Migraine Caused by REFINED SUGAR.

MIGRAINE (And PANIC ATTACKS) Breaking the Sugar Addiction.
Now it's all very well to say cut out the sugar but if the migraineur is addicted, which he or she is almost certain to be. Saturday morning migraines are common for the obvious reason that many people lay in on Saturday so their blood sugar has had longer to fall. If you get out of bed a bit shaky and sweaty your are more likely to be in ketosis, a certain indicator of reactive hypoglycaemia and depending when and what you snacked on before going to bed So its a very good idea to get some Ames Ketostix to test your urine, better still Diastix which also test for glucose although they can't coincide. If you ARE in ketosis this is a sure indicator of poor liver storage of glucose (as glycogen.).
The addictive cycle goes like this. Gets out of bed hanging out for a cuppa with a fair bit of sugar in it, more likely coffee than tea. Blood sugar shoots up, feeling great for a little while then craving starts again as it plunges back down. Another cuppa and so on all day. So first off you've got to cut down the rest period and have a late snack of wholemeal toast with say avocado on it. Now get out of bed early and toast once again, For a sweetener in cuppa cyclemates I suppose although I hate the taste of those things. You could try glycerine as it is very sweet but doesn't trigger an insulin release. Now your blood sugar will rise much more slowly and fall slowly with a much longer cycle. YOU SHOULD HAVE BROKEN THE CYCLE AND NOW BE TOTALLY MIGRAINE/ PANIC ATTACK FREE (as long as you don't backslide)
OKAY NOW SUGARS. Fruit is okay but if you are very sensitive cut out very sweet fruit like pineapple for a coupla weeks. Fruit juices are out as there is no fibre with them and it's just too much sugar.. As much as it's very good for you honey is out for a coupla months as the sucrose in it has been split by the bees digestive system to fructose glucose and there is no fibre in it. Now for the processed food. Chocolate and cola drinks are deadly as they contain sugar, caffeine and threobromine. Now add a cigarette and you have the very worst combination of all. Especially if you are very sensitive you've got to weed out sugars in all other processed food root and branch, Look for SUCROSE (TABLE SUGAR glucose, fructose), GLUCOSE, DEXTROSE (another name for glucose), FRUCTOSE, (although it's supposed not elicit an insulin response), just be on the safe side, CORN SYRUP and MALTOSE (glucose, glucose) . As to the lactose in milk bear in mind that humans are the only animal that drinks milk after being weaned. Just see how you go. Once your liver bounces back you could put things back on the diet like milk but not the refined sugars. Anyway, once you've broken the addiction you'll hate the taste of it.
WHOLEMEAL BREAD, PASTA, SPAGETTI, BISCUITS, BROWN RICE.
BOOZE. Unfortunately ALL out. Meaning no parties, no pub. However, once your mood stabilises and your stress level drops as your liver comes good you won't feel like a drink.
EXERCISE. A lot of migraineurs do nothing one day then go at it like a bull at a gate the next and get a migraine. Obviously exercise is great and NECESSARY but it also gobbles up blood sugar, so just go easy to start off with and increase it a bit at a time.
TYRAMINE. A substance in a lot of foods which triggers the release of NORADRENALIN. I'll deal with that later in a separate post.
{PS When I say blood sugar I meant blood glucose, same thing).
Go for it. Noddy.

Reactive Hypoglycaemia. Low Blood Sugar in Reaction to High Blood Sugar.

If you suggested to a biochemist that refined sugar was a poison he would probably retort indignantly that it has exactly the same molecular structure as the sugar in an apple, and of course he'd be right. However, this misses the point, as refining the sugar removes it from it's natural context of fibre, as well as minerals essential to it's storage and metabolism e.g. zinc. It's all about the way that refined sugar is regulated in the body vs. sugar in it's natural context.
