Insulin is probably the most misunderstood hormone in the body. Insulin's actions are often claimed to be the main culprit for the current epidemic of weight gain. But what many people fail to realize is that, despite its reputation as a fat loss inhibitor, insulin's biological functions are critically important for muscle gain as well as for fat loss. Nevertheless, many people still choose to follow low-carb diets, hoping to minimize insulin activity by chronically restricting carb consumption and thereby forcing the body to burn fat. Low-carb diets, with their extreme restrictions, often lead people to frustration, but seldom to long-term leanness. In the long run, most people on low-carb diets gain more weight than they initially lose.
Insulin plays a critical role in promoting the actions of insulinlike growth factor 1 (IGF1), which facilitates muscle development. Insulin and IGF1 are peptide hormones with almost identical molecular
structures. The difference between them is that insulin can promote fat gain, whereas IGFj stimulates fat loss. Both IGFj and insulin are potent anabolic agents that can transfer amino acids into cells, thus stimulating DNA synthesis and growth.
In addition to the similarity between insulin and IGFj, a collaborative mechanism exists between these two hormones. Metabolically, insulin promotes IGFj actions in the body. To be fully effective, IGFj requires insulin interference. In fact, insulin stimulates IGFj secretion by the liver. Additionally, growth hormone, which stimulates IGFj, is largely ineffective without the influence of insulin, which may explain why diabetes is often associated with low levels of IGFj and depressed growth. Insulin and IGFj work together, however, in a way that may seem contradictory or confusing. In the short run, serum IGFj levels increase when insulin levels decrease. Moreover, IGFj receptors in muscle cells increase significantly during periodic fasting.
Lack of food followed by low insulin levels may force the body to increase the number of IGFj receptors in muscles to maximize performance under conditions of minimal food intake. Researchers believe that the ratio of IGFj receptors to insulin could be an indicator of metabolic efficiency. Obese people often demonstrate a lower ratio of GH and IGFj to insulin. However, as mentioned previously, both GH and IGFj actions can be fully effective only when insulin levels increase, such as when carbs are consumed.
To take full advantage of this complicated way in which insulin affects IGFj, periodic fasting or undereating is recommended in addition to exercise. "Training on empty" enhances the signal to increase both growth hormone and IGFj receptors in the muscles. Then, to induce the effective actions of growth hormone and IGFj, one should have recovery meals immediately after exercise that include protein and carbs, as well as nourish the muscles with full meals that contain all essential nutrients in sufficient amounts.
So as not to compromise the anabolic actions of growth hormone and IGF^s, both of which profoundly affect muscle growth and fat loss, one should avoid chronic carb restrictions. Incorporating periodic cycles of undereating and exercise as well as providing the muscles with complete nutritional meals while avoiding chronic carb restrictions may initially help increase the number of growth hormone and IGFj receptors in the muscles as well as enhance their resulting actions.
Insulin and Thyroid Hormone
Insulin promotes thyroid activity in various ways. Thyroid hormones, particularly T3, play a critical role in energy utilization and body heat regulation. The thyroid hormone's actions are also vitally important for potency, virility, muscle growth, and fat loss. Low thyroid activity may severely impair overall metabolism as well as decrease both mental and physical capacity. Thyroid activity is determined by cellular energy levels, and when cellular energy is low, levels of adenosine triphosphate (ATP) decrease and the conversion of T4 to its active T3 form is severely inhibited. Insulin, which primarily increases cellular energy molecules (ATP) levels, is necessary for fully activating the thyroid hormone T3.
Thyroid hormone activity may be enhanced by the enzyme nitric oxide synthase, which is stimulated by insulin. Nitric oxide synthase is responsible for the production of nitric oxide, which plays an important role in the regulation of vasodilatation, sexual performance, potency, and growth. Therefore, insulin sensitivity and carb ingestion are essentially needed for proper thyroid functioning, thereby supporting virility, growth, and fat metabolism.
Chronic suppression of insulin due to chronic carb restriction may cause chronic elevation of the thyroid-stimulating hormone (TsH). Chronic overexpression of thyroid-stimulating hormone may lead to desensitization of the thyroid's receptors, a condition that may further suppress thyroid hormone synthesis and lead to declined sluggish metabolism. And as if this weren't bad enough, chronically high levels of thyroid-stimulating hormone are associated with increased levels of prolactin, the female lactation hormone. In men, prolactin production can cause profoundly feminizing effects, the least serious of which is overall fat gain.
