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[av_slide_full slide_type=’image’ id=’3689′ video=’http://’ mobile_image=” video_format=” video_ratio=’16:9′ title=’Dr Paul Clayton, Medical Pharmacologist’ custom_title_size=” custom_content_size=” caption_pos=’caption_bottom’ link_apply=” link=’lightbox’ link_target=” button_label=’Click me’ button_color=’light’ link1=’manually,http://’ link_target1=” button_label2=’Click me’ button_color2=’light’ link2=’manually,http://’ link_target2=” font_color=” custom_title=” custom_content=” overlay_opacity=’0.5′ overlay_color=” overlay_pattern=” overlay_custom_pattern=”]
Former President of the Forum on Food and Health at the Royal Society of Medicine
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Dementia including Alzheimer’s Disease
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Dementia is common and becoming more so as our society ages. According to the Alzheimer’s Society, there are about 870,000 people with dementia in the UK, and projected to be 1.8 million by 2050.
These are actually conservative estimates. Obesity and diabetes significantly increase the risk of dementia and Alzheimer’s. If current trends persist, dementia will affect 3 million people by 2050, including 1.5 million cases of Alzheimer’s disease. Quite apart from the personal costs, this is an expensive disease; the annual cost of Alzheimer’s in the UK is already pushing £3 billion.
Given that dementia, Alzheimer’s and the loss of brain cells seem inevitable aspects of the ageing process, these depressing figures seem to loom over all our futures – if we live long enough. But should they?
I think not. Gerontologists now believe that we do not inevitably lose brain cells as we age. There are significant numbers of old and very old people who show no signs of intellectual dimming, and experimental studies have demonstrated that most if not all of the impact of ageing on the brain can be prevented by specific nutritional strategies.
However, before we begin to uncover the secret of retaining mental clarity into your 8th and 9th decades, a little brain biology is essential. There seem to be two quite distinct ways in which we are vulnerable to brain deterioration – the first through the loss of fatty molecules called phospholipids and the second through a protein called beta amyloid and the quaintly named tau tangles!
The importance of phospholipids
You have about 100 billion brain cells (or neurons)! And at the end of each neuron are dendrites – from the Greek for ‘branch’. A thought is an electrical impulse that races down the axon and jumps across to other dendrites on other neurons, via a chemical called a neuro-transmitter, whose function is to temporarily connect them.
Each dendrite is capable of connecting with dozens of other dendrites – which makes the potential number of brain connections virtually limitless.
Maintaining the health and integrity of brain cells is the key to maintaining mental function.
The outer membrane of each axon is made up of phospholipids. Phospholipids are constantly being lost (catabolic action) and repaired (anabolic action) – in the same way as all other cells in the body. Phospholipids are made up of fatty acids, which are vulnerable to oxidation via free radical damage (just as cooking fat is vulnerable to free radical damage i.e. rancidity).
Therefore phospholipid loss is accelerated by oxidation and through the brain’s use of phospholipids for the production of the key neuro-transmitter acetyl-choline.
So to maintain the healthy functioning of brain nerve cells, the rate of repair of the neuron membrane must match the rate of loss. If it doesn’t, brain deterioration takes place.
The only way, therefore, that the rate of repair of phospholipids can keep pace with wear, is if the diet contains the nutritional building blocks for this process. The diet must, equally importantly, contain enough anti-oxidants to slow down the wear caused by oxidation.
Although we will examine them in more detail later, the nutrients that are needed are found in food like eggs, oily fish, and liver which contain the necessary poly-unsaturated fatty acids. Other foods, such as freshwater shrimps, contain methyl group nutrients (such as betaine), which are essential for phospholipid synthesis in the liver.
Under normal circumstances, it is possible to compensate for a lack of phospholipids in the diet by manufacturing them in the liver. But this requires at least 5 co-factors (micro-nutrients like biotin, copper and methyl groups), plus fatty acids like Omega 3. The modern diet tends to be depleted in all of these, impairing our ability to produce phospholipids.
The Amyloid Theory of Alzheimer’s
Anyone who has investigated what is needed to maintain a healthy brain will have come across the term beta amyloid. Here’s how this protein is involved in the development of Alzheimer’s.
