Lasselin · Brain, behavior, and immunity 2020 · randomized crossover trial · n=37

Immunological and behavioral responses to in vivo lipopolysaccharide administration in young and healthy obese and normal-weight humans.

Level 2 - randomized trial

Randomized crossover challenge trial in humans

PubMed 32485294 · doi:10.1016/j.bbi.2020.05.071 · record verified 2026-08-26

What was done

Fourteen obese healthy subjects and 23 normal-weight healthy subjects received intravenous injections of lipopolysaccharide (0.8 ng/kg body weight, adjusted for estimated blood volume in obese subjects) and placebo (saline) in a double-blind, randomized, within-subject crossover design. Measured outcomes included blood concentrations of cytokines (interleukin-6, tumor necrosis factor-alpha, IL-10), body temperature, neuroendocrine markers (cortisol, norepinephrine), and behavioral measures (sickness symptoms, fatigue, negative mood, state anxiety).

What was found

LPS administration induced acute increases in cytokine levels (IL-6, TNF-alpha, IL-10), body temperature, cortisol, norepinephrine, sickness symptoms, fatigue, negative mood, and state anxiety across both groups. Immune and behavioral responses did not differ substantially between obese and normal-weight subjects. Obese individuals demonstrated a strongly attenuated cortisol response to LPS, and higher body fat percentage correlated with a lower cortisol response. The abstract reported no exact numerical values, effect sizes, or p-values.

Why it matters

These findings suggest that young, healthy obese individuals do not display increased behavioral or cytokine sensitivity to acute systemic inflammation compared to normal-weight peers, but they do exhibit blunted hypothalamic-pituitary-adrenal axis reactivity.

Limits

The sample size was small (n = 37 total: 14 obese, 23 normal weight), and the cohort was restricted to young and healthy participants without metabolic comorbidities. No quantitative values or confidence intervals were provided in the abstract. An acute endotoxemia model may not replicate the pathophysiology of chronic low-grade inflammation.