Does height modify the risk of angina associated with economic adversity?

Adult height partly reflects childhood exposures, and we hypothesise that some exposures impairing growth may also increase susceptibility to coronary heart disease--angina pectoris (angina)--risks, such that shorter adults may be more susceptible to some exposures in adulthood that are risks for heart disease. This hypothesis is tested among all adults who participated in the National Health Interview Survey (USA), 1997-2000 [The National Health Survey, 1997-2000. Data file documentation, National Health Interview Survey (machine-readable data file and documentation). National Center for Health Statistics, Hyattsville, Maryland, ]. In the entire study population, height was negatively associated with angina and after adjustment for potential confounding factors; the odds ratio (and 95% confidence interval) for angina risk associated with the tallest height fifth compared with the shortest fifth is 0.77 (0.97, 0.88). The association of low income (less than US 20,000 dollars) with angina was assessed separately in each of five height strata defined by fifths of the height distribution. The magnitude of this association is lower in the shortest than the tallest height fifth, with odds ratios of 1.18 and 1.60, respectively (effect modification). The unexpected results may be explained by the following: childhood adversity resulting in shorter stature may confer resilience against adult economic adversity; the relative disadvantage of low income may be perceived more keenly by those of taller stature thereby increasing stress and thus disease risk; or health-promoting characteristics associated with taller stature may be less effective in the face of adult economic adversity in the low-income group.     

Wealth, inequality, and insolation effects across the 19th century white US stature distribution

Sources associated with 19th century stature variation have been widely considered. Using US state prison records and robust statistics, this paper illustrates that 19th century US white statures were positively associated with a broad combination of wealth, equality, and environmental characteristics. Individuals from geographic areas characterized by low wealth and high inequality had shorter statures. After controlling for various factors, direct sunlight – the primary source of vitamin D – was also positively associated with stature. After controlling for wealth, inequality, and insolation, farmers were taller than workers in other occupations. These wealth, insolation, and socioeconomic relationships are significant across the stature distribution.     

Catch-up growth in females born short for gestational age reduces the risk of giving birth to short-for-gestational-age infants

OBJECTIVES: The aim of the present study was to study the effect of catch-up growth on the offspring's length at birth among females born short for gestational age. METHODS: Data of 1,363 females born short for gestational age (<-2 standard deviation scores) were obtained from the Swedish Birth Register. The females were included in the register both as babies and mothers. The effect of catch-up growth on the offspring's birth length was studied. RESULTS: Short adult stature was associated with a threefold increase in the risk of giving birth to a short infant [OR 3.08 (CI 1.73-5.50)] and smoking increased the risk in a dose-dependent manner. Overweight was associated with a reduced risk [OR 0.46 (CI 0.22-0.96)] of giving birth to a short infant. CONCLUSION: Catch-up growth to normal adult stature among women born short for gestational age is associated with a reduced risk of giving birth to a short-for-gestational-age infant.     

Scaling Vo2 Peak in Obese and Non‐obese Girls

Objective: The conventional ratio method (milliliters O₂ per mass) typically is used to express Vo ₂ peak. The goal of the current study was to compare Vo ₂ peak of obese girls with normal‐weight girls by ratio and allometric scaling methods. Research Methods and Procedures: We compared Vo ₂ peak by ratio and allometric methods in 46 obese and 47 normal‐weight girls. Indirect calorimetry was used to measure Vo ₂ peak during either treadmill running or walking. Regression analysis was used to determine coefficients for mass and stature for each group with ANOVA used to compare data between groups. Results: The obese girls were taller and had higher values of body fatness (p ≤ 0.05). Absolute Vo ₂ peak (liters per minute) was similar between groups ; however Vo ₂ peak relative to mass was 50% lower (p ≤ 0.05) in the obese girls. When Vo ₂ peak (milliliters per minute per kilogram) and mass were correlated, r = ?0.48 was found in the obese group. Allometric scaling of logarithmic transformed stature and mass reduced this to r = ?0.002, thus eliminating the bias associated with the ratio method. Adjusting Vo ₂ peak allometrically scaled for mass, stature, and the combination of mass and stature reduced the difference between groups from 50% (ratio method) to 10% to 11% (p ≤ 0.05) with higher values found in the normal‐weight girls. Discussion: These results demonstrate the bias associated with the ratio method when comparing Vo ₂ peak in obese girls with Vo ₂ peak in normal‐weight girls. Allometric scaling eliminated the bias and thus may reflect a truer comparative response.     

