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Smoking, Alcohol, and Bone Health

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Smoking and alcohol consumption are two lifestyle factors that have important contributions to skeletal health. Deleterious effects of smoking on the skeleton have been recognized for several decades. Smoking adversely affects bone density and increases hip fracture risk in postmenopausal women. In men emerging evidence is suggestive for similar associations but the evidence is not conclusive. Furthermore, the evidence is inadequate to infer a causal relationship between smoking and reduced bone density before menopause in women and in younger men. Previously, the role of alcohol on skeletal health was not as well studied as that of smoking, and results from those studies suggested both beneficial as well as deleterious effects on the skeleton. However, recent studies on the role of alcohol on the skeleton suggest a “J”-shaped curve. Moderate ingestion of alcohol may offer some degree of benefit to the skeleton. Ongoing research further suggests that both ethanol and non-ethanol components of alcohol affect skeletal heath.
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489
M.F. Holick and J.W. Nieves (eds.), Nutrition and Bone Health, Nutrition and Health,
DOI 10.1007/978-1-4939-2001-3_30, © Springer Science+Business Media New York 2015
Key Points
Smoking and alcohol consumption are two lifestyle factors that have important contributions to
skeletal health.
Deleterious effects of smoking on the skeleton have been recognized for several decades. Smoking
adversely affects bone density and increases hip fracture risk in postmenopausal women. In men
emerging evidence is suggestive for similar associations but the evidence is not conclusive.
The evidence is inadequate to infer a causal relationship between smoking and reduced bone den-
sity before menopause in women and in younger men.
Previously, the role of alcohol on skeletal health was not as well studied as that of smoking, and
results from those studies suggested both benefi cial as well as deleterious effects on the skeleton.
However, recent studies on the role of alcohol on the skeleton suggest a “J”-shaped curve. Moderate
ingestion of alcohol may offer some degree of benefi t to the skeleton.
Ongoing research further suggests that both ethanol and non-ethanol components of alcohol con-
taining beverages affect skeletal heath.
Chapter 30
Smoking, Alcohol, and Bone Health
Shivani Sahni and Douglas P. Kiel
S. Sahni , Ph.D. D. P. Kiel , M.D., M.P.H. (*)
Institute for Aging Research, Hebrew SeniorLife and Beth Israel Deaconess Hospital ,
Harvard Medical School , 1200 Centre St. , Boston , MA , USA
e-mail: ShivaniSahni@hsl.harvard.edu; Kiel@hsl.harvard.edu
Keywords Smoking Alcohol Bone mineral density Fracture
30.1 Introduction
Smoking and alcohol consumption are two lifestyle factors that have important contributions to skel-
etal health. Deleterious effects of smoking on the skeleton have been recognized for several decades.
The 2004 Surgeon General’s Report on Bone Health and Osteoporosis [ 1 ] recognized smoking and
heavy alcohol use as signifi cant contributors to reduced bone mass and increased fracture risk. The
2004 Surgeon General’s Report on Women and Smoking [ 2 ] concluded that smoking adversely affects
bone density and increases hip fracture risk in postmenopausal women while the association in men
is suggestive but not conclusive. The evidence is inadequate to infer a causal relationship between
smoking and reduced bone density before menopause in women and in younger men. Recent studies
490
on the role of alcohol on skeletal health suggest a “J”-shaped curve. Moderate ingestion of alcohol
may offer some degree of benefi t to the skeleton. Ongoing research further suggests that both ethanol
and non-ethanol components of alcohol affect skeletal heath.
30.2 Smoking and Bone Health
30.2.1 Smoking Effects on the Skeleton
There are potential direct and indirect effects of smoking on skeletal health and fracture risk. Direct
toxic effects of smoking on bone cells may be related to nicotine effects [ 3 , 4 ] or possibly to toxic
chemicals in tobacco products such as cadmium [ 5 ]. Smoking has direct effects on osteogenesis
including alteration in the RANK–RANKL–OPG system [ 6 , 7 ], collagen metabolism [ 8 ], and bone
angiogenesis [ 9 ] (Fig. 30.1 ). Indirect effects of smoking on bone may result from decreased intestinal
calcium absorption [ 10 ], dysregulation in sex hormone production and metabolism [ 11 ], alterations in
metabolism of adrenal cortical and gonadal hormones [ 1214 ], calciotropic hormones [ 15 ] such as
25-hydroxy-vitamin D [ 11 , 16 ] and parathyroid hormone [ 11 ]. These effects may account for the
generally observed decrease in markers of bone formation, such as osteocalcin, in smokers [ 16 , 17 ].
Smoking may also indirectly infl uence bone density and the risk of fractures through reductions in
body weight. Body weight tends to be lower for smokers than for nonsmokers, and this weight differ-
ence may itself lead to lower bone density and increased risk for fracture [ 18 , 19 ]. Finally, smokers
may be less physically active, which itself may reduce bone density [ 20 ] and increase fracture risk
[ 21 ]. In several analyses involving women, weight explains part of the increased risk of low bone
Fig. 30.1 Pathophysiologic mechanisms due to cigarette smoking that lead to decreased bone mineral density and
increased fracture risk. Tobacco use increases risk through bone mineral density-dependent factors, as well as through
direct effects that are independent of BMD [
15 ]
S. Sahni and D.P. Kiel
491
mineral density (BMD) associated with smoking [ 22 ]; however, there are differences in BMD and
fracture between smokers and nonsmokers, even after adjusting for weight differences [ 17 , 2325 ].
The lower weight in smokers compared to nonsmokers may increase the risk of fractures, such as hip
fractures, through several mechanisms: reduced soft tissue mass overlying the trochanter, resulting in
less energy absorption from a fall on the hip; or even reduced conversion of adrenal steroids into sex
steroids in the adipose tissue. The anti-estrogenic effect of smoking may also contribute to osteoporo-
sis in women [ 26 , 27 ]. Interestingly, although estrogen appears to be a critical hormone for male
skeletal health [ 28 ], smoking does not appear to attenuate the association between estradiol levels and
bone density in men [ 29 ]. Finally, smoking may increase the risk of fracture through a reduction in
physical performance capacity, which itself may increase the risk of falls [ 30 ].
30.2.2 Smoking and Bone Density
30.2.2.1 Skeletal Change Over the Lifespan
In adults, bone mass is dependent on the level achieved at the peak, and on losses due to aging and
other factors. The skeleton grows rapidly in infancy, slows during childhood, and then accelerates
during puberty, such that by age 20–30 years of age, peak skeletal mass is attained [ 31 , 32 ]. Gains in
BMD continue into the third decade and then BMD declines over the remaining decades of life
[ 33 , 34 ]. After menopause, bone loss accelerates compared with premenopausal years. These rates
continue or actually increase with aging [ 35 ] and similar changes are observed in men [ 36 , 37 ].
Because of these age-related patterns, smoking infl uences on bone density may be observed in the
attainment of peak bone mass, in premenopausal women, and in men.
30.2.2.2 Smoking and Attainment of Peak Bone Mass
Data are actually somewhat limited with regard to the negative effects of smoking on the attainment
of peak bone mass because less is known about the skeletal effects of smoking around the time of
puberty [ 3840 ]. A study from Belgium examined 12,446 men aged 25–45 years and reported that
smoking at a young age was associated with unfavorable bone geometry and density and was asso-
ciated with increased fracture prevalence, providing arguments for a disturbed acquisition of peak
bone mass during puberty by smoking, possibly owing to an interaction with sex steroid action
[ 38 ]. Another study of healthy military male recruits ages 16–19, reported that smoking was associ-
ated with preserved bone geometry, but worse BMD and Quantitative Ultrasound (QUS) character-
istics [
41 ].
Few data are available on the role of smoking in the attainment of peak bone mass because of the
relatively rare exposure at very young ages. Some studies have been performed in premenopausal
women initially suggesting that bone density does not differ between smokers and nonsmokers up to
the time of menopause in women. Another study conducted in 1,061 Swedish women, all exactly 25
years of age, reported that among current smokers, negative effects were observed for BMD at the hip
but not at other sites, and it was related to the amount of cigarettes smoked in a dose-dependent man-
ner. Furthermore, young women with a long history of smoking had a higher BMI suggesting that
attainment of peak bone mass is adversely associated with smoking in young women. Previous studies
in young men suggested no real differences in bone density between young male smokers and non-
smokers. However, a recent study from the United Kingdom reported that smoking appeared to be
detrimental to BMD and quantitative bone ultrasound measures, but not proximal femoral geometry
in 723 healthy Caucasian male military recruits (age range 16–18 years) [
41 ].
