Sunday, June 26, 2011

EAT TO GROW : Pump Protector and Fat Ejector by Jerry Brainum

L-arginine has recently emerged as the superstar amino acid, displacing such previous favorites as glutamine and leucine. That’s particularly interesting because L-arginine isn’t even considered an essential amino acid, meaning one that must be provided in food. Like glutamine, it’s a conditionally essential amino: one that’s required in greater amounts during times of growth and stress.

Although arginine has been largely associated with promoting growth hormone release, its present popularity stems from its position as the immediate dietary precursor of nitric oxide. NO is both a gas and a free radical that is short-lived in the body but that performs myriad vital functions.

A recent study featured the Zucker rat, a genetically altered animal that exhibits the same effects of type 2 diabetes and obesity as humans—elevated blood glucose; elevated blood lipids, such as cholesterol andtriglycerides; elevated resting insulin levels; and dysfunction of the lining of blood vessels that leads to atherosclerosis, high blood pressure and cardiovascular disease.1 Researchers gave the fat, diabetic rats arginine because of the relationship between NO and fat metabolism. NO increases the expression of a chemical that leads to increased activity of mitochondria in cells. Fat is oxidized in the mitochondria. When the genes of rats are manipulated so that they don’t produce NO, they always show higher bodyfat levels than ordinary rats, even though they eat the same amount of food. Inhibiting NO in rats also increases blood levels of triglyceride, or fat.

Since NO stimulates fat oxidation in fat cells, the experimenters hypothesized that giving the Zucker diabetic rats, as they’re known, arginine would increase NO production and possibly decrease bodyfat levels. Some rats got arginine as 1.25 percent of their overall caloric intake in drinking water for 10 weeks. Other rats got no additional arginine.

In the arginine rats, blood arginine levels rose 261 percent, and NO was elevated by 70 percent. The bodyweights of the arginine-treated rats were 6, 10 and 16 percent lower than the control rats at weeks four, seven and 10. Abdominal fat dropped by 45 percent. Serum levels of glucose dropped 25 percent; triglycerides dropped 23 percent; free fatty acids dropped 27 percent; homocysteine dropped 26 percent. By the 10th week of the study, NO production had increased in the arginine-treated rats by 71 to 85 percent, fat oxidation had increased 24 percent, and glucose oxidation was boosted by 34 to 36 percent. The genes related to fat oxidation increased considerably in the arginine rats, with two animals showing increases as high as 789 and 500 percent.

The arginine treatment didn’t increase insulin or growth hormone release. No side effects occurred, nor was the uptake or metabolism of any other amino acid adversely affected. Arginine did, however, increase the weight of the rats’ skeletal muscles, heart and brain. Other animal studies also show that arginine benefits protein synthesis, but it doesn’t affect muscle protein breakdown, or catabolism.

One of the substances increased by arginine reduces the availability of malonyl coenzyme-A, which is a primary inhibitor of fat oxidation in the mitochondria. That substance increases in the presence of carbohydrates, which explains why eating carbs just before training blunts fat burning during the workout. Specifically, malonyl coenzyme-A blocks the enzyme that works with L-carnitine in shuttling fat into the mitochondria for oxidation purposes.

Another recent study showed that dietary arginine lowered levels of C-reactive protein in the body.2 CRP is a general measure of inflammation in the body, and inflammation is the cornerstone of most serious diseases, including cancer and cardiovascular disease. Most supplements, even potent antioxidants such as vitamins C and E, have little or no effect on CRP. The effect on CRP may explain why eating nuts and fish protects the cardiovascular system; both foods are rich sources of arginine. Eating 3.6 ounces, or 100 grams, of walnuts provides 2.5 grams of arginine.

Arginine is thought to lower CRP levels through several possible mechanisms. Its antioxidant activity is independent of its role as a NO precursor, since NO itself is an oxidant. Arginine also positively affects immune function, which helps to reduce the inflammation characteristic of high CRP levels.

References

1 Fu, W.J., et al. (2005). Dietary L-arginine supplementation reduces fat mass in Zucker diabetic fatty rats. J. Nutr. 135: 714-721.
2 Wells, B.J., et al. (2005). Association between dietary arginine and C-reactive protein. Nutrition. 21:125-30.

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

Please consider joining this blog by clicking on the blue "join this site" button to the right of this blog. This will ensure that new blogs continue to be published. It costs nothing, and takes only a few seconds. Thank you.

See Jerry's book at       www.jerrybrainum.com

Friday, June 24, 2011

TRAIN TO GAIN : Cardio Brain Strain Does running cause brain damage the way boxing does? by Jerry Brainum

While aerobic exercise tends to be boring and repetitious, at least there are many types to choose from. The main object of any type of aerobic training is to increase your heart rate to a certain level and maintain it at that level for the duration of the session. Most bodybuilders prefer to do nonjarring types of aerobics as a means of preventing joint injuries. Popular forms include treadmill walking, elliptical machines, stair-climbing machines and stationary cycling.

