# Smoking and Acne Inversa: What the Evidence Actually Shows — and Why It’s Complicated

Canonical URL: https://acneinversa.life/en/blog/smoking-acne-inversa-evidence-cessation/
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Language: en
Category: Daily Life
Published: 2026-05-21
Last updated: 2026-05-21
Author: Dr. rer. nat. Dennis Alexander Kwiatkowski (Biochemist, Scientific Writer and Pharma Expert)
Tags: Acne Inversa, Hidradenitis Suppurativa, HS, Daily Life, smoking, tobacco, cessation, nicotine, modifiable risk factors, lifestyle

> Smoking is the single strongest modifiable risk factor for HS in published data. This article explains what the research actually shows, why quitting is harder than it sounds, and what cessation evidence exists specifically in HS.

Medical disclaimer: This website is for general educational information only and does not replace medical advice, diagnosis, or treatment. Please speak with qualified medical professionals about symptoms or treatment decisions.

## Article

The connection between smoking and hidradenitis suppurativa (HS) is one of the most consistently documented modifiable risk relationships in dermatology. Current smokers have roughly three to four times the odds of HS compared to non-smokers across multiple meta-analyses. Disease severity increases with smoking duration. Response to first-line therapy is worse in smokers. Recurrence after surgery is more likely in smokers. By any reasonable reading of the evidence, smoking is the single most well-evidenced modifiable contributor to HS at the patient level.

This article addresses the smoking question directly, without the dual evasions that often surround it in patient education. The first evasion is glib understatement — listing smoking among “lifestyle factors” without conveying the strength of the association. The second is moralistic lecturing — treating cessation as a matter of willpower rather than a difficult behaviour change with its own evidence base. Both are unhelpful. The honest version: the evidence linking smoking and HS is strong, the mechanism is biologically plausible, the benefit of cessation is real if incomplete, and quitting is hard. All of these are simultaneously true.

> **Educational content only.** Smoking cessation strategies should be developed with your general practitioner or a cessation specialist, who can provide appropriate medication, behavioural support, and follow-up.

## Key takeaways

- Current smoking is associated with a 3–4 fold increased odds of HS in pooled meta-analyses; population-based incidence data show roughly doubled HS incidence in smokers compared to non-smokers.
- Disease severity increases with smoking pack-years; response to medical and surgical treatment is worse in smokers.
- The mechanism likely involves both nicotine effects on follicular biology and immune function, and combustion products’ broader inflammatory effects.
- Cessation is associated with reduced HS development risk in new-onset disease and with improved post-surgical outcomes; whether cessation in established disease produces clear improvement is supported by suggestive but limited evidence.
- Combined pharmacotherapy plus behavioural support is the most effective cessation approach. Nicotine replacement therapy, varenicline, and bupropion all have evidence and can be used in HS patients.
- E-cigarettes are not a clean substitute and their long-term effects on HS specifically are not established.

## What the evidence actually shows

The current data on smoking and HS, drawn from multiple sources of varying study quality:

**Meta-analyses of cross-sectional and case-control studies.** The Acharya and Mathur 2020 meta-analysis (published in the Journal of the American Academy of Dermatology) reports an odds ratio of 4.26 (95% CI 3.68–4.94) for current smoking and HS, based on pooled analysis of multiple studies. A more recent 2024 meta-analysis (23 studies, approximately 29.5 million patients across health system datasets) reports a pooled odds ratio of 3.10 (95% CI 2.60–3.69). Both findings are statistically robust and clinically substantial.

**Population-based incidence data.** The Garg et al. U.S. population-based retrospective analysis identified approximately 3.9 million tobacco smokers and 8.0 million non-smokers in healthcare records. HS incidence was 0.20% in smokers versus 0.11% in non-smokers (adjusted odds ratio 1.90, 95% CI 1.84–1.96). The lower odds ratio in this analysis compared to cross-sectional meta-analyses reflects the more conservative incidence framework, but the doubling of incidence is still clinically meaningful.

**Severity correlations.** Several studies have shown that smoking pack-years (a measure of cumulative smoking exposure) correlates with HS severity by Hurley stage. The Dutch cohort analysis reported by Schrader et al. found pack-years as an independent predictor of severity in multivariate analysis. The effect is dose-related: more smoking is associated with worse disease.

**Treatment response.** A retrospective cohort study by Denny and Anadkat (2017) found that current smokers had worse response to first-line therapy for HS than non-smokers. The mechanism is not fully characterized but is consistent with broader observations that smoking impairs response to immunomodulatory therapy across multiple inflammatory diseases.

