TABLE 6.--Continued Hip and/or forearm fractures Reference Population Compartx,n Estimated rebtive risk Comments Paganint-Hill (`ae4: YI pohtmenopau\al women elal.(lYXIl aged 20 with hip fractures Controls: I X2 age. race-matched postmenopausal women Krelgcret al. Car\: OX po.\tmenopausal women aged t IYX1): Krelger 45-74 yr ho\pitalired with hip fracture and Htldnch Trauma Controls: X3 postmenopausd ( IYXh) women hospitali/.ed for trauma Nontrauma Controls: XX4 po\tmenopaussl women hospitalixd for medical illness Williiml\et id. Cnseh: 344 (3%) white women aged (19x2): S(b-74 with hip or forearm fracture Aldc`rman ct al. Controls Sh7 (562) white women from a ( IYXh) hou.xhold atrvey I-lOcig/day vs. none 21 I cig/day Y\. none I .os I .Yh Adjusted for age, age at menopause. Quelelet'\ Index, physical activity, alcohol conxumprion. and exogenous estrogen use Ever vs. never smoker\ Trauma controls Nontram~acornrol\ Among c\tropen nonusers Hip fractures Average weight ever smoker vs obese never smoker Thm ever maker v\. obese never \moher Forearm fracture Thin ever maker v\. obese never moher 51 ppd v\. never > I ppd v\. never I.27 I.?`) 6.Sh 13.Sh S.4h I .o I.2 Adjusted for ape. Quetelet's Index, months breast feeding. ovariectomy, and estrogen use Smokers and nonsmokers were not directly compared; the comparison group for all analyses was obese nonsmokers who had used estrogen for 2 I yr; controlled for hex and race only TABLE 6.--Continued Hip and/or fwxrm frnctutw Kcfcrence Population (`ompariwn E\tlmated relative rl\i\ Smohcr\ v\. nonmoher\ I.3 large samples from the Framingham Heart Study, the Nurses Health Study, and the first National Health and Nutrition Examination Survey. In the largest study by Hemenway and colleagues (1988) 96,508 nurses reported 975 hip or forearm fractures during an average 4 years of observation. The relative risk of fracture was 1 .O in each smoking category (former smokers, smokers of I-14 cigarettes/day, 15-25 cigarettes/day. and >25 cigarettes/day) compared with never smokers. Smoking Cessation and Osteoporosis and Fracture No studies have evaluated the effect of smoking cessation on osteoporosis and fracture, nor are there studies of the risk of osteoporosis or fracture in former smokers compared with continuing smokers. Summary There is insufficient evidence to conclude that smoking decreases bone mineral content and the risk of osteoporotic fractures. Some studies have found lower bone mineral content in smokers compared with nonsmokers, but others have not. Some. but not all, case-control studies have found a higher risk of osteoporotic fracture among smokers. Most negative studies were limited by small sample size, and most positive studies were not designed to control for potentially strong confounding variables. Analysis of data in five cohort studies has found no association of smoking with increased risk of fracture. Skin Wrinkling Introduction Although wrinkling of the facial skin is nearly universal among elderly persons, it is rarely mentioned in textbooks of dermatology or medicine, and little research has been published concerning its etiology or risk factors. Skin wrinkling is associated with sun exposure (Kligman 1969; Allen, Johnson, Diamond 1973; Daniel1 197 1; Knox. Cockerell, Freeman 1962; Rook, Wilkinson, Ebling 1979). Wrinkling occurs with increasing age (Daniel1 1971; Knox, Cockerell, Freeman 1962: Rook, Wilkinson. Ebling 1979), but even among the elderly, wrinkling usually is confined to sun-exposed areas (Kligman 1969; Allen, Johnson, Diamond 1973; Knox, Cockerell. Freeman 1962). There is limited evidence that dramatic weight loss is associated with skin wrinkling (Daniel1 1971). Pathophysiologic Framework It is not clear how cigarette smoking may promote skin wrinkling. Some investigators have concluded that a localized finding such as wrinkling of the face and hands could not be caused by a systemic factor such as the absorbed components of cigarette smoke. TABLE 7.