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Weight Gain, Inflammation and Leptin Resistance by alisaun ..... Leptin Resistance Support Forum

Date:   1/1/2006 5:19:00 PM ( 13 years ago ago)
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Hello,

I also posted this in the Lyme Disease forum, but it deals directly with Leptin resistance, which I find fascinating. Could it be that hormone signalling is at the root of our weight regulation problems? And who knew that fat tissue was so closely related to the immune system! And that fat basically acts as part of the endocrine system because it produces hormones (like leptin!)

For anyone who has, say, an inflammatory disease (Lyme), and who has, say, Leptin resistance (i.e. gained a ton of weight)...

...Like me (not that I'm bitter or anything)! While on my mission to hunt down whoever invented this lousy stealthy disease and caused one of the symptoms to be MASSIVE WEIGHT GAIN (you know who you are), I have been searching for the link or links between Lyme and weight gain. My research led me straight to hormones and I found this amazing article on leptin that I think provides some great leads as to why this happens and how to change it.

Here is the link and I've also pasted the article below:

And P.S.Don't ever secretly engineer a disease that makes women gain a lot of weight because we will find you. And sit on you.

http://www.fatresistancediet.com/chapters/fat-resistance/breakthrough-science...

THE FAT RESISTANCE DIETô :
BREAKTHROUGH Science REVERSES OBESITY

LEO GALLAND, M.D.


Introduction

Americans may be the heaviest nation on the planet, but the rest of the world is following our leadership and catching up quickly. Equally dramaticóand much less knownóis the scientific revolution that is changing our understanding of obesity. New research explains why excess fat by itself causes high blood pressure, diabetes, heart attacks, cancer, strokes and Arthritis and allows us to re-think strategies for achieving and maintaining leanness. Obesity and its related diseases are not just about weight; theyíre about the hormones produced by fat.
Doctors and scientists used to think of fat as no more than a repository of unused calories, an expanding storehouse filled up by eating more than you burn. We now know that fat is a living organ, as active and interactive as the heart or kidneys or liver, and that fat regulates itself by producing its own set of hormones. The hormones produced by fat cells are called ADIPOKINES. They can increase or decrease appetite and metabolic rate, making weight control easier or harder. The discovery of adipokines sparked a revolution in our understanding of obesity. This is the breakthrough Science that is the foundation for my book The Fat Resistance Dietô (Broadway Books, 2005)

