-
1.
Causal relationship between obesity, lifestyle factors and risk of benign prostatic hyperplasia: a univariable and multivariable Mendelian randomization study.
Wang, YB, Yang, L, Deng, YQ, Yan, SY, Luo, LS, Chen, P, Zeng, XT
Journal of translational medicine. 2022;20(1):495
-
-
-
Free full text
Plain language summary
Benign prostatic hyperplasia (BPH) is a common benign disease in middle-aged and elderly men which is often underestimated and underdiagnosed. If patients are not treated in time, it may lead to serious complications, such as urinary retention, renal insufficiency and renal failure. The aim of this study was to evaluate the possible causal associations of abdominal obesity (measured as waist circumference), overall obesity (measured as body mass index), lifestyle factors (dietary habits, smoking, alcohol drinking, and sedentary behaviour) with risk of BPH. This study is a univariable and multivariable mendelian randomised study. Results show that genetic predisposition to higher waist circumference and sedentary behaviour are independently and causally associated with the risk of BPH. However, there isn’t conclusive evidence that genetic predisposition to relative carbohydrate, fat, protein, and sugar intake, smoking and alcohol drinking are causally associated with the risk of BPH. Authors conclude that further studies are needed to identify comprehensive risk factors on BPH and develop freely accessible prediction models for the BPH. These will help to identify individuals at particular risk and provide decision-making supports for individualised intervention.
Abstract
BACKGROUND Obesity (waist circumference, body mass index (BMI)) and lifestyle factors (dietary habits, smoking, alcohol drinking, Sedentary behavior) have been associated with risk of benign prostatic hyperplasia (BPH) in observational studies, but whether these associations are causal is unclear. METHODS We performed a univariable and multivariable Mendelian randomization study to evaluate these associations. Genetic instruments associated with exposures at the genome-wide significance level (P < 5 × 10-8) were selected from corresponding genome-wide associations studies (n = 216,590 to 1,232,091 individuals). Summary-level data for BPH were obtained from the UK Biobank (14,126 cases and 169,762 non-cases) and FinnGen consortium (13,118 cases and 72,799 non-cases). Results from UK Biobank and FinnGen consortium were combined using fixed-effect meta-analysis. RESULTS The combined odds ratios (ORs) of BPH were 1.24 (95% confidence interval (CI), 1.07-1.43, P = 0.0045), 1.08 (95% CI 1.01-1.17, P = 0.0175), 0.94 (95% CI 0.67-1.30, P = 0.6891), 1.29 (95% CI 0.88-1.89, P = 0.1922), 1.23 (95% CI 0.85-1.78, P = 0.2623), and 1.04 (95% CI 0.76-1.42, P = 0.8165) for one standard deviation (SD) increase in waist circumference, BMI, and relative carbohydrate, fat, protein and sugar intake, 1.05 (95% CI 0.92-1.20, P = 0.4581) for one SD increase in prevalence of smoking initiation, 1.10 (95% CI 0.96-1.26, P = 0.1725) and 0.84 (95% CI 0.69-1.02, P = 0.0741) for one SD increase of log-transformed smoking per day and drinks per week, and 1.31 (95% CI 1.08-1.58, P = 0.0051) for one SD increase in sedentary behavior. Genetically predicted waist circumference (OR = 1.26, 95% CI 1.11-1.43, P = 0.0004) and sedentary behavior (OR = 1.14, 95% CI 1.05-1.23, P = 0.0021) were associated with BPH after the adjustment of BMI. CONCLUSION This study supports independent causal roles of high waist circumference, BMI and sedentary behavior in BPH.
-
2.
Psoriasis and cardiovascular disease risk in European and East Asian populations: evidence from meta-analysis and Mendelian randomization analysis.
Zhang, L, Wang, Y, Qiu, L, Wu, J
BMC medicine. 2022;20(1):421
-
-
-
Free full text
Plain language summary
Psoriasis constitutes a chronic, inflammatory skin disease with an immune-genetic basis that has been linked to numerous diseases, including metabolic syndrome, cancer, as well as cardiovascular disease (CVD). The aim of this study was to determine if the relationship of psoriasis with CV events (CVE) risk is congruent with causal associations. This study is a report employing a meta-analysis of observational studies and a two-sample mendelian randomised trial (MR). Results from the meta-analysis show that psoriasis was remarkably associated with a higher risk of incident coronary artery disease (CAD) and myocardial infarction (MI) and was not associated with heart failure risk. Furthermore, the MR approach showed that psoriasis was linked with a higher risk of CAD in both European and East Asian populations. Additionally, psoriasis was also causally linked to an elevated risk of MI in European population. Authors conclude that their findings indicate a causal association of psoriasis with CAD and MI. However, further studies are needed to establish the mechanisms of the causal relationship of psoriasis with CAD and MI.
