History of the Development of Anabolic Androgenic Steroids

  

Few people know of the current state of anabolic androgenic steroids (AAS); it may be rarer still to find someone with knowledge of the history of anabolic steroids. Sadly, the best texts on the subject directly from the pioneers are difficult to locate as they have been out of print for decades, such as Charles Kochakian’s Anabolic Actions of Steroids and Remembrances.¹ One exception is the recent text Testosterone Dreams: Rejuvenation, Aphrodisia, Doping by John Hoberman, which is excellent.² However, policymakers and their clinical gatekeepers (physicians) do not generally take time to read much outside of their specialties, do not refer to popular media, and rely heavily on reviews and research in academic texts.

Considering the conflict that arises between recreational anabolic steroid users and the regulatory agents of medical professionals and legislative policymakers, it should be of interest to learn the history of the development of AAS as it is presented to health care providers and elected officials. A recent review was published in Pediatric Clinics of North America.³ Each issue of Pediatric Clinics of North America is devoted to a single topic, magnifying the impact of each article. This review is interesting in that it focuses on the relatively primitive techniques used to identify a ‘male factor’ and then isolate the responsible molecule.

The review also touches on the pioneering efforts (some misguided, others seemingly barbaric) in applying the male factor and later testosterone to provide restorative therapy to men. It should be of no surprise to anyone that the desired endpoint for many patients was to restore or enhance male sexual prowess. Despite any measurable advance in civilized endeavors over the last 6,000 years, enhancing male sexual prowess remains a driving influence, as demonstrated by the sales of Viagra and related drugs, as well as the comments made on the effect of certain other drugs, such as Melanotan II.^4,5

Recreational and competitive sports did not hold the position in society that they do now, and the display of one’s body was considered vulgar and vain until the relatively puritanical era of the early- to mid-20th century passed. Thus, there was relatively little mention of sports performance enhancement until the 1950s. Of course, physique development and performance enhancement are now considered to be the dominant purposes for the use of testosterone and related anabolic steroids (AAS). However, when questioned in a large survey, most users admitted that attracting potential sexual partners remains the primary reason for steroid use (by improving one’s physique or social status through athletic performance).⁶ The more things change, the more they stay the same.

Myriad Effects of Androgens

The review, authored by Drs. Dotson and Brown, of Columbus Children’s Hospital and The Ohio State University respectively, begins by discussing [some of] the myriad effects of endogenous (natural) androgens— anabolic (tissue-building) and androgenic (masculinizing).³ It is interesting that they label vocal cord-thickening and laryngeal (voice box) enlargement as anabolic, when many consider those to be masculinizing effects.

The history of the pursuit of AAS is acknowledged to have begun over 6,000 years ago as farmers and herders castrated animals to make them easier to domesticate.³ Many married men might jokingly identify with this in a figurative sense, as demonstrated in the comedy routine of the late Sam Kinison: “You’re married now, I guess you won’t be needing this.”

The earliest surviving recorded curatives for impotence or libido problems date back to the Yellow Emperor’s (Huang Ti) Dynasty of China from approximately 2600 B.C. Later, but still ancient cures from the eighth century B.C. are described in writings from India and the Middle East, the ‘cradle of civilization.’ Moving along the timeline, it is revealed that the Egyptians (1600 B.C.), India (eighth century B.C.) and Romans would prepare elixirs and potions, consuming testicles and animal penises to obtain mystical ‘powers.’⁷ Those with a liberal arts education might immediately wonder what psychoanalyst Sigmund Freud would think of such behavior. Interestingly, Freud appears later in the history of AAS.

It was the Greeks who introduced the idea of using the sexual organs of animals or phallus-shaped plants for performance enhancement in sports, at least in Western cultures. Of course, prior to the era of Greek culture, sports took place in gladiatorial arenas where enhancement usually involved heavier armor or more lethal weapons. It is amazing how the Greeks and Romans are revered for their architectural and philosophical advances, but no mention is ever made of their forage into performance enhancement.

The review leaps forward to the late 1700s, a revolutionary time in more ways than one. Scottish surgeon John Hunter was the Royal Surgeon to King George III and a distinguished scholar. He was a strong advocate of observation and experimentation. Some of his rumored behavior is indisputably odd by today’s standards— self-inoculating himself with venereal disease to study the progress of the disease, and displaying the skeleton of a man who suffered from gigantism against his deathbed wishes, after acquiring the remains through bribery.⁸

Hunter is believed by many to be the Scottish equivalent to da Vinci, and one of the United Kingdom’s esteemed professional societies bears his name. Hunter performed the first documented testicular transplant (from a rooster to a hen), resulting in androgenic features in the hen.⁹ Several decades later, German physiologist Arnold Berthold proved that a substance in the bloodstream produced the male features in roosters, but his findings went largely unnoticed.^3,9,10

Pissing Contests and Testicular Transplants

One of the preeminent names in endocrinology is Charles-Édouard Brown-Séquard, who lived from 1817 to 1894. Many tales of his work during his tenure as a Harvard professor abound, including stories of experimenting upon himself with self-injections of testicular extracts from guinea pigs and dogs. Brown-Séquard published a famous report of his [subjective] increased strength, mental abilities, and appetite, relief from constipation and an increased arc in his urine stream.¹¹ On the face of things, it appears that Brown-Séquard was interested in combating aging-related symptoms of androgen deficiency. A close friend whose career is in academics suggests that he might have been involved in performance enhancement, since half of a professor’s time is spent in departmental pissing contests. This comment was made in jest, but it reflects the underlying tension and competition that pervades all levels of modern society— even the hallowed halls of academia.

According to the review, the first people to propose injecting athletes with hormonal substances were Austrian physiologist Oskar Zoth and his physician partner, Fritz Pregl in 1896.³ They self-injected testosterone extracts from bulls and plotted the strength of their middle fingers on ‘fatigue curves.’ Pregl went on to win the Nobel Prize in chemistry in 1923 for unrelated work. Why they chose to use the middle finger is a matter of speculation, though again, Sigmund Freud might offer some insight.

The late 1800s and early 1900s were years of frenetic study in the signaling of the body. Two prominent English physiologists, Bayliss and Starling, coined the term ‘hormone’ from the Greek for ‘to impulse or arouse.’¹²

In 1911, the first suggestion of a dose-response curve was published when André Pézard observed that a rooster developed a more prominent comb with greater doses of extract.^3,10 At this point, physicians began to use rudimentary operations that by today’s standards are bizarre and replete with risks of infection and tissue rejection. The ‘Steinach operation’— basically a vasectomy— was provided to ‘middle-aged and listless’ men. The claimed benefits of the Steinbach operation included hair regrowth, better erections, reduced complaints of premature ejaculation, and improved libido. Critics believed Steinbach’s claims were due to placebo effect, but his list of patients included prominent intellectuals, including Sigmund Freud and William Butler Yeats.³ Again, my esoteric and overeducated friend commented that Steinbach probably whispered, “Your mother loves you” into Freud’s ear during the procedure to ensure his sexual arousal.

