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Decoding Diet & Life Expectancy

A Critical Look at Supplements and the Latest Studies

I did my second podcast on Conquer Aging or Die Trying!


0:00 Introduction

0:47 Diet Quality Impacts Life Expectancy

24:10 Glucosamine

26:20 Bryan Johnson

29:20 NAD: Nicotinic acid vs NMN

32:31 Trigonelline

35:50 Methyl Donors Besides Trimethylglycine (TMG)

38:15 Proline Betaine

41:20 Sauna

50:52 Oral Health

54:45 Alcohol


Previous discussion, Podcast #1

Glyphosate tests in oat cereals and snacks:

Healthy diet reduces premature death by 4-5 years:

Adjusting for many variables reduces premature death by 10 years:

High pesticide fruits and vegetables effect on cancer: Intake of fruits and vegetables according to pesticide residue status in relation to all-cause and disease-specific mortality: Results from three prospective cohort studies

Glucosamine supplement effect on premature death: Associations of regular glucosamine use with all-cause and cause-specific mortality: a large prospective cohort study | Annals of the Rheumatic Diseases

Sauna bathing effects on premature death: Association Between Sauna Bathing and Fatal Cardiovascular and All-Cause Mortality Events

Sauna bathing effects on VO2max: Effects of regular sauna bathing in conjunction with exercise on cardiovascular function: a multi-arm, randomized controlled trial

Sauna suits or hot bath effects on VO2max: Post-Exercise Passive Heating Strategies with Hot Water Immersion and Sauna Suits Improve VO2max, Running Economy, and Lactate Threshold

Hot bath effects on CVD: Habitual tub bathing and risks of incident coronary heart disease and stroke

Dental care effects on premature death: Dental Health Behaviors, Dentition, and Mortality in the Elderly: The Leisure World Cohort Study

Alcohol low or high consumption effect on premature death: The Impact of Healthy Lifestyle Factors on Life Expectancies in the US population

Alcohol effect on premature death by daily amount: Association Between Daily Alcohol Intake and Risk of All-Cause Mortality


Michael Lustgarten: Hey, everybody, welcome back to the channel. Today, we’ve got Crissman Loomis for round two. If you miss round one, it’ll be in the video description. Crissman is the owner and operator of So today, we’re going to talk about a whole bunch of aging-related topics, so let’s jump into it. So, what’s on the agenda today, Criss?

Crissman Loomis: So first, you’re going to talk about a diet life expectancy study. Then I think it would be a good idea for us to talk about supplements and what we think about them. There are a lot of YouTube videos out there of what everyone’s taking, and I want to make sure that you and I put in our two cents worth on it. And then on to healthy habits. Once you get beyond diet and exercise, what else can you do that would make a difference?

ML: So I’ll link to this paper in the video description and I don’t even have the title here. Still, I think it’s impact of healthy lifestyle factors on life expectancies. Then I can’t see what the rest is, but nonetheless gained life expectancy by increasing and then a variety of factors, physical activity, smoking, diet quality, moderate alcohol consumption, and then BMI. So in focusing on diet, people who are in the highest quartile or quantile of the Alternative Healthy Eating Index women and men.

So you can see that women who were in the highest quantile compared to the lowest had about a four-year gain of life expectancy for the highest dietary quality. And then for men, it’s actually, sorry, it’s a five-year gain for women because it’s compared to Q1, which is the reference. And then, for men, it was a four-year gain, so that might not seem too impressive. But then there is another study that was just published so you can see you can see here life expectancy can increase by up to ten years following sustained shifts towards healthier diets. So when it comes to pushing — they don’t have any pretty pictures — I mean, they’ve got them ranked. They looked at hazard ratio all-cause mortality based on individual food groups, and this is actually the case.

So they have in the supplementary data they have, but I don’t remember off the top of my head what they adjusted for. I think this one isn’t fully adjusted. When you look at the fully adjusted data, it’s actually cleaner. So I don’t know. Maybe I’ll share that one too, because I have that open. So, what I’m finding is that the adjustment for as many variables as possible is essential in these epidemiological studies. And I know that may seem superficially obvious. But most epi studies, for example, using LDL as an example, will adjust for the standards of age and sex. BMI, education, and then, like hypertension, glucose levels, basically metabolic health. But then, not all of these studies, whether it’s LDL or this study or others, won’t adjust for all of the comorbidities many of these studies will leave out, like deaths from lung disease or liver disease. And maybe that doesn’t seem like a big deal.

But reverse causation is a big or potentially a big impact on a lot of these associations so like in the case. I mean. I guess we won’t go through the LDL story today, but there’s a study that was recently published with about five million people where they adjusted for like 14 different comorbidities. And when you look at earlier studies that show basically a J-shaped or U-shaped curb for LDL, and all-cause mortality or total cholesterol with LDL driving most of that when you adjust for all of the comorbidities as opposed to some of them, the curve becomes like you know, it flattens out the bottom of that J so that lower LDL is not associated or lower total cholesterol is not associated with an increased cardiovascular disease risk.

So anyway, with that in mind, the paper in the Supplementary data for the Diet Life Expectancy Study, the ten years this is the more fully adjusted model BMI calories or energy age sex, you know, and the full spectrum which reduces their sample size because I think it was probably double or triple this in the larger set. Still, nonetheless, they go through all of the different food groups in terms of the longest reduced all-cause mortality risk versus better survival versus shorter. It’s actually some of it is what you’d expect. Like what’s interesting is not that I’m a pro meat guy. I’m not anti-meat.

But if you look at sugar-sweetened beverages in terms of, you know, all-cause mortality risk, I mean, it’s 65% higher risk. Significantly, you can see the confidence intervals greater than one, and I mean processed meat, too. I mean, Peter Attia is high on his processed meat, and yet 45%, and these are the strongest associations with the process of eating. I guess it probably has no preservatives, and I don’t know how what natural flavors they’re using, but.