Running or jogging is usually not recommended for bodybuilders because of the excessive and cumulative joint trauma that results. Every time your foot hits the ground—even on a soft surface such as grass—you transmit forces equal to three times your bodyweight to your skeletal structure and joints. Running on a hard surface, such as a concrete sidewalk, increases that force to five times bodyweight. Those who run on streets with heavy traffic compound the damage by breathing poisonous auto emissions, such as carbon monoxide. You’re better off sitting in front of the TV and smoking a cigarette than running under those conditions.

Running may have an even more insidious effect, according to one preliminary study.1 It examined the effects of various activities, including both long- and short-distance running, on a specific brain protein called S-100B that also exists in lesser amounts in fat cells, skin-pigment cells (melanocytes) and the testes. Studies show that a rise in this particular protein in the blood is a harbinger of brain deficits.

The study compared the levels of S-100B released by subjects during a number of activities: amateur competitive boxing and sparring, before and after running a 25-kilometer (15.5-mile) race, jogging for 6.2 miles, interval sprinting for two minutes at top speed three times around a track, high-intensity interval stationary cycling—characterized by high-intensity cycling interspersed with one-minute breaks—and heading, or bouncing a soccer ball off the head 20 times.

Boxing is known to cause brain damage, especially among professional boxers. One need look no further than the great former heavyweight champion Muhammad Ali to see what happens when a pro stays in the ring past his prime. Ali suffers from a form of Parkinsonism, marked by damage to the parts of the brain that produce the neurotransmitter dopamine. Lack of sufficient dopamine produces the stiffness, tremors and slow gait evident in Ali, although it doesn’t affect his intellectual capacity.

Other former boxers wind up with dementia pugilistica, which causes brain damage similar to that of Alzheimer’s disease. Again, that’s due to long-term trauma, like being punched in the head. Many neurologists think that no boxer who stays in the ring long enough escapes such damage, though the extent of it varies. One early sign is a marked slurring of speech.

S-100B is an early indicator that something is amiss in the brain. It increases during acute brain events, such as strokes. In the study reported here, as you might expect, boxers fighting without protective headgear showed the highest levels of S-100B. Only one boxer showed no increase in S-100B, and he was also the only boxer who didn’t get hit. Competitive boxing produced higher S-100B levels than sparring.

Despite that, none of the boxers showed levels of S-100B that would point to incipient brain damage. The true surprise was that S-100B levels were similar in all running activities and sparring. To rule out an exercise effect, the authors looked at S-100B in cyclists who trained hard; they showed no increase in the protein.

So why did runners and boxers engaged in sparring show similar levels of S-100B? The theory is that the jarring from running causes a vibration in the brain, leading to a release of the protein. Interestingly, banging the head with a soccer ball didn’t have the same effect, and a previous study showed that not even bungee jumping produced a rise in S-100B.

The unanswered question is whether regular running, since it does increase S-100B, may lead to a type of brain deficit. On the other hand, the fact that similar levels of the protein occur with sparring and running is a bit sobering. The S-100B levels after jogging for 6.2 miles and sparring were nearly the same. Good reason to stick to nonjarring aerobic exercise.


1 Otto, M., et al. (2000). Boxing and running lead to a rise in serum levels of S-100B protein. Int J Sports Med. 21:551-55.

©,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

 

Wednesday, June 22, 2011

EAT TO GROW : Eat to Turn Up the Heat When to eat for maximum fat burning during exercise by Jerry Brainum


Many studies show that eating foods that are rapidly used energy sources, such as carbohydrates, just before a workout blunts the use of fat as a fuel. Carbohydrate drinks do, however, offer a few notable advantages when drunk during the workout. Drinks that contain the proper level of carbs (8 percent or less) combined with some electrolytes (minerals) to speed fluid uptake provide hydration even more efficiently than plain water. Carb drinks maintain energy levels during workouts that exceed an hour and blunt the rise in cortisol that would normally occur after an hour of hard training. But it’s all at the expense of fat burning.

I’ve seen people eat full meals immediately before or even during workouts. Such meals will have a delayed digestion, as blood is shunted from the gastrointestinal area to the working muscles, so the food goes more or less undigested until the workout ends. In addition, weight training is powered mainly by stored muscle glycogen, which is a reflection of what you ate 24 to 48 hours earlier. The only benefit derived from eating just before or during a workout is psychological.

But what’s the time interval after a meal if you want to burn the most fat during a workout? A new study, involving obese women over age 50, examined the issue.1 That group may seem to have little relevance for a younger population, but the principles governing the study apply to anyone, regardless of age.

The women ate meals either one or three hours before exercise. Not only did exercising three hours after a meal result in greater fat oxidation, but the level of fat burning was also similar to what happens after fasting. The three-hour interval led to lower heart rates during exercise and lower glucose, lactate and insulin levels, all of which favor fat burning.

Why did eating a meal one hour before exercise lead to less fat burning? The authors explain that eating so close to a workout increases the carbohydrate content of the blood, resulting in a blunted fat-burning effect. The meal produces higher levels of lactate, which blunts fat burning during exercise. Elevated insulin levels after a meal also block fat release and oxidation during exercise.

The lowered heart rate occurred because of the heart’s role in supplying blood for digestion purposes the first hours after a meal. By the three-hour point the meal was digested, leading to less stress on the heart during exercise.

