Search

Purpose: Coffee intake and apolipoprotein B levels have been linked to gastric, colorectal, and esophageal cancers in numerous recent studies. However, whether these associations are all causal remains unestablished. This study aimed to assess the potential causal associations of apolipoprotein B and coffee intake with the risk of gastric, colorectal, and esophageal cancers using Mendelian randomization analysis. Methods: In this study, we utilized a two-sample Mendelian randomization analysis to access the causal effects of coffee intake and apolipoprotein B on gastric, colorectal, and esophageal cancers. The summary statistics of coffee intake (n = 428,860) and apolipoprotein B (n = 439,214) were obtained from the UK Biobank. In addition, the summary statistics of gastric cancer, colorectal cancer, and esophageal cancer were obtained from the FinnGen biobank (n = 218,792). Inverse variance weighted, MR–Egger, weighted median, and weighted mode were applied to examine the causal relationship between coffee intake, apolipoprotein B and gastric, colorectal, and esophageal cancers. MR–Egger intercept test, Cochran's Q test, and leave-one-out analysis were performed to evaluate possible heterogeneity and pleiotropy. Steiger filtering and bidirectional mendelian randomization analysis were performed to evaluate the possible reverse causality. Results: The result of the inverse variance weighted method indicated that apolipoprotein B levels were significantly associated with a higher risk of gastric cancer (OR = 1.392, 95% CI 1.027–1.889, P = 0.0333) and colorectal cancer (OR = 1.188, 95% CI 1.001–1.411, P = 0.0491). Furthermore, multivariable Mendelian randomization analysis also revealed a positive association between apolipoprotein B levels and colorectal cancer risk, but the effect of apolipoprotein B on gastric cancer risk disappeared after adjustment of coffee intake, body mass index or lipid-related traits. However, we did not discover any conclusive evidence linking coffee intake to gastric, colorectal, or esophageal cancers. Conclusions: This study suggested a causal association between genetically increased apolipoprotein B levels and higher risk of colorectal cancer. No causal relationship was observed between coffee intake and gastric, colorectal, or esophageal cancers. [ABSTRACT FROM AUTHOR]

Background: The prevalence of excess adiposity, as measured by elevated body mass index (BMI) and waist-hip ratio (WHR), is increasing in sub-Saharan African (SSA) populations. This could add a considerable burden of cardiovascular and metabolic diseases for which these populations are currently ill-prepared. Evidence from white, European origin populations shows that higher adiposity leads to an adverse lipid profile; whether these associations are similar in all SSA populations requires further exploration. This study compared the association of BMI and WHR with lipid profile in urban Malawi with a contemporary cohort with contrasting socioeconomic, demographic, and ethnic characteristics in the United Kingdom (UK). Methods: We used data from 1248 adolescents (mean 18.7 years) and 2277 Malawian adults (mean 49.8 years), all urban-dwelling, and from 3201 adolescents (mean 17.8 years) and 6323 adults (mean 49.7 years) resident in the UK. Adiposity measures and fasting lipids were assessed in both settings, and the associations of BMI and WHR with total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were assessed by sex and age groups in both studies. Results: Malawian female adults were more adipose and had more adverse lipid profiles than their UK counterparts. In contrast, Malawian adolescent and adult males were leaner and had more favourable lipid profiles than in the UK. Higher BMI and WHR were associated with increased TC, LDL-C and TG and reduced HDL-C in both settings. The magnitude of the associations of BMI and WHR with lipids was mostly similar or slightly weaker in the Malawian compared with the UK cohort in both adolescents and adults. One exception was the stronger association between increasing adiposity and elevated TC and LDL-C in Malawian compared to UK men. Conclusions: Malawian adult women have greater adiposity and more adverse lipid profiles compared with their UK counterparts. Similar associations of adiposity with adverse lipid profiles were observed for Malawian and UK adults in most age and sex groups studied. Sustained efforts are urgently needed to address the excess adiposity and adverse lipid profiles in Malawi to mitigate a future epidemic of cardio-metabolic disease among the poorest populations. [ABSTRACT FROM AUTHOR]

The article discusses the 1970 British cohort study on the relationship between public care during childhood and the biomedical risk factors in Middle Age. Topics include the association between socioeconomic disadvantages in childhood with cardiovascular disease and adult mortality, the association of care with biomarkers of mortality like glucose metabolism, and the history of early-life public care in Great Britain.

