The Secret Cause of Heart Attacks

Dr. Sal [00:00:00]:

You may end up going to, seeing your doctor. Your EKG is normal, and everything seems fine, and then you all of a sudden you die of a heart attack. And we call that a silent heart attack, which eventually causes death, and that's usually as a result of cardiac autonomic neuropathy, which is as a result of diabetes. A Welcome to the Health Quest Podcast, your guide to God's will us for good health. Hello. My name is doctor Sal, and I've been a practicing physician and surgeon for well over 30 years. And my goal for each episode is that you'll be able to have your mind transformed to God's design for your good health and the way you eat and the way you live. Us and if you're new here, we release a new episode every week.

Dr. Sal [00:00:59]:

And if you enjoy the content, would you please leave us a good review? It really helps our ratings and allows us to reach more people, and in turn, we can help more people as well, and we really appreciate your support. Thank you so much. And on today's episode, we're gonna be talking about diabetic neuropathy. So let's dive right on into today's health a Diabetic neuropathy. Well, in the last few episodes, we talked about insulin resistance. A and it begins with excess sugars such as corn syrup. Now remember a lot of, sugar regular cane sugar has been substituted with corn syrup high fructose corn syrup, in the early nineties and excessive amounts of bad fats. Now the liver eventually converts this extra sugar into fat as well.

Dr. Sal [00:01:54]:

So us gotta remember one thing, the way god designed us. God gave us fat cells to protect us a from lipotoxicity. And it it's that's where all the extra fat gets stored. Now you'll remember, from the previous guess that if the fat cells eventually reach a maximum storage capacity, 2 things can happen to them. Number 1, that extra fat will start to a spill back into the bloodstream, and that's called lipid spillage. The other thing is is that fat cells can expand to the point where it outgrows the blood supply. Now I don't know why we would even allow ourselves to get that big. Us and but when it does that and it outgrows the blood supply, there's not enough oxygen to sustain that, fat cell, and so it breaks a stow, and it goes through what we call necrosis.

Dr. Sal [00:02:53]:

Okay? It just it it just dies. All of a sudden, the cell membranes rupture. A it releases all that fat, and that fat eventually goes back into the bloodstream. So, when a this excess fat can't get stored in the, fat cells. It goes to areas where the fat should not go, and that's into a see the liver, the muscle, the pancreas, and that's how we end up with lipotoxicity. And if you can recall from the previous podcast, lipotoxicity is where the mechanisms, all those chemical reactions, let's say, in the muscle cell, occur. A and in this particular case, insulin will bind to the receptor, and it and it triggers a cascade of these chemical events, a and those get disrupted, and the purpose of of the insulin is to get the gates to open up in the cell to allow that us got sugar to get into that cell, let's say, the muscle cell, where it could use it for energy, or the extra sugar can get stored as glycogen for later usage. At that point, when these gates can't open, it's unable to absorb that sugar from the bloodstream, and we end up with a high fasting blood sugar level.

Dr. Sal [00:04:13]:

When that happens, the body tries to compensate, a and it starts producing more insulin. So insulin goes up, but, again, it's not working because of Vasudy, the cells can't work to function to pull that sugar out of the bloodstream and into the muscle or into the liver, and us we end up with the so called insulin resistance. So insulin takes a the fat and the, sugar, and it causes it to get stored in, the cells, particularly in the fat cells, in the muscle cells, as I said before, the sugar then gets used, as a source of energy. But when the liver so when the liver a becomes insulin resistant. Then the liver starts making its own sugar and starts making its own fat. Us. And the reason being because it says, hey. We've gotta we have to have some fat and sugar for the body to sustain itself.

Dr. Sal [00:05:14]:

A so at this point, the liver starts to think that we're low on sugar and low on fat. It starts making it even though the blood scream, has high levels of fat and sugar. But the insulin is not telling that to the liver because it's now resistant. So now the liver starts thinking that we're starving. And when we're starving, the liver does what it can to maintain because you gotta keep your blood sugar levels at a certain level, a and you have to have so much fat circulating in the body. So when, diabetes starts to set, set in, this progresses even further. A and at that point, as we had fat cells going into the muscle and into the liver and it causes the liver to develop cirrhosis, sudden that's what we call nonalcoholic fatty liver disease, and this happens more so with, fructose or high fructose corn a syrup. This extra fat then starts to deposit in the beta cells of the pancreas, and those become lipotoxic, and they don't function anymore.

