Friday, September 16, 2011

Fat by Pollution: How Environmental Toxins May Be Making You Fat—and What You Can Do About It by Jerry Brainum

Losing excess bodyfat appears to be a straightforward process, involving correcting an out-of-balance energy equation. Superfluous fat represents an excess of stored energy, and if you have too much fat, that means you haven’t balanced your physical activity with your daily calorie intake. Since we know from the laws of physics that energy can be neither created nor destroyed, the basis of all fat-loss diets is to take in fewer calories than you burn through physical activity. That’s what taps into your fat stores.

If losing fat is just a matter of eating less and exercising more, why are Americans fatter than ever? Look at the plethora of foods targeted at dieters, such as lowfat and low-carbohydrate products. Some scientists suggest that an upsurge in processed-foods intake is the enemy in the weight-loss battle. They point to two particular elements: trans fats and high-fructose corn syrup, or HFCS, which increase shelf life and lower manufacturers’ processing costs.

The molecular structure of trans fats is manipulated to a form that is unnatural for the human body. The body handles such fats as if they were saturated fat, which is linked to cardiovascular disease, but they’re even worse for you. Saturated fat doesn’t lower the protective cholesterol carrier in the blood called high-density lipoprotein (HDL), but trans fat does, making it even more potent than saturated fat in promoting cardiovascular disease and cancer.

The production of high-fructose corn syrup starts off with a natural sugar, fructose. Adding glucose produces a rapidly absorbed simple sugar that wreaks havoc in the body by causing an outpouring of insulin. That leads to a dramatic rise in blood triglycerides, or fat, which act as a substrate for increased low-density-lipoprotein cholesterol. When LDL oxidizes in the blood, it promotes atherosclerosis and cardiovascular disease.

The evidence for the fat-promoting effects of trans fats and HFCS is so extensive that many people avoid such processed junk. Still, they either have trouble losing bodyfat or seem to rapidly gain it. Others successfully lose fat through strict dieting and exercise only to see it return. In cases like that a loss of muscle through excessive calorie restriction or lack of weight-training exercise is often to blame. A loss of lean tissue, or muscle, practically guarantees fat regain, since muscle is what maintains the resting metabolic rate.

There’s no shortage of explanations for why so many people are fat. One theory suggests that obesity is an infectious viral disease.1 According to that hypothesis, at least six known pathogens stimulate obesity in animals. Canine distemper virus causes serious disease in dogs but makes mice fat. A virus found in chickens, Rous-associated virus-7, leads to fat chickens if the birds become exposed. A Borna disease virus will fatten a rat, as will scrapie agents. At least two viruses, SMAM-1 and Ad-36, are thought to promote obesity in humans. Sound convincing? The trouble is, no one can explain how those infectious agents promote obesity.

A more plausible theory is that many forms of obesity are related to common toxins that humans are frequently exposed to. Most people are unaware that their bodies harbor countless potentially toxic chemicals. Tens of thousands of such chemicals exist as dyes, pigments, medicines, flavorings, perfumes, plastics, resins and rubber-processing chemicals. Humans get pesticide residue, preservatives and additives in food and water and inhale polluted indoor and outdoor air. Some toxins are absorbed through the skin. The important point is that nearly all such chemicals are fat-soluble, meaning that they’re stored in bodyfat.

Organochlorines, DDT, lindane, organophosphates, carbamate, polychlorinated biphenyl, phthalate, bisphenol A, cadmium and lead, as well as various solvents, are all linked to weight gain because they inhibit activity in the body’s hormonal systems. One animal study showed that the pesticide dieldrin doubled the bodyfat levels of treated mice. Another pesticide led to significant fat gain in mice that ate 50 percent less food!

Toxins cause fat gain by interfering with the activity of hormones involved in body composition and fat oxidation—for example, catecholamines such as epinephrine and norepinephrine, which exert thermogenic effects in stored fat. The chemicals also prevent the conversion of relatively inactive T4 thyroid hormone to the five times more active T3 form, which lowers resting metabolic rate.

Some toxins exert hormonelike effects. Various plastics mimic the effects of estrogen, and excess estrogen is linked to breast and uterine cancer in women. Excess estrogen in men results in increased water retention, increased bodyfat, and gynecomastia, or male breasts. Some studies show that the toxins short-circuit the testosterone synthesis system, leading to lowered testosterone levels. The same is true for growth hormone. The lowering of both those anabolic hormones means less muscle gains for bodybuilders and other athletes.

The toxins reduce training intensity and even the desire to exercise by lowering the levels of such brain neurotransmitters as dopamine and norepinephrine, which stimulate the brain. Toxins also promote direct damage to both nerves and muscle. Net effects: changes in appetite, food metabolism and the desire to exercise.

One system particularly hit hard by toxins stored in fat is the sympathetic nervous system. The SNS is especially involved in fat mobilization through the actions of the catecholamine hormones, epinephrine and norepinephrine, which exert a thermogenic action in fat, leading to a loss of energy as heat, and promote fat oxidation in concert with thyroid and other hormones. When animals are exposed to the various toxins, their excretion of catecholamines increases by 50 percent.

Several drugs promote weight gain. Antidepressants, which happen to be the most prescribed in the world, promote weight gain by affecting brain chemicals that control appetite. Prozac was so powerful that it was suggested as a weight-gain stimulant.