The more alarming trend that was being practiced during this time was testicular transplantation from ‘donors’ into patients. Many of the donors were recently-executed prisoners and the early patients were often fellow prisoners.³ Of course, that sort of treatment is no longer tolerated in the U.S. penal system. One affluent surgeon developed a technique wherein he would slice the donor testicle(s) lengthwise prior to implanting the tissue slices between muscle layers in the abdomen or pelvis. His patients apparently included the well-connected and wealthy, as the case of one patient was reported in The New York Times— Harry F. McCormick, husband of Edith Rockefeller.³ Within years, the supply of testes donors could not meet demand, and certain entrepreneurial surgeons substituted the testicles of rams, boars, chimpanzees, and other mammals. Animal rights activists campaigned against this practice and editorial cartoonists (the early predecessors to Jay Leno) were quick to publish their parodies.

Testes Extracts to Boost Performance?

For modern-day AAS users, the history of AAS begins in the late 1920s when scientists were scrambling to discover the chemical containing the androgenic properties of these testes extracts responsible for providing the improvements in vitality and sexuality. The first related success occurred in 1929 when German chemist Adolf Butenandt isolated the female sex hormone estrone from the urine of pregnant females. Just two years later, Butenandt isolated androsterone.^3,13 As overjoyed as current AAS users may be at hearing of the discovery, Butenandt was likely more ecstatic, as the 15 mg of androsterone was filtered from 15,000 liters of urine from local policemen.^3,9 Androsterone is a metabolite of testosterone, a waste product excreted after testosterone has been enzymatically degraded, removing most of the androgenic and anabolic properties.

The race commenced among pharmaceutical companies, recognizing the unmet demand from men for a treatment for decreased vitality, as well as depressed libido and sexual function. Within months of each other, several chemists published papers on various methods of synthesizing testosterone from chemical precursors, such as cholesterol. Butenandt, one of the primary chemists, received the Nobel Prize in chemistry for his work with sex hormones in 1939.¹³ As material became available, clinical experiments with men suffering from hypogonadism were undertaken, focusing on impotence and sexual desire. It is worthy to note that topical preparations were also formulated to promote sexual desire in women by 1939.³ Remember, this was as the United States was exiting the Great Depression, the only financial crisis worse than today’s economic calamity (so far).

  It was the discovery by Charles Kochakian that the male sex hormone has properties that are anabolic as well as androgenic.^1,3,14 The anabolic function of androgenic steroids captured as much attention as the sexual functions. In 1945, Paul de Kruif published a book titled The Male Hormone, which reported the increased libido and enhanced athletic performance provided by testosterone and related drugs.¹⁵ The world was just recovering from World War II.

Sports and Bodybuilding

From the late 1940s to today, the history of AAS diverts into the realm of sports and bodybuilding. Many of the clinical uses were replaced by more specific treatments; reports of masculinizing side effects in women and liver tumors with chronic use of oral agents caused the class of drugs to fall into disfavor. By the late 1960s, it was suspected that much of the profit from AAS came from black-market distribution. Nonetheless, clinical experimentation on aging men suffering from signs of hypogonadism continued. Paul Niehans, author of the 1960 text Introduction to Cellular Therapy, provided testicle cell injections to prestigious patients such as Pope Pius XII and Aristotle Onassis.^3,16

Despite the unmet demand and growing knowledge base, pharmaceutical companies discontinued AAS production as regulatory and social pressures were applied. This reduction in resource allocation to AAS research coincided with the first Anabolic Steroid Control Act, making the distribution, use and possession of AAS without a physician’s prescription a felony. While the pharmaceutical companies have developed a number of novel (patentable) delivery mechanisms for testosterone, (patches, gels, non-alkylated oral Andriol, long-acting Nebido, and intranasal), the main crux in development has been toward non-steroidal selective androgen receptor modulators (SARMs).¹⁷ This leaves the United States demand for testosterone and other AAS unmet by legitimate, licensed and regulated manufacturers.

This void was quickly filled by the black market. Initially, finished products from Mexican, Pacific Rim, or European pharmaceutical companies were shipped or smuggled into the United States.¹⁸ As the delivery of these compounds became more uncertain due to actions of the Drug Enforcement Administration, U.S. Customs, U.S. Postal Inspectors, Homeland Security, etc., underground labs began meeting demand by purchasing AAS precursors from China, Mexico, India and other countries.¹⁹ These compounds were not monitored as closely and could be imported more easily, particularly if they were mislabeled from the point of origin. Unfortunately, the purity and potency of the precursors and finished products were often well below pharmaceutical standards. Cases of intentional adulteration or frank fraud have been reported, at times resulting in injury to the end user.

Dotson and Brown ended the review discussing the uncertain role testosterone and AAS have in clinical medicine, reported side effects, and the incidence and impact of adolescent drug abuse.³ Though these are all important topics to consider and address, their discussion diverts the reader’s attention away from the original intent of the article, the history of AAS.

The review was interesting and valuable, but it does no service to the readers of this article merely to reiterate the points presented. Instead, it is interesting to look at some of the highlights and consider them in light of the current position of AAS in the clinical, social and economic times.

Ethics, Risks and Gym Rats

AAS are considered by the public, policymakers, and professionals solely as illicit performance-enhancing drugs used by athletes and adolescents without regard of ethics or risks. Legislators, the media, and prosecutors have labeled anyone involved or interested in the field of AAS as unscrupulous pharmacies, rogue physicians, criminals, and scorned athletes. Yet, the history of AAS identification and development includes some of the most notable names in the fields of physiology, chemistry, medicine, surgery and endocrinology. The Nobel Prize has been granted to some who have experimented with and studied the potential of using AAS or related compounds to restore or enhance health and performance. Those who have sought the restorative powers of the humoral or glandular male factor, primarily for decreased libido, impotency, and signs of aging-related decline in androgen status, include notable figures in religion, science, psychology and industry. The demand for a better quality of life prevailed through some of the greatest global and national challenges in history, including the Great Depression and World War II.

It is not only the athletes and ‘gym rats’ buying AAS through the black market for sports titles and larger muscles who are placed in harm’s way by the antithetical turn from the 6,000 year-pursuit of the male factor. It is every man seeking to delay or reverse the deterioration in vitality, independence and esteem that occur almost inevitably with aging. It is every healthy man seeking to improve his social status or sexual attractiveness by improving his appearance and performance, both physical and sexual. These goals may seem vain, but they are an innate driving force, embedded within the nature of mankind, as evidenced by the presence of such demand since recorded time.

The rush to innovate drives America’s competitive place in the international market. Yet, it is the country that is trying to quash, and thus create a black market for, research and development in life-enhancing therapies. The history of AAS should establish that the field has been part of mankind’s recorded history, been nurtured by and advanced through the efforts of some of the greatest minds in medicine, science, religion and industry. Perhaps a better understanding of the history of AAS could alleviate many of the concerns of policymakers and professionals, redirecting development, supporting research and relaxing indications for clinical use.

