L-Arginine and GH Surges by Jerry Brainum

The amino acid L-arginine is most familiar today as the primary active ingredient in popular food supplements aimed at promoting the release of nitric oxide (NO). Arginine is the immediate nutritional precursor of, or raw material for, the body’s synthesis of nitric oxide. The reasoning behind such supplements is that NO is a potent dilator of blood vessels, and dilation can produce a greater degree of muscular pump during training—the muscle benefits through a heightened delivery of oxygen and nutrients.


   But before arginine became linked to nitric oxide-boosting supplements, it was most associated with growth hormone release. While several other amino acids promote the release of growth hormone, arginine is particularly noted for that effect. In fact, an infusion of arginine at a dose ranging from 12 to 40 grams was often used to determine if a GH deficiency existed, especially in children.

   The IV reliably promoted a release of GH in about 20 minutes, except in people deficient in the hormone. That information trickled down to the popular press, with books on longevity declaring that you could effectively promote GH release by taking arginine orally. Several studies appeared to confirm that assertion.

   One such study involved 14 men, aged 15 to 30, who took 1.2 grams of arginine polyglutamate and 1.2 grams of L-lysine. That particular combination of amino acids promoted GH release five times greater than when either amino acid was used alone. Lysine and arginine normally compete for uptake in the body, since they both use the same amino acid transport system. Lysine is often suggested as a natural therapy for treating herpes infections because the virus requires arginine for growth and propagation. Lysine displaces arginine, thereby preventing viral replication.

   Over the years other studies have attempted to test whether oral arginine is an effective GH releaser. No one questions the effectiveness of infused arginine. The problem with oral arginine is that there are a number of formidable barriers to its absorption, starting with the liver enzyme arginase, which degrades it. Another involves methylated arginine by-products of protein digestion that are inactive analogs of arginine but inhibit genuine arginine functions, including the synthesis of nitric oxide.

   A few studies that concluded that oral arginine was ineffective for GH release suffered from flaws. One took only a single blood sample after an oral arginine dose, concluding that arginine showed no apparent GH release. Another was flawed because the researchers used too small a dose of arginine. The fear was that too large a dose would either be degraded in the liver or cause gastrointestinal distress. (Large doses of amino acids draw fluid into the intestine, which can result in nausea and vomiting.)

   One study, however, overcame most of the flaws of previous research and found some interesting results.1 Eight healthy men, aged 18 to 33, were examined on four separate occasions. The men reported to a lab after an overnight fast and were promptly fitted with a catheter in their forearm veins. Blood samples were taken every 10 minutes for five hours by the attending physician, Dr. Dracula (just kidding on that last one).

   A half hour after catheter insertion the men took doses of arginine in six ounces of water ranging from five to nine to 13 grams—or a placebo. Six drops of lemon juice disguised the considerable taste of the arginine (often described as being like dog vomit). The placebo had just the water and lemon juice.

   The five- and nine-gram doses resulted in greater GH release than the placebo, but the 13-gram dose didn’t increase the release beyond that. In fact, the larger dose led to gastrointestinal distress. The GH rise occurred 30 minutes after the subjects took the arginine, compared to 20 minutes after an IV infusion. GH peaked after an hour.

   Arginine primes the pituitary gland to induce the hypothalamus to release GH. It also suppresses the brain hormone somatostatin, which suppresses release of GH. Some scientists suggest that somatostatin release increases with age, explaining the drop in GH secretion that occurs in many older people.

   The study showed that nine grams of arginine produced a GH release 45 percent greater than the five-gram dose, but that was considered statistically insignificant. More important, however, it showed that the pituitary gland can respond to oral doses of arginine.

   The authors suggest that if you want a greater GH release during exercise, you should time your arginine dose with the start of your workout. Begin your workout 30 minutes after taking five to nine grams. They caution that some people don’t respond to any dose of arginine in relation to GH release. Taking a preworkout drink that contains protein or carb, which increases blood glucose, will likely blunt or prevent arginine-induced GH release. Keep in mind, too, that other amino acids compete with arginine for uptake into the body. So take arginine on an empty stomach.

1Collier, S.R., et al. Growth hormone responses to varying doses of oral arginine. Growth Horm IGF Res.2005;15:136-139


