Brain Activity and Heart Disease – a New Mechanism

The amygdala is a key component in the ‘salience network’ of the brain. This network is activated in conditions of fear and stress. A recent elegant paper in Lancet [1] examined the relationship, first, between amygdala activation (measured by PET scanning) and cardiovascular outcomes, and second, between activation of the amygdala and certain mediators of cardiovascular disease concerned with stimulation of bone marrow to produce inflammatory cells and with arterial inflammation. They showed positive correlations in all cases. I am interested in causal modelling,[2] [3] and I was therefore provoked by the authors’ ‘mediation model’, which I take to be a form of structural equation modelling. This suggested that only half of the amygdala’s ‘effect’ on cardiovascular disease could be explained by the two mechanisms proposed above (production of inflammatory cells and arterial inflammation). This paper represents a potential step change in understanding brain-body interactions, but I await replication with interest.

— Richard Lilford, CLAHRC WM Director

References:

  1. Tawakol A, Ishai A, Takx RAP, et al. Relation between resting amygdalar activity and cardiovascular events: a longitudinal and cohort study. Lancet. 2017; 389: 834-45.
  2. Lilford RJ, Girling AJ, Sheikh, et al. Protocol for evaluation of the cost-effectiveness of ePrescribing systems and candidate prototype for other related health information technologies. BMC Health Serv Res. 2014; 14: 314.
  3. Watson SI & Lilford RJ. Essay 1: Integrating multiple sources of evidence: a Bayesian perspective. In: Challenges, solutions and future directions in the evaluation of service innovations in health care and public health. Southampton (UK): NIHR Journals Library, 2016.
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