DIP Episode 328 - B12 Deficiency and The USMLEs (+ 7/29-31 2CK/3/Test Taking Course Reminder)

Okay, welcome. My name is Devine. This is episode 328 of the Divine Intervention podcast. And in this podcast, I'll be talking about vitamin B12 deficiency. Vitamin B12 deficiency is a big topic shows up on the exams in many different ways. And it's just something that unfortunately many people don't really understand as well as they should. So today I'm going to try to break it down and I'm going to focus especially on the things that they love to test on on MBME exams. And before you go into that, I just want to announce as a reminder, if you're taking step two secures, step three, any time soon, I do have multiple review courses coming up this weekend, pretty much every two weeks afterwards. The one that's coming up soon is going to be this starting on Thursday this week with an MBME test against strategy course. It's going to be from two to four 30 p.m. Pacific Standard Time. So that's like five to seven thirty Eastern Standard Time on Thursday. Basically, in that course, we go over very high fidelity means of analyzing exam questions, picking out the correct answers to exam questions, approaching ethics questions. We won't discuss ways to get the answers right, even for questions where you don't really know the content. And then we have a review course is going to be 20 hours long and it's going to be taking place on Friday and Saturday. It's going to be 10 hours each day, at least hopefully that should help people that work or something.

You can probably take Friday off of work and then work, you know, attend the course on Friday and Saturday. Everything is over Zoom. So if you're interested, just just shoot me an email through the website. I still have spots remaining and I'll be glad to sign you up. I'll give you some more information on cost and things of that nature. We cover a ton of material in those courses. And again, if I may be able to take this course, these courses and do extremely well. Okay, so let's just go ahead and jump right into it. Right. So, vitamin B12 deficiency, right? Remember, we also call this cobalming deficiency. I think one thing that we just kind of help is having like a good general review first of numo B12 physiology. So today in today's podcast, I'm going to really try to hone your numo B12 physiology. I'm going to talk about the different causes of vitamin B12 deficiency. I will try, if I can, to discuss on how a B12 deficiency may be diagnosed. And then we'll talk about treatment. And then we'll talk about some pathologies that are associated with B12 deficiency. Right. So the first thing with numo physiology of vitamin B12, right? So the thing is you need to consume animal products, meats, to basically get B12 in your diet. Because remember, full it is from full age, from plants, but B12 is from animals. And then after you consume it, that B12, some of it will bind to some salivary proteins. And then you will make it weed down your stomach, or the way to your stomach.

When it gets to your stomach, the acidity of the stomach is actually pretty necessary in helping you split of vitamin B12 from salivary binding proteins, also in helping you split of vitamin B12 from dietary proteins. That's pretty enough is very important, right? And you need the acidity of the stomach to make that happen. At the same time in the stomach, the parietal cells are making intrinsic factor, but the binding between intrinsic factor and the binding between intrinsic factor and vitamin B12 does not happen until you get to the small intestine. In the small intestine, you actually need pancreatic enzymes as well, again, to basically break off B12 from something called R factor. Because the thing is B12 cannot seepally on its own, make its way from the mouth, all the way to the small intestine. It actually binds to something called R factor. R factor helps it to keep going seepally until it gets to the small intestine. So to get that R factor off of B12, we need pancreatic enzymes to make that happen. And then once B12 is split off from R factor, it can then bind with intrinsic factor. And then there will be reabsorbed through transcobalming two receptors in the terminal Ileon and then it will go into the body. Most of the B12 you have in your body is actually stored in the lever. The lever stores about three to five years worth of vitamin B12. So that is the normal physiology of vitamin B12. That is the normal physiology of vitamin B12.

