There is increasing evidence to suggest that metabolic syndrome affects 60% or more of the U.S. population, a figure that likely reflects its prevalence in the Canadian population as well.

The clinical manifestations of metabolic syndrome include truncal abdominal obesity, elevated blood triglycerides, decreased HDL cholesterol and elevated LDL cholesterol, hypertension atherosclerosis, thrombotic diseases (e.g. deep vein leg thrombosis), hypoglycemia, and non-insulin-dependent diabetes mellitus (NIDDM).Other clinical manifestations may include osteoporosis, clinical depression, cognitive problems (i.e. poor memory and concentration), Alzheimer’s disease, polycystic ovarian disease (PCOD) and erectile dysfunction.

Insulin resistance

Insulin is the body’s primary anabolic or tissue-building hormone, and is secreted by the beta cells of the pancreas. Insulin promotes the uptake and storage of nutrients within the cell, including glucose, free fatty acids, and amino acids. The primary stimulus for insulin secretion is the ingestion of carbohydrates, whereas the consumption of a diet rich in proteins and fats tends to limit the secretion of insulin. When its activities predominate insulin prevents the breakdown of fat and protein.

When a cell does not respond to normal levels of insulin it is said to be insulin-resistant. Such a situation can develop from numerous factors:

  • Consuming foods with high glycemic index. These are foods that contain a relatively large volume of simple sugars, which upon digestion, elevate blood glucose levels and stimulate the release of insulin.
  • Low fat diets. Although widely marketed as being the basis of a healthy lifestyle, low fat diets are not necessarily beneficial. Significant portions of fat in a meal lowers the glycemic index by delaying stomach emptying.
  • Deficiencies of chromium and magnesium. Deficiencies of these nutrients facilitate insulin resistance to create a vicious cycle pattern. Other common nutritional deficiencies include zinc, manganese, and the B-vitamins.
  • Sedentary lifestyle and lack of exercise. Insulin resistance in the liver increases after five days of no exercise. Trained muscle does not require insulin for the uptake of blood glucose, whereas a lack of trained muscle mass in the body promotes systemic insulin resistance.
  • Excess insulin secretion. Chronic excessive insulin secretion promotes insulin resistance in a vicious-cycle relationship. When a cell is exposed to elevated levels of insulin it begins to down-regulate its response to insulin and reduce the number of its insulin receptors. This in turn leads to enhanced insulin secretion.
  • Obesity. Weight gain, particularly truncal-abdominal weight gain, promotes insulin resistance, which in turn, promotes elevated levels of insulin secretion preventing the breakdown of fat.

Not all tissues become insulin resistant at once. The liver, which is exposed to insulin-rich blood from the portal vein, becomes resistant first. Hepatocytes similarly become resistant to the entrance of magnesium, thus creating a relative magnesium deficiency, which can alter the Phase I detoxification pathway. Following this muscle cells become insulin resistant, although adipose tissue sensitivity typically remains high, promoting the truncal-abdominal obesity characteristic of metabolic syndrome. As the condition progresses muscle mass decreases and adiposity increases, but even adipose tissue as well as platelets and other cells eventually become insulin resistant. Skin cells however, are one of the few cell types that don’t become insulin resistant.


As the various tissues of the body become insulin resistant, the uptake of blood glucose becomes more difficult, and as a result blood glucose curves are more elevated and prolonged. The pancreas, in response, puts out progressively more insulin until the nutrients are effectively stored. The net effect of this is that insulin output it not only elevated but is prolonged, such that the total number of hours that the body is exposed to insulin may be elevated by 50-100%.

