Aging males' symptoms in relation to the genetically determined androgen receptor CAG polymorphism, sex hormone levels and sample membership.
Late-onset hypogonadism describes the co-occurrence of a range of physical, psychological and sexual symptoms in aging men, with the implication that these symptoms are caused by androgen deficiency. Previous investigations examined mostly population samples and did not take into account the testosterone modulating effects of the genetically determined CAG repeat polymorphism (CAGn) of the androgen receptor (AR) gene. This is the first study which investigates aging male symptoms (AMS) in relation to the genetically determined androgen receptor CAG polymorphism, estradiol and testosterone levels in men > or =50 years of age in a healthy population sample (n=100), outpatients of an andrological department (n=76) who presented with sexual and "aging male" symptoms and a psychosomatic/psychiatric sample (n=120) who presented with various psychological and medically unexplained somatic complaints. Although the population sample was significantly older than the two patient groups, they reported significantly fewer AMS and had higher testosterone levels and shorter CAG repeats of the AR. Regression analysis revealed influences of CAGn on the AMS global score and the psychological and somatic subscale only in the two patient samples, while testosterone had some impact on the sexual subscale. Our results suggest that the so-called aging male symptoms show a certain association to androgenicity, but that they are rather unspecific and of multifactorial origin. Other factors contributing to AMS need further clarification.
Schneider
Gudrun
G
Department of Psychosomatics and Psychotherapy, University of Münster, Domagkstrasse 22, 48149 Münster, Germany.
Nienhaus
Kathrin
K
Gromoll
Jörg
J
Heuft
Gereon
G
Nieschlag
Eberhard
E
Zitzmann
Michael
M
D017668:Age of Onset; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000097:blood / Q000235:genetics / Q000502:physiology*; D013734:Androgen-Insensitivity Syndrome / Q000097:blood / Q000235:genetics* / Q000503:physiopathology; D016022:Case-Control Studies; D012739:Gonadal Steroid Hormones / Q000097:blood*; D006801:Humans; D007006:Hypogonadism / Q000097:blood / Q000453:epidemiology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000502:physiology; D011602:Psychophysiologic Disorders / Q000097:blood / Q000453:epidemiology / Q000235:genetics; D011944:Receptors, Androgen / Q000235:genetics*; D012107:Research Design; D012494:Sampling Studies; D012735:Sexual Dysfunction, Physiological / Q000097:blood / Q000453:epidemiology / Q000235:genetics; D020018:Sexual Dysfunctions, Psychological / Q000097:blood / Q000453:epidemiology / Q000235:genetics; D019680:Trinucleotide Repeat Expansion / Q000502:physiology
C410798:AR protein, human; D012739:Gonadal Steroid Hormones; D011944:Receptors, Androgen