Nutrition Considerations for Inflammation, Pain, and Rehabilitation
Nutrition Considerations for Inflammation, Pain, and Rehabilitation
David R. Seaman
LEARNING OBJECTIVES
After reading this chapter, you should be able to:
Understand the nutritional approach to inflammation reduction.
Understand how certain foods can promote inflammation in the body.
Understand the impact of excess weight on low back health.
Understand how a pro-inflammatory diet can modify the musculoskeletal system in the same way it modifies the vascular system.
Understand the impact of non-resolving inflammation on musculoskeletal pain.
Understand how to determine whether an antiinflammatory diet will improve musculoskeletal pain.
“Although the world is full of suffering, it is also full of the overcoming of it.
–HELEN KELLER
Introduction
If an unfit individual begins an exercise regimen, they are commonly told to eat a healthy diet. When someone wishes to prevent heart disease or diabetes, they are told to eat a healthy diet. When someone wishes to pursue health throughout their lifetime, they are told to eat a healthy diet. The term “healthy diet” has different meanings depending on the individual or organization involved in promoting the diet. For the purpose of this chapter, the term anti-inflammatory diet or DeFlame Diet refers to a healthy diet. Table 36.1 outlines pro-inflammatory foods versus those that are anti-inflammatory.
I coined the term “DeFlame Diet” for the purpose of simplifying the goal of the diet. We now know that foods are either anti- or noninflammatory versus pro-inflammatory, which will be described in greater detail later in this chapter. The consumption of pro-inflammatory foods creates both acute and chronic inflammation; they inflame the body. Thus, the goal of diet should be to DeFlame the body by replacing pro-inflammatory calories with those that are anti-inflammatory. Making nutrition more complicated than this approach is unwarranted and confusing, and thus, counterproductive in patient care. You will notice that not all possible calorie sources have been mentioned in Table 36.1, such as whole grains, legumes including soy and soy milk, almond milk, yogurt, or regular milk. The reason is straightforward. These calorie sources are less important/nutritious than the foods that create an anti-inflammatory state. Whether these less nutritious calorie sources are consumed should be based on achieving normal levels of inflammatory markers listed in Tables 36.2 and 36.3.
Table 36.1 Pro-inflammatory Foods Versus Anti-inflammatory Foods
Diet That Creates a Pro-inflammatory State
Diet That Creates a DeFlamed or Anti-inflammatory State
Fasting triglyceride/high-density lipoprotein ratio
>3.5 = oxidation of low-density lipoprotein cholesterol
Blood pressure goal
<120/80 = normal
120-139/80-89 = prehypertension
140-159/90-99 = Stage 1 hypertension
≥160/100 = Stage 2 hypertension
Waist circumference goal—men
33 inches or less
Waist circumference goal—women
28 inches or less
Women waist/hip ratio (risk factor for type 2 diabetes = inflammation)
<0.80 = normal
0.81-0.85 = moderate inflammation
>0.85 = high inflammation
Men waist/hip ratio (risk factor for type 2 diabetes = inflammation)
<0.95 = normal
0.96-1.0 = moderate inflammation
>1.0 = high inflammation
Body mass index
18.5-24.9 = normal
25-29.9 = overweight
≥30 = obese
hsCRP in mg/L (general marker of chronic inflammation)
<1.0 = normal
1.0-3.0 = moderate inflammation
>3.0 = high inflammation
25(OH)D (vitamin D)
32-100 ng/mL (goal at least 60-80 ng)
Reprinted with permission from Seaman DR. The DeFlame Diet. Wilmington, NC: Shadow Panther Press; 2016.
This simplified DeFlame approach to nutrition is also consistent with how rehabilitative care is generally practiced. Stabilization exercises are applied to areas of functional instability—a patient’s mental goal is to “stabilize.” Proprioceptive exercises are utilized and related deficits are identified—a patient’s mental goal is to focus on “coordination.” End range loading is performed in the direction that centralizes and abolishes pain—a patient’s mental goal is to “extend” (in most cases). Clearly, the rehabilitative goals and mind-sets are straightforward and not confusing from a practical perspective, which should be the same for diet. If dietary goals and applications are not straightforward and are instead confusing, compliance will be poor.