Leptin

The revolution started in 1994 at New Yorkís Rockefeller University, when Dr. Jeffrey Friedman and his research team discovered that the fat cells of genetically obese mice failed to produce a chemical called LEPTIN. Leptin was the first adipokine, the first hormone shown to be made exclusively by fat cells. Researchers soon discovered that administration of leptin curbed the appetite and stimulated the metabolism of laboratory animals. Injecting leptin into genetically obese mice restored them to normal body weight. Leptin appeared to function as part of what scientists refer to as a negative feedback loop. When an animal is overfed and begins to gain weight, the increase in body fat leads to an increase in production of leptin, which in turn suppresses appetite and stimulates fat burning, restoring the animal to a normal lean weight. This process of internal self-correction is called "homeostasis" and it stabilizes the bodyís internal state, the way a weight at the bottom stabilizes the top of a buoy bobbing in the water.
The discovery of leptin raised great hopes that a natural cure for obesity lay around the corner. Excitement gave way to disappointment. Overweight humans are not leptin deficient: the more body fat, the higher the levels of leptin in blood. For people who are chronically overweight, the problem seems to be that leptin is not doing its job of reducing appetite and stimulating fat burning. The effect of leptin is blocked. Scientists call this state LEPTIN RESISTANCE. Returning to our image of the buoy, itís as if more and more bottom weight is needed to help the buoy stay upright, even when the water remains calm.
Itís easy to see how we created todayís weight crisis. Technology has decreased our level of physical exertion. The ready availability of high calorie, ready-to-eat foods and snacks has increased consumption. Our fat regulatory system, based on leptin, is inefficient at limiting body fat. Its primary function throughout human history has been to sense body fat for survival during famine. Many scientists believe that the main evolutionary role of leptin was not to regulate weight or appetite, but to regulate fertility. Leptin is absolutely necessary for the normal function of reproductive organs. As fat stores fall, leptin levels drop. At a given level of thinness, a womanís ovaries stop working, solely because of leptin deficiency. This effect is seen today in thin young women with very low body fat. Leptin lets the brain know when there is enough food available to support offspring and prevents reproduction when food is scarce.
Fat also appears to regulate the processes by which the body burns fuel for energy, especially in muscle. Adiponectin is the newest fat-produced hormone in the scientific spotlight. It also plays a central role in the biology of fat. Of all the adipokines spewed out by fat cells, adiponectin seems to be the most heroic. Recent studies show that adiponectin curbs appetite and sparks the burning of fat, as does leptin. But unlike leptin, chronically overweight people donít suffer from resistance to the hormone. They have an outright deficiency. A lack of adequate adiponectin is emerging as a significant factor in peopleís inability to melt flab and stay slim.When fat stores are low, fat cells secrete adiponectin, a recently discovered adipokine. Adiponectin helps muscle cells burn fuel for energy more effectively. It acts as a kind of super-charger for maintaining strong and active muscles when stored energy reserves are low. When food is not available and fat stores drop, adiponectin rises, helping muscle cells take up more Sugar from the blood and also enabling them to burn fat more thoroughly as fuel. As fat stores increase, adiponectin levels drop and the burning of fat as fuel actually becomes less complete. Itís a process that allows the body to store fat in times of plenty as a hedge.
Advice about eating less and exercising more has been a resounding failure. Diets, whether theyíre low calorie, low fat or low carbohydrate, all produce initial weight loss but do a lousy job of maintaining leanness. If thereís a way that Science can help us undo the damage technology has caused, then understanding and combating leptin resistance may well be the key.
Of all the theories that attempt to explain leptin resistance and suggest a way to reverse it, the one concept that best knits together everything we know about obesity and has the best chance of stopping this epidemic is the proven link between obesity, leptin and INFLAMMATION.




