Actigraphic sleep and adipokines in older Baltimore adults: cross-sectional and longitudinal links
In 350 adults aged 60 and older, longer average wake bouts were cross-sectionally associated with lower adiponectin and leptin; longer total sleep time predicted a greater rise in adiponectin over time. These are associations, not causes. [1]
Automatic summary · not editorially reviewed
The key findings
The study included 350 adults aged 60 or older from the Baltimore Longitudinal Study of Aging who completed about 6.5 nights of wrist actigraphy and provided fasting plasma for adipokine measurement. [1]
At baseline, longer average wake bout length was associated with lower adiponectin and lower leptin in fully adjusted models. [1]
Longer total sleep time, modeled continuously, predicted a greater increase in adiponectin over time. [1]
The source at a glance
- Study type / format
- Observational study with cross-sectional and longitudinal analyses (abstract).
- Population / context
- 350 adults aged 60 or older (mean 74.8 years, 48.9% female, 19.4% black) in the Baltimore Longitudinal Study of Aging.
- Summary based on
- Study abstract
- Original publication
- July 23, 2026
Sleep and adipokines in 350 older adults
The Baltimore Longitudinal Study of Aging examined whether actigraphic sleep parameters relate to adipokine levels in older adults. Participants were 350 people aged 60 or older (mean 74.8 years, 48.9% female, 19.4% black) who completed about 6.5 nights of wrist actigraphy and gave fasting plasma for adipokine measurement. Predictors were total sleep time, sleep onset latency, wake after sleep onset, sleep efficiency and average wake bout length; outcomes were adiponectin and leptin. The authors explored sex and central obesity as potential moderators.
Supporting source [1]
Wake bouts, sleep time and adipokine findings
At baseline, longer average wake bout length was associated with lower adiponectin (B = -2.02, 95% CI [-3.61, -0.42]) and lower leptin (B = -3.14, [-5.25, -1.03]) in fully adjusted models. Longer total sleep time, modeled continuously, predicted a greater increase in adiponectin over time (B = 0.26, [0.081, 0.44]); short total sleep time showed B = -0.90, [-1.72, -0.079]. Sex and central obesity moderated the baseline wake-bout–adiponectin associations, which were significant in females (B = -3.92, [-6.25, -1.59]) and in those with lower central obesity (B = -6.98, [-10.43, -3.53]).
Supporting source [1]
Cross-sectional and longitudinal scope of the abstract
The abstract reports both cross-sectional baseline associations and longitudinal prediction of adiponectin change, but gives no follow-up duration or number of repeated measurements. It describes associations only; it does not show that sleep changes adipokines or that adipokines cause cardiometabolic effects. The authors suggest sleep may act through adipokines, which remains a hypothesis. Only the abstract was reviewed; the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Follow-up duration and number of repeated measurements are not reported. Findings are associations, not causal effects, and the proposed pathway through adipokines remains a hypothesis.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Wei Z, Yue Y, Rabinowitz JA, Kaizi-Lutu M, Wu MN, Chia CW, Tanaka T, Simonsick EM, Ferrucci L, Spira AP. · europepmc.org · July 23, 2026