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This article studies the effects of 600mg testosterone injections weekly for 10 weeks compared to a placebo. As for the participants for did exercise, the testosterone users had 3x more muscle gain than the placebo group. Serum concentrations data is important to see how much of the testosterone the body retained and how much above baseline it peaked. A further important thing to note is that the wives and parents of the testosterone using participants reported no changes in anger, mood or behavior. With testosterone supplementation being such a huge advantage, roughly tripling muscle gains, it’s hard to believe that top body builders are not using testosterone. References:The Effects of Supraphysiologic Doses of Testosterone on Muscle Size and Strength in Normal Men.
Daniel has a strong interest in evidence supported fitness training, preparation and supplementation. Dr Robin Willcourt was consulted by Essendon's Steve Dank and Dean Robinson last year and outlines what he told them about sports supplements while he also suggests the use of testosterone and hormones to return athletes to their normal levels of those substances should be allowed. LEIGH SALES, PRESENTER: Last year Essendon's Steve Dank and Dean Robertson who you heard mentioned in that story visited Dr Robin Willcourt. This service may include material from Agence France-Presse (AFP), APTN, Reuters, AAP, CNN and the BBC World Service which is copyright and cannot be reproduced.
Late-onset hypogonadism: Current concepts and controversies of pathogenesis, diagnosis and treatment. Age trends in the level of serum testosterone and other hormones in middle-aged men: longitudinal results from the Massachusetts male aging study. Longitudinal changes in testosterone, luteinizing hormone, and follicle-stimulating hormone in healthy older men. Survey for late-onset hypogonadism among old and middle-aged males in Shanghai communities.
Oral testosterone replacement in symptomatic late-onset hypogonadism: effects on rating scales and general safety in a randomized, placebo-controlled study. Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. Effect of male age on fertility: evidence for the decline in male fertility with increasing age. Quantification of the human Sertoli cell population: its distribution, relation to germ cell numbers, and age-related decline.
The relative contributions of aging, health, and lifestyle factors to serum testosterone decline in men. The decline of androgen levels in elderly men and its clinical and therapeutic implications. Measurement of total serum testosterone in adult men: comparison of current laboratory methods versus liquid chromatography-tandem mass spectrometry.
Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study.
Characteristics of androgen deficiency in late-onset hypogonadism: results from the European Male Aging Study (EMAS). This was unique, but it was part of the practice I've got going in Melbourne at the moment, which is to do with anti aging and some sports medicine, getting people in tip-top shape physiologically, so there was no surprise at the end of the day from a chance meeting with Steve Dank that our conversation would just develop into, "What can you do to make your football players as fit as possible?"LEIGH SALES: You mentioned that the blood results showed that the players were under a lot of stress. This does not necessarily mean clinical hypogonadism, because most men with low T remain asymptomatic. What do you mean by that, that they were overtrained or training right to the edge of their capability, what specifically?ROBIN WILLCOURT: I'm sure that was part of it.
It's known that when people are really stressed out both physically or mentally, but particularly physically, things like your testosterone levels will go down, growth hormone levels will go down and it's really a protective device I think that the body is doing to shut down and say "enough is enough". The combination of low T and an array of the above symptoms has been termed with many names, including male menopause or climacterium, partial androgen deficiency of the aging male (PADAM), andropause and late-onset hypogonadism (LOH).
According to a recently formulated definition 'LOH is a clinical and biochemical syndrome associated with advancing age and characterized by symptoms and a deficiency in serum T levels (below the young healthy adult male reference range)'.
Those particular individuals are using the drugs as performance enhancing, meaning they're using massive amounts of those drugs, and it's obvious when you look at them physically. Direct comparisons between the studies from different geographic regions are difficult to make because of heterogeneity of experimental approaches, but it is quite likely that the basic features of LOH are very similar in various geographic and cultural environments.Because the symptoms of LOH are similar to those of hypogonadism in young men, T replacement therapy has become a popular option for its therapy. The diagnostics and evaluation of the effects of T therapy in LOH have largely been based on poorly controlled and underpowered treatment trials, on subjective opinions and experience of physicians and on data that might have been placebo effects. An increase in reliable information about LOH has clarified the diagnostic criteria of LOH.
However, the indications and contraindications for T treatment of LOH, including short- and long-term benefits and risks, still await evidence-based information. I'm very used to what happens in the US with the National Football League and it's not unusual to get saline drips, vitamin C pumped in intravenously; other vitamins to be given intravenously. This review concerns the current facts and controversies in the pathogenesis, diagnosis and treatment of LOH.
It is therefore counterintuitive to draw any parallels between the ageing-related changes in testicular and ovarian function. Spermatogenesis remains upon ageing sufficient to maintain a man's fertility throughout his entire postpubertal life.
