Neuroinflammation and Alzheimer’s Disease
Most of us know someone who has been diagnosed with Alzheimer’s, but how many of us know that research is now categorising it as a ‘disease of civilisation’ – i.e. caused by our modern diet and lifestyle?
Alzheimer’s disease is a specific form of dementia that affects the parts of the brain that control thought, memory, and language. It is the most common cause of dementia and progresses through stages. It’s clearly not an inevitable consequence of old age as 50% of over 85’s show no signs of it. There can be a genetic component, but identical twin studies have proven that having the genes does not make getting the disease inevitable. So what makes one of the twins develop it, and not the other?
It turns out environmental factors that a person has been exposed to during their lifetime, can cause these genetic mutations to express, and diet is now considered to be the most significant, influencing environmental factor of them all, which surely means we can influence and reduce our risk, by our lifestyle and dietary choices.
There is an association between Alzheimer’s disease and type 2-diabetes. Local inflammation and a build up of Amyloid-type plaques occurs in both diseases, and is associated with chronic bacterial infections like periodontitis (gum disease), Borellia (Lyme disease), and H. Pylori (reflux and gastritis). These bacteria tend to be very persistent, evading our immune systems, and once in the blood stream can cross the blood brain barrier, as they have been found in the Amyloid plaques of Alzheimer’s.
Amyloid’s role is normally protective – it is an antimicrobial peptide, and it is effective against E.Coli, Candida, and Streptococcus, but when a bacterial infection is persistent, stealthy and chronic, the resulting amyloid ‘defences’ can build up and become a problem themselves.
The gut may have a contributory part to play here too, as it plays host to vast colonies of microflora, both commensal, beneficial and pathogenic. Many things can cause the gut to become transiently ‘leaky’, or chronically hyper-permeable, allowing bacteria and their toxic byproducts to enter systemic circulation. Once across the blood-brain-barrier they can trigger neuroinflammation.
Where there is immune activation against pathogens, there is always inflammation, and research is looking at the role played by our glial cells – the brain’s immune cells – tasked with editing, pruning and clearing out the brain’s debris at the end of the day. They are our first line of cellular defence against invading pathogens, but when activated, they produce inflammatory cytokines, that invariably cause a certain amount of collateral damage. Studies in the 1990s showed that these glial cells are highly engaged in the formation of Amyloid plaques in the brain’s of Alzheimer’s patients.
So I eagerly anticipated the September 2016 conference: “Why NUTRITION is the key to Alzheimer’s” having just read the extraordinary results of some research led by Professor Dale Bredesen MD, of UCLA who would be presenting, and has spent 30 years researching the treatment and prevention of Alzheimer’s.
At the conference he shared the scientific basis of his hypothesis as well as the unprecedented clinical results demonstrated by a series of case studies using ‘The Bredesen Protocol’, a multi-factorial, lifestyle and nutrition based approach to treating and reversing early stage Alzheimer’s symptoms. His first pilot study involved just 10 cases, but his second – a clinical trial with 110 subjects – all with early stage Alzheimer’s, resulted in more than 90% of them having their symptoms reversed. To date, no drug has come anywhere near this.
“cognition does not exist in isolation”
These results have been questioned by the detractors of nutrition-based therapy, who wonder if Professor Bredesan might be presenting his ‘best cases’, cherry picked from a larger cohort, how else to explain such extraordinary results? One can sympathise to an extent with such cynics, because to date, there is no pharmaceutical cure for even the early stages of the disease. Drugs currently slow disease progression, but none, not one, reverses or cures it. My response to such detractors, were it to be a case of cherry picking, and there’s no suggestion that he has, is that Professor Bredesan has still shown nutrition and lifestyle interventions are capable of reversing signs and symptoms in some cases. Oh – and without any side effects of course.
The key finding of his research is that ‘cognition does not exist in isolation‘. Whereas mainstream medicine a long time ago compartmentalised into organ specialisms, the neurologist would rarely confer with a dermatologist, or the cardiologist, or the gastroenterologist, and the psychiatrist was out on a very isolated branch. Which is a shame, because it turns out ‘cognition’ and ‘metabolism’ actually go hand in hand, so by focussing on the patient as a whole entity, rather than a set of isolated cognitive symptoms, and looking upstream at possible causation, rather than focussing on symptom suppression, Bredesen has achieved some remarkable results.
He likens the disease to having a roof with 36 holes in it, and patients do invariably present with multiple metabolic disturbances alongside the cognitive impairment. So to date, mono-therapy drugs are failing because in reality they need to have dozens of therapeutic routes in their sights, to plug all the different causative holes. If a variety of lifestyle factors conspire to ultimately produce those holes in the roof (resulting in brain degeneration), then it makes sense that multiple lifestyle interventions might be needed to plug those holes, and halt disease progression.
Bredesen’s approach involves many of the old familiar lifestyle enhancements, better sleep, the consumption of healthy dietary fat with less carbohydrate consumption – for improved blood glucose control, stress reduction, exercise to improve insulin sensitivity, management of homocysteine levels, optimising vitamin D3 and the supplementation of other critical nutrients if testing reveals insufficiencies. It also involves investigations of tissue toxicity, genetic errors, soluble/insoluble beta-amyloid, tau tangles, hormone imbalance and inflammation. But crucially, the application of any intervention depends on an individual’s assessment of need, which is based on their own particular habits/dietary shortfalls and test results, so this is not a one size fits all protocol.
The detractors to this holistic approach would prefer to see large, randomised, double-blind, placebo controlled trials – before they will even consider the worth of such a new approach. Such trials work well to test the efficacy of a single drug on a single biomarker, in a controlled setting, but are not best suited to test something as broad and varied as diet and lifestyle factors on what is crucially a multifactorial pathology. And it is the multiplicity of both the causes of the disease and the lifestyle interventions required that is key.
Nutrition science is still viewed as the new kid on the block, but some of the most potent modifiers of systemic and neurological inflammation, including insulin resistance, are dietary, nutritional and lifestyle factors. This much is a proven fact. Evidence from clinical intervention case studies, of the sort conducted by Professor Bredesen, is building and needs recognition as being far better suited to test multifactorial conditions resulting from a multitude of causes.
This is the Functional Medicine model as taught to Nutritional Therapists and endorsement by Dr Rangan Chatterjee of the BBC ‘Doctor in the House’ series and the cardiologist Dr Aseem Malhotra is to be welcomed. They both advocate the use of lifestyle and nutritional interventions in the management of health and chronic disease. Dr Chatterjee will be the lead clinician for the Bredesen Protocol in the UK in collaboration with Cytoplan.
See also ‘The Over-medicated Population’: “Doctors are misinformed, patients are misled and millions of people are taking medication with no benefit for them.” http://bit.ly/2dhCHQz
References
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Bulgaria H et al., (2014) Microbial involvement in Alzheimer disease development and progression. Molecular Neurodegeneration vol 15 (42)
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Bredesen D (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6(9):707-717
