“Our hypothesis was that testosterone would be good for the coronary arteries because we thought that by repleting testosterone to healthy levels there would be an improvement in the cholesterol panel and atherosclerosis burden. But what we found was the opposite, that atherosclerosis actually progresses faster under the influence of testosterone.”
The results of these studies indicate that testosterone treatment in older men with low testosterone may proffer some benefits. However, testosterone treatments may also entail risks. The exact trade-off is unknown. Larger and longer studies need to be performed to clarify the effects of testosterone on heart health, bone health, disability, and more.
^ Butenandt A, Hanisch G (1935). "Uber die Umwandlung des Dehydroandrosterons in Androstenol-(17)-one-(3) (Testosterone); um Weg zur Darstellung des Testosterons auf Cholesterin (Vorlauf Mitteilung). [The conversion of dehydroandrosterone into androstenol-(17)-one-3 (testosterone); a method for the production of testosterone from cholesterol (preliminary communication)]". Chemische Berichte (in German). 68 (9): 1859–62. doi:10.1002/cber.19350680937.
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Finally, there's the question of prostate cancer risk. Research over the past few decades has shown little evidence of a link between testosterone replacement therapy and prostate cancer. However, the question has not been entirely laid to rest. Eisenberg recommends that his testosterone replacement therapy patients get a PSA test once or twice a year to check for possible signs of concern.
To get your levels into the healthy range, sun exposure is the BEST way to optimize your vitamin D levels; exposing a large amount of your skin until it turns the lightest shade of pink, as near to solar noon as possible, is typically necessary to achieve adequate vitamin D production. If sun exposure is not an option, a safe tanning bed (with electronic ballasts rather than magnetic ballasts, to avoid unnecessary exposure to EMF fields) can be used.
One of the few testosterone boosters on the market to feature Eurycoma Longifolia, a patented ingredient that was developed at Massachusetts Institute of Technology (MIT) for the treatment of sexual dysfunction and male fertility, Tongkat Ali supports increased sex drive through multiple pathways, including boosting one’s free testosterone levels. Great as a standalone testosterone booster and a staple in many people’s post cycle after an anabolic cycle.
There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).
Epidemiological evidence supports a link between testosterone and glucose metabolism. Studies in non-diabetic men have found an inverse correlation of total or free testosterone with glucose and insulin levels (Simon et al 1992; Haffner et al 1994) and studies show lower testosterone levels in patients with the metabolic syndrome (Laaksonen et al 2003; Muller et al 2005; Kupelian et al 2006) or diabetes (Barrett-Connor 1992; Andersson et al 1994; Rhoden et al 2005). A study of patients with type 2 diabetes using measurement of serum free testosterone by the gold standard method of equilibrium dialysis, found a 33% prevalence of biochemical hypogonadism (Dhindsa et al 2004). The Barnsley study demonstrated a high prevalence of clinical and biochemical hypogonadism with 19% having total testosterone levels below 8 nmol/l and a further 25% between 8–12 nmol/l (Kapoor, Aldred et al 2007). There are also a number longitudinal studies linking low serum testosterone levels to the future development of the metabolic syndrome (Laaksonen et al 2004) or type 2 diabetes (Haffner et al 1996; Tibblin et al 1996; Stellato et al 2000; Oh et al 2002; Laaksonen et al 2004), indicating a possible role of hypogonadism in the pathogenesis of type 2 diabetes in men. Alternatively, it has been postulated that obesity may be the common link between low testosterone levels and insulin resistance, diabetes and cardiovascular disease (Phillips et al 2003; Kapoor et al 2005). With regard to this hypothesis, study findings vary as to whether the association of testosterone with diabetes occurs independently of obesity (Haffner et al 1996; Laaksonen et al 2003; Rhoden et al 2005).
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Finally, related to the point about competitiveness above, studies have shown that testosterone levels not only go up before a fight or competition, they increase after each win, and this gives the winner a much higher probability of winning his next round, and the next round after that, even against evenly matched competitors. This is called the “winner-effect,” and John Coates, author of The Hour Between Dog and Wolf: Risk Taking, Gut Feelings and the Biology of Boom and Bust, explains why it works:
While testosterone stimulates a man’s sex drive, it also aids in achieving and maintaining an erection. Testosterone alone doesn’t cause an erection, but it stimulates receptors in the brain to produce nitric oxide. Nitric oxide is a molecule that helps trigger a series of chemical reactions necessary for an erection to occur. When testosterone levels are too low, a man may have difficulty achieving an erection prior to sex or having spontaneous erections (for example, during sleep).
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).
“The Andro 400 has been a plus to my daily requirements of energy, stamina and weight loss. I have seen a noticeable reduction in my waistline from a 40" waist to a 37" waist. I am 6'6" and weighed 252, I now weigh 238 and feel much better. Without too much information, my sex drive and performance has been positively enhanced with greater sensitivity and stamina during those intimate times with my wife. Greater sensation, pleasure and results are evident.”
The normal development of the prostate gland is dependent on the action of testosterone via the androgen receptor, and abnormal biosynthesis of the hormone or inactivating mutations of the androgen receptor are associated with a rudimentary prostate gland. Testosterone also requires conversion to dihydrotestosterone in the prostate gland for full activity. In view of this link between testosterone and prostate development, it is important to consider the impact that testosterone replacement may have on the prevalence and morbidity associated with benign prostatic hypertrophy (BPH) and prostate cancer, which are the common conditions related to pathological growth of the prostate gland.
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal. Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling. There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.