Nonetheless, the two strongest associations are processed meat and sugar-sweetened beverages, whereas red meat is not significant, the confidence interval overlaps white meat not significant, and again, I’m not pro or anti-meat. This is just what the data shows, but yet in the pop culture, you know, there isn’t this big drive for, Hey, let’s tax sugar-sweetened beverages, or let’s reduce intake, because now I’m going to sound like the conspiracy theorist. But you’ve got big food, right? Big food, who doesn’t want it, right? So anyway, ten years increased life expectancy with this study, too. So if we’re going to make a dent on pushing that average life expectancy out, we’ve got one study showing four to six years for women and men, this study showing ten years. But then the question is now with the biomarker-based approach, can we push it out 15 to 20, add some circadian alignment in there in terms of when you eat, and a little bit of fasting potentially based on the animal studies, maybe push it out to 25 or 30. I don’t know what the window is, but yeah. I just wanted to. This will probably be in a video at some point, but yeah.

CL: So, just going over it now, like some of the things that jump out.
One is the nuts at 0.45; it looks like it didn’t reach significance, so it’s a bit questionable, but the average result was the largest thing on there. As I’ve talked i think about before and have noted from the epidemiological studies; the nuts dosage is very sensitive, so
basically, getting just what they say here is getting about one small handful or less than an ounce, like almost an ounce a day, is the best, and you see this here.

My statistical analysis of it from another study says it’s a 17% reduction in premature death, and you see here in Quantile 2, it’s 18% right on and significant at that level that one matches expectation. Sugar-sweetened beverages match expectations, though white meat is one that’s kind of strange; right some of these things have strange intermediate results. But then again, you see with the legumes then being healthy generally, but kind of questionable fish also being sort of borderline, which is something I usually think is good. But one of the interesting ones that stands out here also is the milk being actually generally healthy. It is another one that’s a bit of a surprise, especially as you get into the higher amounts. Usually, I see that it is not healthy and that it might be idiosyncratic. This is a UK study.

So that might be something that kind of depends on the UK,
But in general, I think it lines up. It’s something that I’ll be interested in taking a look at and kind of seeing how it matches with the data that we have today.

ML: You’ve got the refined grains too, which I mean across the board you can see Q2 significant. Q3. Q4. Every quantile of higher intake is significantly associated with increased all-cause mortality risk. So, Yeah. I mean, but that’s easy, right for me, that’s the lowest-hanging food. Eat real food and exercise right; it’s not specific enough, and like you were saying about the nuts, where now you’ve got Q2 being significant, whereas the higher intakes are not.

It gets this idea of again specificity like if you look at Q5, okay sure that confidence interval going, you overlapping with one. But when you see so, it raises an interesting thing that the hazard ratio is so low it suggests. But the confidence interval is so high that there was a lot of variability within nut intake and all-cause mortality risk. But on the one hand, and again, I know it’s not significant. So, there is speculation. But it suggests that for a given population, there may be factors where the highest quantile of intake is indeed associated with the largest risk reduction, whereas for whatever reason, people who are eating the most nuts.
There’s some variability in that.

So, for me, it’s a matter of how you can titrate what the variables are. This kind of ties into the alcohol story, too, because there’s a similar effect going on here also, with the hazard ratio potentially suggesting a decreased mortality risk at lower intakes. But it overlaps with one. But it suggests that there may be subpopulations of people, and again, it’s not significant. So it’s just a suggestion.

It suggests that there are subpopulations of people, that if you figure out what the external variables of the other variables are in addition to this, that can impact risk to make it a significant thing. There may be an even bigger benefit, right, but what are those other factors are. I can’t say it has to do deep-dive right so

CL: Well, I mean, off the top of the head, nuts are the high-calorie counter them, right? So then you might be seeing some people who are then eating far too many nuts. My dad often talked about one of his weaknesses: the jar of peanut butter on the counter that he’d come home after eating a tight calorie day and then get a big old globe of peanut butter because he was just hungry. Yeah. I think that’s probably going to be what you’re seeing on the top side.

Podcast Host – The argument against that, though, is they adjusted the model for energy intake. So, but it could be lots of BMI as well. Right, yeah, so even eggs here too. Occasional eggs Q2 significant. And then you can see even Q3 and Q4 right on that borderline of a little bit of eggs potentially being good, but then five highest. I mean, now it’s significant; too many eggs are not good right,

CL: So that matches up exactly with the epidemiological study I’ve seen to date, where it says that on the dosage of about an egg every other day or so is fine and might even be slightly good for you. And this, in fact, shows that Q2 is better for you than being at the lowest egg consumption. But after about an egg a day, then from that, it’s basically break, and after that, now you’re starting to see other effects, and that’s probably going to be the cholesterol, right?

Podcast Host – Yeah, it could be. But so I mean, granted on the outlier and the end of one right. But so I increased egg intake from two per week to four per week, and it didn’t affect anything. No biomarkers, nothing changed.

CL: So that’s sweet spot four per week; you’re about every other day, so that’s exactly in the queue, too. That’s where I’m saying people actually did see benefit from it.

Podcast Host – Right, but you’d expect if that were true. In my case, you’d expect to see some biomarkers with some, you know, just some improvement, moving the needle in some direction and nothing, literally nothing, nothing.

CL: Okay, it had no huh.

ML: Yeah, so, but that goes back to the context-dependent, you know, it could be and no effect obviously, clearly no effect on my total or cholesterol levels. In my case, I’ve got to really jack up my saturated fat, whether it’s from coconut butter or other stuff cacao beans, which is saturated fat too, to get my HDL from or sorry from my LDL in total cholesterol from relatively low 150 and like 180 for total and LDL to get that to like 180 and 200.

So it seems that Eggs, in the context of my high-fiber diet, have no moving the needle on cholesterol, but for the average person who’s probably eating 15 grams of fiber per day because there’s an inverse association between fiber and total cholesterol level. So if you’re on a low-fiber diet relatively and you go to more and more eggs, and I know people are going to say, well, the idea that increasing dietary cholesterol doesn’t impact blood cholesterols.

But for some people, that may not be the case where there is a dose-response relationship depending on the background of other stuff that you’re eating, as I said, including things like fiber. So that could be some of the story here about speculation; I don’t know.

