Circadian rhythms, food timing and obesity

• Published in: Proceedings of the Nutrition Society Vol. 75; no. 4; pp. 501 - 511
• Main Authors: Lopez-Minguez, J., Gómez-Abellán, P., Garaulet, M.
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 01.11.2016
• Subjects: Animals; Chronic illnesses; Circadian Clocks - genetics; Circadian rhythm; Circadian Rhythm - genetics; Circadian rhythms; Conference on ‘Roles of sleep and circadian rhythms in the origin and nutritional management of obesity and metabolic disease’; DNA methylation; Eating behavior; Epigenesis, Genetic; epigenetics; Feeding Behavior - physiology; genes; Genetic diversity; genetic variation; Genetics; Hormones; Humans; Metabolism; mutants; Mutation; Nutrigenomics; Obesity; Obesity - genetics; Obesity - physiopathology; Pacemakers; Physiology; Polymorphism, Single Nucleotide; Shift work; single nucleotide polymorphism; Society; Symposium 4: Influence of lifestyle and genetics; twins; weight loss; Obesity; Food timing; Circadian rhythm; Nutrigenetic; BMAL1 brain- and muscle ANRT-like protein-1; MetS metabolic syndrome; CRY cryptochrome; PER2 Period 2; CD chronodisruption; CLOCK circadian locomotor output cycles kaput; WT wrist temperature
• ISSN: 0029-6651; 1475-2719; 1475-2719
• DOI: 10.1017/S0029665116000628

It is known that our physiology changes throughout the day and that several physiological hormones display circadian rhythmicity. The alteration of this normal pattern is called chronodisruption (CD). In recent years, it has been demonstrated that CD is related to obesity. Although several factors may be causing CD, one important aspect to consider is the failure in our internal clock. Indeed, studies performed in mutant animals have demonstrated that mutations in clock genes are related to obesity. In human subjects, mutations are rare (<1 % of the population). Nevertheless, it is rather common to have genetic variations in one SNP, which underlie differences in our vulnerability to disease. Several SNP in clock genes are related to obesity and weight loss. Taking into account that genetics is behind CD, as has already been demonstrated in twins’ models, the question is: Are we predestinated? We will see along these lines that nutrigenetics and epigenetics answer: ‘No, we are not predestinated’. Through nutrigenetics we know that our behaviours may interact with our genes and may decrease the deleterious effect of one specific risk variant. From epigenetics the message is even more positive: it is demonstrated that by changing our behaviours we can change our genome. Herein, we propose modifying ‘what, how, and when we eat’ as an effective tool to decrease our genetic risk, and as a consequence to diminish CD and decrease obesity. This is a novel and very promising area in obesity prevention and treatment.