S. Hale Shakman
Notes on Psychopharmacology (November 16, 2008)
A preponderance of historical and current information is at a minimum cautionary and is readily viewed as arguing against the use of drugs in psychiatry.
Regarding investigation into the action of psychopharmaceuticals on the underlying cause of neuropsychiatric disorders, a detailed 1955 study by E.C. Rosenow M.D., conducted at the outset of the "psychiatric-drug treatment" era clearly demonstrated that the paradigm-setting drug chlorpromazine (trade name Thorazine) not only failed to eliminate or diminish the implicated causative infection, but actually made it worse. Whereas Rosenow had hoped to disclose a beneficial bactericidal action, (definitive and reproducible) agglutination titer results for both blood serum and urine respectively indicated a "significantly" worsened immunological condition as compared with patients not receiving the drug.
-- Rosenow1955-JNervMentDis122.doc, p. 330.
This early finding of Rosenow is substantiated by the modern realization that so-called "dopamine-blocking" drugs, e.g. metoclopromide, chlorpromazine (Thorazine) and Haldol, very often cause persistent and even permanent neurological damage manifesting as "tardive dyskinesia":
The finding that "the disorder [tardive dyskinesia] ultimately occurs in up to 25% of patients taking dopamine-blocking drugs" seems to clearly indicate how horribly toxic these drugs are. Insofar as permanent physical damage is so prominently evident in a significant portion of these patients, varying lesser degrees of damage with untold implications may readily be projected throughout the "treated" population. It boggles the mind that the state of medicine allows and even encourages such disgraceful, anti-Hippocratic (i.e., "never do harm") practices to continue.
Accordingly Rosenow's work, beyond being confirmed by the aforesaid documented hazards of so-called "dopamine blockers", provides a testable explanation of the underlying cause of these hazards. As such, the tests Rosenow performed with respect to chlorpromazine could well be applied to other drugs in order to determine whether a worsened immunological condition results from their use -- whether or not associated with observable side effects or even a gross disorder such as tardive dyskinesia.
Regarding the many other drugs in use subsequent to chlorpromazine, the very presence of a litany of severe side effects of these newer drugs substantiates at a minimum that they likewise are not addressing the cause (and implies a worsened immunological condition resulting from their use); as summarized by NIMH in 2006, "no [drug for schizophrenia] option improves thought processes or is tolerated well".
Even this acknowledgment grossly understates potential hazards, e.g., the largest cohort [British] study to date indicated a 20-fold increase in suicides in 1994-1998 as compared to the pre-Chlorpromazine years 1874-1925:
In January 2008, the FDA issued an alert reporting an increased risk (double) for suicidal behavior or ideation, consistent among eleven common (epilepsy and psychiatry) drugs when compared to placebo, and with the expectation that this increased risk is shared by all such drugs.
Suicide has often been specifically linked to drug withdrawal, as are other side effects, i.e., the “head in a blender … dizziness, nausea, sweating, insomnia, and electrical shock-like sensations” commonly associated with withdrawal from “antidepressants like Celexa, Cymbalta, Effexor, Paxil, or Zoloft …”:
This last item notes that these “severe side effects [leave] patients virtually addicted to the drug”.
And "...virtually all of the gun-related massacres ... over the past decade ... were perpetrated by people taking ... [an] antidepressant drug."
It is noted that the pharmaceutical industry is seemingly aggressively pursuing new markets, including if not particularly targeting children. For example, psychiatry’s use of drugs in children more than doubled for the decade of 1987 to 1996; and from 1997-2007, the rate of diagnosis for one category, bipolar diagnosis in children under 13, increased almost sevenfold, with a typical treatment regimen of multiple medications.
[It is further noted that the use of drugs in cognitively impaired children is commonplace (e.g., google: "cognitive impairment children medication").]
Certainly suicide and murder are more severe than the other many negative "side"-effects of psychopharmaceuticals; however, at a minimum these issues illustrate something is drastically problematic with the field of psychopharmacology overall, at least as of its present stage of development.
Again we are reminded that the presumed clinical “benefits” of psychopharmaceuticals are themselves not known to have any beneficial effect relative to the underlying physiological cause of a given neuropsychiatric disorder; rather, the action and thus inadvisability of any and all such drugs is arguably properly described by their acknowledged so-called “side effects”, emotional as well as physical.