CL: Right, I’m not sure exactly on the color coding they’re using for this because, like, I look at whole grains Q3, and it’s like 82, and it’s clearly under one. So it’s a significant benefit. But then I look at vegetables Q4, and it’s also green, but it clearly straddles one, so I’m not quite clear how they did the coloring.

ML: Yeah. I agree the color coding here is a disaster like even the blues. The blues are there for their Eat Well recommendations. The UK Eat Well recommendations which just okay, yeah, and then yeah. I don’t. I don’t like what you said. I don’t know why the green would because, yeah, whole greens Q2 and Q4 are significant, so why aren’t those also green? Right, so yeah, screw. That’s one reason I didn’t show this in a video yet because you know it’s just there is some confusion to it. Right.

CL: So, but if you look at it, though. Another interesting thing that is consistent with the epidemiological studies is that vegetables and fruits and vegetables don’t have that big of a boost. Overall. I mean, if you look at, for instance, even just having the Q2 quartile second quartile of nuts, which gave you the 18% reduction in all causes. None of the quartiles for fruits or vegetables give you anywhere more than a 10% reduction in all-cause mortality.

ML: Yeah, to play the devil’s advocate there. I don’t know if it’s because of bias or the published studies drive my bias. But most people are barely eating any fruits and vegetables, so we’re talking about associations for maybe five total servings per day versus one or two, which to me is like, you know, comparing sick against sicker.

I have another. I didn’t open this tab up, but there’s another study on fiber intake and all-cause mortality risk, and off the top of my head. I have to take another look at it, but I think fiber wasn’t significantly associated with reduced risk, which ties into what this data shows and what you’re saying. But vegetable fiber was. But again, that’s still on the lowest side of fiber intake. And I think the highest fiber in that study was like 40 grams like how I’m completely. I’m double that. At least, how do you put me into that context, right? So.

CL: Right, well, I focused on the fiber, getting it from the whole grains and the legumes. The whole grains, as we have seen, have come out strong here. They’re basically one or below in every quartile after the first, and the legumes, though, that’s a mystery one I think I think we’re talking about the rarity thing like the Quantile five, how much legumes that they’re actually eating. But that range is the largest almost of any of the ranges like hazard ratio from 10% to 525% is not clear, but those are the real drivers. I think for most people of, fiber in the diet is whole grains and legumes.

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It’s hard to eat enough fruits and vegetables to get enough fiber before your stomach is full.
I know not everyone is able to put away half a kilo of strawberries like you can. The Legumes are where I’ve been focusing, and also on the whole grains because I find that very underappreciated. Getting like a slice of whole wheat bread is actually a wonderful, healthy thing.

Feels like we kind of forget about it in the rush towards whole foods, it doesn’t look like a food, but it really is. Or some healthy breakfast cereals also can be outstanding, not the Fruit Loops grant you, but like Cheerios or Break nuts or some of those other things, or oatmeal can be excellent healthy foods.

ML: But the argument there for at least someone like me is those foods don’t satiate me at all, and they are processed like it’s not ultra-processed, but like instead of. So if you’ve got a cereal that’s derived from whole Wheat, and it’s quote-unquote whole grain ideally.
You can buy whole wheat berries, you just cook them up, you just put them in whatever you’re cooking, and you just put up the equivalent amount of.

So instead of having a slice of bread, which is like four bites and 100 calories, you put that gran in whole wheat barriers that are still calorie-dense. You know whole grains are about 100 calories an ounce, but at least you’re getting legitimate whole food. Versus, you know, whatever the whole grains, 12 grains of whole grains and Cheerios, right? I mean, literally eat the whole grain, you know. But most doing that most people aren’t doing that.

CL: Right. Well, I’m a big fan of the whole wheat berries as well. I have those every morning. Whole wheat berries, barley, and oatmeal are my standard bowls. So nice, but I actually go and recommend to people, some, and myself as well. Just a granola bar, hyper-processed added sugar, all of those things, but at least it is whole wheat, and the fiber there is quite high.

ML: Yeah, no. I hear you. I hear you on that. I can put it back up. But so yeah, that for me, that’s like the general recommendation versus the, I don’t want to say, the MIC level, which is, you know, eat real food. I just. I see; even the store granola bars are, you know, just that they can be not satiating right. So it’s how many of those are you going to eat. Can you just stick with that one little strip or?

What I learned a long time ago was to know what if I make my own right, and for me, that’s infinitely more satiating than not necessarily. First of all, the oats being rolled oats is, is it so there’s a difference like Quakers? Quakers rolled oats versus steel cut oats glycemic index. There’s a difference, pesticide use like there a, there’s a. I think it’s a. Consumer Reports there’s a website that did a review on pesticides and oatmeal in the rolled oats. And I mean the burden in most rolled oats brands of pesticides. I mean, it was incredibly high, even for some of the organic brands.

So it’s important to know which on the list have no pesticides. You know, I can hear people saying well, so what pesticides? Conventional versus organic. The nutrient quality is not different; that is, there’s data showing that, but I’m trying to limit stuff like pesticides. If I can, whether that makes it dent or not. I take the gamble. But from my experience, the bars that you’re getting.

I mean, just not satiating, and when I make it at home, it’s like, you know. I have cocoa beans in the dates, which I use to make homemade chocolate, and that satiates me to the point where I don’t. I mean, granted. I could probably crush 4 thousand calories as in peanut butter cups. But knowing that I’m eating the natural food, you know, it satisfies that urge versus, you know, I can’t, who can stop eating? You know, even granola bars, right

CL: So well, that’s one key to that I find is not to have too many. There was a time when I was eating. I had a high supply of protein bars, and I found that basically the amount of them that I would eat in one sitting was largely determined by the variety of flavors I had because I would just take one of every flavor. If I had two flavors, I’d have two. If I had five flavors,. I need five. So I currently have two kinds of granola bars, so I usually eat two granola bars.

