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I absolutely love what's just happened. So medicine is full of examples where there's been failure after failure to treat a specific health condition, only for a treatment to appear from a completely different area of research.
So take knee osteoarthritis for example. We haven't had a good treatment option to add to diet and exercise. But then GLP-1 therapies, which were originally designed to help treat type 2 diabetes, started to show significant benefits for arthritis as well.
Then there's penicillin. So its discovery was completely by accident, but then it went on to have enormous positive impacts on a whole range of deadly diseases. So these serendipitous moments are amazing, and it looks like the same thing has happened for dementia.
So recent research has uncovered a surprising beneficial effect from a vaccine developed to help treat a specific problem that, on the surface, it looks completely unrelated to dementia. But we may have never gotten this data without an unusual circumstance that led researchers to run a test that no ethics board would have ever allowed. And if the results hold, this could be one of the biggest breakthroughs in decades when it comes to dementia.
Because after massive investments and hundreds of failed trials, we still lack highly effective preventative measures for dementia or treatments. And there's a lot that we don't know about what causes the condition. But again, recently scientists have turned their attention to an unconventional suspect: viruses.
So, for instance, experiments in mice have shown that these viruses stimulate the production of a protein in the brain that helps to fight off the infection. But it's the same protein that clumps together to form the amyloid plaques that are a key feature of Alzheimer's disease. So the brain's defenses backfire. So yes, it fights off the virus, but it also accelerates the process that contributes to dementia.
And a chief suspect is the varicella zoster virus, which is the same virus that causes chickenpox in childhood. We may hardly remember the infection when we were young. But the problem is that this virus, it lurks quietly in our systems, often reemerging late in life as painful cases of shingles. But even if we don't notice a profound flare-up, as in the case of shingles, the varicella zoster virus can undergo quieter reawakenings that we don't see or are asymptomatic.
So researchers theorize that in both cases, the virus acts as a chronic stressor to our immune system, and that can drive inflammation in our brain and interfere with its immune functioning. So this virus isn't just linked to brain changes like amyloid plaques that drive Alzheimer's disease. It also shows signs of contributing to another kind of dementia, vascular dementia. So that variety of dementia is driven by problems originating in the blood vessels in the brain. So here we're talking about things like high blood pressure, plaque buildup, and strokes.
So the varicella zoster virus is linked to the kind of damage that's usually caused by these factors. So all of these observations, they raise the obvious question: Could preventing the flare-up of the varicella zoster virus that causes shingles also help us to avoid the damage that appears to accelerate the development of dementia?
So observational studies in humans, they have pointed to a positive answer. So in one example, researchers analyzed the health records from two large databases in the USA. They established two groups at the start of the study period: those who'd had a shingles vaccine and those who didn't. So they checked for new diagnoses of dementia in the health records over about an eight-year follow-up period. Participants were at least 65 years of age at the beginning of the study and free of dementia.
So the association between getting the shingles vaccine and a lower dementia risk was pronounced. So the risk reduction was 31 to 35%. But of course, there is a significant problem here. This is just an observational study. And with this kind of study, what's driving the association is always an open question. It's a bit like how autism rates have gone up with increasing organic food sales. Clearly, they aren't related.
So to really know whether the shingles vaccine is protective against dementia, ideally, we want randomized controlled trials. This is when we have a pool of participants that's randomly assigned to get the vaccine or to get a placebo. This is the best way that we have to eliminate the impact of other health factors.
There's just one little problem here, though. We cannot ethically run a study like this. So the shingles vaccine is a standard recommended care for older adults, and that's because previous studies have already proved that the benefits vastly outweigh the risks compared to a placebo. So we cannot assign a group of people to not get the shingles vaccine. And that's left us in the position where there were crucial questions that we wanted to answer but couldn't.
But then a group of researchers spotted a once-in-a-lifetime opportunity. So the state healthcare system in Wales, they made a fateful decision back in 2013. So officials in charge had seen the data on benefits of vaccination to prevent shingles and wanted to make the vaccine broadly available to the population. But as always, you have to balance the costs and the benefits. So they drew a bright red line.
