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Biomedical subjects

S H Wild

Publications and source records attributed to S H Wild.

13 recordsLinked to original sources
PubMed2006

Mortality from all cancers and lung, colorectal, breast and prostate cancer by country of birth in England and Wales, 2001-2003.

Mortality from all cancers combined and major cancers among men and women aged 20 years and over was compared by country of birth with that of the whole of England and Wales as the reference group. Population data from the 2001 Census and mortality data for 2001-2003 were used to estimate standardised mortality ratios. Data on approximately 399 000 cancer deaths were available, with at least 400 cancer deaths in each of the smaller populations. Statistically significant differences from the reference group included: higher mortality from all cancers combined, lung and colorectal cancer among people born in Scotland and Ireland, lower mortality for all cancers combined, lung, breast and prostate cancer among people born in Bangladesh (except for lung cancer in men), India, Pakistan or China/Hong Kong, lower lung cancer mortality among people born in West Africa or the West Indies, higher breast cancer mortality among women born in West Africa and higher prostate cancer mortality among men born in West Africa or the West Indies. These data may be relevant to causal hypotheses and in relation to health care and cancer prevention.

Adult↗
PubMed2006

Diabetes prevalence in England, 2001--estimates from an epidemiological model.

AIMS: To estimate the total prevalence of diabetes mellitus (diagnosed and undiagnosed) at national, regional and local level in England to support health-care planning and delivery. METHODS: An epidemiological model was constructed by applying age-sex-ethnic-specific reference prevalence rates from epidemiological studies to resident populations (2001 census) of England at national, regional, and local authority/Primary Care Trust levels. RESULTS: Estimated prevalence of total diabetes for all persons in England was 4.41% in 2001, equating to 2 168 000 persons. Type 2 diabetes was estimated to affect 2 002 000 persons (92.3%) and Type 1 diabetes 166 000 persons (7.7%). Diabetes prevalence was estimated to be higher in women (5.17%) than men (3.61%). People from ethnic minority groups had higher crude prevalence than White Europeans (4.29, 5.69, 6.63 and 2.13% among White Europeans, Black African/Caribbeans, South Asians and 'other' groups, respectively). Prevalence increased sharply with age (0.33, 3.37 and 13.92%, respectively, in those aged 0-29, 30-59 and 60+ years). The model allows use of user-defined population denominator estimates to derive numbers and prevalence of people with diabetes for a given local population group, such as at ward or general practice level. CONCLUSIONS: Self-reported diabetes prevalence estimates from community surveys underestimate the true burden of diabetes. The model can be used to derive the expected total prevalence of diabetes in health areas that lack reliable data to facilitate the implementation of the National Service Framework for diabetes. It will also allow estimates of future diabetes prevalence to be derived, and can potentially be used for prevalence estimates in all of the UK.

Adolescent↗
PubMed2005

Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects.

AIMS/HYPOTHESIS: We tested the hypothesis that NEFA concentrations are higher in obese subjects with fatty liver than in obese subjects without fatty liver. MATERIALS AND METHODS: We recruited 22 obese (BMI>30 kg/m(2)) men aged 42-64 years, in whom liver fat was assessed by ultrasound and classified into categories of no, mild to moderate and severe fatty liver by two independent radiologists. Regional and visceral abdominal fat were assessed by dual-energy X-ray absorptiometry and magnetic resonance imaging, and endogenous glucose production, whole-body glucose disposal during an insulin clamp, and NEFA concentrations were measured, along with NEFA suppression (percent (%) suppression and insulin sensitivity index for NEFA during an OGTT). RESULTS: Seven subjects had no evidence of fatty liver, nine had mild or moderate fatty liver and six had severe fatty liver. The amount of visceral fat was not associated with the degree of fatty liver. Whole-body glucose disposal was inversely associated with fatty liver (38.4, 26.5 and 23.9 mumol kg(-1) min(-1) for the groups with no fatty liver, mild to moderate fatty liver and severe fatty liver, respectively, p=0.004). NEFA suppression during the OGTT was decreased (62.5, 50.8 and 41%, p=0.03, for no, mild to moderate, and severe fatty liver, respectively) and the insulin sensitivity index for NEFA was decreased (0.80, 0.40 and 0.34, p<0.0001). Regression modelling suggested that NEFA concentrations were associated with fatty liver independently of whole-body glucose production and disposal measurements. CONCLUSIONS/INTERPRETATION: In obese men, NEFA concentrations during an OGTT are associated with fatty liver independently of classic measures of insulin sensitivity determined by the hyperinsulinaemic clamp. The contribution to this association by factors regulating NEFA concentrations requires further study.

