Metabolic syndrome deserves serious attention, for one out of five adult Americans and one out of eight school-age children has it. This dangerous pandemic pushes millions down the slippery slope to heart attacks, stroke, diabetes, and early death.
Profile Of Metabolic Syndrome
What’s involved in the complex mix of unhealthful conditions that make up metabolic syndrome, or MetS, for short?
- Insulin resistance
- High blood cholesterol
If an individual has any three of the above four unhealthful conditions, a doctor can confirm the diagnosis. Significance? Three of these conditions can double one’s risk of heart attack or stroke! And compared to those who have none of these conditions, the risk is tripled! Obviously MetS warrants concern. Because understanding a disease is vital to preventing, curing, or managing it, let’s begin by learning more about the nature and causes of MetS. Other physiologists would include a pro-inflammatory condition, a pro-coagulant state that encourages undesirable clotting and sympathetic nervous system overdrive. Routine blood work would not necessarily indicate these. All persons with MetS should be evaluated on these parameters.
Insulin resistance is the most common of the four major risk factors. This condition results when more insulin than normal is required to do the same job of glucose control in the body. Although more factors may be involved, this impairment of the body’s ability to properly manage blood glucose is the primary feature of insulin resistance.
If you are a lady, and your waist is over 35 inches, or if you are a man, and your waist is over 40 inches—watch out! Excess visceral fat which is stored over the abdominal organs, better known as “potbelly fat” or “apple-shaped fat,” is the most dangerous type. Adipocytes (fat cells) release free fatty acids, the increased number of which interferes with cellular ability to metabolize glucose and damage the insulin-producing cells in the pancreas as well as substances that promote inflammation through out the body.
The level at which total cholesterol is considered normal has been dropping for years. First, it was 240 then—oops!—it was 220, 200, and then 180. So… average is not normal! Two hundred is too high.
High Blood Pressure
Though high blood pressure is not always a pillar of metabolic syndrome, it is still significantly dangerous on its own. Again, what was considered “normal” 10 years ago is no longer normal.. According to the latest consensus, if your systolic reading is 130, you have early hypertension. Actually, we start paying a physiological price at 125 systolic. The old “feel good—feel safe” philosophy is passé. Truth is wiser and much safer!
What Company Does This Syndrome Keep?
As comments our science editor, Dr. Bernell Baldwin, “This new metabolic syndrome is a gang, not a committee!” The more MetS is studied, the wider the ramifications. This would also include psychological, sociological, and even economic aspects.
Complications? You Name It!
If left untreated, MetS will indeed prove deadly, for it affects virtually every system of the body. Not only does it increase the risk of developing and dying from cardiovascular disease, but it also is an independent risk factor in the development of deep vein thrombosis. Heart, lung, kidney, and liver function decline. For example, with MetS, the liver can become sick, as in non-alcoholic fatty liver disease. And unless lifestyle interventions are adopted to reverse the disease process, it can progress into nonalcoholic cirrhosis. MetS also contributes to ovarian or erectile dysfunction. In older individuals it predicts cognitive decline and increases the risk of falling. If obesity and elevated blood sugar are both present, the risk for colorectal cancer is increased. With MetS, the risk for prostate and recurrence of breast cancer also rises.
Unavoidable Risk Factors
Some risk factors for MetS are uncontrollable, including a family history of type II diabetes, hypertension, heart disease, bipolar disorders, and aging. Hispanics and Asians seem to be at greater risk than are other races. Women with fibromyalgia are 5.56 times more likely than healthy controls to have metabolic syndrome.
A pregnant woman’s metabolic state has a powerful influence on whether her child (either male or female) will develop obesity, hyperinsulinemia (elevated insulin), and related conditions. Early studies suggest that children of parents with MetS have higher levels of inflammatory markers which could make their children more susceptible to developing atherosclerosis later.
Modifiable Risk Factors
Lifestyle factors that contribute to MetS include obesity, overeating, snacking, consumption of refined and sugary carbohydrates, and sedentary lifestyle. “The metabolic syndrome is present in about 5 percent of people with normal body weight, 22 percent of those who are overweight, and 60 percent of those considered obese. Adults who continue to gain five or more pounds per year raise their risk of developing metabolic syndrome up to 45 percent.
