Normal, bound and nonbound testosterone levels in normally ageing men: results from the Massachusetts Male Ageing Study

Mohr, Beth A.; Guay, André T.; O’Donnell, Amy B.; McKinlay, John B.

doi:10.1111/j.1365-2265.2004.02174.x

Cited by 238 publications

(179 citation statements)

References 54 publications

(119 reference statements)

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“…Exclusion criteria included outlying total T concentrations (>1,200 ng/dL), use of medications that might influence serum hormone concentrations (determined by an independent endocrinologist as previously reported 18 ), or diagnosis of prostate cancer, for which hormone suppression therapy could not be excluded as a possible external source of reductions in androgen concentrations. Because the focus of the analysis was on SAD transitions (onset or remission), a subject was entered into the analysis only if he contributed data up to at least T2.…”

Section: Analytic Samplementioning

confidence: 99%

“…Whether there exists a threshold at which T levels should be considered "deficient" is still the subject of substantial debate. [14][15][16] Although it is known that comorbidity and health behaviors influence T, 8,17 concurrent changes in health do not appear to account for agerelated declines in T. 8,18 In addition, T levels exhibit substantial random variability over periods of weeks or months. 19,20 The presence or absence of true age-related hypogonadism is therefore difficult to determine.…”

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confidence: 99%

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The Natural History of Symptomatic Androgen Deficiency in Men: Onset, Progression, and Spontaneous Remission

Travison

Shackelton

Araujo

et al. 2008

J American Geriatrics Society

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OBJECTIVES-To describe the onset, progression, and remission of symptomatic androgen deficiency (SAD) using longitudinal data from the Massachusetts Male Aging Study (MMAS).DESIGN-A prospective, population-based study of men living in Boston, Massachusetts. Data were collected in three waves: T1 (1987/89), T2 (1995/97), T3 (2002/04). Onset, progression, and remission were defined in terms of transitions in SAD status from one wave to the next. SETTING-In-person, in-home interviews.PARTICIPANTS-Seven hundred sixty-six community-dwelling men aged 40 to 70 at baseline (T1) contributed data from T1 to T2 and 391 from T2 to T3. MEASUREMENTS-SADwas defined in terms of serum total and free testosterone (T) levels and symptoms associated with low circulating androgens. Total T and sex hormone-binding globulin (SHBG) were measured using radioimmunoassay. Free T was calculated from total T and SHBG measurements. RESULTS-At T2 or T3, the likelihood of SAD was markedly greater for subjects who had exhibited SAD at the previous wave (odds ratio = 3.8, 95% confidence interval = 1.9-7.4), overall 55% of subjects who exhibited SAD experienced remission by the next study wave. The probability of SAD was greater with older age and greater body mass index. Multivariate models demonstrated that the likelihood of remission was at least 50% for most subpopulations.CONCLUSION-Over approximately 15 years of follow-up, SAD did not represent a stable health state. The likelihood of SAD would remit exceeded the likelihood that it Keywords aging; men; androgen; population study Gradual decreases in serum testosterone (T) concentrations are generally believed to accompany male aging. 1-8 Low T levels have been shown to contribute to diabetes mellitus, Address correspondence to: Thomas G. Travison, PhD, New England Research Institutes, 9 Galen St., Watertown, MA 02474. ttravison@neriscience.com. HHS Public AccessAuthor manuscript J Am Geriatr Soc. Author manuscript; available in PMC 2017 August 15. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript low bone and muscle mass, impaired sexual function, and frailty, 9-13 so interventions intended to slow or reverse age-related declines in T have attracted a great deal of attention.Whether there exists a threshold at which T levels should be considered "deficient" is still the subject of substantial debate. [14][15][16] Although it is known that comorbidity and health behaviors influence T, 8,17 concurrent changes in health do not appear to account for agerelated declines in T. 8,18 In addition, T levels exhibit substantial random variability over periods of weeks or months. 19,20 The presence or absence of true age-related hypogonadism is therefore difficult to determine. 21 For these reasons, it has been proposed that a composite measure of T levels and seemingly related symptoms, many of them having to do with mood and self-assessed well-being, may represent a more clinically meaningful assessment of male hormonal status. [22][23][24][25][26][27][28] Implicit in thi...

