In the final part of this trilogy examining the impact of the Western lifestyle on hair health, we will explore a crucial relationship widely recognized as one of the leading factors contributing to the onset of androgenetic alopecia: the connection between smoking and hair loss.
Written by Dr. K. Anastasakis.
Smoking and Hair Loss: Statistical Confirmation of the Link
Smoking is well-known to cause significant damage to overall health, increasing morbidity and mortality among smokers. Specifically, it reduces average life expectancy by about 7 years and healthy life expectancy by 14 years, while also accelerating the aging process. Smoking accounts for 30% of cancer-related deaths in developed countries and is responsible for over 4.8 million deaths annually worldwide from cancer, cardiovascular disease, respiratory illnesses, and degenerative conditions.
These deaths are projected to exceed 10 million by 2030 if current trends continue. Regarding the skin, cigarette smoke induces oxidative stress and promotes immunomodulatory processes in cells, diminishing immune response and triggering the secretion of proteolytic enzymes. This leads to accelerated degradation of collagen and dermal connective tissue, premature skin aging, and reduced wound healing capacity.
The literature establishes a causal link between smoking and various dermatological conditions, including systemic lupus erythematosus (SLE), psoriasis, cutaneous squamous cell carcinoma, palmoplantar pustulosis, hidradenitis suppurativa, and genital warts. Conversely, nicotine has been reported to have potentially beneficial effects in the clinical course of certain systemic diseases (such as Parkinson’s, Alzheimer’s, pregnancy-induced nausea, preeclampsia, endometrial carcinoma, and ulcerative colitis) and skin conditions (including pyoderma gangrenosum, aphthous stomatitis, pemphigus, herpes simplex, and acne). However, these associations remain statistical and epidemiological without established causality.
Cigarette smoke contains genotoxic substances and induces the production of peroxynitrite, which has been shown to cause cellular apoptosis and trigger autoimmune processes.
The Negative Effects of Smoking on the Skin Extend Beyond the Above, Including Premature Skin Aging and Skin Malignancies
In experimental animals, cigarette smoke has been associated with hair loss, hair graying, skin atrophy, and thinning of the subcutaneous tissue. Regarding androgens and smoking, early comprehensive studies investigating this issue found increased androgen levels in the serum of smokers. Specifically, smoking has been shown to raise total testosterone (T) levels by up to 15%, dihydrotestosterone (DHT) by 14%, dehydroepiandrosterone sulfate (DHEA-S) by 13%, and sex hormone-binding globulin (SHBG) by as much as 20%.
A study by Svartberg et al. involving 1,563 men demonstrated that both total and free testosterone increase with smoking—a finding later confirmed by a more recent study by the same group on 3,427 men from the Tromsø Study in the Norwegian population.
Conversely, research by Halmenschlager et al. comparing 90 smokers and 165 non-smokers did not observe similar results, indicating that the correlation between serum testosterone levels and smoking remains inconclusive. Studies with conflicting findings continue to be published.
The most recent and extensive study, conducted in 2009 by Shiels et al., included 1,275 men over 20 years old participating in the NHANES III study. It concluded that current smokers exhibited higher total and free testosterone levels compared to former smokers and non-smokers, as well as elevated estrogen levels, showing a positive correlation between cigarette smoking and estrogen.
Similar increases in testosterone and decreases in SHBG have been reported in female smokers. Furthermore, in both sexes, smoking has been linked to premature hair graying, as supported by a study conducted by Trichopoulos et al. in Greece.
Smoking and Hair Loss: How Hair Follicles Are Affected
Smoking has been directly linked to damage in the vascularization of hair follicles and the skin in general. At the cellular level, studies by Liu et al. have shown that cigarette smoke disrupts mitochondrial function in dermal papilla cells and induces mutations in mitochondrial DNA—likely related to the oxidative effects of peroxynitrite on mitochondria. Clinically, alterations in hair pigmentation and quality have also been reported, as observed in a study by Mosley et al. involving 606 smokers.
Another mechanism by which smoking negatively impacts hair follicles and skin is through increased expression of metalloproteinases MMP-1 and MMP-3 in the epidermis, as well as MMP-2, MMP-8, and MMP-9 not only in the epidermis but also in serum and saliva. At the molecular level, cigarette smoke has been found to act via activation of the aryl hydrocarbon receptor (AhR) and modification of cellular responses to the transforming growth factor-beta (TGF-β), which has been shown to be a key paracrine factor in the development of androgenetic alopecia.
Additionally, Trüeb has proposed a direct link between smoking and hair loss through several pathways: disturbances in the microvascular circulation of the dermal papilla, increased production of oxidative agents, reduced local estrogen levels—which normally protect the hair follicle—and damage to DNA replication in the follicular stem cells caused by toxic smoke derivatives. An in vitro study by Bahta et al. (2008) supports that dermal papilla cells in androgenetic alopecia are particularly sensitive to environmental oxidative stress, such as the biochemical stress caused by smoking, leading to easier cell apoptosis.
Clinically, however, to date, only four studies have directly linked smoking to hair loss.
The Mosley et al. (1996) study, which included 606 patients of both sexes, demonstrated a strong statistical correlation between smoking, premature graying, and hair loss. However, the study did not claim a causal relationship nor did it examine dose-dependent associations between the number of cigarettes smoked and the clinical presentation.
Subsequently, a 2003 study by Matilainen et al. involving 324 postmenopausal women found no positive correlation between smoking and androgenetic alopecia. However, this study was not primarily designed to investigate this parameter, and it lacked detailed data regarding the number of cigarettes smoked or duration of smoking.
A study by Severi et al. on 1,340 men suggested that smoking might even have a potentially positive effect on hair density, although these results were not statistically significant. This study did not provide detailed smoking data and employed an alternative staging system for androgenetic alopecia rather than the classic Norwood-Hamilton scale, making its data less comparable with other research.
The most recent and comprehensive study, Su et al. (2007), which focused specifically on the association between smoking and androgenetic alopecia in 740 men over 40 years old, found that smokers were 77% more likely to exhibit moderate to severe hair loss (Norwood Stage IV or higher). Furthermore, the risk was proportional to both the duration of smoking and the number of cigarettes consumed.
Taken together, these findings support the conclusion that smoking and hair loss are closely interlinked concepts. Smoking systemically affects androgen production and induces cellular and nuclear damage to the hair follicle—a highly metabolically active tissue—and is directly associated with vascular damage to hair follicles.
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