Variation in cardiovascular disease risk factors among older adults in the Hunter Community Study cohort: A comparison of diet quality versus polygenic risk score

My Editor’s Pick for September 2022 is this paper by William Reay, Rebecca Haslam, Murray Cairns, George Moschonis, Erin Clarke, John Attia and Clare Collins.

The interplay of diet and other modifiable lifestyle factors and the genetic and epigenetic predispositions of individuals to disease is the crucial process which determines disease risk profiles. For cardiovascular disease ((CVD) the dietary factors which promote or protect against poor outcomes are well-understood and whilst the genetic basis of CVD risk has not been fully elucidated there are some polymorphisms in genes involved in inflammation, fat metabolism and cholesterol transport which are known to confer higher risk of disease.

The study of Reay and colleagues was an analysis of data from a subset (n=1703) of the Hunter Community Study cohort, comprising 3253 Australian men and women aged 55-85 at recruitment (between 2004 and 2007). Across the cohort there were 138 participants self-reporting that they suffered angina, 176 atrial fibrillation, 689 high cholesterol, 758 hypertension, 129 a heart attack and 164 an arterial bypass surgery. The CVD phenotypes data had a large number of missing data points (only 1678 subjects responding).

Participants in the cohort were genotyped and then allocated a polygenic risk score for CVD based upon gene polymorphisms that were known to be associated with unhealthy LDL, HDL and triglyceride profiles. The study analysis considered the associations between the polygenic risk scores and actual CVD phenotypes in the cohort. Diet quality was assessed using the Australian Recommended Food Score (ARFS) which was determined using a 145-item semi-quantitative food frequency questionnaire. 

The study found that associations between polygenic risk scores for lipid metabolism and transport and both measured lipids and 5 of the 6 studied CVD endpoints (all but atrial fibrillation) were robust, whilst in contrast the ARFS had little association with these outcomes. Moreover, the ARFS did not modify the relationship between polygenic risk score and disease outcomes. Whilst at face value the study suggests that the influence of genetics on disease risk significantly outweighs any influence of diet, there are important limitations of the study which limit the scope for this conclusion. First of all, the ARFS data suggest that dietary quality was poor across the whole cohort. In the absence of a wide distribution of diet quality it is difficult to evaluate the relationship of diet with disease endpoints (i.e. without a lot of participants consuming a healthy diet it is impossible to detect the effects of a healthy diet on lipids and CVD outcomes). Despite the ARFS previously having a association with reduced medicare costs, and fewer medications and hospital admissions, this particular diet quality score was not designed to detect nutrients that likely increase CVD risk. The use of this simple but convenient tool may have compromised the power of this study.

One response to “Variation in cardiovascular disease risk factors among older adults in the Hunter Community Study cohort: A comparison of diet quality versus polygenic risk score

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