[h=1]How to Lose Fat & Boost Testosterone[/h]
Every bodybuilder or athlete understands too much body fat can be detrimental. For the bodybuilder, too much body fat detracts from the physique. The athlete can’t carry too much body fat because it decreases speed and quickness, thus diminishing athletic performance. Although fat tissue can be physically unappealing to the bodybuilder while negatively influencing athletic prowess, fat cells also perform an additional function that can negatively impact the athlete and bodybuilder by drastically decreasing the production of the muscle-building hormone testosterone.
Fat tissue, in addition to storing energy in the form of triglycerides, can be considered an atypical endocrine organ given its ability to secrete several different hormones, known as adipokines, into the bloodstream. The most well characterized adipokine, leptin, is secreted by fat cells after fat cells accumulate triglyceride. Essentially, the more body fat you have the greater the amount of leptin you have circulating in your blood. Leptin is a signal to the brain that decreases appetite and food intake while simultaneously stimulating the rate of fatty acid oxidation, converting stored fat into energy. Unfortunately, leptin’s ability to decrease food consumption while burning fat can be offset by calorically dense foods— leading to increased body fat.
Since leptin is produced at concentrations that parallel the amount of fat reserves, individuals with greater body fat typically have greater levels of circulating leptin. Interestingly, many lines of clinical evidence show that greater body fat, along with correspondingly higher levels of leptin, is frequently associated with low testosterone levels in men. These observations indicate a potential connection between adipokines, such as leptin, and lower testosterone production.
Leptin Decreases Testosterone Production
Intriguingly, several relevant studies demonstrate leptin’s ability to reduce testosterone production. A study by Caprio et al.[SUP]1[/SUP] demonstrated in isolated testicular cells given an excessive amount of leptin, mimicking greater body fat, appreciably decreased testosterone production. Furthermore, in a study by Caprio et al.[SUP]2[/SUP], rats treated with leptin exhibited a diminished response to human chorionic gonadotropin (hCG) stimulated testosterone production. Given that hCG mimics the function of the natural testosterone-stimulating substance known as luteinizing hormone (LH), this result implies that leptin is inhibiting the ability of LH to stimulate testosterone production.
In addition, a study by El-Hefnawy et al.[SUP]3[/SUP] confirmed the presence of a functional leptin receptor in mouse testis that is capable of signal transduction— suggesting a direct effect of leptin on testicular production of testosterone. These observations indicate that leptin directly and indirectly decreases testicular production of testosterone.
Fat cells convert testosterone into estrogen, effectively lowering testosterone levels. Fat cells can also decrease testosterone levels by expressing the aromatase enzyme, which is the catalyst that converts testosterone into the estrogen-like compound estradiol. Because estradiol tells the brain that there are plenty of steroid hormones circulating in the blood, the brain reacts to the high estradiol level by lowering LH secretion. Since LH stimulates the production of testosterone, lower levels of LH decreases testosterone levels as well.
A recent investigation by Håkonsen et al.[SUP]4[/SUP] confirmed fat’s negative influence on testosterone levels by showing that men with high levels of body fat increase their testosterone production after losing body fat. The experiment studied 43 men between 20 and 59 years old with significant body fat. All subjects followed a 14-week diet and exercise regimen to lose fat tissue. At the beginning of the study, the subjects’ hormone levels showed higher body fat levels corresponded to lower testosterone levels and higher estrogen levels, indicating increased aromatase activity. Subsequent to the exercise program and fat loss, hormonal measurements were repeated. The results showed that a decrease in body fat and aromatase levels correlated with an increase in both LH and testosterone levels, along with a decrease in estrogen levels.
Fat Cells Inactivate the Anabolic Effects of DHT
In men, approximately 5 percent of testosterone undergoes biochemical conversion to the more potent androgen, dihydrotestosterone. Despite DHT's appropriate reputation as a potent androgen, it also contributes considerably to anabolic muscle growth by strongly binding to the androgen receptor— which initiates muscle protein synthesis in muscle cells, driving muscle growth and strength. Representing another example of fat’s adversarial effects on testosterone production, it turns out that fat tissue not only converts testosterone into estradiol, but also enzymatically transforms DHT into several different anabolically-inactive metabolites.
Because DHT is a direct metabolite of testosterone, fat cell elimination of DHT will also cause the body to convert additional testosterone into DHT— consequently lowering testosterone as well DHT levels. In a recent investigation by Blouin et al.[SUP]5[/SUP], adipose tissue biopsies were obtained from 21 morbidly obese men and 11 men with lower levels of body fat. The researchers confirmed that several enzymes in fat tissue deactivated DHT in both groups. They also demonstrated that subjects with greater body fat levels showed greater levels of DHT removal. As a result, the more fat you have, the more DHT and testosterone is deactivated in your body— and the best method to mitigate this testosterone removal seems to be losing body fat.