The thing is if you understand the normal physiology of vitamin B12, then understanding the pathology that on the lies B12 deficiency becomes very easy. So what are some things that can potentially cause vitamin B12 deficiency? What are some things that could potentially cause it? Well, the first thing is impaired absorption. The most common causes very high autonone. The most common cause of B12 deficiency is you're not absorbing it properly. And again, your more absorbed it properly can have many many different causes. Again alternatively, I will talk about those causes, but let me talk about the other ones. Or you may not be consuming another vitamin B12. So if you're vegan, if you're vegetarian, I will see vegans especially. These are people that are more likely to develop B12 deficiency again, because they just don't consume adequate amounts of animal products. Another unusual cause of B12 deficiency you may see on your exam is when a person B12, because normally we say that the B12 that you'll live in can store can kind of keep you going for like three to five years. But if you're some reason, right? So just kind of think about it, let's see hospitals. We know that hospitals back in the day before COVID-19 started. Didn't have to use in 95 masks as often, right? It's probably something that was used maybe just in the ICU or if you're taking care of some special patient populations.

With COVID-19, let's say a hospital before the I-95 supply could last them for like 10 years. But then because of COVID-19, that previous 10 years supply of N95s runs out in two days. Obviously they would develop in N95 deficiency very quickly. That's the same thing that happens in people that have these hemolytic anemias. Because normally your ribloces are supposed to live for four months, 120 days. But if something bad really happens, you have a hemolytic anemia, like an autoimmune hemolytic anemia. Remember that's a type 2 hypersensitivity reaction. Or if you have like sickle cell disease, hereditary stress, itosis. In those cases, these people's B12 stores deplete very quickly. And think about it. If your body has about three to five years worth of B12 and about three months or they're about so full it, you can see that those people develop full it a lot quicker, full it deficiency, a lot quicker than their B12 deficiency. This way in general, if you have a hemolytic anemia, you're required daily full it supplementation. That rule does not necessarily apply to B12, but you can already see why these people can develop a B12 deficiency. And also people that have AIDS, because again, their cell turnover is really, really high. Those people can develop a B12 deficiency very quickly. Now, so what are some other causes of B12 deficiency? So I said I'm going to talk about the causes of B12 deficiency that deal with absorption.

Again, if you understand that physiology of B12 deficiency I described, a lot of this should make perfect sense. So a classic one, probably like the most common one that pops up on MBM exams, is when for some reason you have an intrinsic factor deficiency. And what are the things that can cause intrinsic factor deficiency? Well, basically anything that messes up with your stomach will cause an intrinsic factor deficiency. The chief one, obviously, is preneciacinemia, where you make autoantibodies against the pride of cells, or you make autoantibodies against intrinsic factor. The thing that's going to happen in those circumstances is either destroying the pride of cells, the MICIF, or destroying intrinsic factor itself. Then B12 will not have that partner that it needs to be reabsorbed by transcobalming two receptors in the terminal helium of the small intestine. Or think about it, if for some reason you're reset the stomach, like you perform a gastrectin. So they can easily make this a surgery shelf question. That's the thing, B12 deficiency just kind of precolites into many different subjects. So if you perform a gastrectomy, basically you're resetting the part of the stomach again that can cause that havers those are pride of cells. Obviously that's going to cause a B12 deficiency as well. Another classic one is if you do certain kinds of weight loss surgery. So let's see, you do the ROO NY gastric bypass.

That's basically where you pretty much make a small, you essentially divide the stomach into a smaller pouch and a large lower part of the stomach, which is your remnant pouch. Then you essentially make your small intestine connect to both pouches, that small upper pouch and the larger remnant pouch. So the thing is, again, by doing that, you're essentially going to be causing a B12 deficiency because your small intestine doesn't really have much access anymore to that B12 that's coming from the pride of cells. So those things can absolutely cause a B12 deficiency. Or if you, for example, have a problem with the terminal ilium. So say, for example, current disease. When the current disease loves to torch the terminal ilium or if you have some form of... If you have some malabsorbed disorder like celiac disease, webose disease, those things can almost stop your terminal ilium. If you let yourself stop your terminal ilium, again, you're not going to be able to reabsorber by doing B12. And also if a person has a transcobalamin 2 deficiency, decanisly make this a step one question because it's a genetic disease. Transcobalamin 2 deficiency, those are the receptors that you need to be able to get in B12 and intrinsic factor through the terminal ilium into the body. So that can obviously cause a B12 deficiency. Now, if for some reason you also have a low assing in your stomach, that's going to cause a B12 deficiency.

