I was reading in the university health news daily website that a study performed by researchers at the University of Texas M.D. Anderson Cancer Center found that men with prostate cancer who ate 3 tablespoons of milled or ground flax seeds each day had decreased prostate cancer cell proliferation compared to similar men who did not eat flax seeds. According to the American Cancer Society, men who supplement their diets with flax seed have lower PSA levels and slower growth of benign as well as cancerous prostate cells.
The IOM report estimated that a study of whether there is an increased risk of prostate cancer in men on testosterone therapy might require following 5,000 men for three to five years. Before launching such an endeavor, the report recommended more firmly establishing the effectiveness of testosterone-replacement therapy, saying that studies of long-term risks and benefits should be conducted only after short-term efficacy has been proven. That means the male equivalent of the WHI remains far off.
Thomas M. Gill, MD, Humana Foundation Professor of Medicine at Yale University School of Medicine in New Haven, CT, told EndocrineWeb that these trials were needed because “the pharmaceutical industry did a very good job of promoting testosterone, and there have been suggestions of parallels between age-related decreases in testosterone levels in men, and menopause in older women.”
One study showed that six months of zinc supplementation among slightly zinc-deficient elderly men doubled serum levels of testosterone. And another eight-week trial found that college football players who took a nightly zinc supplement showed increased T-levels and increased leg strength that was 250 percent greater than a placebo! Holy quads, Batman! Research has also shown deficiencies in zinc to be a risk factor for infertility caused by low testosterone levels.
Cross-sectional studies have not shown raised testosterone levels at the time of diagnosis of prostate cancer, and in fact, low testosterone at the time of diagnosis has been linked with more locally aggressive and malignant tumors (Massengill et al 2003; Imamoto et al 2005; Isom-Batz et al 2005). This may reflect loss of hormone related control of the tumor or the effect of a more aggressive tumor in decreasing testosterone levels. One study found that 14% of hypogonadal men, with normal digital rectal examination and PSA levels, had histological prostate cancer on biopsy. It is possible that low androgen levels masked the usual evidence of prostate cancer in this population (Morgentaler et al 1996). Most longitudinal studies have not shown a correlation between testosterone levels and the future development of prostate cancer (Carter et al 1995; Heikkila et al 1999; Stattin et al 2004) but a recent study did find a positive association (Parsons et al 2005). Interpretation of such data requires care, as the presentation of prostate cancer could be altered or delayed in patients with lower testosterone levels.

“What on earth do you mean?” Well, I don’t literally mean taking it to the compound. What I mean to say is that you should be incorporating the three most important compound exercises into your routine: bench press, squats, and deadlifts. In case you didn’t know, by training large muscle groups your body releases more testosterone. When you do these three lifts, and perform them properly, then you’ll reap the benefits of not only muscle gains, but also that of an increased release of testosterone and growth hormone.
Like other steroid hormones, testosterone is derived from cholesterol (see figure).[128] The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids.[129] In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.
It doesn’t get more natural than getting a good night’s sleep. Research published in the Journal of the American Medical Association showed that lack of sleep can greatly reduce a healthy young man’s testosterone levels. That effect is clear after only one week of reduced sleep. Testosterone levels were particularly low between 2 and 10 p.m. on sleep-restricted days. Study participants also reported a decreased sense of wellbeing as their blood testosterone levels dropped.
Dr. Resnick and colleagues assessed 788 participants in the cognitive function arm of the TTrials but focused on the 493 participants who were classified as having age-associated memory impairment with a confirmation of both subjective and objective indicators of cognitive decline. The authors detected no significant effect after 1 year of testosterone treatment on either the primary outcome of verbal memory, as measured by delayed paragraph recall or on any of the secondary outcomes of visual memory, executive function, and spatial ability.1
The brain is also affected by this sexual differentiation;[13] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[99]
Men who start using the gels have to come back in to have their testosterone levels measured again to make sure they’re absorbing the right amount. Our target is the mid to upper range of normal, which usually means around 500 to 600 ng/dl. The concentration of testosterone in the blood actually goes up quite quickly, within a few doses. I usually measure it after two weeks, though symptoms may not change for a month or two.

Known as the "male hormone," testosterone is produced primarily by the testicles. "Beginning around age 30, testosterone levels begin to decline naturally and continue to do so as a man ages," says Holly Lucille, ND, RN, a naturopathic doctor, educator, and author, "sometimes leading to low testosterone symptoms such as depressed moods, decreased sex drive, erectile dysfunction, and difficulties with concentration and memory.”