The Couch Potato Syndrome
Research also shows a strong inverse association between physical activity and MetS. Low cardiovascular status is an important risk factor for metabolic syndrome. In Australia, researchers studied 6,241 adults aged 35 years or above who were free from diagnosed diabetes mellitus and self-reported ischemic heart disease. These participants were not taking any lipid-lowering or anti-hypertensive drugs. In women who watched more than 14 hours of TV a week, MetS was twice as prevalent compared to women who watched TV 7 hours or less. The incidence of MetS increased 48 percent for men who watched TV more than 14 hours per week compared with those who watched it less than 7 hours per week. Women who were active 2.5 hours or more per week, had 28 percent less risk of developing MetS. Men who were as active dropped their risk for MetS by 45 percent. Why? Physical inactivity causes the muscle cells to become less sensitive to insulin, and damages the glucose transport in the cells. The number of power plants (mitochondria) in muscle cells also decline; as a result, glucose and fats are not burned as efficiently. An encouraging bit of news is that those who are physically fit, even if overweight, have less risk of developing MetS, than those who are not.
Overeating generates both free radical damage and damage to the tissue proteins. It can elevate blood glucose and lipid levels, thus compromising the ability of insulin to bind to its receptors on cells. When this happens, the blood sugar increases. Overeating also increases the size and number of fat cells.
Obesity And Poor Nutrition Contribute To MetS!
Ninety five percent of individuals who have MetS are overweight or obese. The Framingham study showed that women who were obese and/or had the pattern of consuming empty calories were substantially at risk for developing MetS. It is interesting to note that both the dietary pattern of consuming empty calories and obesity increased the risk of developing MetS whether or not cardiovascular risk factors were present.(5)
The Framingham authors concluded that, while the disease traits in MetS can exist independently of the metabolic syndrome, many of them are the results of it and would be nonexistent without it. Furthermore, suitable amounts of the right diet, particularly a high-fiber diet that emphasizes and almost exclusively consists of fruits, grains, nuts, and vegetables, would prevent the syndrome in most individuals. Might it not even render it essentially obsolete? Let’s look further at how the typical Western diet and obesity prepare individuals to succumb to this deadly syndrome.
Understanding Insulin Resistance
When we eat carbohydrate foods, they are either broken down into glucose or another simple sugar that is converted into glucose. Glucose then enters the blood. Glucose provides the fuel for which the cells, especially the brain cells, make energy. In order for this process to take place, the pancreas produces insulin, a hormone which facilitates the entry of glucose into the cells. Insulin must bind to its receptor sites on cells. To simplify, one could imagine insulin as a key which unlocks the cells’ doors (insulin receptors) so that the glucose can then enter the cell. Normal insulin sensitivity results when the insulin receptors are working optimally and glucose is delivered and utilized effectively.
Both obesity and a high-fat diet damage insulin receptors by impairing their ability to respond to normal amounts of insulin. As a result, blood sugar levels remain high. If this continues, the pancreas is “tricked” into making more insulin in an effort to bring blood glucose within normal range. As long as the pancreas is able to produce enough extra insulin to overcome this problem, blood glucose levels can remain normal. This condition is known as “insulin resistance.”
As insulin resistance continues to builds up, increasingly less glucose is able to enter the cells, and the blood sugar level is again elevated. If not corrected, type 2 diabetes often develops once the overworked pancreas can no longer produce enough insulin, and the blood glucose continues to rise. Even before diabetes 2 occurs or even if it doesn’t occur, high levels of insulin injure the body by encouraging the development of atherosclerosis, high blood pressure, elevated triglycerides (blood fats), abnormal activation of the sympathetic nervous system (“fight or flight”), and increased inflammation throughout the body.
Obesity And Poor Diet Encourage High Blood Pressure
Although many people who develop high blood pressure are not obese, the fact remains that obesity reduces the ability of the blood vessels to dilate and makes the arteries more subject to constriction. Both obesity and overeating increase sympathetic nerve activity, which makes our arteries constrict and our heart rates speed up. This directly contributes to hypertension.
Obesity Promotes Inflammation
Excessive abdominal fat is an arsenal of many pro-inflammatory and pro-atherogenic agents that fuel chronic disease. Inflammation often contributes to insulin resistance, and insulin resistance can trigger inflammation in a vicious cycle. Please note that both weight and percentage of body fat are important. Women who are within their normal weight range, but whose fat mass is greater than 30 percent of the total body weight, have elevated markers for inflammation. Weight alone isn’t enough; the fat percent must be considered as well.
