
“The path to a healthier diet need not be as difficult to navigate as it may appear”
– eeMD
Diet:
Diet and Pain
For many, the role of diet – what and how we eat – is a hugely underestimated variable determining the extent of chronic pain one experiences. The diet one maintains affects not only one’s sensitivity to pain, but also the intensity and the development of the severity of pain. Despite the enormous impact diet has on chronic pain, dietary intervention is extremely underutilized as a means of treating chronic pain and improving quality of life.
The reason for this is largely based on the under-appreciation of the dietary role in chronic pain and the reluctance people have to changing their usual diet. Interestingly, it has also been shown that chronic pain contributes to an impaired sensation of satiation, or feeling full, leading to overeating. Chronic pain also appears to drive higher levels of carbohydrate and fatty food intake.
For those motivated to reduce their chronic pain and enhance their sense of well-being, however, changing one’s diet can be extremely helpful. The basis of dietary effects on pain are primarily based on the role of food intake on the microbiome (the bacteria in the intestinal tract) and on inflammation, both systemic and within the nervous system.The key to reducing pain through dietary management is to emphasize foods that enthance diversity in the microbiome and avoid foods that contribute to systemic inflammation.
And, while supplements play a role in restoring dietary health, they remain supplements, not substitutes, to a healthy diet.
The relationship between nutrition and chronic pain is complex and involve many underlying mechanisms such as oxidative stress, inflammation, and glucose metabolism. But nutrition is the top modifiable lifestyle factor for chronic non-communicable diseases including chronic pain. Optimizing one’s dietary intake and behavior is most important in pain management.
See also:
- An Anti-Inflammatory Diet
- Antioxidants and Oxidative Stress
- Obesity and Pain
- Diet & Diets
- Diet & Fasting
- Diet & Fibromyalgia
- Dysfunctional Eating Behaviors
- Emotional Eating
- External Eating
- Night Eating Syndrome
- Gut Microbiota
- Gut Microbiota and Pain
- Irritable Bowel Syndrome (IBS)
- Food Intolerance & Sensitivity: An Overview
- Food Intolerance & Sensitivity: Gluten
- Elimination Diet – Gluten
- Elimination Diet – FODMAPs
- NRF2 Activators
- Nutrition: Amino Acids
- Nutrition: Carbohydrates
Diet Supplements:
- Supplements – An Overview
- Antioxidants
- NRF2 Activators
- Mitochondrial Dysfunction
- A Quick Review of Vitamins and Minerals,
- Minerals
- Vitamins
Key to Links:
- Grey text – handout
- Red text – another page on this website
- Blue text – Journal publication
Definitions and Terms Related to Pain
Diet & Pain: an Overview
When should someone with chronic pain consider looking at their diet as a means of reducing their pain?
The answer is almost always. Given that Americans generally follow a less-than-ideal diet, there is always room for improvement and in many cases improvements can contribute to reduced pain. However, a more specific answer is when one’s pain or other symptoms are likely to be food-oriented or when one’s symptoms are poorly controlled and not responding to standard care. While the assessment of diet should not be delayed until reaching the point of desperation, this is often the case. But better late than never.
Common chronic pain conditions associated with nutritional factors include osteoarthritis, rheumatic arthritis, fibromyalgia, back pain, irritable bowel syndrome (IBS), pelvic pain (e.g., endometriosis), diabetic neuropathy, migraine headache, post-herpetic neuralgia, and carpal tunnel syndrome.
For the most part, the discussion of diet and pain is a look at the forest, not the trees. While in certain cases of food allergies, food sensitivities and other food intolerances where even small amounts of specific foods can trigger pain and disease, the role of diet is otherwise a look at the big picture. The complete elimination of all “unhealthy” foods is not the goal in planning for a diet to reduce pain. In fact, most “unhealthy” foods become so mainly when they are eaten in excess.
How Pain and Diet are Related
Pain interfaces with diet in a number of ways that often overlap:
- Nutritional Deficiencies and Insufficiencies
- Inflammation and Oxidation (Oxidative Stress)
- Food Intolerances: Allergies and Sensitivities
- Intestinal Wall Integrity
- Gut Microorganisms (Microbiome)
- Impact on Prevention and Control of Painful Medical Conditions
- Pain appears to trigger excessive and/or emotional eating, including pleasure-eating
- High Cholesterol and disrupted lipid metabolism
- Epigenetic Factors, diet and pain
A Quick Summary of an Optimal Diet for Chronic Pain
Since there is no one diet that fits all, this summarizes an optimum diet for pain management. The section on this website that provides a thorough review of the optimal diet recommended for chronic pain is the Anti-Inflammatory Diet (AID). In-depth evaluations of various dietary components are also available including A Quick Review of Vitamins and Minerals, Omega Fatty Acids, Dietary Fiber, Cooking Oils, Green Tea, Chocolate, Chia Seeds, and other subjects are also available.
People experiencing pain generally consume more calories, added sugars, saturated fatty acids, sodium, and caffeine. One third of males and approximately half of female participants in a study consume more than the recommended daily caloric intake, moderate fat intake, and a high saturated fat intake. This study also showed that in people with chronic pain their intake of vitamin D, vitamin E, and magnesium was lower than the recommended daily intake.
To keep things simple, the following food pyramid is based on recent research and is intended to help alleviate chronic pain for most people but should be individualized by one’s physician :
The base of the pyramid includes foods that should be eaten every day:
- 3 portions of carbohydrates with low glycemic index
- 5 portions of fruits and vegetables
- 125 ml yogurt
- extra virgin olive oil
On the next level, foods that should be eaten every week:
- 4 portions of beans, nuts and fish (Salmon, Tuna, Oysters preferred)
- 2 portions of white meat, eggs and fresh cheese
Once per week or less:
- red or processed meats
- Sweets are only allowed occasionally.
Finally, the pinnacle at the top of the pyramid:
Specific, customized foods & supplementation for individuals with chronic pain, that may include:
- Vitamins B9, B12, C and D
- Minerals: Magnesium, Zinc
- Dietary Fiber (Chia Seeds)
- Omega-3 fatty acids (fish oil)
- Avocado
- Matcha Green Tea
Anti-inflammatory and antioxidant supplements:
1. Nutritional Deficiencies and Insufficiencies – a Quick Overview
Nutritional deficiencies and insufficiencies are more common than one might expect. Frank deficiencies are less likely but insufficiencies, or levels that are suboptimal but not actually deficient enough to result in classic deficiency syndromes, are not uncommon and often contribute to pain and/or functional impairment.
