Cross-sectional studies have found a positive association between serum testosterone and some measures of cognitive ability in men (Barrett-Connor, Goodman-Gruen et al 1999; Yaffe et al 2002). Longitudinal studies have found that free testosterone levels correlate positively with future cognitive abilities and reduced rate of cognitive decline (Moffat et al 2002) and that, compared with controls, testosterone levels are reduced in men with Alzheimer’s disease at least 10 years prior to diagnosis (Moffat et al 2004). Studies of the effects of induced androgen deficiency in patients with prostate cancer have shown that profoundly lowering testosterone leads to worsening cognitive functions (Almeida et al 2004; Salminen et al 2004) and increased levels of serum amyloid (Gandy et al 2001; Almeida et al 2004), which is central to the pathogenesis of Alzheimer’s disease (Parihar and Hemnani 2004). Furthermore, testosterone reduces amyloid-induced hippocampal neurotoxity in vitro (Pike 2001) as well as exhibiting other neuroprotective effects (Pouliot et al 1996). The epidemiological and experimental data propose a potential role of testosterone in protecting cognitive function and preventing Alzheimer’s disease.
Testosterone is more than a “male sex hormone”. It is an important contributor to the robust metabolic functioning of multiple bodily systems. The abuse of anabolic steroids by athletes over the years has been one of the major detractors from the investigation and treatment of clinical states that could be caused by or related to male hypogonadism. The unwarranted fear that testosterone therapy would induce prostate cancer has also deterred physicians form pursuing more aggressively the possibility of hypogonadism in symptomatic male patients. In addition to these two mythologies, many physicians believe that testosterone is bad for the male heart. The classical anabolic agents, 17-alkylated steroids, are, indeed, potentially harmful to the liver, to insulin action to lipid metabolism. These substances, however, are not testosterone, which has none of these adverse effects. The current evidence, in fact, strongly suggests that testosterone may be cardioprotective. There is virtually no evidence to implicate testosterone as a cause of prostate cancer. It may exacerbate an existing prostate cancer, although the evidence is flimsy, but it does not likely cause the cancer in the first place. Testosterone has stimulatory effects on bones, muscles, erythropoietin, libido, mood and cognition centres in the brain, penile erection. It is reduced in metabolic syndrome and diabetes and therapy with testosterone in these conditions may provide amelioration by lowering LDL cholesterol, blood sugar, glycated hemoglobin and insulin resistance. The best measure is bio-available testosterone which is the fraction of testosterone not bound to sex hormone binding globulin. Several forms of testosterone administration are available making compliance much less of an issue with testosterone replacement therapy.
Total levels of testosterone in the body are 264 to 916 ng/dL in men age 19 to 39 years,[165] while mean testosterone levels in adult men have been reported as 630 ng/dL.[166] Levels of testosterone in men decline with age.[165] In women, mean levels of total testosterone have been reported to be 32.6 ng/dL.[167][168] In women with hyperandrogenism, mean levels of total testosterone have been reported to be 62.1 ng/dL.[167][168]
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.
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).
The researchers found that the dose of testosterone required to produce different effects in the body varied widely. The influence of testosterone and estradiol also differed. As the testosterone gel dose was reduced, the scientists showed, reductions in lean mass, muscle size, and leg-press strength resulted from decreases in testosterone itself. In contrast, increases in body fat were due to the related declines in estradiol. Both testosterone and estradiol levels were associated with libido and erectile function.
Another effect that can limit treatment is polycythemia, which occurs due to various stimulatory effects of testosterone on erythropoiesis (Zitzmann and Nieschlag 2004). Polycythemia is known to produce increased rates of cerebral ischemia and there have been reports of stroke during testosterone induced polycythaemia (Krauss et al 1991). It is necessary to monitor hematocrit during testosterone treatment, and hematocrit greater than 50% should prompt either a reduction of dose if testosterone levels are high or high-normal, or cessation of treatment if levels are low-normal. On the other hand, late onset hypogonadism frequently results in anemia which will then normalize during physiological testosterone replacement.
Sexual arousal - boosting testosterone can improve sexual arousal, even if you have normal testosterone levels. Higher levels of testosterone can make it easier for you to get aroused and can boost your sex drive generally. While this doesn’t affect the physical action of your erections, if you are not getting hard because you’re not aroused then boosting testosterone could help.

