Bose Einstein condensate and quantum physics in the living systems

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This is a short memo triggered by this paper to alert us to some new ideas emerging in the boundary zone between biology and quantum physics. It could be the next big breakthrough in biology or it it could be off the mark! We shall see.

From Wiki 

See my write-up here:
"Bose Einstein condensate - cold fusion, cellular membranes and neurons."

I have to stress that the above text is a compilation of some speculative ideas and references, not a proof of anything!

For people with a sufficient scientific background, I strongly recommend to read the following references:

Michael A. Crawford, C. Leigh Broadhurst, Martin Guest, Atulya Nagar, Yiqun Wang, Kebreab Ghebremeskel, Walter F. Schmidt, “A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution”; Prostaglandins, Leukotrienes and Essential Fatty Acids 88 (2013) 5–13.

E. Del Giudice, S. Doglia, M. Milani, C. W. Smith, G. Vitiello, “Magnetic Flux Quantization and Josephson Behaviour in Living Systems”; Physica Scripta. Vol. 40, 786-791, 1989.

(P.S. thanks to Edward E. for the links!)

Ketogenic diet slows progression of 5 neuro degenerative diseases

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SCIENCE SUPPORTS THE ANTI-AGING AND ANTI-DEGENERATIVE PROPERTIES OF KETOGENIC DIETS!

Slowing down of neuro-degenerative disease by ketogenic diet was claimed in the recent paper:
Nourishing the Aging Brain, By Morten Scheibye-Knudsen,  The Scientist, March 2015

( in pdf format )


Quotes (see here ):

ALS:
Increased basal metabolism
Caloric restriction exacerbates progression
Ketogenic diet slows progression

ALZHEIMER’S DISEASE:
Normal or lowered basal metabolism
Caloric restriction slows progression
Ketogenic diet slows progression

PARKINSON’S DISEASE:
Increased basal metabolism
Caloric restriction slows progression
Ketogenic diet slows progression

HUNTINGTON’S DISEASE:
Increased basal metabolism
Caloric restriction may slow progression
Ketogenic diet slows progression

COCKAYNE SYNDROME [accelerated aging disease]:
Increased basal metabolism
Caloric restriction exacerbates progression
Ketogenic diet slows progression

[added on 6/03/2015, from the same source]

And the low carbohydrate (or low glucose) nutrition appears to contribute to longevity by increasing the SIRT6 activity (*), according to this paper, from the same issue of The Scientist magazine:

Wrangling Retrotransposons, by Michael Van Meter, Andrei Seluanov, and Vera Gorbunova | March 1, 2015

Quote

Perhaps the best evidence for the retrotransposon’s role in aging comes from the link between the activity of a longevity gene, SIRT6, and the repression of L1 in somatic tissues. SIRT6 encodes an enzyme critical to the forestallment of aging: it maintains telomere length, promotes DNA repair, regulates metabolism, opposes tumorigenesis, and attenuates inflammation—all processes associated with the prevention of age-related decline. Mice lacking SIRT6 suffer from a severe premature aging syndrome, while mice that overexpress SIRT6 enjoy extended life spans.

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One explanation for this failure may relate to SIRT6’s critical role in DNA repair. Several studies have indicated that SIRT6 helps catalyze repair of the damage at numerous types of DNA lesions, including single- and double-strand breaks. A characteristic feature of aging cells is an increase in the amount of DNA damage.

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While overexpression of SIRT6 may not be tractable in a therapeutic context, SIRT6 activity can be increased by caloric restriction, reducing glucose consumption, or increasing NAD+ bioavailability (**) - interventions that have already shown promise in increasing longevity in animal models. (Such interventions are also showing promise in slowing the progress of some age-related neurodegenerative disorders.

Notes:

*) Underexpression or removal of SIRT6 gene is linked to accelerated aging disease, while overexpression of SIRT6 has been shown to extend the lifespan, in mice studies, see Wiki.

**) Niacin is one of the precursors of NAD+, another one is tryptophan.

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