Most of us think of aging as a straight line that’s going steadily downward.
But the truth is, our aging process is more like a straight line interrupted by curves, bumps, and dips at specific points.
Scientists have already identified three points in a person’s life when specific proteins in the blood that affect aging either increase or decrease.
But a more recent study has identified a “turning point” when that acceleration especially ramps up — and how the body is most affected…
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When age-related changes really get going
Compared with other mammals, humans have a remarkably long lifespan.
But we pay the price: the cost of a long life is a decline in organ function, which increases the risk of chronic disease as we age.
To learn more about the patterns of aging and how and when it starts, a team of researchers from the Academy of Sciences built a catalogue of the proteins found in the tissues of organs from seven of the body’s systems.
They collected tissue samples from a total of 76 organ donors between the ages of 14 and 68 who had died of accidental traumatic brain injury. They also obtained blood samples.
In total, they ended up with 516 samples from 13 different tissues covering seven of the body’s systems, including:
- Cardiovascular (heart and aorta)
- Digestive (liver, pancreas, and intestine)
- Immune (spleen and lymph node)
- Endocrine (adrenal gland and white adipose)
- Respiratory (lung)
- Integumentary (skin)
- Musculoskeletal (muscle).
The researchers wrote that, “Based on aging-associated protein changes, we developed tissue-specific proteomic age clocks and characterized organ-level aging trajectories.”
Their analysis revealed an aging inflection around age 50, at which many tissues underwent substantial remodeling, notably the pancreas and the spleen.
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But it was the blood vessels that the researchers described as “a tissue that ages early and is markedly susceptible to aging,” with the most evident changes occurring in the aorta.
They also identified 48 disease-related proteins that increased with age and were linked to cardiovascular conditions, tissue fibrosis, fatty liver disease and liver-related tumors.
The researchers even went a step further, injecting an isolated protein responsible for aortic aging into young mice. Not only did the mice exhibit prominent markers of vascular aging, but also reduced physical performance, decreased grip strength, lower endurance and lower balance and coordination
“These insights may facilitate the development of targeted interventions for aging and age-related diseases, paving the way to improve the health of older adults.”
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Vascular aging kicks off a key component of aging
It’s typical for research like this to take years to develop and apply to human health. But what it can do, right now, is give us a clue about what to pay special attention to…
Previous research has already linked atherosclerosis with accelerated aging.
Using participants from the PESA-CNIC-SANTANDER study, researchers found that low-grade systemic inflammation, also known as inflammaging, spiked in participants with a high burden of atherosclerotic plaques, accelerating epigenetic aging in otherwise healthy adults.
In other words, long before the appearance of symptomatic cardiovascular disease, what’s happening in the arteries is accelerating aging and setting the stage for disease.
Supporting artery health and reducing inflammation sounds like a good place to start to slow down both aging and disease risk, then.
In addition to lifestyle habits that support your body and your heart, like following a Mediterranean-style diet, exercising and managing stress, aim to boost your omega-3 fatty acids.
This special group of nutrients can tackle both inflammation and metabolic disorders, including heart disease, atherosclerosis and fatty liver, while promoting artery health.
Omega-3s are plentiful in fatty fish and in popular supplements.
Sources:
Scientists Reveal Turning Point When Your Body’s Aging Accelerates — Science Alert
Comprehensive human proteome profiles across a 50-year lifespan reveal aging trajectories and signatures — Cell
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