The FDA announced today the recall of a dietary supplement touted for fat loss called Hydroxycut. This is a heavily advertised and popular supplement among bodybuilders and others. I received two e-mails shortly after the FDA announcement about the Hydroxycut recall. Here was my response:
In the most recent study, a case study is presented about a 28-year-old man who showed symptoms indicative of severe liver toxicity. He had ingested Hydroxycut according to product directions, ingesting 2 tablets, 2-3 times daily for 3 months prior to the onset of his symptoms. He also ingested Tylenol and aspirin to treat his “sore muscles.” The man also admitted to drinking an average of 2-3 beers a week, which was described by the study authors as “heavy drinking.” The man showed a high copper level in his urine, which could be indicative of a genetic disease called Wilson’s disease that is characterized by high copper levels. But this was ruled out by the finding of normal serum copper and ceruloplasmin (the protein carrier of copper in the blood) levels. So why did Hydroxycut cause his liver problem? The UCLA physicians who submitted this case study suggest that it may be related to some of the ingredients in the product. This was the third case of liver toxicity linked to Hydroxycut reported in the medical literature. As with this case, the other “victims” also ingested the recommended dose. Three of the ingredients of Hydroxycut, namely Garcinia cambogia, Gymnema sylvestre, and green tea, have all been associated with severe liver toxicity. In one case reported last year, a man used two fat-loss products containing these ingredients (one was Hydroxycut) for only a week, then died of fulminent liver failure. Complicating the case was the fact that he was also ingesting a type of drug called a leukotriene antagonist (used to treat asthma, I take one myself). The theory is that the combination of the drug and the supplement ingredients resulted in rapid liver failure. Green tea extract has been shown to cause liver problems, but it’s difficult to explain why, since the active polypheonols in green tea aren’t absorbed too well, and you would have to ingest far more than is contained in any type of fat-loss supplement. There is the possibility, however, of an idiosyncratic reaction limited to only certain people. The fact that the man was also ingesting Tylenol may have played a role, since the primary ingredient of Tylenol (acetaminophen) is extremely toxic to the liver. Just ingesting 12 tablets at once could alone cause liver failure, and consuming it with alcohol makes it toxic even at lower doses. Since this man admitted a fondness for beer, I suspect that his case of liver failure wasn’t related to the Hydroxycut, but rather to the likelihood that he ingested a large dose of Tylenol with alcohol, which would definitely cause his symptoms. I view this report as alarming, since it reminds me of the previous Ephedrine scare, which was just a conspiracy involving the FDA in collusion with pharmaceutical companies to remove an effective weight-loss product,i.e., ephedrine, that was proven superior in several published studies to existing drugs prescribed to treat obesity. I don’t think the existing medical literature (which I am quite familiar with) justifies pointing an accusatory finger at Hydroxycut or any other existing fat-loss supplement
Studies examining how green tea may be toxic to liver function found the the effect emanates from a parodoxical action of green tea that also exists for other nutrient antioxidants. This involves the fact that large amounts of green tea can act like a pro-oxidant, instead of imparting its usual antioxidant activity. In the liver, the oxidation activity of green tea depletes the primary antioxidant/detoxifyer in the liver, namely glutathione. This suggests that if a person who uses supplements that contain green tea also ingests other nutrients known to increase the liver production of glutathione, such as N-acetylcysteine and milk thistle, the side effects linked to green tea could be blocked.
Learn the truth about anabolic supplements in my e-book, Natural Anabolics, available at www.jerrybrainum.com .
Monday, February 14, 2011
Some interesting new studies from an endocrinology meeting by Jerry Brainum
As this is being written, the 91st annual meeting of the Endocrine society is underway in Washington, D.C. For those of you not familiar with the term “endocrine,” this refers to hormones, and physicians who specialize in the study of hormones are endocrinologists. Among the many studies presented at this meeting of hormone doctors, a few show particular significance for those engaged in bodybuilding and physical activity. For example, one study compared eating the usual 55% carbohydrate diet to a lower intake of carbs, 43% to be exact. The lower carb diet contained more fat (39% versus 27%) than the conventional higher carb diet. The protein intake was identical on both diets, comprising 18% of total calories. While the study authors suggest that his level of protein intake helps to increase feeling of satiety, in truth, most low-carb diets contain over twice that level of protein. Consuming higher protein intakes while on low-carb diets helps to preserve lean tissue, as well as decrease appetite. The results after four weeks showed that eating a lower carb diet led to lower insulin and lower blood glucose levels after a meal. More importantly, those eating the lower carb intake reported far greater feelings of fullness, which would translate into greater dieting compliance.
