One study looking at alcohol consumption found that increasing alcohol consumption led to a higher level of free & total testosterone compared to a non-drinking control group (20). Drinking did however lower SHBG testosterone levels, though this type of testosterone is bound to a protein meaning our bodies cannot use it to build muscle or increase our mood.
In females, this test can find the reason you’re missing periods, not having periods, or having a hard time getting pregnant. Doctors can also use it to diagnose polycystic ovary syndrome (PCOS). That’s a hormone problem that can cause irregular periods and make it hard to get pregnant. A testosterone test can also reveal if you might have a tumor in your ovaries that affects how much of the hormone your body produces.
Ok. So this product is meant to be taken continuously and without side-effects. But my question is, will there be replenishment from this product in aiding the body's natural ability to produce testosterone? In other words, will there ever be a time when I can say well I don't have to take this any more as my body is producing testosterone again on it's own and my muscle mass has been enhanced?
Currently available testosterone preparations in common use include intramuscular injections, subcutaneous pellets, buccal tablets, transdermal gels and patches (see Table 2). Oral testosterone is not widely used. Unmodified testosterone taken orally is largely subject to first-pass metabolism by the liver. Oral doses 100 fold greater than physiological testosterone production can be given to achieve adequate serum levels. Methyl testosterone esters have been associated with hepatotoxicity. There has been some use of testosterone undecanoate, which is an esterified derivative of testosterone that is absorbed via the lymphatic system and bypasses the liver. Unfortunately, it produces unpredictable testosterone levels and increases testosterone levels for only a short period after each oral dose (Schurmeyer et al 1983).
Now that we know chronic insulin spikes lead to lower Testosterone production, I hope I haven’t sent you running into the low carb camp! There are a few studies out there showing that long term low carb or ketogenic dieting leads to higher cortisol levels (especially with subjects who are training), and decreased testosterone levels (28 & 29). I have used low carb diets in the past with successful results (winning a national bodybuilding title), however the key is to use cyclical carb re-feeds. If you’re going to go on a low carb diet for whatever reason, be sure to work in a large carb reefed once a week.
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.[2] In addition, testosterone is involved in health and well-being,[3] and the prevention of osteoporosis.[4] Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss.
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.
The most common "out of balance" testosterone levels are found to be on the low side of normal; this occurs because a male's highest testosterone level usually peaks at about age 20, and then it decreases slowly with age. It has been suggested that a 1% decrease in testosterone level per year is not unusual for middle-aged (30 to 50 years old) and older males. While this decrease may not be noticeable in some men, others may experience significant changes starting in their middle-aged years or more commonly at age 60 and above. This drop in testosterone levels is sometimes termed hypogonadism, "male menopause" or andropause.

Do low levels of testosterone produce symptoms in middle-aged men? Absolutely. In fact, the classic symptoms were first recognized more than 70 years ago when two American physicians, Carl Heller, MD, and Gordon Myers, MD, showed the effectiveness of testosterone treatment for symptoms of fatigue, depression, irritability, low sex drive, erectile dysfunction, night sweats, and hot flashes in men. Over the years, subsequent studies have found that some—but not all—men with low, age-adjusted testosterone levels exhibit symptoms consistent with andropause. All experience improvement with testosterone therapy.
The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. Copyright 1997-2019, A.D.A.M., Inc. Duplication for commercial use must be authorized in writing by ADAM Health Solutions.
Ok. So this product is meant to be taken continuously and without side-effects. But my question is, will there be replenishment from this product in aiding the body's natural ability to produce testosterone? In other words, will there ever be a time when I can say well I don't have to take this any more as my body is producing testosterone again on it's own and my muscle mass has been enhanced?
The production of the stress hormone cortisol blocks the production and effects of testosterone. From a biological perspective, cortisol increases your “fight or flight” response, thereby lowering testosterone-associated functions such as mating, competing, and aggression. Chronic stress can take a toll on testosterone production, as well as your overall health. Therefore, stress management is equally important to a healthy diet and regular exercise. Tools you can use to stay stress-free include prayer, meditation, laughter, and yoga. Relaxation skills, such as deep breathing and visualization, can also promote your emotional health.
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.
Having low T is associated with decreased sex drive and less muscle mass, and one new study even found that lower levels of testosterone may raise the risk of depression. Fortunately, strength training spikes T, and living a healthy lifestyle also goes a long way toward keeping your levels topped off. But there are some completely natural compounds that can help as well.
While testosterone stimulates a man’s sex drive, it also aids in achieving and maintaining an erection. Testosterone alone doesn’t cause an erection, but it stimulates receptors in the brain to produce nitric oxide. Nitric oxide is a molecule that helps trigger a series of chemical reactions necessary for an erection to occur. When testosterone levels are too low, a man may have difficulty achieving an erection prior to sex or having spontaneous erections (for example, during sleep).

A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).


There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
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 the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]
Pine Pollen is an androgen, meaning in theory it can raise testosterone levels – effectively making it a naturally derived source of testosterone. Read more about this on the links below. But like I said I started taking it for a few weeks and did notice a bit more ‘up and go’ so to speak, but it did only last a few weeks. I have tried cycling it but haven’t noticed the same effects as I had when I initially started with it. I’m still experimenting and will keep this page updated. Therefore I recommend doing your own research.
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:
A: Endocrinology is a very difficult subject, some physicians and pharmacists alike have more difficulty with endocrinology than neurology. The reason for this is that there is no clear cut answer. Every hormone interacts with another hormone system in the body whether it be parathyroid hormone, cortisol, follicle stimulating hormone, etc. By in large, testosterone will increases lean body mass, which is to say that it typically increases muscle and or bone mass. We use it in the hospital to put weight on in patients needing to gain weight. That is partially the reason why we refer to testosterone as an "anabolic" hormone; anabolic meaning 'to build'. For more information, please visit us here at: //www.everydayhealth.com/drugs/testosterone Matt Curley, PharmD
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?
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.
Scientists in Italy found that subjects who consumed roughly 3 grams of D-AA for 12 days observed a 42 percent increase in testosterone levels.[12] The researchers also noted that the D-AA group still had 22 percent more testosterone than the placebo group three days after they stopped supplementing. Conversely, a more recent article published in Nutrition Research found no increase in testosterone levels in resistance-trained males after supplementing with 3 grams of D-AA for 28 days.[13]
Having low T is associated with decreased sex drive and less muscle mass, and one new study even found that lower levels of testosterone may raise the risk of depression. Fortunately, strength training spikes T, and living a healthy lifestyle also goes a long way toward keeping your levels topped off. But there are some completely natural compounds that can help as well.
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.
There are a lot of test booster blends out there. A lot of them are junk. I have tried to cover the most effective herbs above. As always, I recommend doing your own research and experiment to see if you notice an effect. If you would like one easy herbal solution I recommend starting with Mike Mahlers Aggressive Strength product purely because I have solid anecdotal evidence of its effectiveness. But again, supplements should be seen purely as that - a supplement to a healthy diet, plenty of sleep, hard training with adequate rest.
At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.
At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.
The participants were seen every 4 weeks. Blood was taken to measure hormone levels, and questionnaires were given to assess physical function, health status, vitality, and sexual function. Body fat and muscle measurements were also taken at the beginning and end of the 16 weeks. The study was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared in the September 12, 2013, issue of the New England Journal of Medicine.
×