What Is Andropause and Low Testosterone

What Is Andropause and Low Testosterone

The Problem – Andropause and Low Testosterone

As men age, their levels of testosterone begin to decline, usually beginning around the mid-40s. This heralds what is commonly known as andropause, the male counterpart to menopause. While this is a natural part of aging, the decline in testosterone production by the testes can be more precipitous in some men than others. Excessive weight gain, stress, lack of exercise, and many medications further contribute to a man’s ability to manufacture testosterone, resulting in even lower testosterone levels and leading to symptoms of andropause. These symptoms may include low libido, irritability, depression, loss of muscle mass and strength, weight gain, metabolic syndrome, erectile dysfunction, sleep disturbances, osteoporosis, and adverse changes in the blood lipid profile. Symptoms of androgen deficiency and low testosterone levels are used to establish a diagnosis of hypogonadism. This low testosterone condition was found to increase significantly with age in the Massachusetts Male Aging Study1 . In the Hypogonadism in Males (HIM) study, hypogonadism was diagnosed in 38.7% of men over 45 years old who presented to primary care offices.

However, while this is certainly an option, the solution to the problem may not be a simple case of restoring testosterone levels. For example, some practitioners find that testosterone therapy may be of little benefit unless problems affecting cortisol production are addressed first. The body’s response to stress is mediated by increased cortisol production, and this prepares the body for “fight or flight” by shutting down other processes, including testosterone production. Correcting disorders such as adrenal fatigue or chronic stress may therefore lead to improved testosterone levels and resolve symptoms, without requiring testosterone therapy. Increasing cortisol levels, along with several other endocrine changes, have been reported in men3 , highlighting the need to obtain a complete hormone profile before initiating any hormone replacement.

The Hormones Tested in our Male Profiles and Why

Estradiol is tested because too much of it, relative to testosterone levels, suppresses testosterone receptors in target tissues and eventually leads to feminizing effects in men, such as breast enlargement. In healthy young men, testosterone is at its highest level and estradiol is very low. However, as men age, this shifts to a higher estradiol/testosterone ratio. Even if testosterone levels are normal, symptoms can indicate a functional testosterone deficiency because of the effects of higher than normal estradiol levels.

There are several mechanisms by which relative levels of estradiol and testosterone can change. Weight gain, whether or not this results from low testosterone, results in increased production of aromatase in fat cells, which converts testosterone to estradiol. Rising estradiol levels also cause the liver to produce more SHBG, which has a greater affinity for testosterone than estradiol. This acts to suppress further the amount of circulating free testosterone. Estradiol also decreases luteinizing hormone (LH) production by negative feedback on the pituitary gland, which in turn acts to decrease testicular testosterone production. High estradiol levels can be controlled by weight loss to decrease the amount of aromatase-producing adipose tissue. There are nutritional and pharmaceutical approaches to aromatase inhibition.

Progesterone is present in men but at a much lower level than found in premenopausal women. Some men supplement with topical progesterone to help with sleep, to support adrenal cortisol production (progesterone is a cortisol precursor), and to counterbalance the effects of estrogens on the prostate. It has also been used as a mild antiandrogen in patients with BPH and to reduce male pattern baldness, because of its competition with testosterone and DHT for androgen receptors. Salivary progesterone levels can, therefore, be useful to monitor supplementation.

Testosterone is the primary indicator of male hypogonadism and andropause. Many things can contribute to low testosterone levels, including high cortisol levels and high estrogen levels, as described above. Testosterone production in the testes is controlled by the hypothalamic-pituitary-testicular axis, and so dysfunctions of the hypothalamus or pituitary can affect levels, as well as the negative feedback effect of estradiol on LH levels to suppress testosterone production.

SHBG binds and transports both testosterone and estrogens in the bloodstream, and it therefore regulates the relative amounts of free and bound hormone and consequently their bioavailability to target tissues. SHBG is a protein produced by the liver in response to exposure to any type of estrogen. Testosterone binds about three times more tightly to SHBG than does estradiol, so this increase in SHBG as a result of estrogen exposure causes the relative proportion of bioavailable testosterone to estradiol to decrease even further, exacerbating the symptoms of testosterone deficiency.

