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Over 75% of young adults who use cannabis also report drinking alcohol, leading to increased risks that include impaired cognition, substance use disorders, and more heavy and frequent substance use. Studies suggest that subjective responses to either alcohol or cannabis can serve as a valuable indicator for identifying individuals at risk of prolonged substance use and use disorder. While laboratory studies show additive effects when alcohol and cannabis are used together, the impact of co‐using these substances, specifically with respect to cannabidiol, on an individual's subjective experience remains unclear. This narrative review explores the effects of simultaneous alcohol and cannabis (SAM) use on subjective drug effects, drawing from qualitative research, laboratory experiments, and naturalistic studies. Experimental findings are inconsistent regarding the combined effects of alcohol and cannabis, likely influenced by factors such as dosage, method of administration, and individual substance use histories. Similarly, findings from qualitative and naturalistic studies are mixed regarding subjective drug effects following SAM use. These discrepancies may be due to recall biases, variations in assessment methods, and the measurement in real‐world contexts of patterns of SAM use and related experiences. Overall, this narrative review highlights the need for more comprehensive research to understand more fully subjective drug effects of SAM use in diverse populations and settings, emphasizing the importance of frequent and nuanced assessment of SAM use and subjective responses in naturalistic settings. [ABSTRACT FROM AUTHOR]

General cognitive ability (also known as general intelligence, or g (18)) is an important human trait. It shows consistent and strong associations with important life outcomes such as educational and [...], Understanding the determinants of healthy mental ageing is a priority for society today (1,2). So far, we know that intelligence differences show high stability from childhood to old age (3,4) and there are estimates of the genetic contribution to intelligence at different ages (5,6). However, attempts to discover whether genetic causes contribute to differences in cognitive ageing have been relatively uninformative (7-10). Here we provide an estimate of the genetic and environmental contributions to stability and change in intelligence across most of the human lifetime. We used genome-wide single nucleotide polymorphism (SNP) data from 1,940 unrelated individuals whose intelligence was measured in childhood (age 11 years) and again in old age (age 65, 70 or 79 years) (11,12). We use a statistical method that allows genetic (co)variance to be estimated from SNP data on unrelated individuals (13-17). We estimate that causal genetic variants in linkage disequilibrium with common SNPs account for 0.24 of the variation in cognitive ability change from childhood to old age. Using bivariate analysis, we estimate a genetic correlation between intelligence at age 11 years and in old age of 0.62. These estimates, derived from rarely available data on lifetime cognitive measures, warrant the search for genetic causes of cognitive stability and change.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.addbeh.2006.03.020 Byline: John M. Starr (a), Ian J. Deary (b), Helen C. Fox (c), Lawrence J. Whalley (c) Keywords: Smoking; Cognition; Memory; Respiratory function Abstract: Previously we reported that smoking is associated with a small relative decline in cognition from childhood to old age. In this study we perform confirmatory analyses on a further wave of data collected from 298 of the participants, all with age 11 IQ scores, at age 66years, 2years after the original observations. Non-smokers scored a mean 4.9 memory test and 2.6 information processing speed test points and ex-smokers 3.5 memory test and 1.9 information processing speed test points higher than current smokers respectively over the two waves of testing, equivalent to 4-8% of mean test scores, adjusted for the effects of childhood IQ. Across tests a 100l/min higher Peak Expiratory Flow Rate was associated with a 3-4% higher test score at ages 64 and 66years. These data confirm the adverse effect of smoking on information processing speed, and provide new evidence for a similar adverse effect on memory for people in their mid-sixties. Author Affiliation: (a) Department of Geriatric Medicine, University of Edinburgh, Scotland, UK (b) Department of Psychology, University of Edinburgh, Scotland, UK (c) Department of Mental Health, University of Aberdeen, Scotland, UK

Smoking as a risk factor for relative cognitive decline from age 11 to 64 years is examined. Multiple linear regression identified childhood IQ, level of education, occupational code, lung function, and smoking history as significant independent predictors of mental function at age 64.

The Scottish Mental Surveys of 1932 and 1947 collected valid IQ-type test scores for almost everyone born in 1921 and 1936 and attending school on June 1, 1932 (N = 89,498) and June 4, 1947 (N = 70,805). These surveys are described. This research, using the surveys' data, examined (a) the stability of intelligence differences across the life span, (b) the determinants of cognitive change from childhood to old age, and (e) the impact of childhood intelligence on survival and health in old age. Surviving participants of the Scottish Mental Surveys were tested, and the surveys' data were linked with public and health records. Novel findings on the stability of IQ scores from age 11 to age 80; sex differences in cognitive aging; the dedifferentiation hypothesis of cognitive aging; and the effect of childhood IQ on all-cause and specific mortality, morbidity, and frailty in old age are presented.