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If there is ONE mechanism central to understanding, panic attacks, schizophrenia, migraine, epilepsy etc. it is THIS. Muscle cells cannot release
glucose back into the bloodstream as they do not express the enzyme
Glucose-6-phosphatase, whereas the liver does, but with impaired
liver storage of glucose as glycogen this cannot happen. Thus when
blood glucose falls the muscles have to take over the role of glucose
storage but because they cannot release it as glucose have to ferment
it to lactic acid instead which is released into the bloodstream and
converted back to glucose by the liver, a process known as
gluconeogenesis.

Now comes a very convoluted process. Adrenalin is required to increase the metabolic rate of the muscles and dilate the blood vessels to wash the lactic
acid out, but the dilated blood vessels supply oxygen which stops
fermentation. Alternatively noradrenalin does constrict the blood
vessel, but has no metabolic effect on muscle cells and of course
restricts blood flow. Enter muscle spasm, hot and cold flushes as
the two hormones alternate. It seems to be hot first followed by
cold

NORADRENALIN is associated with extreme fear, but here it’s not fear in response to an external perceived threat. The threat is internal and NOT
understood by the person experiencing it The crisis is life
threatening cerebral hypoglycaemia (low blood sugar in the brain)
which can only be alleviated by increased lactic acid synthesis by
the muscles. Liver pathology means not just impaired glycogen
storage but also impaired gluconeogenesis (the liver making glucose
from lactic acid) thereby necessitating even more secretion (release)
of adrenalin and noradrenalin by the adrenal glands and in the brain
‘Panic attack’ exacerbated (made worse) by the individual not
understanding what on Earth is going on. ‘I must be going mad (and
all that entails).

THE RUNAWAY
CASCADE OF FEAR.

The brain metabolises 25% of the bodies glucose. The more neural activity, the
more glucose consumption. The more glucose consumption, the worse
the cerebral hypoglycaemia and with it the greater the secretion of
adrenalin and noradrenalin. ‘Jesus, I’m going to die’

Enter HYPERSUGGESTABILITY plus religion, almost universal in schizophrenia.
‘I’m going to burn in Hell. I AM IN HELL. TERROR. I might lose my
mind and go berserk!!! Now frozen stiff in a catatonia trance.
Noradrenalin now predominates to constrict the blood supply to
skeletal muscles persistently, along with immobility of the body to
conserve energy. Catatonia is the worst case scenario and can go for
DAYS ON END.

So how does the individual pull out of the attack? Part of the process of
gluconeogenesis is ketosis where fatty acids from fat cells are
broken down in the liver to ketones, three different kinds. Two of
these come out in the urine and can be tested for using Ames
Ketostix, a good idea straight after a panic attack. One, acetone
comes out in the breath as the “smell of rotting apples”. Most body cell
adapt to using ketones but like ketosis itself this takes time
especially with liver pathology.

body cell adapt to using ketones but like ketosis itself this takes
time especially with liver pathology.

NON ALLERGENIC ASTHMA.
Most
people know that if an asthmatic tries to hyperventilate to overcome the
breathlessness it just makes the attack worse. So they have to slow
their breathing right down/breath into a bag and relax as much as
possible. (Alexander technique) Panic attacks are also alleviated BY
BREATHING INTO A BAG Strange. What’s going on? How can an increase in
oxygen going into the body be detrimental. It’s not the increase in
CO2 that does the trick but the reduction in O2.

Speaking to one asthmatic I knew she said that a cup of tea made it
easier to breath. She thought it was because it was a HOT drink, but I
fixed on the sugar in the tea replacing sugar produced by
gluconeogenesis. With gluconeogenesis turned down there wouldn’t need to
be a noradrenalin-adrenalin reaction on muscle cell to produce lactic
acid.

But what if there was a very weak adrenergic response, especially
noradrenalin and it’s vasocontricting effect to the skeletal muscles
cutting back on their oxygen supply. So, too much oxygen is reaching the
skeletal muscles for fermentation of muscle glucose (as glycogen) to
lactic acid to take place for the liver to make glucose from. So instead
HISTAMINE is released in the lungs to reduce oxygen transport into the
bloodstream instead. Just a hunch, but a big one. Once again the
symptom.