**Post-surgical outcomes.** Smoking is associated with poorer wound healing across surgical specialties generally, and HS surgery specifically. Higher rates of dehiscence, infection, delayed healing, and recurrence have been documented. Smoking cessation peri-operatively (typically at least 4 weeks before and 4 weeks after surgery) is associated with substantial reduction in surgical complications.

**Cessation effects.** A Korean cohort study (Park et al., JAMA Dermatology, 2024) showed that participants who quit smoking and remained smoke-free had reduced subsequent HS development risk compared to continuous smokers; participants who resumed or initiated smoking had elevated risk. This addresses the question of cessation in HS-naive populations rather than established disease, but is consistent with a causal contribution of smoking. For patients with established HS, smaller observational studies suggest that cessation may produce modest improvement in disease activity, but the evidence is less robust than for prevention.

The combined weight of evidence is unusual for a dermatological condition — most lifestyle-disease associations are weaker and more contested. The smoking-HS association is one of the stronger ones in dermatology, comparable in robustness to the smoking-psoriasis-severity link.

## Why smoking aggravates HS: plausible mechanisms

The mechanistic picture is not fully understood but several pathways are well supported.

**Nicotine effects on follicular biology.** Nicotine influences the function of hair follicle keratinocytes and can promote follicular plugging — the early initiating step in HS lesion formation. Nicotine also alters sebaceous and apocrine gland function. These effects are plausibly relevant to HS pathogenesis.

**Effects on neutrophils and innate immunity.** Cigarette smoke alters neutrophil function in ways that may contribute to the abnormal inflammatory response characteristic of HS. Smoking increases neutrophil migration to inflammatory sites and modifies their response to bacterial stimuli.

**Effects on IL-17 and Th17 axis.** The IL-17/Th17 inflammatory pathway is central to HS pathogenesis (and the basis for the IL-17-inhibitor biologics now approved for HS). Smoking has documented effects on Th17 cell differentiation and IL-17 production that are biologically consistent with aggravating IL-17-driven diseases including HS.

**Tissue hypoxia.** Smoking reduces tissue oxygenation through both carbon monoxide binding to haemoglobin and vasoconstriction. Hypoxic skin is more vulnerable to inflammation, impaired wound healing, and impaired immune defence — all relevant to HS.

**Direct toxic effects of combustion products.** Cigarette smoke contains thousands of compounds beyond nicotine, many of which are toxic to skin cells and promote oxidative stress. These effects may explain why smokeless tobacco use, which delivers nicotine without combustion, may be less strongly associated with HS than cigarette smoking — though smokeless tobacco data in HS specifically is limited.

**Microbiome effects.** Smoking alters the cutaneous and oral microbiome in ways that may influence inflammatory skin disease.

Multiple mechanisms operating simultaneously is consistent with the size of the observed clinical effect.

## What cessation does and does not do

The honest framing of what quitting smoking is likely to achieve.

**For people without HS yet:** cessation reduces the risk of developing HS in the future, particularly compared to continued smoking. This is supported by the recent Korean cohort data. For young people with a family history of HS, smoking cessation (or never starting) is one of the more meaningful modifiable interventions available.

**For people with established HS:** cessation likely produces some improvement in disease activity, but the magnitude is variable and not as dramatic as the inverse association in cross-sectional data might suggest. Some patients report substantial improvement after cessation; others see little change in established disease. The reasons for individual variation are not well characterized — possibly the chronicity of the disease at the time of cessation, possibly genetic factors, possibly the contribution of other unaddressed risk factors.

**For people with established HS preparing for surgery:** cessation in the perioperative period substantially reduces surgical complications, wound healing problems, and likely reduces recurrence rates. This effect is robust and is one of the most clearly justified arguments for cessation in HS patients with established disease.

**For people on biologic therapy:** smoking is associated with poorer response to biologics across multiple inflammatory diseases, plausibly including HS. Cessation may improve treatment response, though specific HS data on this is limited.

The realistic framing for an HS patient considering cessation: it is unlikely to be a cure, but it is likely to make every other intervention you try more effective and to reduce the long-term burden of disease. This is a substantive benefit even if it is less than the inverse epidemiological correlation might suggest.

## Why quitting is hard

The empirical reality of smoking cessation: it is one of the most difficult behaviour changes available. Average success rates for unaided cessation attempts run at 3% to 7% sustained at one year. Most people who quit successfully require multiple attempts before success — six to thirty attempts are typical, not unusual.

