81: The Cellular Energy Crisis – How Mitochondrial Dysfunction Fuels Metabolic Disease with Dr. Christian Jenski

The standard of care is downstream and it's the A1C and A hemoglobin. A1C is essentially a hemoglobin molecule, the same molecule that carries oxygen for us, part of the red blood cell, essentially getting glucose slapped onto it. So glucose is sticky, it sticks. So this is glycosylated hemoglobin. The life cycle of a red blood cell is about 90 to 120 days. So it's the average estimated daily glucose over three to four months. So you get that value and if it's below 5.7, they say normal 5.7 to 6.3. Pre diabetes, 6.4 and above diabetes. And if it's like 8, 9, 10, they get really scared. Below 5.7 is not normal. Technically it is, but it's not optimal. Early insulin resistance starts at 5.4. That's well documented. So you want it even below 5.4, but you're not going to be told that. So 5.3. Closer to 5 the better you are.

Welcome back. Once again, everybody, we're super excited to take a deep dive into some of the individual conditions of metabolic syndrome. Point being is that this concept of metabolic syndrome, it's kind of everywhere. It's a myochondrial dysfunction issue. And so we want to take individual diseases, diabetes, sleep apnea, pcos, even cancer, and take some deep dives on how we look at it metabolically. Testing we do. And then part three, we'll talk about some specific mitochondrial therapies that we can do with those. So. So we'll start with. What's the first one on the list here?

Diabetes, insulin resistance.

The diabetes is. Dr. Jensky, I understand it's your soapbox. You have so. So definition of diabetes, if my memory serves me correctly, would be a. A1C over 6.5. It would be a3 fasting glucoses over 126. Or oral glucose challenge tests could be pre diabetic. If you have the three fasting glucoses between 100 and 125 or an A1C. Depends. 5, 7, 5, 8, 5, 7, 6.

4, 8, something like that.

Yeah, no really mention of fasting insulin, insulin, glucagon, C, peptide levels. So. So why don't you talk about that a little bit? Because, you know, you know, typically the only place you're getting a oral glucose challenge test is if you're pregnant. Yeah. To look for gestational diabetes. But no one's really doing all the other stuff. People with minus functional medicine, people like us. So.

So the, the standard of care is downstream. And it's the A1C and A hemoglobin. A1C is essentially a hemoglobin molecule, the same molecule that carries oxygen for us, part of the red blood cell, essentially getting glucose slapped onto it. So glucose is sticky, it sticks. So this is glycosylated hemoglobin. The life cycle of a red blood cell is about 90 to 120 days. So it's the average estimated daily glucose over three to four months. So you get that value. And if it's below 5.7, they say normal 5.7 to 6.3, pre diabetes, 6.4 and above diabetes. And if it's like 8, 9, 10, they get really scared and great. We have criteria. But below 5 for starters, below 5, 7 is not normal. Technically it is, but it's not optimal. Early insulin resistance starts at 5, 4. That's well documented. So you want it even below 5.4, but you're not going to be told that. So 5 3, closer to 5 the better you are. That being said, it's a downstream marker that has many, many moving parts that could influence its value. So if you're not looking at a fasting glucose, if you're not looking at a fasting insulin both upstream of this, if you're not looking at a fasting lepting and adiponectin both upstream of that, then you can't see that full continuum of what's going on metabolically with that person's glucose control or lack thereof. And when you look at those parameters and you get them, and then you have a better idea of what's happening, you know where to intervene. You also can catch someone who has a very normal A1C and they might have high leptin, low adiponectin, they have early upstream metabolic dysfunction. Jump on it then. And then you never have to deal with the A1C versus say that person has an A1C that's in the pre diabetic window and their doctor says, here you go, metformin, that's your option. And they're like, whoa, whoa, whoa, wait a minute. They come see us and I get a fasting glucose, which is 84. That's not only normal, it's optimal. Fasting insulin, that's 6.5. That's not only normal, but it's optimal. Adiponectin and leptin also within normal range. 1 leptin low, adiponectin high. I tell that patient your pre diabetes is not completely predicated on the fact that your metabolism and your Insulin sensitivity versus lack thereof is off. There are other players. What are those other players? It's usually cortisol. So stress, it might be thyroid dysfunction or low testosterone. So hormones play a role. Could be their microbiome, could be toxin buildup. So there's lots of variables. If you're just looking at a downstream A1C and and then trying to treat it as if it's solely metabolic in the sense of insulin resistance, that you're going to miss the boat. So I get all those values that I just mentioned. I also then can calculate what's called a Homa IR score. You typically want that less than 2. And that's using things like glucose and insulin that you can get and just plug into a calculator. I don't do a lot of oral glucose tolerance challenges. I've had a few patients that we've done that on C peptide. Again, something you mentioned that's more if I think the person's having hypoglycemic episodes. But like, this is how it should be worked up. Like, what are your thoughts on that?

