Transcription
Foreign Dr. David Perlmutter here. We're going to talk about mitochondria today. Mitochondria, you know, the energy producers, the powerhouses within every cell. Brain cells may have as many as a thousand mitochondria in each neuron. Mitochondria are seen diffusely throughout the body in virtually all of our cells. Interestingly, not in our red blood cells, but certainly in our white blood cells. Having good mitochondrial function and numbers within our white blood cells is an important player as it relates to proper effective immune function and keeping inflammation in balance.
We know that mitochondrial dysfunction, or problems with the mitochondria, is something that's at the core of some of our most pervasive issues, like cancer and coronary artery disease, cardiovascular disease in general, and certainly as it relates to the brain and things like dementia. The brain is a very energy-hungry organ. The brain weighs, what, three to five percent of the total body weight, and yet at rest may be consuming as much as 25 percent of the caloric expenditure of the entire body. So, the brain does use a lot of energy, and as such, it is highly dependent upon the functionality of the mitochondria.
So, the question that becomes: how can we enhance mitochondrial biogenesis? What a great term that is! It simply means, what can we do to increase the number of mitochondria that are available for energy production? One of the simplest measurements that can be done to look at mitochondria involves looking at the levels of mitochondria within the red blood cells. It's a simple blood draw, and then you evaluate actually the DNA—mitochondrial DNA—which is different from the normal cellular DNA that lives in the white blood cells. That gives you an indication as to how many mitochondria are present within our white blood cells, and it does serve as a surrogate marker for us to make assessments in terms of what mitochondria are doing throughout the rest of the body.
So, as it turns out, there is research that demonstrates that we can, in fact, increase our mitochondrial density—in this case, measured in the white blood cells. This was an interesting study that looked at the effect of a low fructose and low sodium diet on the DNA that was measured of mitochondria in white blood cells in human subjects. And again, it's really very important—at least in this study—they recognize the importance of dysfunction or problems with the mitochondria as being a major risk factor in things like obesity, diabetes, and hypertension. Because it is related to obesity, diabetes, and hypertension, we then know that it is related to the downstream issues that are consequences of obesity and diabetes and hypertension. Things like coronary artery disease, Alzheimer's disease, and even cancer are the downstream manifestations brought about when these mechanisms are activated.
So, we've connected some dots then between mitochondrial dysfunction and some of the most important degenerative conditions on the planet—things like heart disease, cancer, and stroke, for example, and certainly Alzheimer's disease. So, I'd like to consider the statement, however, from a different perspective: from the perspective of down-regulating mitochondria, making mitochondria less functional, and how that may have acted as what we call a survival mechanism.
So, when we have high levels of fructose and/or high levels of sodium in the diet, it really primes the body—or at least the bodies of our ancestors—for survival by down-regulating or making less functional the mitochondria. Why? Because when mitochondria are less functional, we have less energy utilization, and that can be a really powerful advantage when there's not a lot of food around. So, if the mitochondria are not burning as much energy, it might allow survival when the very energy that it would burn is less abundant. In addition, we know that when mitochondrial function is compromised, it leads to the generation of fat, and that, of course, can be a survival mechanism.
Now, let's look at the nuts and bolts of the study. It looked at 36 overweight, pre-hypertensive adults and put them on either a low sodium diet, defined as less than or equal to six grams a day, or an isocaloric—meaning the same number of calories—low sodium and low fructose diet, meaning less than 20 grams a day of the fructose diet. They followed these individuals for eight weeks and compared them to controls. They looked at the measurement of how much DNA related to mitochondria was seen in the blood test, which looked at the white blood cells in a normal blood test. The study went on for an eight-week period of time, again comparing a low sodium diet to a low sodium and low fructose diet.
What did they find? They found that with time, just putting them on a low sodium diet led to, at week eight, you see in the amber color already, the mitochondrial DNA starting to tick up. When you compare that in week eight to being on low sodium and cutting down the fructose to 20 grams a day, there was a dramatic increase—a 70-fold increase—in the mitochondrial DNA, basically the number of mitochondria in the white blood cells that are present now because we're sending less alarm signals to our bodies to make fat, store fat, and to ratchet down mitochondrial function.
Now, the authors of the study proposed a mechanism, and that is that the mechanism for protection could relate—in other words, how did it protect against damaging the mitochondria?—to decreasing oxidative stress, as changes in oxidants parallel the changes in mitochondrial density. What does that mean? Higher levels of oxidative stress threaten the viability, the life, the number of mitochondria. When you put people on a low sodium, low fructose diet, you're putting them on a lower threat, a lower oxidative stress level as it relates to their mitochondria. So, more mitochondria are created, and these mitochondria survive. That's what we want.
What they noted in the low sodium, low fructose group—this gets a little technical—but they noted that the level of something called DNPH (dinitrophenylhydrazine) was decreased by 52 percent. Now, that sounds pretty scientific. Let me tell you what that means: that's a marker of oxidative stress. That's a marker of the damaging action of chemicals called free radicals. It's the reason we take antioxidants. In addition, that number went down quite dramatically. The uric acid level went down by 22 percent in people who were on a low sodium, low fructose diet. Why might that be? Well, fructose directly raises uric acid, and sodium raises uric acid a little bit indirectly because it increases the conversion of glucose into fructose, which then raises uric acid—that's called the polyol pathway.
So, this is really quite a fascinating study that demonstrates that by lowering sodium and reducing fructose consumption, there is a dramatic effect upon the number of mitochondria and therefore mitochondrial function, as we see with less oxidative stress demonstrated by the reduction in the DNPH. That was an interesting study, wasn't it? It showed that low sodium and a low fructose diet combined, after the eight weeks, was associated with a dramatic increase in mitochondrial density, as measured again by the amount of mitochondrial DNA that was found in the white blood cells—again, a surrogate marker basically for DNA of the mitochondria throughout the body.
Therefore, mitochondria throughout the body—we want to do what we can to help our mitochondria work, help them repopulate, help them regrow, enhance what I mentioned earlier called mitochondrial biogenesis, meaning the growth of new mitochondria, and at the same time rid our bodies of defective mitochondria, which is something called mitophagy, part of what the broader term autophagy. Here, we've learned that a low sodium, low fructose diet is really effective in doing that.
I think you know the area that is united by low fructose and low sodium. The mechanism that they share is, of course, this downstream production of uric acid. So, we are upstream of uric acid. We know that uric acid is an instigator of oxidative stress, can damage mitochondria, can compromise cellular function, can increase inflammation, can compromise nitric oxide, therefore lead to poor blood supply, and at the same time compromises insulin sensitivity.
So, the downstream effects of higher levels of sodium in the diet and higher levels of fructose in the diet is an elevation of the uric acid. This was a very dramatic demonstration—a 70-fold increase in mitochondrial DNA in the white blood cells after eight weeks. Very interesting information, and I think for many of you, this will be quite thought-provoking. Hope you enjoyed our time together today. I did. Thanks for joining me. I'm Dr. David Perlmutter. Bye for now.