Obesity Promotes Cardiovascular Events
Obesity, overeating, and junk food all increase low-density lipoprotein (the “bad” cholesterol abbreviated as LDL) that, if elevated, significantly increases the risk of stroke and heart disease. Individuals with MetS often have elevated levels of LDL, small dense LDL, and triglycerides (TGs), but depressed levels of high-density lipoprotein (HDL, the “good” cholesterol). Even obese children have more small dense LDL particles, which are especially dangerous because these penetrate the lining of arteries faster and linger longer. Appropriate weight loss and aerobic exercise improve the HDL level while lowering the small dense LDL level.
Obesity, saturated fats, and empty calories also elevate TGs. This is bad news because even one meal high in saturated fat increases TGs and consequently impairs the ability of the blood vessels to dilate. If these detriments weren’t enough, high TGs also cause the red blood cells to clump, reducing their combined surface area, and thereby decreasing their ability to deliver oxygen. Furthermore, clumped red blood cells have more difficulty squeezing through tiny arteries, and it is impossible for them to squeeze through capillaries.
To make matters even worse, MetS increases the cascade of the body’s agents to form undesirable clots that obstruct blood flow, but decreases the ability of the body to break apart tiny clots.
To successfully treat MetS, one must identify the lifestyle habits that fuel it and its complications and then treat the specific disease traits of that person—obesity, impaired glucose tolerance, elevated lipids, hypertension, inflammation, increased risk of undesirable clotting, and sympathetic overdrive. The combination of problems can vary from one person to another. The good news is that incorporating physiologically- sound principles substantially help to reduce and many times reverse the disease processes underlying MetS.
Nutrition Factors That Speed Recovery
1. Emphasize Plant Foods
Studies show that dietary patterns high in fruit and vegetable content are generally found to be associated with lower prevalence of metabolic syndrome, as well as reduced incidence of inflammation.
Minimally-processed foods and whole grains are also associated with decreased risk of MetS and type 2 diabetes. Diets high in whole grains, fruits, nuts, and green leafy vegetables have been shown to reduce homocysteine levels and several significant inflammatory markers. This is significant because individuals with MetS tend to have elevated homocysteine, which contributes to cardiovascular and inflammatory problems and cognitive decline.
2. A Vegetarian Diet Is Even Better
Research clearly demonstrates that a long-term vegetarian diet is associated with markedly higher fasting plasma antioxidants, and lower levels of triglycerides, uric acid, and inflammatory markers. Long-term vegetarians have a better antioxidant status and coronary heart disease risk profile than do apparently healthy omnivores. Vegetarians generally also have lower systolic and diastolic blood pressures. Further studies demonstrate that vegetarians generally have lower glucose, lower insulin levels, and improved insulin sensitivity than do omnivores.
However, strict vegetarians should be sure to eat foods fortified with vitamin B-12 or take a modest amount of vitamin B-12 in supplemental form. Both B-12 and folic acid decrease insulin resistance, improve the ability of the blood vessels to dilate, and keep homocysteine levels normal in patients with MetS.
3. Easy On The Salt!
Because MetS individuals either have hypertension or are at risk for developing it, they should seriously limit their total salt intake to one teaspoon of salt per day. Too much salt predisposes the arteries to vasoconstriction, stiffens the cerebral arteries, and promotes fluid retention—all of which can contribute to hypertension. Severe salt restriction is seldom needed and in most cases actually increases blood pressure. Keep in mind that 80 percent of our salt intake comes from processed foods. So read labels and choose wisely!
4. The Truth About Carbohydrates
The carbohydrates found in whole grains, nuts, vegetables, and whole fruits contain benefical fiber, which studies show helps to protect against MetS. A high-fiber diet also reduces cholesterol and triglyceride levels, improves insulin sensitivity, reduces some inflammatory markers, helps to control appetite, and is associated with lower incidence of hypertension.
However, simple sugars, candy, pastries, soft drinks, juices, and refined grains should be severely restricted, if not altogether eliminated. Processed, refined sugar encourages inflammation and depletes the body of the minerals magnesium and chromium, both of which improve insulin sensitivity.
Interestingly, a high-fructose diet can rapidly cause MetS in rats, and also raise uric acid (a byproduct of protein metabolism). Lowering uric acid in fructose-fed rats prevents features of MetS. Elevated uric acid levels are associated with new cases of recent onset essential hypertension in children and predict non-alcoholic fatty liver disease in obese children.