Some aspects of secular changes in Hungary over the twentieth century

Growth and maturation are considered the most reliable indicators of health status. Their progression rates in turn are strongly influenced by nutrition and socio-economic status, a well-documented relationship. The pattern of the so-called positive secular changes, i.e. the increase in size and earlier maturation, fits the populations' historical model of economic development very well. The historical, political and economic changes occurring in this century in Hungary have had a remarkably strong impact. Until World War I Hungary was an agrarian part of the Austro-Hungarian monarchy, its ethnic composition was most variegated. Both World Wars caused fundamental changes, namely in respect of post-war Hungary they were associated with marked territorial losses and considerable population mobility. In interpreting the developmental differences in the data collected before and after these wars one should take account of the important facts that, in addition to the changes in socio-economic conditions, affected the gene pool of the populations in Hungary. Over the past 100 years profound changes have occurred in the mean body size, growth rate and timing of maturation of the country's population. This paper is a brief analytic summary of the tendencies observed in adult stature, maturation and some socio-economic conditions. It also compares the cohorts of sub-populations as reflected by the reviewed reports. In summarizing the change in adult stature estimated by the data on recruits, soldiers and students of higher education, it could be stated that adult mean stature had become markedly taller in Hungary since the end of the fifties. However, any estimation of the absolute increment and the exact rate is severely biased by the variable character of the samples' representativeness. Similar problems arose in dealing with sexual maturation, because the retrospective and status-quo methods of assessment were found incomparable. Nevertheless, menarche was observed to have shifted to an appreciably younger age lately, a trend that by the end of the 20th century seemed to have reached a more or less stable level.     

Saturated fat intake and alcohol consumption modulate the association between the APOE polymorphism and risk of future coronary heart disease: a nested case-control study in the Spanish EPIC cohort

The association is still not clear between the common APOE polymorphism and coronary heart disease (CHD) risk, nor its modulation by diet. Thus, our aim was to study the association between the APOE genotypes and incident CHD and how dietary fat and alcohol consumption modify these effects. We performed a nested case-control study in the Spanish European Prospective Investigation into Cancer and Nutrition cohort. Healthy men and women (41?440, 30-69 years) were followed up over a 10-year period, with the incident CHD cases being identified. We analyzed 534 incident CHD cases and 1123 controls. APOE, dietary intake and plasma lipids were determined at baseline. The APOE polymorphism was significantly associated with low-density lipoprotein cholesterol (LDL-C), and gene-alcohol interactions in determining LDL-C were detected. In the whole population, the E2 allele was significantly associated with a lower CHD risk than E3/E3 subjects [odds ratio (OR), 0.58; 95% confidence interval (CI), 0.38-0.89]. The E4 allele did not reach statistical significance vs. E3/E3 (OR, 1.17; 95% CI, 0.88-1.58). However, saturated fat intake modified the effect of the APOE polymorphism in determining CHD risk. When saturated fat intake was low (<10% of energy), no statistically significant association between the APOE polymorphism and CHD risk was observed (P=.682). However, with higher intake (≥10%), the polymorphism was significant (P=.005), and the differences between E2 and E4 carriers were magnified (OR for E4 vs. E2, 3.33; 95% CI, 1.61-6.90). Alcohol consumption also modified the effect of the APOE on CHD risk.In conclusion, in this Mediterranean population, the E2 allele is associated with lower CHD risk, and this association is modulated by saturated fat and alcohol consumption.     

The allometry of metabolism and stature: Worker fatigue and height in the Tanzanian labor market

If the positive wage–height correlation is at least partially biological in origin, one plausible pathway is the effect of stature on energy expenditure in individuals. If metabolism scales proportionately with stature, then relative to short individuals, taller individuals can produce more energy for a given work task. This also suggests that end-of-the-workday fatigue, or lack of energy, varies inversely with stature. We test this hypothesis with data from the 2004 Tanzanian Household Worker Survey in which workers report the extent of their fatigue at the end-of-the-workday. Ordinal latent variable parameter estimates reveal that relative to short workers, taller workers are less likely to report being tired at the end-of-the-workday. This suggests that the positive wage–height relationship also has a biological foundation whereby the energy requirements and metabolic costs associated with work effort/tasks are inversely related to stature.     

