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To determine if there is a significant association between premature hair graying and cigarette smoking. A cross-sectional observational study was conducted in a nonclinical setting on 207 participants on August 24 until 25, 2010. Participants were classified into two groups [premature hair graying (PHG) and normal hair graying]. PHG was defined as the first appearance of gray hair before the age of 30. Data were collected using an interview questionnaire and measurements of body mass index, waist circumference, fasting blood glucose and blood pressure. Collected data were statistically analyzed using SPSS 16, Chicago, IL. Of the 207 subjects, 104 (50.2%) had first appearance of gray hair before the age of 30 (PHG group) while the other 103 (49.8%) were considered normal hair graying group. The prevalence of smokers in the "PHG" group was higher (40.2% vs. 24.7%, P = 0.031). Smokers had earlier onset of hair graying (smokers: 31 (7.4) vs. nonsmokers: 34 (8.6), P = 0.034). Using multiple logistic regression with conditional likelihood, smokers were two and half times (95% CI: 1.5-4.6) more prone to develop PHG. This study suggests that there is a significant relation (with adjusted odds ratio of two and half) between onset of gray hair before the age of 30 and cigarette smoking.
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90 Indian Dermatology Online Journal-
April-June 2013
-
Volume 4
-
Issue 2
Address for
correspondence:
Dr. Ayman A. Zayed,
Department of
Medicine, Jordan
University Hospital,
P.O. Box ‑ 13046,
Amman, Jordan.
E‑mail: baraaayman@
gmail.com
Department of Internal
Medicine, Division
of Endocrinology,
Diabetes and Metabolism,
Faculty of Medicine,
1Department of General
Surgery, Faculty of
Medicine, 2Department
of Anesthesia, Faculty of
Medicine, 3Department
of Biopharmaceutics
and Clinical Pharmacy,
Faculty of Pharmacy,
Jordan University Hospital,
The University of Jordan,
Amman, Jordan
ABSTRACT
Aims: To determine if there is a signicant association between premature hair graying and cigarette smoking.
Materials and Methods: A cross‑sectional observational study was conducted in a nonclinical setting on
207 participants on August 24 until 25, 2010. Participants were classied into two groups [premature hair
graying (PHG) and normal hair graying]. PHG was dened as the rst appearance of gray hair before the age of 30.
Data were collected using an interview questionnaire and measurements of body mass index, waist circumference,
fasting blood glucose and blood pressure. Collected data were statistically analyzed using SPSS 16, Chicago, IL.
Results: Of the 207 subjects, 104 (50.2%) had rst appearance of gray hair before the age of 30 (PHG group)
while the other 103 (49.8%) were considered normal hair graying group. The prevalence of smokers in the “PHG”
group was higher (40.2% vs. 24.7%, P=0.031). Smokers had earlier onset of hair graying (smokers: 31 (7.4)
vs. nonsmokers: 34 (8.6), P=0.034). Using multiple logistic regression with conditional likelihood, smokers
were two and half times (95% CI: 1.5‑4.6) more prone to develop PHG. Conclusion: This study suggests that
there is a signicant relation (with adjusted odds ratio of two and half) between onset of gray hair before the
age of 30 and cigarette smoking.
Key words: Jordan, premature hair graying, smoking
INTRODUCTION
It is well accepted that gray hair is a natural
phenomenon of age in humans.[1] There is
also some evidence that age is associated
with increased graying in mice as well.[2]
Premature hair graying (PHG) has been linked
to certain autoimmune disorders such as
autoimmune thyroid disease and pernicious
anaemia and to several rare premature aging
syndromes (e.g., Werner’s syndrome).[3] In
addition, a link between smoking and gray hair in
both men and women and between smoking and
hair loss in men has been reported.[4‑6] Because
of this, PHG has attracted the attention of the
medical community. Could PHG be a marker
of early aging of organs and thus premature
morbidity and mortality?
Research exploring the relationship of PHG to
smoking has been very little worldwide and does
not exist in the Middle East.
Because of this rarity of studies in this eld, this
particular study was undertaken to determine the
association between PHG and cigarette smoking
in the Jordanian population.
MATERIALS AND METHODS
A cross‑sectional observational study that
aimed at evaluating the association of smoking
with PHG. It was conducted in a nonclinical
setting involving 207 participants (94 men and
113 women) over a period of 2 days from August
24 until August 25, 2010. The participants
represent a random sample of Jordanian people
who participated willingly in this public health
survey.