Beware, then, of soft drinks containing fructose-derived corn syrup!
5. Moderation Does It With Protein
While we certainly do need sufficient protein, there is danger in getting too much. Even though a high-protein diet can promote weight loss, excessive amounts of protein damage the nephrons in the kidneys. These nephrons not only make urine, but also balance the body’s delicate chemistry by eliminating excesses of chemicals and ions that we don’t need, and conserving what we do need. Obesity, hypertension, and high blood glucose all cause damage to the kidneys. So why should those with MetS add insult to injury?
Researchers at the University of Pittsburgh also found that over a period of six years, men who originally had baselines of elevated uric acid in the blood had an 80 percent excess risk for incident hypertension compared with those who did not. This, too, is unfortunate because a high level of uric acid can also accelerate kidney disease.
6. Avoid Harmful Fats; Enjoy The Good!
Saturated fats (found in most animal products and cheese) and trans fat (found in hydrogenated or partially-hydrogenated oils) are seriously implicated in the development of obesity, heart disease, diabetes, and cancer. The preformed omega-3 gamma linolenic fatty acid, found in nuts and leafy greens, shifts the balance in favor of local hormones that combat inflammation. Nuts, seeds, olives, and avocados contain mono-unsaturated fats that help to reduce elevated triglycerides.
A randomized study showed that MetS individuals who increased their consumption of whole grains, fruits, vegetables, olive oil, and foods rich in monounsaturated fats for two years, and were more physically active, lost more weight, had fewer inflammatory markers, and developed less insulin resistance than the controlled group.
Researchers at Columbia University found, even while controlling for other risk factors, that frequent nut and seed consumption was associated with lower levels of inflammatory markers, which may partially explain the inverse association of nut consumption with risk of cardiovascular disease and diabetes. Nuts contain ellagic acid, a phytochemical that protects the pancreas from inflammation and fibrosis. However, because too much fat can reduce the ability of skeletal muscles to transport glucose, moderation is the way to go.
7. Exercise—Preventive and Curative
Regular aerobic exercise improves the elasticity of arteries, slows the resting heart rate, makes the arteries less sensitive to vasoconstriction, and improves insulin sensitivity of the muscles. Even in previously sedentary persons with MetS and elevated triglycerides, mild-to-moderate exercise lowers elevated TGs and improves insulin sensitivity.
Mitochrondria are the cells’ power plants that generate energy by burning glucose and fatty acids. In obesity and diabetes, these powerhouses are smaller than normal in skeletal muscles. A study from the University of Pittsburgh School of Medicine demonstrated that a combination of weight loss and physical exercise increased both the number and volume of mitochondria in skeletal muscles of previously obese individuals. The more power plants, the greater energy production, more efficient burning of fuel, and needful weight loss.
Moderate long-term exercise, especially if accompanied by appropriate, slow, steady weight loss, decreases elevated inflammatory agents but increases adiponectin, an anti-inflammatory protein that reduces cardiovascular risk and improves insulin sensitivity. Long-term exercise also reduces the risk of developing MetS in persons who have cardiovascular problems.
Because MetS is a serious medical problem, individuals who have it should consult with their physicians about what program to pursue. Generally, those with MetS should not engage in competitive or exhaustive exercise, as these contribute to oxygen debt, constrict the arteries, and promote undesirable clotting and increases stress hormones.
Dehydration can prove deadly to an individual with MetS. For one thing, dehydration increases the risk of developing undesirable clots. Drinking adequate amounts of water can reduce the incidence of heart attack between 40 to 50 percent. The MetS individual who has elevated blood sugar, or triglycerides, or obesity is already at risk for unhealthful clot formation. If accompanied by obesity (especially visceral fat), MetS compromises lung and kidney function. Specifically, dehydration increases damage to the nephrons. Sufficient hydration improves the ability of oxygen to permeate cell membranes. This is important because oxygen is needed to release energy, thus adequate water intake aids in increasing energy expenditure. So drink seven glasses of water per day. Eight to ten is better yet, depending on your weight and activity level.