This is not because smokers lack willpower. Nicotine is highly addictive — comparable to or more addictive than several controlled substances. The withdrawal syndrome includes irritability, anxiety, low mood, sleep disruption, difficulty concentrating, and intense cravings, peaking in the first week and resolving over weeks to months. The behavioural component of smoking — the rituals, the social associations, the contexts that trigger urges — persists even after physical withdrawal has resolved.

The implication: cessation is most likely to succeed when approached as a structured project with pharmacological and behavioural support, not as a willpower challenge.

The strongest evidence-based cessation approaches:

**Nicotine replacement therapy (NRT)** — patches, gums, lozenges, inhalers, sprays. Provides nicotine without combustion products, reducing withdrawal severity. Doubles or triples the success rate compared to unaided cessation. Combining a long-acting form (patch) with a short-acting form (gum or lozenge) for breakthrough cravings is more effective than either alone. Available over the counter in most countries; in Germany, NRT products are widely available in pharmacies.

**Varenicline (Champix in Europe, Chantix in the U.S.).** A partial nicotinic receptor agonist. Approximately doubles cessation success rates compared to placebo. Available on prescription. Side effect profile includes nausea, vivid dreams, and (rarely) mood changes that warrant clinical monitoring.

**Bupropion (Zyban for cessation indication).** An atypical antidepressant with established cessation efficacy. Available on prescription. May be particularly useful in patients with depression comorbidity. Contraindicated in patients with seizure history.

**Combined pharmacotherapy and behavioural support.** The Cochrane review and broader evidence base consistently shows that combining medication with structured behavioural support — counselling, group support, telephone quit-lines, structured cessation programs — produces the highest success rates, substantially better than either component alone.

In Germany, smoking cessation support is available through general practitioners, specialty cessation programs, and (partially) covered by statutory health insurance. The German Cancer Research Center operates a national telephone quit-line. Pharmacies offer some cessation counselling.

## E-cigarettes and vaping

The role of e-cigarettes in cessation and in ongoing HS management is genuinely uncertain.

For cessation, e-cigarettes have some evidence supporting their use as a transition tool away from combustible cigarettes. Several large randomized trials, including the U.K. NICE-supported evidence, suggest they can be more effective than NRT for cessation in some users. They deliver nicotine without combustion products, which addresses the combustion-related pathway of harm.

For HS specifically, the evidence on e-cigarettes is essentially absent. Several considerations apply:

- E-cigarettes still deliver nicotine, which has direct effects on follicular biology that may be relevant to HS independently of combustion.
- Some e-cigarette devices (particularly older or illicit-market products) produce significant aerosol contaminants that may have their own toxicity.
- The 2019 EVALI outbreak (vaping-associated lung injury) was strongly linked to illicit cannabis vape cartridges containing vitamin E acetate; regulated nicotine vape products from licensed manufacturers were not implicated, but the episode underscores that not all vape products are equivalent.
- Long-term safety data on chronic e-cigarette use is still accumulating.

A reasonable framing: if e-cigarettes help you successfully transition off combustible cigarettes, the net harm reduction is likely positive. Indefinite continued e-cigarette use without further reduction is less clearly beneficial for HS. Treating e-cigarettes as a temporary cessation tool rather than a permanent substitute is consistent with current public health guidance in most European countries.

## Practical approach to cessation in HS

If you have HS and are considering cessation, the practical structure that tends to work:

1. **Discuss with your general practitioner or a cessation specialist.** A structured approach with appropriate medication and follow-up is substantially more effective than unsupported attempts.
1. **Choose a quit date in advance.** Not so soon that you cannot prepare; not so distant that you postpone indefinitely. Two to four weeks ahead is typical.
1. **Plan for the difficult period.** Identify situations and triggers that will be hard, plan substitutes, arrange social support. The first two weeks are usually the most difficult.
1. **Use pharmacological support.** NRT, varenicline, or bupropion as appropriate to your situation. Combination NRT (patch plus gum or lozenge) for those using NRT.
1. **Engage behavioural support.** Cessation counselling, group programs, telephone quit-lines, or smartphone apps. Multiple sources of support correlate with better outcomes.
1. **Expect and plan for setbacks.** Most successful quitters had multiple attempts before success. A lapse is not failure; it is data about what to do differently next time.
1. **Address other modifiable factors.** Weight management, alcohol moderation, stress management, and other lifestyle factors interact with cessation success. Addressing them together is often more sustainable than addressing them in sequence.
1. **Consider timing relative to other treatment.** If surgery is planned, cessation in the perioperative window has particularly strong evidence. If starting biologic therapy, cessation may improve response.
1. **Use HS-related motivation, but do not rely on it alone.** Specific motivation about HS can help start a cessation attempt; sustained motivation usually comes from broader sources (family, finances, general health) over the months to years required for sustained cessation.

