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 obese
1 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 burned
3, 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 & Folco
8 plus many others
have indicated via their works how science supports obesity as an inflammatory
condition. Calder et all
4 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.
Rayssiguier
10 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 sugar
13 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 kidneys
16, liver
9, pancreas
17, 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).
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.