‘Silver tsunami’ likely to have significant impacts for rheumatology providers
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ORLANDO, Fla. — The aging process can cause a significant decline in the immune system, a process set to impact a growing proportion of the general population and rheumatic patients alike, according to a presenter here.
“We need to recognize the impact of the ‘silver tsunami,’ the rapid growth of our aging population, on our health care system and our society,” Teri Puhalsky, BSN, RN, CRNI, an infusion nurse at Medstar Orthopedic Institute in Alexandria, Virginia, and a member of the board of directors for the Rheumatology Nurses Society, told attendees at the 2024 RNS annual conference.
By 2040, there will be some 80 million individuals in the United States aged older than 65 years, according to Puhalsky.
“About 80% of adults over 65 have one chronic condition, and 50% have at least two,” she said.
There are nine hallmarks of aging for clinicians to consider, according to Puhalsky. They include genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, deregulated nutrient sensing, dysregulation of protein homeostasis, cellular senescence, stem cell exhaustion and altered intercellular communication.
“If we can identify and alter any of these hallmarks, it can delay the aging process,” Puhalsky said.
In addition, each of these hallmarks can contribute to immunosenescence and, consequently, present challenges for rheumatology providers.
“[Immunosenescence] is a gradual deterioration of the immune system,” Puhalsky said. “Immune cells, T/B cells, natural killer cells, neutrophils, dendritic cells and macrophages get confused and they do not know what to do.”
This, in turn, leads to more significant complications for rheumatologists.
“During the aging process, we develop an inflammatory state that produces high levels of pro-inflammatory markers,” Puhalsky said.
She encouraged providers to be vigilant about how these processes can play out in specific disease states.
“In healthy individuals, this decline begins around age 50,” Puhalsky said. “In rheumatoid arthritis, T-cell aging processes are considerably faster.”
Accelerated aging is an immunologic phenotype of RA, Puhalsky added. She noted that the decline of macrophages can also have an impact in RA.
“Macrophages are the most common innate cells in RA,” she said. “There are just not enough.”
On a broader level, aging can cause an imbalance between inflammatory and immune reactions, according to Puhalsky. It also impacts the innate and adaptive immune systems differently. Although both the innate and adaptive immune system decline over time, the innate system tends to be preserved better.
The impact of aging on T cells should also be a point of focus for rheumatology providers. Specifically, although the total number of T cells remains constant, the pool of naïve, undifferentiated cells shrinks, causing less effective immune responses, according to Puhalsky.
“They become the bad guys,” she said.
Looking specifically at immunosenescence in RA, Puhalsky noted that RA T cells carry a high load of DNA double strand breaks, are deprived of energy and produce pro-inflammatory cytokines. Moreover, cells have shortened telomeres, loss of immune tolerance and increased reactivity with self-antigens.
“This whole process occurs prematurely in our RA patients,” she said.
Regarding currently available solutions, Puhalsky said regular moderate exercise can slow down some of these processes, as can a diet heavy on fruits, vegetables and lean proteins, and light on sugar and fats.
“We need that all-elusive sleep,” she added.
Ultimately, though, Puhalsky stressed that aging is a process that differs from person to person. Although replacement of T cells after the age of 40 is a problem, rheumatologists should be aware of how these declines can take place in their patients.
“The adaptive immune system in RA is accelerated in age by more than 20 years,” she said.