Saturday, March 12, 2011

Fat High, Low T by Jerry Brainum

Those interested in increasing their testosterone levels in a completely natural manner—without using any type of drug or even food supplement—may be interested in what follows. One caveat, however: The information applies only if you have excess bodyfat. Studies show that testosterone levels bear a direct relationship to bodyfat levels. Generally, the fatter you are, the lower your total testosterone levels.

That’s due to either a decreased level of a protein that carries testosterone in the blood or a decrease in the pituitary hormones that dictate testosterone synthesis and release. The blood protein that carries testosterone, sex-hormone-binding globulin (SHBG), is usually lower in men who have higher percentages of bodyfat. On the other hand, testosterone isn’t active when it’s bound to this protein. Only unbound, or free, testosterone can interact with cellular steroid receptors.

Most studies show little or no effect of bodyfat levels on free testosterone, but some show an inverse relationship between free testosterone levels and obesity. A lowered free-testosterone level most often reflects a problem with the release of pituitary hormones that control testosterone release, such as luteinizing hormone (LH). Decreased SHBG levels lower total testosterone levels because unbound testosterone is more subject to degradation or conversion into estrogen by aromatase enzymes, which are found in many tissues but particularly in bodyfat.

A new study sought to clear up the confusion over the relationship between testosterone, both free and bound, and bodyfat levels.1 The study featured two groups of obese men, ages 20 to 68. The subjects ate a 1,200-calorie diet for six months, and researchers monitored their hormone levels before and after the diet. To make the dieting process easier for the men, they were also given dexfenfluramine (15 milligrams a day) to help curb their appetites. They were compared to 20 other men who had normal bodyfat levels.

One reason obesity leads to a reduction of total testosterone is that higher levels of bodyfat are associated with elevated insulin levels. Insulin, in turn, decreases the synthesis of SHBG in the liver, leading to the drop in circulating total testosterone. As SHBG drops, free testosterone should increase, but with higher levels of bodyfat it’s simply converted into estrogen by aromatase enzymes in fat tissue. The same holds true for pro-hormone supplements used by people who have higher bodyfat levels.

Losing bodyfat results in lower resting insulin levels, which leads to increased production of SHBG in the liver and, consequently, higher total testosterone levels in the blood. In the study discussed here, total testosterone and insulin levels didn’t differ significantly between massively fat and moderately fat men, but the moderately fat men did show higher free-testosterone levels than the extremely fat men.

Once bodyfat exceeds a certain level, secretion of pituitary hormones that control testosterone release, such as luteinizing hormone, is blunted. Recent studies link that process to increased levels of leptin, a protein released from fat that acts as a fat signal to the brain. Fat people show higher levels of leptin, ostensibly due to a lack of leptin interaction in the brain. Higher leptin levels also interfere with testosterone synthesis in the Leydig cells of the testes, which explains the lower free-testosterone levels in very fat men.

But this study reported that both moderately and massively obese men showed higher total and free-testosterone levels, as well as higher LH levels along with lower insulin levels, after they lost bodyfat by dieting. Despite the decreased level of free testosterone in the very fat men, their sex lives and sex drives weren’t noticeably affected. Free testosterone controls sex drive in both sexes, so the finding indicates that the obese men apparently still had enough free testosterone for sexual functioning.

Steroids and Tendon Injuries

Controversy exists over the effects of anabolic steroids on tendon function and structure. Animal studies, such as those using mice as subjects, show that when rodents are provided with anabolic steroids in doses approximating human use, adverse changes occur in the structure of the animals’ tendons.2 They involve a weakening of tendon fibers, which results in increased susceptibility to injuries.3

The medical literature cites tendon injuries in the thighs, triceps, hands and pectorals linked to anabolic steroid use, though a cause-and-effect relationship has not been proven. A recent case study reported on a 41-year-old competitive bodybuilder who complained about an injured left shoulder that turned out to be a rupture of the teres major tendon in his upper back.4

The bodybuilder was performing what was described as a bench press exercise with a weight listed as 40 kilograms. Since that equals only 88 pounds, we must assume that he was doing dumbbell bench presses. In any case, he heard a snap in his shoulder while doing the exercise. There followed several days of aching pain around the shoulder girdle, made worse by any movement of the area. Examination of the injured area revealed a swelling in the belly of his left teres major tendon, and when felt by the doctors, the free edge of the torn tendon was readily apparent.

The diagnosis was a rupture of the left teres major tendon, and the patient was treated conservatively with anti-inflammatory drugs and physical therapy. A three-month follow-up showed no residual symptoms other than muscle atrophy in the upper-back area.

