Minding your PQQs by Jerry Brainum

Odds are good that you've never heard of a supplement called "PQQ," which stands for pyrroloquinoline quinone. It was first discovered as a growth factor for bacteria in 1979. Later animal studies showed that it also played a role in the growth of animals, too. It may even do this in humans, since human breast milk is known to contain 15 percent PQQ. The human body produces about 100 to 400 nanograms of PQQ a day, which is a very small amount. It's also found in various foods, particularly soy-based foods, such as natto and tofu, as well as in spinach. However, the amount found in foods is also infinitesimal. Still, the fact that it exists in the human body, albeit in very small quantity,indicates that it must do something.
   The fact that it seems to be required for animal growth and reproduction suggested that it could be a new vitamin compound. While PQQ does affect the activity of various body enzymes, which is one requirement of a vitamin, it does not seem to satisfy the other vitamin requirement, in that there is no established deficiency condition associated with PQQ.  Still, it is capable of doing some significant things in the body. Among these are activation of PGC-1A, a substance that promotes the development of new mitochondria. Mitochondria are cigar-shaped structures in the cell where such vital processes as electron transport and beta-oxidation occurs, resulting in the production of the energy factor, ATP, and fat oxidation. A loss of function of mitochondria is thought to be  major cause of aging, since when mitochondria die out, the cell loses its energy source, and cannot function, so it too dies. A loss of mitochondria is also suspected of being a major cause of sarcopenia, the loss of muscle with age.
    While the effects of PQQ in animals are clear-cut and beneficial, the effects on human health are preliminary to say the least. In animals, PQQ lowers triglycerides (blood fat) more efficiently than fish oil, but in the one human study that has tested the effects of PQQ, it had no effect on triglycerides. Animal studies show that PQQ may modify the activity of NMDA brain receptors. These receptors are involved in memory and learning, but when overstimulated, can lead to loss of neurons, or brain cells. PQQ seems able to block such overstimulation. Much of the benefits of PQQ may be ascribed to an antioxidant activity. While antioxidant vitamins, such as vitamins C and E are quickly oxidized and thus no longer capable of exerting anti-oxidant activity, PQQ can be quickly converted back to antioxidant status, and go through thoussands of such cycles, known as redox cycling.
    Articles about PQQ have suggested that it can improve cognitive ability, or brain activity related to memory and intelligence. This could be related to both the increased mitochondria fostered by PQQ or the effect on NMDA brain receptors. However, most of the animal studies that have shown this effect involved PQQ being injected directly into the brain, a method of administration not likely to be popular with humans. Whether the current oral supplement of PQQ does likewise for human brains is not known or proven yet, although some studies did show slight improvements in memory in older adults after PQQ supplementation.
   As noted, there is a dearth of human studies related to PQQ supplementation. In one recent human study, however, a number of beneficial effects did occur.  The study only had 10 subjects, 5 women and 5 men, ages 21 to 34. In the first part of the study, the subjects were provided 0.2 milligrams of PQQ per kilogram of bodyweight in a fruit-flavored drink. This part of the study measured antioxidant effects of PQQ, and found only a slight effect.In the second part of the study, the subjects increased the dose of PQQ to 0.3 milligrams per kilogram of bodyweight. The subjects who ingested this dose showed a lowering of C-reactive protein and interleukin-6, both indicative of decreased body inflammation. The subjects also showed lowered excretion  of TMAO, which was in the news recently because it was implicated as a promoter of atherosclerosis. TMAO is a byproduct of the metabolism of both choline and carnitine that have been acted upon by intestinal bacteria. PQQ also lowered the excretion of a few amino acids, suggesting that it may have a beneficial effect on nitrogen retention. Other indices did show definite beneficial effects on mitochondria.One other thing worth noting: the study was sponsored by the Mitsubishi Gas and Chemical Company--the major supplier of PQQ in supplement form.
   So, is PQQ worth taking as a supplement? Based on the current available human research, the answer would have to be no. On the other hand, for those seeking to maintain healthy mitochondria, PQQ might be useful, but you can get the same effect for free merely by engaging in high intensity aerobic exercise.The  suggested dose of PQQ is 10-20 milligrams a day.



