Last night, I watched an interesting documentary produced by the BBC called” Don’t Grow Old.” As the title implies, this program focused on various ways to slow the aging process. Among the topics discussed was using various supplements, such as resveratrol to slow aging. A leading resveratrol researcher, David Sinclair from Harvard, mentioned that resveratrol appeared to duplicate many of the effects of the only recognized method to slow the aging process, namely caloric restriction (CR). CR involves reducing daily caloric intake by a minimum of 30%. Various animal studies have shown that reducing caloric intake by 30-40% does appear to not only slow signs of aging, but also to ward off various degenerative diseases associated with aging, including both cancer and cardiovascular disease. CR is thought to work by inducing hormesis, which means by imposing stress, in this case fewer calories consumed, the body adapts by upgrading genes related to cellular protection. Among these are genes associated with decreased oxidation.

While animals exposed to decreased caloric diets do live longer, most of these animals are short-lived species. The notion that a considerable reduction of daily caloric intake can produce similar results in humans is still speculative. A few studies show that if CR added anything to human lifespan, the benefits would be modest at best, perhaps 3-7 years. If you stopped smoking, you would live an additional 10 years. On the other hand, the promotion of a lean body with decreased body fat that results from CR without a doubt does promote increased longevity. The main reason for this is probably the decreased level of overall body inflammation that comes with lower body fat levels. Inflammation tends to rise with age, and is now considered to be the cornerstone of most degenerative diseases, including cancer, cardiovascular disease, and Alzheimer’s disease. CR also helps by lowering oxidation, mainly by lowering resting metabolism.

On the BBC program, a couple who’ve used a rigourous CR program for 16 years were interviewed. Both are in their 60s, and follow a strict vegan eating routine. Both think they look much younger than their chronological ages, but the camera revealed otherwise. Both look like they are in their 60s. They do seem content, however, even if they don’t look a day younger than their actual ages. Vegan diets tend to be lower in calories due to the high fiber and water content, which is filling. But vegans also show higher rates of a process that produces advanced glycation end products or AGEs. Without getting into technical details, this process results in older looking skin. Most strict vegans often look older than their actual ages. In addition, following a CR program would be antithetical to anyone seeking added muscle. Every anabolic hormone in the body is significantly lowered on a CR regime. The same holds true for energy levels, making it difficult to exercise intensely enough to build any degree of muscle. CR also raises cortisol levels, the primary catabolic hormone in the body–not good for building muscle.

But the part of the BBC program that I found curious involved antioxidants. Two scientists interviewed on the show discussed animal studies showing that providing antioxidants did zilch to extend longevity. Not mentioned was the amount or the specific antioxidants used in the studies. I found this curious because it is well-known that built-in body antioxidants decline significantly in humans with age. Various inflammatory conditions are related to increased oxidation, including Alzheimer’s disease. The mechanism seems to be an increased activity of nuclear factor kappa-B (NFK-B). This substance is the orchestrator of inflammation in the body. What turns on NFK-B? Oxidation. So you have a scenario in aging that involves lower levels of protective antioxidants in the body, combined with higher NFK-B activity, resulting in increased overall body inflammation and all the diseases that result.

Another theory of aging discussed on the BBC program related to telomeres. Telomeres are found at the end of chromosomes, and act like strings. As you age, the telomere strings shorten. When they disappear, the cell stops replicating and cell repair ends. The cell then commits suicide. Research shows that increased oxidation speeds the shortening of telomeres. Ingesting various antioxidants, including vitamin C, slows the shortening of telomeres. All of this makes me wonder why antioxidants won’t slow the aging process. Perhaps it doesn’t in the short-lived animals in which it showed no effect. To extrapolate this finding to humans doesn’t equate to good science. In the meantime, there is one proven way to promote both endogenous antioxidant production, as well as the leanness linked to increased longevity: exercise. Indeed, some studies show that with the inclusion of regular exercise, a 10% reduction in calories provides similar benefits to the more rigorous 30% plan. It’s also more realistic for most people to exercise more while eating a bit less.