Dr. Sal [00:06:21]:

And what ends up happening is is the beta cells become dysfunctional, a and it reduces the production of insulin. So in the beginning, we have a, an increase in insulin production to compensate for the extra sugar. Us once the cells become resistant, more insulin is produced. But once that fat starts getting deposited in those beta cells, a the beta cells can't produce, and it can't secrete the insulin, and then the insulin starts to drop. And this is what we see when we have advanced type 2 diabetes. So one of the major complications of diabetes is neuropathy. Now what is neuropathy? Well, neuropathy causes pain. This is the the pain symptoms a that the patients with severe diabetes end up developing, and it causes this sharpshooting pain, a start to lose sensation, particularly in the feet.

Dr. Sal [00:07:27]:

And what ends up happening is that sometimes you'll rest your feet on a chair or something, a and you can't feel it and you compress that tissue long enough that over time, that tissue starts to break down a in necrosis. And this is what we call the diabetic ulcers that you see on the bottom of people's feet because they may be standing on it or applying pressure for so long, but because we've lost the sensation, the blood circulation to that area starts to decline, us and then it also affects the the blood vessels as well. We're not getting enough oxygen or nutrients to the tissue, and it starts to break down. A patients with these types of neuropathies also have a higher incidence of injuries because they lose that sense of proprioception. In a sudden words, as we're walking, signals are being sent to our brain continuously to let us know where we're at. It gives us a sense of orientation. A so if we start to feel like we're slipping, we react to it, and we try to protect ourselves from any injury. Well, people with a sudden lose that proprioception, and they're at much higher risk for injury.

Dr. Sal [00:08:36]:

What also ends up happening, folks, because it is the nervous system, us we start to get a decline in cognitive function. Okay? So our brains start to kinda break down too as well. And then in the end, a you may end up going to, seeing your doctor. Your EKG is normal, and everything seems fine. And then you all of a sudden you die of a heart attack. And we call that a silent heart attack, which eventually causes death, and that's usually as a result of cardiac, a, autonomic neuropathy, which is as a result of diabetes. So what is the underlying cause a of these neuropathies or the ideology. Well, as you could see in the photo here, we start to see that, us, we get this high level of blood sugar, and you could see that there are 5 pathways.

Dr. Sal [00:09:31]:

And the causes are usually either metabolic insult. Us there is a neurovascular component to this that, we get more blood circulation to the blood us are to the nerves, and, eventually, those nerves start to break down. There is immune damage. Again, there's that inflammation coming back to haunt us again. Us okay. The we're always especially once we start getting overweight and we're eating the wrong foods, we're always in that low grade chronic inflammatory state. And those, inflammatory cells eventually start causing damage to the tissue. Us and then as the tissue starts to break down, you gotta remember that, nerve tissue creates these growth factors, a.

Dr. Sal [00:10:18]:

And that's usually to help it to repair itself under significant injury, but then over time, even these growth factors become deficient. So as we could see, we have this this diagram here of of hyperglycemia, which means high level of blood sugar. And we see these pathways. So let's go through each one of them 1 at a time. The first one that we have, and now we're gonna go to the 2nd photo, is called the polyol pathway. And there's 2 there's there's 2 reactions in this pathway. A and what ends up happening is we start to see that glucose gets converted to sorbitol, us and it does this through an enzyme. As you recall, enzymes help to catalyze reactions and help they facilitate the reaction.

Dr. Sal [00:11:11]:

And this is as a result of aldose reductase. Now here's the problem with this reaction a is that it uses this NADH, okay, to, provide a hydrogen add them. But then that NADH gets used up a lot in this reaction because we have so much glucose circulating, a and we cannot make this antioxidant, which is called glutathione. Glutathione and for those of you that may have gone to the health food stores and talk are the people there. Glutathione is an antioxidant which decreases oxidative stress. In other words, glutathione binds to a free oxygen radicals or reactive oxygen species, and it neutralizes them so it a sudden cause damage. And so what ends up happening is is we can't make enough of the glutathione. Over time, us all these reactive, species then start causing more and more damage, not only to the nervous tissue, but to other tissues as well.

