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Quantification of the disease burden caused by different risks informs prevention by providing an account of health loss different to that provided by a disease-by-disease analysis. No complete revision of global disease burden caused by risk factors has been done since a comparative risk assessment in 2000, and no previous analysis has assessed changes in burden attributable to risk factors over time. We estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. We estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specific deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden. In 2010, the three leading risk factors for global disease burden were high blood pressure (7·0% [95% uncertainty interval 6·2–7·7] of global DALYs), tobacco smoking including second-hand smoke (6·3% [5·5–7·0]), and household air pollution from solid fuels (4·3% [3·4–5·3]). In 1990, the leading risks were childhood underweight (7·9% [6·8–9·4]), household air pollution from solid fuels (HAP; 6·8% [5·5–8·0]), and tobacco smoking including second-hand smoke (6·1% [5·4–6·8]). Dietary risk factors and physical inactivity collectively accounted for 10·0% (95% UI 9·2–10·8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily affect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient deficiencies, fell in rank between 1990 and 2010, with unimproved water and sanitation accounting for 0·9% (0·4–1·6) of global DALYs in 2010. However, in most of sub-Saharan Africa childhood underweight, HAP, and non-exclusive and discontinued breastfeeding were the leading risks in 2010, while HAP was the leading risk in south Asia. The leading risk factor in Eastern Europe, Andean Latin America, and southern sub-Saharan Africa in 2010 was alcohol use; in most of Asia, most of Latin America, North Africa and Middle East, and central Europe it was high blood pressure. Despite declines, tobacco smoking including second-hand smoke remained the leading risk in high-income north America and western Europe. High body-mass index has increased globally and it is the leading risk in Australasia and southern Latin America, and also ranks high in other high-income regions, North Africa and Middle East, and Oceania. Worldwide, the contribution of different risk factors to disease burden has changed substantially, with a shift away from risks for communicable diseases in children towards those for non-communicable diseases in adults. These changes are related to the ageing population, decreased mortality among children younger than 5 years, changes in cause-of-death composition, and changes in risk factor exposures. New evidence has led to changes in the magnitude of key risks including unimproved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollution. The extent to which the epidemiological shift has occurred and what the leading risks currently are varies greatly across regions. In much of sub-Saharan Africa, the leading risks are still those associated with poverty and those that affect children. Bill & Melinda Gates Foundation.

This bookexamines ways in which cancer health disparities exist due to class and context inequities even in the most advanced society of the world.This volume, while articulating health disparities in the St.Louis, Missouri metropolitan area, including East St.Louis, Illinois, seeks to move beyond deficit models to focus on health equity.

Alcohol is a known carcinogen, yet the evidence for an association with pancreatic cancer risk is considered as limited or inconclusive by international expert panels. We examined the association between alcohol intake and pancreatic cancer risk in a large consortium of prospective studies. Population-based individual-level data was pooled from 30 cohorts across four continents, including Asia, Australia, Europe, and North America. A total of 2,494,432 participants without cancer at baseline (62% women, 84% European ancestries, 70% alcohol drinkers [alcohol intake ≥ 0.1 g/day], 47% never smokers) were recruited between 1980 and 2013 at the median age of 57 years and 10,067 incident pancreatic cancer cases were recorded. In age- and sex-stratified Cox proportional hazards models adjusted for smoking history, diabetes status, body mass index, height, education, race and ethnicity, and physical activity, pancreatic cancer hazard ratios (HR) and 95% confidence intervals (CI) were estimated for categories of alcohol intake and in continuous for a 10 g/day increase. Potential heterogeneity by sex, smoking status, geographic regions, and type of alcoholic beverage was investigated. Alcohol intake was positively associated with pancreatic cancer risk, with HR30-to-<60 g/day and HR≥60 g/day equal to 1.12 (95% CI [1.03,1.21]) and 1.32 (95% CI [1.18,1.47]), respectively, compared to intake of 0.1 to <5 g/day. A 10 g/day increment of alcohol intake was associated with a 3% increased pancreatic cancer risk overall (HR: 1.03; 95% CI [1.02,1.04]; pvalue < 0.001) and among never smokers (HR: 1.03; 95% CI [1.01,1.06]; pvalue = 0.006), with no evidence of heterogeneity by sex (pheterogeneity = 0.274) or smoking status (pheterogeneity = 0.624). Associations were consistent in Europe-Australia (HR10 g/day = 1.03, 95% CI [1.00,1.05]; pvalue = 0.042) and North America (HR10 g/day = 1.03, 95% CI [1.02,1.05]; pvalue < 0.001), while no association was observed in cohorts from Asia (HR10 g/day = 1.00, 95% CI [0.96,1.03]; pvalue = 0.800; pheterogeneity = 0.003). Positive associations with pancreatic cancer risk were found for alcohol intake from beer (HR10 g/day = 1.02, 95% CI [1.00,1.04]; pvalue = 0.015) and spirits/liquor (HR10 g/day = 1.04, 95% CI [1.03,1.06]; pvalue < 0.001), but not wine (HR10 g/day = 1.00, 95% CI [0.98,1.03]; pvalue = 0.827). The differential associations across geographic regions and types of alcoholic beverages might reflect differences in drinking habits and deserve more investigations. Findings from this large-scale pooled analysis support a modest positive association between alcohol intake and pancreatic cancer risk, irrespective of sex and smoking status. Associations were particularly evident for baseline alcohol intake of at least 15 g/day in women and 30 g/day in men.

Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r 2  > 0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer ( P  < 10 -7 ). Four of these contain plausible causative genes ( FGFR2 , TNRC9 , MAP3K1 and LSP1 ). At the second stage, 1,792 SNPs were significant at the P  < 0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach. Novel breast cancer genes Until the genome-wide association study on page 1087 was published online, known susceptibility genes — such as BRCA1 and BRCA2 — accounted for less than 25% of the familial risk of breast cancer. The new study, which involved 21,860 patients and 22,578 controls, has identified four genes positively associated with genetic susceptibility to breast cancer ( FGFR2 , TNRC9 , MAP3K1 and LSP1 ). Most previously identified breast cancer susceptibility genes are involved in DNA repair, but the newly discovered associations appear to relate more to the control of cell growth or to cell signalling. Only one of the genes — FGFR2 — had a clear prior relevance to breast cancer. The identification of these genes opens up new avenues of research into the causes of breast cancer. They may also become part of a new strategy to classify women's risk, paving the way for better disease prevention. Previous work has identified several genes where mutations lead to breast cancer, but other genetic and environmental factors must still be accounted for. A large study of genetic association with breast cancer points to four novel genes and many more genetic markers that should be pursued for their link to cancer susceptibility.

Cancer incidence rates have been shown to vary by ethnicity, and the increasing awareness of and interest in reporting ethnic health inequalities have been growing internationally. The objective of this study was to assess cancer incidence and mortality rates by ethnicity in Canada. The study used the 2006 Canadian Census Health and Environment Cohort, linked to the Canadian Cancer Registry and the Canadian Vital Statistics-Death Database, to determine cancer cases and mortality from 2006 to 2016. Ethnicity was categorized as non-Indigenous North American (NINA); European; Caribbean; Latin, Central and South American (LCSA); African; East Asian; South Asian; and West Central Asian and Middle Eastern. Europeans had the highest standardized incidence rates, while NINA had the highest mortality rates. Rates varied substantially by ethnicity and immigrant status. The top three cancers accounted for 46.5% to 61.9% of all new cancers, while the top three cancer deaths accounted for 36.1 % to 61.9% of all deaths. The distribution of cancers within the top 10 cancers and the top 10 cancer deaths also differed; e.g., stomach cancer was found to be more prevalent in the East Asian, LCSA, African and Caribbean groups. Non-immigrant African males had the highest cancer incidence rates, and non-immigrant South Asian females had the highest mortality rates. There is considerable variability in cancer incidence and cancer mortality rates by ethnicity, and this study addresses the knowledge gap in Canada in this area. Establishing baseline indicators, such as cancer rates by ethnicity, is essential to understanding the differences within the diverse Canadian population and to informing targeted interventions that may help reduce health inequalities.

The spread of “cancel culture” related to sex and gender controversies in North America is examined as part of a larger movement to politicize sex research findings and certain sex and gender narratives as “correct” and “incorrect” from a so-called social justice standpoint. This binary is then used by academic administrators and empowered individuals or self-interest groups to reward or punish scholars for their viewpoints. The cases described by Meyer-Bahlburg, Lowrey, and Hooven are concrete examples of a growing “sexual McCarthyism” where empirical results are challenged by offended social justice “warriors” and embellished on social media into ad hominem attacks, to the point that it can damage—or even cancel—the careers of productive sexual scientists. This occurs largely out of fear on the part of academic administrators and lawyers charged with protecting the university from “brand damage” that might occur if the offending scholar is not dealt with. Sexual scientists are being vilified for research on sex differences, sex/gender assignment and subsequent causes for transitioning and/or de-transitioning, research that shows few or no untoward social or psychological effects of viewing pornography, research that debunks the notion of porn or sex “addiction,” research showing the efficacy of medications to treat sexual desire disorders in women, research on “minor attracted persons” and even animal research that dares to show homologies to human sexual behavior. The silencing of empirical evidence and alternative viewpoints is contrary to the intellectual mission of universities and destructive to academic and political freedoms.