The subject of blood sugar regulation is probably one of the least understood in all of medicine. It is a black hole. The reason for this is that it was suppressed most forcefully in 1972 (no great conspiracy theories). Let me explain. In 1924 a US physician Seale Harris, read a paper put out by the Canadian discoverers of insulin, Banting and Best, in which they described the symptoms of a diabetic injecting too much insulin and the extreme hypoglycaemia (low blood sugar) that ensued (there were no glucose monitors then.) These were tremors, sweats, migraines, convulsions, tachycardia, panic attacks, coma and death in the most extreme case (figures). He knew that many of his patients experienced many of these symptoms, sometimes right out of the blue, like panic attacks. Harris concluded that the culprit was refined sugar in that being stripped of the natural fibre of the cane it was absorbed much too fast into the bloodstream so that the pancreas overreacted, producing far too much insulin which caused the severe hypoglycaemia.
He coined the term for the syndrome 'Reactive Hypoglycaemia', that is, low blood sugar in reaction to high blood sugar or hyperglycaemia. He wrote a paper on migraine which received good acceptance at the time, and this term and the syndrome became orthodoxy for many years. However it eventually began to get up the nose of processed food manufacturers who used refined sugar in their products. By this time the US govt., like so many others, was cutting back on funding of research into health and universities had to rely more and more on said food manufacturers for grants, with large strings attached of course. Principal among these manufacturers were the giant chocolate and soft drink manufacturer and cola manufacturer (you've go no idea of who I mean of course). In 1972 these companies demanded that the US AMA drop the term 'reactive hypoglycaemia' or they would take their money elsewhere. The AMA caved in and the term fell into ridicule even by GP's, as it is today. The 5 hour GTT or glucose tolerance test, a test necessary to clearly demonstrate the abnormal BG swing ceased to exist and of course today no doctor or path lab would do it because of the time involved i.e. the cost. (Actually since I wrote this a number of clinics now do it but it useless as they only test every hour.) I've done quiet a few myself, including a couple on myself. I've added a range of monitors to the test, blood pressure and heart rate monitor, finger temperature monitor, skin conductance monitor, as well as using Ames Multistix to test urine, 8 tests instead of the normal 1 with Glucostix or 2 with Diastix.
Medicare Australia will not fund this test, only the 2 or 3 hr diabetes test which is totally useless because of the short time involved and the infrequency of the tests (one each hour). It is ironic that it was these two companies who were the prime movers in this repression of truth, because BOTH use cocoa and a lot of sugar. Cocoa contains caffeine and a caffeine like substance called threobromine. These three combined cause by far the most unstable blood sugar of all. That giant cola manufacturer buys caffeine from coffee decaffeinators to add to their product to make it even more addictive. Now I've studied this subject extensively for forty years and it is very clear that the main problem is not the pancreas but the inability for the liver to store glucose as glycogen and the extremely convoluted and damaging path that the body has to take to restore the blood sugar level to normal following the fall.
The complete understanding of blood sugar regulation can now only get worse as universities are dumbed down worldwide to attract foreign students and their fees or go bust. I have been told at both the Lorne Vic Aust Cancer and Genome conferences I attended for many years that biochemists no longer study metabolism, which is absolutely absurd. The internet seems to have had a negative effect in this regard as researchers just go online to see just the part of a metabolic pathway they need to conduct an experiment instead of seeing the whole picture. Anyway to work out blood sugar regulation requires a lot more than biochemistry as it also involves at least endocrinology, haematology and physiology The only computer to store all of these pathways is the lump of meat between one's ears. Next, liver pathology.

MIGRAINE Beta Blockers.
