Following our recent visit to the US, and The Buck Institute, we at Cytoplan are excited to announce a collaboration with Professor Bredesen – and The Bredesen Protocol™ – to help bring his work surrounding Alzheimer’s to the UK. The Bredesen Protocol™, a multi-factorial lifestyle and nutrition based approach to treating, and reversing, early onset Alzheimer’s, has so far successfully reversed Alzheimer’s symptoms in 90% of 110 people.
In this week’s blog we look at The Bredesen Protocol™ in more depth, the scale of the concern surrounding Alzheimer’s disease and the failings of monotherapy.
Reversal of cognitive decline – Diet and lifestyle intervention
From the moment we first saw publication of Professor Bredesen’s research paper ‘Reversal of cognitive Decline; a novel therapeutic programme’ in October 2014, and realised the programme involved almost exclusively diet and lifestyle intervention, it was something that excited us greatly.
Why? – because for 25 years we (at Cytoplan) have promoted a philosophy that diet and lifestyle errors are at the heart of most chronic diseases, and conversely if we can adopt a diet and lifestyle that gives our genes the nourishment and environment they need for health, most chronic diseases would no longer be.
It was particularly exciting to see Professor Bredesen’s work demonstrate that a disease such as Alzheimer’s – which is presently viewed as one which cannot be treated, prevented or reversed and is inciting such widespread fear among the population – is indeed not omnipotent and in fact is far more dynamic than popular medical opinion leads us to believe.
Cytoplan are in collaboration with Professor Bredesen and MPI Cognition, and he visited teh UK in 2016 to provide a talk surrounding the ongoing work of MPI Cognition and The Bredesen Protocol™.
Alzheimer’s disease – The Scale of the Problem
Alzheimer’s disease is reaching epidemic proportions and has ‘touched’ most of us through friends and family who suffer, or have died, from the disease. It is a growing problem that has recently been brought to the fore by many world leaders.
30 million people are affected globally (likely to be 160 million by 2050); it is the 3rd leading cause of death in USA and the leading cause of death for women in England and Wales (2nd for men).
The Failure of Drugs & Monotherapy
Drug therapy and monotherapies (single agent drug therapy) for neurodegenerative diseases have failed, hundreds of £millions have been spent worldwide on drugs research and there is presently no effective treatment for Alzheimer’s disease as a result.
This failure is perhaps best explained by recent genetic and biochemical research, which has revealed an extensive network of molecular interactions involved in the pathogenesis of Alzheimer’s disease. Hence a network approach, rather than a single target drug approach, is likely to be more appropriate.
Dozens of biological mechanisms need to be brought into a state where they are enhancing a person’s cognitive health. There is a not a single therapy that exerts anything beyond a marginal, unsustained, symptomatic effect with little or no effect on disease progression. Complexity is therefore the main obstacle with Alzheimer’s disease and the people who have this condition.
Professor Bredesen likens this to a roof with many holes. Monotherapy (single agent drug therapy) plugs just one of these holes and one needs to plug a good number of the holes to have any chance of improving the condition. This latter approach utilised in the Bredesen Protocol™ programme equates to a multiple therapeutic approach, identifying and addressing the areas of imbalance.
Professor Bredesen hypothesises that Alzheimer’s disease, considered by much of medical science to be a single disease, actually consists of three distinct sub-types:
- Inflammatory – in which markers such as C-reactive protein and serum albumin to globulin ratios are increased. These people have biomarkers of systemic inflammation.
- Non-inflammatory – in which these markers are not increased but other metabolic abnormalities are present. This sub-type is known as ‘cold alzheimer’s’ and is often associated with low levels of vitamin D and high homocysteine.
- Cortical/distinctly different – affects mainly young individuals and appears more widely distributed across the brain than the other subtypes of Alzheimer’s. Sufferers of this sub-type are always deficient in zinc – often toxic.
Enter The Bredesen Protocol™
Recently the first success in reversing cognitive decline in early Alzheimer’s disease and its precursors, [Mild Cognitive Impairment] MCI and [Subjective Cognitive Impairment] SCI, was reported (Impact Aging, Bredesen 2014). This published study reported the initial 10 patients treated with a novel, therapeutic approach called The Bredesen Protocol™.
“Of the first ten patients tested, nine showed subjective or objective improvement. These included people with memory loss associated with Alzheimer’s disease and/or varying degrees of cognitive impairment. All six patients who had given up or severely limited work, returned to work or were able to work without difficulty.