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Section: Analytic Samplementioning

confidence: 99%

mentioning

confidence: 99%

The Natural History of Symptomatic Androgen Deficiency in Men: Onset, Progression, and Spontaneous Remission

Travison

Shackelton

Araujo

et al. 2008

J American Geriatrics Society

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“…Another issue is whether an age-specific reference range of testosterone values is appropriate for diagnosing testosterone deficiency in old age. Most population studies show that obesity and/or disease and lifestyle has a profound impact on values of testosterone [16,17]. There is as present no published evidence that use of age-appropriate reference values offers advantages over use of reference values of the general population but it is an important point in the conceptualization of the desirability of testosterone treatment of elderly men.…”

Section: Late Onset Hypogonadism (Loh) Vs Classical Hypogonadismmentioning

confidence: 99%

Androgens and male aging: current evidence of safety and efficacy

Gooren¹

2010

Asian J Androl

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Many signs of aging, such as sexual dysfunction, visceral obesity, impaired bone and muscle strength, bear a close resemblance to features of hypogonadism in younger men. The statistical decline of serum testosterone in aging men is solidly documented. It has been presumed that the above features of aging are related to the concurrent decline of androgens, and that correction of the lower-than-normal circulating levels of testosterone will lead to improvement of symptoms of aging. But in essence, the pivotal question whether the age-related decline of testosterone must be viewed as hypogonadism, in the best case reversed by testosterone treatment, has not been definitively resolved. Studies in elderly men with lower-than-normal testosterone report improvement of features of the metabolic syndrome, bone mineral density, of mood and of sexual functioning. But as yet there is no definitive proof of the beneficial effects of restoring testosterone levels to normal in elderly men on clinical parameters. Few of these studies meet as yet rigorous standards of scientific enquiry: double-blind, placebo-controlled design of the study. The above applies also to the assessment of safety of testosterone administration to elderly men. There is so far no convincing evidence that testosterone is a main factor in the development of prostate cancer in elderly men and guidelines for monitoring the development of prostate disease have been developed. It is of note that there are presently no long-term safety data with regard to the prostate. Polycythemia is another potential complication of testosterone treatment. It is dose dependent and can be managed with dose adjustment.

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“…The mean BT in men aged 40-49 years was 270.9 ng/dl (69.2-469.7 ng/dl) and the mean BT in men aged 70-79 was 144.1 ng/dl (14.4-270.9 ng/dl). 47 As with ED, signs and symptoms of hypogonadism often go unreported to physicians. Therefore, it is important to maintain a proactive dialogue with the patient about possible symptoms such as low…”

Section: Diagnosismentioning

confidence: 99%

“…47 In the MMAS, the threshold for abnormally low total T as established by the 2.5th percentile was 251 ng/dl for healthy men aged 40- In the MMAS, the mean FT in men aged 40-49 years was 14.3 ng/dl, with a range of 3.7 ng/dl (meanÀ2 standard deviations (s.d. )), to 24.9 ng/dl (mean þ 2 s.d.).…”

Section: Diagnosismentioning

confidence: 99%

Male hypogonadism. Part II: etiology, pathophysiology, and diagnosis

Seftel

2005

Int J Impot Res

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Male hypogonadism has a multifactorial etiology that includes genetic conditions, anatomic abnormalities, infection, tumor, and injury. Defects in the hypothalamic-pituitary-gonadal axis may also result from type II diabetes mellitus and treatment with a range of medications. Circulating testosterone levels have been associated with sexual function, cognitive function, and body composition. Apart from reduced levels of testosterone, clinical hallmarks of hypogonadism include absence or regression of secondary sex characteristics, reduced fertility (oligospermia, azoospermia), anemia, muscle wasting, reduced bone mass (and bone mineral density), and/or abdominal adiposity. Some patients, particularly those with partial androgen deficiency of the aging male, also experience sexual dysfunction, reduced sense of vitality, depressed mood, increased irritability, difficulty concentrating, and/or hot flushes in certain cases of acute onset. As many patients with male hypogonadism-like patients with erectile dysfunction-do not seek medical attention, it is important for clinicians to be acquainted with the signs and symptoms of hypogonadism, and to conduct appropriate laboratory testing and other assessments to determine the causes and inform the treatment of this condition.

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Normal, bound and nonbound testosterone levels in normally ageing men: results from the Massachusetts Male Ageing Study

Cited by 238 publications

References 54 publications

The Natural History of Symptomatic Androgen Deficiency in Men: Onset, Progression, and Spontaneous Remission

The Natural History of Symptomatic Androgen Deficiency in Men: Onset, Progression, and Spontaneous Remission

Androgens and male aging: current evidence of safety and efficacy

Male hypogonadism. Part II: etiology, pathophysiology, and diagnosis

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