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Old 08-09-18, 08:46 AM
SB_UK SB_UK is offline

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Vicious Cycles Succ.....

Succinate and the Citric Acid Cycle

--- citric acid cycle
succinate -> fumarate
generating reactive oxygen species

--- Reduced citric acid cycle rate when in ketosis as
succinate -> fumarate -> malate -> oxaloacetate
oxaloacetate <- pulled out into gluconeogenesis
eg 'Conditions that increase gluconeogenesis (diabetes, fasting) slow the citric acid cycle (by drawing off oxaloacetate)'

--- So ketosis slows the citric acid cycle down.

--- Glycolysis slows down also
eg "As a result of limited glucose and enhanced oxidative phosphorylation, reduced glycolytic flux"

--- What results in excess ROS production ?
Bottom Line: Two modes of operation by isolated mitochondria result in significant O2(*-) production, predominantly from complex I:
(i) when the mitochondria are not making ATP and consequently have a high Deltap (protonmotive force) == WHEN THE CELL IS USING GLYCOLYSIS IE NOT USING THE MITOCHONDRIA
(iii) when there is a high NADH/NAD+ ratio in the mitochondrial matrix eg "NADH would be in an oversupply state when glucose overload occurs."

--- Excess ROS production wreaks havoc

--- So - we've multiple lines of pathway which lead us to ketogenesis not glycolysis through succinate.

--- The mitochondria are not in competition with glycolysis.

--- Optimal conditions for mitochondrial electron transport chain are ensured through ketosis lifestyle.

--- For mitochondria to be happy - they need to be used; the energy they generate need be used.
Heat generation and Energy for Movement (aerobic) would be what they like to do.
Shelter (temperature) and Food (ATP) are the only two things that human beings need.

The mitochondrion contributes both.

What happens in an environment of 'stressed' mitochondria ? excess ROS -->-- "According to the free radical theory of aging, oxidative damage initiated by reactive oxygen species is a major contributor to the functional decline that is characteristic of aging."

Why? non-specific damage

Which? can't be repaired / recycled because too much damage is occurring and high C and high N (glucose elevation + protein elevation) prevent autophagy (repair + recycling).
"Insulin and amino acids (through mTOR) are the main regulators of ATGs"

Damage with no means of Repairing the damage.

So - what's the story ?
There are 2 reward systems.
The consumption of blood glucose elevating / protein elevating foods - ALL take-away foods
The acquisition of personal quality - the ketosis lifestyle

Mind + Morality shifts from potential for primitive reward system -> aversion to primitive reward system and adaptation to the higher reward system of personal quality generation (in ketosis).

Personal quality acquisition relates to 'learning' ever better information recognition capacity at the levels which we've defined as being attributable to the neocortex.

True learning does not occur in our current world - what people learn is how to obey.
You are not meant to obey anybody - you're meant to work towards neocortical quality.

The ADDer can not help but operate in this way - and is unable to pay attention to the competitive reward system.
ADHD understood - simple information sensitivity.
Attention geared towards information handling.
Other calls on attention fail to captivate the ADD mind.
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