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Episode 248 – Nootropics Nerd-Out!

In today’s episode of the ATP Project, Matt, Steve, and Elizma nerd out on Nootropics! How they work, the dependence of them to work based on certain neurochemistry pathways, how much you need to feel any effect, all things choline, and why Matt isn’t a genius after consuming eggs… we hope you have your ears tuned in for this one, it’s a nerds dream!

Transcript:

Automated:

Welcome to the ATP Project, delivering the irreverent truth about health, aging, performance, and looking good. If you’re sick and tired of being sick and tired, ready to perform at your best or somewhere in between, then sit back, relax, and open your mind as Jeff and Matt battle the status quo and discuss everything health related that can make you better.

Matt:

As always, this information is not designed to diagnose, treat, prevent or cure any condition, and is for information purposes only. Please discuss any information in this podcast with your healthcare professional before making any changes to your current lifestyle. Stay tuned. The ATP Project is about to start.

Matt:

Welcome to the ATP Project. You’re with your hosts and no guests. So today, we’re talking about-

Steve:

That’s pretty much it.

Matt:

… choline as a nootropic. We’ve got Elizma, Steve and me, by the way. Jeff’s not here.

Steve:

No.

Matt:

No adult supervision.

Steve:

This is bad.

Matt:

And we’re talking about really cool topics. Nootropics, for anyone that doesn’t understand what a nootropic is, they’re basically smart drugs. If anyone’s seen the movie Limitless, and all these things where these people-

Steve:

Great movie.

Matt:

… will take something to make themselves smarter, and by being smarter, it makes you more efficient, better at learning and all that sort of stuff. Technically, a nootropic should also be good for you in the long run. You’re going to make your brain better, improve nerves and structure, blood flows, antioxidant status, hydration. There’s so many aspects to making your brain think better. We talk about things like blood–brain barrier, cerebral blood flow and all that sort of thing.

Matt:

However, over recent years, we’ve discovered that in order to get a nutrient into your brain, you don’t stick it through your ears and up your no… or some people do it up their nose, but you don’t stick things into your brain directly. You take them orally. They got to go from your gut and into your brain. We’ve also realized, recently, that 80% of the chemistry that’s in your brain comes from the gut. With the nerves that connect the gut and the brain axis, 80% of the signals are going from your gut to your brain, not the brain out to your body. So, the gut is extremely important when we’re talking about nootropics and the brain.

Matt:

So, just focusing on what a nutrient does once it’s in the brain, is not as relevant as understanding what happens with the big picture of the whole metabolic fate of that ingredient. So, for example, when we take something orally, we’ve got digestive enzymes and we’ve got things that are going to break it down and convert it. We’ve got the liver’s first pass metabolism. We now know more and more about this microbiome and how the microbiome’s capable of making nutrients, converting nutrients, hijacking nutrients, all depending on what they want to do. So, it’s a really interesting topic because when you talk to people about brain chemistry and moods, everyone is just so different. Some might have a caffeine, and they pick up. Someone has caffeine, and they get all anxious and jittery.

Matt:

We have amphetamines that might make someone drive a truck with mental clarity for 12 hours and keep them buzzing and going and all that sort of stuff, but then it’ll help a child to concentrate, calm down and focus, but then the same drug can be used by someone on the weekend to party and keep up drinking with the boys. Everyone manifests so differently. Now we got mushrooms, we got herbs, we got terms from Ayurvedic medicine such as Brahmi, which means celestial intelligence. It is such a big topic.

Matt:

So, what we’re going to do with our podcast today on nootropics is we’re going to narrow it down to one major field around the nootropics, and that is talking about the nutrient choline. Choline is found in almost all nootropic products. They’ll have some sort of choline in the nootropic, one way or the other, or they’ll at least reference the functions of choline in the brain when they talk about how a herb works. But the big reality is, is choline is very misunderstood. In the sports products in Australia, for example, they’ve regulated choline input down to 10 milligrams. So you can’t-

Elizma:

Oh, what?

Steve:

Yeah, it’s true.

Matt:

… Yeah, hey. You didn’t know that, huh? I just threw that at you.

Steve:

Yeah. We threw it at you.

Matt:

Because you were in here researching how to get choline, and you’re looking at choline sources from foods.

Elizma:

Yeah.

Matt:

We’re looking at how much choline you might find in eggs. There’s 250 milligrams for two eggs or something.

Elizma:

No, no, one egg.

Steve:

One egg.

Matt:

One egg.

Elizma:

One egg is 250 milligrams.

Matt:

250 milligrams of choline.

Steve:

Small eggs are 147 milligrams.

Matt:

But we’re only allowed 10 milligrams of choline in a sports product that might improve your physical/mental performance as a nootropic.

Steve:

Nuts.

Elizma:

Wow.

Matt:

Yeah. The other problem with food is some of it comes from an animal.

Steve:

No.

Matt:

And the animal food that contains choline can make this thing called TMAO, which causes heart disease and that. So, we’re going to talk about animal foods, plant foods, TMA, the metabolic fate of choline, where it goes in the body, where we want it to go, where some people it gets taken. Why I had three eggs for breakfast this morning and I do not feel genius, when I had megadoses. 750 milligrams of choline today.

Steve:

Why not?

Matt:

Now, let’s have a go.

Steve:

All right.

Matt:

So, who wants to tell me about the amazingness of choline? Elizma, you have all sorts of little diagrams and flowcharts, and I want you to tell us what the hell they mean.

Elizma:

Well, I think a good place to start is look at all the different forms of choline. Choline, of course, we do get it from the diet, like you said, plant and animal foods. Grains, nuts, seeds, tofu, kidney beans-

Matt:

Hang on.

Elizma:

… beef.

Matt:

Not just meat and eggs?

Elizma:

No.

Matt:

So, whole grains?

Elizma:

Whole grains. Yeah, all of those kinds of foods. But then choline can kind of be found in different forms. It can be found in lecithin. Lecithin you can get from soy and from sunflower seeds. Lecithin, sometimes we also call it phosphatidylcholine. So, phosphatidylcholine and lecithin, for all intents and purposes, kind of the same thing.

Steve:

Same thing.

Elizma:

They play a huge-

Matt:

Except for price.

Elizma:

… Except for price, yes. Lecithin’s so much cheaper.

Matt:

I mean, you get a bag of leci… so, lecithin in the baking aisle.

Elizma:

Yeah.

Matt:

So, when you go grocery sh… lecithin’s an emulsifier, meaning that it turns big fat bubbles into little fat bubbles.

Elizma:

Yeah, yeah.

Matt:

I don’t know if that’s-

Steve:

That’s terribly accurate, yeah.

Elizma:

That’s pretty accurate.

Matt:

… There you go.

Steve:

Makes oil and water mix.

Matt:

It’s basically available in the bakery aisle. It’s cheap as chips. I mean, probably cheaper than chips. I think two to three bucks a bag.

Elizma:

Yeah, it’s $12, I think, for half a kilo or something like that.

Matt:

Yeah, so it’s really cheap and a really good source of phosphatidylcholine, which is a really good form of choline for various structural sort of purposes.

Elizma:

Cell membranes, yeah.

Matt:

I always have lecithin in my cupboard at home because if I have a fatty meal, I can use lecithin. It’s almost like bile. It helps to cut through those big fat bubbles so I don’t feel nauseous and don’t get a big gut, a big crook in the guts. But tell us about phosphatidylcholine and lecithin.

Elizma:

Well, phosphatidylcholine makes up a huge amount of our bile, so very important in digestion as well. Very important for the brain as well, cell membrane structure and things like that. You also get it in egg yolks. Egg yolks is a big kind of source of phosphatidylcholine as well. Now, then you can also get TMG, or trimethylglycine, which is also sometimes called betaine. That’s another form of choline, but-

Matt:

And not betaine hydrochloride.

Elizma:

… No.

Matt:

Sorry, I’m only interrupting then-

Elizma:

That’s right, yes.

Matt:

… because there’s a lot of people who put betaine into sports products, label it as betaine hydrochloride, which is stomach acid.

Elizma:

That’s stomach acid, that’s completely different. So, with this, I’ve got a little picture of methylation cycle, but… lots of biochemistry, but choline pretty much goes in, it forms betaine or TMG, and this just allows the cycle to continue, in the absence of things like folate and B12. So, when there’s B12 deficiencies, folate deficiencies, then choline, in the form of betaine, can kind of take up the slack there and act as a backup system.

Matt:

Now, does it mask it, though? I’m going to interrupt a lot through this, because there is so much confusion around these things from my end. Because I’m trying to work out how to get a nootropic to really work really well and feel it. So yeah, how does that work? I forgot what I was going to fucking ask there. Did you see that? I mean, I am retarded today.

Steve:

You were asking about betaine.

Matt:

No. Yeah, so for example, I know if I give someone too much B12, I can mask a folate deficiency and stuff like that, by driving through that process. So, would we want to support choline’s methylation capacity with B12s and folates, or is it work independently to B12 and folate?

Elizma:

Well, you’re right. If you, let’s say, had a diet that’s really high in choline, I guess it could mask a folate deficiency because that methylation cycle will still continue to work.

Matt:

What if I’ve got a motherfucker gene, polymorphism? You know, the MTHFR gene, polymorphism? What if I can’t create that form of folate I need? Would, then, the choline work differently for me?

Elizma:

Well, the choline would support that. So, you’d have to probably make a decision whether you want to take a activated folate supplement, or if you kind of just kind of like to support the choline aspect of it. I mean, at the end of the day, I actually see it more as a temporary, short-term adaptation in the biochemistry. So, I don’t like to say, “Well, just take choline and that kind of will-

Matt:

Forever. Yeah.

