Sunday, December 29, 2013

Is this the best diet to promote fat-loss, keep it off, and stay healthy? by Jerry Brainum


Although dieting is never easy, it's nonetheless a truism that it's easier to take weight off, compared to keeping it off.With most dieters, 97 percent of lost weight, especially body fat, quickly returns when the stringent dieting ends. This is particularly true if there is no exercise component, since a rapid weight-loss promotes changes in the body that result in a lowered resting metabolic rate (RMR). The lowered RMR of often ascribed to a loss of lean mass, mainly muscle, that results from a low calorie intake in the absence of exercise. Adding additional protein when calories or carbohydrates are curtailed is absolutely essential for aiding in the retention of lean mass, and is a mistake commonly made by uninformed dieters.
   Keeping lost weight off is difficult because of several factors. First is the aforementioned drop in resting metabolic rate, which means that fewer calories are burned at rest. Thus, if you experience a drop in RME resulting from an extended low calorie intake and low protein intake, combined with lack of resistance exercise, you will quickly regain lost weight when you consume more calories after the diet ends. Dieting also tends to produce changes in some hormones related to appetite control. For example, leptin and insulin resistance,both of which can adversely affect appetite control through an upregulation of  other factors related to appetite,such as a gut hormone called ghrelin, which is the most appetite-boosting substance of all.
     But there may be some hope after all for all those dieters who have lost, but regained body fat. A group of Italian and Greek researchers devised a phased dieting system that takes advantages of two of the best known eating plans: the ketogenic and low carbohydrate diet, and the Mediterranean diet. What they did is manipulate some of the disadvantages of the diets so as to produce maximal compliance with the eating plans. This is a major problem, since most diets fail because people either become bored with them, or are too hungry to continue. The system advocated by these researchers is similar to the type of training suggested by most exercise scientists:periodization, which involves dividing training into phases, where minor changes are made, such as heavier or lighter weights, more sets, less sets, and so on.
    The most effective fat-loss diet for the majority of obese people is the ketogenic diet, which involves a near deletion of carbohydrates from the diet. The popular Dr.Atkins diet also starts with a ketogenic diet, and for good reason. The initial weight loss on such diets consists largely of water, but also includes body fat. However, the loss of water provides an initial psychological boost because of the obvious rapid weight-loss. This phase of the diet also prepares the body for conversion from a largely sugar-burning machine into a fat-burning machine. Very low or ketogenic diets have often been wrongly criticized because of the increase of ketones that occur during the diet. In fact, the rise of ketones during the diet is never dangerous, and isn't comparable to that which occurs during uncontrolled diabetes. Ketones, which are intermediate byproducts of fat metabolism, even provide a number of dieting advantages. They blunt appetite, and can also be used in place of carbohydrates as an energy source. Ketones also provide anti-catabolic effects in muscle, and thus help preserve vital muscle mass under dieting conditions.Ketogenic diets are characterized by a total carbohydrate intake of no more than 50 grams a day. Interestingly, a recent study found that using a ketogenic eating plan immediately following another diet will completely prevent the rise in appetite-stimulating hormones such as ghrelin that normally occurs at the end of a diet, and is chiefly responsible for dieting failures. Dieting success, in contrast, is defined as losing 10 percent of bodyweight, and keeping it off for at least a year after the diet ends.
    The protocol suggested by the scientists consisted of the following:
1) Initial 20 days of very low carb ketogenic diet
2) 20 days of low-carb, but not ketogenic diet
3) Four months of normal caloric intake Mediterranean diet (MD)
4) A second 20-day ketogenic diet phase
5) A second 20-day low carb, not ketogenic diet phase
6) Final 6 months of normal calorie Med diet
     During the ketogenic diet phase, food was limited to beef and veal, poultry, fish, raw and cooked green vegetables (no restriction), dried beef, cured ham, eggs, and some cheese. Drinks permitted were infusion tea, moka coffee, and herbal teas. No alcohol, bread, pasta, rice, milk, yogurt, or other carb sources were permitted during this phase.The subjects were also provided with packaged specialty meals, rich in protein (18 grams per portion) and fiber, but devoid of carbs. To prevent the common side effects that sometimes occur with ketogenic diets, such as fatigue, the subjects also ingested herbal extracts, which are listed below. Thus, the addition of both fiber and the herbal extracts prevented the most common side effects of the ketogenic diet, which encouraged compliance. They also ingested a very weak vitamin and mineral formula, taken once daily.
    With the Mediterranean phase, the subjects consumed a diet composed mainly of whole grains,potatoes, meat, fish, eggs, poultry, vegetables, legumes, fruit, olive oil, whole milk, and red wine.The nutrient intake of this phase was 58% carbs;15% protein, and 27% fat. With the ketogenic phase, the average carb intake was 30 grams a day, with 12% total carb intake;36% protein; and 52% fat. When consuming the low carb phase following the ketogenic phase, the nutrient content was 25% carb;31% protein, and 44% fat. The subjects consisted of 89 male and female obese people, age range of 25 to 65, all healthy but overweight. This diet plan lasted for a year, and at the end, 88.25% of the subjects lost an average of 10% body fat. In the 8 subjects who failed to comply, it was found that they had abandoned the phase protocol and returned to eating high sugar/fat junk foods.Other changes in the dieters who did complete the course included decreases in cholesterol levels, LDL, triglycerides, and glucose levels. No adverse changes occurred in liver or kidney function.  
    Thus, this phase dieting resulted in a high compliance rate,, and a significant improvement in various health measures.By combining the advantages of the proven fat-loss capabilities of the ketogenic and low carb plans with the noted health benefits of the Mediterranean diet, which is the only diet associated with increased longevity, this plan seems to have captured the best of both worlds: rapid and safe fat loss and increased health and vitality.

Paoli, A et al. Long term successful weight loss with a combination biphasic ketogenic Mediterranean diet and Mediterranean diet maintenance protocol.Nutrition 2013;5:5205-5217.



 Plant extracts used in KEMEPHY (ketogenic Mediterranean with phytoextracts) diet
Plant extracts
Week
1-3
Week
4-6
Composition
Extracts A, ml/
day
20 20 Durvillea antarctica, black radish, mint, liquorice, artichoke, horsetail, burdock, dandelion, rhubarb, gentian,
lemon balm, chinaroot, juniper, spear grass, elder, fucus, anise, parsley, bearberry, horehound
Extracts B, ml/
day
20 20 Serenoa, Red clover, Chervil, Bean, Elder, Dandelion, Uncaria, Equisetum, Horehound, Rosemary
Extracts C, ml/
day
50 50 Horsetail, asparagus, birch, cypress, couch grass, corn, dandelion, grape, fennel, elder, rosehip, anise
Extracts D, ml/
day
(only weeks 1
and 2)
40 0 Eleuthero, eurycoma longifolia, ginseng, corn, miura puama, grape, guaranà, arabic coffee, ginger

.Main actives ingredients of used phytoextracts, their reported beneficial effects
Extract Main Active ingredients Reported beneficial effects
Refs
A Mint
black radish
burdock
- indigestion
- antioxidant
- choleretic, increases bile secretion helping digestion
[69]
[70]
B Serenoa Repens (saw
palmetto)
hormonal regulating effects
[71]
White bean
alpha-amylase inhibitory properties and has been reported to aid weight loss and glycemic control [72]
[73]
C Equisetum
Antioxidant
diuretic
glycemic control

Dandelion (Taraxacum
officinale
diuretic

D Ginseng
Miura Puama
Guaranà
Ameliorate the commonly reported symptoms of weakness and tiredness during first phase of ketosis (1-2 weeks).


