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Monday, December 8, 2014
Jerry Brainum, on Eggs.mov
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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.
Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com.
The 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
Monday, November 24, 2014
MYSTERY OF HARD MUSCLE DENSITY : IS TRAINING SLOWER THE BEST WAY BY JERRY BRAINUM
SEE JERRY BRAINUM'S NEWSLETTER...www.appliedmetabolics.com
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.
Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com.
The 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
Sunday, November 16, 2014
Wednesday, October 22, 2014
How often to train each muscle to add maximum size? With Jerry Brainum
Or click on this link to go to Jerry's Video ...https://www.youtube.com/watch?v=1-zcw0AUJkohttps:
©,2017 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited
Uploaded on Jan 16, 2012
Jerry Brainum answers weight-training and nutrition questions: "How often should I train each muscle to build maximum size? Bodybuilders of the past have trained each muscle 2-3 times a week. What does the research say?" More info at http://www.jerrybrainum.com
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©,2017 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
Please share this video on facebook
Saturday, October 18, 2014
Ebola infection: Will melatonin help you to survive? by Jerry Brainum
For Jerry Brainum's newsletter see ...Applied Metabolics Newsletter
To calm increasing national fears, President Obama in his weekly radio address on October 18, 2014 pointed out that in the nation of 300 million people, only three have contracted the Ebola virus, and only one person has died. This, however, is scant solace to those who hear that there is neither a cure nor a treatment for Ebola. This doesn't mean that if you contract the disease you will die, but rather that your chances of death range from 25% to 90% with an average of half those infected succumbing to the virus. The Ebola virus was first identified in the Sudan in 1976. It was thought to have been transmitted to humans by fruit bats, who are immune to the disease, but act as vectors of transmission. Prior to the current outbreak of Ebola, the World Health Organization (WHO) identified a total of 1,716 cases. In contrast, the numbers for the current epidemic involve 9,216 cases, with 4,555 deaths. Again, about half of those who are infected, die.
What is particularly alarming about Ebola is that there currently is no well-defined medical treatment for the disease. The treatment provided is what's called "palliative," which means indirect measures are provided in an attempt to keep the infected person alive long enough for his immune system to combat the infection. In fact, however, it's aberrations in the immune response to the disease that cause many of the problems that do result in mortality. As such, patients are provided with oral rehydration therapy, or sugar and salt water provided intravenously. Some emerging research shows that some common drugs may be able to prevent the Ebola virus from entering cells. One such class of drugs are calcium-channel blockers, normally used to treat high blood pressure. Thus far, however, these drugs have shown efficiency mainly in isolated cell studies, where the cells are infected with Ebola. Other emerging drugs, mostly still experimental, are already being provided to Ebola patients. These drugs are antiivirals, similar to the drugs used to treat viral infections such as herpes. Two such drugs are Favipiravir and Brincidofovir, with the latter drug provided to the one person thus far who had died from the Ebola infection in the United States. Clearly, it is not a cure. There is also an experimental antibody drug approved by WHO called Zmapp that seems capable of successfully treating Ebola infections, but there is not enough available yet to handle the current epidemic. Russia claims to also have an antibody drug that can knock out Ebola, but few details are available, and in any case, that drug isn't yet widely available, either.
The virus is normally acquired by contact with blood and body fluids, including semen. In that latter fluid, it can last for up to 7 weeks, which means it can be sexually transmitted. Ebola can also survive on various surfaces for a few hours, a fact made only too clear after a few Texas nurses acquired the disease by not observing correct sterility procedures following the treatment of an Ebola patient (who died). The symptoms of Ebola usually begin about 2-3 days after being infected. Since the initial symptoms are similar to that of the flu, it's easy to mistake Ebola for the flu. These symptoms include fever, sore throat,muscle aches and pains, and headaches. This is followed by more serious symptoms that include vomiting, diarrhea, and a rash. The infection then progresses to liver and kidney failure, along with internal and external bleeding. Death follows in 6 to 16 days, often from low blood pressure due to excess fluid loss. This explains why rehydration therapy is the initial step in trying to control the disease and prevent death.
Although Ebola isn't epidemic in the United States, and likely won't be, it is in several West African nations, including Guinea, Sierra Leone, Liberia, and Nigeria. The current outbreak in Africa began in December, 2013, and shows no signs of abating.
Although death from Ebola is often caused by excess fluid loss, that's only the tip of the proverbial iceberg as to what really happens in the body with this infection. The primary specific causes of death are a disruption of the vascular endothelium or the lining of blood vessels, which causes the large degree of internal bleeding associated with Ebola; disseminated intravascular coagulation (DIC), which involves an initial overactivity of blood clotting proteins, leading to excess blood clots, followed by a loss of these clotting proteins, resulting in excessive bleeding; fibrinolysis, or the excessive breakdown of blood clots, eventually resulting in extreme bleeding in many internal organs. These major problems begin with the breakdown of the lining of blood vessels, the endothelium.
But it's not the virus itself that attacks the endothelium, but rather is the result of the massive release of several immune mediators usually linked to inflammation in the body. These substances are collectively called cytokines and chemokines, and are released in response to inflammation and infection by immune cells. It is these mediators that activate the coagulation system, revving it to an excessively high level, that causes the endothelial damage. When a specific anticoagulant protein was provided to monkeys infected with Ebola, the monkeys survived the disease, giving credence to the notion that it's the uncontrolled coagulation reactions set off by Ebola that cause death from the disease.
A recent article in the Journal of Pineal Research, suggests that ingesting melatonin, which is synthesized each day in the pineal gland in the brain from the amino acid, L-tryptophan, can protect the endothelium from the damage caused by exposure to the Ebola virus. Melatonin works in this manner by shielding the vulnerable endothelial lining from the damaging effects of the massive release of cytokines and chemokines that would otherwise compromise the integrity of the blood vessel lining. Melatonin also prevents the onset of DIC by upregulating certain natural clotting factors in the blood.
The authors of the new paper also note that some of the effects of Ebola overlap with what occurs during septic shock, which usually causes death by the same route as Ebola, i.e., extreme loss of blood pressure. Providing melatonin appears to block the release of the various inflammatory mediators that are released in such great quantity during both Ebola infection and septic shock. While melatonin is not a cure for the virus itself, it may allow an infected person to survive long enough for their bodies to overcome the initial infection. It does this through preventing the inflammatory cascade that leads to destruction of blood vessels and out of control bleeding and coagulation. According to the authors, melatonin should be given to those diagnosed with Ebola as soon as possible in larger doses of 20 milligrams, several times a day for a prolonged period. It can be provided either orally or intravenously depending on the condition of the patient. In contrast, the body synthesizes melatonin in microgram amounts. One thousand micrograms equal one milligram. The usual dose suggested when melatonin is used as a sleep aid is 1 to 3 milligrams.
As the study authors point out, since there is no current effective treatment for Ebola, it wouldn't hurt to try a course of high dose melatonin, since it may control the underlying mechanisms that overwhelm the body and lead to death.