I agree with everything you said. One additional thing with the A1C is early my diabetes treatment career, we learn about the concept of the area under the curve and that it represents not just your fasting. This is A1C represents the area of the curve. So it's not just. If you can imagine a graph, you can imagine you're the Y axis is your sugar and X axis is time with your meals. When you have a low level glucose then bumps up with a meal and it comes back down and it does that three times during the day. That is area in the curve that the A1C represents. When you see. Also when you see these normal things you mentioned A1C is elevated. What that means the air into the curve is elevated. So you might have normal fasting sugar, but what's your meal look like? Yeah, post granular, pushing it up and it takes you four hours to normalize, you might kind of get back down to that, you know, and so that's where also like knowing what these things actually mean. Not just. And then knowing, okay, you're fasting, insulin is normal, your glucose is normal, ignoring the okay, then the question is okay, that's where. Sometimes either I don't necessarily use a lot of CGMs because people can just get an ACCU check and check it. Fasting in the morning, you know, an hour after breakfast, before lunch, an hour after lunch, before dinner, after. And they pick up this. This phenomena. Yeah. And when they do or you get to see Jim. They. You'll see. And sometimes people are amazed by. It's like a stress test of your meal. You eat breakfast. All I have was oatmeal.

Yeah.

Oh, okay. Yeah.

And she sugar up.

Yeah.

And I see it with apple and beets and carrots and things that are deemed to be very healthy. Yeah.

So that's important as well because it could be as well like you're eating.

Response to the meal. Yeah. That postprandial hyperglycemia after meal high glucose and then the associated and correlated postprandial endotoxemia. If your gut bugs are off, you're releasing a lot of lipopolysaccharide that's also driving up your blood sugar and that's the inflammation is driving that pathway. So they are self perpetuating. They are side by side. But that's the big problem for sure.

And metabolic endotoxemia.

Yeah.

Is metabolic issues driven by these gut toxins that go to the portal circulation can be dragged across. Driven by the food you eat.

Right.

So yeah.

So all of a sudden they're like high ketogenic diets. Like the high fat foods over time will drive up lps.

Yes. I love coconut oil. I love it, I use it. But it can actually draw the drug. And then all of a sudden why is your cholesterol now 280?

Yeah.

And that's when your body's ways of trying to compensate for this metabolic endotoxemia.

So, so how do you treat it? So say you worked it up and someone's got, you know, pre diabetes or maybe even diabetes. Do you dive right into meds? Is it situation specific? What do you like to use from a lifestyle standpoint through supplementations?

I mean, 100 depends on the person, their stage in life. If you're, you know, female in your 20s, I'm going to give you definite recommendations. If you're a female in your 50s, you know, but you got to clean the diet up. You got to remove processed foods, you got to remove industrialized seed oils, you need to remove high fructose corn syrup, environmental toxins and chemicals, all the basic functional mass and stuff. You got to focus on sleep. If you're not sleeping well, if you have sleep apnea and you're not, you know, that's going to affect it and stress levels back to your cortisol thing. Like this is like the foundational stuff that you got. You need to become professional athlete and your health with the basics and not jump to, you know, GLP.1s Nozempic and metformin and berberine or whatever herb, you know, cinnamon chromium, whatever you decide to use. Alpha lipoic acid. Yeah, I know it's like don't do that and keep on, you know, get off artificial sweeteners. Artificial sweeteners actually are, will mess up your hormones. They're called neuroendocrine disruptors. So I start with that. Sometimes, depending on where they're at, I'll use interval fasting. Depends. And I'm not going to do that. Some within some individuals. And then it's like okay, great, you're already doing all that and still off. Cool. Let's do nutritional analysis, fatty acid analysis. Are you deficient in D, which a lot of these people are. Then we address that and then once we get through that, then setting on some of the cool fancy things like your herbs like berberine gymnasta, alpha lipoic acid, nac, I mean all those kind of things.

I love berberine. I think berberine is great for this and I agree with all that and I will do some of these things and I'm sure you do the same concurrently, like get them to commit to lifestyle but also maybe add a little supplemental support along the way. Cuz then they're doing both. That's why supplements are called supplements. They're supplementing as time goes by for your lifestyle to take over. I mean that's just literally what's happening. So berberine is great for metabolic in general because it's, it's basically natural metformin and it doesn't have the side effects or the nutrient deficiencies that go along with it. And in addition it can help with the lipid profile. In addition it can clean up your gut bug. So that's a nice broad sword that I use a lot of alpha lipoic acid because it's insulin sensitizing, it's antioxidant recycles glutathione, your master antioxidant chromium. Only if your chromium's low. If you give someone chromium who has enough chromium, it's not going to budge much. Mag magnesium is necessary for insulin receptor function. If your mag. Yeah, if your mag's not working, if you don't have enough mag, your insulin receptors aren't working. And then there's like, you know, cool formularies. I like some that, that try to stimulate beta islet cells from the pancreas to make more insulin. But yeah, all those other things D like that was really smart to say D time Like D just affects all of this. And if your D is low, like, good luck getting any of this. Right.

And there's all the typical. Of course we're checking your thyroid. Like, I. Yeah, we don't mention everything because we can't mention it all every time, because otherwise. Yeah, but it's like, obviously you want to get your thyroid squared away, but.

