Dr. Bredesen: 08:24 Yeah. My opinion is that we should all get genetic testing to assess Alzheimer's disease, and also biochemical testing. What we recommend is that everyone, 45 years of age or over, should have, just like you would get a colonoscopy when you're 50, you should get a cognoscopy when you're 45 or older. That would look at your biochemistry and genetics, it would look at your function with things like BrainHQ or online assessments of cognitive function. It would, if you're symptomatic, look at your imaging studies.

Dr. Bredesen: 08:58 Of course this would include your genetics and there're many SNPs associated with Alzheimer's disease. Of course the most important genetic association as a risk factor is APOE, the epsilon 4 allele. If you have zero copies, you have about a 9% chance during your lifetime of developing Alzheimer's. Single copy, about 30%. If your hormones are I guess two copies, then you have somewhere between a 50 and 90% chance of developing it.

Dr. Bredesen: 09:26 In the past, people recommended not to check this because you couldn't do anything about it. We disagree with that now, there's a lot you can do about it. There're a lot of studies coming out showing that there is effective prevention, such as the FINGER study that came out of Finland. In our work it shows that you can not only prevent but also reverse, especially early on cognitive decline. Therefore, we recommend that everybody be tested.

Jonathan Otto: 09:56 Can you describe to me what the convectional medical approach is to managing Alzheimer's?

Dr. Bredesen: 00:03 Right. So the conventional medical approach to managing Alzheimer's is to give a monotherapy. It's to give a medication, and typically, what's given is donepezil and/or memantine. And these do not attack the cause of the problem. So you're essentially trying to trick nature, you know, go around it and say, "Okay, we can alter the system." They don't affect the large number of contributors.

Dr. Bredesen: 00:30 We initially identified 36 different contributors, and so we tell people, "Imagine you have a roof with 36 holes in it. You want to close all the holes." Of course, for different people, the holes are different sized. Your Vitamin D, your estradiol, your NGF, your BDNF, these things all tell you something about your risk.

Dr. Bredesen: 00:53 So the conventional approach is to give a monotherapy like donepezil or memantine, and it's been relatively unsuccessful. You can get an improvement, but then you go right back to decline, again.

Jonathan Otto: 01:05 Do you feel that people are given a false hope with using some of these therapies?

Dr. Bredesen: 01:11 You mean the standard therapies?

Jonathan Otto: 01:13 Yeah.

Dr. Bredesen: 01:13 No, I think actually the doctors have been quite good about telling people that these therapies are not terribly effective, that you'll get a small improvement, and that they will not affect the decline.

Jonathan Otto: 01:26 Okay, well, that's good, right? Honesty is a good thing.

Dr. Bredesen: 01:30 It's good, but it then tells people things are hopeless. So unfortunately, what happens is, people know that there's not a lot to be done, so they will wait as long as possible. Instead, what we would like to see is just the opposite. People should come in as early as possible, preferably prevention. But if not prevention, then come in as early as possible for a reversal. The idea of saying, "Since there's very little to be done, I'm going to take some medicine. My driver's license is going to be taken away. I will not be able to get long-term-care insurance, so I'm going to wait as long as possible" is the wrong idea in the long run.

So, as far as an alternative approach, and I think we talk about "alternative medicine." But for so many of these complex, chronic illnesses, whether you're talking about Type II Diabetes or Metabolic Syndrome or a number of the autoimmune diseases or congestive heart failure or atherosclerotic cardiovascular disease ... Instead of calling these "alternative," we should perhaps call them "effective" because they are the most effective things we have now for Type II Diabetes, the most effective things we have for autoimmune diseases, the most effective things we have for some of the gut-health-related diseases.

Dr. Bredesen: 04:06 This alternative or, in this case, first effective approach for cognitive decline involves a very, very different approach. Instead of saying, "We have a small data set. We know that you have Alzheimer's Disease, but we don't know why you got it. And we're going to give you a monotherapy, and you're not going to do well," we've changed everything.

Dr. Bredesen: 04:32 First of all, we want to understand everything about what actually caused the disease therefore we want a much, much larger data set, just as you would do in any sort of functional medicine evaluation. Frankly, the larger the better. We'd like to know all of the potential contributors to system inflammation and to local inflammation. We'd like to know all of the potential contributors to any sort of pathogens that may have contributed, sterile inflammation, all of the potential trophic loss. Why is your BDNF low? Or your NGF? Or Vitamin D? B-12? Why is your homocysteine high? All these sorts of things?

Dr. Bredesen: 05:12 Then we'd like to know, what are all the potential toxins you've been exposed to? These are all critical to understanding. From that, then we have an algorithm. What is actually causing your cognitive decline or your risk for cognitive decline? When you have a much larger data set, then you can look at that. And instead of saying, "Yeah, this is a mysterious illness. We don't know why you got it." This becomes a non-mysterious illness, and you can see the actual contributors to the cognitive decline.

Dr. Bredesen: 05:44 Then what we want to do is address each of these. Again, no differently ... If you went to your cardiologist, and your cardiologist said, "Oh, yeah. You should cut out eating french fries, but go ahead and keep eating the cheeseburgers and the baked goods and things," you'd say, "What kind of a lardy, you know, lousy cardiologist are you?" It doesn't make sense. And so the same idea-

Jonathan Otto: 06:07 That's awesome. You called him a lardy cardiologist.

Dr. Bredesen: 06:09 A lardy, exactly. A lousy cardiologist, exactly.

 

Dr. Bredesen: 06:12 So it's the same idea here, that you want to look at all the different contributors, and then you want to address as many of them as possible. And the good news is, there is, just as there is in cardiovascular disease, there is a threshold. Once you get to a certain threshold, you actually start improving.