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Post by beebs on Dec 25, 2011 9:04:10 GMT -5
DRAFT (fluctuating cognitive dysfunction + brain fog)[bWARNING[/b] : See the short presentation concerning the side effects of Lariam/Mefloquine - indeed damning. [/size] The mention of "irreversible" in the YT vid is contrary for most, in particular, those who abstain from psychotropics, other meds, and invasive procedures, anesthetics, contrast dye, solvents, etc. A major symptom "suicide ideation" or strong impulses to self harm, may appear out of the blue, without psychosis, hallucinations, and not feeling depressed. Neuro/psychiatric symptoms are chemically induced. The vid and most published papers theorize about a previous underlying undiagnosed psychiatric illness. I don't believe this is true. Some papers quote between 40 to 90 percent neuropsychiatric symptoms, mild to severe for most lasting a few months. Those symptoms can last for a few months, or some years, fluctuating. Its difficult at this time to separate unknown triggers, exposure to those triggers, such as local or general anesthetic, other meds, and even some compounds in some foods. Anecdotal: I had a recurrence of neuro symptoms, severe agnosia, and some type of mild seizures, over ten years later after eating raw tumeric (for liver). Found folic acid, and folate or folinic acid exacerbates those symptoms. There are strong links with certain foods exacerbating neuro or psychiatric and joint pains, neuropathy etc.. Do your research. Some may react to fish because of purine, others to chicken perhaps the alanine, for others its foods high glutamic acid, and so on. Pyschosis and hallucinations can take six months to a year to dissipate if NOT taking psychotropics. (anecdotal). One criticism here in this study is the omission of analysis differentiation between those who DID NOT take psychotropics, avoided any medical intervention.Keep optimistic and the belief that you can recover, will lead you towards less harmful solutions, and even if not 100% reversible, to a tolerable level.
Focus on reading recovery stories, for positive reinforcement. Keep a positive frame of mind, will lead to seek valuable information on how to REPAIR (prevent further damage.As for approaches to therapeutic modalities, Choose wisely think of long term consequences, strategize your choice of treatment bearing in mind long term possible damage vs recovery even if partial. Least toxic models. IMHORule No. 1 - avoid psychotropics, valporic acid anesthetics, contrast dye, thallium, asthma inhalers, steroids, solvents, etc. that are known to alter ion channels, neuronal activities, catecholamines and other systems.
Three of my acquaintances tried to commit suicide this past year. They were on psychotropics, none took other meds years preceding psychotropics. They all report that its was a strong urge to self destruct. They could not stop themselves. Quite a leap from being sad, unahppy, inability to cope, to psychotropic = hell.
See: adr-centralreactiontomedications.blogspot.com/search/label/Psychiatry%20-%20Manufacturing Scroll down and read "Marketting of Madness" and list of symptoms from taking psychotropics: adr-centralreactiontomedications.blogspot.com/search/label/Damage%20caused%20by%20psychotropics%20drugs
Rule No. 2 - Put up with symptoms. Seek non toxic models. Keep strong. (As for psychotropics they are known to cause the same symptoms, such as suicide ideation, violent aggressive behaviors and more!!) AVOID (as in Rule No. 1)
Rule No. 3 - INFORM YOURSELVES about foods you should avoid, such glutamate, phenols, soy, sugar, etc... Rationalize symptoms, Your symptoms are chemical toxicity, NOT psychological.
Namid: there is plenty here for further research on NMDA receptors and more mentioned in this vid.
Will post more research over time.
[youtube] www.youtube.com/watch?v=zTUgF3aYGqk&context=C36d4f31ADOEgsToPDskJrr2waDvmZqiSh4hC80ZJg[/youtube]
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Post by beebs on Dec 25, 2011 9:07:43 GMT -5
Aspirin is a well known trig Drug-induced tinnitus and other hearing disorders. Seligmann H, Podoshin L, Ben-David J, Fradis M, Goldsher M.Unit of Clinical Pharmacology, Bnai Zion Medical Center, Haifa, Israel. Tinnitus and hearing loss, both reversible and irreversible, are associated both with acute intoxication and long term administration of a large range of drugs. The mechanism causing drug-induced ototoxicity is unclear, but may involve biochemical and consequent electrophysiological changes in the inner ear and eighth cranial nerve impulse transmission. Over 130 drugs and chemicals have been reported to be potentially ototoxic. The major classes are the aminoglycosides and other antimicrobials, anti-inflammatory agents, diuretics, antimalarial drugs, antineoplastic agents and some topically administered agents. Prevention of drug-induced ototoxicity is generally based upon consideration and avoidance of appropriate risk factors, as well as on monitoring of renal function, serum drug concentrations, and cochlear and auditory functions before and during drug therapy. Ototoxicity, although not life-threatening, may cause considerable discomfort to patients taking ototoxic drugs, and in some cases drug discontinuation may be necessary to prevent permanent damage. Much research has been performed to investigate the causes and mechanisms of ototoxicity, to try to prevent this complication. Despite these efforts, ototoxicity still occurs, and there is much work to be done in order to understand the mechanism of ototoxicity of different drugs and to prevent hearing loss and tinnitus in the future. www.ncbi.nlm.nih.gov/pubmed/89345....ogdbfrom=pubmed