ML: You’re on the marathon. You know you’re on that marathon training diet. So it’s like you need calories; you need quick calories. So

CL: One thing I want to come back around to. I hadn’t seen that. Consumer Reports on the oatmeal. I had seen the Consumer Reports on some of the problems with rice and heavy metals and some of the things. But I haven’t seen the oatmeal from the stuff that I had looked at before. Actually, both legumes and whole wheat.

Whole grains were significantly better on having a very low pesticide burden compared with fruits and vegetables and there was a study that came out. I believe it was in the last few years that they talked about the high pesticide residue fruits and vegetables versus a low pesticide residue, and they found very significant that the high pesticide resident. This is about a third of the total intake.

I had more of a J shape in terms of the all-cause premature death reduction, and my feeling instinct and have no evidence for this is that that’s because of the low dosage; it doesn’t matter, but they were then showing higher cancer rates as people had higher doses of high pesticide residue fruits and vegetables. And I think that’s one of the main reasons why, when we looked at the other pages, you talk about how five servings should be normal for fruits and vegetables. But we don’t actually see that much of a benefit because I don’t think many people are able to get organic.

It’s easy for those of us who are of the means to shop at whole paycheck whole foods every day to think. Oh well, of course, it’s all organic, but anytime you’re going out and eating at someone else’s house or a restaurant or anywhere, anywhere other than your home, where you have had the luxury, perhaps, of paying a premium for the organic food, it’s not something you can count on, which is another reason why I tend to go towards the whole grains and the beans, which just naturally don’t have as much pesticides with them.

ML: So that’s a good point you’ll have to. If you could send the pesticide and the mortality data, that would be great. So it might not be Consumer Reports. But it’s something similar to that where they did an analysis of the pesticides, so we can post that, too the, in the video description.

CL: Okay, cool, Great, so shall we jump then into supplements? Sure, okay. I mean, this is kind of a fast comment. I mean, as I scroll, I do my own scrolling through YouTube and see sort of all the health and nutrition experts. There’s always the question of what nutrients do you take? And I recently wrote a post on Brian Johnson and his blueprint and. Brian Johnson takes over 100 supplements every day, and as I look at that, my general feeling for that is I want to catch all the easy-to-achieve gains through a normal lifestyle through eating whole grains and legumes and a small handful of nuts first and because my benchmark for everything is premature, reducing premature death and reducing that risk.

For so many of these new things, I have no idea there’s no volume that we could get a study for that would tell me whether it actually reduces premature death and my confidence in saying. Okay, well, they’ve taken the study of this particular supplement or this chemical. The joke that I make on the blog is that it’s hard to tell the difference between some of these supplements in the name of Pokemon like Genistein, Taurine, and others.

And they don’t know whether that has a particular impact, whether it’s actually reducing all-cause mortality or just moving a particular biomarker, perhaps in an unhelpful way or something that doesn’t really make an impact, it’s hard for me to see. So, the only supplement that I take on a daily basis is glucosamine chondroitin, which is a knee medicine that’s been around for decades.

Still, it’s commonly prescribed, and as a result, and it’s another UK study from the biobank in the UK, they can show that it has about a 15% reduction in all-cause mortality. It seems to be clustered more around lung diseases such as COPD and pneumonia and other kinds of things, so that reduction just from taking a little completely harmless with no side effects of any kind of medicine is going to give you a better overall result in reduction premature death than maybe even getting restaurant vegetable fruits and vegetables that might have other things with them.

So for the other things like sort of the supplements of the day when you’re talking about Metformin, which is a diabetes supplement. Rapamycin, which targets emptor. These are strong medicines, but they’re strong medicines. They’re prescription only at this point.

So even if you ignore the overhead of trying to get something that requires a doctor’s prescription in the United States, at least they do have side effects with them.

The rapamycin then is going to reduce muscle building, so you need to then cycle it in other things, and I’ve seen some studies that seem to say yes. It’s very beneficial for people who have diabetes. It’s a diabetes medicine.

But if you don’t have diabetes, you’re not going to get the benefit of that, and it’s not really clear. And even if they did, they’re saying that. Maybe it’s like a 5 or 10% reduction in premature death, which I’m saying. Well, I’ve already got glucosamine, which is supple and makes a 15% reduction, so I’m going to stick with that.

But I am interested in the NMN, which is coming up as a new thing. And I know that you’ve been doing a lot of experimentation with NAD. So, with that, I want to pass it over to you and hear what your thoughts are on supplements and also your specific experiments of hacking your own NAD production.

ML: But before then, we can hopefully you can send the glucosamine data, and there may actually be some data that extends the lifespan and mice. I could be wrong about that, but we can put that in the video description, too. So, in terms of the billion supplements that Brian is taking. He unlike I hear your point about all-cause mortality data and extrapolating from the animal studies to humans. I get that. But in his defence, he’s tracking biomarkers, right? He’s doing it rigorously, and he’s doing it.

The right way to see doesn’t make a dent; does it make it not? But I don’t think he has the appropriate control, which is what does my data look like at my current. He can’t start with the pre-blueprint phase. Brian’s data of this is what all my data was, and I was. My body composition was worse, and of all of those things my diet was, his diet was worse, no supplements.

Maybe I don’t know if he’s comparing himself against that. But to take everything like you know. Metformin. I mean, he sees TRT; he’s on Metformin he’s on. I think he may be on a statin, which makes me think, “Dude, does anything in your body normally work without these things, like, you know, do you have?” You’re literally patching the dam like you have so many holes, whatever the situation may be.

So that’s one. The other side of that, though, is, like I said, he’s monitoring biomarkers now. I don’t know, though, what’s the magnitude of the effect. By taking that stuff out? I don’t know if he’s done that experiment.

Which things are actually making a dent? You know what’s the consequence of long-term usage of these things where maybe some of the damage could be irreversible? I don’t know, maybe, and again, I’m speculating there’s no one longitudinal data or even animal studies that have done this well. I don’t know animal studies, but okay, mice, and it’ll extend lifespan and sedentary mice in a cage.