That'S what you meant by like a woman in her 20s versus 50s. In her 20s with this, you're going to be like, I got to look for hypothyroid, I got to look for pcos. Like, that makes sense. It's not that you're not looking for that in the 50s, but like, PCOS would probably be diagnosed by then. And so it's the flip of I'm looking at the person in front of me, I'm listening to their story, that gives me, in my head a mental differential of where I'm going to go with this.

And if they're a mold patient, if they're a long covered patient, they're a Lyme patient, then all of a sudden you're going down a different pathway. You're like, yes, you have metabolic issues and you have these other things we need to address. So that's where this gets fun.

What about the next one? Before we go into pcos, which I'm going to have you jump into? I think we should say. I think we should talk about with regards to diabetes. I mean, do you have patients reverse their diabetes? Do you have patients reverse pre diabetes? Do you see that? Is that. Is that possible?

It is possible. I've had type 1. I had a young man, type 1 diabetic, came to me. He was on pump and he was getting about 80 units of insulin a day. Type 1 diabetes. He's had this ever since he was a kid.

Yeah.

Got him down to 10 units a day of insulin.

Wow.

And we. It was diet, nutrients, exercise.

That's an extreme version of treatment of this. I mean, like, that. That's an autoimmune condition where your pancreas is not making insulin. That person will always need insulin. But you got him down to the minimal amount of insulin that he possibly.

Got him down to. Physiologic doses. Yeah, super physiologic doses to normal physical.

Like, I mean, that's pretty incredible.

Yeah.

But like, Pre diabetes, type 2. All the time, right?

All the time, yeah. Me, I remember, like, one patient who, early on my career, who was actually a truck driver, and he came in, he had an A1C of 11 and for truck drivers, it means you've done. Your career's over. So I was doing his driver's thing. He's like, doc, give me a month. I'm like, okay, whatever, dude. This is what you need to do for a month. We checked his A1C in a month. I know he's supposed to do in three months at the end of the month. And it was eight. Now you can drive. Crud. I'm gonna give this to you for two months, buddy. Keep him hooked in.

Right.

In six months, we had his A1C. Lesson seven.

That's.

And the only drug he was on at the end of that was Metformin.

Metformin, yeah.

Yeah. And he changed every.

Absolutely. It has emerging pro longevity data.

Yes. I'm losing risk for cardiovascular disease, but I've had cases like that. But those situations where we had massive responses that people were all in.

Yeah.

For every one of those, I have five people who come and expect supplements only to do it for them. They don't want to change lifestyle. They don't want to change diet.

Yeah. You got to do all.

They don't want to treat their sleep apnea because I don't like the machine. Yeah. And I don't want to take all those supplements. And why am I not getting better? It's like, you know, I. Sorry I left my magic wand home today.

Yeah. You got to submit. It's what you said. It's. You have to be. That was a great analogy. You have to be a professional athlete at the lifestyle stuff.

Yeah.

And I think that is always what we're about. We talk about these fancy labs and we talk about supplements, and we talk about even medications and compounded things like peptides. But the reality is, is that that is the core of what it is that we do. It's not for everybody.

Yeah.

Some people meet you halfway. Some people are all in. Some people, they just struggle with it. And that's okay. That's their journey. And I always respect and honor that and try not to make them feel bad. But they should also temper expectations if that's the case, because you have to get all in.

I mean, I had one young lady come to see me a while ago who only came to me to get did a surgery pre op evaluation for a gastric bypass surgery. That was the only reason she came to see me. And in a functional clinic. This is my regular. Okay. She's on the functional side now. This is my regular clinic because she saw the power of it. So I was like, look, let's you guys see me every month for three months. We have to say we're trying something. There's this drug, and this is. I used the GLP one. I think it was Victoza. I used Victoza at that point in time. Like, this drug works as well for weight loss, according to literature, as a gastric sleeve, which is what you're. You're looking at. How about we try this while we do a few things? And she rolled her eyes. I was like, okay, whatever. Came back a month later, £15 less. Came back a month later, said £12 less. She lost about £50 over five to six months. She was all in. End up losing close to £100. And she lost actually as much weight as the surgery would have done for her. Without the surgery.

Yeah.

Awesome. And so. So I have all these stories, but unfortunately, for every one of those, I' got five more where it's like, just people aren't quite ready to take the deep dive.

Yeah. Hopefully they will be. All right, let's talk about pcos. So talk about the diagnostic criteria and then, like, how you work this up.

So I love talking about diagnostic criteria. So American College of Obstetricians and Gastro Gynecologists.

Yeah, I keep on trying to say.

I know people try to say gastroenterologist. No, College of obstetricians and gynecologists. There we go. Perfect. Awesome.

Nailed the landing.

Yeah. There we go. Yeah. Oh. So, yeah, it's like, I love going over diagnostic criteria because it let. In a way, it's like, oh, my gosh, this is what I used to do. And it's so little. So what is polycystic ovarian disease? So it's basically having either skipping your cycles or not having cycles, not ovulating. Okay, that makes sense. You know, you have signs of excess testosterone, androgens, which could be like hair growth. Hair on your nipple. The linea alba, which is the line down your belly, gets the hairs get a little darker. And then polycystic ovaries on ultrasound, right? Yeah, that's kind of sort of.

