Inflammation – The deep cause of so much chronic illness and even dementia
It is becoming increasingly accepted that most chronic illness – no matter how different in its expression – has causal roots in inflammation. Much of the early work on this has involved diet. But recently many more aspects of how we live have entered the mix – stress, sleep, relationships, when we eat as well as what we eat.
This post, By James P Watson, with contributions and editorial assistance by Vince Giuliano, is the most comprehensive that I have seen yet and stands as a benchmark for advice on the process and for what each of us can do to reduce our chances of developing chronic illness and dementia.
INTRODUCTION AND OVERALL PRINCIPLES
This is the first of a pair of blog entries concerned with dementias – neurological diseases including Alzheimer’s Disease (AD) and its cousins. This Part 1 write-up was inspired by a recent small, non-randomized clinical trial done by Dr. Dale Bredesen that showed true “Reversal of Cognitive Decline” in 9 out of 10 patients with documented cognitive decline (Bredesen, 2014). Not all of these patients had AD, but all had cognitive decline. Five had AD, two had SCI (subjective cognitive impairment), and two had MCI (mild cognitive impairment). Although this study was too small to allow any statistical conclusions, it is the most positive report in a series of disappointing reports on the recent failures of Big Pharma’s monoclonal antibodies against amyloid-beta. Dale Bredesen’s approach was a multifactorial one – utilizing 24 different approaches to halt or reverse cognitive decline. We explore those 25 interventions here, focusing on the first 19. They do not depend on drugs. The focus of this blog entry is “What can be done about dementias now?”
The forthcoming Part 2 blog entry will provides a detailed discussion of some of the key science related to AD and dementias. This is the “What is science telling us about dementias?” part which gets quite complex. We review major theories related to AD there including the Hardy Hypothesis related to amloid beta, the GSK3 theory and more detail on the neuroinflammation theory which we introduce in this Part 1 blog entry. We expect to emphasize the emerging importance APP (Amloid Precursor Protein). And we will describe some very recent research that appears to establish that a basic cause of AD is the proliferation in aging of vestigal DNA segments in our genomes (known as LINEs which are long interspersed nuclear elements and SINEs which are short interspersed nuclear elements) with encode over and over again for the production of APP and for the failure of its clearance. This could well finally explain the role of beta amyloid in AD.
We have published a number of earlier blog entries relating to AD and dementias. For example, you might want to review my August 2014 blog entry The Amyloid Beta face of Alzheimer’s Disease.
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