Genetics loads the gun. But biology pulls the trigger. Two people with identical family histories of hair loss can experience dramatically different outcomes in terms of onset, severity, and progression. That gap is explained by the biological environment those genes are operating in. Understanding the modifiable factors involved does not guarantee any particular result, but it does clarify what can and cannot be addressed.
The role of DHT in androgenetic alopecia
The most common form of hair loss, androgenetic alopecia, is driven primarily by dihydrotestosterone (DHT). DHT is produced when an enzyme called 5-alpha reductase converts testosterone in the scalp tissue. Hair follicles with a genetic sensitivity to DHT respond by progressively miniaturising over time, producing finer and shorter hairs until the follicle becomes inactive.
This process affects both men and women, though the pattern differs. Men typically experience recession at the temples and crown. Women more often see diffuse thinning across the top of the scalp while the frontal hairline remains relatively intact. The underlying DHT-driven mechanism is similar, but hormonal context shapes how it presents.
Hormonal factors beyond DHT
Thyroid dysfunction is one of the more overlooked contributors to hair loss. Both hypothyroidism and hyperthyroidism can disrupt the hair growth cycle, leading to diffuse shedding across the scalp. Thyroid hormones regulate cellular metabolism throughout the body, and hair follicles are sensitive to that regulation.
Oestrogen fluctuations also play a role. Postpartum hair shedding (telogen effluvium) is common and reflects the sudden withdrawal of elevated oestrogen levels after delivery, which shifts many follicles into the resting phase simultaneously. Perimenopause involves similar dynamics, as declining oestrogen relative to androgens can unmask androgenetic sensitivity that was previously suppressed.
Cortisol is a further factor. Chronic stress elevates cortisol, which can push hair follicles into the telogen (shedding) phase prematurely. This type of stress-related hair loss tends to be diffuse and often presents several months after the stressful period, making the connection easy to miss.
Nutritional factors
Iron deficiency is one of the most common nutritional contributors to hair loss, particularly in women of reproductive age. Ferritin (stored iron) is required for DNA synthesis in rapidly dividing follicle cells. Low ferritin can impair hair production even when haemoglobin levels appear normal on a standard blood test.
Zinc is involved in follicle cycling and protein synthesis. Deficiency disrupts both, and excess zinc supplementation can interfere with copper absorption and create its own problems. Adequate dietary protein matters because hair is predominantly keratin, a structural protein. Insufficient total protein intake reduces the substrate available for hair shaft construction.
Vitamin D receptors are expressed in hair follicles, and deficiency has been associated with alopecia areata as well as general shedding. B12 deficiency can impair red blood cell production and affect oxygen delivery to follicle tissue. Both are common in populations with low sun exposure, restrictive diets, or impaired gut absorption.
Systemic and inflammatory factors
The scalp microbiome is increasingly recognised as relevant to follicle health. Dysbiosis, an imbalance in the microbial populations on the scalp, can contribute to low-grade local inflammation that disrupts the follicle environment. This is distinct from the well-characterised inflammatory mechanisms in conditions like seborrhoeic dermatitis, though there is overlap.
Systemic low-grade inflammation, reflected in markers like elevated CRP or IL-6, can affect follicle cycling more broadly. Alopecia areata is an autoimmune condition where the immune system targets hair follicles directly. It is mechanistically distinct from androgenetic alopecia and responds to different interventions entirely.
Gut health also intersects with hair loss through nutrient absorption. Conditions that impair absorption in the small intestine, including undiagnosed coeliac disease or chronic dysbiosis, can produce deficiencies in iron, zinc, B12, and vitamin D even when dietary intake appears adequate.
What assessment adds
Investigating the biological picture before attempting any intervention is clinically sensible. A practitioner can identify which of the factors above are active contributors in a specific individual, based on blood markers, symptom history, and clinical examination. Not every person with hair loss has a nutritional deficiency or thyroid dysfunction. But some do, and those factors are modifiable.
Without assessment, interventions address symptoms without addressing cause. That may produce temporary improvement while the underlying driver continues. Identifying modifiable factors also helps set realistic expectations about what addressing those factors can reasonably achieve for a given individual.
A practical framing
Some biological contributors to hair loss are modifiable. Others are not. Genetic predisposition to follicle DHT sensitivity cannot be changed. But hormonal imbalances can often be identified and supported. Nutritional deficiencies can be corrected. Inflammatory conditions can be investigated and managed.
Knowing which category applies to your situation is clinically useful. It does not guarantee any particular outcome, and individual variation in response is real. But it changes the decision-making from guesswork to something grounded in your actual biology.