What is a testosterone

The symptoms of low-testosterone are relatively easy to diagnose. They include lethargy, low libido, weakness, depression, and memory loss. Because these symptoms are often diagnosed without blood work as depression or a mood disorder, many people end up on medications that actually will not increase their testosterone, and therefore they won’t see results. The only way to diagnose low testosterone is by getting a blood test to test the actual levels. Once it’s confirmed that testosterone levels are low, then a doctor can prescribe a testosterone supplement in order to treat your symptoms and restore natural levels of testosterone.

Clinical research still hasn’t determined a hard threshold level for when symptoms of low T begin appearing . Some recent research suggests that symptoms of low T might begin appearing in men when their total testosterone level dips below 320 ng/dl . According to anecdotal evidence from the owner of Peak Testosterone,  many men start noticing low T symptoms when their total testosterone dips into the 400s . Of course, it’s anecdotal, so take it for what it’s worth, but it’s probably a good idea to stay above 500 ng/dl if you don’t want to experience symptoms of low T.

The High starch high glucose diet is another important cause of low testosterone. It s one of the reason that low testosterone is a strong predictor of Type 2 Diabetes Mellitus. There is a vicious circle of the High starch diet, such as proposed by most fast food outlets and T2DM, Obesity, Low Testosterone, Brain Atrophy, Hyperglycaemia, heart disease, neuropathies, and even depression. A first thing any police officer should do is to minimize starchy foods in the diet. Digestible starches (amylose and amylopectin) are pure glucose, they are glucose polymer chains. We don’t need carbohydrates to survive, they are an economic luxury of low-cost/high-energy foods but with very little nutrient density, fruits having the most nutrients, and starches the lowest, amongst carbohydrate rich foods (Starches, flours from cereals, score the lowest of all other foods in terms of nutrient density). They were incorporated in the human diets at the beginning of the agricultural organization when humans shifted from a nomadic way of life to a sedentary one some 12,000 years ago. They were appreciated because of their low-cost/high-energy density…not because of their nutrient density. With leafy greens, who are very low-energy/high-nutrient density, their carbohydrate content are mostly fibers (non digestible saccharides, or other complex saccharides). In fact, excessive starchy diets also have a strong chelating effect, this means that the natural chelators (such as phytic acid) found in cereal grains attract nutritional metals such as iron, copper, zinc, etc…a deficiency in zinc is an etiological characteristic of Type 2 Diabetes. This is the reason Food programs sponsored by the UN which usually are based on enriched flours are treated with anti-chelating agents such as phytase, the enzyme that neutralises phytate (also called phytic acid) ( http:///content/130/2/+html ). But the common flours used in the human North American diets are not. before the fast food revolution, North Americans consumed on average less than 10% of starches in their diets. This average is now 25%, and this is the root cause of the metabolic syndrome, diabetes and obesity epidemics, all conditions where low testosterone is a strong marker.

Plasma testosterone levels display circadian variation, peaking during sleep, and reaching a nadir in the late afternoon, with a superimposed ultradian rhythm with pulses every 90 min reflecting the underlying rhythm of pulsatile luteinizing hormone (LH) secretion. The increase in testosterone is sleep, rather than circadian rhythm, dependent and requires at least 3 h of sleep with a normal architecture. Various disorders of sleep including abnormalities of sleep quality, duration, circadian rhythm disruption, and sleep-disordered breathing may result in a reduction in testosterone levels. The evidence, to support a direct effect of sleep restriction or circadian rhythm disruption on testosterone independent of an effect on sex hormone binding globulin (SHBG), or the presence of comorbid conditions, is equivocal and on balance seems tenuous. Obstructive sleep apnea (OSA) appears to have no direct effect on testosterone, after adjusting for age and obesity. However, a possible indirect causal process may exist mediated by the effect of OSA on obesity. Treatment of moderate to severe OSA with continuous positive airway pressure (CPAP) does not reliably increase testosterone levels in most studies. In contrast, a reduction in weight does so predictably and linearly in proportion to the amount of weight lost. Apart from a very transient deleterious effect, testosterone treatment does not adversely affect OSA. The data on the effect of sleep quality on testosterone may depend on whether testosterone is given as replacement, in supratherapeutic doses, or in the context abuse. Experimental data suggest that testosterone may modulate individual vulnerability to subjective symptoms of sleep restriction. Low testosterone may affect overall sleep quality which is improved by replacement doses. Large doses of exogenous testosterone and anabolic/androgenic steroid abuse are associated with abnormalities of sleep duration and architecture.

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What is a testosterone

what is a testosterone

Plasma testosterone levels display circadian variation, peaking during sleep, and reaching a nadir in the late afternoon, with a superimposed ultradian rhythm with pulses every 90 min reflecting the underlying rhythm of pulsatile luteinizing hormone (LH) secretion. The increase in testosterone is sleep, rather than circadian rhythm, dependent and requires at least 3 h of sleep with a normal architecture. Various disorders of sleep including abnormalities of sleep quality, duration, circadian rhythm disruption, and sleep-disordered breathing may result in a reduction in testosterone levels. The evidence, to support a direct effect of sleep restriction or circadian rhythm disruption on testosterone independent of an effect on sex hormone binding globulin (SHBG), or the presence of comorbid conditions, is equivocal and on balance seems tenuous. Obstructive sleep apnea (OSA) appears to have no direct effect on testosterone, after adjusting for age and obesity. However, a possible indirect causal process may exist mediated by the effect of OSA on obesity. Treatment of moderate to severe OSA with continuous positive airway pressure (CPAP) does not reliably increase testosterone levels in most studies. In contrast, a reduction in weight does so predictably and linearly in proportion to the amount of weight lost. Apart from a very transient deleterious effect, testosterone treatment does not adversely affect OSA. The data on the effect of sleep quality on testosterone may depend on whether testosterone is given as replacement, in supratherapeutic doses, or in the context abuse. Experimental data suggest that testosterone may modulate individual vulnerability to subjective symptoms of sleep restriction. Low testosterone may affect overall sleep quality which is improved by replacement doses. Large doses of exogenous testosterone and anabolic/androgenic steroid abuse are associated with abnormalities of sleep duration and architecture.

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