The symptoms of Reflex Sympathetic Dystrophy syndrome typically begin with burning pain, especially in an arm, finger(s), palm of the hand(s), and/or shoulder(s). In some individuals, RSD may occur in one or both legs or it may be localized to one knee or hip. Frequently, RSD may be misdiagnosed as a painful nerve injury. More often, it is associated with a crushing injury typically suffered in an auto accident. The skin over the affected area(s) may become swollen (edema) and inflamed. Affected skin may be extremely sensitive to touch and to hot or cold temperatures (cutaneous hypersensitivity). The affected limb(s) may perspire excessively and be warm to the touch (vasomotor instability). The exact cause of RSD is not fully understood, although it may be associated with injury to the nerves, trauma, surgery, atherosclerotic cardiovascular disease, infection, or radiation therapy.
RSD pathogenesis is unclear to the writers of the below citation. Our experience with trauma injury indicates that high and frequent intake of ascorbic acid will relieve pain and block the dystrophy. Toxic oxygen radicals may be acting long term to destroy injured tissues. Therapeutically high levels of AA (Ascorbic Acid = Vitamin C) in multi (1 to 4) grams doses with frequent (1 to 4) hour intake separation, depending on pain levels) both reduces pain and promotes more rapid healing.
Systemic, sinus, gut, bladder, and respiratory infections with inflammation and infection-produced endotoxin can aggravate the RSD inflammatory state. The need for AA intake is vastly increased.
A 1999 Study that did not go far enough:
Zollinger PE, Tuinebreijer WE, Kreis RW, Breederveld RS. Department of Orthopaedics, Leyenburg Hospital, The Hague, The Netherlands. (1999)
Administer 500 mg daily of AA. For 50 days, with 1 year follow up on final results. A double blind study.
This is a too small dosage, well below Cathcart’s gut tolerance. The results are remarkable and positive, but the treatment is in too small amounts to account for what is now known of AA’s pharmacokinetics when it is used in therapeutic levels of administration. Much better results have been seen by some of our elderly family members when trauma and toxemia pains have been treated with AA in accord with its pharmacokinetics.
Even with these low amounts of AA and mostly depleted systemic AA by the trauma injuries’ oxides, RSD occurred in four (7%) wrists in the vitamin C group and 14 (22%) in the placebo group.
This is a reduction to 1/3 the incidence of RSD. If AA were administered at 2 grams 4x per day, the AA levels would have been in the therapeutic range, absent other systemic infections and toxins.
“This prospective, double-blind study shows that vitamin C was associated with a lower risk of RSD after wrist fractures. Our hypothesis is that this beneficial effect of prophylaxis would be useful in other forms of trauma.”
Comment: The study showed a fantastic reduction to 1/3 the incidence of RSD with modest dosages of AA.
Beneficial results are understated. (Why?)
Higher AA levels should be called for. (Why not?)
No follow up since 1999?
No higher level AA dose trials?
AA Pharmacokinetics Summary
AA is well tolerated in multi gram dosages with intake frequencies of 1 to 3 hours.
The gut to blood transfer efficiency has been estimated to be less than about 15% so about 75 mg can be estimated to make it to the blood each day.
The AA half lifetime was measured in a different pub med study to be ½ hour so after 24 hours the AA concentration can be computed at (½)48th of the original dosage. Thus for the treated study subjects the amount of systemic AA is near zero for most of the day, well below any therapeutic range.
In the presence of oxides and toxins, AA converts from its antioxidant form to dehydroxy AA its oxidizing form. This happens when AA loses two electrons. The reaction is instantaneous. Anascorbemia (Cathcart) results. This is rapid onset scurvy and shares many of the symptoms of anaphylaxis. Anaphylaxis is relived rapidly by systemic infusion of AA.
Adrenaline works as a restorative by releasing several grams of AA from the adrenal glands, destroying adrenal functionality that depends on the stored AA. Adrenaline shots should be accompanied with AA supplementation, preferably by IV or injection.
COPD-related urge to cough is related to AA depletion. Administering several grams of AA can immediately quell the urge to cough and reduce/eliminate the coughing-fit severity. It is suggested that asthma attacks severity and frequency are also an indicator of AA depletion. When the blood levels of AA fall below a critical level, histamine production increases exponentially.
AA intake is generally regarded as safe in any level in the presence of inflammation and toxemia. Too low an AA intake was proven many times by our family experiences to be harmful.
RSD treatment should include therapeutic levels of frequent AA intake in accord with AA pharmacokinetics.
Our experience with trauma (fall) injuries, coincident with an antibiotic (Cipro) induced systemic toxemia state, indicates that pains can be extreme (bursitis and plantar fasciitis) even without trauma in the absence of enough AA (Vitamin C).
With age, hypoglycemia, smoking, toxemia, and trauma, the need for AA rises to a need for greater than 6 grams per day (per 75kg body weight)
AA intake (1-3 grams) every 1-3 hours have quickly quelled pains, reduced the need for analgesics and speeded healing as measured by reduction rates of bruises.