“It’s Genetic”: The Convenient Inheritance of Hair Loss

I’m in a swanky basement in Green Park. It’s a private art awards event, as evidenced by a few canvases lined up along the back wall by the bar.  Within minutes, the host introduces me to James, mid-40s (I think), tallish, musician (former architect he hastens to add) and only just about handsome enough to not be a burning waste of time.  He asks what I do, I say, “I work with hair loss” fixing my gaze firmly on his, and definitely, absolutely not on his receding hairline.  “Oh”, he says, bristling with the energetic confidence that signalled he was about to mansplain my own field to me.  “Well, hair loss, it’s genetic isn’t it?”.  I give a non-commital shrug “everything's genetic” I say.  He looks pleased with himself. I take a small breath and try to ignore the prickle of irritation I get every time I hear the same redundant answer to a question I wasn’t asking.   

James, this is for you, and for every other sheep who bleats “it’s genetic” when the subject of hair loss comes up.  As though it explains something, when in reality it means almost nothing: not an identified gene, poor predictive power, genes identified by statistical association only, not a proposed pathology pathway, not a guaranteed outcome, and certainly not the end of the conversation. 

Where it all started

The idea that male pattern hair loss is inherited goes back at least to 1916, when Dorothy Osborn published Inheritance of Baldness in the Journal of Heredity [1]. In that paper, she argued that common baldness (androgenic alopecia) behaved like a sex-influenced trait and could be influenced by a single gene. A trait is simply a characteristic or physical feature. The paper itself illustrated only five family trees, and even in that measly sample group, some of them incomplete. Osborn proposed that baldness was dominant in men but recessive in women. 

In simple terms, that meant she believed one copy of the baldness gene could be enough for it to appear in a man, whereas a woman would need two copies for the trait to become visible. This fitted older ideas about X chromosome inheritance: men have one X chromosome, inherited from their mother, while women have two X chromosomes, one from each parent. Under that model, the baldness gene was thought to show more easily in men, but to remain hidden in women unless both X chromosomes carried it. She also suggested that women might show only partial baldness if they inherited two baldness genes or if illness helped bring out the trait.

Osborn was writing in the early Mendelian era, when genetics was still in its confident, pattern-hunting phase and researchers were keen to map visible traits into clean dominant and recessive rules. Mendel’s work had recently been re-established in scientific thinking, and family tree analysis became a popular method for inferring inheritance patterns from visible traits, often favouring simplified dominant vs recessive interpretations. A few years earlier, sex-influenced inheritance models had already been discussed for traits such as sheep horns, reinforcing the idea that a trait could behave like “dominant in one sex, recessive in the other.”

Whilst Osborn’s paper became historically important, it really should not have; by modern standards, its investigation methods were flimsy, and its conclusions were far more confident than the evidence allowed.  

The biggest problem is the paper moves from incomplete and unclear family history to an extremely confident Mendelian conclusion.  Missing and uneven data is one of the most serious criticisms of the paper.  If the conclusion rests heavily on incomplete charts, then the discovered inheritance pattern is less convincing.  That kind of weakness is why later authors quietly moved away from Osborn’s simple model toward polygenic (multiple genes) inheritance. 

The 1916 view was too simple.  Osborn’s model treated male pattern baldness as a single inherited trait, whereas later work attempted to show that androgenic alopecia is not a single gene condition, it could potentially be better understood as polygenic.  Meaning that multiple genetic variants may each make small contributions to susceptibility rather than one gene determining the outcome.

A study in 2017 [2] used genetic data from 52,874 White British men aged 40-69 years who self-reported androgenic alopecia in four different categories: no hair loss, slight hair loss, moderate hair loss, and severe hair loss. That analysis identified 287 independent genetic signals associated with male pattern baldness. These were not 287 genes related to baldness, but statistical association signals across the entire genome, often tagging wider regions of linked DNA that may include regulatory, non-coding sequences as well as nearby genes.  The researchers split the men into two groups: one group to identify the signals and build a polygenic risk score, and a second to test how well that score could distinguish men with more severe hair loss from those with none.

This paper had some serious strengths: a genuinely large dataset, genome-wide coverage supplied by UK Biobank, and an attempt to test how well common genetic variants could distinguish different levels of male pattern hair loss. If a genetic model could reliably identify who has hair loss, and how severe it is, that would be powerful evidence for a strong genetic basis. But even with all that data, the model fell short of anything deterministic. 