Granted not to the magnitude of fasting plus circadian alignment. But you know if you take that, okay, if you take that in the short term and you get a trans improvement in biomarkers, and that’s a big. If, what’s the chronic effect of doing that for 30 years like? And if there are things in in your biomarkers that change that may be even more difficult to change. Because you’re taking something in a super physiological dose that you’ve never, you would never see this in the wild.

Are there some negative effects now? Maybe the answer is no, and I’m wrong, which is fine. I’m happy to be wrong about that, but on these things you know. I don’t want. I don’t want my existence to cease to exist because I’ve taken some exogenous agent which I would never see, and basically for a lack of a better term effed myself with some prescription prescription meds. I try to take the lowest, the lowest risk strategy and then you know, add, with the targeted supplementation on top of that. And then even then, even with the targeted supplementation which goes into the NAD NMN Nicotinic story.

Even with that, I may take those things out that may have an improvement in some areas but make other areas worse, right, with the goal of still changing it by diet. So the NAD story is that based on what youthful is in blood cell NAD levels, which the common criticism there is, you don’t know what your tissue levels are, which is a fair point.

But there are studies showing that an increase in blood NAD can link with tissue levels of NAD and we want to have it relatively high in the tissues. We don’t want to have low levels of muscle; we’ll have low levels of muscle energy, and so on. Right.

But I am doing metabolomics data, too, to try to get more insight beyond the blood versus the tissue. It’s not a full picture. We’d have to do muscle biopsies which are impracticable, so relatively low levels of 20 to 25 micromolar without supplementing anything. And this is on my mostly youthful biomarkers, driven even diet.

Exercise training, which is shown to increase NAD, is still relatively low relative to 30 -y yearar olds who have somewhere around 40 median values of 20 to 25 without doing anything. So, I found that nicotinic acid works. I started that experiment with 600 milligrams per day, but on the same day, it was done at pace. The epigenetic pace of aging was like ten standard deviations from my nine-test average without that test suggesting I drove it to outlier status. So then I shifted down 60 milligrams, ten x reduction still got an increase for NAD to the same magnitude as the 1000 milligrams of NMN, which the Internet seems to love NMN and thinking it’s the panacea of all things anti-aging 60 milligrams nicotinic acids same effect on NAD as NMN 1 thousand milligrams. So then I sent blood for any in terms of NAD, which is a low dose. So then, what about is it a high nicotinic acid of 600 milligrams per day and the corresponding high NAD, which was 67 micropolar on that day of the test with the worst need and pace? Is it high in nicotinic acid? Is it high NAD?

That’s potentially messing up with the epigenetic pace of aging. I don’t know. So to test that. I then went with two grams of NMN per day and got my NAD to 61 micromolars. So then the question is all right. If it’s a high story, the need and pace should be messed up. I don’t have that data yet. I sent it should be coming on January 10th. Th. So waiting, yes, still waiting, not much longer, but the pop, you know? The Internet seems to think that it’s going to be a high-dose nicotinic acid story because, in the past, it was around my usual 0.8. 0.78, and 0.76 somewhere in that range.

Then it’s not a high NAD story. It’s a high nicotinic acid story, but the good news is nicotinic acid and lower doses of 60 milligrams per day don’t seem to mess up my eating and pace. I think it was like zero 0.8 two on that day, which is in the ballpark of my, which still is in zero 0.6 like some of these guys like Sealand and others, which is the goal. But so to get around that, I’ve been on the trigger Medline, which I have a recent video about, which potentially could increase NAD. And that’s a dietary change. So it would get better if I could increase NAD and not mess up eating and pace by increasing trigoneline through diet. That’d be a fantastic way to get around this whole nicotinic acid messing up dun eat and paste in my case. So.

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CL: What’s your safest best bet for increasing the NMN or NAD right now with what you know?

ML: Hopefully, trigonelline

CL: Okay, yeah, what’s the dosage?

ML: It’s probably about 20 milligrams per day from the diet, whereas before, it was like zero, almost like five milligrams. And then you could say all right, that’s a 15 milligram per day. The difference is that it is going to make a dent. But remember, 60 milligrams of nicotinic acid raised my NAD by 40%. So what are the dietary sizes of trigonelling again? So you’re going to like this one. Coffee is the most abundant source by far. It’s like 2200 micrograms per gram. But I think that’s dry weight.

CL: I’ve been telling. That’s what I’ve been telling you. You should be drinking that coffee.

ML: Yeah, I’ve been considering it more. But it’s a hard sell for me because coffee blood just. It’s just rank for me. I just brush afterward, but it stays all day. You know, people, if I’m around people that have drank coffee, I’m like God, they just can’t do it. But so then.
Second on that list is chickpeas, which goes to the legume story great,

CL: There you go, ok.

ML: The story gets better there, too, because I have food-elevated IgG food sensitivities against many beans like kidney beans and navy beans. Actually, navy beans and chickpeas have higher levels, but my igG is just way off the chart there. So, I was going to put that data in a video. You know, the screenshots of the igG and the beans. But it would be a too long video. So.

Anyway. So chickpeas are 350 micrograms per gram, so I’ve actually taken them. But then I’ve got to move around calories in my diet because I’m trying to stay caloric or less. So, barley and oats have significantly less trigonelline. Barley has almost none.

CL: Grains, okay, very good.

ML: But so I’m substituting all the whole grains for chickpeas to get that. So whether that makes a dent and the people that have been, you know, saying, where are the legumes, blue zones, and all-cause mortality? Where is that in your data? Now we’re going to see, you know, so will it be enough? I don’t know. But you know, that’s the.

CL: Well, it’s inspiring seeing you kind of pushing the levers and fine-tuning it, so I just wish you could test that stuff faster.

ML: Yeah, yeah, yeah, yeah. I mean, yeah, it’d be great to have that stuff. I could just do it immediately and have the answer like within days. But one can hope right, that’s coming

CL: Right. Okay.