Elizma:

… fix everything,” right? But it can kind of be as a backup. For instance, people who train a lot. I mean, they will burn through their methylating nutrients a lot quicker, or people who have a lot of stress. So, choline can be a real good backup, which I think is probably why they use it in a lot of sports supplements and things like that. So, a good kind of temporary backup, but I wouldn’t like to rely on it instead of also looking at folate as well.

Matt:

Folate. So we need a big variety of all those synergistic nutrients. So, methylation is extremely important for brain and learning and nootropic, but also prevention of all age-related chronic disorders in the brain. But if we have a look at methylation, so methylation for the brain, that’s needed for the DNA production to make new structure, so to actually repair or rebuild or create new synapses and that sort of stuff, methylation is extremely important for that.

Matt:

Methylation is also involved in clearing away metabolic waste, such as homocysteine, that is an acidic, degrading waste that can break down receptors and structural tissue that can contribute to age-related disorders. But methylation, not many people know this, and if they start researching creatine, they’ll see creatine is getting a bit of a reputation as a brain protector, a nootropic ingredient.

Matt:

Now, creatine itself can’t cross the blood-brain barrier, okay? So, it’s actually broken down into its other bits and pieces, and it’s methylation that creates the creatine in the brain. And the reason why creatine is important for the brain is it fuels energy production, makes energy production more efficient. It also holds a lot of water, so creatine will hydrate the brain really well and actually helps a lot with our glymphatic system when we’re sleeping.

Matt:

A really well hydrated brain flushes away all the toxins, and actually allows you to build new synapses and clear away the old crap and that sort of stuff when you’re asleep at night. So, methylation for brain is bloody important. A lot of people are stacking multiple forms of choline together, thinking that we’re going to get acetylcholine release, thinking that the whole concept of nootropics is to actually just change your immediate brain chemistry, almost like a drug, just modifying neurotransmitters. But reality with a naturopath, it’s a kind of slow and steady process to make the brain a better machine, huh?

Steve:

It is.

Elizma:

Absolutely, yeah.

Steve:

It’s incredible, because you’re correct about homocysteine and Alzheimer’s. There was a study very recently, last year, showing that just simple choline can ameliorate homocysteine in the brain, because it gets into the brain, as you correctly pointed out, ameliorates homocysteine, which reduces tau proteins. So, now it’s being touted as a new Alzheimer’s drug. Ironically, since choline was invented in 1905… it was discovered, I should say, not invented, by good old Alfred… what’s his name? Alfred Baeyer, that’s right.

Matt:

Oh, really? Baeyer?

Steve:

Yeah. Oh yeah, and he made a Nobel Prize for it 1905.

Matt:

I was sure it was going to be Alfred Choline.

Steve:

They name it after themselves.

Matt:

Yeah.

Steve:

Although, he had to compete that year with Koch in medicine, who discovered a tuberculosis cure. And he actually was the first to coin the herd immunity, which is very topical at the moment, if you listen to [inaudible 00:12:41]. He first coined that for the Papua New Guineans with plasma in the blood and that sort of thing, with Plasmodium. But anyway, with choline, of course, it does get into the brain because there’s certain chemicals that can drive it in the brain, and certain types of chemicals. You’ve correctly pointed out that choline bitartrate’s got 41% choline, but it doesn’t get into the brain.

Matt:

Yeah.

Elizma:

Yeah.

Steve:

So, this is where they’ll like [inaudible 00:13:02].

Matt:

A lot of people use choline bitartrate in supplements.

Steve:

Because it’s so cheap.

Matt:

It’s 40% choline, which is a massive yield of choline for a little input, and it’s so damn cheap.

Steve:

Yes.

Elizma:

Yes.

Matt:

So, what were you saying? It doesn’t get to the brain?

Steve:

It doesn’t get to the brain.

Elizma:

No.

Steve:

You need things like citicoline, which is a type of choline. It’s only about 18% choline, but-

Matt:

And so bloody expensive.

Steve:

… Yeah, I know.

Matt:

So the citicoline… so, the doses that are required, and that sort of stuff, are quote high. It’s 18%, so it’s only half the yield of choline per input. Man, it is expensive.

Steve:

It’s expensive.

Matt:

What other forms of choline have we got? We’ve got the alpha-GPC, which is a glycerylphosphorylcholine.

Steve:

Phosphorylcholine.

Elizma:

Yep. And then we’ve got the citicoline, or CDP-choline. Both of those, both the alpha-GPC and the CDP-choline, tend to increase the citicoline levels, like Steven mentioned, which is a main neurotransmitter involved in things like dementia and Alzheimer’s, if it becomes low. But it’s also, we have to remember, it’s a parasympathetic kind of chemical, right? And the parasympathetic system is dominant in digestion. So, you need a citicoline also for keeping the digestive system healthy, bile kind of flowing and all of that. At the same time, it’s also been shown to increase dopamine receptor densities.

Steve:

Densities, yeah.

Elizma:

So, dopamine is like our focus and concentration neurotransmitter. So, a lot of kids with ADD, it’s thought that they have issues within that whole dopamine, dopaminergic system. So, dopamine, apart from our focus, concentration, helps us with appetite control, and it’s our reward system as well, helps with depression and things like that. So, these forms of choline, the alpha-GPC and the CDP-choline, which are the two that can cross the blood–brain barrier, and also the more expensive ones, they really have a huge role in kind of upregulating those neurotransmitters in the brain.

Matt:

What about phosphatidylcholine? Does that do that as well? Does that really… because I remember seeing papers in the past with phosphatidylcholine and significant increases in acetylcholine and dopamine release.

Elizma:

Yeah. Yeah, I’ve seen that as well.

Steve:

Yes.

Matt:

That’s so cool. So, how do I know if I’ve got low acetylcholine? I’ll tell you. That was a rhetorical question. I could see he was about to answer it, and it might’ve been a different answer to the one I was going to provide. So, I’ll jump in and give my answer to my question. You mentioned it all before. The acetylcholine drives the parasympathetic nervous system. It’s also heavily involved in short-term memory, concentration span, and dopamine effects. So, the things in the clinic, the symptom picture of a low acetylcholine is typically poor sleep maintenance, poor close vision, poor attention to detail, poor short-term memory, focus and learning ability. You run on gut instincts, intuition, long-term memory and far vision.

Matt:

So, you see how acetylcholine really helps study. It helps with the focus, attention to detail, it gets you into the zone, where you’re remembering. That’s all part of the parasympathetic nervous system, where we’re capable of learning. The sympathetic nervous system runs on short-term survival, long-term memory, gut instincts and intuition, far vision. Really gets in the way of study because you’re struggling to read, you’re struggling to focus, you’re too busy thinking to learn about what you’re reading.

Matt:

So, acetylcholine, short-term memory, focus, concentration span, close vision. Concentration. I couldn’t even speak then, did you hear that? And then, acetylcholine also drives the Vagus nerves for digestion and that sort of stuff. So, the ability to switch into digestion. Also, detoxification. So, detox, sleep maintenance, which, again, links in with that dopamine. But one of the classic symptoms is if you’ve got a deficiency of acetylcholine… because in the clinic, we’re always trying to work out, do you have too much sympathetic or not enough parasympathetic? We try to get people’s lifestyle and balance it out.

Matt:

But if someone doesn’t have enough acetylcholine, they get a couple of very bizarre symptoms. A burning feet syndrome and extremely dry mouth. So, the burning feet syndrome, it’s like this weird, hot, flushing. It’s a sympathetic never flushing. So, it’s the sympathetic nerve system at the extremities that’s driven by… and the Chinese medicine’s cool because they talk about it as an empty heat. Say, because you’ve got a deficiency in your ability to balance and that, you’ve got this emptiness that manifests as this heat. So, you get a dry mouth, burning feet syndrome. So, they are classic signs of low acetylcholine.

Matt:

The old naturopathic way of treating that was B1, B5, choline, and then using herbs that are what we call acetylcholinesterase inhibitors. They stop the breakdown of acetylcholine over time, and they build up acetylcholine. I will just quickly list off some of those because that’s where they fit in there, as nootropics, by preserving acetylcholine. That’s where huperzine works. So, huperzine is probably the most famous one.

Steve:

Huperzine A, yeah.

Matt:

Yeah, Huperzine A. It come from club moss or something, if my memory is right.

Steve:

Yep, that’s right.

Matt:

So, Brahmi is an-

Steve:

Excellent one.

Matt:

… Ayurvedic word, which actually means celestial intelligence, but it could be Bacopa, Centella or Ginkgo. Those sort of things are all listed off as Brahmi, but they’re all acetylcholinesterase inhibitors anyway.

Steve:

That’s right.

Elizma:

Yes, that’s right.

Matt:

So, Ginkgo is an acetylcholinesterase inhibitor, Bacopa and those sort of things, and the huperzine. They actually work as acetylcholinesterase inhibitors, which means they preserve acetylcholine within the synapse. It doesn’t mean they release a blast of acetylcholine. Which means, taking a huperzine in a pre-workout, thinking it’s going to give you this immediate nootropic effect, is actually not the case. You’ve got to take it daily, and sometimes twice a day, for a couple of weeks for it to have that accumulating effect that will improve your memory.

Matt:

So, a lot of people are adding these things into pre-workouts, going, “Man, this is a stimulant. It’s going to blow your mind,” because it’s a nootropic. It’s like, “Man, I had three eggs for breakfast motherfucker, I’m not a genius.” You know what I mean?