Xian-tan, D, et al. Ebola virus disease: Potential use of melatonin as a treatment. J Pineal Res 2014;In press.
Applied Metabolics Newsletter
 | |
| The Ebola virus |
To calm increasing national fears, President Obama in his weekly radio address on October 18, 2014 pointed out that in the nation of 300 million people, only three have contracted the Ebola virus, and only one person has died. This, however, is scant solace to those who hear that there is neither a cure nor a treatment for Ebola. This doesn't mean that if you contract the disease you will die, but rather that your chances of death range from 25% to 90% with an average of half those infected succumbing to the virus. The Ebola virus was first identified in the Sudan in 1976. It was thought to have been transmitted to humans by fruit bats, who are immune to the disease, but act as vectors of transmission. Prior to the current outbreak of Ebola, the World Health Organization (WHO) identified a total of 1,716 cases. In contrast, the numbers for the current epidemic involve 9,216 cases, with 4,555 deaths. Again, about half of those who are infected, die.
What is particularly alarming about Ebola is that there currently is no well-defined medical treatment for the disease. The treatment provided is what's called "palliative," which means indirect measures are provided in an attempt to keep the infected person alive long enough for his immune system to combat the infection. In fact, however, it's aberrations in the immune response to the disease that cause many of the problems that do result in mortality. As such, patients are provided with oral rehydration therapy, or sugar and salt water provided intravenously. Some emerging research shows that some common drugs may be able to prevent the Ebola virus from entering cells. One such class of drugs are calcium-channel blockers, normally used to treat high blood pressure. Thus far, however, these drugs have shown efficiency mainly in isolated cell studies, where the cells are infected with Ebola. Other emerging drugs, mostly still experimental, are already being provided to Ebola patients. These drugs are antiivirals, similar to the drugs used to treat viral infections such as herpes. Two such drugs are Favipiravir and Brincidofovir, with the latter drug provided to the one person thus far who had died from the Ebola infection in the United States. Clearly, it is not a cure. There is also an experimental antibody drug approved by WHO called Zmapp that seems capable of successfully treating Ebola infections, but there is not enough available yet to handle the current epidemic. Russia claims to also have an antibody drug that can knock out Ebola, but few details are available, and in any case, that drug isn't yet widely available, either.
The virus is normally acquired by contact with blood and body fluids, including semen. In that latter fluid, it can last for up to 7 weeks, which means it can be sexually transmitted. Ebola can also survive on various surfaces for a few hours, a fact made only too clear after a few Texas nurses acquired the disease by not observing correct sterility procedures following the treatment of an Ebola patient (who died). The symptoms of Ebola usually begin about 2-3 days after being infected. Since the initial symptoms are similar to that of the flu, it's easy to mistake Ebola for the flu. These symptoms include fever, sore throat,muscle aches and pains, and headaches. This is followed by more serious symptoms that include vomiting, diarrhea, and a rash. The infection then progresses to liver and kidney failure, along with internal and external bleeding. Death follows in 6 to 16 days, often from low blood pressure due to excess fluid loss. This explains why rehydration therapy is the initial step in trying to control the disease and prevent death.
Although Ebola isn't epidemic in the United States, and likely won't be, it is in several West African nations, including Guinea, Sierra Leone, Liberia, and Nigeria. The current outbreak in Africa began in December, 2013, and shows no signs of abating.
Although death from Ebola is often caused by excess fluid loss, that's only the tip of the proverbial iceberg as to what really happens in the body with this infection. The primary specific causes of death are a disruption of the vascular endothelium or the lining of blood vessels, which causes the large degree of internal bleeding associated with Ebola; disseminated intravascular coagulation (DIC), which involves an initial overactivity of blood clotting proteins, leading to excess blood clots, followed by a loss of these clotting proteins, resulting in excessive bleeding; fibrinolysis, or the excessive breakdown of blood clots, eventually resulting in extreme bleeding in many internal organs. These major problems begin with the breakdown of the lining of blood vessels, the endothelium.
But it's not the virus itself that attacks the endothelium, but rather is the result of the massive release of several immune mediators usually linked to inflammation in the body. These substances are collectively called cytokines and chemokines, and are released in response to inflammation and infection by immune cells. It is these mediators that activate the coagulation system, revving it to an excessively high level, that causes the endothelial damage. When a specific anticoagulant protein was provided to monkeys infected with Ebola, the monkeys survived the disease, giving credence to the notion that it's the uncontrolled coagulation reactions set off by Ebola that cause death from the disease.
A recent article in the Journal of Pineal Research, suggests that ingesting melatonin, which is synthesized each day in the pineal gland in the brain from the amino acid, L-tryptophan, can protect the endothelium from the damage caused by exposure to the Ebola virus. Melatonin works in this manner by shielding the vulnerable endothelial lining from the damaging effects of the massive release of cytokines and chemokines that would otherwise compromise the integrity of the blood vessel lining. Melatonin also prevents the onset of DIC by upregulating certain natural clotting factors in the blood.
The authors of the new paper also note that some of the effects of Ebola overlap with what occurs during septic shock, which usually causes death by the same route as Ebola, i.e., extreme loss of blood pressure. Providing melatonin appears to block the release of the various inflammatory mediators that are released in such great quantity during both Ebola infection and septic shock. While melatonin is not a cure for the virus itself, it may allow an infected person to survive long enough for their bodies to overcome the initial infection. It does this through preventing the inflammatory cascade that leads to destruction of blood vessels and out of control bleeding and coagulation. According to the authors, melatonin should be given to those diagnosed with Ebola as soon as possible in larger doses of 20 milligrams, several times a day for a prolonged period. It can be provided either orally or intravenously depending on the condition of the patient. In contrast, the body synthesizes melatonin in microgram amounts. One thousand micrograms equal one milligram. The usual dose suggested when melatonin is used as a sleep aid is 1 to 3 milligrams.
As the study authors point out, since there is no current effective treatment for Ebola, it wouldn't hurt to try a course of high dose melatonin, since it may control the underlying mechanisms that overwhelm the body and lead to death.
Xian-tan, D, et al. Ebola virus disease: Potential use of melatonin as a treatment. J Pineal Res 2014;In press.
 |
| For the latest accurate information on nutrition, health, exercise science, food supplements and more, check out Applied Metabolics Newsletter at www.appliedmetabolics.com |
Friday, October 17, 2014
Jerry Brainum, Arginine and Muscle Pump with Ric Drasin
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, October 11, 2014
Monday, October 6, 2014
Exclusive Newsletter @ www.appliedmetabolics.com
The most important and knowledgeable person that I have encountered during my successful 40-year bodybuilding career is Jerry Brainum.He gave me the edge when it came to preparing for competitions by providing me with vital information related to training and diet. This is the same type of information that will appear in his upcoming newsletter.Jerry gave me the schooling that I needed to develop one of the greatest physiques of all time. His knowledge on the inner workings of the body, along with supplementation, including how to best use these powerful nutrients to build muscle and burn fat, has helped my journey to the winner’s circle to be a frequent one. With Jerry’s advice, I was able to win the Sandow trophy at the first Master’s Mr.Olympia in 1994. That enabled me to achieve “legend” status, and become a member of the Bodybuilding Hall of Fame. If you are serious about your bodybuilding, Jerry’s newsletter will provide you with the information that you need to build your championship physique. I strongly suggest that you subscribe today, and read each issue start to finish.