However, testosterone is only one of many factors that aid in adequate erections. Research is inconclusive regarding the role of testosterone replacement in the treatment of erectile dysfunction. In a review of studies that looked at the benefit of testosterone in men with erection difficulties, showed no improvement with testosterone treatment. Many times, other health problems play a role in erectile difficulties. These can include:

If you have low testosterone, your functional medicine or anti-aging physician will help you diagnose it. There are several different hormones your physician should measure, but the most important two are your free testosterone and estrogen levels, because converting too much testosterone to estrogen is a problem that’s different from not making enough testosterone in the first place. In my case, I wasn’t making very much testosterone, and what I was making my body converted to estrogen way too effectively.
The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[82][83] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.[82] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[84] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.[85][86][87][88][89]
For the 3rd year in a row, DAA Max claims the #1 spot in the Top 10. A product that stands out in all categories with a formula that has been shown in studies to increase free testosterone levels after just 12 days of consistent use. DAA Max’s feedback over the years has shown that this product is not only potent in terms of elevating testosterone and boosting one’s libido, but at its low price it just can’t be beaten.
Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
It's important to understand that your body requires saturated fats from animal and vegetable sources (such as meat, dairy, certain oils, and tropical plants like coconut) for optimal functioning, and if you neglect this important food group in favor of sugar, grains and other starchy carbs, your health and weight are almost guaranteed to suffer. Examples of healthy fats you can eat more of to give your testosterone levels a boost include:
Smoking doesn’t promote maintaining male hormone levels healthy. The study has shown that smoking deprives the body from zinc. Zinc deficiency is dangerous for men because it is fraught with testosterone deficiency. The matter is that zinc is a kind of structural material for building the testosterone molecules. So, smoking combined with unhealthy diet strikes a blow against normal testosterone production.
Zinc: Another potent ingredient to add to any testosterone booster is zinc. This study shows how zinc is able to prevent a decline in testosterone levels during intense and hard workouts performed by wrestlers. Researchers found that the group who was administered with a placebo had a reduction in testosterone, as opposed to the group who were supplemented with zinc. The placebo group had a notable drop in their testosterone count during this process. Zinc has also been shown to increase the number of free testosterone and lower SHBG.

Testosterone may prove to be an effective treatment in female sexual arousal disorders,[52] and is available as a dermal patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.[52]


There have been case reports of development of prostate cancer in patients during treatment with testosterone, including one case series of twenty patients (Gaylis et al 2005). It is not known whether this reflects an increase in incidence, as prostate cancer is very common and because the monitoring for cancer in patients treated with testosterone is greater. Randomized controlled trials of testosterone treatment have found a low incidence of prostate cancer and they do not provide evidence of a link between testosterone treatment and the development of prostate cancer (Rhoden and Morgentaler 2004). More large scale clinical trials of longer durations of testosterone replacement are required to confirm that testosterone treatment does not cause prostate cancer. Overall, it is not known whether testosterone treatment of aging males with hypogonadism increases the risk of prostate cancer, but monitoring for the condition is clearly vital. This should take the form of PSA blood test and rectal examination every three months for the first year of treatment and yearly thereafter (Nieschlag et al 2005). Age adjusted PSA reference ranges should be used to identify men who require further assessment. The concept of PSA velocity is also important and refers to the rate of increase in PSA per year. Patients with abnormal rectal examination suggestive of prostate cancer, PSA above the age specific reference range or a PSA velocity greater than 0.75 ng/ml/yr should be referred to a urologist for consideration of prostate biopsy.

Grape seed extract is another ingredient with not enough research to suggest a dosage. Grape seed extract can interact with drugs like “blood thinners, NSAID painkillers (like aspirin, Advil, and Aleve), certain heart medicines, cancer treatments, and others.” If this sounds like you (or if you ever pop an Advil to clear off a headache), you’ll need to speak with a doctor to make sure this supplement is safe to take.

Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute HPA (hypothalamic–pituitary–adrenal axis) response under dominance challenge.[22] Androgen including testosterone enhances muscle growth. Testosterone also regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.[23][24]
Vitamin D3: Vitamin D3 is actually more hormone than it is a vitamin. Vitamin D is taken in by around 10% of our diets and D3 is mostly absorbed from the sun, which can be linked to greater testosterone production. The link between the two is a result from the luteinizing hormone playing its role. Read more about how vitamin D3 effects testosterone — the evidence is staggering.
Testosterone booster supplements are supplements that are used to either increase the amount of testosterone in someone’s body or increase the amount that can be used by the body without being converted into a different type of hormone. While it is a male sex hormone, women also produce some testosterone. People with low testosterone levels and some athletes choose to use testosterone booster supplements to increase their muscle mass, reduce their fat stores, strengthen their bones, and improve their sex drives, particularly as they approach middle age.
Well, this is another area of confusion and great debate, but I don’t think it’s as confusing as it appears to be in the literature. When most doctors learned about testosterone in medical school, they learned about total testosterone, or all the testosterone in the body. But about half of the testosterone that’s circulating in the bloodstream is not available to the cells. It’s tightly bound to a carrier molecule called sex hormone–binding globulin, which we abbreviate as SHBG.

