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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Monday, November 4, 2013

Can a simple supplement help prevent Alzheimer's disease? By Jerry Brainum

While there are many ways to die, one of the worst has to be Alzheimer's disease (AD). As most people are aware, AD is a neuro-degenerative disease of the brain, where the loss of neurons or brain cells in certain areas of the brain leads to significant cognitive deficits, especially in memory and learning ability. The disease was first noticed by Alois Alzheimer, a physician who described the symptoms in a 55-year-old woman. At that time, the precise cause of AD wasn't known, and even today, with all the advances in science and medicine made since Alzeheimer first described his patient, the precise mechanisms that lead to AD still aren't fully established.
   The characteristic changes in the brain that occur with AD involve a build-up of two proteins: beta-amyloid (BA) and Tau. The increase in BA results in an overabundance of neuritic plaques in the brain that interfere with normal nerve transmission. The other protein, tau, leads to disordered tangles of nerve material, known as neurofibrillary tangles. Interestingly, most older people have both of these proteins in their brains, yet show no symptoms of AD. The reason why others do show symptoms of AD is because the BA and tau increases to abnormal levels in certain parts of the brain.
    The statistics associated with AD are sobering. Currently, 5.3 million people are estimated to be afflicted with AD, and it is the 6th leading cause of death. It tends to strike those over 65 more frequently (13% of those over 65 have AD), although early-onset AD can show up as early as age 40. Every 68 seconds, someone becomes afflicted with AD. By 2050, that figure will rise to every 30 seconds, with 11-16 million people being diagnosed with AD. One in three seniors has AD. Women get it more often than men. Since 2000, the number of deaths from AD has risen by 68%, while deaths from other causes, including cancer and cardiovascular disease, have dropped.
     As to the precise causes, there are many theories, and there may be more than one cause. For example, head trauma is known to increase both forms of abnormal AD proteins in the brain. Some suspect that today's athletes who are involved in sports that feature frequent head trauma, such as boxing and football, will later in life suffer from AD. Indeed, some of the greatest past champions, such as boxing legend, Sugar Ray Robinson, did get severe forms of AD late in life. Having two copies of a gene called APO-E4, increases the chances of acquiring AD  by 80%. Having the genes doesn't guarantee the future development of AD, but does increase the risk. Recent research shows why APOE-4 is linked to AD. It lowers a protein called SIRT-1 that protects neurons. This implies that ingesting substances that may boost SIRT-1, such as resveratrol from red wine and quercetin, may offer some protection to those predisposed to AD because of having two genes for APOE-4. Fish oil offers some AD protection, especially the omega-3 fatty acid, DHA. However, the fish oil protective effect is negated in those with two APOE-4 genes. Green tea has also been shown in some studies to offer some AD protection if ingested chronically. Curcumin, which is contained in turmeric, has been shown in test-tube studies to not only prevent the build-up of BA in the brain, as well as Tau, but also to remove existing excess deposits of BA in isolated brain tissue. The problem with current curcumin supplements, however, is that they are rapidly converted in the liver to inactive metabolites, so that little or none enters the brain.
    The most alarming aspect of AD is that there is no current effective way to prevent or treat the disease. However, the supplements mentioned earlier, through offsetting the buildup of abnormal BA and Tau, may offer some protection against the development of AD. The trick is that you have to start ingesting these supplements before the symptoms begin. Exercise is also effective at helping to prevent AD. It does this through boosting the level of brain-derived neurotrophic factor, which works by maintaining and repairing damaged brain cells. The increase in oxygen delivery to the brain offered by exercise also helps maintain neurons.
    A new study that used mice as subjects found that a common food ingredient, also available in supplement form called phytosterols may offer potent protection against the onset of AD. Not all phytosterols were equally effective in this regard. The one that stood out was stigmasterol,which also happens to be the type of phytosterol least found in food sources. Those food sources include vegetable oils and nuts. Phytosterols are best described as "plant cholesterol,"since plants do not synthesize cholesterol. But phytosterols do have a close physical resemblance to cholesterol to the point where they can displace cholesterol in the intestines, thus reducing cholesterol uptake from food sources. As such, they are capable of lowering blood cholesterol levels by 7 to 10.5% on average, and when used concurrently with statin drugs, boost the cholesterol-lowering effect of statins significantly. At one point, phytosterols were sold as "anabolic" supplements, with the idea that, since cholesterol is the raw material used in the body to synthesize testosterone, phytosterols would do the same. Unfortunately, it doesn't work that way. However, some phytosterols, such as beta-sitosterol, seem to interfere with the activity of DHT, a byproduct of testosterone metabolism linked to prostate enlargement. In fact, beta-sitosterol is the active ingredient in the herb, Saw palmetto, often used to treat BPE.
    In the new mouse study, stigmasterol was found to profoundly interfere with the synthesis of both BA and tau. In fact, it lowered the level of BA in mouse brain by a whopping 68%. It's important to note that while cholesterol is not the major player in cardiovascular disease as it has been long portrayed to be, in the brain, excess cholesterol is a definite stimulant to overproduction of BA. However, too little cholesterol in the brain is also associated with some forms of dementia. Ingesting stigmasterol may prove to be a way to control excess BA without interfering with normal cholesterol metabolism in the brain. Since this was a mouse study, it remains to be confirmed whether the same protective effect that occurred in the mice will also happen in human brains. But if it does, it will be far more effective as a preventive against AD onset than any existing drugs used to treat AD, all of which do little or nothing to halt the progression of the disease.

Burg, VK, et al. Plant sterols the better cholesterol in Alzheimer's disease? A mechanistical study.J Neuroscience  2013: in press.








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