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Background: Cannabis use is common, especially among young people, and is associated with risks for various health harms. Some jurisdictions have recently moved to legalization/regulation pursuing public health goals. Evidence-based ‘Lower Risk Cannabis Use Guidelines’ (LRCUG) and recommendations were previously developed to reduce modifiable risk factors of cannabis-related adverse health outcomes; related evidence has evolved substantially since. We aimed to review new scientific evidence and to develop comprehensively up-to-date LRCUG, including their recommendations, on this evidence basis. Methods: Targeted searches for literature (since 2016) on main risk factors for cannabis-related adverse health outcomes modifiable by the user-individual were conducted. Topical areas were informed by previous LRCUG content and expanded upon current evidence. Searches preferentially focused on systematic reviews, supplemented by key individual studies. The review results were evidence-graded, topically organized and narratively summarized; recommendations were developed through an iterative scientific expert consensus development process. Results: A substantial body of modifiable risk factors for cannabis use-related health harms were identified with varying evidence quality. Twelve substantive recommendation clusters and three precautionary statements were developed. In general, current evidence suggests that individuals can substantially reduce their risk for adverse health outcomes if they delay the onset of cannabis use until after adolescence, avoid the use of high-potency (THC) cannabis products and high-frequency/-intensity of use, and refrain from smoking-routes for administration. While young people are particularly vulnerable to cannabis-related harms, other sub-groups (e.g., pregnant women, drivers, older adults, those with co-morbidities) are advised to exercise particular caution with use-related risks. Legal/regulated cannabis products should be used where possible. Conclusions: Cannabis use can result in adverse health outcomes, mostly among sub-groups with higher-risk use. Reducing the risk factors identified can help to reduce health harms from use. The LRCUG offer one targeted intervention component within a comprehensive public health approach for cannabis use. They require effective audience-tailoring and dissemination, regular updating as new evidence become available, and should be evaluated for their impact.

Additional file 1. Supplementary Material.

Issues\ud \ud Alcohol use has been shown to impact on various forms of liver disease, not restricted to alcoholic liver disease.\ud \ud \ud Approach\ud \ud We developed a conceptual framework based on a narrative review of the literature to identify causal associations between alcohol use and various forms of liver disease including the complex interactions of alcohol with other major risk factors. Based on this framework, we estimate the identified relations for 2017 for the USA.\ud \ud \ud Key Findings\ud \ud The following pathways were identified and modelled for the USA for the year 2017. Alcohol use caused 35 200 (95% uncertainty interval 32 800–37 800) incident cases of alcoholic liver cirrhosis. There were 1700 (uncertainty interval 1100–2500) acute hepatitis B and C virus (HBV and HCV) infections attributable to heavy‐drinking occasions, and 14 000 (uncertainty interval 5900–19 500) chronic HBV and 1700 (uncertainty interval 700–2400) chronic HCV infections due to heavy alcohol use interfering with spontaneous clearance. Alcohol use and its interactions with other risk factors (HBV, HCV, obesity) led to 54 500 (uncertainty interval 50 900–58 400) new cases of liver cirrhosis. In addition, alcohol use caused 6600 (uncertainty interval 4200–9300) liver cancer deaths and 40 700 (uncertainty interval 36 600–44 600) liver cirrhosis deaths.\ud \ud \ud Implications\ud \ud Alcohol use causes a substantial number of incident cases and deaths from chronic liver disease, often in interaction with other risk factors.\ud \ud \ud Conclusion\ud \ud This additional disease burden is not reflected in the current alcoholic liver disease categories. Clinical work and prevention policies need to take this into consideration.

Introduction\ud \ud Nationally representative studies of the combined impact of drinking and body mass (BMI) on mortality outcomes are unavailable. We investigate whether both act together to elevate risk of all‐cause or liver mortality.\ud \ud \ud \ud Methods\ud \ud We obtained self‐reported histories of drinking and BMI from 129 098 women (mean age 47.2 years) and 102 568 men (mean age 45.6 years) ≥18 years interviewed from 1997 to 2004 in the National Health Interview Survey and related these data to the deaths that occurred by 31 December 2006 (women = 8486; men = 7819 deaths). Death hazards among current drinkers in different BMI groups were adjusted for age, education, race and smoking.\ud \ud \ud \ud Results\ud \ud Obese (≥30 kg m−2) adults with consumption of >40 g day−1 (women) or >60 g day−1 (men) pure ethanol were at risk of increased mortality from all‐cause and chronic liver disease (P trend