References:
1. Kochakian C. Anabolic Actions of Steroids and Remembrances. University of Alabama Press, Birmingham, AL;1984. ISBN-13: 9789994291205.
2. Hoberman J. Testosterone Dreams: Rejuvenation, Aphrodisia, Doping. University of California Press, Berkeley, CA;2005. ISBN-13: 9780520221512.
3. Dotson JL, Brown RT. The history of the development of anabolic-androgenic steroids. Pediatr Clin North Am, 2007 Aug;54(4):761-9.
4. Lexchin J. Bigger and better: how Pfizer redefined erectile dysfunction. PLoS Med, 2006 Apr;3(4):e132.
5. Evans-Brown M, Dawson RT, et al. Use of melanotan I and II in the general population. BMJ, 2009 Feb 17;338:b566.
6. Cohen J, Collins R, et al. A league of their own: demographics, motivations and patterns of use of 1,955 male adult non-medical anabolic steroid users in the United States. J Int Soc Sports Nutr, 2007 Oct 11;4:12.
7. Shah J. Erectile dysfunction through the ages. BJU Int, 2002 Sep;90(4):433-41.
8. Kobler J. The Reluctant Surgeon. The Akadine Press, Pleasantville, NY;1999. ISBN-13: 978-1888173963.
9. Freeman ER, Bloom DA, et al. A brief history of testosterone. J Urol, 2001;165:371-3.
10. Medvei VC. The History of Clinical Endocrinology. Parthenon Publishing Group, Pearl River NY;1993. ISBN-10: 1850704279.
11. Brown-Séquard CE: Note on the effects produced on man by subcutaneous injections of a liquid obtained from the testicles of animals. Lancet, 2:105-107:1889.
12. Henderson J. Ernest Starling and 'Hormones': an historical commentary. J Endocrinol, 2005 Jan;184(1):5-10.
13. Karlson P. Adolf Butenandt (1903-1995). Nature, 1995 Feb 23;373(6516):660.
14. Hoberman JM, Yesalis CE. The history of synthetic testosterone. Sci Am, 1995 Feb;272(2):76-81.
15. de Kruif P. The Male Hormone. Permabooks, New York;1948. ASIN: B000KD7ECO.
16. Lambert G. Conquest of Age. The extraordinary story of Dr. Paul Niehans. Rinehart & Company Inc., New York; Clarke, Irwin & Company Limited,Toronto;1959. ASIN: B001UC6GDM.
17. Gao W, Dalton JT. Expanding the therapeutic use of androgens via selective androgen receptor modulators (SARMs). Drug Discov Today, 2007 Mar;12(5-6):241-8.
18. Ryan J. DEA Announces Charges in Largest Ever Steroid Probe. ABC News 2005 December 15. Available at: http://abcnews.go.com/US/LegalCenter/story?id=1411333, accessed April 9, 2009.
19. Schmidt MS. U.S. Arrests 124 in Raids on Global Steroid Ring. The New York Times, 2007 September 24. Available at: http://www.nytimes.com/2007/09/24/sports/24cnd-steroid.html?ref=sports, accessed April 9, 2009.

Ketogenic Diets: Possible Hidden Cardiovascular Risks?

A rhyme originating in the 1600s later appeared in the Mother Goose collection about the dietary habits of the Sprat household. The modern version reads, “Jack Sprat could eat no fat, his wife could eat no lean; and so, between the both, you see, they licked the platter clean.”

Obviously not desirable dinner guests, the Sprats are fine examples of two extremes in dieting that have dominated the American weight loss and healthy eating mania. Low-fat diets have long held the accepted position of being the politically correct and clinically accepted diet. The low-fat approach was originally developed to treat and prevent atherosclerotic cardiovascular disease (ASCVD), commonly visualized by cholesterol-laden plaques within the walls of large and small arteries (blood vessels).¹ The assumption was that by reducing the dietary exposure to fat and cholesterol by discouraging the consumption of meat, eggs, and dairy, serum (blood) cholesterol and triglycerides (fat) would decrease and along with it, the risk of heart attack and stroke.

Unfortunately, low-fat diets do not offer much benefit beyond what would be gained from weight loss by any method. Limiting dietary cholesterol does not address the de novo cholesterol produced by the body, which is the cause of high cholesterol in most people.

Along came the Atkins revolution, an antithetical approach that claims to promote weight loss by restricting carbohydrates rather than fat. Low-fat diets use the approach of reducing the caloric density of the diet to reduce calorie intake; low-carbohydrate diets make it easier for the body to break down and use stored fat for energy by reducing insulin release. Though many assumed the opposite, no evidence of unhealthy changes in cardiovascular markers has been noted. In fact, some components of the lipid profile (fats and cholesterol) improve on low-carbohydrate diets, suggesting they are at least as safe, and possibly safer diets for people at risk for heart attacks and stroke to follow.

The Atkins diet has phases, including the induction phase, which severely restricts carbohydrate consumption. When carbohydrate intake is below 20-30 grams per day, the body enters a state called ketosis.² Weight loss is dramatic and rapid when ketogenic dieting is followed; much of the early weight lost is water, as carbohydrate stores are depleted. Over the long term, weight loss is slower, particularly as people migrate to the more moderate parts of the diet. In time, there appears to be little difference between the various types of diets relative to the number of people who stay on the diet and the amount of weight they lose and keep off.^3-5

Many people get discouraged by slow weight loss, while some people find the mental state associated with ketosis comforting, as a sign of ongoing fat reduction. The brain is highly dependent upon blood sugar and during ketosis, some people experience irritability and difficulty performing mental tasks. However, over time, some people claim they are sharper. Regardless, there is a definite subjective component to ketosis— some people become so committed (obsessive?) that they test their urine for ketones several times a day.

Ketogenic dieting can be followed long term. Many people do so voluntarily; others are directed to do so by their physicians for specific conditions, such as epilepsy.⁶ Some have suggested that ketogenic dieting may not only be as effective as low-fat dieting for weight loss, but more effective and safer. This belief is certainly premature, as very few side-by-side studies have been done and none have followed the subjects long enough to state so definitely.

Bodybuilders and Cardiovascular Health

Cardiovascular health is important for bodybuilders and anabolic steroid-using athletes to consider, as certain anabolic-androgenic steroids (AAS) are associated with adverse changes in cholesterol, and heart attacks and heart failure are some of the most common causes of sudden death or serious injury in this group. Elite bodybuilders and many other AAS users have suffered heart problems. While it is not possible to directly assign AAS as a contributing cause to these cases, there is a strong base building due to several reasons:

 • Use patterns of AAS— dose and duration of cycles— have changed.

• Polypharmacy (the use of multiple medications and/or the administration of more medications than are clinically indicated, representing unnecessary drug use) includes many other anabolic biologics (growth hormones and cytokines) and potent lipolytics (fat-reducers).

• The demographics of AAS users are aging.

‘Cardiovascular’ refers to the heart and the blood vessels. Heart damage is most commonly caused by ischemia (oxygen deprivation) but can also be electrical in nature, as the heartbeat is generated by an internal conduction system that accelerates and decelerates to meet the circulatory demand of the body. When the electrical signal is disrupted, the heart does not beat efficiently or if the disruption is severe enough, may not beat at all. Ischemic damage of the heart (and brain, as well as other tissues) is often due to a buildup of plaque in the arteries, but may also be due to inappropriate vasoconstriction (the blood vessel squeezing shut, as seen in the skin when exposed to cold) or not dilating (opening wider) when oxygen demand requires greater blood flow. Many abusers of cocaine suffered heart attacks due to coronary vasoconstriction, even though their arteries were perfectly healthy.⁷

When ischemia is mild-to-moderate and long-term, the body grows new blood vessels to shorten the distance between active cells and nearby capillaries (the smallest blood vessels and the site where oxygen and factors are diffuse back-and-forth to cells of the body).⁸ A person who lives in the mountains likely has a higher capillary density (a measure of how branched the circulation is to provide oxygen) than a person who lives on the beach at sea level. Many endurance athletes sleep in special chambers that mimic living in the mountains. This increases their red blood cell supply (the cells that carry oxygen) by stimulating the hormone erythropoietin, and likely stimulates new blood vessel growth. Many cancer drugs kill tumors by shutting down blood vessel growth, starving the malignant tumors of oxygen and nutrients.⁹

One final mechanism that affects the buildup of plaque in artery walls is the ability of the blood vessel to maintain an intact lining. Major blood vessels are designed not to leak, and do so by having a lining that prevents red and white blood cells from escaping into the surrounding tissue. With the constant flow of blood rushing through the vessels, the lining wears away but is constantly replaced by new lining cells. If these replacement cells were not available, plaque can more easily build up under the lining in the artery walls.

