A 2-PART SERIES OF SEMINARS BY DR. DOUGLAS WATT, PH.D.
Aging, Calorie Restriction, and the Diseases of Aging - the Promise of Calorie-Restriction Mimetics.
Neurodegeneration - the amyloid hypotheses. A primary failure of proteostasis.
Western healthcare systems are losing a battle against chronic disease, driven in good part by skyrocketing rates of diaobesity (the ubiquitous conjoining of obesity with type II diabetes), and a profound mismatch between our genome and the modern environment. Of the four critical lifestyle variables (diet, exercise, sleep, and social support versus social stress) only two get any attention in primary care, and oftentimes even those are neglected. How can we change a losing game?
- By Douglas F. Watt, Ph.D.
Adjunct Professor Graduate Department of Psychology Lesley University
Clinical Neuroscience Advisor 9th Dimension Biotech, Inc.
PART 1 OF 2
By Dr. Douglas Watt, Ph.D.
Adjunct Professor, Graduate Department of Psychology Lesley University
Clinical Neuroscience Advisor, 9th Dimension Biotech, Inc.
Highlights:
PART 2 OF 2
By Dr. Douglas Watt, Ph.D.
Adjunct Professor, Graduate Department of Psychology Lesley University
Clinical Neuroscience Advisor, 9th Dimension Biotech, Inc.
Highlights:
In Part II, we dive into the Alice-in-Wonderland world of cell signals and the (growing) complexity of how cells regulate and organize a bevy of responses to environmental signals – this is clearly part of evolutionary adaptation to shifting environs. We focus specifically on the calorie restriction (CR) response, which is conserved across phylogeny, and on substances that may at least partially mimic CR, termed CR mimetics. To understand these issues better, we need to review the still young and emerging science of mTOR, and the networks around it, and how AMPK, surtuins, other transcription factors and signals create a catabolic cell signaling space counterposed to the fundamental vectors of mTOR, with long term and major health benefits. Harsh blockade of mTOR may be very bad for us, but long term disinhibition – as in obesity, DMII, CAD, CA, and neurodegenerative disorders (most age-related disease) – looks very bad also. Tonic or pulsatile restraint on mTOR with some permission for growth signals (critical to tissue repair/maintenance and decent neuroplasticity) but with concomitant upregulation of autophagy (cellular ‘trash disposal’) and strong dampening of ‘inflammaging’ appears a difficult but highly desirable ‘sweet spot’ – once again the Greeks were prescient in their advocacy for moderation in all things. We look at Adiponectin as an emerging and fairly recently confirmed critical player in this CR catabolic process, with interactions with AMPK and several PPARs, and how Osmotin may offer critical avenues for agonist effects on AdPN receptor families. Many questions remain, and much scientific and technical opportunity lies ahead.
These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure, or prevent any disease.
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