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© Copyright Paul Clayton and
Accelerated Learning Systems Ltd |
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Purchase your own copy of Dr Clayton’s Health
Defence now
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Alzheimer’s |
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Dementia / 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 780,000 people with dementia in the UK, rising to 870,000 by 2010 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! |
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The importance of phospholipids |
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A brain cell – or neuron looks like this. You have about 100 billion of them! 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. |
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The outer membrane of each axon is made up of phospholipids that can be visualised like this.
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Phospholipids are constantly been lost (catabolic action) and repaired (anabolic action) – in the same way as all other cells in the body. |
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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.
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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.
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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. | | |
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