Robert Clark aka "The Troglodyte" is a 39 year old father of 3, Author, Fitness Trainer, Nutritional Researcher, Obstacle Course Racer, Avid Trail Runner and CrossFit Warrior. He is dedicated to helping others achieve their fitness goals. His extensive work in the field of natural testosterone elevation, inspired the creation of Alpha Wolf Nutrition where he serves as the Lead Product Researcher.
The maximum hormone concentration in the blood is reported immediately after the workout. And the effect lasts throughout the day. However, it’s important to ensure that your physical activity is moderate. The matter is that too much high-intensity exercise can give an undesirable result. But even if for any reason you can’t attend a gym, it’s not a problem. Just move as much as possible during the day. Even simple walking will be of great benefit.
Regardless of the method of testosterone treatment chosen, patients will require regular monitoring during the first year of treatment in order to monitor clinical response to testosterone, testosterone levels and adverse effects, including prostate cancer (see Table 2). It is recommended that patients should be reviewed at least every three months during this time. Once treatment has been established, less frequent review is appropriate but the care of the patient should be the responsibility of an appropriately trained specialist with sufficient experience of managing patients treated with testosterone.
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).
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 rise in testosterone levels during competition predicted aggression in males but not in females. Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression. Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations. Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and physical violence. Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli. Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.
Autopsy studies have found histological prostate cancer to be very common, with one series showing a prevalence of greater than fifty percent in men over age sixty (Holund 1980). The majority of histological cancers go undetected so that the clinical incidence of the disease is much lower, but it is still the most prevalent non-skin cancer in men (Jemal et al 2003). Prostate cancer is also unusual in comparison to other adult cancers in that the majority of those with the disease will die of other causes. Treatment of prostate cancer with androgen deprivation is known to be successful and is widely practiced, indicating an important role for testosterone in modifying the behavior of prostate cancer. In view of this, testosterone treatment is absolutely contraindicated in any case of known or suspected prostate cancer. The question of whether testosterone treatment could cause new cases of prostate cancer, or more likely cause progression of undiagnosed histological prostate cancer that would otherwise have remained occult, is an important consideration when treating ageing males with testosterone.
The confusion is understandable, as one in-vitro study noted that high doses of zinc blocked the enzyme 5-a reductase inside test-tubes. But the studies that don’t see much daylight actually show that oral zinc supplementation on actual living, breathing, humans is able to significantly boost the production of dihydrotestosterone, and it does so even when there’s no deficiency in the mineral.
Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals.
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.
The hormone also plays a role in sex drive, sperm production, fat distribution, red cell production, and maintenance of muscle strength and mass, according to the Mayo Clinic. For these reasons, testosterone is associated with overall health and well-being in men. One 2008 study published in the journal Frontiers of Hormone Research even linked testosterone to the prevention of osteoporosis in men.
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There have been case reports of development of prostate cancer in patients during treatment with testosterone, including one case series of twenty patients (Gaylis et al 2005). It is not known whether this reflects an increase in incidence, as prostate cancer is very common and because the monitoring for cancer in patients treated with testosterone is greater. Randomized controlled trials of testosterone treatment have found a low incidence of prostate cancer and they do not provide evidence of a link between testosterone treatment and the development of prostate cancer (Rhoden and Morgentaler 2004). More large scale clinical trials of longer durations of testosterone replacement are required to confirm that testosterone treatment does not cause prostate cancer. Overall, it is not known whether testosterone treatment of aging males with hypogonadism increases the risk of prostate cancer, but monitoring for the condition is clearly vital. This should take the form of PSA blood test and rectal examination every three months for the first year of treatment and yearly thereafter (Nieschlag et al 2005). Age adjusted PSA reference ranges should be used to identify men who require further assessment. The concept of PSA velocity is also important and refers to the rate of increase in PSA per year. Patients with abnormal rectal examination suggestive of prostate cancer, PSA above the age specific reference range or a PSA velocity greater than 0.75 ng/ml/yr should be referred to a urologist for consideration of prostate biopsy.
Researchers found that the simple act ‘expressing power through open, expansive postures’ (i.e. standing up straight and proud) can increase Testosterone and decrease cortisol (58), along with improving feelings of power and tolerance for risk. Easy! Your mother was right – don’t slouch. This could be a handy trick before making a speech or going on a date!
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.
A blood test may not be enough to determine your levels, because testosterone levels can fluctuate during the day. Once you determine that you do have low levels, there are a number of options to take. There are synthetic and bioidentical testosterone products out on the market, but I advise using bioidentical hormones like DHEA. DHEA is a hormone secreted by your adrenal glands. This substance is the most abundant precursor hormone in the human body. It is crucial for the creation of vital hormones, including testosterone and other sex hormones.
The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
Vitamin C (unnecessary). I don’t know where I first heard about vitamin C’s supposed T-boosting benefits, but it’s one of those things you see all over the internet when you Google “how to increase testosterone.” Without trying to find the research that backs up that claim, I took a vitamin C supplement during my experiment. I later found some research that suggests that vitamin C does increase testosterone levels in diabetic mice, but because I wasn’t diabetic (nor a mouse), I’m not sure how much the vitamin C helped. I’ve actually stopped taking vitamin C supplements. I’m likely getting more than enough with my diet. Unless you have diabetes, you probably won’t see much benefit from this supplement. Don’t waste your money.
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).
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.
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).
A: Androderm comes in the form of a transdermal patch and is used for testosterone replacement therapy in patients who have insufficient levels of testosterone. Testosterone is a hormone produced in the body that plays a key role in many physiological processes in men. In some men, however, the body does not produce enough of the hormone, resulting in a variety of symptoms including decreased libido, erectile dysfunction, muscle loss, anemia and depression, among others. Androderm helps treat these symptoms and raise low testosterone levels by delivering therapeutic amounts of the hormone, which are absorbed through the skin. According to the prescribing information for Androderm, depression was a reported side effect of the medication. Other common side effects of Androderm include itching and redness at the application site, prostate abnormalities, headache, and burning or hardening of the skin at the application site. Less common side effects of Androderm include reduced libido (sex drive), fatigue, high blood pressure, anxiety, confusion, increased appetite, and body pain. For more specific information, consult with your doctor for guidance based on your health status and current medications, particularly before taking any action. Your physician can determine if your dosage of the medication needs to be adjusted or if an alternative medication should be considered. Lori Poulin, PharmD
Our culture sees meat and fat as the enemy, while carbs and sugars are treated like gold. High fructose corn syrup is in almost everything you buy, and this sugar is known to wreak absolute havoc on our endocrine systems. Food companies are well aware that this stuff is destroying you, but as long as people continue to indulge on it they will continue to produce it.
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.
Testosterone is a hormone with multifaceted physiological functions and multiple associations with pathophysiological states. It is an important hormone in male reproductive and metabolic function from intrauterine life to old age. In severe or classical hypogonadal states there is little controversy about the need to administer testosterone by an intramuscular, oral or transdermal formulation. There is controversy about making the diagnosis in the less severe cases of hypogonadism associated with the aging male but the current evidence suggests that this is efficacious in appropriately selected men and that there is little if any risk in giving aging symptomatic hypogonadal men a 6 month trial of therapy to determine whether symptoms will improve.
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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.