And now over 100 patients have been treated, with unprecedented results. A clinical trial is planned in the USA and UK.“
What is the Bredesen Protocol™?
The Bredesen Protocol™ targets the multiple underlying causes of Alzheimer’s disease, with a goal to improve cognitive function. The list below outlines the targets of the programme and the physiological biomarkers that it aims to change to improve cognition.
It simultaneously addresses:
- Insoluble and soluble beta-amyloid
- Tau and tau tangles
- Metabolic issues
- Insufficiency of trophic factors
- Hormone imbalance
- Gut health
- Genetic errors
- Nutrient deficiencies
- Cognitive stimulation
- Lifestyle factors that contribute to the pathology such as poor sleep; stress; lack of exercise; poor diet high in sugar
The same programme can be used by healthy individuals wanting to prevent Alzheimer’s disease and, as Professor Bredesen discovered, it seems to be a protocol that will optimise every area of health.
This is no surprise, really, because it comprises all areas of diet and lifestyle that the human genome needs for optimal health.
Most of the chronic diseases we see today are caused by a mismatch in the diet and lifestyle our genes need for health and the one in which we choose to adopt. We are effectively “fish out of water.”
This situation can only really be remedied by understanding and meeting our genetic needs within our current environment – which is exactly what The Bredesen Protocol™ achieves.
Moreover it permits for individualisation. We humans are all genetically different in the same way as we look different on the outside. We know that “one man’s meat is another man’s poison,” and this exists because variations in genes that impact on metabolic processes dictate this.
For example, some people can drink large quantities of alcohol and recover well whilst others experience long-term effects from very small quantities. In the main this is due to differences in genetic detoxification and methylation pathways.
The science-based conclusions of Professor Bredesen in respect of Alzheimer’s disease include:
- Monotherapy has never worked because Alzheimer’s disease is a condition of multiple aetiology affecting multiple pathogenetic and signalling pathways.
- Alzheimer’s disease involves multiple patho-aetiology that is influenced by both intrinsic and extrinsic factors.
- Alzheimer’s disease is wholly preventable and modifiable up until the late stages of disease.
- Nutrition and lifestyle components are at the heart of the Bredesen Protocol™.
- Inflammation drives metabolism dysfunction. Metabolic dysfunction is at the heart of Alzheimer’s disease.
The Bredesen™ Protocol™ & Cytoplan
Since the publication of Professor Bredesen’s paper on the subject of reversal of cognitive decline using the ‘MEND’ programme (‘metabolic enhancement for neurodegeneration’, now termed ‘The Bredesen Protocol™’), and his subsequent talk in the UK (March 2015), Cytoplan has been in close contact with Professor Bredesen and his team to try and bring the protocol and research to the UK.
Following our recent visit to the US, and the Buck Institute, we are excited to bring you the news that Professor Bredesen will be in England this September, and that he will be giving a talk on behalf of Cytoplan Education on September 8th.
Clinical trials are planned for the US and UK, and health practitioners and their patients are being sought to collaborate on this project.
The most important thing to come out of Professor Bredesen’s research is that Alzheimer’s disease is not an omnipotent neurological disorder over which we have no control, but a metabolic disease which is wholly within our control. This is true right up to the late stages of the disease – which is another factor that underpins the importance of early diagnosis.
With this knowledge we can all be self-empowered about our health, not only for Alzheimer’s disease, but for many other chronic diseases too, as similarities have been identified between the disease process in Alzheimer’s disease and other diseases, such as Cancer, Osteoporosis, Atherosclerosis and Parkinson’s.
Professor Dale Bredesen
A neurologist and Director, Easton Laboratories for Neurodegenerative Disease Research at UCLA, Professor Bredesen trained with Nobel laureate Prof. Stanley Prusiner, and has published over 200 papers focused on the mechanisms and treatment of neurodegenerative disease. He is the founding President of the Buck Institute for Research on Aging in California.
Professor Bredesen has spent over 30 years researching the treatment and prevention of Alzheimer’s disease and is an acknowledged leader in the field of Alzheimer’s research, utilizing therapeutics rather than outmoded mono-therapeutics.
If you have any questions regarding the health topics raised in this article then please do get in touch via phone (01684 310099) or e-mail (firstname.lastname@example.org)
Amanda Williams & The Cytoplan Editorial Team: Joseph Forsyth, Clare Daley and Simon Holdcroft
Last updated on 1st June 2018 by cytoffice