Paul Metz posted:I wonder just how tightly bound to the ACEs project you are? You refer to the material on telomere shortening but I'm wondering if you're really interested in the various other forms of pathophysiology potentially involved in the link between stress (defined more generally than just that caused by ACEs events) and later ill health? Unless the biologists involved in carrying out the research have some sort of special, or especially personal, allegiance to The ACEs Movement, they will be more likely to do research, talk, and think, in terms of the impact of "stress" more generally defined than just ACEs.
Having an ACEs score of 9 many people would consider me a prime candidate for suffering from chronic illness. Hence I wasn't overly surprised, four, nearly five, years ago, to be diagnosed with Parkinson's Disease (many in the US simply call it Parkinson Disease). Adopting this slightly broader perspective brings one to an exploration of a broader range of etiological contributors to illnesses, particularly to an examination of disturbances in mitochondrial functioning -- mitophagy -- and systemic inflammation. Some relevant references would then be
Blaszczyk, anusz W. (2018). The Emerging Role of Energy Metabolism and Neuroprotective Strategies in Parkinson’s Disease. Frontiers in Aging Neuroscience. https://www.frontiersin.org/ar...nagi.2018.00301/full
Chan, Y.-L. E., Bai, Y.-M., Hsu, J.-W., Huang, K.-L., Su, T.-P., Li, C.-T., Lin, W.-C., Pan, T.-L., Chen, T.-J., Tsai, S.-J., & Chen, M.-H. (2017). Post-traumatic Stress Disorder and Risk of Parkinson Disease: A Nationwide Longitudinal Study. Use of Technology in Geriatric Mental Health, 25(8), 917–923. https://doi.org/10.1016/j.jagp.2017.03.012
Hoeijmakers, L., Lesuis, S. L., Krugers, H., Lucassen, P. J., & Korosi, A. (2018). A preclinical perspective on the enhanced vulnerability to Alzheimer’s disease after exposure to stress in early-life. Neurobiology of Stress. https://doi.org/10.1016/j.ynstr.2018.02.003
Kundakovic, M., & Jaric, I. (2017). The epigenetic link between prenatal adverse environments and neurodevelopmental disorders. Genes, 8(3), 104.
Lattin, C. R., Merullo, D. P., Riters, L. V., & Carson, R. E. (2019). In vivo imaging of D2 receptors and corticosteroids predict behavioural responses to captivity stress in a wild bird. Scientific Reports, 9(1), 10407. https://doi.org/10.1038/s41598-019-46845-x
Picard, M., & McEwen, B. S. (2018). Psychological Stress and Mitochondria: A Conceptual Framework. Psychosomatic Medicine, 80(2). https://journals.lww.com/psych...tochondria__A.2.aspx
Schaefers, A. T., & Teuchert-Noodt, G. (2016). Developmental neuroplasticity and the origin of neurodegenerative diseases. The World Journal of Biological Psychiatry, 17(8), 587–599.
Further references could be found as a result of PubMed and Google Scholar searches looking at, say “psychological stress trauma mitochondria”. I hope this has been of some help. Good luck with your studies.
Hi Paul, and thank you for your extensive replay! I appreciate it. Not completely sure what you ment by how tightly I am bound to the ACEs. But if I do understand you correct, it is what I plan on using.
The plan is to use the ACEs questionnaire + A body awareness questionnaire on a population of both prison inmates and prison officers. Almost the priority or main reason is that there is not many papers investigates ACEs in Norway (where I am based), and there is certainly a lack of research on prison inmates in general.. So I have to possibility to do both om my professional interest in my master thesis. Due to the fact that most master thesis´in Norway often involves other perspectives I thought that the perspectives could be phenomenological and biological for instance.
So when Harris mention, in the TEDtalk, that health behavior also had been controlled for - and it still showed that there was a significant alteration in health. Hence my post. I reccon that I very well might have been unclear.
When writing the post I primary thought about that a potensial examiner could ask about how the numbers would add up if I controlled for behavior (e.g. smoking, drinking, or other substance use, lack of exercise etc.) that is deeply connected to poorer life expectancy and health.
Thank you very much for the literature, I start read the papers you linked! 
- Kay