–Robby Robinson, “The Black Prince,” IFBB Mr.America 1975, IFBB Mr.World, 1975, Mr.International, 1976,IFBB Mr.Universe, 1976, Night of the Champions champ, 1978, 1979, NABBA Pro Mr.Universe, 1981, Master’s Mr.Olympia, 1994.
Jerry Brainum's exclusive Newsletter is at www.appliedmetabolics.com
Saturday, September 27, 2014
Friday, September 26, 2014
Wednesday, September 24, 2014
Does boosting Nitric Oxide build muscle? by Jerry Brainum
see Jerry Brainum's newsletter...www.appliedmetabolics.com
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.
Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com.
The 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
Saturday, September 13, 2014
Friday, September 5, 2014
Thursday, August 14, 2014
One set, three sets, or more: Which is best for strength and muscle gains? by Jerry Brainum
Perhaps the most contentious debate among trainers, physiologists, and bodybuilders relates to the volume of exercise that is best to promote muscle hypertrophy (growth) and strength gains.Back in the early days of bodybuilding, pioneers such as the great Eugene Sandow,suggested that those lifting weights should do only one set per exercise. But Sandow also advised the use of light weights to build muscle, probably because he sold light dumbbells. As time progressed, the volume of training gradually increased, too. By the 1940s, men such as Steve Reeves and Clarence Ross, the 1947 and 1945 Mr.Americas respectively, were training three times a week, averaging three sets per exercise. In the late 50s, the volume of exercise increased exponentially, with programs that featured six days a week of training, working varying muscle groups, and as much as 20 or more sets per muscle group.
The increased training volume remained the standard until about 1970. At that time, an eccentric entrepreneur from Florida, Arthur Jones, introduced the "better barbell," namely his Nautilus training machines. These machines, which Jones claimed were the result of about 30 years of development, worked on the principle of variable resistance, made possible by the unique Nautilus cam that was part of every machine. More importantly, however, Jones said that using his machines worked muscles far more intensely than was possible with free weights because the machines placed resistance throughout the full range of exercise motion, unlike free weights, where the resistance at some points was nearly zero. This increased stress on exercised muscles also required a reduction in training volume, lest you exceed a nebulous "recovery ability." Doing so, said Jones, would result in either no gains, or even a loss of muscle through overtraining. As proof, he pointed to the glacially slow gains made by most bodybuilders, who Jones considered grossly overtrained.
Specifically, Jones stated that no one needs to do more than one set per exercise, done to complete muscular failure to ensure a maximal recruitment of available muscle fibers. While the often dogmatic Jones offered some persuasive evidence that training in this high intensity, but low volume manner is superior, in reality his system never captured the complete attention of those in the iron world. Most simply could not accept the notion that doing only one set could ever produce better gains than doing three or more sets per exercise. While Jones disparaged mainstream academic physiology researchers, most of whom he characterized as "idiots," several researchers nonetheless have published studies over the years that sought to either prove or disprove Jones' principles of high intensity, low volume training.
Some studies have indeed found little or no difference in muscle gains when doing one versus three sets of an exercise. Others, in contrast, have found that a minimum of three sets is required to build muscle, although beginners can get away with doing only one set because the initial gains in muscle size and strength that occur with weight-training have more to do with neuromuscular adaptations, rather than actual muscle hypertrophy, which usually doesn't show up until after about three months of regular training. Some studies show that doing a greater volume of training is superior because it promotes a greater release of various anabolic hormones, such as testosterone and growth hormone. This seems a moot point, since recent research shows that the temporary elevations in these anabolic hormones that occur following exercise play no significant role in promoting gains in muscular size and strength. What counts in the way of hormones is producing enough to maintain normal levels, or using drugs, such as anabolic steroids and growth hormone, that result in much higher than normal levels of the hormones, which have definite, unquestionable positive effects on muscle hypertrophy and strength gains.
A major problem with nearly all the past studies that have sought to either prove or disprove the high intensity/low volume style of training is that the subjects in those studies have almost always been untrained college students. While being a college student doesn't matter in this respect, being untrained certainly can affect the results of the study. As noted, when you begin lifting weights, your initial gains result from a more efficient neuromuscular connection. Basically, the exercise makes the connection between your brain and your muscles more efficient, which results in increased muscle strength, followed by increased muscular size. The salient point here is that beginners have a tendency to make gains on any type of training program.So using rank beginners as a way to determine the benefits of any particular style of training is bound to produce skewed results. Not to mention that some beginners are able to train harder than others right from the start, and would likely make faster muscle gains.
A new study that takes still another look at the one versus three set controversy, starts with the premise that three sets are indeed superior to doing one set of an exercise. But unlike prior studies, in this study the subjects all had at least a year of training experience, which is enough to eliminate any of the beginner anomalies discussed earlier. This study lasted for eight weeks, and featured 16 men with an age range of 18 to 21. The men were divided into two groups, with 8 doing an upper body routine that included one set per exercise, done three days per week. The other 8 men did the same routine and workout frequency, but did three sets per exercise. All the subjects ingested their usual diets, but refrained from using any food supplements that may have influenced the study results. At the start of the study, baseline strength tests were done using the bench press and shoulder press exercises. All the exercises done in the routines were standard upper body exercises, using only free weights, not machines (I can hear the ghost of Arthur Jones saying, "idiots!").
The results after 8 weeks of consistent training showed that both groups showed a 20.7% strength gain, with no significant difference between the two groups. The only significant difference between the one and three set groups was in fat loss, as determined by measuring seven skin fold sites before and after the 8-week program. Those in the one set group showed less skinfold thickness compared to the three set group, an indication of greater loss of subcutaneous body fat. This finding surprised the study authors, who expected that the greater number of total reps and volume in the three set group would have produced a better body composition result. The authors suggest that the lower volume training may maintain better muscle glycogen and protein stores, reduce intramuscular damage, and thereby promote greater lean mass formation. On the other hand, skin fold measurements, while accurate when measured by someone who knows precisely the correct measuring technique, isn't as accurate at other methods to determine body fat gains or losses.
The essential point of this study is that it used more experienced subjects, and that with these subjects, doing one set proved as effective as doing three sets per exercise, despite 66 percent less training time. Science decrees that one study doesn't constitute definitive evidence, so this study would have to be replicated with similar results countless times before it's officially accepted as scientific gospel. Even so, I suspect that you cannot eliminate the specter of cognitive dissonance with regard to long held beliefs as to what constitutes the best way to train. In the end, the answer to that question is probably whatever you believe works best for you.
Baker, JS, et al. Strength and body composition changes in recreationally strength-trained individuals: comparison of one versus three sets resistance-training programs.BioMed Res Intern 2013.
