Health Care Burden and Cost Associated With Fetal Alcohol Syndrome: Based on Official Canadian Data.

Health care burden and cost associated with fetal alcohol syndrome: based on official canadian data.

Filed under: Addiction Rehab

PLoS One. 2012; 7(8): e43024
Popova S, Lange S, Burd L, Rehm J

Fetal Alcohol Spectrum Disorder (FASD) is a group of disorders caused by prenatal alcohol exposure. From this group, Fetal Alcohol Syndrome (FAS) is the only disorder coded in the International Classification of Diseases, version 10 (ICD-10). This coding was used to gain an understanding on the health care utilization and the mortality rate for individuals diagnosed with FAS, as well as to estimate the associated health care costs in Canada for the most recent available fiscal year (2008-2009).Health care utilization data associated with a diagnosis of FAS were directly obtained from the Canadian Institute for Health Information (CIHI). Mortality data associated with a diagnosis of FAS were obtained from Statistics Canada.The total direct health care cost of acute care, psychiatric care, day surgery, and emergency department services associated with FAS in Canada in 2008-2009, based on the official CIHI data, was about $ 6.7 million. The vast majority of the most responsible diagnoses, which account for the majority of a patient’s length of stay in hospital, fall within the ICD-10 category Mental and Behavioural Disorders (F00-F99). It was evident that the burden and cost of acute care hospitalizations due to FAS is increasing -1.6 times greater in 2008-2009, compared to 2002-2003. The mortality data due to FAS, obtained from Statistics Canada (2000-2008), may be underreported, and are likely invalid.The official data on the utilization of health care services by individuals diagnosed with FAS are likely to be underreported and therefore, the reported cost figures are most likely underestimated. The quantification of the health care costs associated with FAS is crucial for policy developers and decision makers alike, of the impact of prenatal alcohol exposure, with the ultimate goal of initiating preventive interventions to address FASD.
HubMed – addiction


Chronic sazetidine-A at behaviorally active doses does not increase nicotinic cholinergic receptors in rodent brain.

Filed under: Addiction Rehab

J Pharmacol Exp Ther. 2012 Aug 16;
Hussmann GP, Turner JR, Lomazzo E, Venkatesh R, Cousins V, Xiao Y, Yasuda RP, Wolfe BB, Perry DC, Rezvani AH, Levin ED, Blendy JA, Kellar KJ

Chronic nicotine administration increases ?4?2 neuronal nicotinic acetylcholine receptor (nAChR) density in brain. This up-regulation likely contributes to the development and/or maintenance of nicotine dependence. nAChR up-regulation is believed to be triggered at the ligand binding site, so it is not surprising that other nicotinic ligands also up-regulate nAChRs in brain. These other ligands include varenicline, which is currently used for smoking cessation therapy. Sazetidine-A (saz-A) is a newer nicotinic ligand that binds with high affinity and selectivity at ?4?2* nAChRs. In behavioral studies, saz-A decreases nicotine self-administration and increases performance on tasks of attention. We report here that unlike nicotine and varenicline, chronic administration of saz-A at behaviorally active and even higher doses does not up-regulate nAChRs in rodent brains. We used a newly developed method involving radioligand binding to measure the concentrations and nAChR occupancy of saz-A, nicotine and varenicline in brains from chronically treated rats. Our results indicate that saz-A reached concentrations in the brain that were ~150 times its affinity for ?4?2* nAChRs and occupied at least 75% of nAChRs. Thus, chronic administration of saz-A did not up-regulate nAChRs despite it reaching brain concentrations that are known to bind and desensitize virtually all ?4?2* nAChRs in brain. These findings reinforce a model of nicotine addiction based on desensitization of up-regulated nAChRs and introduce a potential new strategy for smoking cessation therapy in which drugs like saz-A can promote smoking cessation without maintaining nAChR up-regulation, thereby potentially increasing the rate of long-term abstinence from nicotine.
HubMed – addiction


SimSmokeFinn: How far can tobacco control policies move Finland toward tobacco-free 2040 goals?

Filed under: Addiction Rehab

Scand J Public Health. 2012 Aug 16;
Levy DT, Blackman K, Currie LM, Levy J, Clancy L

AIMS: Finland is the first country to stipulate in law that its aim is to end the use of tobacco products containing compounds that are toxic to humans and that create addiction. This paper describes the development of a simulation model examining the potential effect of tobacco control policies in Finland on smoking prevalence and associated future premature mortality. METHODS: The model is developed using the SimSmoke simulation model of tobacco control policy, previously developed for other nations. The model uses population, smoking rates, and tobacco control policy data for Finland. It assesses, individually, and in combination, the effect of seven types of policies: taxes, smoke-free air laws, mass media campaigns, advertising bans, warning labels, cessation treatment, and youth access policies. RESULTS: With a comprehensive set of policies, smoking prevalence can be decreased by as much as 15% in the first few years, increasing to 29% by 20 years and 34% by 30 years. By 2040, 1300 deaths can be averted in that year alone with the stronger set of policies. Without effective tobacco control policies, 23,000 additional lives will be lost due to smoking over all years through 2040. CONCLUSIONS: The model shows that significant inroads to reducing smoking prevalence and premature mortality can be achieved through tax increases, a high-intensity media campaign complete with programmes to encourage cessation, a comprehensive cessation treatment programme, stronger health warnings, and enforcement of youth access laws. Other policies will be needed to further reduce tobacco use.
HubMed – addiction



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