Another study at the meeting presented evidence that a form of the protein, ghrelin, may offer potent anticatabolic effects in muscle. Ghrelin is a potent appetite stimulant, especially for dietary fat intake, but it also promotes growth hormone release. Italian researchers found that a form of ghrelin called des-acyl ghrelin, when provided to mice potently protected the rodents against induced muscle atrophy. How it does this isn’t yet known, but the effect doesn’t work through stimulating other anabolic hormones, such as IGF-1 or testosterone.
Myostatin is a protein that works to inhibit muscle growth. Animals lacking genes for myostatin show huge muscles and a lack of bodyfat, an ideal scenario for bodybuilding purposes. A study presented at the meeting had mice genetically altered to produce a high rate of atherosclerosis breed with other mice also altered to lack the myostatin gene. After 10 generations, they wound up with mice that had both characteristics. Control mice in the study had the genetic predisposition to atherosclerosis, but lacked the myostatin deletion gene. All the mice consumed a high fat diet for 12 weeks. Compared with the control mice, the specially-bred mice showed much less bodyfat, 30% lower fasting blood glucose levels, and 80% lower fasting insulin levels. They also showed 50% lower levels of low density lipoprotein cholesterol, the type most linked to cardiovascular disease, along with 30-60% lower levels of total cholesterol and blood triglycerides. This is a healthy cardiovascular profile that would prevent the onset of cardiovascular disease. One of the study authors commented that he doubts that the supplemental myostatin blockers sold to bodybuilders would have any effect at all.
Learn the truth about anabolic supplements in my e-book, Natural Anabolics, available at
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
Please consider joining this blog by clicking on the blue "join this site" button to the right of this blog. This will ensure that new blogs continue to be published. It costs nothing, and takes only a few seconds. Thank you.
Another study at the meeting presented evidence that a form of the protein, ghrelin, may offer potent anticatabolic effects in muscle. Ghrelin is a potent appetite stimulant, especially for dietary fat intake, but it also promotes growth hormone release. Italian researchers found that a form of ghrelin called des-acyl ghrelin, when provided to mice potently protected the rodents against induced muscle atrophy. How it does this isn’t yet known, but the effect doesn’t work through stimulating other anabolic hormones, such as IGF-1 or testosterone.
Myostatin is a protein that works to inhibit muscle growth. Animals lacking genes for myostatin show huge muscles and a lack of bodyfat, an ideal scenario for bodybuilding purposes. A study presented at the meeting had mice genetically altered to produce a high rate of atherosclerosis breed with other mice also altered to lack the myostatin gene. After 10 generations, they wound up with mice that had both characteristics. Control mice in the study had the genetic predisposition to atherosclerosis, but lacked the myostatin deletion gene. All the mice consumed a high fat diet for 12 weeks. Compared with the control mice, the specially-bred mice showed much less bodyfat, 30% lower fasting blood glucose levels, and 80% lower fasting insulin levels. They also showed 50% lower levels of low density lipoprotein cholesterol, the type most linked to cardiovascular disease, along with 30-60% lower levels of total cholesterol and blood triglycerides. This is a healthy cardiovascular profile that would prevent the onset of cardiovascular disease. One of the study authors commented that he doubts that the supplemental myostatin blockers sold to bodybuilders would have any effect at all.
Learn the truth about anabolic supplements in my e-book, Natural Anabolics, available at
www.jerrybrainum.com
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
Please consider joining this blog by clicking on the blue "join this site" button to the right of this blog. This will ensure that new blogs continue to be published. It costs nothing, and takes only a few seconds. Thank you.
Thursday, February 10, 2011
When Your Brain Has Left the Building
We Americans seem to have an abundance of things to worry about.There is the threat of another attack from crazed, fanatical terrorists looming in our collective psyches, as is the current downward trend in the economy.But there is another threat even more imminent that is facing many of those in the baby boomer generation.That threat is Alzheimer’s disease (AD). The incidence of AD is expected to rise in the coming years as baby boomers get older and approach age 65, when the incidence of AD commonly begins. Some studies suggest that one out of 85 people will have AD in 2050. Clearly, this is an alarming statistic that calls for some action to be taken now. This serious threat has not escaped the notice of researchers around the world, who are working overtime to come up with solutions to the impending threat of epidemic AD. Just two days ago, a consensus report was issued by a blue ribbon gathering of scientists who convened at the National Institute of Health for two days. The report examined all methods suggested to prevent the onset of AD, but before I discuss what they found, it’s probably a good idea to discuss what AD is.
