Showing papers by "Rodolfo Saracci published in 2018"
Queen Mary University of London1, University of London2, Imperial College London3, Seconda Università degli Studi di Napoli4, Academy for Urban School Leadership5, University of Cambridge6, Utrecht University7, University of Naples Federico II8, Umeå University9, University of Florence10, Basque Government11, Lund University12, German Cancer Research Center13, National and Kapodistrian University of Athens14, Prevention Institute15, International Agency for Research on Cancer16
TL;DR: Results are highly suggestive of a true causal link between smoking and PD, although it is not clear which is the chemical compound in cigarette smoking responsible for the biological effect.
Abstract: BACKGROUND: The aim of this paper is to investigate the causality of the inverse association between cigarette smoking and Parkinson's disease (PD). The main suggested alternatives include a delaying effect of smoking, reverse causality or an unmeasured confounding related to a low-risk-taking personality trait. METHODS: A total of 715 incident PD cases were ascertained in a cohort of 220 494 individuals from NeuroEPIC4PD, a prospective European population-based cohort study including 13 centres in eight countries. Smoking habits were recorded at recruitment. We analysed smoking status, duration, and intensity and exposure to passive smoking in relation to PD onset. RESULTS: Former smokers had a 20% decreased risk and current smokers a halved risk of developing PD compared with never smokers. Strong dose-response relationships with smoking intensity and duration were found. Hazard ratios (HRs) for smoking 30 years 0.54 (95% CI 0.43-0.36) compared with never smokers. The proportional hazard assumption was verified, showing no change of risk over time, arguing against a delaying effect. Reverse causality was disproved by the consistency of dose-response relationships among former and current smokers. The inverse association between passive smoking and PD, HR 0.70 (95% CI 0.49-0.99) ruled out the effect of unmeasured confounding. CONCLUSIONS: These results are highly suggestive of a true causal link between smoking and PD, although it is not clear which is the chemical compound in cigarette smoking responsible for the biological effect.
72 citations
International Agency for Research on Cancer1, North-West University2, British Heart Foundation3, Imperial College London4, Utrecht University5, Prevention Institute6, Centre for Health Protection7, University of Helsinki8, University of Tromsø9, German Cancer Research Center10, University of Granada11, Lund University12, University of Rennes13, Cancer Epidemiology Unit14, Aarhus University15, Aalborg University16, National and Kapodistrian University of Athens17, Umeå University18, University of Turin19, Basque Government20, University College London21, University of Ioannina22, University of Cambridge23
TL;DR: Alcohol intake was inversely associated with non-fatal CHD risk but positively associated with the risk of different stroke subtypes, which highlights the opposing associations of alcohol intake with different CVD types and strengthens the evidence for policies to reduce alcohol consumption.
Abstract: Objective To investigate the association between alcohol consumption (at baseline and over lifetime) and non-fatal and fatal coronary heart disease (CHD) and stroke. Design Multicentre case-cohort study. Setting A study of cardiovascular disease (CVD) determinants within the European Prospective Investigation into Cancer and nutrition cohort (EPIC-CVD) from eight European countries. Participants 32 549 participants without baseline CVD, comprised of incident CVD cases and a subcohort for comparison. Main outcome measures Non-fatal and fatal CHD and stroke (including ischaemic and haemorrhagic stroke). Results There were 9307 non-fatal CHD events, 1699 fatal CHD, 5855 non-fatal stroke, and 733 fatal stroke. Baseline alcohol intake was inversely associated with non-fatal CHD, with a hazard ratio of 0.94 (95% confidence interval 0.92 to 0.96) per 12 g/day higher intake. There was a J shaped association between baseline alcohol intake and risk of fatal CHD. The hazard ratios were 0.83 (0.70 to 0.98), 0.65 (0.53 to 0.81), and 0.82 (0.65 to 1.03) for categories 5.0-14.9 g/day, 15.0-29.9 g/day, and 30.0-59.9 g/day of total alcohol intake, respectively, compared with 0.1-4.9 g/day. In contrast, hazard ratios for non-fatal and fatal stroke risk were 1.04 (1.02 to 1.07), and 1.05 (0.98 to 1.13) per 12 g/day increase in baseline alcohol intake, respectively, including broadly similar findings for ischaemic and haemorrhagic stroke. Associations with cardiovascular outcomes were broadly similar with average lifetime alcohol consumption as for baseline alcohol intake, and across the eight countries studied. There was no strong evidence for interactions of alcohol consumption with smoking status on the risk of CVD events. Conclusions Alcohol intake was inversely associated with non-fatal CHD risk but positively associated with the risk of different stroke subtypes. This highlights the opposing associations of alcohol intake with different CVD types and strengthens the evidence for policies to reduce alcohol consumption.
64 citations
TL;DR: A “wise epidemiology” approach is proposed to choose in a context imprinted by Big Data and precision medicine—epidemiological research projects actually relevant to population health, training epidemiologists and clarifying whether today "health" may be redefined—as some maintain in purely technological terms.
Abstract: Big Data and precision medicine, two major contemporary challenges for epidemiology, are critically examined from two different angles. In Part 1 Big Data collected for research purposes (Big research Data) and Big Data used for research although collected for other primary purposes (Big secondary Data) are discussed in the light of the fundamental common requirement of data validity, prevailing over “bigness”. Precision medicine is treated developing the key point that high relative risks are as a rule required to make a variable or combination of variables suitable for prediction of disease occurrence, outcome or response to treatment; the commercial proliferation of allegedly predictive tests of unknown or poor validity is commented. Part 2 proposes a “wise epidemiology” approach to: (a) choosing in a context imprinted by Big Data and precision medicine—epidemiological research projects actually relevant to population health, (b) training epidemiologists, (c) investigating the impact on clinical practices and doctor-patient relation of the influx of Big Data and computerized medicine and (d) clarifying whether today "health" may be redefined—as some maintain in purely technological terms.
43 citations
TL;DR: A workshop to examine the current evidence and identify research priorities for reducing social inequalities in cancer was convened, with participants identifying 3 research priorities.
Abstract: Social inequalities in cancer are a global problem, as has been well documented in the World Health Organization (WHO)/International Agency for Research on Cancer (IARC) publication Social Inequalities and Cancer. Inequalities in income, wealth, education, and power disproportionally impact the most disadvantaged individuals, communities, and countries to produce a social gradient in the incidence, survival, and mortality of many cancers both within and between countries. From April 16 to 18, 2018, the IARC convened a workshop to examine the current evidence and identify research priorities for reducing social inequalities in cancer. International and WHO/IARC experts drawn from many different disciplines presented a series of articles to be published in an IARC scientific publication; extensive discussion in subgroups and plenary sessions resulted in participants identifying 3 research priorities.
37 citations