Although this, you have to be on these drugs for a really long period of time. So if you're on a PPI, like a pertin pump inhibitor, or you're a H2 blocker, like runnytidine, faumotidine, things like that, these things, again, acid reducers in your stomach. Again, if you have low amounts of acid, you're not going to be able to split of it in B12. From... You're not going to be able to split of B12 from your dietary proteins and also from salivary binding proteins. So those things can all give rise to a person having a B12 deficiency. Another classic one is, if for example you have just bacterial overgrowth in your GI tract, right? Bacterial overgrowth in your GI tract, that can absolutely cause a B12 deficiency because bacteria. Many people think it's only the fish tape one, and I'll talk a lot about that in a bit. But it's not only a fish tape one that eats B12. The bacteria in your GI tract, if you overgrow, can become significant enough to pretty much consume your vitamin B12. In fact, there's this thing called a blind loop syndrome. Sometimes it happens after some GI surgeries. This blind loop syndrome, where it happens where, essentially, in these circumstances, the person just has a part of their small intestine that is just kind of static. Nothing seems to be moving along in those places.

When nothing is moving along, bacteria is going to overgrow because the thing is just lay that peristosis, that moment of food through your GI tract literally moves the bacteria along. It keeps everything going smoothly. So the thing is when you have that blind loop syndrome, then you have a build-up of bacteria. And as you build up that bacteria, those got microbes. They can again consume your B12 and cause a lot of B12 deficiency. Metforming that will use to treat diabetes. Time to diabetes can also cause a B12 deficiency. And also, if a person has like, and they will usually give you these people having big time in your sonophilia, for a person has a fish tape one infection, remember, diphidobotramalatum. Those things can all cause a vitamin B12 deficiency. So again, it's very high yield to, and also if your punkers doesn't work. Remember, we said that to cut off vitamin D12 from our binder, you need punk enzymes. So the thing is, if your punkers doesn't work, let's say you have chronic punk retitis, or punkers is dead for some reason, that can cause a B12 deficiency. So you see that there are many potential ways they can test B12 deficiency on an in-bim exam. So the thing is maybe like, okay, define like, why do we care about B12 deficiency? Well, B12 deficiency can certainly cause quite a number of problems. As you'll see, B12 is important for two chemical reactions in the body. The first one is important for is in the formation of methionine.

So again, so far, we've talked about the normal physiology, we've talked about the cause of B12 deficiency. So let's actually go into the diagnostic testing for B12 deficiency, but I want to give some quick background here. So remember that to make methionine with an enzyme called methionine, same phase, you need vitamin B12. You need cobalamine. You need vitamin B12 for that reaction to work. So if you have a B12 deficiency, that's not going to work. So you're not going to be able to convert homocysteine to methionine. So your homocysteine is going to build up, right? One of the most common causes of hyper-homocysteineemia is B12 deficiency. But then remember, if you also want to convert methomalone ochoe to succino ochoe with methomalone ochoe mutees, you need vitamin B12 to make that reaction work, right? The thing is of those two reactions, fully it is also helpful for homocysteine to methionine conversion. So the thing is B12 fully deficiency will both cause hyper-homocysteine. But B12 deficiency is the sole cause, well, besides another genetic disease, but if I mean B12 deficiency is VSO cause, again, besides, I guess, methomalone, methomalone ochoe mutees are deficiency that can cause a person to have a methomalone gastroidemia. So whenever you see a person having hyper-homocysteineemia, check your methomalone gastroid levels. If it's elevated, that tells you it's a bit of deficiency.