Risks for Malnutrition
Malnutrition may occur by not eating enough, not eating the right foods, or being unable to absorb nutrients. Up to 50% of adults >65 years old are malnourished or at an increased risk of malnutrition. A recent study found that older people (>60 years) with chronic pain are almost two times more likely to develop frailty after an average follow up of 5.8 years, compared to those without chronic pain. Frailty is characterised by a decline in physical, mental, and multisystem functions associated with depleted physiological and psychosocial conditions. A serious consequence of frailty is the increased risk of disability and death from minor external stresses, such as a mild infection or facing a stressful event.
Common nutritional deficiencies in America include Vitamin D and Omega-3 fatty acids while common insufficiencies include antioxidants, magnesium, selenium, zinc, vitamin B12, folic acid and Vitamin C, , certain amino acids and dietary fiber.
Omega-3 fatty acids are dietary fats that are important in fighting the systemic inflammation that contributes to chronic pain. Antioxidants are important in combating oxidative stress, which is the build-up of compounds such as free radicals that are destructive by-products of digestion and energy production. These destructive compounds play an important role in the maintenance of chronic pain and in enhancing pain hyper-sensitivity. They also significantly contribute to the development of degenerative diseases, including heart disease, stroke, certain cancers and type-2 diabetes. B vitamins are involved in a multitude of metabolic process that impact pain and deficiencies of Vitamins B1 and B12 lead to painful peripheral neuropathy. Vitamin C is a powerful antioxidant that is often insufficient in smokers and obesity and likely contributes to arthritis pain. Vitamin D, important for maintaining bone density, is also an anti-inflammatory and a significant player in pain.
Magnesium replacement has significant benefit for medical conditions that include muscle spasm and muscle pain, chronic headaches and fibromyalgia. Of particular significance to health and pain is an insufficient intake of the antioxidants found in fruits and vegetables. Omega-3’s and antioxidants impact health in many ways but their insufficiencies are major players in oxidative stress, inflammation and nerve pain.
In addition to fiber’s role in maintaining bowel function, fiber plays an important part in maintaining a healthy microorganism balance in the gut (microbiome – see below), where imbalances contribute to a number of painful conditions. Furthermore, the amount of fiber in one’s diet has been shown to be inversely proportional to the amount of pain associated with knee osteoarthritis. In other words, for those with knee arthritis, the more fiber in the diet, the less pain is likely to be associated with the knee arthritis.
See: Magnesium
See: Nutrition and Oxidative Stress
2. Diet, Inflammation and Oxidative Stress
The “Typical American Diet (TAD) ” is characterized by low intake of fruits, vegetables and fiber along with a high intake of processed grains, carbohydrates , sugars and poor quality fats and oils. In addition, it includes a multitude of additives including artificial sweeteners and preservatives.
The TAD contributes to the two driving forces for chronic pain: inflammation and oxidative stress. Oxidative stress is defined as an excess of certain toxic metabolic compounds (reactive oxygen species – ROS) and a shortage of antioxidative compounds to detoxify ROS in cells and tissues. In addition to other factors (e.g., radiation, smoking, air pollution), dietary induced oxidative stress initiates activation of immune cell that cause inflammation. Ths immune cell activation also raises the amount of the ROS which further contribute to oxidative stress thus creating an oxidative stress—inflammation vicious cycle.
Improvements in diet can cause significant and immediate favorable changes in the PPD. Evidence demonstrates that an increase in dietary antioxidant intake and the increased detoxifying ability of the body can alleviate pain among people with chronic musculoskeletal pain.
Engaging a diet high in minimally processed, high-fiber, plant-based foods including vegetables and fruits, whole grains, legumes, and nuts will markedly reduce the post-meal increase in glucose, triglycerides, and inflammation. Other interventions including intake of specific foods such as lean meat, fish oil, tea, vinegar, ginger and cinnamon, as well as calorie restriction, weight loss and exercise improve PPD. Studies indicate that diets such as the Mediterranean or Okinawan diets that incorporate these types of foods and beverages reduce both inflammation and cardiovascular risk. This anti-inflammatory diet should be engaged for chronic pain as well as for the prevention of coronary artery disease and diabetes (See below).
The Typical American Diet (TAD) , especially with high intakes of saturated animal fats, is associated with increased production of inflammatory cytokines, chemicals that contribute to oxidative stress, pain sensitivity and systemic inflammation, including not just the joints in the extremities and spine but also the organs including the heart, blood vessels and liver.
Cytokines
Cytokines are small proteins released by immune cells that have a specific effect on the interactions and communications between cells and can be either pro-inflammatory or anti-inflammatory. Cytokine is a general name; other names include lymphokine (cytokines made by lymphocyte immune cells), monokine (cytokines made by monocytes immune cells), adipokine (cytokines made by fat cells), and interleukin (cytokines made by one leukocyte immune cells and acting on other leukocyte immune cells).
This persistent pro-inflammatory state decreases the ability of the body’s antioxidants to detoxify cells and tissues (dietary induced oxidative stress) and is an important risk factor for cardiovascular diseases, diabetes mellitus, obesity, cancer, and, especially maintenance of chronic pain.
Pro-inflammatory cytokines are involved in not only the initiation but also the persistence of pathologic pain by directly activating nerves that sense pain (nociceptive sensory neurons). Certain inflammatory cytokines are also involved in nerve injury and inflammation-induced central sensitization, and are related to the development of chronic pain hypersensitivity (hyperalgesia & allodynia).
Neuroinflammation is a localized form of inflammation that occurs in the peripheral and central nervous system. In chronic pain conditions, neuroinflammation is characterized by activation of nerve cells called glial cells, resulting in their increased production of inflammatory cytokines which lead to peripheral and central nervous system sensitization and the development of chronic pain hypersensitivity (hyperalgesia & allodynia). Abnormal glial cell activity drives conditions such as chronic non-specific low back pain, fibromyalgia, migraine, and spinal radiculopathy (sciatica).
Biomarkers for Inflammation
How to effectively measure the degree of systemic inflammation of an individual has been elusive to medical science for decades. Many biomarkers have been identified that appear to be associated with systemic inflammation and often serve as measures of comparism between study groups and study outcomes. An inflammatory biomarker commonly measured in general medical practice is C-Reactive Protein (CRP). It is commonly elevated in obesity and has also been correlated with osteoarthritis and low back pain. While clinically useful, CRP levels are limited in the amount of information they provide or predict. Another clinical biomarker of systemic inflammation is Interleukin-6, one of the Interleukin family of cytokines associated with inflammation. Further information regarding the clinical use of measuring inflammatory biomarkers is forthcoming on this web site.
