Alopecia areata is caused by the immune system attacking hair follicles, but what triggers that immune response varies from person to person. Genetics, stress, infections, and other autoimmune conditions can all play a role. About 2% of the global population is affected, with a lifetime risk estimated between 1.7% and 2.1%. Most cases first appear between the ages of 20 and 34, though it can start at any age.
How the Immune System Turns on Hair Follicles
Hair follicles normally have a form of immune protection, a kind of invisibility cloak that keeps immune cells from noticing them. In alopecia areata, that protection breaks down. When it does, the follicles begin producing stress signals that attract a specific type of immune cell. These cells release inflammatory chemicals that damage the follicle and force it out of its growth phase prematurely. The hair falls out, and the follicle can’t produce a new strand until the immune attack subsides.
This process can happen even if someone has never had an immune problem before. The collapse of that follicle protection and the resulting inflammation are enough to cause hair loss on their own. Once the cycle starts, the inflammatory signals can keep it going, which is why patches of hair loss sometimes expand or persist for months.
Genetics and Family History
Alopecia areata has a strong genetic component. Many of the genes linked to it belong to a family called the HLA complex, which controls how the immune system identifies threats. Specific variants in genes like HLA-DRB1 and HLA-DQB1 have been associated with higher risk. Other implicated genes are involved in inflammation and immune regulation more broadly.
If a close family member has alopecia areata, your own risk is elevated. The condition doesn’t follow a simple inheritance pattern, though. It’s not one gene, one outcome. Dozens of genes contribute small amounts of risk, and they interact with environmental factors to determine whether the disease actually develops. You can carry every known risk variant and never lose a hair, or you can develop it with only a few.
Stress as a Trigger
The link between emotional stress and alopecia areata has been debated for decades. For a long time, many researchers dismissed it as folklore. But clinical observations consistently show that episodes of hair loss follow severely stressful life events, and the biology supports a plausible connection. Stress hormones can disrupt the immune environment around hair follicles, potentially breaking down the protective barrier that normally shields them.
Stress is better understood as a trigger than a root cause. It doesn’t create alopecia areata from nothing, but in someone who is genetically susceptible, a period of intense or prolonged stress can tip the balance. This is why some people experience their first episode after a job loss, a death in the family, or another major life disruption, while others with similar stress levels never develop it.
Linked Autoimmune Conditions
People with one autoimmune condition are more likely to develop another, and alopecia areata frequently overlaps with thyroid disease. Research using genetic analysis has found that Hashimoto’s thyroiditis and hypothyroidism both significantly increase the risk of alopecia areata. The two conditions share overlapping genetic susceptibility, particularly in the same HLA gene variants. One study found that a specific HLA combination appeared at notably higher rates in people who had both thyroid antibodies and alopecia areata compared to controls.
Vitiligo, type 1 diabetes, and other autoimmune conditions also show up more often in people with alopecia areata than in the general population. This clustering suggests a shared underlying tendency toward immune dysregulation rather than a direct cause-and-effect relationship between the diseases.
Viral Infections, Including COVID-19
Viral infections can act as a trigger by overstimulating the immune system. The most extensively documented recent example is COVID-19. Multiple case reports describe new onset, recurrence, or worsening of alopecia areata after SARS-CoV-2 infection, with symptoms typically appearing about four weeks after the initial illness.
The proposed mechanism involves a cascade: the virus causes widespread inflammation and elevated levels of inflammatory chemicals in the blood. Some of these chemicals directly interfere with hair growth. The infection may also cause oxidative stress in hair follicles, which makes them more visible to the immune system. In some cases, cross-reactive antibodies originally directed at the virus may mistakenly target hair follicle tissue.
COVID-19 vaccination has also been linked to new cases in a small number of reports. The suspected mechanism involves the spike protein produced by the vaccine triggering an immune response that, in rare cases, cross-reacts with hair follicle proteins. Additives in the vaccines, such as PEG 2000 in mRNA vaccines and polysorbate 80 in others, have been identified as potential activators of T cells in affected patients. These cases remain uncommon relative to the number of people vaccinated.
Medications That Can Trigger Hair Loss
Certain medications have been linked to alopecia in studies with strong levels of evidence. The most notable category is a class of biologic drugs used to treat other autoimmune conditions, including adalimumab and infliximab, both of which suppress part of the immune system but can paradoxically trigger autoimmune reactions elsewhere. Other medications with documented associations include certain anti-seizure drugs, blood thinners, immune-modulating treatments like interferon and tacrolimus, and several cancer therapies.
If you notice new hair loss after starting a medication, it’s worth flagging with whoever prescribed it. Drug-triggered cases sometimes resolve after the medication is stopped, though recovery timelines vary.
Vitamin D Deficiency
Low vitamin D levels appear more frequently in people with alopecia areata than in the general population, and some research has found a correlation between how low levels drop and how severe the hair loss becomes. Vitamin D plays a role in regulating the immune system, and deficiency is considered an environmental trigger that may contribute to autoimmune conditions generally.
This doesn’t mean low vitamin D directly causes alopecia areata. But in someone with genetic susceptibility, it may be one of several factors that make an episode more likely or more severe. Checking your vitamin D status through a simple blood test is straightforward, and correcting a deficiency is low risk.
The Gut Microbiome Connection
One of the more surprising findings in recent research is the role of gut bacteria. In animal studies, mice whose gut bacteria were depleted with antibiotics were protected from developing alopecia areata. Researchers identified a specific bacterial species that was overrepresented in affected mice before any visible hair loss appeared, suggesting the gut imbalance came first.
In humans, stool samples from people with alopecia areata show a striking difference in gut bacteria composition compared to healthy controls. Certain bacterial families are consistently overrepresented. The connection appears to work through the immune system: gut bacteria influence the behavior of the same type of immune cells that drive the attack on hair follicles. Mice without those gut bacteria had fewer of these destructive immune cells in the lymph nodes near their skin.
This research is still being translated into practical interventions, but it adds an important piece to the puzzle. Alopecia areata isn’t just about what’s happening at the scalp. It reflects a broader immune state that can be shaped by what’s going on in the gut.
Why It Often Takes Multiple Factors
Most people who develop alopecia areata don’t have a single identifiable cause. The pattern that emerges from research is one of layered risk: a genetic foundation that makes the immune system prone to attacking hair follicles, combined with one or more triggers that set the process in motion. Those triggers could be a viral illness, a stressful period, a nutritional gap, a shift in gut bacteria, or some combination.
This layered model explains why the condition is so unpredictable. Two people with identical genetics might have completely different experiences depending on what else is happening in their bodies and lives. It also explains why hair often regrows on its own, only to fall out again later when a new trigger appears. The underlying susceptibility remains, even when the hair comes back.