Currently available testosterone preparations in common use include intramuscular injections, subcutaneous pellets, buccal tablets, transdermal gels and patches (see Table 2). Oral testosterone is not widely used. Unmodified testosterone taken orally is largely subject to first-pass metabolism by the liver. Oral doses 100 fold greater than physiological testosterone production can be given to achieve adequate serum levels. Methyl testosterone esters have been associated with hepatotoxicity. There has been some use of testosterone undecanoate, which is an esterified derivative of testosterone that is absorbed via the lymphatic system and bypasses the liver. Unfortunately, it produces unpredictable testosterone levels and increases testosterone levels for only a short period after each oral dose (Schurmeyer et al 1983).
Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age. The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body. The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.
In fact, studies on vegetarian and low-fat diets both show reduced testosterone levels of about 12 percent. Where higher fat diets of at least 40 percent of calories, with a higher intake of saturated fat, show increased testosterone levels. Why? It’s not rocket science. After all, cholesterol makes up the building blocks from which testosterone is formed; without it, the hormone simply can’t synthesize. Organic eggs are one of the best dietary sources. In addition to essential fatty acids, a whole egg is rich in aspartic acid, an amino acid that triggers production of testosterone.
The doctor regularly measured my levels to be sure they were within the normal range for a male my age. In other words, I wasn’t taking ‘roids to get big; I was getting control of hormones that were not functioning well. This is how you should look at testosterone therapy – it is a gentle nudge to help you be in normal ranges, not a big push to get you huuu-yge. If you’re like me, you want “normal ranges” of a 27-year-old, not of a 60-year-old. It’s my plan to keep my testosterone where it is now (around 700) no matter what it takes. Right now, the Bulletproof Diet and the other biohacks I’ve written about do that! I’m 43.
Statins are some of the most prescribed drugs in the world for reducing cholesterol levels and preventing heart disease. Various studies in the 1990s, including a study published in the ‘European Journal of Clinical Nutrition,’ supported the claim that Fenugreek could help reduce cholesterol levels. One possible explanation is the high fiber content in fenugreek. A fiber-rich diet has been shown to help reduce the levels of LDL (‘bad’ cholesterol) in your blood. (Note: The validity of the various studies from the 1990s have been questioned though because of small sample sizes)
Our Testosterone Therapy Doctors, Urologists and Endocrine Physicians have successfully treated over 25,000 patients. Our Testosterone Therapy Centers utilize the most progressive hormone treatment protocols backed up with training from the Mayo Clinic®, Cenegenics® Clinic and Cleveland Clinic®. Fill out the Quick Info Request Form to speak to a Testosterone Specialist and to receive the best pricing for Testosterone Injections and other hormone replacement medications like HCG and HGH Human Growth Hormone.
AC, I just ran across the thread… definitely start the injections. Should help with levels that low. I’m 36 and have battled low T for 6-7 years. My labs came back to show 90ng/dl when I just turned 30, and I’ve done Testosterone cypionate injections @ 100mg/mL weekly, Testim, Androgel, and Fortesta over the years. I’m actually going to my endocrinologist tomorrow to have new blood work done.
Sustain Alpha is the first ever transdermal testosterone booster to hit the Top 10 and it’s here for good reason. Users have been reporting increased sense of well-being and improved libido just shortly after their first dose with muscular definition and strength improvements after just 2 weeks! The transdermal technology allows users to avoid the traditional route of digesting their supplements and instead allows for them to be absorbed through the skin and directly in the bloodstream. This innovative approach has been delivering and for those looking to try something a bit different, Sustain Alpha is your go to.
Meat. Meat, particularly beef, provides our bodies with the protein it needs to create muscle (more muscle = more T) and the fats and cholesterol to make testosterone. My meat topping of choice was sliced up chuck steak. I grilled two of them on Monday and it lasted me until the next Monday. Every now and then I’d slow-cook some ribs or brisket to use as my meat topping. My philosophy was the fattier, the better.
Hypogonadism is highly prevalent amongst men with diabetes mellitus type 2 or symptoms of the metabolic syndrome, including insulin resistance, impaired glucose regulation, obesity, and hypertension.1,6,13,14,17,18 Low testosterone in many men with diabetes remains undiagnosed and untreated, and current guidelines recommend measurement of testosterone levels in such patients and, equally, that such chronic diseases should be investigated and treated in men with hypogonadism.1,6 It is not yet fully known whether diabetes is a cause or a consequence of low testosterone, and the full effects of testosterone administration on glycemic control in hypogonadal men with diabetes are unclear. However, there are indications that treating hypogonadism may have benefits on metabolic status in men with diabetes, and there is evidence that testosterone replacement therapy has a beneficial effect on risk factors for diabetes such as central obesity, insulin sensitivity, glucose control and blood lipid profiles in hypogonadal men with type 2 diabetes.14,19,20
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.
In fact, high cortisol deals a crushing blow to testosterone in two ways. During, long-lasting stress, high amounts of cortisol release very often and have a direct negative influence on T levels. Thus, cortisol inhibits testosterone synthesis in the testes and hypothalamus. In addition, the production of cortisol is impossible without cholesterol. But testosterone synthesis also demands cholesterol. Since during stress cholesterol is first of all used for making cortisol, T levels simply plummet.
In contrast to steroids, testosterone boosters have a fully different mechanism of action. They are the products which contain the natural ingredients only. These ingredients act by stimulating the man’s body to synthesize own testosterone. So, testosterone levels grow naturally without negative health effects associated with the intake of steroids.
A loophole in FDA regulations allows pharmaceutical marketers to urge men to talk to their doctors if they have certain "possible signs" of testosterone deficiency. "Virtually everybody asks about this now because the direct-to-consumer marketing is so aggressive," says Dr. Michael O'Leary, a urologist at Harvard-affiliated Brigham and Women's Hospital. "Tons of men who would never have asked me about it before started to do so when they saw ads that say 'Do you feel tired?'"