The studies revealed that psychological stress may be a cause as well as a result of HS. As such, it is important for dermatologists to understand the impact of stress on disease flares, as managing psychological conditions may offer disease remission in select patients. There were nine studies on psychological stress. Seven studies were cross-sectional surveys, one was a case-control study, and one was a population retrospective review.^6–14 The studies were observational but showed strong associations, thus resulting in moderate-quality evidence. However, these studies are important to consider because designing a high-quality randomized clinical trial for psychological stress and HS can be met with inherent challenges associated with studying stress factors. One of the proposed mechanisms by which psychological well-being plays a role in HS flares was systemic inflammatory process involved in psychiatric conditions.^9,51 According to previous studies, the hypothalamic-pituitary axis (HPA) is a potent regulator of inflammation and can be disturbed in childhood through different processes, such as traumatic events.⁹ Interestingly, depression and other psychiatric states have also been closely linked to inflammation by altering the HPA axis.^9,51 To assess the link between traumatic events and the development of HS, a case-control study of 17 HS patients and 213 controls was completed. Gielen et al. found that childhood emotional traumatic events were significantly associated with the development of HS (OR 5.03, p <0.05).⁹

On the contrary, the disease itself may be a cause of patients’ psychological stress. The stress induced by patients’ appearance may then play a role in exacerbating the disease. As such, it is important to manage all patient comorbidities. Quality of life is more commonly impaired with HS than other inflammatory cutaneous disorders.^1,12,22 Kouris et al. found that patients with HS had significantly higher anxiety scores than patients without HS (6.41 ± 3.31 vs. 5.00 ± 1.59, p < 0.001).¹² Similarly, they scored higher in depression scales (5.45 ± 2.79 vs. 4.16 ± 1.54, p < 0.001) and in loneliness and social isolation scores (42.86 ± 8.63 vs. 35.57 ± 6.17, p < 0.001). Moreover, their self-esteem scores were significantly lower than healthy controls (18.91 ± 1.79 vs. 19.77 ± 2.53, p = 0.008).¹² These findings are in accordance with the findings in other studies.⁸ For example, the number of lesions on exposed skin plays a vital role in the stigmatization level of patients. However, involvement of different areas of the body affects patients differently. For instance, in a questionnaire study, analysis of respondents revealed that even involvement of the uncovered areas of the body significantly impacts quality of life.¹³

More rare psychological pathologies, such as bipolar disorder and alexithymia (the inability to identify and describe emotions experienced by one’s self), have been observed in HS patients.^6,14 In one cross-sectional questionnaire, the mean score for the Toronto Alexithymia Scale (TAS) was 55.37 compared to 40.96 in the controls (p < 0.001).⁶ In a separate study, bipolar disorder was present in 0.7% of patients with HS compared to 0.1% prevalence in patients without HS.¹⁴ Importantly, there have been studies assessing coping strategies for HS patients with negative psychosocial impacts from HS. Two sets of interviews and focus groups of 12 HS patients revealed that these patients felt “unattractive,” particularly with many/large scars, helpless from limited daily activities caused by the painful lesions, stigmatized and embarrassed by visible scars, and worried other people may find them contagious. Further, the psychological burden was centered around three main themes: shame, pain, and coping mechanisms.^7,10 The interviews revealed that social support was the most beneficial coping strategy, as patients who were acquainted with others who shared their diagnosis valued their understanding of their symptoms.¹⁰ Patients may benefit from the Hidradenitis Suppurativa Foundation (www.hs-foundation.org), which provides a valuable forum and supportive community for HS patients.⁷ However, online support groups may be more suitable for individuals who have longstanding disease. Newly diagnosed patients may find the exposure to the potential severity of HS through the support groups to be distressing. Cognitive-behavioral therapy (CBT) may be a well-suited therapy for HS patients, as it increases individuals’ compassion for themselves and reduces feelings of shame, although it has not been specifically studied in HS patients.¹⁰

In their survey of 143 HS patients, Kirby et al. established that patients with higher resilience levels had a smaller decrease in their health-related quality of life (HRQOL) scores as depressive symptoms increased. The authors proposed that resilience can be taught through online videos, self-guided books or readings, telephone calls with individuals or groups, or in-person small group sessions with exercises and discussions. Hence, there may be a role for resilience training programs for HS patients.¹¹