Abstract
BACKGROUND Psoriasis has been linked to cardiovascular disease (CVD), including coronary artery disease (CAD), myocardial infarction (MI), and heart failure (HF). However, available studies regarding this relationship have shown inconsistent results. Therefore, in this report, we performed a comprehensive review of the literature to assess the effects of psoriasis on risk of these CVDs. METHODS A search of literature until 24 December 2021 was done in PubMed, the Cochrane Library, Web of Science, Google Scholar, and Embase. Within European and East Asian populations, meta-analyses of observational studies assessing correlations between psoriasis and various CVD risk factors were conducted. Mendelian randomization (MR) was then employed to assess the causative impact of genetic pre-disposition for psoriasis on these CVD risk factors. RESULTS The results of the meta-analyses indicated that, in both the European and East Asian populations, psoriasis was significantly linked to an elevated risk in the incidence of CAD (RR = 1.51, 95% confidence interval (CI): 1.04-2.18, p = 0.028 and RR = 1.91, 95% CI: 1.62-2.25, p < 0.001) and MI (RR = 1.23, 95% CI: 1.04-1.46, p = 0.017 and RR = 2.17, 95% CI: 1.44-3.28, p < 0.001). A positive genetic relationship of psoriasis with CAD was found in European individuals (IVW OR1.03; 95% CI: 1.01-1.06, p = 0.005) and in East Asian individuals (IVW OR1.18; 95% CI: 1.03-1.32, p = 0.031). We also established that psoriasis was causally linked with an elevated risk of MI (IVW OR1.05; 95% CI: 1.01-1.09, p = 0.026) in the European population as determined using an MR approach. Moreover, our MR results were congruent with the null findings from the meta-analysis assessing associations of psoriasis with HF risk. CONCLUSIONS This research work provides preliminary evidence that psoriasis and CVD have a common genetic origin and that targeted psoriasis treatment might improve cardiovascular outcomes. These results not only increase our knowledge of the genetic underpinnings linking a comorbidity of psoriasis with CVD but also suggests a novel approach for CVD prevention.
-
3.
Greater risk of severe COVID-19 in Black, Asian and Minority Ethnic populations is not explained by cardiometabolic, socioeconomic or behavioural factors, or by 25(OH)-vitamin D status: study of 1326 cases from the UK Biobank.
Raisi-Estabragh, Z, McCracken, C, Bethell, MS, Cooper, J, Cooper, C, Caulfield, MJ, Munroe, PB, Harvey, NC, Petersen, SE
Journal of public health (Oxford, England). 2020;42(3):451-460
-
-
-
Free full text
-
Plain language summary
The coronavirus disease 2019 (COVID-19) pandemic has to date resulted in over 6 million cases. Growing reports highlight men and Black, Asian and Minority Ethnic (BAME) cohorts as at higher risk of adverse COVID-19 outcomes. The aim of this study was to investigate whether differential patterns of COVID-19 incidence and severity, by sex and ethnicity, might be explained by cardiometabolic, socio-economic, lifestyle and behavioural exposures. This study is a prospective cohort study of over half a million men and women from across the UK. Results showed that male sex, BAME ethnicity, higher body mass index and greater household size were associated with significantly greater odds of a positive result. However, the sex and ethnicity differential pattern of COVID-19 is not adequately explained by variations in cardiometabolic factors, 25(OH)-vitamin D levels, socio-economic or behavioural factors. Authors conclude that investigation of alternative biological and genetic susceptibilities as well as more comprehensive assessment of the complex economic, social and behavioural differences should be prioritised.
