Dr. Anthony’s Notes: Vitamin D has about 100 other beneficial body functions outside of it's impact on testosterone. Make sure you take the active Vitamin D3 (not D2 – from plant sources!) It’s also advisable to get 20 minutes of sunshine daily (weather permitting) – without sunscreen. Verdict: this is one of the natural testosterone supplements that work. Best Food Sources of Vitamin D3: Wild Alaskan Salmon (#1), Sardines, Eggs How To Take Vitamin D3: Using 3000-5000IU of Vitamin D3 per day is a good safe, research supported dose. Your physician can also test your blood for D3 levels for more precise monitoring.
Unlike aerobics or prolonged moderate exercise, short, intense exercise was found to be beneficial in increasing testosterone levels. The results are enhanced with the help of intermittent fasting. Intermittent fasting helps boost testosterone by improving the expression of satiety hormones, like insulin, leptin, adiponectin, glucacgon-like peptide-1 (GLP-1), cholecystokinin (CKK), and melanocortins, which are linked to healthy testosterone function, increased libido, and the prevention of age-induced testosterone decline. When it comes to an exercise plan that will complement testosterone function and production (along with overall health), I recommend including not just aerobics in your routine, but also:

^ Mehta PH, Jones AC, Josephs RA (Jun 2008). "The social endocrinology of dominance: basal testosterone predicts cortisol changes and behavior following victory and defeat" (PDF). Journal of Personality and Social Psychology. 94 (6): 1078–93. CiteSeerX 10.1.1.336.2502. doi:10.1037/0022-3514.94.6.1078. PMID 18505319. Archived from the original (PDF) on April 19, 2009.


While it would be nice to buy a testosterone pill from the local supplement store and have your testosterone levels go up, such a magic pill does not exist. As you can see from the above rundown, while a few supplements may be somewhat effective if your T levels are already low, none will significantly raise your testosterone above a baseline level. Thus, the basics of keeping your T levels high remain pretty simple:
Vitamin D supplementation may potentially boost testosterone levels, but further research is needed to determine if it really has an effect on the testosterone levels of young people and athletes. The truth is likely similar to zinc and magnesium — being in a deficient state causes your testosterone levels to drop below baseline, and supplementing it just takes you right back to baseline (but not any higher).
The biggest change I made to my diet was increasing my fat and cholesterol intake. There’s a reason why old school strong men would drink raw eggs — studies have suggested that higher fat and cholesterol consumption results in increased levels of total T; men eating low-fat diets typically have decreased testosterone levels. The emphasis on increasing fat and cholesterol consumption meant I got to eat like Ron Swanson for three months — bacon and eggs and steak was pretty much the staple of my diet.
Michael T. Murray, ND, is widely regarded as one of the leading authorities on natural medicine. He is the author of many books, including the classic Encyclopedia of Nutritional Supplements. His latest book is What the Drug Companies Won’t Tell You and Your Doctor Doesn’t Know. Visit him online at doctormurray.com.   Article Courtesy of Better Nutrition  
Like most supplements, Beast Sports contains several ingredients with little research about their long-term effects. WebMD describes Suma powder, Rhodiola Rosea, Cissus quadrangularis, Tribulus extract, and ashwagandha extract as possibly safe when taken for a short period of time (usually around 6-10 weeks). However, their long-term safety remains unknown. It also has a few ingredients, like cyanotis vaga root, safed musli, and polygonum cispidatum root extract for which there is a lack of data on even short term safety.
Intramuscular testosterone injections were first used around fifty years ago. Commercially available preparations contain testosterone esters in an oily vehicle. Esterification is designed to retard the release of testosterone from the depot site into the blood because the half life of unmodified testosterone would be very short. For many years intramuscular preparations were the most commonly used testosterone therapy and this is still the case in some centers. Pain can occur at injection sites, but the injections are generally well tolerated and free of major side effects. Until recently, the available intramuscular injections were designed for use at a frequency of between weekly and once every four weeks. These preparations are the cheapest mode of testosterone treatment available, but often cause supraphysiological testosterone levels in the days immediately following injection and/or low trough levels prior to the next injection during which time the symptoms of hypogonadism may return (Nieschlag et al 1976). More recently, a commercial preparation of testosterone undecanoate for intramuscular injection has become available. This has a much longer half life and produces testosterone levels in the physiological range throughout each treatment cycle (Schubert et al 2004). The usual dose frequency is once every three months. This is much more convenient for patients but does not allow prompt cessation of treatment if a contraindication to testosterone develops. The most common example of this would be prostate cancer and it has therefore been suggested that shorter acting testosterone preparations should preferably used for treating older patients (Nieschlag et al 2005). Similar considerations apply to the use of subcutaneous implants which take the form of cylindrical pellets injected under the skin of the abdominal wall and steadily release testosterone to provide physiological testosterone levels for up to six months. Problems also include pellet extrusion and infection (Handelsman et al 1997).