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.


In addition to weightlifting, studies have shown that HIIT workouts can also help boost testosterone levels. For those of you who don’t know, HIIT stands for high-intensity interval training. It calls for short, intense bursts of exercise, followed by a less-intense recovery period. You repeat with the intense/less-intense cycle several times throughout the workout. In addition to increasing T, HIIT has been shown to improve athletic conditioning and fat metabolism, as well as increase muscle strength.
Grape seed extract is another ingredient with not enough research to suggest a dosage. Grape seed extract can interact with drugs like “blood thinners, NSAID painkillers (like aspirin, Advil, and Aleve), certain heart medicines, cancer treatments, and others.” If this sounds like you (or if you ever pop an Advil to clear off a headache), you’ll need to speak with a doctor to make sure this supplement is safe to take.
Many clinical studies have looked at the effect of testosterone treatment on body composition in hypogonadal men or men with borderline low testosterone levels. Some of these studies specifically examine these changes in older men (Tenover 1992; Morley et al 1993; Urban et al 1995; Sih et al 1997; Snyder et al 1999; Kenny et al 2001; Ferrando et al 2002; Steidle et al 2003; Page et al 2005). The data from studies, on patients from all age groups, are consistent in showing an increase in fat free mass and decrease in fat mass or visceral adiposity with testosterone treatment. A recent meta-analysis of 16 randomized controlled trials of testosterone treatment effects on body composition confirms this pattern (Isidori et al 2005). There have been less consistent results with regard to the effects of testosterone treatment of muscle strength. Some studies have shown an increase in muscle strength (Ferrando et al 2002; Page et al 2005) with testosterone whilst others have not (Snyder et al 1999). Within the same trial some muscle group strengths may improve whilst others do not (Ly et al 2001). It is likely that the differences are partly due to the methodological variations in assessing strength, but it also possible that testosterone has different effects on the various muscle groups. The meta-analysis found trends toward significant improvements in dominant knee and hand grip strength only (Isidori et al 2005).

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A side of garlic knots or onion bread can boost your sex drive … just make sure your date has a slice, too! Studies suggest a compound in the stinking rose triggers the release of luteinizing hormone, which regulates production of testosterone. One study showed supplementing with garlic as part of a high-protein diet could substantially boost testosterone levels. And a recent animal study found just 1 gram of onion per kg of body weight could boost T-levels by over 300 percent in just 20 days. Garlic and onions both contain the chemical diallyl disulfide, which stimulates the release of a hormone that spurs the production of testosterone.
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As with cognitive effects, previous studies examining CVD changes following testosterone treatment have been conflicting and inconclusive. Dr. Budoff and his research team used coronary computed tomographic angiography (CCTA) to assess 138 men, including 73 treated with testosterone and 65 receiving placebo, for changes in coronary artery plaque volume after 1 year.
True Grit supplements have absolutely nothing to hide. That’s why there are no proprietary blends in any True Grit product. Proprietary blends are used by some brands to hide that they are using underdosed levels of premium ingredients. That’s not what True GritTM is about. True Grit supplements contain premium, fully dosed key ingredients, so you’ll know exactly what is in the supplement you’re putting in your body.

‘Testosterone boosting’ products  - found online, or in health food or body-building shops, these products claim to boost testosterone levels if you buy them. The majority of these products will not have the effect you want and are not worth spending money on. Any of these products that do have a real effect may have a form of prescription medication in which is both dangerous and illegal.


Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[146] Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[147] Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[148][149][150] Licorice can decrease the production of testosterone and this effect is greater in females.[151]
14. Volek JS, Volk BM, Gómez AL, Kunces LJ, Kupchak BR, Freidenreich DJ, Aristizabal JC, Saenz C, Dunn-Lewis C, Ballard KD, Quann EE, Kawiecki DL, Flanagan SD, Comstock BA, Fragala MS, Earp JE, Fernandez ML, Bruno RS, Ptolemy AS, Kellogg MD, Maresh CM, Kraemer WJ. Whey protein supplementation during resistance training augments lean body mass. J Am Coll Nutr. 2013;32(2):122-35. PMID: 24015719
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
Present in much greater levels in men than women, testosterone initiates the development of the male internal and external reproductive organs during foetal development and is essential for the production of sperm in adult life. This hormone also signals the body to make new blood cells, ensures that muscles and bones stay strong during and after puberty and enhances libido both in men and women. Testosterone is linked to many of the changes seen in boys during puberty (including an increase in height, body and pubic hair growth, enlargement of the penis, testes and prostate gland, and changes in sexual and aggressive behaviour). It also regulates the secretion of luteinising hormone and follicle stimulating hormone. To effect these changes, testosterone is often converted into another androgen called dihydrotestosterone. 
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