One is that they were just taking some supplements, and obviously if the supplements were the same thing that you and I could buy over the counter at GNC it wouldn't matter. Testicular volume reflects closely the quantity of sperm production, and it decreases by about 15% between the ages of 25 and 80-90 years.
So that would imply there was something else going on in there, and I have no knowledge of that so I really can't comment. No, I don't know of any explicit examples in the sporting community here in Australia but the likelihood is if Essendon did something like this, other people are. Moreover, the total number of Sertoli and Leydig cells decreases to around half of that of the young testis.
And one of the things that you cannot possibly rule out is that players could be getting the stuff not sanctioned by the club but just doing it by themselves. Hence the latter decreases more than total T, by about 2%-3% per year although the average free T level still remains within the normal range in most men [Figure 1]. The panels present mean (95% CI in shaded area and vertical lines) levels of (a) total and (b) free testosterone, (c) LH and (d) SHBG. Compared with nonobese men, total and free testosterone was significantly lower in the overweight and obese men at all ages.
Total testosterone and SHBG age trends in the three BMI categories were similar (indicating no interaction between BMI and age).


The free testosterone age trend in the obese group was less steep than in the other two groups (indicating an interaction between BMI and age). Mean LH was not significantly different among the three groups at the median age of 60 years. Moreover, the medications associated with these disorders, such as opiates and glucocorticoids, are partially responsible for the decreased T through actions on LH secretory dynamics.
T production can be considered a good indicator of a man's general health, which decreases in response to a variety of stressors. High body mass index (BMI) can be regarded to provide a read-out for metabolic stress, and its suppressive effect on T levels is much greater than that of chronological age [Figure 1].
Curiously, the decrease in T secretion associated with obesity and chronic illness is not associated with compensatory increase in gonadotropin levels, thus indicating a secondary central mechanism for the disturbance [Figure 1]. Obesity as the cause of low T in ageing men is more common that chronological age; in the EMAS study, 73% of men fulfilling the criteria of LOH (see below) were obese or overweight. They provide usually rapid, economical and reliable information about circulating hormone concentrations.
However, the accuracy and precision of T IAs, especially at the low concentrations detected in children, women and hypogonadal men, remain a concern. However, its technical complexity, cost and suboptimal sensitivity precluded it as a routine method in the clinical chemistry laboratory until very recently. The technical improvements in instrumentation and the wider availability due to falling cost of equipment have made MS now a competitive method with IA, having reached sufficient sensitivity yet maintaining its superior specificity.Now opinions are being widely expressed to promote MS as the only acceptable method for clinical steroid hormone measurements. While it is clear that T measurements by IA are unreliable in children and women, it is uncertain whether MS or IA should be the method of choice for T quantitation in male hypogonadism.Although MS is in general more specific with lower intra- and interassay variability than IA, it faces similar inter-laboratory variability issues as IA.
To what extent MS improves the clinical relevance of steroid measurements requires additional data and experience.
A very recent study comparing total T assays in women concluded that the results obtained by IA and MS were comparable, and there is significant variability and poor precision also between various MS methods at low levels.
Improvements in performance and standardization in platform IAs are feasible alternatives that are already being implemented by some manufacturers. It is a major investment to abandon IA technology in favor of MS, and the reasons for this must be tangible and supported by evidence rather than conjecture.The EMAS study research consortium [42] recently measured T concentrations in the serum samples of a large cohort (n = 3174) of 40- to 79-year-old men using both an established IA and MS method. The conclusion from this comparison was that a validated platform IA is sufficient to detect subnormal T concentrations in the diagnosis of male hypogonadism [Figure 2]. IA can be as good as MS in the clinically important discrimination between eugonadal and hypogonadal men, especially when combined with clinical signs of androgen deficiency.
It seems prudent to conclude that the selection of an assay should be driven by the measurement performance in light of the clinical need and not by assay technology. The similar distribution of the concentrations measured indicates good agreement between the two methods.
There are several consensus statements, based on existing information and expert opinions on limits of normal and hypogonadal T levels of ageing men. This means by definition that 2.5% of normal men have their T levels below the lower limit of normal. Another so far hypothetical, but probably real 'misdiagnosed' group of men are those, whose T decreases within the reference range [Figure 2]. Let us assume, for the sake of argument that a decrease of T of > 50% leads to clinically significant hypoandrogenism. This means that only men whose T is within the lower half of the reference range (10-20 nmol l−1 ) can become 'biochemically hypogonadal' with a 50% decrease in T. In contrast, men with their T between 20 and 30 nmol l−1 still remain 'biochemically eugonadal' after a 50% suppression of T, and their apparent hypogonadism remains undiagnosed. Furthermore, low T levels have to be confirmed at least twice, because T levels near the lower limit of the reference range are often normal upon repeated measurement.
