The past year has seen several new Alzheimer’s drugs fail in clinical trials. That’s no surprise. An effective Alzheimer’s drug is one of the holy grails of drug development, but to date we haven’t discovered one.
For decades, medicine has told us that Alzheimer’s is due to the buildup of beta-amyloid plaque in the brain. If we could just get rid of the plaque, the theory went, we could stop Alzheimer’s in it’s tracks. But it hasn’t worked out that way.
What’s been surprising about the latest round of failed drugs isn’t that they didn’t work. It’s this: they did exactly what they were supposed to do. They did clear plaque out of the brain, or stop it from building up in the first place. But here’s the thing: it had zero effect on symptoms. This should suggest to anyone with half a brain that beta-amyloid plaque is not the problem.
Could it be that this focus on plaques and tangles has distracted us from the real cause of Alzheimer’s? “Alternative” medical practitioners have been saying this for years. They've been dismissed as quacks. Medicine is always reluctant to give up its pet theories, even when the evidence (such as the failed drugs I mentioned above) is overwhelming. However, new research from the University of Adelaide in Australia suggests that the “crackpots” might just be right no matter how much Big Medicine doesn’t like it.
We may have been looking at Alzheimer’s all wrong all these years.
Alzheimer’s isn’t the only thing that causes plaques and tangles in the brain
Not so long ago, the only way to discover these abnormalities was to examine the brain after death. But in recent years we’ve developed ways to look into the living brain. And what we’ve discovered has been somewhat shocking.
We’ve found that many people with amyloid plaques never develop Alzheimer’s. In fact, a surprising percentage of “superagers”—elderly people with exceptional memories—have massive amounts of plaque in their brains, equivalent to someone with end-stage Alzheimers. Yet they suffer no ill effects, and their memories are sharper than people 30 to 40 years younger than them. This alone puts paid to the “plaques-cause-Alzheimer’s” theory.
We’ve also found that beta-amyloid plaques aren’t a feature of Alzheimer’s disease alone. They also occur when we’re sleep deprived. And a growing body of research suggests that amyloid plaques actually form in response to infection—that they’re the brain’s way of trapping invading pathogens.
These and other facts are finally causing mainstream scientists to question whether plaques and tangles really are the root cause of Alzheimer’s. And if not—then what is? The Australian researchers think they may have the answer.
Is Alzheimer’s an autoimmune disease?
When we think of brain diseases, Alzheimer’s, Parkinson’s and Huntington’s diseases spring to mind. These are three of the most common degenerative brain diseases. They have different symptoms—at least at the outset. They begin in different parts of the brain and affect different types of cells. But the scientists involved in the current research note that they also have a lot in common. And as they progress they become even more similar. Researchers believe that these and other degenerative brain diseases may have a single common cause. And it boils down to one word:
In a nutshell, here’s what the researchers suggest:
First the facts: We actually have two types of immune system. Innate immunity is what we are born with, the body’s natural ability to recognize and neutralize threats. Adaptive immunity is when our body is exposed to threats such as bacteria or viruses and learns to recognize them so it can fight them off when it meets them again.
Now the theory: The Adelaide researchers believe that in the case of neurodegenerative diseases the innate immune system has gone haywire. It’s attacking things that aren’t a threat. This results in a storm of inflammation that causes cell death.
This would explain a lot of things. If amyloid plaques are an immune response, it would explain their buildup in Alzheimer’s brains. It would also explain why so many who do have plaque buildup never develop Alzheimer’s. It would explain the links shown between obesity or diabetes and Alzheimer’s. And it would explain why a Mediterranean diet seems to reduce the risk of Alzheimer’s. In short, it would make sense of the whole picture. And if we’re lucky, it might lead to an effective treatment.
Until then, prevention is the best option. And when it comes to reducing or preventing inflammation, we have some very good tools. The number one tool for cooling inflammation is found not in your medicine cabinet but—not surprisingly—in your refrigerator.
The most important thing you can do to reduce chronic inflammation is to change the way you eat. Your diet can turn your body into a walking hotbed of inflammation, or it can cool the flames. Here’s what you need to know:
The biggest drivers of inflammation are processed foods. The most pro-inflammatory things you can eat include:
- Refined carbohydrates like bread and pasta.
- Processed meats like hot dogs and sausages.
- Margarine other products containing trans-fats—which can still be found in products in tiny amounts.
- Oils that are high in omega-6 fatty acids. These are ok in moderation, but should be balanced by omega-3 fatty acids such as those found in fish and flax oil.
In addition, excess weight creates chronic inflammation, so dropping any extra pounds is essential.
On the other hand, there are a variety of foods that calm inflammation, including:
- Olive oil
- Leafy greens
- Nuts—especially walnuts and almonds. These are high in inflammation-fighting omega-3 fatty acids.
- Fresh fruit, especially berries. Strawberries and blueberries at top-notch inflammation-fighters, as are cherries and oranges.
Do we know for sure that inflammation causes Alzheimer’s?
No. But we do know that it plays a role in nearly every other chronic disease out there. And the evidence is very compelling. Reducing your risk of inflammation just makes good sense for every aspect of your health.