What are Natural Bioidentical Hormones? More than that… …how long does it take to work? Low T? Do YOU have low testosterone? Doctors also watch out for high red blood cell counts, which could increase the risk of clotting. Men on long-term using forms of testosterone therapy long term appear to have a higher risk of cardiovascular problems, like heart attacks, strokes, and deaths from heart disease.
For example, in , researchers halted the Testosterone in Older Men study when early results showed that men on testosterone replacement therapy had noticeably more heart problems.
Some physicians also have a lingering concern that testosterone therapy could stimulate the growth of prostate cancer cells. As with the hypothetical cardiac risks, the evidence is mixed. But because prostate cancer is so common, doctors tend to be leery of prescribing testosterone to men who may be at risk. For male patients with low blood testosterone levels, the benefits of hormone replacement therapy for men usually outweigh potential risks.
However, for most other men it's a shared decision with your doctor. It offers men who feel lousy a chance to feel better, but that quick fix could distract attention from unknown long-term hazards. So, keep risks in mind when considering testosterone therapy or other therapies. A large, definitive trial for hormone treatment of men is still to come. Until then, here is how to take a cautious approach to testosterone therapy. Have you considered other reasons why you may be experiencing fatigue, low sex drive, and other symptoms attributable to low testosterone?
For example, do you eat a balanced, nutritious diet? Do you exercise regularly? Do you sleep well? Address these factors before turning to hormone replacement therapy for men.
If your sex life is not what it used to be, have you ruled out relationship or psychological issues that could be contributing? If erectile dysfunction has caused you to suspect "low T" as the culprit, consider that cardiovascular disease can also cause erectile dysfunction. Inaccurate or misinterpreted test results can either falsely diagnose or miss a case of testosterone deficiency.
Thank you for Subscribing Our Housecall e-newsletter will keep you up-to-date on the latest health information. Please try again. Something went wrong on our side, please try again. Show references Qaseem A, et al. Testosterone treatment in adult men with age-related low testosterone: A clinical guideline from the American College of Physicians. Annals of Internal Medicine. Male hypogonadism adult. Mayo Clinic; Gilbert K, et al. Gaps in patient knowledge about risks and benefits of testosterone replacement therapy.
Synder PJ. Approach to older men with low testosterone. Accessed Feb. What is low testosterone? Urology Care Foundation. Snyder PJ, et al. Lessons from the testosterone trials. Endocrine Reviews. Try out PMC Labs and tell us what you think. Learn More. Testosterone has a spectrum of effects on the male organism.
This review attempts to determine, from published studies, the time-course of the effects induced by testosterone replacement therapy from their first manifestation until maximum effects are attained. Effects on sexual interest appear after 3 weeks plateauing at 6 weeks, with no further increments expected beyond. Effects on quality of life manifest within 3—4 weeks, but maximum benefits take longer. Effects on depressive mood become detectable after 3—6 weeks with a maximum after 18—30 weeks.
Effects on erythropoiesis are evident at 3 months, peaking at 9—12 months. Prostate-specific antigen and volume rise, marginally, plateauing at 12 months; further increase should be related to aging rather than therapy. Effects on lipids appear after 4 weeks, maximal after 6—12 months. Insulin sensitivity may improve within few days, but effects on glycemic control become evident only after 3—12 months.
Changes in fat mass, lean body mass, and muscle strength occur within 12—16 weeks, stabilize at 6—12 months, but can marginally continue over years. Effects on inflammation occur within 3—12 weeks. Effects on bone are detectable already after 6 months while continuing at least for 3 years. The time-course of the spectrum of effects of testosterone shows considerable variation, probably related to pharmacodynamics of the testosterone preparation.
Genomic and non-genomic effects, androgen receptor polymorphism and intracellular steroid metabolism further contribute to such diversity. Treatment of hypogonadal men with testosterone is rewarding, for the patients as well as the physician.
The patient experiences, to his satisfaction, profound changes in his physical appearance and his mental makeup. The attending physician observes the changes the patient undergoes and rarely fails to be fascinated by the multitude of functions testosterone appears to have in the process of masculinization in the broadest sense 1. While the effects of testosterone have been described in detail, relatively little attention has been given to the time these effects take to occur and achieve a full expression.