Obesity-Related Pain
Secondary consequences of the SAD is a predisposition to obesity, glucose intolerance and diabetes. Obesity is characterized by an abundance of fat cells that manufacture large amounts of inflammatory cytokines (adipokines) leading to systemic inflammation. Obese patients have, in general, a worse pain profile than the normal weight patients with higher pain intensity, increased pain interference in activities, more sleep disturbances and more constant pain.
Studies show that obesity is an independent predictor of migraine headaches and of severe arthritis progressing to joint replacements of the knees and hips. Obesity is also associated with higher levels of neuropathic pain. Glucose intolerance and diabetes are associated with damages to nerves that leads to worsening of arthritis pain and painful neuropathy.
Adipose tissue (or fat cells (adipocytes) – are now understood to be complex and highly dynamic, with endocrine, metabolic, and immune regulatory activity. Fat cells releases an abundance of bioactive peptides or proteins, immune molecules, and inflammatory mediators named “adipokines” (only produced by the adipose tissue) or “adipocytokines” (primary but not exclusively produced by adipocytes). However, the term “adipokine” is used throughout here to refer to all these mediators, including Interleukins (IL-1, IL-6, IL-8), TNF (Tissue Necrosis Factor), adinopectin, leptin and resistin. A growing number of studies indicate that adipokines are significant contributors to the development of arthritis.
It should also be pointed out that systemic inflammation, obesity and pain are also inter-related with stress. depression, insomnia, sleep apnea, fatigue and physical deconditioning. These conditions interact on levels that sustain and enhance each other and contribute to overall impaired health, physical and emotional.
Weight Loss and Reduced Pain
It is commonly under-appreciated how significant weight loss benefits pain in the obese population. In a study of obese patients with a BMI of 36 or greater experienced a 50% reduction in perceived pain associated with an 11% weight loss over 8 weeks. In patients with obesity and knee arthritis, a simple 5% weight loss resulted in 24% improvement in function and a 30% improvement in pain.
Anti-Inflammatory Diets for Pain Management
There are always many opinions as to what constitutes the healthiest diet and what people should eat. There are a number of proposed diets that are considered to be anti-inflammatory including the Mediterranean diet, the Paleo diet and the Okinawan diet, three currently popular versions. The Paleo diet appears to be a front runner currently but how one defines a Paleo diet is open to a wide range of interpretation and the reader is referred to other sites for more information at this time. The Mediterranean diet is also highly recommended as an anti-inflammatory diet to reduce chronic pain and also to reduce oxidative stress and the risk for atherosclerosis, heard disease and risk for stroke (see handouts below). See: An Anti-inflammatory Diet.
Dietary Fatty Acids, Inflammation and Pain
While most research has focused on the anti-inflammatory benefits of the Mediterranean Diet (MD) on disease development, especially cardiovascular diseases, diabetes, metabolic syndrome, visceral obesity and various cancers, studies have also identified benefits of the MD for rheumatoid arthritis and osteoarthritis. The MD diet appears to reduce the risk of developing rheumatoid arthritis and possibly osteoarthritis. Furthermore, a reduction in arthritis pain has been identified to occur in as little as 2-3 weeks after conversion to a MD.
The MD, which is rich in complex carbohydrates and fibers and low in animal proteins and fats, is able to promote saccharolitic microbiota favouring short-chain fatty acid production. These metabolites have been shown to possess positive immune-modulating activity by modifying cytokine production, promoting intestinal epithelial barrier integrity and resolving intestinal inflammation, Increasing research evidence has emphasized the connection between microbial dysbiosis (an imbalance of the microbiome, or bacterial population of the gut) and many inflammatory arthritic diseases including arthritis of the spine and joints,, lupus, gout, and rheumatoid arthritis.
Many of the anti-inflammatory effects of the MD are related to the intake of foods that are rich in:
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- polyunsaturated fatty acids (PUFA) with a lower omega-6 to omega-3 fatty acid ratio from fish;
- monounsaturated fatty acids (MUFA) from extra-virgin olive oil; and
- non-fat micro-components such as resveratrol from fruits, vegetables and wine.
Foods rich in PUFAs (especially salmon, walnuts and flax seeds) and MUFAs such as extra-virgin olive oil and avocados may offer pain reduction in patients with arthritis.
See: An Anti-inflammatory Diet.
.
Dietary Carbohydrates
Another dietary variable of significance relating to both inflammation and the synthesis of cytokines, especially adipokines, is the intake of carbohydrates. The most notable of dietary carbohydrates are the sugars: sucrose (table sugar), lactose (milk sugar), fructose (fruit sugar) and corn syrup.
According to research, long-term ingestion of sucrose can lead to hyperalgesia, meaning an increased sensitivity to pain, due to potential disruption of the body’s endogenous opioid system which is naturally involved in pain modulation; essentially, prolonged sugar consumption can lead to a decreased ability to naturally manage pain.
Key points about sucrose and hyperalgesia:
Mechanism:
When sucrose is initially ingested, it can trigger the release of endogenous opioids, providing a temporary analgesic effect. However, chronic exposure to high levels of sucrose can lead to a depletion of these opioids, making the body less able to naturally manage pain, resulting in hyperalgesia.
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- Important considerations:
- Dosage and duration: The extent to which sucrose can cause hyperalgesia likely depends on the amount consumed and the duration of high sugar intake.
- Individual variations: Individual differences in metabolism and pain sensitivity can influence how susceptible someone might be to sucrose-induced hyperalgesia.
- Important considerations:
Excessive Carbohydrate Intake
An excessive carbohydrate intake can increase reactive oxygen species (ROS) and trigger oxidative stress (see above). The oxidative stress response activate toll like receptors that initiate inflammatory reactions in the peripheral and central nervous systems. Studies assessing the effect of low-carbohydrate diets, including the ketogenic diet, have shown promising results including improvements in the glucose metabolism. In a study of people with chronic musculoskeletal pain who followed a low carbohydrate diet, a decrease in serum inflammatory biomarkers and pain sensitivity resulted, suggesting high carbohydrate intake plays a role in neuroinflammation and central sensitization.
Carbohydrates can be assessed by their “glycemic load,” the degree to which a carbohydrate impacts blood levels of glucose and insulin. Low glycemic load diets reduce inflammation and are associated with lower levels of CRP (C-reactive protein), a biomarker for systemic inflammation. Furthermore, low glycemic load diets are associated with higher levels of kynurenic acid which acts as an NMDA antagonist which reduces pain (See: Neurobiology of Pain).
See: Carbohydrates
What is not controversial is that one should avoid eating low fiber, calorie-dense, high fat, highly-processed foods. It has been well established that a diet rich in these products contributes to oxidative stress, chronic pai, obesity, cardiovascular disease and possibly some cancers.
