Thursday, July 31, 2014

Muscular Fitness More Important Than Body Weight To Prevent Heart Disease

Exercise protects against heart disease in many ways. One important mechanism is by elevating HDL, a.k.a. the “good” cholesterol. It is well established that high levels of HDL are protective against cardiovascular disease and the National Cholesterol Education Program (NCEP) has emphasized increasing HDL levels to help reduce CHD risk. However, not only HDL levels are important. Emerging research in showing that HDL quality and function is as important, if not more important for health promotion and prevention of cardiovascular and metabolic diseases.

Researchers from the University of California/Los Angeles (UCLA, California, USA) investigated HDL quality in three groups of young men:

  1. overweight untrained (BMI 30 – no training)
  2. overweight trained (BMI 29 – 4 d or more per week resistance training)
  3.  lean trained (BMI 24 – 4 d or more per week resistance training)

It was found that HDL function was significantly better in both trained groups compared with the overweight untrained group. However, HDL function in the overweight trained group was not significantly different from that of the lean trained group.

Thus, muscular fitness is more important than body weight for HDL functionality and could be a potential mechanism by which resistance training may decrease cardiovascular disease risk.

Interestingly, it was noted that some metabolic and hormonal parameters were related to HDL functionality. High HDL function not only correlated with lower oxidized LDL, which is implicated in atherosclerosis, but also with higher testosterone levels. The latter can explain why low testosterone levels are associated with increased cardiovascular disease risk.

Interestingly, it was noted that some metabolic and hormonal parameters were related to HDL functionality. High HDL function not only correlated with lower oxidized LDL, which is implicated in atherosclerosis, but also with higher testosterone levels. The latter can explain why low testosterone levels are associated with increased cardiovascular disease risk.

This is the first study to demonstrate a relationship between HDL redox activity (an aspect of HDL function) and testosterone.

Friday, July 25, 2014

Diabetics live longer with physical exercise

Exercise reduces your chances of developing type-2 diabetes, but even if you already have diabetes exercise is good for you. Definitely if you exercise for longer than the daily half hour that is advised.

At the Lawrence Berkeley National Laboratory, the biostatistician Paul Williams examined data gathered in the National Walkers’ and Runners’ Health Studies. In that project researchers have been following several hundred thousand runners and walkers since the twentieth century – and among them are 2160 men and women who take medication for diabetes.

Williams knew how often the participants walked and ran, and divided them into three groups on the basis of the amount of calories they burned. The first group did the equivalent of 1.07 MET-hours per day. 1 MET-hour is the equivalent of about 1 km running or 1.5 km walking at a brisk pace.

The second group did between 1.07 and 1.8 MET-hours a day. If you manage the 1.8 MET-hours per day, you do exactly the amount of exercise that health experts advise. That means walking briskly for a good half hour every day.

The third group that Williams separated out were those who did more than the 1.8 MET-hours per day, and thus got more exercise than advised.

When Williams then looked at which diabetics had died, he saw that their mortality risk was lower, the higher their MET-hour figure was. In the figure below the mortality risk of the diabetics category with the least exercise.

Diabetics are more likely to die, and this is mainly because the disease damages the heart and blood vessels. Williams discovered that walking and running reduced the risk of dying from cardiovascular disease. In addition, exercise also reduced the chance of dying from an infectious disease or a kidney disease.

“Most people at risk for diabetes are not sufficiently active as defined by the recommendations for the general population, little less the recommendations for diabetic patients”, Williams concludes. “These results identify important additional benefits for diabetic patients to exceed the current general physical activity recommendations for adults.

Reduced Total and Cause-Specific Mortality from Walking and Running in Diabetes

This study aimed to assess the relationships of running and walking to mortality in diabetic subjects.

We studied the mortality surveillance between January 1, 1989 and December 31, 2008, of 2160 participants of the National Walkers’ and Runners’ Health Studies who reported using diabetic medications at baseline. Hazard ratios (HR) and 95% confidence intervals (95% CI) were obtained from Cox proportional hazard analyses for mortality versus exercise energy expenditure (MET-hours per day, 1 MET·h ?1-km run or a 1.5-km brisk walk).