©,2014 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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Saturday, December 21, 2013

New fat reduction factor found in egg yolks by Jerry Brainum


Those who are familiar with my past writings know that I often rant about the common dieting practice of discarding egg yolks and eating only the white of eggs. The ostensible reason for this is that the egg white is nearly pure protein, with no fat or carbohydrates. But what is often overlooked is that nearly all of the nutrients, along with half the protein content. in eggs exist only in the yolks.These nutrients include choline, important for brain health and muscle function since it's the precursor for acetylcholine synthesis. Acetylcholine is thought to be the primary neurotransmitter in the hippocampus area of the brain, a primary site of learning and memory. Indeed, in Alzheimer's disease, the neurons or brain cells that produce acetylcholine are severely damaged, leading to the obvious memory deficits seen with the disease. Acetylcholine is also the neurotransmitter at the myoneural junction, where nerve messages from the brain are sent to muscle,allowing it to contract.  The yolk also contains the most bioavailable form of lutein, a carotenoid and potent antioxidant that offers eye protection, as well as helping to prevent the oxidation of low-density lipoprotein cholesterol that is at the root of cardiovascular disease. That's just two of the nutrients that exist exclusively in the yolk portion of the egg, which is summarily discarded by misguided bodybuilders and dieters. Of more pertinence to those seeking added muscle mass, the yolks also contain half of the available protein in the egg. The cholesterol found in the yolk serves as a precursor for the synthesis of testosterone. Indeed, studies of older people show that those who eat whole eggs, and engage in a resistance exercise program, show greater gains in lean mass compared to old folks who shun eggs or eat only the whites.
     A new study has provided still another reason to consume the yolks. The study identified and isolated a protein found only in the yolks called anti-lipase immunoglobulin (IgY). In the study, this protein was tested on its ability to blunt the activity of pancreatic lipases, or fat-digesting enzymes. If these enzymes are blocked, fat cannot be digested, and thus is excreted out of the body without providing any calories. Since fat, at nine calories per gram, is the most concentrated source of calories among the major nutrients (protein and carbs provide 4 calories per gram), preventing the absorption of these calories could have a major impact on fat loss. Indeed, the primary drug now available to treat obesity is Orlistat, sold under the trade name of Olestra. Six years ago, an over the counter version, Alli, was released.  Orlistat also works by blocking pancreatic lipase activity. But is also comes with some severe possible side effects, These include oily stools, diarrhea, gallstones, and an interference with bile flow in the liver that results in a type of hepatitis or liver inflammation. Those who want to try a natural alternative can turn to green tea polyphenols, which also block lipase activity. However, the amount of green tea capable of providing significant effects in this regard would also place inordinate stress on the liver.
   In contrast, the new IgY factor from hen's egg yolks does the same thing as Orlistat minus any side effects. And it doesn't take much to accomplish this, either. In the study, a level of only 0.2% of IgY proved more effective than Orlistat at blocking lipase in an isolated cell aspect of the study. When it was provided to obese mice made fat from consuming a high-fat diet, IgY resulted in a loss of bodyfat throughout the body of the rodents. Especially noteworthy was the loss of visceral, or deep-lying abdominal fat. This is the most dangerous form of  body fat from a health point of view, since it's linked to the onset of insulin resistance, diabetes, cardiovascular disease, and cancer.
    Another good thing about IgY is that producing it doesn't involve any type of animal cruelty or abuse.It can be painlessly extracted through a certain technique from hen's egg yolks without producing any pain or stress in the birds.
    So those who are throwing out the yolks in favor of eating only egg whites for purposes of fat reduction are paradoxically working against themselves.You might say that the yolk is on them.






Hirose, M, et al. Anti-obesity activity of hen egg anti-lipase immunoglobulin yolk, a novel pancreatic lipase inhibitor.Nut Metabol 2013;10:70.