Coming soon: Jerry Brainum's Applied Metabolics Newsletter, the source of truth for all matters related to health, fitness, nutrition, longevity, and ergogenic aids. It will soon be available at: www.appliedmetabolics.com.
©,2014 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.
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Saturday, July 26, 2014
Does mouth rinsing with carbohydrates boost exercise and sports performance? By Jerry Brainum
Carbohydrates are the most efficient fuel for exercise. While certain amino acids from protein can be converted into glucose, which is the only sugar that circulates in the blood, the conversion of protein or amino acids into glucose is an inefficient process that doesn't yield much glucose. As for fat, only the glycerol portion of the triglyceride structure can be converted into glucose in the liver. Thus, only 10% of fat is capable of being converted into glucose. Carbs are considered the high test fuel to power both exercise and sports. Studies show that carb intake consistently improves performance in activity lasting more than 2 hours. It does this by maintaining glycogen stores, which are the primary fuel for anaerobic exercise, including bodybuilding exercise, and also enhancing carb oxidation, as well as maintaining a high energy level throughout the course of exercise or sports. When it comes to exercise lasted an hour or less, carbs aren't as vital. Studies have even shown that ingesting carbs prior to a high intensity weight workout does not contribute to the intensity level. But this also depends on the existing muscle glycogen state. With a depleted glycogen state, as occurs with a zero carb diet, ingesting the equivalent of one gram of carb per minute does boost intensity level during training.
Some studies suggest that you don't even have to ingest carbs to provide an ergogenic effect. Merely rinsing the mouth with a carb solution for a few seconds is enough to boost energy and exercise performance. One study showed that cyclists who rinsed their mouths with carbs showed a 2.9% improvement in performance. Other studies have shown similar results with running.
Why would just rinsing the mouth with carbs provide an ergogenic effect? Some suggest that rinsing the mouth with carbs activates neural pathways that lower the perception of effort during exercise. A study published two years found that carb mouth rinsing didn't affect strength performance. A new study examined the effects of carb mouth rinsing during multiple sprints, which is a high intensity activity. The study subjects consisted of eight trained men, all with athletic backgrounds. The average age was 21. Anyone who had used creatine supplements, which would affect the outcome of the study was eliminated if they had ingested any creatine within 12 weeks of the study onset. The subjects were also asked to refrain from ingesting any caffeine and to ensure that they were fully hydrated to prevent dehydration-based interference.
The men rinsed their mouths with either a carb solution composed of maltodextrin 6.4% or a placebo. They rinsed their mouths for 30 seconds before engaging in various sprint tests. The results show no improvement in sprint times, perceived exertion, or blood glucose levels in the men that rinsed with the carb solution. As such, the conclusion of the study was that mouth rinsing with carbs is not an effective ergogenic aid. It short, it just doesn't work.
Darling JK, et al. Effect of carbohydrate mouth rinsing on multiple sprint performance.J Int Soc Sports Nutr 2013: 10:41.
©,2014 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.
Coming Soon: Jerry Brainum's Applied Metabolics Newsletter-clearing up the confusion about nutrition, exercise science, anti-aging, ergogenic acids and much more. Look for it at appliedmetabolics.com.
See Jerry's book at www.jerrybrainum.com
Friday, June 20, 2014
Will baking soda help you train harder? By Jerry Brainum
Depending on which study that you look at, sodium bicarbonate (better known as baking soda) is either an efficient ergogenic aid, or just another way to induce nausea. Sodium bicarb acts to alkalinize or reduce acidity. It is made in the body, and used to help maintain a narrow range of acid/base levels in the blood. Either excessive alkaline or acidic blood is very harmful to health. Sodium bicarb is often administered to patients suffering from heart attacks, in which a lack of sufficient oxygen flow to cells results from a failure of the heart to sufficiently pump blood leading to increased blood acidity. From an athletic standpoint, while there are several causes of muscle fatigue, increased acidity is definitely one of them. Increased muscle acidity is the result of anaerobic metabolism, whereby waste products of muscle metabolism boost local acidity in muscles. This, in turn, interferes with the activity of certain energy-related enzymes, which cannot function in an acidic environment.
While lactic acid has often been accused in the past of being the primary instigator of increased muscle acidity, in fact only the acid portion of lactic acid is the true culprit. Lactate itself is a reusable fuel, where it is released into the blood from exercised muscle, sent to the liver, and then reconverted into glucose in a process known as the Cori cycle. The actual process of converting lactate into glucose is known as gluconeogenesis. So the actual acidity from lactic acid are hydrogen ions. These hydrogen ions cause a drop in both muscle and blood pH levels, meaning higher acidity. In the muscle, this leads to lower rates of glycolysis, or use of glucose as a fuel; an interference with the activity of calcium ions required for muscular contraction; and an increased feeling of overall fatigue in the muscle.
Although sodium bicarb doesn't work in the muscle itself, it does impart an alkalosis, or acid-lowering effect in the blood. This lowers levels of hydrogen ions in the blood. But the sodium bicarb also tends to promote exit of lactic acid out of the muscle and into the blood, and this is where the ergogenic effect comes into play. Since the increase of metabolic acid occurs mainly during higher intensity, short-term activity, the ergogenic effect of sodium bicarb is most evident for shorter duration events, such as sprints. But not all studies of sodium bicarb have found a definite improvement after its use. A recent analysis of prior studies that have involved sodium bicarb use in sports found that it was ergogenic in 38% of the studies.
Since weight-training and bodybuilding exercise normally features a short period of high intensity, and since the major cause of fatigue appears to be increased muscle acidity (felt as a burning sensation in the trained muscle), it would initially appear that sodium bicarb would be an ideal ergogenic aid for use in bodybuilding and other weight-training activity. Several studies have examined whether sodium bicarb may be useful for those engaged in weight-training. The results have been mixed, with some studies showing increased repititions done, less feelings of fatigue after using sodium bicarb. Other studies, however, have not shown any improvements.
One primary reason for the lack of response after ingesting sodium bicarb is that since it works by neutralizing excessive acidity, for it to work you need to impose a level of exercise intensity high enough to significantly boost muscle acidity levels. Several of the prior studies that showed no effects after using sodium bicarb did not provide sufficient intensity levels for the bicarb to do anything. In actuality, you would need to use enough weight to stress the muscle, and do each exercise to failure as a means of producing an intensity level high enough to truly test the effects of bicarb.
This was precisely what was done in a new study that involved 8 men experienced in weight training. They ingested either 0.3 milligrams of sodium bicarb per kilogram of bodyweight, which is the standard dose for athletic purposes, or a placebo consisting of salt water. Both treatments were separated by 48 hours, and both drinks were mixed with 5 milliliters per kilogram of bodyweight flavored, sweetened water provided in a opaque flask. The men then did 3 sets of bench press and back squat using 80% of one-rep max weight done to complete muscle failure. The results showed that when the men consumed the sodium bicarb solution, they were able to complete additional reps in the squat compared to the salt water placebo. But when they did the bench press five minutes after the squat exercise, no improvement was noted. The men did a similar number of reps on the first set of both the squat and bench press, but did more reps on the second and third set of the squat. The study authors suggest that the failure protocol used in the exercises explains the clear ergogenic effect of sodium bicarb. Why the bicarb didn't work for the bench press wasn't explained, but it may be related to the larger muscle mass of the legs compared to that used when doing a bench press. More muscle mass means more muscle acidity.