Associations of Serum Ca and Mg Levels with Mental Health in Adult Women Without Psychiatric Disorders

Several lines of evidence from previous studies suggest that Calcium (Ca) and Magnesium (Mg) may be involved in intracellular and interneuronal processes associated with affective disorders. However, there have been inconsistent results on the effect of Ca and Mg on depressive mood disorder. This cross-sectional study was conducted to determine whether serum Ca and Mg levels, as well as serum Ca/Mg ratio, are associated with mental health in relatively healthy, adult women without psychiatric disorders. One hundred and twelve adult women were recruited from the outpatient clinic in a university hospital setting. Serum Ca and Mg levels were measured and indicators of mental health such as depression, anxiety, and stress were evaluated using two validated questionnaires; the Hospital Anxiety Depression Scale and the Modified Brief Encounter Psychosocial Instrument Stress Scale. After categorizing the serum Ca and Mg levels, and the Ca/Mg ratio into tertiles, the mean scores on each mental health scale were compared using analysis of covariance. The risk of depressive mood disorder according to the tertiles of serum Mg level and serum Ca/Mg ratio was assessed using logistic regression analysis. Women in the middle tertile of serum Ca/Mg ratio had significantly lower scores on depression and stress scales (p = 0.004 and p = 0.007, respectively) and a lower odds ratio (OR) for the risk of depressive mood disorder (OR = 0.31, CI_95% 0.10–0.93) than those in the highest tertile. The OR for the risk of depressive mood disorder was higher in women in the lowest tertile of serum Mg than in those in the highest tertile (OR = 3.92, CI_95% 1.11–13.83). Serum Mg level and serum Ca/Mg ratio may be involved in the mechanism for the progression of depressive mood or stress perception in relatively healthy, adult women.     

Influence of Maternal Height and Weight on Low Birth Weight: A Cross-Sectional Study in Poor Communities of Northeastern Brazil

Background

Low birth weight (LBW) is associated with an increased risk of mortality, adverse metabolic conditions, and long-term chronic morbidities. The relationship between LWB and short maternal stature coupled with nutritional status was investigated in poor communities.

Methods/Principal Findings

A cross-sectional population-based study involving 2226 mother-child pairs was conducted during the period 2009-2010 in shantytowns of Maceió, Alagoas, Brazil. Associations between LBW and maternal sociodemographics, stature and nutritional status were investigated. The outcome variable was birth weight (< 2500g and ≥ 2500g). The independent variables were the age, income, educational background, stature and nutritional status (eutrophic, underweight, overweight and obese) of the mother. The frequency of LBW was 10%. Short-statured mothers (1^st quartile of stature ≤ 152cm) showed a tendency of increased risk of LBW children compared to mothers in the 4^th quartile of stature (>160.4cm) (OR: 1.42, 95% CI: 0.96 - 1.09, p = 0.078). Children from short-statured mothers weighed an average of 125g less than those from taller mothers (3.18±0.56kg vs. 3.30±0.58kg, respectively p = 0.002). Multivariate analyses showed that short stature, age < 20y (OR: 3.05, 95% CI:1.44 - 6.47) or were underweight (OR: 2.26, 95% CI:0.92 - 5.95) increased the risk of LBW, while overweight (OR: 0.38, 95% CI:0.16 - 0.95) and obesity (OR: 0.39, 95% CI:0.11 - 1.31) had lower risk for LBW. In taller mothers, lower income and underweight were associated with LBW (OR: 1.88, 95% CI: 1.07 - 3.29 and 2.85, 95% CI:1.09 - 7.47, respectively), and obese mothers showed a trend of increased risk of LBW (OR: 1.66, 95% CI:0.84 - 3.25).

