by Dr. Joseph Debé
Having extra fat around the midsection is much more than just an issue of appearance. It is the tip of a metabolic iceberg. What lies beneath the surface is altered metabolism in virtually all cells, tissues, organs and systems of the body. Abdominal obesity, as it’s called, is the result of abnormal hormonal function, referred to as the metabolic syndrome. The same dysfunction of metabolism that spurs growth of fat cells in the midsection also contributes to poor health, degenerative conditions and premature death. The good news is the metabolic syndrome is reversible through safe natural approaches.
The January 16, 2002 issue of the Journal of the American Medical Association carried an article entitled “Prevalence of the Metabolic Syndrome Among US Adults”. Roughly 1 out of every 5 American adults has the metabolic syndrome, as defined in this article. The definition used was the presence of three or more of the following: “waist circumference greater than 102 cm in men and 88 cm in women; serum triglycerides level of at least 150 mg/dL; high-density lipoprotein cholesterol level of less than 40 mg/dL in men and 50 mg/dL in women; blood pressure of at least 130/85 mm Hg; or serum glucose of at least 110 mg/dL.” I believe the incidence of the metabolic syndrome is actually much higher because the definition used in this study is unrealistically narrow and stringent. It is like defining an elephant by its trunk. Elephants also have tusks and big ears and great memories. Likewise, the metabolic syndrome also has other characteristics. The findings in any given case of metabolic syndrome will be somewhat different due to genetic and environmental factors.
Some of the other findings in the metabolic syndrome include: increased waist to hip ratio (above .8 in women and .95 in men), body mass index (weight in kilograms divided by height in meters squared) greater than 29, elevated fasting insulin levels, elevated ratio of fasting insulin to glucose, elevated insulin and/or glucose after eating, elevated ratio of fasting triglycerides to HDL, abnormalities of stress hormone production (particularly cortisol), increased sympathetic nervous system activity, elevated testosterone in women and low levels in men, low levels of growth hormone, increased leptin, high uric acid, elevated lactic acid levels, high ferritin, high C-reactive protein, electrolyte imbalances, oxidative stress, and unfavorable alterations in blood clotting factors. Interestingly, one of the most important markers of the metabolic syndrome may be carbohydrate cravings. Again, any given case of metabolic syndrome can display various combinations of these. What’s more, although most metabolic syndrome subjects are obese, some are of normal body weight. However, they do have increased body fat, particularly around the midsection.
The metabolic syndrome is an under-appreciated, under-recognized, and under-diagnosed epidemic responsible for more ill health than any other condition. It is also under-treated. Typically, only the manifestations of the metabolic syndrome are addressed. A perfect example of this is a patient of mine who was on one medication for lowering cholesterol, another for lowering blood pressure, another for obesity, and another for arthritic pain. High cholesterol is “treated” by poisoning an enzyme system. High blood pressure is “treated” by blocking calcium channels. Obesity is “treated” by blocking absorption of dietary fat. Pain and inflammation are shut off by poisoning enzyme systems. What I am talking about is the way conventional medicine gives medications to alter endpoints in metabolism – the results of the metabolic syndrome, rather than addressing its upstream cause. This approach can be likened to mopping up the floor without shutting off the running faucet that is flooding the house. Shortly, I will outline an approach to “shut off the faucet” in the metabolic syndrome.
The two key biochemical abnormalities that produce the metabolic syndrome are hyperinsulinemia-insulin resistance and activation of the hypothalamic-pituitary-adrenal (HPA) axis (the stress response system). Insulin resistance is a term that refers to the body’s cells not responding efficiently to insulin’s signals to transport sugar from the blood. The body compensates for this by producing more insulin. Hyperinsulinemia (high blood levels of insulin) and insulin resistance occur together and perpetuate each other. Hyperinsulinemia-insulin resistance produces harmful alterations in metabolism throughout the body. With regard to body composition, these include: increased appetite, increased triglyceride (fat) production, body fat storage, fatty infiltration of muscle cells and reduced burning of body fat.
The importance of the metabolic syndrome in human health was strikingly demonstrated by the results of a study published in 2001, which looked at the connection between insulin resistance and the development of age-associated diseases. 208 healthy men were evaluated for insulin resistance and followed for an average of six years. One out of every three men who had insulin resistance at the start of the study developed either high blood pressure, type 2 diabetes, cancer, heart disease, or stroke within this short time period. All the men with good insulin metabolism remained healthy.
