Gary Womble… Get out of here with your quackery nonsense. No one likes trolls that want to push diet and weight loss pills as a serious solution to low t and ED. Anyone who reads your comment will waste at least 20 seconds of their life. What’s worse, they might listen to you instead of getting real medical advice that might actually help with an issue that is devastating to their lifestyle. And btw, before you decide to respond to this with more quackery, testimonials or fake research, know that I am a pharmaceutical scientist and won’t fall for your bogus statements


Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004).
When I was using the gel my testicles also shrank a bit, but not anywhere near this amount. And when I stopped using the gel they plumbed back up again to their former size. It took some time but their size came back. This may be an issue for the younger guys, but I think most older guys can easily handle this as no big deal, because overall it’s not.
An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations.

Testosterone is responsible for increased muscle mass. Leaner body mass helps control weight and increases energy. For men with low testosterone, studies that treatment can decrease fat mass and increase muscle size and strength. Some men reported a change in lean body mass but no increase in strength. It’s likely you’ll see the most benefits when you combine testosterone therapy with strength training and exercise.


Alcohol has constantly been shown to lower testosterone levels. It’s even worse if you’re a heavy beer drinker. Wanna know why? Because beer raises your estrogen levels due to the phytoestrogens that are produced from the hops used to make beer. If that’s not enough, studies have shown that alcoholics have lower levels of testosterone than non-alcoholics.
Herbalists have used _Trifolium pratense_, red clover, to treat menopausal symptoms like hot flashes. The mechanisms underlying these effects remain unknown. Testosterone decreases hot flashes in some postmenopausal women, so red clover may work in this way. A 2015 paper in the Avicenna Journal of Phytomedicine reviewed the literature testing this idea.

I’m 56 and 5 years ago dropped to 270 with all the side effects listed for low test. After trying shots and not liking the roller coaster effect, I switched to gels. Androgel and Axiron had too low a dosage and far too messy. They need to not call them gels but liquids. If it pours like water it’s a liquid. My doctor recommended a compounding Pharmacy that made a cream and it was perfect. It had a click dispenser that looked like a deoderant that would pre-measure the dosage and I could rub it on my arms and shoulders or on my neck, really anywhere not covered in hair but the thinner the skin the better. It dried instantly so I could get dressed in a couple minutes. My totals never got out of the 400’s until I started the 150mg daily cream dosage, then they hovered around 700. The down side was Insurance didn’t cover it and I had to pay $50 a month vs free shots from the doctors office or $10 for the so-called gels. Bad news is it has now doubled in price due to new Federal production regs on compounding Pharms. Now, I am going back on the shots which I now have to buy the vile for $125 for 10 doses and have to take it to my doctor to administer it every 2wks while I am looking into bioidentical pellet implants.
The use of anabolic steroids (manufactured androgenic hormones) shuts down the release of luteinising hormone and follicle stimulating hormone secretion from the pituitary gland, which in turn decreases the amount of testosterone and sperm produced within the testes. In men, prolonged exposure to anabolic steroids results in infertility, a decreased sex drive, shrinking of the testes and breast development. Liver damage may result from its prolonged attempts to detoxify the anabolic steroids. Behavioural changes (such as increased irritability) may also be observed. Undesirable reactions also occur in women who take anabolic steroids regularly, as a high concentration of testosterone, either natural or manufactured, can cause masculinisation (virilisation) of women.
For example, in February 2017, scientists reported on trials involving men over age 65 who had low testosterone due to aging. Each trial included a different number of men depending on the subject of the research. Roughly half of the participants received testosterone therapy for a year; the rest underwent a placebo treatment. The researchers discovered the following:
Ben has mentioned APOE many times, as in this podcast, with the reference in this transcript as something like 34/44. I’ve always assumed that meant a number of different genes that related to APOE having the homozygous or heterzygous mutations. I’ve only been able to find one rs in my 23andme raw data that seems meaningful to this, rs429358. How do you all figure out your APOE status? Are you getting this from one of the other companies that analyzes part of your raw data for you?
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.
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).
Testosterone boosters are used by many athletes worldwide to achieve a significant muscle mass increase within a short period of time.[1] However; one cannot be completely confident in terms of the quality and efficacy of such products because of several reasons, such as the possibility of bad storage conditions and originating from an unreliable source. Over the years, some consumers of testosterone boosters have complained of kidney and liver abnormalities that could be linked to their use of boosters.[10] Cases of erroneous product administration have occurred in the past as athletes may not follow the instructions on the label fully, which can lead to many side effects.[11] In the present case, a man was admitted to a hospital because of a severe abdominal pain. The pain was later found to be caused by liver injury. The diagnosis confirmed that the levels of the key hepatic enzymes were markedly elevated. The medical complications observed were found to have occurred following the consumption of two courses of a commercial testosterone booster. According to researchers based in the US, about 13% of the annual cases of acute liver failure are attributable to idiosyncratic drug- and/or supplement-induced liver injury.[12] Marked increase in the levels of ALT, AST, and gamma-glutamyl transferase was observed after consuming the first course of the commercial testosterone booster, and they started to decline after the 2nd and 3rd course. This abruptly increases the levels of liver enzymes after the first course may be attributed to the interruption effect of commercial testosterone booster on liver function as a result of the effects of its ingredients.
^ Southren AL, Gordon GG, Tochimoto S, Pinzon G, Lane DR, Stypulkowski W (May 1967). "Mean plasma concentration, metabolic clearance and basal plasma production rates of testosterone in normal young men and women using a constant infusion procedure: effect of time of day and plasma concentration on the metabolic clearance rate of testosterone". The Journal of Clinical Endocrinology and Metabolism. 27 (5): 686–94. doi:10.1210/jcem-27-5-686. PMID 6025472.
There are many Supplements: Zinc for starters about 1/3 of Men have to low Zinc. Make shure you get a good chemical form no oxides best are chelates or citrates. Then there is Arginin and L-Citrullin two amino acids that help Blood flow basacly natural viagra. And then there are things like maca(a plant that you can get in powder form) that hightens libido but not like zinc it doesnt highten the testosteron level. My dad takes the combo of these 3 things kosts you about 30-60$ per Month. Dont be lazy do research on the stuff to make shure you get right dosages and good quality Sups
In a subsequent study of 345 men with normal PSA and low testosterone, we found the cancer rate was similar: 15%. And we had a large enough group to look at the impact of testosterone on cancer risk. For men whose total testosterone or free testosterone value was in the lowest third, the odds of having a positive biopsy were double the odds in the rest of the men. That’s the first evidence that low testosterone may be an independent predictor for the development of prostate cancer.