Pesticides stored in fat promote fat gain by interfering with oxidative enzymes in muscle—the same enzymes that burn fat in muscle. By inhibiting their activity, toxins blunt fat burning during exercise. A recent study confirmed that toxins negatively affect thermogenesis in humans.2 At the cellular level they block the activity of mitochondria, the portion of the cell where a process called beta-oxidation burns fat.

Another recent study found a significant increase in plasma pollutant levels in obese men and women who lost weight through dieting.3 It led to a decrease in resting insulin levels in the men but not in the women. Typically, a decrease in resting insulin levels would be considered favorable, but this study found an interference with normal insulin metabolism. One little-known effect of insulin is that it potently suppresses appetite after meals, and interfering with it may promote increased hunger and excessive eating.

Plasma pollutants may interfere with normal metabolism of long-chain fatty acids. They block the actions of enzymes that convert linoleic acid, an omega-6 fatty acid, into arachidonic acid. Arachidonic acid is the main precursor of a series of hormonelike chemicals synthesized in the body that are collectively known as eicosanoids. While many eicosanoids mediate inflammation in the body, others are essential to both health and muscle—for example prostaglandin F2A, a potent promoter of muscle growth. Arachidonic acid is also involved in testosterone synthesis, and plasma pollutants may interfere with that. The estrogenlike structure of many plastic pollutants, meanwhile, lowers testosterone levels.

Plasma pollutants may explain a frequently encountered problem during fat-loss diets: the dieting plateau. What happens here is that after a few weeks on a decreased-calorie diet, fat and weight loss suddenly stop. The plateau is often attributed to a lowering of the active thyroid hormone, T3, and its conversion into a metabolically inactive form called reverse T3. The usual explanation is that the body perceives a loss of mass and interprets it as a starvation alert. So the body protects itself by lowering metabolism and thus preventing the catabolism, or breakdown, of lean muscle tissue: Production of reverse T3 increases, metabolism drops, and weight loss ceases.

Fat loss brings on a dramatic release of plasma toxins stored in fat. Since they blunt thyroid output and prevent effective SNS hormone activity, it seems reasonable that perhaps the plateau may actually result from the toxin release. The question then becomes what to do to offset the effects of toxin release.

The first thing to do is to avoid becoming fat altogether, since the fatter you are, the more toxins you store in your body. Lean people ingest toxins, but studies show that they release them from their bodies far faster than obese people do. Lean athletes have the lowest levels of stored toxins in their bodies,4 clearly a reflection of their lower bodyfat levels.

If you have a lot of bodyfat, it’s prudent not to attempt to lose more than two pounds a week. Losing weight too rapidly will increase plasma pollutant levels and may interfere with fat loss and oxidation during exercise.

The frequent admonition to increase water intake during dieting serves two purposes: It staves off dehydration and flushes released toxins, which become water soluble in the liver. Make sure, however, that you drink pure water. Drinking water laden with toxins will only add to the problem.

Some evidence shows that fiber speeds the elimination of accumulated toxins released during fat loss. Soluble fiber, found in such foods as oatmeal, beans and fruits, is especially effective because it directly binds to toxins and shunts them toward the exit.

Make sure to include detoxifying nutrients in your diet: the B-complex group of vitamins, such antioxidants as vitamins E and C and selenium and all essential minerals. Nutrients that increase glutathione levels in the body may help the liver detoxify plasma pollutants. Nutritional precursors of glutathione include N-acetyl cysteine, lipoic acid and whey protein supplements.

A primary function of the liver is detoxification. All drugs are degraded by liver enzymes, including hormones, and the liver converts fat-soluble plasma pollutants released from stored bodyfat into water-soluble waste that goes to the kidneys for excretion.

Various nutrients support the liver’s detoxification system. These include the B-complex vitamins; sulfur-containing amino acids, such as cysteine and taurine; and various elements found in fruits and vegetables, such as the ellagic acid found in grapes, strawberries and pomegranates. Cruciferous vegetables, such as broccoli, brussels sprouts and cabbage, contain natural liver-enzyme stimulants such as sulforaphane. Eating foods like that while dieting will diminish the toxic effects of plasma pollutants by promoting their rapid degradation in the liver.

Since plasma pollutants interfere with the metabolism of essential fats, you need to balance intake of both omega-6 and omega-3 fatty acids. That means you need supplements such as flaxseed and fish oil blends. Supplemental amino acids that are precursors of body chemicals blocked by plasma pollutants may also help. Examples include L-tyrosine, the precursor of catecholamine hormones.

In today’s society, it’s difficult to avoid pollutants. The best way to avoid health problems linked to their accumulation in the body is to exercise and stay lean, and try to eat as clean as possible.


1 Dhurandhar, N.V. (2001). Infectobesity: Obesity of infectious origin. J Nutr. 131:2794S-2797S.

2 Trembley, A., et al. (2004). Thermogenesis and weight loss in obese individuals: A primary association with organochlorine pollution. Int J Obes Rel Metab Disord. 28:936-939.

3 Imbeault, P., et al. (2002). Increase in plasma pollutant levels in response to weight loss is associated with the reduction of fasting insulin levels in men but not in women. Metabolism. 51:482-486.

4 Pelletier, C., et al. (2002). Plasma organochlorine concentrations in endurance athletes and obese individuals. Med Sci Sports Exerc. 34:1971S.

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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