Picture a pickup truck bed with a spray-on liner. If the liner gets gouged, rust can develop in the underlying metal— unless a new layer of spray-on lining covers the damage. If neglected, the rust spreads, potentially causing significant damage.

Low-Carb Mice and Ketogenic Diets

This background is provided to put into context the relevance of a newly-published study that unveils some heretofore-unrealized concerns about ketogenic diets. A group of researchers at Beth Israel Hospital and other facilities, all part of the Harvard Medical System, compared the cardiovascular effect of three types of diets— all containing the same amount of cholesterol— in mice bred to be capable of developing atherosclerosis (plaque buildup).¹⁰ The standard chow was low in fat and protein, being 65 percent carbohydrate. The second group received a diet that mimics what most people in the United States consume, (43/15/42— carbohydrate/protein/fat); and the last group was provided with a low-carbohydrate diet of 12/45/43 (carbohydrate/protein/fat).

Mice do not develop atherosclerosis naturally, and the mice fed the standard ‘mouse chow’ had clean arteries after 12 weeks. Mice fed the Western diet had a significant amount of atherosclerosis and the low-carb mice had even more, nearly twice as much.

In looking at the typical lab markers to explain these findings, researchers discovered that there was no real difference in cholesterol, bad cholesterol, or oxidized cholesterol between mice fed the Western and low-carbohydrate diets. Both had a four-fold increase in serum (blood) cholesterol compared to the standard diet. The low-carbohydrate diet was not associated with any increase in oxidative damage (the molecular damage that is protected against by antioxidants). Oxidative damage is proposed to make blood vessels more susceptible to atherosclerosis.¹¹

Another factor involved in atherosclerosis is inflammation. The study looked at two measures of inflammation and found the exact opposite of what would be expected. The low-carbohydrate diet resulted in lower measures of a specific marker for inflammation in the bloodstream— no different from measurements taken from mice fed the standard diet who had essentially no atherosclerosis.¹⁰

The mice fed the low-carbohydrate diet experienced a dramatic decrease in the healing ‘replacement cells’ that normally repair the blood vessel lining. The degree of decrease was greater than 80 percent and also affected precursor cells in the bone marrow.¹⁰ Ironically, one hormone that stimulates the production of the replacement cells, VEGF, actually increased in low-carbohydrate fed mice.^10,12 Failing to directly measure the replacement cells (called endothelial progenitor cells, or EPC) and measuring VEGF instead would misled a clinician to believe that low-carbohydrate dieting was safer for cardiovascular health. The increase in VEGF may be a sign of the body reacting to the EPC-lowering effect of the low-carbohydrate diet in the mice.

EPC plays a role in new blood vessel growth, and corresponding to the decrease seen with EPC, low-carbohydrate fed mice were unable to respond to ischemia (oxygen deprivation).^10,13 One of the factors known to stimulate EPC growth (pAkt) is a ‘downstream’ molecule in the insulin-signaling cascade. ‘Downstream’ means insulin turns on one molecule, which turns on another, which turns on pAkt. Statin drugs (Lipitor, for example), exercise, and estrogen have been shown to counteract impaired EPC production.¹³ Low-carbohydrate fed mice had significantly lowered insulin concentrations compared to other diets, as would be expected. Type 2 diabetics who are insulin-resistant also demonstrated impaired EPC production.¹⁴ Though this is not the entire reason EPC growth is impaired in low-carbohydrate diets, it likely plays a role.

Thus far, low-carbohydrate diets have been shown to markedly increase atherosclerosis, even compared to high-fat diets. This is in a setting that would not raise suspicion. In fact, many measures suggest that cardiovascular health is improved with low-carbohydrate dieting. Also, the ability of the circulatory system (blood vessels) to respond to oxygen deprivation is seriously impaired.

This study did not look at ketogenic dieting, as the carbohydrate content was high enough to prevent ketosis. Thus, it is difficult to determine whether the same concerns would be present during ketogenic dieting. However, another concerning observation has been noted during ketogenic dieting that adds another level of risk.

One study published last year showed that people on a ketogenic diet had impaired dilation, whereas those on a low-fat diet actually demonstrated improved flow-mediated dilation and response to a dilating drug. Similar impairment is again seen in people with insulin resistance.^15,16 This adverse effect may be exaggerated when saturated fat is high, but the balance of research appears to suggest that if mono- and polyunsaturated fats are consumed in sufficient quantities and saturated fats are moderated, blood vessels should respond more appropriately to dilating signals.¹⁷ Research looking at non-ketogenic, low-carbohydrate diets do not demonstrate the same defect, suggesting there may be different risks present during ketosis.^18-20

Moderation Is Sound Advice

This body of research is quite significant, even though it is from a mouse study and has not been duplicated in humans, let alone in a second mouse study. Many people follow a low-carbohydrate diet to reduce their bodyweight, improve conditions associated with the Metabolic Syndrome (high cholesterol, high blood pressure, insulin resistance, etc.) and decrease cardiovascular risk. Further, some who are already at risk for cardiovascular disease or even those in rehab after a cardiovascular event may be following a low-carbohydrate diet, in the belief that it is more effective for weight loss and poses no more (or even less) of a risk to one’s cardiovascular health. Indeed, the blood work performed during studies evaluating the various diets (including Atkins-like, low-carbohydrate diets) suggest that these diets are as safe or safer than the traditional low-fat diet.²¹ Yet, reports of individuals developing cardiovascular disease while following an Atkins-type plan have been published.²²

Given the findings in this study, it is impossible to recommend low-carbohydrate or ketogenic diets to those with a significant personal or family history of cardiovascular disease. In fact, this data supports the recommendation for moderate carbohydrate intake sufficient to maintain a baseline insulin presence. The exact recommendation for carbohydrates remains fuzzy at this time, but it appears that at least 60-100 grams per day of low-glycemic carbohydrates, along with an intake of mono- and polyunsaturated fats to counterbalance saturated fat intake, is the optimal diet plan. Excessive carbohydrate intake should be avoided as well, suggesting that the age-old adage of moderation in all things remains sound advice.

AAS-using bodybuilders and athletes should take note, as hidden damage to the cardiovascular system may make the AAS-using individual more susceptible to heart or brain damage, even sudden death. Certainly, the inability of the circulatory system to develop new blood vessels to feed working and growing muscle would be a detriment to the anabolic effects of training.

There are many approaches to fat loss. Science, the media, and policymakers have so long focused on the dangers of various weight-loss drugs that the hidden dangers of (physiologically) extreme diets may have been ignored.