Recent guidelines recommend 'measurement of free or bioavailable T levels, using accurate and reliable assay, in some men in whom total T concentrations are near the lower limit of the normal range and in whom alterations of SHBG are suspected', [16] and 'particularly in obese men'. Equilibrium dialysis is the best method, but it is expensive, labor-intensive and not generally available. Free T measurements based on analogue displacement are not reliable and should not be used.
However, the commonly used formulae have been recently criticized, [49] and it is possible that a simple reliable way to determine free T is not yet available.
The EMAS study [6] observed that free T improved the LOH diagnosis especially at borderline levels of total T (see below). These men have mainly physical symptoms such as inability to do vigorous exercise, and with time a marked proportion of them seem to progress to genuine primary hypogonadism (EMAS, unpublished observation).Clinical symptoms of late-onset hypogonadismIt is counterintuitive to base the diagnosis of LOH solely on hormone levels, and it has to be supported by clinical symptoms. Conversely, the diagnosis cannot be based only on symptoms, but it has to be supported by information on suppressed androgen levels.
The array of symptoms associated with LOH is wide, covering many, and often nonspecific findings associated with aging, centering around declining bone mass, muscular mass and strength, physical function and frailty, metabolic changes including abdominal obesity, the metabolic syndrome and type 2 diabetes and sexual function. The key question is what, if any, of the wide array of LOH-related symptoms show correlation with low T levels. Various questionnaires have been constructed over the years to monitor the symptoms of LOH and their response to T treatment. These include the Ageing Male Symptom Score (AMS) [55] the Androgen Deficiency in Aging Men (ADAM) [56] and the Massachusetts Male Aging Study Questionnaire. The men were asked about 32 symptoms that other studies have (often without scientific proof) suggested to be related to LOH, and that are being used in the LOH questionnaires mentioned above. Only nine out of the 32 symptoms demonstrated a significant correlation with either total or free T [Table 1]. This has enabled the creation of an algorithm, which could be helpful when assessing patients in whom LOH is suspected [Figure 3]. When assessing patients according to such an algorithm, it is important to note the combination of low T with high gonadotropins, which suggests the presence of primary and age-dependent testicular failure.
If the clinician suspects the patient to have LOH, the diagnosis and choice of treatment can be obtained by following the flow chart from top to bottom, and choosing the next alternative on the basis of the findings. Wu (Manchester University, UK), and data previously published by Huhtaniemi and Forti61 (reproduced with permission). The numeric hormone levels presented are only suggestive, and in the diagnosis the clinician has to use local reference ranges for the assays.Click here to viewAccording to the EMAS data, it is possible to state almost categorically that if a man does not have sexual symptoms he does not have LOH. However, it is noteworthy that even the sexual symptoms have a high background prevalence of 28%-40%, irrespective of T levels, [6] and that not all men who experience sexual dysfunction will report these symptoms to their doctor.
The other LOH symptoms [Table 1] may support the LOH diagnosis, but are not sufficient without the presence of sexual symptoms.
Even LOH fulfilling the strict EMAS criteria can be caused by something else than lack of T, which may explain the relatively modest outcome of T replacement therapy (see below).


One longitudinal study demonstrated that LOH remission occurred in ~ 50% of men, either because the subnormal serum T level normalized or because the patient's symptoms subsided.
Using more relaxed diagnostic criteria, the prevalence of symptomatic LOH has previously been found to be 5.6%-12% in similar cohorts of ageing men. All 40- to 49-year-old men (0.1% of the age group) diagnosed with LOH were clinically overweight. The proportion of ageing-associated (primary) hypogonadism increased gradually to 40% in 70- to 79-year-old men. However, we have to remember that men seeking medical help for sexual problems do not represent the general population.
A report from Italy detected a 15% prevalence of genuine LOH in men visiting andrology clinic. T replacement is an effective therapy for the classic forms of male hypogonadism such as congenital hypogonadotropic hypogonadism, Klinefelter syndrome and anorchia. T treatment of LOH is a much more controversial issue because, as previously mentioned, the symptoms and signs are often unspecific and mild, the T levels are often borderline and low T and high symptom score often do not coincide. Furthermore, there is still no general consensus on the threshold of circulating T below which replacement therapy is recommended. The EMAS definition of LOH [6] supports the recommendations of several international societies.