Conclusions/Significance

Overweight was found to have a protective effect in short-statured mothers, indicating that a surplus of energy may diminish the risk of LBW. Short-statured younger mothers, but not taller ones, showed higher risk of LBW. The mother being underweight, regardless of stature, was associated with LBW.     

Leptin and coronary heart disease risk: prospective case control study of British women

Objective: Prospective studies have shown a positive association between leptin concentrations and coronary heart disease (CHD) in men, but its effect in women is unclear. Our objective was to examine the association of serum leptin levels with CHD in a prospective study of women. Research Methods and Procedures: We conducted a prospective (4 year) case (N = 165) control (N = 335) study nested within a cohort of 4286 British women. Results: With mutual adjustment for each other and age, social class, smoking, and physical activity, leptin was positively associated with BMI, fasting insulin, total cholesterol, low‐density lipoprotein‐cholesterol, triglycerides, and hypertension and was inversely associated with homeostasis model assessment insulin sensitivity. Leptin was not associated with CHD risk (age‐adjusted relative risk for a doubling of leptin: 1.08 [95% confidence interval (CI): 0.91, 1.29]). This changed little with adjustment for childhood and adult social class, smoking, alcohol, and physical activity but attenuated to 1.00 (95% CI: 0.80, 1.26) with further adjustment for other metabolic risk factors (waist‐to‐hip ratio, low‐density lipoprotein‐cholesterol, triglycerides, C‐reactive protein, fasting insulin, hypertension). Discussion: We found no strong statistical evidence that leptin is associated with CHD risk in this study population of older British women. Further research is needed to compare associations of leptin with CHD in men and women and to determine whether the effect varies by gender.     

Long-term interleukin-6 levels and subsequent risk of coronary heart disease: two new prospective studies and a systematic review

Background

The relevance to coronary heart disease (CHD) of cytokines that govern inflammatory cascades, such as interleukin-6 (IL-6), may be underestimated because such mediators are short acting and prone to fluctuations. We evaluated associations of long-term circulating IL-6 levels with CHD risk (defined as nonfatal myocardial infarction [MI] or fatal CHD) in two population-based cohorts, involving serial measurements to enable correction for within-person variability. We updated a systematic review to put the new findings in context.

Methods and Findings

Measurements were made in samples obtained at baseline from 2,138 patients who had a first-ever nonfatal MI or died of CHD during follow-up, and from 4,267 controls in two cohorts comprising 24,230 participants. Correction for within-person variability was made using data from repeat measurements taken several years apart in several hundred participants. The year-to-year variability of IL-6 values within individuals was relatively high (regression dilution ratios of 0.41, 95% confidence interval [CI] 0.28–0.53, over 4 y, and 0.35, 95% CI 0.23–0.48, over 12 y). Ignoring this variability, we found an odds ratio for CHD, adjusted for several established risk factors, of 1.46 (95% CI 1.29–1.65) per 2 standard deviation (SD) increase of baseline IL-6 values, similar to that for baseline C-reactive protein. After correction for within-person variability, the odds ratio for CHD was 2.14 (95% CI 1.45–3.15) with long-term average (“usual”) IL-6, similar to those for some established risk factors. Increasing IL-6 levels were associated with progressively increasing CHD risk. An updated systematic review of electronic databases and other sources identified 15 relevant previous population-based prospective studies of IL-6 and clinical coronary outcomes (i.e., MI or coronary death). Including the two current studies, the 17 available prospective studies gave a combined odds ratio of 1.61 (95% CI 1.42–1.83) per 2 SD increase in baseline IL-6 (corresponding to an odds ratio of 3.34 [95% CI 2.45–4.56] per 2 SD increase in usual [long-term average] IL-6 levels).

Conclusions

Long-term IL-6 levels are associated with CHD risk about as strongly as are some major established risk factors, but causality remains uncertain. These findings highlight the potential relevance of IL-6–mediated pathways to CHD.     