References:
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2. Aoki TT. Metabolic adaptations to starvation, semistarvation, and carbohydrate restriction. Prog Clin Biol Res, 1981;67:161-77.
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4. Gardner CD, Kiazand A, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA, 2007 Mar 7;297(9):969-77.
5. Frisch S, Zittermann A, et al. A randomized controlled trial on the efficacy of carbohydrate-reduced or fat-reduced diets in patients attending a telemedically guided weight loss program. Cardiovasc Diabetol, 2009 Jul 18;8:36.
6. Evangeliou AE, Spilioti M, et al. Branched Chain Amino Acids as Adjunctive Therapy to Ketogenic Diet in Epilepsy: Pilot Study and Hypothesis. J Child Neurol, 2009 Aug 17. [Epub ahead of print]
7. Rezkalla SH, Kloner RA. Cocaine-induced acute myocardial infarction. Clin Med Res, 2007 Oct;5(3):172-6.
8. Yang HT, Prior BM, et al. Training-induced vascular adaptations to ischemic muscle. J Physiol Pharmacol, 2008 Dec;59 Suppl 7:57-70.
9. Ruegg C, Mutter N. Anti-angiogenic therapies in cancer: achievements and open questions. Bull Cancer, 2007 Sep 1;94(9):753-62.
10. Foo SY, Heller ER, et al. Vascular effects of a low-carbohydrate high-protein diet. Proc Natl Acad Sci USA, 2009 Aug 24. [Epub ahead of print]
11. Kondo T, Hirose M, et al. Roles of Oxidative Stress and Redox Regulation in Atherosclerosis. J Atheroscler Thromb, 2009 Sep 14. [Epub ahead of print]
12. Kang LN, Chen Q, et al. Decreased Mobilization of Endothelial Progenitor Cells Contributes to Impaired Neovascularization in Diabetes. Clin Exp Pharmacol Physiol, 2009 Jun 16. [Epub ahead of print]
13. Urbich C, Dimmeler S. Risk factors for coronary artery disease, circulating endothelial progenitor cells, and the role of HMG-CoA reductase inhibitors. Kidney Int, 2005 May;67(5):1672-6.
14. Cubbon RM, Kahn MB, et al. Effects of insulin resistance on endothelial progenitor cells and vascular repair. Clin Sci (Lond), 2009 Aug 3;117(5):173-90.
15. Phillips SA, Jurva JW, et al. Benefit of low-fat over low-carbohydrate diet on endothelial health in obesity. Hypertension, 2008 Feb;51(2):376-82.
16. Ardigo D, Franzini L, et al. Relation of plasma insulin levels to forearm flow-mediated dilatation in healthy volunteers. Am J Cardiol, 2006 Apr 15;97(8):1250-4.
17. Keogh JB, Grieger JA, et al. Flow-mediated dilatation is impaired by a high-saturated fat diet but not by a high-carbohydrate diet. Arterioscler Thromb Vasc Biol, 2005 Jun;25(6):1274-9.
18. Keogh JB, Brinkworth GD, et al. Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. Am J Clin Nutr, 2008 Mar;87(3):567-76.
19. Volek JS, Ballard KD, et al. Effects of dietary carbohydrate restriction vs low-fat diet on flow mediated dilation. Metabolism, 2009 Jul 24. [Epub ahead of print]
20. Keogh JB, Brinkworth GD, et al. Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. Am J Clin Nutr, 2008 Mar;87(3):567-76.
21. Samaha FF, Foster GD, et al. Low-carbohydrate diets, obesity, and metabolic risk factors for cardiovascular disease. Curr Atheroscler Rep, 2007 Dec;9(6):441-7.
22. Barnett TD, Barnard ND, et al. Development of symptomatic cardiovascular disease after self-reported adherence to the Atkins diet. J Am Diet Assoc, 2009 Jul;109(7):1263-5.

TRAIN WITH WAYNE

Is Six Meals a Day Really the Way? Or could fasting have benefits?

You’ve heard the mantra: Eat frequently—five to seven small meals daily, each including a serving of protein, healthy fat and low-glycemic-index, or fibrous, carbohydrates, such as vegetables. Now I’ve heard that maybe it’s a good idea not to eat those frequent meals and instead engage in “intermittent fasting.” In a simple sense, most folks think of this as basically not eating on occasion. And herein is the problem. IF is different things to different people.

If people told me they were doing intermittent fasting, it would mean that one or two days a week they simply didn’t eat. That’s fasting. Fasting is not skipping dinner. It’s not skipping meal number four of your six meals. Fasting is fasting. It’s not not eating a meal. So until the International Group of Fasting Scientists come up with an agreeable definition, it’ll be like judging a bikini contest; it’s all in the eye of the beholder. That said, let’s at least look at some telling statistics on what happens when humans alter their basic patterns of eating.

A recent study from the International Journal of Obesity looked at the feasibility and effectiveness of intermittent continuous energy with continuous energy restriction for weight loss, insulin sensitivity and other metabolic-disease-risk markers.1 In other words, the subjects either cut their calories evenly over a six-month period or restricted calories for only two days per week over the six-month period. Both diets involved a 25 percent calorie restriction overall. The continuous restriction group cut their calories by 25 percent spread evenly over the week, whereas the intermittent group followed a very low-calorie diet two days per week, cutting calories by 75 percent.

Results: both methods were equally effective for weight loss. Both groups had similar reductions in leptin, free androgen index, high-sensitivity C-reactive protein, total and low-density-lipoprotein cholesterol, triglycerides, blood pressure and increases in sex-hormone-binding globulin, IGF-binding proteins 1 and 2; however, the intermittent group had a lower fasting insulin. So the bottom line is that both seemed to produce similar weight loss, with the intermittent method being better for insulin sensitivity. But that was in fat people. What happens to folks who actually exercise?

In a more relevant study, scientists determined whether Ramadan intermittent fasting affects 5,000-meter running performance and other parameters classically associated with middle-distance performance.2 Ramadan is a month of obligatory daily fasting that starts at dawn and ends at sunset, so that to me is “intermittent fasting.” Two experimental groups participated in two experimental sessions, one before Ramadan intermittent fasting and the other at the last week of fasting. The subjects were 18 well-trained, middle-distance runners. At the end of Ramadan fasting, a decrease in maximal voluntary contraction—i.e. strength—was observed as well as a decrease in performance of -5 percent. There was no effect on running efficiency or maximal aerobic power. The study shows that Ramadan intermittent fasting can result in a detriment to performance.

So should you fast or not? Or shall you stick religiously to six meals a day for the rest of your life?

Editor’s note: Jose Antonio, Ph.D., is the CEO of the International Society of Sports Nutrition (www.theissn.org); also check out his site www.TheWeekendWorkout.com.

1 Harvie, M.N., et al. (2011). The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. Int J Obes (Lond). 35(5):714-27.

2 Brisswalter, J., et al. (2011). Effects of Ramadan intermittent fasting on middle-distance running performance in well-trained runners. Clin J Sport Med. 21(5):422-7.

TRAIN WITH WAYNE IS DEDICATED TO BRINGING YOU HEALTH INFORMATION WHICH YOU CAN STUDY AND PICK WHAT BEST WORKS FOR YOU AS AN INDIVIDUAL EXERCISER.

Fat loss and how to keep it off

11 Simple Tips to Lose the Weight and Keep it Off

• Written by  By Jeff Behar, MS, MBA

Losing weight is as simple as eating less and exercising more, right?

If only it were that simple! As most of us know losing weight can be very challenging, both mentally and physically.

There are many things that influence overeating. Stress (stress hormones, like cortisol), environment are major contributors. A basic understanding of when, where can help explain why you may be overeating. Once you know the why, you can than devise a plan to increase your odds of losing weight and keeping it off for good!!

