Sex Hormones and Hair Loss in Men From the General Population of Northeastern Germany

The most common form of human hair loss is androgenetic alopecia. It affects both sexes and at least 50% of men by the age of 50 years.¹ In general, hair grows from androgen-responsive follicles, and invaginations of the superficial epithelium in the skin also show age-dependent changes in androgens. Among genetically predisposed individuals, androgenetic alopecia is characterized by an androgen-responsive hair loss. Pattern alopecia results in a decrease in hair follicle size accompanied by a decrease in the duration of anagen and an increase in the percentage of hair follicles in telogen with follicular miniaturization, which is the histological hallmark of androgenetic alopecia.¹ In vitro, testosterone and estrogen inhibit hair growth, suggesting that scalp hair growth may be controlled by these sex hormones.² Thus, we investigated cross-sectional associations between a panel of liquid chromatography–mass spectrometry (LC-MS/MS)-measured sex hormones and hair loss in men from the general population of Northeastern Germany.

The Study of Health in Pomerania (SHIP-TREND)³ is a cross-sectional, population-based study in Northeastern Germany. Details of the study design, recruitment, and procedures were previously published.³ Written informed consent was obtained from each participant and the ethics committee of the University of Greifswald authorized the study protocol, which is consistent with the principles of the Declaration of Helsinki. We excluded men who received prescribed drugs in the last 7 days (n = 180) and with lacking data (n = 1592). Finally, we investigated a study population of 373 men. We previously published a detailed description of the performed LC-MS/MS sex hormone measurements.⁴ As a part of the clinical examination, a dermatologist screened participants for general hair loss (yes or no), and scalp hair was additionally classified by the 7 stages of the Norwood-Hamilton-Scale.

First, associations of sex hormones with hair loss were analyzed using Poisson regression models, reported as relative risks with their 95% CIs. Second, we implemented age-adjusted and multivariable-adjusted ordered logistic regression models to examine associations of sex hormones with the Norwood-Hamilton Scale. Effects were reported as odds ratios per standard deviation increase and their 95% CI. Multivariable regressions were stratified by low (n = 22) vs normal or high (n = 351) testosterone concentrations with a cut-off of 10.4 nmol/L (to convert to ng/dL, divide by 0.0347). To address potential attrition bias, we included inverse probability weights into the multivariable analyses. All statistical analyses were performed with Stata 13.0 (Stata Corp).

Analysis of sex hormones with hair loss and Norwood-Hamilton Scale revealed no significant associations (Table). Exemplarily, total testosterone was not significantly associated with general hair loss (relative risk, 0.77; 95% CI, 0.96-1.04) or the Norwood-Hamilton Scale (odds ratio, 1.24; 95% CI, 0.93-1.65). Comparing men with and without general hair loss, we also found no significant differences in androgen concentrations, except for lower dehydroepiandrosterone sulfate in men with hair loss (P = .001). Sensitivity analyses did not substantially alter the revealed estimates.

The present cross-sectional, population-based study revealed no associations between sex hormones and hair loss in men from the general population. Previous studies with smaller sample sizes and selected participants yielded similar negative findings with regard to androgenetic alopecia grade severity⁵ and premature balding.⁶ Although higher testosterone concentrations are suggested to increase dihydrotestosterone concentrations converted by 5α- reductase and, thus, to stimulate androgen actions on the dermal papillae cells of hair follicles,⁵ the present study observed no link between serum androgen concentrations and male hair loss. This result confirmed previous research, suggesting that androgenetic alopecia might be attributed to increased androgen sensitivity or androgen receptor density, respectively, rather than to serum androgen concentrations themselves.

Corresponding Author: Hanna Kische, Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Ferdinand-Sauerbruch Str D-17475 Greifswald (kischeh@uni-greifswald.de).

Accepted for Publication: January 25, 2017.

Published Online: April 12, 2017. doi:10.1001/jamadermatol.2017.0297

Author Contributions: Drs Kische and Haring, had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Wallaschofski, Nauck, Haring.

Acquisition, analysis, or interpretation of data: Kische, Arnold, Gross, Wallaschofski, Völzke, Haring.

Drafting of the manuscript: Kische, Nauck, Haring.

Critical revision of the manuscript for important intellectual content: Arnold, Gross, Wallaschofski, Völzke, Haring.

Statistical analysis: Kische, Gross.

Obtained funding: Völzke.

Administrative, technical, or material support: Arnold, Völzke, Haring.

Supervision: Wallaschofski, Nauck, Haring.

Conflict Interest Disclosures: None reported.

Funding/Support: This study was supported in part by the Federal Ministry of Education and Research (grants 01ZZ9603, 01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs, as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania. This work is also part of the research project Greifswald Approach to Individualized Medicine.

Role of the Funder/Sponsor: The funders/sponsors had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.