Testosterone Boosting: The Ultimate Guide

EDIT: I’m turning this blog post into a YouTube series, which can be found here.


This is an overview of how one can influence one’s levels of testosterone, and the body’s androgenic system in general. Testosterone is the primary male hormone, and an androgen is any substance that works through the so-called ‘androgen receptor’, a molecule that is found in cells and produces effects that we conventionally associate with masculinity: muscle mass, bone density, deepening of the voice, risk-taking behaviour, leanness, beard growth, etc.

These effects are split into anabolic and androgenic effects. Anabolic processes are those involved in the growth of new tissue (e.g. muscle), while androgenic effects involve producing male secondary sex-characteristics (beard, deeper voice). The latter effects are mainly mediated through dihydrotestosteone (DHT), a metabolite of testosterone that binds 5x more strongly to the androgen receptor and, unlike testosterone, is not metabolised into estrogen (an anabolic hormone that in excess produces feminising effects in men).


So why would one want to boost testosterone levels and the androgen system?

The answer: to increase the ‘positive’ effects of the hormone — muscle mass, leanness, endurance, confidence/ambition/risk-taking, body width, mood, etc. Basically, all the factors that go awry when androgen deficiency is present. Androgen levels naturally drop with aging, but there has been a large-scale decline of modern men’s testosterone levels — one study found age-controlled levels were dropping 1.2% per year between 1989 and 2005, which would translate (if the trend persisted) to a 36% drop between 1989 and 2019.

One should however be aware of the contraindications (e.g. increased acne, chance of putting estrogen levels out of balance and suffering from breast enlargement etc., temporary infertility, cardiovascular issues, mood swings, etc.) of interfering with this biological system. This article does not advocate any interventions, and readers considering doing such interventions should consult a medical professional on this. This is merely an overview of the topic.


“I do not want the effects mentioned” — This article does not make any prescriptive or advocacy claims.

“Supplements and lifestyle changes don’t work” — I believe this belief has sprung up, because people do not think of the androgen system as a pathway. Simply modifying one component of the pathway means that other rate-limiting/bottleneck components will remain, and therefore simplistic approaches will have a smaller effect than addressing the system as a whole.

“Why not just use exogenous hormones” — While I do not condemn people who take this approach (though I suggest they do it under the supervision of a medical professional), there are a number of issues with introducing exogenous hormones into the body: inconvenient administration, legal issues, doping regulations, inefficiency (simply taking testosterone won’t e.g. increase androgen receptor density, which plays a key role in the system), and more severe androgenic and estrogenic side-effects (testosterone is converted into estrogen, and hence administrating it exogenously can lead to wild fluctuations with concommitant side-effects).

The Androgen System

How is the androgenic system organised in males? The gist is that the brain sends chemicals to the testicles to produce testosterone from cholesterol. This testosterone interacts with the androgen receptors expressed by cells in the body and mediate androgenic effects. The level of testosterone and its metabolites (e.g. estradiol, DHT) are tracked by the brain, and the signal to the testicles is weakened until a steady level of the hormone is present in the blood.

More specifically, the hypothalamus (located in the central part of the brain) sends gonadotropin-releasing hormone (GnRH) to the anterior part of the brain’s pituitary gland. This gland in return releases lutenising hormone (LH) into the bloodstream, which travels to so-called Leydig cells in the testicles. The presence of LH increases the conversion of local cholesterol to pregnelone, which in return is turned into testosterone and other sex hormones.

What happens to this testosterone? It enters the blood-stream, where most of it is bound to sex hormone binding globulin (SHBG) that renders it inactive. The portion that is not bound to SHBG is termed free testosterone. Free testosterone can enter the cytoplasm of cells, where it is for instance further metabolised by the enzyme aromatase into estradiol (E2), an estrogen that then produces signalling effects though estrogen receptors and serves as a negative-feedback to testosterone production through interacting with the hypothalamus. Conversely, a small portion of testosterone is turned into dihydrotestosterone (DHT), a five times more potent androgen, by an enzyme called 5-alpha reductase. Both testosterone and DHT then bind to androgen receptors to mediate their effects.

Upregulating the Androgenic System

This overview of the key-steps of the androgenic system provides a number of factors that influence its activity:

  1. Decreasing aromatisation of testosterone to estrogen — the less aromatisation occurs, the more testosterone is available, and the less the negative feedback-cycle is triggered. The net effect is higher testosterone levels.
  2. Increasing the activity of 5-alpha reductase — the result is higher DHT levels, leading to more potent androgenic signalling due to its five times higher binding strength to the androgen receptor.
  3. Increasing the availability of cholesterol to Leydig cells — as cholesterol is a precursor to pregnelone and thus testosterone.
  4. Increasing Leydig cell activity — the more active Leydig cells are in producting testosterone, the more of the hormone is present in the blood.
  5. Increasing lutenising hormone — increases Leydig cell activity.
  6. Increasing androgen receptor density and signalling — the more androgen receptors are expressed on the surface of cells and the more sensitive they are to androgens, the more cells behave in an androgenic manner.
  7. Decreasing sex hormone binding globulin levels — as SHBG inactivates testosterone, decreasing its levels increases testosterone signalling.

