Peer-reviewed literature notes that alcohol consumption is often discussed or postulated as an environmental risk factor potentially associated with the pathogenesis or early onset of hair loss conditions such as androgenetic alopecia and alopecia areata, but definitive causal proof remains uncertain.
Alopecia areata (AA) is an autoimmune condition that presents with non-scarring hair loss affecting multiple patients worldwide during their lifetime. It ranges from well-defined patchy to diffuse total hair loss, impacting all hair-bearing areas of the body. AA most commonly predominantly manifests on the scalp. The pathophysiology of AA is complex and multi-faceted. The findings of our review article were consistent with the recent literature, delineating autoimmunity, genetic susceptibility, and environmental aspects to be the contributing factors. One of the main causes of AA is believed to be the disruption in the immune privilege of the hair follicles. Multiple genetic loci involved in hair follicle maturation and immune process have been linked to the development of AA as evidenced by several studies. It has been postulated that psychological stressors, smoking, alcohol consumption, sleep disturbances, gut microbiota, and drugs play a role in the pathogenesis of AA by exacerbating the immune response against the hair follicles. AA is a clinically diagnosed disorder. Topical, intra-lesional, and oral corticosteroids, topical and oral minoxidil, cyclosporine, and other immune therapy drugs are widely accepted first-line treatment options, although incomplete remission and relapses are common. Recently JAK-2 inhibitors and mesenchymal stem cell exosomes have shown promising results, potentially treating severe and refractory hair loss. AA has a bidirectional relationship with psychological symptoms as it can lead to social anxiety and depression, which in turn can aggravate hair loss. Hence, it is crucial to implement a holistic approach to managing AA including topical and systemic therapies, psychological counseling, and lifestyle modifications. It is imperative to fully declinate the pathophysiological mechanisms of the disease and formulate therapies in future research to help clinicians and dermatologists devise definitive guidelines to treat the condition
The findings of our review article were consistent with the recent literature, delineating autoimmunity, genetic susceptibility, and environmental aspects to be the contributing factors. One of the main causes of AA is believed to be the disruption in the immune privilege of the hair follicles. Multiple genetic loci involved in hair follicle maturation and immune process have been linked to the development of AA as evidenced by several studies. It has been postulated that psychological stressors, smoking, alcohol consumption, sleep disturbances, gut microbiota, and drugs play a role in the pathogenesis of AA by exacerbating the immune response against the hair follicles.
The disease is primarily caused when the body attacks its own hair follicles through CD8+ T lymphocytes [ 8 ]. Psychological and environmental factors, such as smoking, alcohol
The interplay between cytokines helps each other to sustain the inflammatory response in AA, e.g., IFN-γ can enhance the effects of TNF-α, leading to increased inflammation. These inflammatory cytokines can disrupt the normal cycle of hair growth, especially the conversion from the anagen to the telogen phase, which causes premature regression and hair loss [ 19 ]. The combination of events, i.e., T-cell activation, cytokine release, macrophage activation, etc., leads to a destructive environment for the hair follicles, which results in the weakening of the follicles and hair loss.
CRH and SP cause keratinocyte death via pathways involving TNF-α, concurrently facilitating mast cell degranulation, which results in neurogenic inflammation [ 39 , 40 ]. This inflammation hastens the transition of hair follicles into the catagen phase, resulting in premature hair loss. SP exacerbates hair growth inhibition by diminishing TrkA receptor activation and enhancing pro-apoptotic pathways, elucidating the connection among stress, telogen effluvium, and AA [ 40 ]. A meta-analysis by Toussi et al., which examined 73 studies involving around 414,319 participants, highlights the strong bidirectional relationship between AA and psychological distress.
A meta-analysis found a slight but significant association between smoking and AA, with an odds ratio (OR) of 1.12. Free radicals and pro-inflammatory cytokines caused by smoking may contribute to the loss of hair follicles and IP, while pathways involving Th1, Th2, and Th17 responses are central to AA's pathogenesis [ 43 , 44 ]. Alcohol increases pro-inflammatory cytokines, including IL-6, TGF-α, and IFN-γ, which may aggravate illnesses such as psoriasis and potentially AA. It has been postulated that alcohol can increase TH17-mediated inflammation leading to AA.
