Peer-reviewed research

Since 2017, I've published two peer-reviewed, open access papers about hair loss. You can read these papers for free. The abstracts (and links) are listed below.

I'm also in the early stages of a research partnership with a university. More updates on that in the coming months.

Peer-reviewed publications

Here you'll find my peer-reviewed publications about androgenic alopecia. All manuscripts are open access, so you don't have to pay to read the full texts.

Self-Assessments of Standardized Scalp Massages for Androgenic Alopecia: Survey Results

English, R.S. & Barazesh, J.M. Dermatol Ther (Heidelb) (2019) 9: 167. https://doi.org/10.1007/s13555-019-0281-6

Introduction: Standardized scalp massages (SSMs) improve hair thickness in nonbalding men, but their effects on androgenic alopecia (AGA) have not yet been evaluated. The objective of this study was to investigate the effect of SSMs on self-assessed AGA sufferers (SAGASs).

Methods: Between October 2016 and October 2017, 1899 SAGASs searching online for hair loss treatments beyond AGA management drugs accessed literature explaining SSMs as a potential therapy for AGA, then watched a demonstration video detailing twice-daily, 20-min SSMs segmented by three rotational scalp regions using hand-generated presses, pinches, and stretches. In December 2017, SAGASs were contacted once to participate in a retrospective survey study to assess SSM adherence and hair changes. Age, gender, hair loss region and gradient, diet, supplement and topical use, AGA management drug use, estimations for minutes daily and months of massaging, and self-perceived hair changes were reported. Some participants also submitted photosets documenting hair changes throughout SSM adherence.

Results: A total of 340 (17.9%) respondents completed the survey, and 327 (17.2%) reported attempting the SSMs. SSM participants reported a median daily massage effort of 11–20 min and mean adherence of 7.4 ± 6.6 months, with 68.9% reporting hair loss stabilization or regrowth. Estimated minutes daily, months, and total SSM effort (i.e., minutes daily × months) were positively associated with self-perceived hair changes. On average, perceived hair loss stabilization and regrowth occurred after 36.3 h of SSM effort. Results did not vary across age, gender, Norwood gradient, or concomitant supplement, topical, finasteride, minoxidil, or microneedling use. However, hair change improvements were marginally lower for participants reporting diffuse versus frontal/temporal or vertex thinning.

Conclusions: While further research is warranted, these results align with previous findings and suggest the potential for SSMs to improve AGA.
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A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors

English RS Jr. A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors. Med Hypotheses. 2018;111:73–81.

Abstract: Androgenic alopecia, also known as pattern hair loss, is a chronic progressive condition that affects 80% of men and 50% of women throughout a lifetime. But despite its prevalence and extensive study, a coherent pathology model describing androgenic alopecia’s precursors, biological step-processes, and physiological responses does not yet exist. While consensus is that androgenic alopecia is genetic and androgen-mediated by dihydrotestosterone, questions remain regarding dihydrotestosterone’s exact role in androgenic alopecia onset. What causes dihydrotestosterone to increase in androgenic alopecia-prone tissues? By which mechanisms does dihydrotestosterone miniaturize androgenic alopecia-prone hair follicles? Why is dihydrotestosterone also associated with hair growth in secondary body and facial hair? Why does castration (which decreases androgen production by 95%) stop pattern hair loss, but not fully reverse it? Is there a relationship between dihydrotestosterone and tissue remodeling observed alongside androgenic alopecia onset?

We review evidence supporting and challenging dihydrotestosterone’s causal relationship with androgenic alopecia, then propose an evidence-based pathogenesis model that attempts to answer the above questions, account for additionally-suspected androgenic alopecia mediators, identify rate-limiting recovery factors, and elucidate better treatment targets. The hypothesis argues that: (1) chronic scalp tension transmitted from the galea aponeurotica induces an inflammatory response in androgenic alopecia-prone tissues; (2) dihydrotestosterone increases in androgenic alopecia-prone tissues as part of this inflammatory response; and (3) dihydrotestosterone does not directly miniaturize hair follicles. Rather, dihydrotestosterone is a co-mediator of tissue dermal sheath thickening, perifollicular fibrosis, and calcification – three chronic, progressive conditions concomitant with androgenic alopecia progression. These conditions remodel androgenic alopecia-prone tissues – restricting follicle growth space, oxygen, and nutrient supply – leading to the slow, persistent hair follicle miniaturization characterized in androgenic alopecia.

If true, this hypothetical model explains the mechanisms by which dihydrotestosterone miniaturizes androgenic alopecia-prone hair follicles, describes a rationale for androgenic alopecia progression and patterning, makes sense of dihydrotestosterone’s paradoxical role in hair loss and hair growth, and identifies targets to further improve androgenic alopecia recovery rates: fibrosis, calcification, and chronic scalp tension.

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