Nutritional supplements are often used as part of the treatment program for rehabilitating painful musculoskeletal tissues. As with diet and rehabilitative methods, the approach with nutritional supplements should also be uncomplicated. Table 36.4 lists supplements that can be used for short- and long-term management of inflammation.1,2,3,4,5,6,7,8
Based on Tables 36.1 and 36.4, the nutritional approach to inflammation reduction is to drastically modify dietary behavior, the primary issue being the avoidance of calories from sugar, flour, and n-6 fatty acids, which should be replaced with calories from vegetables, fruit, roots/tubers, nuts. This leads to a normalization of multiple pro-inflammatory chemicals, such as nuclear factor kappa-B (NF-κB), phospholipase A2 (PLA2), cyclo-oxygenase (COX), lipoxygenase (LOX), and cytokines, which will be described in more detail in the next section of this chapter. Supplements should be taken to support or “supplement” the anti-inflammatory diet. In general, diet and supplements should not be viewed in the context of individual named conditions/diseases and this is because most conditions involve excess inflammation. In other words, inflammation is the issue, not the name of the condition that reflects the presence of inflammation in a particular parenchymal tissue.
The next section of this chapter is devoted to diet-induced inflammation. The remaining sections thereafter will describe how to view the issue in the context of rehabilitating patients with musculoskeletal pain syndromes.
Table 36.4 Supplements for Inflammation
Supplement
Dose
Mechanism of Action
Clinical Consideration
For Short-Term Use
Proteolytic enzymes (bromelain, trypsin, and chymotrypsin)
1,000-2,000 mg per day taken on an empty stomach
Antagonizes fibrin and cytokines
Acute inflammation after obvious injury
White willow bark
1,000-4,000 mg per day
Antagonizes free radicals, NF-κB, PLA2, COX, LOX, and collagenase
Pain exacerbation without obvious injury
For Long-Term Use
Ginger, turmeric, boswellia, and other botanicals
1,000-2,000 mg per day
Antagonizes free radicals, NF-κB, COX, and LOX
Chronic inflammation/pain management
Magnesium
200-1,000 mg per day
Involved in hundreds of enzymes; reduces inflammation and regulates central nociception
Chronic inflammation/pain management
Omega-3 fatty acids
1,000-3,000 mg per day
Precursor for anti-inflammatory mediators
Chronic inflammation/pain management
Vitamin D
1,000-10,000 IU based on blood levels
Regulates 2,000 genes including pro- and anti-inflammatory cytokines
Chronic inflammation/pain management
Probiotics
Depends on product
Reduces gut inflammation and associated systemic inflammation
Chronic inflammation/pain management
Coenzyme Q10
100 mg per day or more
ATP production, antioxidant, regulates skeletal muscle gene expression
In 2002, I wrote an article entitled The Diet-induced Pro-inflammatory State.9 It was a challenge to get this paper published because the relationship between diet, inflammation, and pain was just emerging at that time, but to use the colloquial, the writing was clearly on the wall. It is 15 years later now and the research in this area has exploded during this time period, such that it is clearly acknowledged that diet promotes or reduces inflammation.10,11,12,13,14,15,16,17 Review articles are even being published in rehabilitation, translational science, and other journals with titles such as Nutrition and pain18 and Dietary influence on pain via the immune system,19 and Ketogenic diets and pain.20
The average American’s diet is known to be pro-inflammatory, such that very little anti-inflammatory vegetables, fruit, roots/tubers, and nuts are consumed. Instead, approximately 20% of calories come from refined sugar, 20% from refined flour, and 20% from refined omega-6 oils.21 The omega-6 oil sources include corn, safflower, sunflower, cottonseed, peanut, and soybean. Figure 36.1 outlines the general process by which these calories sources generate inflammation.22
Sugar and flour consumption creates a postprandial hyperglycemic response, such that blood glucose will enter cells in amounts greater than normal. This leads to the production of adenosine triphosphate as well as an excess of superoxide free radicals, which activate NF-κB. The nuclear factor subsequently translocates from the cytoplasm to the nucleus, wherein it induces the production of multiple inflammatory proteins. Examples include enzymes such as PLA2, COX, and LOX, which convert dietary omega-6 arachidonic acid into prostaglandin E2 (PGE2) and leukotriene B4 (LTB4). Both PGE2 and LTB4 are referred to as pro-inflammatory eicosanoids, which promote local inflammation.
The same blood glucose surge from sugar and flour consumption causes NF-κB to promote the production of pro-inflammatory cytokines, most notably, interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF). Each of these cytokines promotes local inflammation in conjunction with the pro-inflammatory eicosanoids. Additionally, IL-6 is known to be the cytokine responsible for stimulating the liver to produce C-reactive protein (CRP).
Figure 36.1 The process by which a pro-inflammatory diet can promote inflammation and pain. Reprinted with permission from Seaman DR. The DeFlame Diet. Wilmington, NC: Shadow Panther Press; 2016.
