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Chrononutrition acknowledges the significant relationship between the human biological clock and metabolism. It is known that the circadian rhythm is closely related to metabolic systems such as; glucose and lipid homeostasis, as well as ghrelin secretion and colonic motility (Hideaki Oike, 2014). Intrinsic to the regulation of the human clock is the expression of a number of genes including; CLOCK, BMA11, PER and CRY (J. Lopez-Minguez, 2016).

This has led to discoveries in the field of nutrigenetics identifying a number of genetic variants associated with chronodisruption – whereby regular circadian rhythms are disrupted by environmental influences such as; shift work, jet lag, too much light exposure at rest times or nocturnal eating. Due to the known link to metabolism, chronodisruption may therefore pose an increased risk of metabolic disorders such as; type 2 diabetes, hypertension and obesity (M.D. Corbalan-Tutaua, 2015).

The most extensively researched variant to date is the CLOCK variant 3111T/C. Many studies have shown a correlation between the minor C allele, chronodisruption and obesity. Notably, a study involving 500 overweight and obese participants showed those carrying the C allele were more likely to sleep less than 6 hours a day and were also more resistant to weight loss efforts (Garaulet M, 2010). This may in part be explained by higher plasma concentrations of the hunger hormone, ghrelin, found in carriers of the C variant (Marta Garaulet C. S.-M.-C., 2011). A stronger hunger signal may affect the ability to comply with a dietary programme and therefore result in resistance to weight loss.

Some promising studies have shown how changing diet and lifestyle behaviours may reduce the deleterious effect of the C variant. For example, the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study showed that the deleterious effect of C variants on waist circumference were only apparent when participants consumed more than 11.8% of energy from saturated fat (Marta Garaulet Y.-C. L.-Q., 2009). Furthermore, it has been found that ‘late eaters’ consuming their mid-day meal typically after 3pm were less likely to lose weight effectively compared to ‘early eaters’ (before 3pm) consuming exactly the same amount of calories in a day (J. Lopez-Minguez, 2016).

These findings pose significance in personalised nutrition treatment, particularly with clients who carry the minor C allele, displaying chronodisruption and struggling to lose weight. Such information provides a more than useful predictor for weight loss treatment and assessing the need for chrononutrition therapy as part of treatment. So far, mindful eating, earlier main meal consumption, earlier bed routine as well as increased physical activity are all possible approaches to provide targetted support to variant carriers.

To find out whether your client would benefit from re-setting their circadian clock to help them to lose weight, why not offer them a Genovive test and fine-tune your approach.


Garaulet M, C. M. (2010). CLOCK gene is implicated in weight reduction in obese patients participating in a dietary programme based on the Mediterranean diet. International Journal of Obesity, Mar;34(3):516-23.

Hideaki Oike, c. a. (2014). Nutrients, Clock Genes, and Chrononutrition. Current Nutrition Reports, 3(3): 204–212.

  1. Lopez-Minguez, P. G.-A. (2016). Circadian rhythms, food timing and obesity. Proceedings of the Nutrition Society.

M.D. Corbalan-Tutaua, P. G.-A. (2015). Toward a chronobiological characterization of obesity and metabolic. Clinical Nutrition, 34; 477-483.

Marta Garaulet, C. S.-M.-C. (2011). Ghrelin, Sleep Reduction and Evening Preference: Relationships to CLOCK 3111 T/C SNP and Weight Loss. PLoS ONE, 6(2): e17435. doi:10.1371/journal.pone.0017435.

Marta Garaulet, Y.-C. L.-Q. (2009). CLOCK genetic variation and metabolic syndrome risk: modulation by monounsaturated fatty acids. American Society for Nutrition, 90(6)1466-1475.