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Post by beebs on Dec 25, 2011 9:19:54 GMT -5
Unexpected frequency, duration and spectrum of adverse events after therapeutic dose of mefloquine in healthy adults.[My paper] Pamela Rendi-Wagner, Harald Noedl, Walther H Wernsdorfer, Gerhard Wiedermann, Andrea Mikolasek, Herwig Kollaritsch Department of Specific Prophylaxis and Tropical Medicine, Institute of Pathophysiology, University of Vienna, Kinderspitalgasse 15, A-1095 Vienna, Austria. joy.pamela.wagner@univie.ac.at Abstract The frequency and spectrum of previous adverse events associated with the antimalarial therapeutic regimen of previous floquine (MQ) (750 and 500 mg at an interval of 6 h) was assessed in 22 healthy volunteers who were monitored for 21 days following drug administration. An unexpected high frequency of side effects of any grade were reported by all 22 subjects. The most commonly reported symptoms were vertigo (96%), followed by nausea (82%) and headache (73%). Participants suffering from severe (grade 3) vertigo (73%) required bed rest and specific medication for 1 to 4 days. More females than males reported severe previous adverse reactions. The majority (77.3%) of the participants (f: 8/12, m: 9/10) showed symptom resolution within 3 weeks (510 h) after drug administration. Biochemical and haematological findings stayed within the normal range of values, but showed nevertheless a significant rise of Na, Cl, Ca, bilirubin, GGT and LDH. The unexpectedly high frequency and severity of previous adverse reactions after normal therapeutic dosage of MQ in healthy subjects may influence future recommendations regarding the use of MQ for stand-by treatment of suspected malaria in travellers. lib.bioinfo.pl/pmid:11801224
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Post by beebs on Dec 25, 2011 9:23:39 GMT -5
The hypo of ADRS & S/Es associated with previous neurological and mental illness is refuted and no longer applies. It could happen to anyone. Epileptogenic potential of mefloquine chemoprophylaxis: a pathogenic hypothesis. Nevin RL. Source United States Africa Command, Combined Joint Task Force Horn of Africa, Camp Lemonier, FPO AE 09363, Republic of Djibouti. remington.nevin@us.army.mil Abstract BACKGROUND: Mefloquine has historically been considered safe and well-tolerated for long-term malaria chemoprophylaxis, but prescribing it requires careful attention in order to rule out contraindications to its use. Contraindications include a history of certain neurological conditions that might increase the risk of seizure and other adverse events. The precise pathophysiological mechanism by which mefloquine might predispose those with such a history to seizure remains unclear. PRESENTATION OF THE HYPOTHESIS: Studies have demonstrated that mefloquine at doses consistent with chemoprophylaxis accumulates at high levels in brain tissue, which results in altered neuronal calcium homeostasis, altered gap-junction functioning, and contributes to neuronal cell death. This paper reviews the scientific evidence associating mefloquine with alterations in neuronal function, and it suggests the novel hypothesis that among those with the prevalent EPM1 mutation, inherited and mefloquine-induced impairments in neuronal physiologic safeguards might increase risk of GABAergic seizure during mefloquine chemoprophylaxis. TESTING AND IMPLICATIONS OF THE HYPOTHESIS: Consistent with case reports of tonic-clonic seizures occurring during mefloquine chemoprophylaxis among those with family histories of epilepsy, it is proposed here that a new contraindication to mefloquine use be recognized for people with EPM1 mutation and for those with a personal history of myoclonus or ataxia, or a family history of degenerative neurologic disorder consistent with EPM1. Recommendations and directions for future research are presented. www.ncbi.nlm.nih.gov/pubmed/19656408
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Post by beebs on Dec 25, 2011 9:53:37 GMT -5