30 Smoking, Alcohol, and Bone Health
492
30.2.2.3 Smoking and Bone Density in Mid- and Late Life
In contrast to the results for younger persons, bone density studies performed in populations well
beyond the years of peak bone mass demonstrate signifi cant differences between smokers and non-
smokers (Table 30.1 ). Previous data from longitudinal studies in men and women suggest there may
be a causal relationship between smoking and bone loss in older women and men and that smoking
cessation may slow, or partially reverse, the accelerated bone loss caused by years of smoking.
However, it was unclear if there were sex differences related to smoking effect.
Recent studies examined the impact of smoking characteristics in older men and women. A Co-Twin
Study of 146 female twin pairs (aged 30–65 years) by MacInnis et al. reported that a discordance of
Table 30.1 Studies of BMD and bone loss according to smoking status in women and men
Study Sample, age (year) Smoking status Measurement/site Principal nding
BMD
Tanaka
et al. [
83 ]
325 men aged
50 years
10 % current smokers BMD femoral neck Current smokers at higher risk
of developing osteoporosis
(OR = 6.43).
Tamaki
et al. [
44 ]
1,576 men aged
65 years
17.6 % current smokers;
59.2 % former
smokers
BMD lumbar spine
and total hip
Longer duration of smoking
years was associated with
lower BMD.
Szulc
et al. [
46 ]
719 men aged
51–84 years
11.5 % current smokers;
56.3 % former
smokers
BMD spine, hip,
distal forearm,
ultra distal
radius
Compared to never smokers,
current and former smokers
had lower BMD at most
sites.
Supervia
et al. [
11 ]
74 men and
women; mean
age 32.2 years
29.7 % current smokers BMD lumbar spine,
femoral neck
and total femur
In men smokers had lower
BMD compared to never
smokers.
Muraki
et al. [
84 ]
632 women aged
60 years
20.0 % smokers BMD lumbar spine Ever-smokers had lower BMD
compared to never smokers.
MacInnis
et al. [
42 ]
146 women twin
pairs aged
30–65 years
Pre-menopausal women:
47 % ever smokers
(8.6 mean pack-years
of smoking);
post-menopausal
women: 32 % ever
smokers (14.1 mean
pack-years of
smoking)
BMD spine, total
hip and forearm
10 pack-years smoking related
to 2.3–3.3 % lower BMD at
all sites except forearm.
Effect more pronounced in
post-menopausal women.
Izumotani
et al. [
85 ]
686 Japanese men
aged
40–59 years
Mean smoking (pack-
years) among normal
men: 18.9 ± 20.0;
osteopenic men:
19.1 ± 21.1 and
osteoporotic men:
27.7 ± 29.4
Spine BMD Pack-years of smoking was
associated with lower BMD
Forsmo
et al. [
86 ]
1,652 Norwegian
pre- and
post-
menopausal
women aged
50–59 years
Mean smoking (pack-
years) was 13.9 (95 %
CI: 13.1–14.7); mean
number of daily
cigarettes was 10.8
(95 % CI: 10.3–11.3)
BMD distal and
ultradistal
radius
Pack-years of smoking were
associated with lower distal
radius BMD but not
ultradistal radius
BMD. Marginally
signifi cant interaction for
smoking*coffee ( P = 0.09).
(continued)
S. Sahni and D.P. Kiel
493
Table 30.1 (continued)
Study Sample, age (year) Smoking status Measurement/site Principal nding
Gerdham
et al. [
25 ]
1,032 Swedish
women aged
75 years
14 % current smokers;
20 % former smokers;
66 % never smokers
BMD total body,
spine and hip,
bone mass
assessed by
ultrasound of
the calcaneus
and phalanges
Hip and total body BMD was
low in current vs. never
smokers. This difference
was not detected by
ultrasound measurements.
No difference between
former vs. never smokers at
any bone site.
Baheiraei
et al. [
47 ]
90 Iranian women
aged
35 years
Current smokers 8 %
(pre-menopausal
women); 8 %
post-menopausal
women
BMD spine and
femoral neck
Smoking status associated with
lower BMD. Current
smokers had lower BMD
compared to non-smokers.
Williams
et al. [
87 ]
46 pair of
monozygotic
twins
discordant for
alcohol
consumption
Current smokers vs.
former smokers
BMD hip and
lumbar spine
Current smoking was
negatively associated with
BMD.
Muraki
et al. [
84 ]
632 women aged
60 years
Smokers (20.6 %) vs.
non-smoker
BMD lumbar spine Smoking was negatively
associated with BMD.
Kuo et al. [
43 ] 837 Taiwanese
men aged
46–64 years
30.8 % current smokers;
5.6 % former smokers
BMD spine and
femoral neck
Smoking status and duration of
smoking were deleterious
for spine BMD. The effect
was cumulative with
duration and quantity.
BMD loss
Elgán
et al. [
88 ]
152 Swedish
women (aged
18–26);
average
follow-up
2 years
18.5 % daily smokers;
18.5 % “party”
smokers; 63 %
non-smokers at the
follow-up time
BMD heel bone
(calcaneus)
Baseline smoking associated
with lower BMD at the
follow-up after adjusting
for baseline BMD.
Bakhireva
et al. [
80 ]
507 community-
dwelling men
aged 45–92
years
Current smokers aged:
45–64 years (14.6 %);
65–74 years (7.5 %);
75–92 years (2.2 %)
BMD hip and
lumbar spine
Compared to former smokers,
% BMD loss in current
smokers was increased at
the total hip and femoral
neck.
BMD bone mineral density
10 pack-years of smoking was related to a 2.3–3.3 % (SE, 0.8–1.0) lower lumbar spine BMD, total
hip BMD and total body BMC but not the forearm BMD, with effects more evident in postmeno-
pausal women [ 42 ]. Studies in older Asian men have reported a 3.8 % lower lumbar spine BMD in
heavy smoking (20 cigarette/day) [ 43 ]. The Fujiwara-kyp Osteoporosis Risk in Men (FORMEN)
study reported that the negative impact of smoking on bone status is mainly associated with the num-
ber of years of smoking in older men [ 44 ]. The Male Osteoporosis Study from Hong Kong, a longitu-
dinal study, reported that in older men, current smokers had a 2.0 % decrease in hip BMD (95 % CI:
−3.8, −0.1) while past smokers had a 1.3 % decrease in hip BMD (95 % CI: −2.5, −0.2) compared to
never smokers [ 45 ]. However, some studies report no bone mass differences between former and
never-smokers [ 25 , 46 ]. It has also been suggested that former smokers may not lose or regain BMD
after cessation of smoking [ 46 ].
30 Smoking, Alcohol, and Bone Health
494
Certain factors such as higher body mass index [ 47 ], and higher calcium intake [ 48 ] have been
reported to attenuate the smoking associations with bone. Smoking may also interfere with the treat-
ment of osteoporosis in women using estrogen replacement therapy (ERT), as levels of estradiol are
lower in smokers taking estrogen than in nonsmokers taking estrogen [ 49 ], and bone density values in
women taking estrogen are lower in smokers than in nonsmokers [ 23 ].
These effects on bone density are signifi cant in mid and late life, since for every 10-year increase
in age, the bone density of smokers falls below that of nonsmokers by about 0.14 SD, or 2 % of the
average bone density at the time of the menopause. Because a 1.0-SD decrease in bone density dou-
bles the risk of fracture, and because fracture incidence increases with age, the proportion of all frac-
tures attributable to smoking would be expected to increase as smokers continue smoking into old age.
Attempts to decrease smoking as early in life as possible are likely to reduce fractures that occur in
old age among smokers.
Taken together, cigarette smoking (both dosage and duration of smoking) is associated with lower
BMD and increased bone loss in older men and women. Limited studies have examined if the deleteri-
ous effects of smoking on bone health may be reversible. Furthermore, smoking effects on bone may
not be limited to BMD but may extend to other aspects of bone strength such as bone architecture and
bone geometry, an area that has received little attention.
30.2.3 Smoking and Fracture Risk
Hip fractures, the most frequently studied fractures in relation to smoking, account for a signifi cant
proportion of the morbidity and mortality attributed to osteoporosis. Previous studies suggested that
smoking appeared to increase the risk of hip fracture; however, there were fewer studies of smoking
and fracture risk at other skeletal sites. Because the risk of hip fractures in smokers increases with age,
and hip fracture incidence also increases with age, the proportion of hip fractures attributable to smok-
ing increases with age.
