Mona Jeffreys

Effects of self-reported racial discrimination and deprivation on Māori health and inequalities in New Zealand: cross-sectional study

BACKGROUND Inequalities in health between different ethnic groups in New Zealand are most pronounced between Māori and Europeans. Our aim was to assess the effect of self-reported racial discrimination and deprivation on health inequalities in these two ethnic groups. METHODS We used data from the 2002/03 New Zealand Health Survey to assess prevalence of experiences of self-reported racial discrimination in Māori (n=4108) and Europeans (n=6269) by analysing the responses to five questions about: verbal attacks, physical attacks, and unfair treatment by a health professional, at work, or when buying or renting housing. We did logistic regression analyses to assess the effect of adjustment for experience of racial discrimination and deprivation on ethnic inequalities for various health outcomes. FINDINGS Māori were more likely to report experiences of self-reported racial discrimination in all instances assessed, and were almost ten times more likely to experience discrimination in three or more settings than were Europeans (4.5% [95% CI 3.2-5.8] vs 0.5% [0.3-0.7]). After adjustment for discrimination and deprivation, odds ratios (95% CI) comparing Māori and European ethnic groups were reduced from 1.67 (1.35-2.08) to 1.18 (0.92-1.50) for poor or fair self-rated health, 1.70 (1.42-2.02) to 1.21 (1.00-1.47) for low physical functioning, 1.30 (1.11-1.54) to 1.02 (0.85-1.22) for low mental health, and 1.46 (1.12-1.91) to 1.11 (0.82-1.51) for cardiovascular disease. INTERPRETATION Racism, both interpersonal and institutional, contributes to Māori health losses and leads to inequalities in health between Māori and Europeans in New Zealand. Interventions and policies to improve Māori health and address these inequalities should take into account the health effects of racism.

Ethnic inequalities in cancer survival in New Zealand: linkage study.

We explored the contribution of stage at diagnosis to ethnic disparities in cancer survival in New Zealand. We linked 115811 adult patients with invasive cancer registered on the cancer registry (1994 to 2002) to mortality data. Age-standardized, 5-year relative survival rates were lowest for Maori, intermediate for Pacific people (otherwise known as Pacific Islanders), and highest for non-Maori/non-Pacific people for many cancers. Stage at diagnosis accounted for only part of these differences. Possible factors responsible for ethnic inequalities might include access to specialized cancer services and the quality of care received.

Associations between tooth loss and mortality patterns in the Glasgow Alumni Cohort

Objective: To use data from the Glasgow Alumni Cohort to investigate whether oral health in young adulthood is independently associated with later life cardiovascular disease (CVD) and cancer mortality. Methods and results: Of the original cohort (n = 15 322), 12 631 subjects were traced through the National Health Service Central Register. Of these, 9569 men and 2654 women were 30 years or younger at baseline. During up to 57 years of follow-up, 1432 deaths occurred among subjects with complete data, including 509 deaths from CVD and 549 from cancer. After adjusting for potential confounders, no substantial association was found between the number of missing teeth (as a continuous variable) and all-cause mortality (hazard ratio (HR) for each extra missing tooth  = 1.01; 95% confidence interval (CI) 1.00 to 1.02), CVD mortality (HR = 1.01; 95% CI 0.99 to 1.03) or cancer mortality (HR = 1.00; 95% CI 0.98 to 1.02). When the number of missing teeth was treated as a categorical variable, there was evidence that students with nine or more missing teeth at baseline had an increased risk of CVD (HR = 1.35; 95% CI 1.03 to 1.77) compared with those with fewer than five missing teeth. When the number of missing teeth was transformed using fractional polynomials, there seemed to be a non-linear relation between missing teeth and CVD mortality. Conclusions: Although some evidence was found to support the relation between tooth loss and CVD mortality, causal mechanisms underlying this association remain uncertain.

Body mass index in early and mid-adulthood, and subsequent mortality: a historical cohort study