Many factors, in addition to estrogen exposure, can affect SHBG levels9 . Thyroid hormone increases SHBG production, whereas insulin, on the other hand, decreases SHBG levels. In young men, testosterone levels are usually high and SHBG low, making most of the testosterone bioavailable. However, as men age, gain weight, and their estrogen levels increase, SHBG also rises, decreasing bioavailable testosterone. Measuring SHBG in blood provides an indication of the overall exposure to estrogens, as well as the bioavailable (free) fraction of testosterone (calculated from the ratio of testosterone to SHBG).

PSA is a measure of prostate health and high levels can indicate the presence of BPH or advancing prostate cancer. As prostate cells start to become crowded, they produce PSA, which acts to suppress angiogenesis and therefore reduce the blood supply to the surrounding tissue to prevent it from further growth. High levels are therefore seen only as a result of growth that is fairly rapid. It is important to test PSA levels prior to starting testosterone therapy, as a sharp increase in PSA can indicate prostate problems.

DHEA is a precursor for the production of estrogens and testosterone, and is therefore normally present in greater quantities than all the other steroid hormones. It is mostly found in the circulation in its conjugated form, DHEA sulfate (DHEA-S). Its production, which occurs in the adrenal glands, declines gradually with age. Like cortisol, it is involved with immune function and a balance between the two is essential. Low DHEA can result in reduced libido and general malaise.

Cortisol is an indicator of adrenal function and exposure to stressors. Under normal circumstances, adrenal cortisol production shows a diurnal variation and is highest early in the morning, soon after waking, falling to lower levels in the evening. Normal cortisol production shows a healthy ability to respond to stress. Low cortisol levels can indicate adrenal fatigue (a reduced ability to respond to stressors), and can leave the body more vulnerable to poor blood sugar regulation and immune system dysfunction. Chronically high cortisol is a consequence of high, constant exposure to stressors, and this has serious implications for long-term health, including an increased risk of cancer, osteoporosis, and possibly Alzheimer’s disease10.

Free T4, free T3, TSH, and TPOab tests can can indicate the presence of an imbalance in thyroid function, which can cause a wide variety of symptoms, including feeling cold all the time, low stamina, fatigue (particularly in the evening), depression, low sex drive, weight gain, and high cholesterol.

Contact Connor Wellness Clinic today for more information on how to improve your male hormones and slow aging. Or call our office 916-404-0886

References 1. Araujo AB, O’Donnell AB, Brambilla DJ, Simpson WB, Longcope C, Matsumoto AM,McKinlay JB. Prevalence and incidence of androgen deficiency in middle-aged and older men: estimates from the Massachusetts Male Aging Study. J Clin Endocrinol Metab. 2004;89:5920-6. 2. Mulligan T, Frick MF, Zuraw QC, Stemhagen A, McWhirter C. Prevalence of hypogonadism in males aged at least 45 years: the HIM study. Int J Clin Pract. 2006;60:762-9. 3. Elmlinger MW, Dengler T, Weinstock C, Kuehnel W. Endocrine alterations in the aging male. Clin Chem Lab Med. 2003;41:934- 41. 4. Risbridger GP, Bianco JJ, Ellem SJ, McPherson SJ. Oestrogens and prostate cancer. Endocr Relat Cancer. 2003;10:187-91. 5. Carruba G. Estrogen and prostate cancer: an eclipsed truth in an androgen-dominated scenario. J Cell Biochem. 2007;102:899- 911. 6. Endogenous Hormones, Prostate Cancer Collaborative Group, Roddam AW, Allen NE, Appleby P, Key TJ. Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies. J Natl Cancer Inst. 2008;100:170-83. 7. Risbridger GP, Ellem SJ, McPherson SJ. Estrogen action on the prostate gland: a critical mix of endocrine and paracrine signaling. J Mol Endocrinol. 2007;39:183-8. 8. Tindall DJ, Rittmaster RS. The rationale for inhibiting 5alphareductase isoenzymes in the prevention and treatment of prostate cancer. J Urol. 2008;179:1235-42. 9. Selby C. Sex hormone binding globulin: origin, function and clinical significance. Ann Clin Biochem. 1990;27:532-41. 10. Magri F, Cravello L, Barili L, Sarra S, Cinchetti W, Salmoiraghi F, Micale G, Ferrari E. Stress and dementia: the role of the hypothalamic-pituitary-adrenal axis. Aging Clin Exp Res. 2006;18(2):167-70.

California Locations We Serve:

Auburn | El Dorado Hills | Folsom | Granite Bay | Placerville | Rancho Cordova | Rocklin | Roseville | Sacramento