There are several possible effects of prolonged hyperinsulinemia:

  • Hyperinsulinemia disrupts sodium metabolism and promotes water retention and hypertension.
  • Hyperinsulinemia increases the oxidative load in some tissues, promoting oxidative damage and initiation of atherosclerosis and neoplasia (cancer).
  • Hyperinsulinemia decreases the total daily secretion of growth hormone with negative effects throughout the body. One notable effect of this is to inhibit the conversion of T4 into T3, creating a functional hypothyroidism that is difficult to detect with routine laboratory tests.
  • Chronic hyperinsulinemia may be accompanied by chronic compensatory hypercortisolemia (high blood cortisol levels), poor tolerance to stress, depressed immunity, and eventually, adrenal exhaustion.
  • Chronic,high levels of insulin secretion will eventually exhaust the beta cells of the pancreas, increasing the likelihood of a functional deficit of these tissues, resulting in adult-onset diabetes.

Diagnosis of metabolic syndrome X

The diagnosis of metabolic syndrome is determined by measuring fasting insulin levels, or by measuring insulin changes to a glucose challenge. Unfortunately, most physicians and labs cannot run these tests as there are several practical and technical challenges that make this procedure difficult. Clinicians may determine syndrome X with a fairly large degree of certainty however, based on patient history and physical examination. As a result, clinical guidelines been established by the Adult Treatment Panel III (ATP-III), which is based primarily on data obtained from the Framingham (see atherosclerosis). According to these criteria, in order to qualify a patient must have any three of the following five risk factors:

  1. Abdominal obesity, with a waist circumference 102 cm for men, and  88 cm for women
  2. Elevated serum triglycerides, which is defined here as equal to or greater than 150 mg/dL;
  3. Low HDL cholesterol (under 40 mg/dL for men and less than 50 mg/dL for women)
  4. Raised blood pressure (systolic  130 mm Hg, diastolic 85 mm Hg)
  5. Fasting glucose, equal to or greater than 110 mg/dL (Gotto et al 2002).

Perhaps most important physical feature in metabolic syndrome is is truncal-abdominal obesity. While the ATP-III guidelines provide specific measurements, clinicians will find them somewhat abitrary, and do not accommodate the proportionate degree of truncal-abdominal obesity in people with different frames. As a result, a better method is to compare the ratio between the waist and hips. For men the ratio between these two measurements should be no greater than one, i.e. the abdominal girth should be equal to or less than the waist circumference. For women, the waist-hip ratio should be less than 0.7, i.e. the circumference of the waist should ideally be no more than 70% of the circumference of the hips. Hypertriglyceridemia is good indicator of metabolic syndrome as triglycerides tend to parallel insulinemia.

Holistic treatment

The holistic treatment of metabolic syndrome consists in removing the causes that promote insulin resistance and hyperinsulinemia. This includes dietary changes, nutritional supplementation and exercise, as well as a variety of herbs to support the cardiovascular system and pancreas.

1. Dietary changes.

  • implement a low carbohydrate diet to reduce insulin secretion
  • eliminate grain-fed animal products, hydrogenated fats, and vegetable oils high in n6 PUFAs
  • emphasize above-ground vegetables including leafy greens, cabbage, cauliflower; seaweeds, herbs/spices

2.Supplement for key nutrient deficiencies

  • omega-3 fatty acids, EPA/DHA, equal to 1000 mg each, daily
  • vitamin B complex, 100 mg daily
  • magnesium, 800-1200 mg daily
  • chromium, 200 mcg, thrice daily, with meals
  • zinc, 50 mg daily
  • vitamin D3, 2000-5000 IU daily

3.Botanical support for the pancreas and liver

  • Devil’s Club (Oplopanax horridum), Ginseng (Panax spp. (all), Mesashringi (Gymnema sylvestre), Fenugreek (Trigonella foenum-graecum), Bitter Melon (Momordica charantia), Turmeric (Curcuma longum), Reishi (Ganoderma lucidum), Milk Thistle (Silybum marianum), Katuka (Picrorrhiza kurroa),Triphala, Shilajitu

4.Support cardiovascular function

  • review holistic treatment under atherosclerosis
  • implement antioxidant therapy


  • implement a muscle-building regimen to decrease insulin resistance, i.e.anaerobic exercise (e.g. weight lifting, calisthenics, martial arts, hiking, bicycling etc.) as opposed to aerobic exercise (e.g. jogging, aerobics etc.)