1. A protein in the brain called APP (Amyloid Precursor Protein) is cut by enzymes into smaller pieces. Some of these pieces stay outside and others stay inside the brain cell. One of these pieces is beta amyloid.
2. The rate at which beta amyloid is formed is partly dependent on the level of insulin in the body. High insulin increases the rate at which beta amyloid is formed.
3. Beta amyloid is chemically ‘sticky’. This causes it to form into plaques or ‘clumps’ outside the brain cell or neuron.
4. These clumps can trigger inflammation. If this inflammation is not damped down, immune action may kill the brain cell.
5. Inside the brain cell, tangles called tau tangles can form along the axon – the pathway along which nutrients needed by the brain, and the electrical signals of brain activity normally travel – as long as they are not impeded.
6. The tau tangles, however do interfere with this activity and prevent free movement down the axon. So brain function deteriorates.
7. Many of the dangerous effects of beta amyloid appear to arise from oxidation – free radical – action.
This 7-stage explanation of the Amyloid Theory of Alzheimer’s (it is a theory because it has been accepted by many, but not all researchers) leads to a second strategy for preventing, slowing or just possibly even reversing the process of mental deterioration.
A prevention or amelioration strategy
1. Slow down the production of APP in the first place – and there is evidence that green tea may achieve this.
2. Reduce insulin levels and therefore reduce the rate at which beta amyloid is created. A low GI diet achieves this.
3. Block the production of clumps or plaques of beta amyloid – curcuminoids (turmeric) can achieve this.
4. Reduce inflammation at the plaque sites – again curcuminoids, and flavonoids generally, can achieve this.
5. Inhibit the formation of tau tangles. In my book Health Defence I explain why a supplement that includes manganese (combined with copper, selenium and zinc) and high levels of anti-oxidants may achieve this.
6. Finally, the counter to oxidation caused by free radical action, wherever it occurs, are the anti-oxidants. These include Vitamins C and E, the flavonoids in fruits and vegetables, turmeric, and the minerals that help form anti-oxidant enzymes: zinc, selenium, manganese and copper.
Now that we have understood the different ways in which brain cells may deteriorate we can look at the current pharmaceutical approach and contrast it with the nutritional approach. But first two seemingly false starts.
A False Start?: The Acetylcholine Hypothesis
The oldest hypothesis says that Alzheimer’s begins with impaired production of the neuro-transmitter acetylcholine, followed by the progressive death of brain nerve cells.
Almost all drugs currently in use are based on this hypothesis. They are designed to increase levels of acetylcholine in the brain by blocking the enzymes that break down this important neurotransmitter, or by activating acetylcholine receptors directly.
However, the results of these drugs have been profoundly disappointing. They neither halt nor reverse Alzheimer’s disease, and the overall effect – slight and temporary reduction of symptoms in a few cases, combined with huge costs and not infrequent toxicity – has killed this hypothesis stone-dead.
A False Start?: The Tau Hypothesis
“Tau-ists” believe that tau protein abnormalities (tangles) are the prime cause of Alzheimer’s, while “bA-ptists” believe that beta amyloid deposits are the main culprit.
As we have seen, tangled tau proteins inhibit the transportation of compounds inside the nerve cells. This ‘transport blockade’ is known to kill nerve cells in a way that resembles the pattern of cell death in Alzheimer’s, so it seemed possible that this could be the prime cause of the disease.
As a result, the Tau-ists have proposed various methods of reducing the tau tangles in the hope of re-building the nerve cells’ transport systems, and thus keeping the neurones from dying. Some of the methods of tau regeneration involve trace element supplementation with manganese, others involve drugs.
It is fair to say that neither approach has been very effective, and this has left the Tau Hypothesis somewhat faded – although still supported by some.
bA-ptists in the ascendancy
The ‘bA-ptist’ argument is looking stronger at the time of writing due to a series of recent discoveries.
For example, beta amyloid plaque is now known to be directly neuro-toxic, and beta amyloid turnover in Alzheimer’s brain tissue is disturbed in a way that would inevitably lead to senile plaque formation, and thus nerve death.
Furthermore, food-derived compounds such as the curcuminoids (derived from the spice turmeric) block key biochemical steps in the progression of the disease (Sreejayan and Rao ’97), make beta amyloid plaques dissolve, and slow the progression of Alzheimer’s in animal models (Lim et al ’01, Cole at al ’03, Yang et al ‘04).
