By doctor Francesco Casillo
And we come, in conclusion, to the relationships between exogenous testosterone intake and health problems, such as heart problems, obesity, inflammation, insulin resistance and diabetes.
One of the least contested and most seriously alleged side effects related to androgens is represented by the "acceleration of atherosclerotic cardiovascular disease (ASCVD). By now this knowledge (information, notion) is" gospel "for everyone ... at least until the opposite is proven Fortunately there are still a sufficient number of doctors and researchers who continue to explore the relationship between androgens and ASCVD. Among them are Drs. T. Hugh Jones and Farid Saad, who recently revisited the effects of testosterone on risk factors and mediators. for the ASCVD in the accredited journal "Atherosclerosis" .
Jones and Saad observed the association between low testosterone levels and i markers for ASCVD, as well as the effects induced by testosterone replacement therapy. Low (natural) testosterone levels are unhealthy. Men with low testosterone levels are at high risk for coronary heart disease (CHD), heart attacks and angina. When hypogonadal men (with low testosterone levels) are treated with the male sex steroid there are positive changes associated with a lower risk of CHD. These include: reduction of visceral obesity and insulin resistance, improvement of lipid profile and markers inflammation and improvement in exercise capacity.
An increased risk of myocardial infarction is linked to a number of conditions: smoking, hypertension, high LDL levels, malnutrition, sedentary lifestyle, abdominal-visceral obesity and diabetes. Many of these conditions are related to a low quality lifestyle. In 1981 a constellation of health problems was described as "Metabolic Syndrome". This condition includes: abdominal-visceral obesity, high level of triglycerides and total cholesterol, low HDL levels, hypertension, high fasting glycemic levels. Not all these alterations must necessarily coexist at the same time in the individual, since he can be diagnosed with the Metabolic Syndrome.
Partly also due to the radical change in lifestyle from the 1970s until now, the conditions that make the Metabolic Syndrome possible have progressively increased.In parallel with this, the average testosterone levels, for the same period of time taken into consideration, have also been decreasing. In fact, obesity negatively affects the health of the individual, and this is especially true at the level of heart health. Studies that have analyzed the relationship between obesity and testosterone have shown a negative correlation.
The higher the systemic concentration of testosterone in an individual, the less likely they are to become obese. Conversely, the more obese you are, the lower your testosterone levels will be. Even more convincing are the results showing that a low testosterone concentration is associated with an increased level of abdominal-visceral obesity, as well as a higher percentage of body fat and higher insulin levels. High insulin levels, remember, promote lipogenesis (fat storage) and inhibit lipolysis (destruction of triglycerides).
Body fat and testosterone present a sort of relationship similar to the (proverbial) one of the "chicken and the" egg ": sometimes it is impossible to determine which of the two conditions originates first and, therefore, who generates the second. it stimulates the receptors that reduce the accumulation of fat, increasing lipolytic phenomena as well as diverting the precursors of adipocytes into becoming myocytes rather than mature adipocytes.
Adipocytes are not cells specialized solely in the storage of triglycerides and the release of fatty acids, but they represent a real endocrine system capable of secreting hormones and messengers. Among the messengers there are two cytokines (precisely adipocytokines): resistin and adiponectin.
Resistin increases insulin resistance and inflammation (two conditions that lead to type 2 diabetes, ASCVD and all other diseases related to inflammation itself). Adiponectin, on the other hand, plays a protective role and its secretion increases with decreasing levels of fat and / or in correspondence with limited values of fat; the increase in body fat determines, on the other hand, a decrease in the levels of adiponectin and the simultaneous rise in the levels of other inflammatory adipocytokines.
Insulin resistance and type 2 diabetes are important factors to consider when assessing the risk of myocardial infarction. There is, in fact, an inverse relationship between testosterone levels and insulin resistance and between testosterone and type 2 diabetes. Low testosterone levels are the prelude to the development of type 2 diabetes. As testosterone levels decrease, insulin resistance increases; this causes the body to maintain high insulin levels for obvious homeostatic reasons on glycemic control. If the insulin levels remain high in the long term, the weight loss processes are less, while those that favor an increase in fat mass are strong.
Treatment of type 2 diabetes with testosterone reduces blood glucose and insulin resistance, which is also a beneficial factor in reducing the risk of heart attack in those prone to this condition. Another marker, hemoglobin A1C (HA1C), undergoes a decrease in correspondence with testosterone-based therapy.
Only recently has the collaboration of specialized agencies changed the way diabetes is diagnosed. The diagnosis of diabetes has always been a function of measuring fasting glycemic levels, through the test tolerance to oral glucose load. Such test evaluates and takes into account how the body is able to manage glycemic availability in the short term. Now, however, measuring HA1C allows you to monitor long-term glycemic control.
The mechanism of action within which testosterone would act in the decrease of insulin resistance would be represented by its action in favoring the decrease of visceral fat levels, the event of which determines a decrease in inflammatory processes and in the flow of fatty acids towards the liver - thus inducing a reduction in fat mass and a simultaneous improvement in mitochondrial function.
As mentioned, when the testosterone level decreases, its inhibitory role on adipocytes is lost, thus allowing an increase in fat mass. Unfortunately, the worst is yet to come. As the levels of fat mass increase, the availability of the enzyme “aromatase”, responsible for the conversion of testosterone into estrogen, also increases, thus leading to a negative vicious circle.
In fact, estrogens not only favor the processes of adipose accumulation but in metabolic concert with two adipocytokines and leptin reduce the sensitivity of the chemoceptive system of the hormonal axis HPT (Hypothalamus-Pituitary-Testicles) to low testosterone levels, thus inducing, inhibition of the feedback positive of the same axis in response to low levels of circulating hormone. This leads to the procrastination of low testosterone levels which fuel a vicious cycle in favor of increased levels of obesity and insulin resistance.
A study. In a study a few years ago, 87 male individuals with diabetes and coronary artery disease were "randomized" to 12 weeks of treatment with testosterone undecanoate or placebo, within a "double-blind" protocol. of the intervention, weekly and at the end of the intervention itself: the angina episodes, the number of daily ischemic episodes and the total ischemic load by ECG Holter. Total serum cholesterol levels and blood triglyceride concentrations were also measured.
Results: Compared to the placebo group, the testosterone group reported a 34% reduction in weekly angina episodes; reduction of silent ischemic episodes by 26% and total ischemic load by 21%. Furthermore, after 12 weeks, total cholesterol and triglyceride levels also decreased in the testosterone group compared to the placebo group. Thus, in this case, the therapeutic use of testosterone was positive.
Conclusions
It is disheartening to learn how much of "mass knowledge" is the result of passively acquired information, due to the credit attributed to the repetitiveness with which such "information" is served up, rather than to the "reliability of the same. Reliability that derives from scientific analyzes scrupulous, critical and selective, capable of refuting what is incorrect, or that in a completely altered "socio-cultural" way is spread and propagated and which over time becomes "dogma." Only then can science finally affirming - rightly - one's own truth, and thus founding one's own culture of truth.
The task of the correct disseminators, at every level and in each specific area, is precisely to spread these scientific truths - denying all pseudo-truths. Stay hard!
Article courtesy of the "Cultura Fisica" magazine
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