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

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

The folly of the HCG diet by Jerry Brainum

Back in 1954, British physician A.T.W Simeons proposed in a book entitled Pounds and Inches: A new Approach to obesity that a more efficient way to lose excess body fat involves administering injections of human chorionic gonadotropin (HCG). HCG is a glycoprotein hormone, composed of 244 amino acids attached to a sugar. It has two subunits, termed alpha and beta, with the alpha subunit being identical to luteinizing  hormone (LH), which is involved in pregnancy in women and control of testosterone synthesis in men.In fact, HCG is one of earliest hormones to rise during pregnancy, explaining why most over-the-counter pregnancy tests work by testing for the presence of HCG. During pregnancy, HCG helps to maintain the corpus luteum, which secretes progesterone required for pregnancy to continue.HCG also modifies immune response to protect against a woman's immune system rejecting the fetus. Morning sickness, an early indication of pregnancy is caused by the rise in HCG levels.
    The original drug forms of HCG, which are always injectable, were derived from pregnant women's urine. Typical names of such drugs were Pregnyl and Profasi. A newer form is made through recombinant DNA technology and is sold under the trade name "Ovidrel." Dr.Simeons came up with his HCG weight loss idea after treating young boys afflicted with Frolich's Syndrome, which is caused by damage to the hypothalamus in the brain. Among the symptoms of the disorder are obesity. Simeons found that providing HCG to the boys led to a rapid loss of body fat. Based on this, he believed that HCG would promote rapid fat loss. But to ensure the success of his new treatment, Simeons also prescribed a 500 calorie a day diet plan (see below). While anyone would lose weight eating only 500 calories a day, which is starvation level, the key to Simeons plan was the HCG. Simeons believed that HCG used with the diet not only resulted in a rapid loss of fat( 1-2 pounds a day!) but led to other beneficial effects, including a lack of feeling weak or hungry despite the low caloric intake. In contrast, the usual minimal recommended number of daily calories when dieting for fat loss purposes is 1,500 for men and 1,200 for women.
    Over the years, several studies have examined the HCG plan, and all have concluded that HCG has no advantages over a placebo, and it's only the 500 calories a day that leads to fat loss on the plan. This body of research includes 14 randomized, controlled studies in which HCG has been compared to a placebo (saline or salt water injections), which found no difference in relation to promoting fat loss. The studies have included over 600 patients.While that should have ended the HCG controversy, the idea of using HCG was resurrected with the publication of a 2007 book by Kevin Trudeau. In the book, Trudeau claims that the diet is safe and effective, but that doctors didn't want to let the public know "the truth about HCG." Trudeau's claims were bolstered by Dr.Oz, an  actual physician, on his TV show. Once again, the HCG diet rose in popularity.
     The amount of HCG suggested on the diet is 125 to 150 units daily. As noted, this must be injected and all Internet "HCG supplements" that involve oral intake are an outright fraud. But what isn't publicized is the possible adverse effects from using HCG. In men, HCG, because of its structural similarity to LH, promotes testosterone synthesis. HCG is, in fact, four-times more potent in this regard compared to LH itself. Bodybuilders often use HCG at the end of a steroid cycle to kick-start a lagging endogenous testosterone synthesis in the body that has become blunted by the use of anabolic steroid regimes. In a 2000 study of 40 men over age 60, three months of HCG at a dose of 5000 units, twice weekly resulted in an increase in lean body mass coupled with a significant loss of fat. But the men also showed no increase in strength. Both testosterone and estrogen levels rose by 150% in the men on HCG. Many bodybuilders are not aware that HCG besides boosting testosterone levels, also increases estrogen, too. The men in the study also showed decreased testicular volume. Taking too high a dose of HCG or using it  for too long a time actually has a paradoxical effect in shutting down testosterone due to a reverse feedback loop to the pituitary gland in the brain. This is caused by both elevated estrogen levels produced by the HCG, as well as from the constant bombardment of the Leydig cells of the testes, where testosterone is produced by HCG, which acts like LH. But since LH is normally released in pulsitile fashion, or intermittently, the Leydig cells become paradoxically insensitive to the effects of LH/HCG, so less testosterone is synthesized. Estrogen, however, continues to be produced, setting up possible estrogenic side effects, including water retention and gynecomastia or male breast formation.In addition, a recent study showed that large doses of HCG--meaning any dose higher than 350 units--induces a large degree of oxidation in the Leydig cells, leading to cell death. What this means in practical terms is that using large doses of HCG for more than 4 weeks will result in paradoxical destruction of Leydig cells and an accompanying lowering of testosterone production. A large amount of oxidation in the Leydig cells causes the cells to kill themselves, a process called apoptosis. This explains the lowering of testosterone, since testosterone is produced in the Leydig cells of the testes. The high degree of oxidation is caused by depletion of cellular glutathione, a major antioxidant in the body, and studies have shown that the suicidal oxidative effect of HCG on the Leydig cells can be blocked by ingesting N-acetyl cysteine (NAC) at least twice weekly.NAC works because it's a direct nutrient precursor of glutathione.
      In recent years, direct HCG cell receptors have been found at various sites in the body. What this means is that if you take a drug form of HCG, you will stimulate these receptors. Some of them are in the lining of a woman's uterus, called the endometrium. Overstimulating the endometrium results in endometriosis, a painful disease involving ectopic uterine tissue that responds to monthly hormonal changes in women. Or it could lead to a fibroid tumor forming in the uterus, called a leiomyoma. HCG receptors also exist in the prostate gland, with the implication that using HCG injections can lead to prostate gland enlargement or even prostate cancer.One study linked HCG to gynecomastia or male breast formation and male breast cancer.
      The only thing that isn't explained about the HCG diet  are the reports of those who've used the diet and claimed that they weren't hungry. On a 500 calorie a day diet, most people would be ravenously hungry. The lack of appetite could result from a rapid downgrade in resting metabolic rate. This would also explain the frequent observation that any weight lost while on the HCG plan more often than not is rapidly regained soon after the diet ends.There is also likely a placebo effect involved, which involves having so much faith in the "power"of HCG that dieters talk themselves in believing that they aren't hungry. Another overlooked problem of the HCG diet is the fact that it's impossible to get all required nutrients while consuming only 500 calories a day. Not to mention protein. The lack of protein will lead to catabolic muscle loss, which probably accounts for over half the weight loss seen with HCG diet plans, as well as loss of skin elasticity and hair.

Breakfast:	Tea or coffee in any quantity without sugar. Only one tablespoonful of milk allowed in 24 hours. Saccharin or Stevia may be used.
Lunch:	1.    100 grams of veal, beef, chicken breast, fresh white fish, lobster, crab, or shrimp. All visible fat must be carefully removed before cooking, and the meat must be weighed raw. It must be boiled or grilled without additional fat. Salmon, eel, tuna, herring, dried or pickled fish are not allowed. The chicken breast must be removed from the bird. 2.    One type of vegetable only to be chosen from the following: spinach, chard, chicory, beet-greens, green salad, tomatoes, celery, fennel, onions, red radishes, cucumbers, asparagus, cabbage. 3.    One breadstick (grissino) or one Melba toast. 4.    An apple, orange, or a handful of strawberries or one-half grapefruit.
Dinner :	The same four choices as lunch (above.) ©,2011 Jerry Brainum.Any reprinting in any type of media, including electronic and foreign is expressly prohibited. See Jerry's book at http://www.jerrybrainum.com/

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

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

Kelp: Anti-Estrogen Help? by Jerry Brainum

Competitive bodybuilders—especially male bodybuilders—consider excess estrogen a problem. Among its effects in men is gynecomastia, which is the development of excessive glandular tissue in breasts—make that pecs. It may be responsible for water retention and increased fat deposits under the skin, which obscure muscular definition, especially in the lower body, according to some bodybuilders.


   Hardcore female bodybuilding competitors also consider estrogen a problem. Women have a harder time producing extreme muscular definition in their legs for two reasons. One is that female fat cells in the lower body are marked by a preponderance of alpha-adrenergic receptors. Unlike beta-adrenergic receptors, alpha receptors resist the signals that call for fat mobilization. Some speculate that it has to do with human evolution, since successful pregnancy requires a certain number of calories, and nature locks them into a woman’s lower body.

   The second reason women experience problems in reducing lower-body fat and producing a highly defined appearance is their naturally higher estrogen levels. Estrogen works with the alpha-adrenergic receptors to make fat cells slow to release fat. It promotes processes that result in increased fat deposits in the female body, particularly the thighs, hips and buttocks.

   Elevated estrogen levels aren’t natural in male bodybuilders; however, estrogen could rise naturally through the activity of aromatase, a ubiquitous enzyme that converts androgens, such as testosterone, into estrogen. One-third of women’s entire estrogen production stems from the action of aromatase on adrenal and ovarian androgens. Aromatase is particularly active in peripheral fat stores, such as the ones in the legs. So a man carrying excess fat in his legs would likely produce higher levels of estrogen than a leaner man.

   But estrogen levels don’t usually get high enough to cause distinct estrogen-related problems, such as gyno. For that to occur, they have to be comparable to or higher than what an average woman generates. In reality, that happens either under pathological conditions or through the use of anabolic steroid drugs, such as testosterone injections, that aromatize. Other drugs can also cause gyno, including growth hormone when used by older men.

   While excess estrogen used to be a significant problem for drug-using athletes, the advent of anti-estrogen drugs has considerably blunted the problem. Since gynecomastia is still evident on some bodybuilders, they either aren’t taking pharmacological steps to inhibit estrogen production or are using drugs such as human chorionic gonadotropin, a.k.a. HCG, which increases both testosterone and estrogen production.

   Some drugs, such as Nolvadex, keep estrogen from binding to its cellular receptors. While effective, Nolvadex brings problems of its own. Structurally similar to estrogen, which likely explains why it can bind to estrogen receptors, it can induce paradoxical estrogenic effects if taken too long or in too high a dose. In addition, Nolvadex inhibits two enzymes that the testes require for the synthesis of testosterone.

   The current drugs of choice take a more direct approach by stopping the source of excess estrogen itself—the aromatase enzyme. They’re sold under various trade names, such as Arimidex, Aromasin and Farestan. They all short-circuit the activity of aromatase, and they’re all expensive. They were designed to treat breast cancer in older women whose cancers don’t respond to the older drugs, such as Nolvadex.