Even though the study featured obese older women, the relationship between fat use and exercise applies to anyone, regardless of sex or age. In effect, the longer you wait between your last meal and your workout, the greater the level of bodyfat you’ll burn during the workout.

1 Dumortier, M., et al. (2005). Substrate oxidation during exercise: impact of time interval from the last meal in obese women. Int J Obesity. In press.


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.

 


©,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

 

Which protein source is best for reducing appetite? by Jerry Brainum


Here’s a quick quiz for you. Milk contains two primary types of protein, whey and casein. Studies show that they’re absorbed at different rates, with whey being absorbed rapidly and casein slowly releasing amino acids into the blood for more than seven hours. Which would suppress appetite more? A new study focused on just that question.1 Past studies have shown that protein has a greater satiation effect than fat or carbs. On the other hand, the appetite-suppressing effect of protein is blunted in people who habitually eat a high-protein diet—typical of bodybuilders. That’s most noticeable in those who increase their protein intake from a lower level. With a regular higher-protein intake, amino acids are more rapidly cleared and oxidized from the blood, mitigating its effect on appetite.

That’s also the reason a high-protein diet isn’t likely to lead to increased fat deposition, since all nutrients, including protein, fat and carbs, can be converted into fat. Active people, such as those engaged in regular exercise, burn up excess protein in the liver, thus preventing its conversion into glucose or fat.

One notable difference between whey and casein is that the amino acids in whey are rapidly processed and absorbed into the blood. Casein, on the other hand, curdles in the stomach, leading to a much slower breakdown and release of amino acids. Because a high concentration of amino acids is vital for promoting muscle protein synthesis, some studies suggest that whey’s rapid release of aminos makes it superior to casein for that purpose. On the other hand, casein’s slow release of amino acids makes it more conducive to providing a pronounced anticatabolic effect by maintaining a positive nitrogen balance in the blood over the course of several hours.

The amino acids in the blood dictate the appetite-suppressing properties of protein. Whey is the superior appetite-suppressing protein. In a new study, subjects drank a beverage containing 48 grams of a commercial whey supplement or one containing the same amount of casein and attended an all-you-can-eat buffet 90 minutes later. Those who drank the whey ate 19 percent less food than those who drank the casein.

In the second part of the study researchers wanted to confirm the notion that the quick entry of amino acids made whey more satiating and to figure out if any gut hormones known to affect appetite were affected by whey or casein. That part of the study showed, as expected, that whey increased blood amino acid levels 28 percent more than casein over a three-hour period.

The whey drink increased the levels of several gut hormones that are known to suppress appetite. It increased the blood levels of cholecystokinin (CCK) by 60 percent, glucagonlike peptide-1 by 65 percent and glucose-dependent insulinotropic polypeptide by 36 percent. That last hormone isn’t normally increased by protein alone, but both the whey and casein drinks also contained cream and maltodextrin, a quick-acting carbohydrate.

Thus, whey appears to decrease appetite through its rapid release of amino acids, which in turn promotes the release of several gut hormones known to depress appetite and increase feelings of satiety.

1 Hall, W.L., et al. (2003). Casein and whey exert different effects on plasma amino acid profiles, gastrointestinal hormone secretion and appetite. Brit J Nutrition. 89:239-48.

©,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

 

Sunday, June 19, 2011

BODYBUILDING PHARMACOLOGY : Ephedra Loco by JERRY BRAINUM

Ephedrine and its parent herb, mahuang, are two of the most popular and effective thermogenic food supplements available—but perhaps not for long. Reports concerning the alleged dangers of ephedrine use are appearing regularly in mainstream media, and the deaths of several high-profile professional athletes who used ephedrine supplements have added to the impetus to remove ephedrine and mahuang from over-the-counter sales due to their inherent “toxicity.”

Those reports imply that ephedrine is a dangerous and unpredictable substance for everyone, but that simply doesn’t jibe with most available scientific evidence on ephedrine. In fact, as I’ve said in this column before, most cases of serious health problems involving ephedrine or mahuang are due to idiosyncratic reactions. In short, many of the people who experience serious side effects from using ephedrine or related compounds do so because of either existing health problems that contraindicated the use of ephedrine or from using too high a dose.

Ephedrine is a sympathomimetic drug, meaning that it acts similarly to or promotes the release of sympathetic hormones in the body, such as epinephrine and norepinephrine. Those hormones are also known as “fight-or-flight” hormones because of the reactions they promote during stress, including higher blood pressure due to vascular constriction, release of glucose and release of fat into the blood. A healthy person can easily tolerate those effects, but for someone who already has cardiovascular disease, such reactions could prove dangerous, particularly if he or she used too high a dose.

Since ephedrine shares some properties of other substances known to affect brain function, such as cocaine and amphetamine, it’s reasonable to assume that ephedrine affects behavior. Higher doses of ephedrine produce mental effects that in a broad sense mimic the effects of amphetamines, although published research shows that ephedrine doesn’t share the addictive potential or the immediate cardiac and brain toxicity linked to amphetamines.