©,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, December 15, 2013

Broccoli supplements? Save your money by Jerry Brainum


"I do not like broccoli. And I haven't liked it since I was a little kid and my mother made me eat it. And I'm president of the United States, and I'm not going to eat broccoli anymore."  With those words, President George H.W Bush likely gained the enmity of broccoli growers all across the country. He was not, however, alone in his dislike of broccoli. Many people express a distaste for broccoli, and other vegetables in the cruciferous class. These include cabbage, Brussels sprouts, cauliflower, bok choy, collards, turnips, and watercress. Some studies show that the dislike of these vegetables could have a genetic origin. But one thing is certain: not consuming these vegetables, especially broccoli, amounts to losing some of the most protective elements found in food.
    Although broccoli and other vegetables contain other nutrients, such as folic acid and vitamin C,among others, what makes broccoli stand out as perhaps the most healthful single vegetable that you can eat is its content of substances called isothiocyanates. These include sulforaphane and indole-3-carbinol. Sulforaphane shows spectacular health benefits, and may block the onset of the two primary causes of death: cardiovascular disease and cancer. From an exercise and bodybuilding perspective, sulforaphane was recently found to lower levels of myostatin, a protein that works to block muscular growth. Other studies suggest that sulforaphane can lower the activity of aromatase, the enzyme that converts testosterone and other androgens into estrogen. The other key protective element in broccoli, indole-3-carbinol, is converted in the body into diiolymethane or DIM. DIM has the ability to convert the most active form of estrogen, 17-beta estradiol, into less active forms of estrogen, such as 2-methoxyestrogen. The significant of this is that the converted estrogens don't promote cancer, as does 17-beta estradiol.
    Sulphoraphane (SFN) is considered a nutrigenomic  element, in that it has the ability to influence the activity of genes, either turning them on or off. SFN is actually a weak pro-oxidant, but it is has a potent influence on activating NFR-2.  NFR-2 controls the activity of over 200 genes in the body and serves as a major cell defense element. It is sometimes called "the master antioxidant," since it stimulates the activity of several of the endogenous, or built-in antioxidant systems in the body. These systems are far more protective and powerful than any supplemental antioxidant, and when they decrease with age, many degenerative conditions related to increased oxidation begin to show up. These include Alzheimer's disease, Parkinson's diease, and cancer. A recent study found that the areas of arteries most prone to atherosclerosis are where the artery bifurcates or curves. These areas lack NRF-2, which causes excessive oxidation.According to the new study, providing SFN permits the build-up of NRF-2 in the deficient areas of the artery, thus preventing the onset of atherosclerosis.
      Two problems related to ingesting broccoli are that some people are born with genetic mutations that cause them to excrete all the SFN they ingest. Another problem is that the SFN content of broccoli can vary widely, with some containing lots of SFN, others barely any. The preparation of frozen broccoli destroys the SFN content, thereby making it worthless as a source of SFN. Broccoli does not actually contain SFN. What it contains is glucoraphanin, which is converted by an enzyme in broccoli called myrosinase, into SFN. This is an important point, because without the presence of myrosinase, the precursor substance, glucoraphanin, isn't converted into SFN, and therefore provides zero protective effects. Myrosinase is activated when broccoli is chewed, with the exposure to moisture releasing the myrosinase.
    SFN offers health protection through activating NRF-2, and also by activating phase-2 enzymes in the liver that serve to detoxify various noxious substances that get into the body, including carcinogens. The knowledge of broccoli's SFN content and health benefits has led to the marketing of broccoli extract supplements, which often feature a "standardized" content of SFN. The problem with this is that SFN is very unstable, which means that in these broccoli extract supplements, there is no active SFN left. What you are ingesting are placebo pills with zero activity. You could supply glucoraphanin, the precursor to SFN, which is much more stable than SFN. But the problem here is that you would also need to provide myrosinase to convert the glucoraphanin  into active SFN. Current broccoli supplements do not provide myrosinase, since it, too, would break down and soon disappear.
    Broccoli sprouts contain the highest amount of glucoraphanin , containing 10 to 100-times more than the mature broccoli. The richest source are broccoli seed, and at least one company sells a supplement based on broccoli seeds. Again, however, without the presence of myrosinase to activate the glucoraphanin into SFN, the products are worthless. The seeds also contain erucic acid, a lipid or fat that is linked to causing various types of heart problems. While you would have to ingest a lot of the broccoli seed extract supplements to ingest enough erucic acid to cause heart problems, the fact that it's in there is still a problem. Another substance in broccoli called the epithiospecifier protein or ESP, can convert the glucoraphanin in broccoli into either SFN or SFN nitrile, with the latter having no protective effects. Clearly, any broccoli supplement should be completely devoid of ESP. However, it's not easy to deactivate the ESP in broccoli without also deactivating the myrosinase, or degrading the glucoraphanin content. Cooking broccoli also deactivates SFN. But if you steam broccoli for 1 to 3 minutes, it will destroy the ESP, but preserve the myrosinase, allowing the conversion of glucoraphanin into active SFN. Microwaving the broccoli for about a minute is nearly as good as steaming it for preservation of SFN content.
     So, for a broccoli extract supplement to provide the considerable health benefits of SFN, it must contain glucoraphanin, not preformed SFN, and also include myrosinase to convert the glucoraphanin into SFN. It should also be devoid of ESP to ensure that only the active form of SFN is produced. You would not want to include any other antioxidant nutrients, such as vitamins C or E, because they would nullify the activity of NRF-2, which is stimulated by oxidation. A problem with including both glucoraphanin and myrosinase in the supplement is that myrosinase is turned on by moisture, and a premature onset of myrosinase activity would convert the glucoraphanin in the product into SFN. Since SFN is not stable, it wouldn't last long. Current products contain only glucoraphanin, with no myrosinase, so are inactive and do not provide SFN at all.
    Companies that sell the broccoli seed extract claim that intestinal bacteria is capable of converting glucoraphanin into SFN. But when this effect has been tested, the amount of SFN produced was inconsequential. You need a lot of SFN to help protect against cancer, although smaller amounts do activate NFR-2. The amount produced by intestinal bacteria from ingested glucoraphanin does neither. When I wrote to the major company that produces broccoli seed extract about this problem, they refused to answer me. They are misleading consumers into believing that their product, with a retail cost of over $20 for 60 capsules, does provide active SFN in appreciable amounts. This, however, is a bold-faced lie. As it stands now, the only way to obtain the valuable SFN is to eat either lightly cooked or raw broccoli  and other cruciferous vegetables. All the broccoli extracts now on the market are completely worthless, and do absolutely nothing to improve health.
   

                                                                

                                                 This broccoli supplement is labeled "sulforaphane glucosinolate," which is a meaningless term. In fact, it contains no active sulforaphane at all, just the inactive glucoraphanin precursor.
 


©,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

 


I do not like broccoli. And I haven't liked it since I was a little kid and my mother made me eat it. And I'm President of the United States and I'm not going to eat any more broccoli.
Read more at http://www.brainyquote.com/quotes/quotes/g/georgehw110377.html#ZgD7iYmxtprc1lJy.99

Saturday, December 7, 2013

No-Bull Amino by Jerry Brainum





Proteins are composed of various combinations of amino acids, and all dietary proteins are eventually converted into amino acids. The amino acids, which number about 22, are classified as either essential or nonessential. Essential amino acids are so-named because your body can’t synthesize them and so it’s essential that you get them in your diet.
     The balance of essential amino acids in any particular protein determines its biological value. Since animal protein sources are higher in essential amino acids and more closely duplicate the amino acid pattern found in the human body, they’re considered superior to plant-derived proteins, which often have either low or no amounts of essential aminos.
    Recent research proves that from the perspective of muscle protein synthesis, essential aminos are extremely important. In fact, some studies show that getting as little as six grams a day of an essential amino acid mixture promotes muscle protein synthesis following resistance exercise, such as weight training. But watch out: Information on the importance of essential amino acids may lead you to conclude that the so-called nonessential amino acids are not very important.
      That would be incorrect. Some nonessential amino acids have been reclassified as “conditionally” essential because under certain circumstances, such as high-stress conditions, the body cannot sufficiently synthesize them and their status changes from unessential to essential.
     Examples of conditionally essential amino acids include glutamine and arginine. Normally, the body can synthesize them if you’ve taken in a sufficient supply of essential aminos. Sometimes, however, that synthesis can’t take place rapidly enough.
    Glutamine and arginine are among the most popular amino acid supplements with athletes and bodybuilders today. Research on glutamine was originally derived from hospitalized patients, especially burn patients, who lose vast amounts of protein as a result of their injuries. Giving them glutamine reversed or halted the cascading catabolic effects on muscle that can result in death. Thanks to the anticatabolic effect, glutamine earned a place in the supplement regimen of intensely training athletes. Later studies showed that it also appeared to prevent the immune-suppression effects of extended exercise—endurance events, for instance.
    Arginine was initially promoted as a growth hormone releaser because doctors gave it intravenously to patients to treat growth hormone deficiency. Forms of arginine used for other purposes have also turned up in various food supplements, notably those that increase nitric oxide.
Many of the food supplements that contain glutamine and/or arginine also contain another amino acid, taurine—particularly creatine supplements. That’s because creatine is thought to encourage the cellular hydration that signals increased muscle protein synthesis. Glutamine and taurine also appear to promote cellular hydration, which makes them synergistic with creatine.
If taurine did nothing more than promote cellular hydration, it would likely still be considered a useful supplement. But taurine—conditionally essential like glutamine and arginine—is far more essential to those engaged in exercise.
                                                      What Is Taurine?