Inflammation

Inflammation is part of the bodyís protective response to injury or infection. The ancient Greeks described it as an internal fire. The Romans recognized it by four attributes: redness, heat, swelling and pain. We see those attributes in medical conditions that end in "-itis": arthritis, tonsillitis, appendicitis. During the Nineteenth Century, scientists discovered that inflammation was produced by white blood cells that migrate from the blood stream and enter areas of infection or injury. Recent research has linked heart attacks and strokes to microscopic inflammation of the blood vessels. Although inflammation produces many of the symptoms associated with being sick or injured, it is a necessary part of healing.
During the Twentieth Century, scientists uncovered the chemical basis of inflammation. It became clear that inflammation could exist without redness, heat, swelling or pain and without a migration of white blood cells. Today, in the Twenty-first Century, inflammation is seen as a chemical state that can exist in all or part of your body without necessarily producing symptoms. Its presence is most accurately determined by measuring the levels of inflammatory chemicals in the inflamed tissue, or sometimes in a blood sample. Many of the chemicals associated with inflammation actually cause damage to cells. They are referred to as "mediators" of inflammation. Other chemicals are just signals that indicate inflammation is present. They are "markers" of inflammation.
The biochemical understanding of inflammation has allowed scientists to recognize that your body controls the degree of inflammation by producing anti-inflammatory substances that damp down the pro-inflammatory signals. This is the normal response of your body to all kinds of stress: a stimulus provokes a reaction and that reaction acts as a stimulus to a counter-reaction that slowly returns your body to the state that existed before the initial stimulus. The whole process is called homeostasis and the pattern involves negative feedback loops. Homeostasis requires that all components of the negative feedback loops are in working order. Chronic inflammation results from the failure of homeostasis.
How does fat itself cause inflammation? Many adipokines, even leptin itself, are mediators of inflammation. They promote and encourage the inflammatory response, wherever it might be occurring. The more fat in your body, the higher the levels of these mediators in your blood and the greater the level of inflammation in your body. Hereís a fascinating example:
Weíve known for a long time that being overweight is associated with the development of osteoarthritis, especially in the knees. Osteoarthritis is the commonest form of Arthritis and is thought to result from wear and tear on the cartilage that lines joints. Osteoarthritis produces an overgrowth of bone that narrows the space in the joint and increases the likelihood of damage when the joint is moved. Doctors have thought that the reason osteoarthritis is associated with obesity is that being heavy increases the wear and tear on your knees, a simple physical explanation. Recent research has found a chemical connection. Joint fluid in the knees of overweight people contains high levels of leptin, which is produced by fat, not by the joints themselves. Leptin in the joints causes inflammation. Leptin also triggers the production of an anti-inflammatory chemical called TGF-beta (transforming growth factor-beta). TGF-beta is part of a negative feedback loop to damp down inflammation. But one of the effects of TGF-beta is to stimulate the growth of bone, in this case producing the bony overgrowth characteristic of osteoarthritis. So the relationship between obesity and osteoarthritis is not just created by how much you weigh. It is a hormonal relationship in which the bodyís normal homeostatic mechanisms go awry and produce disease.
Everyone experiences trauma to their knees during the course of their lives. Lean people, like athletes, who experience extensive, repetitive trauma, are at risk for osteoarthritis because the stimulus to inflammation and counter-inflammation is so intense. People who are overweight develop osteoarthritis because excess body fat causes an excessive inflammatory response to minor injury, which then triggers an increase in the counter-inflammatory response. The result is that both inflammatory and anti-inflammatory mediators are increased in obesity. The end result is no longer homeostasis but disease, which develops because of the unbridled activity of chemical mediators that fail in their effort to heal.
The plot gets even thicker. The inflammatory nature of fat is not only due to fat cells themselves. In addition to fat cells (adipocytes), fat also contains blood vessels and white blood cells. Fat specifically attracts a type of white blood cell called a macrophage. Macrophage literally means "large eater" and macrophages are large white blood cells that gobble up cellular debris. They are scavengers, sometimes called "garbage men of the immune system." The macrophages found in fat are major producers of inflammatory mediators, especially a substance called Tumor Necrosis Factor (TNF). TNF is well-known in medicine, because high levels of it produce much of the tissue damage and pain associated with Rheumatoid Arthritis and other autoimmune diseases. Fatty tissue can be laden with TNF-producing macrophages. In some animal studies, over 40% to 50% of cells found in adipose tissue were macrophages.
