HS triggers, without the guesswork.

The only controlled study on this question (a 1982 case-control of 40 people with HS and matched controls) found no significant difference in deodorant use before disease onset. Guidelines consider the evidence insufficient to recommend avoiding deodorants routinely. HS is not caused by hygiene, in either direction.

Individual products can still irritate individual skin: fragrances, alcohol and baking soda are common culprits on skin that is already inflamed. That is an irritation question, not an HS-cause question.

Read "neutral" as a reported signal, not a rule (the only controlled study found no link with onset). It does not mean deodorant and antiperspirant works the same way for everyone with HS.

Choosing a deodorant with HS: the full guide →

The same 1982 case-control study found no significant difference in razor or depilatory use before HS onset. In a retrospective series, 57.5% of patients shaved but only three considered it aggravating.

Cuts and irritation can locally worsen skin that already has lesions. Gentle-shaving advice from dermatology organizations is prudential, not trial-based.

Read "neutral" as a reported signal, not a rule (controlled and retrospective data show no causal role). It does not mean shaving and hair removal works the same way for everyone with HS.

Shaving with HS: the full guide →

In a 110-person questionnaire study, tight clothing and friction were among the most frequently perceived aggravating factors. A mechanistic review proposes mechanical stress, occlusion and shear forces as plausible promoters of lesions in predisposed areas.

No controlled clothing intervention exists. Guidelines consider the evidence insufficient for a formal recommendation, while noting it is reasonable to avoid friction that is individually problematic.

Read "worsening" as a reported signal, not a rule (patient-reported aggravation and mechanical plausibility). It does not mean friction and tight clothing works the same way for everyone with HS.

Luca's experience · one person, not a prediction. Waistbands and tight sleeves on active areas were something I learned to notice early. Small change, real difference in comfort for me.

Heat and sweating are frequently reported aggravators in patient surveys. A small 2022 study found no objective excess sweating in HS, but a pro-inflammatory profile in patients' sweat and a higher subjective burden.

Sweat, heat, occlusion and friction are hard to separate from each other. Inflammatory molecules in sweat do not demonstrate that sweat causes flares.

Read "mixed" as a reported signal, not a rule (frequently reported, with discordant findings). It does not mean sweat and heat works the same way for everyone with HS.

Gut barrier. In a controlled human hyperthermia study, raising core temperature by 2 degrees C produced a modest increase in the lactulose/rhamnose permeability ratio in both younger and older adults. The exposure reflects heat stress rather than sweating itself and was not an HS outcome.

Luca's experience · one person, not a prediction. Summer was reliably harder for me for years. Whether that was sweat, friction or both, my notes never fully settled.

A 2007 open-label pilot gave 22 people zinc gluconate 90 mg/day: 8 complete and 14 partial remissions, mostly in early-stage disease. A retrospective series of 66 people combining zinc with topical triclosan saw fewer nodules and flares. A systematic review calls the signal promising but unproven.

There is no randomized placebo-controlled trial. High-dose zinc over time can cause copper deficiency and gastrointestinal effects, which is why medical supervision matters.

Read "beneficial" as a reported signal, not a rule (small non-randomized clinical studies). It does not mean zinc works the same way for everyone with HS.

Gut barrier. In a small human intervention, 12 people with Crohn's disease in remission and elevated permeability had a lower lactulose/mannitol ratio after eight weeks of zinc supplementation. The uncontrolled disease-specific result does not establish an effect in the general population and was not an HS outcome.

Zinc and HS: the full evidence page →

Turmeric is one of the supplements people with HS use most: in a 303-person survey it was among the most common complementary approaches. That tells us about popularity, not efficacy.

No HS-specific clinical study of curcumin exists. General anti-inflammatory findings from lab research do not transfer automatically to HS.

Gut barrier. In an animal study of methotrexate-induced enteritis, curcumin reduced markers of intestinal barrier injury and permeability in rats. This is a disease-model finding, not human evidence and not an HS outcome.

Turmeric and HS: what we actually know →

Vitamin D deficiency is very common in HS (75-100% of samples in a 2024 systematic review). A small pilot supplemented 14 deficient patients for six months and reported fewer nodules in most of them.

No randomized trial exists. Obesity, skin pigmentation, season and reduced sun exposure can explain part of the deficiency association.

Read "beneficial" as a reported signal, not a rule (a small pilot in deficient patients and deficiency associations). It does not mean vitamin d works the same way for everyone with HS.

Gut barrier. In a human randomized placebo-controlled trial in 27 people with Crohn's disease in remission, vitamin D maintained permeability measures while permeability increased in the placebo group over three months. The sample was small and disease-specific, and intestinal permeability was not an HS outcome.

Luca's experience · one person, not a prediction. Vitamin D was one of the first things my blood tests flagged. I wrote a full article about it.

Vitamin D and HS: full article →

In a 303-person survey, 47.7% of Epsom salt bath users perceived them as helpful, but that does not establish an effect of magnesium. A separate 20-person controlled study tested oral liposomal magnesium only as part of a combination with myo-inositol and folic acid alongside antibiotics and a normocaloric diet; the supplement group had a significant within-group reduction in Sartorius score.

The study cannot isolate magnesium from myo-inositol, folic acid, antibiotics or diet, and it was not a randomized placebo-controlled trial. There is still no HS study of oral magnesium alone.

Gut barrier. Animal and cell-model evidence found that dietary magnesium availability influenced mucosal integrity and tight-junction repair in DSS colitis, with supplementation improving restoration after injury. This does not directly establish permeability effects in humans and was not an HS outcome.

In a case-control study of 41 people with HS and 41 controls, higher dietary n-3 polyunsaturated fatty acid intake correlated with lower Sartorius severity after adjustment for sex, age, BMI and total energy intake.

