Just support for the fact that metals especially aluminum inhibits the ability to regenerate BH4 and that’s why we worry so much when we see those A1298C mutations where we may have intrinsic problems with generating BH4 in addition to the presence of aluminum.
The reason aluminum is putting vaccines is that it helps to stimulate your immune system. But it can over stimulate the immune system. Aluminum also can play havoc on your lipid profiles and your phospholipids that are so important for membrane fluidity. And in a little while we’re gonna also talk about the role of the PEMT enzyme – that’s a new snip that we’ll be looking at and how that seems to affect the membranes. Also looking again at the role of aluminum and myelin, and we need to be able to read re-myelinate these nerves.
So taking a break from all the information again, just looking at some excretion of aluminum and again these are unprovoked metal tests, and all we’re doing is supporting the body to get around mutations in the methylation cycle as well as supporting the body to be able to deal with bacteria in the system as well as Viroqua.[00:43:18.25]
And so we’re looking at the excretion of a tremendous amount of metals by addressing and balancing the methylation cycle, as well as applying some of the techniques that we’re going to talk about in a few minutes to deal with the bacteria. And I spoke this morning and I’ve talked about before, plotting your excretion, looking for the bell-shaped curve, looking for what’s going on and when you’re at a sufficient endpoint. And I’ll just run through these tests very quickly, but again getting the metals out because leaving them in the system that’s where I think we’re getting the low muscle tone, seizure activity as well as the problems with language and cognition.
Now when we look at adults, and we’ve been working with a lot more adults recently on the chat group – it can take longer for an older individual and sometimes the amount of excretion isn’t as stellar as some of those black ones across the page that we saw just now. But we can look at something more subtle and so here we’re dealing with an adult. We’re not seeing any aluminum over time okay. So from year to year we’re not seeing aluminum excretion at all, Ok, nothing
At this point we added in a compounded mitochondrial support supplement. And once we start to support the mitochondria we are starting to see aluminum excretion for the first time in years. And we are maintaining that aluminum excretion. And even though it’s not as impressive as those black lines across the page, the fact that we had no excretion, and now we’re seeing consistent excretion supports the fact that you want to be looking at dealing with the bacteria in your system and supporting the mitochondria in the body.
Again dealing with the mitochondria – in this case will looking at a major increase in tungsten excretion – and if you look at the difference in creatinine and you account for those differences, this is probably more than a four-fold increase in tungsten excretion simply by supporting the mitochondrion in the body. Okay, so where are we at this point? Bacterial loads can be related to iron levels, we want to be paying attention to the SHMT plus. Other nutrigenomic markers that play a role in this gut environment in the swamp, ACAT, BHMT, A1298C.
Bacteria have the capacity to hold onto metals. And when we’re addressing chronic bacterial issues we want to be looking at excretion of any number of metals on a UTN, a UEE, a fecal metal as well as a hair test OK.
And now I want to get into more of the specifics of the interaction between aluminum and the mitochondria and oxidative stress.
So the mitochondria are the energy producers in your body, they are what help to generate the energy for the ATP that your body needs to drive reactions, okay. And they’re doing it by moving electrons back and forth through the cytochromes that we looked at before, but in the process they generate oxygen radicals. And this energy cycle, this Krebs cycle that we’re used to looking out on a map test, is related to ACAT mutations because they can’t feed in, and we need to be able to come from this cycle and feed in to this part of the pathway to generate the energy we need ATP to drive reactions in your body.
Thallium disrupts the Krebs cycle and affects ATP production and that’s why anyone who is running tester through our office when I see thallium I’m telling you to add ATP. When we’re seeing unbalanced amounts of sodium, potassium and phosphorus on a UEE, I’m suggesting we need to look at more ATP because thallium may be a problem.
And so ATP and thallium have a…aah.. an antagonistic relationship. So when you’re seeing thallium you want to be thinking about ATP and the mitochondria and energy in the body okay.
Aluminum directly affects the cycle were looking at. Aluminum directly interferes with it, so that we have a problem at this point in the cycle as a result we end up with additional oxidized species and the TCA cycle isn’t working correctly. Which means we can’t generate the ATP that we need, so that when you are looking at one of those tests that show you what’s going on in the cycle, if you’re finding lower numbers here and higher numbers here, one of the first things you want to think about is aluminum toxicity.