People who are unaffected by mental illness experience a slight sense of euphoria coupled with a feeling of heightened energy when they use ephedrine. That effect is amplified in the mentally ill, who often overdose on ephedrine-containing supplements, since they’re more readily available than cocaine or amphetamines. In fact, ephedrine is so close in structure to amphetamines that if a person takes it before a drug test, he or she will test positive for speed. A follow-up test can distinguish the two drugs.

Recent reports in the medical literature cite adverse mental effects supposedly induced by ephedrine. One report described a 19-year-old man who suffered from decreased sleep, increased aggression and disorganized behavior after using two of the most popular ephedrine-containing food supplements.1 He was using so much of the supplements that he decided to open up the capsules and snort them like cocaine. Yet he was described as having no previous psychiatric history.

In another case a 21-year-old man took increasing doses of a popular thermogenic supplement and soon developed mania and psychosis, along with delusions. No dosages were mentioned, other than that he increased the dose regularly. A brain scan showed cerebral atrophy—not a usual finding in someone his age—a condition that could cause adverse mental symptoms.

Previous reports linking ephedrine to mental problems show that the typical dose used before symptoms occurred was 510 milligrams daily. Contrast that with the maximum suggested safe dose of 90 milligrams a day or the typical 25 milligrams found in a single capsule of most ephedrine supplements. The symptom most commonly linked to ephedrine use appears to be mania, and again, in nearly all cases the people had the condition before they took any ephedrine or mahuang supplement. In most cases they overdosed, which could cause similar problems in anyone. As the saying goes, “Only the dose determines the poison.”

Another recent case study documented a rare possible side effect of using ephedrine: priapism.2 That’s an extended, involuntary penile erection. It sounds good initially, until you realize that erections are the result of trapped blood that, if not released within a certain time, can cause serious damage and, paradoxically, lead to loss of sexual function.

Those case studies involved the use of cocaine and ephedrine supplements, though not at the same time. Cocaine causes priapism by inhibiting the reuptake of norepinephrine, which extends the vasoconstrictive activity of sympathetic nerves. Interestingly, using cocaine often leads to temporary impotence because an erection depends on an orderly balance between the parasympathetic and sympathetic nervous systems. Initially, the parasympathetic system is dominant, promoting erection by dilating blood vessels in penile tissues. Once the penile tissues are engorged with blood, the sympathetic system takes over to constrict the blood vessels, in effect trapping the blood in penile tissues to maintain the erection. Under normal circumstances the vasoconstriction is abated by the muscular pelvic contractions and rapid release of trapped blood that are linked to orgasm. But coke and ephedrine can block that effect, keeping the tissues engorged and causing the uncomfortable effect of being sexually aroused yet unable to perform. (I’ve always wondered why they refer to sex as a “performance.” Perhaps it’s connected to the reason gonorrhea is called “the clap.”)

In the cases described in the study, men who used OTC ephedrine supplements experienced erections that lasted seven and nine hours. Ouch, that ain’t no Viagra!

Nevertheless, the cases must be considered idiosyncratic, since many men use the same ephedrine supplements with no evidence of prolonged, painful erections. The men involved in the studies may have had hidden health or circulatory problems that made them particularly susceptible to that effect. After all, if this were a common occurrence, it would have no doubt received a great deal of publicity.

Amid the reports in the scientific literature of ephedrine’s adverse effects, a positive study emerges.3 Thirteen male subjects took in caffeine (four milligrams per kilogram of bodyweight), ephedrine (0.8 milligrams per kilogram of bodyweight), a combination of ephedrine and caffeine or a placebo. Ninety minutes later they did three sets each of leg presses and bench presses.

Those on either the caffeine-and-ephedrine combo or the ephedrine alone showed increased muscular endurance, but only during the first set of each exercise. The subjects on the supplements lifted more weight than those on the placebo on all three sets, and the blood pressure of those using the ephedrine increased before training. They showed a 48 percent improvement on the leg press and a 16 percent improvement on the bench press that would normally have taken four to 12 weeks of training to achieve. The researchers noted that caffeine plus ephedrine didn’t do anything for the subjects that ephedrine didn’t accomplish by itself, which contradicts recent statements that ephedrine doesn’t provide any ergogenic benefits.

 Insulin Abuse

 If you’d asked competitive bodybuilders 20 years ago about the possibility of injecting insulin as an anabolic drug, most of them would have said that insulin is for diabetics only. Indeed, insulin does treat diabetes, which comes in two forms. Type 1 diabetes is characterized by a complete failure of the beta cells of the pancreas to synthesize insulin. That’s why people who have that form of the disease must use insulin injections. Type 2, or adult-onset, diabetes, so named because it most often becomes apparent after age 40, may be controlled with other drugs, along with weight loss and proper diet, although in some cases insulin is required for maintaining normal blood glucose levels.

Insulin is vital for several aspects of nutrient storage and processing. It’s required for glucose uptake into cells and aids in amino acid entry into muscles. Insulin promotes the activity of glycogen synthetase, the rate-limiting enzyme for glycogen synthesis. On the dark side, insulin is the most potent fat-promoting hormone in the body.

