October 30, 2012
Alzheimer’s is one of the major medical problems of our age.
A ghastly disease that condemns millions to years of confusion and fear, it also threatens to bankrupt our health system — yet doctors don’t really know what causes it, or how to treat it effectively.
But could that be about to change?
Scientists increasingly believe Alzheimer’s is linked to type 2 diabetes — so closely linked, in fact, it’s even being called ‘brain diabetes’ or type 3 diabetes.
This surprising new theory holds out hope that treatments already available for diabetes may also be able to help dementia sufferers, slowing down or stopping the progression of the disease.
When it comes to type 2 diabetes, there’s no mystery about what’s behind the soaring rates — eating too much, especially junk food that’s packed with sugar, refined carbohydrates and fat.
This leads to damagingly high levels of sugar in the blood and high levels of insulin needed to clear it away.
The rising levels of glucose and insulin affect the blood vessels of the heart and extremities, potentially leading to blindness and amputations.
But it seems raised insulin levels also affect the brain.
Recent research has found this hormone plays a much more important role in the brain than once thought — protecting cells and helping to lay down memories.
The key to diabetes, and very possibly to Alzheimer’s, is insulin resistance.
This is when your body becomes so used to extra insulin in the bloodstream that it needs more and more to have the same effect.
If you constantly eat high glycaemic foods, such as cakes and white bread, this pushes up the amount of sugar in your blood.
Insulin has to work overtime, turning glucose into fat and sweeping it into storage.
The favourite storage areas — fat cells, muscles and the liver — start to reject insulin’s fat deliveries. Gradually, things start to go wrong.
Your body has to keep making more insulin to make the normal store areas respond.
This is turning out to be especially damaging in the brain.
Insulin is so important to the proper function of the brain that it makes its own supplies.
The hormone keeps the brain’s blood vessels healthy and also helps brain cells (neurons) absorb the sugar they need to function.
This allows them to change in response to learning and to lay down memories.
The hormone is also involved in making some of the chemicals that pass messages around the brain.
But if glucose levels keep shooting up after meals, insulin resistance kicks in, and the relationship between neurons and insulin starts to break down — and the brain suffers damage.
For instance, insulin resistance is being linked with formation of the plaques — deposits of damaged protein — that are a classic sign of Alzheimer’s.
In a study at Brown University in the U.S., when insulin supply in rats’ brains was blocked — mimicking the effects of insulin resistance — the animals became disoriented and plaques appeared in their brain cells.
The effects of raised sugar are not limited to rats.
Last year, a small study from the U.S. Department of Veteran Affairs looked at healthy volunteers who had been on a junk-food diet for only four weeks.
They had a raised level of the markers for plaque in their spinal fluid.
Scientists are still finding out what happens when insulin levels in the brain rise.
‘But we know it is much more important than we thought,’ says Professor Jennie Brand-Miller, a biochemist at the University of Sydney and world authority on insulin (she helped develop the glycaemic index).
High levels of insulin could also be having a damaging effect on neurons, she says.
‘This is because insulin comes partnered with another hormone, amylin, which makes the same sort of plaques as those found in the brains of dementia patients, except in the pancreas.
‘It could be contributing to plaque formation in the brain.’
High sugar levels don’t just push up insulin — they can also damage the brain directly.
Last May, researchers at the University of California showed for the first time that eating high levels of fructose, the concentrated sweetener found in many processed foods, reduced brain function in rats.
‘A high fructose diet over the long term alters your ability to learn and remember information,’ says research leader, Fernandez Gomez-Pinilla, a professor of neurosurgery.
Earlier this year, an Australian team scanned the brains of 300 older people who didn’t have dementia.
The brains of those with diabetes shrank up to two-and-a-half times faster than normal.
This shrinking occurred most in the frontal lobe that controls many functions damaged by Alzheimer’s — decision-making, emotional control and long-term memory.
What makes the theory linking type 2 diabetes and Alzheimer’s so convincing is that both are increasing at similar rates.
In other words, it’s very likely the same process is behind the two.
Dr Suzanne de la Monte, a neuropathologist at Brown University, says: ‘Before 1980, there was little overlap between Alzheimer’s and diabetes.
‘In fact, until then diabetes rates had been declining.’
Then something changed.
‘In every age group, the death rate from both diseases in 2005 is much higher than in 1980.
‘I believe Alzheimer’s starts with insulin resistance,’ says Dr de la Monte.
If, indeed, the links between diabetes, insulin and Alzheimer’s stand up, the good news is that it will give us more treatment options.
Drugs already used to treat diabetes might benefit Alzheimer’s patients or even stop the disease developing.
As it happens, it’s not the usual diabetes drugs — such as metformin — that may help.
‘So far, giving the older insulin drugs to Alzheimer’s patients hasn’t proved effective,’ says Dr Callum Sutherland, a specialist in insulin action at Dundee University.
The latest approach, in fact, is to boost insulin levels in the brain directly.
A small-scale trial last year found that dementia patients’ memories improved after nasal sprays of insulin.
A larger trial on 240 patients with early signs of dementia is under way at Washington University, in Seattle, to see if it can slow the disease down.
Research with a new type of diabetes drug, known as GLP-1, is promising.
It slows down brain damage in mice with dementia.
Of course, the insulin theory also gives us even more incentive to eat a diet that keeps refined carbohydrates to a minimum.
There is still work to be done to understand all the connections, as not everyone with diabetes develops Alzheimer’s and vice versa, says Dr Sutherland.
But finding out exactly how this link works could mark a turning point in the fight against this dreadful disease.