Yeah. Now, there are some serum. Serum markers of hyperandrogenism as well. So I can elevate testosterone on a blood panel. And you're assuming they even get blood, which usually doesn't happen typically.

And they might do some additional labs if things come off. And there's this thing called congenital adrenal hypoplasia, which I don't think I've ever had a patient with it.

I've had one. It doesn't hide like they're diagnosed. By the time they see you, they're already followed by endocrinology. Yeah, they're on all the right steroid, hormones and other things that they need like that. Get all the things. Like when we talk about these conditions, we're talking about excluding the obvious bad stuff like prolactinomas and CAH and other things. And then it's like, okay, this is looking more like pcos. Okay. Do they meet diagnostic criteria? Okay, do I even need that? I don't. I mean, if they want to label, sure. But if they don't meet diagnostic criteria, but they have, let's say one out of the three or maybe one and a half. Like there's a soft history of hyperandrogenism, but their T is currently fine. But they have the metabolic derangements that go along with it. I'm still treating it as such. Right. Like I'm still using the same things that I would use because it's only going to help them.

Well, how many people do you see come and I see this all the time. They went to the ob, they went to endocrinologist, they told that they have fertility issues. I've got some endometriosis, maybe a fibroid. Yeah, pcos. And you're like, okay, you don't necessarily meet all the criteria for this one, but you've got endo, you've got some fibroids and you have infertility. And many, many times young women, the way their PCs gets diagnosed is they're trying to start a family and can't start it. And that's an unfortunate way to find out. But it's interesting how, you know, one of the medications that we'll get started on to help with fertility is metformin. Which is what, an insulin sensitizer, Right?

Yeah, they say metformin and then hormones, usually birth control. Or if they need their cycles regulated.

Yeah. Or if they're not trying to have a family out, which is unfortunate because the oral estrogen will drive estrogen dominance even further through the range, which can drive yeast overgrowth. And strangely enough, that also suppresses your androgen production, which brings the androgen down. But then all of a sudden, now the outer third of the vaginal vault in your labia are antigen dependent tissues. So now you get cystitis, uncomfortable down there, painful intercourse, recurrent bladder things. The urines are normal. You don't realize this is all induced by your suppressed androgens now and estrogen dominance. And so it's like, well, I fixed one problem and now we have two more. So it's. Anyway, so labs, we do labs alike, you know, free and total testosterone, sex hormone, globulin, fsh, lh, progesterone, estradiol. Doing a full hormone panel, but also metabolic labs. I want to know fasting, insulin, A1C, thyroid status, you know, also because PCOS is an autoimmune spectrum disorder, I'm looking for thyroid antibodies, thyroid peroxidate, thyroglobulin. Exactly, yes. But I'm also looking for ana. I'm looking for celiac markers, anti gliadin markers. I'm looking at your HSCRP. Do you have a marker? Because CRPs are interesting because it's also an antimicrobial peptide. And when that's elevated, that can go along with low grade infections, whether it's dental or whatnot. Looking at your sed rate, looking at your white count, if the. I've had several come in, the white count's nine, which is normal. But we know white count. Yeah, it's pretty high. Yeah. And so all of a sudden, what other inflammation is going on in your body that can go along with this PCOS that if we get those markers to come down. I mean my experiences pretty much universally. The other stuff comes down. Yeah, it comes down as well.

I sometimes do expanded hormone testing. We just did a, a few pieces on hormones so we don't have to belabor that. But I might do a rhythm kit. I might try to capture what their cycle looks like. I might get. I actually usually mostly most of the time get like an essential estrogens detox kit. Cause if they're estrogen dominant, I wanna see that they're breaking it down. Usually they're not. I mean they are, but they're not neutralizing it appropriately. And if their gut's not working, they're not clearing it appropriately. So you work there too. And that's like working really upstream because then that's helping the problem in general. That then might autocorrect some of these other issues. So how would you treat it?

Treat it? Always, Always the basics, you know, the triangle of health, gut stress, sleep, environment. I'm looking for environmental toxins and chemicals as they're mold in your house. I almost always put these young ladies on blood dose naltrexone. It's great for dealing with that autoimmune spectrum phenomena and inflammation. If your tregs are off TH17, TH2, TH1, which you've got, you love diving in that and going into that, getting nerding out on that here.

If it's off, your adaptive teeter totter is imbalanced.

Your little teeter totter is off. Right. If those are off, guess what Lotus Naltrexone. It's a tonic. It just kind of balances things.

And if it's normal, puts the kid on the side of the teeter totter. That balances it out.

There we go. Fair enough.

It's kind of what it does.

I will use metformin.

Yeah.

Because metformin increases Akkermansia mesenophylla, which is one of the particular bacteria associated with Medlock syndrome. Like low levels associate up to tenfold.

They make short chain fatty acids like butyrate rich does. What does GLP1 does?

This nature, it's a natural part of jail one. It also helps to prevent some sensitivity. So if you're having the hair issues, you're having polycystic ovary stuff, you can help with that.

Yeah.

Strangely enough, metformin also helps with weight loss. It's one of the weight loss drugs. Caveat is can deplete CoQ10 and B vitamins. So I'll make sure people are taking B12 in particular. And then you've got to work on some kind of detox. There's almost always atoxic components are N acetylcysteine, milk thistle, silomeric extract, glutathione if necessary. This is on top of checking the fatty acids. We're checking the status. How many of these young ladies do you see have sibo?

