Smoking is not only a preventable cause of major systemic diseases, but also affects the growth cycle and pigmentation in hair and hair follicles. Exposure to tobacco smoke in the environment causes nicotine to accumulate in the hair follicles and hair shaft.
Alopecia (hair loss) is among the most common disease groups that apply to dermatologists. The etiology of androgenetic alopecia (AGA),which is the most common cause of hair loss, is multifactorial. Testosterone has been shown to play a role in the pathogenesis of AGA by causing hair miniaturization and transforming terminal vellus hairs. The role of environmental factors, such as smoking, negatively affects hair growth and cause hair loss. Hair transplantation is permanent treatment modality in hair loss.
Smoking is a risk factor for many preventable diseases, including cerebrovascular, lung disease, cancer, and oral mucosal diseases. More recently,the role of smoking in skin aging and hair loss has been the subject of great interest and research. Animal studies in mice have shown that environmental factors, including exposure to tobacco smoke, can lead to hair loss and premature graying. Chemical components found in tobacco smoke, such as nicotine, can accumulate in the hair and become reliable biomarkers for detecting smoke exposure.
While genetic factors play an important role in alopecia environmental factors such as smoking, and nicotine exposure should also be considered. Current scientific evidence, primarily from cross-sectional studies, shows a positive association between length of smoking history and severity of alopecia in patients with androgenetic alopecia. Severe presentations of androgenetic alopecia were observed in subjects who smoked larger amounts of cigarettes per day. Several studies have reported no association between smoking and alopecia. Among them, a cross-sectional retrospective study reported a higher prevalence of scarring alopecia, severe frontal fibrosing alopecia in patients with no previous tobacco exposure .
Various hormonal irregularities, including decreased prolactin, are linked to chronic tobacco exposure and may explain the higher prevalence of frontal fibrosing alopecia non-smokers. A possible association between female androgenetic alopecia (FAA) and acute telogen effluvium has been observed in previous studies. Furthermore, a retrospective analysis identified triggering causes such as iron deficiency and thyroid dysfunction, with a higher risk of developing concomitant FAA and acute telogen effluvium. In addition, a report has provided support that some cases of telogen effluvium may progress rapidly to female androgenetic alopecia . Hair transplant Turkey is popular location to resolve hair loss problem.
An earlier onset and higher prevalence of graying hair were also observed in smokers compared to controls. A positive smoking history has also been shown to increase the risk of graying hair for each year a person continues to smoke. This correlation was not found to be true for smokers under the age of 21, possibly due to the shorter duration of smoking and the time frame of the study. Although the mechanism responsible for hair loss in people exposed to nicotine or tobacco smoke is unknown, it is thought to be similar to the mechanism by which smoking increases skin aging.
Nicotine is known to cause constriction of the dermal hair papilla and local ischemia, accumulation of DNA damage, dysregulation of protease/antiprotease systems involved in the hair growth cycle, and upregulation of local proinflammatory cytokines associated with follicular inflammation and fibrosis. There is a hypothesis that exogenous nicotine from smoking may cause overstimulation of cellular nicotinic acetylcholine receptors, resulting in receptor desensitization. This contributes to hair follicle destruction by activation of programmed cell death pathways found in keratinocytes [42-44]. Studies in C57BL/6 mice, a species prone to hair loss, may explain increased hair loss in smokers. When mice were exposed to whole body, environmental tobacco smoke (ETS) for 3 months, they showed evidence of hair loss and PHG with reported circular alopecia patches and graying on their backs. The patches grew larger with longer exposure to ETS and at 4 months all mice exposed to ETS developed patches of patchy and messy gray hair. Neither hair loss nor PHG was observed in the control group. On histology, alopecia areas showed fewer and shorter hair follicles and reduced hair bulbs with reduced and uneven pigmentation, along with markers of cellular apoptosis. These findings were thought to be secondary to metabolic changes caused by inhaled smoke-associated genotoxins, leading to a dystrophic anagen pattern. Long-term, high-dose nicotine treatment, which is commonly used in A/J mouse models, is associated with hair loss to investigate the carcinogenic effects of nitrosamines, a downstream metabolite produced by nitrosation of nicotine. Mice treated with daily subcutaneous injection of nicotine began to lose their hair in separate patches after 8-9 months of treatment.
Another study in nicotine-vaccinated mice showed evidence of hair follicle fibrosis, chronic inflammatory infiltrate, and extravasation of erythrocytes . Health image is negatively affected by hair loss and graying . More recently, “smokeless tobacco” products have been heavily marketed, but these too contain high doses of nicotine, and this new and growing trend may also pose a significant risk to hair health. This review was limited by the lack of randomized control studies or case series in the literature, association reports rather than causality, lack of scalp biopsies to confirm the link between smoke-induced oxidative stress and AGA and recall bias due to use. In addition, the use of small sample sizes and hospital- or outpatient-based studies rather than community-based studies make it difficult to integrate data into the general population. Results supporting no association between smoking and hair loss could not be properly interpreted due to the small sample size, incomplete smoking histories, and unequal control groups.
The 1996 study of Mosley and Gibbs is often referenced when it comes to smoking and hair loss studies. This is one of the first reports to meaningfully address the relationship between smoking and hair loss. The authors examined 606 patients (268 males and 338 females) aged 30 years and older who presented to the surgical outpatient clinic during the three months of the study. The risk of hair loss was approximately twice as high in smokers compared to non-smokers.
The next important study, is a 2007 study by Dr. Su and Dr. Chen. These investigators studied 740 patients aged 40 to 91 years over a 2-month period. They found that smokers generally had worse androgenetic alopecia compared to nonsmokers. In fact, smokers have almost twice the risk of having moderate or severe genetic hair loss compared to non-smokers. Additionally, the early development of male hair loss was seen as more likely in smokers.
Many additional studies have been published since these 2 early studies, supporting the idea that smoking accelerates the hair loss process. It is important to emphasize to our smoker patients the importance of quitting smoking, not only to reduce hair loss, but also to reduce the risk of cardiovascular disease. Androgenetic patients are at risk of developing cardiovascular disease, heart attack and stroke, even if they do not smoke, and smoking further increases these risks.
Androgenetic alopecia is chronic hair disease. Civas hair transplant that is best hair transplant clinic in Turkey is right choice for hair disorders. You can contact with us to resolve hair problems.