Sweet potatoes, white potatoes, russets, red potatoes, purple potatoes, etc. If it’s a potato, you should be eating it. Potatoes are excellent no-gluten source of testosterone boosting carbohydrates, and also very dense in nutrients. Stock pile your pantry full of them, and make potatoes your main carbohydrate source. Heck, if you can find potato chips that haven’t been laden with polyunsaturated fats, go for those too.
Once you have surpassed your early twenties, natural testosterone levels slowly begin to decline. This is a natural occurrence which occurs in all men, however can be prevented to some extent by ensuring your diet is rich in vitamins, minerals and quality fats. You can also supplement with a Natural Testosterone Booster which will work by encouraging your body to produce more Testosterone, back up to levels you could produce in your younger years.
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).
"Low T" is anything but inevitable. BMJ's Drug and Therapeutics Bulletin says that around 80 percent of 60-year-old men, and half of those in their eighties, have testosterone levels within the normal range for younger men. It concluded, "The evidence that an age-related reduction in testosterone levels causes specific symptoms is weak." The Food and Drug Administration (FDA) meanwhile has not approved testosterone use to improve strength, athletic performance, physical appearance, or prevent aging. And a 2004 report from the Institute of Medicine ("Testosterone and Aging: Clinical Research Directions") called TRT for age-related testosterone decline a "scientifically unproven method."
Epidemiological data has associated low testosterone levels with atherogenic lipid parameters, including lower HDL cholesterol (Lichtenstein et al 1987; Haffner et al 1993; Van Pottelbergh et al 2003) and higher total cholesterol (Haffner et al 1993; Van Pottelbergh et al 2003), LDL cholesterol (Haffner et al 1993) and triglyceride levels (Lichtenstein et al 1987; Haffner et al 1993). Furthermore, these relationships are independent of other factors such as age, obesity and glucose levels (Haffner et al 1993; Van Pottelbergh et al 2003). Interventional trails of testosterone replacement have shown that treatment causes a decrease in total cholesterol. A recent meta-analysis of 17 randomized controlled trials confirmed this and found that the magnitude of changes was larger in trials of patients with lower baseline testosterone levels (Isidori et al 2005). The same meta-analysis found no significant overall change in LDL or HDL cholesterol levels but in trials with baseline testosterone levels greater than 10 nmol/l, there was a small reduction in HDL cholesterol with testosterone treatment.
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch. Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone. These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry. Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.
The mineral zinc is important for testosterone production, and supplementing your diet for as little as six weeks has been shown to cause a marked improvement in testosterone among men with low levels.1 Likewise, research has shown that restricting dietary sources of zinc leads to a significant decrease in testosterone, while zinc supplementation increases it2 -- and even protects men from exercised-induced reductions in testosterone levels.3
Testosterone is the primary male sex hormone and an anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair. In addition, testosterone is involved in health and well-being, and the prevention of osteoporosis. Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss.
For example, the study published in Obesity Research tells that the scientists measured testosterone levels in two groups of middle-aged men with obesity. One group underwent a 16-week weight loss program, while the second group did nothing. Each participant of the first group lost 20 kg on the average. And these participants experienced a significant increase in testosterone levels. So, the fight against overweight is very important for those who want to overcome testosterone deficiency. But starvation is strictly forbidden because this is a stressful situation which leads to the sharp decline in T levels.
Português: Aumentar Naturalmente os Níveis de Testosterona, Español: aumentar tus niveles de testosterona de manera natural, Italiano: Aumentare i Livelli di Testosterone in Modo Naturale, Français: augmenter naturellement son taux de testostérone, Deutsch: Den Testosteronspiegel auf natürliche Weise erhöhen, 中文: 提高睾酮水平, Русский: естественными способами повысить уровень тестостерона, Čeština: Jak přirozenou cestou zvýšit hladinu testosteronu, Nederlands: Je testosteron op natuurlijke wijze laten toenemen, Bahasa Indonesia: Meningkatkan Tingkat Testosteron Secara Alami, العربية: زيادة معدّلات هرمون التستوستيرون بالجسم طبيعيًّا, हिन्दी: टेस्टोस्टेरोन लेवल बढायें (Gharelu Nuskhe, Sex Power, Kaise Kare), Tiếng Việt: Tăng Testosterone Tự nhiên, ไทย: เพิ่มระดับฮอร์โมนเทสโทสเทอโรนด้วยวิธีธรรมชาติ, 한국어: 테스토스테론 수치 자연적으로 늘리는 방법
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:
Other side effects include increased risk of heart problems in older men with poor mobility, according to a 2009 study at Boston Medical Center. A 2017 study published in JAMA found that treatments increase coronary artery plaque volume. Additionally, the Food and Drug Administration (FDA) requires manufactures to include a notice on the labeling that states taking testosterone treatments can lead to possible increased risk of heart attacks and strokes. The FDA recommends that patients using testosterone should seek medical attention right away if they have these symptoms:
As we age, the body undergoes multiple degenerative changes at multiple sites and in multiple systems. The changes of aging are inevitable and inexorable and represent the march toward ultimate death. We are mortal beings whose destiny it is to die. As we come to learn about the processes of life we can better prepare ourselves for the finality of death and on the way perhaps retard the degenerative process, or repair it (for however long we may enjoy this repair), or substitute chemical compounds that our bodies once produced in abundance, an abundance which fades with the advance of age.
