Alzheimer’s disease (AD) is a poorly understood, progressive neurological condition that affects approximately 30 million people worldwide. It can be seen to be a disease of modern civilization, and while conventional thinking labels it as irreversible, recent research suggests that with the right approach, this may not be the case.
AD is also one of most feared diseases, and rightly so, with a very low success rate of conventional medication in controlling the condition. With growth rates accelerating year on year, it is predicted that there will be 160 million sufferers globally in 2050.
Symptoms of Alzheimer’s disease (AD)
• Getting lost and losing items
• Taking longer to complete daily tasks
• Repeating questions
• Personality and behavioural changes
• Difficulty thinking and understanding
• Difficulty carrying out normal tasks
• Inability to recognise people
• Impulsive behaviour
• Aggression and agitation
• Paranoia, hallucinations and delusions
• Inability to communicate
• Increased time spent sleeping
• Groaning and grunting
Genetic susceptibility is thought to play a part in the incidence of AD, in particular the ApoE4 gene, because it impacts on lipid metabolism, lipid absorption, and increases activation of inflammatory processes.
The Bredesen Protocol
While conventional medicine has focused on singular areas of treatment, recent research has shown that the development of AD is complex, involving multiple pathways and biochemical changes. Professor Dale Bredesen, an acknowledged leader in the field of Alzheimer’s research, has developed a multi-factorial approach to AD, called The Bredesen Protocol. It incorporates diet and lifestyle changes individual to the sufferer and their underlying pathologies, and success rates based on small samples have so far been encouraging, with 90% of 110 participants experiencing a reversal in their Alzheimer’s symptoms.
Professor Bredesen states that there has been a lot of work based on amyloid plaques being ‘the cause’ of AD, and pharmacological approaches have focused on getting rid of this plaque. He states, however, that it’s imperative to know what is causing this amyloid plaque in the first place rather that just removing it. Recent research has indicated that amyloid plaque is anti-microbial, suggesting that while the plaque itself is thought to cause harm, its presence may be protective at the same time. Dr Bredesen has categorised AD into three main subtypes, which while complex in nature, can be summarized as follows:
1. Inflammatory – ongoing infections and other causes of systemic inflammation and an increase in inflammatory markers such as C-reactive Protein, ESR and fasting insulin. Amyloid plaque is liberated as part of the antimicrobial protective response.
2. Non-inflammatory – including high homocysteine, low vitamin D, insulin resistance. These are related to a withdrawal of trophic support. The survival of neurons is regulated by trophic factors, and axons that don’t receive enough trophic support die by apoptosis. Neurons produce amyloid as part of their programmatic downsizing when trophic support is unavailable.
3. Cortical – displaying general cortical atrophy. There may be early onset in this subtype despite being ApoE4 negative. Sufferers may experience trouble with simple calculations and also problems with executive functions and organisation. They always appear to be deficient in zinc. There tends to be toxin exposure such as mycotoxins or Lyme disease, and while there can be some crossover with type 1 in terms of inflammation, these sufferers tend to present differently.
There is also an extra subtype – type 1.5, which has been identified to capture those individuals who fall into both types one and two – those with insulin resistance and perhaps glycotoxicity leading to inflammation, as well as a withdrawal of trophic support. Insulin is one of the most important trophic supports for the brain, and those suffering from insulin resistance will be resistant to its protective effects.
As a key part of the protocol, extensive testing is carried out to collect as much data as possible in order to find out what is driving the process in each individual. The results reveal an individual’s subtype, which in turn directs the specific diet, supplement and lifestyle recommendations. The earlier the changes can be made, the better the chances of success.
While the protocol is extensive and highly individualized, it includes:
• Low glycaemic dietary approach including reduction in inflammatory foods like grains
• High intake of antioxidants through diet and supplements
• Overnight fasting
• Stress reduction practices
• Optimal sleep
• Regular exercise
• Brain stimulation
• Supplements to reduce homocysteine such as folate and vitamin B12
• Supplements to reduce inflammation such as curcumin and vitamin D3
• Supplements to optimise mitochondrial function such as CoQ10 and ALA
• Reduced exposure to heavy metals and treatment if necessary
Written by Emma Rushe