The unsexy truth is that increasing T naturally simply comes down to making some long-term changes in your diet and lifestyle. As you’ll see, what I did to increase T largely boils down to eating better, exercising smarter, and getting more sleep. That’s pretty much it. But as with most things in life, the devil is in the details, so I’ll share with you exactly what I did and provide research that explains why the things I did helped boost my testosterone.
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Afrisham, R., Sadejh-Nejadi, S., SoliemaniFar, O., Kooti, W., Ashtary-Larky, D., Alamiri, F., … Khaneh-Keshi, A. (2016, November 24). Salivary testosterone levels under psychological stress and its relationship with rumination and five personality traits in medical students. Psychiatry Investigations, 13(6), 637–643. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5128352/
In many of the studies we found, those who saw the most improvement in health, testosterone, or muscle gain were those with existing nutrient or vitamin deficiencies. This means that some gains may be due more to dietary changes and generally restoring nutrient and vitamin levels than any one magic ingredient, but also that making sure your diet includes healthy amounts of nutrients should be your first step.
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.
Male hypogonadism is a clinical syndrome caused by a lack of androgens or their action. Causes of hypogonadism may reflect abnormalities of the hypothalamus, pituitary, testes or target tissues. Increases in the amount of testosterone converted to estrogen under the action of the enzyme aromatase may also contribute to hypogonadism. Most aspects of the clinical syndrome are unrelated to the location of the cause. A greater factor in the production of a clinical syndrome is the age of onset. The development of hypogonadism with aging is known as late-onset hypogonadism and is characterised by loss of vitality, fatigue, loss of libido, erectile dysfunction, somnolence, depression and poor concentration. Hypogonadal ageing men also gain fat mass and lose bone mass, muscle mass and strength.
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.
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.
I highly recommend using a great essential amino acid mix post-exercise in order to boost testosterone. These essential amino acids and especially the concentrated branched chain amino acids leucine, isoleucine and valine stimulate muscle protein synthesis. Getting these amino acids in the post-workout window dramatically boosts testosterone production (14). I like using our Amino Strong and will often recommend a scoop pre-workout and post-workout for the best muscle building, testosterone boosting benefits.
Stick to protocols that stress large degrees of muscle mass and are moderate- to high-intensity. Additionally, more seasoned gym-goers may want to incorporate forced repetitions periodically into their programs, as testosterone increases have been observed with this type of training.14 Incorporating other post-failure training techniques such as dropsets or partials may similarly be associated with higher T production.
The largest amounts of testosterone (>95%) are produced by the testes in men, while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta. In the testes, testosterone is produced by the Leydig cells. The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).
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The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about 2.5 times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
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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.
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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.
Both testosterone and 5α-DHT are metabolized mainly in the liver. Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order. Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone. The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile. Only a small fraction (2%) of testosterone is excreted unchanged in the urine.
4. Foods rich in vitamin A. Vitamin A is more commonly known for its association with eyesight improvement, but it is also a vitamin supplements the production of testosterone. The June 2004 issue of the Clinical Endocrinology journal published research conducted by Israel’s Kaplan Medical Center. This study involved Israeli boys that had delays in puberty. These boys were given Vitamin A supplements and foods rich in Vitamin A over the course of 6 months, and most of them showed an improvement with their testosterone levels. If you want to boost the level of testosterone in your body, food types that are rich in Vitamin A are carrots, sweet potatoes, squash, cantaloupe and eggs.
In contrast to steroids, testosterone boosters have a fully different mechanism of action. They are the products which contain the natural ingredients only. These ingredients act by stimulating the man’s body to synthesize own testosterone. So, testosterone levels grow naturally without negative health effects associated with the intake of steroids.
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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?
Testosterone is a stimulant of hematopoiesis in the bone marrow and consequently, increases the hematocrit (Shahidi 1973). Men with unexplained anemia should have their testosterone measured and if reduced, these men should be treated with testosterone. Because of the erythropoietin stimulating effect of testosterone, one of the parameters to be monitored during testosterone treatment is hematocrit since a small percent of testosterone-treated men develop polycythemia.
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.
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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.
"The Journal of Clinical Endocrinology and Metabolism" published that males who switched from a high-fat diet to a low-fat diet also saw a decrease in their testosterone levels. If you want to put some fat back into your diet without fearing cardiac implications, plant-based saturated fat like coconut is just the ticket. Meat-based fat is also acceptable if kept to less than 10% of your dietary fat intake.
Prostate hyperplasia (BPH), or simply an enlarged prostate, is a serious problem among men, especially those over age 60. As I’ve pointed out, high testosterone levels are not a precursor to an enlarged prostate or cancer; rather, excessive DHT and estrogen levels formed as metabolites of testosterone are. Conventional medicine uses two classes of drugs to treat BPH, each having a number of serious side effects. These are:
The definition of the metabolic syndrome continues to be a work in progress. Within the last decade a number of definitions have emerged each with its own set of criteria although there is considerable overlap among them. The most recent definition seems to enjoy considerable consensus. It requires central adiposity (>94 cm waist circumference) plus two of, increased triglycerides, decreased HDL cholesterol, hypertension, insulin resistance as evidenced by impaired glucose tolerance, or frank diabetes (Alberti 2005). Almost immediately on the heels of this consensus, came a number of specific chemical markers which have been proposed to complement the basic definition of the metabolic syndrome (Eckel et al 2005).
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It may also become a treatment for anemia, bone density and strength problems. In a 2017 study published in the journal of the American Medical Association (JAMA), testosterone treatments corrected anemia in older men with low testosterone levels better than a placebo. Another 2017 study published in JAMA found that older men with low testosterone had increased bone strength and density after treatment when compared with a placebo.
First, it’s important to note that these tactics and practices to boost testosterone naturally probably won’t work with men who have hypoandrogenism. If the glands and cells responsible for producing testosterone are damaged or defective, no amount of eggs or sleep will help you raise testosterone levels. You’ll likely need to use testosterone replacement therapy to get your T levels to a healthy place.
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.
If you’re a frequent reader here in AM, you already know that increased dietary fat intake is directly correlated with increased testosterone production. And not only that, but the types of fat that increase T seem to be saturated fats (SFAs) and monounsaturated fats (MUFAs), while polyunsaturated (PUFAs) actually tend to lower testosterone (more here).
There are supplements out there that promise to increase your libido while also upping your testosterone. There are over the counter testosterone supplements and prescription supplements. There are supplements that market themselves as T-boosters, while also touting themselves as an aphrodisiac. And then there are companies that claim to have developed a testosterone pill that contains the triumvirate of male-enhancing properties: T-boosting, libido-enhancing, and even fertility-increasing. These supplement makers sometimes throw in an additional claim of muscle gain as well.
Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age. The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body. The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.
It may be unlikely to completely eliminate products with EDCs, but there are a number of practical strategies that you can try to limit your exposure to these gender-bending substances. The first step would be to stop using Teflon cookware, as EDCs can leach out from contaminated cookware. Replace them with ceramic ones. Stop eating out of cans, as the sealant used for the can liner is almost always made from powerful endocrine-disrupting petrochemicals known as bisphenols, e.g. Bisphenol A,