AD was first described by German physician, Alois Alzhemier in 1906, based on his post-mortem examination of a female patient who had been showing various mental symptoms, including memory loss, language problems, and unpredictable behavior. His autopsy examination of her brain revealed abnormal protein clumps, later called beta amyloid plaques, along with tangles of another brain protein, later called tau. These two abnormalities became the basis of AD.The incidence of AD has risen over the years, to the extent that it now constitutes 60 to 80 percent of all dementia cases. It’s estimated that 5.3 million Americans suffer from AD, and it’s the sixth leading cause of death in the U.S, and the fifth leading cause of death in people over age 65. The greatest risk factor for AD is age, with the majority of cases showing up after age 65, although there is a version that strikes younger people, which is far more rare.
The blue ribbon science panel looked at randomized, controlled trials of various factors thought to be related to AD prevention. They noted that having the apolipoprotein A4 gene increases your likelihood of acquiring AD, although it doesn’t mean that the disease is inevitable. Not mentioned in the report is the fact that undergoing head trauma, as occurs in various sports, such as boxing and mixed marital arts, is especially dangerous for those with the APOA4 genes in relation to the development of AD. Other health factors related to AD onset include long-term high blood pressure, diabetes (or more specifically, high resting insulin levels) , and having elevated blood cholesterol readings in middle age.While various nutrients have been suggested as protective against AD onset, according to the report, ingesting many of these suggested protective nutrients, including fish oil, and B-complex vitamins including folic acid, shows limited evidence of efficacy because some studies show beneficial effects, while others do not. There is also limited evidence for a diet that is low in saturated fat and rich in vegetable intake. They do suggest that preliminary evidence points to exercise as being protective in the preservation of cognitive (thinking) ability.
So what they are saying in essence is that there in no definitive evidence that any of the suggested methods to prevent AD will help prevent the disease. But nearly all the studies they base this assertion on lasted no longer than two years, and AD is a process that likely takes many years before it becomes evident. Thus, studying preventive techniques for only two years or less will not yield any definitive results. But there is abundant evidence that AD has a large inflammatory component, and may even be the underlying basis of the disease. As such, techniques that lower brain inflammation should offer preventive effects against AD onset. One way to do this is to avoid obesity, especially beginning at about age 40. Exercise lowers inflammation, as does consuming diets rich in such protective factors as antioxidants. One study found that eating a Mediterranean-style diet that is low in saturated fat, but rich in antioxidants, leads to a 40% decreased risk of AD. Preliminary evidence shows that DHA, one of the omega-3 fatty acids, prevents the accumulation of beta amyloid protein in the brain that is the hallmark of AD. Curcumin from turmeric has been shown to not only prevent beta amyloid accumulation in the brain, but also seems to help remove it through activating certain immune system components. Even drinking 5-6 cups of coffee daily significantly lowers AD risk because of the antioxidant effect of compounds found in coffee. The same holds true for green tea, and one study showed that the antioxidants in green tea can reduce AD risk by 78%. One of the most important things you can do to prevent AD is to maintain cardiovascular health, since this is related to the activity of the APO-A4 genes found to be a risk factor for AD development. Exercise and maintaining healthy blood pressure levels will also prevent the other type of primary dementia, vascular dementia, which looks a lot like AD. Nicotinamide, a B-complex vitamin, can significantly lower levels of the Tau protein that forms the basis of the nerve tangles of AD, as can an increase in heat shock protein 70, which is increased by exercise. Exercise also increases levels of brain-derived neurotropic factor, which can repair damaged neurons in the brain.
So although the consensus report issued by the NIH panel offers a rather bleak perspective on AD prevention, the thing to remember is that these conclusions are based on the “scientific method.” In short, this means that nothing is accepted in science until results have been replicated numerous times by different scientists or researchers. This could take decades before it’s completely accepted as scientific gospel. In the meantime, I suggest it would be prudent not to wait for definitive scientific consensus, but rather adapt some of the preliminary preventive techniques mentioned above,since at least they will improve total health, and you can’t go wrong with that.