If it's not elevated, that tells you it's likely going to be some kind of full-eat deficiency, right? So the thing is you may wonder, oh, the vine, if methomalone gastroid builds up, it's not a big deal. Well, it's a big deal. One is it can give you metabolic acidosis, that's one. But two, methomalone gastroid when it builds up makes your myelin more fragile, makes it less stable, right? So those people begin to have like the myelinative problems, right? Because the aneurys don't work right, because again, remember, you need myelin to help you with that solitary conduction business with your neurons. So your anal transmission becomes a huge issue, right? So how do we diagnose B12 deficiency? Again, I've pretty much talked about it already, right? You can check the person's homocysteine levels, you can check their vitamin B12 levels, you can check their methomalone gastroid levels. The thing is checking the vitamin B12 levels, right? It's obviously like a smart easy thing to do, right? But again, it would make sense that the mb-me will not put that on an exam. It would make more sense that you make you do the chemical analysis with these homocysteine levels and the methomalone gastroid levels. So that's something I'd expect more on your exam. And then there's one smart thing our friends at the mb-me love to do. They love to talk about this thing called the shilling test. The thing is most people these days, most clinicians do not perform the shilling test.

The shilling test is kind of a high-ealtest to understand because it's like a B12 deficiency localized deletion test, right? It's like a B12 deficiency localized deletion test. They still put these things on exams whether they like it or not, they put it on step one, put it on step 2, see how you put it on step 3. So it doesn't mean that no one performs it but very few people perform it, right? So it's something you kind of want to understand because it really, really helps you localize why a person has a vitamin B12 deficiency, right? So the thing is the test has many different variants but I'm just going to give you the variant that will help you on your exam. So what's the variant? So how do we do this step? This test, right? This test is kind of done in a lot of process. So the first step in set process is to give the person like intramuscular vitamin B12. The reason you do that is you want to basically saturate all the persons B12 stores, right? You just want to tell the body that oh B12 is saturated, right? The reason you do that is again, if you give that I am vitamin B12, it will saturate basically all the B12 receptors or stores, you know, like in the lever and stuff like that, right? So the thing is for a normal human being, if I saturate all your B12 stores and then I give you oral vitamin B12, that oral vitamin B12 is going to get reabsorbed in the terminal helium and then it's going to shop in your urine.

Usually you're looking for about 10% of what you took early. So let's see, it took a hundred milligrams of vitamin B12, you want about 10 milligrams of it roughly in your urine, above 10 milligrams of it, 10 milligrams or more in your urine. If you don't see that much in your urine, then that means something is going on, right? So again, in the first step, you're going to give that I am vitamin B12 too. Again, pretty much saturate the body with vitamin B12, right? And then in the second step, you're then going to go ahead and give those people oral vitamin B12. And it would be like, oh, divine, how do you track these B12 they are given? How do you differentiate it from the one that was given by I am injection? Well, the thing is the one given by I am injection is going to be normal vitamin B12, the contains normal cobalt. But then the one you give already is radio labeled, right? Because remember, vitamin B12 is also called cobalamine, the coastance for cobalt. Cobalt, they actually some radioactive isotopes of cobalt is pretty low radioactivity. So it's not that big of a deal. But basically, this bit person will get radio labeled cobalt. And then that radio labeled cobalt will be the thing that goes in the oral B12. So if for example, you give the person, so if for example, you give the person, that I am vitamin B12. And then after that, you give them the oral B12. And you notice that, I mean, I don't see any of this vitamin B12 in the person's urine.

