In November last year, new figures from the Office for National Statistics showed that dementia is now the leading cause of death in England and Wales, replacing ischaemic heart disease. It is the leading cause for women and overall, heart disease remains the leading cause for men.
There isn’t a week that passes where Alzheimer’s or dementia is not in the news – a new drug offers hope, a new drug has failed, a well loved celebrity has the disease, a therapy has shown promise. Nevertheless, although over 244 drugs have been approved for dementia, they have failed to make any real, lasting difference, other than perhaps some short term symptom improvement.
On the other hand, work in the United States is showing promising results – Professor Bredesen who has spent his life in Alzheimer’s research has developed The Bredesen ProtocolTM with which he has, so far, reversed symptoms of Alzheimer’s in more than 90% of his patients. Cytoplan’s Technical Director Amanda Williams read Professor Bredesen’s landmark 2014 paper “Reversal of Cognitive Decline: A novel therapeutic program” and saw him speak in London in 2015. Since then, Amanda and Cytoplan have been working to bring his work to the UK through a number of projects. This blog focusses on one of the projects we have launched – the Action Against Alzheimer’s programme.
What is The Bredesen Protocol™?
Professor Bredesen likens Alzheimer’s pathology to a ‘roof with many holes’. There are dozens of biological mechanisms that need to be optimised (brought into balance) in order to return a person to health. Monotherapy (single agent drug therapy) plugs just one of these holes, however, 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™ equates to a multiple therapeutic approach, identifying and addressing the areas of imbalance.
The Bredesen Protocol™ is a programme that is used by Doctors in a clinical setting. The programme diagnostics rely on input from numerous blood and other tests (including scans) for input into a software algorithm from which patient programmes are produced. You can find more information in our previous blog on The Bredesen Protocol™.
The protocol uses a functional medicine approach that aims to identify the root causes of the disease. Functional Medicine recognises that whilst two individuals may have the same disease and pathology, the underlying causes may be different. Functional medicine asks “why has this person got this disease”? and looks for clues in their current and past environment, diet, lifestyle, medical history and family history.
What is the Action Against Alzheimer’s Programme?
Whilst Alzheimer’s and dementia may be diagnosed in our 70’s or 80’s, the processes that eventually result in dementia occur much earlier – in our 30’s, 40’s, 50’s, and 60’s. The Action Against Alzheimer’s Programme is for people BEFORE they develop dementia; it is an upstream workshop programme based on the diet and lifestyle elements of the Bredesen Protocol™. The Action Against Alzheimer’s programme is being delivered by Cytoplan Licensed Nutritional Therapists to small groups of the general public through a series of 8 workshops.
The workshops are designed to help people engage with each aspect of the programme and understand what they need to do to optimise cognitive function, thus the workshops cover: Nutrition, Gut Health, Stress, Sleep; Exercise & Brain Training. A homestudy module – the Self Care Journey – runs alongside the workshops and is designed to support the change process.
Nutrition is at the heart of the programme
The links between nutrition and brain health are many and include:
- B vitamins which are needed for methylation and homocysteine reduction; in particular vitamins B6, B12 and methylfolate. Methylation reactions are needed for the production and metabolism of brain neurotransmitters important for memory and mood. In addition, if the methionine cycle is properly supported then homocysteine levels will be kept low. High homocysteine is a risk factor for dementia.
- Vitamin A – concentrations of vitamin A have been reported as lower in cerebrospinal fluid and plasma of Alzheimer’s patients. In vitro studies have demonstrated vitamin A inhibits the formation and extension of beta-amyloid fibrils. Vitamin A’s role in maintenance of mucous membranes is also important as this helps maintain integrity of the gut lining which is important for reducing inflammation. Inflammatory mediators, as a result of leaky gut, have the potential to cross the blood-brain barrier and activate immune cells in the brain. Neuroinflammation is a risk factor for the development of Alzheimer’s (and other neurodegenerative diseases).
- Vitamin D receptors are widely expressed in the brain and evidence has linked serum vitamin D deficiency to cognitive impairment and dementia. In vitro studies show that vitamin D can stimulate the clearance of amyloid plaques. Vitamin D also reduces amyloid-induced cytotoxicity, apoptosis (cell death), and inflammatory responses in neurons.
- Magnesium is an enzyme cofactor for more than 300 enzymes. In the brain it acts as a modulator of synaptic plasticity. Plasticity refers to the ability of tissue to strengthen and weaken and change shape according to need and the signals/nourishment it receives. Magnesium’s roles in energy (ie ATP) synthesis and insulin signalling are also important in the brain.
