Page 69 - Petelin, Ana, Nejc Šarabon, Boštjan Žvanut, eds. 2017. Zdravje delovno aktivne populacije ▪︎ Health of the Working-Age Population. Proceedings. Koper: Založba Univerze na Primorskem/University of Primorska Press
P. 69
Researching the neuroprotective properties of nutrition is by nature re- ketogenic diet and its impact on mental processes of working population 67
ductionist, regardless of the mechanism (epigenetic, direct or indirect modu-
lation of individual physiological substances). Research is also mostly direct-
ed at improving known pathologies. To understand potential preventive effects
some backwards deduction should be made.
Conclusion
Our insight into KD is barely scratching the surface. A lot of research both in
humans and in animal models looks promising as expansion of our current
nutritional knowledge and potentially as a paradigmatic shift in understand-
ing what is “healthy diet” in general.
When the nervous system is in question, KD appears to have more ef-
ficient bioenergetics. We presented the research that deals with pathologies
where the underlying hypometabolism is potentially the key to understand
AD, Parkinson’s disease, head trauma etc. Ketosis seems to be especially ben-
eficial for mitochondria dysfunction. KB reduce the damaging effect of ROS,
help body’s own antioxidant capacity, while the ketone metabolism itself poses
decreased oxidative stress to the tissues.
Neuroprotective effect of KD for now seems irrefutable, despite the lack
of thorough understanding of the underlying mechanisms. Further research,
especially in the form of clinical trials, is needed.
References
AMARAL, A.I. 2013. A ketone ester diet exhibits anxiolytic and cognition-spar-
ing properties, and lessens amyloid and tau pathologies in a mouse model
of Alzheimer‘s disease. Journal of Inherited Metabolic Disease, vol. 34, no.
6, pp. 1530-1539.
BARBANTI, P. et al. 2017. Ketogenic diet in migraine: rationale, findings and
perspectives. Neurological sciences: official journal of the Italian Neurologi-
cal Society and of the Italian Society of Clinical Neurophysiology, vol. 38, no.
Suppl 1, pp. 111-115.
BAXTER, P., CHEN, Y., XU, Y. and SWANSON, R.A. 2014. Mitochondrial dys-
function induced by nuclear poly(ADP-ribose) polymerase-1: a treatable
cause of cell death in stroke. Translational Stroke Research, vol. 5, no. 1, pp.
136-144.
BAZZANO, L. et al. 2015. Effects of low-carbohydrate and low-fat diets: a ran-
domized trial. The The American Journal of Clinical Nutrition, vol. 102, no.
4, pp. 780-790.
BOISON, D. 2013. Adenosine kinase: exploitation for therapeutic gain. Pharma-
cological Reviews, vol. 65, no. 3, pp. 906-943.
BUENO, N., VIEIRA DE MELO, I., LIMA DE OLIVEIRA, S. and DA ROCHA
ATAIDE, T. 2013. Very-low-carbohydrate ketogenic diet v. low-fat diet for
ductionist, regardless of the mechanism (epigenetic, direct or indirect modu-
lation of individual physiological substances). Research is also mostly direct-
ed at improving known pathologies. To understand potential preventive effects
some backwards deduction should be made.
Conclusion
Our insight into KD is barely scratching the surface. A lot of research both in
humans and in animal models looks promising as expansion of our current
nutritional knowledge and potentially as a paradigmatic shift in understand-
ing what is “healthy diet” in general.
When the nervous system is in question, KD appears to have more ef-
ficient bioenergetics. We presented the research that deals with pathologies
where the underlying hypometabolism is potentially the key to understand
AD, Parkinson’s disease, head trauma etc. Ketosis seems to be especially ben-
eficial for mitochondria dysfunction. KB reduce the damaging effect of ROS,
help body’s own antioxidant capacity, while the ketone metabolism itself poses
decreased oxidative stress to the tissues.
Neuroprotective effect of KD for now seems irrefutable, despite the lack
of thorough understanding of the underlying mechanisms. Further research,
especially in the form of clinical trials, is needed.
References
AMARAL, A.I. 2013. A ketone ester diet exhibits anxiolytic and cognition-spar-
ing properties, and lessens amyloid and tau pathologies in a mouse model
of Alzheimer‘s disease. Journal of Inherited Metabolic Disease, vol. 34, no.
6, pp. 1530-1539.
BARBANTI, P. et al. 2017. Ketogenic diet in migraine: rationale, findings and
perspectives. Neurological sciences: official journal of the Italian Neurologi-
cal Society and of the Italian Society of Clinical Neurophysiology, vol. 38, no.
Suppl 1, pp. 111-115.
BAXTER, P., CHEN, Y., XU, Y. and SWANSON, R.A. 2014. Mitochondrial dys-
function induced by nuclear poly(ADP-ribose) polymerase-1: a treatable
cause of cell death in stroke. Translational Stroke Research, vol. 5, no. 1, pp.
136-144.
BAZZANO, L. et al. 2015. Effects of low-carbohydrate and low-fat diets: a ran-
domized trial. The The American Journal of Clinical Nutrition, vol. 102, no.
4, pp. 780-790.
BOISON, D. 2013. Adenosine kinase: exploitation for therapeutic gain. Pharma-
cological Reviews, vol. 65, no. 3, pp. 906-943.
BUENO, N., VIEIRA DE MELO, I., LIMA DE OLIVEIRA, S. and DA ROCHA
ATAIDE, T. 2013. Very-low-carbohydrate ketogenic diet v. low-fat diet for