What are all these macrophages doing in a personís layers of fat? Biologists donít yet have all the answers, but one theory is that the bloated fat cells of people who are overweight actually leak or break open. Macrophages are then mobilized from the blood to move into the leaky fat tissue and clean up the mess. Once embedded in adipose tissue, macrophages begin spewing out inflammatory chemicals, especially TNF and a related mediator called Interleukin-6 (IL-6). Chemical mediators like TNF and IL-6 produced by white blood cells are called cytokines, because they increase the activity of white blood cells. (Cyto- is Greek for "cell" and kinesis means "movement or activity". Adipokines are cytokine-like chemicals produced by fat cells). Attracted by the cytokines in fatty tissue, more white blood cells move in to assist in mopping-up, releasing more cytokines and increasing the level of inflammation.
One of the more radical research findings in fat biology suggests that fat cells are actually cousins of macrophages. It appears that very young fat cells (called pre-adipocytes) can be transformed into TNF-spewing macrophages, rather than maturing into normal adipocytes. A group of French researchers discovered that pre-adipocytes become macrophages when prompted to do so by cytokines. Their finding is another example of the dynamic complexity of fat. Fat cells are intimately connected to and sometimes interchangeable with cells of the immune system. They both create and react to a wide range of hormones and mediators. Fat can be thought of as part of the immune system and part of the endocrine (hormone) system. TNF, in fact, is both a cytokine (a mediator produced by macrophages) and an adipokine (a hormone produced by fat cells). Whatever its source, TNF and its inflammatory relatives can wreak havoc with our fat-storage-and-management systems. TNF interferes with the operation of insulin, and is therefore a major contributor to insulin resistance. So, too, is another adipokine called resistin.
What we see in obesity is the swelling of fat tissue accompanied by a cacophony of cellular activity, most of it pushing the body toward a state of excess inflammation. Among the pro-inflammatory substances made by fat cells themselves are leptin, TNF, IL-6, and resistin. Add the contribution of fat-embedded macrophages and their own payload of TNF and IL-6, and biologists are beginning to view fat as a brewery of inflammatory chemicals.
The whole body is affected by this state of affairs, since inflammatory activity is not limited to fat tissue but spills over into the bloodstream. Thus, overweight people become subject to a body-wide state of chronic, low-grade inflammation, induced by fat itself.
The effect of fat on inflammation is just half of the cycle. The effects of inflammation on fat are equally intense.
When inflammation is severe, as in a life-threatening infection, it can cause tremendous weight loss. With severe inflammation, the body cannibalizes itself and both fat and muscle cells are destroyed. This is not a good way to lose weight. The breakdown of muscle is always greater than the breakdown of fat.
When inflammation is mild and chronic, producing few symptoms and only subtle changes on blood tests, inflammation has a very different effect on your metabolism. Chronic low-grade inflammation makes your brain and body resistant to the normal regulatory effects of leptin and other hormones, including insulin and cortisol. Insulin and cortisol are not adipokines. Insulin is made in the pancreas and cortisol is made in the adrenal glands. In excess, either can have a devastating effect on your attempts to lose weight. I discussed insulin in Chapter 2. High insulin levels prevent the breakdown of fat. Cortisol actually causes fat cells to grow.
One marker of inflammation that has received considerable attention over the past two years is "C-reactive protein" or CRP. Mild elevation of the level of CRP in blood is associated with obesity and with weight gain. Weight loss, on the other hand, produces a decrease in CRP. In people with a history of heart disease, mild elevation of CRP predicts an increased risk of heart attacks and strokes. In adults who develop diabetes, elevated CRP occurs before the onset of diabetes. In people with normal blood pressure, elevated CRP predicts the future development of high blood pressure. In aging adults, high CRP is associated with muscle weakness and frailty. Studies of CRP have proven the close relationship between silent, chronic inflammation and the development of the most common chronic diseases of modern society.
Inflammation and fat share a complex relationship. When inflammation is severe, as in a life-threatening infection, it can cause tremendous weight loss. With severe inflammation, both fat and muscle cells are destroyed; the breakdown of muscle is always greater than the breakdown of fat. When inflammation is mild and chronic, however, producing few symptoms and only subtle changes on blood tests, inflammation has a very different effect on your metabolism. It disrupts hormones. Acting through the complex networks of chemicals involved in homeostasis, inflammation makes your cells resistant to the normal regulatory effects of leptin and other hormones, including insulin and cortisol. Iíll say more about insulin and cortisol later. These hormones are not adipokines, but they can have a devastating effect on your attempts to lose weight. First, I want you to understand the vicious cycle that keeps you from living lean: FAT ITSELF CAUSES INFLAMMATION.
Many adipokines, even leptin itself, are chemical mediators of inflammation. Remember what I said about mediators. They are chemicals associated with inflammation that actually cause damage to cells. The more fat in your body, the higher the levels of these mediators in your blood and the greater the level of inflammation in your body. Not only does this fat-derived inflammation prevent leptin from helping you lose weight, it causes other hormonal effects that interfere with permanent weight loss. Inflammation raises the level of insulin and cortisol, two hormones that actually cause your body to make more fat.