Taurine was discovered in 1827 as a component of ox bile, which explains its name; taurus is Latin for bull. Taurine is not incorporated into muscle and other tissues of the body like other amino acids but instead is found as a free, or unbound, amino acid or as part of short chains of aminos known as peptides. The significance of taurine wasn’t recognized until studies in the 1970s found that it was an essential nutrient for cats. Without it, cats develop retinal degeneration leading to blindness and serious heart problems, which explains why cat food labels prominently display the taurine content.
    Research on cats led some scientists to investigate whether taurine had any use for human nutrition. Initial studies found that babies fed on formula instead of mother’s milk often developed taurine deficiency, since their bodies lacked the enzymes needed to synthesize it. Normally, taurine is synthesized from two other amino acids—the essential methionine and the nonessential cysteine—both of which contain sulfur.
     In fact, some scientists suggest that taurine isn’t a true amino acid, since it contains a sulfonic acid group; other aminos contain a carboxylic acid group. Taurine is found abundantly in the body, in brain, skeletal and heart muscle tissue. In muscle, it’s the second most abundant free amino acid, behind glutamine. Taurine’s presence in muscle suggests that it must be there for a reason.
    The body can synthesize taurine from methionine and cysteine but not without the presence of the activated form of vitamin B6, or pyridoxine. So a lack of B6 in the diet can impair taurine synthesis. Controversy exists about just how well the body is able to make taurine. The main enzyme involved is not that active in either humans or cats. That’s why some theories suggest that many people can benefit from taking supplemental taurine.
    The most recognized function of taurine is its role in the production of bile salts. Bile, composed mainly of cholesterol, is a substance manufactured in the liver and stored in the gallbladder. In fact, the primary way the body rids itself of excess cholesterol is by shunting it into bile production. Bile itself promotes the digestion of fat by reducing its surface area, which makes it more digestible by lipases, or fat-digesting enzymes.
Even so, bile isn’t soluble enough to work unless it’s conjugated, or combined with other substances. When that happens, bile becomes bile salts, and the two main conjugating agents are the amino acids glycine and taurine. So taurine helps create bile salts and lower blood cholesterol, keeping it from floating through the bloodstream as low-density lipoprotein (the bad kind of cholesterol). High levels of LDL are a major risk factor for cardiovascular disease, especially oxidized LDL. The less LDL in the blood, the less chance of cardiovascular disease.
     Taurine accelerates bile salt synthesis by boosting the genes responsible for making an enzyme called 7-alpha hydroxylase. The increased use of cholesterol for bile synthesis lowers blood levels of cholesterol, which in turn opens up LDL receptors on cells, also lowering cholesterol levels.
    One study examined the effects of providing either three grams a day of taurine or a placebo to 30 overweight college students for seven weeks.1 Those in the taurine group had lower triglyceride levels in the blood, along with a reduced atherogenic index, a measure of the ratio of HDL cholesterol (the good kind) to triglycerides in the blood. Taurine increases HDL production by boosting the activity of the protein carrier of HDL, apolipoprotein A-1.
    A beneficial side effect also occurred in the students who took the taurine supplements: They all lost bodyfat. Studies done with diabetic rats show that taurine prevents buildup of abdominal fat, which is considered the most dangerous to health, being linked to insulin resistance, heart disease and diabetes.
Taurine also functions as an antioxidant, which protects against such diseases as cardiovascular disease and cancer. When certain immune cells destroy invading organisms, they release a stream of free radicals, which are unstable oxygen by-products that destroy the invading organism’s cellular membrane, killing it. Free radicals can also damage normal tissue. When the body has sufficient taurine, however, the taurine soaks up the excess free radicals, rendering them neutral.
     Smoking damages arterial linings and leads to cardiovascular disease. A 2003 study, however, found that in smokers who took taurine, the function of the lining, or endothelium, rapidly improved to the point where it worked similarly to that of nonsmokers. That occurred after only five days on a 1.5-gram dose of taurine, about the same amount found in a 100-gram serving of fish.
    Although omega-3 fats are considered the health-promoting component in fish, its high taurine content also offers protective benefits that are frequently overlooked. Some studies show that the taurine content of fish helps lower blood pressure and reduce the negative effects of a high salt intake.2 Stress also increases blood pressure by increasing the release of such hormones as epinephrine and norepinephrine, which constrict blood vessels. Taurine counteracts that effect, leading to lower blood pressure. Interestingly, the populations with the lowest rates of cardiovascular disease in the world, those of Japan and the Mediterranean countries, also get the greatest amounts of taurine in their diets.
     Still another way that taurine protects the heart is by modulating electrolyte function. Excess calcium can rapidly lead to cellular death, but taurine prevents that. It also favorably affects the balance of sodium and potassium in heart tissue, thus maintaining proper heart function.
     Highly refined sugars, such as in high-fructose corn syrup, are thought to be responsible for the rising epidemic of obesity, especially in younger people.While HFCS is chemically the same as sucrose, or table sugar, the fact that it is ubiquitous in so many processed foods leads to overconsumption.Eating excess fructose causes sugar to be deposited into protein tissues, an effect called glycation that’s considered a major cause of aging and the prime cause of the stiffness and lack of mobility many people experience as they get older.
     In a recent experiment rats were put on a 60 percent fructose diet but also got a 2 percent taurine solution for 30 days. That prevented the formation of glycation end products while also enhancing the use of glucose.3 Taurine worked with insulin to affect glucose, although it worked independently of insulin in promoting glucose use. Some studies show that taurine may help prevent some serious diabetic complications, including neuropathy (nerve degeneration) and retinopathy (blindness).
                                    
                                     Can Taurine Help Your Workouts?

     Slow-twitch muscles have higher levels of taurine than fast-twitch muscles. That’s likely because slow-twitch fibers have a greater oxidative capacity, and taurine has antioxidative properties. Studies show that the body loses the greatest amount of taurine after intense anaerobic exercise, such as weight training.
Experiments done with rats demonstrate that taurine increases exercise capacity, especially in older animals.4 Another study found that taking taurine may help protect against exercise-induced muscle injuries.5 The authors of that study observed that taurine supplementation reversed “certain types of functional deficits in skeletal muscle. Our results suggest that taurine supplementation may facilitate exercise performance and reduce some limited aspects of muscle injury caused by exercise.”
    A later study that used human subjects confirmed the protective effects of taurine during exercise.6 Because of the increased oxygen intake that occurs, exercise also ups the production of dangerous free radicals, and rampant free-radical release can damage DNA in cells, leading to mutations that may cause cancer and other diseases. In this study, however, giving men supplemental taurine before exercise significantly prevented DNA strand breakage, an effect attributed to taurine’s antioxidative properties. In addition, the subjects who took taurine also showed increased VO2-max, an indicator of increased endurance, increased time to exercise exhaustion and increased maximal workload. That effect could come from taurine’s role in increasing the pumping power of the heart and improving the electrical and contractile properties of skeletal muscle.
    In muscle, taurine stabilizes cell membranes, including the sarcolemma, the membrane that surrounds muscle fibers. By controlling calcium entry into muscle, it promotes muscle contraction as well.
Taurine’s effect on electrolyte functions in muscle may also explain why it helps prevent severe muscle cramps. One theory suggests that exercise-induced loss of sodium and calcium may precipitate such cramps. By stabilizing those minerals during exercise, taurine may help prevent postworkout muscle cramps. The transport of taurine into muscle is promoted by sodium and chloride and decreased by lactate and beta-alanine.
    A recent study found that taurine content in fast-twitch muscle significantly decreased during extended exercise sessions and noted that it enhances the enzymes in muscle that regulate energy production and fat oxidation.7 Taurine also stimulates cyclic AMP, which leads to a greater release of catecholamines, such as epinephrine and norepinephrine. The latter two substances activate the enzyme hormone-sensitive lipase in fat cells, which leads to the release of fat for use as energy during exercise.