Background: The relationship between physical fitness and risk markers for type 2 diabetes (T2D) in children and the contribution to ethnic differences in these risk markers have been little studied. We examined associations between physical fitness and early risk markers for T2D and cardiovascular disease in 9‐ to 10‐year‐old UK children. Methods: Cross‐sectional study of 1445 9‐ to 10‐year‐old UK children of South Asian, black African‐Caribbean and white European origin. A fasting blood sample was used for measurement of insulin, glucose (from which homeostasis model assessment [HOMA]‐insulin resistance [IR] was derived), glycated hemoglobin (HbA1c), urate, C‐reactive protein (CRP), and lipids. Measurements of blood pressure (BP) and fat mass index (FMI) were made; physical activity was measured by accelerometry. Estimated VO2 max was derived from a submaximal fitness step test. Associations were estimated using multilevel linear regression. Results: Higher VO2 max was associated with lower FMI, insulin, HOMA‐IR, HbA1c, glucose, urate, CRP, triglycerides, LDL‐cholesterol, BP and higher HDL‐cholesterol. Associations were reduced by adjustment for FMI, but those for insulin, HOMA‐IR, glucose, urate, CRP, triglycerides and BP remained statistically significant. Higher levels of insulin and HOMA‐IR in South Asian children were partially explained by lower levels of VO2max compared to white Europeans, accounting for 11% of the difference. Conclusions: Physical fitness is associated with risk markers for T2D and CVD in children, which persist after adjustment for adiposity. Higher levels of IR in South Asians are partially explained by lower physical fitness levels compared to white Europeans. Improving physical fitness may provide scope for reducing risks of T2D. [ABSTRACT FROM AUTHOR]

Type 2 diabetes (T2D) is a complex disorder characterized by high blood sugar, insulin resistance, and relative lack of insulin. The collective effects of genome wide minor alleles of common SNPs, or the minor allele content (MAC) in an individual, have been linked with quantitative variations of complex traits and diseases. Here we studied MAC in T2D using previously published SNP datasets and found higher MAC in cases relative to matched controls. A set of 357 SNPs was found to have the best predictive accuracy in a British population. A weighted risk score calculated by using this set produced an area under the curve (AUC) score of 0.86, which is comparable to risk models built by phenotypic markers. These results identify a novel genetic risk element in T2D susceptibility and provide a potentially useful genetic method to identify individuals with high risk of T2D. [ABSTRACT FROM AUTHOR]

Ever more evidence associates short sleep with increased risk of metabolic diseases such as obesity, which may be related to a predisposition to non-homeostatic eating. Few studies have concurrently determined associations between sleep duration and objective measures of metabolic health as well as sleep duration and diet, however. We therefore analyzed associations between sleep duration, diet and metabolic health markers in UK adults, assessing associations between sleep duration and 1) adiposity, 2) selected metabolic health markers and 3) diet, using National Diet and Nutrition Survey data. Adults (n = 1,615, age 19–65 years, 57.1% female) completed questions about sleep duration and 3 to 4 days of food diaries. Blood pressure and waist circumference were recorded. Fasting blood lipids, glucose, glycated haemoglobin (HbA1c), thyroid hormones, and high-sensitivity C-reactive protein (CRP) were measured in a subset of participants. We used regression analyses to explore associations between sleep duration and outcomes. After adjustment for age, ethnicity, sex, smoking, and socioeconomic status, sleep duration was negatively associated with body mass index (-0.46 kg/m2 per hour, 95% CI -0.69 to -0.24 kg/m2, p < 0.001) and waist circumference (-0.9 cm per hour, 95% CI -1.5 to -0.3cm, p = 0.004), and positively associated with high-density lipoprotein cholesterol (0.03 mmol/L per hour, 95% CI 0.00 to 0.05, p = 0.03). Sleep duration tended to be positively associated with free thyroxine levels and negatively associated with HbA1c and CRP (p = 0.09 to 0.10). Contrary to our hypothesis, sleep duration was not associated with any dietary measures (p ≥ 0.14). Together, our findings show that short-sleeping UK adults are more likely to have obesity, a disease with many comorbidities. [ABSTRACT FROM AUTHOR]

