Statin medications were approved for use in the US in 1987. As of 2009, the revenue for these drugs was approximately 29 billion dollars (that year).
Suggested guidelines from 2015 say that 56 million American adults, or almost half those age 40 to 75, should be advised to take statins. A large percentage, about half, of these do.
Although they do work very successfully at lowering LDL cholesterol (the main carriers of cholesterol in the body) – which is what they are made to do – cholesterol does not directly give you heart disease (see post ‘some clarity on cholesterol’). Researchers say statins have failed to substantially improve cardiovascular outcomes, stating that ‘statistical deception’ was used to inflate claims about their effectiveness. The effect of the drugs on the population is called the ‘absolute risk,’ which has shown that statins benefit only about 1% of the population. Sellers, however, don’t present the 1% effect to the public. Instead they transform the 1% effect using another statistic, called the “relative risk,” which creates the appearance that statins benefit 30-50% of the population.
This is how they were sold to doctors, and to the public.
Along with the myths that were sold to us regarding cholesterol was the idea that statins would reduce Alzheimer’s. But one look at an actual mechanism the body uses to prevent Alzheimer’s-related plaque build up tells a very different story.
It remains unclear what causes Alzheimer’s, and there are various theories. But we do know a few things: there is a build-up of amyloid beta plaque in the brain and twists of tau proteins inside the neurons, leading to eventual damage and death of neurons.
Amyloid beta plaques are present in small quantities in a normal brain, and though the function is unclear, they appear to be related to protection from oxidative stress as well as providing protection from microbes. In a normal brain amyloid beta rises while we are awake, then falls during sleep.
The mechanism the body uses to clear the plaques is key to understanding where the potential danger of statins seems to lie in relation to Alzheimer’s.
The body uses a protein called ApoE to target the removal of these apparently dangerous plaque build-ups from the brain. ApoE comes in 3 genetically different forms, 2, 3, and 4, and the ApoE4 form is directly linked to higher rates of Alzheimer’s.
When the body needs to clear amyloid beta plaque from the brain, it calls on ApoE protein. At the same time it raises the level of cholesterol in the blood. I will repeat that: it raises the level of cholesterol in the blood.
The reason it does this is because it is only the ApoE joined with cholesterol that allows the clearance mechanism to function. I will repeat that too: higher levels of cholesterol are necessary for the body to clear excess amyloid beta plaques from the brain to prevent plaque buildup, a hallmark of Alzheimer’s.
In the case of ApoE4, the 4 type is less successful at joining with the cholesterol. This may be the reason why the body tends to carry higher levels of LDL in people with the ApoE4 type.
So let’s go back to the approximately 32 million Americans who lower their cholesterol with statins. Statins are not a drug that you take to make you better and then you stop taking it. Statins are drugs that are often prescribed for life. That means a large number of that 32 million have been on them for many years. Those who were prescribed statins in the 1990s when they were 50 are now 70.
What is going to happen to all of those people – the one’s who have potentially had their plaque clearing mechanism crippled from low blood cholesterol – are their cholesterol levels consistently too low to effectively trigger plaque clearance? I don’t know the answer but I’m afraid we are about to find out.
In the population of America, 1 in 9 people over 65 presently have Alzheimer’s. Two thirds of these are women. By 2025, the number of people age 65 and older with Alzheimer’s disease is estimated to reach 7.1 million — almost a 40 percent increase over 2016. By 2050, the number of people age 65 and older with Alzheimer’s may nearly triple, from 5.2 million to 13.8 million, with some projections suggesting this number may be as high as 16 million. How many of these will be from impaired plaque-clearing mechanisms due to statins? We don’t know, because no one is looking at this.
We don’t know what causes Alzheimer’s, and we don’t know the complexity of the mechanisms involved. But we do know how the body tries to protect itself. And in this very important instance we appear to be working directly at odds to the basic mechanisms of the body.