Abstract
BACKGROUND We examined whether the greater severity of coronavirus disease 2019 (COVID-19) amongst men and Black, Asian and Minority Ethnic (BAME) individuals is explained by cardiometabolic, socio-economic or behavioural factors. METHODS We studied 4510 UK Biobank participants tested for COVID-19 (positive, n = 1326). Multivariate logistic regression models including age, sex and ethnicity were used to test whether addition of (1) cardiometabolic factors [diabetes, hypertension, high cholesterol, prior myocardial infarction, smoking and body mass index (BMI)]; (2) 25(OH)-vitamin D; (3) poor diet; (4) Townsend deprivation score; (5) housing (home type, overcrowding) or (6) behavioural factors (sociability, risk taking) attenuated sex/ethnicity associations with COVID-19 status. RESULTS There was over-representation of men and BAME ethnicities in the COVID-19 positive group. BAME individuals had, on average, poorer cardiometabolic profile, lower 25(OH)-vitamin D, greater material deprivation, and were more likely to live in larger households and in flats/apartments. Male sex, BAME ethnicity, higher BMI, higher Townsend deprivation score and household overcrowding were independently associated with significantly greater odds of COVID-19. The pattern of association was consistent for men and women; cardiometabolic, socio-demographic and behavioural factors did not attenuate sex/ethnicity associations. CONCLUSIONS In this study, sex and ethnicity differential pattern of COVID-19 was not adequately explained by variations in cardiometabolic factors, 25(OH)-vitamin D levels or socio-economic factors. Factors which underlie ethnic differences in COVID-19 may not be easily captured, and so investigation of alternative biological and genetic susceptibilities as well as more comprehensive assessment of the complex economic, social and behavioural differences should be prioritised.
-
4.
A Systematic Review of Organic Versus Conventional Food Consumption: Is There a Measurable Benefit on Human Health?
Vigar, V, Myers, S, Oliver, C, Arellano, J, Robinson, S, Leifert, C
Nutrients. 2019;12(1)
-
-
-
Free full text
Plain language summary
The demand for organic products has risen rapidly over the last decades. The reasons why consumers may favour organic over conventional products are varied. They may be for personal health and wellbeing, environmental considerations, animal welfare or perceived higher nutritional profile - which is true for some, but not all components. While the long-term safety of pesticide consumption through conventional food production has been questioned, organic foods clearly show lower levels of toxic metabolites, like heavy metals and synthetic fertilizer and pesticide residues. This systematic review aimed to assess the current evidence of organic diet consumption and human health compared to conventionally produced foods. Included were 35 papers on clinical trials and observational studies. The clinical trials studied pesticide and phytochemical excretion, antioxidant capacity, body composition, lipids and inflammatory markers. The observational studies were focused on fertility, foetal and childhood development, pregnancy, lactation and levels of pesticides in children and adults, as well as nutritional biomarkers and cancer risk in adults. An increased intake of organic produce in long-term studies appeared to reduce the incidence of infertility, birth defects, allergies, middle ear infection, pre-eclampsia, metabolic syndrome, high BMI, and non-Hodgkin lymphoma. Organic intake was also linked to reduced urinary levels of organophosphorus pesticides and herbicides. Yet, the author highlighted that organic consumers are more likely to be health conscious, physically active, eat a more plant-based diet, have higher education levels and income, and therefore are not representative of the general population. They also argue that the possible benefits from an organic diet may be partially due to the quality and composition of the diet rather than a direct effect of organic food consumption. Whereby a growing number of findings demonstrate the health benefits of organic food consumption, according to the authors, the current evidence does not yield a solid and definitive answer.
Abstract
The current review aims to systematically assess the evidence related to human health outcomes when an organic diet is consumed in comparison to its conventional counterpart. Relevant databases were searched for articles published to January 2019. Clinical trials and observational research studies were included where they provided comparative results on direct or indirect health outcomes. Thirty-five papers met the criteria for inclusion in the review. Few clinical trials assessed direct improvements in health outcomes associated with organic food consumption; most assessed either differences in pesticide exposure or other indirect measures. Significant positive outcomes were seen in longitudinal studies where increased organic intake was associated with reduced incidence of infertility, birth defects, allergic sensitisation, otitis media, pre-eclampsia, metabolic syndrome, high BMI, and non-Hodgkin lymphoma. The current evidence base does not allow a definitive statement on the health benefits of organic dietary intake. However, a growing number of important findings are being reported from observational research linking demonstrable health benefits with organic food consumption. Future clinical research should focus on using long-term whole-diet substitution with certified organic interventions as this approach is more likely to determine whether or not true measurable health benefits exist.
-
5.
Lifestyle Risk Factors for Serrated Colorectal Polyps: A Systematic Review and Meta-analysis.
Bailie, L, Loughrey, MB, Coleman, HG
Gastroenterology. 2017;152(1):92-104
-
-
-
Free full text
-
Plain language summary
Colorectal cancer (CRC) is a heterogeneous disease thought to result from the accumulation of various aberrant mutations in the cells lining the colorectal mucosa. The aim of this systematic review and meta-analysis was to evaluate modifiable and lifestyle factors and the risk of serrated polyps (a type of growth that stick out from the surface of the colon or rectum) of the colorectum. A search of 3 databases yielded a potential 2446 studies for inclusion, from which 43 remained for systematic review. Results indicate that smoking, alcohol consumption, body fatness, dietary fat and meat consumption increased the risk of developing serrated polyps. Whereas, nonsteroidal anti-inflammatory drugs, aspirin and dietary folate decreased this risk. Authors conclude that their findings strengthen public health messages promoting awareness and change in order to reduce the risk of these precancerous lesions and consequently CRC.
