What your DNA can tell us

DNA contains information about biological variation. Some genetic variants have well-established biological consequences; others are associated with small changes in the probability of a disease or trait; many have uncertain or no presently useful interpretation.

That distinction matters.

DNA is evidence, not destiny

For most common diseases and complex traits, genetics is only part of the explanation.

Health and longevity can also be influenced by:

• age and sex;
• family history;
• lifestyle and behaviour;
• environment;
• socioeconomic circumstances;
• medical history and treatment;
• interactions among many genes; and
• chance.

A genetic association therefore usually changes probability, not certainty.

Different genetic findings mean different things

Not all genetic evidence has the same character.

Some variants can have comparatively large biological effects. Others make only a small contribution to a complex trait. Still others become meaningful only when combined with many variants or with non-genetic information.

For example, research has identified genetic evidence relating to areas such as:

• lipid metabolism and cardiovascular health;
• glucose regulation and metabolic disease;
• inflammation and immune response;
• thrombosis;
• neurodegenerative disease susceptibility;
• cellular stress response and healthy ageing;
• muscle composition and physical performance;
• medication metabolism; and
• multiple other biological pathways.

Bioanalytix should not interpret these categories as equivalent.

Longevity is especially complex

There is no single "longevity gene."

Some genes and variants — including research involving FOXO3 and APOE — have repeatedly been associated with longevity or age-related outcomes. But human lifespan is a complex phenotype influenced by many genetic and non-genetic factors.

A longevity-associated variant therefore does not tell an individual how long they will live.

Its value to Bioanalytix is as one piece of evidence that may contribute to a broader view of biological and longevity uncertainty.

From individual variants to polygenic evidence

Many common conditions are polygenic: genetic susceptibility is distributed across large numbers of variants, each often contributing only a small effect.

Genome-wide association studies, or GWAS, search across the genome for statistical associations between variants and traits. Polygenic risk scores can then combine effects across many variants to estimate part of an individual's genetic susceptibility.

These methods are advancing rapidly, but they have limitations. Their predictive performance can vary between populations, they do not capture every source of genetic risk, and they should generally be considered alongside non-genetic risk factors.

Why the evidence changes

Genomic science is not static.

Larger biobanks, more diverse research populations, whole-genome sequencing, improved statistical methods and better understanding of biological pathways continually change what can reasonably be inferred from genetic information.

For that reason, Bioanalytix treats the scientific evidence behind an observation as something that can evolve.

A genetic observation does not change.

Our understanding of what that observation means can.