BACKGROUND: The aim of this study was to investigate the associations between body mass index (BMI) in early and mid-adulthood, and BMI change between these ages, and mortality.METHODS: Historical cohort study of 629 men, who had height and weight measured at the Student Health Service of the University of Glasgow in 1948–1949 (median age 22 y) and who reported their weight in a postal questionnaire in 1963–1966 (median age 38 y). The participants were followed up until April 2002 (mean follow-up: 35 y). During this time, 124 men died, 68 of cardiovascular disease (CVD) and 33 of cancer.FINDINGS: Mean BMI increased from 21.4 kg/m2 (standard deviation (s.d.): 2.2 kg/m2) in early adulthood to 24.2 kg/m2 (s.d.: 3.0 kg/m2) in mid-adulthood. All-cause mortality was associated with being overweight (BMI≥25 kg/m2) at age 22 but not at age 38, adjusted hazard ratio (HR): 1.85 (95% confidence interval (CI) 1.09–3.13) and 1.05 (95% CI: 0.73–1.52), respectively. BMI at age 22 y was more strongly associated with CVD mortality than was BMI at age 38 y, adjusted HR22 y: 2.41 (95% CI: 1.26–4.60) and HR38 y: 1.33 (95% CI: 0.82–2.16). There was no clear relationship between cancer mortality and BMI at either age: HR22 y: 0.68 (95% CI: 0.16–2.91), HR38 y: 0.90 (95% CI: 0.44–1.84), although relatively few men died of cancer in the follow-up period. Similar patterns were seen for obesity (BMI≥30 kg/m2) as for being overweight. Analyses of weight patterns indicated particularly detrimental effects of overweight persisting from early to mid-adulthood.CONCLUSIONS: BMI in early adulthood is positively related to CVD mortality in later life in men. The risk associated with early adulthood adiposity appeared to be greater than that in mid-adulthood. We did not demonstrate an association between weight gain and later mortality. These results reinforce the need to stem the obesity epidemic in children and young adults.

Life course breast cancer risk factors and adult breast density (United Kingdom)

Objective To determine whether risk factors in childhood and early adulthood affect later mammographic breast density. Methods: Subjects were 628 women who attended a medical examination at the University of Glasgow Student Health Service (1948–1968), responded to a questionnaire (2001) and had a screening mammogram in Scotland (1989–2002). Mammograms (median age of 59years) were classified using a six category classification (SCC) of breast density percent. Logistic regression was used to determine associations between risk factors and having a high-risk mammogram (≥25 dense). Results: In multi-variable analyses, high-risk mammograms were associated with parity (adjusted odds ratio (OR) per child: 0.77 (95 confidence interval (CI) 0.61–0.99)), age at first birth, OR per year: 1.05 (0.99–1.11), smoking at university, OR smokers versus non-smokers: 0.58 (0.36–0.92) and body mass index (BMI) while at university, OR per 1kg/m20.75 (0.69–0.82). No associations with SCC were found for age at menarche, birth weight, oral contraceptive (OC) use, height, leg length or exercise at age 20. Conclusions: We confirm previous findings that breast density is affected by reproductive events and some anthropometric measures, however most of the risk factors acting throughout the life course which we examined were not closely related to adult breast density.

Cancer disparities in indigenous Polynesian populations: Māori, Native Hawaiians, and Pacific people

Polynesia consists of several islands that are scattered across a vast triangle in the Pacific, and include New Zealand, Hawaii, and the Pacific islands. There are reported differences in the types of cancer and epidemiologies seen among communities in these islands, the reasons for which are diverse and complex. In this Review, we describe patterns of cancer incidence, mortality, and survival in indigenous populations compared with populations of European origin in Polynesia, and highlight the limited available data for Pacific populations. Additionally, we document the current knowledge of the underlying biology of cancers in these populations, and report risk factors that differ between ethnicities, including smoking, viral infections, and obesity. Disparities in measures of health are highlighted, as are evident differences in knowledge of tumour biology and cancer management between majority and minority populations.

Association between sibship size and allergic diseases in the Glasgow Alumni Study.

Background: Recent epidemiological studies consistently report an inverse association between sibship size and allergic disease, but evidence from individuals born before the 1980s is inconsistent. As information on relative permanence of this finding may offer clues to its biological explanation, the association between sibship size and allergic disease in individuals born between 1918 and 1952 was investigated. Methods: Cross sectional surveys conducted by the Student Health Service at the University of Glasgow (1948–68) provided data on 14 140 men and women aged 16–30 years at the time of examination. The main outcome measures studied were self-reported asthma, eczema-urticaria, and hay fever. Results: A total of 1677 individuals (11.9%) provided a positive history of at least one of the three allergic diseases: 457 (3.2%) asthma, 594 (4.2%) eczema-urticaria, and 885 (6.3%) hay fever. Compared with those without siblings (reference odds ratio = 1), the odds ratios (95% confidence intervals) for having any allergic disease among those with one, two or three siblings were 0.86 (0.75 to 0.99), 0.80 (0.69 to 0.93), and 0.70 (0.60 to 0.83), respectively (ptrend<0.001). Increasing birth order and low socioeconomic position in childhood were associated with a lower risk of allergy. Adjustment for birth order, year of birth, age, sex, socioeconomic position in childhood, and family history of allergy did not materially alter the results. Conclusions: There is a robust inverse association between sibship size and allergic disease even among people born in the first half of the 20th century. These results favour relatively time-independent explanations for this phenomenon (such as the hygiene hypothesis or parity related changes in the intrauterine environment) over new environmental exposures.

