A 2010 study published in the journal Hormones and Behavior first suggested this when researchers evaluated the “dual-hormone hypothesis” clinically. (11) They discovered that when cortisol is elevated, testosterone responds by elevating as well but soon after bottoms out at a much lower level than before cortisol kicked in! That means you want to find ways to relieve stress to keep your testosterone levels up.
In fact, testosterone supplements might cause more problems than they solve. Studies have suggested a connection between supplements and heart problems. A 2010 study reported in The New England Journal of Medicine showed that some men over age 65 had an increase in heart problems when they used testosterone gel. A later of men younger than 65 at risk for heart problems and heart-healthy older men showed that both groups had a greater risk of heart attack when taking testosterone supplements.
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).
A large number of side-effects have been attributed to testosterone. In our clinical experience, the incidence of significant adverse effects with treatment producing physiological testosterone levels is low, and many side effects attributed to testosterone are mainly relevant to supraphysiological replacement. Some adverse effects are specific to a given mode of delivery and have already been described. Potential adverse effects concerning the prostate have also been discussed and require appropriate monitoring of symptoms, PSA and digital rectal examination. Other tumors which may be androgen responsive include cancer of the breast and primary liver tumors, and these are both contraindications to testosterone treatment
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).

A team led by Dr. Joel Finkelstein at Massachusetts General Hospital investigated testosterone and estradiol levels in 400 healthy men, 20 to 50 years of age. To control hormone levels, the researchers first gave the participants injections of a drug that suppressed their normal testosterone and estradiol production. The men were randomly assigned to 5 groups that received different amounts (from 0 to 10 grams) of a topical 1% testosterone gel daily for 16 weeks. Half of the participants were also given a drug to block testosterone from being converted to estradiol.


To get a good dietary source of selenium, you can eat shellfish or Brazilian nuts. 1-2 Brazilian nuts is enough to get 200% of your daily intake. You don’t need any more than that. Read more about increasing testosterone with Brazilian nuts here. It’s a good idea to get your selenium levels checked before hand and then adjust your diet as needed to avoid selenium toxicity.

At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.


The reliable measurement of serum free testosterone requires equilibrium dialysis. This is not appropriate for clinical use as it is very time consuming and therefore expensive. The amount of bioavailable testosterone can be measured as a percentage of the total testosterone after precipitation of the SHBG bound fraction using ammonium sulphate. The bioavailable testosterone is then calculated from the total testosterone level. This method has an excellent correlation with free testosterone (Tremblay and Dube 1974) but is not widely available for clinical use. In most clinical situations the available tests are total testosterone and SHBG which are both easily and reliably measured. Total testosterone is appropriate for the diagnosis of overt male hypogonadism where testosterone levels are very low and also in excluding hypogonadism in patients with normal/high-normal testosterone levels. With increasing age, a greater number of men have total testosterone levels just below the normal range or in the low-normal range. In these patients total testosterone can be an unreliable indicator of hypogonadal status. There are a number of formulae that calculate an estimated bioavailable or free testosterone level using the SHBG and total testosterone levels. Some of these have been shown to correlate well with laboratory measures and there is evidence that they more reliably indicate hypogonadism than total testosterone in cases of borderline biochemical hypogonadism (Vermeulen et al 1971; Morris et al 2004). It is important that such tests are validated for use in patient populations relevant to the patient under consideration.


We kept it simple, and followed the premise of testosterone boosters: testosterone affects muscle gain, weight loss, and libido, so by increasing the amount of testosterone in the body, we can improve on each of those goals. This meant that we looked for ingredients proven to increase testosterone levels, not ingredients that might increase libido or help build muscle mass independently of testosterone (like having a healthy diet and feeling good about yourself). In addition, we dove deep into the specific ingredient lists of our finalists and cross-checked them against WebMD and the National Institutes of Health (NIH) database to make sure that they did not contain ingredients known to be harmful.
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.
We kept it simple, and followed the premise of testosterone boosters: testosterone affects muscle gain, weight loss, and libido, so by increasing the amount of testosterone in the body, we can improve on each of those goals. This meant that we looked for ingredients proven to increase testosterone levels, not ingredients that might increase libido or help build muscle mass independently of testosterone (like having a healthy diet and feeling good about yourself). In addition, we dove deep into the specific ingredient lists of our finalists and cross-checked them against WebMD and the National Institutes of Health (NIH) database to make sure that they did not contain ingredients known to be harmful.
Testosterone is a hormone that is secreted in both men and women. It is responsible for sex drive, as well as protein processing for muscle mass development and strength. Testosterone declines with age, illness and poor nutrition in both genders, though this change may be more marked in men. Synthetic hormone replacement therapy can cause adverse side effects. A natural way to raise the body’s testosterone levels safely include supplementing the diet with specific nutrients and physical exercise.