                                                Words of Caution


    For those considering supplementing taurine, several caveats are in order. The precise optimal dose of taurine for increasing exercise performance has been calculated—in rats.8 It’s between 100 and 500 milligrams per kilogram (2.2 pounds) of bodyweight. The dose depends on body size and would be considerably lower in a human. Good food sources of taurine include most animal protein foods, particularly fish. Oysters are a superior source.
     Those who use the drug clenbuterol should be aware that it causes a rapid and severe depletion of taurine from muscle and heart tissue. That could explain the heart damage and muscle cramps that can occur with its use.9 Ephedrine and mahuang supplements also reduce taurine muscle content.
    The amino acid beta-alanine is now being added to various food supplements because it’s the precursor of L-carnosine synthesis in the body. Beta-alanine and taurine compete for the same uptake carrier into the body, and beta-alanine can block taurine uptake by 50 percent or more. Best to use the two amino acids at different times. While the beta alanine and taurine conflict is possible, it almost never occurs, since you would need to ingest relatively massive amounts of beta-alanine to cause this interference with taurine uptake.
    Finally, be aware that taurine functions in the brain as an inhibitory neurotransmitter—meaning that it has a depressant action on brain function. So taking too much taurine in a single dose can lead to feelings of fatigue and lack of energy. Smaller doses of taurine, less than a gram, have a reverse effect: providing energy. That’s ostensibly why taurine is a major ingredient of a popular energy drink that includes the word bull in its name. But since the drink also contains caffeine, the taurine addition could indeed represent a lot of bull.
                                                                
                                                               




                                                         Cats deficient in taurine can go blind





                                                               References


1 Zhang, M., et al. (2004). Beneficial effects of taurine on serum lipids in overweight or obese non-diabetic subjects. Amino Acids. 26:267-71.
2 Nara, Y., et al. (1978). Effects of dietary taurine on blood pressure in spontaneously hypertensive rats. Biochem Pharmacol. 27:2689-92.
3 Nandhini, A.T., et al. (2004). Stimulation of glucose utilization and inhibition of protein glycation and AGE products by taurine. Acta Physiol Scand. 181:297-303.
4 Pierno, S., et al. (1998). Chronic administration of taurine to aged rats improves the electrical and contractile properties of skeletal muscle. J Pharmacol Exp Therap. 286:1183-90.
5 Dawson R, et al. (2002). The cytoprotective role of taurine in exercise-induced muscle injury. Amino Acids. 22:309-24.
6 Zhang, M. et al. (2004). Role of taurine supplementation to prevent exercise-induced oxidative stress in healthy young men. Amino Acids. 26:203-7.
7 Matsuzaki, Y., et al. (2002). Decreased taurine concentration in skeletal muscles after exercise for various durations. Med Sci Sports Exer. 34:793-97.
8 Miyazaki, T., et al. (2004). Optimal and effective oral dose of taurine to prolong exercise performance in rat. Amino Acids. 27:291-98.
9 Doheny, M.H., et al. (1998). The effects of the beta-2 agonist drug clenbuterol on taurine in heart and other tissues in the rat. Amino Acids. 15:13-25.

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Saturday, November 30, 2013

Alternate day fasting: healthy and good for weight-loss?



Diet fads tend to come and go, and few of them ever have a sound scientific basis, which is one reason why they don't last. Sooner or later, unanticipated side effects often crop up, including fatigue, muscle loss, and even failure to lose body fat. A recent diet trend that has been making its way around the Internet is alternative day or intermittent fasting.As the name implies, this involves eating normally one day, followed by eating far less the next. The fasting day doesn't involve complete avoidance of food and drink, but rather consuming an average of 25 percent of normal daily caloric intake.
   The notion that eating less improves health and fosters longer life is the cornerstone of the classic caloric restriction diet. With this diet, you consume 30% less calories then your normal intake every day. Animal studies show that eating in this manner is the only established way to maximize life span. One recent study involving monkeys, however, showed no actual life extension benefits from CR. Other primate studies have shown slowed aging effects, such as low insulin and glucose, lack of insulin resistance, along with lower rates of various diseases, such as diabetes, cardiovascular disease, cancer, and cognitive disease, such as Alzheimer's disease.
   But the truth is that there is no actual human evidence that CR styles of eating can extend human life. There are people who eat in this manner based on the findings of benefits in animals. Such people do tend to show lower resting insulin, blood pressure, lipids and so on. But they are also painfully thin, with a catabolic appearance suggesting a loss of muscle mass. They are also often frequently cold and tired. Clearly, there must be a better way.
    Animal studies that compared intermittent fasting with the standard daily CR regime, found that the animals lived just as long when following the IF plan as when eating the far more restrictive CR style. Indeed, in some ways the IF animals were healthier, showing lower resting insulin and glucose levels compared to their CR peers. Other animal studies, usually involving rats and mice, show that IF exerts protection against strokes, and slows cognitive loss or brain function deficits. IF also boosts the levels of chaperon proteins, which repair misfolded proteins in the body that are linked to various diseases, including Alzheimer's. IF appears to increase the level of brain-derived neurotrophic factor, which is involved in neuron repair, by 50 to 400%.   Autophagy is a process by which old cells are broken down to allow room for new cells. When this process is impaired, aging ensues. IF is known to boost autophagy.
    Of course, eating less would also promote loss of excess body fat, as well as increased insulin sensitivity. In one mouse study, the mice were permitted to eat unrestricted amounts of high fat foods for 8 hours, followed by not eating for the next 8 hours. Despite the initial overeating,none of the mice got fat or showed elevated insulin levels. Studies of humans who followed short-term IF regimes showed moderate fat loss, but a significant improvement in several health values, such as increased HDL cholesterol, lower triglycerides, lower insulin and so on.
   The latest human study on IF involved 32 subjects randomly selected for either a IF group, or a control group for 12 weeks. The IF group ate normally one day, followed by eating 25% of their normal intake the next day. The subjects in this study included both normal weight and overweight people. The results after 12 weeks showed an average 6% weight loss. But more significantly, several health benefits were also evident. These included lower blood triglycerides, lower CRP (a measure of inflammation), lower leptin (lower hunger), and an increase in LDL particle size, which is associated with a decreased risk of cardiovascular disease. Levels of adiponectin, linked to increased insulin sensitivity, also rose in the IF group. The adherence to the IF diet was high, although the subjects did confess to moderate hunger on the fasting days. Most impressive, however, was that none of the fasting subjects loss any lean mass or muscle. That is an important consideration, since loss of lean mass is a common side effect of most diet plans, and is the main cause of weight regain after such diets.
     It appears that, if you can handle it, following a IF regime may help you lose some body fat quickly, without losing muscle. As for using the IF plan continuously, this is possible, but the long-term effects are as yet, not known. I suspect that one notable advantage of IF over CR regimes is that with CR regimes, you experience a significant drop in all anabolic hormones, including testosterone, growth hormone, and IGF-1. With IF, because you are still eating normal amounts of food every other day, these hormones are maintained, so no muscle loss ensues. In addition, you get all the benefits of the CR without the constant starvation. One note of caution, however: in rats who followed long-term IF regimes, their hearts showed a stiffening effect that could result in future congestive heart failure.