It performed reasonably well when separating the cleanest extremes, severe hair loss versus no hair loss, correctly distinguishing between the two about 78 times out of 100. Performance was weaker for moderate hair loss versus no hair loss, at about 68 out of 100, and weaker still for slight hair loss versus no hair loss, at about 61 out of 100, which is only a little better than chance. In other words, the model was better at separating the extremes than at identifying the subtler, clinically messier middle ground. 

Men below the midpoint for genetic risk were not protected: 14% still had severe hair loss, while 39% had none. By contrast, of those with a polygenic score in the top 10%, 58% reported moderate-to-severe hair loss. The age range also limits how strongly the findings can be relied upon.  Because the men were aged 40 to 69, this was a mid-life snapshot, meaning the model predicted hair status only at assessment time, meaning those with no hair loss or slight hair loss could go on to develop severe hair loss, this would significantly change the predictive value. 

The hair loss categories were also self-reported as part of a wider UK Biobank questionnaire, based on each man’s own perception of his hair loss rather than clinical grading, trichoscopy, or standardised scalp photography. We therefore do not know exactly how consistently participants interpreted the categories, or how they were instructed to distinguish slight, moderate, and severe hair loss.

A study carried out in 2018, is one of the largest fully published Genome Wide Association Study analyses of male pattern baldness using UK Biobank individual-level data [3]. The study included 205,327 European men who self-reported male pattern baldness on a scale of 1 to 4. The researchers measured DNA markers across the genome to ask how much of the variation in baldness could be explained by common genetic variants.

In plain English, the study found: if a younger man was already bald, having a bald father stood out as a stronger risk signal. But as men got older, baldness became more common across the whole group anyway, so the father’s baldness became less useful for explaining who was bald and who was not. Once a trait becomes common with age, family history can look less distinctive, because more men are affected regardless of whether their father was recorded as bald.

In this dataset, brothers resembled each other in baldness more strongly than fathers and sons did. Brothers usually share more than DNA: they are often raised in the same household, exposed to similar diets, grooming habits, life-stage conditions, and broader environmental influences. In family-based data, looking at what is inherited can therefore make baldness, or any trait in question, appear more strongly genetic than it really is, because shared environment can be loaded into the overall measure of inheritance.

Understanding Polygenic Risk

A polygenic score can tell us that inherited genetic variation contributes to risk, yet it still fails to predict individual outcomes reliably, and twin studies makes the limitation obvious: identical genetic background does not guarantee identical hair loss. That is exactly where metabolism and energy regulation become relevant. 

Genetics may shape baseline sensitivity, but systemic factors such as insulin resistance, inflammatory tone, microvascular function, and hormonal signalling influence whether that susceptibility is expressed, how early it appears, and how aggressively it progresses. In other words, the strongest reading of the evidence is not that androgenic alopecia “is genetic,” but that it is genetically influenced and metabolically modulated, which is a very different claim and far more clinically useful.

One genome multiple phenotypes

Cells may contain the same DNA but behave very differently because they do not express the same genes in the same way. Genes can be switched on or off at different times, in different patterns, and at different intensities depending on the cell type, tissue environment, hormones, inflammation, age, and other biological signals.  Epigenetics describes how the environment chemically modifies the machinery that reads DNA so that the ways genes are expressed changes without changing the underlying sequence.  

Science shows a genetic susceptibility dependent on environmental factors, what it does not show is genetic predetermination.  If hair loss were genetically predetermined in any simple sense, identical twins would be expected to lose hair in the same way and to the same degree, yet twin data show otherwise, with differences in whether hair loss occurs at all and with severity linked to factors such as smoking, stress, alcohol exposure, multiple marriages and BMI.  The broader hair loss literature supports this non-deterministic view. Twin data is important in genetic research because identical twins provide a literal test of genetic determinism: if the same DNA does not reliably produce the same outcome, genes cannot be at the determining factor.

Fraga and colleagues showed that identical twins can become increasingly different at the level of gene regulation as they age [4]. In other words, the genes are the same, but genetic output drifts, which is exactly why genetic susceptibility does not translate into fixed outcomes.  The study notes that increased money spent on hair loss products was associated with hair loss.  This is a clear example of how study results can be misread, especially when researchers are trying to isolate meaningful signals from millions of genetic variations.  The increased expenditure on hair loss products was a consequence, not a cause.