Dr. Sal [00:12:15]:

Us that NADH or NADPH, actually, is also needed to make nitric oxide. A nitric oxide is released in the, blood vessels to actually cause the blood vessel to dilate. So they're vasodilators. Us, everybody's big on the beet juice right now because beet juice helps the blood vessels to produce more nitric oxide. It relaxes the blood vessels that helps dilate them to improve the blood circulation, and it also it also lowers your blood pressure too as well in a natural fashion. A so we get the buildup of this, Sorbitol, and eventually, us we start to see that any tissues that don't have the sorbitol dehydrogenase, which starts to take us to the 2nd phase, us are areas such as the kidneys, the retina, and the Schwann cells, which are the Schwann cells are these cells that cover a the the the axons or the nerve fibers. So they're like the coat that protects have that nerve fiber. So we get a buildup of this sorbitol, which is a sugar alcohol.

Dr. Sal [00:13:30]:

Oh, and by the way, sorbitol is used as an, artificial sweetener that they put in gums or even candies. And so the sugar alcohol starts to accumulate, a and what does it do? It starts to glycate nitrogens. Now nitrogens, as you know, is a is an atom. Okay? Nitrogen. A and when it's a part of a molecule, it makes it a protein. Okay? So a so nitrogens if you see a nitrogen on a molecule, you pretty much can determine that it's a protein like an amino acid. Us well, it glycates it. In other words, it adds the sugar moiety to this protein.

Dr. Sal [00:14:11]:

And us one of the proteins that I'm referring to in this case is collagen, and collagen lines a the outside part of the blood vessels. And so advanced glycosylated end products, as the term we're called, ages, okay, us then starts to, bind to the nitrogen in the collagen molecules of the vessels as well as a sudden, nerves. And then all of a sudden, we start to see, some damage occurring. So, you gotta remember, the cells of these organs of the kidneys, the retina, and the Schwann cells, they're basically insulin a independent. And what that means is that it doesn't require insulin to allow the sugar to move a into that cell. So sugar just moves freely across that cell membrane. What ends up happening is is that it doesn't work when the blood sugar levels are normal. A but once the blood sugar starts getting elevated, it starts to activate it.

Dr. Sal [00:15:14]:

It starts turning in, it starts creating an exorbitant amount a sudden of the sorbitol. So once we have that, we start to see that it glycates, the collagen molecules on the blood vessels. And at that point, you start causing damage to the blood vessels and the neural tissue, particularly in the areas of the kidneys, the eyes, a and the nerves. And that's how we end up with the neuropathy. The 2nd reaction, as I said, the sorbitol then gets converted into fructose as you could see in the diagram. A now fructose is 10 times better substrate of becoming glycated. And so now this leads us. Now we can go back to the original, hyperglycemia, diagram, and we see the next one is glycated us products or the advanced glycated end products.

Dr. Sal [00:16:12]:

And so what we start to see is this is when sugar binds to protein products, and it does it without the use of an enzyme. And if anything, it uses iron and copper to help that a reaction, proceed. So, again, it starts to glycate these, these structures, a and it it makes it abnormal. And so the blood vessels don't function or they start to get stiff. The blood, the nerves start break down. And the second thing about the ages or the advanced glycated end products is that they bind to receptors. Us and one of the receptors they, bind to is called RAGE, which is the receptor for the aegis. And what it does is it activates that nuclear factor kappa b.

Dr. Sal [00:16:57]:

Now a sudden hear that comes back, that NF kappa b then promotes proinflammatory mediators like tumor necrosis factor alpha, interleukin 6, interleukin 1 beta. Remember, these are these inflammatory mediators that we talked about, us that occur as a result of having, excessive amount of fat storage, and it promotes this nuclear factor kappa b to promote these mediators. And these are also a key target for atherosclerosis, and we'll talk about that in a later podcast. The other thing is is that when you have high levels of these ages, it polarizes the macrophages into the classically activated macrophages. Remember what we talked about before in inflammation us that you have 2 types of macrophages in the fat cells, the m one or macrophage 1 or the m two, the macrophage 2. Us. Right? The m ones are the ones that, in the initial trauma, go in and they destroy bacterial infections. Us, they they take away dead tissue.