Statistical Methods
Collected data were entered into Statistical
Package for Social Sciences (SPSS16, Chicago,
IL). Data were expressed as mean (SD). Data
were subdivided between two groups (PHG and
normal hair graying). PHG was dened as the
rst appearance of gray hair before the age of
30. Whereas in the literature, other denitions
were used. (See discussion section).
Smokers’ hair: Does smoking cause premature
hair graying?
Ayman A. Zayed, Awni D. Shahait1, Musa N. Ayoub2, Al‑Motassem Yousef3
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DOI: 10.4103/2229-5178.110586
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Original Article
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Data of continuous nature [age of rst appearance of gray hair,
height, weight, body mass index (BMI), waist circumference,
fasting blood glucose, systolic blood pressure and diastolic
blood pressure] were compared between the two groups by
independent Student t‑test. Data of categorical nature (gender,
smoking behavior and medical history of hypertension,
diabetes, and dyslipidemia) were compared between the two
groups by Chi square. Despite its importance, family history
was not included in this survey, because it was subjected to
recall bias since the onset of hair graying in the family members
was not exceptionally remembered by the participants. Multiple
logistic regression was utilized to discern the relationship
between signicant variables and the susceptibility to PHG.
A nonsmoker was dened as someone who never smoked.
However, the range of smoking among the smokers in this
study was between one to 70 cigarettes per year. Those who
had smoked in the past were not included in the study.
BMI was calculated by dividing the body weight in kilograms
by the height in square meters.
RESULTS
The total number of people who agreed to participate was
207 subjects, half of them had PHG (n=104) [Table 1]. Men
and women were equally represented in the whole sample
(men: 94 (45.4%)) and in the two subgroups (men in PHG
group: 51 (49%), P=0.29). The participants covered a wide
range of age categories with an average age of 44 (11.6)
years (range: 18‑65 years). One quarter of recruits was below
the age of 35.3 years, one quarter above the age of 53.7 and
with a median age of 44.5 years.
The average age for the rst appearance of gray hair was
31.7 years with one quarter was below the age of 25, one quarter
above the age of 40 and a median age of 30 years. There was
15 years difference in age at which hair graying was rst noted
between the two groups [25.0 (4.7) vs. 40 (5.3), P<0.001].
There was no statistically significant difference in the
demographics between the two groups. There were no
differences in their body weight [78.8 (15) vs. 78.0 (15.3) kg,
P=0.73]; height [1.67 (0.09) vs. 1.65 (0.09) m, P=0.11];
BMI [28.9 (5.3) vs. 28.1 (5.3) kg/m2, P=0.3]; waist
circumference [95.6 (14.4) vs. 96.5 (12.6) cm, P=0.67]; fasting
blood glucose [104.3 (26.8) vs. 108.5 (25.9) g/dL, P=0.29];
systolic blood pressure [121.6 (11.3) vs. 123.7 (16.7) mmHg,
P=0.32] and diastolic blood pressure [80.1 (7.5) vs.
82.0 (8.2) mmHg, P=0.11] [Table 1].
The prevalence of physician‑diagnosed diabetes was
similar between the two groups (5.8% vs. 11.7%, P=0.13).
The prevalence of hypertension was lower in subjects with
PHG (7.7% vs. 28.2%, P<0.001). The prevalence of smokers
in the “PHG” was higher (40.2% vs. 24.7%, P=0.031).
Smokers had earlier onset of hair graying [smokers: 31 (7.4)
vs. nonsmokers: 34 (8.6), P=0.034] in the whole sample.
Backward stepwise multiple logistic regression with conditional
likelihood was used to nd out the best subset of variables
to predict PHG. The logistic regression was specied for
signicance level of 0.05 for entry and at level of 0.1 for removal.
The different models were compared by conditional logistic
regression, and minus two log likelihood ratio statistic was used
in comparing the tness of combined models. Two variables
were evaluated for susceptibility; smoking behavior and medical
history of hypertension. Smoking behavior remained statistically
signicant with adjusted odds ratio of 2.5 (95% CI: 1.5‑4.6).
DISCUSSION
Besides being a well‑known risk factor for cardiovascular
disease, smoking was reported to be associated with an
increase in apparent biological age over chronological age.[7]
Model D. indicates that people who smoke have characteristic
facial changes similar to those seen in premature aging.[8]
Smoking was also linked to PHG. Mosley and Gibbs reported
a signicant relation between gray hair and smoking.[4] Of their
606 patients aged over 30 years, 152 of each sex, smoked.