Levels of apolipoprotein M are not associated with the risk of coronary heart disease in two independent case-control studies

Apolipoprotein M (apoM), a 25 kDa plasma protein belonging to the lipocalin protein family, is predominantly associated with HDL. Studies in mice have suggested apoM to be important for the formation of pre-beta-HDL and to increase cholesterol efflux from macrophage foam cells. Overexpression of human apoM in LDL receptor-deficient mice reduced the atherogenic effect of a cholesterol-rich diet. The aim of the present study was to investigate whether the apoM levels in man predict the risk for coronary heart disease (CHD). ApoM was measured in samples from two separate case-control studies. FINRISK '92 consisted of 255 individuals, of whom 80 developed CHD during follow-up and 175 were controls. The Copenhagen City Heart Study included 1,865 individuals, of whom 921 developed CHD during follow-up and 944 were controls. Correlation studies of apoM concentration with several analytes showed a marked positive correlation with HDL and total cholesterol as well as with apoA-I and apoB. There was no significant difference in mean apoM level between CHD and control subjects in either study. In conditional logistic regression analyses, apoM was not a predictor of CHD events, [odds ratio (95% CI) 0.97 (0.74-1.27) and 0.92 (0.84-1.02), respectively]. In conclusion, no association between apoM and CHD could be found in this study.     

Insight into the role of CYBA A640G and C242T gene variants and coronary heart disease risk. A case-control study

The CYBA gene variants have been inconsistently associated with coronary heart disease (CHD) risk. A case-control study was conducted genotyping 619 subjects to explore the contribution of C242T and A640G to CHD risk in the population. A significant risk was found associated with GG homozygosity (odds ratio (OR) 2.132, 95% confidence interval, 1.113-4.085). The C242T variant was associated with CHD risk in women. Bias due to population stratification was analysed. Phenotype changes linked to these polymorphisms were evaluated. Superoxide measurements revealed higher production as indicated by the presence of the G and T alleles. Differences in mRNA concentration in heterozygous A640G samples were analysed. Higher levels of G allele mRNA compared with A allele mRNA were found. NAD(P)H oxidase p22phox sub-unit expression was evaluated with Western blot. Experiments revealed a gradual relationship in p22phox protein expression according to genotypes of the analysed variants. Those GG TT double homozygous showed increased p22phox protein expressions regarding AA CC double homozygous. This study has demonstrated increased expression and activity of the NAD(P)H system components during atherogenesis and the results could help explain the relevance of the A640G variant as a CHD marker.     

Instability of the insertional mutation inCftr TgH(neoim)Hgu cystic fibrosis mouse model

Background

There have been inconsistent results from case-control studies assessing the association of the PON1 Q192R polymorphism with coronary heart disease (CHD). Most studies have included predominantly men and the association in women is unclear. Since lipid levels vary between the sexes the antioxidant effect of PON1 and any genes associated with it may also vary by sex. We have examined the association of the PON1 Q192R polymorphism with CHD in a large cohort of British women and combined the results from our cohort study with those from all other published studies.

Results

The distribution of genotypes was the same among women with CHD and those without disease. The odds ratio (95% confidence interval) of having CHD comparing those with either the QR or RR genotype to those with QQ genotype (dominant model of association) was 1.03 (0.89, 1.21) and the per allele odds ratio was 0.98 (0.95, 1.01). In a meta-analysis of this and 38 other published studies (10,738 cases and 17,068 controls) the pooled odds ratio for the dominant effect was 1.14 (1.08, 1.20) and for the per allele effect was 1.10 (1.06, 1.13). There was evidence of small study bias in the meta-analyses and the dominant effect among those studies with 500 or more cases was 1.05 (0.96, 1.15). Ethnicity and reporting of whether the genotyping was done blind to the participants clinical status also contributed to heterogeneity between studies, but there was no difference in effect between studies with 50% or more women compared to those with fewer women and no difference between studies of healthy populations compared to those at high risk (with diabetes, renal disease of familial hypercholesterolaemia).

Conclusion

There is no robust evidence that the PON1 Q192R polymorphism is associated with CHD risk in Caucasian women or men.     