The primary feature of HPA axis activation is elevated levels of the stress hormone, cortisol. Cortisol opposes the action of insulin on glucose storage. When insulin lowers blood sugar past a certain point, cortisol levels increase to raise blood sugar. With fluctuating blood sugar levels, insulin and cortisol levels seesaw. Insulin resistance causes high levels of cortisol and high cortisol in turn causes more insulin resistance. The metabolic syndrome actually is characterized by many such self-sustaining vicious cycles interconnected in a web-like fashion. If targeted intervention to break the cycle of insulin resistance and high cortisol levels is not instituted, a downward spiral of declining health is inevitable.
Hyperinulinemia-insulin resistance and HPA axis activation are the destructive dynamic duo of the metabolic syndrome. The initiating dysfunction in many cases may be the HPA axis activation. Metabolic syndrome patients have been found to have a more sensitive stress response system-they get stressed more easily and produce more cortisol in response to stress. Cortisol receptors are found in virtually every tissue in the body. When cortisol levels are chronically elevated (as in the metabolic syndrome), the whole body suffers. Like insulin, cortisol increases hunger. High cortisol levels directly stimulate storage of body fat in the midsection and cause derangement in physiology of other hormones that result in intensification of this effect: high insulin along with low levels of growth hormone and altered levels of leptin and testosterone – all seen in the metabolic syndrome.
Fat cells in the abdomen are different than fat cells on the hips and thighs. The visceral or abdominal fat cells are more active in producing and metabolizing hormones. The large amount of abdominal fat, characteristic of the metabolic syndrome produces more cortisol, which further impairs insulin sensitivity, resulting in higher insulin levels. Insulin and cortisol cause the fat cells to produce more cortisol (and more estrogen in men). Thus, abdominal fat helps to sustain itself and worsens and perpetuates the metabolic syndrome.
Probably the most destructive aspect of elevated cortisol levels is its effect on muscle. Cortisol reduces protein synthesis while increasing protein break down. Cortisol breaks down muscle to be converted to glucose. Elevated cortisol causes a loss of muscle mass – a process one researcher has referred to as “autocannibalism”. Loss of muscle mass worsens insulin resistance, which in turn causes further increases in cortisol. What exactly causes the metabolic syndrome? Genetics play a minor role. Acquired in-utero factors also play a role. These include prenatal malnutrition, toxin exposure and exposure to high levels of maternal cortisol. These conditions appear to produce “metabolic syndrome programming”. For example, prenatal malnutrition, exemplified by a birth weight below 5.5 pounds, is associated with persistence of abnormal cortisol metabolism and insulin resistance into adulthood. Loss of a parent and poor care taking in childhood are also associated with lifelong excessive elevations in cortisol upon exposure to stress.
For most people, the metabolic syndrome results primarily from lifestyle factors. The three most important factors underlying most cases of the metabolic syndrome are probably chronic stress, inadequate exercise and excessive eating of refined carbohydrates. Other contributing factors include: overeating, under eating, eating too infrequently, imbalanced eating (with regard to protein, fat and carbohydrate), nutrient insufficiencies, too much exercise, inadequate rest, decreased muscle mass, inflammation, oxidative stress, toxicity, excessive caffeine, excessive alcohol, smoking, anabolic steroids, and certain medications.
An important facet of the metabolic syndrome is abnormal carbohydrate metabolism. Eating large amounts of refined carbohydrates (bread, pasta, cookies, cakes, muffins, crackers, bagels, soda, fruit juice, cereals, French fries, etc.) causes a rapid rise in blood sugar levels that cause the body to release large amounts of insulin. Chronically elevated insulin levels will result in cellular insulin resistance. The other contributing factors previously mentioned impair carbohydrate metabolism in various ways. With regard to carbohydrate metabolism, people are not simply either normal or diabetic. There is a continuum between normal glucose metabolism and type 2 diabetes. Largely due to the aforementioned lifestyle factors, metabolic changes occur in people of normal metabolism that gradually develop into the metabolic syndrome. The metabolic syndrome in turn can deteriorate into type 2 diabetes. Type 2 diabetes is the label that is used when the pancreas can no longer produce enough insulin to overcome the cellular resistance, resulting in elevated blood glucose levels. A significant minority of people with the metabolic syndrome eventually becomes diabetic. The importance of preventing diabetes is underscored by the fact that about 14% of all health care expenditures in the United States is for diabetes-related illness (including blindness, kidney failure and amputation of diseased limbs). Recognizing the continuum between normal metabolism and overt pathology is an important 21st century health care concept that applies to all degenerative conditions.