--Summary of cohort studies of smoking and fractures Keference JeflV31 (14X6) Populatlon/out~on~~ Population-bawd study of 70-year-old women in Copenhrigen. Denmarh: 77 smohed daily for 220 yr: 103 never \mohed 0utc0111r: all fractures Hemenway et al. (IYXX) 0630X nurwb aged 35-50 31 hahellnc ( IYXO) followed fur 4 yr. Outcome: self-report of Y7S fracture\ of hip or fwxrm Felson et al (IYXX) Holbrook. Barrett-Connor. Wingard (IYXX) Farmer et al. (19X0) 52OY men and women m the Framingham Heart Study followed retrr)qxxtively for about 30 yr. Outcome. ? I7 documented hip fracture5 Y7S men and women aped S(b7Y at haaeline followed for I4 yr, Outcome: 33 documented hip fractures 3,595 white women in NHANES-I aped 4&77 at baseline ( lY71-75) followed fur an uvernge of IO yr, Outcome: X4 documcntrd hip fractuw Comparison `% smoker\ with fracture vs. % nonsmokrr~ with fracture: All po\tmenopauwl fractures O~troporot~c frscturesh Age-adjusted fracture rate compared to: never smoher\ Ex-smokrrx Smokers I I4 tip/day IS-24 c@day 23 cig/d/dny Bawd on ciglday Smohrrs vs. nonsmoker\ I.1 Bawd on number of yr smoked at huwlinr exam Relative risk Comments All wbject\ were 70.yr-old women: no control for other confounders I .o I .o I .o I .o No incrrase No mcreasr A very large cohort study producing narrow Cl3 (upper hmn I .2.5). hut most women were mlddlr-aged or younger; controlled for age only Cox re@re%ion model. adJusted for age. wx. body ma\\ Index, dietary calcium. and alwhol conwmptwn No data given. hut reported no significant 35wiation: ilnaly~a adJusted for age. body muss Index. menopausal Qtuh. citlcium conwmption. and activity However. facial skin, and to a lesser extent, the skin of the hands contain an intradermal elastic tissue mesh that is denser and more complex than in other areas (Shelley and Wood 1974). Thus. the toxic effect of both sunlight and smoking may be most damaging in these more susceptible areas. Alternatively. damage from sunlight and smoking may simply be additive. and the threshold for clinically apparent changes from smoking may not be reached in sun-protected areas of the skin. Histopathologic examination of sun-exposed skin commonly shows abnormalities of collagen in the dermis that decrease the elastic properties of the skin. a condition known as elastosis (Marks 1976: Shelley and Wood 1974). However. the mechanism by which sunlight might cause these changes is uncertain, and there is no evidence that smoking is associated with elastosis. Cigarette smoking has been shown to decrease capillary and arteriolar blood flow in the skin acutely (Klemp. Staberg. Thomsen 1982: Reus et al. 1984: Richardson 1987). and hence. may cause tissue hypoxia. However. there is no evidence that this causes changes in skin transparency and turgor or produces wrinkles. Smoking and Skin Wrinkling Several studies have reported that smoking is associated with prominent skin wrin- kling, particularly in the periorbital or "crow's foot" area of the face. lppen and Ippen (1965) defined "cigarette skin" as appearing pale. grayish. and wrinkled. especially on the cheeks. with thick skin between the wrinkles. In an examination of women aged 35 to 84.66 of the 84 .;mokers had cigarette skin compared with 27 of the 140 nonsmokers (relative risk=4. I. pltr.,ia/ oJ`Gtrsrr.oerlre,.~~/~J,~~ (Supplement X3):6 l-68. 1983. CONSENSUS CONFERENCE. Osteoporosis. .lorw/7c~/ of/he Anler-iwn Mrdir u/ Assoc~iutior7 252(6):799-X02. Augubt IO. 19X-t. COOPER. C.. BARKER. D.J.P.. WICKHAM. C. Physical activity, muscle stren_eth. and calcium intake in fracture of the proximal femur in Britain. Bri/i.sh Mdicd Jo7o~nul 297:1443-1446. December 3. 19Xx. CRAWFORD. F.E.. BACK. D.J.. L'EORME. M.. BRECKENRIDGE. A.M. 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January 1982. 468 CHAPTER 10 SMOKING CESSATION AND BODY WEIGHT CHANGE CONTENTS Introduction ..................................................... ..47 3 Amount of Weight Gain After Smoking Cessation and-Likelihood of Gaining Weight ....................................................... ..47 3 Causes of Postcessation Weight Gain ................................... 483 Food Intake ................................................... 4x4 Physical Activity .............................................. 486 Energy Expenditure ............................................... 487 Relationship Between Overweight and Adverse Medical and Psychosocial Outcomes .................................................... Change in Weight-Related Health Risks After Smoking Cessation ......... Strategies to Control Postcessation Weight Gain ....................... Behavioral Methods for Reducing Postcessation Weight Gain .......... Pharmacologic Methods for Reducing Postcessation Weight Gain ....... Conclusions .................................................... ... References ..................... ................................ 