Note that anyone can suffer from Mefloquine/Lariam ADRs, not only those with a history of neuro or mental illness, its ANYBODY.. The Antimalarial Potential of 4-Quinolinecarbinolamines May Be Limited due to Neurotoxicity and Cross-Resistance in Mefloquine-Resistant Plasmodium falciparum Strains Geoffrey S. Dow,1* Michael L. Koenig,2 Lesley Wolf,2 Lucia Gerena,1 Miriam Lopez-Sanchez,1 Thomas H. Hudson,1 and Apurba K. Bhattacharjee1 Divisions of Experimental Therapeutics,1 Neurosciences, Walter Reed Army Institute of Research, Silver Spring, Maryland 209102 Received 16 September 2003/ Returned for modification 25 November 2003/ Accepted 3 March 2004 /… Background Mefloquine (Lariam/Mefloquine®) is a commonly prescribed anti-malarial. Although historically the long-term use of mefloquine for malaria chemoprophylaxis has been considered safe and well-tolerated [1,2], careful prescribing is needed to minimize the potential for severe neurological adverse events, including myoclonus and seizure, for which individuals with certain neurological histories appear to be at highest risk [3]. In particular, case-report [4], case-series [5], and retrospective cohort [6,7] studies define a well-characterized pattern of increased susceptibility to seizure and other movement disorders including nystagmus and ataxia [4] with use of mefloquine among those with a personal [4-6] or family history [7] of such conditions. Additional case-reports describe, in the absence of personal or family history, the occurrence of multifocal myoclonus [8], convulsions, and seizures following both therapeutic [9] and prophylactic doses [10-12] when mefloquine is co-administered with other medications such as fluroquinolones [13], or occasionally when mefloquine administration is preceded by non-specific neurologic prodrome [14]. The U.S. package insert cautions that mefloquine "should not be prescribed for prophylaxis in patients with active depression, a recent history of depression, generalized anxiety disorder, psychosis, or schizophrenia or other major psychiatric disorders, or with a history of convulsions" [15]. The prevalence of these contraindications is approximately 9–10% in both military [16] and civilian [17] populations that present for malaria chemoprophylaxis, which underscores that clinicians must exercise significant care prior to prescribing and dispensing mefloquine….// Adverse central nervous system (CNS) events have been associated with mefloquine use. Severe CNS events requiring hospitalization (e.g., seizures and hallucinations) occur in 1:10,000 patients taking mefloquine for chemoprophylaxis (22). However, milder CNS events (e.g., dizziness, headache, insomnia, and vivid dreams) are more frequently observed, occurring in up to 25% of patients (22). The rate of adverse neurological events associated with mefloquine is higher than for Malarone (20), and subjects receiving mefloquine in clinical trials are more likely to withdraw from the trial than those receiving placebo (8). The higher incidence of adverse events observed when the drug is used at the higher doses needed for malaria treatment (22, 23) implies a dose effect. There is no accepted biochemical basis for the neurotoxicity of the drug; [b ]However, we recently showed that mefloquine severely disrupts calcium homeostasis in rat neurons in vitro at concentrations in excess of 20 µM, an effect closely related to the acute neurotoxicity of the drug in terms of dose effect and kinetics (10)[/b] Peak plasma levels of mefloquine are 3.8 and 2.1 to 23 µM after prophylaxis and treatment, respectively (16, 25). However, the drug crosses the blood-brain barrier and accumulates as much as 30-fold in the central nervous system and mefloquine brain concentrations as high as 50 µM have been reported in human postmortem cases (14, 21). Mefloquine brain concentrations as high as 90 µM have been reported in rats given a therapy-equivalent dose rate, with concentrations in subcompartments in the brain exceeding 100 µM (2). Since it has long been known that a prolonged disruption of neuronal calcium homeostasis may lead to neuronal cell death and injury (6, 13), it is reasonable to suppose that such events may contribute to the clinical neuropathy of the drug. Mefloquine remains a useful antimalarial drug for many patients who are able to tolerate the drug or are unable or unwilling to take doxycycline or Malarone. However, the neurotoxicity associated with mefloquine is such that some have questioned its clinical utility as a prophylactic drug (7). There are several approaches to the amelioration of this problem, including (i) administration of neuroprotective drugs such as physostigmine (26), (ii) reformulation of mefloquine as a pure isomer (24), and (iii) reengineering of the mefloquine molecule to yield derivatives that are less neurotoxic but retain their antimalarial activity. Bhattacharjee and Karle (3) earlier showed that the in vivo potency of 4-quinolinecarbinolamines was correlated with key stereoelectronic features, including electrostatic potential and lipophilicity. However, the issues of neurotoxicity and drug resistance were not addressed. In the present report, we show that the antimalarial potential of 4-quinolinecarbinolamines may be limited by their neurotoxicity and cross-resistance of mefloquine-resistant parasites. We also describe the generation of a reliable function-based three-dimensional (3D) quantitative structure activity relationship (QSAR) pharmacophore model for neurotoxicity of this class of compounds which may be useful for selecting new quinoline analog candidates devoid of such toxicity. Cont/… www.ncbi.nlm.nih.gov/pubmed/15215119
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Post by beebs on Dec 30, 2011 15:42:10 GMT -5
Many suffer from neuropathy post Lariam, sometimes delayed, and don't make the connection... Yet, if someone takes a herb and suffers from side effects, the medical establishment is very quick at pointing the finger!!