Hair loss on the scalp, eyebrows, and body can deeply impact a person's perception of their body image, identity, and self-worth. Because hair loss is visible, it leads to social withdrawal and alienation. Hair loss can cause significant emotional distress and serves as a persistent reminder of the patient's diagnosis. This heightened awareness often increases feelings of anxiety and depression, which makes it difficult for individuals to participate in social and work settings due to insecurities and discomfort. Therefore, the disease's physical symptoms may lead to psychological scarring, and this may cause further exacerbation.
This anxiety could stem from a fear of societal judgment or relapses, thus incurring a vicious cycle [ 2 ]. Experiencing anxiety may cause more hair loss and alopecia replated flare-ups. Anxiety surrounding AA regarding children may stem from social consequences [ 88 , 89 ]. Children often get victimized, which challenges their self-esteem and causes lasting trauma. Psychological treatments such as cognitive behavioral therapy (CBT) and mindfulness-based stress reduction are effective in reducing anxiety in AA patients. Furthermore, early implementation of support-rich psychological approaches and various treatments may benefit patients diagnosed with AA.
<p class="abstract"><strong>Background:</strong> Androgenetic alopecia (AGA) is the most common form of hair loss affecting up to 80% of the men. It manifests mostly after puberty and is evident by the age of 30. Nowadays the onset of AGA is much earlier and most of them develop AGA in early twenties. Risk factors such as smoking, alcohol consumption and prevalence of AGA in the family are considered to contribute to the early onset. Aims: To estimate the prevalence of and to determine risk factors for AGA in adult males.</p><p class="abstract"><strong>Methods:</strong> A total of 103 patients above 18 years of age attending the dermatology OPD were included in the study. Epidemiological data was collected using a standard questionnaire.<strong></strong></p><p class="abstract"><strong>Results:</strong> In the study population, 68% patients were in the age group 21-30 years. No association was noted between smoking and the age of onset of AGA. An early age of onset was associated in patients with history of alcohol consumption (73.3%). Prevalence of familial AGA was seen in 68% and had a paternal inheritance (62.8%) more than maternal (8.6%). Associated systemic diseases were seen in 12.6% of the patients and hypertension was the most common.</p><p><strong>Conclusions:</strong> AGA is a very common presenting complaint in the younger population. The early onset of AGA itself causes anxiety and apprehension in the patients that further contribute to the hair loss. The presence
It commonly begins by 20 years of age and affects nearly 50% of men by the age of 50 years and 50% of women by the age of 60 years.1,2 The propensity to develop AGA is polygenic and not Mendelian.3 In general, sons of fathers who have no alopecia are at a low risk of hair loss themselves. Risk increases in men with a positive maternal grandfather history and even more so in men with a history of paternal alopecia. 4 Environmental factors such as smoking and alcohol intake may play a role in the pathogenesis of AGA.
The association between smoking and AGA has been addressed earlier in a few studies with inconsistent results.5-7 ABSTRACT Background: Androgenetic alopecia (AGA) is the most common form of hair loss affecting up to 80% of the men. It manifests mostly after puberty and is evident by the age of 30. Nowadays the onset of AGA is much earlier and most of them develop AGA in early twenties. Risk factors such as smoking, alcohol consumption and prevalence of AGA in the family are considered to contribute to the early onset. Aims: To estimate the prevalence of and to determine risk factors for AGA in adult males.
Conclusions: AGA is a very common presenting complaint in the younger population. The early onset of AGA itself causes anx iety and apprehension in the patients that further contribute to the hair loss. The presence of a family history in the patients’ needs for an early management of the disorder. Environmental factors like smoking and alcohol consumption thought to play a role in the aetiology of the disease. Keywords: Androgenetic alopecia, Smoking, Inheritance, Alcohol Department of Dermatology, Venereology and Leprosy, Yenepoya Medical College, Yenepoya University, Mangalore, Karnataka, India Received: 10 March 2017 Revised: 01 April 2017 Accepted: 04 April 2017 *Correspondence: Dr.