Genetics vs Gene Expression 

Genes can be upregulated and downregulated depending upon the environment.  Most genes are switched on and off, turned up and down, depending on context. The technical term is gene expression. A gene can be present, but barely used, or heavily used, depending on signals the cell is receiving.

Cells respond to their environment through signalling pathways. Those signals can come from:

• hormones (androgens, cortisol, insulin, thyroid hormones)

• inflammatory cytokines

• oxidative stress and nutrient status

• mechanical stress

• circadian rhythm and sleep disruption

• medications and toxins

These signals change which genes are expressed, that is why two people can carry identical genes, but express it differently.  Epigenetics is the layer of chemical regulation that influences gene expression without changing the physical DNA. 

The big mechanisms are:

• DNA methylation

• histone modifications

• regulatory RNAs

These do not rewrite the genome, but they can make certain genes easier or harder to read. Some epigenetic marks are relatively stable, some are dynamic and change with environment and age. In complex traits, epigenetics is one of the key ways “environment” gets under the skin and into our biology.

So what does it mean?

That brings us to the real issue with the phrase “it’s genetic.” In common use, it implies that there is a specific gene, or a fixed polygenic inheritance that explains androgenic alopecia. That is not what science shows.  There is no single gene that reliably determines how the condition appears or progresses in the way one would expect in a true single-gene disorder, and even the polygenic evidence points to risk association rather than a determination of outcome.

Instead, there are statistical associations, heritable tendencies, and risk-modifying variants with incomplete and inconsistent predictive value. The phrase therefore becomes clinically blunt and scientifically misleading. It compresses a dynamic, multifactorial process into a story of inherited inevitability.

Osborn, who introduced the concept of genetic inheritance, concluded that heredity “explains away the difficulties” which is revealing in the worst way.  It suggests heredity is being used as a neat bow on a messy problem rather than being rigorously weighed against alternative explanations.  

When we look at a patient with hair loss, research has shown a broader physiology that often travels with it: insulin resistance, chronic inflammation, high cholesterol, increased visceral fat, low vitamin D, low zinc, fibrosis of the scalp, altered androgen metabolism, oxidative stress, and microvascular strain. If you live in a way that repeatedly pushes the body into those states, it will express itself somewhere. For some people that may be weight gain, for others acne, fatigue, blood sugar instability, or hair loss. In that context, hair loss becomes the visible output of modifiable biological drivers acting on a susceptible system.  

So the more accurate statement is not “it’s genetic,” but “genetics may increase susceptibility, while onset, expression and severity are shaped by multiple interacting factors that have nothing to do with genetics.” It’s not as catchy or convenient, but that distinction matters.  It matters because if we look at someone with hair loss and just say “it’s genetic”, clinicians and patients stop looking for modifiable drivers that improve overall health and metabolism and will influence the course of hair loss conditions.

The real clinical question is not whether hair loss can run in families, but what is making it active, visible, accelerated or harder to recover from in the person sitting in front of us.

1. Osborn D. Inheritance of baldness. Journal of Heredity. 1916 Aug 1;7(8):347-55.
2. Hagenaars SP, Hill WD, Harris SE, Ritchie SJ, Davies G, Liewald DC, Gale CR, Porteous DJ, Deary IJ, Marioni RE. Genetic prediction of male pattern baldness. PLoS genetics. 2017 Feb 14;13(2):e1006594.
3. Yap CX, Sidorenko J, Wu Y, Kemper KE, Yang J, Wray NR, Robinson MR, Visscher PM. Dissection of genetic variation and evidence for pleiotropy in male pattern baldness. Nature communications. 2018 Dec 20;9(1):5407.
4. Fraga, M.F., Ballestar, E., Paz, M.F., Ropero, S., Setien, F., Ballestar, M.L., Heine-Suñer, D., Cigudosa, J.C., Urioste, M., Benitez, J., Boix-Chornet, M., Sanchez-Aguilera, A., Ling, C., Carlsson, E., Poulsen, P., Vaag, A., Stephan, Z., Spector, T.D., Wu, Y.Z., Plass, C. and Esteller, M. (2005) ‘Epigenetic differences arise during the lifetime of monozygotic twins’, Proceedings of the National Academy of Sciences, 102(30), pp. 10604–10609. doi: 10.1073/pnas.0500398102.