                                                                       

Harris, CB, et al. Dietary pyrroquinoline quinone (PQQ) alters indicators of inflammation and mitochondrial-related metabolism in human subjects.J Nut Biochem 2013;24:2076-84.

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Toxic Cinnamon? By Jerry Brainum

Next to black pepper, cinnamon is the most common spice used today. Cinnamon is derived from the bark of small evergreen trees grown in South and Southeast Asia, especially Sri Lanka. However, there are different kinds of cinnamon, and this can have an impact on health. For example, what's called true cinnamon, also known as Ceylon cinnamon comes mostly from Sri Lanka. The other predominant types include various forms of cassia, which includes Indonesian Cassia, Vietnamese Cassia, and Chinese Cassia. These look and smell like cinnamon, but they aren't true cinnamon, and this is where the health effects enter the picture.
    Cinnamon has a long history of use, dating back the Biblical times. It's mentioned in the Bible several times. Then, as now, it was primarily used as a spice for flavoring purposes.More recently, cinnamon has been suggested as a natural way to support healthy blood glucose levels. This, if true, could have a major significant impact on health, since the incidence of diseases related to poor glucose control, including insulin resistance, or "pre-diabetes," and type-2 diabetes, are are the rise worldwide. Type-2 diabetes was formerly called "adult-onset diabetes" to distinguish it from type-1 diabetes, which is caused by a destruction of the cells in the pancreas that produce insulin. The adult-onset form usually does not involve destruction of the pancreatic cells that produce insulin, but rather features a resistance of cells to insulin activity. The usual treatment involves a combination of oral drugs and exercise, or if the disease progresses, use of insulin itself to overcome the cellular resistance to the hormone. Type-2 diabetes is no longer referred to as "adult onset diabetes,"since it shows up in children as young as 12. The reasons for this are multifactorial, but relate mostly to a combination of lack of sufficient physical activity and excess body fat.
    Those who suffer from insulin resistance, which is characterized by elevated resting glucose levels, are often able to prevent the progression to full-blown diabetes if they lose excess body fat through a combination of exercise and diet. Low carbohydrate diets are particularly effective in this regard, since they tend to significantly reduce elevated resting insulin levels, as well as lower elevated blood glucose levels. Several natural supplements are also suggested as a safe way to help control elevated insulin and glucose levels. These include the trace mineral, chromium. Chromium is thought to work through boosting the effectiveness of insulin. It does this by modifying the cellular receptors for insulin, more or less providing a tighter bond of insulin to its cellular receptor. However, more recent studies have found that an excess of chromium produces the paradoxical effect of increasing insulin resistance. Even worse, the most recently published study found that chromium exerted little or no effect on elevated blood glucose levels. That, however, is just one study, and it would not be wise to cease consuming any chromium based on the findings of a single study.