Abdomen↗
PubMed2005

Criteria for previously undiagnosed diabetes and risk of mortality: 15-year follow-up of the Edinburgh Artery Study cohort.

AIMS: To compare risk of all-cause and cardiovascular mortality associated with different criteria for undiagnosed diabetes and glucose tolerance. METHODS: A population-based cohort of 758 men and 738 women of 55-74 years of age who had an oral glucose tolerance test or known diabetes at baseline were followed up until death or for 15 years. Mortality outcomes were compared by baseline diabetes status using people with normal glucose tolerance (i.e. those without diabetes, impaired fasting glucose or impaired glucose tolerance) as the reference group. RESULTS: Prevalence of undiagnosed diabetes using World Health Organization (WHO) criteria (fasting glucose of > or = 7.0 mmol/l and/or a 2-h post-challenge glucose of > or = 11.1 mmol/l) was 6.6%, of which 81% was associated with fasting glucose > or = 7.0 mmol/l and 19% was associated with isolated post-challenge hyperglycaemia. Hazard ratios (95% CI) for all-cause mortality adjusted for age and sex were 1.51 (1.09-2.08) for new diabetes by the American Diabetes Association (ADA) criterion (fasting glucose of > or = 7.0 mmol/l regardless of post-challenge glucose), 1.60 (1.20-2.13) for new diabetes by WHO criteria and 1.98 (1.14-3.44) for isolated post-challenge hyperglycaemia. Hazard ratios (95% CI) for cardiovascular mortality adjusted for age and sex were 1.89 (1.17-3.00), 1.73 (1.12-2.66) and 1.08 (0.34-3.40) for new diabetes by ADA and WHO criteria and for isolated post-challenge hyperglycaemia, respectively. CONCLUSIONS: Undiagnosed diabetes was associated with increased risk of all-cause mortality by any criteria but significantly increased cardiovascular disease mortality was only associated with diabetes diagnosed using the fasting glucose criterion. Mortality risks were similar in this population using either ADA or WHO criteria for diagnosis of diabetes.

Aged↗
PubMed1998

Mortality of women with polycystic ovary syndrome at long-term follow-up.

Metabolic disturbances associated with insulin resistance are present in most women with polycystic ovary syndrome. This has led to suggestions that women with polycystic ovary syndrome may be at increased risk of cardiovascular disease in later life. We undertook a long-term follow-up study to test whether cardiovascular mortality is increased in these women. A total of 786 women diagnosed with polycystic ovary syndrome in the United Kingdom between 1930 and 1979 were traced from hospital records and followed for an average of 30 years. Standardized mortality ratios (SMRs) were calculated to compare the death rates of these women with national rates. The SMR for all causes was 0.90 (95% CI, 0.69-1.17), based on 59 deaths. There were 15 deaths from circulatory disease, yielding an SMR of 0.83 (95% CI, 0.46-1.37). Of these 15 deaths, 13 were from ischemic heart disease (SMR 1.40; 95% CI, 0.75-2.40) and two were from other circulatory disease (SMR 0.23; 95% CI, 0.03-0.85). There were six deaths from diabetes mellitus as underlying or contributory cause, compared with 1.7 expected (odds ratio 3.6; 95% CI, 1.5-8.4). Breast cancer was the commonest cause of death (SMR 1.48 based on 13 deaths; 95% CI, 0.79-2.54). We conclude that women with polycystic ovary syndrome do not have markedly higher than average mortality from circulatory disease, even though the condition is strongly associated with diabetes, lipid abnormalities, and other cardiovascular risk factors. The characteristic endocrine profile of women with polycystic ovary syndrome may protect against circulatory disease in this condition.

Adult↗
PubMed1997

A prospective case-control study of lipoprotein(a) levels and apo(a) size and risk of coronary heart disease in Stanford Five-City Project participants.