As supporting evidence, in parts of the world where high levels of these compounds are eaten, the incidence of Alzheimer’s disease is very much lower.
One of the lowest age-adjusted Alzheimer’s rates in the world was recorded in a rural community in northern India. The incidence of Alzheimer’s there was 4.7 per 1000 person-years, compared to 17.5 per 1000 person years in Pennsylvania (Chandra et al ‘01).
This is a huge 73 percent reduction – and it holds out real hope of an even greater risk reduction through dietary and life-style change.
To summarise, the drug-based model of Alzheimer’s treatment has thus far been lamentably unsuccessful because the drugs have been aimed at the wrong target.
As our understanding of the disease develops, however, it has become obvious that there are multiple abnormalities in the dementing brain – yet almost every one of them can be modified by lifestyle and dietary changes. It is highly unlikely that any drug could address all the abnormalities, and highly unlikely that the next generation of drugs will be free of toxicity.
Let us look therefore at an alternative model of treatment.
Risk Factors / Disease Mechanisms in Dementia
It is impossible to design effective risk reduction or treatment programmes for a disease without a detailed understanding of how the disease starts and progresses. We have already looked at the biology – let’s now look for clues by studying risk factors.
Although genetic susceptibility is involved in about 1 in 10 of Alzheimer’s patients, most cases are “sporadic”, ie there is no clear family history, and in these cases environmental factors predominate.
For example, it helps to start with the largest possible number of brain cells; individuals with larger cranial diameters (largely determined by maternal and infant nutrition) have a lower risk of Alzheimer’s than those with smaller heads, presumably because larger brain-cases contain greater spare neuronal capacity. It also helps to look after those brain cells you do have; head injury (which kills brain cells) increases the risk of Alzheimer’s in later life.
Cardiovascular risk factors – diabetes, hypertension, high cholesterol and smoking – in middle age are very strongly associated with later-life dementia (Whitmer et al ’05). But is this cause or association? In other words, do these risk factors themselves injure the brain and drive the disease process of Alzheimer’s? Or are they merely symptoms of a more fundamental set of problems that drive both vascular disease and Alzheimer’s? The answer is likely to be both.
Smoking imposes a high oxidative stress on nerve cells which contributes to their ageing and death. It also damages nutritional status, which harms nerves directly, inflames blood vessels and increases the risk of stroke.
Hypertension, high cholesterol and Type 2 diabetes are largely caused by poor nutrition and poor nutrition undoubtedly causes nerve and blood vessel damage. Hypertension increases the risk of strokes, as does high cholesterol and diabetes; and in patients who have Alzheimer’s, micro-strokes make their condition very much worse (Riley at al ’05).
Diabetes is a strong risk factor for strokes and vascular dementia (Hassing et al ’02), and will therefore exacerbate Alzheimer’s.
To make things even more complicated, insulin is directly involved in brain function. Recent work has found that insulin is both produced and utilised in the brain, where it acts as a vital nerve growth and support factor (Steen et al ’05), and is broken down by the same enzyme that breaks down beta amyloid (see below).
The metabolic changes that occur in diabetes appear to drive the disease process in Alzheimer’s (see above); and because of the insulin connection, leading researchers are increasingly describing Alzheimer’s disease as ‘Type 3 diabetes’ (Steen et al ’05).
This is a tangled web of causes and effects – and it strongly suggests that the best way to avoid dementia is not to rely on drugs, but to stop smoking, lose weight if necessary, take more exercise and eat a better (low GI) diet, which reduces insulin levels.
These are general steps to better health, but there are a number of specific additional nutritional steps that should reduce the risk of dementia even further.
Reducing the risk of vascular dementia caused by stroke
Strokes occur when the blood supply to an area of the brain is disrupted, so that the tissue supplied by that artery dies.
Stoppages affecting the blood supply to the brain can be caused by either the rupture of a blood vessel (haemorrhagic stroke), or by a blockage in a blood vessel (thrombo-embolic stroke).
Haemorrhagic stroke is generally due to hypertension which is in turn largely caused by Endothelial dysfunction (ED). ED is a chronic sub-clinical inflammation of the arteries and/or veins.