Steve:

Yes. I should be a genius. You got to remember that the nootropic is a term from 1964 that means forward minds. That’s what it means literally, the translation.

Matt:

Yeah, right.

Steve:

Forward minds, so it’s actually taking your mind forward. It’s not stimulating your mind.

Matt:

No.

Steve:

It’s driving your mind forward. So, a lot of people who are trapped in their comfort zones, or know what they know and don’t learn anything new, that’s a classic choline deficiency as well. And you find that in conditions, severe conditions, like Alzheimer’s, where people only remember old things, can’t learn new things.

Matt:

Yeah.

Steve:

And this is the classic choline deficiency. Also, major depression. There’s a great paper on this that talked about all of this. It’s titled Brain choline in major depression, obviously, and it talks about how these people regress back to their comfort zone. They don’t go out. They just sit there. They don’t learn anything new. It’s all miserable. It’s all dark. This is a classic choline deficiency in the brain.

Matt:

Yeah, and they can’t let go.

Steve:

Can’t let go.

Matt:

Because you’re stuck with the sympathetic, which is long-term memory, gut instincts, intuition. What did I do the last time I felt this way, that I survived, and what is my gut instinct telling me to go? Plus, reading this, if I needed to read that and understand that to survive a stress, I’d be dead. Yeah, so typically during an acute stress, it’s like I’m seeing straight past that, I found the exit, I’m off. Your gut instincts is like, “Man, my spider senses are tingling. I’m just going to get the fuck out of here.” And you’re not going to stop… I’m swearing a lot today. Sorry, it’s the eggs.

Steve:

It’s the eggs. The eggs make him swear.

Speaker 1:

It is the eggs for breakfast.

Matt:

The TMA… I interrupted while we were talking about choline hijacked down the TMAO pathway. TMAO is a bad thing, so we should probably talk a little bit more about that as well.

Elizma:

Yeah. No, there’s obviously a lot of… there’s been a lot of talk about TMAO, like if you have a high meat diet, then you will tend to convert a lot of that choline into TMAO. TMAO being complicit or implicit in atherosclerosis, heart disease and things like that. But the interesting thing is, is that TMAO is also found in things like fish. And fish-

Matt:

Main source is fish, isn’t it?

Steve:

Yeah.

Matt:

Yeah.

Elizma:

… Main source is fish, and that’s supposed to be heart friendly and all that, right?

Matt:

Yeah.

Steve:

Yeah, it is.

Elizma:

So, it seems that when we do have TMAO production in the body, we tend to clear about 50% of the stuff anyway, through the urine. The 50% that we don’t clear will tend to convert to TMA back and forth, depending on how the enzyme is functioning and also depending on the gut bacteria. What they’re finding is that, specifically more Prevotella type species, if you have an overgrowth of Prevotella type species, you tend to produce more TMAO, or convert more of the TMA to TMAO. Just to clarify, choline converts to TMA, and then TMA can then be converted into TMAO.

Steve:

In the liver. It’s oxidized in the liver.

Elizma:

Yeah. That’s right.

Steve:

Because TMA is trimethylamine, and then you oxidize it to trimethylamine oxides, and that’s in the liver, that last bit.

Elizma:

Yeah, it’s in the liver. There’s an enzyme called FMO3, which is a [inaudible 00:22:03] enzyme. Yeah, flavin-

Steve:

That’s right.

Matt:

Or [inaudible 00:22:05].

Steve:

FMO3, yeah, that’s right.

Elizma:

… enzyme. That’s the enzyme that’s responsible for converting that TMA into TMAO.

Steve:

It’s in the liver, it’s oxidized there, yeah.

Elizma:

So, then, it would make sense if that enzyme was working really fast or being upregulated, but you’re going to get more TMAO, right?

Steve:

Mm-hmm (affirmative).

Elizma:

But the things that makes an enzyme work faster is insulin resistance, low insulin levels, and iron overload and salt overload.

Matt:

I love the way you say iron.

Elizma:

Iron overload.

Matt:

I love it.

Elizma:

Is that how you say it?

Matt:

I don’t care.

Steve:

Iron. I’m going to say iron from now on.

Elizma:

But yeah, those kinds of things can upregulate FMO3, which can then make more TMAO. Now, the things that can actually prevent that conversion from TMA to TMAO is antigens and testosterone. So, it’s more likely to kind of… think about it that men, as they age, and their testosterone levels drop off, that’s when they’re… we could say well, maybe it’s because of that protective effect that testosterone has against-

Matt:

So, who gets the heart attacks?

Elizma:

… Well, older men.

Steve:

Yeah, men do, all throughout their life-

Matt:

Because there’s a definite-

Steve:

… and then women catch up at menopause.

Matt:

… So, that’s why… so, men are more likely to die of heart attacks-

Steve:

Yes.

Elizma:

Yes yeah.

Matt:

… young or old?

Steve:

Well, all throughout their age.

Matt:

Yeah.

Steve:

It’s linear. It just goes up like that. But women go protective, protective, menopause, it kicks up like that. So, men are… I’ll put it to the camera, it’s just going up like that. So, you still got a chance at younger, but women, very protective, and then they catch up at menopause age, 51, and it spikes because they lose their protective progesterone.

Matt:

Wow. And what were you saying about the hormones?

Elizma:

Well, so antigens or testosterone slows down FMO3, so that slows down conversion to TMAO and lowers the TMAO.

Matt:

Yeah, right oh.

Elizma:

The reason why women could probably be more at risk as they reach menopause is because of bile acid issues-

Steve:

And progesterone is an antigen-

Elizma:

… and progesterone and things like that, yeah.

Steve:

… in women.

Elizma:

So, that’s potentially one mechanism. There was something I was going to say around that, and I forgot. Oh yeah, the Prevotella bacteria. So, Prevotella bacteria is a big one that seems to be linked to high levels of TMAO. But Prevotella bacteria is more likely to increase with whole grain diets than it is with meat diets. Red meat have been getting the bad rap about the more red meat you eat, the more choline you’re getting, the higher your TMAO levels will go-

Matt:

And that’s why meat is evil.

Elizma:

… And that’s why meat is supposedly evil. But, as we saw with the studies, TMAO gets pushed with Prevotella bacterial overgrowth, and whole grains feed Prevotella bacteria.

Matt:

Prevotella.

Steve:

This is where the protective effects of the old classic Atkins style diets, with the low grains or no grains and the high meats. We’re actually protective against atherosclerosis.

Matt:

So, I tell you, something else cool with that, Steve, is that in the research that we’re doing on the microbiome, is there’s a particular profile in the microbiome that may be obesogenic or can contribute to insulin resistance and inflammation and obesity. So, the diabetic profile and the microbiome, the inflamed, and the obese profile. All of the same risk factors associated with cardiovascular disease, are exactly the same microbes that potentially could be hijacking the choline and converting it through to TMAO that causes heart disease. Which is why people that are predisposed to obesity, inflammation, diabetes, and heart disease, when they do a meta-analysis and find that they’re eating eggs, they go, “Oh, the eggs are causing your heart disease.” Is this the kind of like-

Elizma:

Well, that’s the rhetoric that goes on, right?

Matt:

… Yeah.

Elizma:

But there was another study that I looked at, where they looked at eggs, and they looked at about 42 different foods, I believe. The eggs did not increase the TMAO levels in this study, but there was about 21 other foods that did, and 18 or 19 of them, I believe, were fish. Fish products.

Matt:

Yeah, wow.

Elizma:

So, the eggs didn’t increase TMAO, but fish did, and halibut was, I think, the biggest one and increased-

Steve:

It was the worst, yeah.

Matt:

And it’s supposed to be the healthiest one.

Elizma:

… and supposed to be the healthiest.

Steve:

And herring. Herrings too. And this [inaudible 00:26:07] study, called it, It’s a Red Herring. It’s titled Love, Beautiful Love-

Matt:

[crosstalk 00:26:12].

Steve:

… Microbial TMAO as a marker. Something fishy? Because it says, “Hang on, we’re eating all these beautiful fish. We’re getting very low heart disease, but it’s increasing our TMAO. Is it causing heart disease?” So, there’s a real double standard. And I believe, and this paper supports it, where it talks about the [inaudible 00:26:29]. They’re very, sorry, small ticks there. But all the ones with the little ticks here are the ones that increase TMA, not TMAO because that’s in the liver. You’ll see it’s all Firmicutes and the Protavella bacteria. And they’re the ones that cause the TMA production. Because, remember, the bugs didn’t cause TMAO, the liver-

Matt:

And do you know what’s cool?

Steve:

… What?

Matt:

I’ll tell you another cool link. This is why I love our podcast, where we don’t prep too much, because one of the wickedest links that we’re seeing here is the polyphenol foods.

Steve:

TMAO. That’s it.

Matt:

So, the things like the grape pomace, and that’s all the skins and peels and seeds and shit out of the grape. Asparagus is a really good one. Fenugreek is a really good one. And how cool is that? If you consider fenugreek, fenugreek’s other benefits is regulating blood sugar-

Steve:

And…

Matt:

… and that sort of stuff, and insulin resistance, and maintaining testosterone levels.

Steve:

That’s it.

Elizma:

Absolutely.

Matt:

I have no idea why he just pointed at your ear.

Steve:

My bicep. I was showing you my big bicep.

Matt:

Oh, your bicep. No, I thought you were pointing at your ear.

Steve:

My rippling bicep.

Matt:

But he was trying to do his bicep curl. Sorry. I thought you were going, “Look at my ear.”

Steve:

You couldn’t see my rippling bicep, so small from back there.