Meanwhile, even these presumed “benefits” may be somewhat suspect, considering that allegations abound of drug companies routinely playing down risks, aggressively marketing drugs, and attempting to create markets, buy influence, etc. An introductory summary article discussing these issues (from google search for: pharmaceutical companies psychiatric drugs withholding facts):
The importance of marketing within the field overall is evident in the suggestive use, ironically, in positive psychological nomenclature; e.g., "Celexa" (suggesting "celebrate"), "Cymbalta" ("cymbals"), "Effexor" ("effective), "Luvox" (suggesting "love"), Paxil ("peace"), Prozac ("pro", versus "con"), "Remeron" ("remedy"), "Topamax" ("top", "maximum"), "Wellbutrin" ("wellness"), etc. Considering that none of these actually have been shown to have a direct beneficial impact relative to the underlying cause of the involved nervous system disorder; and all seem to have notable derogatory "side effects", i.e. all are toxic/poison to some extent; the use of such psychological inducements in conjunction with aggressive promotional campaigns may be viewed as problematic at a minimum (and, arguably, pejoratively speaking, even somewhat "sleazy").
The field of psychiatry is seemingly perpetually describing, or arguably devising, new categories of controversial “mental illnesses”, a process that has been criticized as an ever expanding quest to gain patients and sell drugs:
A particularly notable example of the arguably systemic state of collusion between psychiatry and the drug companies, with incontrovertible conflict-of-interest implications, involves a (now-former) department chairman, who was demoted (but not discharged) -- not for taking income from drug companies, but rather for getting caught failing to report it. The act of taking income from drug companies, disclosed or not, is a clear conflict of interest for any and all medical practitioners or teachers, in any and all disciplines, and in a sane society would be strictly prohibited.
Notwithstanding the presumptive overwhelming predominance of well-intentioned honorable researchers, the prestigious New England J. of Medicine has recently discussed deception and even fraud pervading the very foundation of medical research. This 2008 article disclosed an apparent general pattern whereby unfavorable studies are distorted or ignored while only favorable ones are published; see particularly the third item in this article, entitled “Negative drug trials unreported”:
And finally, if there is any credence to the above documentation of issues relevant to the field of psychopharmacology, we seemingly go off the deep end of rationality with the recent publication of a Cambridge U. Press text on "Ethno-Psychopharmacology" -- a treatise on differentiation of effects of these drugs on different ethnic groups. Thus the current sad trend, away from animal experimentation and toward human experimentation, arguably spirals downward into utter nonsense, which the March 4 2009 JAMA reviewer (Mark H. Fleisher, MD, U. Nebraska) recommends "be required for all academic libraries ..." and various researchers and clinicians. Hopefully it will properly be filed under "fiction".
Given the extensive proofs by Rosenow that a range of neuropsychiatric conditions are infectious and can be ameliorated if not eliminated on this basis (see particularly Shakman-History-Rosenow and Rosenow1955-JNervMentDis122.doc), it is unlikely that any current or prospective future pharmaceuticals can possibly succeed in having a comparable result (without inclusion of Rosenow's protocols (i.e., vaccine and foci removal), in which case any such proposed pharmaceuticals would be irrelevant). In any case it is clear that no pharmaceuticals currently in use come even remotely close to a proper and sensible solution (to say nothing of inherent dangers in all).
There is, of course, always the hope that some new pharmaceutical will indeed target and eliminate the causative organism; either in the circulation, thereby disallowing it to spread; or in the source (oral) nest, thereby healing infections in teeth etc.; or preferably both. A prospective first step in evaluating any such prospective pharmaceutical intervention would be replication of those agglutinative titer experiments described in the above-discussed Rosenow article (Rosenow1955-JNervMentDis122.doc). For prospective researchers wishing to proceed along these lines, detailed associated culture methodology recipes are posted at http://instituteofscience.com/Ro-recip.html .
P.S.: Possible efficacy of antibiotics in infective conditions that may be secondary to oral foci:
In 1916, Rosenow had first demonstrated that stomach ulcers were caused by infection. This finding has been more recently validated through identification of a phase of the causative organism, i.e., Helicobacter pylori, by Barry Marshall of Australia. Whereas Rosenow's work was accomplished well prior to the advent of antibiotics, Marshall's recent re-discovery has fostered a new protocol for treatment through the use of antibiotics.
Consistent with this approach is the use of low-dose long term antibiotic therapy for a range of chronic, systemic conditions (e.g., google: chronic disease low dose antibiotics). Insofar as the action of many antibiotics (e.g., penicillin, amoxicillin, etc.) does not actually destroy the organism per se but rather causes dissociation by removing its cell wall, a process that is reversible, presumably the intended effect of long term antibiotics would be prevention of reversion to the harmful phase and thus prevention of harmful effects.