Insulin and cortisol

Insulin is a hormone produced in your pancreas. Its best known effect is to lower blood Sugar by driving Sugar and other nutrients into cells, especially muscle cells. Your muscles need insulin to help them produce energy and recover from the effects of exercise. Inflammation interferes with the effect of insulin on your muscles. Just as inflammation causes leptin resistance, it is a major cause of INSULIN RESISTANCE. With insulin resistance, your muscles are not fully responsive to insulin, so they donít efficiently burn the sugar that circulates in your blood. As a result, your blood sugar starts to rise. Your pancreas responds by releasing more insulin. When the degree of insulin resistance outpaces the ability of your pancreas to produce more insulin, diabetes occurs. Whether or not you actually develop diabetes, high levels of circulating insulin can have seriously negative effects. There are some actions of insulin that occur outside of muscle and are not impaired during insulin resistance. As insulin levels increase, these effects of insulin are felt. High insulin levels make your kidneys retain fluid, raising your blood pressure and creating that feeling of being bloated and swollen. High insulin levels prevent cells from breaking down fat, making it harder to lose weight through dieting. Insulin also turns on genes that produce a number of mediators of inflammation, so with high insulin, as with high leptin, the level of inflammation in your body increases.
Your brain and your adrenal glands are attuned to the level of inflammation in your body. As inflammation increases, your brain sends a signal to your adrenal glands to produce more of a hormone called cortisol. You may be familiar with cortisone, a drug used to relieve symptoms of inflammation like itching, redness or pain. Cortisol is the natural equivalent of the drug, made in your own adrenal glands in response to stress. Cortisol naturally combats inflammation, but at a high price. Cortisol increases the amount of belly fat. It also causes fluid retention, muscle weakness, memory loss, high blood pressure, and further raises your blood sugar. The increase in blood sugar then stimulates a further increase in insulin.
Insulin is a hormone produced in your pancreas. Its best known effect is to lower blood sugar by driving sugar and other nutrients into cells, especially muscle cells. Your muscles need insulin to help them produce energy and recover from the effects of exercise. Inflammation interferes with the effect of insulin on your muscles. Just as inflammation causes leptin resistance, it is a major cause of INSULIN RESISTANCE. With insulin resistance, your muscles are not fully responsive to insulin, so they donít efficiently burn the sugar that circulates in your blood. As a result, your blood sugar starts to rise. Your pancreas responds by releasing more insulin. When the degree of insulin resistance outpaces the ability of your pancreas to produce more insulin, diabetes occurs. Whether or not you actually develop diabetes, high levels of circulating insulin can have seriously negative effects. There are some actions of insulin that occur outside of muscle and are not impaired during insulin resistance. As insulin levels increase, these effects of insulin are felt. High insulin levels make your kidneys retain fluid, raising your blood pressure and creating that feeling of being bloated and swollen. High insulin levels prevent cells from breaking down fat, making it harder to lose weight through dieting. Insulin also turns on genes that produce a number of mediators of inflammation, so with high insulin, as with high leptin, the level of inflammation in your body increases. Your brain and your adrenal glands are attuned to the level of inflammation in your body. As inflammation increases, your brain sends a signal to your adrenal glands to produce more of a hormone called cortisol. You may be familiar with cortisone, a drug used to relieve symptoms of inflammation like itching, redness or pain. Cortisol is the natural equivalent of the drug, made in your own adrenal glands in response to stress. Cortisol naturally combats inflammation, but at a high price. Cortisol increases the amount of belly fat. It also causes fluid retention, muscle weakness, memory loss, high blood pressure, and further raises your blood sugar. The increase in blood sugar then stimulates a further increase in insulin.

HOW DOES INFLAMMATION CAUSE LEPTIN RESISTANCE?