Three hundred and thirty-one diabetic individuals died during a 9.8-yr average follow-up. Merely meeting the current exercise recommendations was not associated with lower all-cause mortality (P = 0.61), whereas exceeding the recommendations was associated with lower all-cause mortality (HR = 0.64, 95% CI = 0.49–0.82, P = 0.0005). Greater MET-hours per day ran or walked was associated with 40% lower risk for all chronic kidney disease-related deaths (HR = 0.60 per MET·h·d?1, 95% CI = 0.35–0.91, P = 0.02), 31% lower risk for all sepsis-related deaths (HR = 0.69, 0.47–0.94, P = 0.01), and 31% lower risk for all pneumonia and influenza-related deaths (HR = 0.69, 95% CI = 0.45–0.97, P = 0.03). Running or walking ?1.8 MET·h·d?1 was associated with 57% reduction in cardiovascular disease (CVD) as an underlying cause of death and 46% lower risk for all CVD-related deaths versus <1 .07="" d="" h="" met="" nbsp="" p="">
All results remained significant:

  1. adjusted for baseline BMI and 
  2. excluding all deaths within 3 yr of baseline.

These results suggest that

  1.  exercise is associated with significantly lower all-cause, CVD, chronic kidney disease, sepsis, and pneumonia, and influenza mortality in diabetic patients and:
  2. higher exercise standards may be warranted for diabetic patients than currently provided to the general population.

Friday, July 18, 2014

Muscle mass extends life expectancy

If you do heavy physical work or weight training, you’ll not only make your body more muscled and stronger, but you’ll also make it last longer.

Researchers used to think that overweight elderly people had a higher risk of dying, but recent studies have shown that both overweight and underweight elderly people are more likely to die. More and more epidemiologists are therefore coming to the conclusion that it’s not bodyweight that determines how long you are likely to live, but lean body mass.

In other words: the muscles.

Preethi Srikanthan tested this theory by examining data on 3695 over 55s gathered for the National Health and Nutrition Examination Survey III. Srikanthan followed the participants from the period 1989-1994 until 2004. When the study started the men were over 55 and the women older than 65. Srikanthan noted which of the participants died in the 10-16-year period.

There was no relationship between the participants’ amount of non-muscle mass and their survival chances, Srikanthan discovered when he divided the participants into four equal-sized groups (quartiles) on the basis of their non-muscle mass, and then calculated their mortality risk.

But when Srikanthan divided the participants into quartiles based on muscle mass, he did find a relationship. Participants with lots of muscle mass were 20 percent less likely to die than participants with little muscle mass. Srikanthan is not sure how muscle mass increases our survival chances. Perhaps it protects against high glucose levels, perhaps it reduces the amount of dangerous fat in the body, or perhaps muscles produce protective substances. But he does have a word of advice. “Get up and start moving”, the researcher said.

Clinical study to assess the efficacy and safety of a citrus polyphenolic extract of red orange, grapefruit, and orange on weight management and metabolic parameters in healthy overweight individuals.

Friday, July 11, 2014

Gynecomastia: Causes & Cures

Out of all the side effects a steroid user could potentially experience, gynecomastia (aka bitch tits) is one of the worst…and it certainly tops the list when it comes to cosmetic side effects. Being heavily associated with womanhood, the very nature of this side effect is an affront to our masculinity. Not only is it embarrassing, but in some cases it can destroy the entire appearance of one’s physique. We have all seen pictures of the more extreme cases, where the  bodybuilder literally looks like he has grown a small pair of tits on an otherwise normal body. The severity of this condition can range from only slight swelling, which is often imperceptible from a visual standpoint, to the more extreme cases, as mentioned above Fortunately, gynecomastia does not develop over night and its progression is easily halted and reversed if the proper steps are taken in a timely fashion. There really isn’t any good excuse for a steroid user to experience permanent, visible breast tissue growth. Those that do either don’t care or rather (and much more likely), they weren’t prepared and/or educated to deal with this side effect ahead of time. While there are numerous potential causes of this condition, the  bodybuilder generally only has to worry about a few of them and the available treatment options are simple in their application. Through minimal self-education and a small financial investment we have all the tools we need to keep this side effect at bay.

