Treatment of Degenerative Neurological Conditions such as Parkinson's Disease (PD), Alzheimer's, Motor Neurone Disease (MND) and Creutzfeldt-Jakob's

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Treatment of prion disorders

The problem with prion disorders is a similar problem to cancer. A pathological process has been switched on which then has a momentum of its own. Stopping the smoker from smoking does not cure his lung cancer! However one should be able to slow down the progression of the disease hopefully to an extent where healing and repair exceeds damage. There has to be a reason why Stephen Hawking was able to survive motor neurone disease for over 50 years when for most the prognosis is much worse! See Stephen Hawking Wikipedia Entry

1. Identify the initiator - identify toxic exposures and detox. See Chemical poisons and toxins. Deal with these specifically - see Detoxification - an overview and Detoxing - Far Infrared Sauna (FIRS). Heavy metals are commonly implicated and the best test for these is to measure urinary toxic metals following DMSA challange - see - Comprehensive Urine element Profile

2. Do the The general approach to maintaining and restoring good health

3. Because there is an element of autoimmunity in prion disorders, tackle Autoimmune diseases - the environmental approach to treating

4. Anything to reduce inflammation is likely to be helpful See Inflammation especially high dose vitamin D.

5. There is now evidence that many neurological conditions may also be a symptom of mitochondrial failure. The idea here is that if one doesn't have the raw materials for energy production in cells, then the cells go slow and if cells go slow then production of neuro-transmitters will be slow and result in their low levels. We also know that all the prion disorders are associated with toxic stress (see above) and these toxins can cause damage by inhibiting mitochondrial function. For example, organophosphates severely inhibit oxidative phosphorylation (because they get in the way of phosphate metabolism) and therefore could easily impair mitochondrial function in the brain. So there is a good argument to try the package of treatment which supports mitochondria, namely co-enzyme Q 10 300mg daily, D-ribose 15g daily, acetyl-L-carnitine 2g daily, vitamin B3 (niacinamide) 500mg daily combined with magnesium 400mg daily. See CFS - The Central Cause: Mitochondrial Failure See also Neurological disorders and mitochondria which concludes that:

...mitochondrial dysfunction is a central aspect of many adult-onset neurological diseases, including stroke, ALS, Alzheimer's, Huntington's, and Parkinson's diseases.

A major cause of damage to nerve cells is calcium influxing into cells. This happens when mitochondria go slow. The reason for this is that 40% of resting energy does nothing but fire the ion pumps that pump calcium out of cells and magnesium into cells. So having a low red cell magnesium may well be symptomatic of mitochondrial failure. However, the point here is that giving magnesium by injection reduces the work of these ion pumps, reduces toxic calcium influxing into cells and therefore may well reduce nerve damage further. Therefore, this explains why magnesium injections are sometimes very helpful in patients with neurological degenerations. They can be given in a similar way to the B12 by daily subcutaneous injections.

6. The brain is largely made up of fats. It is enormously demanding of energy and it needs fats to deliver energy as well as requiring fats as an energy source - see Brain fog - poor memory, difficulty thinking clearly etc. Our present infatuation with low fat diets, low cholesterol and statins are, I believe, fueling the current epidemic of degerative brain disorders. A high fat diet is a vital part of improving brain function and Phospholipid exchange a sucessful therapy. Eat a high fat diet.

Particular problems have particular triggers

BSE - Mark Purdey's convincing theory on BSE taught me a huge amount about prion disorders generally. He makes a compelling case for BSE being initiated in the brain of the cow by the cumulative action of toxins such as organophosphate pesticides and manganese. These toxins are made more toxic where there is a copper deficiency. He also suggets that infrasound may be an additional trigger and the epidemiology fits! I do recommend his book "Animal Pharm". See Mark Purdey Wikipedia Entry and its related links to his many published medical papers, and Link for Animal Pharm Sadly Mark Purdey died of a brain tumour, aged 52, in 2006 - see The Guardian Obit - Mark Purdey

CJD - this may be acquired in the same way - ie the cumulative action of toxins such as organophosphate pesticides and manganese. Since prions once created become infectious in their own right, it is also possible that it is acquired when material from cows is injected into humans (many vaccinations were made from cows - not something the vegetarians were told). I think it is highly unlikely that CJD is acquired though eating beef.

Alzheimer's - poisoning by mercury and aluminium and possibly other heavy metals or chemicals.

Parkinson's - poisoning by pesticides (high incidence of Parkinson's in agriculture and horticultural workers) and manganese (manganese miners get PD) and probably other toxins (some drugs cause PD).

Multi system atrophy (MSA) - I have one patient with MSA possibly triggered by organophosphate exposure.

Drug therapy of PD.

In PD the substantia nigra (the black stuff) in the ascending reticular formation of the brain stem fails to produce adequate dopamine. It is the balance between dopamine and acetylcholine that keeps us normal. An imbalance results in the many symptoms of PD such as muscle stiffness, tremor, mask-like face, slow reactions, a tripping gait and, in advanced cases, dementia. The idea of drug therapy is either to increase the level of dopamine in the brain, or to reduce the level of acetylcholine and so correct the balance. There is no doubt that in the short term the dopamine agonists (such as L-dopa) work. However, they only work for a certain length of time. In the longer term they stop working and the clinical situation becomes unstable with so-called on-off effects. I'm suspicious that taking dopamine agonists accelerates the progression of PD because it makes the cells of the substantia nigra lazy and switches off endogenous dopamine production. My view is to postpone use of these drugs for a long as clinically possible.

Specific causes of Motor neurone disease

Motor neurone disease - poisoning by plant toxins (cycad) is a known cause. The cycad seed is consumed on the Island of Guam and caused motor neurone disease which killed 10% of its inhabitants. See The Emerging Science of BMAA (β-methylamino-ʟ-alanine ): Do Cyanobacteria Contribute to Neurodegenerative Disease? which, among other fascinating observations, states that:

The trail of clues began soon after U.S. forces recaptured Guam from the Japanese in 1944. A Navy neurologist noticed the Chamorro people succumbed to a strange neurodegenerative illness that caused paralysis, shaking, and dementia at 50–100 times the incidence of ALS worldwide.

I have two patients for whom I suspect aspartame was the cause - both had done massive slimming regimes involving high intakes of aspartame. Having said that, acute weight loss would also mobilise toxins from fat and cause an acute poisoning.

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