For many years, scientists have believed that Alzheimer’s disease (AD) is passed through the family line and is genetic due to the possession of a particular gene called Apo E. Through our research, we have clearly demonstrated this cannot be the case.
If AD was purely genetic, we would expect four natural consequences to be true:
1. Global Distribution of Alzheimer’s disease.
Given that the Apo E gene is found in people all over the world, we would expect AD to have a random and uniform distribution pattern – i.e. to see the same incidences of the disease in countries in Europe as in South America. However, this is not the case; there are clear patterns of this disease across the globe.
In fact, in some areas of the world, there are really low incidences of AD, like in Maracaibo, Venezuela where there has only been one case of AD was found in a decade. Maracaibo has an AD mortality rate of 1 per 10,000,000 per year. Conversely, in Norway, AD is diagnosed in 6 - 109 per 100,000 women and 4 - 55 per 100,000 men every year, ranking Norway as having the highest incidence of this disease. Therefore, AD is thousands of times more common in parts of Norway than in Maracaibo, Venezuela.
2. Earlier and rapidly increasing onset of Alzheimer’s disease.
Human genes do not change quickly, they remain constant over long periods of time which means that if AD was genetic we would not expect to see fast increasing incidences of the disease in younger people.
However, the opposite is true, we are seeing the rates of AD increasing faster than the population is aging (almost to epidemic proportions), particularly in the USA, Canada, England, Norway and Australia. We often hear the term ‘early onset Alzheimer’s’ which must mean other factors are causing the disease, rather than genes.
3. Migration would not alter incidence.
If AD was genetic, migration would not alter the incidence of the disease. However, the evidence supports the opposite as being true, e.g. Japanese Americans who leave Japan and move to the US have far higher prevalence rates than Japanese remaining in Japan; and we see double the incidence of AD in African Americans (i.e. Nigerians) than seen in Nigerians remaining in Nigeria.
4. Changes in diet would have no Impact.
There are two documented cases of AD patients, who fully recovered by significantly altering their diets. This is obviously anecdotal evidence, however it is interesting as it opens an opportunity for further study. A Russian scientist at the III World Congress on Vitamin C in 2001, presented further interesting results from a clinical study on a significant sample of elderly people in Moscow who had recently suffered memory loss. Memory loss was reversed after several months of a specific nutrient protocol taken daily by the patients.
In conclusion, Foster Health’s research deduced that an individual’s geographic location, lifestyle, diet and exposure to specific environmental factors are the principle ‘root causes’ of AD and dementia. Our work has examined, in depth, the foods and environmental toxins which appear to be causative factors of AD. We have also investigated the key nutrients which in combination with a specific diet are protective and can alleviate the symptoms of AD and other forms of dementia.
From this exhaustive research we have designed a nutrient supplement, Neuron Plus which has been shown in clinical practice to improve memory and cognitive function in patients with Alzheimer’s disease. We are now sourcing physicians and research institutions to develop a double-blind, controlled clinical trial for Neuron Plus. If you are interested, please contact us.