Sigh, He might say that he knows William White personally and he is not a scientist but a moderator at his other small board and his 'hypothesis' on Olney's Lesions has been roundly discredited for 'quite some time'.
He might also say that 'Bill' has since
retracted his 'hypothesis' regarding Olney's Lesions. Since the overwhelming evidence suggests that he was simply incorrect. Not only has it been studied for neuroprotection (antithetical to this suggested damage) but actually, the lesion in question has NEVER been seen in a human EVER, or a primate for that matter.
> How dangerous/harmful would you say DXM is to our brains
> and health?
Used infrequently and in responsible doses, I'd say that DXM is considerably less dangerous than many other commonly used drugs (such as, say, cocaine, methamphetamine, and possibly MDMA).
> There's very little information on it
Incorrect. Try going here and doing searches for "dextromethorphan" and "dextrorphan":
Helpful Site
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
You will find such interesting study abstracts as:
Drug Alcohol Depend. 2002 Jul 1;67(2):177-83.
A randomized, double-blind, placebo-controlled safety study of high-dose dextromethorphan in methadone-maintained male inpatients.
Cornish JW, Herman BH, Ehrman RN, Robbins SJ, Childress AR, Bead V, Esmonde CA, Martz K, Poole S, Caruso FS, O'Brien CP.
Veteran's Affairs Medical Center, University & Woodland Aves., Philadelphia, PA 19104, USA.
[email protected]
from abstract:
"Male participants received daily methadone (50-70 mg/day) and either DM (n=10) or placebo (n=5) during the 12-day active medication phase of the study. DM participants received doses of 120, 240, and 480 mg/day in increasing order (4 days each). ... Overall, DM was well-tolerated by the methadone-maintained opiate-dependent subjects studied here. These results support the further exploration of DM as an adjunct medication during methadone replacement therapy."
Methods Find Exp Clin Pharmacol. 1999 Dec;21(10):673-8.
A phase I clinical trial of dextromethorphan in intractable partial epilepsy.
Kimiskidis VK, Mirtsou-Fidani V, Papaioannidou PG, Niopas I, Georgiadis G, Constadinidis TC, Kazis AD.
3rd Department of Neurology, Aristotle University of Thessaloniki, Greece.
from abstract:
"After an 8-week baseline period, DM was added to the existing antiepileptic drugs at a dose of 40 and 50 mg every 6 h (160 and 200 mg/day). Each treatment period lasted 8 weeks. Seizure control improved after administration of DM, especially in the group of intermediate and slow metabolizers. Two patients, however, experienced increased seizure frequency and withdrew from the study. Adverse effects during DM administration were mild and transient. DM was well tolerated even in patients with high plasma levels of the drug (up to 15020 ng/dl). Our results indicate that DM is safe and effective in the treatment of comedicated patients with intractable partial epilepsies."
J Pediatr. 1998 Apr;132(4):709-13.
Long-term use of high-dose benzoate and dextromethorphan for the treatment of nonketotic hyperglycinemia.
Hamosh A, Maher JF, Bellus GA, Rasmussen SA, Johnston MV.
Center for Medical Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
from abstract:
"We administered benzoate (at doses of 500 to 750 mg/kg/day) and dextromethorphan (at doses of 3.5 to 22.5 mg/kg/day) to four infants with nonketotic hyperglycinemia with follow-up of 3 months to 6 years. ... Benzoate reduced to normal the glycine concentration in plasma and substantially reduced but did not normalize the glycine concentration in cerebrospinal fluid. Dextromethorphan was a potent anticonvulsant in some but not all patients. There was remarkable interpatient variability in dextromethorphan metabolism. Three patients are living (ages ranging from 4 to 6 years) and are moderately to severely developmentally delayed; two are free of seizures. The third patient, with the slowest development, had intractable seizures for nearly a month before diagnosis, and although seizure-free for 30 months, now has grand-mal seizures. One patient died of intractable seizures at 3 months."
Neuropediatrics. 1997 Aug;28(4):191-7.
The effect of the N-methyl-D-aspartate receptor antagonist dextromethorphan on perioperative brain injury in children undergoing cardiac surgery with cardiopulmonary bypass: results of a pilot study.
Schmitt B, Bauersfeld U, Fanconi S, Wohlrab G, Huisman TA, Bandtlow C, Baumann P, Superti-Furga A, Martin E, Arbenz U, Molinari L, Turina M, Boltshauser E, Schmid ER.
Department of Pediatrics, University of Zurich, Switzerland.
from abstract:
"Thirteen children age 3-36 months undergoing cardiac surgery with expected CPB of 60 minutes or more were randomly assigned to treatment with dextromethorphan (36-38 mg/kg/day) or placebo administered by naso-gastric tube. Dextromethorphan was absorbed well and reached putative therapeutic levels in blood and cerebrospinal fluid. Adverse effects were not observed."
Neurology. 1997 May;48(5):1212-8.
High-dose oral dextromethorphan versus placebo in painful diabetic neuropathy and postherpetic neuralgia.
Nelson KA, Park KM, Robinovitz E, Tsigos C, Max MB.
Pain and Neurosensory Mechanisms Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892-1258, USA.
from abstract:
"Dosage was titrated in each patient to the highest level reached without disrupting normal activities; mean doses were 381 mg/day in diabetics and 439 mg/day in postherpetic neuralgia patients. In diabetic neuropathy, dextromethorphan decreased pain by a mean of 24% (95% CI: 6% to 42%, p = 0.01), relative to placebo. In postherpetic neuralgia, dextromethorphan did not reduce pain (95% CI: 10% decrease in pain to 14% increase in pain, p = 0.72). Five of 31 patients who took dextromethorphan dropped out due to sedation or ataxia during dose escalation, but the remaining patients all reached a reasonably well-tolerated maintenance dose."