Eighteen years ago when I was selling my little migraine book on the footpath in the middle of town a chap of around 25 told me something that I still find hard to believe. He said that he had migraines so excruciating that he'd been given a prescription to get his own morphine so that could inject himself as they came on too quickly to get to a doctor. Then came the bombshell. On the advice of the doctor he was drinking about twelve cups of coffee each day with SIX teaspoons of sugar in each. Now I thought he must have been pulling my leg and replied, 'You're joking.' and he got a bit upset at this and said, 'No I'm NOT joking'. This is an example of what I mean about the black hole in medicine about blood sugar regulation. It would seem to me that the doctor assumed that this bloke had chronic hypoglycaemia, it was there all the time, it wasn't periodic hypoglycaemia in response hyperglycaemia. Then I asked him what medication he was on and he replied Beta-Blockers, not for chronic hypertension but as prophylaxis against the acute hypertension of the migraine, the reasoning being I assume that by reducing blood pressure the blood vessel dilation, when a migraine took place, wouldn't be as severe with less pressure to distend them. He would further reason that if he got a migraine it was because he went too long without having his next drink of hot glue, his blood sugar fell, vomiting started and so he was unable to have another cup to bring it back up again. The migraines lasted up to 3 days. Now to the beta blockers. The drug molecule binds the the beta receptors on the cells of the myocardium, (heart muscle cells}. There are alpha an beta receptors on the RAS pathway I described earlier. The beta is the stimulatory receptor and the alpha in the inhibitory. The beta receptor his the highest affinity for the ligand, in this case adrenalin, thus it saturates first and if the concentration of ligand increases the alpha receptor begins to saturate and puts on the brake. Very neat. Adrenalin belts up the metabolic rate of the heart muscle, increasing its contraction and thus increases blood pressure. Sympathetic nervous stimulus increases the RATE of contraction. The beta blocker is an antagonist in that it prevents adrenalin binding but has no stimulatory effect itself.
Fine, but what the doctor hadn't realised is that adrenal binds lots of other receptors, including those on skeletal muscle cell and fat cells, the very tissue that has to supply substrate for gluconeogenesis in the liver to restore BG to normal so that the blood vessels to the brain can normalise. Fatty acids and glycerol from fat cells and lactic acid from the muscles are needed. Cortisol has this affect however it is weak without adrenalin as there is a synergy between the two hormones. So blood sugar falls through floor, vomiting stops drinking more sugar, stops taking vasoconstrictor drug such as ergotamine tartrate, so any gluconeogenisis is very weak due both to the lack of substrate combined with liver pathology. He was very fortunate to still be alive.
Okay, what about a migrainer taking beta blockers for hypertension. Go off the sugar and the beta blocker is going to inhibit gluconeogenesis which normally comes on after glucose storage to metabolise excess amino acids from the diet. I'm not gonna advise someone to go off their beta blocker if they've got bad hyper tension. However, what if a lot of the hypertension is renal hypertension so that they could switch to an ACE (angiotensinogen converting enzyme) inhibitor, temporarily. Meantime get some omega 3 oil, flaxseed oil. Omega 2 is the precursor for the prostaglandin PGE 2 a general vasodilator, kidneys included. Omega 3 is the precursor for PGE 3 more important for blood vessels close to the skin in winter. These polyunsaturated fatty acids are a common deficiency for a range of reasons, being saturated in processed food so they wont oxidise, converted to trans fatty acids, (swivelled around at a double bond due to the heat of cooking). Our bodies can only make Omega 1, oleic acid. So get a bottle of good quality flax seed oil in a dark bottle to protect it from light and refrigerate it, oh yea and take it daily. Now go and buy a blood pressure gauge and heart rate monitor and check daily, better to do it at the same time each day probably before breakfast.
Now what to do about reversing the hypertension. A lot of hypertension in poorly managed diabetics is due to huge surges in BG. This causes so called nonenzymatic glycosation of protein, i.e. blood vessels gunked up with glucose mixed with cholesterol. A migrainer has big surges in BG as well, not as bad as the poorly managed diabetic but bad enough. With a now much lower BG peak and the normal regeneration of blood vessel epithelia this gunk should gradually dissolve and disappear and blood vessels become more flexible. Look at the gap between systolic and diastolic. That will widen as blood vessels improve. Now go and do your tax returns, take the neighbour's lawn mower back that you've had for weeks. Pay what bills you can, patch up all the petty blues you've had with people, get the car up to roadworthy standard, etc. etc. etc. so that the ceaseless chatter of the drunken monkey, as Hindus call it, will start to quieten down and blood pressure will drop accordingly. Cut back on the ACE inhibitor until blood pressure comes back to normal then flush them down the toilet where they belong..