Am J Trop Med Hyg. 2011 Dec;85(6):1008-9. Peripheral polyneuropathy and mefloquine prophylaxis.Chester AC, Sandroni P. Source Department of Medicine, Georgetown University Hospital, Washington, DC; Department of Neurology, Mayo Clinic, Rochester, Minnesota. Abstract Abstract. We describe a case of a woman who developed a peripheral polyneuropathy shortly after completing 4 weekly doses of mefloquine hydrochloride (250 mg) malaria prophylaxis. Although mefloquine-related central nervous system neuropathy is well described in the literature, peripheral polyneuropathy similar to this case has been documented only once before, to our knowledge. www.ncbi.nlm.nih.gov/pubmed/22144435
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Post by beebs on Dec 30, 2011 16:50:27 GMT -5
An earlier study showed Mefloquine in tissues post mortem years later... This paper makes a correlation with the lack of P-Glycoprotein at the blood brain barrier. See this horrific theory about regulating the P-Gycoprotein to enable the effectiveness of psychotropics. www.ncbi.nlm.nih.gov/pmc/articles/PMC2634288/?tool=pmcentrez It boggles the mind... Oh, I forgot to mention another study which mentions using Mefloquine as a possible psychotropic in future, and this is science for you (will post it when I find it). Question: if indeed it was due to the lack of P-Glyco, Why some experience no side effects for many months or years taking Lariam on/off, to suddenly develop serious CNS side effects??? Oooops Harefuah. 2010 Sep;149(9):583-4, 620, 619. [Polymorphism at the MDR1 locus as a cause of mefloquine-induced psychosis].[Article in Hebrew] Zaigraykina N, Potasman I. Source Infectious Diseases Unit, Bnai Zion Medical Center, Haifa. natalia.zaigraykin@b-zion.org.il Abstract The use of mefloquine for malaria prophylaxis has been hampered by the drug's adverse effects. Foremost among the latter are neuropsychiatric adverse effects such as dizziness, vivid dreams, epilepsy and psychosis. Recent evidence from studies in mice has implicated the lack of P-glycoprotein at the blood-brain barrier as the cause of these adverse effects. The authors present the case of a 60 year-old man who was hospitalized for psychosis following ingestion of mefloquine for malaria prophylaxis. Genetic studies have found polymorphism at the MDR1 gene with genotypes 3435TT and 2677TT which underlie high levels of mefloquine in the brain.Now read this & explain how can those scientists get away with such flagrant pseudo-science? Modulation of P-glycoprotein at the Blood-Brain Barrier: Opportunities to Improve CNS PharmacotherapyDavid S. Miller, Björn Bauer, and Anika M.S. Hartz Laboratory of Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC (B.B., A.M.S.H., D.S.M.) College of Pharmacy (B.B.) and Medical School (A.M.S.H.), University of Minnesota, Duluth, MN Corresponding Author: Dr. David S. Miller Laboratory of Pharmacology and Chemistry National Institute of Environmental Health Sciences National Institutes of Health Research Triangle Park, NC 27709, USA Phone: 919 541 3235 Fax: 919 541 5737 ; Email: miller@niehs.nih.gov Small right arrow pointing to: The publisher's final edited version of this article is available free at Pharmacol Rev Small right arrow pointing to: See other articles in PMC that cite the published article. * Other Sections▼ o Abstract o I. Introduction o II. The Blood-Brain Barrier o III. P-glycoprotein, A Critical Element of the Selective/Biochemical Barrier o IV. Modulation of P-glycoprotein Transport Activity o V. Perspectives o References Abstract Pharmacotherapy of CNS disorders, e.g., neurodegenerative diseases, epilepsy, brain cancer, and neuro-AIDS, is limited by the blood-brain barrier. P-glycoprotein, an ATP-driven, drug efflux transporter, is a critical element of that barrier. High level of expression, luminal membrane location, specificity and high transport potency make P-glycoprotein a selective gate-keeper of the blood-brain barrier and thus a primary obstacle to drug delivery into the brain. As such, P-glycoprotein limits entry into the CNS for a large number of prescribed drugs, contributes to the poor success rate of CNS drug candidates and likely contributes to patient-to-patient variability in response to CNS pharmacotherapy. Modulating P-glycoprotein could therefore improve drug delivery into the brain. Here we review the current understanding of signaling mechanisms responsible for the modulation of P-glycoprotein activity/expression at the blood-brain barrier with an emphasis on recent studies from our laboratories. Using intact brain capillaries from rats and mice, we have identified multiple extracellular and intracellular signals that regulate this transporter; several signaling pathways have been mapped. Three pathways are triggered by elements of the brain's innate immune response, one by glutamate, one by xenobiotic-nuclear receptor (PXR) interactions and one by elevated β-amyloid levels. Signaling is complex, with several pathways sharing common signaling elements (TNF-R1, ETB receptor, PKC, NOS), suggesting a regulatory network. Several pathways utilize autocrine/paracrine elements, involving release of the proinflammatory cytokine, TNF-α, and the polypeptide hormone, ET-1. Finally, several steps in signaling are potential therapeutic targets that could be used to modulate P-glycoprotein activity in the clinic. Cont/... www.ncbi.nlm.nih.gov/pmc/articles/PMC2634288/?tool=pmcentrez
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Post by beebs on Dec 30, 2011 16:53:39 GMT -5