Then that makes your life easy. That tells you that you know what this person likely has some kind of B12 deficiency. It tells you that there is some reabsorption defect with B12 deficiency. So that's the second step, right? Because again, if I give you an oral B12, you were a normal human being, then that B12 should show up in your urine. But if it doesn't show up, then there is something going on. There is something going on. So what are you doing the third step? In the third step, what you're going to do is you're going to give intrinsic factor. You're going to give oral intrinsic factor, right? If you give oral intrinsic factor, well, they are one of two results you can get. You can get the fact that, oh, I give you oral intrinsic factor, I give you that radio labeled oral B12. And voila, the vitamin B12 deficiency results, right? You see it in the urine, right? You notice that, wow, okay, I'm seeing more than 10% of what I give oral in the urine. Then that's good. Then that tells you that it's an intrinsic factor deficiency. That caused the presence vitamin B12 deficiency. So that pretty much tells you the person has prenecious anemia and you're done. But if for some reason you notice that, gee, I give this person oral vitamin B12 and I gave intrinsic factor and I didn't see that B12 show up in the urine. Then that tells you that, hmm, it's not intrinsic factor deficiency that is causing this person's problem.

You've pretty much crossed off prenecious anemia as the cause of the person's vitamin B12 deficiency. So typically after that, what are you going to do next? Many times, the thing that's done next, and again, to be honest with you, this part where you give intrinsic factor about 99.9999, 99% of the time is where the endemic will stop. But for completeness seek, some other primetitions that I used, like the next stage, typically is you'll give that oral vitamin B12 and antibiotics. Because again, some people as I described, bacterial overgrowth can cause B12 deficiency. Give them like a two-course of antibiotics. They'll kill off all that bacteria. And then hopefully, if you give B12 an intrinsic factor, that should fix the problem. So given antibiotics, again, can help you rule out bacterial overgrowth as the cause of the person's B12 deficiency. Many times in the next stage, after that, let's say you give antibiotics, he still doesn't fix the problem. Then one thing that's classically done is you can give the person like pancreatic enzymes. They give you like three days worth of pancreatic enzymes. Because again, remember, you need pancreatic enzymes to split a vitamin B12 from from our binder. So if you give pancreatic enzymes, and then you notice that, oh, you now see the B12 in the person you're in. Again, you give pancreatic enzymes plus your own, you know, radio labeled B12.

Then that tells you that, okay, this person likely has a pancreatitis or something weird with a pancreas that's causing them to have that B12 deficiency. So, but again, the part of to where I describe the intrinsic factor, it's kind of like the big thing is you're basically what you're doing with the shilling test is, you're giving ORO B12, and then you're just sobbing out different things to see if, oh, if I change this one variable, if fix it, you see B12 in the urine, that basically tells you, helps you localize the lesion as tool, why the person has a B12 deficiency. So hopefully you understand the shilling test again. It's one of these diagnostic tests you can use for B12 deficiency. But again, they don't, people don't really use it clinically, but it shows up abundantly on NV Me exams. Now, the next thing I want to talk about is the pathology of B12 deficiency. So why is B12 deficiency a problem? Well, again, I told you that first things first, you need B12 to make methionine. Methionine is kind of necessary for making neurotransmitters, right? So many times we would have B12 deficiency, they tend to have like depression, they tend to have these neuropsych disorders, right? Because again, the neurotransmitters are not being made in adequate quantity. Second one is remember you need B12 again to make methionine, which is necessary, right? In B in a purine and a thymidine synthesis. So if that doesn't work, then you're going to be in big trouble, right?

Because the person is not going to have like DNA synthesis, right? So your cells can keep getting big. Because many times remember when you're about on the go cell division, the cell will almost like double in size, right? And then it will double its DNA content, and usually that doubling in size happens before the doubling in DNA content. So if your cell doubles in size, like gets bigger, but then you notice that, wow, I can't make the DNA, right? Your cell will be big with like little DNA to meet that new big cell requirement, right? So these people tend to get like megaloblastic anemia. And the thing is many people for some reason think that it's only like these people's are neutrophils. I mean, these people's are red blood cells that get big. No, that's not true, right? Many other cells in the body get big, like literally epithelial cells in multiple tissues of the body will get big in people that have a vitamin B12 deficiency. So that's just something to keep in mind, right? And then remember again, as I said, you need B12 to make sure that myelins integrity is preserved, right? So if for example, again, you have a B12 deficiency methamalonic acid will build up and make your myelin more fragile. And your myelin will not work as well, right? So you begin to affect different parts of the body, right? The big, big thing I want you to keep in mind here is subacute combined degeneration of the spinal cord. Well, what do I mean by subacute combined degeneration?