They indicated a signicant association between gray hair
and smoking for all age groups in both sexes with overall
odds ratio of 4.40 (3.24‑5.96). However, they did not mention
their denition of gray hair. Our cross‑sectional observational
study showed similar results. Smokers had earlier onset of
hair graying [smokers: 31 (7.4) vs. nonsmokers: 34 (8.6),
P=0.034] in the whole sample with adjusted odds ratio of 2.5
Table 1: Clinical characteristics of participants by the
onset of first appearance of gray hair
Variable Premature hair
gray (
N
=104)
mean±SD or
N
(%)
Normal hair
gray (
N
=103)
mean±SD or
N
(%)
P
value
Age (years) 40.5±12.8 52.9±11.9 <0.000
Height (m) 1.67 ±0.09 1.65±0.09 0.11
Weight (kg) 78.8±15 78±15.3 0.73
BMI (kg/m2) 28.9±5.3 28.1±5.3 0.3
Waist
circumference (cm)
95.6±14.4 96.5±12.6 0.67
Fasting blood
glucose (mg/dl)
104.3±26.8 108.5±25.9 0.29
Diabetes 6 (5.8) 12 (11.7) 0.13
Systolic blood
pressure (mmHg)
121. 6±11 .3 123.7±16.7 0.32
Diastolic blood
pressure (mmHg)
80.1±7.5 82±8.2 0 .11
Hypertension 8 (7.7) 29 (28.2) <0.001
BMI: Body mass index
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April-June 2013
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Volume 4
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(95% CI: 1.5‑4.6). On the other hand, there was no signicant
association between PHG and BMI, waist circumference,
fasting blood glucose or blood pressure. It should be noted
that the prevalence of hypertension was lower in subjects
with PHG (7.7% vs. 28.2%, P < 0.001), despite being
smokers. This could be related to the fact that PHG group
was signicantly younger than the normal hair graying group
[40.5 (12.8) vs. 52.9 (11.9) years, P<0.000].
To our knowledge, there is no universal denition of PHG. Gould,
et al. and Glasser dened PHG if 50% of hair is gray before the
age of 50.[9,10] On the other hand, others considered participants
to have PHG if all or most of their hair is gray before the age of
40.[11,12] Whereas Trueb adopted the threshold of PHG to be at
the age of 20 in Caucasian and at the age of 30 in Africans, but
he did not specify the percentage of gray hair.[13] In our study, we
considered participants to have PHG if the onset of visible gray
hair is before the age of 30. The reason that this age was chosen
because it has been proposed that for every decade after the
age of 30, there is a decrease of 10‑20% in pigment‑producing
epidermal melanocytes.[14,15] This melanocyte decrease is one
of the proposed mechanisms of hair graying.
The mechanisms by which smoking causes hair graying are
incompletely understood. The color of hair mainly relies on
the presence or absence of melanin pigment produced by the
melanocytes.[13] It has been indicated that smoking could be
associated with generating huge amounts of reactive oxygen
species leading to increased oxidative stress.[6] This pro‑oxidant
effect of smoking could lead to damage the melanin‑producing
cells, the melanocytes. This theory is supported by the observation
that melanocytes in gray hair bulbs are frequently highly
vacuolated, a common response to increased oxidative stress.[13]
A limiting factor throughout this study was that there is no
temporal relationship and it is impossible to distinguish between
cause and effect. For this reason surveys such as this can be
regarded as hypothesis‑generation and not hypothesis‑testing.
Other limitations include left censorship, and the potential that
nonresponders are of different quality than the responders.
CONCLUSIONS
This hypothesis‑generating study suggests that there is a
signicant relation (with adjusted odds ratio of two and half)
between onset of gray hair before the age of 30 years and
cigarette smoking in a random sample of Jordanian people.
We think that the results of this study are important for young
smokers especially females and for policy makers in the elds
of public health and preventive medicine in their continuous
war against smoking.
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Cite this article as: Zayed AA, Shahait AD, Ayoub MN, Yousef A. Smokers'
hair: Does smoking cause premature hair graying?. Indian Dermatol Online
J 2013;4:90‑2.
Source of Support: Nil, Conict of Interest: None declared.
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... A positive correlation between smoking and PHG, defined as presence of gray hair <30 years, was described in 7 studies [3,7,[28][29][30][31][32]. In an observational study, Mosley and Gibbs [3] reported a higher incidence of hair graying in smokers over 30-year old than in nonsmokers regardless of age-group or gender (n = 606). ...
