The chronic inflammatory hypothesis for the morbidity associated with morbid obesity

Implications and effect of weight loss

Daniel R. Cottam, Samer G. Mattar, Emma Barinas-Mitchell, George Eid, Lewis Kuller, David E. Kelley, Philip R. Schauer

Research output: Contribution to journalArticle

292 Citations (Scopus)

Abstract

Background: Obesity is a worldwide pandemic that causes a multitude of co-morbid conditions. However, there has been slow progress in understanding the basic pathophysiology that underlies co-morbid conditions associated with obesity. Recently, there has been intense interest in the role of inflammation in obesity. Using the inflammatory hypothesis, many of the mechanisms by which co-morbid conditions are associated with obesity are being elucidated. Methods: We searched the literature and reviewed all relevant articles. We focused on hormones and cytokines that have been associated with other inflammatory conditions such as sepsis and systemic inflammatory response syndrome. Findings: Angiotensinogen (AGT), transforming growth factor beta (TGFβ), tumor necrosis factor alpha (TMFα), and interleukin six (IL-6) are all elevated in obesity and correlate with several markers of adipocyte mass. These mediators have detrimental effects on hypertension, diabetes, dyslipidemia, thromboembolic phenomena, infections, and cancer. Weight loss results in a reduction of inflammatory mediators and a diminution of the associated co-morbid conditions. Conclusions: The success of weight loss surgery in treating the complications associated with obesity is most probably related to the reduction of inflammatory mediators. While some aspects of bariatric physiology remain unclear, there appears to be a strong association between obesity and inflammation, thereby rendering obesity a chronic inflammatory state. A clearer understanding of the physiology of obesity will allow physicians who treat the obese to develop better strategies to promote weight loss and improve the well-being of millions of individuals.

Original languageEnglish (US)
Pages (from-to)589-600
Number of pages12
JournalObesity Surgery
Volume14
Issue number5
DOIs
StatePublished - May 2004
Externally publishedYes

Fingerprint

Morbid Obesity
Weight Loss
Obesity
Morbidity
Inflammation
Bariatrics
Systemic Inflammatory Response Syndrome
Angiotensinogen
Interleukins
Pandemics
Dyslipidemias
Adipocytes
Transforming Growth Factor beta
Interleukin-6
Sepsis
Tumor Necrosis Factor-alpha
Hormones
Cytokines
Hypertension
Physicians

Keywords

  • Angiotensin
  • C-reactive protein
  • Cancer
  • Hypertension
  • Infection
  • Inflammation
  • Insulin resistance
  • Interleukin
  • Leptin
  • Morbid obesity
  • Obesity
  • Serum amyloid A
  • Transforming growth factor
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Surgery

Cite this

Cottam, D. R., Mattar, S. G., Barinas-Mitchell, E., Eid, G., Kuller, L., Kelley, D. E., & Schauer, P. R. (2004). The chronic inflammatory hypothesis for the morbidity associated with morbid obesity: Implications and effect of weight loss. Obesity Surgery, 14(5), 589-600. https://doi.org/10.1381/096089204323093345

The chronic inflammatory hypothesis for the morbidity associated with morbid obesity : Implications and effect of weight loss. / Cottam, Daniel R.; Mattar, Samer G.; Barinas-Mitchell, Emma; Eid, George; Kuller, Lewis; Kelley, David E.; Schauer, Philip R.

In: Obesity Surgery, Vol. 14, No. 5, 05.2004, p. 589-600.

Research output: Contribution to journalArticle

Cottam, DR, Mattar, SG, Barinas-Mitchell, E, Eid, G, Kuller, L, Kelley, DE & Schauer, PR 2004, 'The chronic inflammatory hypothesis for the morbidity associated with morbid obesity: Implications and effect of weight loss', Obesity Surgery, vol. 14, no. 5, pp. 589-600. https://doi.org/10.1381/096089204323093345
Cottam, Daniel R. ; Mattar, Samer G. ; Barinas-Mitchell, Emma ; Eid, George ; Kuller, Lewis ; Kelley, David E. ; Schauer, Philip R. / The chronic inflammatory hypothesis for the morbidity associated with morbid obesity : Implications and effect of weight loss. In: Obesity Surgery. 2004 ; Vol. 14, No. 5. pp. 589-600.
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