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Ultra Body Works


A Deadly Epidemic
Written by By Elizabeth J. Hall   
By Elizabeth J. Hall
Elizabeth Hall has taught and researched health topics for more than 25 years at Wildwood Lifestyle Center & Hospital, Wildwood, Georgia.

 

metabolicSyndrome_1WHAT HAPPENS IN A SYNDROME-LADEN SOCIETY? Do we tend to “tune it out” when another one is named? 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
• Obesity
• High blood cholesterol
• Hypertension

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

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.

OBESITY

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.

CHOLESTEROL

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.

metabolicSyndrome_3HIGH 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. 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 FISK 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.(1)

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.”(2)

As weight and body mass index (BMI)* increases, the risk for developing MetS increases in a dose-related fashion. Marie-Pierre St-Onge, PHD and associates studied a total of 7,602 adult participants of the Third National Health and Nutrition Examination Survey, a nationally representative cross-sectional analysis. However, the average norms aren’t everything. Individuals even in the upper normal-weight and slightly overweight BMI range have a relatively high incidence and are at increased risk of having the MetS. It should be noted that a high prevalence of women that have a large waist circumference (even though not obese) are also insulin resistant.(3) In Denmark, researchers also found that even a minor accumulation of adipose tissue in the abdominal region in otherwise non-obese men was associated with a considerably adverse metabolic risk profile.

By far, though, it seems that MetS is predominately a disease resulting from poor lifestyle choices and habits. This article will focus on how obesity and the typical Western diet—low in fiber, high in fat, refined carbohydrates, and animal protein— impacts the development of MetS and then we will present bonafide solutions. But first, let us summarize the relationship between sedentary living and exercise.

*Body mass index (BMI) is a measure of body fat based on height and weight that applies to adult men and women.

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 whowere 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.(4) 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

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 DO 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, which  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.

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 remains 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.

*Other factors such as excess estrogen, progesterone, use of steroids, stress, chronic inflammation, and infections can damage insulin receptors.

**It is also possible that some cases of insulin resistance arise from defective glucose transport post insulin receptors.

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.(6)

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

(except the thoroughfare channels)to deliver their goods. (Thoroughfare channels are shortcuts within the capillary network that allow blood to pass directly to the venule from the arteriole).

CLOTS AHEAD

To make matters even worse, MetS is also a prothrombotic state. It 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.

SOLUTIONS!

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.

metabolicSyndrome_7NUTRITION FACTORS THAT SPEED RECOVERY

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. (7) 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.

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.(8)

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!

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.(9)

Beware, then, of soft drinks containing fructose-derived corn syrup!

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. (10) This, too, is unfortunate because a high level of uric acid can also accelerate kidney disease. (11)

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.(12)

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.

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. (13)

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.

metabolicSyndrome_10WATER

 

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.

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

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.

REST

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 cytokines, decrease parasympathetic and increase sympathetic tone, increase blood pressure, and increase evening cortisol levels, as well as elevate insulin and blood glucose.” (15)

*For an in-depth discussion of how alcohol affects the cardiovascular system, see The Journal of Health & Healing, Vol. 26:3.

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:

1. Recognize that metabolic syndrome is a growing set of unhealthful dangerous conditions.

2. Get a serious in-depth diagnosis. It saves lives.

3. 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.

4. 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.

5. 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.”15

6. 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.

metabolicSyndrome_147. 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.”(16)

Could wiser counsel be found? Let’s follow it, and reap the Giver’s blessed rewards! 

REFERENCES

1. Loevinger, B.L., et al., Metabolic syndrome in women with chronic pain. Metabolism, 56(1):87-93, 2007.

2. Gill, Colleen, Medicine Net.com, Metabolic Syndrome, Denver and Health Sciences Center.

3. St-Onge, M., et. al., Metabolic Syndrome in Normal-Weight Americans. Diabetes Care, 27(9):2222-2228, 2004.

4. Dunstan, W., et al., Lipids Online, Watching television risk factor for metabolic syndrome. Public Health,121: 83-91, 2007.

5. Sonnenberg, L., et al., Dietary Patterns and the Metabolic Syndrome in Obese and Non Obese Framingham Women. Obese Res, 13:153-62, 2005.

6. De Lorenso, A., et al., Normal-weight obese syndrome: early inflammation? Am J Clin Nutr, 85(1):40-5, 2007.

7. 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.

8. 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.

9. Feig, D.I, et al., The role of uric acid in pediatric hypertension. J Ren Nutr, 17(1):79-83, 2007.

10. Krishnan, E., et al, Hyperuricemia and incidence of hypertension among men without metabolic syndrome. Hypertension, 49(2):298-303, 2007; Epub 2006 Dec 26.

11. Crillo, P, et al., Uric Acid, Metabolic Syndrome, and Renal Disease. J Am Soc Nephrol, 17(12 Suppl 3):S165-8, 2006.

12. 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.

13. Zang, J.O., Effect of exercise on postprandial lipemia in men with hypertriglyceridemia. Eur J Appl Physiol, 98(6):575-82, 2006.

