Page 67 - 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
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nitive function [tiab]) OR (memory [mesh] OR memory [tiab]) OR (mem- ketogenic diet and its impact on mental processes of working population 65
ory disorders[mesh] OR (memory [tiab] AND disorders [tiab])) OR (Memory
Disorders/diet therapy[Mesh])) NOT epilepsy [mesh]. Google Scholar search
results, found by using the string »ketogenic diet, low carbohydrate, cognitive
function, memory creation, neuroprotective«, were added to initial Pubmed
search. Some results were excluded based on weak connection to the topic.
Results
Neuronal hypometabolism appears to be foundation in pathogenesis of many
ND (Castellano et al., 2015): consequences of metabolic disorders set off in the
preclinical stages of the disease. This is a common ground for new therapies
for ND, especially in those where neuroprotection is the key (Stafstrom et al.,
2012). Ketosis could be the opportunity to open paracrine and autocrine signal-
ling mechanisms to influence cometabolism within the nervous system and tu-
mours as a way to achieve therapeutic ends (Puchalska et al., 2017).
Mitochondria do not only supply cells with energy; they control the apop-
tosis, calcium levels and production and elimination of reactive oxygen species
(ROS) (Milder et al., 2012). Nutrition based therapies are not only an option for
rare mitochondriopathies but also for a spectrum of ND associated with aging
(Procaccio et al., 2014). Mitochondrial dysfunction and the consequential hy-
pometabolism of the nervous system that is a part of aging can be a source and
a consequence of inflammatory processes (Currais, 2015).
KD is efficient with ameliorating symptoms of AD, Parkinson’s disease
and other ND (Hartman, 2012, Liśkiewicz et al., 2012, Mandla et al., 2013).
KD can have a profound effect on neuronal plasticity, reduces inflammation,
and improves bioenergetics in the brain … (Procaccio et al., 2014). Mitochon-
drial function is impaired in ND – both systemically as well as in the brain
(Wilkins et al., 2017). Nervous system’s glucose dependency poses a risk to cog-
nitive health (Farias et al., 2014). Neurons are adapted to using many differ-
ent substrates for energy: glutamine, glutamate, lactate, pyruvate, KB. This
is especially useful for people with regular hypoglycaemic episodes (Amaral,
2013), causing cognitive dysfunction, sensory disturbances and memory de-
fects (Costantini et al., 2008), verbal memory, digit symbol coding, digit span
backwards, and map searching (Page et al., 2009).
Lack of energy due to hypometabolism and mitochondriopathies can be
replaced by KB (Currais, 2015). Nutritional ketosis provides replenishment of
the TCA cycle, restoration of neurotransmitter and ion channel function, and
enhanced mitochondrial respiration. It helps cellular homeostasis by enabling
signal pathways, developed as sensors of the energy state of the cell (Gano et al.,
2014). These antiseizure, neuroprotective and antitumor properties of KD are
not yet well understood (Maalouf et al., 2009, Thio, 2012).
Use of ketosis looks promising most prominently in AD (Grom, 2016).
Decrease in glucose utilization has a very early onset with AD – much earli-
ory disorders[mesh] OR (memory [tiab] AND disorders [tiab])) OR (Memory
Disorders/diet therapy[Mesh])) NOT epilepsy [mesh]. Google Scholar search
results, found by using the string »ketogenic diet, low carbohydrate, cognitive
function, memory creation, neuroprotective«, were added to initial Pubmed
search. Some results were excluded based on weak connection to the topic.
Results
Neuronal hypometabolism appears to be foundation in pathogenesis of many
ND (Castellano et al., 2015): consequences of metabolic disorders set off in the
preclinical stages of the disease. This is a common ground for new therapies
for ND, especially in those where neuroprotection is the key (Stafstrom et al.,
2012). Ketosis could be the opportunity to open paracrine and autocrine signal-
ling mechanisms to influence cometabolism within the nervous system and tu-
mours as a way to achieve therapeutic ends (Puchalska et al., 2017).
Mitochondria do not only supply cells with energy; they control the apop-
tosis, calcium levels and production and elimination of reactive oxygen species
(ROS) (Milder et al., 2012). Nutrition based therapies are not only an option for
rare mitochondriopathies but also for a spectrum of ND associated with aging
(Procaccio et al., 2014). Mitochondrial dysfunction and the consequential hy-
pometabolism of the nervous system that is a part of aging can be a source and
a consequence of inflammatory processes (Currais, 2015).
KD is efficient with ameliorating symptoms of AD, Parkinson’s disease
and other ND (Hartman, 2012, Liśkiewicz et al., 2012, Mandla et al., 2013).
KD can have a profound effect on neuronal plasticity, reduces inflammation,
and improves bioenergetics in the brain … (Procaccio et al., 2014). Mitochon-
drial function is impaired in ND – both systemically as well as in the brain
(Wilkins et al., 2017). Nervous system’s glucose dependency poses a risk to cog-
nitive health (Farias et al., 2014). Neurons are adapted to using many differ-
ent substrates for energy: glutamine, glutamate, lactate, pyruvate, KB. This
is especially useful for people with regular hypoglycaemic episodes (Amaral,
2013), causing cognitive dysfunction, sensory disturbances and memory de-
fects (Costantini et al., 2008), verbal memory, digit symbol coding, digit span
backwards, and map searching (Page et al., 2009).
Lack of energy due to hypometabolism and mitochondriopathies can be
replaced by KB (Currais, 2015). Nutritional ketosis provides replenishment of
the TCA cycle, restoration of neurotransmitter and ion channel function, and
enhanced mitochondrial respiration. It helps cellular homeostasis by enabling
signal pathways, developed as sensors of the energy state of the cell (Gano et al.,
2014). These antiseizure, neuroprotective and antitumor properties of KD are
not yet well understood (Maalouf et al., 2009, Thio, 2012).
Use of ketosis looks promising most prominently in AD (Grom, 2016).
Decrease in glucose utilization has a very early onset with AD – much earli-
