One would think that eating too much would result in an abundance of nutritional support for cells. But being overweight and undernourished at the same time is a reality that is just beginning to be understood. It is quite strange to say to people that the more they eat, the more malnourished they are destined to be.
Overweight people more often than not suffer from gross malnutrition because the nutritional values of the basic foods available to us have been steadily dropping for the last 50 years even as toxic exposures increase. Obese people tend to eat too many processed white foods with the fiber removed along with many of the vitamins and minerals. Not enough fiber is another common problem with the obese.
Excessive calorie intake is the fast track to leptin resistance. Since it’s hard to eat excess of the so-called “clean” foods, excess calories usually come from junk foods as do magnesium deficiencies.
Jennifer Welsh, a LiveScience staff writer explains that when dieters starve themselves of calories, they starve their brain cells as well. New research finds that these hungry brain cells then release “feed me” signals, which drive up hunger, slow down metabolism and thus cause diets to fail. Neurons sense nutrients in the body and tell the body when it’s time to eat and time to stop eating. The point is that dieters are not just starving themselves of calories, they are starving themselves of vital minerals and this comes on top of already existing mineral deficiencies that are characteristic of overweight and obese populations.
Obesity is Starvation
Obese people generally have hyperinsulinemia (high levels of insulin in the blood) and insulin causes fat to be stored in fat cells. Obese people in general cannot satisfy their body’s demands for energy or nutrients by eating. In this scenario, lethargy, hunger and stress are not a cause of obesity; they are the effects or results of it (due to the internal starvation). Syndrome X, also known as metabolic syndrome is a combination of insulin resistance, leptin resistance and glucose intolerance. All of these conditions are precursors to diabetes, heart disease, obesity and cancer.
Leptin and Magnesium
The new fashion in obesity is to look at the role of leptin, but what we are going to do in this essay is look not just at leptin but also at the leptin-magnesium axis that speaks volumes more than looking at either of these substances alone. High levels of leptin seem to be related to increased urinary magnesium loss in patients with type-1 diabetes.
Hypomagnesaemia and hyperleptinemia are common in patients with diabetes. Moreover, it has been demonstrated that leptin stimulates diuresis and natriuresis causing the urinary magnesium loss in type-1 diabetes. Human leptin is a protein of 167 amino acids. It is manufactured primarily in the adipocytes of white adipose tissue, and the level of circulating leptin is directly proportional to the total amount of fat in the body.
Magnesium makes dieting easier by supporting the brain’s sensitivity to leptin. Magnesium’s benefits go on forever it seems. Now we have to get serious and introduce it to the world of diet, weight loss and the medical science of obesity and diabetes.
Studies have shown that leptin and magnesium both play significant if not primary roles in heart disease, obesity, diabetes, osteoporosis, autoimmune diseases, reproductive disorders, and perhaps the rate of aging itself.Many chronic diseases are now linked to excess inflammation such as heart disease and diabetes. High leptin levels and low magnesium levels are extremely pro-inflammatory.,
Leptin is a hormone that triggers your sense of feeling full. A leptin deficiency can cause overeating, leading to obesity and obesity-related disease. Most people don’t have a leptin deficiency—they have lost their sensitivity to leptin, which is called leptin resistance. Much like insulin resistance, it’s possible to have enough leptin, but because your body doesn’t use it effectively, you still feel hungry. Leptin resistance is a serious health issue. Essentially you are overfeeding your body but the perception from your brain is that you are starving because you actually are missing vital nutrients such as magnesium.
The journal Circulation showed that men with established heart disease had blood leptin levels 16% higher than men considered heart healthy. Every 30% increase in leptin increased the risk of a heart attack or a vascular event by 25% (Wallace et al 2001).
Obesity and type-2 diabetes epidemics have joined forces ravaging the health of hundreds of millions of people around the world who have been significantly affected by this deadly pair. It is extremely important to understand how these two epidemics are intertwined.
The popular belief is that if one eats too much sugar, they’ll get fat and develop diabetes, but this is only half the truth. There’s more to the obesity-diabetes connection than what most doctors and just about everyone else typically believe.
When leptin is working properly it prevents nutrient spillover by telling insulin to shut off after your tank is full. Every time you eat excess food (more than what your body needs for energy), leptin and insulin levels surge. Leptin resistance leads to insulin resistance which further establishes leptin resistance. Leptin levels correlate with insulin levels (both are high in hyperinsulinemia). With insulin resistance, you no longer have insulin sensitivity. When you are insulin sensitive, you only need to secrete a small amount of insulin to get glucose (glycogen) into the muscles and liver.
Researchers have discovered that a proper diet and regular exercise have the greatest impact on reversing the damage done by leptin resistance. Too little sleep can lower the appetite-control hormone leptin and increase the appetite-stimulating hormone ghrelin. Now research reports that sleep loss may increase dangerous belly fat. Get a good night’s sleep should be standard doctor’s orders but sleep does not come on command for a large segment of people.