- Zinc deficiency has been shown to affect neurogenesis and increase neuronal apoptosis (cell death) which can lead to learning and memory deficits.
- Essential fatty acids – the brain is 60% fat, so adequate healthy dietary fats are important, including omega-3 fatty acids – both EPA and DHA. DHA is the predominant omega-3 found in the brain and is important for neurotransmission and neurogenesis, synaptic plasticity and neuroinflammation. Blood levels of DHA have been inversely correlated to mild cognitive impairment and dementia.
- Antioxidants – the brain is particularly susceptible to oxidative stress and due to its high metabolic rate produces a high load of free radicals; this is coupled with the fact the brain’s natural antioxidant capacity declines with age. Oxidative stress and inflammation are key factors that can contribute to cognitive decline.
- A low glycaemic load diet in order to prevent the development of insulin resistance. The brain can become insulin resistant 20 years before the rest of the body – this has a number of effects – for example, brain cells can become starved of fuel because glucose cannot effectively enter cells and high brain glucose levels result in the production of Advanced Glycation End Products (AGEs) which cause damage to lipids and proteins within cell membranes.
- In addition to the above, there are many specific nutrients from diet and supplements that are being researched and used to support brain health including curcumin, glutathione, resveratrol and others.
Gut Health –There is a link via several mechanisms between gut health and brain health. One mechanism is through the gut barrier function. Compromised gut barrier function, or ‘leaky gut’, may underpin the chronic low grade inflammation observed in many disorders. The gut microbiota can modulate brain development, function and behaviour by immune, hormonal and neural pathways. Endotoxins (eg LPS) that derive from certain gut bacteria are often found in the plaque lesions characteristic of Alzheimer’s. Animal studies have shown that increased LPS is linked to cognitive dysfunction and elevated levels of inflammatory cytokines and beta-amyloid in the hippocampus. Certain species of gut bacteria can increase Brain Derived Neurotrophic Factor and the brain neurotransmitter GABA (a calming ‘brain chemical’).
Stress – persistently high levels of the stress hormone cortisol can cause death of brain cells. Stress also affects brain function through other mechanisms including its effects on raising blood sugar which over time can lead to insulin resistance.
Sleep – sleep is when beta-amyloid plaque, one of the proteins responsible for blocking cell communication etc in Alzheimer’s, is cleared from the brain. Melatonin, the hormone released prior to and during sleep, upregulates antioxidant enzymes and helps break down beta-amyloid plaques, inhibits tau tangles from forming and helps promote Brain Derived Neurotrophic Factor. Poor sleep can also result in insulin resistance.
Exercise – upregulates and synchronises metabolic and catabolic processes. Research has shown that physical activity reduces hippocampal atrophy in the elderly and helps maintain cognitive function. The mechanism for this is less well understood but exercise reduces neuro-inflammation and aids the release of BDNF, which promotes growth and regeneration of new nerve cells. Exercise increases insulin sensitivity, increases blood flow to the brain (and thus the delivery of oxygen and nutrients) and reduces plaque formation.
Brain Training – Challenging and stretching the brain allows new connections to be created and maintained. It maintains brain plasticity – this refers to the brain’s lifelong capacity for physical and functional change. The adult brain continuously adapts to relevant sensory stimuli so activities which challenge all the senses will help maintain positive plasticity and processing speed.
The Self Care Journey – This runs alongside the workshop programme and includes a series of practical activities and exercises to be carried out at home. The activities will help workshop participants understand their goals, barriers to change, limiting beliefs, behaviours and motivation and will support people’s capacity to make sustainable changes to their diet and lifestyle.
Become a Licensed Action Against Alzheimer’s Nutritional Therapist
Cytoplan has produced all workshop and support materials needed to deliver the Action Against Alzheimer’s workshop programme including powerpoint presentations, speakers notes and handouts and is looking for self-employed nutritional therapists to become Licensed Action Against Alzheimer’s Practitioners.
We are seeking nutritional therapists with:
- Minimum 2 years’ experience
- CNHC registered
If you are interested in becoming a Cytoplan Licensed Action Against Alzheimer’s Nutritional Therapist, as a first step, you will need to attend our 1-day training – our next training date is 15 February at The Hive in Manchester.
