» Articles » PMID: 35141821

Adiposity and Smoking Mediate the Relationship Between Depression History and Inflammation Among Young Adults

Overview
Journal Int J Behav Med
Publisher Informa Healthcare
Date 2022 Feb 10
PMID 35141821
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Depression is associated with inflammation, but the mechanisms underlying this association are unclear. We examined adiposity and smoking as potential pathways through which childhood depression may lead to an elevated inflammatory status among young adults.

Methods: The sample included 294 subjects with histories of depression (probands), 270 never-depressed siblings of probands (high-risk siblings), and 169 controls. C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1) were assessed in serum samples. An adiposity score was computed from body mass index and waist circumference. Smoking behavior was evaluated during an interview. Mixed-effects models were used to test whether adiposity and smoking mediate the relationship between depression and inflammation.

Results: Probands (p = .004), but not siblings (p = .071), had higher levels of sICAM-1 compared to controls. However, depression history and risk status had no direct effects on CRP (ps > .13) or IL-6 (ps > .16). Importantly, adiposity indirectly mediated the effect of group (probands vs. controls; siblings vs. controls) on all three inflammatory markers. Smoking indirectly mediated the effect of group (probands vs. controls; siblings vs. controls) on sICAM-1 only.

Conclusions: Among young adults, the adverse inflammatory consequences of depression history are significant for sICAM-1. Adiposity and smoking are pathways through which depression can indirectly impact several inflammatory markers, suggesting possible preventive interventions to improve the immunologic and cardiovascular health of depression-prone individuals.

Citing Articles

Neuroinflammation Profiling of Brain Cytokines Following Repeated Blast Exposure.

Heyburn L, Batuure A, Wilder D, Long J, Sajja V Int J Mol Sci. 2023; 24(16).

PMID: 37628746 PMC: 10454588. DOI: 10.3390/ijms241612564.

References
1.
Howren M, Lamkin D, Suls J . Associations of depression with C-reactive protein, IL-1, and IL-6: a meta-analysis. Psychosom Med. 2009; 71(2):171-86. DOI: 10.1097/PSY.0b013e3181907c1b. View

2.
Kiecolt-Glaser J, Derry H, Fagundes C . Inflammation: depression fans the flames and feasts on the heat. Am J Psychiatry. 2015; 172(11):1075-91. PMC: 6511978. DOI: 10.1176/appi.ajp.2015.15020152. View

3.
Elovainio M, Keltikangas-Jarvinen L, Pulkki-Raback L, Kivimaki M, Puttonen S, Viikari L . Depressive symptoms and C-reactive protein: the Cardiovascular Risk in Young Finns Study. Psychol Med. 2006; 36(6):797-805. DOI: 10.1017/S0033291706007574. View

4.
Ford D, Erlinger T . Depression and C-reactive protein in US adults: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2004; 164(9):1010-4. DOI: 10.1001/archinte.164.9.1010. View

5.
Copeland W, Shanahan L, Worthman C, Angold A, Costello E . Cumulative depression episodes predict later C-reactive protein levels: a prospective analysis. Biol Psychiatry. 2011; 71(1):15-21. PMC: 3586231. DOI: 10.1016/j.biopsych.2011.09.023. View