Melatonin, the hormone that regulates your body’s internal clock, is closely linked with leptin production. Your body produces the most leptin overnight while you sleep. Anything that disrupts your sleep can disrupt leptin production. Nothing will disturb sleep more than a serious magnesium deficiency, except for pharmaceutical medications for sleep disorders. It is vitally important to sleep in the dark—any artificial light sources will seriously curtail melatonin production during sleep.
One potential cause for lower serum magnesium in obese youth is low dietary magnesium intake. Studies do show that the calorie-adjusted magnesium intake in obese children was lower compared with lean children. Hypomagnesemia (serum magnesium 0.78 mmol/l) was present in 27% of healthy lean children and 55% of obese children.
One of the causes of magnesium deficiency is over-medicating with synthetic pharmaceutical drugs approved by the FDA and prescribed by doctors. They prevent the body from absorbing magnesium. It’s a cruel reality that diabetics are prescribed medicines that further reduce their magnesium reserves putting them into a fatal tailspin.
The body requires magnesium to absorb and utilize nutrients. Without magnesium our bodies cannot properly use the fats, proteins and carbohydrates we eat every day. When we aren’t getting what we need from our diet, we will crave more food in an effort to obtain those vital nutrients. By activating hundreds of enzymes in the body, magnesium helps you get the most from what you eat so you can be satisfied with no more than the amount of food you genuinely need.
Since conditions like insulin resistance and diabetes are strongly associated with obesity, controlling blood sugar levels is a key factor in maintaining a healthy weight. When enough magnesium is present in the body, insulin can function properly and blood glucose is used for energy. A magnesium deficiency causes insulin to function poorly, resulting in high blood sugar and fat storage.
Magnesium is a co-factor of many enzymes involved in glucose metabolism. Magnesium has an important role in insulin action, and insulin stimulates magnesium uptake in insulin-sensitive tissues. Magnesium is required for both proper glucose utilization and insulin signaling. Metabolic alterations in cellular magnesium, which may play the role of a second messenger for insulin action, contribute to insulin resistance. Magnesium is needed to extract energy from food and for optimal insulin function. The more energy you extract from food the less you have to eat to feel great.
There are co-factors that the body needs in order to utilize vitamin D properly. Magnesium is the most important co-factor for vitamin D. In fact, it is common for rising vitamin D levels to exacerbate an underlying magnesium deficiency. If one is having difficulty maintaining vitamin D levels, a magnesium deficiency could be the reason. Magnesium is a mineral that is essential to all cells of all known living organisms. We also see research showing that low serum magnesium levels can be raised by injections of vitamin D. Vitamin D supplementation of 2000 mg/day also reduces the incidence of type-2 diabetes.
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Stress management is one of the most important keys in fighting obesity, and magnesium is a vital nutrient for reducing stress. This is because magnesium supports healthy adrenal glands. These are the glands that control the release of adrenaline and cortisol, two hormones related to the stress response. While these hormones are vital to living, too much of them can cause weight gain and other health problems. Magnesium helps regulate these hormones so they are not overproduced.
Magnesium also regulates nervous system response. When we have a magnesium deficiency, our nervous system is over-stimulated, leading to irritation, nervousness and stress. When there is plenty of magnesium, the mind and body are finally able to relax and reverse the effects of stress.
Optimizing hormone levels is critical because hormones influence our moods, thought patterns (negative and positive), behaviors, appearance, and our ability to handle stress.
“Eating throws powerful hormonal switches and when you eat is just as important as what you eat,” states Byron Richards, leptin expert of Wellness Resources. He provides five simple rules to getting the leptin in our systems to work properly for you and help you lose weight:
Following a Leptin Diet
Combining this with adequate magnesium levels and vitamin D will together significantly impact the problems of obesity, metabolic syndrome and outright diabetes as well as many other diseases of aging.
Essential Role in Health, Disease and Aging; Dr. Ron Rosedale;
pro-inflammatory and immunomodulatory emerging role of leptin; Otero et
al; Rheumatology 2006;45:944–950;
affects food intake and body weight by actions on the hypothalamus.
Although leptin resistance is common in obesity, mechanisms have not
been identified. Specuation holds that the consumption of high amounts
fructose causes leptin resistance and elevated
triglycerides in rats. It’s been suggested that the major
physiological role of leptin is not as a “satiety signal” to prevent
obesity in times of energy excess, but as a “starvation signal” to
maintain adequate fat stores for survival during times of energy deficit
and that leptin resistance in overweight individuals is the standard
feature of mammalian physiology which possibly confers a survival
 Results: Baseline concentrations of serum Magnesium and 25 hydroxy vitamin D in obese individuals was lower than non obese individuals, the former being significant. Twenty seven percent of obese women versus 15% of non obese women were Magnesium deficient. Vitamin D injection caused a significant increase in serum Magnesium concentration in obese subjects but not in non obese subjects. There was also a significant increase of serum 25 hydroxy vitamin D in both groups. Mean elevation in serum Magnesium level among women who had Magnesium deficiency was higher than women with Magnesium adequacy (P<0.05). Conclusion: Low serum Magnesium concentration in obese individuals can be modified by vitamin D injection (JPMA 59:258; 2009).