Those born on or after September the 2nd, 1933, would be eligible for the vaccine. It would be available beginning of September 1st, 2013. But those who were born before that September 2nd cutoff back in 1933 would never be eligible. In 2013, they would be 80. And the logic was this: At that age, there was a diminishing chance of seeing a benefit from the vaccine.
But this policy gave researchers an opportunity that they wouldn't have had any other way. Here was something that closely resembled a randomized controlled trial. So what the researchers did was assemble two groups. One included those individuals born one week before the cutoff date, so they weren't eligible for the vaccine. But the other group, those were born one week after the date, they were eligible for the vaccine. And the researchers reasoned that it was extremely unlikely that there would be any important differences between these two groups because they were essentially the same age.
So researchers could rule out one problem that we mentioned about health-conscious individuals. They could rule out other possible biases as well. It was the perfect natural experiment. All they had to do was wait for the data to roll in.
Now, the first thing that they needed to see was whether the shingles vaccine rates differed substantially between the two groups. So, that's a real question because while the state healthcare system wasn't going to pay for the vaccine for the older group, they weren't preventing them from getting it either. So, they could always pay for it themselves and receive it. But luckily for the study, most of them didn't.
So for those born before that cutoff date, the probability that they ever got the vaccine during the study period was 0.1%. In contrast, for those born after the cutoff date, the probability was just over 47%. So here's the critical question: How much did that higher rate of shingles vaccination use impact new cases of dementia?
Comparing the groups as a whole, those who were eligible for the vaccine had a 1.3% lower absolute risk and an 8.5% lower relative risk of a new dementia diagnosis over the seven-year follow-up period. But as we've seen, only about half of the eligible group actually got the vaccine. So the impact here is diluted compared to those who weren't vaccinated.
So researchers used a statistical technique to estimate the true impact for those who received the vaccine. So for that group, there was a 3.5% lower absolute risk reduction and a nearly 20% relative risk reduction in dementia diagnoses. That 3.5% absolute risk reduction might not sound like much, but in clinical research, that's a major finding. At a population level, that would translate to thousands of cases of dementia prevented using a simple, cheap intervention, and it's a game-changer. And remember, that is only the absolute risk reduction during the seven-year follow-up period. It's highly likely that their benefit would grow as time progresses.
Now, the researchers were ready for some potential objections. Do we really know that there were no important differences between the two groups? Well, maybe, for instance, the eligible group on average was more engaged in preventative care. They checked for that, though, and there was no difference. Or maybe there was some other important intervention that was used around that cutoff date. So, they checked that too, but nothing else used that date.
They even addressed the issue that we noted earlier for observational studies. So in those studies, the group receiving the vaccine had a cluster of other unrelated health benefits that seemed to point to other factors apart from the vaccine as being decisive. But in this study, however, the two groups didn't differ when it came to other common health problems. The only divergence between them was in dementia rates.
But as exciting as those results were, important questions do remain. And one key one is this: Was the vaccine just something that prevented the development of dementia? Or could it also slow the progression of the disease? Well, the same group of researchers just published a follow-up analysis drawing on the same population in Wales to answer that question. And what they found is that the protective effects of the vaccine extended further than what we might have thought in two directions.
So on one hand, not only did the vaccine appear to prevent new dementia diagnoses, but it also appeared to reduce the cases of new diagnoses of mild cognitive impairment. That is an earlier transitional stage on the path to dementia. But on the other end of the spectrum, the vaccine also appeared to have the ability to slow down disease progression. And here the impact was dramatic.
So they looked at those individuals who'd had a diagnosis of dementia before the vaccine program began. So for this high-risk group, the death rate over the nine-year follow-up period was almost 50%. But the vaccinated group, they slashed their risk by nearly 30 percentage points, which is a remarkable reduction.
