Recent Research on Lariam
Mefloquine Induces Dose-Related Neurological Effects in a Rat Model. GS Dow et al., Walter Reed Army Institute of Medical Research (WRAIR), March 2006. This study documents that at treatment levels, the concentration of mefloquine in the bloodstream (reached in women after the 4th or 5th preventive dose) “caused degeneration of specific brain stem nuclei.” Also see Dow’s earlier research (below) which further documents mefloquine’s neurotoxicity.
“Effectiveness of antimalarial drugs” (scroll to letter #3), Croft, Beer, Herxheimer, New England Journal of Medicine, Nov 28, 2005.
The antimalarial potential of 4-Quinolinecarbinolamines may be limited due to neruotoxity and cross-resistance in mefloquine-resistant plasmodim flaciparum strains. Dow, GS et al., Walter Reed Army Institute of Research (WRAIR), Antimicrobial Agents Chemotherapy, 48(7):2624-2632 (2004).
Malaria drug blocks brain conduits. Brown University Press Release. Brown researchers have discovered that mefloquine, an anti-malarial drug, blocks two gap junction proteins, or connexins, in low doses and with very few side effects in the brains of laboratory mice. The work opens an important door: Connexins found in high concentrations in the brain are believed to play a critical role in movement, vision and memory. August 7, 2004. Study follows.
Potent block of Cx36 and Cx50 gap junction channels by mefloquine. Cruickshank, Connors, et al., Proceedings of the National Academy of Science, 101(33): 12364-12369). PDF REPRINT.
Schlagenhauf Patricia et al., Tolerability of malaria chemoprophylaxis in non-immune travellers to sub-Saharan Africa: multicentre,
randomised, double blind, four arm study. BMJ 2003;327:1078 (8
November).
The acute neurotoxicity of mefloquine may be mediated through a disruption of calcium homeostasis and ER function in vitro. Dow, GS et al., WRAIR, Malar J. 2003; 2: 14. Published online 2003 June 12.
Overbosch, David, et al. 2001. Atovaquone-proguanil versus mefloquine for malaria prophylaxis in nonimmune travelers: Results from a randomized, double-blind study. Clinical Infectious Diseases 33 (1
Oct):1015-1021.
Response to Overbosch from UK medical experts Croft and Herxheimer, Tolerability of Antimalarial Drugs, with authors’ reply, Clinical Infectious Diseases, 2002;34:1278.
van Riemsdijk MM, et al., Atovaquone plus chloroguanide [Malarone] versus mefloquine [Lariam] for malaria prophylaxis: a focus on neuropsychiatric adverse events. Clin Pharmacol Ther, 2002 Sep;72(3):294-301. “Prophylactic use of mefloquine was associated with significantly higher scores on scales for depression, anger, and fatigue and lower scores for vigor than prophylactic use of atovaquone plus chloroguanide.” [randomized, double blind study]
van Riemsdijk MM, et al. “Neuropsychiatric events during prophylactic use of mefloquine before travelling”, Published online: 27 July 2002, Springer-Verlag
“Neurological Effects of Mefloquine a Trans-Atlantic Debate”, by RPCV Rebecca Brodsky, Returned Peace Corps Volunteer, October 2, 2001, A review of research to date.
MASTA (Malaria Advisory Services for Travelles Abroad) study: Comparison of adverse events associated with use of mefloquine and combination of chloroquine and proguanil as antimalarial prophylaxis: postal and telephone survey of travellers P J Barrett, P D Emmins, P D Clarke, D J Bradley, BMJ, 7056, Vol 313, August 31, 1996.
World Health Organization (WHO) review:
Review of Central Nervous System Adverse Events Related to the Antimalarial Drug, Mefloquine, 1985 – 1990 Report by the Malaria Control Unit, Division or Control of Tropical Diseases, WHO, in cooperation with the Drug Safety Unit, F. Hoffmann-La Roche. Issued in 1991.
World Health Organization (WHO) report: Central Nervous System Reactions Related to the Antimalarial Drug, Mefloquine, Report from Geneva, 17 July 1989; includes list of participants.
For more scientific studies about Lariam, see Medical Research References.