Matt:

I hurt my arm a little bit.

Steve:

With these gym [inaudible 00:27:51], it’s…

Matt:

Yeah, so the fenugreek, how cool is fenugreek? Because it will stop TMAO production from choline significantly, but also works on blood sugar, testosterone. Gynostemma, which is your poor man’s ginseng. It’s actually a very powerful vasodilator. It regulates nitric oxide and vasodilation and improves sports and performance and mental performance. It also stops TMAO from choline.

Matt:

The grape was one of the other good ones I mentioned. So, the cranberries, the [inaudible 00:28:23], asparagus. Also, the skins of the nut, so, in particular, the almonds and the peanuts can shunt it. You know how they talk about peanut contributed to heart disease and cholesterol or whatever, but the peels on the outside stops TMAO production. So, how cool is it that the same herbs that would fix that microbiome profile, that have got a reputation preventing cardiovascular disease, metabolic disorders, and now also showing up as the ones that stop the TMAO production?

Steve:

Yep.

Elizma:

Absolutely, yeah.

Matt:

My favorite one. My favorite story in regards to TMAO. You know fish, they smell fishy because of the TMAO. TMAO smells like fish. That’s what makes fish smell like fish.

Steve:

Like a fishy smell, yeah.

Matt:

So, they’re very high in it compared to everything else because they’re the fishiest smelling of all the animals, like… you know what I mean?

Steve:

Funny though, isn’t it?

Matt:

Funny that fish smell more like fish than a chicken would. Now… Got to speak some shit up. But I’ll tell you what’s interesting, the Chinese wet markets have been in the news a bit lately for different reasons. But one cool thing that’s come out of the wet markets, and that sort of stuff globally, is that when you put fish on the bench, they start to smell fishy quite quickly because the microbes… the same microbes that live in our gut, are everywhere. That’s why they’re in our gut. So, when they get on the fish when it’s on the bench, they start breaking down the choline in the fish and making it more fishy smelling. That’s how you know how fresh the fish is and how much microbial exposure it’s had, is by how fishy it smells. That’s why you want your seafood to smell like the ocean, you know?

Steve:

Yes.

Elizma:

Yeah.

Matt:

Not necessarily that fishy. That’s the TMAO. So, what they did in the Asia wet markets to preserve the shelf life of fish, was to actually marinate it with green tea and citrus. They used to say, “Well, it masks the smell of the fish.” Well, and they’d say, “It just stops the fish from smelling fishy or going fishy.” Well, they’ve now recently tested that and found that green tea and citrus were a couple of the best things at preventing TMAO production. It all went back from, well, we might as well have a look at this because it’s been used for thousands of years to stop things smelling fishy. We now know that fish smell comes from TMAO. Maybe it does something. And it’s like one of the most potent ones. So, how is cool is this that-

Steve:

It’s the essence.

Matt:

… Yeah, anyway. I get a little bit excited about it. They’re synergies, you know?

Steve:

No, that’s exciting. It goes back to the acids.

Matt:

And the polyphenols.

Steve:

The polyphenols, like epigallocatechin-gallate is great for that. And also, the acid is what’s found in the gut, like the acids like the other acids, propionic acid, valerenic acid.

Matt:

Are you talking about the short-chain fatty acids-

Steve:

Short-chain fatty acids.

Matt:

… made in the large inte… not stomach acid?

Steve:

No, no, not stomach acid, the…

Matt:

Colon acid.

Steve:

The colon acid. There we go, we’ll call them the colon acids. There we go. Butyric acid-

Matt:

That’s what I’m going to call my next cocktail.

Steve:

… That inhibits, particularly clostridia, which are the ones that particularly drive TMA production. That’s why we-

Matt:

No, you know that noise. I just made that [inaudible 00:31:25]. I only did that because I just had a genius epiphany for my cocktail. If I add absinthium to it, so absinthe, which is Chinese wormwood, which also stops TMA production, and kind of makes you feel like you’re on acid. So, I could do that.

Steve:

What’s that stuff?

Matt:

So, I could do that. We could do colon acid based on absinthe. That’s my cocktail. Anyway, back to your story.

Steve:

The great thing about the colon is that it regulates these bad bugs, the clostridia bugs, which are the ones that are linked here that cause the TMA production.

Matt:

So, hang on. So, you’re saying choline… supplementing choline controls the microbiome.

Steve:

No, no. The acids, the short-chain fatty acids control the microbiome, specifically the ones that cause TMA production.

Elizma:

Butyrates, specifically.

Matt:

Yeah, right.

Steve:

So, that’s why putting acid with fish is an excellent idea, and why lemons go so well with fish, and also it’s used as a preservative. That’s why a lot of traditional medicines, or if I call-

Matt:

It’s kind of cool, eh?

Steve:

… It is. Because they’ve worked it out. They didn’t know the biochemistry, but they’ve worked it out. Reverse engineered. Which is why I love it. Which is another reason why good old TMAO, that’s normally naturally found in fish, is not the problem. It’s probably when it’s being reacted with some sort of microbial [crosstalk 00:32:30].

Matt:

Isn’t just… are we talking again, antioxidant defense?

Steve:

Yeah.

Matt:

Are we talking about just this waste that might build up while it’s in transit on our way to the kidneys to be eliminated that it might be degrading? You know, arterial integrity, triggering plaque formation or something. Is that kind of how TMA makes… how does TMAO make an atherosclerotic plaque? I think was my question.

Elizma:

Well, I’ve got a-

Steve:

I’ve got a chart here.

Elizma:

… All right. I’ve got a theory on it.

Matt:

I want to hear your theory-

Steve:

I’ve got a beautiful chart here.

Matt:

… and then I’ll see your picture and see if it matches up. Quiz. Go. Your theory. He’s got a reference. No pressure.

Steve:

Poor thing.

Elizma:

It kind of like matches in with-

Matt:

If you’re wrong, you’re off the podcast.

Elizma:

… [inaudible 00:33:07]. It kind of like matches in a little bit with what Steve said about clostridia bacteria and all of that. So, we also know that clostridia bacteria is involved in making secondary bile acids, right? So, what they found is they found that there’s a link between TMAO levels and bile acid dysregulation. So, what they found is that TMAO can actually inhibit CYP701 enzyme, which is the rate-limiting enzyme involved in bile acid synthesis. So, cholesterol has to go through that enzyme, CYP701, to become bile acids. There’s 14 other enzymes, or something like that, and we won’t worry about that because this is the important one. Now, TMAO can inhibit that enzyme by about 40%, which means it’ll slow down cholesterol being used for bile acids.

Matt:

Wow.

Elizma:

So, now you’re going to have more cholesterol sitting there not being used.

Matt:

A backlog. Yeah.

Elizma:

So, you’re going to get metabolic syndrome. You’re going to get the plaque formation, which is the monocytes and the foam cells and all of that kind of stuff. So, that, I think, kind of made… when I looked at that, that made more sense to me, in terms of how it could possibly be involved in something like heart disease or atherosclerosis, but more really to do with that interference of bile acid synthesis than necessarily a direct effect from the TMAO.

Matt:

I like that. What’s [inaudible 00:34:26] in this journal thing?

Steve:

This journal thing. There’s five mechanisms, and you’ve hit two on the head perfectly-

Elizma:

Oh, cool.

Matt:

Well, there you go.

Steve:

… so that’s really good.

Elizma:

I passed.

Matt:

You can stay.

Steve:

There’s CYP701 and CPY2701 are the two that [crosstalk 00:34:38] bile acids.

Matt:

I was thinking 2701.

Steve:

That’s bile acid. Also, it increases macrophages to increase foam cell formation.

Matt:

Oh, yeah, yeah.

Steve:

This is TMAO’s mechanisms on [crosstalk 00:34:47].

Matt:

Hey, can I tell people what a foam cell is because it’s fucking cool?

Steve:

Go for it.

Matt:

They’re really cool, and normally people don’t know what they are because I didn’t know what they were, so I read about it.

Steve:

Oh, okay.

Matt:

And they’re nothing to do with foam. I thought they’d be frothy.

Steve:

Foamy, yeah?

Matt:

I thought there’d be some sort of a foamy froth involved, but it’s the exact opposite. So, what they do, it’s immune cells roaming around in your arteries looking for shit all the time. Foreign particles and bugs and viruses or whatever. Cholesterol is normally really smooth and round and slippery. Then when it gets oxidized, it gets all spiky and changes its shape, and then doesn’t resemble cholesterol anymore. So, the immune cells see it and go, “What are you, you mong, you’re not supposed to be here.” They got to engulf it and remove it. So, they actually engulf it like it’s a bug or a bacteria or an infection or a bacterial fragment, like lipopolysaccharide or something. So, they’ll engulf it to remove it, and then they basically eat it and then they just beep, beep, reverse into the artery wall and then cover themselves in calcium.

Steve:

That’s it, that’s it.

Elizma:

Yeah.

Matt:

And that’s like a foam cell. So, they’ll like hold the bug, take it… Cholesterol’s not bad, but if it’s oxidized, it’s no longer cholesterol, and the body has to do something with it. And it has to remove it, and it’s the immune cells that do that.

Steve:

And it’s worse now because it doesn’t just go-

Matt:

Worse?

Steve:

… behind the thing. Yeah, because it also leaves a lump.

Matt:

One upmanship.

Elizma:

Yeah. Is that the blob of cement in the-

Steve:

So, it leaves a lump in your artery.

Elizma:

… you have potholes and you just blob a bunch of cement on it.