   Some natural anti-estrogens exist. Soy, like Nolvadex, is molecularly similar to estrogen and can interfere with its actions. High intakes of soy are thought to explain the lower incidence of estrogen-related cancers that occur in Asian than in Western women. Soy, however, presents problems for men; above a certain level it acts like an estrogen in them.

   Other natural substances inhibit aromatase. An example is green tea, but the activity is weak, not comparable to the anti-aromatase drugs by any standard. Brown kelp, however, is another matter.1

Kelp was a popular supplement among bodybuilders around the time Arnold was king of the posing platform. The idea was that it helped increase muscular definition by stimulating the thyroid gland. Kelp, or seaweed, is rich in the trace mineral iodine, which makes up two-thirds of thyroid hormone. What bodybuilders at the time didn’t realize was that kelp was also loaded with sodium, a mineral known for its water-retaining property.


   As for thyroid stimulation, a deficiency of iodine can impair thyroid activity, but too much can do the same thing. Since kelp was thought to be a natural, innocuous substance, it wasn’t unusual for bodybuilders to pop as many as 30 to 50 tablets a day, which may have had the paradoxical effect of inhibiting thyroid hormone synthesis.

   Where estrogen is concerned, kelp has promise. In fact, some scientists now think that it wasn’t the soy that prevented all those cancers in Asian women; it may have been their high kelp intake.

   A recent study examined the effects of kelp in both rats and isolated human cells derived from female ovaries. Giving rats kelp led to an 18 to 33 percent reduction in circulating levels of 17-beta estradiol, the most potent form of estrogen. The amount of kelp they got was comparable to the daily human intake in Asian populations. In the human cells, kelp resulted in a 23 to 35 percent reduction in active estrogen. The experimenters think that kelp may either directly inhibit estrogen production or enhance its rapid metabolic breakdown. Kelp showed no effects on aromatase.

   The researchers also found that kelp binds to estrogen cell receptors much in the manner of Nolvadex. The question that remains is what in kelp is responsible for what looks like anti-estrogen activity.

   Several constituents of kelp are candidates: bioactive polyphenols, which have potent antioxidant activity; sulfated polysaccharides, a combination of sulfur and sugar; and substances called fucosterols. As a practical matter, depending on kelp to neutralize the effects of drug-related high estrogen levels would be foolish. From a health perspective, however, the effects are worth a look.

The Arginine-Testosterone Connection

Although it’s considered a conditionally essential amino acid, arginine has always been a popular supplement among bodybuilders and other athletes. That’s because it was considered a potent promoter of growth hormone release, a notion based on provocative use of arginine to cause release of GH from the pituitary gland in the brain. The problem was that the effect required average arginine infusions of 30 grams, a level that, taken orally, usually led to nausea and vomiting. Taking too much at one time also activated arginase, a liver enzyme that rapidly degraded it.

   Recently, forms of arginine have enjoyed a resurgence as active constituents of nitric oxide food supplements. Nitric oxide is a natural body chemical—a free radical, in fact. It has many functions in the body, its most familiar being to dilate blood vessels. The rapid widening of blood vessels induced by nitric oxide fosters an exorbitant muscle pump, and as the Governator noted in the film “Pumping Iron,” the pump is where it’s at in bodybuilding.

   Arginine is the direct precursor of nitric oxide synthesis in the body. No arginine, no nitric oxide. It’s also involved in other important body functions. It’s required for synthesis of growth-promoting compounds called polyamines and is the primary amino acid precursor of creatine synthesis in the body.

   Perhaps its least known property is its effect on testosterone. A recent study using rats as subjects focused on the not so apparent metabolic partnership between arginine and testosterone.2 A key finding was that testosterone was required for the production of enzymes that regulate kidney function. When arginine was omitted from the rats’ diets, the anabolic activity of testosterone in their bodies significantly declined. The effect was noted in the animals’ kidneys and muscles.

The authors aren’t sure of the precise connection between arginine and testosterone, but they think it’s related to the protein-binding property of insulinlike growth factor 1. They observed that when arginine is deficient in the body, IGF-1 production is blunted in the kidneys and liver. Previous studies have showed that testosterone and IGF-1 have an anabolic partnership in muscle, and this study’s authors suggest that supplementing with arginine may improve the anabolic results of testosterone. If the rat-based findings hold true for human subjects, it could cast a whole new light on arginine.


 Another designer Steroid Emerges



The World Anti-Doping Agency recently announced the seizure of a mysterious-looking vial from a car traveling from Montana across the Canadian border. While the incident occurred in December 2003, the results of an analysis of the vial’s contents were just announced. Ostensibly, WADA held back the information until the drug could be identified and a drug test instituted.

   The vial contained a designer steroid, so designated because it had never appeared on the commercial market and was likely conjured by a renegade chemist somewhere. But WADA officials also said that unlike THG, the notorious designer steroid from the Balco drug scandal, the new drug is more sophisticated.

   It was called desoxy-methyl-testosterone, or DMT. According to the Canadian lab that identified and developed a test for the drug, it hasn’t yet found its way into professional sports, perhaps because it contains markers that would show up in a normal anabolic drug screen. Which makes you wonder just how sophisticated the drug actually is.

   The drug bust was the result of an “anonymous tipster,” according to WADA, as was the discovery of THG. The fact that DMT hasn’t yet reached any market and contains elements that would arouse suspicion during a plain-wrap drug test makes you wonder about the legitimacy of the bust. The entire episode may in fact be a ruse, intended to warn renegade chemists and dastardly purveyors of designer steroids that the intrepid WADA enforcement apparatus is on the job.
      DMT eventually did find its way into a number of OTC "pro hormone" supplements. I used one myself, not being aware at the time that the supplement contained the notorious DMT designer steroid, since the label didn't reflect this extra added ingredient. I must admit that the "supplement" worked spectacularly: Both my strength and muscle size increased significantly, and I also lost enough bodyfat to reveal a set of abs that had been on sabbatical for years. That's the good part. The bad part is that when I had my testosterone level tested, I showed a level of 90. Clinical hypogonadism starts at a level of 250. I had a testosterone level less than that of a young girl, according to the test. Actually, what was happening was that the designer steroid that I was unknowingly using had completely suppressed my endogenous or natural testosterone production. The most curious aspect of this episode was that while a Kaiser doctor called me to warn me of my "very low testosterone" level, he also refused to prescribe any testosterone replacement therapy, noting that "testosterone causes prostate cancer." He was a clear example of how you can acquire an advanced education and still be an abject moron.
     The same source that provided the DMT-laced supplement also provided another supplement that I was told would help me to both lose excess bodyfat, as well as build muscle. Once again, this product contained an unlisted anabolic steroid that I wasn't aware was in it at the time I used it. This product contained an old, discarded steroid that was developed in the early 60s. It was never released to the market, likley because of excess toxicity, especially in the liver. This supplement, which went by the name "Jungle Warfare" was later analyzed by German scientists, and found to contain delta-6-methyltestosterone, the old steroid. It contained 12 milligrams per capsule, and later versions of the product didn't contain the unlisted steroid. Similarly to the DMT supplement, I made considerable muscle gains on this stuff, and did lose fat in my abdominal area with no change in exercise or diet. It also raised my liver enzymes to astronomical levels, which led one doctor to suggest a liver biopsy. But I got off the supplement, and my liver enzymes reverted to normal levels.My feelings about this idea of adding surreptitious anabolic steroids without full disclosure is that it borders on criminal behavior. It certainly is unethical.