Now, it's important to add some qualifications here. The confidence intervals were wide in the study. So that means that there's low certainty about the exact magnitude of the impact. Moreover, the study analyzed a population in a very narrow age range at baseline. They were only between the ages of 79 to 80. So we don't know how those results might translate to younger age groups. So there is more research to be done, but these studies in Wales give us compelling evidence that the shingles vaccine can help to slow down or prevent dementia across the disease course. And given the vaccine is already widely available, the benefits vastly outweigh the risks. And it's a simple one-time intervention. This is of great significance for all of us at risk of dementia as we age.
But there's one more lingering question when it comes to these studies. So the vaccine that was used in that study is being replaced by a different one. So that new one is what we use in my clinic today. So would that new vaccine be as effective? Well, the type of vaccine that was used in the Wales study, it involves a live virus that was weakened before it was injected. The newer shingles vaccine is called a recombinant vaccine, and it just uses a small part of the virus.
So here's the worry: Some researchers found that the broader health benefits sometimes associated with vaccines seem to be much stronger for live virus type vaccines. But fortunately, there was an opportunity in the US to test this worry. So the circumstances were similar to those in Wales. After 2017, there was a rapid shift from the old live virus vaccine to the new recombinant one. And the results here were reassuring. The newer vaccine was associated with an even lower risk of dementia.
Overall, this is super exciting because potentially we've got another way that we can prevent and treat dementia. Plus, other recent developments are giving us more potential strategies to reduce our dementia risk. So, for instance, there's exciting evidence that a specific form of lithium called lithium orotate could help to slow down Alzheimer's development. A study in mice found that it blocked both key hallmarks of disease progression.
And we've learned that addressing hearing loss also plays huge dividends. So, a systematic review in humans found that people with hearing loss who used hearing aids had a significantly lower risk of cognitive decline and dementia compared to those who didn't. So, that's a really simple intervention that can make a huge difference.
And there's even some supplements that research suggests may protect our brains and possibly lower our dementia risk. So, let's take a look at four of them briefly. A large trial analyzed the effects of taking the first supplement daily over a two-year time period. Researchers discovered relative improvements in overall cognition scores and memory. The effect on cognition was equivalent to reducing the speed of aging of the brain by two years. So the supplement was a multivitamin and mineral.
Then there are omega-3 fatty acids. So they're naturally abundant in food sources like fatty fish. And these substances are critical for brain health. And an important study published in 2019 found that omega-3 supplements improved brain performance by 7.1% and reduced dementia symptoms by 22.3%. Now, there's an important note here for that study. The researchers found that adequate B vitamins were important for seeing those benefits. So, that's another consideration in favor of using a multivitamin and mineral supplement.
The third supplement is one that we've been using for decades to boost exercise performance and muscle building. The supplement is creatine. And yes, a lot of creatine is found in our muscles, but it's also found in the brain, and our brains need a lot of energy to function correctly. So, creatine helps to produce this energy quickly, and it supports critical brain processes like memory and thinking. And some research has suggested that creatine supplements can increase the amount of creatine in the brain. And a recent meta-analysis published in 2022 showed that creatine supplementation improved memory performance compared to a placebo. And that effect was particularly strong in older adults.
And the final supplement is one that's also linked to exercise, but it also seems to show promise when it comes to brain health. And that supplement is TMG. So it's got an interesting link to Alzheimer's disease. In 2020, a large review of the risk factors for Alzheimer's disease found that high levels of homocysteine, which is an amino acid, was strongly linked to Alzheimer's. And that analysis went on to say that homocysteine-lowering treatment may be a promising intervention for Alzheimer's disease prevention. And TMG lowers homocysteine. So in other words, TMG may lower a key risk factor for Alzheimer's by lowering homocysteine levels. Now, that's not a guaranteed way to prevent Alzheimer's, but it's a really promising area of research and another potential benefit of a TMG supplement.
So personally, I take a multivitamin and mineral along with creatine and TMG as part of a microvitamin plus powder. But just because I take a supplement does in no way mean that you should as well.
And there's one final factor linked with dementia that might surprise you, and that's cholesterol. So, make sure to check out this next video here for the details of a huge study that shows how significant the impact can be of lowering our cholesterol levels.