GSTT1 null genotype contributes to coronary heart disease risk: a meta-analysis

Many studies have investigated the association between glutathione S-transferase T1 (GSTT1) null genotype and risk of coronary heart disease (CHD), but the impact of GSTT1 null genotype on CHD is still unclear owing to the obvious inconsistence among those studies. This study aims to quantify the strength of association between GSTT1 null genotype and risk of CHD. We searched the PubMed, Embase and Wangfang databases for studies relating the association between GSTT1 null genotype and risk of CHD. We estimated summary odds ratio (OR) with their 95 % confidence interval (95 % CI) to assess the association. 24 case-control studies with 13, 884 CHD cases and 30, 719 controls were included into this meta-analysis. Meta-analysis of total 24 studies showed GSTT1 null genotype was not associated risk of CHD (random-effects OR = 1.17, 95 % CI 0.97-1.42, P = 0.101). After adjustment for heterogeneity, meta-analysis showed GSTT1 null genotype was associated increased risk of CHD both in total population and Caucasians (for total population, fixed-effects OR = 1.12, 95 % CI 1.05-1.21, P = 0.001; for Caucasians, fixed-effects OR = 1.10, 95 % CI 1.02-1.19, P = 0.010). There was no significant association in the other populations. No evidence of publication bias was observed. Meta-analyses of available data suggest the GSTT1 null genotype contributes to increased risk of CHD in Caucasians.     

Lifecourse Adversity and Physical Performance across Countries among Men and Women Aged 65-74

Background

This study examines the associations between lifecourse adversity and physical performance in old age in different societies of North and South America and Europe.

Methods

We used data from the baseline survey of the International Study of Mobility in Aging, conducted in: Kingston (Canada), Saint-Hyacinthe (Canada), Natal (Brazil), Manizales (Colombia) and Tirana (Albania). The study population was composed of community dwelling people between 65 and 74 years of age, recruiting 200 men and 200 women at each site. Physical Performance was assessed with the Short Physical Performance Battery (SPPB). Economic and social adversity was estimated from childhood adverse events, low education, semi-skilled occupations during adulthood and living alone and insufficient income in old age.

Results

A total of 1995 people were assessed. Low physical performance was associated with childhood social and economic adversity, semi-skilled occupations, living alone and insufficient income. Physical performance was lower in participants living in Colombia, Brazil and Albania than in Canada counterparts, despite adjustment for lifecourse adversity, age and sex.

Conclusions

We show evidence of the early origins of social and economic inequalities in physical performance during old age in distinct populations and for the independent and cumulative disadvantage of low socioeconomic status during adulthood and poverty and living alone in later life.     

Height, wealth, and health: An overview with new data from three longitudinal studies

This overview, based on a literature review and new data from the three cohorts (Whitehall Studies I and II, and the Vietnam Experience Study), has four objectives: (a) to outline the major determinants of height, so providing an indication as to what exposures this characteristic may capture; (b) to summarise, by reviewing reports from large scale studies, the relation between adult height and a range of disease outcomes – both somatic and psychiatric – with particular emphasis on coronary heart disease (CHD) and stroke; (c) to discuss why these relationships may exist, in particular, the role, if any, of socioeconomic position in explaining the apparent associations; and, finally (d) to outline future research directions in this field.The large majority of evidence for predictors of height, and its health consequences, comes from observational studies. While genetic predisposition is a major determinant of height, secular rises in childhood and adult stature across successive birth cohorts suggest that early life environment also has an important impact. Plausible non-genetic determinants of height include nutrition, illness, socioeconomic status, and psychosocial stress. Evidence for an association between height and a series of health endpoints is accumulating. Thus, shorter people appear to experience increased risk of CHD, and these associations appear to be independent of socioeconomic position and other potentially confounding variables. For stroke, and its sub-types, findings are less clear. In contrast to CHD, some cancers, such as carcinoma of the colorectum, prostate, breast (in women), central nervous system, skin, endometrium, thyroid and blood (haematopoietic) are more common in taller people. While height may be negatively related to the risk of completed suicide, conclusions about the links between stature and other health endpoints is problematic given the paucity of evidence, which should be addressed.Ultimately, for want of better data, investigators in this area have used height as a proxy for a range of pre-adult exposures. In future, research should aim to explore the predictive capacity of direct measures of diet, psychosocial stress, childhood chronic illness and so on, rather than focus on height or its components. The problem is that extended follow-up of child cohorts with such data are required, and studies which hold these data are not currently available, although several are either maturing to the point where they offer sufficient clinical outcomes to facilitate analyses or are in the advanced planning stage.     