References

1 Skibola, C., et al. (2005). Brown kelp modulates endocrine hormones in female Sprague-Dawley rats and in human luteinized granulosa cells. J Nutr. 135:296-300.

2 Cremades, A., et al. (2004). Influence of dietary arginine on the anabolic effects of androgens. J Endocrino. 183:343-351.

 

                                       Applied Metabolics Newsletter 

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

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

 

Guzzling Drinks and Bar Hopping by Jerry Brainum

The glycemic index, or G.I., is a method of predicting how soon the sugar in food will enter the bloodstream. Glucose, the only type of sugar that circulates in the blood, is assigned a value of 100. The higher the glycemic-index number, the faster the food enters the blood.


The system was initially designed for diabetics, since the rapidity of carbohydrate entrance into the blood is critical for insulin use or any other medication designed to control elevated blood glucose. Eventually, the G.I. was used to determine the different metabolic effects of various carb foods.

The idea is that foods with higher G.I. numbers enter the blood faster and, by doing so, provoke a greater release of insulin. In someone who’s not diabetic, excess insulin can be a problem because it tends to promote and perpetuate bodyfat stores. Insulin blunts the body’s fat-mobilization and oxidation processes.

Expert consensus is that carbohydrate foods promote the greatest release of insulin, particularly so-called high-glycemic-index foods, or simple sugars. Protein is supposed to incur a minimal insulin release, since it doesn’t have much effect in increasing blood glucose levels. That’s the cornerstone of most high-protein, low-carb diets: the idea that by limiting carb intake you can control insulin and burn fat more efficiently. The high-protein intake inhibits appetite and conserves lean body mass—mainly muscle—that might be catabolized during low-calorie or low-carb diets.

Many energy bars and drinks have a high-protein, low-carb formula. The idea is that carbs promote an insulin release that rapidly lowers blood glucose, and prior to training that may result in hypoglycemia, or low blood sugar, or lead to premature exhaustion of limited muscle glycogen reserves, which are needed to power bodybuilding workouts.

A recent study that compared the glycemic effects of sugars and proteins came up with some paradoxical findings.1 Twelve healthy men, none of whom lifted weights or did any other type of exercise, got a 50-gram glucose drink, a white-flour bagel (high-G.I. food), peanuts (low-G.I. food), a protein bar containing 29 grams of protein and three grams of carbs or a protein drink containing 30 grams of protein and eight grams of carbs. The men then lay down, and the scientists drew their blood every 10 minutes for two hours to measure their glycemic responses to the foods.

The glucose drink, the protein bar and the protein drink elevated plasma insulin levels above baseline, or resting, levels starting at 10 minutes and lasting through 60 minutes. The bagel, a high-G.I. food, elevated insulin levels above baseline from 30 to 75 minutes. No change in insulin levels occurred in those who ate the peanuts. All the participants’ insulin levels returned to baseline by the 90-minute mark.

When insulin levels rise at the start of exercise, there’s a huge increase in muscle glucose uptake, a result of the interaction between insulin and the increase in muscle glucose transporter, or GLUT-4, that’s caused by the muscle contraction. The net effect is a drop in blood glucose levels so dramatic in some people that they nearly become hypoglycemic when they start exercise. For many the start of exercise releases catecholamines, such as epinephrine, which lower blood glucose levels and break down the liver glycogen that releases glucose into the blood. In low-carb dieters, liver glycogen may already be low. Result: premature fatigue during training.

The study highlights a few overlooked facts. The high-protein, low-carb diets that are supposed to work by limiting insulin release don’t work as advertised. That doesn’t mean low-carb plans don’t work, just that their insulin effect is overplayed. Certain amino acids are nearly as potent as sugar in promoting insulin release. That makes sense, since insulin is known to promote the entry of amino acids into muscle, an anabolic effect. In fact, insulin is only anabolic in the presence of a high blood amino acid level. The difference between carbs and protein is that carbs, especially the simple, or high-G.I., carbs, will promote an increase in blood glucose, and a protein meal doesn’t. Simple carbs and protein, however, have similar effects on insulin.

In practical terms, that means drinking a high-protein, low-carb shake prior to training may not be a good idea for many people. As the study shows, the high protein content will promote a considerable insulin release, which may cause low blood glucose at the start of exercise—not good for high-energy training.


Is there a solution? Eat protein with carbs, particularly low-G.I. carbs. Adding some form of soluble fiber, such as psyllium or guargum, to the drink, will slow the entry of nutrients into the blood. Of course, you may also increase your production of intestinal gas, which can be either an advantage or a disadvantage, depending on how crowded the gym is that day. The most practical option is simply to add an essential fat source, such as flaxseed oil, to the drink. That, too, will considerably lower the G.I. and insulin-releasing effect while providing some important essential fats.

One note here: Don’t add fish oil. By far the best source of the important omega-3 fatty acids, fish oil also blocks the synthesis of an important substance called prostaglandin F2A, which has anabolic effects in muscle. Aspirin and other over-the-counter pain relievers do the same thing and can inhibit muscle gains.


1 Parcell, A.C., et al. (2004). Glycemic and insulinemic responses to protein supplements. J Am Diet Assoc. 104:1800-1804.


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

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

Growth Hormone K.O by Jerry Brainum

Boxing is undeniably brutal—the goal is to knock out your opponent, the sooner the better. Films and novels have depicted the sad postboxing lives of many fighters. Some of the greatest champions of the ring have ended up broke and in poor health, despite having earned millions in their prime. It doesn’t happen only to the pugs without a punch, either.


Sugar Ray Robinson held the middleweight title of the world five times and won the welterweight title once. Considered by most boxing experts the best pound-for-pound fighter ever, Robinson was untouchable in his younger days. His punches came fast and hard, and by the time his opponent realized what hit him, Sugar Ray had danced away, often leaving his opponent lying on his back.

Financial pressures, however, made Sugar Ray stay in the ring too long. He was still fighting at 40 and began to lose to men who wouldn’t have lasted three rounds with him in his younger days. Ray took a lot of punches in those last fights, and the resulting head trauma may have contributed to the severe case of Alzheimer’s disease that eventually caused his death.

A more recent example of the effect boxing can have on the brain is Muhammad Ali, who may be the greatest heavyweight champion ever and who was voted second to Robinson in an Associated Press poll of the greatest boxers of the 20th century. Ali doesn’t have Alzheimer’s, but it’s clear from his slurred speech and slow gait that the once lightning-fast fighter is suffering. In his case it’s Parkinson’s; the brain cells that produce the neurotransmitter dopamine have been severely damaged.

Ali was born with an abnormally small substantia nigra, the area of the brain where dopamine is produced, and that area seems to have been selectively damaged by blows to the head. Of course, Ali didn’t realize that, and it certainly didn’t affect his earlier boxing skills. Like Robinson, however, Ali fought past his prime and consequently took many head punches that would never have landed in his younger days.

Traumatic brain injury (TBI) can lead to severe damage to the pituitary gland. Located just behind the nose in the brain, the gland produces many vital hormones, including growth hormone, thyroid-stimulating hormone and gonadotropins such as luteinizing hormone, which controls testosterone synthesis.

Statistics show that more than 1.5 million Americans have suffered some form of TBI. Often it’s the result of head trauma, as from a violent car accident, but anything that violently hits the head can lead to TBI. About 40 percent of patients with moderate or severe head injury show damage to the pituitary gland. The hormones most affected by TBI are growth hormone and gonadotropins, the two primary anabolic hormones in the pituitary.

