Chronic inflammation has been linked to multiple health issues that plague our society, including obesity, diabetes, cardiovascular disease, some cancers plus a range of autoimmune diseases. Here we’ll highlight what chronic inflammation is and some simple lifestyle changes to help reduce the toll it takes on your body.
Acute inflammation is the body’s response to tissue injury. It is the first line of defense against injury and is characterized by changes in microcirculation, leakage of fluid and migration of white blood cells from blood vessels to the area of injury. Typically of short duration, acute inflammation is primarily aimed at removing the injurious agent. Most of the time it is self-limiting. Clinically, acute inflammation is characterized by five cardinal signs: rubor (redness), calor (heat), tumor (swelling), dolor (pain), and functio laesa (loss of function). The acute inflammatory process is essential for tissue healing and repair.
Chronic inflammation, on the other hand, serves no function and has been linked to many of the chronic illnesses that are epidemic today, such as: diabetes, cardiovascular diseases, autoimmune diseases, arthritis, some cancers, allergies, asthma and obesity. (Khansari, N et al. 2009)
SPEED is an acronym for five major lifestyle factors that can be manipulated to mitigate and/or reverse some of the effects of chronic inflammation:
- Psychological stress
A number of studies have reported an association between poor sleep and inflammation. Alterations in sleep have been shown to increase a range of inflammatory markers. In addition, several of these inflammatory processes have been associated with reduced health status and inflammation-based diseases such as cardiovascular disease, diabetes, arthritis and obesity. Maintaining adequate sleep duration and quality through good sleep habits may reduce inflammatory processes and increase wellness. (Miller, M.A. 2007) (Simpson, N.,2007)
Chronic exposure to stress is associated with an increased risk of disease and the expression of proinflammatory genes via the sympathetic nervous system. (Powell, N.D., et al. 2013) Many of the symptoms of chronic inflammation are aggravated by ongoing repeated stress. Chronic repeated stress exerts different effects on the inflammatory response than short-lived acute stress does. The ongoing repetition of a mild stressor can induce adverse effects on the inflammatory process that might otherwise be innocuous acutely. Clinically, there is an association between repeated stress and the aggravation of inflammatory disease symptoms. (Strausbaugh, H.J., et al. 1999)
Persistent organic pollutants (POPs) are toxic compounds that persist in the environment, enter into the food chain, and accumulate in adipose tissue due to their high lipophilicity. POPs include some organochlorine pesticides, polychlorinated biphenyls (PCBs), brominated flame retardants and polycyclic aromatic hydrocarbons.
POPs have been shown to perturb health due to their disrupting effects on the endocrine, immune, and reproductive systems. Many studies show an association between POP exposure and insulin resistance, as well as metabolic disorders like obesity, diabetes, and metabolic syndrome. Inflammation is a known mechanism arising in tissues exposed to POPs. (Mostafalou, S. 2016)
Neurogenic inflammation is another consequence of exposure to environmental toxins. Chemical exposure results in the release of inflammatory mediators (neuropeptides) from nerve cells. Neurogenic inflammation appears to play an important role in the pathogenesis of numerous chronic inflammatory diseases, including migraines, psoriasis, asthma, rhinitis, arthritis, fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivites. (Meggs, W.J. 1993)
Phthalates (AKA plasticizers) are another group of chemicals used to make plastics as well as being used as solvents (dissolving agents). Phthalates are used across a large range of products, including such items as personal-care products (e.g., hair, nail and soap products), detergents, vinyl flooring, adhesives, lubricating oils, and automotive plastics.
Additionally, phthalates are widely used in polyvinyl chloride plastics, These are used in products such as packaging film, garden hoses, toys (inflatable and even some children’s toys), and somewhat surprisingly, blood-storage containers and medical tubing. Phthalate exposure can result in inflammation and oxidative stress and has been associated with a wide range of adverse health outcomes. (Ferguson, K.K., et al. 2011)
Regular exercise protects against diseases associated with chronic low-grade systemic inflammation. These effects may be ascribed to the anti-inflammatory response elicited by muscle-derived cytokines such as interleukin 6 (IL-6). IL-6 inhibits the production of the proinflammatory cytokine Tumor Necrosis Factor (TNF-α). Additionally, IL-6 stimulates lipolysis and fat oxidation and may offer protection against TNF-induced insulin resistance.
In addition to their local effects, IL-6 and other cytokines, which are produced and released by skeletal muscles (AKA myokines), have been shown to exert their effects in other organs of the body, and may play important roles in the protection against numerous diseases associated with low-grade inflammation. (Petersen, A.M.W., & Pedersen, B.K. 2005)
Should You Take NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) After Strength Training?
Resistance training leads to skeletal muscle hypertrophy. Satellite cells (the stem cells of skeletal muscle) are essential for physiological adaptations during muscle hypertrophy and for muscle regeneration after injury. Their role is to provide new myonuclei during hypertrophy and assist in the repair of damaged muscle fiber segments for successful regeneration.