A meta-analysis by Kanis et al. [ 50 ] included 59,232 men and women from ten prospective cohorts
from across the world. This study reported that a smoking history was associated with a signifi cantly
increased risk of fracture compared with individuals with no smoking history. The highest risk was
observed for hip fracture (84 % increased risk, 95 % CI: 1.52–2.22) while the risk of osteoporotic
fractures considered as a group was marginally higher (29 % increased risk, 95 % CI: 1.13–1.28). The
authors concluded that a history of smoking results in fracture risk that is substantially greater than
that explained by the risk of lower BMD. A study by Olofsson et al. using data from the Uppsala
Longitudinal Study of Adult men [ 51 ] supported these fi ndings, and further clarifi ed that the risk of
fracture in older men depends both on recency of smoking and on the daily amount of tobacco smoked,
rather than smoking duration (Table
30.2 ). However, Samelson et al. reported no signifi cant associa-
tions of smoking (number of cigarettes/day compared to never smokers) and 25-year cumulative
incidence of radiographic vertebral fracture in men and women [ 52 ].
Interventions aimed at helping smokers quit are likely to result in a signifi cantly reduced number
of hip fractures. Although hip fractures carry the greatest risk of mortality, morbidity, and cost, other
fractures also contribute signifi cantly to these outcomes. Further research is necessary to quantify the
risk of these fractures in smokers.
S. Sahni and D.P. Kiel
495
Table 30.2 Studies of smoking and relative risk of fractures of the hip and other sites
Type of
fracture/study Study design Sample Results
Hip fracture
Lau et al. [
89 ] Case–control 451 Asian men and 725 Asian women with
hip fracture; aged 50 and older (mean,
72.0 for men, 73.7 for women) 1,162
healthy controls (456 men, 706 women)
without hip fracture; mean age, 70.8 for
men, 72.7 for women
Current smoking: Men, RR = 0.7
(95 %, CI, 0.5–1.0); women,
RR = 0.5 (95 %, CI, 0.3–0.7)
Former smoking: Men, RR = 2.1 (95 %
CI, 1.5–2.9); women, RR = 1.4
(95 % CI, 0.9–2.0)
Baron
et al. [
82 ]
Age-matched,
case–control
1,328 Swedish postmenopausal women
with hip fracture; aged 50–81 years
(mean, 72.5) 3,312 Swedish
postmenopausal without hip fracture;
mean age, 70.5
Current smokers had increased risk of
fracture, OR = 1.35 (95 % CI,
1.12–1.64); Duration of smoking,
particularly postmenopausal
smoking was more important than
the amount smoked
Du et al. [
90 ] Cross-sectional
study
703 community-dwelling Chinese men and
women (226 men, 467 women) aged
90 years (mean, 93.5)
Current or former smoking had no
association
Porthouse
et al. [
91 ]
Prospective
cohort study
703 community-dwelling English women
aged 70 years (mean, 76.9)
Current smoking not related to fracture
risk
Olofsson
et al. [
51 ]
Prospective
cohort study
2,322 community-dwelling Swedish men
aged 49–51 years
Current smoking (RR = 3.03; 95 % CI
1.02–3.44), former smoking
(RR = 1.87; 95 % CI 1.02–3.44);
ever smoking (RR = 2.12; 95 % CI
1.18–3.81) were associated with
hip fracture
Jutberger
et al. [
92 ]
Prospective
cohort study
3,003 men aged 69–80 years from the
Swedish MrOs Study ( n = 209 incident
fractures over a follow-up of
3.32 years)
Current smokers had an increased risk
of hip fractures (HR: 3.16, 95 % CI
1.44–6.95)
Vertebral fracture
Jutberger
et al. [
92 ]
Prospective
cohort study
3,003 men aged 69–80 years from the
Swedish MrOs Study ( n = 209 incident
fractures over a follow-up of
3.32 years)
Current smokers had an increased risk
of clinical and radiographic
vertebral fractures (HR: 2.53, 95 %
CI 1.37–4.65)
Klift
et al. [
93 ]
Prospective
cohort study
3,001 men and women aged 55 years
with 6.3 years of follow-up; 157
vertebral fractures (men, 44; women,
113)
Current smoking was associated with
incident vertebral in women
(RR = 2.1; 95 % CI 1.2–3.5)
Samelson
et al. [
52 ]
Prospective
cohort study
Community-dwelling American men (252);
women (452) aged 47–72 years; 92
(women) and 20 (men) new
radiographic vertebral fractures
occurred over 25 years follow-up
Smoking was not associated with
25-years cumulative incidence of
radiographic vertebral fracture
Ankle fracture
Valtola
et al. [
94 ]
Prospective
cohort study
11,798 Finnish women aged 47–56 years
with 5 years of follow-up; 194
malleolar fractures
Smoking had a dose–response
effect with HR: 1.73 (95 % CI
1.11–2.71) in those smoking 1–19
cigarettes/day, and 2.94 (95 % CI
1.53–5.62) in those smoking 20
cigarettes/day
(continued)
30 Smoking, Alcohol, and Bone Health
496
30.3 Alcohol and Bone Health
30.3.1 Alcohol Effects on the Skeleton
The mechanisms by which alcohol acts on the skeleton are poorly understood. This is due to the fol-
lowing factors: First , it is diffi cult to isolate the specifi c contribution of alcohol from other comorbid-
ity factors known to infl uence bone health [ 53 ]. Second , it is diffi cult to isolate ethanol effects from
other nutritional factors within alcoholic beverages, which usually differ by beverage type (for exam-
ple silicon present as orthosilicic acid in beer and resveratrol in wine). Third , methods of assessing
exposure to alcohol are inconsistent, especially in observational studies in humans. Additionally, the
defi nition for moderate alcohol is not clear and the guidelines on acceptable intakes of alcoholic bev-
erages is different between nations [ 54 ]. Fourth , the effect of alcohol on fracture outcomes is compli-
cated, as it may be infl uenced by other factors such as age, drinking patterns, and alcohol effect on
falls [ 55 ]. Fifth , ethanol-related health effects vary between populations because genetic background
greatly infl uence the metabolism of alcohol [ 54 ].
Nevertheless, the direct effects of alcohol on bone and mineral metabolism have been described in
both rats and in humans. Studies of chronic alcohol consumption in growing male and female rats
have indicated that bone growth is suppressed, leading to a failure to acquire a normal peak bone mass
[ 56 ]. Bone loss in adult rats fed ad libitum a liquid diet containing increasing concentrations of etha-
nol until receiving the appropriate percentage of total caloric intake, resulted in a dose-dependent
decrease in trabecular thickness, bone turnover, and bone formation rate [ 57 ]. When equated to
humans, the doses used in the adult rat experiments ranged from the low end of moderate (3 % of
caloric intake) to alcoholic levels comprising 35 % of caloric intake. These fi ndings in rats suggest
that even moderate levels of alcoholic beverage consumption in humans may have the potential to
reduce bone turnover and possibly to have deleterious effects on the skeleton. In rats fed ethanol over
long periods, Peng et al. reported a greater risk of tibial fractures and a decrease in trabecular bone
volume and bone strength [ 58 ]. Turner et al. reported that alcohol-consuming rats had decreased bone
turnover after 4 months of treatment. Furthermore, an imbalance between bone formation and bone
resorption at higher levels of alcohol consumption resulted in trabecular thinning [ 57 ].
Table 30.2 (continued)
Type of
fracture/study Study design Sample Results
Wrist fracture
Porthouse
et al. [
91 ]
Prospective
cohort study
703 community-dwelling English women
aged 70 years (mean, 76.9)
Current smoking not related to
fracture risk
Any nonvertebral fracture
Porthouse
et al. [
91 ]
Prospective
cohort study
703 community-dwelling English women
aged 70 years (mean, 76.9)
Current smoking not related to fracture
risk
Jutberger
et al. [
92 ]
Prospective
cohort study
3,003 men aged 69–80 years from the
Swedish MrOs Study (nonvertebral
fractures defi ned as humerus, radius,
pelvis, and hip fractures over a
follow-up of 3.32 years)
Current smokers had an increased risk
of nonvertebral osteoporotic
fractures (HR: 2.14, 95 % CI
1.18–3.88)
Any fracture
Jutberger
et al. [
92 ]
Prospective
cohort study
3,003 men aged 69–80 years from the
Swedish MrOs Study (nonvertebral
fractures defi ned as humerus, radius,
pelvis, and hip fractures over a
follow-up of 3.32 years)
Current smokers had an increased risk
of all new fractures (HR: 1.76,
95 % CI 1.19–2.61)
S. Sahni and D.P. Kiel
497
In humans, alcoholics have been shown to have low BMD that is due to an inhibition of bone
remodeling by a mechanism independent of the calciotropic hormones [ 59 , 60 ]. Others have com-
pared alcoholics to controls and found that serum concentrations of 25-hydroxyvitamin D
3 and
1,25-dihydroxyvitamin D
3 were signifi cantly reduced among the alcoholics as compared to the con-
trols [ 61 , 62 ]. These low levels have been suggested to be the result of a defi cient diet, reduced expo-
sure to sunlight, malabsorption of vitamin D, increased biliary excretion of 25-hydroxyvitamin D
metabolites, or to be the result of reduced reserves of vitamin D owing to a reduction of adipose and
muscle tissue in alcoholics [ 63 ]. Laitenen and colleagues demonstrated that the low serum levels of
vitamin D metabolites in non-cirrhotic alcoholics were not because of nutritional defi ciency, and
hypothesized that there was increased degradation of vitamin D metabolites in the liver. However,
they showed that high calcium intake could counteract the vitamin D abnormalities [ 64 ]. Alcohol may
also have deleterious effects on bone homeostasis through increased excretion of calcium and magne-
sium [ 65 ]. Consistent with the observations of reduced bone formation in alcohol-fed rats, reductions
in osteoblastic activity have been observed in acute alcohol intoxication and in moderate use over 3
weeks time in humans [ 66 , 67 ].