Various case reports have reported mechanical stress as an inciting factor for HS flares, especially in high-friction areas, whether from clothing or skin-skin contact. A total of eight studies on mechanical stress were found. Seven were case studies, and one was a cross-sectional study.^15–22 The evidence is limited by the low-quality evidence of case reports and cross-sectional studies. It is widely documented that HS is more prevalent in obese patients. Still, the role of friction as an independent environmental factor in the pathogenesis of HS has been implicated in only a few case studies and series. Mechanical stress independent of obesity has only been studied in the form of case reports and case series.

Several case reports have described the development of recurrent HS lesions in friction-bearing areas, suggesting that mechanical stress itself can be an inciting factor for HS.^15–19,21 Case reports have documented lesions arising around the band of wired brassieres, on the feet of a patient with tight-fitting work shoes, waistbands, and from leg prostheses.

Moreover, there was a report of a 4-month-old child that developed HS-like lesions in an inguinal nevus comedonicus after mechanical stress of the region.²⁰ HS caused by mechanical stress in atypical areas not characterized by apocrine sweat glands may be caused by mechanical friction and a warm, humid, occlusive microclimate favorable to bacteria.¹⁹ To minimize mechanical friction and pressure in HS patients, ideal undergarments include sports bras or camisole tanks with built-in bras that lack thin straps, tight elastic, and metal wires. Loose-fitting underwear (seamless or laser-cut underwear lacking elastic bands) made from gentle fabrics are favorable for patients with HS. In one questionnaire, 16 of 110 (16%) patients reported tight clothing and friction as an aggravating factor of HS and 11 of 110 (11%) reported loose clothing as a relieving factor of HS.²² Men should be encouraged to opt for loose-fitting boxers rather than tight briefs. Education about appropriate undergarment styles and fabrics can empower patients to choose clothing options that reduce friction and irritation, decreasing the likelihood of HS flares.

Observational studies have shown increased sleep disturbances in HS patients, likely due to the pain and pruritus. In addition, poor sleep can contribute further to the inflammatory state of HS. Of the five studies, two were cross-sectional, one was a prospective study, and two were retrospective studies.^23–27 Sleep is a fundamental physiological process governed by homeostatic sleep drive and circadian rhythm. Since skin plays a role in core body temperature control and thermoregulation, it contributes to proper sleep activity, onset, and awakenings. Sleep quality can be disturbed by chronic inflammatory dermatoses such as atopic dermatitis, plaque psoriasis, prurigo nodularis, chronic spontaneous urticaria, and HS.^24,52 The pain, pruritus, and unpleasant odor caused by HS lesions may also amplify sleep disturbance.

A study in The Netherlands found that 121 of 211 HS patients (57.3%) had pruritus based on a numerical rating scale (NRS, 0 – 10), with a mean NRS score of 6.1 ± 2.0. The eosinophilic granulocytes may explain the increased pruritus in HS patients and a perineural infiltrate in the affected skin. In turn, these patients reported decreased quality of sleep and activities of daily living in the 5-D itch scale questionnaire.²⁶ Using the Athens Insomnia Scale (AIS) and Pittsburgh Sleep Quality Index (PSQI) questionnaires on 108 HS patients and 50 control patients, Kaaz and colleagues found that itch and pain had a significant impact on insomnia frequency, and pain significantly affected sleep quality, sleep duration, and daytime dysfunction.²⁴