So lets jump into supplements and lifestyle changes that can influence these seven factors.

1) Decreasing aromatisation of testosterone to estrogen

Aromatisation of testosterone into estrogen occurs largely in fat tissue, and as such weight-loss can significantly reduce the amount of conversion into estradiol that occurs [1]. BMI has been found to have a negative 0.36 correlation with total testosterone levels [2].

Chamomille tea contains so-called aromatase inhibiors like chrysin and apigenin [3][4], which reduce the conversion rate.

More potent aromatase inhibitors include nicotine, which however also reduces levels of ‘good estrogens’ involved in anabolic signalling [5].

While likely not aromatase mediated, consumption of yacon syrup has been found in a rat study to reduce the degradation of testosterone. [6]

[1] — https://clinicaltrials.gov/ct2/show/NCT03490513

[2] — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667256/

[3] — https://examine.com/supplements/apigenin/

[4] — https://examine.com/supplements/chrysin/

[5] — https://examine.com/supplements/nicotine/

[6] — https://examine.com/supplements/yacon/

2) Increasing the activity of 5-alpha reductase

Note: Increasing 5-alpha reductase will increase DHT levels, and DHT is a primary contributing factor to male pattern baldness in those predisposed to it.

Creatine, a safe sports supplement, possibly increases 5-alpha reductase [1].

A study found that low (but not high) doses of zinc can increase 5-alpha reductase [2].

[1] — https://examine.com/nutrition/does-creatine-cause-hairloss/

[2] — https://www.ncbi.nlm.nih.gov/pubmed/6200703

3) Increasing the availability of cholesterol to Leydig cells

The amount of cholesterol and saturated fats has been found to directly influence testosterone levels [1] (see two graphs below) — as these fats are the precursors to sex hormone production in Leydig cells.

Shilajit, a Himalayan mineral pitch supplement, has been found to increase testosterone levels, probably by increasing levels of the testosterone precursor DHEA [2].

[1] — http://pan.olsztyn.pl/repbiol/docs/pdfs/repbiol_vol6_supp2_num_page13.pdf

[2] — https://www.ncbi.nlm.nih.gov/pubmed/26395129

4) Increasing Leydig cell activity

Thyroid hormone regulates the activity of Leydig cells, and as such suffcient iodine intake (necessary for thyroid function) should maintain their activity [1].

Taurine is an anti-oxidant amino acid that is found in high concentration in the testicles, and has a protective effect there [2].

Vitamin D is involved in upregulating hundreds of genes, many of which are implicated in sex hormone production [3].

Deficiency of vitamin A has been found to reduce testosterone levels in rats [4].

Gingerol (and active ingredient of ginger) reliably increases testosterone levels in animal studies and has a protective effect on the testis [5].

The anti-oxidant N-acetyl-cysteine (NAC) has been found to reduce DNA damage in the testicles of infertile men, and boost testosterone 12% in one study [6].

[1] — https://www.ncbi.nlm.nih.gov/pubmed/8182361

[2] — https://examine.com/supplements/taurine/

[3] — https://www.spandidos-publications.com/10.3892/ijmm.2016.2576

[4] — https://www.ncbi.nlm.nih.gov/pubmed/7227300

[5] — https://examine.com/supplements/ginger/

[6] — https://rbej.biomedcentral.com/articles/10.1186/s12958-019-0468-9?subid1=20210110-0014-0222-a406-15c46c864cf3

5) Increasing lutenising hormone

D-aspartic acid (DAA) reliably increases LH levels — though the body adjusts after some time and hence this supplement is often taken intermittently [1].

Forskolin is a plant extract that raises levels of a signalling molecule CREB, that mimics the effects of LH [2], and directly raises testosterone by modulating enzymes necessary for testosterone production (e.g. StAR, Cyp11a, 3 -HSD ,and Cyp17 [3]).

← Tangent beginning →

In fact, this CREB pathway is also a secondary, bone-regulated and brain hypothalamo-pituitary-axis independent pathway through which the body increases testosterone [3]. Osteoblasts (i.e. bone cells) secrete a hormone called osteocalcin. Insulin secretion in the body leads to osteoblast cells in bone tissue secreting more osteocalcin. Osteocalcin thence travels to the testicles, and communicates with osteocalcin receptor Gprc6a on the surface of Leydig cells, increasing CREB levels, and thus testosterone production. In other words, increasing insulin levels (e.g. by eating enough carbohydrates and calories) will promote testosterone production independently of the brain’s hormone axis. Aside from insulin, vitamin K2 has been found to be a direct regulator of osteocalcin levels, increasing osteocalcin-dependent testosterone production in both rats and testicle-derived cell-lines [4].