    There are various other natural substances often suggested to control blood glucose levels, such as soluble fiber, which delays the absorption of simple carbohydrates, and thus lowers the insulin release effect. But among the various natural supplements touted to control glucose levels and possibly help to prevent the development of diabetes, cinnamon is the most often mentioned supplement. The research to prove this effect of cinnamon, however, is contradictory at best. One study published in 2003 provided 60 diabetic patients of both sexes with doses of 1, 3, or 6 grams of cinnamon powder. The treatment duration was 40 days, the results showed that cinnamon decreased fasting blood glucose levels, as well as lowering elevated blood lipid levels. Another study from 2006 featured 65 diabetic patients  who ingested 3 grams of a water extract of cinnamon for four months. The results of this study showed that while cinnamon did lower fasting blood glucose levels, it didn't affect blood lipid levels, nor did it affect hemoglobin A1C,a measure of long-term glucose usage in the body. Two other studies published the same year, found no effect of  cinnamon on blood glucose or other measures. Two studies published in 2007 likewise also found no effects of cinnamon when provided at a dose of one gram a day. Another study published the same year found that 6 grams of cinnamon delayed gastric emptying following a meal, which delayed the entrance of glucose into the blood. A Cochran review (which accessed previous studies) found that "cinnamon produces no more effects than a placebo." In other words, the review suggested that cinnamon was worthless in terms of glucose control.
    But that's not the biggest problem with cinnamon. It turns out that all of the commercial cinnamon on the market doesn't contain true or Ceylon cinnamon, but rather contains a variety of the cassia form. The problem here lies in a natural constituent of the cassia, but not Ceylon cinnamon, namely coumarin. The fact is that 90 percent of commerical cinnamon used in spices and supplements is the Indonesian cassia form, and in some cases, the Chinese cassia. Both of these forms contain significant amounts of coumarin. Why is that a problem?
    Coumarins can cause severe liver problems in animals, less so in humans. Some humans show liver abnormalities after consuming it, while others don't for unknown reasons. It is also a possible carcinogen, linked to causing tumors in animal studies. Coumarin also serves as a precursor for the production of the drug, Coumadin, trade name, Warfarin. Warfarin is a vitamin K antagonist that helps to prevent blood clots. It's often prescribed to treat people with atrial fibrillation, a defect of heart conduction that is a risk factor for strokes. The hope is that providing these people with Warfarin will lower stroke risk by preventing clot formation, which is often the cause of the strokes. Warfarin is also commonly used to kill rats.
   A recent study analyzed the levels of coumarin in both commercial cinnamon supplements, and cinnamon used for flavoring, spices, and so on. It found levels of coumarin that exceed the amount allowed by various health organizations to exist naturally in  food. True or Ceylon cinnamon was found to contain only trace amounts of coumarin. But all the cassia versions contained far more, and in some causes, possibly toxic levels of coumarin.
   The obvious solution to this problem would be to use only Ceylon cinnamon. The problem with this is that Ceylon cinnamon is virtually non-existent in the United States, where only the cassia forms are used. Another option is to use only special water-soluble cinnamon extract supplements, which are sold under various names. These supplements do not contain any coumarin, but they do contain the polyphenol substances thought to account for the beneficial effects of cinnamon. From an anecdotal point of view, I've tried both forms of cinnamon supplement, although the ones that I used were likely the cassia versions. Neither form, either the usual cinnamon or the far higher priced water-soluble form, did anything at all to control my blood glucose levels. Since I was insulin resistant at the time I used the supplements, I was a good test subject. I used the suggested doses, and regularly checked my resting blood glucose level, but found no changes whatsoever with use of either form of cinnamon. Am I saying that cinnamon is useless? Not at all. I think cinnamon tastes great, and I love it as a flavoring agent. But for treating insulin resistance and diabetes, well, let's just say I'm highly skeptical about that.