What foods and supplements will really help you increase muscular size and strength? Find out in my e-book, Natural Anabolics at http://www.jerrybrainum.com/
AD was first described by German physician, Alois Alzhemier in 1906, based on his post-mortem examination of a female patient who had been showing various mental symptoms, including memory loss, language problems, and unpredictable behavior. His autopsy examination of her brain revealed abnormal protein clumps, later called beta amyloid plaques, along with tangles of another brain protein, later called tau. These two abnormalities became the basis of AD.The incidence of AD has risen over the years, to the extent that it now constitutes 60 to 80 percent of all dementia cases. It’s estimated that 5.3 million Americans suffer from AD, and it’s the sixth leading cause of death in the U.S, and the fifth leading cause of death in people over age 65. The greatest risk factor for AD is age, with the majority of cases showing up after age 65, although there is a version that strikes younger people, which is far more rare.
The blue ribbon science panel looked at randomized, controlled trials of various factors thought to be related to AD prevention. They noted that having the apolipoprotein A4 gene increases your likelihood of acquiring AD, although it doesn’t mean that the disease is inevitable. Not mentioned in the report is the fact that undergoing head trauma, as occurs in various sports, such as boxing and mixed marital arts, is especially dangerous for those with the APOA4 genes in relation to the development of AD. Other health factors related to AD onset include long-term high blood pressure, diabetes (or more specifically, high resting insulin levels) , and having elevated blood cholesterol readings in middle age.While various nutrients have been suggested as protective against AD onset, according to the report, ingesting many of these suggested protective nutrients, including fish oil, and B-complex vitamins including folic acid, shows limited evidence of efficacy because some studies show beneficial effects, while others do not. There is also limited evidence for a diet that is low in saturated fat and rich in vegetable intake. They do suggest that preliminary evidence points to exercise as being protective in the preservation of cognitive (thinking) ability.
So what they are saying in essence is that there in no definitive evidence that any of the suggested methods to prevent AD will help prevent the disease. But nearly all the studies they base this assertion on lasted no longer than two years, and AD is a process that likely takes many years before it becomes evident. Thus, studying preventive techniques for only two years or less will not yield any definitive results. But there is abundant evidence that AD has a large inflammatory component, and may even be the underlying basis of the disease. As such, techniques that lower brain inflammation should offer preventive effects against AD onset. One way to do this is to avoid obesity, especially beginning at about age 40. Exercise lowers inflammation, as does consuming diets rich in such protective factors as antioxidants. One study found that eating a Mediterranean-style diet that is low in saturated fat, but rich in antioxidants, leads to a 40% decreased risk of AD. Preliminary evidence shows that DHA, one of the omega-3 fatty acids, prevents the accumulation of beta amyloid protein in the brain that is the hallmark of AD. Curcumin from turmeric has been shown to not only prevent beta amyloid accumulation in the brain, but also seems to help remove it through activating certain immune system components. Even drinking 5-6 cups of coffee daily significantly lowers AD risk because of the antioxidant effect of compounds found in coffee. The same holds true for green tea, and one study showed that the antioxidants in green tea can reduce AD risk by 78%. One of the most important things you can do to prevent AD is to maintain cardiovascular health, since this is related to the activity of the APO-A4 genes found to be a risk factor for AD development. Exercise and maintaining healthy blood pressure levels will also prevent the other type of primary dementia, vascular dementia, which looks a lot like AD. Nicotinamide, a B-complex vitamin, can significantly lower levels of the Tau protein that forms the basis of the nerve tangles of AD, as can an increase in heat shock protein 70, which is increased by exercise. Exercise also increases levels of brain-derived neurotropic factor, which can repair damaged neurons in the brain.
So although the consensus report issued by the NIH panel offers a rather bleak perspective on AD prevention, the thing to remember is that these conclusions are based on the “scientific method.” In short, this means that nothing is accepted in science until results have been replicated numerous times by different scientists or researchers. This could take decades before it’s completely accepted as scientific gospel. In the meantime, I suggest it would be prudent not to wait for definitive scientific consensus, but rather adapt some of the preliminary preventive techniques mentioned above,since at least they will improve total health, and you can’t go wrong with that.