This seems relevant. To the attending physician, monitoring the effects of administration of testosterone will be facilitated when it is known when certain effects can and should be expected.
Patients like to receive information when the effects will set in. If patients have not been exposed to testosterone at the usual time of puberty, they must be prepared and counseled about the emergence of sexual thoughts and dreams, an increase in erections and seminal emissions, and when to expect them.
Furthermore, this information is relevant for the design of clinical trials on testosterone replacement therapy.
It is important to have information when an effect can be expected and when its maximum has been attained. Data to compile a time-course for the diverse actions of testosterone are not easily available. They originate from studies analyzing the effects of testosterone administration to hypogonadal men or, alternatively, from studies on androgen deprivation.
The main source of information will be the former category. Nearly all of these studies were not specifically designed to address the onset or time-dependency of effects of testosterone, nevertheless a number of controlled studies with different design and scheduled follow-up, allow a reasonable estimation. Studies were identified by a computerized search of MEDLINE, the Cochrane Library, EMBASE, and Current Contents for the past 35 years — , by searching the bibliographies of all retrieved articles and examining references of review articles found during the search to identify additional studies.
The search was focused on trials published later than , because at that time testosterone assays became widespread and more reliable. The search was limited to trials performed with testosterone, including testosterone esters and dihydrotestosterone preparations, independently of delivery. Only articles published in peer-reviewed medical journals were used; no abstracts were used. There is now evidence that the spectrum of complaints of testosterone deficiency cannot be related to a specific threshold of testosterone concentrations, but that thresholds vary with the various symptoms of testosterone deficiency 2.
Symptoms related to androgen deficiency in this study could be subdivided into three independent groups: psychosomatic complaints, metabolic disorders, and sexual health problems.
Patients suffering from one of these three groups exhibit distinct features in terms of androgen levels, age, and body mass index. So, complaints are not only linked to androgen levels but age and body mass index carried weight as well in the manifestation of signs and symptoms of androgen deficiency 2.
To further complicate the matter of the relationship between testosterone levels on the one hand and symptoms of testosterone deficiency on the other hand, there is the multifactorial impact on certain androgen-related functions 2. Erectile dysfunction may serve as an example of a composite dysfunctionality in which arterial endothelial function, neuronal integrity, testosterone concentrations, and psychological factors play pivotal roles 3, 4 , almost precluding establishing a straightforward relationship between testosterone levels and erectile dysfunction.
Given that the clinical manifestations of testosterone deficiency do not occur at a definitive threshold value of circulating testosterone, but vary with the target organ, associated symptoms and underlying conditions, it is even more complicated to establish a time-course since a reversal of these symptoms of deficiency is not only dependent on restoring serum testosterone to normal. In fact, at least two new variables are to be entered into the model: pharmacodynamics of the testosterone preparation and pharmacogenomics of the treated subject.
The latter varies inversely with the starting concentration of testosterone and predicts the magnitude and rapidity of response to treatment.
The time-course for the spectrum of effects of testosterone may vary considerably, as testosterone actions are exerted through a cascade of many different pathways. Most of the actions of testosterone take place via the androgen receptor as a transcription factor activated by testosterone. The bound androgen receptor acts as transcription regulatory element by binding to specific DNA response elements in target gene promoters, causing activation or repression of transcription and subsequently protein synthesis.
Over the past two decades evidence of rapid responses to androgens, dependent or independent of the androgen receptor, occurring at the cellular and organ level has accumulated. Examples are actions of testosterone on the brain and on vascular tone 7.
In addition to the time-course of actions of testosterone on androgen-dependent biological variables, Table 1 presents an indication of quantitative changes associated with testosterone administration.
Observed mean range of changes in selected measurable outcomes of testosterone administration to hypogonadal men in reviewed studies. In a series of studies, Bhasin et al. In a later study, the same group of authors concluded that the anabolic response to testosterone can largely be predicted by the dose administered 9. If the dose administered is too low, no effects may be demonstrable In a study that combined testosterone with GH, total lean body mass increased, as did appendicular lean tissue.