On the other hand, recent studies have also focused on non-ethanol components of alcohol bever-
ages such as silicon and resveratrol. Recent reviews by Jugdaohsingh [ 68 ] and more recently by Price
et al. [ 69 ] have provided extensive research on silicon’s effect on bone and connective tissue. While
the exact mechanisms are still unclear, various mechanisms were suggested in these reviews. Silicon
improves bone matrix quality, facilitates bone mineralization, and plays a role in collagen synthesis
and/or its stabilization as well as in the utilization (i.e. gastrointestinal uptake and metabolism) of
essential elements that are required for bone and collagen synthesis. Available epidemiological data
also supports silicon’s role in BMD [ 70 , 71 ] in humans. Research on health effects of resveratrol is
limited and primarily comes from studies of animals. One study in an ovariectomized rat model
showed that rats treated with resveratrol had signifi cantly greater BMD than those not treated [ 72 ]
suggesting that resveratrol could play a role in protecting against bone loss induced by estrogen defi -
ciency. A recent study of male rats showed that trans-resveratrol supplementation (12.5 mg/kg body
weight/day) appeared to preserve the skeletal system during disuse and age-related bone loss [ 73 ].
30.3.2 Alcohol and Bone Density
Most studies investigating alcohol intake and bone health suggest a “J”-shaped curve such that the
infl ection point is at moderate ingestion, which offers maximum protection. Increased intake beyond
this level shows negative effects on the skeleton. Wosje et al. reported bone benefi cial effects of mod-
erate alcohol consumption (measured as drinking occasions/month) using the data from the Third
National Health and Nutrition Examination Survey (NHANES III, 1988–1994) [
74 ]. This study
reported that total hip BMD in men and FN-BMD in postmenopausal women were higher among
those with >29 drinking occasions/month compared to abstainers. However, no associations were
observed in premenopausal women or with binge drinking (Table 30.3 ). Results from the Cardiovascular
Health Study (subgroup of 1,567 men and women with BMD measures) showed that alcohol intake
(measured as drinks/week) was associated with hip BMD in a U-shaped relationship, with approxi-
mately 5 % higher BMD among participants with 14 drinks/week compared to abstainers [ 75 ].
Cawthon et al. examined the association of alcohol intake and problem drinking history with BMD
in a cross-sectional study of 5,974 men (aged 65 years) [ 76 ]. Alcohol intake categories were defi ned
as non/infrequent (<12 drinks/year, abstainers), light (12 drinks/year to <13 drinks/week), and mod-
erate to heavy (14 drinks/week). Alcohol intake was positively associated with hip and spine
BMD. Although the absolute differences in BMD levels across categories of alcohol were modest
(3.5 % for total hip BMD). Men with problem drinking also had higher hip and spine BMD. The type
of alcohol consumed was not ascertained.
30 Smoking, Alcohol, and Bone Health
498
Tucker et al. further attempted to identify the different classes of alcohol in relation with BMD in
older men and women (1,182 men, 1,289 postmenopausal women, and 248 premenopausal women)
from the Framingham Heart Study [ 77 ]. This study sample of predominantly beer-drinking men, and
predominantly wine drinking women, supported the earlier fi ndings that moderate consumption of
alcohol is associated with higher BMD in men and postmenopausal women. This protective effect
peaked at one to two drinks/day for men (the benefi ts declined with higher intakes). However, for
unclear reasons and contrary to the current guidelines for women, this protective effect peaked at a
higher limit (>2 drinks/day) in women. No associations were observed in premenopausal women,
perhaps due to low power. Interestingly, men with high liquor intakes (>2 drinks/day) were associated
with signifi cantly lower BMD. The authors concluded that stronger associations with beer or wine,
relative to liquor, suggest that other constituents (such as silicon in beer) rather than ethanol may
contribute to bone health.
Table 30.3 Studies of bone density and bone loss according to alcohol use
Study Sample, age (year) Alcohol status Measurement/site Principal nding
BMD
Wosje
et al. [
74 ]
14,646 men and
women aged
20 years
Frequency of alcohol
consumed in past 1
month
BMD total hip
and femoral
neck
Alcohol intake was positively
associated with BMD in men
and postmenopausal women
but not in premenopausal
women. No associations
with binge drinking.
Williams
et al. [
87 ]
46 pair of
monozygotic
twins discordant
for alcohol
consumption
Units per week, defi ned as
half a pint of beer; a
glass of wine or one
measure of spirits
BMD hip and
lumbar spine
Alcohol consumption was
positively associated with
BMD.
Tucker
et al. [
77 ]
1,182 men, 1,289
postmenopausal
women and 248
premenopausal
women aged
29–86 years
Drinks/day, defi ned as
356 mL beer; 118 mL
wine; 42 mL liquor
BMD Spine
and hip
Moderate alcohol intake was
positively associated with
BMD in men and
postmenopausal women but
not premenopausal women.
Kouda et al.
[
78 ]
1,421 Japanese men
aged 60 years
Grams of absolute ethanol
per day calculated
from current alcohol
intake by beverage
type
BMD Spine
and hip
Alcohol intake <55 g/day was
associated with higher BMD
and intake of 55 g/day was
associated with lower BMD.
Cauley et al.
[
95 ]
5,995 men aged
65 years
Drinks/week BMD Spine
and hip
A 1 SD (approximately seven
drinks/week) increase in
alcohol consumption was
associated with a 1 % higher
hip and spine BMD.
Muraki et al.
[
84 ]
632 women aged
60 years
Alcohol drinker vs.
nondrinker
BMD lumbar
spine
Alcohol consumption was
positively associated with
BMD.
BMD loss
Macdonald
et al. [
79 ]
891 women aged
45–55 years
Alcohol intake in
quartiles
BMD lumbar
spine and
femoral neck
Modest alcohol intake was
associated with less bone
loss.
Bakhireva
et al. [
80 ]
507 community-
dwelling men
aged 45–92
Frequency of alcohol
consumption (drinking
3 vs. 2 days/week)
BMD lumbar
spine, total hip
and femoral
neck
Moderate alcohol intake was
associated with less bone
loss.
BMD bone mineral density
S. Sahni and D.P. Kiel
499
Using data from the baseline survey for the Fujiwara-kyo Osteoporosis Risk in Men (FORMEN)
study, Kouda et al. reported a positive association between alcohol intake (g/day) and BMD as well as
with bone markers (serum levels of osteocalcin and tartrate-resistant acid phosphatase 5b (TRACP5b)
[ 78 ]. However, they reported an infl ection point for the relation between alcohol intake and BMD as
55 g/day. Thus the range of positive association in this study was larger than the previous studies.
Only two longitudinal studies examined alcohol intakes with bone loss. One study from the
Aberdeen Prospective Osteoporosis Screening Study examined the association of alcohol intake (in g/
day) with recent bone loss around menopause in 891 women aged 45–44 years at the baseline and
50–59 years at the follow-up (5–7 years later) [ 79 ]. MacDonald et al. reported that participants in the
highest quartile of alcohol intake (median intake of 13.6 g/day) had signifi cantly lower bone loss
(calculated as annual percentage change) at the lumbar spine bone loss compared to nonalcohol drink-
ers. These differences remained signifi cant after adjustment for appropriate confounders and covari-
ates. The other study from Rancho Bernardo in Southern California, examined 507 older men aged
45–92 years. This study reported moderate alcohol consumption of 3 times/week to be associated
with less bone loss at femoral neck over 4 years [ 80 ].