First tip: right down everything you eat...and I mean everything, in a food log. Note time, and any contributory factor you can identify (running late, ate fast food, stressed at work, grabbed some junk food, etc.)

Next, determine how many calories you need to maintain your current weight.

This can be done using one of the tools available to you at www.mybesthealthportal.com, or you can do a few simple calculations.

For the simple calculation you do not need to be a math wiz. Here is a simple way to find out how many calories your body requires to maintain your current weight.

Multiply your current weight by 15. This is roughly the number of calories per pound of body weight needed to maintain your current weight if you are moderately active. Moderately active means getting at least 30 minutes of physical activity a day in the form of exercise (walking at a brisk pace, climbing stairs, or active gardening). Let's say you're a man who is 5 feet, 8 inches tall and weighs 200 pounds, and you need to lose about 20 pounds to put you in a healthy weight range. If you multiply 200 by 15, you will get 3,000, which is the number of calories per day that you need in order to maintain your current weight (weight-maintenance calories). To lose a 2 pounds of body weight per week, you will need to lose 7000 calories less, or 1000 per day.

If you are sedentary, you will also need to build more activity into your day. In order to lose at least a pound a week, try to do at least 45 minutes of physical activity on most days, and reduce your daily calorie intake by at least 500 calories.

Because your body will soon adapt to restricted calories as a survival mechanism it is important that you average and cycle your calories to reach the desired deficit (7000 per week in the example above).  That would mean decreasing your calories in a manner such as this:

1500

2000

2500

1500

3000

1500

2000

Using the example above you have reduced your caloric intake from an average of 3000 calories a day to an average of 2000 calories a day. That would be 7000 calories less a week for a loss of 2 pounds per week.

Meeting your calorie target

How can you meet your daily calorie target? The best approach iis to add up the number of calories per serving of all the foods that you eat, using a food log like a menu.   You can buy books at a book store or find information on the web that lists calories per serving for many foods.  You can also find some of this information at mybesthealthportal.com under the tools/resources tab in the tool bar.

Also take heed to the nutrition labels on all packaged foods and beverages. They will provide calories per serving information, and often also provide grams of carbs, fats, protein and more.  Ingredients listed are usually in the orderf of amounts as well.

Reading Before Eating

Always read the labels before eating. This will not only start to educate you about what you are putting into your body, but it will also help prevent you from eating the wrong things in error.

Do Not Forget Counting the Drinks

Drinks can have calories as well, and are often not tacked by dieters, and these same dieters often wonder why they are not losing weight!!

When tracking your calories always noteg the number of calories and the serving sizes.

Hate Counting?

If you hate counting calories, there are different approaches where you choose certain meals, foods and eat at specific times using specific portions (like the Weight Watcher points system).

The Sensible Approach

Whichever method you choose, research shows that a regular eating schedule - with meals and snacks planned for certain times each day - makes for the most successful approach.

This is also important for your long term success in keeping the weight off for good. Sticking with an eating schedule increases your chance of maintaining your new weight.

If you decide to not count calories (which personally I believe is the best way), and plan on trying a common sense approach it is important that you follow a few simple guidelines which will help increase your chances and success in losing and keeping off the weight.

1. Minimize the bad fats. Fats are 9 calories a gram more than double that of protein and carbohydrates.

2. Minimize empty calories such as gravies and other toppings.

3. Eat foods that are filling and low in calories. That means meals and snacks made with whole grains, such as brown rice, whole-wheat bread, and oatmeal, as well as legumes, such as lentils and other beans.

4. Consider fish and poultry over meat.

5. When you eat meat, choose lean cuts of meat and modest amounts - about 3½ or 4 ounces per serving.

6. Avoid fried foods. For stovetop cooking, it's better either to stir-fry foods in nonstick pans lightly coated with a cooking-oil spray or to braise them in broth or wine. Baking, broiling, and roasting add no extra fat to your meals.

7. Use low-fat or nonfat dairy foods. Milk, yogurt, and cheese are good sources of protein and calcium, but the whole-milk versions of these dairy products are very high in fat, so substitute them for the low fat or fat free varieties whenever possible.

8. Eat slowly. For more than 30 years, dieters have been told to eat slowly to reduce their intake of food. This idea "It started in about 1972 as a hypothesis that eating slowly would allow the body time for the development of satiety [fullness] and we would eat less," according to Kathleen Melanson, assistant professor of nutrition and food science at the University of Rhode Island. "Since then we've heard it everywhere and it has become common knowledge. But no studies had been conducted to prove it." Not until recently!!! In  a laboratory study of college-age women over the past year led by Melanson confirmed the long-held belief. In the study, 30 women made two visits to Melanson's lab, and each time they were given a large plate of pasta and told to eat as much as they wanted. When they were told to eat quickly, they consumed 646 calories in nine minutes, but when they were encouraged to pause between bites and chew each mouthful 15 to 20 times, they ate just 579 calories in 29 minutes. The study demonstrated that satiety signals  need time to develop. The women took in fewer calories when they ate more slowly, and they had a greater feeling of satiety at meal completion and 60 minutes afterwards!!! This data strongly suggests benefits to eating more slowly. The study also interviewed the participants who stated that they enjoyed the meal more when they ate slowly than when they ate quickly. Of important note, One potentially confounding factor in the study was that the volunteers were provided water to drink with their meal, and when eating slowly they had considerably more time to drink before completing their meal. The greater consumption of water might have contributed to satiety under the slow condition. However, Melanson said that this factor reflects the real-world situation, since eating slowly allows more time for water consumption.

9. Drink lots of water. Water can help you lose weight and feel full (see above) while also being very good for the body as well. Drinking cold water is best. Studies show that drinking cold water rather than tepid water can burn calories; drinking about 8 ounces of ice-cold water (1 degree Celsius) would cause the body to expend about 9 calories. Although this is not a huge deal, if you drank 100 ounces a day this way you could lose a pound a month, besides the calories you might not eat while drinking the water which would also help you feel fuller.  You can read more about it at : How Stuff Works: "Does drinking ice water burn calories?"

http://science.howstuffworks.com/question447.htm.

10.  Avoid fast foods. Hamburgers, tacos, fried chicken, hot dogs, chicken nuggets, French fries, and other fast-food meals and snacks tend to promote weight gain for two reasons. First, they are high in fat, calories, or both. Second, the "value meals" are often excessively large and tempt you to overeat.

11. Minimize beverages that contain calories. Why? because they can add up quickly and often leave you feeling hungry.

Diabetes and Heart Health

Diabetes makes people more likely to have congestive heart failure by pumping up their blood sugar. High blood sugar can cause fatty materials to clog blood vessels. As the blood backs up like cars on the highway, the heart is forced to pump even harder to keep the traffic moving. That leads to the heart getting worn out and quitting.
Many people with diabetes are also overweight. That’s another contributor to heart disease. When the bloodstream has extra fat, also known as cholesterol and triglycerides, even more cars are added to the congestion of the blood system.  People with diabetes must hold their long-term blood sugar below 7 percent and carefully monitor cholesterol to keep their blood freely flowing. The danger of congestive heart failure is significant. About 65 percent of diabetes deaths are related to the heart.