In some cases the damage is caused by direct injury to the pituitary gland. Or the damage may ensue from vascular injury, which limits blood flow to the gland, leading to the death of cells. A common cause of TBI is a concussion, an injury to the brain that often involves a temporary loss of consciousness and that has occurred in 40 percent of people diagnosed with TBI. The injury is common in contact sports, such as boxing, football and ice hockey. In fact, a boxer’s primary objective is to induce a concussion, which usually means knocking out the opponent.

No boxer walks away from the sport without suffering some form of brain injury. While a series of knockouts results in the greatest degree of brain damage, even being hit in the head repeatedly causes a shearing effect in the brain—because brain tissue is thrust violently against the skull—leading to an actual loss of brain cells. The cumulative effect can be devastating and may take years to show up. Early symptoms include slurred speech and slowed movement.

   The worst aftermath of being hit in the head repeatedly, as in boxing, is a type of dementia that looks like Alzheimer’s disease: pugilistica dementia. Jerry Quarry, a great heavyweight of the ’70s who fought Ali, died from it, as have countless other fighters.

All fighters know the risk of brain damage, and most try to end their ring careers before they lose their marbles. But a lesser known consequence of years spent in the ring has recently been recognized. Since boxing is a definite risk activity for the development of TBI and since TBI is known to lead to damage in the pituitary gland, researchers tested 11 recently retired or still competing boxers to check their growth hormone levels.1


None of the boxers could be considered bums, since all were current or former world champions. Their average age was 38, with an age range of 18 to 55. None reported any serious illness, and none were taking any type of medication. But seven of the fighters complained of memory impairment, while another four complained about fatigue. None showed any symptoms that would suggest pituitary gland problems, such as a tendency to sleep, cold intolerance, low blood pressure, low blood glucose levels, reduced body hair, decreased sex drive, excessive urination and thirst.

Even so, 45.4 percent of the subjects had a growth hormone deficiency—rare in men that young. In another 36.4 percent the status of their growth hormone release was uncertain. Based on that finding, the authors suggest that GH deficiency is probably a common occurrence in boxers at all levels and occurs at a significantly younger age than it normally does.

Many readers are probably thinking that while this information is interesting (or maybe not), it doesn’t apply to them since they aren’t boxers. But consider the fact that any type of concussion, which always involves some brain injury, can damage the pituitary gland and result in a permanent loss of GH release. That could happen to an 18-year-old engaged in some form of martial arts, where head trauma results in a knockout. Or a car accident in which you get knocked out. That can injure the brain enough to cause pituitary trauma, either as a result of direct injury to the gland or through damage to the blood vessels that serve it.

Another aspect to consider is that the product of growth hormone, insulinlike growth hormone 1 (IGF-1), is known to be vital for the maintenance of neurons, the functioning cells of the brain. Recent studies show that GH itself exerts a protective effect on brain cells. A lack of adequate GH may promote brain degeneration.


Restoring Growth Hormone:


A New Method?

Growth hormone and IGF-1, which is stimulated by GH, drop about 14 percent with each decade of life. By age 60 many people are deficient in GH, a condition that’s called “somatopause.” Changes in the body that occur with a GH deficiency are typical of the physical decline associated with aging. They include a reduction in skeletal muscle mass and strength; increased bodyfat, especially in the abdominal area; an increase in low-density-lipoprotein cholesterol, which is the type most linked to cardiovascular disease; impaired blood clotting, which also predisposes them to heart attacks and strokes; increased blood pressure; reduced heart power; lowered immune response; and lower bone mass.

A lack of GH and IGF-1 is also associated with mental decline, including the loss of memory common with age. IGF-1 is involved in maintaining energy processes in the brain, the formation of new neurons, nerve stimulation reactions and other vital brain functions. Without GH and IGF-1 a toxic metabolite of the essential amino acid methionine, homocysteine, increases in the brain, resulting in further degenerative changes.

Knowledge that those adverse effects are linked to a deficiency of GH and IGF-1 has led to the concept of GH therapy. As a peptide hormone, GH must be injected. Another possible alternative treatment features the use of growth hormone secretagogues. When GH-replacement therapies are provided to people deficient in the hormone, the effects of GH deficiency diminish.

Providing GH therapy presents some formidable problems, however, starting with its high cost—potentially thousands of dollars. Since it’s not an officially accepted form of therapy, it isn’t covered by medical insurance. Side effects are also common, most often with higher-than-normal physiological replacement dosages: edema, or water retention, muscle pain and carpal tunnel syndrome, which pinches nerves in the wrists and hands. In addition, the long-term life-extension effects of GH remain speculative at best. Some scientists even suggest that long-term use of GH may shorten life span, though the evidence for that is sparse.

The reason GH declines with age has to do with the two hormones that control its release in the brain, growth-hormone-releasing hormone and somatostatin. GHRH promotes GH release, while somatostatin blocks it. With age somatostatin becomes dominant. The pituitary gland still continues to synthesize GH and exhibits no defects unless affected by trauma. That explains why drugs such as GH secretagogues work in older people; they bypass somatostatin.


GH release is also affected by brain neurotransmitters, which are the chemicals that regulate nerve impulses in the brain. One neurotransmitter linked to GH release is acetylcholine, which is also linked to memory and learning functions. In Alzheimer’s disease, nerve cells that synthesize acetylcholine are destroyed, which results in the intellectual deficit characteristic of Alzheimer’s disease.

The present medical treatment of Alzheimer’s involves drugs that inhibit the primary enzyme that degrades acetylcholine in the brain. But since acetylcholine also promotes GH release, a group of researchers looked at whether the same drugs used to treat AD could also promote GH release.2

For eight weeks 24 older men were put on either a placebo or the drug donepezil, trade name Aricept, which is used to treat Alzheimer’s disease. They took a five-milligram dose for the first four weeks, 10 milligrams for the second.

There was a 53-percent increase in GH and a 31 percent increase in IGF-1 in the drug group. That change equals a shift to hormone levels typically seen in men 20 years younger, or about age 40. Still unclear is whether that level of GH increase would reverse some the negative effects seen with a GH deficiency. If this drug does work, it would dramatically reduce the current cost of GH therapy and also produce little or no side effects.

One point to consider is that the drug therapy would be useful only for those with a full-blown GH deficiency. For all others, using it would have little or no effect on GH release.


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

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

Growth Factors and Muscle Subtractors : Myostatin, IGF-1 and your workouts by Jerry Brainum

Myostatin, a protein discovered by scientists at Johns Hopkins Medical School in 1997, prevents muscular growth. It also works in concert with cortisol and thyroid hormones to increase muscle catabolism, or the breakdown of muscular tissue. Insulinlike growth factor 1 (IGF-1), so named because it has a structure similar to that of insulin, provides potent anabolic effects in muscle, just as insulin does. A condition that favors a decrease in myostatin with an increase in IGF-1 should result in increased muscular growth—shouldn’t it?


   A recent study examined the relationship between myostatin, IGF-1 and muscular growth.1 The study featured two groups of men. Group one trained all the major muscles of the body, while group two trained only their biceps. The subjects trained twice a week for 10 weeks. The hypothesis was that training a larger percentage of muscles would lead to greater levels of growth-promoting hormones, in this case IGF-1. In light of recent studies examining the effect of weight training on myostatin, the authors figured that myostatin levels would decrease.