... Furthermore, a questionnaire in Korean patients ages 12-91 years reported a 14.9% increased risk of developing premature gray hair for every year a subject smokes (n = 522 M, 480 F, p < 0.001), and an overall 1.99 times higher risk of graying prematurely compared to nonsmokers [29]. Premature graying in subjects with a Skin Appendage Disord 2021;7:251-264 DOI: 10.1159/000512865 reported history of smoking was also observed in a crosssectional study conducted by Zayed et al. [30] (n = 207, p = 0.031), and a case-control study of chronic smokers compared to subjects with no smoking history (n = 236, p = 0.031) [31]. In 2 similar studies by Sharma and Dogra [7] and Shin et al. [32], a significant number of patients with PHG also confirmed a history of smoking, with a correlation reported with a minimum smoking history of 5 pack-years (n = 240). ...
... An earlier onset and higher prevalence of hair graying were also observed in smoker groups compared to controls [7,28,30,31]. A positive smoking history was also shown to increase the risk of hair graying each year a subject continued to smoke [29]. ...
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... The association between PGH and smoking is reported in many studies and case series 21,25,32,33,48,50 among which four studies reported the smoking status of PGH and non-PGH patients. While combining the results of all the studies by meta-analytic technique (Figure 2), significant association was found between smoking and PGH (RR 1.56 [1.08-2.27]). ...
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... 2 However, a daily hair fall that exceeds the said limit, is then labelled as "balding". 3 The incidence of hair loss is increasing globally and both men and women are equally affected by a hair loss, 4 that is related to several factors such as family trajectories, aging, hormonal changes, telogen effluvium (hair shedding due to illness), etc. 5 The psychological disequilibrium has been on the rise amongst the young male members of the society, who directly associate their physical appearance with feelings of low self esteem or insecurity, due to the hair loss that they have experienced. 6 Interestingly, stress or psychological distress is also considered to be one of the most significant factors that lead to baldness in both males and females, which eventually causes loss of sleep and appetite, previous empirical literature found this association. ...
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Experimental evidence supports the hypothesis that oxidative stress plays a major role in the ageing process. Reactive oxygen species are generated by a multitude of endogenous and environmental challenges. Reactive oxygen species or free radicals are highly reactive molecules that can directly damage cellular structural membranes, lipids, proteins, and DNA. The body possesses endogenous defence mechanisms, such as antioxidative enzymes and non-enzymatic antioxidative molecules, protecting it from free radicals by reducing and neutralizing them. With age, the production of free radicals increases, while the endogenous defence mechanisms decrease. This imbalance leads to the progressive damage of cellular structures, presumably resulting in the ageing phenotype. Ageing of hair manifests as decrease of melanocyte function or graying, and decrease in hair production or alopecia. There is circumstantial evidence that oxidative stress may be a pivotal mechanism contributing to hair graying and hair loss. New insights into the role and prevention of oxidative stress could open new strategies for intervention and reversal of the hair graying process and age-dependent alopecia.
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Premature graying of hair is associated with several endocrine disorders, vitiligo, and the aging process. Although the pathophysiology of melanin depletion in hair follicles is unknown, genetic factors regulate the expression of this trait. As acquisition of bone mass is also genetically determined, we performed an exploratory case control study of the association between premature graying of hair and osteopenia (lumbar bone density t score, below -1.0). Subjects were recruited from a single metabolic bone clinic. Premature graying of hair in 36 men and women with osteopenia (cases) was compared to that in 27 men and women without osteopenia (controls). Subjects with premature graying but no other identifiable risk factor were 4.4 times as likely to have osteopenia as subjects without premature graying (P = 0.02). Subjects with osteopenia and premature graying in their teens and twenties had a stronger family history of osteoporosis than those who had osteopenia and graying later in their thirties (P = 0.06), but bone density and other characteristics were not different. The association between premature graying and low bone mass could be related to genes that control peak bone mass or factors that regulate bone turnover. Premature graying of hair may be an important risk marker for osteopenia.
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Hypertension, diabetes mellitus, hypercholesterolemia, and smoking are known coronary risk factors. It has been our impression that premature graying of the hair also predisposes individuals to myocardial infarctions. To test this hypothesis, we evaluated all of the patients under the age of 50 who were admitted to the coronary care unit between 1974 and 1976 with a proven diagnosis of a myocardial infarction. There were 50 patients. Thirty-eight did not have premature graying. Twelve of the male patients (24%) had virtual total graying of the hair which made them appear older than their stated age. The graying in these patients started on the average at 29 years. Five of these patients state that other family members had premature hair graying. The incidence of diabetes, hypertension, and smoking was similar in those with and without premature hair graying. This preliminary study suggests that premature graying of the hair is associated with premature cardiovascular disease. It should probably be regarded as a coronary risk factor and used to identify patients at increased risk.