Varady, KA, et al. Alternate day fasting for weight loss in normal weight and overweight subjects: a randomized controlled trial. Nutrition Journal 2013; in press.

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Friday, November 22, 2013

JFK: steroid user by Jerry Brainum



The 1960 presidential election was considered one of the closer elections in American history. Many historians say that the turning point came on September 26, 1960, with the advent of the first televised presidential debates. John F.Kennedy was the democratic candidate, a United States Senator from Massachusetts. Incumbent vice-president Richard Nixon represented the Republican party. Both men presented clear and cogent arguments and brought up important issues. If you went by content alone, you would have to declare a tie, with no clear winner. However, those debates turned the tide for Kennedy. It wasn't anything particular that he said, but rather how he looked that made the difference. Kennedy appeared tan and rested, while his opponent Nixon looked pale and sweaty; in fact, he was sick. Nixon had refused make-up, and the cameras caught every bead of sweat and bags under his eyes. In contrast, Kennedy seemed to present a picture of youthful vigor and energy. In fact, nothing could be further from the truth. Nixon was by far the healthier of the two candidates.
      Kennedy had more personal medical issues that any United States president, before or since. The extent of his health problems became apparent with the complete release of his medical history eleven years ago. What Kennedy was afflicted with falls under the broad medical term of autoimmune polyendocrine syndrome, type-2 (APS-2). What this refers to is a failure of several endocrine organs, or organs that release hormones, caused by  the body's immune system turning upon itself, and attacking those organs as if they were foreign disease organisms. The syndrome was initially described by Thomas Addison in 1849. The type-2 form that JFK had is characterized by a failure of his adrenal glands, along with a failure of the thyroid gland.
     Kennedy was known to suffer from Addison's disease, named after that same Dr.Thomas Addison, who first described it. With Addison's disease, the adrenal glands stop producing hormones. This aspect of Kennedy's health was kept secret for years, and the full disclosure only emerged with the publication of a book in 1976. There were signs of problems long before that, however. In September, 1947, JFK, then a U.S Congressman, collapsed while on a visit to England. A local doctor diagnosed Kennedy's illness as "adrenal crisis" and remarked to a friend of Kennedy "that young man doesn't have a year to live." Kennedy left for New York accompanied by a nurse, and was admitted to the Lahey clinic in Boston. The press was told that the reason for Kennedy's illness was a severe recurrence of the malaria he had contracted while serving in the Pacific during World War two.
    In reality, JFK was being treated at the Lahey Clinic by an endocrinologist, who gave JFK an early corticosteroid drug, namely desoxycorticosterone (DOCA). This was in pellet form, which was implanted in the skin of his thigh every three months. In 1950, oral cortisone became available, and Kennedy began ingesting 25 milligrams daily in addition to continuing the DOCA treatment. He had to do this because with the Addison's disease, he wasn't producing any cortisol, which is essential to life. He wasn't actually diagnosed with Addison's until  September, 1947. When he first ran for congress in 1945, JFK weighed only 150 pounds at a height of 6-foot, and as the campaign went on, he was descibed as appearing "tired, hollow-eyed, and anemic" by his staff workers. Despite this, JFK seemed indefatigable, and won the election. But the day prior to the election, he had marched in the annual Bunker Hill parade, and at the end of the 5-mile walk, he collapsed. One aid said that he looked "yellow and blue, like a man having a heart attack."
     Back in 1940, when he was only 23, JFK was given a medical examination by a doctor, who told JFK's father than his son had hypotension, or very low blood pressure. This was an early sign of his adrenal failure.Kennedy's celebrated tan was also a manifestation of his adrenal failure. It was hardly a"healthy tan."
    In 1954, as a U.S Senator, JFK had back surgery to correct long standing pain that may have been caused by long term use of steroids (not anabolic steroids), which can cause bone resorption and thus weaken spinal bones. The doctors who operated on him had to take special precautions because of his Addison's disease, since JFK's body was incapable of handling stress. He survived the surgery, which was written up in a medical journal--without identifying the patient.JFK still suffered from back pain the rest of his life, and was wearing a back brace on the day of his assassination.That brace, which allowed him to keep his upper body erect, may also have inadvertently led to his death in Dallas on November 22, 1963. JFK's erect body and lack of flexibility allowed the second bullet that smashed into his skull to efficiently find its target. This was the bullet that blew the back of his skull off and proved fatal. Had he been able to move more without the brace, the bullet might have missed, and JFK would have survived.  
    Kennedy's political opponents were aware of Kennedy's Addison disease, and tried to go public with the disclosure that JFK was in fact, a sick man. But his condition was covered up by Dr.Janet Travell, who later became the White House physician. In 1955, JFK was diagnosed as having hypothyroidism, or low thyroid output.During his presidencny, JFK took 25 micrograms of liothyronine, better known by its trade name of Cytomel, twice a day. Cytomel is a T3 thyroid drug, considered the fastest acting and most potent of thyroid medications.  The diagnosis of both adrenal and thyroid failure is indicative of APS-2. Again, this stems from the body producing an immune reaction that attacks the adrenal and thyroid glands. At Kennedy's autopsy,it was noted that his adrenal glands had atrophied to the point of non-existence, which is indicative of severe Addison's disease.  Half of those with APS-2 have relatives who also suffer from autoimmune disease. Kennedy's sister, Eunice, mother of Maria Schriver, also had Addison's disease, while Kennedy's son, JFK Jr, had Graves disease, which is characterized by excessive thyroid output, and is considered an autoimmune disease.
    Those who suffer from APS-2 show an incidence of hypergonadotropic hypogonadism of 4 to 9 percent. This could lead to infertility, which clearly wasn't the case with JFK, who sired four children, with two surviving infancy.However, the syndrome can also affect the gastrointestinal system, and JFK suffered from recurrent symptoms of intestinal cramping, diarrhea, and inability to gain weight for most of his life.
  A list of medications prescribed by Dr.Travell on October 12, 1961 for JFK consisted of the following: Vitamin C, 500 mgs, twice daily;hydrocortisone, 10 mgs daily;prednisone, 2.5 mgs, twice daily;methyltestosterone 10 mgs daily;  25 mcg twice daily of Cytomel for thyroid; fludrocortisone, 0.1 mgs daily;diphenoxylate HCL and Atropine (Lomitol), 2 tablets as needed to treat diarrhea. Kennedy used testosterone daily during his entire presidency. He usually used 10 mgs of the anabolic steroid, methyltestosterone, one of the only orally available anabolic steroids at that time, and sometimes boosted the dose to 25 milligrams. In 1962, his doctors put him on between 50 and 75 milligrams of testosterone aqueous suspension, an injection, for four days. He later began taking fluoxymesterone,another oral anabolic steroid available as Halotestin, at a dose of 5 to 10 milligrams.
   With Kennedy's autoimmune condition, it's possible that antibodies could attack the Leydig cells in the testes, where testosterone is synthesized. While JFK may have had this effect, it didn't destroy his fertility, as evidenced by his ability to produce children (with his wife's assistance). But the probable reason why Kennedy used testosterone preparations was to counter the catabolic effects on muscle produced by his necessary use of corticosteroid drugs, which are catabolic hormones, in that they produce muscle tissue loss. In addition, regular use of cortisol-based drugs can result in pituitary suppression of gonadal hormone output. In other words, using cortisol drugs can blunt the synthesis of testosterone in the body, necessitating an outside source of the hormone. Kennedy would often request higher doses of his testosterone or anabolic steroid drugs because they made him feel more alive and clear-headed, while reducing his ever-present feeling of fatigue. His inability to gain weight because of the Addisons also made testosterone drugs a useful option, since they allowed JFK to gain weight and improve his appearance. Before he used the drugs, he appeared gaunt and very skinny.He actually first started using testosterone when he ran for president in 1960, again to improve his appearance and sense of vigor, which it did.
    JFK also used vitamin B12 injections throughout his presidency. The APS-2 condition, because of adverse effects on the gastrointestinal system, often leads to a B12 deficiency, which JFK did have, hence the B12 injections.
    Just like a Hollywood facade, JFK wasn't the picture of youthful health and vigor that he appeared to be.But without his hormone treatments, including the corticosteroids he had to use to stay alive, and the testosterone preparations that made him look healthy despite his illness, history may well have not been the same.


