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~ s, ...i':. 862' Circulation Vo185; Vo 2 February 1992' 1 Dietary Fat Intake and Carotid Artery Wa17 Thickness: The ARIC Study Grethe S. Te11, Gregory W. Evans, Tomoko Shimakawa; Aaron R. Folsom, Myra Carpenter, Gerardo Heiss„ for the ARIC Investigators. Bowman Gray School of Medicine, Winston.Salemi NC We report preliminary results on the association between dietary fat intake and carotid artery wall thickness (WT) (measured by B-mode ultracound) in 2114 black women (BW), 1316 black men (BM)„ 5193 white women (WW)' and 4614 white men (Wlvf) ages 45-64 years, examined by the Atherosclerosis Risk in Communities (AR1C). Study. A food frequency questionnaire was used to assess habitual dietary intake. Shown below are age- and energy,adjusted beta coefficients for the relation between WT (in mm) and average daily intake (see table for units)r , ~ '•'~' Passive Smoking and Carbtid Artery Wall Thickness: The ARIC Study 3 George Howard, Moyes SrYlo, Gregory, Evans, Grethe Tell, John Eckfcldt, Gerardo Heiss Bowman Gray School of Medicine, Winston Salem, NC. The association between passive and active cigarette smoking with carotid'artery wall thickness was studied'in 12,863 men and women ages 45 to 64 examined by the Athcrosclerosis Risk in Communicies (ARIC) Study. Of these, 3,509 were current smokers, 4.276 past smokers, 3,316 had never smoked but reported ezposure to environmental1 tobacco smoke (ETS or 'passive smoke'), and 1,762 had never smoked and reported no exposure to ETS. Carotid artery wall thickness was measured by $-mode ultrasound. Increasing exposure to cigarette smoke across the gradient from never smoking to current smoking was consistently associated with increases in carotid artery wall thickness within 5-year age groups (shown below adjusted for race and'gender, mean = S.E., in mm.); Animal fat (100 gfday) DEW .056' IIM .055 WW .101' YYM .070' Age rou No sure ETS n) PAST Smoker! CURRENT Smoker Yegetable fat (100 g/day) -.074' -.081 -.069T -.080- 45-50 0.66=0:005 0.6720.003 0.68=0;004 0.70=0.004 Mooamsauramd fat (900 g/day) i .005 -.018 .082 .056 51-55 0.71_0.007 0.71= 0.005 0.73_0:005 0.76_0.006. Saturated fat (100 glday) .065 .036 .1337 .031 56-60 0.75z0.007 0.76x0.006 0:79=0:007 0.83=0.008'. Polvuas.nu.ted fat (J00 g/day) -.110 ' -.248 -.163' -.151 61-65 0.79=0.009 0.80z0.008 0:85±0:009' 0.89_0.012 Cbolesterol (100 mglday) .005 .006 .010r .005 'p<0.05 - p<0.01 -p<0:001 'p<0.0001 Thus, elements of habitual dietary intake are consistently associated with WT in all four race-gender groups, consistent with their putatively atherogenic and anti= atherogenic properties. 2 Comparison of IntracerebraJ Arterioneerosis in Japanese Men in Japan and Hawaii Dwayne Reed. David Jacobs. Takup Hayashi. Hiroyasu Iso; Masamitsu Konishi. James Ndlon, Jack Strong Honolulu Heart Program. Honolulu, HI In eadien reports we showed that the ineidenee and mortality rates of all',types of stroke were threefold greater in Japanese men in Japan compared to those n Hawaii, and: that this difference was not related to atherosclerosia n the Cirde of VHilis: bn this sttrdy,, brain specimens from 232 man from a Hiroshima oohort. and 175 men in a H'aw.i'cohort wens aaamaed by three pathdoqirts for the prasance of d'dMerentt stages of arterionecrosis in small intracersbraa arteries. Most measures of srterion.crosis were higher in all aqe groups in Japan, than Hawali: were higher among men who died of stroke compared to nontardiovaswla causes; and; were higher amonp men with cerebral infsrction at autopsy. Risk factor analysas for the Hawaii cohort indicated that blood pressure and some aspect of, the Asian diet ware associated with arterionecrosis. These data indicate thartlre difference n stroke frequency bmreen Japan and Hawaii Is retated to intracerebral arterioneerosis. mate lal may be Th~s ~~ p~o~~ted rN u, ~e 11 The ETS gToup had thicker arterial'walls than never smokers; these differences were statistically signi6canr (p s 0.0001) only at younger ages. Also, the ETS participants showed an increase (p = 0.03) in arterial wall thickness with an increasing number of hours per week of ETS exposure. Thus exposure to ETS may contribute to atherogenesis. 4 Depression Amplifies the Association Between Carotid Atherosclerosis and Age, Hypertension, Low Density Lipoproteins, and Platelet Aggregability. George A. Kaplan, Richard D: Cohen, Thomas W: Wilson, Jussi Kauhanen, Riitu Salonen, Jukka T. Salonen. California Depart- ment of Health Services, Berkeley, CA Extensive data on cardiovascular risk factors, ultrasound read• ings of the intimal-media thickness (IMT)'of the common carntid artery; and MMPI depressive status were obtained from 825 participants in the Kuopio Ctebemic Heart Disease Risk Factor Study, a population-based study of 42-60 year old men in Eastern Finland. In multiple regression models predicting IMT, there were significant interactions between MMPl1 depression (above vs. below median) and age (p=.049) and LDL (pm.028)i An 18 year difference in age was associated with 40% greater increase in IMT in the depressed' than in the noa-0eprossed. A median split in LDL levels was associated with a 2-fold increase in IMT among the depressed. Three way interactions in predicting IMT were found for age'depression'platdet aggregability (p-.072), and age`de- pression'hypertencion (p=.078). Depression was associated with 79 x greater age-related increase in IMT for those with high platelet aggregabUity and a 9% greater increase in hypertensives. There were no significant interactions between depressive status and fibrinogen, smoking, alcohol eonsumption+ or physical activity and IMT. The results indicate thara psychosocial factor, depression,,may contribute to the development of atherosclerotic vascular disease by increasing the impact of other risk factors on atherogenesis.