   Both programs led to significant increases in muscular growth of the biceps, but neither group showed any changes in IGF-1. The researchers were measuring systemic release of IGF-1, but it’s also produced locally in muscle, which appears to account for its anabolic effects in muscle. The fact that both groups showed significant decreases in myostatin levels underscores other findings indicating that weight training is an effective natural myostatin inhibitor. Interestingly, both groups—those doing the isolated biceps exercises and those training their entire bodies—had about the same decrease in systemic myostatin.

   Another study, involving rats as subjects, found that a high-protein diet leads to a greater production of myostatin.2 At the same time that myostatin is increasing, so is another factor, called myogenin, that would normally promote muscle growth. The increase in myostatin cancels the effects of myogenin. Does that mean that those who seek more muscle growth are working against themselves if they’re on a high-protein diet?

   Not at all. The increase in myostatin is only a small part of the picture. Other hormones also increase. Exercise generates localized production of IGF-1 in the muscle, which would cancel myostatin’s inhibition of muscular growth. In fact, protein is the primary nutrient that regulates IGF-1 production.

   Another study looked at two types of exercise to figure out which produced the greatest response of IGF-1 release.3 Twenty-four male subjects divided into two groups exercised three days a week for six weeks. The first group used pure strength training with maximum muscular contractions. The second used a combination program involving maximum contractions and ballistic and stretch exercises.

   Those in the strength-only group showed a 475 percent increase in IGF-1 mRNA, while those in the combo group showed a 135 percent increase. Since the combo group used lighter weights, this study shows that a primary impetus to increased IGF-1 release is exercising with heavier weights.


1 Walker, K.S., et al. (2004). Resistance training alters plasma myostatin but not IGF-1 in healthy men. Med Sci Sports Exerc. 36:787-93.

2 Koichi, N., et al. (2004). A high-protein diet stimulates myostatin mRNA expression in rat skeletal muscles. Med Sci Sports Exer. 36:S193-S194.

3 Necker, A., et al. (2004). IGF-1 responses in human muscle to strength training. Med Sci Sports Exerc. 36:S184.

 

Want more evidence-based information on exercise science, nutrition and food supplements, fat-loss,ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com.

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Grape Expectation: This Fruit Has Got It Going On! by Jerry Brainum

  A noted scientist once observed that humans don’t wear out—they rust out. What he meant was that many diseases, as well as the aging process itself, are likely related to out-of-control oxidation reactions in the body. No one argues about the necessity of oxygen for human life. Try breathing without it. Oxygen is necessary to power cellular processes involved in energy production, and without energy, you cannot live.


   The way the body uses oxygen isn’t a perfect process. In the course of it noxious by-products known as free radicals are unavoidably released. Free radicals go by different names, but they’re all unpaired electrons seeking to pair with other electrons. When a free radical finds paired electrons, it locks onto them, creating cellular havoc. Substances prone to oxidation are particularly effective at producing free radicals. Polyunsaturated fats, which play structural roles in various organs and tissues in the body, including cellular membranes and organs that are largely composed of fat, such as the brain, come under that heading. When attacked by free radicals, susceptible structures break down and fail. That, in turn, can lead to myriad diseases, including cardiovascular disease and cancer, the two primary killers.

   Luckily, nature and evolution have created a built-in defense system against free-radical cellular terrorism. It consists of various enzyme systems that neutralize free radicals, often by contributing an electron to stabilize the renegade free radical. Even so, free radicals are voracious in their appetite for pairing with another electron, and thousands of attacks occur at any time. It’s easy for the body to be overwhelmed.

   Once again, nature provides antidotes: dietary antioxidants. Vitamins C and E are the antioxidants familiar to most people, but many other nutrients provide potent protection, including the hundreds of flavonoid chemicals found in various fruits and vegetables. The frequent recommendation to eat at least five servings a day of fruits and vegetables is largely based on their fiber and antioxidant contents, which play definite roles in warding off degenerative diseases.

   The power of antioxidant protection is reflected in what’s known as the French paradox. Although the French habitually eat a considerable amount of saturated fat, the type of fat most linked to cardiovascular disease, they don’t have a high rate of that kind of health problem. Scientists who’ve studied the effect think that their fondness for drinking red wine with most meals is what enables the French to eat saturated fat with impunity.

   Red wine contains flavonoids called polyphenols. They’re potent antioxidants that can protect against cardiovascular disease with a number of mechanisms, including their ability to prevent the internal blood clotting that initiates most heart attacks. Polyphenols also stabilize low-density lipoprotein, the primary cholesterol carrier in the blood. That’s significant because LDL, which is known as the bad cholesterol, is dangerous mainly when oxidized.

   What if you just don’t want to drink wine? Can you get the benefits of its polyphenol content from any other source? A good candidate source is grape-seed extract, which also has powers above and beyond those found in a fine merlot.

Grape-Seed Power

   While common dietary antioxidants such as vitamins C and E do offer potent protective effects, they pale in comparison to grape-seed extract. Studies show that the active components of GSE are 20 times more potent than vitamin C and 50 times more potent than vitamin E in antioxidant activity. The functions of GSE, however, go beyond mere antioxidant protection. For example, it inhibits enzymes that promote the release of histamine from cellular mast cells. Histamine plays a dominant role in the symptoms associated with allergies and inflammation in the body.

   Another name for the active ingredients found in GSE is oligomeric proanthocyanidins. OPCs exist naturally in such fruits as apples, pears and grapes and in chocolate, red wine and tea. In supplement form they’re available as either grape-seed extract or an extract from pine bark known as pycnogenol, which is touted as being the superior source and usually costs nearly twice as much as grape-seed extract.

The truth, however, is that most of the research on the effects of OPCs used grape-seed extract. Even Jacques Masquelier, credited with discovering pycnogenol, says that grape-seed extract is superior. That’s because GSE contains gallic esters not found in pycnogenol that give it greater antioxidant activity. Similar to what happens with another popular antioxidant, lipoic acid, GSE works in both fat and water media, giving it a greater range of protection. In contrast, vitamin C works only in a water medium, while vitamin E functions only in a fat medium.


   Most of the studies showing a beneficial effect, however, were isolated-cell studies, also known as in-vitro, or test-tube, studies. That’s significant because flavonoids tend to be difficult for the human body to absorb. Studies tracking the fate of ingested grape-seed extract found that it was indeed difficult for the body to absorb the active ingredients, but about 25 percent was absorbed, and since they are potent antioxidants, it appears to be enough.

   As noted above, GSE neutralizes many of the problems that lead to cardiovascular disease, including the oxidation of LDL. It also protects vital organs, such as the liver and brain. The OPCs in grape-seed extract have a particular affinity for vascular and connective tissue. They inhibit enzymes that would otherwise degrade those tissues, and in doing so they maintain the integrity of various structural proteins of connective tissue and skin, such as collagen, elastin and hyaluronic acid. When those substances break down in the skin, visible signs of aging, such as wrinkles, appear. One study showed that a topical form of GSE offered protection against the oxidative damage caused by exposure to the sun.

   Pumping Up with GSE

   Nitric oxide has been getting extensive publicity lately. Various supplements have come on the market that increase the effect of nitric oxide synthesis. Among other functions, nitric oxide dilates blood vessels, which would increase the sensation of a muscular pump during training. GSE also increases nitric oxide synthesis, and it does so even more effectively than many of the high-priced supplements currently available. In addition, GSE stimulates vascular endothelial growth factor, which plays a role in wound healing.

