What is known about tobacco industry efforts to influence tobacco tax? A systematic review of empirical studies.

OBJECTIVE: To systematically review studies of tobacco industry efforts to influence tobacco tax policies. METHODS: Searches were conducted between 1 October 2009 and 31 March 2010 in 14 databases/websites, in relevant bibliographies and via experts. Studies were included if they focused on industry efforts to influence tobacco tax policies, drew on empirical evidence, were in English and concerned the period 1985-2010. In total, 36 studies met these criteria. Two reviewers undertook data extraction and critical appraisal. A random selection of 15 studies (42%) was subject to second review. Evidence was assessed thematically to identify distinct tobacco industry aims, arguments and tactics. RESULTS: A total of 34 studies examined industry efforts to influence tax levels. They suggest the tobacco industry works hard to prevent significant increases and particularly dislikes taxes 'earmarked' for tobacco control. Key arguments to counter increases are that tobacco taxes are socially regressive, unfair and lead to increased levels of illicit trade and negative economic impacts. For earmarked taxes, the industry also frequently tries to raise concerns about revenue allocation. Assessing industry arguments against established evidence demonstrates most are unsupported. Key industry tactics include: establishing 'front groups', securing credible allies, direct lobbying and publicity campaigns. Only seven studies examined efforts to influence tax structures. They suggest company preferences vary and tactics centre on direct lobbying. CONCLUSIONS: The tobacco industry has historically tried to keep tobacco taxes low using consistent tactics and misleading arguments. Further research is required to explore efforts to influence tax structures, excise policies beyond the USA and recent policies

Tcf4 Regulates Synaptic Plasticity, DNA Methylation, and Memory Function

Human haploinsufficiency of the transcription factor Tcf4 leads to a rare autism spectrum disorder called Pitt-Hopkins syndrome (PTHS), which is associated with severe language impairment and development delay. Here, we demonstrate that Tcf4 haploinsufficient mice have deficits in social interaction, ultrasonic vocalization, prepulse inhibition, and spatial and associative learning and memory. Despite learning deficits, Tcf4(+/−) mice have enhanced long-term potentiation in the CA1 area of the hippocampus. In translationally oriented studies, we found that small-molecule HDAC inhibitors normalized hippocampal LTP and memory recall. A comprehensive set of next-generation sequencing experiments of hippocampal mRNA and methylated DNA isolated from Tcf4-deficient and WT mice before or shortly after experiential learning, with or without administration of vorinostat, identified “memory-associated” genes modulated by HDAC inhibition and dysregulated by Tcf4 haploinsufficiency. Finally, we observed that Hdac2 isoform-selective knockdown was sufficient to rescue memory deficits in Tcf4(+/−) mice