                                                                

Wang, YH, et al. Cassia cinnamon as a source of coumarin in cinnamon-flavored food and food supplements in the United States.J Agric Food Chemistry 2013: in press.

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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Are vitamin and mineral supplements a waste of money? By Jerry Brainum

An article published in the December 17, 2013 issue of the Annals of Internal Medicine made the bold claim that vitamin-mineral supplements are a waste of money for most people. The article authors noted that the evidence that vitamins and minerals have any preventive effect against the onset of the major killer diseases, including cardiovascular disease and cancer, is scant to non-existent. Furthurmore, asserts the doctors who wrote the article, vitamins and minerals will do nothing to help you live longer. Of course, since so many people, even those who aren't into using food supplements, still ingest a basic vitamin and mineral formulation as "nutritional insurance," this story merited being picked up by the popular media, who preceded to produce stories with such headlines as "Vitamin and minerals are worthless and a waste of money."
   However, as is typical with popular science reporting, several important points were not mentioned in the Internet and newspaper reports. For one, the assumption of the medical journal article was that most people are consuming enough nutrients in food, and therefore don't need any supplements. This further makes the assumption that most people consume a balanced diet that is replete in all necessary nutrients. That notion is nothing less than a fantasy on the part of the medical journal authors. Had they bothered to look at the latest government nutritional surveys, they would quickly have noted that the majority of Americans are in fact, not even meeting the minimal suggested daily intake of many vitamins and minerals.
   One reason for this is the reliance on processed and fast foods, which are devoid of many essential nutrients, but are top-heavy in carbohydrates and fats. Few people consume even the minimal suggested intake of five servings a day of fruits and vegetables, and without eating these foods, they will not be getting some of the essential nutrients. The obvious question is: if they aren't obtaining these required nutrients from food sources, where are they getting them? The answer is no where. And contrary to what was wrongly stated in the medical journal article, a long-term lack of nutrients is indeed linked to disease onset, even if it involves just a nutrient deficiency.
    The authors also overlooked individual requirements for certain nutrients. The concept of biochemical individuality states that, due to certain slight gene differences, some nutrients may be more required than others in some people. One example of this involves the production of a byproduct of amino acid metabolism called homocysteine . Homocysteine is produced from the metabolism of the essential amino acid, methionine. Normally, the body deals with it without a problem. But in some people, again likely due to slight genetic differences, homocysteine can accumulate in the body. When this happens, a few toxic effects may accrue. This includes acceleration of both cardiovascular disease and brain degeneration. The good news is that homocystine is capable of being broken down into harmless substances, as long as three nutrients are present: vitamins B6, B12, and folic acid. If a person who overproduces homocysteine isn't consuming enough of these three nutrients from food sources, eventual health disaster is likely.
    Then there is the case of the obese. Studies show that those with high body fat levels tend to sequester nutrients in their body fat, where the nutrients are inert. This is particularly true of the fat-soluble class of vitamins, such as vitamins E and D. In fact, studies conclusively show that obese people need to ingest higher doses of vitamin D just to reach an optimal blood level of the nutrient. A recent study examined the nutrient intake of obese subjects, both before and after being placed on special weight-reduction plan. This plan was designed to deliver all required vitamin and minerals in optimal amounts for health promotion. In fact, the plan actually delivered a level of vitamins and minerals that was slightly above suggested intakes.
     Prior to starting the special diet plan, the obese people were examined for any pre-existing nutrient deficiencies. This revealed deficiencies for vitamin D, vitamin C, selenium, iron, beta-carotene, and lycopene. The researchers conducting the study determined this by taking buccal or inner cheek smears from the subjects, since this method was more reflective of nutrient uptake and long-term intake of the nutrients, rather than a blood sample, which would just provide a more immediate picture.
   As noted, these obese subjects were placed on a special formula diet that at its strictest phase, provided only 800 calories a day. But they also were provided enough protein and other nutrients to prevent any problems.Despite this, while on the formula diet for three months, the obese subjects still showed deficiencies of vitamin C, selenium, iron, zinc, and lycopene. And this was true despite the fact that they were supplied these nutrients based on suggested daily requirements. So why were they still deficient?
    When losing fat in large quantities, the level of oxidation in the body increases significantly. As such, the minimal level of nutrients that the subjects ingested, most of which were antioxidants, were being used up to decrease the potentially dangerous byproducts of increased oxidation from the fat utilization.In addition, the fat-soluble vitamins, instead of being circulated in the blood, were instead shunted into fat reserves, which not only neutralized their effectiveness, but also increased the oxidation effect. The fat cells also exert an inflammatory effect, which adversly affects iron metabolism by boosting levels of hepcidin, a substance that controls iron uptake into the body.
   So, as this study shows, obese people show a definite increased need for certain vitamins and minerals that is above the recommended suggested intake of these nutrients. This is particularly true under dieting conditions, when increased oxidation effects will use up existing levels of minimal vitamins and minerals in the blood. Also, the fat sequestration effect must also be considered. Obese people need to ingest higher amounts of fat-soluble vitamins to get the same protective effects as their leaner peers.
    The absolute stupidity of suggesting that vitamin-mineral supplements are a waste of money is obvious. For the tiny minority of people that truly do ingest a balanced diet, they aren't as necessary, unless there is a genetic quirk that demands higher intake of certain nutrients. For all the rest, vitamins and mineral supplements can represent the difference between long-term health and disease. The salient question really comes down to this: Who stands to gain if people stop ingesting vitamins and minerals, and eventually become afflicted with health problems related to the lack of those nutrients?

                                                                  

Damms-Machado, A, et al. Micronutrient deficiency in obese subjects undergoing low calorie diet.Nutrition Journal 2012;11;34.


