Zoe Nutrition is Wrong About DNA Diets

At GeneFood, we use genetic data to offer customers personalised recommendations on diet and health, informed by the latest genome wide association studies (GWAS).

However, genes are not the only factor that affects our metabolism. It is clear that internal and external environments, such as climate (X), air quality (X), our stress levels (X) and our gut microbiome (X) also play a role.

But how much of an impact do our genes have compared to these other factors? A study (X) in the prestigious journal Nature Medicine attempted to address this question, focusing on the levels of key metabolites: glucose, triglycerides and C-peptide (indicative of insulin secretion) at specific times after having a meal (known as “postprandial” levels).

The director of the PREDICT-1 study, Tim Spector, built a business on the study’s findings, called, Zoe Nutrition.

The “UK Twins” study

To address the contribution of genetics to these traits, the authors took advantage of a large cohort of UK twins. Twin cohorts provide powerful opportunities to study the heritability of a trait – that is, the contribution of genes to the variability of this trait across individuals. This is because in monozygotic twins, the genes are essentially the same, and so most of the observed differences between them are down to non-genetic factors. 

The authors invited study participants to a clinic, where they were given the same meal and had  blood samples taken at regular intervals. They were then sent home and asked to take standardized breakfasts and lunches for another 12 days, while their metabolite levels and gut microbiome were monitored with blood and stool tests.

Based on these data, the authors could estimate the effects of genes on the levels of glucose, insulin and triglyceride following a meal. They found that genetic factors accounted for nearly half (48%) of the variability in how much glucose levels rose 2h after a meal. In contrast, they found that genes explained only ~10% of the variability in how much insulin levels rose at the same time point and none of the variance in triglyceride levels 6h after a meal.

Importantly, this analysis predicted the overall heritability of a trait, but not the specific genetic variants (such as SNPs) that drive it. Looking at a subset of known SNPs for glucose levels that the authors established to be largely heritable, the authors estimated that they explained only a fraction (about 20%) of this heritability. 

Zoe’s Conflict of Interest

The authors thus delivered a rather damning verdict on nutrigenomics and so called, DNA Diets: “The modest heritability of postprandial traits means that, even in an unrealistically optimistic scenario in which most of this trait variance is explained by known DNA variants, it is unlikely that prediction algorithms using DNA variant data alone, which many direct-to-consumer nutrigenomics companies advocate, would succeed”.

What are our thoughts on this statement?

First, it is important to mention an obvious conflict of interest. Many of the study’s authors are affiliated with a consumer health startup. Zoe Nutrition, that provides personalized nutrition services based on the analysis of blood metabolites (fat and sugar), as well as microbiome – but not genetics. 

Given their own commercial interests at Zoe, inserting this statement in a scientific paper is, in my view, totally unacceptable.

Was PREDICT-1 Conclusive?

Focusing on the science, however, it is also hard to say that the study was conclusive.

Measuring postprandial lipids in a precise, reproducible and interpretable way is a more challenging task than for glucose (X), and any flaws in these measurements could reduce the detected heritability. Secondly, even if postprandial lipid levels aren’t particularly heritable (for example, because our gut microbiome plays an important role in how quickly and effectively we digest food), fasting lipid levels certainly are heritable (X; X) and affect the risk of developing cardiovascular disease, which also has a clear genetic component (X).

So lipid levels after a meal may simply not be the easiest or most relevant trait to look at when considering the contribution of our genes to disease risk and how we can reduce it through lifestyle and diet.

The Bottom Line

In conclusion, while it is important to bear in mind that our lipid metabolism depends on many factors, it is in our view incorrect to take our genetic makeup off this list.

In my view, genetic predispositions for cholesterol absorption, saturated fat metabolism, foundational micronutrient deficiency, histamine degradation, basic food sensitivity, carbohydrate response, and many more sit at the foundation of a personalized approach to health and wellness. DNA isn’t the whole story, but does provide valuable insight for those looking in earnest for helpful dietary advice that goes beyond dogma.

And as new associations between genetic variants and metabolic traits are continuously reported through larger, more diverse and better controlled studies (X, X, X, X, X), they become increasingly more precise and interpretable.