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by Ron Rosedale, M.D.
The underlying cause of any of the chronic diseases of aging including Type II diabetes, CV disease, obesity, osteoporosis, and cancer will always be a derangement in the signals, the instructions, that tell your body how to turn energy into life. The two most important signals we know of today are given by insulin and leptin.
People have heard quite a bit about insulin, but what is leptin?
Leptin is a very powerful and influential hormone produced by fat cells that have totally changed the way scientific researchers looks at fat, nutrition, and metabolism in general. Prior to leptin’s discovery in 1994, fat was viewed as strictly an ugly energy storage depot that most everyone was trying to get rid of. After it was discovered that fat produced the hormone leptin (and subsequently other very significant hormones), fat became an endocrine organ like the ovaries, pancreas and pituitary, influencing the rest of the body and in particular, the brain. Leptin, as far as science currently knows, is the most powerful regulator of the brain’s two most important biological prerogatives: eating and reproduction. Your fat, by way of leptin, tells your brain whether you should be hungry, eat and make more fat, whether you should reproduce and make babies, or (partly by controlling insulin) whether to “hunker down” and work overtime to maintain and repair yourself; in other words live longer. I believe I could now make a very convincing and scientifically accurate statement that rather than your brain being in control of your body—your body, specifically its fat and leptin, controls your brain.
In our ancestral history, it was advantageous to store some fat to call upon during times of famine. However, it was equally disadvantageous to be too fat. For most of our evolutionary history, it was necessary to run, to hunt, and most importantly, to avoid being prey. If a saber tooth tiger chased a clan of cavemen it would catch the slowest one who could not make it up the tree—the fattest one whose genes would then be eliminated from the gene pool.
Thus, fat storage had to be highly regulated and it is. When one typically tries to lose weight the body tries to gain it back and results in what is commonly known as “yo-yo” dieting. It has long been theorized that there is a so-called “set point” and there must be a hormone that determines this. Science points now to leptin as being that hormone. To break the yo-yo cycle one must control leptin.
If a person is getting too fat, the extra fat produces more leptin that is supposed to tell the brain there is too much fat stored, more should not be stored, and the excess should be burned. Signals are therefore sent to an area of the brain in the hypothalamus to stop being hungry, to stop eating, to stop storing fat and to start burning some extra fat off. Controlling hunger is a major (though not the only) way leptin controls energy storage. Hunger is a very powerful, ancient, and deep-seated drive that, if stimulated long enough, will make you do all you can to eat. Asking somebody to not eat, to voluntarily restrict calories even though they are hungry, is asking the near impossible. The only way to eat less in the long-term is to not be hungry, and the only way to do this is to control the hormones that regulate hunger, the primary one being leptin. More recently, it has been found that leptin not only changes brain chemistry, but can also “rewire” the neurons in very important areas of the brain that control hunger and metabolism to do its bidding. This is quite “mind bending”.
The inability of the body to properly hear leptin’s signals, in other words leptin resistance plays significant, if not primary roles in heart disease, obesity, diabetes, osteoporosis, autoimmune diseases, reproductive disorders, cancer, and perhaps the rate of aging itself.
Remember the laboratory changes seen in animals on caloric restricted diets...and in those people who follow “The Rosedale Diet.” The longest-lived animals share the following traits:
- Low fasting glucose
- Low fasting insulin levels
- Lower body temperature
- Low percentage of body (visceral) fat
- Reduced thyroid levels
- Low triglycerides
- Low leptin
Let’s examine this further.
“Sugar is bad for you.” Your grandmother told you this, and she was absolutely correct (though the American Diabetes Association hasn’t figured this out yet). Why do the longest living humans and animals have low blood sugar levels for their age?
Glucose literally AGEs you. In a process called glycation, glucose reacts with protein resulting in sticky, sugar-damaged proteins called advanced glycated end products, or AGEs for short. When protein is damaged, it cannot function or communicate properly. AGEs also promotes excessive inflammation and free radical damage. AGEs, along with free radicals from oxidation are two of the major molecular mechanisms whereby damage accrues that leads to aging. AGEs cause skin and the lining of arteries to wrinkle and inflame contributing to plaque and heart attacks. It can promote the formation of cataracts and macular degeneration and eventual blindness. The glycation process has also been linked to the destruction of proteins and nerve cells that can lead to Alzheimer’s disease, memory loss and various neuropathies. Glycation, along with oxidation are two of the major molecular mechanisms whereby damage accrues, disease occurs, and death results. Making caramel by adding sugar to cream is a form of glycation. When fat oxidizes it turns rancid. As we age, we caramelize and turn rancid. I’d prefer to minimize that.
High blood sugar can suppress your immune system, making you more vulnerable to infection and cancer. Highly aggressive cancers outpace the availability of oxygen and therefore must use an anaerobic fuel—glucose. Elevating glucose feeds cancer.
Finally, high blood levels of sugar from nonfiber carbohydrates and excess protein send leptin and insulin levels soaring. It’s well documented in laboratory animals that high insulin accelerates aging.