Dr Black, an ethical doctor not worried about his career, voiced my sentiments. LARIAM SHOULD BE WITHDRAWNIts not life saving...to say the least! Lariam and HalfanJohn Black Retired Paediatrician, Victoria Mill House, Framlingham, IP13 9EG E-mail dorothyblack@suffolkonline.net Small right arrow pointing to: See "A lesson learnt: the rise and fall of Lariam and Halfan" on page 170. * Other Sections▼ o References Ashley Croft1 has performed a service in exposing the disgraceful failure to test properly the antimalarial drugs Lariam (mefloquine) and Halfan (halofantrine) (JRSM 2007;100:170-174). The side-effects of these drugs were not widely recognized until the mid-1990s, but incredibly, a randomized controlled study was not undertaken until 2001!2 In 1995, my wife and I, on our way back from Tristan da Cunha, were on board RMS St Helena, which called at The Gambia, where we had a day ashore. For this reason we had been advised to take malaria prophylaxis. We shared a table with the ship's doctor, who remarked on the number of passengers, mainly women, who were complaining of depression: he attributed this to the Lariam which they had been prescribed. We had put our faith in chloroquine and proguanil instead. Unfortunately, the ship's doctor did not think to send an adverse reaction report, which was a pity since such a report might have produced action earlier than 2001. I was astonished to find that mefloquine (but not halofantrine) was still listed in the September 2006 issue of the British National Formulary with an entry identical to that of March 2001—a mild warning about neuropsychiatric disorders, depression, convulsions and hypersensitivity to quinine. In both issues of the BNF there is a 17-line list of side-effects! I cannot agree with Croft's plea for more research on mefloquine and halofantrine on the grounds that they are ‘undoubtedly lifesaving drugs.’ In my view, Lariam should be withdrawn, as has presumably occurred with Halfan. www.ncbi.nlm.nih.gov/pmc/articles/PMC1939950/?tool=pmcentrez
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Post by beebs on Jun 6, 2012 7:14:21 GMT -5
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Post by beebs on Jun 15, 2012 7:21:46 GMT -5
Drip by drip odd studies published now and then about resulting symptoms and illnesses, caused by Lariam/mefloquine, Anecdotal, shows higher frequency of cascading symptoms and disease process...Despite all the evidence, its near impossible to obtain a lariam toxicity diagnosis. Int J Clin Pharmacol Ther. 2010 Sep;48(9):577-81. Postural orthostatic tachycardia syndrome: a case report of palpitations and dizziness following prophylactic mefloquine use.Bhanji A, Atkins C, Karim M. Source Department of Renal Medicine, Norfolk and Norwich University Hospital, Norwich, UK. Abstract OBJECTIVE: The antimalarial agent mefloquine has been reported to cause a number of possible side effects. Here we describe a case demonstrating a previously unreported complication, the postural orthostatic tachycardia syndrome (POTS). CASE HISTORY: A 44-year-old woman presented with symptoms of severe orthostatic intolerance (palpitations and dizziness) in combination with postural tachycardia (but no fall in blood pressure) following the use of mefloquine prophylaxis. Investigations revealed evidence of autonomic dysfunction (with loss of ECG R-R interval variation) consistent with POTS. Her symptoms responded well to beta-blockade with propranolol. CONCLUSION: The possibility of POTS should be considered in patients presenting with symptoms of palpitations, dizziness, presyncope or other features suggestive of autonomic dysfunction following the use of mefloquine. www.ncbi.nlm.nih.gov/pubmed/20860911
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Post by beebs on Jun 17, 2012 6:30:53 GMT -5
Lariam should be withdrawn from the market. Most common strains of Plasmodium falciparum are resistant to treatmen. I haven't checked geographical areas and various strains recently, but if this was the case btween 2002-2004 .. Observation is that the local population in mosquitoes infested area take precautions, such as chewing various leaves; they do not suffer as high infections portrayed in the press. Furthermore, those parasites are not unique in central nervous system/cerebral infection, it applies to most infectious pathogens. The propaganda to justify usage of Lariam/Mefloquine & other prophylaxis is profit driven... Excerpts of an "Open Letter addressed to General Tacket" “This further investigation may throw light upon the Guantanamo SOP wherein all detainees were subjected to a never-before-attempted use of mass administration of treatment doses of the controversial anti-malaria drug mefloquine (Lariam), as also reported in a special investigation by Jason Leopold and myself last December. The scandal was also the subject of an independent investigatory report published at the same time by Seton Hall University Law School’s Center for Policy and Research. In a 2002 report on mefloquine adverse events, “Unexpected frequency, duration and spectrum of adverse events after therapeutic dose of mefloquine in healthy adults,” published in top medical journal Acta Tropica, it was noted that 73% of the participants suffered “severe (grade 3) vertigo …” which “required bed rest and specific medication for 1 to 4 days.” Nevertheless, DoD maintains that the use of mefloquine was for public health purposes, to prevent malaria from spreading in Cuba. But as our investigation showed, talking with military medical experts, and examining other military responses to malaria threat, including in Cuba, no such use of such mass treatment doses, with its attendant dangers, was ever used or even proposed. Nor did DoD medical officers at Guantanamo demand the same protocols be used on foreign workers from malarial areas brought into the camp at this same time to work on building Camp Delta and other facilities at the naval base. The workers were employed by Kellogg Brown and Root, a subsidiary of Halliburton.” Cont/.... nuclearnuttery.com/2011/05/01/the-mefloquine-letter-open-letter-to-general-tackett-one-missing-link-between-gitmo-ptsd-sufferers-and-returning-us-vets-with-ptsd-shocking/
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Post by beebs on Jun 21, 2012 5:20:18 GMT -5