30.3.3 Alcohol and Fracture Risk
Despite the suggestion from some of the above studies that alcohol may have benefi cial effects on the
skeleton, the vast majority of previous studies examining alcohol consumption and risk of fractures
either showed no signifi cant association, or in some cases, an increased risk of fracture among those
men and women with high intakes of alcohol. Higher intakes may predispose to trauma-associated frac-
ture outcomes. Finally, alcoholics appear to have low bone density and metabolic abnormalities that
threaten bone health. However, recent studies suggest that moderate alcohol consumption may be pro-
tective against hip fracture risk [ 75 ] and one study on alcoholic showed that the increased lifetime preva-
lence of fractures among problem drinkers could be due to factors other than the acute intoxication [ 81 ].
Cawthon et al. examined the association of alcohol intake and problem drinking history with frac-
ture risk in 5,974 men (aged 65 years, 256 nonvertebral fractures, and 46 hip fractures over 3.65-
year follow-up) in a prospective cohort study of MrOs [ 76 ]. The authors reported no signifi cant
association between alcohol intake and risk of nonspine and hip fractures among older men
(Table 30.4 ). There were however, weak protective trends for greater weekly alcohol intake and lower
relative hazard of hip fracture. History of problem drinking, heavy drinking, or current episodic drink-
ing were also not related to risk of nonspine or hip fractures. Similar weak inverse associations were
also observed for alcohol intake and hip fracture risk from a case–control study in Swedish postmeno-
pausal women [
82 ].
Results from the Cardiovascular Health Study (5,865 men and women, 412 cases of hip fracture
over 12 years follow-up) showed a U-shaped relationship between alcohol intake (measured as drinks/
week) and hip fracture. Compared with long-term abstainers, the hip fracture risk was 22 % lower
(HR: 0.78; 95 % CI: 0.61–1.00) among consumers of up to 14 drinks/week and the risk was 18 %
(HR: 1.18; 95 % CI: 0.77–1.81) higher among those with 14 drinks/week [ 75 ]. However, it was
unclear if the increased fracture risk with higher alcohol intake was mediated through an increased
risk for falls or other types of trauma. Increased vertebral fracture risk in men but not women was also
reported in the Framingham Study where the increased risk was observed even at lower intakes of
1–4 oz/week (~1.5–6.5 drinks/week) and at higher intakes of 4 oz/week (6.5 drinks/week) [ 52 ].
Clark et al. examined the differences in self-reported lifetime fracture prevalence in Caucasian
women ( n = 834, aged 18–70 years) in treatment for alcohol abuse, in recovery and nonalcohol-
dependent women [
81 ]. Women in treatment and recovery reported more fractures during childhood
and adolescence than nonalcohol-dependent women. Women with histories of alcohol dependence
30 Smoking, Alcohol, and Bone Health
500
Table 30.4 Studies of alcohol and relative risk of fractures of the hip and other sites
Type of
fracture/study Study design Sample Results
Hip fracture
Lau et al. [
89 ] Case–control 451 Asian men and 725 Asian women
with hip fracture; aged 50 and
older (mean, 72.0 for men, 73.7
for women) 1,162 healthy controls
(456 men, 706 women) without
hip fracture; mean age, 70.8 for
men, 72.7 for women
Occasional alcohol consumption:
associated with lower risk in women,
RR = 0.5 (95 %, CI, 0.3–0.9)
Daily alcohol consumption (7 days/week)
associated with higher risk: men,
RR = 2.0 (95 % CI, 1.3–3.1); women,
RR = 2.1 (95 % CI, 1.0–4.7)
Number of alcoholic drinks/week 14;
RR = 2.9 (95 %, CI, 1.2–7.1)) and years
of alcohol consumption 25; RR = 3.0
(95 %, CI, 1.7–5.2) was associated
with higher risk in men
Baron et al.
[
82 ]
Age-matched,
case–control
1,328 Swedish postmenopausal
women with hip fracture; aged
50–81 years (mean, 72.5) 3,312
Swedish postmenopausal without
hip fracture; mean age, 70.5
Drinkers had lower risk, OR = 0.70 (95 %
CI, 0.60–0.82). All types of alcoholic
beverages were protective except for
light beer, which showed no
association
Du et al. [
90 ] Cross-sectional
study
703 community-dwelling Chinese
men and women (226 men, 467
women) aged 90 years (mean,
93.5)
Former alcohol consumption was
associated with higher hip fracture risk
(OR = 2.5; 95 % CI 1.0–5.5)
Mukamal
et al. [
75 ]
Prospective
cohort study
5,865 community-dwelling American
men and women aged 65 years;
412 fractures occurred over
12 years follow-up
U-shaped relationship with lower risk
among consumers of <14 drinks/week,
HR: 0.78 (95 % CI, 0.61–1.00) and
higher risk among consumers of 14
drinks/week, HR: 1.18 (95 % CI,
0.77–1.81)
Cawthon
et al. [
76 ]
Prospective
cohort study
5,974 community-dwelling American
men aged 65 years; 46 hip
fractures occurred over 3.65 years
follow-up
Alcohol not signifi cantly associated with
hip fracture
Osteoporotic fracture
Clark et al.
[
81 ]
Cross-sectional
study
831 Caucasian women aged
18–70 years
Percent osteoporotic fractures: Women in
treatment for alcohol abuse: 25 % vs.
non-alcohol abusers: 15 % ( P < 0.01)
Women in recovery and abstainer: 25 %
vs. non-alcohol abusers: 15 %
( P < 0.01)
Vertebral fracture
Samelson
et al. [
52 ]
Prospective
cohort study
Community-dwelling American men
(252); women (452) aged
47–72 years; 92 (women) and 20
(men) new vertebral fractures
occurred over 25 years follow-up
Alcohol consumption (4 oz/week) was
associated with increased 25-years
cumulative incidence of vertebral
fracture
Non-vertebral fracture
Cawthon
et al. [
76 ]
Prospective
cohort study
5,974 community-dwelling American
men aged 65 years; 256
non- vertebral fractures occurred
over 3.65 years follow-up
Alcohol not signifi cantly associated with
hip fracture
RR relative risk, CI confi dence interval, OR odds ratio, HR hazard ratio
S. Sahni and D.P. Kiel
501
had higher lifetime prevalence of fractures, including time periods before the onset of problem drink-
ing and following abstinence, suggesting that factors other than the acute intoxication contributed to
the greater fracture prevalence.
30.4 Conclusion
Smoking and alcohol consumption are two lifestyle factors that have important contributions to skeletal
health. Smoking adversely affects bone density and increases hip fracture risk in postmenopausal
women. However, the association in men is not conclusive while the evidence is inadequate for premeno-
pausal women and younger men. The role of alcohol on skeletal health can be both benefi cial as well as
deleterious depending upon the level of intake. Recent studies on the role of alcohol on the skeleton
suggest a “J”-shaped curve and report that moderate ingestion may offer benefi ts to the skeleton, and
both ethanol and non-ethanol components of alcohol may be involved in affecting skeletal heath.
References
1. Offi ce of the Surgeon General. Bone health and osteoporosis: a report of the Surgeon General. Rockville, MD: US
Department of Health and Human Services, Offi ce of the Surgeon General; 2004.
2. The health consequences of smoking: a report of the Surgeon General. Atlanta, GA: U.S. Department of Health and
Human Services, Offi ce of Surgeon General, Centers for Disease Control and Prevention, National Center for
Chronic Disease Prevention and Health Promotion, Offi ce on Smoking and Health; 2004.
3. Riebel GD, Boden SD, Whitesides TE, Hutton WC. The effect of nicotine on incorporation of cancellous bone graft
in an animal model. Spine. 1995;20(20):2198–202.
4. Fang MA, Frost PJ, Iida-Klein A, Hahn TJ. Effects of nicotine on cellular function in UMR 106-01 osteoblast-like
cells. Bone. 1991;12(4):283–6.
5. Bhattacharyya MH, Whelton BD, Stern PH, Peterson DP. Cadmium accelerates bone loss in overiectomized mice
and fetal rat limb bones in culture. Proc Natl Acad Sci U S A. 1988;85:8761–5.
6. Tang TH, Fitzsimmons TR, Bartold PM. Effect of smoking on concentrations of receptor activator of nuclear factor
kappa B ligand and osteoprotegerin in human gingival crevicular fl uid. J Clin Periodontol. 2009;36(9):713–8.
