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).
The converse is also true; there is an increased incidence of rheumatic/autoimmune disease in men with hypogonadism. Jimenez-Balderas et al (2001) carried out neuroendocrine, genetic and rheumatologic investigations in hypogonadal men. Of the 13 hypogonadal patients, 8 (61%) had rheumatic autoimmune disease (ankylosing spondylitis, systemic lupus erythemetosus, rheumatoid arthritis, dermatomyositis). There is a low frequency of those diseases (0.83%) in the general population.
Dobs and colleagues found that men with an increased body mass index had both reduced testosterone and reduced high density lipoprotein (HDL) levels. Treatment with testosterone increased the levels of HDL (Dobs et al 2001). Rising levels of HDL are not a consistent finding with TRT. More often, however, one finds reduced total cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels with TRT (Zgliczynski et al 1996; Whitsel et al 2001).
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.
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:
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Testing is the only way you can validate a low-T diagnosis and measure treatment progress. I always say, "Test, don’t guess!" Your doctor may "suspect" you have hormone imbalances by your symptoms, but you should ask that they do testing to confirm unhealthy levels. Testing also ensures your doctor rules out other issues that may simply have similar symptoms. With your test results in hand, your physician can best determine what the optimal levels are for you and determine the best course of treatment.
These researchers took saliva samples from recreational women athletes before and after playing 10 minutes of flag football. The data showed that this short, intense burst of competitive sport triggered the immediate release of testosterone. Interestingly, the subjects' mental state also contributed to the data. Self-rated performance scores were directly related to testosterone levels.
Individuals with metabolic syndrome are at increased risk for developing coronary artery disease and diabetes mellitus. Predicting who might develop the metabolic syndrome would allow preventive measures to be taken in addition to weight control and other lifestyle modifications such as cessation of smoking and increased exercise. It is known that with decreasing testosterone availability in aging males there is an increase in fat mass and decrease in lean body mass (van den Beld et al 2000), there are disorders of insulin and glucose metabolism (Haffner et al 1996) and dyslipidemia (Tsai et al 2004). Kupelian and colleagues (2006) in analyzing data from the Massachusetts Male Aging Study demonstrated that men with low levels of testosterone, sex hormone-binding globulin, or clinical androgen deficiency, especially men with a BMI of greater than 25, were at increased risk of developing the metabolic syndrome and hence, diabetes mellitus and/or coronary artery disease.
“About 2 weeks after starting Andro400, I noticed my belly fat disappearing. Now, after only one month, I've lost about ten pounds all in my mid section. What a miracle! I have more energy and don't have to hold my gut in any longer. I'm more relaxed and my libido has increased 5 fold! I'm 58 years old and beginning to feel like a teenager again! Your product has delivered exactly as advertised. I'm elated!”
Some boys even develop enlarged testicles and penis, armpit or pubic hair, as well as facial hair as early as age nine! Early puberty is not something to be taken lightly because it can significantly influence physical and psychological health, including an increased risk of hormone-related cancers. Precocious sexual development may also lead to emotional and behavioral issues, such as:
A diagnosis of low testosterone is typically made if a man’s free testosterone hormone level is below 300 ng/dL. But as a doctor specializing in sexual health, I typically consider optimized male testosterone levels somewhere between 600 to 800 ng/dL—rarely above or below those numbers. The tests that I routinely recommend to my male clients can be found in this test panel and include biomarkers associated with testosterone, free and total (this includes sex-hormone binding globulin [SHBG]), estradiol, estrogen (total and serum), cortisol, DHEAs, thyroid-stimulating hormone (TSH), hemoglobin A1C, and vitamin D.
That testosterone decreases with age has been clearly established by many studies over many years in several different populations of men (Harman et al 2001; Feldman et al 2002; Araujo et al 2004; Kaufman and Vermeulen 2005). Of even greater significance is the steeper fall of the most biologically active fraction of total testosterone, non-sex hormone binding globulin (SHBG)- bound testosterone, or bioavailable testosterone (bio-T). The classical, but not the only approach to measuring bio-T, is to precipitate out SHBG (and hence the testosterone which is strongly bound to it as well) and measure the remainder as total testosterone (Tremblay 2003). Vermeulen et al (1999) have devised a less tedious and less expensive method of measuring a surrogate for bio-T, namely calculated bio-T, inserting total T, albumin, SHBG and a constant into a mathematical formulation. There is a strong correlation between actual bio-T and calculated bio-T (Emadi-Konjin et al 2003).
Zinc is involved in virtually every aspect of male reproduction, including testosterone metabolism. Several studies support the use of zinc for treating low sperm counts, especially when accompanied by low testosterone levels. In these studies, zinc has shown an ability to raise both sperm counts and testosterone levels. Many men may be suffering from low testosterone simply because of a zinc deficiency. Taking 30–45 mg of zinc per day is recommended; balance with 2–3 mg of copper for best results.
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.
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 studies suggest that many significant clinical findings and important disease states are linked to low testosterone levels. These include osteoporosis (Campion and Maricic 2003), Alzheimer’s disease (Moffat et al 2004), frailty, obesity (Svartberg, von Muhlen, Sundsfjord et al 2004), diabetes (Barrett-Connor 1992), hypercholesterolemia (Haffner et al 1993; Van Pottelbergh et al 2003), hypertension (Phillips et al 1993), cardiac failure (Tappler and Katz 1979; Kontoleon et al 2003) and ischemic heart disease (Barrett-Connor and Khaw 1988). The extent to which testosterone deficiency is involved in the pathogenesis of these conditions, or to which testosterone supplementation could be useful in their treatment is an area of great interest with many unanswered questions.
There is an increased incidence of hypogonadism in men with rheumatoid arthritis. Tengstrand et al (2002) studied hormonal levels in 104 men with rheumatoid arthritis and 99 age-matched healthy men. They divided their subjects into 3 age groups: 30–49, 40–59, 60–69. Mean non-sex hormone binding globulin-bound testosterone (bioavailable testosterone) was lower in men with rheumatoid arthritis for each of the three groups. LH was also found to be lower in the patients with rheumatoid arthritis suggesting a hypothalamic-pituitary cause of the reduced bioavailable testosterone. Of the 104 men with rheumatoid arthritis, 33 had hypogonadism compared to 7 of the 99 healthy controls.
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:
"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.