Telomeres are DNA sequences at the end of chromosomes in eukaryotes that preserve genome information. Telomere length may mark an individual’s biological age as opposed to their calendar age, acting as a mitotic clock indicative of cellular aging. Thus, telomere shortening is a hallmark sign of cellular aging.
While telomere length normally decreases with age, this process may be affected by chronic disease, chronic stress, and lifestyle factors.
We are interested in cellular aging in persons with heart failure and in family caregivers of persons with chronic disease. Our studies are described below.
While telomere length normally decreases with age, this process may be affected by chronic disease, chronic stress, and lifestyle factors.
We are interested in cellular aging in persons with heart failure and in family caregivers of persons with chronic disease. Our studies are described below.
The Effects of Exercise on Telomere Length in Persons With Heart Failure
Telomere length is reduced in persons with heart failure (HF). Inflammation is a putative mechanism contributing to telomere shortening. Although physical activity is known to increase telomere length, its effects in HF are unknown.
Objective: The aim of this study was to examine the effects of exercise on telomere length and its relationship with interleukin (IL)-1β in persons with HF.
Methods: This secondary analysis of a 3-month home-based aerobic exercise intervention measured total telomere length and IL-1β levels in persons with HF (69% with reduced ejection fraction).
Results: Total telomere length increased and plasma IL-1β levels decreased in the exercise group from baseline to 3 months. Total telomere length was negatively associated with IL-1β at baseline (r = -0.441 P = .001).
Conclusions: The association between telomere length and IL-1β suggests a relationship between inflammation and cellular aging. Moderate-intensity exercise may help maintain cellular functions. Further research is needed to examine the effects on outcomes in persons with HF.
Butts B, Hope C, Herring C, Mueller K, Gary RA. The Effects of Exercise on Telomere Length in Persons With Heart Failure [published online ahead of print, 2023 Oct 6]. J Cardiovasc Nurs. 2023;10.1097/JCN.0000000000001044.
Objective: The aim of this study was to examine the effects of exercise on telomere length and its relationship with interleukin (IL)-1β in persons with HF.
Methods: This secondary analysis of a 3-month home-based aerobic exercise intervention measured total telomere length and IL-1β levels in persons with HF (69% with reduced ejection fraction).
Results: Total telomere length increased and plasma IL-1β levels decreased in the exercise group from baseline to 3 months. Total telomere length was negatively associated with IL-1β at baseline (r = -0.441 P = .001).
Conclusions: The association between telomere length and IL-1β suggests a relationship between inflammation and cellular aging. Moderate-intensity exercise may help maintain cellular functions. Further research is needed to examine the effects on outcomes in persons with HF.
Butts B, Hope C, Herring C, Mueller K, Gary RA. The Effects of Exercise on Telomere Length in Persons With Heart Failure [published online ahead of print, 2023 Oct 6]. J Cardiovasc Nurs. 2023;10.1097/JCN.0000000000001044.
Cardiovascular disease risk and cellular aging among heart failure and Alzheimer’s disease family caregivers.
The purpose of this study is to evaluate the risk of cardiovascular disease (CVD) and cellular aging among dementia and heart failure family caregivers.
In the United States, around 50 million persons provide care for a chronically ill, disabled or aged family member during any given year. Although serving an essential role, the impact of caregiving in chronic illness can take a toll on the health of family caregivers. Elderly spousal caregivers with a chronic illness who experience caregiving related stress demonstrate premature aging and have a 63% higher mortality rate when compared with non-caregivers of the same age.
The effects of these psychosocial and physiological attributes on cardiovascular risk and cellular aging on family caregivers is not well addressed. Furthermore, there is little research relating the impact of caregiver stress on telomere length and telomerase activity. Using stored samples from the COOL-HF and COOL-AD studies, this study will address current gaps in the science of family-focused care in chronic illness by evaluating FCG risks for cardiovascular disease and cellular senescence by addressing the following aims:
Aim 1: Examine the relationships between caregiver stress and CVD outcomes in FCG.
H1: Higher levels of perceived stress and caregiver burden are associated with: a. Higher levels of inflammatory biochemical markers (IL-6 and CRP); b. Shortened telomere length and lower telomerase activity; c. Poor cardiovascular reactivity.
Aim 2: Examine the relationships between intermediate outcomes (emotional, health status and neuroendocrine) and CVD outcomes in FCG.
H2: Poor long term (risk) outcomes of increased inflammatory biochemical markers (IL-6 and CRP), shortened telomeres and lower telomerase activity will be associated with: a. Increased levels of depression (CESD); b. Increased levels of anxiety (STAI); c. Increased caregiver burden (BCOS, and OCBS [HF only]); d. Decreased health status (physical function).
Exploratory Aim: Explore the mediating relationship of coping style on intermediate outcomes.
RQ1: Does coping style (WOC) mediate the relationship between caregiver stress (PSS) and the intermediate outcomes of depression (CES-D), anxiety (STAI), caregiver burden (BCOS and OCBS), health status (SF-36 and treadmill test) and cortisol levels?
In the United States, around 50 million persons provide care for a chronically ill, disabled or aged family member during any given year. Although serving an essential role, the impact of caregiving in chronic illness can take a toll on the health of family caregivers. Elderly spousal caregivers with a chronic illness who experience caregiving related stress demonstrate premature aging and have a 63% higher mortality rate when compared with non-caregivers of the same age.
The effects of these psychosocial and physiological attributes on cardiovascular risk and cellular aging on family caregivers is not well addressed. Furthermore, there is little research relating the impact of caregiver stress on telomere length and telomerase activity. Using stored samples from the COOL-HF and COOL-AD studies, this study will address current gaps in the science of family-focused care in chronic illness by evaluating FCG risks for cardiovascular disease and cellular senescence by addressing the following aims:
Aim 1: Examine the relationships between caregiver stress and CVD outcomes in FCG.
H1: Higher levels of perceived stress and caregiver burden are associated with: a. Higher levels of inflammatory biochemical markers (IL-6 and CRP); b. Shortened telomere length and lower telomerase activity; c. Poor cardiovascular reactivity.
Aim 2: Examine the relationships between intermediate outcomes (emotional, health status and neuroendocrine) and CVD outcomes in FCG.
H2: Poor long term (risk) outcomes of increased inflammatory biochemical markers (IL-6 and CRP), shortened telomeres and lower telomerase activity will be associated with: a. Increased levels of depression (CESD); b. Increased levels of anxiety (STAI); c. Increased caregiver burden (BCOS, and OCBS [HF only]); d. Decreased health status (physical function).
Exploratory Aim: Explore the mediating relationship of coping style on intermediate outcomes.
RQ1: Does coping style (WOC) mediate the relationship between caregiver stress (PSS) and the intermediate outcomes of depression (CES-D), anxiety (STAI), caregiver burden (BCOS and OCBS), health status (SF-36 and treadmill test) and cortisol levels?