The most important factor in the prevention of gyno is knowing how it occurs in the first place. Since this article is targeted mainly towards the steroid-using bodybuilder, we will only address the causes which are directly attributable to PED usage. There are 4 types of steroids which can cause gynecomastia , the most prominent of which are the aromatizable steroids. Aromatizable steroids are those anabolic sterods which are capable of converting to estrogen. This includes many steroids, such as Testosterone, Methyltestosterone, Methandrostanolone (Dianabol), and to a lesser degree, Nandrolone (Deca), and Boldenone (EQ). This conversion process is initiated when aromatizable anabolic steroids interact with aromatase, which is an enzyme necessary for the biosynthesis of estrogen. See below for a depiction of this interaction:

When low dosages of these steroids are administered, the degree of conversion is not sufficient to cause this side effect. However, this threshold is regularly crossed by BB’rs who utilize dosages well in excess of those required to avoid estrogenic side effects. The problem with being able to pin-point the dose at which this side effect occurs is that not all individuals are affected equally by the same dose. Some can get away with using fairly large dosages of highly aromatizing drugs, such as testosterone, while others seem to develop problems even with minimal use. I know a powerlifter who was able to use a full gram of pharmaceutical-grade testosterone per week without experiencing any gyno symptoms, while other people have encountered early signs of gynecomastia at only 250 mg weekly. For this reason, assumptions should not be made beforehand regarding personal tolerance. When it comes to learning your limit, real-world experience must be your teacher. However, if I had to guess, I would say that most individuals will begin to experience the early stages of gyno by the time they reach 400-500 mg per week when using testosterone, assuming preventative action is not taken.

The 2nd type of steroid which can potentially cause gyno are those which appear to exhibit inherent estrogenic activity, despite lacking the ability to aromatize. One example would be Oxymetholone (Anadrol). This steroid is not capable of converting to estrogen to any degree, yet it causes gyno in a moderate percentage of users. The most plausible explanation for this side effect is that the Anadrol molecule itself demonstrates estrogenic activity, likely by attaching directly to the estrogen receptor. While we cannot yet conclusively state this to be fact, it seems more probable than the other theories which have been put forward over the years.

The 3rd type of anabolic sterods associated with the development of gynecomastia are the progestin-based steroids, which promote their effects through direct stimulation of the progesterone receptor. Two examples which fit this description would be trenbolone and nandrolone. However, these drugs differ from the previously mentioned anabolic sterods  in that they rarely cause gyno on their own. Typically, they require the presence of estrogen (usually at above normal levels) in order to have an impact on the growth of breast tissue. In essence, their progestagenic effects tend to exacerbate the effect of estrogen, thereby acting more as a contributor rather than the primary offender.

The last category of AAS with a history of exhibiting this side effect are those which result in estrogen-rebound. Anticipating the effects of these drugs can be difficult, as they are much less predictable in their behavior. Not only does personal response vary tremendously between individuals, but there is often a lack of consistency even among the same individual. For example, a particular steroid may be employed multiple times without incident, only to cause troubling gyno symptoms under nearly identical circumstances at a later date.

We’ve looked at particular types of anabolic sterods and how they work to cause gyno, but there are other causes which should not be overlooked, one of which is an out of balance androgen to estrogen ratio. DHT itself, as well as many DHT derivatives, possess natural anti-estrogenic activity. Therefore, even in the face of stable estrogen levels, a reduction in these hormones may lead to the appearance of estrogenic side effects. In turn, an increase in DHT or its related metabolites will enable an individual to more effectively deal with increased levels of estrogen. This is why a steroid user is much more likely to encounter estrogenic side effects using testosterone alone, compared to a combination of testosterone and Drostanolone (Masteron), which was developed specifically for the management of female breast cancer.

The last cause of gyno in the steroid user is prolactinemia, which is an elevation of prolactin levels outside of the normally recognized limits. The most common cause of prolactinemia in the general population is prolactinoma (tumor of the pituitary gland), although this condition can be caused by administering prolactin elevating steroids, such as trenbolone and nandrolone. However, just like progesterone, prolactin rarely causes gyno by itself. This is not because prolactin is not able to accomplish this. Rather, anabolic sterods generally aren’t able to elicit elevations in prolactin adequate for causation. Most of the time, prolactin acts to exacerbate the effects of estrogen (similar to progesterone), making it a contributing factor and not the primary cause in the large majority of cases. Still, there have been instances in which these steroids were able to cause gyno and/or lactation independent of aromatizable anabolic sterods. I want to emphasize the fact that lactation rarely occurs in steroid users, but when it does, it is almost always attributable to excessive dosing with the offending steroids, in combination with poor personal response.