How, exactly, does chronic inflammation cause leptin resistance? The question and the answer lie at the very heart of the Fat Resistance Dietô.
Fat biology researchers have uncovered what many believe to be the key mechanisms of leptin resistance. Dr. Jeffrey Flier and his colleagues at Harvard Medical School have led these efforts. They have discovered that a group of molecules involved in reducing inflammation also interfere with leptin signaling on the cell surface and inside the cell. These molecules are known as SOCS, which stands for suppressors of cytokine signaling. Two specific SOCS molecules, SOCS-1 and SOCS-3, have been shown in many animal studies, first by Flierís group and later by other research teams, to jam the signals that leptin is supposed to deliver to brain cells and muscle cells.
What is the significance of the fact that SOCS molecules are key causes of leptin resistanceóthe fundamental factor in stubborn overweight? SOCS-1 and SOCS-3 are both part of the bodyís response to inflammation. When working properly, our levels of inflammation are kept in balance by overlapping feedback loops. When particular arms of the inflammation system go into gear, provoked, for example, by the presence of a bacterial invader or a sudden injury, another set of chemicals is released to make certain that the chemistry of inflammation doesnít spiral out-of-control, causing excessive damage to cells and tissues. SOCS molecules represent the message-carriers in one of these negative feedback loops. Their message to inflammatory cells and cytokines is: "Cool down!" SOCS proteins are an essential part of the bodyís system of checks and balances. When they work as they should, SOCS molecules succeed in checking excess inflammation. As inflammation subsides, levels of SOCS subside.
Immunobiologists believe that overweight people with chronic inflammation have chronically high levels of SOCS, released in a continual effort to damp down their body-wide inflammation. Indeed, elevated SOCS proteins have been found in the brain, liver, muscle, and to a lesser extent, the fat tissue of obese animals. High SOCS levels are a sign that the overweight animal is "over-inflamed" and trying to tone the inflammation down. Studies done at Harvard have found SOCS molecules in the hypothalamus, a walnut-sized structure at the base of the brain that regulates mood, thirst, and hunger. The Harvard studies show that SOCS-1 and SOCS-3 jam leptinís signal at the internal portion of the leptin receptor. Bottom line: SOCS molecules interrupt leptinís message to suppress hunger, and they are primary causes of leptin resistance in the brain.
Other studies suggest that SOCS-1 and SOCS-3 also interfere with leptinís effects in muscle and other organs outside the brain. In these sites, jamming of the leptin signal can lead to sluggish metabolism. Remember, an active SOCS system is strong evidence that the person is already suffering from chronic inflammation that the body is trying to get under control.
Adding more fuel to the fire of inflammationís role in fat, another research team from Harvardís Joslin Diabetes Center showed that the exact same molecules, SOCS-1 and SOCS-3, play a distinctly similar role in hampering insulin sensitivity. Their research, published in 2004, demonstrated how these molecules trigger insulin resistance by interfering with the successful connection of insulin to its matching receptor on the surface of your cells.
Under the influence of chronic inflammation, hormones that should function to protect your health are thrown into disarray. As their levels increase, they begin to destroy your health, encouraging weight gain and more inflammation. If you have a chronic weight problem, this is the vicious cycle you face whenever you try to lose weight and keep it off. Donít ever let anyone tell you that weight problems are not the result of hormones. They are totally dependent upon hormones that misfire. Breaking the vicious cycle of obesity, inflammation and hormone disruption is the greatest nutritional challenge in the world today.
Drugs will not fix this problem. The problem with drugs is: there arenít any that do the right thing. Drugs that are used to treat the kind of inflammation associated with pain, like aspirin and ibuprofen, donít act on the part of inflammation that produces hormone resistance. At high doses, they cause fluid retention, which only increases the bloating you feel.
There is something that can counter the kind of inflammation associated with obesity: FOOD.
A major problem of the modern, obesity-causing dietóoften overlookedóis that the natural, inflammation-fighting components of food have been removed. Itís true that our food supply is loaded with concentrated high calorie ingredients, like added sugar and added fats, which are easy to slurp down. Just as important is what has been removed from our food: nutrients that fight inflammation. What are they? There are two major categories: GOOD FATS and PHYTONUTRIENTS.

