Higher smoking exposure and alcohol consumption associated with increased arterial stiffness in adolescents
Early vascular damage from smoking and alcohol in teenage years: the ALSPAC studyLiterature - Charakida M, Georgiopoulos G, Dangardt F et al. - Eur Heart J 2018; doi:10.1093/eurheartj/ehy52
Introduction and methods
Cigarette smoking and alcohol consumption are positively associated with CV risk in adults [1-2]. Moreover, smokers have a two-fold risk of suffering a myocardial infarction compared to non-smokers, whereas the dose-effect relationship of alcohol intake and CV risk remains contradictory . Most adults who use alcohol or tobacco begin in their early teenage years [4,5]. This study assessed the impact of smoking and alcohol exposure on arterial stiffness in young adulthood.
This sub-analysis of the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort study included 1266 participants with measured carotid-to-femoral pulse wave velocity (PWV) at 17 years and data on both smoking exposure and alcohol use at 13, 15 and 17 years.
Smoking exposure and alcohol consumption were measured by questionnaires. Participants were classified by smoking status (smokers and non-smokers), and intensity in lifetime smoking (high [>100 cigarettes], moderate [20–99 cigarettes], and low/never smokers [<20 cigarettes]). For alcohol use, participants were classified by frequency (drinkers and not-drinkers), and intensity of drinking (heavy [>10 drinks], medium [3-9 drinks], and light [<2 drinks]) on a typical day that they were drinking alcohol. The outcome was aortic stiffness, measured by carotid to femoral PWV.
- Current smokers showed increased arterial stiffness, compared with non-smokers (mean difference: 0.176 [0.058–0.293] m/s, P=0.003).
- A significant positive association was observed between smoking intensity and PWV. High intensity smokers showed higher PWV, compared with low/never-smokers (mean difference: 0.104 [0.01–0.199] m/s, P=0.032), which remained significant after adjustment for CV risk factors.
- Never smokers had lower PWV at 17 years, compared with participants who had been smoking since they were 13 years old (-0.313 [-0.01 to -0.618] m/s, P=0.044) and to current smokers (-0.196 [-0.034 to -0.357] m/s, P=0.018).
- The longitudinal effect of smoking between 13–17 years on PWV was consistent across groups of increased duration (mean increase in PWV 0.143 [0.047–0.239] m/s per category, P-linearity=0.004), compared with never smokers.
- No difference in PWV was observed between subjects who smoked between 13 and 17 years but who subsequently stopped and never smokers (mean difference -0.152 [-0.364 to 0.06], P=0.160).
- Compared with participants who had never smoked, adolescents who smoked since 13 or 15 years showed an adjusted increase of 0.157 [0.01–0.308] m/s in PWV (P=0.042).
- Age of starting to drink alcohol or frequency of drinking and PWV were not significantly associated, whereas high intensity drinking was associated with increased PWV (HI 5.85 ± 0.8 vs. LI 5.67 ± 0.604 m/s, mean difference 0.182 [0.019–0.346] m/s, P=0.029), which remained significant after adjustment for CV risk factors.
- Increased drinking intensity (>10 drinks/typical drinking day) correlated with increased arterial stiffness (5.85 ± 0.8 vs. 5.7 ± 0.625 m/s, mean increase 0.147 [0.016–0.279], P=0.028), also after adjustment.
- In longitudinal analysis, drinking intensity was not associated with PWV (P>0.05 for all categories).
Smoking exposure and alcohol consumption
- Higher alcohol and smoking intensity had additive effects on arterial stiffness compared with never smoking and low alcohol use (5.89 ± 0.857 vs. 5.61 ± 0.589, mean increase 0.277 [0.028–0.525] m/s, P=0.029). This combination remained an independent predictor of PWV after adjustments.
Drinking intensity and smoking was independently and additively associated with arterial changes relevant to atherosclerosis progression in adolescents in a large cohort study. Interestingly, an association between smoking cessation and normalization of aortic stiffness in adolescence was observed. These results provide further support to discourage young adults adopting smoking and drinking habits, and discontinue these unhealthy behaviors.
In their editorial , Münzel, Hahad and Daibe characterize the Charakida et al. data as ‘somewhat surprising’ and ‘worrisome’ since the numbers of cigarettes smoked by teenagers are far below those considered to be harmful in adults. They note that the interpretation of the results would have been easier if the nicotine degradation product cotinine was measured, rather than subjective questionnaire-based assessment. Next, they discuss how politicians and healthcare providers can protect young adults from smoking- and alcohol-driven vascular damage, including the provision of age verification systems on cigarette machines, ban of tobacco smoking in public areas and prohibition of cigarette advertising.