Should you consider regular use of sodium bicarb to enhance workout performance? While baking soda is not expensive compared to high priced "pre-workout" supplements, routine use of sodium bicarb would not be a good idea because of the high sodium content of baking soda. In fact, it is the high sodium content of baking soda that has limited its use among athletes, since many have experienced gastrointestinal distress following the use of sodium bicarb. But there are ways around this. If you ingest a high carb meal, 120-150 minutes prior to exercise, and at that time consume a dose of 0.3 grams of sodium bicarb per kilogram of bodyweight mixed with 7 milliliters of water per kilogram of bodyweight, the risk of gastrointestinal distress drops significantly. Most of the problems that have occurred with ingestion of sodium bicarb have involved ingesting it too close to exercise or sports activity.
Recent research suggests that sodium bicarb is synergistic with beta alanine, which works to boost levels of carnosine, an intramuscular buffer in muscle. Creatine also lowers muscle acidity, and the combination of sodium bicarb and creatine offers a potent weapon against premature training fatigue, and would likely allow you to train with an increased level of intensity, which translates into increased muscle and strength gains. Adding caffeine to the mixture would make it even more potent, with the amount of caffeine being 300-400 milligrams.
Duncan, M.J, et al. The effect of sodium bicarbonate ingestion on back squat and bench press exercise to failure. J Strength Cond Res 2013: in press.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
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Sunday, June 1, 2014
Does fasting high intensity interval training burn more fat? by Jerry Brainum
There are two basic types of aerobic training, long-slow distance (LSD) and high intensity interval training (HIIT). With the long-slow distance, you exercise at a constant level of intensity, usually based on your age and fitness level, for a set amount of time. The HIIT training is characterized by short bursts of high intensity exercise, as shown by a higher pulse rate and exercise intensity, interspersed with brief recovery periods, where you slow down, and let your pulse drop down. The main advantage of doing HIIT training as opposed to the more conventional LSD type of aerobics, is that you get the same, or better results with far less investment of training time. Indeed, studies show that just 6 HIIT training sessions over a 2-week period resulted in the same changes in muscle oxidative capacity as doing continuous moderate intensity aerobics that required 3-fold as much training time, and 9-times more training volume. A recent study showed that doing HIIT of 10x 60 second intervals at 90% of maximum heart rate led to an immediate increase in insulin sensitivity as measured by a lower resting glucose level in diabetics.
So it appears that you can get the same, or even superior benefits with HIIT compared to conventional LSD training. The notable advantage of HIIT is far less time in the gym. In addition, from a bodybuilding perspective, you also are less likely to slip into an overtraining state from doing HIIT compared to hours of conventional aerobics.
A current issue of aerobic training is whether you should exercise in a fasted state, or eat something prior to training. Some believe that exercising in a fasted state permits more fat oxidation, especially when done first thing in the morning. The idea here is that glycogen levels are low in the when you awaken, and thus it's easier to tap into fat stores when you exercise at that time. One study found that 6 weeks of conventional aerobic exercise in the fasted state produced changes that resulted in greater muscle oxidative enzymes (required for fat oxidation or "burning."), and also increased glucose and fatty acid transport capacity. Young men who engaged in fasted aerobics didn't gain weight despite consuming a higher fat and calorie intake.
Based on these findings, a new study had 16 overweight, obese women engage in HIIT for 6 weeks. They used the 10x 60 seconds HIIT protocol, during which they raised their heart beat levels to 90% of maximum for 60 seconds, followed by a recovery period in which they slowed down (they were on stationary bikes) for another 60 seconds. They did 10 bouts of this per session, three times a week for a total of 18 sessions. But eight of the women consumed a meal prior to the exercise session, while the other eight did the exercise in a fasted state. The women who ate consumed a meal an hour prior to exercise, while the fasted women ate their last meal before exercise the evening before, but did eat a meal an hour after the exercise. The meals consisted of 439 calories, with 74% of the calories derived from carbohydrates.
The results showed that both groups showed similar beneficial changes, and that eating the meal prior to training had no effects on these changes.Specifically, the women showed reduced fat in their thighs and abdominal regions. And they got this from only 30 minutes of exercise a week. HIIT may be more efficient at lower body fat levels because of increased release of hormones that promote fat mobilization, such as epinephrine and norepinephrine. HIIT also leads to a higher post-exercise oxygen consumption, which means a higher resting metabolic rate compared to conventional aerobics. One recent study also suggested that HIIT produces a greater decrease of appetite after training, which means less total food consumption.
One change that didn't occur was an increase in insulin sensitivity. This effect more often happens in men, and is related to a greater depletion of existing glycogen stores. When women exercise, they are more efficient at preserving glycogen levels. In fact, they use up to 50% less glycogen then men during high intensity exercise. In addition, about 25% of people just don't get any change in insulin sensitivity following exercise, and another 15% show a decline in insulin sensitivity. But since abdominal fat, especially the deep-lying visceral fat, is related to insulin sensitivity, and since all the women in this study did lose significant amounts of abdominal fat, the odds are that their insulin sensitivity was improved, but the effect was more subtle.The women also showed lean mass gains in their legs, which never occurs with conventional aerobics.Gains in lean mass, or muscle, are known to boost insulin sensitivity.
So for those who lack the time to engage in long aerobic sessions in an effort to reduce excess body fat levels, HIIT may be the best way to go.
Gillen, JB, et al. Interval training in the fed or fasted state improves body composition and muscle oxidative capacity in overweight women.Obesity 2013;21: 249-2255.
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Monday, May 5, 2014
Minding your PQQs by Jerry Brainum
Odds are good that you've never heard of a supplement called "PQQ," which stands for pyrroloquinoline quinone. It was first discovered as a growth factor for bacteria in 1979. Later animal studies showed that it also played a role in the growth of animals, too. It may even do this in humans, since human breast milk is known to contain 15 percent PQQ. The human body produces about 100 to 400 nanograms of PQQ a day, which is a very small amount. It's also found in various foods, particularly soy-based foods, such as natto and tofu, as well as in spinach. However, the amount found in foods is also infinitesimal. Still, the fact that it exists in the human body, albeit in very small quantity,indicates that it must do something.
The fact that it seems to be required for animal growth and reproduction suggested that it could be a new vitamin compound. While PQQ does affect the activity of various body enzymes, which is one requirement of a vitamin, it does not seem to satisfy the other vitamin requirement, in that there is no established deficiency condition associated with PQQ. Still, it is capable of doing some significant things in the body. Among these are activation of PGC-1A, a substance that promotes the development of new mitochondria. Mitochondria are cigar-shaped structures in the cell where such vital processes as electron transport and beta-oxidation occurs, resulting in the production of the energy factor, ATP, and fat oxidation. A loss of function of mitochondria is thought to be major cause of aging, since when mitochondria die out, the cell loses its energy source, and cannot function, so it too dies. A loss of mitochondria is also suspected of being a major cause of sarcopenia, the loss of muscle with age.