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An office and autopsy study was performed to see if early graying was associated with increased morbidity, earlier age at death, and specific cause of death. 195 consecutive office patients over the age of 40 were studied to see if premature graying of scalp hair (50% or more gray before age 50) was associated with increased incidence of disease before age 50 (P = ns). Their parents' mean ages at death, prematurely gray or not, were compared. For fathers, mean age at death if prematurely gray was 68.27 years; if not prematurely gray, 66.03 years (P = 0.35). For mothers, the values were 70.55 years and 70.37 years respectively (P = greater than 0.50). 874 autopsy patients dying over a 23-year period (1966-1989) were studied to see if the median age at death (of patients 50% or more gray) differed for any of the six categories of disease (myocardial infarction, congestive heart failure, cancer, stroke, pneumonia/bronchitis, or cirrhosis of the liver/GI problems) when compared to the entire autopsy sample of 19 categories of disease (P = ns for each comparison). This dual office and autopsy study provides no evidence to support the contention that early gray hair is a risk factor.
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Some strains of C57BL/10 H-2-congenic mice were found to exhibit greying with age, whereas others did not. Two patterns of greying were observed, diffuse greying beginning at 4 to 6 months of age and patterned greying beginning at 4 to 6 weeks. Strains exhibiting either greying pattern expressed high levels of infectious ecotropic and mink cell focus-inducing murine leukemia viruses (MuLV) in tests of thymus and spleen and in cultures from skin or tail biopsies, whereas nongreying strains expressed little virus until late in life. Electron microscopy demonstrated large accumulations of MuLV in grey, but not in black areas, of skin from a mouse with patterned greying. Infectious MuLV was produced spontaneously by embryos of greying, but not of nongreying, mice and pups of nongreying strains fostered on greying mothers turned grey after 3 months. These results suggest that greying with age results from melanocyte dysfunction that occurs subsequent to pre- or early postnatal infection with MuLV.
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In a prospective survey of patients attending a general medical outpatient clinic roughly half the current cigarette smokers who had smoked for 10 years or more were identified, using defined criteria, by their facial features alone. These facial features, designated "smoker's face," were present in three (8%) of those who had smoked cigarettes for 10 years or more in the past and in none of the non-smokers. The association of smoker's face with current smoking that had continued for 10 years or more was significant (p less than 0.001) and remained after the patient's age, social class, exposure to sunlight, recent change of weight, and estimated lifetime consumption of cigarettes were controlled for. Smoker's face may be a helpful indicator in antismoking campaigns.
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The Journal of Investigative Dermatology publishes basic and clinical research in cutaneous biology and skin disease.
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Indicators of ageing were measured in 397 male and 130 female London Civil Servants aged from 37 to 58 years of age. Grey hair, skin inelasticity, and arcus senilis were strongly and independently related to chronological age. Also independently related were serum albumin (negatively related in both sexes), baldness, serum creatinine, systolic blood pressure, serum calcium (negatively) and ESR in men, and serum cholesterol in women. Chronological age was regressed on the above variables for men and women separately to provide regression equations. Biological age for an individual was calculated by entering his or her results and calculating the residuals. Biological age in those who stopped smoking tended to be younger than chronological age by an average of 12-13 months in men and 1-4 months in women. Men and women who had never smoked had higher biological than actual ages but not after adjusting for regression dilution bias. Men who currently smoked had higher biological ages of 2-3 months but not women smokers (4-6 months lower). Similarly, men of lower employment grades had an average biological age 13 months older and women 8 months, compared with higher employment grades. These differences between employment grade appeared to be due to ESR, arcus senilis, systolic blood pressure and serum cholesterol. These four measurements may be markers of biological rather than chronological age, and the value of attempting to measure biological age is discussed.
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Premature graying of hair is associated with several endocrine disorders, vitiligo, and the aging process. Although the pathophysiology of melanin depletion in hair follicles is unknown, genetic factors regulate the expression of this trait. As acquisition of bone mass is also genetically determined, we performed an exploratory case control study of the association between premature graying of hair and osteopenia (lumbar bone density t score, below -1.0). Subjects were recruited from a single metabolic bone clinic. Premature graying of hair in 36 men and women with osteopenia (cases) was compared to that in 27 men and women without osteopenia (controls). Subjects with premature graying but no other identifiable risk factor were 4.4 times as likely to have osteopenia as subjects without premature graying (P = 0.02). Subjects with osteopenia and premature graying in their teens and twenties had a stronger family history of osteoporosis than those who had osteopenia and graying later in their thirties (P = 0.06), but bone density and other characteristics were not different. The association between premature graying and low bone mass could be related to genes that control peak bone mass or factors that regulate bone turnover. Premature graying of hair may be an important risk marker for osteopenia.