                                                                      


                                                               



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Friday, November 15, 2013

IGF-1 protects muscles against statin-induced toxicity by Jerry Brainum


Statin drugs are among the most frequently prescribed drugs in medicine. They are used to lower high levels of blood cholesterol, and secondarily to lower inflammation within blood vessel walls. Ironically, it's become clear recently that the primary preventive effect of statin drugs against the onset of cardiovascular disease (CVD) is their effect on lowering excess inflammation, rather than high blood cholesterol. The notion that lowering blood cholesterol alone is sufficient to prevent CVD is dubious at best, and simplistic. Cholesterol itself is an important substance produced in the liver. It's vital for cell membrane integrity, and serves as the raw material for a variety of hormones, all in the "steroid" category, which means that they are made using cholesterol as the precursor substance. These include testosterone, cortisol, estrogen, activated vitamin D, and others.
   Despite the importance of cholesterol, most physicians who treat patients with high blood cholesterol levels will provide a prescription for a statin drug. While higher plasma cholesterol levels can be effectively managed through dietary and exercise modalities, many people aren't motivated enough to engage in these practices. As such, statin drugs are thought to offer an easy mode of protection against the onset of heart attacks and strokes. Again, this is a very dubious concept, since many other things can cause a heart attack or stroke besides an elevated plasma cholesterol level.
    But, like any other drugs, statins are not side-effect free. Side effects related to the use of statins can include eye problems, liver abnormalities, and muscle breakdown. In regard to the latter, studies have shown that many people on statin drugs cannot produce any muscular progress from exercise because of an inhibitory effect induced by their statin use. The extent of this effect varies with dose, the specific statin drug used, and individual response to the drugs. This effect of statins on muscle function is known as myopathy, and is more likely to occur with certain statins, most notably simvastatin (Zocor) and mevastatin (Compactin). In contrast, another popular statin, provastatin (Pravachol) rarely causes myopathy.
     The cause of statin-induced myopathy is generally attributed to an interference with the synthesis of coenzyme Q10, which is important in the function of mitochondria, local cell structures that, among other functions, produce energy and oxidize fat in muscle. Statins work by inhibiting an enzyme in the liver called HMB-COA-Reductase, which is the rate-limiting enzyme for cholesterol synthesis. But this enzyme is also involved in the same pathway that also produces COQ10, and by inhibiting this pathway, statins prevent the synthesis of Q10, which results in myopathy.
    This suggests that anyone who is using statin drugs should also supplement their diet with pre-formed Q10. Despite this obvious solution to the statin/myopathy problem, most cardiologists do not often suggest that their patients on statins also use Q10 supplements. The reason for this is that some studies show that the myopathy side effect of the drugs is relatively rare. But the interference with muscle progress from exercise is far more common and subtle, and is often blamed on things other the statin drugs. Why doctors would be reluctant to suggest that patients on statins consider using Q10 supplements is strange, considering the low expense and side effect profile of Q10.
    One study published two years ago found another solution to the statin-myopathy problem that isn't well-known. This study involved exposing isolated muscle cells first to statin drugs alone, then to cells exposed to statins, followed by exposure to insulinlike growth factor-1 (IGF-1). IGF-1 is an anabolic hormone, produced both in the liver under the aegis of growth hormone release, as well as directly in muscle. The local IGF-1 produced in muscle plays a primary role in promoting the activity of satellite cells, muscle stem cells required to repair and build muscle. In the new study, when muscle cells were exposed to statin drugs, the drugs reduced muscle proliferation an average of 50 percent. But when the muscle cells were then treated with IGF-1, all statin-induced negative effects on muscle were completely blocked.
   While providing Q10 supplements to those on statin drugs would be the simplest solution to the statin-induced myopathy problem, it may not work for everyone. However, IGF-1 may be the ultimate solution to the problem. And you may not need to inject actual IGF-1 to get the benefits. IGF-1 is also significantly boosted by resistance exercise, as well as DHEA supplements. Indeed, various published studies have shown that initial muscle problems induced by exercise in people using statin drugs is often ameliorated within a short time after starting a resistance exercise program. My guess is that it's the IGF-1 from the exercise that is kicking in and thus preventing the excess muscle damage caused by the statin drugs.








Harfmann, BD, et al. IGF-1 protects against statin myotoxicity. Med Sci Sprts Ex 2011;43:372-373.