This was dietary intake within a broader Mediterranean pattern, not a fish-oil trial. No HS-specific study establishes the effect of an omega-3 supplement, a formulation or a dose.

Read "beneficial" as a reported signal, not a rule (dietary-intake associations in observational studies). It does not mean omega-3 fatty acids works the same way for everyone with HS.

Gut barrier. In an exploratory human analysis of the randomized LIBRE trial, higher plasma DHA was inversely associated with LBP and fecal zonulin during a Mediterranean-diet intervention. Omega-3 effects were not isolated from the broader diet, and this was not an HS outcome.

Human studies report differences in the gut microbiome of some people with HS compared with controls. These observations provide a research rationale for microbiome-directed approaches, but they do not show that a probiotic changes HS activity.

No HS-specific clinical trial of an oral or topical probiotic was identified. Microbiome differences may reflect antibiotics, diet, obesity, inflammation or the disease itself, and results vary across studies.

Gut barrier. A systematic review and meta-analysis of 26 human randomized trials reported improvements across several intestinal-barrier markers with probiotics, although effects varied by strain, population and endpoint. This review did not evaluate HS outcomes.

A 2010 report described people with inflammatory bowel disease and suppurative dermatoses, including biopsy-confirmed HS, whose suppuration decreased during vitamin B12 treatment. A later micronutrient review found only a few such cases.

There is no randomized trial in HS and the reported HS cases also had inflammatory bowel disease. The evidence does not establish an effect in people with HS alone or show that baseline B12 status predicts response.

Gut barrier. In animal studies using Drosophila recurrent gut injury and mouse acute colitis models, vitamin B12 maintained epithelial junctions and reduced barrier disruption. These preclinical findings are not human evidence and were not HS outcomes.

In a 20-person controlled study of HS with impaired glucose metabolism, 10 participants received myo-inositol, folic acid and liposomal magnesium alongside the same background of antibiotics and a normocaloric diet. The supplement group had a significant within-group reduction in Sartorius score and HOMA-IR.

The groups were tiny and not reported as randomized. The design cannot separate the three supplement ingredients from each other or from concurrent antibiotics and diet, and it does not establish the effect of folic acid alone.

This is the strongest association in the whole trigger list. A 2024 meta-analysis of 23 studies found smoking associated with HS at an odds ratio of 3.10. A national cohort of 6.2 million people found lower risk of new HS in former smokers versus persistent smokers, with the benefit emerging after about 3-4 years. A 1,689-person cohort correlated pack-years with more affected sites, more pain and worse quality of life.

These are epidemiological data, not randomized trials. The evidence that quitting improves already-established HS is weaker than the evidence linking smoking to developing it and to severity.

Read "strongly worsening" as a reported signal, not a rule (meta-analysis and national cohort data). It does not mean smoking works the same way for everyone with HS.

Gut barrier. In an animal study, chronic cigarette-smoke exposure increased small-bowel permeability, bacterial translocation and tight-junction damage in mice, with no comparable barrier change in the colon. This is preclinical evidence and was not an HS outcome.

Smoking and HS: the full evidence page →

A 2024 meta-analysis found obesity associated with HS at an odds ratio of 2.48. In a survey of 249 people after bariatric surgery, 35% reported reduced symptoms, and weight loss above 15% was associated with significantly lower severity. A nationwide study found bariatric surgery associated with less new-onset HS.

HS affects people at every BMI, and weight-loss results in existing HS are mixed: in the nationwide study, the reduction of recurrences in pre-existing HS was not statistically significant. Post-surgical skin excess and nutritional deficiencies can even worsen some patients.

Read "worsening" as a reported signal, not a rule (association with severity and mixed weight-loss data). It does not mean body weight works the same way for everyone with HS.

Gut barrier. In a small human weight-loss intervention, elevated lactulose/mannitol ratios in adults with severe obesity and liver steatosis fell into a previously reported normal range during weight reduction. The study was uncontrolled, cannot isolate body weight from diet and metabolic changes, and did not assess an HS outcome.

Body weight and HS: the full evidence page →

Stress is one of the aggravators patients report most: 50% in one retrospective series, and it appeared among the most cited factors in the earliest natural-history survey. A 2024 cross-sectional analysis found higher perceived stress in people with HS.

The relationship is almost certainly bidirectional: HS itself generates stress. No prospective trial shows that a stress-reduction intervention reduces flares.

Read "worsening" as a reported signal, not a rule (patient self-reports, relationship likely bidirectional). It does not mean stress works the same way for everyone with HS.

Gut barrier. In a human experimental study, acute psychological stress increased paracellular permeability in rectal biopsies from healthy volunteers. This was an acute laboratory stressor, not chronic everyday stress, and intestinal permeability was not an HS outcome.

Luca's experience · one person, not a prediction. My worst flares and my worst months at work overlapped more than once. I wrote a full article about what I changed.

HS and stress: full article →

In a 283-person survey, 62.4% reported perimenstrual worsening, with the flare most often in the week before menstruation. A second survey found worsening with menses in 76.7% of respondents. A small 1986 crossover trial tested two hormonal regimens with improvement in some patients.

The pattern is consistent across surveys but not universal (about one in five report no change), and the data are self-reported. Contraception, PCOS, pregnancy and menopause can shift HS in different directions.

Read "worsening" as a reported signal, not a rule (consistent survey reports of perimenstrual flares). It does not mean menstrual cycle and hormones works the same way for everyone with HS.

Gut barrier. A human translational study found that physiological progesterone increased barrier resistance in primary colon tissue and that higher progesterone correlated with lower plasma LPS during pregnancy. It did not test menstrual-cycle phases or HS outcomes, so relevance to cyclical HS flares remains indirect.

HS and the menstrual cycle: full article →