Sleep disturbance in the form of obstructive sleep apnea (OSA) has a higher prevalence in HS patients than in healthy controls.²⁵ OSA is an independent risk factor for the development of cardiovascular disease, increasing the risk of morbidity and mortality in HS patients. In a small study, Kelly et al. used the Berlin, STOP-Bang and Epworth Sleep questionnaires as well as overnight sleep studies to assess the prevalence of OSA in HS patients and found that the probability of OSA in HS patients is higher than that of the general population (50% in HS patients, versus 10% of males and 3% of females in the general population).²⁵ However, this comparison does not control for the confounder of weight in HS populations. In a population-based analysis, Werteneil et al. found an increased incidence of OSA in HS patients, 3.5% (n = 695/19 945) vs. healthy controls 2.5% (n = 7400/296 170; p < 0.001).²⁷ Lastly, Cohen et al. also found an increased incidence of OSA in HS patients vs. health controls (OR= 1.60, 95% CI 1.36-1.86; p < 0.0001). In their study, Cohen et al. also found an association between other sleep disorders besides OSA and HS. Specifically, there was a 32% increased chance that patients with HS had a non-OSA sleep disorder (95% CI 1.12-1.57; p < 0.001).²³ While observational studies can not determine causation, authors have proposed that HS and sleep disorders are associated through pro-inflammatory states. Additional interventional studies investigating the presence and role of OSA in HS patients are required to establish the temporal association between this modifiable cardiovascular risk factor and HS.

Observational studies have shown strong associations between smoking and an increased risk of HS.^1,2,33,36 Although the studies discussed have been observational in nature, the strong associations result in moderate-quality evidence. Smoking may contribute to the pathophysiology of HS through follicular occlusion, inflammation, and dysregulated immunity. Nicotine, polyaromatic hydrocarbons, arsenic, and dioxin-like compounds in tobacco smoke activate keratinocytes and cells of the immune system via nicotinic acetylcholine receptors.²⁸ Skin samples from HS patients have shown a significantly thicker epidermis in the presence of nicotine in vitro compared with controls and an increased expression of acetylcholinesterase receptors surrounding the follicular infundibulum.²⁹ Further, alkaloids such as nicotine stimulate the growth of Staphylococcus aureus, which consequently enhances the expression of choline acetyltransferase, the rate-limiting enzyme in the synthesis of acetylcholine, which may play a role in the pathway of infundibular hyperkeratosis and follicular occlusion via autocrine and paracrine signaling of the acetylcholine receptors.³³ Various inflammatory interleukins (IL’s) such as IL-36α, IL-36β, and IL-36γ are increased in active smokers, contributing to HS exacerbations.⁵³

Numerous studies indicate that a high percentage of HS patients, approximately 70-90%, currently smoke or have previously smoked cigarettes.^1,25,29,51 Akdogan et al. investigated 40 patients with HS and 40 matched controls and found smoking was associated with a 14.87-fold increase in the risk of HS (95% CI 2.82—78.56). Active cigarette smoking increased the likelihood of HS, which was further increased by the length of time smoking.² Among 7,860 patients with HS, Garg et al. showed that the incidence of HS was doubled among tobacco smokers compared to nonsmokers. Tobacco smokers diagnosed with HS were most commonly aged 18–39 years, women, white, and those with body mass index (BMI) ≥ 30.³³ Additionally, a Danish study suggested that tobacco smokers may be less likely to achieve remission, or the absence of inflammatory lesions for at least 6 months, than non-smokers.¹ In another population of Danish blood donors, active smoking was associated with lower remission rates (HR = 0.49, 95% CI 0.32-0.76) as well as the development of HS (HR = 1.72, 95% CI 1.15-2.50).³⁶ A meta-analysis of observational studies found that HS was significantly correlated with active smoking (OR 4.34, 95% CI 2.48–7.60, p < 0.001) and with a history of smoking (OR 6.34, 95% CI 2.41–16.68, p < 0.001).⁴³

Although smoking has been extensively studied as a trigger for HS, its association with the clinical severity of the disease has been less clear.⁵⁴ A study comparing the differences in the epidemiology of HS in Western countries and East Asia did not find an association between tobacco smoking and disease severity.³⁹ Dessinioti et al. found that smoking did not affect the severity of HS through Hurley staging, but smoking did increase the number of affected body areas in HS patients, with an increased risk for current or former smokers to have more than two body areas affected compared to non-smokers.²⁹ However, early-onset HS was associated with less frequent smokers when compared to adult-onset HS.³⁰ In contrast, Liakou and colleagues, as well as a study of Dutch patients with HS by Schrader et al. did, however, conclude that active smoking and increased pack-years may be associated with more severe HS.³⁷ Further, Sartorius et al. showed that according to the Hidradenitis Suppurativa Scoring (HSS), smokers had more severe HS compared with former smokers and non-smokers.⁴¹ In a survey study, 17% of respondents indicated that their HS improved upon smoking cessation. Although this was a small proportion reporting severity improvement compared to other interventions, these patients had the most subjective and Hurley staging improvement in their HS compared to other lifestyle interventions.³⁸