Background: Diabetes, obesity and metabolic syndrome are highly prevalent in patients with severe mental illness and can impose a major physical health burden. Objective: To determine how anthropometric and metabolic features changed over time in a retrospective cohort of people with Severe Mental Illness living in Cheshire, UK. Methods: In all, 1307 individuals on the severe mental illness Register were followed up between 2002 and 2012 in UK general practice. Subjects were identified through a pseudanonymised search of general practice registers. Results: Baseline body mass index was 28.6 kg/m2 increasing to 31.0 at 10-year follow-up (r² = 0.84; p = 0.0002). There was a significant increase in fasting blood glucose from 5.72 to 6.79 mmol/L (r² = 0.48; p = 0.026). Correspondingly, there was a strong positive univariate relation between increase in body mass index and fasting blood glucose (r² = 0.54; p < 0.0001) taking into account all measurements. Fasting blood glucose also increased slightly with age (p = 0.028). With increasing use of statins, total cholesterol fell from 4.5 to 3.9 mmol/L (r² = 0.88; p = 0.0001), as did low-density lipoprotein cholesterol from 3.43 to 2.35 mmol/L (r² = 0.94; p = 0.0001). In multivariate models, adjusting for age, gender, smoking and blood pressure, each unit increase in body mass index (odds ratio = 1.07 [1.01, 1.13]; p = 0.031) and triglycerides (odds ratio = 1.28 (1.06, 1.55); p = 0.009) was independently associated with an increased risk of having type 2 diabetes. Conclusion: Increasing body mass index relates to increasing rates of dysglycaemia over time. Measures to encourage weight reduction should be key strategies to reduce dysglycaemia rates in severe mental illness. Prescribing statins may have been effective in improving the lipid profile in this group. [ABSTRACT FROM AUTHOR]

The article discusses a study that discusses the role of a workplace-based risk assessment in improving a lifetime cardiovascular disease risk in male steelworkers in Great Britain. It informs that the study included a sample of male employees from a local steelworks in Carmarthenshire, South Wales, and undergone cardiovascular disease (CVD) and diabetes risk assessment and the results showed that workplace-based CVD initiatives were beneficial to shift workers.

Aims To establish whether an 8-week very-low-calorie diet could improve glycaemic control in Type 2 diabetes of long duration. Methods A total of 29 people with Type 2 diabetes [short-duration group (diabetes duration < 4 years), n = 15; long-duration group (diabetes duration > 8 years), n = 14] completed an 8-week very-low-calorie diet, with assessments of fasting anthropometry, blood tests and blood pressure at baseline and weeks 1, 4 and 8 of the diet. Results Similar weight loss was achieved in the short- and long-duration groups (14.8 ± 0.8% and 14.4 ± 0.7% respectively; P = 0.662). The glucose response to acute calorie restriction was heterogeneous in the long-duration group with some responding similarly to those in the short-duration group, some responding, but only slowly, and others not responding at all. Overall, HbA1c concentration in the short- vs. long-duration groups fell to 44 ± 2 vs. 64 ± 6 mmol/l (6.2 ± 0.2 vs. 8.0 ± 0.5%; P = 0.002). Fasting plasma glucose levels decreased to 5.8 ± 0.2 vs. 8.4 ± 1.1 mmol/l ( P = 0.024) respectively. A total of 87% of the short-duration group and 50% of the long-duration group achieved non-diabetic fasting plasma glucose levels at week 8. Clinically significant improvements in blood pressure and lipid profile were seen regardless of diabetes duration. Conclusion In people with Type 2 diabetes of > 8 years' duration, a therapeutic trial of a very-low-calorie diet may be undertaken with a 50% chance of achieving non-diabetic fasting glucose levels off all antidiabetic therapies. [ABSTRACT FROM AUTHOR]

