Nexus - 0705 - New Times Magazine-pages

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Several clinicians have remarked that their MS patients’ enters the brain in higher concentrations and also increases brain conditions were made worse following exposure to dietary acetylcholine, necessary for normal memory function. While excitotoxins. I have seen this myself. It is logical to assume that these particular substances are found to boost brain energy func- the conditions of patients with other neurodegenerative disorders, tion significantly, they are not alone in this important property. such as Alzheimer's disease, Parkinson's disease and ALS, will be Phosphotidyl serine, ginkgo biloba, vitamin B12, folate, magne- made worse on diets high in excitotoxins. Barrier disruption has sium, vitamin K and several other substances are also shown to be been demonstrated in the case of Alzheimer's disease.** important. Recently it was shown that not only can free radicals open the While mitochondrial dysfunction is important in explaining why blood-brain barrier, but excitotoxins can as well.” In fact, gluta- some people are more vulnerable to excitotoxin damage than oth- mate receptors have been demonstrated on the barrier itself“ Ina ers, it does not explain injury in those with normal cellular carefully designed experiment, researchers produced opening of metabolism. There are several conditions under which energy the blood-brain barrier using injected iron as a free radical genera- metabolism is impaired. We know, for example, that approxi- tor. When a powerful free radical scavenger (U-74006F) was mately one-third of Americans suffer from reactive used in this model, opening of the barrier was significantly hypoglycaemia; that is, they respond to a meal composed of either blocked, but the glutamate blocker (MK-801) acted even more simple sugars or carbohydrates (that are quickly broken down into effectively to protect the barrier. The authors of this study con- simple sugars, i.e., a high glycaemic index) by secreting excessive cluded that glutamate appears to be an important regulator of amounts of insulin, which causes a dramatic lowering of the blood brain capillary transport and stability, and that overstimulation of sugar. When the blood sugar level falls, the body responds by NMDA (glutamate) receptors on the blood-brain barrier appears releasing a burst of epinephrine from the adrenal glands in an effort to play an important role in breakdown of the barrier system. to raise the blood sugar. This release is felt as nervousness, palpi- What this also means is that high levels of dietary glutamate or tations of the heart, tremulousness and profuse sweating. aspartate may very well disrupt the Occasionally we can have a slower fall normal blood-brain barrier, thus in the blood sugar that will not pro- allowing more glutamate to enter the duce a_ reactive release of brain, creating a vicious cycle. Recently it was shown that epinephrine, thereby producing few not only can free radicals open symptoms. This can be more danger ous, since we are unaware that our CELLULAR ENERGY Excitotoxin damage is heavily the blood-brain barrier, but glucose reserve is falling until we cell” Cells with a normal enersy excitotoxins can as well. toms, suchas difculty thinking and generation system are very resistant In fact, glutamate receptors a sensation of lightheadedness. wave ovine whence | ave been demonstrated fT ein i one of ts mest cause—hypoxia, starvation, metabol- on the barrier itself. since it has a limited ability to ic poisons, hypoglycaemia—they metabolise other substrates such as become infinitely more susceptible to fats. There is some evidence that excitotoxic injury or death. Even several of the neurodegenerative normal concentrations of glutamate are toxic to energy-deficient diseases are related to either excessive insulin release, as with cells. Alzheimer's disease, or impaired glucose utilisation, as we have It is known that in many of the neurodegenerative disorders, seen in the case of Parkinson's disease and Huntington's disease.* neuron energy deficiency often precedes the clinical onset of the It is my firm belief, based on clinical experience and physiolog- disease by years, if not decades.” This was demonstrated in the ical principles, that many of these diseases occur primarily in the case of Huntington's disease and Alzheimer's disease, using the face of either reactive hypoglycaemia or "brain hypoglycaemia", a PET scanner which measures brain metabolism. In the case of condition where the blood sugar is normal and the brain is hypo- Parkinson's disease, several groups demonstrated that one of the — glycaemic in isolation. In at least two well-conducted studies, it early deficits of the disorder is an impaired energy production by was found that pure Alzheimer's dementia was rare in those with the complex I group of enzymes within the mitochondria of the normal blood sugar profiles, and that in most cases Alzheimer's substantia nigra.*'*? Interestingly, it is known that the complex I _ patients had low blood sugar and high CSF (cerebrospinal fluid) system is very sensitive to free radical damage. insulin levels.***’ In my own limited experience with Parkinson's Recently it was shown that when striatal neurons are exposed to and ALS patients, I found a disproportionately high number suf- micro-injected excitotoxins, there is a dramatic and rapid fall in fering from reactive hypoglycaemia. energy production by these neurons. In this model, co-enzyme I find it interesting that several ALS patients observed an asso- Q10 was shown to restore energy production but not to prevent ciation between their symptoms and gluten: when they adhered to cellular death. But, when combined with niacinamide, both cellu- a gluten-free diet, their clinical symptoms improved. It may be lar energy production and neuron protection was seen.* For those that by avoiding gluten-containing products, such as bread, crack- with neurodegenerative disorders, I recommend a combination of _ ers, cereal, pasta, etc., they are also avoiding products that are high CoQ10, acetyl-L carnitine, niacinamide, riboflavin, methylcobal- on the glycaemic index, i.e., that produce reactive hypoglycaemia. amin and thiamine. Also, all of these food items are high in free iron. Clinically, hypo- One of the newer revelations of modern molecular biology is glycaemia worsens the symptoms of most neurological disorders. the discovery of mitochondrial diseases, of which cellular energy | We know that severe hypoglycaemia can in fact mimic ALS both deficiency is a hallmark. In many of these disorders, significant clinically and pathologically.* It is also known that many of the clinical improvement is seen following a similar regimen of vita- symptoms of Alzheimer's disease resemble hypoglycaemia, as if mins combined with CoQ10 and L-carnitine. Acetyl L-carnitine the brain is hypoglycaemic in isolation. not only can free radicals open the blood-brain barrier, but excitotoxins can as well. In fact, glutamate receptors have been demonstrated 42 = NEXUS Recently it was shown that on the barrier itself. AUGUST - SEPTEMBER 2000