For men with low blood testosterone levels, the benefits of hormone replacement therapy 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. "I can't tell you for certain that this raises your personal risk of heart problems and prostate cancer, or that it doesn't," Dr. Pallais says.
With the decline of ovarian function in menopause, not only do estrogen levels decline, but so does testosterone availability, since the ovaries contribute, either by direct secretion or through precursor production, about 50 percent of circulating testosterone. The other 50 percent is supplied by the adrenal glands. Many post-menopausal or oophorectomized women are symptomatic as a consequence of reduced testosterone, the leading symptom being loss of libido (Sherwin and Gelfand 1987; Simon et al 2005). There is an increasing trend toward testosterone supplementation in these women. Such supplementation may also lead, not only to increased libido, but to increased bone mineral density and an improvement in general overall sense of well-being including energy, strength, motivation and mood (Davis et al 1995; Davis et al 2000).
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.
6. Foods rich in vitamin D. If you’ve been thinking of increasing your testosterone levels, you better stock up on those mushrooms, salmon and milk. Clinical Endocrinology’s August 2010 issue published a study that was conducted by Austria’s Medical University Graz. According to the researchers, mushroom, salmon and dairy products are examples of food that are rich in Vitamin D. These researchers also found a relationship between Vitamin D and testosterone. Their study has shown that individuals with high levels of Vitamin D also had high testosterone levels. The obvious inverse relationship was true as well.  Click here for a convincing study on HUMAN BEINGS to back this up.

Now you know I prefer studies conducted on human participants instead of rodents, but often there is no choice.  A Japanese study on rats that you can read here: http://jn.nutrition.org/content/131/8/2150.short has demonstrated pretty convincingly that garlic supplementation significantly increases testosterone.  I wish there were more tests on humans but it turns out garlic isn’t patentable (sorry Monsanto) which means there isn’t enough financial interest to warrant human studies.  Maybe I’ll conduct one.  Any volunteers?
Take 250 mg of Forskolin, standardized to 10 percent, twice a day. Take one serving before training and the other with a meal. According to "Natural Anabolics," Forskolin decreased body fat and increased free testosterone levels in training individuals as compared to a placebo. Forskolin comes from the herb coleus forskohlii and is also known as Forslean.
Testosterone is included in the World Health Organization's list of essential medicines, which are the most important medications needed in a basic health system.[107] It is available as a generic medication.[10] The price depends on the form of testosterone used.[108] It can be administered as a cream or transdermal patch that is applied to the skin, by injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.[10]
Kostic TS, Stojkov NJ, Bjelic MM, Mihajlovic AI, Janjic MM, Andric SA: Pharmacological doses of testosterone upregulated androgen receptor and 3-Beta-hydroxysteroid dehydrogenase/delta-5-delta-4 isomerase and impaired leydig cells steroidogenesis in adult rats. Toxicol Sci. 2011 Jun;121(2):397-407. doi: 10.1093/toxsci/kfr063. Epub 2011 Apr 6. [PubMed:21427060]

Overall, it seems that both estrogen and testosterone are important for normal bone growth and maintenance. Deficiency or failure of action of the sex hormones is associated with osteoporosis and minimal trauma fractures. Estrogen in males is produced via metabolism of testosterone by aromatase and it is therefore important that androgens used for the treatment of hypogonadism be amenable to the action of aromatase to yield maximal positive effects on bone. There is data showing that testosterone treatment increases bone mineral density in aging males but that these benefits are confined to hypogonadal men. The magnitude of this improvement is greater in the spine than in the hip and further studies are warranted to confirm or refute any differential effects of testosterone at these important sites. Improvements seen in randomized controlled trials to date may underestimate true positive effects due to relatively short duration and/or baseline characteristics of the patients involved. There is no data as yet to confirm that the improvement in bone density with testosterone treatment reduces fractures in men and this is an important area for future study.
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.[151] 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.[2][151][157][158] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[159] skin, hair follicles, and brain[160] and aromatase is highly expressed in adipose tissue, bone, and the brain.[161][162] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[152] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[163] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[164]
Testosterone is the primary sex hormone in men, and it is responsible for the development of many of the physical characteristics that are considered typically male. Women also produce the hormone in much smaller amounts. Testosterone, part of a hormone class known as androgens, is produced by the testicles after stimulation by the pituitary gland, which is located near the base of the brain, and it sends signals to a male's testicles (or to a woman's ovaries) that spark feelings of sexual desire. (1)
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.
Natural remedies for treating erectile dysfunction Erectile dysfunction has many causes, can affect any male, and is often distressing? Some people advocate several different natural remedies, mostly herbs and other plants. Here, we look at their merits and side effects, plus lifestyle changes, and alternative therapies that may bring relief for erectile dysfunction. Read now
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