Every vitamin, mineral, and ingredient that affects the human body can be taken in enough quantities that they are harmful, or toxic, even the ones that — at lower levels — are beneficial or necessary. Unfortunately, testosterone boosters contain a lot of ingredients that are not well understood. This means in addition to not being able to confirm whether certain ingredients increase testosterone, the scientific and medical communities also don’t know at what levels many ingredients become toxic. On the up side, you might need to eat several pounds of a particular leafy plant before it becomes harmful. On the down side, it could be significantly less that pushes you over your body’s limit. We simply don’t know how little or how much the human body can tolerate. We recommend keeping your doctor in the loop when you add any supplement with unproven ingredients into your diet — they’ll be able to help you find and track any undesired side-effects that these ingredients might cause.
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.
Does the diminution that age brings with it in both total and bioavailable T have any clinical significance? This question leads us to the theme of this paper, “The Many Faces of Testosterone”. If testosterone were simply a “sex hormone” involved only with sexual desire and arousal we might tend to dismiss testosterone treatment in the aging man as merely a “life-style” therapy without any substantive basis for broad physiological necessity. The fact is, however, that the sexual attributes of testosterone are the least of its physiological necessities and that testosterone has a broad spectrum of demonstrated physiological functions as well as a wide variety of physiological and pathophysiological associations about which we are just learning.
In order to discuss the biochemical diagnosis of hypogonadism it is necessary to outline the usual carriage of testosterone in the blood. Total serum testosterone consists of free testosterone (2%–3%), testosterone bound to sex hormone binding globulin (SHBG) (45%) and testosterone bound to other proteins (mainly albumin −50%) (Dunn et al 1981). Testosterone binds only loosely to albumin and so this testosterone as well as free testosterone is available to tissues and is termed bioavailable testosterone. Testosterone bound to SHBG is tightly bound and is biologically inactive. Bioavailable and free testosterone are known to correlate better than total testosterone with clinical sequelae of androgenization such as bone mineral density and muscle strength (Khosla et al 1998; Roy et al 2002). There is diurnal variation in serum testosterone levels with peak levels seen in the morning following sleep, which can be maintained into the seventh decade (Diver et al 2003). Samples should always be taken in the morning before 11 am to allow for standardization.
Testosterone treatment is unequivocally needed in classical hypogonadism for reasons discussed in subsequent subsections. In classical hypogonadism, testosterone production is usually clearly below the lower limit of normal and patients are highly symptomatic; the various symptoms are easily related to the deficiencies in various bodily systems where testosterone action is important. Symptoms of testosterone deficiency are listed in Table 2. A few prominent causes of classical hypogonadism are listed in Table 3.
The natural production of DHEA is also age-dependent. Prior to puberty, the body produces very little DHEA. Production of this prohormone peaks during your late 20’s or early 30’s. With age, DHEA production begins to decline. The adrenal glands also manufacture the stress hormone cortisol, which is in direct competition with DHEA for production because they use the same hormonal substrate known as pregnenolone. Chronic stress basically causes excessive cortisol levels and impairs DHEA production, which is why stress is another factor for low testosterone levels.
This evidence, together with the beneficial effects of testosterone replacement on central obesity and diabetes, raises the question whether testosterone treatment could be beneficial in preventing or treating atherosclerosis. No trial of sufficient size or duration has investigated the effect of testosterone replacement in primary or secondary prevention cardiovascular disease. The absence of such data leads us to examine the relationship of testosterone to other cardiovascular risk factors, such as adverse lipid parameters, blood pressure, endothelial dysfunction, coagulation factors, inflammatory markers and cytokines. This analysis can supply evidence of the likely effects of testosterone on overall cardiovascular risk. This has limitations, however, including the potential for diverging effects of testosterone on the various factors involved and the resultant impossibility of accurately predicting the relative impact of such changes.

There is also solid research indicating that if you take astaxanthin in combination with saw palmetto, you may experience significant synergistic benefits. A 2009 study published in the Journal of the International Society of Sports Nutrition found that an optimal dose of saw palmetto and astaxanthin decreased both DHT and estrogen while simultaneously increasing testosterone.6 Also, in order to block the synthesis of excess estrogen (estradiol) from testosterone there are excellent foods and plant extracts that may help to block the enzyme known as aromatase which is responsible producing estrogen. Some of these include white button mushrooms, grape seed extract and nettles.7

