The journal of pain : official journal of the American Pain Society
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Omega-3 and omega-6 fatty acids are biosynthetic precursors of endocannabinoids with antinociceptive, anxiolytic, and neurogenic properties. We recently reported that targeted dietary manipulation-increasing omega-3 fatty acids while reducing omega-6 linoleic acid (the H3-L6 intervention)-reduced headache pain and psychological distress among chronic headache patients. It is not yet known whether these clinical improvements were due to changes in endocannabinoids and related mediators derived from omega-3 and omega-6 fatty acids. We therefore used data from this trial (N = 55) to investigate 1) whether the H3-L6 intervention altered omega-3- and omega-6-derived endocannabinoids in plasma and 2) whether diet-induced changes in these bioactive lipids were associated with clinical improvements. The H3-L6 intervention significantly increased the omega-3 docosahexaenoic acid derivatives 2-docosahexaenoylglycerol (+65%, P < .001) and docosahexaenoylethanolamine (+99%, P < .001) and reduced the omega-6 arachidonic acid derivative 2-arachidonoylglycerol (-25%, P = .001). Diet-induced changes in these endocannabinoid derivatives of omega-3 docosahexaenoic acid, but not omega-6 arachidonic acid, correlated with reductions in physical pain and psychological distress. These findings demonstrate that targeted dietary manipulation can alter endocannabinoids derived from omega-3 and omega-6 fatty acids in humans and suggest that 2-docosahexaenoylglycerol and docosahexaenoylethanolamine could have physical and/or psychological pain modulating properties.
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Using a simple approach for coding pain severity, the present study describes self-reported pain in U.S. adults. Data are included for 8,781 adults who completed the Functioning and Disability Supplement of the 2012 National Health Interview Survey. An internationally piloted pain severity coding system was used to group participants into 5 discrete ordered pain categories based on their pain persistence (days with pain in the last 3 months) and bothersomeness (little, a lot, somewhere in between): pain free and categories 1 (low) to 4 (high). It is estimated that 126.1 million adults reported some pain in the previous 3 months, with 25.3 million adults (11.2%) suffering from daily (chronic) pain and 23.4 million (10.3%) reporting a lot of pain. Based on the persistence and bothersomeness of their pain, 14.4 million adults (6.4%) were classified as having the highest level of pain, category 4, with an additional 25.4 million adults (11.3%) experiencing category 3 pain. Individuals with category 3 or 4 pain were likely to have worse health status, to use more health care, and to suffer from more disability than those with less severe pain. Associations were seen between pain severity and selected demographic variables including race, ethnicity, preferred language, sex, and age. ⋯ U.S. estimates of pain prevalence are presented using a simple approach for assigning pain severity developed by the Washington Group on Disability Statistics. Concurrent validity is assessed. Although this approach is promising, additional work is required to determine the usefulness of the Washington Group pain categories for pain research or clinical practice.
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Population-based studies suggest that pain in the lower body is common and that pain at multiple sites is more prevalent than single-site pain. Obesity is a risk factor for multisite musculoskeletal pain, but there are limited data on the role of body composition. Therefore, we sought to determine whether body composition is associated with multisite musculoskeletal pain involving the low back, knee, and foot. A total of 133 participants were recruited for a study examining the relationship between obesity and musculoskeletal disease. Participants completed validated questionnaires that examined levels of pain at the low back, knee, and foot. Body composition was assessed using dual-energy x-ray absorptiometry. Multisite pain was common, with 26.3% of participants reporting pain at 2 sites and 31.6% at 3 sites, and only 20% were pain free. The low back was the most common site of pain (63%). Greater fat mass and fat mass index, but not fat-free mass, were associated with pain at a greater number of sites, independent of age, gender, and fat-free mass (P < .01). Longitudinal studies exploring the mechanism of action by which increased fat mass is associated with pain may provide important insights into therapeutic strategies for the prevention of multisite pain. ⋯ Greater fat mass and fat mass index were associated with a greater number of lower body pain sites, with no association observed for fat-free mass. Understanding the mechanism by which increased fat mass is associated with pain may provide important insights into therapeutic strategies for the prevention of pain.
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Randomized Controlled Trial
Effects of Milnacipran on Clinical Pain and Hyperalgesia of Patients With Fibromyalgia: Results of a 6-Week Randomized Controlled Trial.
Milnacipran is a serotonin-norepinephrine reuptake inhibitor that was approved by the U.S. Food and Drug Administration as effective therapy for fibromyalgia (FM) symptoms. However, its analgesic mechanism of action is not well understood. We hypothesized that improvement of mechanical and heat hyperalgesia would be a critical component of overall milnacipran efficacy in FM. We used a novel quantitative sensory testing protocol for assessment of mechanical and heat pain sensitivity that can be used for testing of peripheral and central pain mechanisms and their impact on clinical pain over time. We applied tonic mechanical and heat pain stimuli to 46 patients with FM during a randomized controlled trial with either 50 mg milnacipran (n = 23) or placebo (n = 23) twice daily over 6 weeks. During this trial, mean clinical pain (standard deviation) was evaluated daily, and mechanical and heat pain sensitivity every 2 weeks. At study entry, clinical pain was 5.0 (1.8) and 5.5 (1.8) visual analog scale units for patients with FM randomized to placebo and milnacipran, respectively (P > .05). Over 6 weeks, clinical pain of patients with FM significantly declined by 15%, but this improvement was not statistically different between milnacipran and placebo. However, repeated measures of mechanical and heat pain sensitivity reliably predicted up to 80% of the variance in clinical FM pain at every time point. Clinical pain and mechanical/heat pain sensitivity of patients with FM steadily declined during this trial, but the effects of milnacipran were not found to be superior to placebo. Repeated measures of mechanical/heat hyperalgesia reliably predicted large amounts of the variance in clinical pain across all participants, indicating their relevance for FM pain. ⋯ Although clinical pain and hyperalgesia decreased during this 6-week trial, the efficacy of milnacipran was not superior to placebo. The high correlations between clinical pain and hyperalgesia ratings at every time point seem to emphasize the relevant contributions of mechanical and heat hyperalgesia to clinical FM pain.