Many years ago I found a little second hand book in a book store about autopsies performed at the Queen Ann Hospital in London on people who had been migraine sufferers and who had taken a variety of medications. It was not a pretty tale. The major lesion was extensive blood vessel damage, necrotic zones and benign tumours. I don't remember if there had been some malignant tumours. As far as the drugs were concerned the worst offender were those derived from ergot, a fungus that grows on rye flour and the plant I assume. These are blood vessel constrictors, but the problem is that they cause irreversible constriction when used over a pronged time. Thus the prolonged hypoxia induced by this constriction would be the primary cause of the necrotic zones and the tumours. LSD25 is derived from from ergot, and is just one of the LSD's and I think that the ergot drugs belong to that category, but not hallucinogenic.
St Trinian's Fire. In about the sixteenth century a baker somewhere in Massachusetts in the US baked bread, probably over some time, from rye flour that had gone mouldy in a damp cellar, and contained ergot fungus. Then what happened to that town was just so bizarre. People began to experience hallucinations and had accidents as they lost control. Over a much longer period people had to have limbs amputated that had become gangrenous. What had happened was that the combination of the ergot fungi in the flour and the heat of the oven had produced a wide range of LSD's from LSD25 to vasoconstrictors. Obviously the witches (gnostic Christian women, probably the most benign kind) were to blame and were rounded up and burned at the stake.
Migraine drugs fall into main categories, constrictors and dilators. Now obviously that sounds completely contradictory, However, the dilators are used prophylacticly to prevent the first first phase of the vasomotor, the constriction, No constriction, no reflex dilation in response to the hypoxia and hypoglycaemia induced by the constriction. No dilation no migraine or one of reduced severity. The idea of using these drugs prophylacticly is to get around the vomiting problem as a migraine begins where it becomes impossible to imbibe them (naturally)
The constrictors, including the ergot derived ones. These are used by migraineurs who don't have the vomiting problem or when the migraine is a slow onset so they can take them before vomiting starts. In other words they have to take them ideally before the dilation phase begins but not too early as this would exacerbate the constriction of the vasospasm.
The basic philosophy of the Naturopath is that the symptom is Nature's way of trying to alleviate an underlying cause and that to suppress the symptom is to make the underlying cause worse over time. Couldn't agree more. Trouble is because the naturopath is low on physiology, biochemistry. etc. but big on flying saucers he cops flack from the allopaths who treat the symptoms. However allopaths seem to be adopting flying saucers whilst sticking with treating the symptoms.
If you read my Part on the Vasospasm and if it makes sense it must be obvious that the vasospasm has a clearly identifiable cause, i.e. to alleviate said underlying cause and thus minimise the damage resulting from the cause, osmotic pressure imbalance followed by severe hypoglycaemia and hypoxia.. Thus to suppress the symptoms MUST make the underlying cause much worse and do a lot of damage in the process and the autopsies mentioned above are pretty clear evidence of same. The pain is there for a reason, to warn of a problem so that it can be fixed.
These drugs fall into a different category to the beta blockers in that getting straight off them before starting on the change of diet should be no problem.
General Analgesics. If you are having problems getting off the sugar or there are other complications so that migraines of reduced severity persist for a while so that you have to take an analgesic then think about these choices. Panadol or Paracetamol is hepatoxic. Codeine being made from naturally occurring opium is not. Panadeine is a mixture of both so no go.. Thus Codeine must the analgesic of choice but causes constipation. So take a naturally occurring laxative which is a mixture if fruit and senna (in Australia that's Nu Lax). A few prunes each day helps a lot.