Lipoprotein(a) [Lp(a)] is formed by the assembly of LDL particles and a carbohydrate-rich protein, apolipoprotein(a) [apo(a)], which has a high degree of structural homology with plasminogen. While the majority of retrospective studies have found an association between Lp(a) level and cardiovascular disease (CVD), the few prospective studies to date have reported contradictory results. We conducted a nested case-control study using the participants in the Stanford Five-City Project, a long-term CVD prevention trial. Participants with an incident possible or definite myocardial infarction or coronary death were matched to a single control subject for age, sex, ethnicity, residence in a treatment or control city, and time of survey. This process yielded 134 case-control pairs, 90 male and 44 female, for whom plasma was available for analysis of Lp(a). Lp(a) values in nanomoles per liter were determined by an enzyme-linked immunoassay that measures Lp(a) independently of apo(a) size polymorphism. Apo(a) size isoforms were determined by SDS-agarose gel electrophoresis. Median Lp(a) level in male cases was almost double that in control subjects (41.8 versus 21.2 nmol/L; P < .01); in female cases, median Lp(a) was 34% higher than in control subjects (32.5 versus 21.2 nmol/L), but this difference was not statistically significant. Among the male cases, there was an increased frequency of small apo(a) isoforms, while no significant difference was found in apo(a) size between female cases and control subjects. The association between Lp(a) level and case-control status in men was independent of total, HDL, and non-HDL cholesterol levels, as well as apo(a) size isoform, cigarette smoking, blood pressure, and obesity. In men, the most efficient threshold value of Lp(a) concentration for separating cases and control subjects was 35 nmol/L; the odds ratio for being a case above this level compared with below was 2.84 (95% confidence interval: 1.53-5.27, P < .001). This study provides strong evidence that Lp(a) level is a prospective, independent risk factor for developing coronary artery disease in men and indicates that the size of apo(a) may also play a role. The lack of a significant association in women deserves further evaluation in larger studies.

Adolescent↗
PubMed1995

Mortality from coronary heart disease and stroke for six ethnic groups in California, 1985 to 1990.

Coronary heart disease and stroke death rates were compared for six ethnic groups (non-Hispanic white, Hispanic, African-American, Chinese, Japanese, and Asian Indian) by sex and age (25 to 44, 45 to 64, 65 to 84, and 25 to 84 years old) using California census and 1985 to 1990 death data. African-American men and women in all age groups had the highest rates of death from coronary heart disease, stroke, and all causes (except for coronary heart disease in the oldest men). Hispanics, Chinese, and Japanese in all age-sex groups had comparatively low death rates for coronary heart disease and stroke, although stroke was proportionally an important cause of death for Chinese and Japanese groups. Coronary heart disease was an important cause of death for Asian Indians although death rates were generally not higher than those for other ethnic groups. Ethnic differences were most marked for women and younger age groups.

Adult↗
PubMedDate not supplied

Glycemic control and cardiovascular disease in type 2 diabetes: a review.

Cardiovascular disease is the major cause of morbidity and mortality in people with Type 2 diabetes, and risk of atherosclerotic disease is markedly increased in people with diabetes compared to people with normal glucose tolerance. The excess risk can not be completely explained by increased prevalence of other cardiovascular disease risk factors such as hypertension and hyperlipidaemia in people with diabetes. This review examines the role of hyperglycemia and glycemic control in cardiovascular disease in people with Type 2 diabetes. The results of prospective observational studies and randomized controlled trials are summarized. We conclude that control of hypertension and hyperlipidemia are important to reduce risk of cardiovascular disease in people with diabetes and may be more easily achieved than tight glycemic control.

Cardiovascular Diseases↗
PubMedDate not supplied

Lipoprotein(a) in health and disease.

Elevated plasma levels of Lp(a) do seem to influence the progression of atherosclerosis. Evidence is emerging that certain apo(a) isoforms may be more atherogenic than others, and in transgenic mice free apo(a) has been shown to be associated with accelerated atherosclerosis. Currently it is not known whether treating elevated Lp(a) levels will reduce progression of atherosclerosis and, as therapeutic options are limited, mass screening of Lp(a) levels in populations is not indicated. The presence of raised Lp(a) levels, however, warrants aggressive treatment to reduce other cardiovascular risk factors. Continuing research to investigate the relationship of the apo(a) gene to other genes, including the plasminogen gene and apo(a)-related genes, will add further information pertaining to the evolution, function, regulation and clinical implications of Lp(a).

Arteriosclerosis↗