   A recent study confirmed the effect of OPCs derived from pycnogenol in helping to alleviate impotence in men.1 The subjects took 120 milligrams a day of either pycnogenol or a placebo for three months in a double-blind protocol, meaning that neither the subjects nor the researchers knew who was taking what. After three months the men who got the pycnogenol showed significant improvement.

   The researchers attributed that result to pycnogenol’s ability to promote nitric oxide synthesis. Nitric oxide is required for the dilation of blood vessels that lead to an erection. Most of today’s so-called impotence drugs, such as Viagra, work through the same mechanism.

   GSE may aid workout recovery by decreasing various chemical initiators of inflammation in the body. Hard training leads to a localized inflammation in muscles, and muscles cannot fully recover until it’s doused. The inflammation is caused by a number of chemicals associated with immune function, such as cytokines, interleukins and tumor necrosis factor-alpha. By neutralizing their excess activity, GSE helps to heal muscle inflammation after intense training, thereby speeding recovery.

GSE: Immunity Booster

   GSE helps protect against various types of cancer. In isolated-cell studies it destroyed several types of cancers, such as those affecting the breasts, lungs and stomach. GSE also reduces the side effects of chemotherapy drugs, which are designed to destroy cancer cells by increasing free-radical production in tumors—an undesirable activity in normal cells. Other research shows that GSE inhibits the virus that causes AIDS, but, once again, the studies involved were test-tube studies.

   A recent study found that GSE may offer benefits in the treatment of advanced prostate cancer, the number-one killer of men.2 Many prostate tumors are initially androgen-sensitive; that is, their growth is stimulated by the presence of testosterone and other androgens. The treatment is to block androgen production, hoping the tumor will recede. In some cases, however, it returns, and this time it’s androgen-independent. Advanced prostate tumors like that are harder to treat and have a greater tendency to metastasize, or spread.

   In the new study GSE strongly inhibited advanced prostate tumors. The researchers believe it accomplished that through at least two mechanisms: It prevents the release of a chemical that enables tumors to spread in the body, and it increases a binding protein for IGF-1, which promotes tumor growth. As a result the tumor winds up killing itself, a process known as apoptosis.


Girlieman Terminator

   Another study found that substances in GSE can inhibit aromatase,3 the ubiquitous enzyme that converts androgens, such as testosterone, into estrogen. From a medical point of view, that means that GSE may help prevent estrogen-related cancer. Inhibiting aromatase in men leads to increased testosterone and lower estrogen—and lower estrogen equals less subcutaneous bodyfat, less water retention and less likelihood that excess-estrogen-related conditions, such as gynecomastia, or male breasts, will occur.

   GSE also exerts insulinlike activity in aiding glucose uptake into cells.4 It appears to lower elevated glucose levels, such as those that occur in people who have diabetes and those who use human growth hormone, as well as increasing the activity of cellular proteins that aid in getting glucose into cells, such as GLUT-4.

   Another interesting isolated-cell study found that a combination of aged garlic and pycnogenol caused a potent release of growth hormone.5 The study used skin cells that had been genetically engineered to react to substances touted as growth hormone releasers. The results showed that pycnogenol is about 1,000 times more potent in its ability to promote GH release than the other substances tested, including amino acids.

   Isolated-cell studies also show that both GSE and pycnogenol inhibit enzymes called lipases, which are required to absorb dietary fat.6,7 Orlistat, a drug that’s currently used to treat obesity, works in the same manner, with the result that about 30 percent less fat is absorbed during a meal. That means fewer fat calories taken in, possibly leading to fat losses.

Safety Issues

What about toxicity? Grape-seed extract is remarkably safe. It shows no mutagenic effects—i.e., links to tumor formation—and has no known interaction with drugs. It does, however, help prevent liver failure if someone takes too much acetaminophen (Tylenol). The best dosage for health effects is about one milligram per kilogram (2.2 pounds) of bodyweight. So someone weighing 200 pounds should take about 100 milligrams of GSE daily. Another method is to begin with a loading dose of 300 milligrams a day in divided doses for about a month, then switch to the one-milligram-per-kilogram-of-bodyweight maintenance dose.

References

1 Durackova, Z., et al. (2003). Lipid metabolism and erectile function improvement by pycnogenol extract from the bark of Pinus pinaster in patients suffering from erectile dysfunction—a pilot study. Nut Res. 23:1189-98.

2 Singh, R., et al. (2004). Grape-seed extract inhibits advanced human prostate tumor growth and angiogenesis and unregulated insulinlike growth factor binding protein-3. Int J Cancer. 108:733-40.

3 Eng, E.T., et al. (2003). Suppression of estrogen biosynthesis by procyanidin dimers in red wine and grape seeds. Cancer Res. 63:8516-22.

4 Pinent, M., et al. (2004). Grape-seed-derived procyanidins have an antihypoglycemic effect in streptozotocin-induced diabetic rats and insulinomemetic activity in insulin-sensitive cell lines. Endocrinology. In press.

5 Buz’Zard, A., et al. (2002). Kyolic and pycnogenol increase human growth hormone secretion in genetically engineered keratinocytes. Growth hormone and IGF-1 Research. 12:34-40.

6 Moreno, D.A., et al. (2003). Inhibitory effects of grape-seed extract on lipases. Nutrition. 19:876-79.

7 Hasegawa, N. (2000). Inhibition of lipogenesis by pycnogenol. Phytotherapy Res. 14:472-473.


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

Have you been ripped off by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com

 
 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

Can leucine spare muscle lost from aerobic training? by Jerry Brainum

Many bodybuilders fear doing aerobics because they think it will lead to a loss of hard-earned muscle mass. Looking at long distance runners, with their anorexic-appearing bodies, seems to confirm this notion. In addition, some studies that have involved human subjects have indeed found several catabolic processes at work with extended aerobic work. These studies show that doing excessive amounts of aerobics boosts levels of cortisol, the primary catabolic hormone in the body. As cortisol levels rise, testosterone levels tend to drop. Since testosterone helps to build and maintain muscle mass, it's not hard to understand why going overboard with aerobics can lead to muscle mass losses.
    But the key word here is "overboard." Cortisol levels don't begin to rise during aerobics until after about an hour of steady aerobics. If you do less than that in one session, the rise in cortisol is negligible. There is an exception to this, however. Those on either restricted low calorie diets, or diets very low in carbohydrate, would have a higher release of cortisol during aerobics because of the restricted energy intake features of both diets. In addition, just lifting weights also boosts cortisol, particularly near the end of the workout. This workout-induced rise in cortisol, however, tends to occur more in less experienced trainees. With training experience, the body tends to adapt to regular exercise, and as a result less cortisol is produced during and after the workout session.
     Another reason why there's a greater chance of losing muscle with aerobics is because muscle protein synthesis ceases during aerobics (and weight-training as well). The reason for this is that as far as the body is concerned, energy production is more vital than muscle protein synthesis. So the primary focus during exercise is maintaining energy to power the muscle activity. One way the body does this, besides cortisol release, is through the release of a protein called AMPK. AMPK functions as an energy sensor in muscle, and when levels of ATP decline in muscle, AMPK is secreted. Among other functions, AMPK promotes the use of fat as a fuel, which is a primary goal of aerobic exercise. But the other side of the coin is that AMPK also abruptly halts all protein synthesis. Since the body mantains a balance between anabolic and catabolic processes, if protein synthesis ceases during exercise, catabolic or breakdown processes begin to dominate.
     But there may be a easy nutritional antidote to this dilemma. A new study had 10 subjects who ingested a protein drink containing 10 grams of protein, with either 1.87 or 3.5 grams of added leucine during a cycling test. Leucine is one of three branched-chain amino acids, and is the amino acid most associated with increased muscle protein synthesis. It does this by promoting the activity of another protein called mTOR. Another group of subjects drank an essential amino acid drink with no added leucine. Those in the leucine group showed a 33% increase in muscle protein synthesis. The leucine group also showed less muscle protein breakdown during exercise. It's important to note that this effect is mainly associated with aerobic exercise of extended duration, not weight-training. But it also means that those who fear losing muscle from doing aerobics while in restricted calorie or carb diets can supplement with leucine prior to the aerobic session, and not only not lose any muscle, but actually boost muscle protein synthesis by a third.