©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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Does a higher protein intake increase the risk of death? by Jerry Brainum

High protein diets have always been controversial. Critics of the diets often predict dire consequences for those foolish enough to stay on such diets long-term.These consequences include kidney disease and bone mass loss. However, more recent analysis of such possible risks show that they exist more on paper than in reality. When examined in healthy, active adults, higher protein intakes have consistently been shown not to impose any undue risks on kidney function, bone mass, or other factors. Athletes and others engaged in regular physical activity have long been advised to ingest a higher protein intake. In some cases, the level of protein intake is extreme. Some bodybuilders have stated that they regularly ingest as much as 600 grams of protein a day. It's doubtful that this degree of protein intake contributes anything useful to their goal of boosting muscle mass. Most excess protein is merely degraded and oxidized in the liver.
    But two alarming new studies, both published in the March 4, 2014 issue of the journal, Cell Metabolism, assert that a higher protein intake is not only not necessary,but could shorten lifespan if consumed during middle-age. The first study analyzed data from a nationwide nutrition study, and specifically looked at the protein intake of 6,831 middle-aged adults.The data showed that adults with an average age of 50 who consumed a diet that contained more than 20% of calories as protein were 4-times more likely to die of cancer or diabetes, and more than twice as likely to die from any cause in the next 18 years. Even a moderate protein diet of 10 to 19% protein was still associated with a 3-fold increase in death from cancer. Interestingly, the effect was only associated with consumption of animal proteins. Consuming protein from plant sources, such as beans, did not result in any negative effects on health. Even more intriguing was the finding that this effect was reversed in people over age 65; that is, those consuming a higher protein diet showed a 28% reduced risk of mortality from any cause, and a 60% reduced risk of dying from cancer. The effects of consuming a higher protein diet during middle-age on mortality were comparable to smoking!
     This, of course, is very bad news for anyone who ingests a high protein diet, especially those who are middle-age. But let's take a closer look at these findings. What, for example, is it about a high protein diet that seems to increase mortality? According to the study authors, the likely explanation is that a high protein (and higher calorie) diet boosts levels of a hormone called Insulinlike growth-factor-1 or simply, IGF-1. IGF-1 is produced both locally in muscle, where it functions as a major arbiter of promoting muscle growth, and in the liver, where it provides systemic body effects. These effects include helping to preserve lean mass, bone, neurons in the brain, and heart muscle. Without sufficient IGF-1, these tissues and organs degenerate. But IGF-1 has also been implicated in the cancer process because it promotes mitosis, or cellular division. Cancer involves uncontrolled cell division. But scientists still quibble over the precise role that IGF-1 plays in cancer. Among other effects, IGF-1 prevents a process called apoptosis, a type of cellular suicide. One theory suggests that tumors upgrade local IGF-1 synthesis as means of survival.Other theories say that it's the circulating IGF-1 itself that promotes cancer spread. On the other hand, IGF-1 travels in the blood bound to six different binding proteins, with IGFBP-3 being the predominant form. An important point is that IGF-1 can only interact with cells when it is unbound, or free. Bound IGF-1 is basically inert.So the question then arises: what can cause IGF-1 to be released from its binding protein? One thing that does this is insulin, as well as estrogen. When these two hormones are released in greater amounts in the blood, you also get a higher level of free IGF-1, which may be capable of interacting with existing tumors.
   An important point to consider about this new study is that no mention is made of what other nutrients the subjects ingested. If they had excess bodyfat, which is linked to higher levels of estrogen, that would account for their elevated IGF-1 levels. If they consumed excess carbohydrates, and were also pre-diabetic, this, too, would lead to higher free IGF-1 levels. The study authors implicated protein because protein is known to boost IGF-1 levels, but not necessarily the free or active form. But the mere fact that the data was derived from an epidemiological survey brings the findings into question, since such surveys are notoriously unreliable.    
    The study authors note that mice on restricted protein diets show a 45% decrease in tumor mass after two months. But they also say that consuming a higher protein diet protects people over age 65. This relates to the prevention of frailty associated with a lack of IGF-1, which is a major cause of death in older people. Yet, who has the highest rates of cancer? People over age 65. So why would a high protein diet, which is known to boost IGF-1, lead to less mortality in the older people? According to the study authors' suggestion, the higher IGF-1 induced by a higher protein intake should result in a greater incidence of cancer in an older population, especially since such older people usually have an abundance of damaged DNA in their cells--a scenario highly favorable to cancer onset. Would this same information apply to active people, who use or metabolize a higher protein intake differently compared to those who are sedentary?
   The other study exclusively used mice as subjects, and found that a low protein, high fat diet was most detrimental to health. But they also found that a very high carbohydrate intake of 70% of ingested calories, along with a low protein intake, was most conducive to longevity!  The most surprising aspect of the study, however, was the finding that reducing calories had no effect on longevity. This is contrary to dozens of previously published studies, which did find increased lifespan among various species who ingested a lower caloric intake. On the other hand, the stated mechanism for the increase in longevity linked to the high carb, low protein diet was a decrease in mTOR. mTOR is a protein that is crucial to protein synthesis, and is increased by a higher protein intake. But it is also associated with faster aging and spread of cancer in later years. But mTOR can easily be controlled by far less extreme measures than restricting protein while shoveling in high amounts of carbohydrates. The latter is disastrous for the estimated 50 million Americans who have insulin insensivity or "pre-diabetes," and would, without a doubt, result in an increase in mortality, rather than longevity, if ingested. The study authors did note that the mice who consumed a low protein, high carb diet not only consumed far more calories, but were also significantly fatter than mice who consumed a higher protein, lower carb intake. How being fat and overeating can boost lifespan is a type of metabolic magic that I doubt that anyone can explain, but it may work for mice, certainly not for humans!


