This indicates that a “one-size fits all” approach to nutrition is perhaps insufficient, and that individualised nutrient guidelines may improve population health. However, in those with the risk (TT) genotype, intakes of greater than the recommended daily allowance (RDA) of folate are associated with a lowering of homocysteine to reference values. As an example, variation in MTHFR C677T genotype leads to alterations in plasma folate status, which can increase the risk of hyperhomocysteinemia, potentially increasing the risk of cardiovascular disease. Prior studies suggest that specific genetic variants may increase susceptibility to certain disease states, but that this increased risk can be reduced or completely mitigated with dietary modification. This has been demonstrated in recent years in studies on gene-diet interactions and the emergence of nutrigenetics, a goal of which is to add a level of personalization to standard nutrition by adjusting it according to genetic variation.

Emerging research suggests that the ability to place obese subjects on a personalised nutrition regime using genetic information may increase both adherence to that diet and subsequent post-diet nutrition, enhancing health outcomes. In terms of dietary interventions, the efficacy of these trials is mixed, with a sizeable proportion of dieters regaining more weight than they initially lose. Ī considerable number of health interventions have been trialled to reduce obesity.

The causes of obesity are not simply the consumption of a greater amount of energy than is utilised instead, obesity is a complex disorder, with many biological, psychological, and sociological factors combining in its development. Obesity is also associated with several health issues, including the development of metabolic syndrome, hypertension, cardiovascular disease, arthritis, and various cancers. Obesity is characterised by excessive fat accumulation, and it is well established that the percentage of the population that is either obese or overweight is rising over time. NCT04330209, Registered, retrospectively registered. This suggests that personalising nutrition has the potential to enhance long-term weight loss and changes in cardiometabolic parameters. However, at 18-month follow up, the personalised nutrition group (lowGI/NG) lost significantly more weight and experienced significantly greater improvements in measures of cholesterol and blood glucose. These findings demonstrate that the ketogenic group experienced enhanced weight loss during the 24-week dietary intervention. Additionally, after the 24-week diet and 18-month follow up the low-GI nutrigenetic diet group had significantly greater (p < 0.0001) improvements in total cholesterol (ketogenic − 35.4 ± 32.2 mg/dl low-GI nutrigenetic − 52.5 ± 24.3 mg/dl), HDL cholesterol (ketogenic + 4.7 ± 4.5 mg/dl low-GI nutrigenetic + 11.9 ± 4.1 mg/dl), and fasting glucose (ketogenic − 13.7 ± 8.4 mg/dl low-GI nutrigenetic − 24.7 ± 7.4 mg/dl). However, at 18-month follow up, the subjects in the low-GI nutrigenetic diet had lost significantly more weight (− 27.5 ± 8.9 kg) than those in the ketogenic diet who had regained some weight (− 19.4 ± 5.0 kg) ( p < 0.0001). 2) After the 24-week diet period, the subjects were monitored for an additional 18 months using standard guidelines for the Keto group vs standard guidelines modified by nutrigenetic advice for the low-Glycaemic Index nutrigenetic diet (lowGI/NG) group. The subjects self-selected whether to follow a standardized ketogenic diet ( n = 53), or a personalised low-glycemic index (GI) nutrigenetic diet utilising information from 28 single nucleotide polymorphisms ( n = 61). The investigators followed 114 overweight and obese subjects from a weight loss clinic in a 2-stage process. There is evidence that the provision of genetic information may enhance long-term weight loss, either by increasing dietary adherence or through underlying biological mechanisms. Many different weight loss interventions have been trialled with mixed efficacy, as demonstrated by the large number of individuals who regain weight upon completion of such interventions. Obesity and its related metabolic disturbances represent a huge health burden on society.

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