ML: Maybe the trigonelline doesn’t make a dent at all. And then I just have to go with, you know, a small dose of nicotinic acid. But the trick there, too, is the methyl donor thing you get just going. This goes to the idea of supplementation, too. So if for people supplementing with Nnemin, Nr, or niacin, nicotinamide, or nicotinic acid, that’s well known to deplete methyl donors, so it’s all over the internet, too. And there is published data that supports this that when supplementing with pre-our cursors, it can deplete methyl donors, leading to increases in things like homocysteine, which could potentially affect methylation age too. Because methylation age is clear, it’s a hyper or hypomethylation process.

CL: Right, so it is one of the leading indicators for overall cardiovascular. Right?

ML: Yeah, that’s right. Definitely, the RCTs don’t show any improvements, though, which is tricky because, you know, so reducing homocysteine doesn’t show from my reading of the literature, and it’s not a comprehensive review. But that’s generally the argument against Homocyinas as biomarkers. What did the RCT show? But these are generally in already sick populations who have some pre-existing condition. So maybe less, sintering, lowering in that case isn’t a big deal. But my goal is prevention and minimization of risk. So you know, can I delay any vascular-related complications from elevated homocysteine rather than I have elevated homocysteine, now I’m going to try to improve my mortality, so I’m trying to prevent it. So I think it’s a different story.

But so the TMG triethyl glycine is what people are like. Take TMG, take TMG. Well, I’ve done that experiment. It didn’t work for me. I took up to three grams per day. Homocysteine didn’t bulge. I’ve also done the serine plus B six to pull homocysteine down away toward glutathione. That didn’t work either. Six grams of serine, like 40 or 50 milligrams of which is like 13x, might be that didn’t work either on homocysteine. Methyl b-twelve does reduce my homocysteine by a bit, but it goes to this idea of, you know, what are the methyl donors that are specific that you can take if you’re trying to improve NAD or you have elevated homocysteine?

That is specific for you. Maybe it’s not TMG. Everybody thinks TMG. It may not be now along those lines. I’ve also added, which again is going to seem like a simple change or addition. But I’ve added oranges into the approach. I actually cut the strawberries down and added an equivalent amount of oranges. And I did that because oranges have proline beetle, which is at the end; you have a couple of methyl groups now. Can that act as a methyl donor? I don’t know. And that’s not.

The only amino acid that is dye or trimethylated, like trimethylglycine, has three methyl groups attached to its nitrogen. There’s tryptophan bean, which has methyl groups. So, many amino acids besides glycine are demethylated or trimethylated that can potentially act as methyl donors. Is that going to be enough from 100 grams or so of oranges per day? I don’t know, I’ll find out.

CL: What are you hoping to see in your metabolism that would change as a result of moving from the strawberries over to the oranges, like which of the hooks are going to see in the homocysteine you’re thinking, or where are you going to see that show up?

ML: So that’s an interesting question. Because I looked at correlations between diet and the blood biomarkers and in a panel of 25 biomarkers, strawberries have a net positive correlative score with 11 of those in terms of how they change during aging and all-cause mortality risk. Now, that’s an unadjusted correlation; I haven’t adjusted for body weight. Body weight may drive some of that as strawberry intake has increased as I’ve cut body weight down, and body weight seems to be a big driver of improving biomarkers in my data. So the risk, though, is if strawberries are driving some of those correlations, I’ve reduced their intake and now increased it with oranges. So, I may get some reduction of positive effects by reducing strawberries with a small isolated effect, if any, for oranges.

But home assisting is the primary driver just through the proline betaine to increase proline betaine, which my diet had basically none of beforehand. And if you look, if you look at my horvat, that genetic age and my homocysteine data without any B-12 or additional folate, it does suggest I have some methyl donor inadequacy or deficiency, so I’ve got to try to, and then it gets to this idea of diet specificity.

CL: In a vegetarian diet, the deficit of B-12 is one of the first things that you’re warned about with a vegetarian diet or a vegan diet. You might not be getting enough vitamin B-12, so that’s completely understandable. Yep,

ML: But in my case, I’ve got fish every day. In terms of B-12 intake compared to the RDA. I meant like 5x the RDA without supplements. So it’s not a vegan diet and actually a little bit more right, yeah, but it goes to the idea of it, and it may not be a B-12 issue at all. It may just be methyl B-twelve has some methyl donors. I need to have a boost in methyl donors for whatever reason, and I’m not really fixing the problem. I’m open to even taking out the methyl B-12 at some point and just trying to. They’ll tweak the diet and get more methyl donors.

CL: Okay, great. So let’s continue on and talk about some of the other things that we have beyond the food and beyond the exercise. So. I’ll start off on this to sort of give an example because it’s something I’ve been thinking about: what are the things that we can talk about as habits that are healthy but are beyond going to the gym and the kitchen? So.

One of the things, for example, that has become popular lately is the sauna as a term for all causes of mortality reduction. The studies of this, and we’ll link them below, are mostly from Finland because they have a strong sonic culture there, but the data is quite compelling. They have RCTs that show things like improved lactate threshold and VO2 max, which is a really good measure of cardiovascular overall health, and they say they have studies there that show that going to the sunna about four to seven times a week and they have the baseline is quite funny because there aren’t any people they could find like in a city of 4 thousand people. They could only find two people who didn’t go to the sauna at least once a week. So, the baseline they’re comparing to is people who go once a week. But even so, the people who went four to seven times had a 40% reduction in premature death. So, one of the things that I’ve added to my overall schedule is that I go to the sauna regularly here where I live down the street. There’s a local bath I’m in Japan, so there’s a local bath that actually has a sauna in it. But the thing.

Interestingly, I found some other studies that show similar effects for other ways of heating the body, so it seems like the sauna is actually a way for your body to fool your body. Hack it, if you will, in the thinking that you’re still doing exercise. So the study and the study refers to wearing a sauna suit, which is basically wearing a trash bag so that you continue to sweat even after you exercise. And it compares going to the sauna wearing a sauna suit and also just taking a hot bath. So, sitting in a hot bath of that nice toasty bath for a long time, and in the last actually couple of years, they’ve had a study that’s been released in Japan that showed similar cardiovascular benefits not as strong as the sauna but similar where they’re showing increased benefit as far as reduced.