Thrombo-embolic stroke is generally a sequel to disturbances in clotting mechanisms, which are largely caused by the same factors that predispose to endothelial dysfunction.
A pharmaco-nutritional programme designed to alleviate endothelial dysfunction, therefore, will do a great deal to reduce the risk of micro-strokes and dementia.
Working from an evidence base of many hundreds of research papers, such a programme should start with a diet rich in fruits and vegetables, containing only low levels of meat and dairy foods. It should also have a low Glycemic Load (ie low in potatoes, baked goods, confectionery and non-diet carbonated beverages).
This should be supplemented with flavonoids, anti-inflammatory agents which target the arteries and are linked to a reduced risk of Alzheimer’s (Borenstein et al ’05); as is folic acid (Seshadri et al ’02, Kruman et al ’02) and probably the other B vitamins B6, B12 and B10, aka betaine.
A broad-spectrum micronutrient support programme is also recommended (see ideal supplement), as are improved food storage and cooking techniques. For a full report on these topics see my books Health Defence and After Atkins.
Reducing the risk of Alzheimer’s Disease
The nutritional approach starts by identifying of as many of the metabolic errors involved in driving the disease as possible. It then assembles a programme of food derivates (vitamins, minerals and phyto-nutrients, ie nutrients derived from fruits and vegetables), designed to rectify as many of the errors as possible. This multiple-agent metabolic support strategy is safe, and likely to be highly effective.
Problem 1 : Beta amyloid formation
Beta amyloid is formed inside the cell when the protein APP, a protein which protects the nerve cell membrane, is broken down by a family of enzymes. One of these enzymes BACE produces beta amyloid, which is then excreted out of the cell.
Solution
Inhibit BACE and therefore reduce the formation of beta amyloid with green tea flavonoids (Jeon et al ’03, Okello et al ’04).
Problem 2 : Toxicity
Accumulation of beta amyloid outside the cells (in plaques) causes neurotoxicity.
Solution
Increase the removal of beta amyloid with curcuminoids.
Problem 3 : Insulin
Insulin and beta amyloid are both broken down by the same enzyme (Insulin-Degrading Enzyme or IDE). Raised levels of insulin increase the rate at which beta amyloid is excreted from the brain cell (Gasparini et al ’01), and prevent it from being broken down.
When less beta amyloid is broken down, more of it accumulates (Watson et al ’03, Watson & Craft ’03, Shiiki et al ’04). This explains why diabetics, with high insulin levels, have an increased risk of Alzheimer’s, although the increased risk of mini-stroke is also involved.
Solution
Reduce the levels of insulin, so that more beta amyloid can be broken down by IDE. This can be achieved using oral anti-diabetic drugs, but lifestyle change is more effective (Knowler et al ’02). This involves changing to a low-GL diet, losing weight if appropriate, and adopting a modest exercise regime
Problem 4 : Plaques
When beta amyloid molecules accumulate outside the cell they may be altered in a way that makes them bind together in clumps, forming plaque.
Solution
The change in beta amyloid molecules which triggers the clumping mechanism is thought to involve stress involving nitrous oxide, but this can be inhibited by curcuminoids (Sreejayan & Rao ’97).
The process of clumping is accelerated by excess copper (Cherny et al ’99) and by excess zinc, which therefore exacerbates Alzheimer’s (Bush et al ’94).
This process can again be blocked with curcuminoids which bind to beta amyloid molecules and prevent them from clumping together (Ono et al ’04, Yang et al ’05). This may in part be due to the curcuminoids’ ability to bind to copper ions (Baum & Ng ’04).
The curcuminoids also appear to have another valuable role: they reportedly increase the rate at which macrophages remove beta amyloid plaque (Yang et al ’05).
Problem 5 : Free radicals from beta amyloid plaque
Beta amyloid that has clumped into plaque is neurotoxic, and a potent generator of free radicals.
Solution
Neutralise the neurotoxicity caused by beta amyloid plaque (Lim et al ’01) through anti-oxidant flavonoids (like curcuminoids), vitamins C and E plus carotenoids which thus counteract the oxidation of blood fats (lipids) (Schroeter et al ’00).
Problem 6 : Local inflammation
Local increase in inflammation (Rogers ’95).