For more information, please see the following handouts:
1.Wellness (Anti-inflammatory) Diet: Overview
2.Wellness Diet: Menu Examples
3. Food Intolerances Contributing to Pain: Allergies and Sensitivities
Specific foods can play a significant role in the health of certain individuals, leading to a wide range of mild to severely incapacitating symptoms, including gastrointestinal symptoms, neurological symptoms, fatigue and, importantly, pain. These symptoms may be the consequence of impaired digestion of a particular food, an allergic or antibody response to a food or simply a nonspecific intolerance due to inability to metabolize or other unknown mechanisms.
Food Intolerance – immune-related
Intolerance to food can be immune-related, the result of a reaction to either IgE or IgG antibodies. IgE antibody reactions result in typical, immediate-onset allergic reactions characterized by hives and/or life-threatening anaphylaxis. IgG antibody reactions (technically not allergic reactions) are more subtle and avoid obvious recognition in many cases. Immune-related food intolerances can be tested for by measuring IgE and/or IgG antibody levels for various foods commonly associated with intolerances. However, IgG testing is not very specific in identifying food sensitivities and may lead to incorrect conclusions.
See: Example of IgG Food Antibody Test
Food Intolerance – Digestion and Metabolism Related
Food intolerance can also be related to the inability to digest or metabolize a nutrient. Food intolerance is not uncommon and includes lactose intolerance (due to insufficient lactase enzyme), histamine and tyramine (related to genetics or metabolic overload) intolerance. For those with symptoms of Irritable Bowel Syndrome (IBS), intolerance to FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) is common FODMAPs are commonly found in a wide variety of vegetables, fruits, beans, dairy products and teas. To identify specific FODMAP intolerances requires testing with an Elimination Diet (see below). Food intolerance symptoms are usually limited to g.i. complaints such as abdominal pain or cramps, bloating, nausea and diarrhea.
Food sensitivity is a catch-all term for a negative reaction to food. It can take many forms but is not an immunologic reaction to food. A useful approach for identifying immune-related and digestion and metabolism-related food intolerances and other food sensitivities is use of the Elimination Diet (see below).
4. Intestinal Wall Integrity
When certain foods cannot be digested, often due to genetic factors, they can interact with the lining of the intestinal wall which can cause the release of a protein called zonulin, resulting in a loosening or disruption of the tight junction between the cells lining the intestine. This disruption contributes to greater permeability of the gut, called “Leaky Gut,” that allows foreign elements including undigested food, microorganisms and toxins in the gut to cross the intestinal wall barrier into the blood and systemic system. These foreign elements in turn can trigger the release of cytokines, proteins that stimulate inflammation and contribute to pain sensitization and/or trigger an immune response with the formation of antibodies. These antibodies then often interact with various tissues in the body, including joints, muscles and other organs causing inflammation, tissue destruction and other responses leading to illness and pain.
The hallmark of this type of reaction is Celiac Disease or Sprue, a genetically influenced condition in which sensitive individuals cannot digest gluten, a protein found in many grains, especially wheat, rye and barley. Celiac disease is characterized by many systemic symptoms including fatigue, arthritis and peripheral neuropathy amongst many others. Blood tests are available and fairly reliable for diagnosing Celiac Disease but other similar conditions lack specific tests. To identify other foods that might be responsible for such food sensitivities, the use of an Elimination Diet (see below) can be helpful.
Leaky Gut has been implicated in many medical conditions ranging from chronic migraine headaches to depression. Leaky Gut can be initiated by many triggers including the use of NSAIDs (non-steroid anti-inflammatory drugs including ibuprofen and naproxen) as well as by disruptions of the bacterial balance in the gut, the microbiome (See below).
See Leaky Gut
5. The Gut Microorganisms (Microbiome) and Pain
The Typical American Diet (TAD) is associated with shifts and loss of diversity and disruption of rhe healthy balance in the species of bacteria and other microorganisms referred to as the “gut microbiome.” The bacterial balance of the microbiome affects pain and other conditions through toxin production and candida (yeast) overgrowth. While our understanding of the role of gut bacteria in systemic health is still in it’s infancy, it has been recognized that these microbiome changes contribute to chronic pain and such diverse conditions as diabetes, depression, headaches, arthritis and other painful conditions including chronic prostatitis and chronic pelvic pain. Research indicates there is a role for modifying diet to improve the balance of the microbiome as a means of pain management.
Microbiome-Gut-Brain Axis
The gut microbiome plays an important role in the human body and contributes to many metabolic functions and is essential in the maintenance of general health. The gut and brain share a bidirectional communication pathway referred to as the “Gut-Brain Axis” in which intestinal the microbiome can modify brain functions. This link occurs through a connection between the vagus nerve and brainstem, via spinal nerve pathways. The population of the gut microbiome is influenced by various factors, including medications, mental health, infection, and nutrition which can result in an imbalance or dysregulation of the gut microbiome.
Dysregulation of the microbiome-gut-brain axis is associated with many pathologic conditions including chronic pain and conditions such as inflammatory bowel disease, diabetes, obesity, autism and depression. The effect of nutrition on the microbiome-gut-brain axis can have a modifying effect in both acute and chronic pain.
Microbes residing in the gut can be modified by nutritional factors. Thus, the microbiome–gut-brain axis is a target for nutritional interventions. Differences in the diversity of the microbiome are associated with dietary patterns, such as vegetarian, vegan, and omnivorous diets. Energy dense, proinflammatory dietary patterns that are nutrient poor and high in unsaturated fats, refined carbohydrates, and low in fruits and vegetables can cause a diet-induced inflammation in the gut. Proinflammatory cytokines released in response to unhealthy dietary patterns, activate the vagus nerve receptors located in the gastrointestinal tract. Upon activation, the vagus nerve can trigger glial cell activation and the neuroinflammation process in the central nervous system. These resulting peripheral and central proinflammatory responses, including pathologic glial cell activity, contribute to the maintenance of chronic pain. Targeting the gut microbiome with nutritional interventions in chronic pain populations is an important approach for pain management.
Studies indicate that the diversity of the microbiome is quickly subject to change, with a change in diet resulting in significant shifts in the microbiome in as little as 24 hours. It does not take long to improve the microbiome when an anti-inflammatory diet is engaged.
Opioids and the Microbiome
In addition to the gut microbiome contributing to pain, there is evidence that the chronic use of opioids induces changes in the microbiome, a condition called Opioid-Induced Dysbiosis (OID), that contribute to loss of gut integrity and subsequent systemic inflammation.