Fat Cells Can Weaken Anabolic Steroids
Anabolic steroids are testosterone derivatives, making them equally susceptible to fat cell-driven aromatization into estrogen-like compounds. Therefore, lowering body fat should produce a more potent response to anabolic steroid use— resulting from less aromatization of the anabolic steroid into estrogen. In addition, lower levels of aromatized steroids into estrogen-like compounds will reduce the inhibition of endogenous testosterone that occurs from anabolic steroid consumption.
Substantiating the above idea, a group of endocrinologists from Muenster, Germany[SUP]6[/SUP], gave 40 healthy men a single injectionof testosterone propionate and four weeks later, two injectionsof 1,000 milligrams of testosterone undecanoate six weeks apart. The test subjects with higher body fat showed a greater decrease in natural testosterone levels, most likely from the fat cell-stimulated conversion of the injected anabolic steroid into estrogen— which has been shown to strongly inhibit natural testosterone production. Therefore, reducing body fat should improve anabolic steroid potency— potentially diminishing the need for megadosing anabolic steroids.
In conclusion, carrying extra body fat is so much more detrimental than just the extra pounds you have to carry around. Fat tissue has a remarkable grip on testosterone production and muscle growth by generating a seemingly endless feedback loop that not only diminishes muscle growth, but favors further accumulation of fat tissue. Ironically, the best way to repress the anti-testosterone features of fat tissue is apparently by increasing testosterone levels. Of course, getting as lean as possible will also help combat fat’s dastardly grip on muscle growth.
For most of Michael Rudolph’s career he has been engrossed in the exercise world as either an athlete (he played college football at Hofstra University), personal trainer or as a Research Scientist (he earned a B.Sc. in Exercise Science at Hofstra University and a Ph.D. in Biochemistry and Molecular Biology from Stony Brook University). After earning his Ph.D., Michael investigated the molecular biology of exercise as a fellow at Harvard Medical School and Columbia University for over eight years. That research contributed seminally to understanding the function of the incredibly important cellular energy sensor AMPK— leading to numerous publications in peer-reviewed journals including the journal Nature. Michael is currently a scientist working at the New York Structural Biology Center doing contract work for the Department of Defense on a project involving national security.
Every bodybuilder or athlete understands too much body fat can be detrimental. For the bodybuilder, too much body fat detracts from the physique. The athlete can’t carry too much body fat because it decreases speed and quickness, thus diminishing athletic performance. Although fat tissue can be physically unappealing to the bodybuilder while negatively influencing athletic prowess, fat cells also perform an additional function that can negatively impact the athlete and bodybuilder by drastically decreasing the production of the muscle-building hormone testosterone.
Fat tissue, in addition to storing energy in the form of triglycerides, can be considered an atypical endocrine organ given its ability to secrete several different hormones, known as adipokines, into the bloodstream. The most well characterized adipokine, leptin, is secreted by fat cells after fat cells accumulate triglyceride. Essentially, the more body fat you have the greater the amount of leptin you have circulating in your blood. Leptin is a signal to the brain that decreases appetite and food intake while simultaneously stimulating the rate of fatty acid oxidation, converting stored fat into energy. Unfortunately, leptin’s ability to decrease food consumption while burning fat can be offset by calorically dense foods— leading to increased body fat.
Since leptin is produced at concentrations that parallel the amount of fat reserves, individuals with greater body fat typically have greater levels of circulating leptin. Interestingly, many lines of clinical evidence show that greater body fat, along with correspondingly higher levels of leptin, is frequently associated with low testosterone levels in men. These observations indicate a potential connection between adipokines, such as leptin, and lower testosterone production.
Leptin Decreases Testosterone Production
Intriguingly, several relevant studies demonstrate leptin’s ability to reduce testosterone production. A study by Caprio et al.[SUP]1[/SUP] demonstrated in isolated testicular cells given an excessive amount of leptin, mimicking greater body fat, appreciably decreased testosterone production. Furthermore, in a study by Caprio et al.[SUP]2[/SUP], rats treated with leptin exhibited a diminished response to human chorionic gonadotropin (hCG) stimulated testosterone production. Given that hCG mimics the function of the natural testosterone-stimulating substance known as luteinizing hormone (LH), this result implies that leptin is inhibiting the ability of LH to stimulate testosterone production.
In addition, a study by El-Hefnawy et al.[SUP]3[/SUP] confirmed the presence of a functional leptin receptor in mouse testis that is capable of signal transduction— suggesting a direct effect of leptin on testicular production of testosterone. These observations indicate that leptin directly and indirectly decreases testicular production of testosterone.
