Mrs. D -

But the papers on morphine glial cells do not explain the vasodilation/edema of CRPS, whereas high levels of CGRP might, don't you think?

From my perspective, any theory of CRPS, not simply one's garden-variety back pain, that can't address vasodialation, can only explain how too high an opioid comsumption can only make our pain worse. And beyond that, may not worth the paper it's printed on, at least as to CRPS per se. Unless it can. Please discuss.

Mike

You are right up to a point.

What I see, is that the glia which holds the spinal cord and
brain together, is an active promoter of inflammatory cytokines. The RSD response is complex. Certainly the vaso effects are obvious. But then there is the PAIN part...some of that IS mediated in the brain centrally. I have been reading here some members who have had tolerance to opiates and also new pain/burning--the Opana posts by Dew. These responses are in addition to the regional damage, IMO. So I put this up because....because use of opiates for all chronic pain is on the table now, and may be very altered in the future. Based on the attitude of the specialist neurologists I heard discuss many chronic pain states, opiates are not going to be popular in the near future. That is unless Big Pharma finds a way to block this glial response, soon.

It just might be that the anti-inflammatory diet, helps with these issues as well as those in the periphery. I know myself that certain foods trigger my PN pain and burning significantly.
It stands to reason that others with chronic pain are also in a similar situation.
(I don't use opiates, BTW)

I've been away for a while.Just dropping in to see whats up with everyone.
I thought I'd repost the RSD Diet for those that may have missed it and still might be interested.
My best to you all. Di


01-14-2009, 03:39 PM #2
DianaA
Member




Join Date: Jun 2007
Posts: 260
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RSD Diet

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Quote:
Originally Posted by screwballpookie
Hey you all,
I see everybody talks about the rsd diet and I don't know what it is. Can anyone help me? I would like to know what it is to see if it will help me as well. I am willing to try anything at least once to see if it helps. If it doesn't then I know what not to do. So please help me.

I also have another question. Can anyone explain in short form what HBOT is? If maybe it is something I can try to see if it helps with my pain. Thanks and you all take care.

Sincerely,
Tracy(screwballpookie)

Tracy, I hope this helps. Here's the copy I have. I picked this up on the interent,
All the best! Diana

RSD Diet Guidelines

Dr. Hooshmand states this diet isn't for losing or gaining weight. The purpose of this particular diet of his, is to exclude foods that are harmful to one's health and that aggravates chronic pain such as with RSD.

The Five C's you need to avoid are: cookies, cakes, chocolates, cocktails and Candy. Other foods that should be avoided are internal organ meats like: liver, sauage and hot dogs. There are certain foods that help the inhibitory nerve cells that suppress the pain input, and they are the Four F's: Fresh Fruit, Fresh Veggies, Fish and Fowl.

Four F's-

Fresh Fruit (not canned) Fresh Vegetables(Olive Oil is best to cook with) Fish-DOn't use margarine. Baked or broiled Fowl-Skinned. not fried.(baked, roasted or grilled is fine)

Foods that are allowed rarely or sparingly

Tea, Lamb, Pulp of potato

Foods To Avoid

Coffee, soft drink with sugar crystalline sugar ,Pies, Bologna, Salami, Hot Dogs, Sherbert ,Ice Cream, Enriched Flour(bleached) ,Syrups, Mayonnaise, All fried foods, Canned fruits packed in syrup, Candies, Bacon, or pork, Donuts, Margarine, Nondairy cream substitutes ,Alcohol, Cake Mixes ,Potato Chips, Dips ,Crisco & other shortenings(replace with olive oil), Lard, Sweetrolls and Cakes.

FOODS YOU CAN HAVE

Diet drinks(low to no sodium, no sugar or caffine) ,Nuts-salted & raw, Honey(natural) ,Skim Cheese, Apples, All Fresh Fruits, Unsweetened orange juice, Natural fresh squeezed orange or grapefruit juice ,Apple juice(natural), All Fresh Vegetables, Veal ,Chicken & Fowl(skinned) ,Lobster(no butter), Lean Roast Beef(moderation), Raisins ,Skim Milk, Tuna(packed in water). Drink 6-8 glasses water daily. Fruits(dried), Shrimp ,All Fish Cereals(low sugar , whole grain) Sardines Sweet Potatoe & skin Lowfat plain yogurt(add yoour own fruit), Lowfat cottage cheese, Oatmeal(plan and unflavored) ,Crab

here is the link to Dr Hoosmands Diet

http://www.rsdrx.com/four_f's_diet.htm

Dear Mrs. D -

I think that we are in full agreement that the CRPS patient is at equal risk with any other patient of developing Opioid Induced Hyperalgesia. I particularly enjoyed your posting of "Glial Cells—A New Target for Chronic Pain Treatment," with it's interview with Linda Watkins, Ph.D. For another treatment of the subject, check out, "Opioid Guidelines in the Management of Chronic Non-cancer Pain," Trescot AM, Boswell MV, Atluri SL, et al, Pain Physician, 2006; 9: 1 - 40 at 17, free full text at http://www.rsds.org/2/library/articl...ician2006.pdf:

Hyperalgesia or abnormal pain sensitivity manifests as increased pain from noxious stimuli and as pain from previously non-noxious stimuli. Long-term use of opioids may be associated with the development of hyperalgesia. Experimental and clinical studies describe that cellular mechanisms of neuropathic pain may be similar to opioid-induced hyperalgesia. In an experimental setting, NMDA-receptor-mediated changes that cause abnormal pain sensitivity have been shown to occur in animals in the spinal cord dorsal horn cells of animals after repeated exposure to opioids. Similarly, these changes have been observed in the spinal cord in animal models of neuropathic pain. Consequently, interactions between neural mechanisms of opioid tolerance and neuropathic pain involving spinal and supraspinal neural circuits may have important clinical implications.