Pasiakos, SM ,et al. Leucine-enriched essential amino acid supplementation during moderate  steady state exercise enhances leucine-enriched muscle protein synthesis, Am J Clin Nutr 2011;94:809-818.

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

Have you been ripped off by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com

 
 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

Are bodybuilders slowly killing themselves? By Jerry Brainum

Bodybuilding encompasses two divisions: those who compete in bodybuilding contests, and those who live weights recreationally. While not everyone who lifts weights aspires to be Mr or Ms. Olympia, I'd venture a guess that all who regularly go to a gym and heave iron want to look good and be healthy. Lifting weights offers a number of important health benefits, most of which have been recognized only recently. In the past, many health professionals took a dim view of weight-training. Lifting weights was said to be bad for the heart because it raised resting blood pressure. In fact, while blood pressure does go up temporarily when lifting, it rapidly returns to normal when the exercise ends. In fact, those who engage in weight-training regularly show lower blood pressure readings. Other studies show that lifting weights duplicates many of the favorable effects of aerobics on cardiovascular fitness, including lower blood lipids, lower blood pressure, and so on. Resistance exercise is particularly important as you age. Without exercise, muscle mass begins to degenerate at age 40, and you will lose strength each year. The body works on a "use it or lose it" principle, and when muscles aren't challenged with increased resistance, they will gradually atrophy. This loss of muscle is associated with loss of mobility and increased onset of cardiovascular disease and mental degeneration.
     So bodybuilding, with its emphasis on eating right and regular exercise, can be considered a healthy practice. But some alarming recent research suggests that while we are building up our muscles, we may also be short-circuiting our longevity. It's important to point out that at present, the evidence for this is mostly circumstantial. It comes from animal research, and much of it may not apply to humans. So what are the habits of bodybuilders that may lead to decreased longevity?
       The only tentatively accepted way to extend life is through calorie restriction. This entails lowering daily caloric intake about 30-40%. It appears to work in many animal species, but the evidence that it will extend life for humans is not definitive by any means. Still, based on the favorable animal studies, many humans have opted to use caloric restriction  (CR) regimes in the hope of extending their life. Initial studies of these human CR self-experiments show some favorable changes in their physiology. They show low body fat levels, low resting insulin and glucose levels, and lower blood pressure and blood lipids. But they are also constantly cold, have no energy, and are very hungry. It takes an enormous amount of willpower to adhere to typical CR regimes. Most CR diet plans emphasize fruits and vegetables because of their lower caloric density. These CR humans also have lower levels of testosterone, although their IGF-1 levels don't seem to be affected by their lack of calories. They also usually look quite gaunt, lacking any semblance of muscularity.
       In an effort to gain muscle, many bodybuilders still resort to the old "bulking up" technique, involving a high intake of calories. If the CR theory is true, then eating in this manner for extended times will take a toll on future longevity. On the other hand, the dieting phases of bodybuilding fit right in with CR theories. It's all a bit moot, since longevity scientists have calculated that CR is most effective when begun at birth! If you start a strict CR regime at age 48, and stay on it the rest of your life, you will extend your life by 2.8 years. That's a weak trade for years of being tired, hungry, weak, and yes, small.
       Other animal studies show that restricting protein intake will extend life. Of course, eating a high protein diet is a staple of any bodybuilding nutrition program, since protein is the key for promoting muscle protein synthesis. In fact, it isn't protein that is the problem. The animal studies show that eliminating only one amino acid--methionine-- extend animal longevity by about 15%. But methionine is an essential amino acid, which means that it's a required nutrient. Completely eliminating it from a diet can spell trouble for humans.
     Speaking of muscle protein synthesis, a key player in that process is a protein known as mTOR. Branched-chain amino acids, especially leucine, are known to promote mTOR activity, and by doing so,they upgrade MPS. But mTOR also plays a role in accelerating aging and even promoting the spread of cancers in the body. The good news is that mTOR can be controlled by promoting the release of another protein that opposes its actions: AMPK. You raise AMPK when you do aerobics, and using drugs such as metformin also boost AMPK. While AMPK blocks MPS through its interference with mTOR, it also boosts fat oxidation in muscle. A number of natural substances also boost AMPK, including  resveratrol, caffeine, chromium, cinnamon, CLA, creatine, curcurmin, DHA from fish oil, garlic, and grape seed extract. Including some of these in the diet should offset the negative effects of mTOR without interfering with the MPS effects.
    Bodybuilders often purposely raise their insulin levels, such as following a workout by consuming a simple carb and protein drink. Boosting insulin after the workout aids recovery by promoting amino acid uptake into muscle and also increasing the activity of the enzyme that synthesizes glycogen. Other bodybuilders inject insulin as an anabolic drug. The problem here is that lower insulin levels are associated with life extension. Studies of people who have lived to 100 or more show that such people always have both low resting insulin levels, as well as lower blood glucose levels. They also usually show lower levels of insulinlike growth factor-1 (IGF-1). IGF-1 is produced in the liver as a result of growth hormone release. It's also produced directly in muscle after exercise, where it exerts potent anabolic effects. Animals that lack receptors for IGF-1 live longer lives than normal animals. On the other hand, a lack of IGF-1 in human studies has shown an increase in mortality. Among other functions, IGF-1 helps to maintain both heart and brain cells. Growth hormone itself lowers oxidation at normal levels, but raises it when taken in larger doses, as is the practice of some competitive bodybuilders.
     Then there is the resting metabolic rate. Some of the longest lived animals on Earth show low resting metabolic rates. These include certain mollusks known to live over 450 years, as well as tortoises that live to over 200. But other long-lived animals, such as bats and birds, have very high metabolic rates. Bodybuilders use supplements that boost metabolism for purposes of losing bodyfat, and some also use thyroid drugs for the same reason. Whether habitually boosting resting metabolic rate will limit longevity is anyone's guess.
      When you add it all up the choice is clear: you can eat less protein, less calories and walk around small, weak, but healthy. Or you can continue the "risky" bodybuilding practices and look big, healthy and feel great. You may not live as long, but you'll get a lot more life out of those years compared to the pathetic CR cultists who are living on lettuce.


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

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The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

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Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 
This is a photo of Lisa Walford, who has been a CR advocate for many years. She is 50 years old in this photo.