13. 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.

14. McEwen, B.S, Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load. Metabolism, 55(10 Suppl 2):S20-3, Review, 2006.

15. The Bible, 2 Peter 1:4.

16. White, E.G. The Ministry of Healing, p. 127.

 
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Global Physiology
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Improving Your Brain Power
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brainPower_1Natural Ways to Increase Brain Cell “Fertilizer”
Elizabeth Hall
Excerpted from Keys to Optimal Health and Happiness


Lifestyle habits shape our brain power. How do they do so? Which lifestyle factors boost our brain power and which ones impair our mental functioning? To understand this we must consider where action happens in the brain? Synapses are microscopic points of communication between nerve cells that are heavily involved in memory, learning, habit formation, and the development of talent and character. We can, by our lifestyle choices, influence them positively or negatively. A neural circuit is composed of neurons and their synapses. Recurrent use of a particular neural circuit for learning (i.e. learning a musical instrument) increases the size, number, and efficiency of the involved synapses. Repeated use of a brain circuit results in easier and faster learning, and therefore, practice may indeed make perfect. Non-use, however, causes atrophy of the synapses that will eventually be manifested in slower reaction times and less rapid processing of information in the inactive areas of the brain. In other words, disuse of a neural circuit causes the synapses in that particular circuit to atrophy. These two features are known as synaptic plasticity.

BRAIN CELL FERTILIZER: BDNF

Brain-derived nerve growth factor (BDNF) is a protein that acts as a “fertilizer” to the synapses, protects brain cells, and in certain areas of the brain, regenerates brain cells. The abundant presence of BDNF predicts the ease of learning, whereas when it is in short supply, learning is more difficult; it also exerts anti-depressive actions.(1) Scientific evidence now suggests that brain-derived nerve growth factor and its precursor are decreased in the early stages of Alzheimer’s disease and that BDNF levels in depressed individuals are often low.(2) Therefore, BDNF can be beneficial in the treatment of depression. BDNF is also reduced in chronic or acute stress(3), especially in the hippocampus. This area, embedded in the temporal lobes, is important for storing memories and retrieving them, learning, and mood regulation. It can be significantly decreased in individuals with eating disorders, such as anorexia nervosa and bulimia.(4),(5)   

LIFESTYLE FACTORS THAT REDUCE BDNF


Overeating and a diet high in saturated fat and sugar decrease brain-derived nerve growth factor.(6) Animal experiments, however, suggest that voluntary physical exercise somewhat counteracts the effects of a high fat diet on BDNF.(7) Rodents fed a high-fat, high-glucose diet supplemented with high-fructose corn syrup for eight months demonstrated actual alterations in energy and lipid metabolism similar to clinical diabetes, such as elevated fasting glucose and increased cholesterol and triglycerides. The rats showed negative microscopic changes to the neurons in the hippocampus, a major area in the temporal lobes, which is involved in memory, learning, and mood regulation. They also exhibited less response activity and reduced levels of BDNF after repetitive nerve stimulation.(8)

LIFESTYLE FACTORS THAT INCREASE BDNF:

Wise calorie restriction (if obese) and intermittent fasting(9) (skipping supper, for example) stimulates the production of proteins that enhance the growth, size, and efficiency of synapses, increase brain-derived nerve growth factor, and help to increase neuron resistance to oxidative and metabolic insults from aging, Alzheimer's disease, Parkinson's disease, Huntington's disease, stroke, and chronic diseases, and increases the brain’s capacity for self-repair.(10) Of course, it is essential that we get adequate vitamins and minerals, complex carbohydrates, essential fats, and protein. Malnutrition also damages the brain.
Omega-3 fats, an assortment of whole plant foods,(11) physical exercise,(12) a variety of positive mental activities,(13) and quality sleep all improve the production of BDNF and subsequently, improve our brain power. Studies show that individuals with diabetes have a significant decline of BDNF in the brain, which may explain why diabetics are more at risk for dementia.

VITAMIN D

Animal studies show that vitamin D deficiency in newborns results in lower BDNF and reduced thickness of the brain cortex.(14) Animal studies also show that vitamin D deficiency during pregnancy disrupts the pattern of thirty-six major proteins in the mental development of the offspring. These proteins make up part of several biological pathways, including those involved in synaptic development and the transmission of impulses between brain cells. Nearly half of the molecules in the above experiment are disrupted, damaged, or malfunctioning in animal models of schizophrenia and multiple sclerosis.(15) Because breast milk does not necessarily supply an adequate amount of vitamin D, nursing mothers must be sure that their infants receive adequate sunlight and be sure that their own vitamin D levels are within normal range.

Autism, a complex developmental disability that includes an impaired synaptic network, is more common in areas of less ultraviolet light penetration (i.e. latitudes near the poles, urban areas, areas with high air pollution, and areas of high precipitation). Autism is also more prevalent in persons with dark skin, and severe maternal vitamin D deficiency is exceptionally common in dark-skinned individuals.(16) Please note: I am not saying that vitamin D deficiency is the sole cause of autism, multiple sclerosis, or schizophrenia; however, individuals with these problems or those who are at risk for these serious conditions should certainly have their vitamin D levels checked.