In overweight or obese men, lifestyle counseling to achieve sustained weight loss should be the mainstay of management, even if T treatment is likely to induce a small increase of the total lean body mass and a small decrease of total body fat (see also below). The recent EMAS data show that weight gain or loss have clear inverse correlation with circulating T [Figure 4]. Moreover, the risk of experiencing adverse effects associated with T treatment was reported to increase in obese subjects. We still lack randomized, placebo-controlled studies on T replacement in men aged ≥60 years, and the existing trials have low numbers of subjects, and are often of insufficient duration. However, the evidence for a beneficial effect of T on erectile function was tempered by the progressively smaller effect with increasing baseline T levels and by the declining effect of the treatment over time. Some studies in healthy older men have reported improvements in grip strength, whereas others have not, and limited data are available on the beneficial effects of T on lower limb muscle strength. Altogether, there is still no convincing proof that these effects at safe doses would translate into clinically significant improvement in muscle performance and quality of life. Effects of T treatment in these conditions have been evaluated in a few controlled trials, and two meta-analyses [91],[92] have reported some beneficial effects of T treatment on glycemic control and visceral obesity.
However, the short duration of the trials and the limited number of enrolled subjects mean that firm conclusions cannot be drawn from these studies, and T treatment is not yet be recommended for these conditions. Androgenic-anabolic steroids are also associated with the coagulation cascade, hemostasis as well as damaged endothelial and myocardial function. However, numerous studies, albeit relatively small in size, on the association of androgens and CAD have found no adverse effect of T.
Neither have significant beneficial effects of androgen treatment been reported in primary or secondary prevention.
The answer to this question is crucial for the feasibility of T replacement in the prevention and therapy of CAD. It is probably bidirectional, therapeutic reduction of T in prostate cancer patients increased in an observational study on the CAD risk, [98] but also numerous comorbidities in ageing men reduce T levels.
T replacement therapy decreases the symptoms of heart failure and improves the exercise capacity.
Their aim is to test the hypothesis that T treatment for one year compared to placebo will improve walking speed, sexual activity, vitality and verbal memory and correct anemia.
Two recent meta-analysis have shown significant effects of T treatments over placebo on its appearance. However, no difference was observed in the rates of any of these events between the two groups.
The man-years of exposure in these trials were too small to allow reliable risk assessment. It has been estimated that randomization of approximately 6000 men aged 65-80 years with low T levels to placebo or T treatment for 5 years would be required to detect a 30% difference in prostate cancer incidence rates between T-treated and placebo-treated men.
However, once again the short duration and the low number of subjects enrolled in most studies limits the final conclusions.According to recent recommendations, men with untreated congestive heart failure should not be treated with T. Even if the cardiovascular events were not planned as primary or secondary outcome and the health conditions of the recruited men were rather poor in comparison to other trials, these findings suggest caution in T replacement of aged men with poor health, low mobility and multiple risk factors for cardiovascular events. Admittedly, pharmacological doses of T were used in this study, and we do not know whether the findings are applicable to a situation where low T levels are returned to the physiological range.The effects of T on lipids in comparison to placebo have also been examined in a meta-analysis, [111] which showed that T decreased total cholesterol in men with lower T levels, and that it could reduce high density lipoprotein (HDL)-cholesterol, but only in men who had high baseline T levels.
The evidence that T replacement can cause sleep apnea is rather weak.Finally, we do not know whether decreased T levels in ageing men, and especially in those with comorbidities, is a protective mechanism with beneficial effects of the homeostasis of the ageing organ systems with reduced functional capacity. This is a caveat that has to be kept in mind when considering the benefits and risks of T replacement therapy of LOH.Duration and monitoring of T treatmentImprovement of symptoms should be assessed after a few months of T treatment.
If no benefit is reported by the patient, treatment should be terminated and other causes of symptoms should be investigated. It should also be kept in mind that the initial benefits of T could be a placebo effect, although such improvements are short-lived. However, it is likely to be much higher in the selected group of men who seek medical help for their LOH symptoms. When diagnosing LOH and choosing the most appropriate treatment, it is important to consider the general situation of the patient. In this situation, it would seem most logical to begin treatment with lifestyle modification and weight reduction, and to optimize the treatment of comorbidities, before T supplementation, which is expensive and of uncertain benefit.If the clinician decides, after excluding contraindications, to initiate T treatment, the patient must be informed about the experimental nature of T therapy, as no evidence-based information is available regarding the long-term risks and benefits, and there are no specific guidelines for its use. When assessing the results of T treatment, it must be kept in mind that even placebo treatment of LOH can achieve statistically significant effects.
T should not be prescribed for the treatment of symptoms that are not specific to LOH, and that can be caused by other conditions - such as obesity, metabolic syndrome, depression, diabetes or other chronic diseases - even though low T is associated with these conditions. T replacement should be considered only for men with clear LOH diagnosis, but the beneficial effects of this treatment, as well as its potential risks are currently unknown. Only larger multicenter, long-term clinical trials will settle the current controversies surrounding the diagnosis and treatment of LOH.



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