Solution
The curcuminoids and flavonoids in general are potent anti-inflammatory agents (Hong et al ’99).
Additional nutritional protection
Berry flavonoids
The curcuminoids clearly have potent and appropriate anti-Alzheimer’s effects, which help to explain why Alzheimer’s is relatively uncommon in areas where the diet contains large amounts of turmeric.
There is good data to suggest that the closely related flavonoid compounds in berry fruits and other vegetables, may be just as protective.
Strawberry, blueberry and spinach have all been shown to prevent and reverse age-related cognitive decline in mice (Joseph et al ’99, Skrecky ’03), and a high intake of fruit juice appears to be protective in humans also (Borenstein ’05).
Colostrinin
Colostrinin is a highly functional polypeptide derived from cows’ milk. This compound has a series of protective effects that broadly resemble those of the curcuminoids.
It reduces nitrosative stress (Zablocka et al ’05), reduces plaque formation (Schuster at al ’05) and may even accelerate plaque dissolution and removal (Schuster at al ’05).
Colostrinin has been shown to be effective in improving symptoms in Alzheimer’s patients in at least 3 clinical trials (Leszek et al ’99, ’02, Bilikiewicz & Gaus ’04). Interestingly, colostrinin has also been shown to improve learning ability in rats (Popik et al ’99, ’01) via a mechanism which probably also operational in humans.
At least two drug companies are working to develop synthetic drugs which will act in the same way as colostrinin. Colostrinin, as a food derivate, appears to be completely non-toxic. The drugs will almost certainly carry a risk of adverse effects.
NB Colostrinin and curcuminoids / flavonoids may not be a particularly good combination. Colostrinin is rich in the amino acid proline (Janusz et al ’81), and many flavonoids have a high affinity with proline (Baxter at al ’97). There is a distinct possibility that if colostrinin and berry flavonoids are taken together they will bind to each other to form inactive complexes.
I would recommend you chose which route to go – and on balance would probably opt for increased intake of flavonoids and curcuminoids as the latter have proven positive effects on other health issues – including arthritis, cardio-function and hypertension.
Other Risk Factors and Nutritional Solutions
1. Phospholipids
The membranes of all our body’s cells are dynamic ie structural molecules in the membranes are continually being broken down and replaced by new ones. If the rate of loss is balanced by the rate of replacement, membranes remain functional and cells remain viable.
On a poor diet, however, losses increase and the rate of repair falls – ie catabolic rates outstrip anabolic rates. This leads to increasing neuronal malfunction, membrane breakdown and the death of the cell.
Lipids (ie fats) account for 60% of the brain’s dry weight, and the bulk of these are polyunsaturates. As we have seen, the membranes of nerve cells contain (as do all cell membranes) molecules called phospholipids. These molecules contain fatty acids, a high proportion of which are poly-unsaturated. And poly-unsaturated fatty acids are very vulnerable to oxidative stress or oxidation.
To make matters worse, there is a lot of oxygen about, as the brain takes up to a quarter of the body’s oxygen intake, even though it is only 3% of body weight.
This is a recipe for cumulative oxidative damage which, if unchecked, would lead to loss of nerve cell membranes and eventual cell death. This helps to explain why diets high in anti-oxidants are associated with a reduced risk of dementia (Zandi et al ’04).
When phospholipids are destroyed by oxidative stress or any other mechanism, they must be replaced if the cell membrane is not to fail. Replacement phospholipids are either derived from the diet or manufactured in the liver.
Levels of phospholipids in the diet have fallen markedly in the last century, as the main sources of these compounds – crude vegetable oils and offal meats – have largely disappeared from the food chain. Eggs, the other main source, have been stigmatised as sources of salmonella and cholesterol, and as a result egg consumption fell throughout the ’90s.
Under normal circumstances it is possible to compensate for a dietary lack of phospholipids by manufacturing them in the liver. But this requires at least 5 co-factors (micro-nutrients like biotin, copper and methyl groups such as betaine), and fatty acids including the omega 3 polyunsaturates. The modern diet tends to be depleted in all of these, impairing our ability to produce phospholipids.
All this helps to explain why the risk of dementia increases with age. As we age we tend to take in less protective anti-oxidants (from fruits and vegetables) and less of the nutritional building blocks for brain cells.