The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)".[180] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.[181][182]
As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone. 
Autopsy studies have found histological prostate cancer to be very common, with one series showing a prevalence of greater than fifty percent in men over age sixty (Holund 1980). The majority of histological cancers go undetected so that the clinical incidence of the disease is much lower, but it is still the most prevalent non-skin cancer in men (Jemal et al 2003). Prostate cancer is also unusual in comparison to other adult cancers in that the majority of those with the disease will die of other causes. Treatment of prostate cancer with androgen deprivation is known to be successful and is widely practiced, indicating an important role for testosterone in modifying the behavior of prostate cancer. In view of this, testosterone treatment is absolutely contraindicated in any case of known or suspected prostate cancer. The question of whether testosterone treatment could cause new cases of prostate cancer, or more likely cause progression of undiagnosed histological prostate cancer that would otherwise have remained occult, is an important consideration when treating ageing males with testosterone.
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.
Recently, a panel with cooperation from international andrology and urology societies, published specific recommendations with regard to the diagnosis of Late-onset Hypogonadism (Nieschlag et al 2005). These are summarized in the following text. It is advised that at least two serum testosterone measurements, taken before 11 am on different mornings, are necessary to confirm the diagnosis. The second sample should also include measurement of gonadotrophin and prolactin levels, which may indicate the need for further investigations for pituitary disease. Patients with serum total testosterone consistently below 8 nmol/l invariably demonstrate the clinical syndrome of hypogonadism and are likely to benefit from treatment. Patients with serum total testosterone in the range 8–12 nmol/l often have symptoms attributable to hypogonadism and it may be decided to offer either a clinical trial of testosterone treatment or to make further efforts to define serum bioavailable or free testosterone and then reconsider treatment. Patients with serum total testosterone persistently above 12 nmol/l do not have hypogonadism and symptoms are likely to be due to other disease states or ageing per se so testosterone treatment is not indicated.
In males, testosterone is synthesized primarily in Leydig cells. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase.[128]
There are several supplements on the market claiming to be natural testosterone boosters. I get these sorts of things in the mail all time. The companies that produce these products claim that the herbs (typically stinging nettle and tribulus) in their pills increase free testosterone by reducing SHBG. They also throw in some B vitamins for “increased energy and vitality.”
Vitamin C (unnecessary). I don’t know where I first heard about vitamin C’s supposed T-boosting benefits, but it’s one of those things you see all over the internet when you Google “how to increase testosterone.” Without trying to find the research that backs up that claim, I took a vitamin C supplement during my experiment. I later found some research that suggests that vitamin C does increase testosterone levels in diabetic mice, but because I wasn’t diabetic (nor a mouse), I’m not sure how much the vitamin C helped. I’ve actually stopped taking vitamin C supplements. I’m likely getting more than enough with my diet. Unless you have diabetes, you probably won’t see much benefit from this supplement. Don’t waste your money.

Vitamin D supplementation may potentially boost testosterone levels, but further research is needed to determine if it really has an effect on the testosterone levels of young people and athletes. The truth is likely similar to zinc and magnesium — being in a deficient state causes your testosterone levels to drop below baseline, and supplementing it just takes you right back to baseline (but not any higher).

Unlike aerobics or prolonged moderate exercise, short, intense exercise was found to be beneficial in increasing testosterone levels. The results are enhanced with the help of intermittent fasting. Intermittent fasting helps boost testosterone by improving the expression of satiety hormones, like insulin, leptin, adiponectin, glucacgon-like peptide-1 (GLP-1), cholecystokinin (CKK), and melanocortins, which are linked to healthy testosterone function, increased libido, and the prevention of age-induced testosterone decline. When it comes to an exercise plan that will complement testosterone function and production (along with overall health), I recommend including not just aerobics in your routine, but also:
Men can experience a range of symptoms if testosterone decreases more than it should. Low testosterone, or low T, is diagnosed when levels fall below 300 nanograms per deciliter (ng/dL). A normal range is typically 300–1000 ng/dL, according to the U.S. Food and Drug Administration. A blood test called a serum testosterone test is used to determine your level of circulating testosterone.

Hypogonadism is a disease in which the body is unable to produce normal amounts of testosterone due to a problem with the testicles or with the pituitary gland that controls the testicles. Testosterone replacement therapy can improve the signs and symptoms of low testosterone in these men. Doctors may prescribe testosterone as injections, pellets, patches or gels.
×