Steve:

Yeah. So, it leaves a lump in the artery like that, and you get a few of those, and you get the lump, lump, and eventually the artery closes off and you die.

Matt:

And the lump is covered in what we call adhesion molecules. That’s when the next thing comes through and it sticks to the lump. Then, it oxidizes because in that area you’ve got inflammation and oxidative stress. Then, that cholesterol goes mong, then another immune cell grabs it, reverses in, covers itself in calcium, and the plaques build up onto each other.

Steve:

Called VCAMs, if you want to look it up, everyone. It’s called vascular adhesion molecules.

Matt:

Don’t Google VCAM.

Steve:

Do you want to know the other mechanisms?

Elizma:

Yes.

Steve:

It increases platelet activity. Simple. It causes clots.

Matt:

Oh, wow. [Brooklyn 00:36:52], you’re useless.

Steve:

So, TMA also damages the vascular endothelium. So, you get endothelial damage. This is what can be measured when you do those calcium scans that Matt was talking about before, when you got those big coronary calcium scans to see how much heart disease you’ve got. They give you a calcium score. That’s what the calcium score is. That’s difficult.

Matt:

Good, Steve.

Steve:

Brooklyn’s crying over there.

Matt:

So, TMAO…

Steve:

Gosh.

Elizma:

Just a bit like homocysteine, right? So, like in terms of damaging the endothelial walls.

Steve:

Yeah.

Elizma:

It’s that inflammation and all of that.

Steve:

Of course.

Elizma:

But, ironically, you need choline to remove homocysteine-

Steve:

Yes.

Elizma:

… and things like that.

Matt:

So, if you’ve got a choline deficiency, you can’t methylate things, so you build up homocysteine. That’ll contribute to the conversion of… it incr… fucking [inaudible 00:37:42] lost the [inaudible 00:37:42].

Elizma:

Well, the conversion of homocysteine, yeah, to [inaudible 00:37:45] in all of that.

Steve:

Of course, the other symptom is fatty livers. This is where it ties in with… I’m trying to… it ties in with carnitine. Because carnitine and choline, those very good for treating fatty livers.

Matt:

And carnitine is another nootropic because it stimulates the release of acetylcholine and dopamine and all the acetyl… How does a carnitine work in nootropics?

Steve:

[crosstalk 00:38:04].

Elizma:

If it’s acetylcholine, yes.

Steve:

It works and it increases dopamine.

Matt:

Is that just that the acetyl part of the carnitine joins up with the choline to make acetylcholine? Is that too simple?

Steve:

Well now, yeah. When you acetylize something, it can cross the blood-brain-barrier.

Matt:

Yeah, right oh.

Steve:

So, it’s like acetylcholine, brain, acetylcarnitine brain, so acetylcarnitine activates the D1 receptors. If we talk about the different five receptors. Do you want me to talk about those?

Matt:

Oh, we have to talk about dopamine receptors because it-

Steve:

Do you want me to?

Matt:

… Yeah, do it because it bugs the hell out of me. And I’ll tell you why it bugs the hell out of me. Everyone says dopamine is this amazing, bloody nootropic that makes you smarter and amazing. Vitex is a herb that we use for hormones that has all these effects on progesterone. It’s the most [inaudible 00:38:47] compound I can think of and it doesn’t make you a genius.

Steve:

It doesn’t. There’s five different receptors I’ll briefly do. One activates cyclic AMP and cyclic adenosine monophosphate.

Matt:

So, that’s an on switch for cells?

Steve:

Yes.

Matt:

That’s basically stimulates activity.

Steve:

And the D2 receptor downregulates-

Matt:

Yeah, right oh.

Steve:

… cyclic adenosine monophosphate. So, that means that it’s like an off switch. So, you have to be very careful which dopamine receptors you activate. This is the same with [inaudible 00:39:15] receptors.

Matt:

What does Vitex work on then?

Steve:

D2 receptors.

Matt:

Well I’ll be buggered.

Steve:

So, it’s very good for calming PMS.

Matt:

Yeah, right.

Steve:

Which is why it’s got that well known traditional use for that. So, it’s different sort of receptors… it’s the same chemical. It’s dopamine. But it just… lock and keys with a different receptor.

Matt:

Is this also why someone might have something that stimulates a release of dopamine?

Steve:

Yep.

Matt:

And in one person, they go manic-

Steve:

Yep.

Elizma:

Yeah.

Matt:

… and in another person, they just go have a nice, deeper sleep.

Steve:

It’s almost like the caffeine things, where it switches off adenosine. And people don’t have much adenosine, so it has no effect on them anyway.

Matt:

Yeah, right.

Steve:

This is why… because caffeine’s not a stimulant. I used to fail my students if they said caffeine is a stimulant. Because I’d say, “No, no, it just switches off the off switch.” Off the off. It’s a double negative, I know, but that’s how it works. We have to know how things work in the body if we’re going to prescribe them. When I was teaching, I was a bit of a anal about that. Because the practitioner had to know what they were giving and how it worked.

Matt:

Yeah, right.

Elizma:

Yeah.

Steve:

So, it’s important to know there’s different dopamine receptors.

Elizma:

Yeah, because I think DRD2 is also more the one involved in addictions, right?

Steve:

Yes, very much so.

Elizma:

So, it’s interesting where you say like that’s the one that downregulates or-

Steve:

All right. So, you have cancer stick, we’ll call it. That activates the D2 receptors, which is why it settles people down. They go, “I need a cigarette.” That’s activating the D2 receptors for cigarettes, so don’t have to call-

Matt:

Is that why it’s so addictive?

Steve:

… Yeah, it’s very addictive because it’s an off switch for your brain, otherwise your brain goes nuts and you need the drug to settle yourself down.

Matt:

So, how do these things help someone study? I mean, this is what confuses me so much about the whole nootropic. Because, I mean, stimulants, you think so much, you’re wide awake, you’re buzzing around, but does that make you more efficient, smarter, or anything?

Steve:

It does.

Matt:

I find, personally, if I’m in a state of zen, if I reduce my excessive mental chatter, if I actually calm down, and, if anything, use sedatives, I’m actually smarter.

Steve:

Well, you got to remember, this is not a stimulant. Choline doesn’t stimulate your brain. You’ve had three eggs this morning, and you weren’t stimulated.

Matt:

No. I had three coffees with it, I still wasn’t stimulated.

Steve:

It’s good for your brain. It’s making the chemistry work. There is a thing called Hebb’s law of learning, which is forming new neural pathways, and acetylcholine works with that.

Matt:

Yeah, right.

Steve:

So, it forms new memories in the brain. That’s how it works. If you’ve all seen a nerve cell, it’s got little tentacles coming out of it. Well, they’re all new pathways, and that helps you learn all different new connections. That’s what acetylcholine does. It doesn’t stimulate your brain.

Matt:

So, we want to stimulate more synapses.

Steve:

Yes.

Elizma:

… Yeah.

Matt:

We want to stimulate more architecture.

Steve:

Synaptic stimulation.

Matt:

So we’re looking for things that… that brain derived nootropic factor and things that drive that.

Steve:

Yes.

Elizma:

Yes.

Steve:

You got to remember that-

Matt:

Like a stroke.

Steve:

… Like a stroke. Well-

Matt:

No, I mean, ultimately, like, damage encourages healing.

Steve:

… It does, it does.

Matt:

That’s probably what I was just trying to think of what the highest amount of BDNF in anyone is someone that’s recovering from some sort of trauma or brain injury.

Elizma:

Yeah, that’s true.

Steve:

Brain-derived neurotrophic factors.

Matt:

So, there’s other ways of manifesting those same things. The reason why I said like a stroke or like a brain injury is what the signaling factors for BDNF release in production. And those sort of things are, is typically swelling, inflammation, and nitric oxide. So, things that enhance nitric oxide, things that increase the hydration in the brain, manifests the same pathways that trigger extra healing and regrowth. In the same way, that’s a way nitric oxide stimulates muscle growth as well by manifesting the same sort of scenario as an injury, and then needing to recover with more.

Steve:

[inaudible 00:43:02].

Matt:

So, those sort of things are kind of cool, eh? That’s where a lot of the people talk about the mushrooms. That’s where a lot of the herbs, as well, get a lot of things, but you can also train that. For example, my study technique. I’d had this trick… I don’t know, I just started doing it in high school because it worked for me, and then I read something once about it later that, I think Buzan or someone said it’s a good idea. And I thought, “Oh, I fluked it.”

Matt:

So, when we’re talking about being smarter in learning, it’s being able to access the information. So, everything we’ve ever seen, heard, smelt, done, should be in there somewhere, which is why hypnotists can access it or something. So, it’s a matter of accessing it. So, when you learn something new… this is my study trick. Whenever I learn something that I want to remember, I’ll learn it on a day, I’ll remind myself of it the next day, seven days later, so one week later, I’ll just quickly remind myself, and then 21 days, and then three months.

Elizma:

I did exactly the same thing, yeah.

Matt:

Yeah. And then you learn it. And once it’s there, you’re tricking your brain into thinking this is important information I need to recall on a regular basis. Then it brings it to the front. That’s my imagination of it bringing it to the front. But what we’re talking about is making shortcuts, like nerves synapse shortcuts from where you are now to a piece of information that might be relevant and useful. The problem is, is if we’re running in a state of angst, stress and anxiety, it goes down a different pathway to survival stuff. And survival stuff is not conducive to learning.

Elizma:

Well, that’s the cerebellum and not the cerebrum, isn’t it? That’s the… yeah, where all the emotional stuff sits.