Problem Foods. Spontaneously Forming Hallucinogens
1 TYRAMINE. Found in broad beans, fermented cheeses, some wine etc. (Check online) This compound used to be a big problem for people taking Mono Amine Oxidase (MAO) Inhibitors for depression. These fell out of favour with the introduction of the SRI (serotonin reuptake inhibitors) such as Prozac. The MAO pathway breaks down the catecholamines, adrenalin, noradrenalin and dopamine, and by inhibiting MAO these hormones, associated with arousal, are maintained in the bloodstream for a much longer period. What Tyramine does is to trigger a big release of noradrenalin and with MAO inhibited the noradrenalin can't be broken down and causes a sharp rise in blood pressure, presumably because noradrenalin is a vasoconstrictor in many tissues, and could cause a stroke.
While it is a vasoconstrictor there is another factor associated with noradrenalin FEAR. A few years ago I saw a doco about Antarctic researchers being tested for their cold response by being immersed in icy water. One of the things they were injected with was noradrenalin without being told what sort of response they might get which was PANIC ATTACKS without any sort of external threats to trigger them. Noradrenalin is secreted as part of the gluconeogenesis response and the less able the liver is to store glucose as glycogen the greater the secretion of noradrenalin. Fear, right out of the blue, 'I must be going crazy'. Thus we can add a powerful sympathetic nervous response to further elevate blood pressure. Tyramine is an analogue of one of the catecholamines as they are made in the adrenals from the amino acid tyrosine So tyramine is an amine of tyrosine and broken down by MAO mostly in the liver.
But you don't have to be taking MAO inhibitors to have inhibition of MAO. MAO is contained in the mitochondria and because numerous detoxification enzyme systems are contained in the mitochondria it is susceptible when things go awry. A major mitochondrial damaging toxin is acetaldehyde from the breakdown of alcohol (ethanol). The pathway is alcohol dehydrogenase (zinc dependant) acetaldehyde dehydrogenase (copper dependant) the end product being acetate. If acetaldehyde dehydrogenase is downregulated due say to a copper deficiency, then acetaldehyde builds up in the bloodstream and, with heavy drinking, probably causes more liver mitochondria damage than anything else. It is the compound which causes hangover.
So liver damage is MAO impairment and thus Tyramine sensitivity.. Now it gets even nastier. The cause of the hallucinations associated with DT's due to liver cirrhosis, from chronic alcoholism is impaired MAO. If the outlet end of the pathway if blocked then intermediate molecules between the enzyme steps pile up and some of these can combine by condensing reactions to form hallucinogenic neurotransmitters. This indicates that MAO doesn't have a feedback loop from the outlet to the inlet to inhibit it when the outlet is blocked for whatever reason. I don't remember the names of these compounds but there are a couple I do that also result from MAO inhibition, Now remember that there is a big secretion of the catecholamines in response to a fall in by associated with livers inability to store glycogen, one being noradrenalin.
Now add an inability to break them down due to impaired MAO also due to liver damage. Further add an inability to take up amino acids from the bloodstream by the damaged liver, and turn them into nonsense proteins for storage. One of those amino acids is methionine, the number one methyl donor associated with DNA methylation. Then there is the catecholamine, dopamine piled up in the bloodstream. Dopamine comes into contact with methionine and is spontaneously methylated to ORTHOMETHYL DOPA, the active ingredient in the hallucinogenic cactus mescal. Many years ago asthmatics were having freak outs after injecting adrenalin as an antihistamine. It turned out that being in a clear bottle next to a window exposed to the Sun the adrenalin turned pink. It had oxidised to an hallucinogenic compound called adrenochrome and it turns out that if adrenalin remains in the bloodstream for a long time due to MAO inhibition the same thing happens, yet another hallucinogen. Add them all up, noradrenalin, adrenochrome, orthomethyl dopa and the other two resulting from MAO intermediates, and you've got factors in panic attacks, schizophrenia etc. Then add Tyramine as another trigger for noradrenalin and most of this pathology is down to liver damage, the blood sugar instability. Now that was a bit long winded for just one compound but is sheds light on so many others, hence choosing tyramine to get the ball rolling.. MSG won't be as long I haven't boned up on that one

VASOSPASM. The OSMOTIC PRESSURE HYPOTHESIS.