While leafing through a bodybuilding magazine in the library, I noticed a small item concerning the effects of the popular herbal supplement, ginkgo biloba extract (GBE) on testosterone levels. For those who aren’t familiar with Ginkgo, the ginkgo tree, from which the extract is derived, is often referred to as a “living fossil” because it has been around since the days when dinosaurs walked around. Numerous studies show that elements found naturally in Ginkgo, such as various flavonoids, provide some beneficial health effects. For example, GBE is known to increase blood flow and is also a potent free radical inhibitor, meaning that it inhibits out-of-control oxidation in the body. Both of these qualities can boost brain power, and ginkgo’s main claim to fame is that it may help prevent the onset of dementia, and in other cases may increase brain function and alertness through an increased circulation effect. There are many other claims made for ginkgo, however. The item that I read in the bodybuilding magazine was taken from an abstract of a Chinese medical journal, and the study itself was published in Chinese. The study involved providing GBE to either normal or diabetic rats. Humans afflicted with type-2 diabetes often show low testosterone levels, and conversely, there are new studies linking the onset of both the metabolic syndrome and diabetes to low testosterone levels. The connection is that low testosterone levels promote an increased level of visceral, or deep-lying abdominal fat stores. These particular fat stores, in turn, are associated with a greater incidence of cardiovascular disease and diabetes. Sure enough, the study with rats showed that the diabetic rodents were lower in enzymes related to testosterone synthesis in the body, as well as a lower volume of cells in the Leydig cells of the testes, where testosterone is synthesized. But when diabetic rats were provided GBE for 12 weeks, most of the negative effects on testosterone synthesis were reversed or blocked. The conclusion of the study was that GBE enhanced testosterone synthesis in type-2 diabetic rats. Based on this conclusion, whoever wrote the article in the bodybuilding magazine extrapolated this study to human usage, suggesting that bodybuilders use GBE to boost testosterone levels.

There are several problems with this suggestion. For one, humans aren’t rats, and what works in a rat doesn’t always also work in humans. In addition, these were diabetic rats, and we do know that human diabetics tend to have lower testosterone levels, but this doesn’t apply to those who don’t have diabetes. Had the author of the bodybuilding article scrolled down the Pub Med page where he or she probably found the Chinese rat study, they would have found an earlier study, published in 2005 that featured human subjects. The purpose of the prior human study was to determine if using ginkgo significantly altered levels of steroid hormones, including free testosterone,cortisol, DHEA, and others. The subjects ingested 240 milligrams a day of GBE for 14 days. Before ingesting the GBE, all subjects provided baseline hormone levels for comparison purposes. The results showed that the GBE had no effect on any steroid hormones, including testosterone. This study included six men and five women, but no rats. So while GBE may indeed raise testosterone levels in diabetic rats, the odds are good that it does not provide comparable effects in humans.

The take home message from this little episode is that you should be suspicious of those who directly extrapolate animal research to humans in definitive terms. While some animal studies do prove transferable to humans, many do not. When I write my articles that involve animal research, I always end by noting that future studies  should determine if the effect shown in animals is applicable to humans. And that can only be done through studies with humans, and not just one study, either.

It would not be an exaggeration to say that creatine is one of the most popular and effective sports supplements. Studies show that about 70% of those who use creatine supplements obtain definite ergogenic benefits, including increased body mass, strength, and upgraded muscle endurance. Most of the published studies attesting to creatine efficacy have involved creatine monohydrate, which is composed of 99% creatine and 1% water.While forms of creatine were routinely used by Russian and East German athletes in the 60s, the use of creatine as a popular sports supplement began in 1993. The ongoing popularity of creatine has led to a variety of supplemental forms of creatine. Some creatine supplements contain simple sugars, based on studies showing that promoting an insulin release boosts muscle uptake of creatine. In actuality, the efficiency of muscle creatine uptake is dependent on the creatine transporter protein found in muscle. With continued use of creatine, this muscle transporter eventually downgrades, and when that happens, most of the ingested supplemental creatine is rapidly converted into the creatine metabolic byproduct, namely creatinine. Creatinine, however, provides no ergogenic effects, although it does provide a minor antioxidant effect. In recent years, many ads for various creatine products suggest that creatine monohydrate is difficult for the body to absorb. Other ads suggest that the harsh acidic enviroment of the stomach rapidly degrades creatine into creatinine. In fact, several good studies show that creatine is completely absorbed into the gastrointestinal tract. The conversion of creatine into creatinine is negligible, contrary to some ad claims. In fact, the availability of creatine in the blood after oral ingestion approaches 100% of the dose, and you can’t get much better than that. Then why do so many products claim to be vastly superior to plain old creatine monohydrate (CM)?

