A recent study has tried to bring to light characteristics that affect longevity, which can help us add years to our lives through diet!

We have dealt with Mendelian randomization and in the past.

In short, the use of human genetic data (as for example in Mendelian randomization) allows the evaluation of possible causal associations by exploiting natural genetic variations so that we can study impartially the risk that may arise from exposure to an agent.

We can therefore say that Mendelian randomization is not subject to many of the biases of observational studies, such as reverse causality or random measurement error, and is less prone to spurious correlations and reverse causality.

So let's see what some of these characteristics are that affect longevity and what we can do to add years to our lives.


Starting with the easy ones, one of the findings was that circulating metabolites such as amino acids are doubtful to be causally related to longevity, which supports the theory that elevated blood concentrations of amino acids result from their defective catabolism in people with metabolic syndrome and type 2 diabetes, as we explained and in a previous article.

Going straight to the part that shows us what interventions we can make to our diet to live longer.

Here we can see the dramatic impact that lipids have on longevity.

All apolipoprotein B-carrying particles (i.e. LDL, VLDL and IDL), or what is not an HDL particle, have a negative impact on longevity, while the contribution of so-called "good cholesterol" is minimal.

Indeed, the findings concerning apolipoprotein B are consistent with previous Mendelian randomization research, which implicates it in many major diseases, including heart disease, stroke and type 2 diabetes.

We move on to the slightly more complex findings:

In this analysis, the only protein that showed a significant association in genome-wide MR studies was haptoglobulin (Hp), which binds free haemoglobin and facilitates its removal from the bloodstream.

Haptoglobin also reduces the oxidation of apolipoprotein E (encoded by the longevity gene APOE which also has links to cognitive decline and Alzheimer's disease), with a previous study finding that exon deletion in HP to be associated with lower LDL-c levels.

It should be noted here that the association between LDL-c, APOE and haptoglobulin may have implications beyond longevity, as the APOE gene also has associations with cognitive decline and Alzheimer's disease.

So, let's try to make sense of the findings and how we can use them to live longer:

  • We need to keep non-HDL cholesterol levels low. It is proven that saturated and trans fats are the ones that affect it the most, with dietary cholesterol following.
  • We need to keep haemoglobin levels relatively low, but obviously within normal limits. This can be achieved by moderating iron from the diet, mainly from animal sources, as plant sources of iron are usually not as bioavailable.

-Suprastratum: The authority on health, fitness and nutrition

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Author: Nick Krontiris

Founder, Suprastratum

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