A lot of them. Most of them.

Tell us about SIBO and pos.

And going back to the toxin component, there was a study that showed 40% of women diagnosed with PCOS have evidence of elevated BPA levels. So all these plastics, endocrine disrupting chemicals, these pops, persistent organic pollutants, these all play a role. Clearly. Placebo, small intestinal bacterial overgrowth is a gut issue. Your small intestine should only house about a couple thousand bacteria. They're basically peacekeepers. It's all about nutrient extractions, processing and packaging your food, and then you kick the rest down the pipe to go to the colon, where trillions of bacteria exist to do all the things they do. Fermentation, short chain fatty acid production, stool formation, water resorption, et cetera. When bacteria from the colon translocate to the small intestine where they do not belong, even some commensal bugs, oftentimes bad players, that's called sibo, or small intestinal bacterial overgrowth, where you're Making lots of gases that can cause symptoms like diarrhea, constipation, bloating, upper GI symptoms. But more importantly, the immune issues that occur secondary to that, like autoimmunity, like inflammation. And the toxins that are being elicited will get into the portal circulation, which is the liver, that then affect you systemically, which means gut translating into body translating into inflammation. Or the fire started my gut, now it's system wide. Now I am metabolically dysfunctional. Maybe my mitochondria taking a hit and my hormones go wonky. And now I have a diagnosis of pcos. So I mean, when in doubt, it can, you can tie it to the gut, but sibo's incredibly predominant. And if these individuals have chronic stress from their issues, the stress of trying to get pregnant, not being able to, and being told you're infertile, or stress around other things or their hypothyroid, those are also setups for sibo because of the decreased migratory motor complex or poor vagal tone that makes the gut go slower, that leads to that translocation of bacteria. So, yeah, I mean, you gotta look at, in these patients, just gotta look at top down approach, right? The hormone hierarchy, look at gut, that's bare minimum. Then expanded detox, all the while look at metabolic stuff. That's kind of how I would handle it too.

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What about gout and kidney stones?

Yeah, we'll put gout and key stones together.

They kind of go together.

Yeah. As far as lab evaluation on these people, I'm obviously doing uric acid during a conference of metabolic Panel, a cbc. I'm doing all the metabolic stuff we already mentioned, so I'm not going to belabor that point.

Yeah.

With oxalates, you know, with kidney stones, it's like, typically, you want to make sure they've had the evaluation because there are uric acid, kidney stones. There are different kinds of kidney stones. You'll get from bacteria. Calcium struvite, but they're 90% of them are calcium oxalate. Correct. So by the time they get to us, they've already had that evaluation done. Sometimes these individuals, actually, you'll do a urine on them and see oxalate crystals in the urine.

Yeah. And you can get those on the neutral and the metabolomics. The organic O testing.

Yeah, they'll show you. That's if you want to. Okay, let me see where they're at. Now, if the urine's not showing it up, give me a number. Because the urine dip is not a number. It's like a plus plus, you know, kind of thing. And then let's work on your metabolism. And it's really interesting how with your kidneys, things like alkalinizing your urine for a bare minimum, that minimizes the chance of making stones. And that's really relatively easy to do, whether it's using potassium citrate, magnesium citrate. There's a potassium citrate, magnesium combo.

I use adequate hydration, which.

Okay, so, yeah, obviously, adequate hydration. Strangely enough, actually, our house, our water was actually out, was actually acidic. So we actually had to alkalinize the water at our house, you know, which was easy to do, but you have to check it.

Right.

If you're still.

Would you have these patients drink alkaline water?

No. Yeah. Alkaline water, I think, is a good concept gone awry.

Yeah.

You know, alkaline water in nature is basically coming from a mountain. The stream is going through rock, it's picking up bicarb and coming alkalinized. You know, it's important. You know, you don't want to be consuming acidic water. But ultimately, when you're trying to alkalinize your body, the question is which? The acidity of your urine and the acidity of your saliva, you know, how do you get that to improve? You know, I tried eating lots of green leafies. I tried green smoothies. The only way I eventually got my urine alkalinized was using bicarbonate citrate and potassium magnesium. And now I wake up in the morning and my little strip is dark blue.

What's your cutoff? Greater Than you want your urine to be greater than 6.5, greater than 7.

If this day I just wanted to turn. Yeah. Like it starts turning bluish. Like about that seven mark. Yeah. And the reality is I'm gonna eat protein, I'm gonna do whatever. It's gonna go downhill. The interesting thing about my. My mouth, it's never been acidic. It's always been alkaline. And I don't really make cavities. I don't make cavities. I've never had a cavity. I don't make tartar. And it's interesting people who have oral microbiome issues when you have them start checking their oral microbiome. It's acidic.

Yeah.

And just changing the ph.

How do you keep your mouth so alkaline?

For me, it's my diet. The hard part for me maintaining is my. You're to check it. You get a little P hit test strips. It's 5.5 to 8 rates.

Do you use buffered vitamin C at all to alkalinize?