Bodybuilders and other athletes use insulin for several purposes. It promotes rapid muscle glycogen storage, thus increasing energy stores and muscle fullness. Its role in amino acid uptake is key because the aminos are used for muscle protein synthesis reactions, and it provides an anticatabolic effect in muscle, preventing excessive muscle tissue breakdown.

Insulin also is synergistic with other anabolic hormones, such as testosterone and growth hormone. In fact, the combination of those three hormones is chiefly responsible for the massive appearance of today’s professional bodybuilders. All three hormones amplify one another’s anabolic effects. Unfortunately, that same combination is also responsible for the bloated abdomens that are so frequently seen on bodybuilders today. The combination of insulin and IGF-1 (from GH use) appears to foster internal organ growth and a thickening of the abdominal wall musculature.

Various forms of insulin are available without a prescription, to make it convenient for diabetics to obtain required medication. Athletes favor two types of synthetic insulin, both which are produced with recombinant DNA technology: Humalog, a quick-acting form that peaks in two hours and is out of the body by the four-hour mark, and Humulin-R, which also acts rapidly and is out of the body in six to eight hours. As a polypeptide composed of long chains of amino acids, insulin is always injected; taking it orally would lead to rapid inactivation. Insulin must also be injected subcutaneously, or right under the skin. Users rotate injection sites.

A full cc of insulin equals 100 I.U., and the doses used by bodybuilders average 1 I.U. per 15 pounds of bodyweight. The usual suggested protocol involves taking a minimum of 10 grams of simple, or rapidly acting, carbohydrates within 20 to 30 minutes of the insulin injection. Not following the carb protocol can lead to rapid hypoglycemia, or a drop in blood glucose levels. Symptoms include sleepiness, drowsiness, hunger, blurred vision, dizziness, sweating, slurred speech, inability to concentrate, tingling in hands and feet and other effects. If a simple sugar isn’t immediately ingested when those symptoms arise, the brain is deprived of its primary fuel—glucose—and coma can ensue.

Several bodybuilders have fallen into comas through injudicious use of insulin. In the most recently reported case in the medical literature, a 31-year-old bodybuilder went into a coma after switching to a rapidly acting insulin injection.4 He had previously used longer-acting forms of insulin and was apparently unaware that he needed a timely and correctly proportioned infusion of simple carbs. In another case a 21-year-old bodybuilder suffered severe brain damage after using insulin.5

“Incorrectly administered, insulin can kill you stone dead or leave you as a vegetable,” notes Peter Sonksen, a British medical researcher.

As for when to use insulin, for those of you intrepid or foolish enough to consider it, the best suggested times are first thing in the morning and following an intense training session. During those periods levels of cortisol, the primary catabolic hormone in the body, are high, and insulin opposes its effects.

You should also be aware that a hyperinsulinemic environment, or elevated insulin levels, has serious long-term health consequences, besides the considerable immediate dangers already cited. Elevated insulin promotes a process in the body known as glycation, or sugar deposition in tissues, thought to be one of the primary causes of aging. Diabetics, whether on insulin therapy or not, are known to age at an accelerated rate. Recent animal-based studies show that lifelong insulin control may be a key factor for healthy aging and maintenance of vigor with passing years.

One study shows that insulin use promotes the oxidation of low-density lipoprotein (LDL), the bad kind of cholesterol.6 That would promote atherosclerosis and subsequent cardiovascular disease. Another study shows that using large doses of insulin can cause a vasospasm in the coronary arteries, resulting in a heart attack.7

A study published earlier this year points to the possibility that high insulin levels are related to the onset of Alzheimer’s disease.8 The mechanism involves increased release of and inhibited degradation of beta-amyloid protein, which builds up in the brains of people afflicted with the disease and is thought to be a root cause of Alzheimer’s. Oddly enough, insulin appears to increase memory function in younger people, but a researcher involved in the study said that “high insulin levels are bad for your brain as well as your body.” By the way, the doses of insulin used in that study were higher than diabetics use but comparable to what’s suggested for “anabolic” effects in bodybuilders.

The one aspect of insulin use that I find curious is that in the usual protocols suggested for athletes, there’s never any mention of amino acid use with the drug. Yet evidence clearly shows that insulin promotes muscle protein synthesis only in the presence of elevated amino acid levels. So it would appear prudent to take amino acids—not a whole-protein source—with simple carbs shortly after a rapidly acting insulin injection, since the insulin will “push” those aminos directly into muscle, producing a pronounced muscle protein synthesis effect.

You should also be aware that if you’re already insulin-insensitive from carrying too much bodyfat, the insulin-and-simple-carb protocol will make you appear about as muscularly defined as John Goodman. Using insulin and high simple carbs under that condition is tantamount to attempting to put out a fire with gasoline. Recall that insulin promotes bodyfat synthesis by turning on every system in the body for that purpose while simultaneously turning off fat-oxidizing systems. The lesson here is to avoid even considering using insulin—unless you are diabetic—until you diet and train away that excess bodyfat. Insulin is also a potent water- and sodium-retaining hormone, which may increase blood pressure in some people.