9. Healing Sunshine
As mentioned before, metabolic syndrome significantly increases the risk for type 2 diabetes. Italian researchers found that individuals with diabetes had a higher rate of vitamin D deficiency than non-diabetics. Participants with diabetes and low levels of vitamin D had a marked increase in common carotid intima-medial thickness (an early sign of atherosclerosis) when compared with their vitamin D-sufficient counterparts. These individuals also had significantly higher hemoglobin A1C (a marker for diabetes,) fibrinogen (a proclotting, pro-inflammatory protein) and C-reactive protein (hs-CRP, an inflammatory marker) concentrations.
Nutrition epidemiologists estimate that 50 percent of the populations in North America and Europe are vitamin D deficient! Adequate amounts of vitamin D can reduce complications of MetS, such as reducing the risks for colon cancer and inflammatory processes. It should be noted that exposure to sunlight increases vitamin D-2 synthesis, and both obesity and kidney disease compromise the ability of the body to convert vitamin D-2 into its active hormone form. Therefore, a select group of individuals with vitamin D deficiency and chronic kidney disease require vitamin D-3 supplementation.
Temperance, the habitual avoidance of that which is harmful, and moderation in all that is good, is another key to preventing or overcoming MetS.
- Appetite control is essential for preventing, correcting, and hopefully reversing MetS and its components. Wise calorie restriction improves the balance between the parasympathetic and the sympathetic nervous systems. The sympathetic nerves help to mobilize us to action in times of stress. Blood pressure, heart rate, and blood sugar increase while digestive processes slow down. The parasympathetic nerves slow the heart rate, stimulate the digestive process, and help us to take care of our daily needs. We actually need a balance of both systems. However, excessive sympathetic tone and decreased parasympathetic tone can contribute to high blood pressure, diabetes, and electrical disturbances of the heart’s rate and rhythm.
- Fasting, as in eliminating the last meal of the day, improves melatonin production. Melatonin is an anti-oxidant, immune-bolstering, cardiovascular-protective hormone synthesized in the pineal gland. It improves the production of growth hormone, a hormone synthesized in and released from the pituitary gland, which encourages the burning up of fat. A short fast can also reduce sympathetic nervous system activity. However, total fasts that last longer than 48 to 72 hours can actually have adverse effects on the liver, and increase cortisol levels. This extra cortisol inhibits protein synthesis in the body and elevates blood sugar. Yes indeed, slow, gradual, but permanent weight loss, if one is overweight or obese, improves HDL levels and reduces sympathetic nervous system activity, triglycerides, pro-clotting, and pro-inflammatory agents.
- Avoid caffeine. Caffeine seems to enhance the mood and is often incorporated into over-the-counter pills for weight loss because it increases metabolism. However, caffeine magnifies the actions of the sympathetic nervous system, which is already a problem in MetS. Caffeine also increases both glucose and insulin levels. Preliminary animal studies indicate that chronic caffeine consumption has an adverse effect on the kidneys. (14) This is a definite concern, as MetS already significantly increases the risk of kidney damage.
- Refrain from alcohol. It is true that some studies show that light-to-moderate drinking affords some protection from cardiovascular diseases.* However, alcohol damages the brain, liver, and pancreas. Insulin resistance, which many MetS individuals have, provides a metabolic pathway to chronic liver diseases. Chronic alcohol consumption damages the heart muscle and elevates triglycerides. Alcohol also depletes the body of magnesium and the B vitamins needed to combat MetS.
Research shows that sleep-deprived people typically increase their caloric consumption by as much as 15 percent. Chronic loss of sleep may increase the risk of diabetes because the insulin secretion can be impaired by up to 30 percent. A study involving 28,000 children and 15,000 adults showed that sleep deprivation doubles the risk of obesity in both children and adults. Lack of sleep increases the hormone grehlin, which stimulates the appetite, and reduces leptin, a hormone that promotes satiety, reduces appetite, and helps us to burn up the calories we eat. Another adverse effect of sleep deprivation is that of reduced growth hormone production.
This critical substance not only assists in the repair of our bodies, but also in the burning up of fat. “Chronic sleep deprivation in young healthy volunteers has been reported to increase appetite and energy expenditure, increase levels of proinflammatory chemicals, decrease parasympathetic and increase sympathetic tone, increase blood pressure, and increase evening cortisol levels, as well as elevate insulin and blood glucose.”
12. Mental Influences
Mental factors should not be overlooked in MetS. If obesity, insulin resistance, or hypertension is present, the sympathetic nervous system is in overdrive. The “flight or fight” response can promote a state of insulin resistance both in the liver and skeletal muscles. Together, excess insulin and excess cortisol encourage this extra energy to be stored in visceral fat. Chronic activation of stress causes the suppression of the regulation of growth and thyroid hormones that are involved in burning up of fat.