7. Lappin DF, Sherrabeh S, Jenkins WM, Macpherson LM. Effect of smoking on serum RANKL and OPG in sex, age
and clinically matched supportive-therapy periodontitis patients. J Clin Periodontol. 2007;34(4):271–7.
8. Sorensen LT, Toft BG, Rygaard J, Ladelund S, Paddon M, James T, Taylor R, et al. Effect of smoking, smoking
cessation, and nicotine patch on wound dimension, vitamin C, and systemic markers of collagen metabolism.
Surgery. 2010;148(5):982–90.
9. Ma L, Zheng LW, Sham MH, Cheung LK. Uncoupled angiogenesis and osteogenesis in nicotine-compromised
bone healing. J Bone Miner Res. 2010;25(6):1305–13.
10. Krall EA, Dawson-Hughes B. Smoking increases bone loss and decreases intestinal calcium absorption. J Bone
Miner Res. 1999;14(2):215–20.
11. Supervia A, Nogues X, Enjuanes A, Vila J, Mellibovsky L, Serrano S, Aubia J, et al. Effect of smoking and smoking
cessation on bone mass, bone remodeling, vitamin D, PTH and sex hormones. J Musculoskelet Neuronal Interact.
2006;6(3):234–41.
12. Baron JA, Comi RJ, Cryns V, Brinck-Johnsen T, Mercer NG. The effect of cigarette smoking on adrenal cortical
hormones. J Pharmacol Exp Ther. 1995;272(1):151–5.
13. Khaw KT, Tazuke S, Barrett-Connor E. Cigarette smoking and levels of adrenal androgens in postmenopausal
women. N Engl J Med. 1988;318(26):1705–9.
14. Michnovicz JJ, Hershcopf RJ, Naganuma H, Bradlow HL, Fishman J. Increased 2-hydroxylation of estradiol as a
possible mechanism for the anti-estrogenic effect of cigarette smoking. N Engl J Med. 1986;315(21):1305–9.
15. Yoon V, Maalouf NM, Sakhaee K. The effects of smoking on bone metabolism. Osteoporos Int.
2012;23(8):2081–92.
16. Brot C, Jorgensen NR, Sorensen OH. The infl uence of smoking on vitamin D status and calcium metabolism. Eur J
Clin Nutr. 1999;53(12):920–6.
30 Smoking, Alcohol, and Bone Health
502
17. Bjarnason NH, Christiansen C. The infl uence of thinness and smoking on bone loss and response to hormone
replacement therapy in early postmenopausal women. J Clin Endocrinol Metab. 2000;85(2):590–6.
18. Cummings SR, Nevitt MC, Browner WS, Stone K, Fox KM, Ensrud KE, Cauley J, et al. Risk factors for hip fracture
in white women. Study of Osteoporotic Fractures Research Group. N Engl J Med. 1995;332(12):767–73.
19. Kiel DP, Felson DT, Anderson JJ, Wilson PW, Moskowitz MA. Hip fracture and the use of estrogens in postmeno-
pausal women. The Framingham Study. N Engl J Med. 1987;317(19):1169–74.
20. Bolam KA, van Uffelen JG, Taaffe DR. The effect of physical exercise on bone density in middle-aged and older
men: a systematic review. Osteoporos Int. 2013;24(11):2749–62.
21. Feskanich D, Willett W, Colditz G. Walking and leisure-time activity and risk of hip fracture in postmenopausal
women. JAMA. 2002;288(18):2300–6.
22. Bauer DC, Browner WS, Cauley JA, Orwoll ES, Scott JC, Black DM, Tao JL, et al. Factors associated with appen-
dicular bone mass in older women. The Study of Osteoporotic Fractures Research Group (see comments). Ann
Intern Med. 1993;118(9):657–65.
23. Kiel DP, Baron JA, Anderson JJ, Hannan MT, Felson DT. Smoking eliminates the protective effect of oral estrogens
on the risk for hip fracture among women. Ann Intern Med. 1992;116(9):716–21.
24. Kiel DP, Zhang Y, Hannan MT, Anderson JJ, Baron JA, Felson DT. The effect of smoking at different life stages on
bone mineral density in elderly men and women. Osteoporos Int. 1996;6:240–8.
25. Gerdhem P, Obrant KJ. Effects of cigarette-smoking on bone mass as assessed by dual-energy X-ray absorptiometry
and ultrasound. Osteoporos Int. 2002;13(12):932–6.
26. Jensen J, Christiansen C. Effects of smoking on serum lipoproteins and bone mineral content during postmeno-
pausal hormone replacement therapy. Am J Obstet Gynecol. 1988;159(4):820–5.
27. Jensen J, Christiansen C, Rodbro P. Cigarette smoking, serum estrogens, and bone loss during hormone- replacement
therapy early after menopause. N Engl J Med. 1985;313(16):973–5.
28. LeBlanc ES, Nielson CM, Marshall LM, Lapidus JA, Barrett-Connor E, Ensrud KE, Hoffman AR, et al. The effects
of serum testosterone, estradiol, and sex hormone binding globulin levels on fracture risk in older men. J Clin
Endocrinol Metab. 2009;94(9):3337–46.
29. Amin S, LaValley MP, Zhang Y, Evans SR, Sawin C, Wilson PWF, Hannan MT, et al. Is the effect of smoking on
bone mineral density (BMD) in elderly men mediated through estradiol (E2)? The Framingham Osteoporosis Study.
J Bone Miner Res. 1999;14 Suppl 1:S147.
30. Nelson HD, Nevitt MC, Scott JC, Stone KL, Cummings SR. Smoking, alcohol, and neuromuscular and physical
function of older women. Study of Osteoporotic Fractures Research Group (see comments). JAMA. 1994;272(23):
1825–31.
31. Kroger H, Kotaniemi A, Vainio P, Alhava E. Bone densitometry of the spine and femur in children by dual-energy
x-ray absorptiometry. Bone Miner. 1992;17(1):75–85 (published erratum appears in Bone Miner 1992 Jun;17(3):429).
32. Lu PW, Cowell CT, Lloyd-Jones SA, Briody JN, Howman-Giles R. Volumetric bone mineral density in normal
subjects, aged 5–27 years. J Clin Endocrinol Metab. 1996;81(4):1586–90.
33. Kanis JA, Delmas P, Burckhardt P, Cooper C, Torgerson D. Guidelines for diagnosis and management of osteopo-
rosis. The European Foundation for Osteoporosis and Bone Disease. Osteoporos Int. 1997;7(4):390–406.
34. Wasnich RD. Perspective on fracture risk and phalangeal bone mineral density. J Clin Densitom.
1998;1(3):259–68.
35. Ensrud KE, Palermo L, Black DM, Cauley J, Jergas M, Orwoll E, Nevitt MC, et al. Hip and calcaneal bone loss
increase with advancing age: longitudinal results from the study of osteoporotic fractures. J Bone Miner Res.
1995;10:1778–87.
36. Jones G, Nguyen T, Sambrook P, Kelly PJ, Eisman JA. Progressive loss of bone in the femoral neck in elderly
people: longitudinal fi ndings from the Dubbo osteoporosis epidemiology study. BMJ. 1994;309(6956):691–5.
37. Hannan MT, Felson DT, Dawson-Hughes B, Tucker KL, Cupples LA, Wilson PW, Kiel DP. Risk factors for longi-
tudinal bone loss in elderly men and women: the Framingham Osteoporosis Study. J Bone Miner Res.
2000;15(4):710–20.
38. Taes Y, Lapauw B, Vanbillemont G, Bogaert V, De Bacquer D, Goemaere S, Zmierczak H, et al. Early smoking is
associated with peak bone mass and prevalent fractures in young, healthy men. J Bone Miner Res. 2010;25(2):
379–87.
39. Ortego-Centeno N, Munoz-Torres M, Jodar E, Hernandez-Quero J, Jurado-Duce A, de la Higuera Torres-Puchol
J. Effect of tobacco consumption on bone mineral density in healthy young males. Calcif Tissue Int. 1997;60(6):
496–500.
40. Lorentzon M, Mellstrom D, Haug E, Ohlsson C. Smoking is associated with lower bone mineral density and
reduced cortical thickness in young men. J Clin Endocrinol Metab. 2007;92(2):497–503.
41. Eleftheriou KI, Rawal JS, James LE, Payne JR, Loosemore M, Pennell DJ, World M, et al. Bone structure and
geometry in young men: the infl uence of smoking, alcohol intake and physical activity. Bone. 2013;52(1):17–26.