Opioid-Induced Dysbiosis (OID) is a specific condition that results from chronic opioid use effects on the bacterial composition of the gut. Opioids impact the epithelial barrier in the gut and modulate inflammatory pathways, which in turn may affect opioid tolerance. Changes in the gut’s epithelial barrier allows invasion and proliferation of pathologic bacterial colonies.
The integrity of the gut epithelial barrier is linked to the integrity of blood-brain barrier, referred to as the gut-brain axis. Disruption of the blood-brain barrier affects the emotional and cognitive functions of the brain and can affect mental health. In effect, disruption of the gut epithelial barrier therefore may impact not just intestinal diseases such as Irritable Bowel Syndrome but central nervous system functioning as well, including depression and Parkinson’s disease.
The impact of opioids on gut microbial dysbiosis can result in the development of tolerance to the analgesic benefits of opioids for pain. By altering the gastrointestinal tract’s microbial composition, opioids contributes to bacterial transport across the gut epithelial barrier resulting in inflammation within the gut wall and possible alteration of sensory nerves resulting in tolerance development.
Diets to Support a Healthy, Diverse Microbiome
The best approach to maintaining an optimal microbiome – although the specifics concerning “optimal” remain ill-defined – is to maintain a high fiber diet, consuming 30 grams of fiber/day. The Paleo Diet has also been proposed to be supportive of a healthy gut microbiome. Early studies indicate that probiotic supplementation may be helpful.
Probiotics are live, nonpathogenic microorganisms that improve microbial balance, especially in the gut. Probiotic therapy should be considered with chronic opioid use to counteract opioid-induced increased gut permeability and associated neuroinflammation.
While the use of prebiotics and probiotics is gaining popularity, it is too early to make specific recommendations as to choices of species and doses.
For more information regarding probiotics, see:
1.A Gastroenterologist’s Guide to Probiotics
2.Probiotic Candian Clincial Guide to Probiotics
6. Dietary Impact on Prevention and Control of Painful Medical Conditions
While diet plays a large role in the development of diabetes and obesity, two conditions that are major contributors to chronic pain, diet also plays a large role in reducing the pain associated with these conditions. Diet is often a very effective tool for reducing or preventing chronic headaches. The pain and inflammation associated with chronic arthritis can often be significantly reduced with dietary changes, especially when accompanied by weight loss.
Other conditions in which modification of diet can have significant benefit in reducing pain include fibromyalgia, interstitial cystitis, endometriosis, irritable bowel syndrome (IBS) and inflammatory bowel conditions including Crohn’s disease and ulcerative colitis.
For condition-specific dietary approaches including the use of nutritional supplements, see:
- Arthritis
- Fibromyalgia
- Headaches
- Interstitial Cystitis
7. Pain change appetite, satiety and palatability of food
Chronic pain, especially in association with obesity has also been identified as triggering excessive eating through multiple mechanisms. Pain is linked to changes in satiety, in that it takes more food to feel full which contributes to overeating. Furthermore, pain appears to reduce how tasteful food can be. In contrast, hedonic hunger (appetite triggered by the seeking of pleasure from eating) is associated with chronic pain as well as emotional or binge-eating. A third variable, low mood or depression may also contribute to chronic pain and obesity and impact eating habits.
8. High Cholesterol and Disrupted Lipid Metabolism
Lipids (fats) are essential for several bodily functions, and are one of the body’s main energy sources. However, excessive intake of saturated fats, dietary fructose, and an overall TAD style of eating affects lipid biomarkers including increasing low-density lipoprotein (LDL), triglycerides, and decreasing high-density lipoprotein (HDL). A high LDL cholesterol level increases the risk of cardiovascular disease (CVD) and is commonly known as “bad cholesterol”, while a high HDL cholesterol level is protective, reduces the risk of CVD, and is often referred to as “good cholesterol”.
A healthy intake of omega-3 unsaturated fatty acids and antioxidants, intermittent fasting, and adherence to an anti-inflammatory diet, can have the reverse effects on these lipid biomarkers. The role of a disrupted lipid metabolism in chronic pain is gaining more attention and targeting this mechanism with diet is a promising approach for chronic pain management.
For example, low back pain is prevalent among individuals with a decreased lumbar blood supply. The relationship between the decreased lumbar blood supply and spinal pain is a basis for the atherosclerosis theory of the persistent non-specific low back pain. Prevalence of low back pain is inversely associated with the levels of HDL cholesterol and positively associated with serum triglycerides and LDL cholesterol, suggesting that atherosclerosis contributes to low back pain.
Additionally, fibromyalgia patients with a disrupted serum lipid profile has been found to be positively associated with pain sensitivity. Also, in a systematic review, the biomarkers of the serum lipid metabolism, including decreased serum HDL cholesterol and increased LDL cholesterol, and triglycerides, was found to be strongly associated with musculoskeletal pain arising from tendinopathy.
9. Epigenetic , Diet and Pain
Epigenetics refers to changing the expression of a gene without actually changing the DNA)structure of the gene. This includes impacting the gene in such a way as to turn it off or turn it on. Almost every cell in the body has the same DNA but the genes in each cell have different profiles of which genes are turned on, or activated, and which genes are turned turned off, or deactivated. These epigenetic changes can alter the expression of the gene and many epigenetic mechanisms are reversible and modifiable which make them an attractive therapeutic target.
Unfortunately, our understanding of genetics remains in early infancy, and our ability to induce epigenetic changes is limited at best. Research shows that epigenetic changes can alter the expression of pain-related genes to suppress or enhance pain. For example, epigenetic dysregulation can play a role in the transition from acute to chronic pain.
Epigenetic mechanisms are divided into three main categories:
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- DNA methylation
- Histone modifications
- Non-coding ribonucleic acid (RNA) interference
Nutrition is a major modifiable lifestyle factor that has the ability to alter the epigenetic regulation including causing epigenetic dysregulation. Additionally, epigenetic markers also have the ability to alter the body’s response to certain dietary intake and patterns. Dysregulation of the epigenetic markers can alter the gene expression, protein synthesis, cell function, and metabolism and can lead to chronic diseases.
DNA methylation – For better or for worse
Nutrients and foods with anti-inflammatory properties, such as omega-3 polyunsaturated fatty acids, extra virgin olive oil, curcumin, and polyphenols show anti-inflammatory effects via their effects on the DNA methylation processes in immune cells.
Alternatively, preclinical studies have shown an increase in inflammation via DNA methylation after the consumption of diets rich in saturated fats or high in carbohydrates. The DNA methylation of genes that promote inflammatory cytokines, especially TNF-alpha, has been associated with obesity and with a dietary intake high in omega-6 polyunsaturated fatty acids. Saturated fatty acids are known for their inflammatory characteristics and a higher intake of saturated fatty acids has been associated with DNA methylation of genes that play an essential role in the inflammatory biomarker synthesis and insulin resistance.