The list of health conditions caused (at least in part) or worsened by the metabolic syndrome is staggering. A partial list includes: stress, fatigue, inflammation, fibromyalgia, depression, increased appetite, increased fat around the midsection (“apple-shape” or visceral adiposity), sleep apnea, gout, heart disease, stroke, osteoporosis, Alzheimer’s disease, certain cancers, fatty liver, liver fibrosis and cirrhosis, kidney dysfunction, parasympathetic nervous system dysfunction, type 2 diabetes, impaired wound healing, immune suppression, sarcopenia (age-associated loss of lean healthy body tissue), and reproductive disorders. Additionally, the elevated cortisol levels, typical of the metabolic syndrome, can also contribute to irritability, fluid retention, high blood cholesterol, insomnia, impaired detoxication, stomach ulcers, memory and learning impairment, skin wrinkles, arthritis, weakness, and reduced thyroid function, resulting in decreased metabolism, lowered body temperature, and reduced vitality. The combination of reduced R.E.M. (rapid eye movement) sleep and lowered growth hormone release at night diminishes mental and physical regeneration, which results in acceleration of the aging process.
The sex hormone alterations (primarily testosterone and estrogen) and reproductive disorders that often result from the metabolic syndrome deserve further discussion. Young girls with the biochemical alterations of the metabolic syndrome develop premature pubarche – appearance of pubic hair or breasts before age 8. One out of 7 Caucasian girls develops premature pubarche. The figure is nearly 1 out of 2 for African American girls. Premature sexual development happens in boys much less frequently. If a girl has premature pubarche, it’s a safe bet that she has altered insulin and adrenal hormone metabolism producing biochemical changes that result in abnormally high levels of androgenic hormones. The androgens initiate the sexual development and can also produce male-pattern hair growth.
Premature pubarche is a precursor of the condition affecting adult women, called polycystic ovary syndrome. This condition is characterized by cessation of periods or infrequent and scanty blood flow, chronic lack of ovulation, ovaries with multiple cysts, weight gain and increased fat around the midsection, infertility, mood swings, fatigue, increased blood triglycerides and reduced HDL cholesterol, scalp hair loss, male pattern hair growth, and acne. Elevated insulin increases adrenal and ovarian production of androgens (“male” hormones like testosterone) and reduces the liver’s production of sex hormone binding globulin. Lower sex hormone binding globulin results in increased levels of free (biologically active) testosterone.
Some women with the metabolic syndrome will develop increased levels of biologically active and disease-promoting estrogens. The end result can be premenstrual tension syndrome, painful periods, tender breasts, worsening of uterine fibroids, endometriosis, cervical dysplasia (abnormal pap smears), and increased risk of certain cancers.
In men, the metabolic syndrome leads to low levels of testosterone. The stress component lowers testosterone levels, and the abdominal fat cells that are so plentiful in the metabolic syndrome, produce enzymes that convert testosterone into estrogen. The effects of this altered testosterone-estrogen balance include: fatigue, depression, lack of motivation and aggression, anxiety, irritability, reduced strength, bone loss, prostatic hypertrophy and cancer, low sex drive and erectile dysfunction. Low testosterone in men contributes to heart disease. What’s more, low testosterone in men contributes to perpetuation of the metabolic syndrome through alteration of body composition: decreased muscle mass and increased abdominal fat.
The good news is that the metabolic syndrome can be avoided and reversed in most cases. Interventions to improve insulin metabolism and stress physiology are needed. Weight (body fat) loss is both a treatment and a goal for metabolic syndrome patients. Many dietary variables have the potential to help. Eat within a 12 hour window, having only water and unsweetened, non-caloric beverages the other 12 hours. Don’t over eat. The majority of the diet should be whole foods; limit consumption of refined carbohydrates. When you do “cheat” with carbohydrates, make sure it is part of (or at the end of) a mixed meal (containing fat and protein) in order to minimize blood sugar fluctuations and have it earlier in the day when the body’s circadian rhythm creates better insulin sensitivity. Avoid partially hydrogenated oils. Eat plenty of omega 3 fatty acid-rich foods such as cold – water fish and flaxseeds. Eat avocados, olives, and raw nuts. Limit consumption of fructose. Eat your fruit rather than drink too much fruit juice. Engage in moderate exercise. Exercise can be overdone, contributing to the metabolic syndrome. Cardiovascular exercise can lower cortisol levels. Both cardiovascular and resistance training can improve insulin sensitivity. Weight training is probably the most important exercise for preventing or reversing the metabolic syndrome. Weight training is uniquely effective in building muscle, which is critical to improving insulin sensitivity. The vast majority of insulin receptors are found on muscle. Get adequate sleep and practice some form of stress reduction (such as deep breathing, meditation, yoga, massage, herbs).