BSN Evotest the next ranked testosterone booster and is a unique option in that it’s available in both capsule and powdered drink form. For those who dislike swallowing pills, this will be a better route to go. There are mixed reports on the taste quality of the product, however, this is an individual preference and should not be something that deters you from purchasing it. It mixes fairly well by most reports, so is something that you should be able to easily take with you to the gym for use during the workout session.
D-Aspartic acid is a natural amino acid involved in the synthesis and release of testosterone, which research shows can be used as a testosterone booster for infertile men. One 90-day study gave D-Aspartic acid to men with impaired sperm production, and found their sperm count rose from 8.2 million sperm per ml to 16.5 million sperm per ml, more than a 100 per cent increase.
Side note, insurance rarely will cover it and cause a long paper trail to even approve it which is unfortunate and disheartening. Especially when it is done out of network. Currently I have found a place to supply all of the aboue sent to my house at approximately $200.00 per month. Still an unfortunate cost for a medical reason that the insurance companies don’t approve. Best of luck to all of you.
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.
Sprinting has been shown numerous times that it has positive effects on testosterone levels. One 2011 study (ref 84) looked at weightlifters who performed 4x35m sprints twice a week. In contrast to the control group (who continued lifting but did not sprint), it was found that “After the 4-week training program, total testosterone and the total testosterone/cortisol ratio increased significantly in the (sprinters) EXP group”.

