Featured Student: Sundus Malik

Sundus Malik is a medical student at the University of Missouri–Kansas City School of Medicine and a Master of International Health candidate. Her academic interests span internal medicine and dermatology, with a focus on the metabolic and systemic factors that influence cutaneous disease. She also served as Executive Director of the Sojourner Health Clinic, where she leads initiatives aimed at improving access to comprehensive, patient‑centered care.

Androgenic alopecia (AGA) is the most common form of hair loss in adults and represents a significant source of psychosocial distress for patients. Traditionally, AGA has been conceptualized as a hormonally mediated disorder driven by dihydrotestosterone‑dependent follicular miniaturization in genetically susceptible individuals. However, emerging evidence suggests that metabolic factors may also play a meaningful role in disease pathogenesis. A 2024 review of major dermatologic studies highlighted a Mendelian‑randomization analysis demonstrating that elevated lipid‑related metabolites are causally associated with increased risk of androgenic alopecia. This finding reframes AGA as not only a hormonally influenced condition but also one with important metabolic underpinnings, opening new avenues for prevention and treatment.

The study employed a Mendelian randomization (MR) design, a method that uses genetic variants as instrumental variables to infer causality between an exposure and an outcome. This approach helps overcome limitations of observational studies, such as confounding and reverse causation. By integrating large‑scale genomic and metabolomic datasets, the investigators identified specific lipid‑related metabolites whose genetically predicted elevations increased the likelihood of developing AGA. The causal nature of this association strengthens the hypothesis that lipid dysregulation contributes directly to follicular miniaturization rather than merely co‑occurring with hair loss.

These findings align with a growing body of literature linking metabolic syndrome, dyslipidemia, and cardiovascular risk factors with hair disorders. Prior observational studies have reported higher rates of insulin resistance, hypertension, and abnormal lipid profiles among individuals with AGA. However, such studies cannot establish whether metabolic abnormalities cause hair loss or simply share common risk factors. The MR approach used in this 2024 study provides stronger evidence that lipid abnormalities may play a mechanistic role in AGA pathophysiology. This insight is clinically meaningful, as it suggests that metabolic health may influence the onset and progression of hair loss.

The study’s strengths include its use of large, well‑characterized genomic datasets and the methodological rigor inherent to Mendelian randomization. By relying on genetic instruments, the analysis reduces confounding and strengthens causal inference. Additionally, the identification of specific lipid‑related metabolites provides a more granular understanding of metabolic pathways that may influence follicular 

biology. These findings may help guide future mechanistic studies exploring how lipid metabolism interacts with androgen signaling, inflammation, and follicular cycling.

However, several limitations warrant consideration. First, MR analyses depend on the validity of the selected genetic instruments. If the genetic variants influence AGA through pathways unrelated to lipid metabolism, the results may be biased. Second, the study population likely consisted predominantly of individuals of European ancestry, which may limit generalizability to more diverse populations. Third, while MR can establish causality, it cannot delineate the precise biological mechanisms linking lipid metabolites to hair follicle miniaturization. Further laboratory and clinical research is needed to clarify these pathways and determine whether modifying lipid levels can meaningfully alter disease course.

Despite these limitations, the study has important implications for dermatologic practice. If lipid abnormalities contribute causally to AGA, clinicians may consider incorporating metabolic screening into the evaluation of patients presenting with early hair thinning. This could include lipid panels, assessment of metabolic syndrome components, and counseling on lifestyle modifications. Moreover, the findings raise the possibility that lipid‑lowering therapies—such as statins, PCSK9 inhibitors, or dietary interventions—could serve as adjunctive treatments for AGA. While such interventions are not yet evidence‑based for hair loss, the study provides a strong rationale for future clinical trials exploring metabolic‑targeted therapies alongside established treatments such as minoxidil, finasteride, and low‑level laser therapy.

In conclusion, the 2024 study identifying lipid‑related metabolites as causal contributors to androgenic alopecia represents a significant advancement in understanding the pathophysiology of this common condition. By demonstrating a metabolic component to AGA risk, the research expands the conceptual framework of hair loss beyond androgen signaling alone and highlights the importance of systemic health in dermatologic disease. As the field continues to integrate insights from genomics, metabolomics, and epidemiology, studies such as this underscore the value of interdisciplinary approaches in improving patient care and developing novel therapeutic strategies.