In response to the same postprandial glucose surge, NF-κB produces many other proteins such as matrix metalloproteinases (MMPs) and growth factors, such as vascular endothelial growth factor (VEGF). Collagenase, elastase, and stromelysins are examples of MMPs, which function to degrade connective tissue, such as in joint cartilage, nucleus pulposus, annulus fibrosis, and tendons. VEGF promotes angiogenesis, which is associated with disc herniation and the development of osteoarthritis (OA).
Unlike sugar and flour, the consumption of refined omega-6 oils does not stimulate mitochondria to produce free radicals. Instead, the oils by themselves, or in combination with sugar and flour, cause lipopolysaccharide (LPS) to be released from the cell wall of gram-negative bacteria located in the small intestine release. LPS, which is also known as bacterial endotoxin, is absorbed into circulation where it, like superoxide free radicals, stimulates NF-κB to produce inflammatory proteins.
It should be understood that the inflammatory response described above occurs immediately after sugar, flour, and lipid calories are consumed.23,24,25,26 Test meals that have been used to measure this “acute dietary injury response” in healthy normal weight subjects include three slices of buttered white toast (900 calories) and a typical McDonald’s breakfast that consisted of an egg muffin, sausage muffin, and two hash brown patties (910 calories).27,28 When eating these pro-inflammatory calories on an occasional basis, it is not likely that long-term pro-inflammatory changes will occur. However, if sugar, flour, and lipids are consumed on a regular basis, and the diet is otherwise limited in polyphenol- and carotenoid-rich vegetation, multiple pro-inflammatory changes can develop.22
Chronic exposure to a pro-inflammatory diet leads to inadequacies of omega-3 fatty acids and magnesium, and because most individuals have been scared out of the sun for fear of skin cancer, vitamin D insufficiency or deficiency is the norm, rather than the exception. Each of these nutrients is known to support gut barrier integrity, which when compromised allows for a leaky gut state that permits greater absorption of LPS.27,28,29,30,31,32,33,34,35,36 The leaky gut state is also promoted by the overconsumption of sugar, flour, and oils, because each promotes the overgrowth of gram-negative bacteria in the small intestine.37,38 This dysbiosis state is further promoted by a lack of dietary prebiotics (vegetables, fruit, nuts, and roots/tubers) and probiotics from fermented foods. The net outcome is a greater absorption of LPS into circulation as illustrated in Figure 36.1.
The chronic overconsumption of sugar, flour, and omega-6 oils, coupled with a lack of exercise, will eventually lead to a reduction in high-density lipoprotein (HDL) cholesterol, which is one marker for the metabolic syndrome (see Table 36.1). Although HDL is most well known for its relationship to cardiovascular disease (CVD), it plays a key role in trapping and eliminating LPS molecules that are absorbed from the gut.39 Practically speaking, this means that weight gain and the expression of the metabolic syndrome correlate with increasing levels of circulating endotoxin, which has been associated with the eventual expression of type 2 diabetes and depression.39,40
Notice the term “adiposopathy” in Figure 36.1, which refers to sick fat or inflamed fat syndrome. Adiposity refers to the accumulation of fat mass, which initially occurs without measurable systemic inflammation. At some point during the accumulation of body fat, a pro-inflammatory shift occurs within adipose tissue.41,42 Lean adipose tissue consists of adipocytes and an anti-inflammatory profile of immune cells including T-helper 2 cells, T-regulatory cells, and M2 nonactivated macrophages These immune cells release anti-inflammatory mediators such as IL-10.
As adipocytes swell in size, there is an associated reduction and eventual disappearance of anti-inflammatory immune cells, which are replaced with pro-inflammatory T-helper 1 cells, cytotoxic T-cells, M1-activated macrophages, and mast cells. These pro-inflammatory immune cells chronically release pro-inflammatory mediators, such as the cytokines IL-1, IL-6, and TNF, as indicated in Figure 36.1, which act on NF-κB to perpetuate inflammation. Although not as robust, it should be understood that this immune profile associated with adiposopathy is similar to the immune profile associated with an infection or autoimmune disease.
Notice in Figure 36.1 that pro-inflammatory cytokines are also released by macrophages/monocytes in local tissues and in circulation, due to an insufficiency/deficiency of omega-3 fatty acids, magnesium, and vitamin D.43,44,45 The outcome is an additional source of stimulation of NF-κB and augmented inflammatory mediator release and related communication among various cell types, such as macrophages, fibroblasts, and sensory C neurons.
Described thus far are the chemical changes that occur during the “flame-up” process, which can take years to develop. It is reasonable to be curious as to when this progressively increasing inflammatory state may cause pain and other symptoms/conditions. Figure 36.1 does illustrate that sensory C neurons generate pain; however, this is not an all or nothing phenomenon.
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