Occupational physical activity and risk of coronary heart disease among active and non-active working-women of North Dakota: a Go Red North Dakota Study

Currently less than half of the US adults meet physical activity (PA) recommendations, yet many more are sedentary in their occupations. Sedentary workers may therefore be at elevated risk for coronary heart disease (CHD). Therefore, the objective of the study is to examine the relationship of CHD risk with occupational PA (OCPA) and leisure time PA (LTPA) among working-women. The 10-year CHD risk and relative risk scores were calculated for 642 working-women. Self-report questionnaire determined levels of OCPA and LTPA. Biometric data were directly collected on all women. No direct relationship for OCPA and 'high risk' of CHD was determined. Insufficient LTPA was significantly associated with greater prevalence of 'high risk' of CHD. No dose response relationship was determined with PA and CHD risk. The odds of being 'high risk' were significantly greater for sedentary workers with insufficient LTPA compared to sufficient LTPA. The odds for being 'high risk' were similar among moderately active or heavy working women completing insufficient LTPA compared to women doing sufficient LTPA. For women with sedentary occupations, a sufficient amount of LTPA is essential to reduce CHD risk. Women in moderate to heavy working occupations may be acquiring adequate amounts of PA to minimize CHD risk.     

Inequality in the American South: evidence from the nineteenth century missouri state prison

The use of height data to measure living standards is now a well-established method in economic history. Moreover, a number of core findings in the literature are widely agreed upon. There are still some populations, places and times, however, for which anthropometric evidence remains thin. One example is 19th century African-Americans in US border-states. This paper introduces a new data set from the Missouri state prison to track the heights of comparable black and white men born between 1820 and 1904. Modern blacks and whites come to comparable terminal statures when brought to maturity under optimal conditions; however, whites were persistently taller than blacks in the Missouri prison sample by two centimetres. Throughout the 19th century, black and white adult statures remained approximately constant, while black youth stature increased during the antebellum period.     

The association of C-reactive protein and CRP genotype with coronary heart disease: findings from five studies with 4,610 cases amongst 18,637 participants

Background

It is unclear whether C-reactive protein (CRP) is causally related to coronary heart disease (CHD). Genetic variants that are known to be associated with CRP levels can be used to provide causal inference of the effect of CRP on CHD. Our objective was to examine the association between CRP genetic variant +1444C>T (rs1130864) and CHD risk in the largest study to date of this association.

Methods and Results

We estimated the association of CRP genetic variant +1444C>T (rs1130864) with CRP levels and with CHD in five studies and then pooled these analyses (N = 18,637 participants amongst whom there were 4,610 cases). CRP was associated with potential confounding factors (socioeconomic position, physical activity, smoking and body mass) whereas genotype (rs1130864) was not associated with these confounders. The pooled odds ratio of CHD per doubling of circulating CRP level after adjustment for age and sex was 1.13 (95%CI: 1.06, 1.21), and after further adjustment for confounding factors it was 1.07 (95%CI: 1.02, 1.13). Genotype (rs1130864) was associated with circulating CRP; the pooled ratio of geometric means of CRP level among individuals with the TT genotype compared to those with the CT/CC genotype was 1.21 (95%CI: 1.15, 1.28) and the pooled ratio of geometric means of CRP level per additional T allele was 1.14 (95%CI: 1.11, 1.18), with no strong evidence in either analyses of between study heterogeneity (I² = 0%, p>0.9 for both analyses). There was no association of genotype (rs1130864) with CHD: pooled odds ratio 1.01 (95%CI: 0.88, 1.16) comparing individuals with TT genotype to those with CT/CC genotype and 0.96 (95%CI: 0.90, 1.03) per additional T allele (I²<7.5%, p>0.6 for both meta-analyses). An instrumental variables analysis (in which the proportion of CRP levels explained by rs1130864 was related to CHD) suggested that circulating CRP was not associated with CHD: the odds ratio for a doubling of CRP level was 1.04 (95%CI: 0.61, 1.80).

Conclusions

We found no association of a genetic variant, which is known to be related to CRP levels, (rs1130864) and having CHD. These findings do not support a causal association between circulating CRP and CHD risk, but very large, extended, genetic association studies would be required to rule this out.