Licensed Action Against Alzheimer’s Nutritional Therapists have access to the workshop materials to run Action Against Alzheimer’s workshops which aim to support people optimise their cognitive health. It is not a licence to work with Alzheimer’s patients using the Bredesen ProtocolTM. To find out more about the training and book please follow this link or email Clare (email@example.com).
Alternatively, if you would like to find a Licensed Action Against Alzheimer’s practitioner near you, then please contact me, Clare@Cytoplan.co.uk and I will send you details when we have someone in your area.
CoQ10 Multi – Our most comprehensive Wholefood Multivitamin and mineral formula available incorporating antioxidant CoQ10, Beta Glucan for immune support, and good all round vitamin & mineral levels including optimal levels of vitamin D3 & vitamin B12. This formula now includes additional phytonutrients and Acerola Cherry rich in vitamin C and flavonoids.
Mixed Tocopherols – Containing the full spectrum of vitamin E as it occurs in nature; alpha, beta, delta, gamma tocopherol and alpha, beta, delta, gamma tocotrienol.
R-Omega – R-Omega is a phospholipid rich DHA and EPA omega 3 supplement from herring roe. The DHA and EPA from herring roe is highly bio-available and has shown to be three times more bio-effective compared to standard fish oils.
Liposomal Glutathione – A powerful antioxidant formula designed to help protect cells from free radicals and delay the signs of aging. Comprising; N-Acetyl L Carnitine, Alpha Lipoic Acid, Gingko Biloba, Rosemary Leaf Extract, Liposomal Glutathione and Resveratrol.
For our full range of Supplements to support The Bredesen Protocol please request our new catalogue by contacting firstname.lastname@example.org or by calling our team on 01684 310099
If you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Clare) by phone or email at any time.
email@example.com, 01684 310099
The Cytoplan editorial team: Clare Daley and Joseph Forsyth.
Bannerjee A et al (2015) – Vitamin D and Alzheimer’s Disease: Neurocognition to Therapeutics. International Journal of Alzheimer’s Disease, 1-11.
Bitra V R et al (2015) – Prediabetes and Alzheimer’s Disease. Indian J Pharm Sci, 77, 5, 511-514
Bredesen D et al (2014) – Reversal of Cognitive Decline, A novel therapeutic program. Ageing, 6, 1-11.
Cassani B et al (2012) – Vitamin A and immune regulation: role of retinoic acid in gut-associated dendritic cell education, immune protection and tolerance. Molecular aspects of medicine, 33, 1, 63-76.
Cunningham C & Hennessy E (2015) – Co-morbidity and systemic inflammation as drivers of cognitive decline: new experimental models adopting a broader paradigm in dementia research. Alzheimer’s research and therapy, 7(1), 33.
Haan M N et al (2007) – Homocysteine, B vitamins and incidence of dementia and cognitive impairment: results from the Sacramento Area Latino Study on Aging. Am J Clin Nutr, 85, 511-7
Kelly et al (2015) – Breaking down the barriers the gut microbiome, intestinal permeability and stress related psychiatric disorders, 14, 9, 392. Front Cell Neurosci, 9, 392
Musiek E S et al (2015) – Sleep, circadian rhythms and the pathogenesis of Alzheimer’s Disease. Exp Mol Med, 3, e148.
Noble E et al (2011) – The Lighter side of BDNF. Am J Phsiol Regul Integr Comp Physiol, 300, 5, R1053-R1069.
Ono K & Yamada M (2012) – Vitamin A and Alzheimer’s disease. Geriatrics and Gerontology International, 12, 2, 180-8
Slutsy I et al (2010) – Enhancement of learning and memory by elevating brain magnesium. Neuron, 65, 165-177
Szewczyk B (2013) – Zinc homeostasis and neurodegenerative disorders. Front Aging Neurosi, 5, 33
Vyas S et al (2016) – Chronic stress and glucocorticoids: from neuronal plasticity to neurodegeneration. Neural Plast.
Weiser M J et al (2016) – Docosahexaenoic acid correlates with cognitive impairment in Alzheimer’s disease. PLoS One, 5, 9
Wilson R S et al (2013) – Life-span cognitive activity, neuropathologic burden and cognitive ageing. Neurology, 81, 4, 314-21.
Zhu B et al (2014) – Chronic lipopolysaccharide exposure induces cognitive dysfunction without affecting BDNF expression in the rat hippocampus. Exp Ther Med, 7, 3, 750-54