J Neurosurg. 1996 May;84(5):860-6.
Dose escalation safety and tolerance study of the N-methyl-D-aspartate antagonist dextromethorphan in neurosurgery patients.
Steinberg GK, Bell TE, Yenari MA.
Department of Neurosurgery, Stanford University Medical Center, California, USA.
from abstract:
"One hundred eighty-one patients received a total of 212 courses of DM treatment in dose ranges of 0.8 to 9.64 mg/kg. ... In 11 patients, brain and plasma levels of DM were comparable to levels that have been shown to be neuroprotective in animal studies. Frequent side effects occurring at neuroprotective levels of DM included nystagmus (64%), nausea and vomiting (27%) distorted vision (27%), feeling "drunk" (27%), ataxia (27%), and dizziness (27%). All symptoms were reversible and no patient suffered severe adverse reactions. This study demonstrates that potentially neuroprotective doses of DM can be administered safely to neurosurgical patients. ... Side effects, even at the highest levels, proved to be tolerable and reversible. Administration of DM to patients at risk for cerebral injury should be further explored."
Drug Saf. 1992 May-Jun;7(3):190-9.
Dextromethorphan. An overview of safety issues.
Bem JL, Peck R.
Pharma Division, F. Hoffmann-LaRoche Ltd, Basel, Switzerland.
from abstract:
"In summary, the safety profile of dextromethorphan is reassuring, particularly relating to overdose in adults and children."
Ann Neurol. 1994 Dec;36(6):920-4.
High-dose dextromethorphan in amyotrophic lateral sclerosis: phase I safety and pharmacokinetic studies.
Hollander D, Pradas J, Kaplan R, McLeod HL, Evans WE, Munsat TL.
Department of Neurology, Tufts University School of Medicine, Boston, MA.
from abstract:
"Thirteen patients were given DM in an escalating dose fashion, to a target of 10 mg/kg/day or the maximum tolerable dose, and then maintained on this dose for up to 6 months. Total daily doses ranged from 4.8 to 10 mg/kg (median, 7 mg/kg). Side effects were dose limiting in most patients. The most common side effects were light-headedness, slurred speech, and fatigue. Detailed pharmacokinetic and neuropsychology studies were performed. This study demonstrates the feasibility of long-term administration of high-dose DM in ALS, as well as in other conditions associated with glutamate excitotoxicity."
From a different helpful website:
Safety, Tolerability, and Pharmacokinetics of the N-Methyl-D-Aspartate
Antagonist Dextrorphan in Patients With Acute Stroke
G.W. Albers, MD; R.P. Atkinson, MD; R.E. Kelley, MD; D.M. Rosenbaum,
MD; on behalf of the Dextrorphan Study Group
Stanford Stroke Center, Stanford University Medical Center, Palo Alto, CA 94304.
(Stroke. 1995;26:254-258.)
© 1995 American Heart Association, Inc.
From paper:
"Patients typically became confused and frequently had vivid auditory and visual hallucinations, often of religious or death-related content. ... The maximum total dose of dextrorphan administered was 3310 mg over 24 hours. ... There was no evidence of systemic toxicity, and means of routine laboratory tests (complete blood count, chemistry panel, coagulation studies) were within the normal ranges at 24 and 48 hours after infusion. In addition, no significant electrocardiographic changes were noted on routine monitoring. There was one death 30 days after drug infusion (the patient with the occult carcinoma) due to respiratory failure secondary to the carcinoma."
That last study involved DXO, not DXM, but as DXM metabolizes almost completely into DXO (given normal doses in extensive metabolizers) this study demonstrates the relative safety of doses of DXO as high as 3 grams over 24 hours(i.e., many, many times the antitussive dose) in stroke patients. Some patients did experience hypotension when the IV infusion of DXO was too rapid, but this effect was easily treated. The highest doses administered were associated with apnea, which is a good argument for not eating three grams of DXM. Finally, please consider, from a University of Maryland pharmacology link that is now unfortunately dead:
"Despite these concerns, dextromethorphan is considered to be a safe drug overall. Ingestion of greater than 10 mg/kg might produce toxic symptoms, but doses in excess of 100 times the usual adult dose have not been fatal. Mortality from dextromethorphan is rare unless there are co-ingestants (such as MDMA, monoamine oxidase inhibitors, antidepressants, or antihistamines)."
As you can see, DXM doses in the recreational range have been used experimentally without serious adverse consequences, sometimes daily for months.
> If you would like some definate answers, donate a chimp and
> 100g of DXM powder to Mr. William White.
(1) Chimps are not humans, so a chimp getting NAN would not definitively prove that humans do.
(2) One chimpanzee is not an adequate statistical sample for a scientific experiment.
> Is it as bad as an opiate addiction or a benzo addiction?
No.
This would be a classic example of D.A.R.E. campaign using incorrect scientific information, for years now they both attacked Bill White for writing the DXM faq and then they cite a mistake of his repeating it saying it will eat holes in people's brains.
Which, as everyone has known for years was simply his own hypothesis that had zero proof but sounded good in the way he wrote it. It is quite simply incorrect as he has admitted several times.
If you do not believe me, simply ask William White who made that whole brain lesion thing up. He is a moderator at
www.dextroverse.org and I PMd with him last night. His handle is bwhite.
The moral of the story is, just because it is written does not make it true, of course, WHAT IF?? William White is Brothabill, hmmmm??
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