Heart Failure Side Effects of Diabetes Medication
Certain medications also make people with diabetes more likely to have congestive heart failure. The type 2 diabetes drug Avandia was essentially banned for heart-related side effects. Its sister drug, Actos, now carries the black-box warning from the Food and Drug Administration (FDA) for its congestive heart failure risk and other Life Threatening Side Effects. The black-box warning is applied to drugs that can cause serious injury or death.
Actos is still for sale in the United States, even though it makes patients 30 percent more likely to have congestive heart failure. Recent studies have found it also increases the risk of bladder cancer. This has lead to several thousand Actos Lawsuits.  It’s still unclear exactly how these medications contribute to blood vessel congestion. The drugs have been linked to about an 18 percent increase in LDL cholesterol. LDL is cholesterol that’s bad for the body. Most people should try to keep their LDL levels below 100 mg/dL.
People with diabetes need to work hard at heart health because they’re at higher risk. They should monitor blood glucose, blood pressure, cholesterol and medication side effects. Speaking to a doctor will help patients understand their cardiovascular health. A physician can also provide health improvement strategies.

William Richards researches and writes about prescription drugs and medical devices for Drugwatch.com.

Can You Overdose On Vitamin C

It is one of the most common vitamins that is talked about and definitely the most popular. But what is this vitamin and what does it do? In the scientific terminology, vitamin c is known as l-ascorbic acid. This acid is one of the more necessary nutrients that us humans need in our bodies. Without it, you could end up with a very bad case of the disease scurvy, something that was quite common in the olden days.

This vitamin consists of ascorbate, or an ion of the ascorbic acid. It is key to the functioning of the metabolism in both animals and plants. This ascorbate is necessary in the bodies of living organisms, since it is an anti-oxidant. Without it, the process of oxidation would cause far too much stress on our cells and tissue, which can be damaging in nature. There are a number of reactions and processes that are enzymatic in nature (related to enzymes) that need the ascorbate to function. In order to study them further, the year 1933 saw the isolation of ascorbic acid and its synthesis in 1934.

This of course begs the question – is it possible to have too much of a good thing?

Can you overdose on vitamin c?

Research has suggested that you can in fact overdose on vitamin C. In fact Vitamin C has an upper limit of 2000mg and over-consuming vitamin C to this amount can bring about certain symptoms.

The two most common symptoms of a Vitamin C overdose are nausea and Diarrhea as a result of an overdose on vitamin c. Although these are not symptoms that can be seen with some overdoses of serious medications and pharmaceutical products these can still be concerning. If a person becomes very sick and is constantly vomiting or unable to gain any nutrients from their food they could become dehydrated and have their immune systems functions lowered putting them at risk to further sickness.

The best way to be certain you will not overdose on vitamin C is to track your consumption of vitamin c daily. Vitamin C can be found in many common foods such as apples and blackberries but actually getting to the upper limit level for safe consumption cannot usually be done without some form of vitamin supplement. An apple maybe contains about 8-9 mg of vitamin C so reaching the upper limit would require eating hundreds of apples in a day. A vitamin C supplement however can contain a few hundred mg up to even 1000mg of vitamin C all in one tablet.

Should a child get a hold of a bottle or you accidentally take more than one supplement in a day there is a small chance that you could feel the symptoms of an overdose on vitamin c. Unfortunately many vitamin C tablets are flavored and have quite a sweet taste similar to candy. For kids these can be irresistible and it is important that they do not take more than one a day. A child’s body will have an even lower tolerance for vitamin C and they may begin to feel the symptoms of a vitamin C overdose with only half the amount of an adult upper limit for consumption.

Even though there are risks involved with vitamin C consumption there is no reason why a person should abstain from taking a supplement or trying to get their daily dose of vitamin C. Vitamin C deficiency in fact will leave a person more worse off than the symptoms of an overdose on vitamin C. Not getting enough vitamin C can result in muscle loss, joint pain and health problems in general.

The safe consumption for vitamin C intake has been determined as somewhere between 500 and 1000mg of vitamin C a day. It has been critically proven that by taking vitamin C you can reduce your risk for heart disease and improve maintain your health which will allow you to live longer.

Although there is a danger of potentially having an overdose on vitamin C, by tracking your intake and making sure to only take the recommended amount, you can ensure that your body will maintain its current level of health and never be deficient of vitamin C. The benefits greatly outweigh the risks and taking vitamin C is still recommended by physicians everywhere.

Minor Symptoms of  a vitamin c overdose

Vitamin c overdose can manifest in a number of ways. If you’re currently taking vitamin c, and discover any with the following signs and symptoms, lower your dosage instantly, as these are all minor signs of a light vitamin c overdose:

Nausea
Sturdy smelling Urine
Mouth ulcers
Gas
Bloating
Upset stomach

Diarrhea can also be a sign that you simply are taking an excessive amount of vitamin c and many doctors recommend utilizing this sign to gauge your tolerance to vitamin c. Diarrhea resulting from excessive amounts of vitamin c is viewed as just below potentially risky levels, and strangely enough can impart certain benefits to your well being and health, for example a lowered risk of colon cancer.

Serious signs and symptoms of vitamin c overdose

The risk of overdosing and serious side effects is very relevant for people who take over 6000mg each day, or those that take extra supplements along with high doses of vitamin c. Significant signs and symptoms of a hazardous vitamin c overdose involve:

Kidney stones
Vitamin B-12 deficiencies
Copper deficiencies
Increased want for oxygen

If you are experiencing any of the above then it is prudent to go and see a medical professional. Significantly altered levels of vitamin c in the body can result in numerous health hazards.

Mega dosing vitamin c.

Even with the continuing research and data stating the hazards of excessive vitamin c, there are many professionals who do not comply with the findings. There are a  number of researchers and medical personnel who recommend mega doses of the vitamin. Under such a circumstance, a person can see an intake of up to 20 grams or more of vitamin c each day. The use of this practice is to work towards a healthier body and curing various illnesses and disorders.

There are many ways in which these doses can be taken. The common form is to divide the dosage throughout the day and portions are to be consumed at specific intervals of time. One of the methods used is to inject the vitamin c straight into the body, in the measure of hundreds of grams. This has been advocated as a form of  healing for bodily trauma, poisoning of the system and certain body disorders. Others find it easier to depend on pill use through the day. One can also use a pure form of vitamin c, which is crystallized. This can be dissolved in water or juice to make a drink that lasts through the day

There are a number of research works on Vitamin C at the moment and the effects have been widely studied. Some of these are:

Effects on the Common Cold

One of the more common old wives tales includes the use of citrus fruits as a way to prevent or cure common cold. The high levels of vitamin C are supposedly effective on the condition and helps to dispel it faster. Studies have been conducted to verify this theory. A 3 meta-analyses has suggested that a dosages of the order 200 mg to 2 grams are seen to decrease the duration of the cold. This is effective when taken prophylaxis (before infection) rather than post infection. The actual rates of infection showed no changes. The appearance of the cold was shown to have fallen by 50% in certain demographics of adults under duress such as athletes, soldiers and those in cold environments. There was no reduction of symptoms to be seen or diminished duration when taken during the first few stages of infection.
By the conclusion of a 2010 Cochrane Review, it is shown that intake of Vitamin C in varied dosages does little to reduce the incidence of the common cold. However, it is seen that for the population exposed to severe strain during physical exercise and brief but considerable exertion, Vitamin C is a helpful supplement. Dosages of the vitamin prior to the onset of cold and similar symptoms has shown to be effective – mostly in alleviation of the symptoms. However, such results have not been again in therapeutic trails. This demands further therapeutic RCTs.