Major depression and anxiety disorders increase inflammation within the body. By increasing the ability of the blood to clot, making the heart more susceptible to arrhythmias, and increasing sympathetic activity, depression also increases the risk of developing heart disease. Stress management and power to cope successfully with life’s problems are vital components of any therapeutic plan for overcoming MetS. A daily quiet time with God will work wonders!
In summary, Dr. Baldwin provides a winning strategy:
- Recognize that metabolic syndrome is a growing set of unhealthful dangerous conditions.
- Get a serious in-depth diagnosis. It saves lives.
- Each unhealthful condition should be changed. Other people around you, who are sliding into heart attacks, strokes, and diabetes are not your criteria, models, or standards. If you are too fat around the middle, get Divine and human help to eat less and exercise more. If you can’t do this at home, go to a lifestyle center and deal with the issues. The later in life you get serious the harder it will be to stop, turn around, and start living in health instead of presumption.
- Bad habits can kill; good habits are pillars of the abundant life. Learn them. Survival is no accident. The will is the governing power in our natures. Arise and use it. Choose to live and not die.
- Cooperate with your Creator and with nature to help you. The crutch of drugs won’t build power of self-control to solve your problems. Serious regular prayer builds personal power over bad habits. Find, write down, and use promises, “…exceeding great and precious promises; that by these ye may be partakers of the Divine nature, having escaped the corruption that is in the world through lust.”
- The results of years of violations won’t evaporate. Re-establish right living, eating, working, and resting habits that can help restore a normal weight, good insulin sensitivity, normal lipid levels, normal blood pressures and risk factors, so that you can face the future in faith.
- Be of good courage. Continual, faithful effort make for an easy habit, and doing what one should do is its own reward.
“Disease is an effort of nature to free the system from conditions that result from a violation of the laws of health. In case of sickness the cause should be ascertained. Unhealthful conditions should be changed, wrong habits corrected. Then nature is to be assisted in her efforts to expel impurities, and to re-establish right conditions in the system.”
Could wiser counsel be found? Let’s follow it, and reap the Giver’s blessed rewards!
- Baxter, A.J., et al., Dietary Patterns and Metabolic Syndrome—A Review of Epidemiological Evidence, Asia Pac J Clin Nutri, 15(2):134-142, 2006.
- Crillo, P, et al., Uric Acid, Metabolic Syndrome, and Renal Disease. J Am Soc Nephrol, 17(12 Suppl 3):S165-8, 2006.
- De Lorenso, A., et al., Normal-weight obese syndrome: early inflammation? Am J Clin Nutr, 85(1):40-5, 2007.
- Dunstan, W., et al., Lipids Online, Watching television risk factor for metabolic syndrome. Public Health,121: 83-91, 2007
- Esposito, K., et al., Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA, 22;292(12):1440-6, 2004.
- Feig, D.I, et al., The role of uric acid in pediatric hypertension. J Ren Nutr, 17(1):79-83, 2007.
- Gill, Colleen, Medicine Net.com, Metabolic Syndrome, Denver and Health Sciences Center.
- Krishnan, E., et al, Hyperuricemia and incidence of hypertension among men without metabolic syndrome. Hypertension, 49(2):298-303, 2007; Epub 2006 Dec 26.
- Loevinger, B.L., et al., Metabolic syndrome in women with chronic pain. Metabolism, 56(1):87-93, 2007.
- McEwen, B.S, Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load. Metabolism, 55(10 Suppl 2):S20-3, Review, 2006
- Setoli, E, et al, Insulin resistance and endothelial function are improved after folate and vitamin B12 therapy in patients with metabolic syndrome: relationship between homocysteine levels and hyperinsulinemia. Eur J Endocrinol, 151(4):483-9, 2004
- St-Onge, M., et. al., Metabolic Syndrome in Normal-Weight Americans. Diabetes Care, 27(9):2222-2228, 2004.
- Tofovic, S.P., Long-term caffeine consumption exacerbates renal failure in obese, diabetic, ZSF1 (fa-fa(cp) rats.Kidney Int, 61(4):1433-44, 2002.
- Zang, J.O., Effect of exercise on postprandial lipemia in men with hypertriglyceridemia. Eur J Appl Physiol, 98(6):575-82, 2006.
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