My book How Not to Age is all about the mechanisms of aging and how we can affect them through diet and lifestyle.

Can looking at epigenetics, modifiers of gene expression help predict our health span and lifespan?

Watch to find out.

Epigenetics.

The differential expression of genes both establishes the character and function of a cell

and maintains that identity over time through round after round of cell division.

So our heart cell stays a heart cell and divides to make more heart cells instead of skin cells or kidney cells,

even though all of our main cells have the same entire complement of DNA to potentially be anything.

This is accomplished by methylation, chemical markers that silence inappropriate genes in a particular cell. The fidelity of that

maintenance of methylation is good, 97% to 99.9% every division, but not perfect. Over time,

those tiny errors may add up and may help explain why the methylation patterns of identical

twins drift apart as they age.

The epigenetic markers of young identical twins are essentially indistinguishable,

but then diverge over time.

Identical twins have the same DNA, the same genes,

but the difference in gene expression among older identical twin pairs were found to be

about four times greater than those observed in young pairs.

This may result in them each getting different diseases.

An age-related disease like Alzheimer's only has an identical twin concordance rate of about 50%, meaning if one twin gets it, there's only about a coin-flip chance that the other will too, despite identical DNA.

Or even if they do both get it, the disease may manifest decades in part.

Any epigenetic differences that may contribute to differential disease rates may arise

from having different diets and lifestyles, or maybe a result of random epigenetic drift.

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