Although rats handle insulin in a manner similar to humans, a study of human subjects would likely add more weight to the theory that insulin does indeed promote fat accretion. As we don’t breed humans without insulin fat-cell receptors, the best way to test the effects of insulin on bodyfat would involve a drug that modulates or inhibits insulin release in response to food.
Determining whether such a drug exists was the objective of a study that did involve human subjects.1 For 24 weeks, 44 severely obese adults were injected with octreotide-LAR, a drug that works by inhibiting the early secretion of insulin from the pancreas, as would normally occur in response to a meal. The subjects ate whatever they wanted, and their physical activity was unrestricted. They also took a drug to prevent gallstone formation, a common side effect when very fat people lose fat rapidly.
Eighteen percent of the subjects experienced marked fat loss, while another 57 percent dropped more modest but still significant amounts of fat. None of the subjects had any side effects. More important, they also experienced both a significant reduction in appetite and a reduced craving for carbohydrates. Those subjects showing the greatest reduction in insulin release also dropped daily carb consumption by 40.7 percent. That suggests that excess insulin perpetuates obesity by promoting hunger and craving for carbs, a vicious cycle that leads to further insulin release and even more fat synthesis in the body.
Most obese people do oversecrete insulin in response to a meal, a process called hyperinsulinemia. The debate in medicine is whether the excess insulin is a cause or effect of obesity. Losing bodyfat appears to curb excess insulin secretion, but insulin resistance could be caused by a failure of cells to properly use the hormone, with the body compensating by secreting even more insulin.
In a study that compared lean to obese people, insulin inhibited its own release in the lean people but was secreted excessively in the obese group.2 So the fatter you get, the more insulin insensitive you become. The body compensates by secreting even more insulin, which, ironically, only perpetuates obesity.
Insulin is the body’s primary storage hormone. It stores carbs as glycogen and promotes activity in muscle that leads to a type of protein storage referred to as increased amino acid uptake. Insulin works in fat tissue by increasing the activity of enzymes that promote fat synthesis while simultaneously inhibiting other enzymes that stimulate fat release and mobilization and possible oxidation.
Increased bodyfat, particularly in the body’s trunk, feeds aberrant metabolic and hormonal behavior that helps insulin maintain bodyfat. An example is increased cortisol, which not only promotes muscle loss but also works with insulin to perpetuate further fat increases in the central portion of the body, especially the gut area. Increased insulin and cortisol, in turn, inhibit the activity of hormones like growth hormone and testosterone, which promote fat losses in the area. The net effect: Insulin promotes a negative hormonal cascade that makes obesity hard to deal with.
While some researchers deny the insulin/bodyfat effect, still chanting the old mantra that only calories count, emerging studies appear to confirm the effects of excess insulin on fat synthesis. The latest such studies were recently reported in the prestigious New England Journal of Medicine. They compared low-carb diets, which lower insulin output, with the usually suggested lowfat diets. Subjects on lower-carb diets not only lost twice as much fat as those on lowfat diets but also showed more beneficial changes in cardiovascular risk factors.
Since insulin does show potent fat-promoting effects, how does that jibe with the experience of bodybuilders who inject insulin for anabolic purposes?
Injecting insulin alone is a good way to get fat as a pig, unless you eat practically nothing. That doesn’t apply to diabetics, who inject insulin because either their bodies don’t make the hormone (type I) or they can’t properly use the insulin their bodies do make (type II). Bodybuilders inject insulin in concert with other anabolic drugs, such as growth hormone and testosterone, both of which modulate insulin’s fat-producing effects. In fact, insulin is the yang to the yin of growth hormone; each tends to cancel out the major side effects of the other. Without the presence of insulin, growth hormone shows zero anabolic activity. Taking larger doses of GH, as some bodybuilders and other athletes do, may necessitate an increase in insulin for purposes of promoting maximum anabolic activity.
Insulin itself shows little or no protein-synthesizing effects in the blood unless accompanied by a higher-than-usual level of amino acids. In that case it makes no difference whether the dose of insulin is large or small: no aminos, no protein synthesis. That explains why taking a protein-and-carb drink following a workout is so effective—it maximizes insulin release at the most opportune time, during the so-called anabolic window, when muscle is most conducive to anabolic activity.