The Cure

Once you’ve indentified the root of the problem, deciding on the best course of action is relatively simple. With that said, let’s get right to the nuts-n-bolts of how to get rid of gyno. When excess estrogen levels are the culprit (aromatizable anabolic sterods), there are multiple treatment methods available to us. Ideally, you want to stop the problem before it even begins. Therefore, when planning your cycle, if you know you will be using a dose of aromatizable drugs likely to raise estrogen into a problematic range, the concomitant administration of an A.I. (anti-aromatase) from the outset of your cycle is the best bet. By making an A.I. an integral component of your program right from the start, you will never find yourself in an emergency situation.

While A.I’s can be used in either the prevention or reversal of gyno symptoms, they are best employed as a preventative measure…and with good reason. You see, the job of an A.I. is to prevent testosterone from aromatizing into estrogen, which it does very well, but the problem is that it does absolutely nothing to prevent currently circulating estrogen from continuing to cause problems. As long as A.I’s are utilized as a preventative measure and not for the treatment of an emergency situation, they are preferable to other gyno remedies, but that is not all. The primary mechanism by which A.I’s inhibit gyno formation (management of systematic estrogen) also provides numerous other benefits not found elsewhere, such as: reduced water retention, lowered blood pressure, decreased fat storage, and others. Lastly, A.I.’ do not reduce IGF-1 levels, as will Tamoxifen (Nolvadex).

Should you find yourself in a situation where gyno symptoms manifest unexpectedly, you should turn to Tamoxifen (Nolvadex) for assistance. Why? The body is programmed to convert a percentage of our naturally produced testosterone into estrogen. This is a necessary and healthy process, as estrogen is required for a variety of male physiological functions. However, as the dose of androgens continues to rise, the body continues to convert roughly the same amount of androgens into estrogen. This becomes a problem once we begin administering supraphysiological quantities of these drugs. The much greater amounts of estrogen now floating through the bloodstream are free to attach to any estrogen receptor sites they come in contact with, including those in breast tissue. The end result is gyno formation…also known as “growing boobs”. This is great in teenage girls, but not in grown men.

The only way to put an immediate stop to this is by deactivating estrogen in breast tissue. Tamoxifen does just that. Due to its greater binding affinity, Tamoxifen is able to dislocate estrogen from the receptor site and take its place, leaving the estrogen with nowhere to attach. The main downside of Tamoxifen relative to the A.I.’s, aside from its IGF-1 lowering effect, is that it is powerless to reduce systematic estrogen levels. Because whole-body estrogen levels remain elevated, the user is subject to side effects such as water retention, increased fat storage, increased blood pressure, etc.

The 3rd way to treat estrogen-induced gyno is through the use of anti-estrogenic steroids, such as Masteron or Proviron. Of this we can be certain, as Masteron has been proven effective, in a clinical setting, at modulating estrogen levels in breast tissue. In fact, Masteron was originally designed for use in women afflicted with breast cancer. Like A.I.’s, Masteron and gang work to keep estrogen levels low by preventing aromatization. As mentioned above, this is a decisive advantage compared to a drug like Tamoxifen, which is completely ineffective at managing whole-body estrogen. This also means it is best used as a preventative measure and not in emergency situations. As a whole, anti-estrogenic steroids are not as potent as the A.I’s. Therefore, these steroids should be utilized right from the start of a cycle, at a dosage commensurate to the amount of aromatizable drugs being used. In my opinion, Masteron is usually the best steroid for this purpose, as it not only provides an anti-estrogenic punch similar to Proviron, but it also increase the muscle-building value of a cycle, unlike Proviron, which has virtually no muscle building effect. Lastly, Masteron provides the additional benefit of enhanced sex drive.

We’ve spoken a lot on estrogen-induced gyno, but not all gyno is estrogen dependent. Prolactin has the ability to cause gyno if levels get high enough, as does progesterone. While anabolic sterods do not directly increase progesterone levels, some steroids themselves are progestins (ex. trenbolone & nandrolone), exhibiting progestagenic effects on the body. Generally, this progestagenic effect is not strong enough to cause gyno by itself, but it can certainly exacerbate the effects of estrogen, making the problem worse. In the same way, anabolic sterods are generally not able to increase prolactin high enough in order to cause gyno by itself, yet it can certainly contribute to the problem. In extreme cases, individuals using large doses of Trenbolone have been known to lactate. Although this is rare and typically only occurs in heavy users with an unfavorable response, it does occasionally happen.