For those who—wisely—prefer to avoid using a drug as potentially dangerous as insulin, you can get a similar, if less dramatic, muscle protein synthesis effect simply by taking in a rapid-acting protein source (such as whey) with simple carbs immediately following a workout. That combination maximizes your own output of insulin, leading to increased amino acid uptake into muscle, coupled with quicker muscle glycogen replenishment. And the great part about it is that you don’t have to worry about falling into a coma.

 References

1 Walton, R., et al. (2003). Psychosis related to ephedra-containing herbal supplement use. Southern Med J. 96:718-20.

2 Munarriz, R., et al. (2003). Cocaine and ephedrine-induced priapism: case reports and investigation of potential adrenergic mechanisms. Urology. 62:187-92.

3 Jacobs, I., et al. (2003). Effects of ephedrine, caffeine, and their combination on muscular endurance. Med Sci Sports Exer. 35:987-94.

4 Evans, P.J., et al. (2003). Insulin as a drug of abuse in bodybuilding. Brit J Sports Med. 37:356-7.

5 Elkin, S., et al. (1997). Bodybuilders find it easy to obtain insulin to help them in training. Brit Med J. 314:1280.

6 Quinones, A., et al. (1999). Evidence that acute insulin administration enhances LDL cholesterol susceptibility to oxidation in healthy humans. Aterioscler Thromb Vasc Biol. 19:2928-2932.

7 Kamijo, Y., et al. (2000). Myocardial infarction with acute insulin poisoning. Angiology. 51:689-693.

8 Watson, G.S., et al. (2003). Insulin increases CSF Ab42 levels in normal older adults. Neurology. 60:1899-1903.

©,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

 

Saturday, June 18, 2011

LAB TEST SERIES: PART 3: YOU GOTTA HAVE HEART(CARDIOVASCULAR TESTS) by JERRY BRAINUM


Metaphorically speaking, cardiovascular disease is comparable to a health terrorist. The factors that promote cardiovascular disease increase slowly and without knowledge, often causing no apparent symptoms until disaster strikes. Cardiovascular disease (CVD), represented by various diseases, including myocardial infarctions (heart attacks), strokes, and various other disorders related to the heart and circulatory system, remain the number one killer worldwide.

This dubious distinction of being the top killer in the world is reflected by the latest statistics released 3 years ago by the American Heart Association. According to those statistics, 61,800,000 Americans have one or more forms of CVD. These include 50,000 with high blood pressure;7,600,000 with heart attacks;and 4,700,000 with strokes. A total of 945,836 people died from the effects of CVD in 2000, or 39.4 of all deaths from any cause. Viewed from another perspective, 1 out of every 2.5 deaths resulted from CVD.

The most tragic aspect of these cold statistics is that although it’s the number one killer, CVD is largely both preventable and treatable. This involves paying attention to various CVD risk factors. Such risk factors include smoking, high blood pressure, obesity, lack of exercise, and a high saturated fat diet. Other risk factors aren’t as controllable, such as genetic predisposition, age, and sex. Males are generally more at risk for CVD compared to younger women.

The bodybuilding lifestyle, with its emphasis on exercise and proper nutrition, offers many protective effects against CVD onset. An example of this is how exercise increases levels of a protective cholesterol-carrier in the blood called high density lipoprotein (HDL). Another cholesterol-carrier, called low density lipoprotein (LDL) is closely linked to CVD onset, particularly when oxidized. But bodybuilders who consume a generous intake of various antioxidant nutrients, such as vitamin E and selenium, confer added CVD protection. Other nutrients likewise play protective roles in CVD, but a discussion of these nutrients is beyond the scope of this article.

You cannot ascertain the degree of your cardiovascular status by outward appearance. Thus, some obese people may have lower total cholesterol levels than their thinner counterparts for various reasons. The only effective way to access your CVD status is through blood testing. Yet, it’s amazing considering the number of people that are stricken with CVD, how few people even bother to have regular blood tests.

   Another factor that makes many avoid CVD blood testing is the notion that only older, out-of-shape people have CVD. But autopsies performed on soldiers as young as 19 killed during the Korean and Vietnam conflicts revealed a surprising level of atherosclerosis, which involves a narrowing of the arteries, and is considered a primary harbinger of impending heart attacks and strokes. A recent study of 141 young men, ages 17 and 18, confirmed that the process of CVD begins early.[i] Age offers no real protection against CVD.

The usual way to ascertain your CVD status is through standard blood tests, collectively known as a lipid panel. Many of these tests are not included in a standard blood panel, and must be specifically ordered. Otherwise, you will likely see only your blood value for total cholesterol. While total cholesterol levels are still important, knowing this value only provides you with a small sample of your total cardiovascular status. The only tests included in a common lipid panel include total cholesterol,  HDL, LDL, and triglycerides. All of these are important, but again, they reveal only a partial picture of your cardiovascular status.

The major breakthrough in cardiovascular lab testing occurred at the Berkeley Lab in California in 1949. That’s when scientists at the lab first isolated and developed tests for lipoprotein and lipoprotein subclasses, allowing doctors to determine the ratio between lipid fractions such as HDL and LDL, and thus get a more accurate idea of patient status in relation to CVD. Since then, several other tests have been developed, and these tests do provide the clearest picture of how you stand in your cardiovascular status.

