Poor diet quality may prolong recovery following injury

Obesity is often the result of excess energy intake that is stored in adipose tissue (fat). Obesity is a condition with significant social, economical and medical impact worldwide. The risk of developing cardiovascular disease, stroke, Type 2 Diabetes and chronic pain is raised by obesity. As such, it is imperative that we gain an understanding of the relationship between the cause of obesity (diet) and the negative health outcomes that accompany it.

Because the signals sent by excess adipose tissue (i.e. leptin) to the rest of the body initiate an inflammatory response, obesity is considered a pro-inflammatory state1,2. In addition, specific items in the diet can increase inflammation as well. We, and others, have reported that foods containing high levels of saturated fats or omega-6 fatty acids trigger an inflammatory response3-5. On the other hand, foods high in omega-3 fatty acids and food additives that include ginger, ginseng and turmeric have known anti-inflammatory effects5. Together, this information suggests that both diet and fat tissue can have negative effects on health. Our study in mice was designed to study these effects related to pain.

In the mid-2000s a large-scale study was completed in the US that investigated the levels of micro- and macronutrients in a typical American diet: the National Health and Nutrition Examination Survey (NHANES). Based on these findings, a rodent diet was created that used the average values for all of the nutrients in the NHANES. This diet is referred to as the Total Western Diet (TWD). In our study, recently published in the Journal of Pain, we used this TWD to see what effects the diet had on sensitivity to touch and heat as well as physiological effects of the diet. Finally, we were interested in whether the animals on the TWD responded differently to CFA-mediated (Complete Freund’s Adjuvant) chronic pain induction compared to animals on a diet of standard laboratory animal food.

We found that the animals eating the TWD became less sensitive to heat and touch. This was initially surprising, but it is similar to what is observed in obese humans who show higher thresholds for peripheral pain6. While it may seem plausible that fat deposits under the skin provide more insulation, we know that nerve cells are actually closer to the surface than the adipose tissue deposits making that explanation unlikely. In addition to the changes in sensitivity, the mice showed significantly elevated levels of inflammatory cytokines in their blood. This suggested that they were in an inflammatory state that is not unlike that seen in obese humans. When we assessed the composition of their body tissues after 12 weeks on the diet, the animals eating the TWD showed significant elevations in body fat, without showing elevated body weight! That is to say, the poor quality TWD changed the animals’ body composition without making them heavier or noticeably obese, suggesting that any effects were not due to the animals being heavier.

Finally, we used a standard method to induce a recoverable pain condition and this is where we really saw some startling effects. When animals were made hypersensitive to touch and heat using CFA, control animals (n = 8) recovered in the expected 5-8 days. However, animals that were eating the TWD (n = 10) took 11-14 days to fully recover. This diet effectively doubled their recovery time in a blinded assessment of sensitivity. In addition, these animals showed more hypersensitivity than control animals.

Taken together, we believe that our results suggest that poor diet and the physiological changes that arise because of it could be an underlying mechanism that contributes to chronic pain in humans. While we agree that increased weight causes significant stress in weight-bearing joints (knees, back), obese humans develop pain in other areas that are not weight-bearing (neck, fingers, shoulders) suggesting other factors may also contribute7. Currently we are examining the impact of poor diet on immune system activity and whether an anti-inflammatory diet can reverse the negative effects of a poor diet. It is our hope that, in the near future, diets can serve as a healthy alternative to pharmaceuticals when treating chronic pain.

About Stacie Totsch

Stacie TotschStacie Totsch is a PhD student at the University of Alabama at Birmingham and is currently working under the supervision of Dr. Robert Sorge. Her work aims to understand the relationship between diet and pain as they interact with immune system cells. Stacie is interested in fitness and health and, as an Alabama native, is concerned with the rise in obesity.

 References

  1. Agrawal S, Gollapudi S, Su H, Gupta S. Leptin activates human B cells to secrete TNF-alpha, IL-6, and IL-10 via JAK2/STAT3 and p38MAPK/ERK1/2 signaling pathway. Journal of clinical immunology. 2011;31(3):472-8. doi: 10.1007/s10875-010-9507-1. PubMed PMID: 21243519; PubMed Central PMCID: PMC3132280.
  2. Fernandez-Riejos P, Najib S, Santos-Alvarez J, Martin-Romero C, Perez-Perez A, Gonzalez-Yanes C, et al. Role of leptin in the activation of immune cells. Mediators of inflammation. 2010;2010:568343. doi: 10.1155/2010/568343. PubMed PMID: 20368778; PubMed Central PMCID: PMC2846344.
  3. Joffe YT, Collins M, Goedecke JH. The relationship between dietary fatty acids and inflammatory genes on the obese phenotype and serum lipids. Nutrients. 2013;5(5):1672-705. doi: 10.3390/nu5051672. PubMed PMID: 23698162; PubMed Central PMCID: PMC3708344.
  4. Lee JY, Sohn KH, Rhee SH, Hwang D. Saturated fatty acids, but not unsaturated fatty acids, induce the expression of cyclooxygenase-2 mediated through Toll-like receptor 4. The Journal of biological chemistry. 2001;276(20):16683-9. doi: 10.1074/jbc.M011695200. PubMed PMID: 11278967.
  5. Totsch SK, Waite ME, Sorge RE. Dietary Influence on Pain via the Immune System. Progress in molecular biology and translational science. 2015;131:435-69. doi: 10.1016/bs.pmbts.2014.11.013. PubMed PMID: 25744682.
  6. Khimich S. Level of sensitivity of pain in patients with obesity. Acta chirurgica Hungarica. 1997;36(1-4):166-7. PubMed PMID: 9408331.
  7. Vincent HK, Heywood K, Connelly J, Hurley RW. Obesity and weight loss in the treatment and prevention of osteoarthritis. PM & R : the journal of injury, function, and rehabilitation. 2012;4(5 Suppl):S59-67. doi: 10.1016/j.pmrj.2012.01.005. PubMed PMID: 22632704; PubMed Central PMCID: PMC3623013.

 

Comments

  1. Very interesting.

    I agree to the research findings from my anecdotal experience.

    It will be interesting to look at the difference in prevalence of chronic pain in between low socio economic (presumably bad eating habits) and mid to high socio economic background.

    Also it may also reinforce your point if you look at the difference in prevalence of chronic pain between western countries and particular part of ethnic people across globe who eat well.