Cross-sectional and longitudinal studies were performed in a rural population living in The Gambia to examine the relationship between several in vitro assays of the host immune response to asexual stages of Plasmodium falciparum and protection from malaria in vivo. Assays included an enzyme-linked immunosorbent assay for antibodies to schizont antigens; an indirect immunofluorescence assay for total antiblood-stage antibodies; an immunofluorescence assay on glutaraldehyde-fixed parasites to detect antibodies to antigen Pf 155; an assay for serum inhibition of red blood cell invasion; a micro-agglutination assay to detect antibodies to neo-antigens on the surface of infected red blood cells; and an assay using polymorphonuclear leucocytes to detect antibodies capable of opsonizing schizont infected red blood cells. There were marked differences in the age-related pattern of response for different assays performed on sera obtained at a cross-sectional survey of 280 individuals. Examination of the correlation between the various immune responses and malariometric indices at the population level and at the individual level provided no evidence that any of the in vitro assays were related to protective immunity. The relationship between in vitro measurements of the anti-malarial immune response and protection from clinical episodes of malaria was examined in a group of 134 children aged 11 years and under who were monitored weekly throughout an entire malaria transmission season. The only immune factor to show a consistent protective effect against clinical malaria was the titre of antibodies to neo-antigens on the infected erythrocyte surface (P = 0.01). The same longitudinal techniques were used to examine the effect of two non-immunological factors, sickle cell trait and mosquito net usage, both of which showed significant protection against clinical episodes and malaria.

A ten-year community survey was undertaken to investigate the high coronary heart disease (CHD) incidence among people of Indian (South Asian) descent in Trinidad, West Indies. Of 2491 individuals aged 35-69 years, 2215 (89%) were examined and 2069 (83%) found to be clinically free of CHD at baseline. After exclusion of 71 of minority ethnic groups, 786 African, 598 Indian, 147 European and 467 adults of Mixed descent were followed for CHD morbidity and mortality. In both sexes, adults of Indian origin had higher prevalence rates of diabetes mellitus, a low concentration of high-density lipoprotein (HDL) cholesterol, and recent abstinence from alcohol than other ethnic groups. Indian men also had larger skinfold thicknesses than other men. In participants free of CHD at entry, the age-adjusted relative risk of a cardiac event believed due to CHD was at least twice as high in Indian men and women as in other ethnic groups. In men, blood pressure, diabetes mellitus and low-density lipoprotein (LDL) cholesterol concentration were positively and independently related to risk of CHD, whereas alcohol consumption and HDL cholesterol concentration were inversely associated with risk after allowing for age and ethnic group. The ethnic contrasts in CHD persisted when these characteristics were taken into account. In the smaller sample of women, only ethnic group was predictive of CHD as defined. The failure of point estimates of risk to explain the high CHD incidence in Indians calls for focus on age of onset of risk and examination of other potential risk factors such as insulin concentration.

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