This hypothesis is based on two things. All of the evidence points to it and 2. Things don't just happen as the neurologist suggests. Like all of my stuff it is based on my research and is, as far as I know, unique as to a valid EXPLANATION of the vasospasm. It is written more for the MD or researcher as a way of VALIDATING my overall hypothesis.

The migrainer might start to experience symptoms of an impending migraine in a couple of days prior to the attack. I'd suggest a series of reactive hypoglycaemia of ever shortening duration as being responsible here. The migrainer wakes up with a sugar craving and is in ketosis, perhaps. Has a sugary breakfast or just a cup of coffee with 2 or 3 teaspoons of sugar in it. But not necessarily so as the person suffering reactive hyper hypoglycaemia seems to become increasingly sensitive to sugar over time, sometimes exquisitely so. Perhaps it's the caffeine. (I'm just thinking out loud). Within a couple of hours the craving returns. Then the same again but sooner as the swings get bigger, finally a migraine. FEAR of an impending migraine as early symptoms appear obviously exacerbates this vicious cycle, worsening symptoms more fear and vicky verka. Finally up goes the BG to an astronomical high and begins to plunge rapidly.

OSMOSIS and the VASOSPASM..
We can divide tissue up into 3 basic osmotic compartments, intervascular, interstitial or between tissue cells, and intercellular. The intervascular department is a bit different as it contains albumin made by the liver. Referred to as a colloid albumin transports a range of different molecules on different charged sites and exerts a lot of osmotic pressure. With liver failure, as with cirrhosis, albumin production drops and fluid increasing leaks out of the blood vessels into the interstitial spaces
A range of ions and polar molecules exert osmotic pressure in solution. These obviously include some whole proteins. Whilst the concentration of the different ions is different between the inside of a cell and the outside, e.g. more sodium outside and more potassium inside, as is necessary to achieve an electrical gradient across the plasma membrane, osmotic pressure is balanced between compartments. If it were not so the compartment with greatest pressure would obviously swell up and burst or just leak badly. A range of cell plasma membrane pumps pump some things in and some things out, some like the sodium potassium pump pumps sodium out and potassium in whilst potassium gradually leaks out by passive diffusion. There is also a pH gradient across the membrane, for instance when red blood cells exchange oxygen for carbon dioxide there is a pH swap on which, what becomes their carbhaemoglobin, a site which ionically binds sodium ions swaps this for a hydrogen ion whilst bicarbonate ions in the cell are exchanged for chloride ions outside the cell. You could say that ionised sodium bicarbonate is exchanged across the membrane for ionised hydrochloric acid when oxygen is off loaded and carbon dioxide is taken onboard. Alkaline oxyhaemoglobin become acidic carbhaemoglobin. Hydrogen ions and chloride ions diffuse into the cell in exchange for sodium and bicarbonate ions which diffuse out, and of course the opposite takes place in the lungs. All well and good. Does that mean that venous blood is more alkaline than arterial blood? From memory not so as free carbonic acid makes venous blood more acidic. Normal arterial blood has a pH of 7.4, however, with very severe metabolic acidosis it can fall to life threatening 6.8. The patient is breathing very heavily as the body to get rid of excess carbon dioxide as it forms carbonic acid in solution
Glucose, being a polar molecule, also exerts osmotic pressure and as long as blood glucose regulation is performing properly, then everything has evolved to be in balance. However, lets say that the BG level shoots up 300% in a half hour. Neurons in the brain do not store glucose as glycogen and thus have no insulin receptors on them. Glucose enters neurons by passive diffusion to be immediately metabolised.. So how does the brain control how much glucose enters neurons to match their fluctuating metabolic rate? The brain controls the ENTIRE BG regulatory system TO SUIT ITSELF, modulating pancreas, adrenals, liver etc. with parasympathetic and sympathetic signals, modulating blood vessels etc. etc. Thus brain cells are bathed in the precise glucose concentration needed to suit their immediate metabolic demands. Localised areas of the brain control blood vessels to match the degree of localised metabolism. Many neurotransmitter (if not all) are also prostaglandin activators,