The second objective was to also to explore possible risk factors associated with early onset of AGA. METHODS Male patients attending the Yenepoya Medical College Hospital with complaints of patterned hair loss. This study was conducted from January 2015 to September 2016 from the male patients with AGA at Yenepoya Medical Colleg e Hospital, Deralakatte, Mangalore. We analysed 103 patients who attended the outpatient department with complaints of hair loss and were diagnosed with AGA. We excluded patients with other causes of non - scarring alopecia or with precipitating factors suc h as high fever, emotional stress, surgery or drugs.
RESULTS Age distribution and age of onset Among the patients attended with AGA, 68% to the age group 21-30 years followed by 20% in the age group 31 - 40 years, 7% in the age group 41 -50 years and 1% in above 50 years of age (Figure 1). Out of the 103 patients, 51 (49.5%) patients had hair loss between 19 -
Figure 2: Distribution of cases based on the smoking and alcohol consumption with the age of onset of hair loss. 4% 68% 20% 7% 1% Percentage 20 and below 21 - 30 31 - 40 22 13 11 0 6 4 0 5 10 15 20 25 <20 (cigarettes/day) >20 (cigarettes/day) Alcohol consumption No of patients Risk factors <35 years >35years Nargis T et al. Int J Res Dermatol. 2017 Jun;3(2):267-271 International Journal of Research in Dermatology | April-June 2017 | Vol 3 | Issue 2 Page 269 Family history A positive family history for AGA was present for 70 (68%) of the 103 male patients.
The mechanisms by which smoking causes hair loss may be multifactorial: it may be deleterious to the microvasculature of the dermal hair papilla, as a genotoxicants may damage DNA of the hair follicle or may cause an imbalance in the follicular protease or antiprotease system. Smoking may induce oxidative stress leading to release of pro -inflammatory cytokines that, in turn, results in follicular microinflammation an d fibrosis or may yield a relative hypoestrogenic state by increased hydroxylation of estradiol and inhibition of aromatase.
There is also need to quantify the amount and duration of alcohol intake and smoking to accurately comment on their effect on the early onset of hair loss. Nargis T et al. Int J Res Dermatol. 2017 Jun;3(2):267-271 International Journal of Research in Dermatology | April-June 2017 | Vol 3 | Issue 2 Page 271 CONCLUSION In our study, we noticed the prevalence of AGA in the younger age group thu s signifying its importance in diagnosing it and the need for early treatment. There was no association between risk factors such as smoking, increased BMI and systemic diseases with early onset of AGA.
Abstract: BACKGROUND: Androgenetic alopecia (AGA) is a patterned hair loss occurring due to systemic androgen and genetic factors. It is the most common cause of hair loss in both genders. In recent years, many studies investigating the relation between systemic diseases and androgenetic alopecia presented controversial results. OBJECTIVES: In this study we aimed to investigate the frequency of androgenetic alopecia, the presence of accompanying systemic diseases, the relation between body mass index and androgenetic alopecia severity and the association of hyperandrogenemia signs with androgenetic alopecia in patients who referred to our outpatient clinic. METHODS: Patients who referred to our clinic between October 2013 and May 2014 were included in the study. Diagnosis of androgenetic alopecia was made upon clinical findings. Presence of seborrhea and acne in both genders, and hirsutism in women, were examined. Age, gender, smoking habit and alcohol consumption, age of onset of androgenetic alopecia, family history, accompanying systemic diseases and abnormalities of menstrual cycle were recorded. RESULTS: 954 patients (535 women, 419 men) were included in the study. Androgenetic alopecia prevalence found was 67.1% in men and 23.9% in women. Androgenetic alopecia prevalence and severity were correlated with age in both genders (p=0,0001). Frequency of accompanying systemic diseases were not significantly different between patients with and without androgenetic alopecia (p=
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