No, I don't use buffered. I've actually done the testing myself. The best, if you're looking for things like that, the natural calm magnesium citrate is the best for that because it's basically bicarb and it's mag bicarb with citrate. If you're looking for that, that can be helpful with bowel movements as well as sleeping at night. But what it comes down a lot to is just minerals. Mineral deficiency.

And you'll clear these things out then. I mean the whole point of all this conversation is that you're then going to lower these oxalate levels. You're going to lower these uric acids.

Well, you're extrude them better when you extrude them. Because here's the thing. If oxalates. Uric acid is in your blood and your. It's in all the tissues in your body. I had a GAL flare that's not just in your gout, it's actually in your heart. They can actually do biopsies of people's hearts. We'll see these little crystals. It's really interesting you mentioned about like GAL flares where you get the crystals in your joints all the time. But for some trigger makes the PMNs, the polymorphonuclein attack them and eat them up and they release these hydrogen peroxide, which causes the whole gal flare thing. We don't know why the process stops. It'll eventually go away on its own. We can speed that up by slowing white Cell migration, which is what colchicine does, that blocks the micro stuff. But we ultimately don't know what causes the flare and what makes it your body just naturally immune dysregulation, whatever, you know. But you have these tissues everywhere in your body. Aches and pains, fascial pains, general inflammation. Yeah. The thing is, okay, kidney stone's great. Whatever. I'm worried about kidney function. And build up either oxalates or uric acid is correlated in the elderly with CKD stage chronic kidney disease. And so for me at 52ish now, I'm like, I want my kidneys working while I'm 80.

Right.

Anyway, alkalization minerals, and then those are kind of like general. Obviously, if your uric acid level is over six and you have gout sometimes, that does require allopurinol.

Yeah, allopurinol or colchicine. And if you're in pain, they do NSAIDs, which I don't love. Steroids are actually the new standard of care. You get a course of prednisone or sodium Medrol instead of endometh.

Propensal. I learned that, you know, 20 years ago. Knocks it out so quickly. Depends on the patient. You know, it depends on where they're at.

And then. Tart cherry, low purine diet.

Yeah. Avoiding high fructose.

Fructose is the evil. All right, let's move on to dyslipidemia. This is a pet peeve.

Well, we talked about this a bunch before. I don't know if I want. Because we talked about this elsewhere. I don't know how much I want to talk about, you know, looking at triglycerides and L.P. and your apolipid protein and particle number, particle size and non HDL, which correlates with APOB and oxidative.

Stress markers like, say, isoprosteins, oxidized LDL, myeloperoxidase, Lp, PLA2, which inflammatory markers. So you gotta get an expanded profile. It's the short version. And then have someone help you to get the moving in the right direction. It's complex. We can do an entire cardiovascular lecture. It's part diet, part gut hormones, genetics, part toxins. Like it's your body responding to something.

I'm gonna put this out there. I was actually talking with one of my friends a week or two ago, and he sees, you know, high level functional person gets peptides and we're talking about his numbers. He had never had a calcium score done. I mentioned it to him. He was like, what's that?

It's crazy.

And I was kind of like, what do you mean a calcium score is. Yeah, I mean, okay, how do I apply this? Like you need to work with someone else maybe.

Yeah, you need to work with someone.

Else who's actually going to take care of.

Yes. So it's the continuum. Again, my favorite analogy.

Yeah.

If you have risk, don't you want to know if you have early disease? How do you know if you have early disease? Get a CACCT if it's zero, Great, you have no calcification done. Go even deeper and consider getting a cimt. Study carotid intimal medial thickness, ultrasound, estimate your vascular age, maybe a surrogate for soft plaque. If someone can do an endopat, get an endopat done. Or go and get a clearly study. It's like an external catheterization. And now you know exactly where you are in the continuum. Do I have any disease? No. Great. Let's keep really working on this risk before I get that disease. Because once you get it, it's hard.

To get rid of it when those individuals. That's key because if all those things are normal, you've done these anatomical evaluations and you don't have any blockage in your arteries, there's no thickness intimal wall, you don't have any soft plaques in your. Clearly your calcium score is zero. Then we're chasing numbers. It does take decades to develop cardiovascular disease. So we're in this realm here. And if we get those numbers down, ain't got to worry about this.

And it also guides your therapy. If they're being browbeaten about taking certain drugs that you don't think they need and then you have some proof that they don't need based on the absolute risk. Right. The number needed to treat if you're doing primary prevention. If I have a patient who has a csect that's a 0 and a CIMT that's equivalent with their age or even younger than them. And their cholesterol is 250 and their LDL is 150. No, you don't need a statin because 1% of people in that group will get benefit. One out of a hundred people for primary prevention. The number needed to treat for secondary prevention is 1 out of 37. Best case scenario. So 36 people aren't getting benefit from statin therapy alone. What else you gotta do? What are some of the things that you use? I mean for lowering lipids, omegas. I mean it's fiber.