If there is a known single marker for long life, as found in the centenarian and animal studies, it is low insulin levels. Insulin’s purpose is not to regulate blood sugar as believed by the general public and the medical profession alike; that is for cortisone, epinephrine, glucagon, and growth hormone to do. Insulin has other purposes. One is to store excess energy for future times of need. It lowers blood glucose levels as a side effect from storing it away, not regulating it. Our ancestors were forced to sometimes survive for days, weeks or even months on little food. High glucose was not a problem back then. Insulin helped our ancestors store away fat for the proverbial rainy day when they would need it.
Today, high glucose is the norm, not the exception and as a result, our insulin levels are typically much higher than they were among our ancestors. When your cells are constantly bombarded with insulin, they become insulin resistant, meaning they stop hearing insulin’s important messages; they lose their hearing so to speak. Insulin levels rise to try to be heard. Insulin resistance may even be a defense mechanism on the part of cells to protect against the toxic effects of excess insulin and glucose. However, this creates a hormonal derangement that has a catastrophic effect on your metabolism.
High insulin contributes to making you fat. Why? First, high insulin is telling your cells to store fat rather than burn it. More importantly repeated high levels of insulin cause insulin resistance and there is a loss in the orchestration of its signal. Not all cells become insulin resistant at the same time. Liver cells may be the first to become insulin resistant. Since one of insulin’s effects is to suppress production of sugar by the liver, if the liver is no longer listening to insulin, it makes lots of sugar. Eventually muscle cells become insulin resistant and can’t effectively burn sugar. Your fat cells are among the last to become insulin resistant, which is a problem because insulin promotes the making and storage of fat. All that excess sugar that hasn’t been burned is now socked away as fat. At this point one could consider the making of fat and obesity the price one pays to keep from becoming diabetic. Eventually, your fat cells become insulin resistant, and your fat production slows. But then you have no place to stuff excess sugar and it starts building up in your blood, and finally, after decades of hormonal dysfunction, you get diagnosed with diabetes. Incidentally, two of the most popular diabetic medications today, Actos and Avandia, work by multiplying fat cells, creating more wastebaskets to store sugar as fat, making you fatter, more leptin resistant, and accelerating your rate of aging.
High insulin causes retention of sodium, fluid retention, excretion of magnesium, elevated blood pressure, congestive heart failure, blood clotting, and arterial plaque formation. Heart attacks are much more likely to happen after a high carbohydrate meal, than after a high fat meal. The immediate effect of raising your blood sugar from a high carb meal is to raise insulin and leptin. This in turn, magnified by low magnesium, triggers the “stress response” which can cause arterial spasm, constriction of the arteries, elevated blood pressure, irregular heartbeat and sudden death. Insulin resistance accompanied by low magnesium prevents you from metabolizing important fatty acids such as EPA and DHA, which are vital to your heart and health in general.
In most species of caloric restricted animals, life span increases primarily as a result of a reduction in cancer rates (cancer being the number one killer in most animals). This is not surprising. Insulin is closely related to another hormone, IGF-1, or insulin-like growth factor. IGF’s primary function is to promote growth and cellular reproduction. There is a strong link between IGF levels and cancer (which is not much more than excessive cellular reproduction). Because of its molecular similarity to IGF, insulin can trigger the same genetic message, promoting cellular reproduction...and cancer. IGF, derived from growth hormone, is normally low in caloric restricted animals. Elegant studies published by a friend of mine have shown that bringing those IGF levels up to just average levels totally negates the benefits of caloric restriction on longevity. I question the use of growth hormone as an antiaging therapy; it may do the opposite.
Most significantly, the first, and perhaps still the most powerful genetic pathway that researchers from the University of Colorado, Harvard, MIT, and the University of California, have been able to manipulate to greatly extend life span is the insulin pathway. Genetically forcing insulin and its cousin IGF to remain low greatly extends life span in virtually all species tested. That may be insulin’s main purpose; to help coordinate energy stores and life span.
I have spoken about insulin’s critical role in health for over 15 years and I am even more convinced now.
However, as critical as insulin is in your health, leptin may even be more so. New research is revealing that long-term glucose and insulin signals may be largely determined by leptin. Leptin, through the brain and hypothalamus, also controls thyroid levels and body temperature. It largely determines the accumulation of belly fat and the ability to burn fat as indicated by triglyceride levels. It largely controls all of the other markers of longevity.
Leptin plays a significant role in obesity, heart disease, osteoporosis, autoimmune diseases, inflammatory diseases and cancer. These are the so-called “chronic diseases of aging”. Could it perhaps directly affect the rate of aging itself? Remember, there are two endeavors, two drives that life has been programmed, since its inception, to succeed at, to eat and to reproduce. All of your morphological characteristics from your hair to your toenails are designed to help you succeed at those two activities. If every one of our ancestors had not succeeded in eating and reproducing we would not be here, and this paper would be moot. Leptin plays a major role, maybe the major role, in both of those prerogatives. Nature’s purpose is not necessarily to have you live a long and healthy life, but to perpetuate the instructions for life. Even so-called “Paleolithic” diets, though undoubtedly far better than what is generally eaten today, were not designed by nature to help us live a long and healthy post-reproductive life, but at best to maximize reproductive success. Nature appears to not care much about what happens to us after we have had a sufficient chance to reproduce. That is why we die. But there are clues as to how to live a long and healthy life. And that brings us once again to fat—and leptin, and how to control it—which will be discussed in the next issue of totalhealth.
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