Serum lipids, apoproteins and nutrient intake in rural Cretan boys consuming high-olive-oil diets

A high intake of olive oil has produced high levels of high-density and low levels of low-density lipoprotein cholesterol in short-term dietary trials. To investigate long-term effects of olive oil we have studied the diet and serum lipids of boys in Crete, where a high olive oil consumption is the norm. Seventy-six healthy rural Cretan boys aged 7–9 years were studied. The diet was assessed by a 2-day dietary recall. Blood was collected according to a standardized protocol and sera were analyzed in a rigidly standardized laboratory. The mean daily intake of energy was 11.0 MJ (2629 kcal). The intake of fat (45.0% of energy) and oleic acid (27.2% of energy) was high, and that of saturated fat low (10.0% of energy), reflecting a high consumption of olive oil. The high consumption of olive oil was confirmed by a high proportion of oleic-acid (27.1 %) in serum cholesteryl fatty acids. Mean concentration of serum total cholesterol was 4.42 mmol 1−1 (171 mg dl−1 ), of HDL-cholesterol 1.40 mmol 1−1 (54 mg dl−1), of serum triglycerides 0.59 mmol I−1 (52 mg dl−1 ), of apo-A1 1210 mg 1−1 and of LDL apo-B 798 mg 1−1. The body mass index of the Cretan boys (18.2 kg m−2) was on average 2 kg m−2 higher than that of boys from other countries. Contrary to our expectation, the Cretan boys did not show a more favourable serum lipoprotein pattern than boys from more westernized countries studied previously using the same protocol. Our hypothesis that a typical, olive-oil-rich Cretan diet causes a relatively high HDL- to total cholesterol ratio is not supported by the present findings

Family resemblance for plasma lipids and lipoprotein concentrations in blacks. Cincinnati Lipid Research Clinic Family Study.

Our specific aim in this study was to assess the family resemblance for lipids and lipoproteins in blacks randomly selected from the Princeton School District's Family Study cohort, and compare the family resemblance of lipids and lipoproteins between the blacks and whites from the same cohort. There were 160 white and 59 black nuclear families ascertained through randomly selected family study probands. Familial correlations were estimated by the method of maximum likelihood. Father-child and sib-sib correlations were of larger magnitude in whites than blacks for each lipid and lipoprotein, with the exception of high density lipoprotein cholesterol, where the correlations in blacks were higher than in whites. Estimates of genetic heritability were larger in whites than in blacks for each lipid and lipoprotein, with the exception of high density lipoprotein cholesterol. Whereas environment has a substantial effect on high density lipoprotein cholesterol levels in both blacks and whites, there may be a greater genetic effect accounting for higher levels of high density lipoprotein cholesterol in blacks. This is highlighted in our current study by the consistent observation in blacks of increased measures of within-family resemblance for high density lipoprotein cholesterol alone, of all lipids and lipoproteins.</jats:p

The Cincinnati Lipid Research Clinic family study: Bivariate path analyses of lipoprotein concentrations

SUMMARYMethods for the analysis of the joint transmission of two phenotypes are described and used to determine the extent to which lipoprotein concentrations share a common genetic and/or environmental background. Analysis of data on 160 Caucasian nuclear families revealed that the observed phenotypic association between high-density cholesterol (HDL) and low-density cholesterol (LDL) could be accounted for in terms of common family environmental effects alone (estimated genetic correlation, ρG = −0·132±0·136; estimated residual environmental correlation, ρR = 0·065±0·230). The association between HDL and very-low-density cholesterol (VLDL) could not be accounted for in terms of family environmental effects alone. For HDL and VLDL the residual environmental correlation was significant while the genetic correlation was not (ρG = −0·111±0·214, ρR = −0·421±0·172). The correlation between LDL and VLDL also could not be accounted for in terms of common family environmental effects alone, although here a genetic relationship appears to be the important factor (ρG = 0·330±0·192, ρR = 0·010±0·217).</jats:p