490 497 -500 500 502 SOS so7 INTRODUCTION Cigarette smoking is associated with decreased body weight. and many smokers report that a major reason they smoke is to reduce body weight (Grunberg 1986: Klespes et al. 1989; US DHHS 19gXa). However. as documented in this Chapter. the weight gain associated with smoking cessation is generally small and poses a minimal health risk. This Chapter is organized into six sections. Drawing from prospective investigations meeting specific criteria. the first section of this Chapter determines average weight gain following smoking cessation compared with continued smoking. assesses the percentage of continuing smokers and quitters gaining weight. and calculates the risk of gaining weight after smoking cessation versus continued smoking. The next section of this Chapter discusses the mechanisms responsible for weight gain after mohing cessation. The available literature is reviewed on dietary,. activity. and metabolic changes after smoking cessation The third section reviews the relationship between body weight and adverse medical and psychosocial outcomes. The fourth section examines whether weight-related health effects accompany weight gain in ex-smokers. The fifth section presents potential treatments for reducing postcessation weight gain. including pharmacologic (e.g.. nicotine polacrilex gum. phenylpropanolamine. and d-fenfluramine) and nonpharmacologic approaches. The sixth section presents con- clusions regarding smoking cessation and body weight change. AMOUNT OF WEIGHT GAIN AFTER SMOKING CESSATION AND LIKELIHOOD OF GAINING WEIGHT To evaluate postcessation weight gain and to determine the likelihood or relativ,e risk of gaining weight after smoking cessation, longitudinal investigations after 1970 of postcessation weight gain were examined. Only studies that included a control group of continuing smokers were evaluated. Requirements for studies in this review included a minimum followup period of 1 month and at least IO smokers who quit. Studies were excluded if a weight loss component or severe caloric restriction was part of the intervention or if an agent known to affect body weight (e.g., nicotine polacrilex gum) was used; however, placebo conditions within drug trials were considered. A few studies were excluded for methodologic or interpretive reasons, such as relapsed subjects included in data analysis along with quit subjects or whenever a weight change could not be calculated. Table I summarizes the IS studies that fulfilled the\e inclusionary and exclusionary criteria. The following information is included for each study listed in Table 1: the study reference, the followup or period of abstinence. the mean weight gain among in dividuals whoquit smoking, the mean weight gain of subjects whodid not quit smoking. the percentage of subjects quitting smoking who gained weight from baseline to the followup period, the percentage of nonabstinent subjects who gained weight during the same period, and the relative risk of gaining any weight after smoking cessation versus continued smoking. Adjusted averages of weight gain are provided to summarize across all studies. These adjusted averages control for differing sample sizes and assign 173 TAHIX I.--Summary of prospective studies on smoking and body weight 5 yr ! yr I qr I Yr h yr 6.3.5 7.5 5.15 I I.1 3.1X (1. I I .h (1.94 7.7 2.01 - 2.2 0.04 76.9 JO.3 I.66 7.3 x7.0 60.7 I .a3 0.r) - 0.3 0.9 - - 7x.0 Sh.0 I ..I9 0.44 - - 2.4 X0.6 61.7 1.31 TABLE I.--Continued Krference Sample Number of \i7c quitters Quit period Mean weight % continuing Relative ri\h gain (lb) `2 quitter\ who gain \moher\ who of gaining Qumer\ Continuing \moher5 weight gain weight weight Puddry et al. (IYXS) zx Kabhin ( lYX4h) 107 Kotlin 42 (lYX7) Scltfrr (l'J73) 31X Tuomilehto et al. ( IYX6) 3Yh I..( mn 3 mo I .5 mo 5 yr s yr 2.Y7 4.4 3.1x 7.`) 6.02 Median l'ollowup period=7 yr Avcragc ~elght gain among quitter\=l.h: N=J.h47 0.44 0.7 0.70 5X.3 33.3 I .75 33 I .57 Avcragc wclght gain among continumg w~oker\=O.X: N= 15.046 Averq!e Average Average `I$ of quitter\ % ot cclntirlulng relntive rlah uho gain \mcrher\ who olgaming wcighk7Y";: gain \cright=Wk: weight= I.451 Numhcr ot Numhcrot Numher ot \tudie\ reportlng=5: dud~c\ \tudie\ N=714 reporting=5: rcpwmg=S: N=l,l I3 N= I.77