This review focuses on the lived experiences of chronic conditions among African communities in the Global North, focusing on established immigrant communities as well as recent immigrant, refugee, and asylum-seeking communities. We conducted a systematic and narrative synthesis of qualitative studies published from inception to 2022, following a search from nine databases—MEDLINE, EMBASE, PsycINFO, Web of Science, Social Science Citation Index, Academic Search Complete, CINAHL, SCOPUS and AMED. 39 articles reporting 32 qualitative studies were included in the synthesis. The studies were conducted in 10 countries (Australia, Canada, Denmark, France, Netherlands, Norway, Sweden, Switzerland, United Kingdom, and the United States) and focused on 748 participants from 27 African countries living with eight conditions: type 2 diabetes, hypertension, prostate cancer, sickle cell disease, chronic hepatitis, chronic pain, musculoskeletal orders and mental health conditions. The majority of participants believed chronic conditions to be lifelong, requiring complex interventions. Chronic illness impacted several domains of everyday life—physical, sexual, psycho-emotional, social, and economic. Participants managed their illness using biomedical management, traditional medical treatment and faith-based coping, in isolation or combination. In a number of studies, participants took ‘therapeutic journeys’–which involved navigating illness action at home and abroad, with the support of transnational therapy networks. Multi-level barriers to healthcare were reported across the majority of studies: these included individual (changing food habits), social (stigma) and structural (healthcare disparities). We outline methodological and interpretive limitations, such as limited engagement with multi-ethnic and intergenerational differences. However, the studies provide an important insights on a much-ignored area that intersects healthcare for African communities in the Global North and medical pluralism on the continent; they also raise important conceptual, methodological and policy challenges for national health programmes on healthcare disparities.

Background Personalized medicine (PM) aims to tailor disease prevention, diagnosis, and treatment to individuals on the basis of their genes, lifestyle and environments. Patient and interest organizations (PIOs) may potentially play an important role in the realization of PM. This paper investigates the views and perspectives on PM of a variety of PIOs. Methods Semi-structured telephone interviews were conducted among leading representatives of 13 PIOs located in Europe and North-America. The data collected were analysed using a conventional content analysis approach. Results The PIO representatives supported the realization of PM but feared that many financial, structural and organizational challenges may delay its realization. They encouraged strategies to modernize drug licencing mechanisms, develop research and data sharing infrastructures, and educate patients and health care professionals in PM. Notably, they emphasized the importance of developing PM in an equitable way and taking into consideration the patients’ needs, values and personal situation. Despite varying levels of awareness regarding PM, the PIO representatives expressed willingness to engage in the PM agenda and recommended that PIOs work closely with policy-makers to design PM in a way that truly addresses the needs and concerns of patients. Conclusions PIOs have the potential to become central drivers of the PM agenda. Collaborations should be further developed between PIOs, researchers, drug developers and health care authorities.

Studies of the defence capacity of ancient hominins against toxic substances may contribute importantly to the reconstruction of their niche, including their diets and use of fire. Fire usage implies frequent exposure to hazardous compounds from smoke and heated food, known to affect general health and fertility, probably resulting in genetic selection for improved detoxification. To investigate whether such genetic selection occurred, we investigated the alleles in Neanderthals, Denisovans and modern humans at gene polymorphisms well-known to be relevant from modern human epidemiological studies of habitual tobacco smoke exposure and mechanistic evidence. We compared these with the alleles in chimpanzees and gorillas. Neanderthal and Denisovan hominins predominantly possess gene variants conferring increased resistance to these toxic compounds. Surprisingly, we observed the same in chimpanzees and gorillas, implying that less efficient variants are derived and mainly evolved in modern humans. Less efficient variants are observable from the first early Upper Palaeolithic hunter-gatherers onwards. While not clarifying the deep history of fire use, our results highlight the long-term stability of the genes under consideration despite major changes in the hominin dietary niche. Specifically for detoxification gene variants characterised as deleterious by epidemiological studies, our results confirm the predominantly recent appearance reported for deleterious human gene variants, suggesting substantial impact of recent human population history, including pre-Holocene expansions.