Effects on Heart Illness

There are currently a number of clinical trials being conducted to test the correlation between vitamin C use and the affect on coronary diseases. The relation between vitamin C usage and prevention of strokes or coronary heart problems has seen results showing neutral, negative and some positive outcome. There is no clear answer as of now, seeing how challenges of selection of test subjects, methodology and direction of study are hard to keep similar and further difficult to interpret.

Effects on Cancer

One of the first studies concerning cancer and the use of vitamin C was published by Pauling and Cameron in 1976. Using data from a hundred cancer patients, the trial was conducted to check whether intravenous dosage could affect the life expectancy and increase it. The results were positive. However, the results were not replicated in independent studies conducted in 1979, 1983 and 1985. These trials were conducted with oral vitamin C, as compared to the earlier one with ascorbic acid delivered through intravenous methods and were placebo-controlled. There are flaws found in the earlier study, with the patients not being picked in a randomized or controlled manner.
Most current trials have been limited in their scope to simply finding appropriate dosages. However, these Phase 1 clinical trials and researches have been able to determine that patients who have cancer will not suffer toxicity caused by vitamin C. For a dosage of less that 1.5 grams of ascorbic acid per each kg of the body weight, there is little scope that vitamin C has as therapy. At the same time, there are certain in-vitro cell lines testing that are indicative of problems. Mainly, the possible problems that may occur during chemotherapy due to dehydroascrobic acid (DHA) which is an ascorbic acid in an oxidized form.
There is little evidence to support that vitamin C has any sustained impact on the treatment of cancer. 33 long years of research and trials culminated in a 2010 consultation, which revealed that the evaluation of vitamin C and other antioxidants revealed no major difference in effects during chemotherapy for cancer. Vitamin C has not been shown to cause a major decrease in the tumor activity nor does it act against specific kind of cancers. At the same time, the appropriate dosage is still not known and how any specific quantities of vitamin C can help in engaging the body systems in an anti-tumor response.

Effects on Phencyclidine Psychosis Treatment

One of the proven areas of effectiveness is the treatment of phencyclidine psychosis. A dosage of some 1000-2000 mg that is supplied intravenously has been seen to complement the use of an antipsychotic drug. It can also be provided along with a DA-2 antagonist in a mixed form. Common antagonists used are haloperidol and risperidone, which can be administered through the muscular tissue. Cases of PCP (acute phencyclidine psychosis) are seen to recover thanks to the supplement of vitamin C as it is seen to be interacting synergistically with the occurrence of phencyclidine and metabolites of the same.

Effects on Gout

Whether in the form of supplements or taken through natural form, Vitamin C consumption in large quantities has been linked to lower rates of incidence in Gout. A research study conducted in the year 2008 showed that serum uric acid levels went down and so the possibility to developing symptoms of gout by 45%. The intake amount was chalked up to more than 1500 mg for this study.

Effects on Burns

The role of Vitamin C is seen to be important during the treatment of serious burns. It is considered to be an adjuvant treatment to dose patients with intravenous vitamin C for small periods of time. This is done since certain metabolic changes related to the conditions of burns. As of now, the American Burn Association has been considered the administration of ascorbic acid to be an adjacent form of therapy rather than an actual treatment method. The quantity of the dose has been settled upon 110 grams (66 mg per kilogram per hour for a day) by one study conducted. However, these results remain isolated and have not seen further enquires and studies to prove the same. A number of trials and studies will have to be conducted with positive results before vitamin C becomes a form of treatment. This is because the ABA finds no substantial benefit from the dosage.

There are however, also numerous studies that support the consumption of higher doses of vitamin c.

The blood plasma vitamin c concentration among vitamin c supplement users is about 60 to 70 percent larger than adults who do not take supplements (75-80 vs. 45-50 micromole). [J Am College Nutrition 13: 22-32, 1994] A daily intake of 1000 mg is needed to maintain plasma vitamin c concentration in the range of 75-80 micromole. Only 4.2 percent of the US population 3 to 74 years of age is probably to have plasma vitamin c levels above the 80 micromole point. [National Wellness Survey, Series 11, No. 232, DHHS Publication No 83-1682, 1982]

One particular broadly acclaimed study published in 1992 indicated that vitamin c, in oral doses exceeding 750 milligrams per day, increased the lifespan of males by about 6 years. [Epidemiology three: 194-202, 1992]

A study published inside the March 2004 issue with the American Journal of Epidemiology indicates males taking high-dose vitamin c exhibit a 2.68 less chance of calcification in their arteries compared to males who consume low doses of vitamin c. The risk for angina among adults who consume considerable amounts of alcohol could be cut in half with high doses of vitamin c. [Ann Epidemiology. 9: 358-65, 1999] One study concluded that 3000 mg of oral vitamin c everyday even increases the frequency of sexual intercourse. [Biological Psychiatry. 2002 52:371-4, 2002]

Safety will not be an issue in terms of mega-dose vitamin c supplements. Eight placebo-controlled, double-blind scientific studies and six non-placebo controlled clinical trials in with up to 10 000 milligrams of vitamin c was consumed every day for up to three years, confirm the safety profile of vitamin c pills in excess in the RDA. [J Am College Nutrition 14: 124-36, 1995] Frequent allegations are produced that vitamin c supplements might encourage the formation of kidney stones, but are poorly founded. Moreover, the false notion that withdrawal from high-dose vitamin C may well result in “rebound scurvy” has also been dispelled. Whilst vitamin c increases the absorption of iron, it has not been shown to induce iron overload in humans. [Nutrition Reviews 57: 71-77, 1999]

Anecdotal and unverified uses of vitamin c

Mega doses of intravenous vitamin c have been used successfully in some cases for coma recovery.
Linus Pauling and Dr Hugh Riordan advocated and claimed to have successfully treated cancer with high doses of vitamin c.
Anecdotal reports suggest that vitamin c may help in reducing scar tissue in the body (scarring from accidents, acne etc).
Anecdotal reports of vitamin c reducing angina pains and clearing plaque deposits in the arteries.

Protein Drink Dangers: Investigation Finds Several Protein Powders and Protein Drinks Toxic

 

Are Ready-to-Drink Protein Powders and Protein Liquids are Contaminated?

A new "Consumer Reports" Investigation finds that some ready-to-drink protein powders and protein liquids are contaminated with dangerous metals that pose serious health risks and can have toxic effects on the body's organs.

The Consumer Reports investigation appearing in Consumer Report's July issue, included the testing of 15 protein drinks, as well as a review of government documents and interviews with health and fitness experts, and consumers.
The report found that most people already get enough protein and that even people who do not can find "far better and cheaper ways to add more protein to their diet if it's needed."
All 15 of the protein drinks tested by Consumer Reports had one or more the following contaminants: arsenic, cadmium, lead and mercury.
Specifically, "Consumer Reports" found that Muscle Milk Chocolate, Muscle Milk Vanilla Crème and EAS Myoplex Original Rich Dark Chocolate can expose users to elevated levels of heavy metals when they consume three servings a day.
If consumed in excess, arsenic, cadmium, lead and mercury can have toxic effects on the body and its organs. Chronic, low-level exposure to heavy metals can build up in the body and cause serious health conditions, including but not limited to central nervous system damage, reproductive damage, organ failure and even death.