Repeated administration of opioids not only results in the development of tolerance but also hyperalgesia. In fact, opioid-induced abnormal pain sensitivity has been observed in patients treated for both pain and addiction. It also has been postulated that there may be correlation between tolerance which is a desensitization process, and hyperalgesia which is a pro-nociceptive process or sensitization. In prolonged opioid therapy, desensitization and sensitization together may contribute to tolerance or an afferent decrease in analgesia, regardless of the progression of the pain. Ballantyne and Mao stated that the need for dose escalation during opioid therapy – that is, the development of “afferent” opioid tolerance – may result from pharmacologic opioid tolerance, opioid-induced abnormal pain sensitivity, or disease progression. The potential use of NMDA antagonists in the treatment of neuropathic pain, opioid tolerance, and opioid-induced hyperalgesia is the subject of multiple investigations. [Citations to references omitted.]

That said, I see no reason, following the results of the 2009 article by Schinkel et al, referred to in my prior post, to assume that chronic CRPS has the same "inflammatory signature" as does - say - PN or back pain, where only a single pro-inflammatory cytokine - calcitonin gene related peptide (CGRP) - was observed to stand out to any level of statistical significance in chronic CRPS patients. If that's the case, I would suggest that we have to consider at least the possibility that a diet with wonderful anti-inflammatory properties in general, might have little or no effect on chronic CRPS unless it happens to effect the regulation of the CGRP gene, which:

. . . is in part controlled by the expression of the mitogen-activated protein kinases (MAPK) signaling pathway, cytokines such as TNFα and iNOS. 5HT1 agonists such as sumatriptan increase intracellular calcium which cause decreases in CGRP promoter activity. Botulinum toxin type A is able to prevent stimulated release of CGRP through the cleavage of SNAP-25 protein. Receptor antagonists such as telcagepant, which is in phase III from Merck Pharmaceuticals, also has promise in limiting the effects of CGRP. [Citations omitted.]

http://en.wikipedia.org/wiki/Calcito...elated_peptide

You have stated that you believe "It stands to reason that others with chronic pain are also in a similar situation." But you have to acknowledge that is only an assumption, which may or may not be correct. All that I am suggesting is that we be prepared to think of this analagously to the manner in which CRPS has been shown to produce patterns of gray brain matter atrophy and white matter structures on structural MRIs that are wholly unlike those observed in patients with either chronic back pain or fibromyalgia. See, "The Brain in Chronic CRPS Pain: Abnormal Gray-White Matter Interactions in Emotional and Autonomic Regions," Paul Y. Geha, Marwan N. Baliki, R. Norman Harden, William R. Bauer, Todd B. Parrish, and A. Vania Apkarian, Neuron 60, 570–581 at 574 - 575 (November 26, 2008), free full text at http://www.apkarianlab.northwestern....S_Neuron08.pdf

As such, I simply submit that if Schinkel et al are correct, the most amazing anti-inflamatory diet in the world may or may not have an effect on chronic CRPS, depending on its effect on the regulation of the CGRP gene. And one of the things that makes me feel that they are are on the right track is if you do a PubMed search under "CRPS calcitonin gene related peptide" you get only 5 articles, but written by some of the best minds in the field, e.g., two by Frank Birklein and one co-authored by Anne Louise Oaklander.

Still, nothing would make me happier to know that if I stuck to Diet X for six weeks, there would be a 50% reduction in my pain and all of my edema would resolve.

Mike

PS It's unfortunate that Merck had to put telcagepant on hold in April of this year, perhaps permanently, due to issues of elevated liver enzymes when migraine patients started taking it on a daily basis - as any CRPS patient would have to - as opposed to the episodic use for which it was planned, but word has it that Merck and perhaps others may be trying to tweak the molecule even in the present moment, so there may be more news yet on that front. http://www.thedailyheadache.com/2009...rmanently.html

I guess when we find out what is unique to RSD patients compared to those who do not develop this, we will have our answers.

This seems similar to Fibromyalgia, which is becoming obvious, as an inherited problem. Once triggered by an injury, trauma, Fibro does not go away either.

The central pain sensitization is similar in Fibro patients and PN patients, as well as RSD patients. PN patients also have demyelination that is now being tested for. The new skin biopsies, are proving this condition. It might be that PN has several subsets, of peripheral degeneration + central pain perceptions.

Right now MS is being looked at as a multiple process. Beginning with an inflammatory phase and followed by a disruption in astrocytes --
http://ms.about.com/b/2009/06/09/cou...sease.htm?nl=1

So we are all in the same boat, waiting for research to point the way, more clearly.