^ Jump up to: a b Sapienza P, Zingales L, Maestripieri D (September 2009). "Gender differences in financial risk aversion and career choices are affected by testosterone". Proceedings of the National Academy of Sciences of the United States of America. 106 (36): 15268–73. Bibcode:2009PNAS..10615268S. doi:10.1073/pnas.0907352106. PMC 2741240. PMID 19706398.
We all remember the time during our teens where our body underwent majority of its changes that led us into adulthood. As far as testosterone levels go, this period of time is where the production of this hormone peaked. Testosterone levels during these teenage years remain high and consistent, and therefore it is not advisable to use a testosterone boosting supplement during this time. This is because, Natural Testosterone Boosters work by encouraging your body to increase it;s natural levels back to their maximum capacity. If your body is already producing it’s maximum amount of Testosterone, these products will be ineffective for you. You should be prioritising quality, intense training sessions with adequate nutrition, rich in protein and carbohydrates to elicit growth and repair.
Unfortunately, in the modern world, stresses and emotional exhaustion lie in wait for men at every step. Nowadays, burnout is a constant state for many men. Of course, this causes great harm to the men’s health. Stresses drain of vitality and affect emotional state. Besides, they are also very dangerous for the nervous system. The nature is wise. And the body of a man who is not subject to stress can produce more testosterone.
As you cut these dietary troublemakers from your meals, you need to replace them with healthy substitutes like vegetables and healthy fats (including natural saturated fats!). Your body prefers the carbohydrates in micronutrient-dense vegetables rather than grains and sugars because it slows the conversion to simple sugars like glucose, and decreases your insulin level. When you cut grains and sugar from your meals, you typically will need to radically increase the amount of vegetables you eat, as well as make sure you are also consuming protein and healthy fats regularly.
Withania Somnifera is another name for Ashwagandha which is an ancient herb used as a medicine. It is an adaptogen because it helps the body to handle anxiety and stress. It improves T levels along with increasing sperm production. Other than improvement in sexual performance it also helps in fat loss, strength, and stamina. It reduces the stress by reducing the output of the cortisol hormone, which acts antagonist to testosterone. This reduction helps to body to trigger the testosterone production.
Directions — SUGGESTED USE: As a dietary supplement take 3 capsules daily, preferably with a meal, or as directed by a healthcare professional. — Take two capsules with a meal twice a day. On days that you are not training, take two capsules in the morning and two capsules at night. On days that you train, take two capsules about an hour before workouts and take two capsules in the morning or at night depending on when you train.
Dr. Anthony's Notes: When evaluating the efficacy of a product, it’s tough to balance the currently available human research with thousands of years of anecdotal evidence of efficacy. Tongkat Ali is a perfect example. All of the current studies are on animal models (not humans) – this DOES NOT mean that Tongkat Ali doesn’t work with humans. It simply means more research is needed. Personally, the strong experience of thousands of men (myself included) using this herb can confirm it’s libido enhancing effects. Also, this herb is DAMN BITTER. It makes Maca powder seem like a walk in the park. Hide in a smoothie or you will be sorry haha! How To Take Tongkat Ali: 200-300mg (of a 100:1 extract) 1-2 times per day. If you are using the raw powder (recommended below) that is NOT encapsulated, definitely hide the powder in a fat burning smoothie like the “Fit Father Fat Burning Shake Recipe” we recommend in FF30X. Again, I cannot understand how damn nasty this powder tastes. Beware!
Total levels of testosterone in the body are 264 to 916 ng/dL in men age 19 to 39 years,[165] while mean testosterone levels in adult men have been reported as 630 ng/dL.[166] Levels of testosterone in men decline with age.[165] In women, mean levels of total testosterone have been reported to be 32.6 ng/dL.[167][168] In women with hyperandrogenism, mean levels of total testosterone have been reported to be 62.1 ng/dL.[167][168]
A: According to the NIH, normal values for testosterone levels in men can range from 300 to 1,200ng/dL. There can be many different causes of low testosterone including age, diseases, accidents, and medications. Symptoms of low testosterone may include: loss of sex drive, erectile dysfunction, depressed mood, and difficulty concentrating. Low testosterone levels may also bring around body changes including: hair loss, decrease in blood cells possibly leading to anemia, fragile bones, and a decrease in muscle mass. There are different testosterone replacement therapies including patches, such as Androderm; gels, such as Androgel and Testim; and injections, such as testosterone cypionate. Only your health care provider can decide if and what kind of testosterone replacement therapy is appropriate for you. Testosterone replacement therapy is not right for everyone. Patient with certain prostate issues or breast cancer should not take testosterone. For more specific information, consult with your doctor for guidance based on your health status and current medications, particularly before taking any action. Kristen Dore, PharmD
So, how does one ensure that testosterone levels remain in balance? Some doctors suggest that monitoring testosterone levels every five years, starting at age 35, is a reasonable strategy to follow. If the testosterone level falls too low or if the individual has the signs and symptoms of low testosterone levels described above, testosterone therapy can be considered. However, once testosterone therapy is initiated, testosterone levels should be closely monitored to make sure that the testosterone level does not become too high, as this may cause stress on the individual, and high testosterone levels may result in some of the negative problems (described previously) seen.
Testosterone is an essential hormone for men, and a decline in the levels can occur due to many reasons, but these natural supplements are great. They are safe to use and don’t have any side effects, that’s why you can take these supplements without doctor consultations. But if you have any other health issues, then consult a doctor before taking them.