With reactive hypoglycaemia the brain LOSES CONTROL. So up shoots the BG in the fluid bathing the neuron and because it has no control over it's ingress it turns on an emergency pathway call a Polyol Pathway (multiple alcohol). The idea is to get the glucose in the cell out of solution as quickly as possible. So first it's converted to sorbitol then to fructose and because fructose precipitates out at a lower concentration than glucose, fructose crystals begin to form in the cytoplasm.. However, unlike glycogen which is aosmotic (doesn't exert osmotic pressure) fructose does and when the BG outside the neuron begins to plummet precipitously the fructose crystals begin to pull a lot of water into the cell. The entire brain swells in a migraine and this is why. A lot of neurons may be permanently damaged. Unable to repair themselves, and unable to turn on apoptosis, they 'inappropriately' express MHC2(?) receptors, thereby behaving like an APC (antigen presentation cell) and so initiate an immune response against themselves. Auto immune 'attack' maybe. Just a hunch!!
In a desperate attempt to limit the osmotic pressure imbalance and limit the damage the brain must secrete a vasoconstrictor in blood vessels supplying it, even though this constriction will worsen the already severe hypoglycaemia and create hypoxia just at a time when cells need both glucose and oxygen to make ATP to DRIVE THE BAIL OUT PUMPS. As noradrenalin is a constrictor in blood vessels in which adrenalin is a dilator, then I'd nominate it, but not coming from the adrenals, but from the brain itself in order to limit this constriction to just these blood vessels alone. This is purely a hypothesis and the reason I believe that it does this is to retain as much electrolyte, calcium, sodium etc. in the interstitial fluid to compensate for the loss of glucose. It is a desperate attempt to balance one crisis against another. If the migrainer is very frightened and is considering the possibility of a stoke, even death, then the extra neural activity of fear (the brain on average uses 40% of the body's glucose) further exacerbates the overall problem. Fear also creates hypersuggestability, or the ability to imagine even worse consequences, Hellfire, thus even more fear ad infinitum. Blacking out would be protective against this runaway fear and that is why, I believe, an epileptic blacks out before an attack.
Finally the hypoxia added to the hypoglycaemia becomes the predominant problem and flood of vasodilator is released and these blood vessels massively dilate instead. One important dilator is ADP which builds up in cells unable to phosphorylate it to ATP and is released from these cells. Bradikinin sensitises pain receptors so it is possibly involved as well. MIIIIIIIGRAINE!!!!!
Now consider other factors which must contribute to the mental confusion as the blood sugar falls. A huge imbalance in the concentration of ions across the plasma membranes of a neuron, must drastically alter it's depolarisation/repolarisation when it fires, thereby altering the firing potential of it's synapses, along with the drastic shift in pH gradient also having a negative affect.
Next, the gyrations of the rest of the soma. Noddy (Paul Hill)

The term sugars covers a wide range of compounds, however, I just want to cover the hexoses (6 sided) normally found in food. All dietary sugars are either dimers (2 joined together) or the polymer starch, the exception being honey in which the double sugar sucrose has been hydrolysed by the bees digestive system into single sugars. Fruit sugar sucrose is fructose glucose, milk sugar lactose is galactose, glucose and starch is a long chain of glucose molecules with side branches sticking out from the main trunk. Glycogen, the form of glucose polymer which acts as a storage medium in animal cells is much the same as plant starch except the side branches are located in a different place and cannot be digested in a human's gastro-intestinal tract. Starch digestion begins in the mouth by the enzyme ptyalin and it is broken down to the double glucose molecule maltose by the time it enters the duodenum.