What foods and supplements will really help you increase muscular size and strength? Find out in my e-book, Natural Anabolics at http://www.jerrybrainum.com/
Occlusion training boosts muscle gains in older men
Occlusion training involves restricting blood flow to working muscles by way of a cuff or tourniquet. Originally developed in Japan, this style of training has been shown to increase anabolic factors related to muscle growth. Even more interestingly, training in this manner allows you to lift much lighter weights, yet gain similar benefits compared to high intensity, heavy training. As such, this type of training may be particularly suitable to promote muscle gains in older people. Many older people, through years of inactivity, have developed joint problems that prevents them from lifting the amount of weight needed to foster significant gains in muscular size and strength. The question is, can occlusion training help such people?
A recent study involved studying changes in the thigh muscles of seven older men, average age, 70, when they engaged in light weight leg extensions with and without inflatable cuffs on their thighs. The cuffs were used to restrict blood flow to the thigh muscles while the subjects did leg extensions. The results showed that when training with the cuffs on, the older men responded to the exercise in a manner similar to that of young men doing high intensity exercise. The occlusion exercise increased muscle protein synthesis pathways associated with gains in muscle size and strength. Why the occlusion exercise did this isn’t certain, but it could be that training in this manner permitted the older men to activate type-2 muscle fibers more amenable to growth. Normally, these fibers can be activated only by lifting heavier weights. Previous studies of occlusion exercise with younger subjects showed that it increases several anabolic factors in muscle, including IGF-1. IGF-1, when produced locally in muscle, activates muscle satellite cells required for muscle repair and growth. In older people, it’s more difficult to activate these satellite cells, usually because of a age-related loss of neuromuscular function. If occlusion exercise can bypass this age limitation, it could be a useful protective exercise against the development of sarcopenia, or loss of muscle with age. Sarcopenia is the primary cause of weakness and disability with age, so this could be quite significant. Older people would need to be closely supervised when doing occlusion training, since blocking blood flow too long can present some serious problems, such as the development of a blood clot.
Fry, CS, et al. Blood flow restriction exercise stimulates mTOR1 signaling and muscle protein synthesis in older men.J Appl Physiol 2010;108;1199-1209.
What anabolic nutrients really promote gains in muscular size and strength? Find out in my e-book, Natural Anabolics at www.jerrybrainum.com.
A recent study involved studying changes in the thigh muscles of seven older men, average age, 70, when they engaged in light weight leg extensions with and without inflatable cuffs on their thighs. The cuffs were used to restrict blood flow to the thigh muscles while the subjects did leg extensions. The results showed that when training with the cuffs on, the older men responded to the exercise in a manner similar to that of young men doing high intensity exercise. The occlusion exercise increased muscle protein synthesis pathways associated with gains in muscle size and strength. Why the occlusion exercise did this isn’t certain, but it could be that training in this manner permitted the older men to activate type-2 muscle fibers more amenable to growth. Normally, these fibers can be activated only by lifting heavier weights. Previous studies of occlusion exercise with younger subjects showed that it increases several anabolic factors in muscle, including IGF-1. IGF-1, when produced locally in muscle, activates muscle satellite cells required for muscle repair and growth. In older people, it’s more difficult to activate these satellite cells, usually because of a age-related loss of neuromuscular function. If occlusion exercise can bypass this age limitation, it could be a useful protective exercise against the development of sarcopenia, or loss of muscle with age. Sarcopenia is the primary cause of weakness and disability with age, so this could be quite significant. Older people would need to be closely supervised when doing occlusion training, since blocking blood flow too long can present some serious problems, such as the development of a blood clot.
Fry, CS, et al. Blood flow restriction exercise stimulates mTOR1 signaling and muscle protein synthesis in older men.J Appl Physiol 2010;108;1199-1209.
What anabolic nutrients really promote gains in muscular size and strength? Find out in my e-book, Natural Anabolics at www.jerrybrainum.com.
L-carnosine
Not to be confused with L-carnitine, which I also use. Carnosine is a dipeptide, or linkage of two amino acids, histidine and alanine. In muscle it acts as a primary intramuscular buffer, reducing the acid that leads to muscle fatigue. Carnosine also blunts glycation, so culpable in the aging process. I take 1,000 milligrams daily on an empty stomach, usually in the morning.
www.jerrybrainum.com
www.jerrybrainum.com
Subscribe to:
Posts (Atom)