Dear Dr. Tennant,
The topic of dietary considerations when delivering treatment for pain conditions in your recent edition was a pleasant surprise.1 Thank you. Although it fell short in a very important area, I think the contribution is nonetheless a valuable one.
During decades of work in facilitating reduction of discomfort in patients with chronic pain, I have almost routinely observed amelioration of a large part of the pain condition when foods and beverages with pro-inflammatory agents are eliminated. This consideration is especially vital to good treatment outcome when the presentation includes a related intractable inflammatory response. I believe pain ought to be viewed like a pie chart, in which the clinician tries to determine how big a piece of the pie is nerve insult or nerve disease, the inflammatory component, psychogenic pain, mechanical exacerbation, and so forth. A narcotic for osteoarthritis is like a Swiss cheese umbrella for protection against raining substance P.
Prescribing nonsteroidal anti-inflammatory drugs and then sending the patient home to unwittingly self-medicate with products rich in caffeine and 1,3,7-trimethyl-xanthine (coffee), l-phenylalanine and purines (beef), and phenylethylamine (chocolate) is a common—and probably the chief—cause of numerous iatrogenic disorders. Moreover, a diet with stimulants often negates the therapeutic effect of central nervous system depressants.
Proteins may be classified as stimulants, just as carbohydrates and starches are tranquilizers. Why raise the speed limit on the somatosensory highway to, say, the limbic system when the traffic is jammed with excitatory neurotransmitters in a subject with intractable pain?
I encourage you to look at my compilation, to which I refer as “Friends & Foes” of anyone suffering physical or emotional discomfort, under the “autoimmune” section at my site. All of my patients suffering from osteoarthritis are able to not only dramatically reverse the progress of the disease but also resolve Heberden’s and Bouchard’s nodes up to 90% by embracing their “Friends” and eschewing their “enemies,” identified in the list.
—Gerard J. Taylor, PhD
Neurobehavioral Medicine Center
New Port Richey, FL
Dear Dr. Taylor,
Your suggestion to remove pro-inflammatory elements from a pain diet is most intriguing, and I thank you for sharing it.
As physicians, we frequently encounter patients with chronic pain, particularly those who have central pain, hardly eat protein, and demonstrate muscle wasting. Consequently, my personal approach has leaned toward a high-protein diet to reverse a catabolic state. My thinking, however, in many patients may be misguided and counterproductive, as you imply. In view of the fact that you describe patients who have peripheral pain, is it possible that we need a different diet for patients with central pain?
Our dietary issue of Practical Pain Management was our first,1 and much of our motivation was to stir interest and debate.
Can you tell us more about your anti-inflammatory diet? Hopefully, other readers will weigh in on this important issue.
Thank you for your help.
Dr. Taylor’s response:
I’m most grateful for your response and interesting comments. I receive a number of medical journals but find myself reading yours more often than any other.
My background is in pain management, studying the effects of emotion on pain and vice versa. My interest in the inflammatory piece of the pain pie chart is fueled in large part by the observation that it is the part least attended to by pain specialists (some prescribe narcotics for inflammation). For decades, I have seen an almost consistent improvement in this population when they are compliant with a diet limited in protein intake. A loss of 1% of muscle mass per year is a fair trade-off for regaining a productive lifestyle—the unavoidable two-edged sword.
You may download a printable chart of my “Friends & Foes” (includes dietary information) from my Website. Scroll down on the “Downloads” page or look under “Autoimmune Disorders” in the menu (www.mednetconnection.com).
Pardon me for the lengthy reply, but I am still euphoric after recently overcoming what almost led me to follow my orthopedic specialist’s recommendation to have my C5-C6 vertebrae fused following a period of excruciating pain when I was unable to stand longer than 15 seconds before falling to my knees or passing out, or to concentrate on what my patients were saying. The MRI [magnetic resonance imaging] showed a severely herniated disk, pushing one-third of the way into the spinal cord. You could not convince me a dagger was not lodged in my left “winged” scapula. Another colleague, a neurologist, stated that surgery was unequivocally unavoidable.
But even my physiatrist, who is a Johns Hopkins graduate/Harvard fellow, was unable to explain the mechanics of my debilitating pain. How did the stenosis actually cause the crippling trigger points in the supraspinatus? After brushing up on Travell & Simons’ approach to myofascial pain syndrome and figuring out the puzzle, I managed to be 100% pain free in less than 2 weeks and off the morphine and acetaminophen and hydrocodone (Vicodin) in another 2. Had I not specialized in psychophysiology, I doubt I would be writing this letter or continuing to run my practice. What an alarming realization that we have become so specialized that we can no longer put the jigsaw-like puzzle together—everybody has a piece of the map, but nobody knows the way. I now wonder how many iatrogenic cases of disabling treatment are generated every day.
Although the subject of chronic pain is admittedly far too complex for me—especially after scientists in Tel Aviv discovered chemical pathways transmitting pain in a post-rhizotomy case—I have observed that in most individuals, proteins have as much of a stimulant effect as carbs have a tranquilizing effect. Whether through dietary- or anxiety-driven sympathetic arousal, the speed limit on the pain highway to the brain is raised.
The apparent paradox of the red meat–eating hunter enjoying a higher pain threshold than the frail carb/starch academic may be explained not so much by a greater production of endogenous opioid peptides or decrease in synaptic enkephalinase activity, but by the fact that the higher brain centers in the physically stronger individual are governed or redirected by a different cognitive process. Hence, loading up on precursors to enkephalins for pain is like loading up on melatonin for insomnia—neither is better than placebo.
—Gerard J. Taylor, PhD
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