Polygenic risk scores (PRS) and blood protein measurements can estimate personal risk for dozens of diseases more accurately than standard clinical information. The methods are promising but have limitations: they concern probabilities, not certainties, and accuracy is lower outside European populations.
Your DNA contains millions of small variations (also called 'variants') that together determine how large your risk of certain diseases is. The most widely used method to measure this is the polygenic risk score (PRS). It adds up the effects of sometimes more than a million of these variants into a single number. The higher that number, the greater your genetic risk. For heart disease (coronary artery disease), the top 20% of the score distribution was found to have a more than fourfold higher risk than the bottom 20% (PMID 30309464). For five common diseases simultaneously, including atrial fibrillation, type 2 diabetes, inflammatory bowel disease and breast cancer, such a score could identify 1 to 8 percent of the population with a more than threefold elevated risk (PMID 30104762).
An important limitation of this DNA method is that most scores have been built using data from people of European descent. For people with a different background, the scores are therefore less accurate and sometimes even misleading (PMID 31765077). Moreover, it always concerns probabilities, not certainties: a high PRS does not mean you will definitely develop the disease, and a low score does not rule it out.
Beyond purely genetic testing, there are also blood tests that measure proteins (proteomics). Proteins are the building blocks that your genes produce, and their presence in the blood reflects what is happening in your organs. A large-scale study showed that measuring 5 to 20 proteins could predict the 10-year risk of 67 different diseases better than standard clinical information alone, with an average improvement of 0.07 in predictive precision (PMID 39039249). A related method looks at which organs are ageing faster than expected based on protein profiles. Nearly 20% of people turn out to have one organ that is ageing at a strongly accelerated rate, which increases the risk of death by 20 to 50%. Accelerated heart ageing even gave a 250% greater risk of heart failure (PMID 38057571).
For people with type 2 diabetes, a protein model was built that could predict future heart disease with an accuracy (AUC) of 0.819, based on nine specific proteins associated with both diabetes and heart disease (PMID 40087642). This is an example of how proteins and genetics together provide a sharper picture than either does separately.
Finally, there is genomic testing in newborns, in which the complete DNA is read out to detect rare, serious single-gene mutations. This can be useful, but the interpretation is complex: by no means do all variants found have a clear meaning, and there are ethical questions about what to report back to parents when risks only become relevant later in life (PMID 30576641).
In summary: yes, from your DNA and via blood proteins you can get a reasonably good picture of your disease risks. But these are probabilities, not predetermined outcomes. The methods are strongest for heart disease and a handful of other common conditions, and least reliable in people of non-European descent. Blood protein measurements complement DNA analyses and can sometimes even outperform them for specific diseases.
Based on 7 claims with PMIDs: 30309464, 30104762, 31765077, 39039249, 38057571, 40087642, 30576641. Three claims have strong evidence quality (large cohort studies), two moderate, two moderate with ethical considerations. All findings are associative; none of the DNA/PRS methods has been proven causal in an interventional sense.