While the effects of PQQ in animals are clear-cut and beneficial, the effects on human health are preliminary to say the least. In animals, PQQ lowers triglycerides (blood fat) more efficiently than fish oil, but in the one human study that has tested the effects of PQQ, it had no effect on triglycerides. Animal studies show that PQQ may modify the activity of NMDA brain receptors. These receptors are involved in memory and learning, but when overstimulated, can lead to loss of neurons, or brain cells. PQQ seems able to block such overstimulation. Much of the benefits of PQQ may be ascribed to an antioxidant activity. While antioxidant vitamins, such as vitamins C and E are quickly oxidized and thus no longer capable of exerting anti-oxidant activity, PQQ can be quickly converted back to antioxidant status, and go through thoussands of such cycles, known as redox cycling.
Articles about PQQ have suggested that it can improve cognitive ability, or brain activity related to memory and intelligence. This could be related to both the increased mitochondria fostered by PQQ or the effect on NMDA brain receptors. However, most of the animal studies that have shown this effect involved PQQ being injected directly into the brain, a method of administration not likely to be popular with humans. Whether the current oral supplement of PQQ does likewise for human brains is not known or proven yet, although some studies did show slight improvements in memory in older adults after PQQ supplementation.
As noted, there is a dearth of human studies related to PQQ supplementation. In one recent human study, however, a number of beneficial effects did occur. The study only had 10 subjects, 5 women and 5 men, ages 21 to 34. In the first part of the study, the subjects were provided 0.2 milligrams of PQQ per kilogram of bodyweight in a fruit-flavored drink. This part of the study measured antioxidant effects of PQQ, and found only a slight effect.In the second part of the study, the subjects increased the dose of PQQ to 0.3 milligrams per kilogram of bodyweight. The subjects who ingested this dose showed a lowering of C-reactive protein and interleukin-6, both indicative of decreased body inflammation. The subjects also showed lowered excretion of TMAO, which was in the news recently because it was implicated as a promoter of atherosclerosis. TMAO is a byproduct of the metabolism of both choline and carnitine that have been acted upon by intestinal bacteria. PQQ also lowered the excretion of a few amino acids, suggesting that it may have a beneficial effect on nitrogen retention. Other indices did show definite beneficial effects on mitochondria.One other thing worth noting: the study was sponsored by the Mitsubishi Gas and Chemical Company--the major supplier of PQQ in supplement form.
So, is PQQ worth taking as a supplement? Based on the current available human research, the answer would have to be no. On the other hand, for those seeking to maintain healthy mitochondria, PQQ might be useful, but you can get the same effect for free merely by engaging in high intensity aerobic exercise.The suggested dose of PQQ is 10-20 milligrams a day.
Harris, CB, et al. Dietary pyrroquinoline quinone (PQQ) alters indicators of inflammation and mitochondrial-related metabolism in human subjects.J Nut Biochem 2013;24:2076-84.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
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Friday, April 11, 2014
Toxic Cinnamon? By Jerry Brainum
Next to black pepper, cinnamon is the most common spice used today. Cinnamon is derived from the bark of small evergreen trees grown in South and Southeast Asia, especially Sri Lanka. However, there are different kinds of cinnamon, and this can have an impact on health. For example, what's called true cinnamon, also known as Ceylon cinnamon comes mostly from Sri Lanka. The other predominant types include various forms of cassia, which includes Indonesian Cassia, Vietnamese Cassia, and Chinese Cassia. These look and smell like cinnamon, but they aren't true cinnamon, and this is where the health effects enter the picture.
Cinnamon has a long history of use, dating back the Biblical times. It's mentioned in the Bible several times. Then, as now, it was primarily used as a spice for flavoring purposes.More recently, cinnamon has been suggested as a natural way to support healthy blood glucose levels. This, if true, could have a major significant impact on health, since the incidence of diseases related to poor glucose control, including insulin resistance, or "pre-diabetes," and type-2 diabetes, are are the rise worldwide. Type-2 diabetes was formerly called "adult-onset diabetes" to distinguish it from type-1 diabetes, which is caused by a destruction of the cells in the pancreas that produce insulin. The adult-onset form usually does not involve destruction of the pancreatic cells that produce insulin, but rather features a resistance of cells to insulin activity. The usual treatment involves a combination of oral drugs and exercise, or if the disease progresses, use of insulin itself to overcome the cellular resistance to the hormone. Type-2 diabetes is no longer referred to as "adult onset diabetes,"since it shows up in children as young as 12. The reasons for this are multifactorial, but relate mostly to a combination of lack of sufficient physical activity and excess body fat.
Those who suffer from insulin resistance, which is characterized by elevated resting glucose levels, are often able to prevent the progression to full-blown diabetes if they lose excess body fat through a combination of exercise and diet. Low carbohydrate diets are particularly effective in this regard, since they tend to significantly reduce elevated resting insulin levels, as well as lower elevated blood glucose levels. Several natural supplements are also suggested as a safe way to help control elevated insulin and glucose levels. These include the trace mineral, chromium. Chromium is thought to work through boosting the effectiveness of insulin. It does this by modifying the cellular receptors for insulin, more or less providing a tighter bond of insulin to its cellular receptor. However, more recent studies have found that an excess of chromium produces the paradoxical effect of increasing insulin resistance. Even worse, the most recently published study found that chromium exerted little or no effect on elevated blood glucose levels. That, however, is just one study, and it would not be wise to cease consuming any chromium based on the findings of a single study.
There are various other natural substances often suggested to control blood glucose levels, such as soluble fiber, which delays the absorption of simple carbohydrates, and thus lowers the insulin release effect. But among the various natural supplements touted to control glucose levels and possibly help to prevent the development of diabetes, cinnamon is the most often mentioned supplement. The research to prove this effect of cinnamon, however, is contradictory at best. One study published in 2003 provided 60 diabetic patients of both sexes with doses of 1, 3, or 6 grams of cinnamon powder. The treatment duration was 40 days, the results showed that cinnamon decreased fasting blood glucose levels, as well as lowering elevated blood lipid levels. Another study from 2006 featured 65 diabetic patients who ingested 3 grams of a water extract of cinnamon for four months. The results of this study showed that while cinnamon did lower fasting blood glucose levels, it didn't affect blood lipid levels, nor did it affect hemoglobin A1C,a measure of long-term glucose usage in the body. Two other studies published the same year, found no effect of cinnamon on blood glucose or other measures. Two studies published in 2007 likewise also found no effects of cinnamon when provided at a dose of one gram a day. Another study published the same year found that 6 grams of cinnamon delayed gastric emptying following a meal, which delayed the entrance of glucose into the blood. A Cochran review (which accessed previous studies) found that "cinnamon produces no more effects than a placebo." In other words, the review suggested that cinnamon was worthless in terms of glucose control.