Matt:

Yeah, so that’s important for people with a nootropic stuff and brain and learning and even looking after brain long-term, is to not be confused with thinking a lot. It is not the same as learning, you know?

Steve:

Exactly. Because if you’re overstressed and you’re trying to learn something, you can’t. It’s really tricky. This is why it’s called forward brain. It’s not stimulant brain nootropic. It’s a really interesting term. So, it was only coined in the 60s, so these new, we’ll call them drugs. There’s a beautiful rat study here that I want to show you. Now, rat studies are rat studies, they’re on rats, but the beautiful thing about rats is you can control their environment 100%. There’s a beautiful graphical representation on aging rats, where they gave choline and piracetam, not paracetamol, piracetam, which was the very first smart drug developed.

Matt:

Or piracetam.

Steve:

Or it could be piracetam.

Matt:

They call them racetams. There’s a whole group of them. Yeah, a very popular one.

Steve:

There’s a beautiful… and I’ll show you guys and then I’ll show the camera. Look at the performance enhancing when you gave them with choline and piracetam.

Elizma:

Oh, wow.

Matt:

It’s true.

Steve:

It just shows you that they got a heck of a lot smarter. These were old, old rats. You can see here that it just showed it. That doesn’t matter what their variables was, it was actually retention latency, so to how quick they remember things. So, you can see that that’s what it’s all about. Not about stimulating the brain or anything like that. So, there’s some beautiful work done on that.

Matt:

So, without choline, so, I mean, which of the… so, we’ve said choline bitartrate is probably more likely to make TMAO because it really sucks at getting into the brain, so it’s less likely to go down an acetylcholine pathway, more likely to be hijacked by our gut microbes and converted into TMAO, or TMA and then TMAO, from the liver. So, choline bitartrate is probably the not ideal one. Lecithin, phosphatidylcholine forms, that’s pretty cool.

Elizma:

Yeah.

Steve:

Yeah, it’s good.

Matt:

Not only does it support acetylcholine, but it also works towards myelin sheath and other structural components of choline, which in regards to cell walls and cell membranes. They did a really cool study combining it with krill. And because the krill also has that form of fish oil that’s required for cell membranes, the two of them together worked quite well and reduced the production of TMAO. Had a protective effect of against TMAO causing sclerotic plaque. So, Lecithin’s is a cool one. Alpha-GPC. What do we reckon about alpha-GPC?

Steve:

I’m a fan.

Elizma:

Yeah, that’s a good one.

Matt:

It’s about 18%.

Steve:

I like it. There’s a couple of studies on that. They did it in… [inaudible 00:47:11] clinical trials have shown that it’s been very, very beneficial in memory. So, that one is well tested.

Matt:

Yep. That citicoline is probably, I’d say, the most popular or the most common one used as a choline supplement.

Elizma:

Yeah.

Matt:

And it’s a combination of choline with cytidine. And cytidine itself has its other effects.

Steve:

It stimulates glutamate out of the brain, which is a [inaudible 00:47:31], so it stimulates your brain.

Matt:

So, glutamate, it’s exo-tertiary, yeah.

Steve:

Yeah, so you’ll feel that one. That’s the one you’ll go whee.

Matt:

Whee.

Steve:

I’ll do it again. Whee.

Matt:

So, it’s the opposite to GABA.

Elizma:

Opposite to GABA.

Matt:

So, glutamic acid makes you whee.

Steve:

And GABA makes you go [inaudible 00:47:43].

Elizma:

That’s right.

Matt:

How is it? Do the GABA again, Steve.

Steve:

I’m just doing graphical for the people watching.

Matt:

Yeah, now it’s just… it’s good.

Steve:

It’s just makes me [inaudible 00:47:53] stroke. So, it just sedates you, of course. GABA’s when you drink too much beer, that stimulates you, GABA receptors.

Matt:

Really?

Steve:

Yeah.

Matt:

I like beer.

Steve:

How does it make you feel?

Matt:

Sleepy.

Steve:

Yes.

Elizma:

That’s right, yeah.

Steve:

[inaudible 00:48:05] GABA.

Matt:

That’s cool. So, we’ve got alpha-GPC, citicoline… so, all those are kind of cool. I’d avoid the choline bitartrate. I really like the lecithin. I really just like it because it’s-

Elizma:

Food sources.

Matt:

… food. People would probably tend to go towards the sunflower rather than the soy because soy is now a dirty word. But apart from the GMO aspects in that, it’s the same bloody stuff, isn’t it?

Steve:

Yeah.

Elizma:

Yeah.

Matt:

So, if you can’t… I know, in the grocery stores, it’s really hard to get the Sunflower Lecithin sometimes, and the soy is available. It shouldn’t matter too much for there, in regards to the lecithin ingredients.

Elizma:

No, unless you have allergies or reactions to soy. Because remember, it’s the fatty part of soy. It’s not the protein part.

Matt:

And you can add a big dose of lecithin granules. So, you can add like a-

Steve:

Spoonful, yeah.

Matt:

… couple of teaspoons and that sort of stuff. Like I said, I always have it in a bit of warm water with a bit of lemon juice to help digestion and that sort of stuff. But it will also add to the… put it in all the milkshakes for the kids and that sort of stuff. It’s really kind of cool.

Elizma:

Yeah.

Steve:

It’s good stuff. And you’ll see it around. You stop breaking down acetylcholine by taking acetylcholinesterase inhibitors, like Brahmi. And the great thing is the newer drugs for Alzheimer’s are acetylcholinesterase inhibitors. They’re drugs.

Matt:

But just to be aware that they work over an accumulation.

Elizma:

Yeah.

Steve:

Yes.

Matt:

You’re not going to have them and feel something straight away unless you take a megadose, and that’s a different effect.

Steve:

It is.

Matt:

The acetylcholine thing takes a good 10 days to kick in. It’s this weird trend of adding acute doses of huperzine is strange. Doing the huperzine in a pre-workout is not going to have the nootropic effects that we talk about with the huperzine, especially if you’re doing your pre-workout three times a week or something like that, and not twice a day.

Elizma:

Yeah.

Matt:

Because huperzine is supposed to be used… you usually use it by itself just daily. I imagine like an antidepressant. You know when people do the antidepressants to preserve serotonin. Well, these acetylcholine things preserve acetylcholine, they just take a little while to kick in.

Steve:

That’s a good analogy, yeah.

Matt:

So, acetylcholinesterase inhibitors, different forms of choline, alpha-GPC. If I was to find a nootropic and just go, “Look, I’ve listed off five nootropic ingredients today. Choline bitartrate, alpha-GPC, citicoline. If I stack five different forms of choline together, do I make a super nootropic drug?”

Steve:

No.

Elizma:

No.

Matt:

No, man. You want synergy, huh? So, we’d want to use a good source of choline, one of those, or a combination, maybe, if you wanted to, but understand it’s only doing the choline aspect. Stack them, then, with an acetylcholinesterase inhibitor to preserve the acetylcholine into the brain. And then, look after your gut.

Steve:

That’s important.

Matt:

Because if you’re not combining good holistic protocols and realizing you didn’t take these things early, you’ve focused all your research on brain chemistry, and you realized the bugger’s not going to get there. It’s going to get hijacked and taken down a different pathway. So, then adding in things like eating lots of asparagus, garlic. That’s why garlic is good for the heart. Garlic stops TMAO.

Steve:

It does.

Elizma:

Yeah.

Matt:

It goes great with lemon and fish. You see these synergies in recipes. Hey. So, anyway, and garlic, so the fenugreeks, and all those sort of things. Put those in with the choline to stop it. Maybe reduce the exposure to whole grains and other lactobacilli stuff… what am I… I’m trying to think of all the-

Elizma:

It stimulates the Firmicutes.

Matt:

The Firmicute production, yeah. Increase polyphenols and reduce the amount of Firmicute support you’re giving, which is typically sugars, carbs, and lactose sort of things.

Steve:

Yes. And also, eat a lot of choline-rich foods. You start with that. The healthy eggs, the healthy fish.

Matt:

Especially when you see a supplement of… if you consider a supplement of a choline supplement might cost you 80 bucks. And it, in a capsule… like, if I fill up a capsule… if I do pure CDP-choline in a capsule, say I can fit and I can really push it in there with no [inaudible 00:51:53]. I might get a gram into a double-layered capsule. I’m only doing that because it’s a round number. I’ll be getting 150 to 180 milligrams of choline from that CDP-choline. That’s less than one egg.

Steve:

Yeah. Still less than one egg.

Matt:

So, for a bit of perspective that we could have a couple of eggs, we could throw a couple of teaspoons of lecithin granules, and we’re actually getting equivalent to probably 10 capsules of a choline supplement, and we’ve had it for breakfast. And we can do that every day, and not be geniuses.

Steve:

No.

Matt:

You know what I mean? So, it’s not… just for that bit of perspective.

Steve:

And lecithin’s also found in egg yolk too.

Matt:

Yeah.

Elizma:

Yeah.

Steve:

Naturally. So, it’s a great breakfast. You cut it up with some nice greens and polyphenols for your gut. It’s a great breakfast, you know?

Matt:

Yeah.

Steve:

We can have a nice smoothie.

Matt:

Yeah, but my point is, I mean, it’s equivalent to like 10 of some of these brain drugs that are on the market. We all do it all the time. We don’t feel… it’s not that significant. So, the strategy is all about combining-

Elizma:

Synergy.

