When I told people that I was doing an experiment to increase my testosterone, the question that people would invariably ask in hushed tones was, “So, did it, you know, improve your sex life?” Honestly, I didn’t see too much change. I had a robust and healthy sex life before the experiment and continued to do so afterwards. I guess I was a bit more randier than usual, but not much. I’d imagine if you had been suffering from low T for a long time and took steps to increase it, you’d likely see improvement in the bedroom department.
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When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a female's).
Sportsmen are permitted to use the boosters to trigger the mechanism of testosterone synthesis in the body. These products won a wide popularity among the sportsmen. The matter is that the supplements work by substantially enhancing sports performance, reviving strength, boosting endurance, coping with excessive stress levels, and decreasing time necessary for recovery after exhausting exercises.
In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them. The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.
In addition to its role as a natural hormone, testosterone is used as a medication, for instance in the treatment of low testosterone levels in men and breast cancer in women. Since testosterone levels decrease as men age, testosterone is sometimes used in older men to counteract this deficiency. It is also used illicitly to enhance physique and performance, for instance in athletes.
It may also become a treatment for anemia, bone density and strength problems. In a 2017 study published in the journal of the American Medical Association (JAMA), testosterone treatments corrected anemia in older men with low testosterone levels better than a placebo. Another 2017 study published in JAMA found that older men with low testosterone had increased bone strength and density after treatment when compared with a placebo.
Testosterone. During adolescence and early adulthood, testosterone levels in men are naturally high resulting in a feeling of strength, sexual charge and vitality. But as men get older, the aging process causes testosterone levels to decline, often resulting in a decrease in sexual desire, decrease in muscle mass, excessive weight gain, feeling tired all day, extreme mood swings, insomnia, depression and hair loss.
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Inaccurate or misinterpreted test results can either falsely diagnose or miss a case of testosterone deficiency. Your testosterone level should be measured between 7 am and 10 am, when it's at its peak. Confirm a low reading with a second test on a different day. It may require multiple measurements and careful interpretation to establish bioavailable testosterone, or the amount of the hormone that is able to have effects on the body. Consider getting a second opinion from an endocrinologist.
Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues. Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase. 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides), skin, hair follicles, and brain and aromatase is highly expressed in adipose tissue, bone, and the brain. As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression, and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone, it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.
Testosterone plays a role in certain behaviors, including aggression and dominance. It also helps to spark competitiveness and boost self-esteem. Just as sexual activity can affect testosterone levels, taking part in competitive activities can cause a man’s testosterone levels to rise or fall. Low testosterone may result in a loss of confidence and lack of motivation. It can also lower a man’s ability to concentrate or cause feelings of sadness. Low testosterone can cause sleep disturbances and lack of energy.
For example, testosterone can increase the hematocrit, the percentage of red blood cells in the bloodstream. If the hematocrit goes up too high, we worry about the blood becoming too viscous or thick, possibly predisposing someone to stroke or clotting events. Although, frankly, in a review that I wrote in the New England Journal of Medicine* where we reviewed as much of this as we could, we found no cases of stroke or severe clotting related to testosterone therapy. Nevertheless, the risk exists, so we want to be careful about giving testosterone to men who already have a high hematocrit, such as those with chronic obstructive pulmonary disease, or those who have a red-blood-cell disorder.
The oldest form is an injection, which we still use because it’s inexpensive and because we reliably get good testosterone levels in nearly everybody. The disadvantage is that a man needs to come in every few weeks to get a shot. A roller-coaster effect can also occur as blood testosterone levels peak and then return to baseline. [See “Exogenous vs. endogenous testosterone,” above.]
After years of low libido,ED and just general lack of energy I found a urogist will to look at my symptoms. Turned out my testosterone level was 135 so I started on testosterone. Had a great improvement on everything I was having issues plus just a lot happier. My Dr. did PSA every 6 months and my PSA over almost 2 years went from 1.16 to 1.67, still pretty low for 56YOA He wanted to do a biopsy and he found 1 out of 12 cores 60%, GS3X3. I had an MRI and found a .5cm cancer, clean margins, perfectly round and dead center of the prostate.I’m doing active surviellance and the DR wants to start me on Finasteride and continue TRT. I like to believe that the years of low testosterone help the cancer to develope and the twice yearly testing of PSA by the doctor because of therapy caught it very early.I’m not too sure about TRT and Finasteride together.
