Why Is Age a Risk Factor for Cardiovascular Disease?

Cardiovascular disease (CVD) encompasses a range of conditions affecting the heart and blood vessels. While lifestyle choices and genetics play a role, age stands as a primary, non-modifiable risk factor for developing CVD. As individuals grow older, their bodies undergo complex biological changes that directly contribute to an increased susceptibility to these heart and vascular conditions.

Age-Related Changes in Blood Vessels

As the body ages, blood vessels experience significant physical and functional alterations. Arteries, which are typically elastic, undergo arteriosclerosis, characterized by stiffening and thickening of their walls. This loss of elasticity means arteries become less efficient at regulating blood pressure, leading to increased pressure within the circulatory system.

This stiffening is partly due to changes in the composition of the arterial wall, including increased collagen deposition and cross-linking, alongside decreased production of elastin. The altered structure contributes to higher pulse pressure and an increased workload for the heart. The inner lining of blood vessels, the endothelium, can become impaired (endothelial dysfunction). This impairment reduces the vessels’ ability to dilate and constrict, making them more vulnerable to fatty deposits and plaque (atherosclerosis).

Inflammation and Oxidative Stress

Aging is associated with chronic low-grade inflammation, often called “inflammaging.” This systemic inflammation can continuously damage cells and tissues throughout the body, particularly within the vascular system. Such ongoing inflammatory processes contribute to the deterioration of blood vessel walls, making them more susceptible to injury and cardiovascular issues.

Increased oxidative stress also accumulates with age. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (free radicals) and the body’s ability to neutralize them. These free radicals can cause damage to cellular components, further compromising the integrity and function of cardiovascular tissues. The combined effects of chronic inflammation and oxidative stress promote vascular dysfunction and accelerate cardiovascular disease.

Metabolic and Hormonal Imbalances

Age-related shifts in metabolism and hormone levels significantly influence cardiovascular disease risk. Lipid profiles change with aging, showing an increase in low-density lipoprotein (LDL) cholesterol, often referred to as “bad” cholesterol, and triglycerides, while levels of high-density lipoprotein (HDL) cholesterol, or “good” cholesterol, may decrease. These alterations create a less favorable lipid environment, promoting plaque accumulation in arteries.

Insulin resistance also becomes more prevalent with age, meaning the body’s cells do not respond as effectively to insulin. This can lead to higher blood sugar levels and, over time, the development of type 2 diabetes, which is a major risk factor for cardiovascular disease.

Furthermore, age-related declines in certain hormones, such as sex hormones like estrogen and testosterone, and growth hormone, can have implications for cardiovascular health. For instance, the drop in estrogen after menopause can affect how the body uses insulin and contributes to increased cardiovascular risk in women.

Decline in Cellular Maintenance and Repair

The body’s capacity for cellular maintenance and repair naturally diminishes with advancing age, rendering tissues more susceptible to disease. One aspect of this decline involves reduced efficiency in DNA repair mechanisms. Over time, accumulated DNA damage can compromise cellular function and contribute to the aging process of cardiovascular cells.

Another factor is the accumulation of senescent cells. These cells have stopped dividing but remain metabolically active, releasing substances that can harm neighboring healthy cells and promote inflammation.

The efficiency of cellular waste removal processes, such as autophagy, decreases with age. This reduced cellular “housekeeping” leads to the build-up of cellular debris, contributing to cumulative damage that underlies age-related cardiovascular conditions and reduces the body’s resilience to various stressors.