Matt:

… combinations of things. And then, also, trying to get the zen. It’s a holistic thing. We always go back to the same bloody holistic thing. You got to be in that state with no angst, you got to be in that focus, you got to be comfortable, you got to be happy, you’ve got to be relatively symptom free from other sources of oxidative stress, inflammation, immune dysregulation, and stress. Nootropic stuff is holistic. We can’t just go through and say, “I’m going to manipulate my brain chemistry.”

Matt:

Then, there’s a lot of other stuff out there that might have data showing that it increases brain-derived neurotrophic factor. Therefore, will be the greatest smart drug on earth. Like, a lot of the new mushrooms that we’re still starting to research, still trying to get an understanding around. You got to realize… what did I say before? The main cause of BDNF is concussion and stroke. At this point in time, with inadequate research, you don’t know what things are increasing brain chemistry and a response to brain damage. It’s got to be very careful with what you’re over dosing on and what you’re trying on. Because you can get these weird feelings, doesn’t mean that you’re now limitless, you know what I mean?

Elizma:

Yeah.

Matt:

It’s just so many factors with it that you want to treat the people. That’s why I’m really skeptical about anything that’s just a straight out smart drug. Because we don’t treat the brain, or we don’t treat smart, and we don’t treat dumb, you know? We kind of treat people, and trying to work out each person’s hand brake and that sort of stuff.

Steve:

It’s true. And you got to remember, with the TMAO, we’ve talked about that a lot today, and is that the cause of heart disease? Is it a factor? Is it a marker? Is it-

Matt:

Is it an association?

Steve:

… Is it an assoc… Remember, a correlation doesn’t mean causation. The greatest lesson that I could teach people is that just because it’s there and you get heart disease and the more of it, it could be the microbes. It could be just a marker of the bad microbes that cause heart disease. Or it could be the actual chemical causing it. It could be-

Matt:

Now, in regards to the hierarchy in the body, if you get a trigger to your sympathetic nervous system, from anything, smell, memory, vision, whatever, something you’ve studied and read, or just something you got excited about, like we do in the podcast, sometimes we get excited, we totally forget what we were about to say because we got too excited. You know what I mean?

Elizma:

Yeah, yeah. Yeah.

Steve:

… Yes.

Matt:

So, we got to have a look at that sort of aspect and realize that… I’ve totally forgot what I was talking about then because I got excited. You see what I mean? It is so easy, we switch out of the… the sympathetic nervous system will just take over and it’ll get you running on gut instincts, long-term memory, intuition, in response to a trigger of some sort. So, more than anything, to drive that parasympathetic nervous system, it’s one thing to build it up, build up acetylcholine, acetylcholinesterase inhibitors, but unless you can get rid of the sympathetic nervous system, you can’t get into that full smart drug zone. So, that’s the challenge, in my opinion-

Steve:

It’s true.

Matt:

… because a lot of people add nootropics with stimulants.

Elizma:

Yeah.

Matt:

And even that glutamic acid aspect you said before. Glutamic is exo-tertiary.

Steve:

Very much so.

Matt:

For me personally, I would study better after a GABA and [inaudible 00:56:29] than I would with glutamic acid because I just get too much excessive mental chatter. But if I’m not actually trying to learn something, if I’m just trying to stay awake and be alert, then the glutamic acid’s fine. If I’m going to be-

Steve:

Probably good for a movie.

Matt:

… or gaming and stuff.

Steve:

Gaming, yeah.

Matt:

So, you have to look at it as some things… Why’d I pause? Gaming is another aspect for nootropics. These people play the Xboxes and those are… a lot of that is gut instincts, intuition, long-term memory, back to my training. Fighters. So, UFC fighters and all that sort of stuff. A lot of that is back to the training. I know a lot of fighters that actually train better when they’re almost unconscious, and they fight better because now all of a sudden they stop thinking and they go back to their training. So, you’ll find, in some aspects of nootropics, so gaming, fighting, maybe extreme sports, your Red Bull guys in the planes and all that sort of stuff. Their learning ability, their concentration and focus is not as important as long-term memory, gut instincts and intuition.

Matt:

So, again, the nootropic category, you need to split it up and understand what your objective is. Am I trying to be alert, awake, running on autopilot for as long as possible, which is what we might find with gaming, sports, fighters, those sort of things. Or am I trying to get into the zone to dissect a paper, to learn, to… a totally different form of the brain that you’d need to learn, to study new things and remember it, is totally different to an extreme sport. So, we can have totally different forms of nootropics. Crazy, huh?

Steve:

It’s crazy, isn’t it, eh? It really is. If you want to smash it out at the gym, with the HyStim stuff, it may work for you, but you’re right, learning is all about nootropic, and that’s a completely different topic to stimulants, it really is.

Matt:

Yeah.

Elizma:

Yeah.

Steve:

They’re totally different and people don’t understand.

Matt:

So, my understanding it, because that’s where I always get caught up, it’s always like these nootropics are… people talk about nootropics like amphetamines. And I said, “No, that’s the worst thing-

Steve:

It’s a stimulant, yeah.

Matt:

… that’s the last thing that I want to do.” I want to be zen and I want to be in the zone. I want to be focused. I want to listen to classical music, not angry stuff, you know?

Steve:

Can you imagine reading papers… Yeah, yeah. You don’t want to be reading a [inaudible 00:58:32] paper on amphetamines. You’d be going, “Oh, buggered, I’ll go out for a run.”

Elizma:

Yeah.

Matt:

Yeah. So, if I’m trying to discover something, if I’m trying to learn something new, I will totally change my learning environment to if I’m actually just trying to get some work done. So, if I’m actually trying to get some work done, that, to me, is like autopilot, that I’ve been doing for years, I’ll actually raise my desk up, I’ll stand up, I’ll have my coffee, and I’ll play my drinking music. Actually, that’s what my playlist title is. Drinking music.

Steve:

It’s good music, too.

Matt:

And I’ll get out all the Radio Birdman and all that sort of stuff and play that and I’ll be in that zone. I’ll be bouncing around like an idiot. It’ll just be bulk amount of work getting done. All of it’s coming from somewhere. I have no idea where. Seminars. When I’m doing a seminar, I’m not learning something new, typically, when I’m presenting. I’m in a zone.

Steve:

Recalling, yeah.

Matt:

Often, I disassociate, I forget the whole thing. I’m running the whole thing on autopilot, long-term memory, gut instincts, and intuition. That’s my zone I need to be in. But when I want to invent a new product, create some educational material, discover a new thing, I need to be… I get the classical music, I sit down, I calm down, I make sure there’s less distractions. Is that what you guys-

Elizma:

I did that in high school. So, I was lucky enough to… kind of like I have a photographic memory, so for me, it was very easy to kind of remember stuff. But the way I studied was through classical music. I would play classical music, and that’s when I studied. It just really, really worked very well.

Matt:

… Yeah.

Steve:

I found playing the guitar and then learning, was better for me. Like, actually playing. You play for about three or four minutes and then you read something. I don’t know, the playing action did something to my brain. It made it work better.

Matt:

Yeah. A little bit of left and right brain. You’re getting it all working together and that sort of thing.

Steve:

It did something or other. And when I would swim, after swimming, my brain would be more alive.

Matt:

That might be that left and right too because-

Elizma:

Yeah, could be.

Matt:

… that cross crawling action, that anything that you can get your left and right brain. So, left brain is for analytical sort of stuff, just data collection. But right brain is all the problem solving and working out where it goes.

Matt:

Man, how often do you guys learn something new, and then have this little epiphany and remember shit that you haven’t thought of for years. It happens all the time in these podcasts, hey. So, you’ll be going along, and someone will say something, and all of a sudden this memory, and then all of a sudden the things start piecing together. We’ve got lots of data sitting in the back of our brain that we thought was irrelevant and useless, or was filed there, but we haven’t been able to use it. Then, all of a sudden, you learn a piece of information, and it might go to three or four different filing cabinets in your brain, piece it all together, and you’re having your aha moment, “Oh my gosh, this is where it all fits in.” You know?

Elizma:

Yeah.

Steve:

[crosstalk 01:01:05] all the time.

Matt:

That’s where these synapses and everything form. So, I think the point of my story here is that we… there’s no, like, a smart drug. There’s no, a drug, for anything. That’s why we have holistic, and that’s why we treat people, we create synergistic formulas, and what works for one person, may not work for the next person. You can stop shit from working, through simple things like angst, bad posture, bad lifestyle, and that sort of stuff. You can be taking all the right stuff, like I did for breakfast this morning, and I still don’t feel any different because my brain is in a different place, you know what I mean?

Elizma:

Yeah.

Steve:

Yeah.

Matt:

So, it’s holistic. So, stack up your cholines, but also add some other shit. You might want to add… when you’re looking for a good choline product, it synergizes well with B vitamins, the B12, the folates, and that sort of stuff, for the methylation. It synergizes with B1 and B5 for acetylcholine production. So, we’ve got-

Elizma:

Acetylcarnitine.

Matt:

… lots of B vitamins. A good carnitine, amazing. So, it stacks with carnitine, choline, all your B vitamins are good. Definitely understand that you’re going to need some sources of polyphenols when you’re taking these things early to regulate the gut flora, and typically in your diet, you wouldn’t want to be having too many sugars. You want to have the higher fat diet, which is why we always study better in keto. That’s a bit of a big statement, but I find-

Steve:

I do.

Matt:

… if I go into ketosis, I’m a hell of a lot smarter. It’s a preferred source of fuel for my brain anyway. So, everyone’s a little bit different there.

Steve:

Same here.

Matt:

So, lots of polyphenols. And of the polyphenols that we’ve researched, they’re all pretty good. In fact, your green teas, the ones coming out of citrus peels, are really excellent, which is also a source of other racetams, come out of the citrus peels and that sort of stuff as well.