Well, it's a degeneration of two things, right? The first one is going to be the drossal columns, right? And the second thing is going to be a lateral corticospinal tract. Those things depend heavily on appropriate myelin function. So these people have lots of pain, pain, no, not pain prick. So pain, no, not even pain or pain prick. Whoops. Sorry. Touch vibration and perception, right? They'll have losses of touch, vibration and perception. And then they'll also have opamodoneuransim, some things like the babinski sign, hyperreflexia, muscle hypertonia, things like that, right? And again, because their drossal columns don't work, right? Those people have a positive rumberg test, right? Because remember, the rumberg test is a test of drossal column function, not cerebral function. Basically, once the rumberg test, essentially what the rumberg test is is you pretty much need three things. There are three things in the body that tell your joints where they are in space. And of those three things, you need to be working at every single point in time for it to not topple over, right? So what are those three things? Well, one is your vision, two is your drossal columns, and then three is screen on the earth, eight, your vestibular cochlear nerve. So if, for example, presence drossal column doesn't work, right? Let's see, because they have a bit of deficiency, or they have tertiary syphilis with TB's, or psilos, or whatever, right?

Then those people are still going to be able to stand up straight, no big deal, right? Because their vision is still there, cranial E, it is still there. But then if you call them into your office, tell them to close your eyes, then they're going to topple over. Because now their vision is gone, right? There are drossal columns already gone. So the only thing that's left is cranial nerve, eight, the vestibular cochlear nerve. And you need two out of three, no one out of three. So those people fall over. That's a very good test for drossal column function, right? So those are the different pathologies that are associated with a person having a B12 deficiency. And there's many, many other things that are caused by B12 deficiency, but we're not really going to go into that because they're not particularly high old to know for the, for the USML exams. And again, how do you treat B12 deficiency? Many times you're just going to start off with like a big mega dose of B12, and then after that you go to like a smaller dose. That's again, essentially how you're going to treat B12 deficiency on MIMI exams. So I think I'm going to go ahead and stop here. Again, as I do at the end of every podcast, I do offer one on one, two, or in for many USML exams. Step one, step two, see key, step three, pre-clinical medical exams, third year shelf exams. And also, if you need help with your ERAS applications, again, I know ERAS season has essentially kind of got in full gear.

I mean, I've been booked out already for many sessions with people for these ERAS applications, right? So like personal statements, editing your ERAS app, stuff like that, mock interviews. Again, I do this with people. And again, it's probably even more realistic now, especially with the Zoom cycles that we're going to be going through, probably for the possible future. So if you're interested in any of those things, or even the step two CK course that I have coming up for this week, step two CK step three course, just shoot me an email and I'll give you some more details on cost and how my teaching modalities are. Again, I've worked with tons of students that are marching through many competitive specialties for many years, right? And again, I have admissions committee experience, right? So I'm very good with these processes. I'm very good with kind of making sure your application is as high as possible, focuses on things that will make you more marketable, more desirable with programs. And then again, many of you know that I'm a Christian. So I have this, you know, I used to talk about life lessons at the end of my regular podcast and I was still continuing to do those. But I have a divine intervention on life lessons at .com website that you can go to and you'll find life lessons. In fact, so far, I think I've made like eight podcasts, all of them are under 10 minutes long. And you know, you just learned some very good Bible based teaching.