Creatine is not very water soluble, and also doesn’t easily penetrate cellular membranes. Based on these known characteristics of creatine, a few creatine supplemental variants have emerged with the goal of overcoming these creatine barriers. One in particular, creatine ethyl ester (CEE) even makes the formidable claim that it bypasses the creatine transport protein limitation. It allegedly does this because the ethyl part of CEE is alcohol, which is known to easily penetrate fatty cell membranes. The theory behind CEE is that the ester protects it against premature degradation in the gut, while also speeding uptake into muscle. As such, you would need to ingest far less creatine, and the amount you do ingest would increase muscle uptake considerably. According to CEE advocates, enzymes in the gut called esterases remove creatine from its ester, thereby producing free and active creatine. But the proof for this supposed enhanced creatine uptake with CEE had little or no evidence to back up the many grandiose ad claims about CEE, such as that it provided 400% or more better uptake compared to CM. Some recent studies have tested CEE and compared it to CM. The results are not going to make those who sell CEE too happy.

For example, one study, published in Journal of the International Society of Sports Nutrition, featured 30 untrained men, divided into placebo, CM, and CEE groups. The study, which lasted for seven weeks, had the men in the creatine groups ingest 20 grams a day for 5 days, followed by 5 grams a day for 42 days. Throughout the course of the study, all the subjects trained with weights on a 4-day split routine. The results showed high blood levels of creatine in the placebo and CM groups compared to the CEE group. On the other hand, blood levels of creatinine was higher in the CEE group compared to the other groups. Both creatine groups showed higher muscle levels of creatine compared to the placebo group, but there wasn’t any significant difference between the creatine groups in this regard. While ad claims for CEE suggest that this form of creatine results in less extracellular water retention, this study showed that CEE, in fact, produced the highest level of extracellular water retention. The main conclusion of the study was that not only wasn’t CEE superior to CM, but most of ingested CEE appears to rapidly degrade into creatinine.

Another recent study, published in the International Journal of Sports Medicine tested the notion that intestinal esterase enzymes cleave the ester off of CEE, thereby liberating the creatine portion for use in muscle uptake. The study found that the esterase enzymes did not convert CEE into active creatine to any significant degree. Instead, nearly all of the creatine took a direct route into relatively useless creatinine. All of this information should not be surprising. CEE was initially formulated in the 1920s. A 1955 study found that CEE was too inherently unstable to be of any practical use. Which begs the question: Why was CEE introduced to the sports supplement market?  The answer is that the mechanism for the higher efficacy of CEE seemed initially plausible–but untested. A darker motivation for some was unabashed greed. The bottom line, however, is that all forms of supplemental CEE are considerably more expensive than CM, yet paradoxically is far less effective for its intended purpose. Perhaps it’s time to relegate CEE to the list of ineffectual  supplements that appeared promising but proved to be a bust. In that sense, CEE has plenty of company, with such notable past failures as boron to boost testosterone, HMB, and numerous others.

For more information about creatine and various other sports supplements, check out my e-book,Natural Anabolics. Information is available at: jerrybrainum.com.

References

Spillane, M, et al. The effects of creatine ethyl ester supplementation combined with heavy resistance training on body composition, muscle performance, and serum and muscle creatine levels.J Int Soc Sports Nutr 2009;6:6

Giese MW, et al. Qualitative in vitro NMR analysis of creatine ethyl ester pronutrient in human plasma.Int J Sports Med 2009: in press.

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.