Composite maximum voluntary strength of upper and lower body muscles had increased after 16 weeks A study investigating the effect of a week long-acting testosterone administration on maximal exercise capacity and muscle strength found an increase in quadriceps isometric strength, maximal voluntary contraction, and isokinetic strength peak torque Testosterone administration for 20 weeks was associated with dose-dependent increases in skeletal muscle mass, leg strength, and power A study similar in design found an increase in lean body mass and an improvement of lower limb muscle strength after 6 months It can be concluded that the effects of testosterone on muscle strength are demonstrable after 12—20 weeks and that depending on the achieved testosterone levels, the maximum effects are attained after 6 or 12 months.
The data are summarized in Fig. The effects of testosterone on bone mineral density are in part mediated by estrogens, derived from testosterone via aromatization Testosterone improves bone mineral density at the lumbar spine compared with placebo, but at the femoral neck improvements are less certain Testosterone produces a consistent reduction in bone resorption markers Effects on bone mineral density have been shown in studies of 6 months duration 21, 22 , 8 months duration 23 , or 1 year duration From studies analyzing the effects of testosterone administration over as long as 36 months 25, 26 an increase was observed over that time period and it did not become clear whether the maximum effects of testosterone improving bone mineral have been attained after 36 months.
Testosterone plays a significant role in obesity, glucose homeostasis, and lipid metabolism Testosterone regulates lineage determination in mesenchymal pluripotent cells by promoting their commitment to the myogenic lineage and inhibiting their differentiation into the adipogenic lineage through an androgen receptor-mediated pathway.
The observation that differentiation of pluripotent cells is androgen dependent provides a unifying explanation for the reciprocal effects of androgens on muscle and fat mass in men 28, Upon testosterone administration there is a decrease in fat mass and an increase in lean body mass and the net result is often, but not always, that total body weight does not show major changes. An increase in total mass was found after 3 months 14 and an increase in weight in elderly men after 3 months A decrease in weight has been observed after 3 months 31 and 6 months 17 , with further progressive decrease over 24 months An increase in total body mass, lean body mass, and a decrease in fat mass were found after 3 months 14, 30 or 6 months A decrease in fat mass has been widely reported after 3 months 14, 30, 31 or 6 months 17 , and a decrease in percent fat mass equally after 3 months 14, It is now commonly accepted that a preferential accumulation of fat in the abdominal region is associated with an increased risk of type 2 diabetes mellitus and cardiovascular disease, not only in obese subjects but even in non-obese subjects Therefore, the effects on trunk fat, often measured as changes in waist circumference 34 , are very relevant effects of testosterone treatment.
A decrease in trunk fat or waist circumference was noted in a number of studies after 3 months 35, 36 with continuous decline over 24 months 32 and a decrease in the waist hip ratio after 3 months 31, 36 or after 6 months and 30 weeks respectively A continued decline up to weeks was reported Body mass index as a widely used measure of body composition declined after 6 months with further improvement during an observation period of 2 years Decreases in serum total cholesterol have been noted as quick as after 4 weeks 38, 39 but most studies have reported a decrease after 3 months 35, A decrease after 24 weeks was observed in a recent study 40 , others have found this to occur after 9 months 41 or 12 months 42 with a maximum reached after 12 months The decrease in serum triglycerides follows a similar pattern: after 4 weeks 38 , after 3 months 35 , and with further decrease over 9 months 41 or 12 months The decrease in low-density lipoprotein cholesterol seems somewhat slower: after 3 months 35 , after 40—44 weeks, 44 or after 12 months 42 with a maximum observed after 24 months Studies have found both an increase and decrease in high-density lipoprotein cholesterol.
An increase was found to occur after 3 months increasing further during 12 months 43 , after 6 months, 35 or close to 1 year Continuous increase was observed over 24 months Several studies indicate that upon testosterone administration, serum glucose is reduced after 3 months in men with impaired glucose tolerance 31, 36, An early study reported a decrease in glucose and glucose disposal rate after 9 months
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