Aims In the UK, lifestyle intervention is first-line management in Type 2 diabetes. It is unclear what type of diet is most efficacious for improving glycaemic control. This study investigated the effects of an oat-enriched diet on glycaemic control, postprandial glycaemia, inflammation and oxidative stress compared with standard dietary advice. Methods In a randomized crossover design, 27 volunteers with Type 2 diabetes, managed on diet and lifestyle only, were observed for two consecutive 8-week periods following either the oat-enriched diet or re-enforced standard dietary advice. Volunteers attended at baseline (habitual intake) and 8 and 16 weeks. Measurements included basic clinical measurements and fasted and postprandial (3-h) glucose and insulin in response to a healthy test meal. Markers of inflammation and oxidative stress, including high-sensitivity C-reactive protein, interleukin 6, interleukin 18, tumour necrosis factor-alpha, adiponectin, thiobarbituric acid reactive substances, oxygen radical antioxidant capacity, oxidized LDL and urinary isoprostanes, were also measured at fasting and in the postprandial period. Results There were no diet-related effects on glycaemic control or glycaemic or insulinaemic responses to the test meal. Total cholesterol (5.1 ± 1.0 vs. 4.9 ± 0.8 mmol/l, P = 0.019) concentrations declined following the oat-enriched diet compared with standard dietary advice. There was a postprandial decline in adiponectin concentration ( P = 0.009), but no effect of dietary intervention. None of the measures of oxidative stress or inflammation were altered by the oat-enriched diet compared with standard dietary advice. Conclusion The oat-enriched diet had a modest impact on lipid lowering, but did not impact on oxidative stress or inflammation in these volunteers with Type 2 diabetes. [ABSTRACT FROM AUTHOR]

Abstract: Here the impact of APOE genotype on CHD risk in UK adults is reported, along with an analysis of APOE genotype×BMI/age/sex interactions. APOE genotype had a significant impact on fasting total:LDL-cholesterol (TC:LDL-C) ratio, triglycerides, % HDL3, and the Framingham 10-year CVD risk score (P <0.05), with an overall trend towards lower and higher risk in E2- and E4-carriers, respectively, relative to the wild-type E3/E3 genotype. A greater impact of genotype on TC:HDL-C was observed in females, which explained 16% of the variability in this outcome versus 6% in males. APOE genotype was also associated with plasma C-reactive protein and adhesion molecule concentrations (P <0.05), with significant genotype×BMI interactions observed. Our observations indicate that the association between the APOE genotype and CHD risk is unlikely to be homogenous and highlights the risk of inaccurate estimations of genotype–phenotype associations in population subgroups without appropriate stratification for sex and adiposity. [Copyright &y& Elsevier]

Purpose: Why early puberty is associated with worse cardiovascular outcomes is unknown. The relationship between puberty and lipids is unclear. Our aim was to assess whether age at puberty was associated with triglyceride and total low-density lipoprotein and high-density lipoprotein cholesterol at age 53 years. Methods: Participants in a national birth cohort were examined at 15 years, when pubertal stage for boys was assessed and age at menarche reported by the girls'' mothers. At 53 years, 3035 were interviewed in their homes by research nurses, where blood was taken. Results: There was a significant inverse relationship in women but not men between age at puberty (in years) and triglycerides (regression coefficient −0.2.9, 95% confidence interval −5.5, to −0.04, p = .02), age at puberty, and age at puberty and adult body mass index (BMI; p < .001). Relationships between puberty and lipids were completely explained by BMI or waist circumference at 53 years. Conclusions: In both sexes earlier maturation was associated with greater BMI and waist circumference in later life, which resulted in greater triglycerides and cholesterol in women. We suggest that intervention after puberty to help avoid obesity in early maturing women may improve their later cardiovascular health. [Copyright &y& Elsevier]