Deilhes et al. conducted a retrospective review investigating the benefits of a smoking cessation program (SCP) combining behavioral and pharmacological treatments on 51 HS patients (20 males, 31 females). All patients were daily smokers with an average of 13 pack-years and 13.8 cigarettes per day. Forty-eight patients followed up after a mean time of 11.6 months, with 70% of patients attending the SCP. One-third continuously stopped smoking and 44% reduced their consumption, with a mean reduction of 2.4 cigarettes per day. Among quitters in this time period, 93% attended the SCP.²⁸ Similarly, HS patients who attended a smoking cessation program in an interdisciplinary intervention study by Touhouche et al. decreased their mean number of cigarettes per day.⁵⁵

There are also other HS populations at risk for increased smoking habits, such as pregnant women and the pediatric population. In one study on Swedish pregnant women, 41% of the 1,724 pregnancies belonged to smokers. This is compared to only 13% in the reference population who were smokers.³⁵ The pediatric population must also be regarded when considering smoking as a risk factor for their HS. Interestingly, Garcovich et al. found that in a cross-sectional review of 870 pediatric patients with HS, 23.9% of the cohort were smokers, which is higher than the referenced general population (11.8% of the general pediatric population are smokers).³²

Interestingly, smokers are less likely to respond to first-line therapies for HS, including oral antibiotics, topical antibiotics, intralesional corticosteroids, or antibacterial washes, creams, and lotions.³ A recent study published by Iannone et al. revealed that smoking seems to be a predictive factor for poor response to clindamycin and rifampin therapy. There was a positive correlation between acne inversa severity index (AISA) and smoking (Spearman’s rho= 0.57, p=0.36).³⁴ A case series by Simonart et al. suggested that smoking cessation has decreased the severity of HS in two women, aged 24 years and 37 years, as well as helped them achieve remission and may do so in other patients with HS.⁴²

Factors increasing smoking cessation success in HS patients included motivation, level of nicotine dependency, access to interventions, and psychological comorbidities such as depression and anxiety.²⁸ A multidisciplinary intervention including social services, nutrition, psychology, and pharmacological treatments such as nicotine replacement and varenicline may aid in establishing quitting goals in this population.²⁸

A rare finding, Foolad et al.’s chart review on HS patients from the University of California Medical Center found that more than half of their cohort were never smokers (57.7%). These findings are contrary to other evidence in the literature regarding HS and smoking. Importantly, their study was a descriptive analysis from a single center. Although the majority of their HS patients were never smokers, they did not test for an association between smoking and HS.³¹

There is evidence that substance use disorders are more prevalent in patients affected by HS. While the eight studies described associations between HS and SUD, they failed to answer whether substance use affects HS disease state, severity, or flares.^40,44–50 Additionally, the quality of the evidence is low because some studies have shown minor or no associations. As alluded to previously, patients with HS often endure chronic pain, which can lead to anxiety and depression. For instance, studies have shown that these patients score higher on anxiety and depression scales.^8,12 These psychiatric conditions may lend themselves as precursors for substance use disorders (SUD) in these individuals. For example, a cross-sectional analysis of HS patients revealed that the prevalence of SUD in HS patients compared to non-HS patients was significantly different (4% in HS patients vs. 2% in non-HS patients, p < 0.001). SUD cases were from alcohol (47.9%), opioids (32.7%), and cannabis (29.7%).⁴⁴ Similar findings were seen in a French cohort, where the prevalence of cannabis use among HS patients was 34% compared to 11.6% in psoriasis patients (p < 0.001). Interestingly, the majority of the patients in the HS cannabis use cohort had begun to use cannabis before disease onset, indicating that cannabis may be implicated in disease pathogenesis.⁴⁵ Patel et al. found that HS was two times more likely to be associated with a primary/secondary diagnosis of mental health disorder, including SUD, than patients without HS.⁴⁶

Some studies found conflicting evidence regarding alcohol and drug dependence in patients with HS. Shlyankevich et al. found that there were significantly lower odds of having alcohol dependence in HS patients compared to non-HS patients.⁴⁷ Additionally, Revuz et al. did not find a significant difference in alcohol intake between patients with HS and non-HS patients.⁴⁰ Riss et al. found a difference in wine and spirits intake among Danish patients with HS compared to non-HS patients, but there was no difference in beer intake.⁴⁸ Specifically, HS patients drink significantly less wine than non-HS patients but significantly more hard liquor.

