09 Dec Chronic Pain and Diet. Is There a Connection?
Does normal activity lead to the release of inflammatory mediators? Is this related to chronic pain? And is there a dietary connection? Dr. David Seaman is a popular and prolific author of numerous nutrition and neurology articles, and of the text Clinical Nutrition for Pain, Inflammation, and Tissue Healing. His recent article discusses the role of inflammatory mediators and their link to diet, arthritis, and the central nervous system. My comments in brief summary of the key concepts:
According to Dr. Seaman, “acute inflammation” occurs after injury, which is then followed by the repair and remodeling phases. Pain supposedly should resolve as acute inflammation subsides, so long as care is taken not to mechanically strain the injured tissues. He goes on to say that many blame chronic pain on a “sensitized” or hyperactive central nervous system. But what about understanding the “biomechanical” chemistry of normal musculoskeletal tissues as it relates to pain and inflammation? According to Dr. Seaman, science shows us “prostaglandins participate in the generation of peripheral nociceptive signals. Typically, prostaglandin E2 (PGE2) is incorrectly viewed solely as a pain/inflammation producer released as a consequence of tissue injury. Research published over the past decade demands that we reconsider this notion.”
In a study where researchers collected fluid from the Achilles tendon from subjects who performed intermittent isometric plantar flexion exercises that mimicked the force generation that normally occurs during walking. They found an increase in PGE2(prostaglandin E2) which can create inflammation, but is also normally released because it creates vasodilation to increase blood flow to exercising muscles. Researchers also showed that fibroblasts also release PGE2 which shows that connective tissue cells release inflammatory mediators during normal activity. Researchers also studied inflammatory COX enzymes, COX1 and COX2. COX2 are blocked by anti-inflammatory drugs such as Celebrex and other NSAID’s (non steroidal anti-inflammatories). They showed that both COX1 and COX2 could convert Omega 6 fatty acids (bad fats) to arachodonic acid, which causes inflammation. It is also known that the same COX enzymes can convert the dietary omega 3(good fats) EPA and DHA into anti-inflammmatory mediators. This means that “anti-inflammatory” activity of the COX enzymes can be affected by the presence of omega 6 and omega 3 fatty acids within the cell membrane. In other words, according to Dr. Seaman, “we are always producing a mediator that is typically viewed to be inflammatory and pain promoting, and it makes no difference whether the tissue is injured or not”. Dr. Seaman notes that “osteoarthritis is known to be associated with increased levels of arachodonic acid within the tissues”. These levels are not seen in young people, but increase as we age because of dietary excess of omega 6 fatty acids. Dr. Seaman states “It is certainly possible that a critical threshold will be reached regarding diet-derived arachidonic acid levels in musculoskeletal tissues. At this point, the “normal state” is pro-inflammatory and pro-nociceptive, which is why a patient will continually rescue with NSAIDs. In this case, the sensitized dorsal horn would be perpetually stimulated by ongoing nociceptive input in the absence of overt pathoanatomy”. Therefore it appears that diet can be attributed, at least in part, to creating a sensitized central nervous system and play a major role in chronic pain.
To read more from Dr. Seaman about diet and it’s role in inflammation and pain visit deflame.com