Strokes and heart attacks and other things from just people who are getting lots of baths every night in the evening as traditional here. So that’s one of the things that I do. That’s further than that. The other things are would be the dental care is another thing where they have strong reductions of premature death. And I especially like this one because it’s different from the other studies. Oftentimes, people think, well, yes, of course, if someone takes good care of teeth, they’re taking care of their body as a whole. They’re seeing the doctor all the time and all these things. But actually, the specificity about it is that brushing your teeth is helpful for longevity when done in the evening.

And only in the evening, like if you brush your teeth in the morning, that’s great. It helps for fresh breath. Maybe gets rid of the coffee smell in your breath, but it does nothing for your longevity. It’s only.

When you brush it in the evening before you go to bed, and there are other things as well; flossing your teeth once a day, at least, is healthy and prevents premature death, and then there are other ones that are sort of not what you’d expect for instance, mouthwash, and you recommend Bristle on Youtube channel quite often for measuring the oral microbiome and I’ve talked with the scientists there and they echo this that actually a mouthwash doesn’t show any benefit in terms of improving the oral biome in general and the all premature death studies find that as well, is that yes, it’s great to brush your teeth that will extend your lifespan. But doing a mouthwash doesn’t seem to have any effect at all. So those are two habits that I find to be quite helpful in terms of all cause mortality that have the numbers to back them up, that I make sure to incorporate into my daily routine.

ML: So, wait, starting with the sauna, I was just taking notes because I didn’t want to interrupt. But I haven’t focused on the sauna in terms of videos or information because it’s already so saturated, like, you know, Rhonda’s hours of content on the sauna. The initial flags that pop up in my mind are: what’s the BMI of that study? What’s the BMI? Because I think the data is probably an overweight, overweight people who maybe have hypertension or pre-hypertension, and I can see a road where that may be.

The sauna would have benefits for that specific group of people, especially those who are overweight or obese. Just, you know, be a might greater than 25, probably not fit or active. So in that case, it’s like when you exercise, you’re going to get the increase in body temperature and then the increase in body temperature may be part of a vasodilation program where you’re you should be able to reduce blood pressure over time, whether that’s because of the heat or other health-promoting effects of exercise.

Just and then this is again speculation, but I haven’t read those studies. I haven’t paid attention to it, but I hear the sauna story everywhere right. But from my experience, at least here in the States, the people who are most likely to use the sauna are these overweight, don’t exercise out of shape, and again, maybe have some. So I can see a road where that’s beneficial. But then it gets the idea that if you take someone who’s not hypertensive, not overweight, already lean and fit, if you have that group and now they’re in the sauna four to seven times per week and maybe even like a randomized crossover trial where know you have them sauna, then you have them go out of the sauna for a few weeks. So you know you’re seeing if there’s an effect of improvement, and then if it does, come back to baseline. I don’t know do those studies exist?

CL: I mean, they have the studies. There are the interventional ones where they’re doing an RCT, and these are standard RCT. So these are being done probably on honestly college students. I haven’t actually reviewed. That doesn’t mean they’re not 25 over 25 BMI, but of course they’re all controlled for BMI. That’s standard right.

So it’s an interesting thing. But for instance, the studies that are talking about bathing in Japan, which is one of the thinnest countries in the world, are not going to be subject to that. That’s probably going to be fairly clean as far as most of the people are low-weight. So I think there’s something in it beyond just sort of dealing with a higher BMI, and it does seem to be beneficial to do it after aerobic exercise, in particular the sweatsuit and hot bath and sauna. A study that I saw was talking about specifically about doing 15 minutes after going for like a 30-minute run or so, but It’s something worth looking at.

ML: And then the other question is which biomarkers besides blood pressure and I guess maybe you could look at. I mean, the ideal if it’s a cardiovascular disease risk kind of thing where it’s reducing that risk. You would look at soft plaques or even calcification like I just don’t know if. There are studies showing some effects on those cardiovascular-related outcomes besides blood pressure.

I just don’t know what biome, how would you know so subjectively? It feels good when you heat the body up like that. And even after a song like. But for someone to say. Oh, it works because it makes me feel good. Okay, that’s a different story than what the objective data actually shows in terms of well there.

CL: I mean, I’ve actually doubled down and have increased my sauna at times as I’m getting ready for this marathon because of the benefits on the V̇O2 max, which is your cardiovascular respiratory health, which is a key driver of marathon performance, so I’ve been doing that and also it raises the lactate threshold which is sort of the point at which you start to get your muscles get sore from overexertion.

The other endpoint that they’ve been looking at aside from premature death is also in the sauna studies they’ve been looking at specifically cardiovascular death, so death from cardiovascular disease, heart attacks, and other things, and in the Japanese bath study, they were then looking at just stroke or cardiovascular events not going so far as death and I think that’s probably because they don’t have is quite as strong. I think probably the sauna is more effective, but just a hot bath is a good measure and much more convenient for the great majority of people than firing their way to the sauna after doing exercise.

ML: Yeah, so that ties into probably blood pressure and some slowing atherosclerosis if it does, but what if your blood pressure is already normal? I get the argument for the V̇O2 max potential benefits there. I mean, probably pro athletes should be doing this stuff, you know, pushing your view two max. Even a few units higher will benefit in that case, right? But if my V̇O2 max is 50 versus 52, is that going to really make a difference on longevity versus the time commitment? You know, and not just that? What’s crazy is I see some people; I’m not anti-sauna, and I’m just being skeptical, right, you know, what’s that? That guy’s, you know? Robert Schirmer. I think his name is the skeptic anyway, that guy is just always a skeptic about everything. I’m not trying to be that guy, but so. I just had something in terms of sauna. Anyway just playing the Skeptic. So oral care. Yeah, so. In terms of so, yeah. I get you on the brushing and the flossing regular cleaning, too. How often, whether it’s every six months or every year, can contribute to the plaque buildup? You want to get rid of that, keep that at a minimum. But yeah, taking that a step further, it’s, you know, in my case, trying to, well, in the first case, get rid of this bacterium.