This evidence, together with the beneficial effects of testosterone replacement on central obesity and diabetes, raises the question whether testosterone treatment could be beneficial in preventing or treating atherosclerosis. No trial of sufficient size or duration has investigated the effect of testosterone replacement in primary or secondary prevention cardiovascular disease. The absence of such data leads us to examine the relationship of testosterone to other cardiovascular risk factors, such as adverse lipid parameters, blood pressure, endothelial dysfunction, coagulation factors, inflammatory markers and cytokines. This analysis can supply evidence of the likely effects of testosterone on overall cardiovascular risk. This has limitations, however, including the potential for diverging effects of testosterone on the various factors involved and the resultant impossibility of accurately predicting the relative impact of such changes.
The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
Today we take a look at some of the physical and psychological benefits that come with having optimal testosterone levels (I’ll talk about what “optimal” means regarding T later this week). You probably know about some of the benefits already, but some of the ones I discuss may surprise you. When appropriate, I’ll report any health benefits that I experienced during my own 90-day testosterone boosting experiment.
A4M, which stands for “The American Academy of Anti-Aging Medicine” is dedicated to the advancement of tools, technology, and transformations in healthcare that can detect, treat, and prevent diseases associated with aging. They promote the research of practices and protocols that have the potential to optimize the human aging process. The organization is also dedicated to educating healthcare professionals and practitioners, scientists, and members of the public on biomedical sciences, breakthrough technologies, and medical protocols through our advanced education entity: Metabolic Medical Institute (MMI). Their event in Vegas each year is, in my opinion, well worth checking out.
A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
In this podcast, I will review the key biomarkers for achieving peak male health, along with the most potent and effective practices for optimizing biological variables for men's fertility and longevity. I will also unveil a host of little-known biohacks proven to enhance or restore peak testosterone and drive, along with how to practically implement a blend of ancestral wisdom and modern science to amplify sexual performance.
I can report that I saw decreased body fat during my three-month testosterone experiment. I started off with 18% body fat and ended the experiment with 12% body fat. I almost have a six-pack! This is the leanest I’ve ever been in my entire life. The funny thing is, I wasn’t even trying to shed body fat. It just happened. All hail, mighty testosterone!
“Before taking Andro400, my husband weighed 290 lbs. He's a diabetic and his blood pressure was through the roof. I purchased Andro based on the reviews, and he's lost 60 - 70 lbs! It's enhanced him health-wise in a lot of aspects too. He used to be depressed because of his weight. The fact that he was losing weight like crazy gave him a lot of relief. He's not depressed now, he's really happy. He's more loving. And it's so exciting for me as a wife to see him happier -- it made me happier! So I'm really grateful. Andro400 gave him a lot of energy too because of the testosterone boost. The 3 main things everybody's noticing are: no more depression, a lot more energy and the huge weight loss. He went from size 42 to 38, so it's like, oh my God it's WORKING!! Trust me, we've tried a lot of other things that didn't work. And that's why I'm so excited because it's actually, literally changing our lives!”
For years, the recommendation has been to get a testosterone value early in the morning because levels start to drop after 10 or 11 a.m. But the data behind that recommendation were drawn from healthy young men. Two recent studies showed little change in blood testosterone levels in men 40 and older over the course of the day. One reported no change in average testosterone until after 2 p.m. Between 2 and 6 p.m., it went down by 13%, a modest amount, and probably not enough to influence diagnosis. Most guidelines still say it’s important to do the test in the morning, but for men 40 and above, it probably doesn’t matter much, as long as they get their blood drawn before 5 or 6 p.m.
The authors reported statistically significant increases in both noncalcified and total coronary artery plaque in patients receiving testosterone treatment. Participants’ coronary artery calcium scores, another measure of calcified plaque, were not significantly affected by testosterone treatment. Although these results are potentially a cause for concern, additional studies are required to determine the clinical relevance of this increase in plaque volume.
Sharma, R., Oni, O. A., Gupta, K., Chen, G., Sharma, M., Dawn, B., … & Barua, R. S. (2015, August 6). Normalization of testosterone level is associated with reduced incidence of myocardial infarction. European Heart Journal, 36(40), 2706-2715. Retrieved from https://academic.oup.com/eurheartj/article/36/40/2706/2293361/Normalization-of-testosterone-level-is-associated