Okay, now to a VERY IMPORTANT POINT. In the natural world all sugars (except in honey) arrive in the duodenum for digestion as DOUBLE sugars, sucrose, lactose and maltose and cannot be absorbed into the body until cleaved into single sugars by the enzymes sucrase, lactase and maltase which are secreted into the duodenum by the EXocrine pancreas. This is where regulation comes in and is so important in stabilising the blood sugar level, The ENdocrine pancreas, located inside the body and which produces insulin in it's beta cells and glucagon in it's alpha cells, monitors blood sugar and it communicates with the exocrine pancreas via the GIP (gastro inhibitory peptide) axis. The idea is that the exocrine pancreas does not secrete the digestive enzymes into the duodenum until it the endocrine pancreas is ready and the exocrine pancreas monitors the presence and level of sugars in the duodenum telling the endocrine pancreas when to begin making insulin. THUS THERE IS VERY TIGHT CONTROL
Insulin takes about twenty minutes to synthesise. However, in the healthy individual there is a residue of insulin remaining in the cells from the previous release, so that there is a so called biphasic release. This residue is to nip in the bud any premature release of sugar into the bloodstream until de nova synthesis has finished and it is lost with reactive hypoglycaemia, as with migraine, because the pancreas is forced to overreact all the time. This loss of biphasic release is destabilising as I will cover in the next chapter.
Now we come to fibre. Plant fibre is composed of lignin, cellulose, hemicellulose and pectin. Fibre exerts strong osmotic pressure in solution and when present in the digestive tract pulls against the absorption of the monosaccharides resulting from the cleavage of the disaccharrides by the digestive enzymes. The monosaccharrides, glucose and galactose are actively transported in to the bloodstream, whereas, from memory, fructose enters by passive diffusion, So active transport also acts as a regulator.

REFINED SUGARS.
Now I want to leave the subject of digestion and assimilation and talk about the sugars of the concrete jungle. It is harmful to eat monosaccharides as they disturb blood sugar regulation. Processed foods contain the monosaccharides fructose, glucose, dextrose (another name for glucose) and food manufacturers are desperate to shove as much of this stuff into their 'foods' as possible. Sucrose or refined sugar put into a boiling cup of tea or coffee is hydrolysed into the monosaccharides by the heat whilst the caffeine accelerates the rise in blood sugar.
Caffeine poisons the enzyme phosphodiesterase located on the G stimulatory protein of the RAS (rat sarcoma) signalling pathway thereby preventing the pathway from turning off. Let's say that adrenalin binds to the RAS beta receptor outside the cell and activates it. Inside the cell the (C terminus) part of the receptor, now activated, draws the G protein to it and the G protein is diphosphorylated and thus activated. Activated G protein then migrates to adenylate cyclase and activates it and adenylate cyclase then begins to make cyclic AMP or cAMP which in turn activates the rest of the signal transduction pathway.. Within milliseconds or seconds phosphodiesterase on the G protein dephosphorylates the G protein and it migrates back to a position midway between the adenylate cyclase and the RAS beta receptor. Thus by caffeine poisoning phosphodiesterase an adrenalin response remains switched on for some time after adrenalin is withdrawn from the bloodstream. As adrenalin raises blood sugar in a number of ways it is obvious that caffeine is destabilising to blood sugar regulation. RAS pathways are ubiquitous in the body and stimulators include embryonic hormones, hence the suggestion that caffeine can be a promoter of cancer once started and it's cells dedifferientated.
Threobromine is the other blood sugar raiser in Coca Cola and chocolate. It's a xanthine like uric acid, and is essentially caffeine with one less methyl group on it (caffeine has 4). So, boiling coffee, sugar, a lump of chocolate, a swig of Coke and an hour or so the mouth is spewing and the head is thumping, tremors, sweats, no bloody good at all and very destructive.
In part 4 I want to get into the subject of blood sugar regulation INSIDE the body (the GI tract is officially outside the body). This will begin to touch on panic attacks, epilepsy, asthma and schizophrenia.. I might also start on the subject of how to break the addictions.
In veritas Noddy. Paul Hill.