While insulin is a potent anabolic hormone, the drug form is associated with serious potential problems. If carb intake isn’t balanced with insulin injections, hypoglycemia, or low blood glucose, can rapidly ensue. As the brain is deprived of glucose, that can lead to anything from fainting to coma.
Insulin injections are a necessary and healthful evil for diabetics, though insulin is known to cause arterial lesions that can eventually result in cardiovascular complications. More recent studies show a direct relationship between higher insulin levels and the onset of colon cancer. Insulin also initiates a cascade that results in both sodium and water retention and high blood pressure. What’s more, insulin is thought to be partially responsible for the now-familiar bloated-gut appearance of some pro bodybuilders (GH and IGF-1 are also involved).
Shedding Light on Testosterone
Bodybuilders are always on the lookout for anything that can increase the body’s testosterone levels. That makes sense, since testosterone is a primary anabolic hormone, and anabolic steroids, recognized inducers of muscle growth, are merely synthetic versions of testosterone altered to prevent rapid breakdown in the liver (if they’re taken orally) or manipulated to extend useful therapeutic peak times (if they’re injected).
Several natural methods for increasing testosterone levels have been suggested. Examples are the various pro-hormone supplements, which are precursors to testosterone that exist naturally in the body or in natural sources. Occasionally, potential testosterone-increasing methods or substances turn up unexpectedly. That’s what happened in a study involving high-intensity light exposure.3
The researchers began with the premise that light controls sexual cycles in types of animals described as photoperiodic. Studies of human subjects have found that during the summer, when the sun is brighter, luteinizing hormone (LH), a pituitary hormone that controls testosterone synthesis in the body, increases. In a disease called seasonal affective disorder, or SAD, people become depressed during the winter months, when sunlight decreases. Normal light has an illumination intensity of 200 to 500 LUX, or lumens per square meter; SAD is treated with a minimum of 2,500 LUX.
Based on those observations, researchers exposed 11 healthy young men, ages 19 to 30, to either bright light, at an intensity of 1,000 LUX, or a placebo light between 5 a.m. and 6 a.m. for five days. The LH levels of the young men exposed to genuine bright light rose by 69.5 percent. That’s significant because when LH rises, so does testosterone, and bright light is thought to decrease levels of melatonin, a hormone produced in the pineal gland from the amino acid precursor tryptophan. Higher melatonin levels are thought to play a role in SAD, but in this study melatonin didn’t affect the way bright light increased LH release.
Another study did find an intriguing effect of melatonin in human male subjects, however.4 Past studies with animals show that melatonin controls animals’ sexual cycles by altering the level of sex hormones, such as testosterone. Studies of human subjects have failed to show similar effects, but melatonin exists naturally in human semen, and this six-month study tried to determine what happens when you provide supplemental melatonin to healthy men.
Eight male subjects in a double-blind, crossover protocol took a three-milligram dose of either melatonin (commonly used by consumers as a sleep aid) or a placebo. In six of the men no changes occurred in either hormone levels or sperm concentration or motility (movement). In two subjects, however, sperm levels declined significantly, and motility decreased by about 30 percent, an index of decreased fertility. Both men also showed a drop in estrogen and an increase in testosterone levels. After six months of getting off melatonin, one of the men’s sperm levels and hormone levels returned to normal, but the other man still showed abnormalities.
How did melatonin do it? It turns out that the hormone may inhibit local production of estrogen in the testes by inhibiting the activity of aromatase, an enzyme that converts testosterone into estrogen. Few people realize that estrogen is necessary for full maturation and sperm activity. This study shows that while estrogen has garnered a bad reputation among bodybuilders, men still need it for specific reactions in the body.
References
1 Mieyer-Velasquez, P.A., et al. (2003). Suppression of insulin secretion is associated with weight loss and altered macronutrient intake and preference in a subset of obese adults. Int J Obesity. 27:219-26.
2 Muscelli, E., et al. (2001). Lack of insulin inhibition on insulin secretion in non-diabetic morbidly obese patients. Int J Obesity. 25:798-804.
3 Yoon, I.Y., et al. (2003). Luteinizing hormone following light exposure in healthy young men. Neuroscience Letters. 341:25-28.
4 Luboshitzky, R., et al. (2002). Melatonin administration alters semen quality in healthy men. J Andrology. 23:572078.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
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