©,2014 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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Do fat-burning supplements really work? by Jerry Brainum

When I first began bodybuilding, the choices for "fat burners" was strictly limited. In those days, you relied on what was called "lipotropics," which means "fat loving."The primary lipotropics were two nutrients, namely choline and inositol. The notion that they help rid the body of excess fat was based on the fact that when you are deficient in choline, your liver reacts by increasing the storage of fat in the liver. This is the first step of liver failure. Choline helped to rid the fat of liver by offering what chemists call methyl donors, which allow the liver to effectively process excess fat through transporting them out of the liver through the production of lipoproteins. Choline aided in the production of these lipoproteins. Somehow, the choline-associated process of liver fat reduction transmogrified into an overall body fat loss effect. In fact, however, neither choline or inositol were ever shown to promote systemic fat loss.
   The other popular "fat loss" supplement years ago were kelp tablets. Kelp is a rich natural source of iodine. Iodine, in turn, is essential for the production of thyroid hormone, which primarily controls the resting metabolic rate. So the idea was that if you took enough kelp tablets, you would boost thyroid hormone output, which would lead to increased resting metabolism, and then--presto!--you lost body fat. Unfortunately,none of us who gobbled handfuls of kelp tablets knew at the time that excess iodine intake had a paradoxical reverse effect of inhibiting thyroid hormone synthesis.
   In recent years, the category of "fat burning" supplements has become a big business, garnering a large percentage of the profits of the billion dollar food supplement business. One reason for this is that unlike other supplements targeted to bodybuilders and athletes, fat burners are a crossover supplement, appealing to anyone with a desire to lose excess body fat. Since so many people are obese, the market for such supplements is immense. Adding to this is the fact that there are no current effective pharmaceutical weight-loss products available.  Most of the weight-loss drugs work by either suppressing appetite, or blunting enzymes that digest dietary fat. Not only are such drugs ineffective for most people, but they also produce frequent unpleasant side effects.
   Thus, if you could offer a safe, over-the-counter fat-loss supplement, it would be very appealing. Probably the most effective supplement in the category was the combination of ephedrine and caffeine. Some formulas also added a form of aspirin, natural or otherwise, because it extended the effectiveness of the ephedrine/caffeine duo. Such products did work because they provided an enhanced thermogenic effect, which simply means that they converted calories into heat, which also involved a rise in the resting metabolic rate. In addition, ephedrine and caffeine also promoted the conversion of inactive thyroid hormone into the active form, which as noted, would favorably affect fat loss by maintaining an elevated resting metabolism. But in 2004, ephedrine and caffeine were removed from the commercial market due to concerns about toxicity, especially in relation to causing heart attacks and strokes. In fact, ephedrine and caffeine had a long history of safety, and when used in suggested doses, were safe, with the notable exception of those with pre-existing cardiovascular disease. Warnings on all product labels advised that those with CVD should not use the product, but many ignored the warning to their peril. In other cases, people overdosed, thinking that if two pills worked, ingesting eight or ten would speed fat loss. Small wonder why such idiots experienced health problems.
    So ephedrine was banned, but caffeine went on to become the number one active ingredient in current fat loss supplements. There is no doubt that caffeine does modestly boost resting metabolic rate. It also boosts the release of catecholamines, hormones such as epinephrine and norepinephrine, which do promote fat mobilization. But a frequently overlooked fact is that caffeine itself does not burn or oxidize fat. It merely promotes the exit of stored fat into the blood. If you do nothing to burn the fat, such as exercise, the fat is simply sent right back to be restored in the fat cells. This is a key point regarding fat loss supplements. While they may aid the process of fat loss through a heightened release of fat, they do not themselves actually burn fat. Most ads for such products are deceptive, in that they lead unwary consumers to believe that the product itself burns fat. It doesn't.