42. MacInnis RJ, Cassar C, Nowson CA, Paton LM, Flicker L, Hopper JL, Larkins RG, et al. Determinants of bone
density in 30- to 65-year-old women: a co-twin study. J Bone Miner Res. 2003;18(9):1650–6.
S. Sahni and D.P. Kiel
503
43. Kuo CW, Chang TH, Chi WL, Chu TC. Effect of cigarette smoking on bone mineral density in healthy Taiwanese
middle-aged men. J Clin Densitom. 2008;11(4):518–24.
44. Tamaki J, Iki M, Fujita Y, Kouda K, Yura A, Kadowaki E, Sato Y, et al. Impact of smoking on bone mineral density
and bone metabolism in elderly men: the Fujiwara-kyo Osteoporosis Risk in Men (FORMEN) study. Osteoporos
Int. 2011;22(1):133–41.
45. Lau EM, Leung PC, Kwok T, Woo J, Lynn H, Orwoll E, Cummings S, et al. The determinants of bone mineral
density in Chinese men—results from Mr. Os (Hong Kong), the fi rst cohort study on osteoporosis in Asian men.
Osteoporos Int. 2006;17(2):297–303.
46. Szulc P, Garnero P, Claustrat B, Marchand F, Duboeuf F, Delmas PD. Increased bone resorption in moderate smok-
ers with low body weight: the Minos study. J Clin Endocrinol Metab. 2002;87(2):666–74.
47. Baheiraei A, Pocock NA, Eisman JA, Nguyen ND, Nguyen TV. Bone mineral density, body mass index and ciga-
rette smoking among Iranian women: implications for prevention. BMC Musculoskelet Disord. 2005;6:34.
48. Ilich JZ, Brownbill RA, Tamborini L, Crncevic-Orlic Z. To drink or not to drink: how are alcohol, caffeine and past
smoking related to bone mineral density in elderly women? J Am Coll Nutr. 2002;21(6):536–44.
49. Komulainen M, Kroger H, Tuppurainen MT, Heikkinen AM, Honkanen R, Saarikoski S. Identifi cation of early
postmenopausal women with no bone response to HRT: results of a fi ve-year clinical trial. Osteoporos Int.
2000;11(3):211–8.
50. Kanis JA, Johnell O, Oden A, Johansson H, De Laet C, Eisman JA, Fujiwara S, et al. Smoking and fracture risk: a
meta-analysis. Osteoporos Int. 2005;16(2):155–62.
51. Olofsson H, Byberg L, Mohsen R, Melhus H, Lithell H, Michaelsson K. Smoking and the risk of fracture in older
men. J Bone Miner Res. 2005;20(7):1208–15.
52. Samelson EJ, Hannan MT, Zhang Y, Genant HK, Felson DT, Kiel DP. Incidence and risk factors for vertebral frac-
ture in women and men: 25-year follow-up results from the population-based Framingham study. J Bone Miner Res.
2006;21(8):1207–14.
53. Kanis J, Johnell O, Gullberg B, Allander E, Elffors L, Ranstam J, Dequeker J, et al. Risk factors for hip fracture in men
from southern Europe: the MEDOS study. Mediterranean Osteoporosis Study. Osteoporos Int. 1999;9(1):45–54.
54. Jugdaohsingh R, O’Connell MA, Sripanyakorn S, Powell JJ. Moderate alcohol consumption and increased bone
mineral density: potential ethanol and non-ethanol mechanisms. Proc Nutr Soc. 2006;65(3):291–310.
55. Iwaniec UT, Turner RT. Intraperitoneal injection of ethanol results in drastic changes in bone metabolism not
observed when ethanol is administered by oral gavage. Alcohol Clin Exp Res. 2013;37(8):1271–7.
56. Turner RT, Greene VS, Bell NH. Demonstration that ethanol inhibits bone matrix synthesis and mineralization in
the rat. J Bone Miner Res. 1987;2(1):61–6.
57. Turner RT, Kidder LS, Kennedy A, Evans GL, Sibonga JD. Moderate alcohol consumption suppresses bone turn-
over in adult female rats. J Bone Miner Res. 2001;16(3):589–94.
58. Peng TC, Kusy RP, Hirsch PF, Hagaman JR. Ethanol-induced changes in morphology and strength of femurs of rats.
Alcohol Clin Exp Res. 1988;12(5):655–9.
59. Bikle DD, Genant HK, Cann C, Recker RR, Halloran BP, Strewler GJ. Bone disease in alcohol abuse. Ann Intern
Med. 1985;103(1):42–8.
60. Crilly RG, Anderson C, Hogan D, Delaquerriere-Richardson L. Bone histomorphometry, bone mass, and related
parameters in alcoholic males. Calcif Tissue Int. 1988;43(5):269–76.
61. Bjorneboe GE, Bjorneboe A, Johnsen J, Skylv N, Oftebro H, Gautvik KM, Hoiseth A, et al. Calcium status and
calcium-regulating hormones in alcoholics. Alcohol Clin Exp Res. 1988;12(2):229–32.
62. Feitelberg S, Epstein S, Ismail F, D’Amanda C. Deranged bone mineral metabolism in chronic alcoholism.
Metabolism. 1987;36(4):322–6.
63. Laitinen K, Valimaki M. Alcohol and bone. Calcif Tissue Int. 1991;49(Suppl):S70–3.
64. Laitinen K, Valimaki M, Lamberg-Allardt C, Kivisaari L, Lalla M, Karkkainen M, Ylikahri R. Deranged vitamin D
metabolism but normal bone mineral density in Finnish noncirrhotic male alcoholics. Alcohol Clin Exp Res.
1990;14(4):551–6.
65. Kalbfl eisch JM, Lindemann RD, Ginn HE, Smith WD. Effects of ethanol administration on urinary excretion of
magnesium and other electrolytes in alcoholic and normal subjects. J Clin Invest. 1963;42:1471.
66. Laitinen K, Lamberg-Allardt C, Tunninen R, Karonen SL, Ylikahri R, Valimaki M. Effects of 3 weeks’ moderate
alcohol intake on bone and mineral metabolism in normal men. Bone Miner. 1991;13(2):139–51.
67. Garcia-Sanchez A, Gonzalez-Calvin JL, Diez-Ruiz A, Casals JL, Gallego-Rojo F, Salvatierra D. Effect of acute
alcohol ingestion on mineral metabolism and osteoblastic function. Alcohol Alcohol. 1995;30(4):449–53.
68. Jugdaohsingh R. Silicon and bone health. J Nutr Health Aging. 2007;11(2):99–110.
69. Price CT, Koval KJ, Langford JR. Silicon: a review of its potential role in the prevention and treatment of postmeno-
pausal osteoporosis. Int J Endocrinol. 2013;2013:316783.
70. Jugdaohsingh R, Tucker KL, Qiao N, Cupples LA, Kiel DP, Powell JJ. Dietary silicon intake is positively associated
with bone mineral density in men and premenopausal women of the Framingham Offspring cohort. J Bone Miner
Res. 2004;19(2):297–307.
30 Smoking, Alcohol, and Bone Health
504
71. Macdonald HM, Hardcastle AC, Jugdaohsingh R, Fraser WD, Reid DM, Powell JJ. Dietary silicon interacts with
oestrogen to infl uence bone health: evidence from the Aberdeen Prospective Osteoporosis Screening Study. Bone.
2012;50(3):681–7.
72. Liu ZP, Li WX, Yu B, Huang J, Sun J, Huo JS, Liu CX. Effects of trans-resveratrol from Polygonum cuspidatum on
bone loss using the ovariectomized rat model. J Med Food. 2005;8(1):14–9.
73. Durbin SM, Jackson JR, Ryan MJ, Gigliotti JC, Alway SE, Tou JC. Resveratrol supplementation preserves long bone
mass, microstructure, and strength in hindlimb-suspended old male rats. J Bone Miner Metab. 2014;32(1):38–47.
74. Wosje KS, Kalkwarf HJ. Bone density in relation to alcohol intake among men and women in the United States.
Osteoporos Int. 2007;18(3):391–400.
75. Mukamal KJ, Robbins JA, Cauley JA, Kern LM, Siscovick DS. Alcohol consumption, bone density, and hip fracture
among older adults: the cardiovascular health study. Osteoporos Int. 2007;18(5):593–602.
76. Cawthon PM, Harrison SL, Barrett-Connor E, Fink HA, Cauley JA, Lewis CE, Orwoll ES, et al. Alcohol intake and
its relationship with bone mineral density, falls, and fracture risk in older men. J Am Geriatr Soc.
2006;54(11):1649–57.