Okay so again, we have that cycle where you still looking at. We need to feed in to this pathway in the mitochondria so that we can bounce electrons back and forth across this membrane, generate in energy potential and in doing so, have ATP that we need to drive reactions. And in doing so we generate oxygen, which can create oxidative stress and damage if we don’t have sufficient antioxidants in the body. And the same thing that goes on in our mitochondria is what goes on in bacteria and this is a nice graphic to help to show you that. We’re moving back and forth through this membrane. We generate that membrane potential, and that’s what drives the energy for that ATP that we need to drive reactions. And so when you go back and you read that Times article that came out this week and they talk about the voltage gated calcium channel and seeing a higher prevalence of that snip in that mutation in autistic boys, what they’re talking about is something very similar to this for calcium, that that voltage gated means using that kind of energy and that kind of potential, in order to control calcium in and out of the body.
And so the way we measure this energy and evaluate it in mitochondria, is the same as what I did twenty years ago measuring this energy and bacteria. And so we’re looking at very similar problem whether we are looking at microchondria or looking at bacterial at this energy gradient and actually how it impacts on uptake of glutamate into the body, okay. And so looking at the membrane potential’s and how they play a role in transport and antibiotic resistance and bacteria and energy generation. And so just another graphic to show you that in the mitochondria we’re generating oxidative damage in the process of having this energy potential that helps for transport, into the body and you want to be using antioxidants, whether it’s melatonin or whether it’s CoQ10, [00:52:31.22] or whether it’s NADH, to try to help to pull the oxidative damage down.
And so mitochondria are major source of reactive oxygen species and are particularly prone to oxidative damage okay.
Going back to BH4 again, we want to be thinking about the fact that the relationship between the ability to have adequate BH4 levels in the body, the A1298C mutation, if we have aluminum and it affects our BH4 levels, and when we want to layer in hyperbaric oxygen. I’m not averse to adding it in to help with anaerobes, but we want to be thinking about when is the best time to be adding oxygen to the system. My personal preference is look at a CSA. Let’s get it a clean CSA, let’s get rid of the bacteria that may be holding onto some of this aluminum, let’s pull the oxidative stress down, let’s get rid of the aluminum so that we can repair the damage, and then let’s look at adding in a little more oxygen to deal with the anaerobic bacteria.
And just a slide to reiterate and remind you in case you haven’t seen it before I have forgotten that the amount of BH4 that you have in the body controls what type of species in terms of reactive oxygen molecules that you’re going to have. And so when you had two molecules of BH4 we handle these radicals very efficiently. But if we only have one or we have none that’s when we’re generating some of these very dangerous radicals that then cause neural damage.
And again whether were talking about an aging system or a damaged system that the mitochondria in the process of generating the energy they need, cause these free oxygen radicals that can play a role in aging, and in the case we are looking at, making it more difficult to be able to get rid of heavy metals from the body. And this was a very nice visual and science recently mitochondrial gone badly. And the counter side of mitochondria that we need them to be able to generate energy but in doing so we’re generating these oxygen radicals and so we need to this energy, we can’t survive without ATP and we need to be able to move these electrons back and forth to get that membrane potential. But in doing so we’re creating oxygen radicals which layer onto the problem of the aluminum that’s already causing that oxidative stress and nickel.
And if we look at the ability of nerves to be able to grow the way they need to. We are looking at what happens in the absence of antioxidants versus the presence of antioxidants. So mitochondria and the oxidative stress can be a key to getting some of the repair we need, and the importance of the use of antioxidants and controlling this oxidative stress and getting rid of the bacteria they’re holding onto the aluminum and other problems that they’re causing with respect to oxidative stress.
And so again going back to the schematic we want the TCA cycle functioning properly and aluminum can inhibit that directly. We need to be able to generate this energy. And when do so, we create oxygen free radicals that we need to be in a position to deal with. Methionine directly helps to deal with oxidative stress. And I can’t tell you how many UAAs I’ve looked at where methionine is all the way to the left. We’re way too low on methionine. Methionine is right in the middle of the methylation cycle that we look at all the time. If we’ve got mutations in that cycle, especially in a case let’s say where we have a CBS up regulation, and all the intermediates of our cycle are draining out through taurine. Methionine is essentially in the toilet. So if we’ve got aluminum, and we’ve got oxidative stress and we’ve got no methionine we’re in a position where we can’t even deal with some of that stress. That’s why again I’m not spending a lot of time in the genetics today but what I’m assuming is you’re gonna look at those mutations, you’re gonna bypass those, you’re gonna support that cycle so we can get those methionine levels where we need them, and if simply bypassing mutations alone doesn’t get us there, then we want to be supporting with low doses of methionine or using some of that methionine RNA. Get those levels up there because methionine is so central when it comes to oxidative stress. And in a few moments I’m going to give you one of those things when you… one of those light bulb moments… when you look at it and say, “Where does the sky end?” and just believe me that methionine is so critical basically for life itself, that we really need to keep that cycle in balance as well as the role that it’s playing for oxidative stress.