The most effective treatment for normalizing prolactin levels are the anti-prolactin drugs, such as cabergoline, pramipexole, or bromocriptine. Bromocriptine is a 1st generation anti-prolactin drug. It is not as potent as the other two and since it is less specific in its actions, it comes with an increased risk of side effects. There is no longer any good reason to choose bromocriptine when seeking relief from elevated prolactin. While cabergoline and pramipexole will both get the job done, in terms of compatibility and ease of use, caber is usually preferred due to its reduced side effect profile and longer active life. If there is one downside, it would be its greater cost. Pramipexole must be dosed daily, while cabergoline is usually only administered once every 2-3 days, depending on need. As for the progestagenic effects of anabolic sterods, a stated above, gyno is rarely ever a concern as long as estrogen levels are properly managed. Therefore, no specific treatment is indicated. Rather, you indirectly treat the problem by maintaining a normal estrogen level.

That about sums it up, guys. If there is one take home message here, it is that prevention is preferable to correction. Stop gyno before it starts by keeping your estrogen level stable and it is very unlikely that you will ever have gyno issues. For those who are very sensitive to the effects of prolactin, yet like to use high doses of trenbolone or nandrolone, you may require the additional use of an anti-prolactin drug. However, most of us will not need these in order to avoid gyno.

Obviously, personal experience will play a key role in showing us what we can and cannot do as we attempt to stay gyno-free, so as you go about experimenting with different steroids & dosages, make sure you have the appropriate ancillaries on hand just in case they are needed. It is always wise to have a back-up supply of Tamoxifen lying around, simply because it’s almost universally effective for stopping gyno, regardless of the cause.

Friday, July 4, 2014

How to Protect the Liver During Anabolic Steroid Use

Q: “What can I do with my anabolic steroid cycle planning to help protect my liver?”

A: First, liver harm from anabolic steroids comes principally or entirely from alkylated anabolic steroids. Where the steroids are non-alkylated and estradiol levels remain normal, there’s almost never harm to the liver from steroid use. (A handful of apparent cases exist in the medical literature, so I don’t rule out that it could occur in very rare cases. Example non-alkylated steroids are testosterone, Masteron, Trenbolone, Boldenone (Equipoise), Nandrolone (Deca Durabolin), and Primobolan.

Keeping liver safety in mind, an effective cycle should have one or more of these steroids as the base, or even as the entirety of the cycle. About 350-700 mg/week of a steroid stack, though, may be an alkylated compound.

The most common alkylated steroids are Dianabol, Anadrol, oxandrolone (Anavar), and Winstrol. Alkylated steroid use is preferably limited to only six weeks at a time, though of course many who go longer don’t suffer lasting harm. However, sustained use of oral anabolic steroids absolutely can cause undetected formation of scar tissue in the liver. This effect can be cumulative, as the scar tissue does not heal. And thoroughly excellent gains can be achieved without “pushing” the 6-week rule.

If cycle length is greater than 6 weeks, then appropriate amounts of testosterone can substitute for the orals. I replace Anadrol or Winstrol with testosterone on a milligram for milligram basis. I replace Dianabol on a three-to-two basis, or in other words, 50 mg/day Dianabol is replaced by about 75 mg/day of testosterone. Oxandrolone, on the other hand, is replaced with Masteron on a three-to-two basis, or trenbolone on a two-to-three basis. Each period of alkylated steroid use should be followed by about twice as much time not using alkylated steroids, or longer. Estradiol preferably will be kept in the normal range, or not much above it, as elevated estradiol is slightly liver toxic. In and of itself estradiol toxicity is not greatly important, but in combination with alkylated steroid use, it adds to the toxicity.

Obviously hepatotoxic drugs and excessive alcohol use should be avoided, as should heavy use of NSAID’s, aspirin, or acetaminophen. Cautious use is fine. In terms of supplementation for liver health, lecithin may be taken in amounts such as 3-7 g/day together with B vitamins. With regard to milk thistle, steroid-induced cholestasis results from reduced activity of the bile salt export pump, and silymarin and silibinin (components of milk thistle) act at this point and can partially block the adverse effects of steroids. However, cheap milk thistle products don’t provide much of these substances. As for liver antioxidants, the problem does not seem to be one of oxidation and I don’t think they make a difference.

Liver protection supplementation may safely be omitted when the above principles are followed. Supplementation shouldn’t be a license to use alkylated steroids less carefully. I would treat supplementation only as a backup.