Our bodies make testosterone while we sleep. In one study, men who got five hours of sleep a night had testosterone levels 10 to 15 percent lower than when they got a solid eight hours. The study, conducted by the University of Chicago, found that skimping on sleep reduced the men’s T levels by an amount equivalent to aging 10 or more years. While it can be challenging to change your sleep habits, says Natasha Turner, ND, you can “start going to bed 15 minutes earlier each week until you reach your target time.”
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:
Although it’s rare to see swelling caused by fluid retention, physicians need to be careful when prescribing testosterone to men with compromised kidney or liver function, or some degree of congestive heart failure. It can also increase the oiliness of the skin, so that some men get acne or pimples, but that’s quite uncommon, as are sleep apnea and gynecomastia (breast enlargement).
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).
Ten healthy men aged around 24 years old spent 1 week sleeping for 8 hours per night at home, they then spent the next 11 nights in a lab. They slept for 10 hours per night for 3 nights, followed by 8 nights of restricted sleep, when they slept for only 5 hours. Doctors checked their blood every 15 to 30 minutes during the last night that they slept 10 hours, as well as on the sleep-restricted session.
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.
The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
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There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
Fenugreek is often found in Indian, Turkish, and Persian cuisine. Multiple studies have found it to improve testosterone levels, and in particular, sexual performance. Scientists at Babu Banarasi Das University and King George’s Medical University in India have found that fenugreek improved testosterone levels. Testosterone levels increased for 90% of the volunteers, sperm morphology (the size and shape of sperm) improved for 14.6%, and more than 50% of volunteers experienced improvements in mental alertness, mood, and libido.
In fact, there is increasing evidence of the potential benefits of testosterone replacement therapy on multiple cardiovascular risk factors. This evidence recently has been comprehensively reviewed by Traish et al. in the Journal of Andrology.16 Although the full effects of testosterone replacement therapy on cardiovascular risk are yet to be established, the balance of emerging evidence from clinical studies suggests that testosterone replacement therapy in hypogonadal men may improve endothelial function, reduce proinflammatory factors, reduce hypertension, and improve the lipid profile.
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Finally, we looked at the proprietary blends of our remaining boosters, and dug into their ingredient lists. Supplements frequently include ingredients known for their “folk-lore” value; they’re believed to work, even when there isn’t any scientific background to prove it. Though we didn’t ding points if an ingredient wasn’t proven to be good (just so long as it wasn’t proven to be bad), we didn’t want to include any ingredient with evidence of causing harm.

For facts sake I am 51yr old male and I am fat. I do have a large and muscular fat, but I also have a good amount of at on top of that. My body shape is not the typical huge “beer belly” gut that is hard and dangerous, rather, I am fat all over proportionally, but still considered obese. The fat on my body and around my middle is quite soft compared to male friends who have those large and hard bellies. Still, my doctor and reading indicate that fat has an effect on T potentially lowering the overall level that my T would be if I lost a good amount of that fat.
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Leafy green vegetables such as spinach are rich sources of folic acid. Low levels of folate can give rise to distorted sperm shapes such as ones with two heads or two tails. The sperm are also at an increased risk of chromosomal abnormalities. This means that firstly your sperm will find it difficult to reach an egg and even if it does reach an egg, it will not be able to fertilize it. Furthermore, even if these sperms are able to fertilize an egg, the chances of birth defects are quite high in such cases.


In many of the studies we found, those who saw the most improvement in health, testosterone, or muscle gain were those with existing nutrient or vitamin deficiencies. This means that some gains may be due more to dietary changes and generally restoring nutrient and vitamin levels than any one magic ingredient, but also that making sure your diet includes healthy amounts of nutrients should be your first step.
Testosterone is an androgen hormone produced by the adrenal cortex, the testes (in men), and the ovaries (in women). It is often considered the primary male sex hormone. Testosterone stimulates the development of male secondary sex characteristics (like body hair and muscle growth) and is essential in the production of sperm. In women, testosterone plays a role in egg development and ovulation.
The researchers found that men who received hormone treatment experienced an increase in bone strength and density. Strength increases were greater in the spine than they were in the hip. However, as with other T Trials, more research needs to be done. A larger study over many years would need to be performed to determine whether testosterone could decrease risk of bone fracture.
If testosterone deficiency occurs during fetal development, then male characteristics may not completely develop. If testosterone deficiency occurs during puberty, a boy’s growth may slow and no growth spurt will be seen. The child may have reduced development of pubic hair, growth of the penis and testes, and deepening of the voice. Around the time of puberty, boys with too little testosterone may also have less than normal strength and endurance, and their arms and legs may continue to grow out of proportion with the rest of their body.
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