Not long ago, I wrote a two-part article on the benefits of green tea for Ironman. I’ve used green tea (GT) myself for quite some time. It contains some of the most potent natural antioxidants yet discovered, which explains why it offers a myriad of health benefits. While leafing through a magazine that touts itself as being the “premier” bodybuilding science magazine, I noticed an item with the heading “Green tea lowers testosterone.” The way the short item was written appeared to offer convincing evidence that using green tea supplements, or drinking the tea itself, would lower testosterone levels. The item ended by suggesting that perhaps bodybuilders should avoid anything with green tea. Such a suggestion is problematic, because most “fat-loss” supplements sold today contain green tea as a primary active ingredient. On the other hand, attempting to produce any appreciable gains in muscle mass while also consuming a substance that lowers testosterone amounts to working against yourself. You simply cannot build muscle without a certain amount of testosterone. This is an established fact. So what to do about the green tea problem?

I mentioned in my Ironman green tea article how some rat studies in which the rodents were given large doses of green tea antioxidants via intravenous route did appear to lower testosterone in the animals. It also lowered other hormones, including estrogen. But the study showed that when provided orally, green tea had no effect on the hormones.In addition, the rats in the study lost a considerable amount of weight, and it was conjectured that the weight loss, rather than the green tea exposure, is what led to the lowered hormone levels. Losing large amounts of weight rapidly produces similar effects in humans due to a high stress effect.   In addition, other studies with mice and rats show that green tea appears to boost testosterone levels. One mechanism may be an inhibition of the aromatase enzyme that converts androgens, such as testosterone, into estrogen. Test tube studies of rodent cells show that green tea may also inhibit 5-alpha-reductase, the enzyme that converts testosterone into its metabolite, dihydrotestosterone (DHT). The latter causes male pattern baldness, acne, and prostate gland problems.

To  examine the  question of whether new information does suggest an anti-testosterone mechanism associated with green tea , I looked at the actual study, which was published in the Asian Journal of Andrology. This was the same journal that first published articles about an African herb called Fadogia, which was soon followed by some people attempting to peddle fadogia as a potent testosterone producer. My reaction to that was that the evidence for the efficacy of fadogia consisted of folk tales from Nigeria, along with one–count em’– one study of rats. A follow up study by the same researchers found that long-term use of the herb could cause testicular toxicity, which is not exactly amenable to higher testosterone production. Of course, the purveyors of fadogia never mentioned that later study. But back to green tea and testosterone.

The article in the bodybuilding magazine indicated that the study used intact rats. First, what happens in rats doesn’t necessarily also happen in humans. But the study didn’t involve live rats. Instead, it examined isolated Leydig cells obtained from rats. The Leydig cells are the portion of the testes where testosterone is synthesized. The cells were incubated with the active antioxidant constituents of green tea for three hours, along with the testosterone precursor, androstenedione. Some may recall that andro was one of the first prohormones released, and gained fame when baseball slugger, Mark McGwire admitted using it. Of course, now we know what McGwire really used, and it wasn’t an over-the-counter prohormone! The study showed that exposing isolated cells to large amounts of green tea interfered with several pathways of testosterone synthesis. But this involved doses far larger than would be obtained by an oral intake of green tea. In addition, humans can only absorb a small percentage of ingested green tea polyphenols (antioxidants). So in effect, this study was similar to the one that I described in my green tea article. To suggest that consuming green tea in supplement form would produce the same effect is a huge leap of scientific logic. If this were true, most bodybuilders who use green tea supplements in any form would have low testosterone levels, and that is simply not the case. Also, consider that in Asian countries, the average intake of green tea is 10 cups a day. Again, if this were lowering testosterone levels, China would be a vast, uninhabited wasteland. Ditto for Japan. The level of Leydig cell exposure to green tea polyphenols that occurred in the study would never happen in the human body.

So much for the “premier science” bodybuilding rag, er, I mean mag.

While I strongly advise eating plenty of fruits and vegetables, there is one notable problem with such foods. Many are laced with various pesticides. These pesticides are linked to everything from cancer to interference with hormone activity in the body. Below you’ll find the fruits and vegetables containing both the highest level of pesticides, along with the lowest. You should still eat the “tainted” fruits and veggies, since many of these contain valuable phytochemicals and antioxidants that help to prevent a myriad of diseases, including cardiovascular disease and cancer. Some, such as broccoli, can even lower active levels of estrogen in both men and women. This prevents estrogen-related cancers in women, and lower estrogen in men helps to maximize the effects of testosterone in the body. Just ensure that you thoroughly rinse the “dirty” ones before eating them.  Here’s the list:

Highest in pesticide content:

1. Peaches

2. Apples

3. Bell peppers

4. Celery

5. Nectarines

6. Strawberries

7. Cherries

8. Kale

9. Lettuce

10. Imported grapes

11. Carrots

12. Pears

13. Broccoli

14. Tomatoes

15. Sweet potatoes

Lowest pesticide levels

1.Onions

2. Avocados

3. Sweet corn

4. Pineapple

5. Mango

6. Asparagus

7. Sweet peas

8. Kiwi

9. Cabbage

10. Eggplant

11. Papaya

12. Watermelon

Although I’ve written over 3,000 published articles during the last 30 years, I have not, until now, ventured into the world of book writing. But recently, with the encouragement of Ironman editor-in-chief, Steve Holman, and publisher John Balik, I’ve finally decided to make the leap  to the book world. To be precise, my first book is an E-book, which of course stands for electronic book.

The title of the book is Natural Anabolics, and it covers in concise fashion most of the more popular ergogenic aid sports supplements available on the market. What sets this book apart from others, however, is the total lack of commercial nonsense and outright lies too often seen on books on nutrition that are supposed to be objective.

This book answers many of the common questions that people have asked me over the years, such as are there any supplements that actually boost testosterone levels, and others.

This is not my first venture into the world of total truth. About a decade ago, Ironman published a newsletter that I wrote called Applied Metabolics. I was originally supposed to write this with a medical doctor and a well-known exercise physiologist. The medical doctor backed out of the project after signing a contract with a supplement company. The physiologist had recently begun working for another magazine, and backed out of participating in the newsletter because of fear of repercussions from the publisher of the magazine. So I wrote the whole thing myself.

This was the type of publication that supposedly would appeal to a wide range of intelligent readers, since it contained no advertising, and I had no limits in regard to writing the whole truth and nothing but. That is also true of the new e-book.

I think it will serve as a handy antidote to the crap that is regularly published in some magazines, and is rampant in ads pertaining to various supplements. Somebody had to step up to the plate about this flood of B.S falling on the public, and I was happy to take the bat. Those who’ve read my work over the years know that it is devoid of lies and commercial ties. I usually avoid writing about studies that push particular products, knowing how easy it is to manipulate studies, and also because I refuse to be an unpaid shill for supplement companies. If you want to know the truth about the most popular sports supplements and sports nutrition, check out jerrybrainum.com for info on my e-book.

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.

According to a study just presented at the annual Experimental Biology 2009 conference in New Orleans, women who use oral contraceptives, better known as birth control pills, may experienced hampered muscle gains when they lift weights. The study consisted of 73 healthy women, ages 18 to 31, who were assigned to either a birth control pill group (BCP), or a non-birth control group (NBCG). All the women participated in a 10-week weight-training program, training 3 days a week under the supervision of physiologists. They did both standard upper and lower body exercises, all for 3 sets of 6-10 reps, using weights equal to 75% of their maximum one-rep lift. Body composition in the women was measured by hydrostatic weighing. In addition, blood samples were obtained prior to, and after the training to measure various hormones, including DHEA, DHEA-S,  and IGF-1.

The results showed that those not taking BCP gained 60% more lean mass compared to those taking the pills. On the other hand, strength gains and arm and leg circumferences were similar between the groups. The levels of the anabolic hormones, DHEA and IGF-1, were significantly lower in the women on the pill, while levels of the catabolic hormone, cortisol were higher in the pill users. The OCP also showed decreased levels of DHEA at the end of the study. In contrast, no change occurred in DHEA levels in the non-pill users.

The researchers who conducted this study were at a loss to explain the results, other than suggesting that BCP can impede muscle gains in women. On the other hand, while the pill users gained 60% less lean mass compared to their non-pill peers, both groups gained similar levels of strength and size in the legs and arms. This, of course, is a quite contradictory finding, and makes you wonder if much of the lean mass gains experienced by the non-pill users consisted of water. Curiously, testosterone wasn’t measured in the study, which would have somewhat clarified the results. Instead, only DHEA levels were measured. DHEA, however, is an adrenal androgen that tends to convert into testosterone in women far more readily that it does in men. But recent studies also show that DHEA doesn’t appear to promote muscle gains in exercising women. Since the women trained under supervision, we have to assume that they trained with an equal level of intensity, which would have influenced muscle gains. The elevated cortisol levels in the pill users likely played a major role in why they gained less lean mass, since the non-pill users didn’t show such elevations. The women were told to ingest at least 0.5 grams of protein per pound of bodyweight. Normally, a high protein intake would offset much of the muscle catabolic effects linked to higher cortisol levels, but this level of protein may not have been enough to overcome the catabolic effects probably induced by the OC.