                                   The cardio blood tests and what they mean

1) Total cholesterol- normal values are below 200 milligrams per deciliter of blood, though optimal protective levels are 140-150 mg/dl. Most people consider cholesterol an evil substance because of its association with cardiovascular disease. But cholesterol, of which about 80 percent% is made in the liver, is an essential element for cell membrane structure, hormones (including testosterone, which is synthesized from cholesterol and carried to the testes in men on LDL in the blood), and bile acids needed for fat digestion. Cholesterol itself cannot freely circulate in the blood, and must be attached to lipoproteins,such as HDL and LDL to circulate in the blood. Other lipoproteins include chylomicrons, which carry mostly triglyceride or fat; very-low density lipoprotein (VLDL), also primary a fat or triglyceride carrier; and intermediate-density lipoprotein (IDL). Although total cholesterol levels have been downplayed in recent years, a recent study found that total cholesterol levels do point to a lifetime risk of coronary heart disease.[ii]

(2) Low density lipoprotein cholesterol (LDL)- as noted, LDL is considered the primary bad guy in CVD onset, especially when oxidized. Ideal levels are below 100 mg/dl. LDL is the primary cholesterol carrier in the blood, where it transports cholesterol made in the liver to body tissues. When circulating LDL gets trapped in lesions in arteries, it tends to get oxidized. When LDL is oxidized, a series of events occurs inside the arterial wall that culminates in atherosclerosis.

Food high in saturated fat tend to lower the level of LDL cell receptors, thus increasing the level of LDL in the blood and increasing the risk of CVD. The other reason that saturated fat is considered bad in terms of CVD is that it acts as a precursor or starting substance for cholesterol synthesis in the liver. While having a LDL level of 100 or less is good, it isn’t a guarantee that you won’t suffer the effects of CVD.
(3) High density lipoprotein (HDL)- any level below 40 mg/dl is considered abnormal, and the higher the level,the better. HDL is considered the good cholesterol carrier, since it transports cholesterol out of the blood, back to the liver, where the cholesterol is degraded into bile. This represents the only way the body can rid itself of excess cholesterol, since cholesterol cannot be oxidized or burned like fat.

HDL also carries a unique and potent antioxidant called paroxanase that helps to douse the oxidant effects occurring in arteries that initiate the process of atherosclerosis. This natural antioxidant nullifies much of the effects of oxidized LDL. Exercise is closely linked to HDL levels, effectively increasing HDL levels in the blood. Most studies, however, show that you must exercise frequently and at a higher level of intensity to derive this exercise benefit of increased HDL. Losing bodyfat also increases HDL. Alcohol may increase HDL, too, but not necessarily the most protective subfraction of HDL.

(4) Triglycerides- Anything above 140 mg/dl is abnormal. Again, the lower the value,the better. Triglycerides are fat in the blood, and the dietary aspects that consistently increases blood triglycerides are carbohydrate intake, along with excess alcohol intake. For years, triglycerides weren’t considered particularly important in CVD. But recent studies show that higher triglycerides often leads to higher levels of both total cholesterol and LDL. Again, losing fat helps lower elevated blood triglycerides. Fish oil supplements can lower elevated triglycerides by about 60 percent.

The above listed tests are the standard lipid blood
tests. But these do not provide a complete picture of cardiovascular status. Studies show that as many as 50 to 80 percent of people with normal cholesterol levels still develop CVD. Determining the true status of your cardiovascular system requires several other tests. Many of these tests focus on inflammatory markers, such as C-reactive protein. This is related to the recognition that CVD is a largely inflammatory disease state in the arteries. Finding this out early enough to do something about it can spell the difference between life and death.

        
                   The additional CVD markers

                      Small LDL

Small, dense LDL is considered the most dangerous LDL of all.   Having much of this small LDL circulating in the blood is known as LDL pattern B. Those with larger LDL particles have pattern A. People with a predominance of pattern B or small LDL have a 3-times increased risk of CVD. Those with a lot of such small LDL show a 6-times increased risk. Small LDL is related to genetic predisposition, but also shows up in those who consume high carb diets, gain a lot of weight (fat), and don’t workout.

Smaller LDL can more easily become oxidized and thus play a greater role in CVD onset. Interestingly, those with Pattern B LDL can lower their risk by reducing fat intake, but in those with pattern A, a low-fat diet can make things worse by promoting the onset of the unhealthy smaller, denser LDL pattern B. This is one example of why a low-fat diet isn’t suitable for everyone, but you wouldn’t be aware of this unless you were tested for your specific LDL pattern. The good news about pattern B is that while such people show the most rapid progression of CVD, it’s also the most treatable pattern.

