Early vascular damage from smoking and alcohol in teenage years: the ALSPAC study

Abstract

Aims: To determine the impact of smoking and alcohol exposure during adolescence on arterial stiffness at 17 years.

Methods and results: Smoking and alcohol use were assessed by questionnaires at 13, 15, and 17 years in 1266 participants (425 males and 841 females) from the ALSPAC study. Smoking status (smokers and non-smoker) and intensity ('high' ≥100, 'moderate' 20-99, and 'low or never' <20 cigarettes in lifetime) were ascertained. Participants were classified by frequency (low or high) and intensity of drinking [light (LI <2), medium (MI 3-9), and heavy (HI >10 drinks on a typical drinking day)]. Carotid to femoral pulse wave velocity (PWV) was assessed at 17 years [mean ± standard deviation and/or mean difference (95% confidence intervals)]. Current smokers had higher PWV compared with non-smokers (P = 0.003). Higher smoking exposure was associated with higher PWV compared with non-smokers [5.81 ± 0.725 vs. 5.71 ± 0.677 m/s, mean adjusted difference 0.211 (0.087-0.334) m/s, P = 0.001]. Participants who stopped smoking had similar PWV to never smokers (P = 0.160). High-intensity drinkers had increased PWV [HI 5.85 ± 0.8 vs. LI 5.67 ± 0.604 m/s, mean adjusted difference 0.266 (0.055-0.476) m/s, P = 0.013]. There was an additive effect of smoking intensity and alcohol intensity, so that 'high' smokers who were also HI drinkers had higher PWV compared with never-smokers and LI drinkers [mean adjusted increase 0.603 (0.229-0.978) m/s, P = 0.002].

Conclusion: Smoking exposure even at low levels and intensity of alcohol use were associated individually and together with increased arterial stiffness. Public health strategies need to prevent adoption of these habits in adolescence to preserve or restore arterial health.

Figure 1

Study population. Flow chart shows the number of participants who responded to questionnaires exploring smoking and alcohol use from 13 to 17 years.

Figure 2

The longitudinal association between smoking exposure and arterial stiffness. Increased smoking exposure was associated with higher aortic pulse wave velocity compared with those who had never smoked. Participants who quit smoking had similar pulse wave velocity compared with those who never smoked. *P < 0.05. PWV, pulse wave velocity.

Figure 3

The combined effect of smoking over lifetime and intensity of drinking on arterial stiffness. The combination of high-intensity drinking with lifetime smoking exposure is shown. Pulse wave velocity measurements are expressed as mean values and 95% confidence intervals around the mean on the x-axis. The participants who had ‘high’ drinking intensity and ‘high’ smoking exposure had the highest pulse wave velocity compared with the ‘low lifetime smoking exposure’ and ‘low drinking intensity’. *P < 0.05.

Take home figure

Unhealthy behaviours in adolescents (drinking and cigarette smoking) are associated with increased carotid to femoral pulse wave velocity (stiffer arteries) and accelerated atherosclerosis. Stopping smoking in adolescence and reducing binge drinking has potential for reversibility of arterial stiffening.