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).
In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them. The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.
Using steroids eventually trains your body to realize that it doesn’t have to produce as much testosterone to reach its equilibrium, so to reach the same highs you’ll need to take more steroids, and when you stop taking them, your body will need to readjust — you’ll be living with low testosterone for a while (and you’ll need to see a doctor if your body doesn’t readjust on its own). Forcing your body to stay above your natural testosterone, even if you’re naturally low, can create this kind of dependency which ultimately decreases the amount of testosterone your body will produce on its own.
When your testosterone levels go up, so does your libido. Unfortunately, the inverse is not true — your libido levels can go up without your testosterone levels also going up. And that’s how most supposed T-boosters “work”: they make you feel ornery, leading you to think that your T levels are appreciably higher, when they actually aren’t. In rare cases, supplementation will result in a 20% testosterone increase. This kind of improvement may sound impressive, but is irrelevant for practical purposes.
The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (see figure to the right). When testosterone levels are low, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH. These latter two hormones stimulate the testis to synthesize testosterone. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively.
Dr. Anthony’s Notes: I use Maca often in cycles throughout the year. I typically buy the raw Maca powder, which has a VERY “dirt-like” earthy taste. Beware if you are a bit squeamish on tastes! How To Take Maca: 1500-3000mg of Maca powder is a typical dosage take daily alongside food. From personal experience, I've found that it’s best to buy the Maca powder as a standalone supplement and throw it into a blended protein shake to mask the taste.
That there is an association between depression and testosterone concentration seems possible because of the observation that depression may be associated with reduced testosterone concentrations, hypogonadal men may have their symptoms of depression relieved by TRT and that testosterone itself may have anti-depressant properties (Pope et al 2003). The evidence, however, is inconsistent. Seidman and colleagues (2002), for example, found that there was no relationship between testosterone and depression but there was an association of testosterone with dysthymia. McIntyre and colleagues (2006), on the other hand, found that middle-aged men with depression did have a reduction in bio-available testosterone.
Total levels of testosterone in the body are 264 to 916 ng/dL in men age 19 to 39 years, while mean testosterone levels in adult men have been reported as 630 ng/dL. Levels of testosterone in men decline with age. In women, mean levels of total testosterone have been reported to be 32.6 ng/dL. In women with hyperandrogenism, mean levels of total testosterone have been reported to be 62.1 ng/dL.
Topical testosterone, specifically gels, creams and liquids, may transfer to others. Women and children are most at risk of harmful effects from contact with them. You should take care to cover the area and wash your hands well after putting on the medication. Be careful not to let the site with the topical TT touch others because that could transfer the drug.
This causes your body to burn fat for the next 36 hours to replace your body’s vital energy stores. It addition to increasing your T-levels, it can help burn between 3–9 times more fat, lower your resting heart rate, lower blood pressure, keep your brain young by increasing circulation, and aids in detoxification by stimulating the lymphatic system.
In Australia, where it is illegal for drug makers to advertise directly to consumers—as it is everywhere except the United States and New Zealand— Dr. Vitry told me via e-mail that the country's FDA-like regulatory body, Medicines Australia, fined Bayer a minuscule, but symbolic, 10,000 Australian dollars for breaching MA's code of conduct in its TRT disease-awareness campaign. Although Bayer implied that low testosterone was the most prevalent cause of the symptoms described, and that there was a high incidence of low T, Vitry said Medicines Australia didn't nail Bayer for illegal direct-to-consumer advertising because its campaign "did not encourage patients to seek a prescription for a specific testosterone product."
"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.