Well, it depends what's elevated. Yeah, the total cholesterol if it's between 200 and 240. According to Japanese research, that actually has the lowest alcohol's mortality. So if it's mine, mine runs about 220. So what are all my other ones? So I want to get the LDL particle number down. Lots of ways to do that. Nice. In Omega 3s, I've had great results with getting really high quality extra virgin cold pressed olive oil. I've had some patients drop their numbers like 20, 30% just with 3 tablespoons of olive oil from the olive oil tap room here in Richmond. You know, if their LP is up, I'm gonna use some garlic, niacin. It really depends on what numbers are off. If they're homocysteine, zelevated, they're getting, you know, methylated B vitamins, mag. Yeah. Choline, yes. All that kind of stuff. So it really depends on what's elevated. That's one of the things cool about metabolic cardiology is once you do all these things, then you're like, okay, cool. What knobs do I turn?

Yeah.

It's all on top of diet and lifestyle, of course.

Yeah. Start with every single one of these patients with two things and I say it over and over again until they, they go from laughing to kind of looking at me like I'm crazy. And it's official. And fiber. Why? Because most people are low in omega 3s and don't eat enough fiber. And those are the two lowest hanging fruits that are gonna have the most bang for buck. You get over 40 grams a day of fiber, you get your omega check like greater than 8 and a nice ratio of threes to sixes. You're changing a lot physiologically in a very beneficial way. Then you layer other stuff in, or if it's really bad, you can concurrently do so. But it should be based on the literature. I like red yeast rice. I like plant sterols. I don't use a lot of citrus bergamot. I definitely use niacin. So you just kind of pick and choose what, what you need. You give it a trial, you follow the numbers, then you pivot like that's how it should be.

Before we move on, the one thing I want to say about the fish oil, you know, taking omega 3s lowers your risk of sudden cardiac death. 50%.

Yeah.

Which is huge. And if your omega 3 levels are low, you have an equivalent risk for heart disease as a smoker with normal omega 3 levels.

Yeah. That's crazy. That's exactly right. That's why I say it like A lunatic.

Let's skip to. Because we don't want to spend too much time. I don't want to hear us ramble. Actually is the truth. Fatty liver disease. I feel like this is something we can do. I've had patients have their elastography testing normalize, which is a marker for fibrosis. Normalized people have their ggts and ASD alts. Besides all the basic stuff, you know, we assume, what are other things that you're using for metabolic associated fatty liver diseases?

Yeah, I was £230. I'm currently £167. I had gut dysfunction, including sibo. I had heavy metal toxicity. I had sirs. I was not managing my stress. So I clearly had fatty liver disease. I was on blood pressure medication. I was pre diabetic. I wouldn't take metformin. My lipids were high. None of that's the case now. And I reversed my fatty liver disease. So clearly you can do it. That being said, for me, it was a drastic lifestyle change. Starts with foundations. I think we're beating that to death, but I think it's on purpose. I don't eat gluten, I don't eat dairy. I don't eat processed food. I don't drink alcohol. Completely detoxified my home and my lifestyle. Heavy metal chelated. Based on testing, got my dentition right. Purify my air, filter my water. And then I take things that are naturally detoxifying in my diet, like cruciferous vegetables, like artichoke, like asparagus, like parsley, like cilantro. Things that are literally helping modified citrus pectin. So eating citrus, peeling the fruit and eating that pith, that great part, getting enough fiber in my diet, sweating with exercise, sweating with sauna, all those things are important. And then things like vitamin E have good reports in the literature. Things like milk thistle, which the key component is called silymarin, globe artichoke nac, glutathione, PC, which is phosphatidylcholine. These are all things that are incredibly important to help the liver heal and reverse fatty liver disease into normal liver function, not disease.

And those are all great. You know, when we started our training early on, we've learned about lipid therapy with mold, stuff with water damage, building exposure. Yeah.

Patricia Kane stuff.

Yes, exactly. And it's interesting how a lot of stuff to help us. The peroxisomes clean out toxins also help with the peroxisomes in the fatty liver. Yeah.

So plasmaogens have a role.

Yeah. Butyrate And I'm now using Ursa Dial because the local gi. Well, not the local. The GI Doctors. Nih. I'll copy the NIH doctors. But it's literal on your sodiol. Which is. Which is a. Which is a bile acid extract that actually ramps up peroxisome function. So what that does is all these dysfunctional fats, these dysfunctional lipids. It's like burning off your old engine, burning off battery, burn the stuff off.

You're prescribing that?

Yes.

And you're getting it covered.

Yeah. Awesome. Yeah.

Because isn't the indication for that gallstone resolution, which I've never seen happen, so I just never even try it.

Well, we start using it for gallstones back in the 50s. When having the surgery for gallstones, it's like, we can do this laparoscopically robot da Vinci in 45 minutes, and you can go home in the afternoon. It's like, well, you're gonna take these couple pills that might elevate your lymphoma a little bit for the next two to three years, or you're gonna just go into the. You know.

Yeah.

So, no, I don't know if that many people do that anymore, but for the fatty liver stuff, it's huge in the primary barrel cirrhosis world. In the liver transplant world, they're using this accident to maintain liver function, to prevent. In the autoimmune liver disease world, to prevent a secondary autoimmune process from attacking the liver. So it just is like. It's. For me, it's like a very small jump to be like, okay, metabolic stuff. Let's. Let's do this.

Yeah.