In summary, early research shows that there is an interaction between nutrition and the epigenetic factors have important roles in chronic pain and their associated conditions, such as obesity, disturbed glucose metabolism, and gut microbiota diversity. Although the use of genetic and epigenetic data in chronic pain management is still in a very early phase, the potential for the development of personalized epigenetic treatment may be available in the future.
Identifying Specific Foods that Affect Pain
As noted above, diet can affect pain through a number of mechanisms. When assessing diets, however, the focus is on the forest, not the trees. Emphasis is placed on minimally processed foods, fruits and vegetables, lean meats, nuts etc. The next step is to evaluate individual foods. Are their individual foods one might emphasize or avoid over another? The answer depends on the mechanism by which the food interacts with each individual as reviewed above. Obviously certain foods that are highly refined and calorie-dense for example are easily identified and best minimized in one’s diet. Somer foods may specifically increase or decrease inflammation and oxidative stress based on their inherent characteristcs while other foods do so based on a person’s individual food sensitivity or intolerance.
For more information regarding the rating of the inflammatory nature of individual foods, see resources below:
1. Anti-Inflammatory Food Ratings – A resource
2. Anti-Inflammatory Food – About Formula for Rating Foods and Link to Phone Apps
Specific Foods that Increase Pain Due to Their Inherent Characteristics
While a complete list of foods that contribute to increased pain is beyond the scope of this web site, certain foods should be mentioned.
Advanced Glycation End Products
Advanced glycation end products (AGEs), also known as glycotoxins, are a diverse group of highly oxidant compounds with pathogenic significance in diabetes and in other chronic diseases. AGEs are created through a nonenzymatic reaction between reducing sugars and free amino groups of proteins, lipids, or nucleic acids. This reaction is also known as the Maillard or browning reaction.The presence of AGEs in food depend on the nature of how they are cooked since cooked.
Dry heat contributes to new dietary AGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and are prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dietary AGEs during cooking can be significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar.
The formation of AGEs is a part of normal metabolism, but with excessively high levels of AGEs they can cause problems due to their ability to promote oxidative stress and inflammation. This occurs when AGEs bind with cell surface receptors or with body proteins, altering their structure and function. Dietary levels of AGEs correlate with biomarkers for inflammation and oxidative stress.
Diet rich in grilled or roasted meats, fats, and highly processed foods are likely to be associated with high levels of dietary AGE intake. Comparatively, diets with lower-meat meals prepared with moist heat (such as soups and stews) as part of a diet rich in plant foods could realistically consume half the daily AGE intake.
Also, it has been shown that sinigrin, a glucosinolates component of cruciferous vegetables (cabbage, broccoli, cauliflower, mustard greens and brussel sprouts) may offer protection against AGEs. The crucifers are known to be a rich source of the glucosinolates, a class of compounds containing glucose and sulphur whose enzyme breakdown products are known for their pungency. Epidemiological evidence also supports the possibility that glucosinolate breakdown products derived from cruciferous vegetables may protect against human cancers, especially those of the lung and gastrointestinal tract (stomanch, colon and rectum).
Tannins in tea may also offer protective effects, suggesting that their may be a benefit of adding tea or cruciferous vegetable to a steak or hamburger meal.
Individuals advised to consider limiting their dietary intake of AGEs would include those with pre-existing high levels of increased systemic inflammation and/or oxidative stress such as those with chronic pain. Additionally, those individuals with obesity, diabetes and/or kidney disease would also be advised.
For more information about diet and AGEs including an extensive list of AGE content of more than 500 foods,
See: Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet – 2010
Specific Foods that Reduce Pain Due to Their Inherent Characteristics
Many claims are made for the health-aspects of a wide variety of foods so, again, a complete list is beyond the scope of this web site, but certain foods should be mentioned. (More information forthcoming)
- Alliums – garlic, onions, scallion, shallot, leeks, and chives
- Avocado (Hass)
- Cinnamon
- Cruciferous Vegetables – cabbage, broccoli, cauliflower, mustard greens and brussel sprouts
- Fiber
- Ginger
- Omega-3 Fatty Acids – fish oil
- Tea
- Turmeric – See Curcumin
Dietary Fatty Acids, Inflammation and Pain
While most research has focused on the anti-inflammatory benefits of the Mediterranean Diet (MD) on disease development, especially cardiovascular diseases, diabetes, metabolic syndrome, visceral obesity and various cancers, studies have also identified benefits of the MD for rheumatoid arthritis and osteoarthritis. The MD diet appears to reduce the risk of developing rheumatoid arthritis and possibly osteoarthritis. Furthermore, a reduction in arthritis pain has been identified to occur in as little as 2-3 weeks after conversion to a MD.
Many of the anti-inflammatory effects of the MD are related to the intake of foods that are rich in: 1) polyunsaturated fatty acids (PUFA) with a lower omega-6 to omega-3 fatty acid ratio from fish; 2) monounsaturated fatty acids (MUFA) from extra-virgin olive oil; and 3) non-fat micro-components such as resveratrol from fruits, vegetables and wine.
Foods rich in PUFAs (especially salmon, walnuts and flax seeds) and MUFAs such as extra-virgin olive oil and avocados may offer pain reduction in patients with arthritis. The MD, which is rich in complex carbohydrates and fibers and low in animal proteins and fats, is able to promote saccharolitic microbiota favouring short-chain fatty acid production. These metabolites have been shown to possess positive immune-modulating activity by modifying the cytokine production profile of TH cells, promoting intestinal epithelial barrier integrity and resolving intestinal inflammation, Increasing research evidence has emphasized the connection between microbial dysbiosis and many inflammatory rheumatic diseases including spondyloarthropathies, lupus, gout, and rheumatoid arthritis.
For more information: See: Mediterranean Diet (MD)
Specific Foods that Increase Pain Due to Their Inherent Characteristics
- Saturated Fats
- Trans Fats
- Cholesterol
Specific Foods that Increase Pain Due to Individual Food Sensitivity or Intolerance
Unfortunately, it is seldom obvious what, or even if, a food sensitivity or intolerance is a significant contributor to a patient’s chronic pain, fatigue or other symptoms. How does one investigate a person’s symptoms or pain as to whether a particular food or diet is a significant contributor? The first step is to begin moving towards an anti-inflammatory diet such as the Mediterranean, Paleo or Okinawan diets by eliminating or reducing foods known to contribute to inflammation and oxidative stress. If this move is inadequate to reduce symptoms to an acceptable level a more aggressive approach is indicated.