But that's not the biggest problem with cinnamon. It turns out that all of the commercial cinnamon on the market doesn't contain true or Ceylon cinnamon, but rather contains a variety of the cassia form. The problem here lies in a natural constituent of the cassia, but not Ceylon cinnamon, namely coumarin. The fact is that 90 percent of commerical cinnamon used in spices and supplements is the Indonesian cassia form, and in some cases, the Chinese cassia. Both of these forms contain significant amounts of coumarin. Why is that a problem?
Coumarins can cause severe liver problems in animals, less so in humans. Some humans show liver abnormalities after consuming it, while others don't for unknown reasons. It is also a possible carcinogen, linked to causing tumors in animal studies. Coumarin also serves as a precursor for the production of the drug, Coumadin, trade name, Warfarin. Warfarin is a vitamin K antagonist that helps to prevent blood clots. It's often prescribed to treat people with atrial fibrillation, a defect of heart conduction that is a risk factor for strokes. The hope is that providing these people with Warfarin will lower stroke risk by preventing clot formation, which is often the cause of the strokes. Warfarin is also commonly used to kill rats.
A recent study analyzed the levels of coumarin in both commercial cinnamon supplements, and cinnamon used for flavoring, spices, and so on. It found levels of coumarin that exceed the amount allowed by various health organizations to exist naturally in food. True or Ceylon cinnamon was found to contain only trace amounts of coumarin. But all the cassia versions contained far more, and in some causes, possibly toxic levels of coumarin.
The obvious solution to this problem would be to use only Ceylon cinnamon. The problem with this is that Ceylon cinnamon is virtually non-existent in the United States, where only the cassia forms are used. Another option is to use only special water-soluble cinnamon extract supplements, which are sold under various names. These supplements do not contain any coumarin, but they do contain the polyphenol substances thought to account for the beneficial effects of cinnamon. From an anecdotal point of view, I've tried both forms of cinnamon supplement, although the ones that I used were likely the cassia versions. Neither form, either the usual cinnamon or the far higher priced water-soluble form, did anything at all to control my blood glucose levels. Since I was insulin resistant at the time I used the supplements, I was a good test subject. I used the suggested doses, and regularly checked my resting blood glucose level, but found no changes whatsoever with use of either form of cinnamon. Am I saying that cinnamon is useless? Not at all. I think cinnamon tastes great, and I love it as a flavoring agent. But for treating insulin resistance and diabetes, well, let's just say I'm highly skeptical about that.
Wang, YH, et al. Cassia cinnamon as a source of coumarin in cinnamon-flavored food and food supplements in the United States.J Agric Food Chemistry 2013: in press.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
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Sunday, March 23, 2014
Are vitamin and mineral supplements a waste of money? By Jerry Brainum
An article published in the December 17, 2013 issue of the Annals of Internal Medicine made the bold claim that vitamin-mineral supplements are a waste of money for most people. The article authors noted that the evidence that vitamins and minerals have any preventive effect against the onset of the major killer diseases, including cardiovascular disease and cancer, is scant to non-existent. Furthurmore, asserts the doctors who wrote the article, vitamins and minerals will do nothing to help you live longer. Of course, since so many people, even those who aren't into using food supplements, still ingest a basic vitamin and mineral formulation as "nutritional insurance," this story merited being picked up by the popular media, who preceded to produce stories with such headlines as "Vitamin and minerals are worthless and a waste of money."
However, as is typical with popular science reporting, several important points were not mentioned in the Internet and newspaper reports. For one, the assumption of the medical journal article was that most people are consuming enough nutrients in food, and therefore don't need any supplements. This further makes the assumption that most people consume a balanced diet that is replete in all necessary nutrients. That notion is nothing less than a fantasy on the part of the medical journal authors. Had they bothered to look at the latest government nutritional surveys, they would quickly have noted that the majority of Americans are in fact, not even meeting the minimal suggested daily intake of many vitamins and minerals.
One reason for this is the reliance on processed and fast foods, which are devoid of many essential nutrients, but are top-heavy in carbohydrates and fats. Few people consume even the minimal suggested intake of five servings a day of fruits and vegetables, and without eating these foods, they will not be getting some of the essential nutrients. The obvious question is: if they aren't obtaining these required nutrients from food sources, where are they getting them? The answer is no where. And contrary to what was wrongly stated in the medical journal article, a long-term lack of nutrients is indeed linked to disease onset, even if it involves just a nutrient deficiency.
The authors also overlooked individual requirements for certain nutrients. The concept of biochemical individuality states that, due to certain slight gene differences, some nutrients may be more required than others in some people. One example of this involves the production of a byproduct of amino acid metabolism called homocysteine . Homocysteine is produced from the metabolism of the essential amino acid, methionine. Normally, the body deals with it without a problem. But in some people, again likely due to slight genetic differences, homocysteine can accumulate in the body. When this happens, a few toxic effects may accrue. This includes acceleration of both cardiovascular disease and brain degeneration. The good news is that homocystine is capable of being broken down into harmless substances, as long as three nutrients are present: vitamins B6, B12, and folic acid. If a person who overproduces homocysteine isn't consuming enough of these three nutrients from food sources, eventual health disaster is likely.
Then there is the case of the obese. Studies show that those with high body fat levels tend to sequester nutrients in their body fat, where the nutrients are inert. This is particularly true of the fat-soluble class of vitamins, such as vitamins E and D. In fact, studies conclusively show that obese people need to ingest higher doses of vitamin D just to reach an optimal blood level of the nutrient. A recent study examined the nutrient intake of obese subjects, both before and after being placed on special weight-reduction plan. This plan was designed to deliver all required vitamin and minerals in optimal amounts for health promotion. In fact, the plan actually delivered a level of vitamins and minerals that was slightly above suggested intakes.
Prior to starting the special diet plan, the obese people were examined for any pre-existing nutrient deficiencies. This revealed deficiencies for vitamin D, vitamin C, selenium, iron, beta-carotene, and lycopene. The researchers conducting the study determined this by taking buccal or inner cheek smears from the subjects, since this method was more reflective of nutrient uptake and long-term intake of the nutrients, rather than a blood sample, which would just provide a more immediate picture.
As noted, these obese subjects were placed on a special formula diet that at its strictest phase, provided only 800 calories a day. But they also were provided enough protein and other nutrients to prevent any problems.Despite this, while on the formula diet for three months, the obese subjects still showed deficiencies of vitamin C, selenium, iron, zinc, and lycopene. And this was true despite the fact that they were supplied these nutrients based on suggested daily requirements. So why were they still deficient?
When losing fat in large quantities, the level of oxidation in the body increases significantly. As such, the minimal level of nutrients that the subjects ingested, most of which were antioxidants, were being used up to decrease the potentially dangerous byproducts of increased oxidation from the fat utilization.In addition, the fat-soluble vitamins, instead of being circulated in the blood, were instead shunted into fat reserves, which not only neutralized their effectiveness, but also increased the oxidation effect. The fat cells also exert an inflammatory effect, which adversly affects iron metabolism by boosting levels of hepcidin, a substance that controls iron uptake into the body.