Childhood body mass index and later cancer risk: a 50-year follow-up of the Boyd Orr study.

Associations between childhood BMI and adult cancer risk were investigated in a historical cohort study based on the Carnegie (“Boyd Orr”) Survey of Diet and Health in Pre‐War Britain (1937–9). In 14 centres in England and Scotland, children had their height and weight measured. We included 2,347 individuals aged between 2 and 14 years 9 months at the time of measurement, who were traced through the National Health Service Central Register. Relative cancer risk (registration or death) was estimated in relation to age‐ and sex‐specific BMI SD scores. We studied associations with (i) all cancers, (ii) cancer groups stratified according to their relationship to smoking and (iii) certain site‐specific cancers. In the 50 years of follow‐up, 188 men and 192 women developed cancer. There was a 9% increase (95% CI –3 to 22%) in risk of cancer in adulthood per SD increase in BMI measured in childhood. There was no evidence of confounding by childhood or adulthood socioeconomic position, other anthropometric variables, childhood energy intake or birth order. There was a 30% increase (95% CI 10–54%) in risk of smoking‐related cancers per SD increase in childhood BMI. There was no relationship between BMI and cancers not related to smoking. Associations for all cancers and non‐smoking‐related cancers tended to be stronger in children who were measured at an older (>8 years) rather than a younger (≤8 years) age. We conclude that childhood BMI is related to increased risk of cancer in later life, particularly smoking‐related cancers.

Do lifestyle or social factors explain ethnic/racial inequalities in breast cancer survival?

Despite numerous studies documenting ethnic inequalities in breast cancer survival between minority and majority ethnic groups worldwide, reasons for these inequalities remain unclear. The authors performed a systematic review of published literature to identify studies that investigated the explanatory power of smoking, alcohol consumption, body mass index (BMI), and socioeconomic position (SEP) on ethnic inequalities in breast cancer survival. Sixteen studies were included in the review. From 5 studies, the authors found that differences in breast cancer survival between ethnic groups may be in part explained by BMI, but there was little evidence to implicate smoking or alcohol consumption as explanatory factors of this inequality. From 12 studies, the authors found that SEP explains part of the ethnic inequality in all-cause survival but that it was not evident for breast-cancer-specific survival. SEP explains more of the disparities among African-American versus white women in the United States compared with other ethnic comparisons. Furthermore, given social patterning of BMI and other lifestyle habits, it is possible that results for SEP and BMI are measuring the same effect. In this review, the authors make suggestions regarding the role of epidemiology in facilitating further research to better inform the development of effective policies to address ethnic differences in survival.

Socioeconomic inequalities in cancer survival in New Zealand: the role of extent of disease at diagnosis.

We examined socioeconomic inequalities in cancer survival in New Zealand among 132,006 people ages 15 to 99 years who had a cancer registered (1994-2003) and were followed up to 2004. Relative survival rates (RSR) were calculated using deprivation-specific life tables. A census-based measure of socioeconomic position (New Zealand deprivation based on the 1996 census) based on residence at the time of cancer registration was used. All RSRs were age-standardized, and further standardization was used to investigate the effect of extent of disease at diagnosis on survival. Weighted linear regression was used to estimate the deprivation gap (slope index of inequality) between the most and least deprived cases. Socioeconomic inequalities in cancer survival were evident for all of the major cancer sites, with the deprivation gap being particularly high for prostate (−0.15), kidney and uterus (both −0.14), bladder (−0.12), colorectum (−0.10), and brain (+0.10). Accounting for extent of disease explained some of the inequalities in survival from breast and colorectal cancer and melanoma and all of the deprivation gaps in survival of cervical cancer; however, it did not affect RSRs for cancers of the kidney, uterus, and brain. No substantial differences between the total compared with the non-Māori population were found, indicating that the findings were not due to confounding by ethnicity. In summary, socioeconomic disparities in survival were consistent for nearly all cancer sites, persisted in ethnic-specific analyses, and were only partially explained by differential extent of disease at diagnosis. Further investigation of reasons for persisting inequalities is required. (Cancer Epidemiol Biomarkers Prev 2009;18(3):915–21)