NSAID use during and after exercise has been shown to suppress the exercise-induced increase in the number of satellite cells for up to eight days after exercise, suggesting that NSAIDs negatively affect satellite cell activity and muscle repair/adaptations. (Mikkelsen, U.R., et al. 2009)
The influence of energy balance, macro and micronutrients, and the gut microbiome on diet-induced inflammation has been well established.
Excessive energy intake induces obesity, which in turn creates a state of chronic, low-grade inflammation.
Adhering to a balanced diet with healthy carbohydrates (low glycemic), anti-inflammatory fats (omega-3 polyunsaturated fatty acids and monounsaturated fats), adequate protein and nutrient dense foods high in vitamins, minerals, and flavonoids are effective ways to ¨deflame” the body and reduce the incidence and morbidity of inflammatory diseases.
The influence of diet on inflammation is related to how different nutrients affect inflammatory substances such as C-Reactive Protein (CRP), eicosanoids and cytokines (e.g., TNF-α and Interleukins).
Carbohydrates are our main dietary energy source and can be evaluated according to their glycemic response. Glycemic Index (GI) is a ranking of foods based on their postprandial blood glucose responses and a measure of carbohydrate quality. Glycemic Load (GL) is a measure that incorporates both the quantity and quality of dietary carbohydrates. Studies have shown an association between dietary GI/GL and inflammatory cytokines.
A number of different fatty acids, including polyunsaturated (PUFA), saturated, and trans-fatty acids have been studied for their effects on inflammatory status.
Polyunsaturated Fatty Acids (PUFAs)
The omega-6 (n-6) and omega-3 (n-3) PUFA families are precursors to eicosanoids, which play an important role in the immune response. The anti-inflammatory effects of n-3 PUFA (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) have been observed in numerous studies, which have shown that the intake of n-3 fatty acids (e.g., cold water fish) is inversely associated with biomarkers of inflammation, such as CRP, IL-6, and TNF-α. Other studies indicate that humans evolved on a diet with a ratio of omega-6 (e.g., vegetable and seed oils) to omega-3 essential fatty acids (e.g. cold water fish, flax and walnuts) of ~1:1, whereas in Western diets the ratio is closer to 15:1. While both omega-6 and omega-3 fats are essential fats (i.e., they need to come from the diet), a high omega-6:omega-3 ratio promotes the pathogenesis of many inflammatory based diseases, including cardiovascular disease, cancer, osteoporosis, and autoimmune diseases, whereas increased levels of omega-3 (a lower omega-6:omega-3 ratio), exert suppressive effects. (Simopoulos, A.P. 2006)
Trans and Saturated Fats
Observational and interventional studies suggest that trans and saturated fats are significantly related to the immune response. Trans fat consumption has been associated with high levels of CRP and IL-6.
Vegetables and Fruits
Numerous studies have reported an inverse association between high vegetable/fruit consumption and CRP levels. Some vitamins and minerals (e.g., vitamins A and C, and magnesium) have been shown to have a beneficial effect on oxidative stress and immune responses and are associated with decreased levels of inflammatory markers such as CRP, TNF-α, and IL-6.
Flavonoids are polyphenolic compounds that are present in plant-based foods such as vegetables, fruits and herbs, that have shown clear antioxidant, anti-inflammatory and immunoregulatory effects. High consumption of dietary flavonoids is inversely associated with plasma CRP concentration and plasma levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-8).
Phytoestrogens are plant-derived compounds found in a wide variety of foods, such as beans, seeds, and grains. Phytoestrogens are recognized to have anti-inflammatory properties that significantly reduce plasma CRP concentrations.
Probiotics and Prebiotics
Probiotics are living microorganisms that have health benefits for their host. Orally ingested probiotic bacteria are able to modulate the immune system and have beneficial effects on inflammatory markers. Prebiotics are nondigestible food components that have a health benefit associated with the modulation of microbiota in the gut. There is a convincing association between prebiotic supplementation and inflammatory markers. (Lee, H., 2013) (Galland, L. 2010).
Can diet affect pH and low-grade chronic inflammation?
The human body requires a tightly controlled pH level in the blood of about 7.4 (slightly alkaline) to survive. In the past century, increased industrialization has adversely affected the pH of our oceans and the soil in which plants are grown. Consequently, this has had considerable influence on the mineral content of the food we eat. Acidic soil results in a reduction in the bioavailability of essential nutrients such as calcium, magnesium, iron, manganese, copper and zinc, thereby affecting the mineral content of some of our foods.
When it comes to the pH and net acid load in the human diet, there has also been considerable change from the hunter gather civilization to the present Both the agricultural revolution (last 10,000 years) and industrialization (last 200 years), has resulted in a decrease in potassium (K) compared to sodium (Na) and an increase in chloride compared to bicarbonate found in the diet. The ratio of potassium to sodium has reversed. K/Na previously was 10 to 1, whereas the modern diet has a ratio of 1 to 3. It is generally accepted that our current diet is poor in magnesium, potassium and fiber and high in saturated fat, simple sugars, sodium, and chloride as compared to the pre agricultural period. Consequently, the modern diet may induce a relative metabolic acidosis which is mismatched to our genetically determined nutritional requirements.