A study, quoted in the authoritative book called Modern Nutrition in Health and Disease found that 76% of dark-skinned women at the time of delivery were vitamin D deficient, and 81% of their children were also deficient in the same vitamin. Obesity before pregnancy often predicts vitamin D deficiency in mothers and their neonates. Pregnant women should have their vitamin D levels checked at least twice during their pregnancy and get regular exposure to sunlight. They should also take an appropriate amount of vitamin D supplement to prevent vitamin D deficiency and insufficiency.

COMPANIONSHIP

Researchers at the University of Veterinary Medicine Vienna found that social interactions have more influence on BDNF concentrations in the cerebral parietotemporal cortex of aging rodents than physical exercise and food restriction. Early social interactions actually help to shape the adult brain.(17)

Other studies show that social isolation decreases acetylcholine, a major neurotransmitter in the brain. Selective deprivation of social contact and of language during the critical period of brain development, especially in childhood, also has profound consequences for the structure and function of the adult brain. Researchers at Queen’s University in Canada discovered that animals that are reared in isolation show increased anxiety, avoid new situations, and exhibit poorer performance in learning and spatial memory tasks. However, providing social interactions during their adolescent period partially reversed these adverse effects of isolation.(18)

MY TESTIMONY:

Abilities can be developed and talents improved by persistent practice. When I (Liz) first came to Wildwood, I felt that I had not been given many natural talents, and I did not seem to have the capacity to excel in any area. In fact, I was so ignorant that some of the school’s administration did not think I would last at Wildwood. However, others believed that as I learned to work, study, investigate, and take the initiative, God would help me to enlarge the underdeveloped talents I did have. For example, in high school, science was definitely not my forte. I memorized key sections of the biology book with little, if any, comprehension. When I came to Wildwood and enrolled in physiology, I literally had to take it three times before mastering it. The more I shared what I learned in class and shared the information with others, the easier it became to remember the material. Now I can read medical textbooks of physiology without trouble, and can easily lecture on physiology without any notes. Yes, indeed, the more we share, the more personally develop.

REFERENCES

1. Thakker-Varia, S. and Alder, J., Neuropeptides in depression: role of VGF. Behav Brain Res, 197(2):262-78, 2009.
2. Lee, B.H., et al, Decreased plasma BDNF in depressive patients. J Affect Disord, 101(1-3):239-44, 2007.
3. Ibid, Thakker-Varia S, Alder J.
4. Monteleone, P., et al, Circulating brain-derived neurotrophic factor is decreased in women with anorexia and bulimia nervosa but not in women with binge-eating disorder: relationships to co-morbid depression, psychopathology and hormonal variables. Psychol Med, 35(6):897-905, 2005.
5. Hashimoto K., et al, Role of brain-derived neurotrophic factor in eating disorders: recent findings and its pathophysiological implications. Prog Neuropsychopharmacol Biol Psychiatry, 29(4):499-504, 2005.
6. Molteni, R., et al, A high fat-refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience, 112(4):803-14, 2002.
7. Molteni, R., et al, Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor. Neuroscience, 123(2):429-40, 2004.
8. Stranahan, A.M., Diet-induced insulin resistance impairs hippocampal synaptic plasticity and cognition in middle-aged rats. Hippocampus, 18(11):1095-8, 2008.
9. Mattson, M.P., Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms. J Neurochem, 84(3):417-31, 2003.
10. Mattson, M.P., Neuroprotective signaling and the aging brain; take away my food and let me run. Brain Res, 886(1-2):47-53, 2000.
11. Venna, V.R., et al, PUFA induce antidepressant-like effects in parallel to structural and molecular changes in the hippocampus. Psychoneuroendocrinology, 34(2):199-211, 2009, epub Oct 10, 2008.
12. Vaynman, S., et al, Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition. Eur J Neurosci, 20(10):2580-90, 2004.
13. Hubka, P., Neural network plasticity, BDNF and behavioral interventions in Alzheimer's disease. Ratisl Lek Listy, 107(9-10):395-401, 2006, review.
14. Feron, T.H.J., et al, Developmental vitamin D3 deficiency alters the adult rat brain. Brain Research Bulletin, 65(2):141-148, 2005.
15. Almeras, L., et al, Developmental vitamin D deficiency alters brain protein expression in the adult rat: Implications for neuropsychiatric disorders, http://doi.wiley.com/10.1002/pmic.200600392.
16. Cannell, J.J., Autism and vitamin D. Med Hypotheses, 70(4):750-9, 2008.
17. Branchi, I., Early social enrichment shapes social behavior and nerve growth factor and brain-derived neurotrophic factor levels in the adult mouse brain. Biol Psychiatry, 60(7):690-6, 2006.
18. Hellemans, K.G., et al, Adolescent enrichment partially reverses the social isolation syndrome. Brain Res Dev Brain Res, 150(2):103-15, 2004.
 
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