Tears of the teres major tendon have been associated with chronic kidney failure, gout, diabetes, rheumatoid disease and obesity, but the bodybuilder had none of those conditions. Though his specific regimen wasn’t discussed, he did use anabolic steroids. Lack of any previously identified risk factors led the examining physicians to suggest that his use of anabolic steroids had set him up for the injury. The good news is that he healed well, showing no residual loss of function or mobility in his shoulders or upper back.

The case study shows only circumstantial evidence linking a tendon rupture to previous and continuing use of anabolic steroid drugs. Absent microscopic observation of the man’s tendons, his injury is impossible to link definitely to steroid use. He might just as easily have incurred the injury by not warming up or by using poor exercise form. Proving a cause-and-effect relationship requires many cases and much examination to find changes in tendon structure that could precipitate an injury.

Steroid Side Effects: Past and Present

Gathering information on illicit steroid use is often difficult. Anabolic steroid drugs require a medical prescription, and obtaining them through black market sources is illegal. Stigma attaches to being an open, admitted steroid user—even if it’s obvious that you are. The drugs are banned by all international sports federations, including bodybuilding, though actual steroid-testing procedures are instituted in relatively few competitions.

A group of Australian doctors decided to work around the usual barriers to obtaining accurate steroid use information by setting up a three-year clinic at an inner-city hospital in Sydney.5 They provided free physical exams and follow-ups to steroid users on an anonymous basis to ensure participation without fear of public exposure. Subjects reporting to the free clinic were identified only by a number. No steroids or other drugs were prescribed at the clinic, nor was their use encouraged. The goal was to gather facts about actual anabolic drug use and related side effects.

The doctors managed to get 58 male participants, consisting of 27 past steroid users, 14 current users and 17 potential users, the potential users acting as a control group. The age range of users and nonusers was 16 to 36. Nearly all of them cycled steroids for an average of six weeks to six months, with the cycles numbering from one to nine. Researchers tracked the use of oral, injectable, human and veterinary drugs. The dose usually involved a pattern of increased use during the first half of the cycle that was maintained for a few weeks, then gradually tapered off.

The most popular drugs were Deca 50, a 50-milligram veterinary injectable containing nandrolone decanoate (also found in Deca-Durabolin); veterinary injections of stanazol, also known as Winstrol; Sustanon, a human injectable containing four testosterone esters; and Anapolon, a 50-milligram oral drug also known as Anadrol-50. Seven of the men reported using Nolvadex, an estrogen-blocking drug, to help prevent gynecomastia, a common side effect of steroid use. Other drugs included clenbuterol, thyroid drugs, HCG injections, growth hormone injections and diuretics. Reportedly, the majority of the drugs—85 percent—were obtained from black market sources.

Of the various side effects reported, 25 steroid users mentioned mood changes while taking the drugs. Some effects were beneficial, such as increased feelings of well-being and self-confidence, while others were adverse, such as increased paranoia, anxiety and depression. Among past and present steroid users, most reported a pattern of both increased and decreased sex drive while on the same steroid cycle. Nine reported problems with getting erections either just before or just after getting off the drugs.

Current steroid users showed shrunken testicles and suppression of the pituitary hormones that dictate testicular function, including testosterone synthesis. Gynecomastia, caused when testosterone-based drugs are aromatized, or enzymatically converted, into estrogen, occurred in two current and 10 former users. Another 19 had acne, usually on the face and back, a common side effect due to overactive sebaceous (oil) glands in the skin. Elevated blood pressure is considered a major cardiovascular risk, and 10 past steroid users and five present users showed higher blood pressure. On the other hand, electrocardiogram measurements showed no evidence of any undetected heart attacks or other cardiovascular problems in either past or present steroid users. The same held true for liver disease. Participants in each group, including the drug-free controls, showed minor elevations in liver enzyme levels, likely the result of muscle damage from weight training.

In addition to sustained higher blood pressure readings, the major side effect observed in this survey was gyno. While other side effects were mentioned by past and present steroid users, none could be specifically related to their steroid use, since such effects involved only 2 percent of participants. Future editions of this column will discuss common anabolic drug side effects in depth, including possible remedies and treatments.


1 Lima, N., et al. (2000). Decreased androgen levels in massively obese men may be associated with impaired function of the gonadostat. Int J Obesity. 24:1433-1437.

2 Bach, B.R., et al. (1987). Triess rupture: a case report and literature review. Am J Sports Med. 15:285-289.

3 Wood, T.O., et al. (1988). The effect of exercise and anabolic steroids on the mechanical properties and crimp morphology of the rat tendon. Am J Sports Med. 16:153-158.

4 Davies, J.P., et al. (1998). Rupture of the teres major tendon associated with anabolic steroid use. Sports Exercise and Injury. 4:210-211.

5 O’Sullivan, A., et al. (2000). Anabolic-androgenic steroids: medical assessment of present, past and potential users. Med J Australia. 173:323-327.

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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