This new information does not apply to women using anabolic steroid drugs, which would make any effects of OC on muscle growth negligible. As the study authors suggest, there may be other, as yet unidentified mechanisms as work here, too. In the meantime, I doubt that many women would be willing to toss those birth control pills as a means of promoting muscle gains. Becoming pregnant when you don’t want to is a far more serious proposition than sacrificing some muscle gains in rational women.

February 12 marked the bicentennial of the birth of Abraham Lincoln, the 16th and greatest president of the United States.  Most people know that on the night of April 14, 1865, Lincoln was assassinated by John Wilkes Booth while viewing a play at Ford’s theatre in Washington. Shortly after being shot by Booth, Lincoln was attended to by two young physicians, one of whom had graduated from medical school just a month earlier. The doctors did what they could for Lincoln, but the medical techniques available at the time could do little to save the president. The question arises: could modern medical techniques have made a difference in Lincoln’s prognosis?

I recently found an article that featured comments from Thomas A Scalea, M.D., who is associated with the nation’s oldest trauma center, the R.Adams Cowley Shock Trauma Center in Baltimore. In the article, the precise nature of Lincoln’s wounds are described, along with how he would be treated today.

Booth’s bullet entered the left side of Lincoln’s skull, and the two attending physicians soon probed the open wound with their fingers, which certainly isn’t advisable due to possible exposure to sepsis. They noted that at age 56, Lincoln still had the “chest and arms of an athlete.” Lincoln’s robust physique led the doctors to believe that if he hadn’t been in such strong condition, he would have died in 10 minutes.

The force of the bullet caused Lincoln to have an intracerebral hemorrhage and a subdural hematoma (blood clot) in the brain. If it happened today, Lincoln would have been rushed to a local trauma center, where he would have immediately been intubated to assist his breathing. The treatment would next have focused on relieving Lincoln’s intracranial pressure. This would involve providing a blood expansion effect by administering hypertonic saline (salt solution), along with modest hyperventilation. He would be given a chest X-ray, along with a CT scan of his head to observe the full extent of his injury.

To relieve the blood clot in his brain, Lincoln would have undergone surgery within 15 minutes of his arrival at the trauma center. The main thrust of Lincoln’s treatment would have involved relieving his elevated intracranial pressure. After the surgery, Lincoln would have been given antibiotics to prevent infection, along with a drug to prevent post-operative seizures.

Since brain injury is a highly catabolic event, Lincoln would have also been provided with parenteral nutrition or “tube feeding.” To prevent deep vein thrombosis, he would have been given blood thinners.

Lincoln’s injury would have resulted in some permanent deficits. He would have been paralyzed on his right side, suffer partial blindness, and would have been unable to read, write, or speak. But since the frontal lobe of his brain was uninjured, he would have retained his intellectual capacity. In short, he may have survived Booth’s bullet, but his quality of life would have been quite low.

Several other physicians have remarked that even if he had not been shot by Booth, Lincoln would not have lived long anyway. Based on Lincoln’s body structure, some doctors have suggested that Lincoln suffered from Marfan’s disease, which often results in a premature death from heart failure. Another physician, Dr.John G.Sotes, a cardiologist who has studied the health of American presidents, published a book last year based on years of research into the state of Lincoln’s health. In his book, The Physical Lincoln, Sotes says that Lincoln  had a rare (one person in a million) genetic disorder called multiple endocrine neoplasia, type 2B. Having this genetic defect results in cancers of endocrine organs, especially the thyroid and adrenal glands. Sotes suggests that Lincoln already showed signs of advanced cancer at the time of his death, and wouldn’t have survived much longer, since there was no treatment of cancer at the time.