← Tangent End →

So back to the brain and LH.

Substances that increase activity of the neurotransmitter dopamine can increase LH, as dopamine supresses prolactin, a hormone that itself suppresses GnRH and thus LH [5]. Noteworthy, as a tangent, is that ejaculation leads to a spike in prolactin (responsible for the refractory period after sex), which lends credence to claims that abstaining from ejaculation raises testosterone (corroborated by studies [6]). Hence dopamine signalling enhancers like dopamine receptor agonists, dopamine reuptake inhibitors (makes dopamine signal for longer before being recycled by neurons), tyrosine (dopamine precursor), or monoamine oxidase inhibitors (metabolises dopamine) will tend to suppress prolactin and increase LH.

Cortisol, a stress hormone, decreases LH release [7], and also suppresses LH pulses by suppressing GnRH by increasing (along with glucocorticoids and melatonin) a hormone called gonadotropin-inhibitory hormone (GnIH)[8]. Hence reducing stress levels and being well rested (without using too much melatonin) can stop this suppression from occuring. Supplements like ashwagandha have been found to maintain healthy cortisol levels [9]. Being assertive and winning confrontations and competions has been found to lead to higher testosterone and androgen receptor levels in hamsters [10] and also in some human studies [11].

[1] — https://examine.com/supplements/d-aspartic-acid/

[2] — https://examine.com/supplements/coleus-forskohlii/

[3] — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3850748/

[4] — https://lipidworld.biomedcentral.com/articles/10.1186/1476-511X-10-158

[5] — https://www.ncbi.nlm.nih.gov/pubmed/18477617

[6] — https://www.ncbi.nlm.nih.gov/pubmed/12659241

[7] — https://www.ncbi.nlm.nih.gov/pubmed/14576178

[8] — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902780

[9] — https://examine.com/supplements/ashwagandha/

[10] — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294220/

[11] — https://pubmed.ncbi.nlm.nih.gov/25463514/

6) Increasing androgen receptor density and signalling

Saturated fatty acids increase androgen receptor transcription (production from DNA) [1].

Resistance exercise, e.g. weight-training or sprints, increases androgen receptor density [2].

Exposure to heat (e.g. sauna) increases the levels of heat-shock protein, that is involved in increasing androgen receptor density, stability, and trafficking (moving androgen receptors from the center of the cell where they are produced, to its surface) [3].

Insulin-like growth factor 1 (IGF-1) increases androgen receptor potency [4]. IGF-1 is increased by high carbohydrate and protein consumption — hence it makes sense to have high-carb days (without gaining fat mass — remember aromatase) and to eat sufficient protein.

Abstaining from sex has been found to increase androgen receptor density in some areas of the brain, in rat studies [5].

Though there is evidence that Omega-3 fatty acids lead to androgen receptor breakdown and reduced androgen receptor density acutely [6], a study wherein male buffalo [7]were fed with a high Omega-3 diet found increases in testosterone and a human study [8] found increases in strength and muscle mass (indication of possible androgen signalling).

The substance L-Carnitine has been found to increase androgen receptor expression within muscle cells [9].

A combination of supplementation with vitamin E, and oxidative stress (for example seen in smokers), has been postulated to reduce the transcription of androgen receptors [10]

[1] — https://www.pnas.org/content/116/2/631

[2] — https://www.ncbi.nlm.nih.gov/pubmed/15354030

[3] — https://www.ncbi.nlm.nih.gov/pubmed/17974989

[4] — https://www.ncbi.nlm.nih.gov/pubmed/19251054

[5] — https://www.ncbi.nlm.nih.gov/pubmed/17268169

[6] — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271270/

[7] — https://www.sciencedirect.com/science/article/abs/pii/S0378432016303955

[8] — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480667/

[9] — https://pubmed.ncbi.nlm.nih.gov/16826026/

[10] — https://cancerres.aacrjournals.org/content/68/9_Supplement/5479

7) Decreasing sex hormone binding globulin (SHBG) levels

Boron, a trace mineral, stops SHBG from binding to sex hormones as much [1]. Stinging nettle, vitamin D, and IGF-1 (see above) have been found to have similar effects [2][3][4].

[1] — https://examine.com/supplements/boron/

[2] — https://examine.com/supplements/stinging-nettle/

[3] — https://examine.com/supplements/vitamin-d/

[4] — https://www.ncbi.nlm.nih.gov/pubmed/2946133

Summary Table

Thank you for reading! For a guide how to avoid unneccessary factors that suppress your testosterone, you might enjoy the second part of this series:

You may also enjoy our other articles:



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