A step in the right direction! Brain injury tied to malaria drug, doctor saysAn Army physician who spent his career studying the malaria drug mefloquine, also known as Lariam, asked Congress on June 6 to support research on brain injuries he says can be caused by the medication. Speaking before the Senate Appropriations Committee, Maj. Remington Nevin requested funding for a mefloquine research center at a civilian medical or public health school to investigate the “physiology, epidemiology, clinical diagnosis and treatment” of health issues related to mefloquine. “Given our research commitments to post-traumatic stress and traumatic brain injury … this observation calls for a similarly robust agenda into mefloquine neurotoxic brain injury to ensure that patients with these conditions are receiving accurate diagnoses and the very best medical care,” Nevin said. An epidemiologist and preventive medicine expert, Nevin published a case study in March of a sailor who developed psychosis, short-term memory loss, confusion and personality change after taking mefloquine. Nevin believes the drug caused lesions to form in the patient’s brain stem. He has published previous work similarly raising concerns about mefloquine, developed under the Army’s malaria drug discovery program from 1963 to 1976 to prevent and treat malaria. Anecdotal reports of severe mefloquine reactions abound, including one presented in May at the American Psychiatric Association meeting in Philadelphia by Army Maj. Jerald Block, who discussed the case of a previously normal soldier who developed psychoses while deployed to Afghanistan. According to Block, the service member reported vivid dreams of a frightening dragon — which later appeared to him during the daytime as the soldier cleaned his weapon. Suspecting an adverse reaction to mefloquine, Block prescribed an alternative malaria therapy and the atypical antipsychotic quetiapine, or Seroquel, to halt the psychotic episodes. The patient recovered. The Pentagon’s top doctor, Jonathan Woodson, in January directed the Army, Navy and Air Force and the commander of Joint Task Force National Capital Region Medical to provide their data and policies related to mefloquine prescriptions. In the Defense Department, mefloquine is supposed to be a last-choice drug after doxycycline, chloroquine or Malarone, but it remains in use because it is taken weekly while the others are taken daily. Some physicians believe that troops are more likely to take a weekly dose. DoD published a memo in 2009 saying doxycylcine and mefloquine may be used in areas where malaria is resistant to chloroquine, but doxycycline is the preferred choice. In 2011, U.S. Central Command and U.S. Africa Command issued memos barring mefloquine use except when doxycycline or Malarone cannot be taken. The drug first drew concerns in 2002, when it was noted that four soldiers who killed their wives had been taking mefloquine. Two of those troops committed suicide. Concerns over the medication’s side effects resurfaced in March, when a former Army psychiatrist listed it among the medications possibly taken by Army Staff Sgt. Robert Bales, charged in the shooting deaths of 16 Afghan civilians. Nevin, who is on terminal leave from the Army and will pursue a research career at Johns Hopkins University, told appropriations committee members that while the damage caused by a toxic dose of mefloquine cannot be reversed, he believes research can improve the lives of those with brain damage. “I have personally treated a number of patients whose conditions have proven fairly responsive to rehabilitation, including vestibular physical and neuro-optimetric therapy. Speech therapy and cognitive rehabilitation also hold promise. “However, obtaining access to such therapy requires that mefloquine neurotoxic brain injury be correctly diagnosed,” he said. Last year, 124 service members contracted malaria — 91 in Afghanistan, 24 in Africa and nine elsewhere. The year before, 113 troops contracted malaria; one died. Nevin said his testimony was as a private citizen and that he did not speak for the Army. www.airforcetimes.com/news/2012/06/military-brain-injury-tied-to-malaria-drug-doctor-says-061312/
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Post by beebs on Jun 25, 2012 19:23:51 GMT -5
Excellent concise presentation from Dr Remington Nevin:
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Post by beebs on Sept 5, 2012 16:19:13 GMT -5
This drug should be banned, there is no scientific understanding of its neurotoxicity. SIMPLE. Shocking that it was given to Guantanamo Bay prisoners, complained of PSTD symptoms Limbic encephalopathy and central vestibulopathy caused by mefloquine: a case report.Nevin RL. Source Department of Preventive Medicine, Bayne-Jones Army Community Hospital, 1585 Third Street, Fort Polk, LA 71459, USA. remington.nevin@us.army.mil Abstract Mefloquine is a 4-methanolquinoline anti-malarial that in recent years has fallen out of favor for use as chemoprophylaxis against infection with chloroquine-resistant Plasmodium falciparum malaria owing in part to growing concerns of side effects and potential neurotoxicity. Despite over 20 years of licensed use, the pathophysiological mechanisms underlying mefloquine's neuropsychiatric and physical side effects and the clinical significance of the drug's neurotoxicity have remained poorly understood. In this report, an adverse reaction to mefloquine chemoprophylaxis is described characterized by prodromal symptoms of anxiety with subsequent development of psychosis, short-term memory impairment, confusion and personality change accompanied by complaints of disequilibrium and vertigo, with objective findings of central vestibulopathy. It is posited that these effects represent an idiosyncratic neurotoxic syndrome of progressive limbic encephalopathy and multifocal brainstem injury caused by the drug. This case provides insights into the clinical significance of mefloquine neuronal gap junction blockade and neurotoxicity demonstrated in animal models, points to recommendations for the management of affected patients including diagnostic considerations and appropriate referrals, and highlights critical implications for the continued safe use of the medication. www.ncbi.nlm.nih.gov/pubmed/22494697