A list of natural supplements that can help in various ways to reverse the metabolic syndrome includes: whey protein, vitamins B1, B5, B6, C, D & E, biotin, inositol, magnesium, chromium, vanadium, calcium, zinc, copper, potassium, manganese, selenium, creatine monohydrate, arginine, glutamine, taurine, soluble fiber (such as pea, oat, guar gum, pectin, and glucommonan), HMB, 5-HTP, carnitine, DHEA, Co Enzyme Q10, reduced glutathione, N-Acetyl-L-Cysteine, fish oil, conjugated linoleic acid, alpha lipoic acid, berberine, green tea, cinnamon extract, Gymnema Sylvestre, Siberian ginseng, and phosphorylated serine. An especially effective supplement is a new one called Insinase. It is the result of extensive research and development. It combines extracts from hops and acacia, and has been demonstrated to improve blood sugar and insulin levels about as well as two diabetes medications: Metformin and Avandia. What’s more, it lowers triglyceride levels about 45 points. Best of all, there appear to be no side effects.
What can one expect from a natural program to manage the metabolic syndrome? Let’s take one of my patients as an example. “Joe” was under a lot of psychological stress. He had a previous diagnosis of sleep apnea. He had a history of elevated liver enzymes, which made prescription of medication to lower his elevated cholesterol problematic. In mid July, 2001 he developed a rapid pulse and heart palpitations. He went to a hospital emergency room and subsequently saw a private medical doctor. His blood pressure was elevated at 160/85. The medical doctor prescribed medication to lower the blood pressure and slow the heart rate. His waist measurement was slightly elevated, and waist to hip ratio was borderline. His body mass index was elevated at 32.5. On 7/28/01 he had the following abnormal lab values: Total cholesterol – 296, triglycerides – 133 (above what I consider optimal), HDL cholesterol – 33, LDL cholesterol – 236, Total cholesterol/HDL – 8.97.
I told Joe I was fairly sure what was going on with him and suggested we jump right into treatment. I believe the metabolic syndrome is the most common cause of elevated blood cholesterol levels; the high insulin levels characteristic of the metabolic syndrome stimulate the liver to produce more cholesterol. The simple-minded approach to lower blood cholesterol by reducing the amount of cholesterol one eats displays an ignorance for how the body actually functions. Only about 1 in 10 people experience significant elevations in blood cholesterol by consuming large quantities of dietary cholesterol.
Joe wanted confirmation for himself; so he opted to have the most sensitive test for identifying the metabolic syndrome – a carbohydrate challenge test. The carbohydrate challenge test is like an endocrine system stress test. It picks up subtle insulin resistance that can be missed with fasting glucose and insulin. The carbohydrate challenge test is performed at a blood drawing facility in the following way: A high carbohydrate meal, consisting of white bread, a banana, and orange juice, is eaten in the morning, after taking a blood and saliva sample. Over the next three hours, additional blood and saliva samples are taken. Glucose, insulin and cortisol are measured from these samples. Heart rate is also monitored during the test, as an indication of autonomic nervous system function. An abnormality in any of these parameters points to the underlying cause of the dysfunction in carbohydrate metabolism. Because the test uses whole food, it can point to delayed emptying of food from the stomach, impaired carbohydrate digestion, and malabsorption as root causes of abnormal blood sugar levels. Natural treatments are customized, based on the exact nature of the results. The carbohydrate challenge test can pick up problems early – before damage has been done – even before symptoms are present.
Joe’s carbohydrate challenge test results revealed insulin resistance, reactive hypoglycemia and a pre-diabetic state. His fasting glucose of 103 was above what I consider optimal and his elevated fasting insulin of 14 was in the metabolic syndrome range. His blood sugar increased way too much half an hour after eating and his body had to continue to increase its insulin levels to transport the sugar into the cells. His sympathetic nervous system became activated in an attempt to avoid a reactive hypoglycemia. However, his adrenal glands, apparently weakened by chronic stress, were not producing enough cortisol to aid in regulating the dropping blood sugar.
I got Joe started on a comprehensive program of diet, nutritional supplementation, exercise and stress reduction. A blood test on August 22, 2001, showed significant improvement in his blood lipids. It also showed elevated liver enzymes: AST of 56 and ALT of 128. This caused his medical doctor to refer him to a gastroenterologist. I told Joe I felt the elevated liver enzymes might be a part of the metabolic syndrome and could improve with our program.
On 10/11/01, we did a blood test to see how our natural program had worked. His fasting glucose was now an acceptable 92 and his fasting insulin was a normal 5.4. Total cholesterol was down 103 points from 7/28/01 – to 193, Triglycerides were down to 61, LDL cholesterol was down 42% to 138, HDL cholesterol was up 30 % to 43, and the Total cholesterol/HDL was down to a safe 4.49. His liver enzymes were much improved: AST was 39 and ALT was 61. During this same period Joe lost 30 pounds. His blood pressure normalized and he discontinued his medication. His digestion improved and he reported more endurance. These results were accomplished through a natural lifestyle modification program of diet, exercise, stress reduction and nutritional supplementation.