Medical conditions that are most likely to be improved by dietary intervention include arthritis (osteoarthritis or rheumatoid arthritis), chronic headaches, fibromyalgia, chronic fatigue and those with symptoms related to the gut, including irritable bowel syndrome and inflammatory bowel conditions including Crohns and ulcerative colitis. Recommended dietary considerations for these conditions, including specific Elimination Diets will be forthcoming.
In order to identify specific foods that may be contributing to pain or other multiple, unexplained symptoms, the most effective approach is to engage an Elimination Diet. An Elimination Diet removes all suspicious foods from the patient’s diet for a period of 3-4 weeks at which point the patient reassesses their level of symptom control. The foods on the “most suspicious” list includes lactose and dairy products, gluten and the artificial low-calorie sweetener, aspartame. An Elimination Diet requires careful planning, guidance and execution to be successful.
For more information, see Food Intolerance & Sensitivity: An Overview
Making the Changes
Small Steps
For those reluctant to commit to making “big” changes in how they eat, there are some simple steps one can start with that are effexive:
- Eat more slowly
- Reduce portion size
- Substitute healthier favorite food choices
1. Eat More Slowly
Studies show that finishing a meal in less than 15 minutes is associated with higher caloric intake, higher cholesterol levels and greater systemic inflammation. Spending more time chewing improves digestion and slower eating leads to arresting the appetite with eating less food.
In recent studies eating rate was significantly and positively associated with the development of metabolic syndrome, a collection of conditions associated with increased risk of heart disease and stroke (High blood pressure, Elevated sugar, Central obesity, Low HDL (good cholesterol) and High triglycerides ). This trend may be of greater significance in men than women, at least in the Japanese population. Of metabolic syndrome components, abdominal obesity showed the strongest association with eating rate. The association of slow eating with lower odds of high blood pressure (men and women) and high blood sugar (men) and that of fast eating with higher odds of lipid (cholesterol) abnormality (men) is statistically significant.
A study indicated that self-reported faster eating is positively associated with visceral fat accumulation, independently of subcutaneous fat accumulation. Visceral fat, the fat surrounding organs within the abdomen, is known to contribute more to development of systemic inflammation than fat distributed over the rest of the body in the subcutaneous layers.
Another finding associated with fast eating is that of increased likelihood of elevated blood levels of ALT (alanine aminotransferase), a liver enzyme that is a biomarker for liver damage and can be seen with fatty liver.
2. Reduce Portion Size
Serve yourself smaller than usual servings – and commit yourself to it. Especially if combined with eating more slowly, this practice will retrain appetite and restore healthier levels of food intake.
3. Substitute Healthier Favorite Food Choices
Ultimately, the successful reduction in pain will require significant changes in foods most people in America eat. By starting slowly with choosing healthier favorite foods, it facilitates a start in the right direction. Every journey begins with a single step – when this step is more likely to be successful, it allows for a build-up of the momentum of change.
Diet and Individual Pain Diagnoses
Diet and Migraine Headaches
Omega Fatty Acid Intake
A 2021 study evaluated the impact of improving the omega fatty acid intake as comparted to the average American diet. In this study, three diets were designed evaluating Omega-3 fatty acids [eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA)], and Omega-6 fatty acids (linoleic acid).
- H3 diet- increased Omega-3 (EPA+DHA) to 1,500 mg (1.5 g)/day and maintain Omega-6 (linoleic acid) at around 7% of energy;
- H3-L6 diet – increased Omega-3 (EPA+DHA) to 1,500 mg (1.5 g)/day and decrease Omega-6 (linoleic acid) to ≤1.8% of energy
- Control diet – The control diet was designed to match the average US dietary intakes of EPA+DHA (<150 mg/day) and Omega-6 (linoleic acid) (7.2% of energy). A typical US diet has a linoleic acid intake of 7% of energy. The study sought to decrease linoleic acid in the H3-L6 group to achieve intakes of 1.8% of energy (as 1.8% is the amount in US diets before the addition of concentrated vegetable oils, so ubiquitous in the American diet).
Results of study:
The authors noted that the two dietary changes resulted in “large, robust reductions in frequency and severity of headaches.” Compared with the control diet, both the H3-L6 and H3 diets decreased total headache hours per day, moderate to severe headache hours per day and headache days per month. Also, the H3-L6 diet decreased headache days per month more than the H3 diet, suggesting additional benefit from lowering dietary Omega-6 (linoleic acid). Importantly, the H3-L6 diet produced twice the reduction in headache days as the H3 diet, consistent with the hypothesis that lowering dietary Omega-6 (linoleic acid) is a key component contributing to maximal pain reduction.
Both diets resulted in changes in biomarkers consistent with decreased pain. Both diets also produced measurable changes in red blood cell membranes as measured by the Omega-3 Index blood test.
How omega dietary changes influence migraine headaches
Omega-6 fatty acids, Prostaglandins, and Leukotrienes
The H3 and H3- L6 diets significantly decreased the levels of the omega-6 arachidonic acid. Omega-6 fatty acids, in addition to their mostly inflammatory actions, are also precursors to compounds (oxylipins) such as leukotrienes and prostaglandins that are linked to immune activation and facilitation of pain. Leukotrienes are potent activators of inflammation and have been linked to triggering migraines.
Prostaglandins are hormone-like substances that can also trigger migraines and can cause pain by promoting inflammation and nerve excitability. They play a role in the body’s natural healing process and are produced in response to injury or infection. Excessive prostaglandins, however, can act on nerve endings the peripheral and central nervous system to promote pain sensation and lead to the sensitization that magnifies chronic pain over time (see: Sensitization – Peripheral and Central). Central sensitization is often associated with chronic migraines as well as other chronic pain conditions including neck and back pain and especially fibromyalgia.