Boron, a mineral, keeps the cell walls of plants strong. Eating dried fruits and nuts gives you abundant amounts of boron. You can also take boron supplements. It's important to keep your daily boron intake at less than 20 mg, however, according to a current factsheet available from the U.S. National Library of Medicine. High doses of boron can cause serious side effects such as skin inflammation and peeling, irritability, tremors or depression.


Binge drinking on the other hand does impact Testosterone levels – especially on a short term basis. Two studies (22 & 23) show that large acute quantities of alcohol consumption in a short period led to decreases in Testosterone levels by a whooping 20-23% after 24hours! Note however this is drinking to extreme excess! Likewise, chronic alcohol abuse is known to reduce testosterone more notably (as seen in alcoholics).
Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition.[77] The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression.[77] Thus it is the challenge of competition among males of the species that facilitates aggression and violence.[77] Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels.[77] The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.[77]

There is a negative correlation of testosterone levels with plasminogen activator inhibitor-1 (PAI-1) (Glueck et al 1993; Phillips 1993), which is a major prothrombotic factor and known to be associated with progression of atherosclerosis, as well as other prothrombotic factors fibrinogen, α2-antiplasmin and factor VII (Bonithon-Kopp et al 1988; Glueck et al 1993; Phillips 1993; De Pergola et al 1997). There is a positive correlation with tissue plasminogen activator (tPA) which is one of the major fibrinolytic agents (Glueck et al 1993). Interventional trials have shown a neutral effect of physiological testosterone replacement on the major clotting factors (Smith et al 2005) but supraphysiological androgen administration can produce a temporary mild pro-coagulant effect (Anderson et al 1995).
Anabolic–androgenic steroids (AASs) are synthetic derivatives of testosterone that are commonly used among athletes aged 18–40 years, but many reports have demonstrated the presence of numerous toxic and hormonal effects as a result of long-term use of an AAS.[9] Testosterone-foods act as natural libido boosters. Due to the growing interest in herbal ingredients and other dietary supplements worldwide, the use of testosterone boosters is becoming more and more mainstream among athletes, but several side effects were documented. Hence, this study established to help in the assessment of the side effects and health risks which could occur among athletes consuming testosterone boosters.
Testosterone boosters are a class of herbal supplements aimed at naturally increasing your testosterone levels. Usually, they contain micronutrients that men are commonly deficient in, such as zinc, and which have been connected in research to healthy testosterone levels. They also may contain adaptogens, which are a class of supplement that are thought to help the body adapt to stress, or ingredients which have been connected to improved sleep. Sleep restriction has been shown to reduce testosterone in healthy young men, and as Chris Lockwood, Ph.D., notes, disturbed sleep is a common symptom of low T-levels.[1]
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:
This evidence, together with the beneficial effects of testosterone replacement on central obesity and diabetes, raises the question whether testosterone treatment could be beneficial in preventing or treating atherosclerosis. No trial of sufficient size or duration has investigated the effect of testosterone replacement in primary or secondary prevention cardiovascular disease. The absence of such data leads us to examine the relationship of testosterone to other cardiovascular risk factors, such as adverse lipid parameters, blood pressure, endothelial dysfunction, coagulation factors, inflammatory markers and cytokines. This analysis can supply evidence of the likely effects of testosterone on overall cardiovascular risk. This has limitations, however, including the potential for diverging effects of testosterone on the various factors involved and the resultant impossibility of accurately predicting the relative impact of such changes.
Like other steroid hormones, testosterone is derived from cholesterol (see figure).[124] 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.[125] 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.

Testosterone is a steroid sex hormone found in both men and women. In men, testosterone is produced primarily by the Leydig (interstitial) cells of the testes when stimulated by luteinizing hormone (LH). It functions to stimulate spermatogenesis, promote physical and functional maturation of spermatozoa, maintain accessory organs of the male reproductive tract, support development of secondary sexual characteristics, stimulate growth and metabolism throughout the body and influence brain development by stimulating sexual behaviors and sexual drive. In women, testosterone is produced by the ovaries (25%), adrenals (25%) and via peripheral conversion from androstenedione (50%). Testerone in women functions to maintain libido and general wellbeing. Testosterone exerts a negative feedback mechanism on pituitary release of LH and follicle-stimulating hormone (FSH). Testosterone may be further converted to dihydrotestosterone or estradiol depending on the tissue.
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.
Testosterone was first used as a clinical drug as early as 1937, but with little understanding of its mechanisms. The hormone is now widely prescribed to men whose bodies naturally produce low levels. But the levels at which testosterone deficiency become medically relevant still aren’t well understood. Normal testosterone production varies widely in men, so it’s difficult to know what levels have medical significance. The hormone’s mechanisms of action are also unclear.
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