If insurance won't cover your sodiola torso deoxy, the dosing equivalents. I looked this up a while. The 250 milligrams, you need to dose the TUCA a little higher than the. Based on what the literature is the equivalent dosing. So you're looking at probably 750 to thousand of the Tucker, which is what Dr. Kane recommends with the lipid protocol stuff. So all of a sudden it's like. This all kind of makes sense.

Yeah. Also, besides helping with detox through what you just described, it's also a natural antiseptic, so it's keeping balance in the small intestine. So there's that SIBO link again.

It does help with controlling. Yeah. So cool. And type three Alzheimer's. We'll briefly talk about this. You know, the whole Dale Brinson recode protocol should be its own kind of thing because Yes. I mean, I did that training years ago. It's literally its own kind of thing. But let's talk about briefly, if someone has cognitive decline, their MOCA score is going down, many cogs going down, or just they're forgetting things and they're worried about it. What kind of labs are we doing to figure out if these person's a potential type 1, type 2, type 3, type 4?

All the labs, if you're working the Bredesen protocol, you have to count for all the subtypes. Now, that being said, you might rule a subtype out by history. Right? Like someone's never had trauma. You know, it's not traumatic. Okay, great. But vascular, glycotoxic, traumatic, inflammatory, cold, hot. There's all these different subtypes. And like ultra trophic, I think, is one of them. So essentially I'm looking. Do they have nutrient deficiencies? Do they have hormone imbalances? Do they have metabolic dysfunction? Do they have inflammation? Do they have biotoxins? Do they have chronic infections? Do they have heavy metals? Like, you're doing that whole workup. I'm doing that whole workup. So that's all the labs that we've talked about and more. But then I'm considering other parameters, like the genetic component APOE. I'll look at their APOE status. Are they E3, E3, which is same risk as general population, or do they have an E4, which increases risk? And if you have two exponentially more and there is a new blood test out or blood tests that are out now, it's, I believe, called AD Detect. And really it's two labs in one. And it's looking at a beta 4240 ratio. And then P Tau 217. There's another lab called neurofibrillary light chains. And then there's another lab that I think only LabCorp does, called GFAP. It's a LEO, fibrillary associated protein, I think is what it is. So there's emerging data on each of these tasks correlating with specific cognitive decline. Not all Alzheimer's dementia, some others like ALS or TBI. But the 80 detect one is one that's showing good emerging evidence. And when you see someone whose score is off, it rates it as low likelihood, indeterminate or high likelihood. I mean, if that's off and they have the genetics and they have the clinical presentation, like they got to get an amyloid PET to see what's going on, you know, and so then you're doing that workup usually a neurologist is doing that workup a little beyond my scope, but that's how I'm working those up.

And the reality is here in Richmond, usually they're going up to D.C. to get a spec scan. We can do the neurops here, but most neurologists aren't ordering. They might order a scan. They think they have Parkinson's. I've had to happen with a few patients, but that was actually at the university, not the local neurological group.

I have a patient who had a DAD scan and I'm not sure where she got it. She comes down from Fredericksburg. Either way, both my Parkinson's patients are biotoxin patients. By the way, it'll be interesting to see if that diagnosis is true or not.

Many of mine were several patients who retired, went to long term care. They were retirement communities. They were these really great retirement communities and they started having issues and you know, a year into it, it's like they had mold in their unit and the air conditioner in their unit. So you move to this place to take care of the rest of your life and then you start going downhill, just molding the place.

I was 39 when I started my medical journey. I'm 50 now. I thought I had dementia. My brain stopped working. That's when I got scared. That's why I sought you out. You think I wanted to hang out with you?

Of course you did.

My brain was broken and clearly it was related to something else. So there's a large percentage of people out there probably being misdiagnosed. If you look at the statistics with regards to what's true when you say dementia, what's vascular, what's senile, what's Alzheimer's like? Depending on who you ask, you're gonna get a different set of numbers. There's no uniformity, meaning that there's a lot of overlap and there's a lot of misdiagnoses. So the key is if you suspect it, work it up. And if you can't handle it, get them to the right place. But there's more and more tools now just basically understand that this is a metabolic disease.

I've had a couple of patients that they got this thing called collagen. One got collagenous colitis, one got microscopic colitis. And those diagnoses occurred about a year and year and a half before they start having some cognitive decline. Yeah, and it was really interesting to see how that gut new diagnosis preceded their cognitive decline.

I mean, that's what the amyloid is. It's an immune defense against some agent that it thinks is attacking. So antimicrobial peptide, like is this bacteria, is this yeast, is this a virus? So it's your body's defense mechanism is what it is. All right, cool.

Let's wrap this up. So these are a deep dive into considerations for the different conditions of metabolic syndrome. Next, let's talk about mitochondrial function because ultimately all these things come down to mitochondrial function. So I want to talk about that in relationship to metabolic production and then what are some things we can do for addressing mitochondria which ultimately comes the root cause of even aging now?

Everything. I mean cancer it all, it's all mitochondria. Yeah.

So cool. Well, if you have questions, please post them below. Otherwise, hope this information is educational. Please like share, subscribe all things I forgot to say at the beginning and otherwise we will talk to you all later.