References:
Anti-Inflammatory Diet – Resources
InflammationFactor.com
- Anti-Inflammatory Food Ratings – A resource
- Anti-Inflammatory Food – About Formula for Rating Foods and Link to Phone Apps
- An extensive bibliography of research on the effects of individual nutrients on inflammation
Diet
Anti-Inflammatory Diet
-
- Cytokines, Inflammation and Pain – 2007
- Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet – 2010
- Glucosinolates in the human diet – Bioavailability and implications for health – 2002
- Glucosinolates in Ghinese Cabbage
- Sinigrin, a major glucosinolate from cruciferous vegetables restrains non-enzymatic glycation of albumin. – PubMed – NCBI
- Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. – PubMed – NCBI
- Hass avocado modulates postprandial vascular reactivity and postprandial inflammatory responses to a hamburger meal in healthy volunteers. – PubMed – NCBI
- The associations between dietary fibers intake and systemic immune and inflammatory biomarkers, a multi-cycle study of NHANES 2015–2020 – 2023
- Nutritional Assessment – StatPearls – NCBI Bookshelf
- The Importance of Nutrition as a Lifestyle Factor in Chronic Pain Management- A Narrative Review – 2022
- Nutritional Risk Screening and Assessment – 2019
- Nutritional Risk, Micronutrient Status and Clinical Outcomes- A Prospective Observational Study in an Infectious Disease Clinic – 2016
- The Role of an Anti-Inflammatory Diet in Conjunction to COVID-19 – 2021
- Role of Resolvins in Inflammatory and Neuropathic Pain – 2023
- Nutrition and Chronic Pain – International Association for the Study of Pain (IASP)
Low Glyccemic Diet
Diet Sweeteners
Western Diet – Overview
Diet – Fibromyalgia
-
- A low fermentable oligo-di-mono-saccharides and polyols (FODMAP) diet is a balanced therapy for fibromyalgia with nutritional and symptomatic benefits – PubMed – NCBI
- Dietary interventions in fibromyalgia- a systematic review – 2019
- Vegetarian and Vegan Diet in Fibromyalgia – A Systematic Review – 2021
- A systematic review of the association between fibromyalgia and functional gastrointestinal disorders – 2020
- Dietary Interventions in the Management of Fibromyalgia – A Systematic Review and Best-Evidence Synthesis – 2020
- Nutritional Interventions in the Management of Fibromyalgia Syndrome – 2020
- The Role of Nutrient Supplementation in the Management of Chronic Pain in Fibromyalgia A Narrative Review – PubMed
- Fibromyalgia – Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update – 2021
- Coenzyme Q10 supplementation alleviates pain in pregabalin-treated fibromyalgia patients via reducing brain activity and mitochondrial dysfunction – PubMed – 2019
- Fibromyalgia and Nutrition An Updated Review – PubMed – 2020
Diet – Migraine headaches
Diet – Pain
-
- Food-Derived Natural Compounds for Pain Relief in Neuropathic Pain – 2016
- Food pyramid for subjects with chronic pain: foods and dietary constituents as anti-inflammatory and antioxidant agents. – PubMed – NCBI – 2018
- Dietary Patterns and Interventions to Alleviate Chronic Pain – 2020
- Neuroprotective Effect of Antioxidants in the Brain – 2020
- Neuropathic Pain – Delving into the Oxidative Origin and the Possible Implication of Transient Receptor Potential Channels – 2018
- Do Nutritional Factors Interact with Chronic Musculoskeletal Pain? A Systematic Review – 2020
- Nutraceutical Supplements in the Management and Prevention of Osteoarthritis – 2016
- Food for Special Medical Purposes and Nutraceuticals for Pain – A Narrative Review – 2021
- Nutritional Supplements for the Treatment of Neuropathic Pain – 2021
- Food Implications in Central Sensitization Syndromes – 2020
- Influence of pro-algesic foods on chronic pain conditions – 2016
- Food in Chronic Pain – Friend or Foe? – 2020
- Mood Components in Cocoa and Chocolate – The Mood Pyramid – 2018
Diet – Water
Diet – Fast Eating
-
- Self-reported faster eating associated with higher ALT activity in middle-aged, apparently healthy Japanese women. – PubMed – NCBI
- Self-awareness of fast eating and its impact on diagnostic components of metabolic syndrome among middle-aged Japanese males and females. – PubMed – NCBI
- Self-reported faster eating is positively associated with accumulation of visceral fat in middle-aged apparently healthy Japanese men. – PubMed – NCBI
- Association Between Eating Speed and Metabolic Syndrome in a Three-Year Population-Based Cohort Study – 2015
- Self-reported eating rate and metabolic syndrome in Japanese people – cross-sectional study -2014
Eating – Appetite, Satiation and Pain
Body Composition
The Microbiome – Overview
The Microbiome – Arthritis and Rheumatic Diseases
The Microbiome – Inflammatory Bowel Disease
The Microbiome – Obesity
-
- Innate sensors of pathogen and stress: linking inflammation to obesity. – PubMed – NCBI
- Microbiota, inflammation and obesity. – PubMed – NCBI
- Obesity-Driven Gut Microbiota Inflammatory Pathways to Metabolic Syndrome – 2015
- Gut microbiota as a key player in triggering obesity, systemic inflammation and insulin resistance. 2014 – PubMed – NCBI
The Microbiome – Opioids
-
- Chronic Opioid Use Is Associated With Altered Gut Microbiota and Predicts Readmissions in Patients With Cirrhosis – 2017
- Opioid-induced gut microbial disruption and bile dysregulation leads to gut barrier compromise and sustained systemic inflammation – 2016
- Pain and Opioid-Induced Gut Microbial Dysbiosis – 2022
The Microbiome – Probiotics
The Microbiome – Pain
The Microbiome – Surgery
Food Sensitivities – Overviews
Food Sensitivities – Gluten
Miscellaneous
- Kaempferol, a dietary flavonoid, ameliorates acute inflammatory and nociceptive symptoms in gastritis, pancreatitis, and abdominal pain. – PubMed – NCBI
- Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet – 2010
Obesity – Pain
- Obesity-related adipokines predict patient-reported shoulder pain – 2013
- Adipokine Contribution to the Pathogenesis of Osteoarthritis – 2017
- Relationship between Neuropathic Pain and Obesity – 2016
- “The more pain I have, the more I want to eat” – obesity in the context of chronic pain – 2012
- Weight loss – the treatment of choice for knee osteoarthritis? A randomized trial – 2004
Emphasis on Education
Accurate Clinic promotes patient education as the foundation of it’s medical care. In Dr. Ehlenberger’s integrative approach to patient care, including conventional and complementary and alternative medical (CAM) treatments, he may encourage or provide advice about the use of supplements. However, the specifics of choice of supplement, dosing and duration of treatment should be individualized through discussion with Dr. Ehlenberger. The following information and reference articles are presented to provide the reader with some of the latest research to facilitate evidence-based, informed decisions regarding the use of conventional as well as CAM treatments.
For medical-legal reasons, access to these links is limited to patients enrolled in an Accurate Clinic medical program.
Should you wish more information regarding any of the subjects listed – or not listed – here, please contact Dr. Ehlenberger. He has literally thousands of published articles to share on hundreds of topics associated with pain management, weight loss, nutrition, addiction recovery and emergency medicine. It would take years for you to read them, as it did him.
For more information, please contact Accurate Clinic.
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