The solution is to increase flavonoid and anti-oxidant intakes via fruits and vegetables (and a comprehensive supplement) and increase Omega 3 (fish oil) intake and methyl group intake eg betaine.
The proof is that a diet rich in micronutrients is linked to a reduced risk of developing Alzheimer’s, as are increased intakes of the fish oils (Morris et al ’03) which are essential for phospholipid synthesis.
In animal models, supplements containing DHA (one of the fatty acids in fish oil) significantly reduced the development of beta amyloid plaque (Lim et al ’05).
2. Cholesterol
When phospholipids decrease in the neuron membrane, other fatty substances can accumulate there to take their place, including cholesterol, and a by-product of oxidation called ceramide (Cutler et al ’04). High levels of cholesterol impair neuronal function, and high levels of ceramide are neurotoxic (Jarvis & Grant ’98).
The solution is to increase intake of omega 3 polyunsaturates to aid phospholipid replacement and to increase antioxidant intake, such as vitamin C and E and flavonoids, to reduce ceramide production (Cutler et al ’04).
High levels of LDL cholesterol increase the risk of Alzheimer’s, and abnormally high levels of cholesterol are found in specific areas of the brains of Alzheimer’s patients (Cutler et al ’04).
Cholesterol-lowering drugs are reported to give some protection against developing the disease (Wolozin et al 2000), and to improve symptoms in patients with mild to moderate Alzheimer’s (Rockwood et al ’02, Sparks et al ’05).
However, as cholesterol-lowering drugs carry a significant risk of adverse effects, a safer and more natural alternative strategy would be an increased intake of oat-based foods – including porridge! These foodstuffs contain a resistant starch called beta glucan, which lowers LDL cholesterol very effectively (Uusitupa et al ’92, Braaten et al ’94, Behall et al ’97, Nicolosi et al ’99, Bell et al ’99).
3. Mitochondrial decay
As tissue ages, the power-generators of the cell – the mitochondria – start to show signs of progressive damage. They become less able to produce ATP (the cell’s basic energy molecule), and start instead to generate too many free radicals. As this happens the cell becomes damaged and less able to perform its normal functions.
If levels of ATP production fall below a certain point, the cell dies.
This pattern of cellular decay and death undoubtedly affects brain cells and, although not necessarily directly involved in Alzheimer’s disease, anything that impairs brain cell function and viability will exacerbate loss of memory and acuity and bring dementia a little closer.
Work carried out by Professor Bruce Ames has shown that mitochondrial ageing can be partly reversed. Using a combination of acetyl-l-carnitine and alpha lipoic acid, his team demonstrated that mitochondrial efficiency can be improved (Liu Atamna et al ’02, Hagen et al ’02, Liu Killilia Ames ’02, Ames ’04) and energy levels, memory and learning ability improved in tandem (Liu Head et al ’02).
My own work suggests that Coenzyme Q10 and beta carotene are also key nutrients in a defence against mitochondrial decay – to which acetyl-l-carnitine and alpha lipoic acid can be added as they all protect different parts of the mitochondrion and should work well in combination.
Prevention strategy for everyone from age 40
Prevention is always better than cure. There is good evidence that we begin to lose our cognitive ability in early mid-life (Crook et al ’93); and so if you have a particular concern about dementia, or simply prefer to hold on to your intelligence, it does not make much sense to wait until symptoms emerge and the doctor is ready to prescribe anti-Alzheimer’s drugs.
My preference would be to put a neuro-protective programme in place from about the age of 40.
That would include boosting fruit and vegetable intakes, oily fish twice a week and a comprehensive supplement that includes flavonoids, omega 3, Q10, and optimum levels of the vitamins and minerals that are either anti-oxidant in their own right – beta carotene, Vit C, and E, or that are needed to boost the bodies own anti-oxidant defences – like zinc, selenium, manganese and copper.
Treatment as soon as symptoms appear
Increase your intake of:
* Berry fruits – and flavonoids/anti-oxidants from fruits and vegetables generally
* Green tea
* Curcuminoids from turmeric, and to a lesser extent ginger
* Low GI foods
* and finally consider supplementing with acetyl-l-carnitine and alpha lipoic acid
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