Insulin's actions are also necessary for thyroid production. Thyroid hormone synthesis is an intense biochemical process that involves iodinization via brutal oxidative reactions catalyzed by the molecule NADPH. NADPH is a product of glucose metabolism in the so-called pentose phosphate pathway, which is an essential metabolic process derived from insulin-related glucose utilization. High thyroid hormones have a steroidlike activity, in particular, mediating the hormone actions of other anabolic steroids. This leads to the following conclusions:
• Insulin interference is critical for effective thyroid hormone activity, thereby potentially enhancing growth and fat loss.
• Chronic carb and calorie restrictions may impair thyroid function and overall metabolism.
• Insulin sensitivity is paramount for thyroid hormone synthesis via the pentose phosphate pathway.
In summary, by supporting thyroid hormone actions, insulin proves to be a fat-burning enhancer and growth promoter.
The pentose phosphate pathway is an essential insulin-related process that utilizes glucose for various critically important metabolic functions affecting muscle gain and fat loss. Impaired glucose utilization due to insulin resistance or the accumulation of serum lipids may adversely affect the pentose phosphate pathway, with devastating effects on overall metabolism.
The pentose phosphate pathway is primarily an anabolic pathway. It utilizes glucose to synthesize the five-carbon sugar pentose, which plays an essential role in cell membrane, nucleic acid, and steroid hormone biosynthesis. The pentose phosphate pathway is responsible for the utilization of large amounts of the essential energy molecule NADPH. NADPH is required for the synthesis of cell nucleus material, including DNA and RNA. This energy molecule is also vitally required for the enhancement of the body's self-defense against DNA damage, as well as protection from oxidant radicals and toxins. NADPH is necessary for the recycling of the body's most powerful immune protector, the antioxidant peptide glutathione enzyme, which protects the body from overall oxidative stress.
Glutathione enzymes are responsible for protecting nucleic acids from damage, a fact that is of utmost importance because it directly relates to cancer prevention and antiaging. The importance of the pentose phosphate pathway is often overlooked. Biologically, it serves critical
purposes, including the oxidation of glucose to energy. Nonetheless, the primary functions of this pathway are as follows:
• To generate the energy molecule NADPH for steroid hormone biosynthesis as well as to facilitate antioxidant reactions.
• To provide ribose 5 phosphate for the synthesis of nucleotides and the nucleic acids DNA and RNA.
• To regenerate glucose from pentose.
Certain organs such as the liver, adipose tissue, and the adrenal cortex contain high levels of PPP enzymes. In fact, 30 percent of glucose oxidation in the liver occurs via the pentose phosphate pathway.
In summary, insulin sensitivity is required for proper glucose utilization and the full activation of its related pentose phosphate pathway. Any intervention in pentose phosphate activity may adversely affect the body's ability to handle increased oxidative stress such as that from intense or prolonged exercise. Additionally, through its mediating actions, insulin helps protect the body from genetic damage, thus enhancing immunity and promoting an overall antiaging effect.
Methods that may help protect against insulin resistance including daily detoxification, minimizing carb consumption to no more than one meal per day, and minimizing simple sugars (particularly fructose) are all beneficially important because of their enhancing effect on glucose utilization and the pentose phosphate pathway. The foods richest in pentose and PPP enzymes are legumes, particularly mung beans. Animal foods, especially meat and liver, are abundant in dietary pentose, which initially stimulates PPP activity.
Finally, crash diets, prolonged fasting, starvation, and chronic carb restrictions may compromise the pentose phosphate pathway's anabolic actions, forcing it to oxidize glucose into energy instead. As long as the body is insulin-sensitive and sufficiently nourished, it will induce proper glucose utilization and its related pentose phosphate pathway.
However, as noted, prolonged restrictions of carbs and calories may waste PPP actions to utilizing energy, compensating for the lack of
dietary carbs and calories. Nevertheless, frequent and overconsumption of carbs may be as bad as carb restriction, and sometimes worse. Eating too many carb-containing meals during the day may lead to insulin insensitivity, a condition that may adversely inhibit the pentose phosphate pathway and all its related actions.
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