In addition, as we age, there is a gradual loss in renal acid-base regulatory function and a resultant increase in diet-induced metabolic acidosis when adhering to a modern diet. The pH in our body may vary considerably from one area to another, with the highest acidity in the stomach (pH of 1.35 to 3.5) to aid in digestion and protect against opportunistic microbial organisms. The skin is also acidic (pH 4–6.5), providing a protective barrier to the environment against microbial overgrowth. The urine may have a variable pH from acid to alkaline depending on the need for balancing the internal environment.
Foods can be categorized by the potential renal acid loads. Fruits, vegetables, fruit juices, potatoes, and alkali-rich and low phosphorus beverages (e.g., red and white wine, mineral soda waters) have a negative acid load, whereas grains, meats, dairy, fish, and alkali poor and low phosphorus beverages (e.g., pale beers, cocoa) have relatively high acid loads.
There may be some value in considering an alkaline diet in reducing morbidity and mortality from chronic diseases. Some of the research in this area has focused on:
- Chronic Acidosis and Bone Disease
- Alkaline Diets and Muscle (Sarcopenia)
- Alkaline Supplementation and Growth Hormone
- Alkaline Diets and Back Pain
- Alkalinity and Chemotherapy
From an inflammatory perspective, eating alkalizing foods may have many of the same anti-inflammatory properties mentioned above due to the quality and type of macro, micro and phyto nutrients naturally present in these foods. More studies are warranted in this area of medicine. (Schwalfenberg, G. K. 2011)
Practical Tips to Reduce Chronic Inflammation
- Adults should aim for 7-9 hours/night
- Keep your bedroom dark and minimize/eliminate electronics
- Get a routine going (and stick to it)
- Try a light snack 30 minutes before bed
- Cognitive Behavioral Therapy
- Daily meditation
- Acupuncture and massage
- The Environmental Working Group is a great resource to identify the toxic load exposure from your diet and self-care products.
- Follow the NASM – Optimum Performance Training ™ (OPT™) model to get the most out of your exercise though an integrated, evidence-based exercise plan
- Adhere to a balanced diet consisting of healthy carbohydrates (low glycemic), “good” fats (omega-3 polyunsaturated fatty acids and monounsaturated fats), adequate protein, and cultured and nutrient dense foods
Ferguson, K. K., Loch-Caruso, R., & Meeker, J. D. (2011). Exploration of oxidative stress and inflammatory markers in relation to urinary phthalate metabolites: NHANES 1999–2006. Environmental science & technology,46(1), 477-485.
Galland, L. (2010). Diet and inflammation. Nutrition in Clinical Practice, 25(6), 634-640.
Khansari, N., Shakiba, Y., & Mahmoudi, M. (2009). Chronic inflammation and oxidative stress as a major cause of age-related diseases and cancer. Recent patents on inflammation & allergy drug discovery, 3(1), 73-80.
Lee, H., Lee, I. S., & Choue, R. (2013). Obesity, inflammation and diet. Pediatric gastroenterology, hepatology & nutrition, 16(3), 143-152.
Meggs, W. J. (1993). Neurogenic inflammation and sensitivity to environmental chemicals. Environmental health perspectives, 101(3), 234.
Mikkelsen, U. R., Langberg, H., Helmark, I. C., Skovgaard, D., Andersen, L. L., Kjær, M., & Mackey, A. L. (2009). Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise. Journal of Applied Physiology, 107(5), 1600–1611. http://doi.org/10.1152/japplphysiol.00707.2009
Miller, M. A., & Cappuccio, F. P. (2007). Inflammation, sleep, obesity and cardiovascular disease. Current vascular pharmacology, 5(2), 93-102.
Mostafalou, S. (2016). Persistent Organic Pollutants and Concern Over the Link with Insulin Resistance Related Metabolic Diseases.
Petersen, A. M. W., & Pedersen, B. K. (2005). The anti-inflammatory effect of exercise. Journal of applied physiology, 98(4), 1154-1162.
Powell, N. D., Sloan, E. K., Bailey, M. T., Arevalo, J. M., Miller, G. E., Chen, E., … & Cole, S. W. (2013). Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via β-adrenergic induction of myelopoiesis. Proceedings of the National Academy of Sciences, 110(41), 16574-16579.
Schwalfenberg, G. K. (2011). The alkaline diet: is there evidence that an alkaline pH diet benefits health?. Journal of Environmental and Public Health, 2012.
Simopoulos, A. P. (2006). Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases.Biomedicine & pharmacotherapy, 60(9), 502-507.
Simpson, N., & Dinges, D. F. (2007). Sleep and inflammation. Nutrition reviews, 65(suppl 3), S244-S252.
Strausbaugh, H. J., Dallman, M. F., & Levine, J. D. (1999). Repeated, but not acute, stress suppresses inflammatory plasma extravasation. Proceedings of the National Academy of Sciences, 96(25), 14629-14634.