Dr. Sal [00:18:03]:

So it's a very destructive state. And then after that's done, later on, the inflammatory process switches over to a more reparative state. Well, in this particular case, what ends up happening is it activates more of the m one stages. So a higher m one to m two ratio is a major determinant for plaque formation in, the microvasculature that supplies the nerves and then the nerves become, hypoxic or have a have less oxygen, and it starts to break down. Oxidative stress, as we talked about before, is basically where blood sugars or excessive amount of sugars us start to oxidize, molecules and they become these so called free oxygen radicals such as superoxides, sides lipid hydroperoxides, conjugated dienes. These then almost like radiation. They start shooting around your body, and they start doing damage to the cells and even to the DNA, which can cause mutations to the DNA. In the end, it ends up in the nerves, especially the dorsal nerves, a sympathetic ganglion.

Dr. Sal [00:19:14]:

And this is what causes what we're what is known as myelopathy, and that's the breakdown of the protective sheath over the nerve fiber or the axon. The other thing that it does is that it breaks down, the mitochondria, and the mitochondria is the energy producing factories in our cells. And if you destroy your your power plant and you can't produce enough energy for that cell to use, the a cell starts to break down. It can't do its function, and things at at point start to spiral downwards. And then remember, we're made up of a 100, a trillion cells. So if you do it to 1 cell, it's one thing. But once these start to accumulate, this is where all the problems come in, especially in the nerve damage and neuropathy then start to set in. One of the ways to prevent this us is with alpha lipoic acid.

Dr. Sal [00:20:10]:

Now, again, I advise that you take alpha lipoic acid, but you really gotta change your diet, man. You gotta get rid of those bad us, which we're gonna talk about on a later podcast. But you gotta reduce the sugar and carb consumption. Okay. Now the 4th thing in the diagram that we show, it says DAG, diacylglyceride, and it's a type of fat sudden can build up. Now in the nerve tissue, if it decreases, then it decreases this this enzyme which allows for sodium and potassium to flex in and out of the cell, which helps with the nerve conduction. And if the nerve conduction sudden now starts to slow down, then signals aren't being sent to the brain appropriately, and they could be or inappropriately, a and you start to experience pain or you lose sensation. In the vascular tissue now, a if you have an increase of this, DAG, which is the fat, it increases the so called protein kinase, and that also in the, us, vascular tissue decreases the sodium potassium pump, and that's where you start getting problems as far as us helping the blood vessel, to build the protein scaffold that it needs to maintain, its integrity.

Dr. Sal [00:21:34]:

Us and so as a result, it starts to break down. You start getting this fat and sugar interaction in the cell walls of the, of the vascular system or the small a tiny microvasculature, and that's when you start to have complications. The last 1 on the list is the essential fatty acid impairment. Us, diabetics or people with high levels of, blood sugar have an impaired conversion of linoleic acid to gamma linoleic acid, and this is just one of the essential fatty acids. And it's the GLA, let's call it the gamma linoleic acid is GLA, is important have for nerve structure and function. And it's required for normal neuronal membranes, which is the membranes of the cells, and it's required for normal regulation of the nerve conduction. So that means the sending of the proper signals down the nerve fiber. Us now some of the best treatments for that is really primrose oil that you could buy at the health food store.

Dr. Sal [00:22:32]:

Now they have other oils like borage, a blackcurrant and fungal oil that actually high have higher levels of, gamma linoleic acid or GLA. But somehow, us, they don't work as well because what they've determined is there's something inside that oil that counteracts the effects of the GLA, and they don't know what that is. So Primrose oil is also a benefit. So alpha lipoic acid, primrose oil. These help to, counteract the, the detrimental effects. But the bottom line is is you gotta cut those sugars, us and you gotta cut out those, those bad fats. And we're gonna go over that in one of our, podcasts yet to come. So I wanna thank you so much for for joining us on our show today.

Dr. Sal [00:23:19]:

If you enjoyed this episode, please be sure to leave us a good review, and visit our website and social media accounts to connect with us see even more. And if you'd like to see any of the sources, for this research in the episode, it'll be available in the show notes listen to the prescription. Until next time. I'm doctor Sal. Have a great day, and god bless.