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Post by beebs on Apr 1, 2013 10:26:52 GMT -5
A Guantanamo Connection? Documents Show CIA Stockpiled Antimalaria Drugs as "Incapacitating Agents" A Truthout analysis of historical records concerning government research and nonmedical use of antimalarial medications has revealed that such drugs were the objects of experimental research under the CIA's MKULTRA program. Even more, one of these drugs, cinchonine, was illegally stockpiled by the CIA as an "incapacitating agent." Antimalarial drugs were studied as part of the CIA's mind control program MKULTRA. Cinchonine, an antimalarial drug derived from chichona bark, was one of the drugs used by the operational components of MKULTRA, code-named MKNAOMI and MKDELTA. The CIA worked with researchers for the Army's Special Operations Division, a secret component of the US Army Chemical Corps based at Fort Detrick, to develop delivery systems for the drugs. Revelations concerning CIA interest in use of antimalarial drugs would be of historical interest, as it has never been written about before. But such interest gains contemporary significance in the light of actions taken by the Department of Defense (DoD) in the "war on terror," and the fact that a key DoD expert on antimalarial drugs was a psychiatrist involved in training personnel for Guantanamo interrogations. In January 2002, the DoD deliberately decided that all incoming detainees at Guantanamo would be given a full treatment dose of the controversial antimalarial drug mefloquine, also known as Lariam. The purpose was supposedly to control for a possible malaria outbreak, in deference to concerns from Cuban officials. Cont/... truth-out.org/news/item/9601-a-guantanamo-connection-documents-show-cia-stockpiled-antimalaria-drugs-as-incapacitating-agents
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Post by beebs on Apr 22, 2013 11:50:39 GMT -5
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Post by Admin on Sept 15, 2014 18:14:55 GMT -5
The media focuses on PSTD, rather than Lariam being a trigger for psychiatric symptoms at Guantanomo.
Trop Med Int Health. 2012 Oct;17(10):1281-8. doi: 10.1111/j.1365-3156.2012.03063.x. Epub 2012 Aug 12.
Mass administration of the antimalarial drug mefloquine to Guantánamo detainees: a critical analysis. Nevin RL. Author information Department of Preventive Medicine, Bayne-Jones Army Community Hospital, Ft. Polk, LA, USA.
Abstract Recently, evidence has emerged from an unusual form of mass drug administration practised among detainees held at US Naval Station Guantánamo Bay, Cuba ('Guantánamo'), ostensibly as a public health measure. Mefloquine, an antimalarial drug originally developed by the US military, whose use is associated with a range of severe neuropsychiatric adverse effects, was administered at treatment doses to detainees immediately upon their arrival at Guantánamo, prior to laboratory testing for malaria and irrespective of symptoms of disease. In this analysis, the history of mefloquine's development is reviewed and the indications for its administration at treatment doses are discussed. The stated rationale for the use of mefloquine among Guantánamo detainees is then evaluated in the context of accepted forms of population-based malaria control. It is concluded that there was no plausible public health indication for the use of mefloquine at Guantánamo and that based on prevailing standards of care, the clinical indications for its use are decidedly unclear. This analysis suggests the troubling possibility that the use of mefloquine at Guantánamo may have been motivated in part by knowledge of the drug's adverse effects, and points to a critical need for further investigation to resolve unanswered questions regarding the drug's potentially inappropriate use.
Published 2012. This article is a US Government work and is in the public domain in the USA.
KEYWORDS: Cuba; Estados Unidos; Etats‐Unis; Malaria; Medicina Militar; Mefloquina; United States; malaria; mefloquine; military medicine; médecine militaire; méfloquine; paludisme
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Post by Admin on Sept 16, 2014 10:47:39 GMT -5
Yet, again, another article which focuses on psychiatric lariam ADRs. The fact is that it can cause other life threatening health issues such as cardiac, hypothyroidism, diabetes and so forth. Whilst, its known Lariam can cause serious neuro damage, some researchers, promote Lariam as possible management for psychiatric illnesses & MS. <<smile>> The article below discusses the darker side of neuropsychiatric symptoms linking with the sentencing of Staff Sgt. Robert Bales, who killed 16 Afghan civilians in 2012. www.nytimes.com/2013/07/30/business/fda-strengthens-warnings-on-lariam-anti-malaria-drug.html?_r=0
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Post by Admin on Nov 20, 2014 10:35:10 GMT -5