Steve:

Yes, they do.

Matt:

Which is an interesting little link. Yeah, so, choline, B vitamins, acetylcholinesterase inhibitor herbs. It could be huperzine, Ginkgo, Brahmi, Bacopas. They’re the sort of things that you want to look for to maximize acetylcholine. You also want to understand acetylcholine does other jobs, which is structural jobs. We want to support that with other sorts of EPA, DHAs, and that sort of thing as well.

Elizma:

There’s another one that I kind of quickly want to mention because I saw it a lot at my clinic, is acetylcholine is also involved in muscle contractions and stuff like that. So, things like… what’s the word? You have bladder problems.

Matt:

Incontinence.

Elizma:

Incontinence.

Matt:

Yeah.

Elizma:

There you go.

Matt:

Why would you do that with a bladder problem? What were you doing then?

Elizma:

I was trying to make my brain [crosstalk 01:03:36].

Steve:

She could’ve just done right.

Elizma:

I was trying to make brain go forward.

Steve:

Left brain here.

Matt:

Toilet paper or something.

Elizma:

Well, anyway. So, things like incontinence responds very well to choline and an acetylcarnitine.

Matt:

Yeah.

Steve:

No, I see, of course it would.

Matt:

Yeah, it would.

Elizma:

Yeah. And that’s kind of what you see when people get older. It’s not just the dementia and the Alzheimer’s. It’s loss of bladder control and-

Matt:

So, if we think about it. The acetylcholine deficient symptom picture, or a sympathetic nervous system dominant picture, would manifest as that needing to wee all the time and that sort of stuff. An inability to hold, which is something we talk about with stress.

Steve:

It’s true.

Matt:

And it’ll be worse with stress. So, under stress, you’re going to need to wee even more. So, dry mouth, dry skin, burning feet syndrome, a weird flushing to the skin, fatigue, and-

Elizma:

… It was almost like [inaudible 01:04:29].

Steve:

Chronic depression.

Matt:

… Yeah, chronic… I was about to say spastic muscles then, and I was like-

Elizma:

Well it is. I had that actually.

Matt:

… “Is that the technical term?” Spasming.

Elizma:

No, I had them when I was… no, my body broke down from over training when I was doing a lot of training. I got exactly that thing, where I started losing control of my muscles. So, it’s like I was running, but it’s like my feet forgot how to run.

Matt:

Yeah. And that’s acetylcholine stuff.

Elizma:

That’s acetylcholine because that all improves-

Matt:

Myasthenia gravis. Did anyone treat myasthenia gravis in your clinic?

Steve:

Never had one.

Elizma:

… No.

Matt:

That’s an autoimmune condition that wipes out the acetylcholine receptors.

Steve:

Yes.

Matt:

And they just get droopy muscles. So, they’ll have like sections of the body of just… it looks like they’ve had a stroke and that sort of stuff. But it’s not, it’s an autoimmune that’s wiped out acetylcholine and their muscles can’t contract. If that happens, [inaudible 01:05:12] can’t think or that organ can’t function.

Steve:

Awful, eh?

Elizma:

Yeah, terrible.

Matt:

Yeah, it’s wild, man.

Steve:

Nasty.

Matt:

So, that’s a cool thing. So, choline, we can get lots of dietary choline from both animals and plant origin. That, again, goes back to the same thing, not too much sugar, increase your polyphenols.

Matt:

The cool thing is, is you can pick from those list of polyphenols, something that suits you. Do you want a polyphenol that helps with your blood sugar control from fenugreek? Do you want the polyphenol from Garnastema that helps with your circulation? Do you want your polyphenols from asparagus that just makes your wee stink? But asparagus has got a lot of other interesting features in Ayurvedic medicine, that it helps to regulate the downward flowing movement of all hollow organs.

Steve:

Whoa. [inaudible 01:06:06].

Matt:

And it also helps to move water through the body, so very important for the fluid migration through the brain stem, just like it is regulating kidneys, urinary tract… I don’t why she just pointed at you.

Elizma:

No, I don’t know.

Matt:

Just the incontinence stuff.

Steve:

Yes.

Matt:

There’s a lot of antioxidant compounds, such as resveratrol and that sort of stuff. Resveratrol is really good for this TMAO.

Steve:

[crosstalk 01:06:40].

Matt:

But I’ve found that it stimulates a lot of antioxidant defense mechanisms by acting as a poison.

Elizma:

Yeah.

Matt:

So, it’ll come through and trigger an oxidative stress that the body will manifest a antioxidant defense mechanism for.

Elizma:

It’s like your body needs that little bit of stress to kind of… that may even be the way that alcohol works as well. If you look at the French paradox. You got the antioxidants in there, but you also have the alcohol that may stimulate a kind of a small stress, but then have the antioxidants to kind of-

Steve:

It’s like going for a run this morning. That was a small stress on my body and that beneficial my body.

Matt:

It would’ve killed me. That small stress on your body. I would’ve died.

Steve:

It was only 12k’s. You would’ve made it.

Matt:

No, I’d still be going. I’d make it, but I’d still… I might be a bit late to work.

Steve:

We’re nothing like Elizma when it comes to running. God, she’s… many, many kilometers, don’t you?

Elizma:

… I used to, yeah. 30 kilometers, et cetera, but-

Steve:

I used to do that too, many years ago.

Matt:

Why?

Elizma:

… not anymore.

Matt:

No one’s going to be chasing you still after 30k’s.

Elizma:

It’s an amazing feeling like when you run like that and you don’t get tired.

Matt:

Yeah, it would be.

Elizma:

You feel-

Steve:

Well, also the persistent hunting in Africa, where they chased animals for 30 to 40 kilometers and they drop dead and you catch them and eat them.

Matt:

Hunters?

Steve:

Persistent hunters they were called. They just hunt them for hours.

Matt:

I’d just follow the hunter. Wait for them to drop.

Steve:

Because the animals couldn’t sweat, and humans can, so we had this ability to catch the animals and kill them. Persistent hunting.

Matt:

You’re a horrible person, Steve.

Steve:

I didn’t ever persistent hunted anything.

Matt:

Anyway.

Steve:

Yes.

Matt:

What the fuck is he talking about?

Elizma:

I don’t know.

Steve:

You don’t… the… I’m trying to remember the name of the hunting tribe thing because they’re from Africa.

Elizma:

Well, yeah, but.

Steve:

What’s the name of the tribe there? The famous tribe.

Matt:

You’re so racist, Steve. You meet an African and all of a sudden…

Elizma:

Oh, is it the Bushmen… the Khoi… the Khoisan.

Steve:

Yeah, that’s it.

Elizma:

Yeah, the Khoisan.

Steve:

Khoisan. Yeah, they were the persistent hunters.

Matt:

So, you did actually know?

Elizma:

I guess so.

Steve:

I thought you did. All right.

Matt:

A grudge to me is just a place to park my car. Any who. Nootropics. Good stuff. All right. Let’s finish this out.

Steve:

I think our brains are better for that.

Steve:

Good.

Matt:

Because there is so much more I want to say that’s a little bit different, but it’s not directly driving down the nootropic angle, so that’s cool. I’ll save that for another day.

Steve:

Good.

Matt:

I reckon this is a great idea. We got to realize that food is the best. Not only is food a shit load more than you can fit into a capsule, and you can dose it up, but you can actually structure a proper recipes to get into proper big bloody doses, and you can do it consistently daily. So, I still think food is the best.

Elizma:

Absolutely.

Matt:

And when it comes to these nootropics, if you aren’t considering the whole holistic picture, you’re really only covering a small fraction. I was going to say that you’re only covering half the… it’s not even close to half. Like, if you’re looking at what brain chemistry is, and focusing your research on supplementing things that are going to get into your brain, you’re kidding yourself to think that the body’s not a whole holistic system. It’s going to do exactly what it wants with those nutrients. If you’ve taken something that works something a certain way for you, don’t assume it’s going to do the same thing for someone else.

Elizma:

Yep.

Matt:

So, you got to understand, treat everyone individually, a holistic approach, and really focus on the foods.

Steve:

Awesome.

Matt:

You guys cool with that?

Elizma:

Yep.

Steve:

Absolutely. That’s the perfect way to-

Matt:

Anything else you want to add?

Steve:

… No, that’s perfect.

Elizma:

No.

Matt:

Done. That was pretty easy. That’s goodbye from us. That’ll do.

Elizma:

That’ll do.

Steve:

See you in Detroit.

Elizma:

Cheers.

Automated:

Thanks for listening. And remember; question everything. Well, except what we say.

 

References:

  1. https://elizmalambert.com/atherosclerosis/
  2. Effect of Grape Pomace Polyphenols With or Without Pectin on TMAO Serum Levels Assessed by LC/MS-Based Assay: A Preliminary Clinical Study on Overweight/Obese Subjects

  3. Choline nutrition programs brain development via DNA and histone methylation

  4. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk.
  5. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa

  6. Maternal choline supplementation ameliorates Alzheimer’s disease pathology by reducing brain homocysteine levels across multiple generations

  7. Trimethylamine N-Oxide Generated by the Gut Microbiota Is Associated with Vascular Inflammation: New Insights into Atherosclerosis.
  8. History of nootropics ” an accidental discovery” 
  9. why choline is so important to our health 
  10. cdo choline vs alpha gpc vs centrophenoxine
  11. Microbial trimethylamine-N-oxide as a disease marker: something fishy?
  12. Trimethylamine N-Oxide and Risk of Cardiovascular Disease and Mortality.