In their meta-analysis, Phan et al. documented an association between substance-related disorders, alcohol abuse, and HS. Similar to the findings by Garg et al, the most cited substances were alcohol, opioids, and cannabis. The authors hypothesized that the increased association between substance-related disorders and HS may be largely due to the pain that these patients experience.⁴⁹ The pain these patients experience also serves as an explanation behind the increased opiate prescriptions in HS patients in a retrospective cross-sectional study. The finding of increased opiate prescriptions in these patients lends a focus on the poor management of these patients and serves as an argument for increased treatment strategies to alleviate flares.⁵⁰

Psychiatric conditions such as depression are hypothesized to cause an inflammatory state, which could worsen the cutaneous inflammation in HS, regardless of medication regimen.⁹ However, there is no strong quality evidence suggesting that control of psychiatric conditions improves HS flares, as may be suggested by the inflammatory hypothesis. Regardless, a large proportion of HS patients suffer from a psychiatric condition. Therefore, clinicians may consider screening for anxiety and depression during a dermatology visit and facilitate an interdisciplinary partnership with a psychiatrist, psychologist, or primary care provider.

It is important to consider the role that mechanical stress plays on HS severity. Case reports have reported that the friction induced by clothing and other objects may play a critical role leading to HS exacerbations. Clinicians can screen for disease activity in body locations susceptible to friction and advise patients to modify their choice of clothing to help control flares, in favor of loose undergarments.

Since skin plays a role in core body temperature control and thermoregulation, it contributes to proper sleep activity, onset, and awakenings. Increased sleep disturbances including OSA were observed in HS patients. Therefore, sleep quality measures can be assessed for each patient, as this can negatively impact the quality of life for HS patients and is a pathway that increases the inflammatory state. In the case of suspected OSA, a referral to diagnose and treat this potentially serious condition would be important.

There is strong evidence that smoking is associated with increased odds of HS.^2,3 Smoking has also been associated with reduced response to HS treatment.^2,3,28,33 Assessment for smoking status is recommended in each HS patient, and referrals to smoking cessation programs should be offered when appropriate.

Although there is no evidence of SUD being a trigger for HS, HS patients are more likely to suffer from SUDs than non-HS patients.⁴⁷ Consequently, it is important for dermatologists to understand that this may be a comorbidity and screen for such disorders, whether it is through specific SUD questionnaires or a review of systems.

Our review has several limitations which are inherent to the studies included. First, a meta-analysis of these studies could not be completed due to the broad objective of the study and the paucity of specific studies on the matter with common variables. There is a large body of evidence on the effects of nutrition and weight on HS. However, the purpose of this review was to provide the scientific community with an overview of the less-frequently discussed lifestyle behaviors that are important in HS. Many of these studies are cross-sectional in design and rely on observational methods, which limits the extent of causation between lifestyle and HS.^{1,4,9–11,14,23,28–31} The optimal method to determine causation would be with a randomized-controlled trial, which may be challenging to conduct due to the variables in question. Additionally, several included studies relied on questionnaires for their results, which makes the study susceptible to errors in self-reported diagnoses, recall bias, and selection bias.^{9,12,22,30,36,38} Lastly, several studies were limited by their small sample sizes.^{8,10,14,25,29}

This review highlights how an integrated multidisciplinary care model for HS is needed to optimally manage HS symptoms and comorbidities. Additionally, our work features other lifestyle factors beyond weight and diet that are infrequently discussed as factors for HS disease severity. Addressing these lifestyle behaviors may lead to an increased quality of life for HS patients and improve HS symptoms and individuals’ comorbidities.

The authors have no financial or personal conflicts of interest that may influence the work or reduce transparency. Funding was not received for this project.