Roche removed pdf documents listing side effects, including liver toxicity, cardiac toxicity, dermatological, allergies, neurological, and other toxicites. Future post will include these documents. See the article in reference to liver toxicity post Lariam/Mefloquine. Note that in spite of inserts advising liver damage, studies focus on variables such as heat and alcohol, undiagnosed pathology, and other. All medications containing quinoline, including some antibiotics, are known to cause long term hepatic toxicity, not detectable on the usual diagnostic tests, except for fluctuating raised liver enzymes and sometimes a biopsy. due toda mage to polymorphisms of CYPs enzymes. Patients report inability to metabolize medications, anesthetics (local & GA) herbs, chemicals in foods, and more, due to polymorphisms in liver CYPs leading to toxicity from the afore mentioned even at very low dose, allergies, MCS, etc Mefloquine and the liver Mefloquine is an aryl amino alcohol which accumulates in both the liver and the lungs, and is subject to enterohepatic circulation. [29] It has recently been found to cause acute hepatitis.[30] Mefloquine does not appear to cause florid signs of liver disease. However, transient subclinical disturbances of liver function are a common feature of many drugs metabolised in the liver, and this may explain the frequent finding of transaminase changes in safety studies of new drugs; these biochemical findings are usually dismissed as meaningless noise, but they may in fact be sensitive or oversensitive markers of vulnerability, of low specificity. That mefloquine induces liver enzymes is well documented. Jaspers et al reported significantly raised transaminases in Dutch marines who took mefloquine during 3 months in Cambodia, and who were not drinking alcohol at the time. [31] Takeshima found that of a cohort of healthy Japanese soldiers who took prophylactic mefloquine for 36 weeks without drinking alcohol, one-quarter developed symptoms compatible with liver pathology and four showed disturbed liver function. [32] Reisinger et al observed the same phenomenon in a cohort of short-stay European travellers to Africa, but it is not clear whether alcohol could have contributed to this effect.[33] One of the travellers, who was concurrently taking a liver-damaging agent, sulfadoxine,[34] showed gross morphological changes in his liver which were attributed to his use of prophylactic mefloquine. Liver biopsy showed intralobular cellular infiltrates consisting of macrophages and eosinophils as well as sporadic eosinophilic cell necroses; virology was negative. [33] Grieco et al described a 46-year-old woman who drank wine daily while taking mefloquine, and who became nervous and depressed, with nausea, vomiting and diarrhoea. She was dehydrated and in severe liver failure, with negative virology. Liver biopsy showed diffuse macrovesical hepatic steatosis. [35] ‘Heavy sun exposure’ is noted in a case report of a 60-year-old Frenchman who reacted acutely to his second mefloquine tablet; it is likely that this sun exposure would have caused dehydration.[5] A 20-year old French traveller, concurrently taking an oral contraceptive, had epileptic seizures in her sixth week of mefloquine prophylaxis, directly after ‘severe exertion’.[5] It seems likely that in some mefloquine users dehydration will impose an added burden on the liver, and that this could contribute to a severe reaction to the drug. Many long-haul travellers using mefloquine are mildly dehydrated from in-flight alcohol and air conditioning, followed by hot and dry conditions, and more alcohol consumption, at their holiday or business destination. Of the 516 case reports we reviewed, eleven cited alcohol as possibly contributing to the adverse drug effects described. Wittes et al reported a remarkable challenge-rechallenge experiment where a healthy male geologist took both his third and his fourth weekly mefloquine tablet together with half a bottle of whisky, and on both occasions experienced acute paranoid delusions, depression and suicidal ideation; a fellow geologist who shared the same whisky bottle (and who was taking no antimalaria medication) experienced no such effects.[36] Vuurman et al, sponsored by Hoffmann-La Roche, tested in healthy volunteers whether or not alcohol might interact adversely with mefloquine.[37] They found psychomotor performance unimpaired, but their study design had important limitations. Only 20 participants took mefloquine and of these, two women dropped out due to adverse events (one with nausea, vomiting and dizziness, the other with malaise, fever and headache). The study protocol forbade ‘strenuous physical activity’ and any prescribed medications. Alcohol was given under strict laboratory conditions 24 h after mefloquine ingestion, and then in small and interrupted doses, such that the blood alcohol concentration in any participant never exceeded 0.50 mg ml-1. The authors admit that their study did not address ‘the question of what might happen should (mefloquine users) consume intoxicating amounts of alcohol. [37] Their findings can thus not be generalised to the broad population of tourists and business travellers. Approximately half of the case reports listed in the Cochrane review note some co-medication taken along with mefloquine.[26] Other quinoline derivatives (chiefly chloroquine and quinine) are the commonest co-medications mentioned in the case reports. After antimalaria drugs, an oral contraceptive (noted in 8 reports) is the next most commonly reported co-medication, followed by sodium valproate (7) and diazepam (4). All these drugs can cause liver damage.[34] Diazepam is also a thyroid hormone antagonist, and we discuss below the possible significance of this. Meszaros et al reported a male traveller who in addition to mefloquine took thioridazine, amitriptyline and fluphenazine (all capable of damaging the liver), and whose mefloquine-associated neuropsychiatric symptoms persisted for over a year. [38] Gullahorn et al reported a series of patients who experienced delirium on emerging from anaesthesia, possibly because in addition to mefloquine they had received isoflurane, an anaesthetic known to cause hepatocellular necrosis. [34,39] One report describes an acute reaction in a man who took one mefloquine tablet each week together with two aspirin tablets. One hour after taking his fifth mefloquine tablet he experienced acute amnesia lasting approximately one hour.[40] Aspirin can cause hepatocellular necrosis,[34] and in addition can aggravate acute thyroid disturbance (discussed below) by competing with thyroid hormones for sites on binding proteins.[53] homecomingvets.com/2010/08/02/mefloquine-lariam-linked-to-liver-and-thyroid-damage/
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