Fat cells convert testosterone into estrogen, effectively lowering testosterone levels. Fat cells can also decrease testosterone levels by expressing the aromatase enzyme, which is the catalyst that converts testosterone into the estrogen-like compound estradiol. Because estradiol tells the brain that there are plenty of steroid hormones circulating in the blood, the brain reacts to the high estradiol level by lowering LH secretion. Since LH stimulates the production of testosterone, lower levels of LH decreases testosterone levels as well.
A recent investigation by Håkonsen et al.[SUP]4[/SUP] confirmed fat’s negative influence on testosterone levels by showing that men with high levels of body fat increase their testosterone production after losing body fat. The experiment studied 43 men between 20 and 59 years old with significant body fat. All subjects followed a 14-week diet and exercise regimen to lose fat tissue. At the beginning of the study, the subjects’ hormone levels showed higher body fat levels corresponded to lower testosterone levels and higher estrogen levels, indicating increased aromatase activity. Subsequent to the exercise program and fat loss, hormonal measurements were repeated. The results showed that a decrease in body fat and aromatase levels correlated with an increase in both LH and testosterone levels, along with a decrease in estrogen levels.
Fat Cells Inactivate the Anabolic Effects of DHT
In men, approximately 5 percent of testosterone undergoes biochemical conversion to the more potent androgen, dihydrotestosterone. Despite DHT's appropriate reputation as a potent androgen, it also contributes considerably to anabolic muscle growth by strongly binding to the androgen receptor— which initiates muscle protein synthesis in muscle cells, driving muscle growth and strength. Representing another example of fat’s adversarial effects on testosterone production, it turns out that fat tissue not only converts testosterone into estradiol, but also enzymatically transforms DHT into several different anabolically-inactive metabolites.
Because DHT is a direct metabolite of testosterone, fat cell elimination of DHT will also cause the body to convert additional testosterone into DHT— consequently lowering testosterone as well DHT levels. In a recent investigation by Blouin et al.[SUP]5[/SUP], adipose tissue biopsies were obtained from 21 morbidly obese men and 11 men with lower levels of body fat. The researchers confirmed that several enzymes in fat tissue deactivated DHT in both groups. They also demonstrated that subjects with greater body fat levels showed greater levels of DHT removal. As a result, the more fat you have, the more DHT and testosterone is deactivated in your body— and the best method to mitigate this testosterone removal seems to be losing body fat.
Fat Cells Can Weaken Anabolic Steroids
Anabolic steroids are testosterone derivatives, making them equally susceptible to fat cell-driven aromatization into estrogen-like compounds. Therefore, lowering body fat should produce a more potent response to anabolic steroid use— resulting from less aromatization of the anabolic steroid into estrogen. In addition, lower levels of aromatized steroids into estrogen-like compounds will reduce the inhibition of endogenous testosterone that occurs from anabolic steroid consumption.
Substantiating the above idea, a group of endocrinologists from Muenster, Germany[SUP]6[/SUP], gave 40 healthy men a single injectionof testosterone propionate and four weeks later, two injectionsof 1,000 milligrams of testosterone undecanoate six weeks apart. The test subjects with higher body fat showed a greater decrease in natural testosterone levels, most likely from the fat cell-stimulated conversion of the injected anabolic steroid into estrogen— which has been shown to strongly inhibit natural testosterone production. Therefore, reducing body fat should improve anabolic steroid potency— potentially diminishing the need for megadosing anabolic steroids.
In conclusion, carrying extra body fat is so much more detrimental than just the extra pounds you have to carry around. Fat tissue has a remarkable grip on testosterone production and muscle growth by generating a seemingly endless feedback loop that not only diminishes muscle growth, but favors further accumulation of fat tissue. Ironically, the best way to repress the anti-testosterone features of fat tissue is apparently by increasing testosterone levels. Of course, getting as lean as possible will also help combat fat’s dastardly grip on muscle growth.
For most of Michael Rudolph’s career he has been engrossed in the exercise world as either an athlete (he played college football at Hofstra University), personal trainer or as a Research Scientist (he earned a B.Sc. in Exercise Science at Hofstra University and a Ph.D. in Biochemistry and Molecular Biology from Stony Brook University). After earning his Ph.D., Michael investigated the molecular biology of exercise as a fellow at Harvard Medical School and Columbia University for over eight years. That research contributed seminally to understanding the function of the incredibly important cellular energy sensor AMPK— leading to numerous publications in peer-reviewed journals including the journal Nature. Michael is currently a scientist working at the New York Structural Biology Center doing contract work for the Department of Defense on a project involving national security.