EPILEPSY.
I always ask myself what do symptoms do. Okay, now
add a black out and convulsions, ie a grand mal epileptic fit, as an
alternative to the above runaway cascade. The unconsciousness of
blackout shuts off the panic cascade thereby conserving glucose and
the CONVULSIONS PUMP LACTIC ACID OUT OF THE SKELETAL MUSCLES.

Veins
have non return valves along them so that by the convulsions
stretching and contracting them they act as a series of pumps to
speed up the delivery of lactic acid back to the liver. I’ve had a
few fits myself years ago and with one massive fit I was fully
conscious during the entire fit. That was very enlightening. I was
extremely paranoid, with the very obvious visual distortions
mentioned above which got increasing more obvious. Then projectile
vomiting followed by the very violent convulsions, which changed in
pattern from the last. Now a period of calm in which the visuals
distortions were minimal but gradually built up to another round of
vomiting and convulsions. This confirmed what was known that when
schizophrenics, who also suffer epilepsy, have a fit it dramatically
reduces the symptoms. It was this factor that inspired ECT to induce
convulsions.

Brain tumours don’t directly trigger seizures. They use a lot of
glucose the more malignant they become (what’s called the Warburg
effect)and so exacerbate (make worse) the cerebral hypoglycaemia. I
believe that the majority of these tumours are caused by the severe
hypoxia in the brain associated with the vasoconstriction phase of
migraine or simply severe reactive hypoglycaemia

COMING DOWN FROM THE PANIC ATTACK..
So how does the the individual pull out of the attack? By going into ketosis. You go into ketosis when you fast or eat a carbohydrate restricted diet.
Carnivorous animals in the wild go in and out of ketosis all the time
as they miss 4 out of 5 attempts to catch prey. A schizophrenic
coming out of panic attack might be too paranoid to eat, believing
their food is poisoned, or contains a hidden hallucinogen put there
by whoever the conspiracy theorists online tell them put it in their
coffee/food. How much of this stuff did Holmes read, lots I bet.
How many video games include these types of conspiracies. Plenty of
movies do.

Ketosis is associated with the process of gluconeogenesis whereby
the liver makes glucose from lactic and amino acids supplied by the
muscles and glycerol supplied by fat cells. Ketosis is where fatty
acids from fat cells are broken down in the liver to ketones, three
different kinds. Two of these, betahydroxybutyric acid and diacetate,
when in excess, come out in the urine and can be tested for using
Ames Ketostix, a good idea straight after a panic attack. One,
acetone, comes out in the breath as the “smell of rotting apples”.
Most body cells adapt to using ketones but like ketosis itself this
takes time especially with liver pathology.

Gluconeogenesis is also impaired thus delaying restoration of BG
to normal. It is a complex process, requiring 3 substrates, lactic
acid and amino acids from the muscles and glycerol from fat cells.
Fatty acids are also released from the adipose fat cells, not as
substrate for gluconeogenesis, but to provide the energy to drive the
process, as gluconeogenesis is an energy negative process unlike
glycolysis which uses the same pathway, but in the opposite
direction, and has a net production of 2 ATP’s. Fatty acids are
first beta oxidised to ketones in liver cells, then to acetylCoA
which enters the TCA (tricarboxalic acid, Kreb, citric acid) cycle to
produce the ATP (the energy currency of the cell) needed to drive
gluconeogenesis. Carbon skeletons from some skeletal muscle derived
amino acids, after deammination, also enter the TCA cycle as
intermediates and are also metabolised to produce ATP..

Glycerol from adipose fat cell triglycerides and other skeletal
muscle derived amino acid carbon skeletons, enter the gluconeogenesis
pathway as substrate for the synthesis of glucose. Ketone production
by the liver by far exceeds that needed to drive gluconeogenesis and
excess ketones poor into the bloodstream for use by most body cells
ONCE THEY ADAPT by up regulating the associated genes. However that
adaption is also delayed, so body cells might continue to require
glucose for days. Obviously transcription, splicing, translation ect.
of the associated genes requires energy but as the BG is so low there
is not enough fuel for these processes to take place.

The two main endocrine hormones required for the process of
ketosis and gluconeogenesis are cortisol and adrenalin. Cortisol acts
on the skeletal muscles to get them to release amino acids whilst
adrenalin acts on adipose fat cell to get them to break down
triglycerides to fatty acids and glycerol for release into the
bloodstream. Whilst not necessary for fat catabolism, cortisol also
acts in synergism with adrenalin in this task and greatly increases
the supply of fatty acids and glycerol to the liver.