longevitywatch

Do some people age primarily through their heart and others through their metabolism?

Yes, people age through different organ pathways. The science needed to map this precisely for each individual is promising, but still at an early stage.

Ageing unfolds differently in every person. Genes, lifestyle, environment and psychological factors together determine whether you are more likely to develop heart problems first, or instead metabolic or kidney problems. That is not an exception -- it is a core feature of how ageing works1.

Blood tests that measure hundreds of substances simultaneously show that people have their own metabolic profile. In people with coronary artery disease, 23 blood markers were linked to heart problems in general. But which type of heart problem a person develops varies from individual to individual. Certain fats in cell membranes specifically predicted heart failure, not a heart attack or stroke. This suggests that people develop heart problems through different pathways2.

Individual variation also plays a role within the heart itself. Immune cells are involved in the formation of scar tissue in heart muscle at older ages. How those cells behave differs from person to person3. At the cellular level, the energy centres of the cell play a role in both cardiac and metabolic ageing4.

Clinical research confirms this picture. SGLT2 inhibitors, a class of diabetes medications, reduce the risk of hospitalisation for heart failure by 23% and slow kidney disease by 45%. The effect on heart attack, however, was limited to people who already had atherosclerosis. The same pill therefore delivers much more benefit in one person than in another5.

GLP-1 medications such as semaglutide show something similar. Weight loss is accompanied by loss of muscle mass: 15% to 60% of total loss, depending on the person and the drug. In younger people this is relatively harmless. In frail older adults, excessive muscle loss is a real risk6. Blood tests can already point a doctor in a certain direction, but truly personalised care at the molecular level is not yet standard practice1.

The evidence
6 studies

Sources: one conceptual-theoretical review article (PMID 40250404), one metabolic study in coronary artery disease patients (PMID 38977723), one review on immune cells in the heart (PMID 38816371), one large cardiovascular trial of SGLT2 inhibitors with thousands of participants (PMID 30424892), one review on GLP-1 medications and muscle mass (PMID 38937282), and one mechanistic study on cellular energy centres (PMID 28711444).

Last updated: June 2026
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