Omega-3 fats

Good fats are starting to receive the attention they deserve. They are known as OMEGA-3 FATTY ACIDS, because of their unique chemical structure. They are found in fish, green leafy vegetables, and some nuts, beans and seeds. Some of the popular weight loss diets of the past few years have talked about good fats, usually in conjunction with "good carbs". Most of them have you get your supply of omega-3ís from fish oil supplements rather than from food. Thatís a shame, because foods containing omega-3ís also contain other natural inflammation fighters.
Most of the fat we eat is composed of fatty acids, which are made from long strings of carbon atoms linked together. Itís the type of fatty acids in the fat that determine its nature. SATURATED FAT is solid at room temperature, like butter or coconut oil or the fat you trim from a steak. Itís called "saturated" because all of the carbon atoms are surrounded by hydrogen atoms. Every possible chemical linkage is filled There are no potential chemical bonds unfilled. They are literally saturated. Saturation makes the string of carbons straight and stiff. UNSATURATED FAT is composed of fatty acids in which some of the carbon atoms have chemical bonds that are not filled by hydrogen. Unsaturated fatty acids tend to curve and get softer. Unsaturated fat is liquid at room temperature, like most vegetable oils. The more unsaturated an oil becomes, the more liquid it is. Olive oil, for example, is mostly monounsaturated. It is liquid at room temperature but congeals and gets goopy when refrigerated. Some corn oils are polyunsaturated. They stay liquid in your refrigerator, but will start to thicken in your freezer. Fish oil is the most unsaturated of all the fats you consume. A high omega-3 fish oil concentrate will remain a liquid, even in your freezer.
Whatís important about omega-3 fats is not only their fluidity, but their name. Omega-3 refers to a special characteristic of their chemical structure. Our bodies are not able to produce omega-3ís or to turn other kinds of fat into omega-3ís. We have to get them from food. There are no substitutes. Of all the foods that actively fight inflammation, omega-3 fatty acids have been the most studied. I started using omega-3 oils in my medical practice over 25 years ago. At first, we thought that omega-3ís acted like aspirin to reduce the levels of inflammatory mediators called PROSTAGLANDINS. Recent research has shown that omega-3ís do far more. The mechanisms of their protective anti-inflammatory effects extend beyond aspirinís. They are a natural and intrinsic component of numerous complex regulatory systems in the cells of our bodies. Conditions in which omega-3 fats have proven value, either for treatment or prevention include arthritis, colitis, diabetes, high blood pressure, heart attacks, heart arrhythmias, asthma, dementia, depression, and schizophrenia.
Stone Age humans got most of their omega-3ís from wild game. Wild animals that feed on grass and leaves store omega-3 fats in their flesh and organs, which are eaten by hunters. Todayís cattle are raised on corn or manufactured feed that supplies no omega-3ís for the animal to incorporate into its meat. With the development of agriculture and fishing, the major sources of omega-3ís became wild fish, beans, nuts, seeds and leafy greens vegetables. Navy beans, kidney beans and soy beans all supply omega-3ís. Walnuts are a delicious source of these. Flax seed, an excellent source of omega-3ís, was the health food of the Romans. Purslane supplied them for the ancient Greeks. The Twentieth Century witnessed a progressive depletion of omega-3 oils from diets of people all over the world. Because omega-3ís have a short shelf life, they were systematically removed from processed foods and animal feed. The result is a widespread global deficiency of omega-3ís, in industrialized nations and developing countries alike. Any successful solution to the twin problems of obesity and chronic inflammation must correct this deficiency by incorporating omega-3 containing foods, like flax seed, walnuts, salmon, tuna and other cold water fish, beans and leafy greens. Feeding flax seed or seaweed to chickens allows them to lay eggs with omega-3 fatty acids in the yolk.

Phytonutrients

"Phyto" means plant and the term "phytonutrient" applies to nutritional substances found in plants that improve the way your body functions. The plants we eat contain thousands of phytonutrients. The appetizing colors of fresh fruits and vegetables derive from the presence of anti-inflammatory phytonutreints known as carotenoids and flavonoids. Carotenoids are fat-soluble compounds that range in hue from light yellow to deep orange. The best known carotenoid is beta-carotene, the orange pigment evident in carrots and cantaloupe. But other carotenoids, like lutein, lycopene and zeaxanthin, have recently received considerable attention for their benefits in preserving vision and fighting cancer. I recommend a diet high in mixed carotenoids, which includes many different varieties of fruits and vegetables: carrots, broccoli, spinach, tomatoes, winter squash and papaya. Flavonoids typically range from bright yellow to deep purple in hue. Important anti-inflammatory flavonoids are found in blueberries, cherries, pomegranate, citrus fruits, purple grapes, green tea, onions, dark chocolate and many herbs and spices. In the U.S., perhaps more than in any other country, food has gotten blander and blander. American palates have grown accustomed to the taste of sugar, fat and salt. A major defect of almost every weight loss diet is its reliance on sugar substitutes, fake fats and artificial flavors to reduce caloric intake. If you use these manufactured ingredients in an effort to lose weight, you are reinforcing the brainwashing of your appetite, which believes it can only be satisfied by a sweetness or oiliness or saltiness that overpowers all other flavors of food, subtle or piquant. As much as you need to avoid empty calories and junk foods, you need to embrace the herbs and spices that lend amazing taste to meals and snacks.



Copyright © Leo Galland 2005



 

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