The human body doesn’t age at a steady pace throughout adulthood. Instead, a new study reveals that it speeds up dramatically around ages 44 and 60. This research, published in the journal *Nature Aging*, involved measuring over 11,000 molecules in the adult body over time and discovered that 81% of them undergo significant changes at these two ages.
This type of aging research focuses on tracking “biological age.” This refers to changes that occur in the body throughout a lifetime, impacting proteins, metabolites, and gene activity. This concept is distinct from the “chronological age” we celebrate on our birthdays.
The finding that biological aging accelerates at two points in midlife could help researchers understand why the risk of certain illnesses increases in bursts as we age. For instance, approximately 6.5% of people between ages 40 and 59 have coronary artery disease, but this prevalence rises sharply to 19.8% in those between 60 and 79 years old.
For their study, researchers at Stanford University recruited 108 participants from diverse ethnic backgrounds, ranging in age from 25 to 75. Every three to six months, for up to seven years, the scientists collected blood samples from these participants to assess how various factors like gene activity and blood sugar levels changed over time.
Many of the factors that shifted around ages 44 and 60 were related to heart health. For example, a protein linked to atherosclerosis (plaque buildup in arteries) increased in the blood of participants during their 40s and 60s. These age groups also showed declines in their ability to metabolize caffeine, which temporarily raises blood pressure, and alcohol, which initially lowers but then raises blood pressure.
The body’s pathway for producing unsaturated fatty acids, which lower “bad” cholesterol, also decreased at these two ages. While the study’s multiple links to cardiovascular health were only correlative, they point to potential reasons why heart disease becomes more common with age.
Beyond heart health, blood sugar levels peaked in participants in their 40s and 60s, suggesting a possible link to age-related type 2 diabetes. However, scientists don’t yet know why body chemistry changes so drastically at these ages. The study didn’t account for lifestyle factors, such as diet or exercise, which could play a role.
Juan Carlos Verján, an aging researcher at the National Institute of Geriatrics in Mexico, who was not involved in the study, suggests that the 60-year inflection point might be due to inflammation. For instance, participants over 60 accumulated antioxidant enzymes in their blood. These enzymes neutralize chemical triggers for inflammation, suggesting that inflammation could be accumulating in this age group.
The aging boost at age 44 also coincides with the time some women begin perimenopause. However, the study found the same trigger points for both women and men, suggesting that sex-specific hormonal changes are not responsible for these aging boosts. “There should be another reason to cause the same change in men and women,” says study co-author Xiaotao Shen, a computational biologist now at Nanyang Technology University in Singapore. What this shared factor is remains a mystery.
The study had some limitations. The participants ranged from ages 25 to 75, preventing the researchers from assessing significant shifts that occur at other key moments in life, such as during puberty or at very advanced ages. The small sample size of 108 participants from California, which is unlikely to represent all humans globally, was another limitation.
While the study focused on changes in molecules in the blood, this doesn’t necessarily reflect all the organs in the body. Aging is tissue-related, meaning that different organs age at different rates. For example, some people experience the fastest aging in their heart, while others see it in their kidneys.
Shen’s team discovered a number of changes that correlate with the timing of age-linked diseases, but they still need to confirm a causal link to these factors. Do the changes seen in the blood actually drive disease, or are they more of a byproduct of the aging process? Animal experiments could help answer this question.
Verján speculates that epigenetic changes, which modify the activity of genes without altering their underlying code, might be driving these dramatic shifts. These findings provide a deeper understanding of the human body’s aging process and could lead to future research into slowing down the aging process and preventing age-related diseases.
