Circadian clock gene variants and their link with chronotype, chrononutrition, sleeping patterns and obesity in the European prospective investigation into cancer and nutrition (EPIC) study

Aug 12, 2022Clinical nutrition (Edinburgh, Scotland)

Circadian clock gene differences linked to daily timing preferences, eating habits, sleep patterns, and obesity in a European health study

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Abstract

The variant rs2735611 in the PER1 gene is associated with an 11.6% decrease in long-term weight gain.

Three variants of the CLOCK gene are linked to a ∼20% decrease in waist circumference gain.
After adjusting for multiple comparisons, significant associations were only observed for waist-to-hip ratio with specific CLOCK gene variants.
No significant associations were found between genetic variants and chrononutrition variables, chronotype, or sleep duration/quality.
A weighted genetic risk score is associated with an evening/late chronotype and an increased risk of overweight/obesity in both early and late adulthood.
The odds of being overweight or obese are approximately 2.2 times higher for individuals with an evening chronotype compared to those with a normal weight.

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BACKGROUND & AIMS: The circadian clock is involved in the control of daily rhythms and is related to the individual's chronotype, i.e., the morningness-eveneningness preference. Knowledge is limited on the relationship between circadian genes, chronotype, sleeping patterns, chronutrition and obesity. The aim was to explore these associations within the EPIC-Spain cohort study.

METHODS: There were 3183 subjects with information on twelve genetic variants of six genes (PER1, PER2, PER3, CRY1, NR1D1, CLOCK). Their association was evaluated with: chronotype and sleeping duration/quality (assessed by questionnaires), chrononutrition (number of meals and timing of intake assessed by a diet history), and also anthropometric measures of obesity at early and late adulthood (in two points in time), such as weight and waist circumference (assessed by physical measurements). Multivariable logistic and linear regression as well as additive genetic models were applied. Odds ratios (ORs), β coefficients, and p-values corrected for multiple comparisons were estimated. Genetic risk scores (GRS) were built to test gene-outcome associations further.

RESULTS: At nominal significance level, the variant rs2735611 (PER1 gene) was associated with a 11.6% decrease in long-term weight gain (per-allele β = -0.12), whereas three CLOCK gene variants (rs12649507, rs3749474 and rs4864548), were associated with a ∼20% decrease in waist circumference gain (per-allele β ∼ -0.19). These and other associations with body measures did not hold after multiple testing correction, except waist-to-hip ratio and rs1801260, rs2070062 and rs4580704 (CLOCK gene). Associations with chrononutrition variables, chronotype and sleep duration/quality failed to reach statistical significance. Conversely, a weighted GRS was associated with the evening/late chronotype and with all other outcomes (p < 0.05). The chronotype-GRS was associated with an increased overweight/obesity risk (vs normal weight) in both early and late adulthood (OR = 2.2; p = 0.004, and OR = 2.1; p = 0.02, respectively).

CONCLUSION: Genetic variants of some circadian clock genes could explain the link between genetic susceptibility to the individual's chronotype and obesity risk.

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Circadian clock gene variants and their link with chronotype, chrononutrition, sleeping patterns and obesity in the European prospective investigation into cancer and nutrition (EPIC) study

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