77. Tucker KL, Jugdaohsingh R, Powell JJ, Qiao N, Hannan MT, Sripanyakorn S, Cupples LA, et al. Effects of beer,
wine, and liquor intakes on bone mineral density in older men and women. Am J Clin Nutr. 2009;89(4):1188–96.
78. Kouda K, Iki M, Fujita Y, Tamaki J, Yura A, Kadowaki E, Sato Y, et al. Alcohol intake and bone status in elderly
Japanese men: baseline data from the Fujiwara-kyo osteoporosis risk in men (FORMEN) study. Bone. 2011;49(2):
275–80.
79. Macdonald HM, New SA, Golden MH, Campbell MK, Reid DM. Nutritional associations with bone loss during the
menopausal transition: evidence of a benefi cial effect of calcium, alcohol, and fruit and vegetable nutrients and of
a detrimental effect of fatty acids. Am J Clin Nutr. 2004;79(1):155–65.
80. Bakhireva LN, Barrett-Connor E, Kritz-Silverstein D, Morton DJ. Modifi able predictors of bone loss in older men:
a prospective study. Am J Prev Med. 2004;26(5):436–42.
81. Clark MK, Sowers MF, Dekordi F, Nichols S. Bone mineral density and fractures among alcohol-dependent women
in treatment and in recovery. Osteoporos Int. 2003;14(5):396–403.
82. Baron JA, Farahmand BY, Weiderpass E, Michaelsson K, Alberts A, Persson I, Ljunghall S. Cigarette smoking,
alcohol consumption, and risk of hip fracture in women. Arch Intern Med. 2001;161(7):983–8.
83. Tanaka T, Latorre MR, Jaime PC, Florindo AA, Pippa MG, Zerbini CA. Risk factors for proximal femur osteopo-
rosis in men aged 50 years or older. Osteoporos Int. 2001;12(11):942–9.
84. Muraki S, Yamamoto S, Ishibashi H, Oka H, Yoshimura N, Kawaguchi H, Nakamura K. Diet and lifestyle associ-
ated with increased bone mineral density: cross-sectional study of Japanese elderly women at an osteoporosis out-
patient clinic. J Orthop Sci. 2007;12(4):317–20.
85. Izumotani K, Hagiwara S, Izumotani T, Miki T, Morii H, Nishizawa Y. Risk factors for osteoporosis in men. J Bone
Miner Metab. 2003;21(2):86–90.
86. Forsmo S, Schei B, Langhammer A, Forsen L. How do reproductive and lifestyle factors infl uence bone density in
distal and ultradistal radius of early postmenopausal women? The Nord-Trondelag Health Survey, Norway.
Osteoporos Int. 2001;12(3):222–9.
87. Williams FM, Cherkas LF, Spector TD, MacGregor AJ. The effect of moderate alcohol consumption on bone min-
eral density: a study of female twins. Ann Rheum Dis. 2005;64(2):309–10.
88. Elgan C, Dykes AK, Samsioe G. Bone mineral density changes in young women: a two year study. Gynecol
Endocrinol. 2004;19(4):169–77.
89. Lau EM, Suriwongpaisal P, Lee JK, Das De S, Festin MR, Saw SM, Khir A, et al. Risk factors for hip fracture in
Asian men and women: the Asian osteoporosis study. J Bone Miner Res. 2001;16(3):572–80.
90. Du F, Birong D, Changquan H, Hongmei W, Yanling Z, Wen Z, Li L. Association of osteoporotic fracture with
smoking, alcohol consumption, tea consumption and exercise among Chinese nonagenarians/centenarians. J Nutr
Health Aging. 2011;15(5):327–31.
91. Porthouse J, Birks YF, Torgerson DJ, Cockayne S, Puffer S, Watt I. Risk factors for fracture in a UK population: a
prospective cohort study. QJM. 2004;97(9):569–74.
92. Jutberger H, Lorentzon M, Barrett-Connor E, Johansson H, Kanis JA, Ljunggren O, Karlsson MK, et al. Smoking
predicts incident fractures in elderly men: Mr OS Sweden. J Bone Miner Res. 2010;25(5):1010–6.
93. van der Klift M, de Laet CE, McCloskey EV, Johnell O, Kanis JA, Hofman A, Pols HA. Risk factors for incident
vertebral fractures in men and women: the Rotterdam Study. J Bone Miner Res. 2004;19(7):1172–80.
94. Valtola A, Honkanen R, Kroger H, Tuppurainen M, Saarikoski S, Alhava E. Lifestyle and other factors predict ankle
fractures in perimenopausal women: a population-based prospective cohort study. Bone. 2002;30(1):238–42.
95. Cauley JA, Fullman RL, Stone KL, Zmuda JM, Bauer DC, Barrett-Connor E, Ensrud K, et al. Factors associated
with the lumbar spine and proximal femur bone mineral density in older men. Osteoporos Int. 2005;
16(12):1525–37.
S. Sahni and D.P. Kiel
... Sex differences in smoking behavior are established in adolescence, with apartheid era prevalence rates of 27.3% in SAB boys but only 0.8% in SAB girls (Strebel, Kuhn, & Yach, 1989). While smoking is a potential risk factor, its negative effects on the attainment of peak bone mass are not yet well understood (Sahni & Kiel, 2015). ...
... No signifi cant associations were reported among women. Smoking is an established risk factor of osteoporosis as outlined in our recent review [ 31 ]. ...
Chapter
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Dietary and lifestyle factors have important contributions to skeletal health. Fruit- and vegetable-specific antioxidants, such as vitamin C, might help in preventing osteoporosis because vitamin C may decrease oxidative stress and subsequent bone-resorption. Vitamin C is an essential cofactor for collagen formation (an important component of bone matrix) and potentiates vitamin E activity in cells by regenerating α-tocopherol from its oxidized derivative. In this chapter, we highlight findings from previous studies on vitamin C intake and bone measures to underscore our current understanding and emphasize the importance of vitamin C on skeletal health. Taken together, previous studies showed a positive association between dietary vitamin C and bone mineral density. Very few examined serum vitamin C status, vitamin C supplementation or bone loss. The reported associations were complex due to multiple interactions with smoking, calcium and vitamin E intakes and current estrogen use in women. One longitudinal study reported that higher vitamin C intake may be protective against bone loss in men with low calcium or vitamin E intake. There is an urgent need to replicate these findings in larger cohorts with data on bone loss over time. Studies have also suggested that vitamin C intake may be protective against hip fracture as well as other fractures, especially among current smokers and estrogen using women. Larger prospective cohort studies are required to further clarify these interactions. Lastly, good-quality randomized controlled trials are needed to confirm these epidemiological findings to ascertain optimal intakes for osteoporosis prevention.
... A review of studies investigating alcohol intake and bone health suggested a BJ^-shaped curve, where moderate ingestion of alcohol may offer maximum protection; however, intakes beyond this level show negative effects on the skeleton [113]. The above observations emerging from studies of alcohol containing beverages suggest that specific components found in these beverages in addition to the alcohol may also have effects on skeletal health. ...
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The aims of this study were to determine common international risk factors for hip fracture in women aged 50 years or more. We studied women aged 50 years or more who sustained a hip fracture in 14 centers from Portugal, Spain, France, Italy, Greece, and Turkey over a 1-year period. Women aged 50 years or more selected from the neighborhood or population registers served as controls. Cases and controls were interviewed using a structured questionnaire on work, physical activity, exposure to sunlight, reproductive history and gynecologic status, height, weight, mental score, and consumption of tobacco, alcohol, calcium, coffee, and tea. Significant risk factors identified by univariate analysis included low body mass index (BMI), short fertile period, low physical activity, lack of sunlight exposure, low milk consumption, no consumption of tea, and a poor mental score. No significant adverse effects of coffee or smoking were observed. Moderate intake of spirits was a protective factor in young adulthood, but otherwise no significant effect of alcohol intake was observed. For some risks, a threshold effect was observed. A low BMI and milk consumption were significant risks only in the lowest 50% and 10% of the population, respectively. A late menarche, poor mental score, low BMI and physical activity, low exposure to sunlight, and a low consumption of calcium and tea remained independent risk factors after multivariate analysis, accounting for 70% of hip fractures. Excluding mental score and age at menarche (not potentially reversible), the attributable risk was 56%. Thus, about half of the hip fractures could be explained on the basis of the potentially reversible risk factors sought. In contrast, the use of risk factors to “predict” hip fractures had moderate sensitivity and specificity. We conclude that variations in lifestyle factors are associated with significant differences in the risk of hip fracture, account for a large component of the total risk, and may be of some value in selecting individuals at high risk.
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