So, as this study shows, obese people show a definite increased need for certain vitamins and minerals that is above the recommended suggested intake of these nutrients. This is particularly true under dieting conditions, when increased oxidation effects will use up existing levels of minimal vitamins and minerals in the blood. Also, the fat sequestration effect must also be considered. Obese people need to ingest higher amounts of fat-soluble vitamins to get the same protective effects as their leaner peers.
The absolute stupidity of suggesting that vitamin-mineral supplements are a waste of money is obvious. For the tiny minority of people that truly do ingest a balanced diet, they aren't as necessary, unless there is a genetic quirk that demands higher intake of certain nutrients. For all the rest, vitamins and mineral supplements can represent the difference between long-term health and disease. The salient question really comes down to this: Who stands to gain if people stop ingesting vitamins and minerals, and eventually become afflicted with health problems related to the lack of those nutrients?
Damms-Machado, A, et al. Micronutrient deficiency in obese subjects undergoing low calorie diet.Nutrition Journal 2012;11;34.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
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Tuesday, March 4, 2014
Does a higher protein intake increase the risk of death? by Jerry Brainum
High protein diets have always been controversial. Critics of the diets often predict dire consequences for those foolish enough to stay on such diets long-term.These consequences include kidney disease and bone mass loss. However, more recent analysis of such possible risks show that they exist more on paper than in reality. When examined in healthy, active adults, higher protein intakes have consistently been shown not to impose any undue risks on kidney function, bone mass, or other factors. Athletes and others engaged in regular physical activity have long been advised to ingest a higher protein intake. In some cases, the level of protein intake is extreme. Some bodybuilders have stated that they regularly ingest as much as 600 grams of protein a day. It's doubtful that this degree of protein intake contributes anything useful to their goal of boosting muscle mass. Most excess protein is merely degraded and oxidized in the liver.
But two alarming new studies, both published in the March 4, 2014 issue of the journal, Cell Metabolism, assert that a higher protein intake is not only not necessary,but could shorten lifespan if consumed during middle-age. The first study analyzed data from a nationwide nutrition study, and specifically looked at the protein intake of 6,831 middle-aged adults.The data showed that adults with an average age of 50 who consumed a diet that contained more than 20% of calories as protein were 4-times more likely to die of cancer or diabetes, and more than twice as likely to die from any cause in the next 18 years. Even a moderate protein diet of 10 to 19% protein was still associated with a 3-fold increase in death from cancer. Interestingly, the effect was only associated with consumption of animal proteins. Consuming protein from plant sources, such as beans, did not result in any negative effects on health. Even more intriguing was the finding that this effect was reversed in people over age 65; that is, those consuming a higher protein diet showed a 28% reduced risk of mortality from any cause, and a 60% reduced risk of dying from cancer. The effects of consuming a higher protein diet during middle-age on mortality were comparable to smoking!
This, of course, is very bad news for anyone who ingests a high protein diet, especially those who are middle-age. But let's take a closer look at these findings. What, for example, is it about a high protein diet that seems to increase mortality? According to the study authors, the likely explanation is that a high protein (and higher calorie) diet boosts levels of a hormone called Insulinlike growth-factor-1 or simply, IGF-1. IGF-1 is produced both locally in muscle, where it functions as a major arbiter of promoting muscle growth, and in the liver, where it provides systemic body effects. These effects include helping to preserve lean mass, bone, neurons in the brain, and heart muscle. Without sufficient IGF-1, these tissues and organs degenerate. But IGF-1 has also been implicated in the cancer process because it promotes mitosis, or cellular division. Cancer involves uncontrolled cell division. But scientists still quibble over the precise role that IGF-1 plays in cancer. Among other effects, IGF-1 prevents a process called apoptosis, a type of cellular suicide. One theory suggests that tumors upgrade local IGF-1 synthesis as means of survival.Other theories say that it's the circulating IGF-1 itself that promotes cancer spread. On the other hand, IGF-1 travels in the blood bound to six different binding proteins, with IGFBP-3 being the predominant form. An important point is that IGF-1 can only interact with cells when it is unbound, or free. Bound IGF-1 is basically inert.So the question then arises: what can cause IGF-1 to be released from its binding protein? One thing that does this is insulin, as well as estrogen. When these two hormones are released in greater amounts in the blood, you also get a higher level of free IGF-1, which may be capable of interacting with existing tumors.
An important point to consider about this new study is that no mention is made of what other nutrients the subjects ingested. If they had excess bodyfat, which is linked to higher levels of estrogen, that would account for their elevated IGF-1 levels. If they consumed excess carbohydrates, and were also pre-diabetic, this, too, would lead to higher free IGF-1 levels. The study authors implicated protein because protein is known to boost IGF-1 levels, but not necessarily the free or active form. But the mere fact that the data was derived from an epidemiological survey brings the findings into question, since such surveys are notoriously unreliable.
The study authors note that mice on restricted protein diets show a 45% decrease in tumor mass after two months. But they also say that consuming a higher protein diet protects people over age 65. This relates to the prevention of frailty associated with a lack of IGF-1, which is a major cause of death in older people. Yet, who has the highest rates of cancer? People over age 65. So why would a high protein diet, which is known to boost IGF-1, lead to less mortality in the older people? According to the study authors' suggestion, the higher IGF-1 induced by a higher protein intake should result in a greater incidence of cancer in an older population, especially since such older people usually have an abundance of damaged DNA in their cells--a scenario highly favorable to cancer onset. Would this same information apply to active people, who use or metabolize a higher protein intake differently compared to those who are sedentary?
The other study exclusively used mice as subjects, and found that a low protein, high fat diet was most detrimental to health. But they also found that a very high carbohydrate intake of 70% of ingested calories, along with a low protein intake, was most conducive to longevity! The most surprising aspect of the study, however, was the finding that reducing calories had no effect on longevity. This is contrary to dozens of previously published studies, which did find increased lifespan among various species who ingested a lower caloric intake. On the other hand, the stated mechanism for the increase in longevity linked to the high carb, low protein diet was a decrease in mTOR. mTOR is a protein that is crucial to protein synthesis, and is increased by a higher protein intake. But it is also associated with faster aging and spread of cancer in later years. But mTOR can easily be controlled by far less extreme measures than restricting protein while shoveling in high amounts of carbohydrates. The latter is disastrous for the estimated 50 million Americans who have insulin insensivity or "pre-diabetes," and would, without a doubt, result in an increase in mortality, rather than longevity, if ingested. The study authors did note that the mice who consumed a low protein, high carb diet not only consumed far more calories, but were also significantly fatter than mice who consumed a higher protein, lower carb intake. How being fat and overeating can boost lifespan is a type of metabolic magic that I doubt that anyone can explain, but it may work for mice, certainly not for humans!
©,2014 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
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