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

Ageing does not follow the same path in everyone. Genes and molecular pathways that accelerate or slow ageing interact with lifestyle, environment and psychological factors. The result is that one person develops heart problems earlier, while another is confronted mainly with metabolic disorders or kidney problems. This is not an exception but a core feature of how ageing works, as described by research published in 2025¹.

Metabolomics research, in which hundreds of substances in the blood are measured, shows that people have a clearly individual metabolic profile that is associated with the risk of heart, kidney and metabolic conditions simultaneously, also known as cardiovascular-kidney-metabolic syndrome. More concretely: in people with coronary artery disease, 23 blood markers were linked to cardiovascular problems in general. However, which type of heart problem a person develops differs from person to person: changes in glycerophospholipids, a type of fat found in cell membranes, specifically predicted heart failure, while that relationship did not hold for heart attack or stroke. This suggests that people develop heart problems via different metabolic routes².

At the level of the immune system within the heart itself, there is also evidence of individual variation. Macrophages, cells of the innate immune system, play a central role in scar tissue formation in heart muscle (fibrosis) at older ages. How those macrophages behave differs from person to person, and according to research this contributes to the variation in how the heart ages³. At the cellular level, the condition of mitochondria, the energy powerhouses of the cell, also plays a role in both cardiac and metabolic ageing, although individual variation in this has not yet been directly measured⁴.

The idea that each ageing pathway requires its own treatment also receives support from clinical drug research. SGLT2 inhibitors, a class of diabetes medications, reduce the risk of hospitalisation for heart failure by 23% and slow kidney disease by 45%, regardless of whether a person already had heart disease. The effect on classic atherosclerotic complications such as heart attack or stroke, however, was limited to people with pre-existing atherosclerosis. This concretely illustrates that the same treatment works well for some people and poorly for others, depending on which organ is most severely affected⁵.

Another example is the use of GLP-1 medications such as semaglutide (Ozempic/Wegovy). With weight loss, a portion of the lost weight also comes at the expense of muscle mass, somewhere between 15% and 60% of the total weight loss, depending on the person and the agent. In younger people this can be relatively harmless because muscle quality and insulin sensitivity improve at the same time. In older people, however, the risk of excessive muscle loss is real and warrants extra attention, especially if someone is already frail⁶. This is an example where the metabolic ageing route collides with the muscle route, and the end result can turn out very differently from person to person.

Precision medicine for ageing, in which comprehensive molecular profiles are used to determine per individual which pathways are most active, is promising but still experimental. Large-scale clinical trials and regulatory approval are still lacking. At present, a physician can already provide some guidance on the dominant risk organ based on available blood tests, but truly tailoring the management of ageing at the molecular level is not yet standard care¹.