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Sunday, November 10, 2013

Low sodium intake: beneficial or toxic? By Jerry Brainum



No one thinks much about salt or sodium chloride these days, except in what happens when you consume too much. Sodium is linked to water retention and a bloated appearance. Medical doctors warn their patients that consuming too much sodium will raise blood pressure, and thus increase the risk of heart attacks and strokes. In fact, having hypertension or high blood pressure is the number one risk factor for strokes. But the concern about sodium or salt hasn't always been this way. In ancient times, salt was considerable so valuable that wars were fought over it. It was considered more valuable than gold at one point.Indeed, the word "salary," is derived from the Latin word for salt, and Roman soldiers were paid with salt. Small wonder that the popular phrase,"worth his salt" is said of a particularly productive person.  Homer (the Greek poet, not the TV cartoon character) called salt "a divine substance." His opinion was echoed by the philosopher, Plato, who noted that "salt is especially dear to the gods." The word "salt" appears more than 50 times in the bible. So it's clear that at times, salt has been revered in history.
   Not so today. Despite sodium being an essential mineral, health warnings abound about the consequences of too much sodium in the diet. At first, these warnings seem accurate, since sodium is ubiquitous in the food supply, particularly in processed and fast foods, which are packed with salt. The question is: how much sodium do we actually need to ingest to stay healthy?  According to the Center for Nutrition Policy and Promotion, the daily intake of sodium should be less than 2,300 milligrams a day in normal people, and 1,500 milligrams a day in those at greater risk for cardiovascular disease, including people over 50, black people, and those with existing high blood pressure, type-2 diabetes, and kidney disease. The American Heart Association recently suggested that ideal cardiovascular health could be achieved for most people by 2020, and one way to do this is to limit sodium intake to less than 1,500 milligrams a day. The average person ingests 3,300 milligrams of sodium a day, while our paleolithic ancestors averaged only 768 milligrams daily intake of sodium. The minimal sodium requirement is thought to be around 500 milligrams.
  Sodium regulates extracellular fluid, including that found in the blood, which is 98% water. Sodium is also vital for nerve transmission, and nerve signals are propagated when sodium and potassium are exchanged in nerve cells. This explains one of the primary signs of low sodium: muscle cramps, as the nerve conductivity to muscle is blunted with lack of sufficient sodium intake, or by using drugs such as diuretics that promote sodium excretion. Besides muscle cramps, other symptoms of sodium depletion include loss of appetite,  nausea, and fatigue. The initial fatigue often felt during low carbohydrate diets occurs because of a loss of stored glycogen caused by the lack of carb intake. Glycogen is stored with water, and as glycogen is depleted the water portion is excreted, along with various minerals, including sodium. The lack of minerals adversely affects nerve transmission and brain function, leading to fatigue.
   It's not common to be deficient in sodium, but it's possible if you engage in certain practices. For example, drinking excessive distilled water can lead to hyponatremia, or low sodium body stores. This has happened to long distance runners who consume copious amounts of sodium-free water during a race. In 2007, a young woman rapidly drank two gallons of distilled water during a radio contest, then promptly died from brain edema due to sodium depletion. Of course, using diuretic drugs, which work by promoting the loss of water through fostering sodium and other mineral excretion, can also rapidly cause sodium depletion. This can lead to either intense muscle cramps, or in a worst-case scenario, death. Several deaths in bodybuilders has occurred because of their use of potent diuretic drugs combined with lack of sodium intake.
  Contrary to popular belief, however, the body normally tightly controls sodium levels. With a high intake of sodium, the extracellular fluid intake expands, leading to a temporary rise in blood pressure. The higher blood pressure increases perfusion of blood through the kidneys (which depend on a higher blood pressure to properly filter the blood) this increased blood perfusion then stimulates the kidneys to excrete sodium. The body prevents the excretion of too much sodium through the release of an adrenal hormone called aldosterone, which retains sodium and water, while promoting potassium excretion. In fact, the human body has evolved to retain sodium, while promoting potassium excretion.
   It's important to note that in all the studies that have shown protective effects induced by a reduction in sodium intake, the proof was in the form of surrogate or indirect markers of sodium metabolism, such as increased excretion of sodium. The degree of blood pressure lowering by diets designed to lower sodium has been trivial at best, with no proof that such diets actually prevent high blood pressure or cardiovascular disease (CVD). However, there is evidence that a low sodium diet can be detrimental under certain conditions, such as if a person has type-2 diabetes. Persons with diabetes who ingest low sodium diets show higher rates of cardiovascular disease and mortality. How can this be? A low sodium intake stimulates activity of the sympathetic nervous system, which then overstimulates the heart.In addition, low sodium activates the  renin-angiotensin-aldosterone axis, which paradoxically increases, rather than lowers blood pressure, and also exerts direct damage to the arteries, thus promoting atherosclerosis. Perhaps the most curious effect of all, however, is that low sodium intake increases insulin resistance. Diabetics already have a problem with insulin resistance, which itself is known as "pre-diabetes." Thus, having a diabetic ingest a low sodium diet is like putting oil on a fire.
   People with congestive heart failure are often advised to follow a low sodium diet, since a primary cause of congestive heart failure is long-standing high blood pressure. Yet those afflicted with CHF show reduced blood perfusion in the kidneys, which activates the sympathetic nervous system, along with the renin/angiotensin/aldosterone axis. This causes a retention of water at the expense of sodium, which is then rapidly excreted, leading to possible hyponatremia. Studies show that CHF patients who ingest a low sodium diet have a higher mortality rate compared to those who consume a normal sodium intake. Consider that in rat studies, the rodents show a 4-times greater rate of arterial plaque formation when on a low sodium intake compared to normal intakes. The effect is blocked when the rats are provided with an ACE-inhibitor drug, which blocks the renin/angiotensin effect.  Mouse studies show that a low sodium diet increases vascular inflammation and promotes atherosclerosis.
   A recent review of 167 studies that examined the effects of a low sodium diet found that such diets increased renin, aldosterone, noradrenaline, adrenalin, cholesterol and triglycerides, thus painting a picture showing increased CVD risk from low sodium diets. Consider that prior to the introduction of iodized salt, thyroid disease due to lack of sufficient  dietary iodine, which is required for the synthesis of thyroid hormones, was prevalent in the United States, especially in the so-called "goiter belt," in the midwest. Salt in food not only increases palatability,but also exerts an antimicrobial effect. Decreasing salt intake may lead to increased food-borne infections.
   So how should you handle sodium intake? For most people, a normal intake of up to 4 to 6 grams of sodium a day won't cause any problems. This is especially true if you also ingest sufficient potassium, which balances the effects of sodium in the body. In fact, potassium will speed the excretion of excess sodium intake if you ingest a 2:1 ratio of sodium to potassium. Thus, if you consume 2,000 milligrams of sodium, ingesting 1,000 milligrams of potassium will offset any possibly deleterious effects of the sodium intake, including effects on water retention and blood pressure. Adding other minerals, especially calcium and magnesium, will further completely neutralize any possible problems associated with a high sodium intake. And consider one other fact about sodium: sodium is the primary activator of the amino acid transport in muscles that permits uptake of amino acids for use in muscle protein synthesis reactions. Thus, protein supplements that feature "low sodium" is idiotic. Sodium also activates the sodium/potassium pump in muscle that turns on the creatine transport protein, which determines how much creatine is taken up into muscle.

                                                                     
                                                           Sodium occurrence in foods



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