## A note on the moral framing

Smoking cessation discussions in medical settings can drift toward moralism — explicit or implicit messaging that the patient is harming themselves through personal failing. This framing is unhelpful and counterproductive.

Smoking is a behaviour shaped by addiction, social context, life history, mental health, and structural factors. Patients who smoke have usually heard repeatedly that they should quit and are aware that smoking is bad for their health. What is generally missing is not awareness or motivation but access to effective cessation support delivered in a non-judgmental framework.

If you are an HS patient who smokes and your dermatologist’s primary engagement with this is to lecture you about it, that is not maximally helpful clinical practice. A more useful conversation focuses on whether you are interested in attempting cessation, what would help, what previous attempts have looked like, and what specific support could be arranged.

If you are an HS patient who has tried to quit and not succeeded, that is the typical pattern rather than a personal failure. The next attempt, with better support and adjusted strategy, has reasonable prospects.

## FAQ

### Will quitting smoking cure my HS?

No. Smoking cessation is associated with improved disease activity in some patients, particularly those with newer-onset disease, but it does not cure HS. The underlying inflammatory tendency remains and other contributors persist.

### How long after quitting should I expect to see improvement?

This is variable and not well characterized. Some patients report subjective improvement within weeks to months; others see little change in established disease over the first year. Disease activity has multiple inputs (medication, weight, hormonal factors, friction, infection control), and smoking cessation is one input among several.

### What if I cannot quit completely — does cutting down help?

Reducing cigarettes per day has some health benefit but is substantially less effective than complete cessation. For HS specifically, the threshold effect of complete cessation appears more important than dose reduction. Approaches that allow continued nicotine through cleaner delivery (NRT, possibly e-cigarettes) while eliminating combustion may be a useful intermediate step toward complete cessation.

### Is smokeless tobacco a safer alternative?

Smokeless tobacco (snus, chewing tobacco) eliminates combustion-related harm and may be associated with lower HS risk than smoking. However, it carries its own significant health risks (oral cancer, cardiovascular disease, nicotine dependence) and is not generally recommended as a cessation strategy. Its specific effect on HS is poorly studied.

### Can I be prescribed cessation medication on GKV in Germany?

Pharmacological cessation aids (varenicline, bupropion for cessation indication) require prescription. Reimbursement under GKV varies; some sickness funds cover cessation aids under specific structured cessation programs, others require self-payment. The German Cancer Aid (Deutsche Krebshilfe) and other health organizations offer free counselling resources.

### Does smoking affect biologic therapy for HS?

Smoking is associated with poorer response to biologic therapy across multiple inflammatory diseases. The effect in HS specifically is plausible but less directly documented. Optimizing all modifiable factors (smoking, weight, friction, etc.) is reasonable when starting expensive long-term therapy where response matters substantially.

### What if I am exposed to second-hand smoke at home or work?

Second-hand smoke exposure has been less directly studied in HS, but the broader evidence on second-hand smoke and inflammatory disease is consistent with adverse effects. Reducing household exposure (designating smoking outside the home, requesting workplace smoke-free policies) is reasonable.

## References

1. Acharya P, Mathur M. *Hidradenitis suppurativa and smoking: a systematic review and meta-analysis.* Journal of the American Academy of Dermatology, 2020.
2. Garg A, Papagermanos V, Midura M, Strunk A. *Incidence of hidradenitis suppurativa among tobacco smokers: a population-based retrospective analysis in the U.S.A.* British Journal of Dermatology, 2018.
3. Park S et al. *Smoking Cessation and Risk of Hidradenitis Suppurativa Development.* JAMA Dermatology, 2024.
4. Denny G, Anadkat MJ. *The effect of smoking and age on the response to first-line therapy of hidradenitis suppurativa: an institutional retrospective cohort study.* Journal of the American Academy of Dermatology, 2017.
5. Stead LF et al. *Combined pharmacotherapy and behavioural interventions for smoking cessation.* Cochrane Database of Systematic Reviews.
6. Deutsches Krebsforschungszentrum (DKFZ). *Rauchertelefon und Tabakentwöhnungsressourcen.*