    The other frequent ingredient often seen in current fat-loss supplements is green tea. Green tea contains a number of potent antioxidants, with the primary one being EGCG, that do seem to provide a mild thermogenic effect. One suggested way that green tea helps burn fat is through blunting an enzyme that degrades catecholamines called COMT. If you extended the time of catecholamine activity, you would theoretically burn more fat if you also exercised. However, this effect of green tea remains a theory, rather than a proven commodity. More recent studies of green tea provided alone show little or no fat-reduction effect. On the other hand, green tea may be synergistic with other substances, including caffeine, and some studies have indeed shown this. The main problem with green tea is that some people have experienced severe liver problems after using it. Some suggest that it was the green tea content of a popular fat loss supplement called Hydroxycut that resulted in users showing severe side effects, many of whom experienced liver problems. This has never been verified, however. Indeed, some formulations of green tea were found to be tainted with the herb, germander, which has been shown to be toxic to the liver. In fact, germander was banned in France in 1992 after 26 cases of hepatitis were reported in users of the herb.
     After ephedrine was banned, companies hustled to find an appropriate substitute. One candidate was the similarly structured compound, synephrine. Synephrine, like ephedrine, acts as a sympathomemetic, meaning that it works like catecholamines to promote fat release from fat cells. The initial advertising suggested that synephrine worked by promoting the activity of beta-3 adrenergic receptors. The only problem with this was that this particular fat-cell receptor is most active in brown adipose tissue, which, while existing in humans, is far more active in rodents. Indeed, attempts by drug companies to produce a beta-3 activating drug for human use has uniformly failed to promote significant fat loss, but has produced significant side effects.
    Some of the most recent fat-loss supplements list esoteric herbs that few people have ever heard of. If you check the medical literature for information about the efficacy of such herbs, you'll find that there is a dearth of human research, and in many cases, there is none. The inclusion of such substances in fat loss supplements is based entirely on a few animal studies, in which the animal subjects are often supplied inordinately large doses to promote fat loss. How humans would react to ingesting similar doses is anyone's guess.
   Another, more alarming, problem related to fat loss supplements is possible contamination with ingredients not listed on the label. This came to light recently, when it was revealed that certain OTC fat loss supplements contained a prescription drug linked to heart problems. The lack of quality control in the supplement industry makes this a genuine risk. In other cases, the production of supplements is farmed out to Chinese companies, where quality control is non-existent. This is far more common than is realized. I recently found out that a popular online supplement company's house brand of supplements is manufactured entirely in China. When I wrote to the company for confirmation about this, they refused to answer me.
   One way to prove the efficacy of any food supplement is through quality research. But such research is expensive, and since the ingredients in most supplements are not patent-protected, many companies do not sponsor such research. Those that do often produce studies that aren't very convincing, involving too few subjects, no placebo, no controls, and no comparison to similar products. As such, such "studies" are merely ads for the company product.
   So will fat burners fulfill their promise? The best way to view them is as minor adjunctive diet aids. They do boost resting metabolism for about 6 hours following ingestion, and when combined with a suitable diet and exercise program, will help promote some additional fat loss. Will they produce such body composition change without exercise or diet? Absolutely not. There is only one substance that I am aware of that will promote extensive fat loss without exercise or diet. That substance is called dinitrophenol or DNP. It works by inhibiting energy production in the cell. The good news is that it often produces a fat loss of a half-pound of fat a day. The bad news is that it's highly toxic, and has caused several recent deaths.Those seeking an easy road to effortless fat loss will find a road that never ends.


                                                                  

©,2015 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited

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