Abstract
BACKGROUND & AIMS Certain subsets of colorectal serrated polyps (SP) have malignant potential. We performed a systematic review and meta-analysis to investigate the association between modifiable lifestyle factors and risk for SPs. METHODS We conducted a systematic search of Medline, Embase, and Web of Science for observational or interventional studies that contained the terms risk or risk factor, and serrated or hyperplastic, and polyps or adenomas, and colorectal (or synonymous terms), published by March 2016. Titles and abstracts of identified articles were independently reviewed by at least 2 reviewers. Adjusted relative risk (RR) and 95% confidence interval (CI) were combined using random effects meta-analyses to assess the risk of SP, when possible. RESULTS We identified 43 studies of SP risk associated with 7 different lifestyle factors: smoking, alcohol, body fatness, diet, physical activity, medication, and hormone-replacement therapy. When we compared the highest and lowest categories of exposure, factors we found to significantly increase risk for SP included tobacco smoking (RR, 2.47; 95% CI, 2.12-2.87), alcohol intake (RR, 1.33; 95% CI, 1.17-1.52), body mass index (RR, 1.40; 95% CI, 1.22-1.61), and high intake of fat or meat. Direct associations for smoking and alcohol, but not body fat, tended to be stronger for sessile serrated adenomas/polyps than hyperplastic polyps. In contrast, factors we found to significantly decrease risks for SP included use of nonsteroidal anti-inflammatory drugs (RR, 0.77; 95% CI, 0.65-0.92) or aspirin (RR, 0.81; 95% CI, 0.67-0.99), as well as high intake of folate, calcium, or fiber. No significant associations were detected between SP risk and physical activity or hormone replacement therapy. CONCLUSIONS Several lifestyle factors, most notably smoking and alcohol, are associated with SP risk. These findings enhance our understanding of mechanisms of SP development and indicate that risk of serrated pathway colorectal neoplasms could be reduced with lifestyle changes.
-
6.
Risk factors for pancreatic cancer: a summary review of meta-analytical studies.
Maisonneuve, P, Lowenfels, AB
International journal of epidemiology. 2015;44(1):186-98
-
-
-
Plain language summary
Pancreatic cancer (PC) is one of the four or five most common causes of cancer mortality in developed countries. The aim of this review was to summarize results from pooled analyses and meta-analyses to estimate the fraction of PCs attributable to many different risk factors. A comprehensive review of the literature was carried out by searching for meta-analytical studies on the association between specific risk factors and PC risk or multiple cancer sites. Results indicate that PC has a multifactorial aetiology. All identified factors can be combined into a specific aetiological (the philosophy or study of causation) pathway for PC. The main pathways include insulin resistance (central adiposity, diabetes, metabolic syndrome), inflammation (tobacco, alcohol, pancreatitis), DNA damage (tobacco, red meat) and haemostasis (blood group, history of thrombosis). Authors conclude that about two-thirds of the major risk factors associated with PC are potentially modifiable, affording a unique opportunity for preventing one of our deadliest cancers.
Abstract
BACKGROUND The aetiology of pancreatic cancer (PC) has been extensively studied and is the subject of numerous meta-analyses and pooled analyses. We have summarized results from these pooled and meta-analytical studies to estimate the fraction of PCs attributable to each of the identified risk factors. METHODS Using a comprehensive strategy, we retrieved 117 meta-analytical or pooled reports dealing with the association between specific risk factors and PC risk. We combined estimates of relative risk and estimates of exposure to calculate the fraction of PCs caused or prevented by a particular exposure. RESULTS Tobacco smoking ('strong' evidence) and Helicobacter pylori infection ('moderate' evidence) are the major risk factors associated with PC, with respective estimated population attributable fractions of 11-32% and 4-25%. The major protective factors are history of allergy ('strong' evidence) and increasing fruit or folate intake ('moderate' evidence), with respective population preventable fractions of 3-7% and 0-12%. CONCLUSIONS We summarized results of 117 meta-analytical or pooled data reports dealing with 37 aetiological exposures, to obtain robust information about the suspected causes of PC. By combining these estimates with their prevalences in the population, we calculated population attributable or population preventable fractions. About two-thirds of the major risk factors associated with PC are potentially modifiable, affording a unique opportunity for preventing one of our deadliest cancers.