You can almost use like a devotional to just use key things about life. Just key life lessons that are applicable, not just to medical professionals, but to pretty much everyone. And I also have a You Tube channel, divine intervention, you have some many podcasts and videos. And that's where I put all my videos. Although the slides that go with those videos on the website, under the respective episodes, right, divine intervention podcasts. .com. So subscribe to the You Tube channel. If I make any new podcasts, I mean, if I make any videos, they're going to be on there. And then again, if you subscribe to the website, divine intervention podcast.com, you'll get an email notification whenever I make a new podcast. And also every podcast from episode one, all the way to this one episode three, twenty eight is there. Because by the way, I also have these podcasts on Google podcasts, on Apple podcasts, on Spotify. So you can get them on there. The only problem is is the most recent 150 podcasts you'll get. So since this episode, three hundred and twenty eight, if I'm doing my math right, everything from episode one to episode one hundred and seventy seven, it won't be on the podcast apps, right. So you can find those on the website. It's a Word Press role. It is really not there's really not much I've tried. Trust me, there's really not much I can do to circumvent those roles. And again, the divine intervention life lessons podcast is on Apple podcast as well.

So the life lesson I just want to share today is the importance of working in the secret place, right. So what do I mean by working in the secret place? Working in the secret place just means keeping a level head, doing good work, even when no one is watching, right. So the thing is many times people want the glory of life without going through the story of life. What do I mean by that? The thing I mean by that is when people see for example, LeBron James coming out and just really crushing it on the court or Anthony Davis coming out and really crushing it on the court or Steph Curry coming out and just switching all those threes. They think it just happened because they just have some natural ability. Yes, they probably have some natural ability. But the thing is natural ability is not going to do you much if you don't spend time building up your craft. So you need to work in the secret place. Many people are not willing to do that secret place work. That work that almost looks mundane, looks dry, looks boring, right. That work that no one is seeing them, right. But the thing is they know how big they want to perform on the world stage. So they put in that work in the secret place, right. They put in that work in the secret place or you see a person that has like good shape, good physique, good weight, very healthy. Again, those people are putting in work in the secret place. It may not always feel good, again, the thing is doing the right thing may not always feel right.

But doing the right thing is always the right thing to do. So those people you see them attending to their diets and working out every day. No one may be seeing them. But then you see them outside. They have good weights, good BMI, it's good everything. And they wonder what's happening, right. And they become jealous. Don't get jealous. No, go and perform your own life story. Go and work hard in the secret place and you'll get similar results, right. Or you see people doing well on step two, CK, step three, step one, getting two, seven days and stuff, right. And you're feeling jealous. And you're like, ah, and then you're trying to draw these things to subdue those people. No, those people worked hard in the secret place. They crank through those on key decks. They watch those videos. They listen to those podcasts. They read those things. They did all those Q banks. They spent time on those MMI practice exams. They did all that analysis, right. The thing is many times in life, you can achieve big things by just doing mundane boring things consistently that other people do not want to do. So I'll encourage you to do that secret place work. And you will succeed on the big stage. And we got on your side. You can do some really, really great things. So thank you for listening to the podcast. I'll see you next time. God bless you. Thank you.

Animal products (meat).

The terminal ileum.

Stomach acidity and parietal cells producing intrinsic factor.

Splitting B12 from R-factor, which requires pancreatic enzymes.

Homocysteine.

The Shilling Test.

Elevated homocysteine (hyperhomocysteineemia).

Because B12 is a necessary cofactor for methylmalonyl-CoA mutase, which converts MMA to succinyl-CoA.

The terminal ileum (via Transcobalamin II receptors).

Pernicious anemia, Gastrectomy, Roux-en-Y gastric bypass, Crohn's disease (if involving the terminal ileum), Celiac disease.

Subacute Combined Degeneration (SCD).

The excess bacteria consume/utilize the available Vitamin B12.

Elevated homocysteine (hyperhomocysteineemia).

Because B12 is a necessary cofactor for methylmalonyl-CoA mutase, which converts MMA to succinyl-CoA.

The terminal ileum (via Transcobalamin II receptors).

Pernicious anemia, Gastrectomy, Roux-en-Y gastric bypass, Crohn's disease (if involving the terminal ileum), Celiac disease.

Subacute Combined Degeneration (SCD).

The excess bacteria consume/utilize the available Vitamin B12.