                                                             

                         Lipoprotein (a)

Lipoprotein (a) acts in a manner similar to LDL. In fact, it’s just LDL with a small protein fraction added to it. Having elevated lipoprotein (a) increases the chances of CVD three-fold. This blood protein isn’t tested in normal blood tests. One interesting aspect of lipoprotein (a) is that testosterone lowers it, but growth hormone elevates it. Anything above 20 mg/dl is abnormal. Studies show that elevated lipoprotein (a) levels occur in one-third of all coronary patients, and 15 to 30 percent of people who suffer heart attacks or strokes have elevated levels of this blood protein. Even if all your other lipid levels are good, having an elevated lipoprotein (a) level alone increases your risk of coronary artery disease by 300 percent.

                                              Apolipoprotein B (ApoB)


Apo B is a protein attached to LDL particles. Apo-B measurements provide a more accurate assessment of LDL status than even LDL itself. This relates to the fact that LDL is an indirect test, measured in relation to total cholesterol levels. But measuring apo-B is like doing a direct head count of LDL levels in the blood, thus providing a more accurate picture. Knowing precisely how much LDL is in the blood allows you to determine whether a person falls into the dangerous small LDL pattern or the safer larger LDL pattern. In addition, when LDL is oxidized, the portion oxidized is apo-B, thus making it in important risk factor for CVD. Desirable levels of apo-B are 40-60 mg/dl.

                                                         HDL2b

HDL2B is the type of HDL considered the most protective against CVD onset. This is the type increased by exercise and decreased bodyfat levels. HDL2B is the engine that makes HDL remove excess cholesterol from the arteries, and also carries the potent natural antioxidant, paraoxanase. People of Asian decent, as well as those who are fat and don’t exercise, often are deficient in this subfraction of HDL.

                                               C-reactive protein (CRP)

C-reactive protein is a general marker of inflammation in the body, and as noted, CVD is now considered an inflammatory disease. Since all forms of inflammation in the body can increase CRP levels, scientists developed a test more specific to CVD, known as a high sensitivity CRP test. CRP is also known as an acute phase reactant, because it’s released so rapidly after an inflammatory event in the body. The body releases such substances to help fight inflammation. Higher levels of HS-CRP point to an inflammation indicative of CVD. Those with high levels of HS-CRP have a 4-7 times increased risk of CVD.

Recent studies show that HS-CRP may be the most predictive test of all in relation to CVD. An elevated HS-CRP is twice as likely to predict the onset of a heart attack compared to LDL cholesterol levels. An estimated 20 to 30 million Americans have elevated HS-CRP, despite also having normal total cholesterol levels.

Having a HS-CRP level of greater than 3 mg/dl is considered a high risk for a heart attack. Elevated levels of CRP also show an increased risk of type-2 or adult-onset diabetes mellitus. Those who smoke, have high blood pressure, are fat, and fail to exercise, tend to have elevated CRP levels. People who regularly exercise show lower levels. In fact, a recent study[iii] showed that exercise was effective in lowering CRP levels even in obese people.

                                                        Fibrinogen

Fibrinogen is another acute phase reactant, involved in blood clotting reactions. Having an elevated fibrinogen level points to an increased tendency for internal blood clots. This is significant because most heart attacks and strokes are initiated by such internal clots that block arteries occluded by atherosclerosis. The normal blood range is 200 to 400 mg/dl.

                                                     Homocysteine


Homocysteine is a metabolite of the amino acid, methionine. Numerous studies show that this amino acid incurs direct toxic effects against arteries. Again, many people with normal blood lipid values may still have higher homocysteine levels. Studies show that having a high blood level of homocysteine puts you at the same risk of having a stroke as smoking a pack of cigarettes each day. Elevated homocysteine levels in the blood promote atherosclerosis by irritating the arteries and promoting a smooth muscle proliferation in the walls of arteries that leads to narrowed arteries.

The good news is that homocysteine levels are easily controlled by ingesting three nutrients: vitamin B6, folic acid, and vitamin B12. These nutrients convert homocysteine into a safe substance excreted from the body. Normal levels of homocysteine are below 14 micromoles per liter of blood. Steroid users should know that using these drugs increase homocysteine levels in the blood.

Other useful tests include those for resting insulin, since excess insulin can damage the internal linings of arteries, leading to atherosclerosis. Another good test is for apolipoprotein E, which exists in normal and abnormal genetic forms. Knowing which form you have can not only be a prognostic indicator of future CVD, but also of Alzheimer’s disease.

While many of these tests may appear exotic, they nonetheless provide the most accurate portrait of your cardiovascular status. They provide you the needed information that allows you to offset the sneaky effects of CVD to help yourself from becoming just another sad victim of the hidden terrorist within: CVD.


[i].Knoflach M, et al. Cardiovascular risk factors and atherosclerosis in young men.Circulation 2003;108:1064.
[ii].Lloyd-Jones D, et al. Lifetime risk of coronary disease by cholesterol levels at selected ages.Arch Internal Med 2003;163:1966-72.
[iii].Tomaszewski M, et al. Strikingly low circulating CRP concentrations in ultramarathon runners independent of markers of adiposity.Arter, Thromb, Vasc Biol 2003;in press.

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

Please consider joining this blog by clicking on the blue "join this site" button to the right of this blog. This will ensure that new blogs continue to be published. It costs nothing, and takes only a few seconds. Thank you.

See Jerry's book at       www.jerrybrainum.com