Obesity is a chronic inflammatory disease: An evolving paradigm

The following is my first guest post.  Dr. Joseph Gentzel is a recent graduate from USD tDPT program that I do adjunct faculty work for.  He has done extensive study in the area of obesity and chronic diseases, especially related to diet and exercise (you can see why I thought he would have some great insights to share on this blog).  He graciously offered to do a post (after a little begging and pleading with him).  Here it is and you can follow more of his post at his blog Senior Physical Therapist's Blog.

Obesity is a chronic inflammatory disease:
An evolving paradigm

Dr. Joseph B. Gentzel, PT, DPT

With the most recent announcement that by 2030 forty-two percent of us will be obese¹ that translates to 9 out of ten ² of us being overweight or obese by 2030; it is imperative that we dismiss the information cascades that have failed so completely these past 40-50 years. There are many information cascades, but none bigger than the notion that obesity is caused by consuming too many calories in relation to the calories we burn; thus resulting in the deposition of fat stores in our body. Science has documented for us sufficiently that the weight reduction benefits of exercise is not restricted to calories burned³, but to other dramatic physiological changes made to the body’s physiology by a diet low in advanced glycation end products ( AGE poor diet)⁴  and exercise^5,6.

In 2001 Das asked the rhetorical question: Is obesity an inflammatory condition? ⁷ Ronca & Folco⁸ plus many others have indicated via their works how science supports obesity as an inflammatory condition. Calder et all⁴ describe many dietary factors associated with chronic disease inflammation that includes obesity. Roncal-Jimenez et all drive one of the many nails in coffin of the calories in calories out paradigm.⁹ May it rest in peace to never return again. By employing a model that fails so completely, we insure failure in addressing this mammoth public health problem. Failure, by any rational measure, has occurred in dramatic fashion with this paradigm.

Rayssiguier¹⁰ et all note that “studies have been published that implicate subclinical chronic inflammation as an important pathogenic factor in the development of metabolic syndrome”.  With multiple components comprising metabolic syndrome, this is an important point. Metabolic syndrome is comprised of combinations of visceral obesity, dyslipidaemia, hyperglycaemia, and hypertension.¹¹

So what? The clinical picture over these past 10 plus years seems to be clearing up to support that obesity is at least associated with and potentially caused by systemic inflammation. This is inflammation that we can measure with inflammatory markers such a C reactive protein, interleukin 6, possibly tumor necrosis factor, and many others. Being able to quantify the systemic inflammation offers objective measures of the condition and our interventions with same.¹²

This presents some novel approaches to addressing the disease that somehow we always knew worked but never understood how/why and too often got sidetracked by the clutter and noise that has bombarded the scene these past 40-50 years. The Centers for Disease Control and Prevention (CDC) appear to have little understanding of this and continue to apply invalid models. Nowhere is this more glaring that the USDA food pyramid that misses the point as illustrated by its continued advocacy of the toxin sugar¹³ and other nutritional areas that have ignored the science of the past 10 years.¹⁴ The Harvard School of Public Health agrees.¹⁵ The science is in and piling up to lead us away from the old information cascades. Information cascades that need to take their place alongside bloodletting and the like.

Sugar creates inflammation.⁴ Sugar causes injury to kidneys¹⁶, liver⁹, pancreas¹⁷, GI system^4,18,19, and virtually every system in the body. We should therefore not be surprised to find that obesity induced chronic inflammation damages the brain circuits that are involved with reward and feeding behaviors.²⁰

References

1.         Finkelstein EA, Khavjou OA, Thompson H, Trogdon JG, Pan L, Sherry B. Obesity and severe obesity forecasts through 2030. Am J Prev  Med. June 2012;42(6).

2.         Melville K. 9 out of 10 americans obese or overweight by 2030. [ONLINE]. 2008; 29 July, 2008:http://www.scienceagogo.com/news/20080629010344data_trunc_sys.shtml. Accessed May 7, 2012.

3.         Cannon B, Nedergaard J. Thermogenesis challenges the adipostat hypothesis for body-weight control. Proc Nutr Soc. Nov 2009;68(4):401-407.

4.         Calder P, Ahluwalia N, Brouns F, et al. Dietary factors and low-grade inflammation in relation to overweight and obesity. Br J Nutr. Dec 2011;106(Suppl 3):s5-s78.

5.         Kawanishi N, Yano H, Yokogawa Y, Suzuki K. Exercise training inhibits inflammation in adipose tissue via both suppression of macrophage infiltration and acceleration of phenotypic switching from M1 to M2 macrophages in high-fat -diet-induced obese mice. Exerc Immunol Rev. 2010;16:105-118.

6.         Petersen A, Pedersen B. The. anti-inflammatory effect of exercise. J Appl Physiol. Apr 2005;98(4):1154-1162.

7.         Das U. Is obesity an inflammatory condition? Nutrition. Nov-Dec 2001;17(11-12):953-966.

8.         Rocha V, Folco E. Inflammatory concepts of obesity. Int J Inflam. 2011 2011;2011:529061.

9.         Roncal-Jimenez C, Lanaspa M, Rivard C, et al. Sucrose induces fatty liver and pancreatic inflammation in male breeder rats independent of excess energy intake. Metabolism. Sep 2011;60(9):1259-1270.

10.       Rayssiguier Y, Gueux E, Nowacki W, Rock E, Mazur A. High fructose consumption combined iwth low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnes Res. Dec 2006;19(4):237-243.

11.       Alberti K, Zimmet P, Shaw J, IDF_Epidemiology_Task_Force-Consensus_Group. The metabolic syndrome--a new worldwide definition. Lancet. Sep 24-30 2005;366(9491):1059-1062.

12.       Ploeger H, Takken T, Greef Md, Timmons B. The effects of acute and chronic exercise on inflammatory markers in children and adults with a chronic inflammatory disease: a systematic review. Exerc Immunol Rev. 2009;15:6-41.

13.       Johnson R, Sanchez-Lozada L, Nakagawa T. The effect of fructose on renal biology and disease. J am Soc Nephrol. Dec 2010;21(12):2036-2039.

14.       Chiuve S, Willett W. The 2005 food Guide Pyramid: an opportunity lost? Nat Clin Pract Cardiovasc Med. Nov 2007;4(11):610-620.

15.       Willett W, McCullough M. Dietary pattern analysis for the evaluation of dietary guidelines. Asia Pac J Clin Nutr. 2008;17(Suppl 1):75-78.

16.       Nakayama T, Kosugi T, Gersch M, et al. Dietary fructose causes tubulointerstitial injury in the normal rat kidney. Am J Physiol Renal Physiol. Mar 2010;298(12-20).

17.       Ryu S, Ornoy A, Samuni A, Zangen S, Kohen R. Oxidative stress in Cohen diabetic rat model by high-sucrose, low copper diet: inducing pancreatic damage and diabetes. Metabolism. Sep 2008;57(9):1253-1261.

18.       Ding S, Lund P. Role of intestinal inflammation as an early event in obesity and insulin resistance. Curr Opin Clin nutr Metab Care. Jul 2011;14(4):328-333.

19.       Kawada M, Anihiro A, Mizpguchi E. Insights from advances in research of chemically induced experimental models of human inflammatory bowel disease. World J Gastroenterol. 2007;13(42):5581-5593.

20.       Cazettes F, Cohen J, Yau P, Talbot H, Convit A. Obesity-mediated inflammation may damage the brain circuit that regulates food intake. Brain Res. 2011;Feb 10(1373):101-109.