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That’s consistently 95% of my oral microbiome, which I think to me is a potential time bomb ticking time bomb, where maybe my mouth and system won’t be able to keep it limited. You know it can cause sepsis some; anyway trying to eliminate this thing, and then people like want you to take antibiotics all right, so maybe I kill it off. First of all, it’s oral; it’s not a topically applied antibiotic, I would eat it; it goes to my gut. I will obliterate my gut microbiome, which is a problem allowing potential.

CL: You’ve built that up over the years.

ML: Right, I built that garden. Over the years, I don’t want to just get rid of it, but then, you know, some of it will indeed impact my oral microbiome, potentially eliminating that bacteria. But the other side is antibiotic resistance Serratia, which is an even bigger nightmare. And I say that as someone who studies the microbiome and, you know, getting rid of antibiotic-resistant bacteria on its own is a problem that’s like a particularly nasty bacterium once it’s antibiotic resistance, so the race is on to get rid of it. But then, assuming I didn’t have that in my oral microbiome, there are certain bacteria that have been linked with it.

Alzheimer’s disease cardiovascular disease. You know whether they’re found in the brains of Alzheimer’s disease patients or found in the plaques in cardiovascular disease or can specifically cause it in mice like p. gingivalis.

Yeah, I am making sure that I get rid of the Serratia, and then once I’m back to a normal microbiome, keep these bacteria linked with poor systemic health atop the list. To me, that’s the cutting edge it goes beyond. You know, brushing and flossing, which you know. But the idea of mouthwashing the store is too. Mouthwashs contain things like alcohol, which many do, which you know. There are published studies showing that that can affect blood pressure, so basically, you’re killing off oral bacteria, and those oral bacteria have some positive role in regulating blood pressure systemically. So yeah, alcohol bases mouthwash is; I’d stay away from those, right?

CL: I stay away from the mouthwashes in general because some of the other ones that aren’t alcohol-based are still kind of based off kind of strip and basically kill the entire microbiome, which is where, as we’ve talked about, you want to cultivate the positive bacteria as opposed to just nuking everything and then hoping the good ones grow back right.

ML: But that kind of gets into the idea that, okay, alcohol and mouthwash are bad. But then you know toothpaste is loaded with sudsing agents, sodium doecco, sulfate, and other stuff like that. So I haven’t done a deep dive there, and I’m sure there’ll be people in the comments saying. Just take some coconut butter or coconut oil mix it with sodium bicarbonate and brush your teeth.

I don’t know that that’s the best either. There are no RCTs on that right, but there are things in toothpaste know that whether it’s additives or preservatives like, for example, the whole preservatives impacting gut bacteria, and that could be true too in terms of the oral microbiome because it’s so understudied, they’re just you who knows what’s good or what’s wrong in terms of what a toothpaste should even look like right. So yeah, figuring that out is on the to-do list.

CL: Okay, Right, so what else should we cover today? What do we get? I want the list. Alcohol is all right. Let’s see, you’ve got a share screen as long as we’re talking about something more serious than just the alcohol in your mouthwash.

ML: Yeah, first in one of the life expectancy studies, that’s this one. Let’s start off there.

This is the study where was and again it’ll be linked in the comments. Five factors increase life expectancy for men and women. So here, gained or lost life expectancy compared to moderate alcohol consumption. So that was the reference, right? No alcohol, and then you’ve got the highest intake, so light blue and red. So, for women.

What was it here? You can see that there’s a loss of life expectancy for the highest alcohol intake, 30 grams per day. So what is that? A glass of wine is about 12 grams per 100 mill. So you know, it’s like three drinks per day. Reduced life expectancy similarly for men. But in men, you can see well actually for women, too light blue, no alcohol almost just as bad for life expectancy as two and a half or so drinks per day. But even there, even in this study, you know there’s no gain in life expectancy with alcohol intake. It’s just minimizing a small loss, if any, two years or so for the abstainers, which is a very mild effect. But okay, this is just one study. And then I’ve got another here that was recently published. Right association.

There we go right now: we’re in business. Meta-analysis published in March 2023. And this is the largest meta-analysis that I’ve come across. 100 and seven studies on alcohol all-cause mortality in 4.8 million people. So.

In contrast with the earlier meta-analyses, low-volume alcohol drinking is not associated with protection from death from all causes. So scrolling, I know I got the perma scroll here, but let’s see.

So they separated it all right. I don’t know if you can see this now. So I don’t know why this data is slightly different from what their main results are in the paper. I mean, they i’d have to go through the tables. I know in one of the tables. They defined the groups differently. So you’ve got non-drinker occasional, which is like one drink per week, less than 1.3 grams per day. So you can see that compared to a non-drinker, very occasionally not associated with a reduced all-cause mortality risk.

But you can see the, and that’s the. You want to see the fully adjusted right, so this is a solid line that would be here, and then the confidence interval, you can see it just barely crosses one, so not significant, so that’s one, maybe one drink per week. Then you can see the low volume group for the fully adjusted model up to two drinks per day, which is a significant reduction in all mortality risk. So, but then above that 25 to 44 grams per day, we’ve got increased risk, so you can see that’s above the hazard ratio of one of the confidence intervals. And then you’ve got significant increases for greater than 45 grams of alcohol per day, which is like four drinks per day. So, but.

In the study in the main study here, I don’t know why I can’t open this as a PDF, but the way they define the groups, you know whether they define. If they define the reference as the occasional drinker, then the low dose for.

Up to 25 grams per day wasn’t significant, and the reason they used the occasional drinker is because I guess there is some selection bias in abstainers where they used to drink. Maybe they stop because they’re sick and there’s some reverse causation in that, whereas if you go with the occasional drinker. I guess that’s minimized. So, when the reference group is the occasional drinker, the low-volume group wasn’t significantly associated with reduced risk. But I think, like the plot showed, there is a trend towards having a lower risk. With the low volume alcohol intake, you can see it’s just outside the confidence interval being less than one, which again goes to the idea of what the other variables are where a low, very low intake of alcohol? What are the other variables that help you actually reduce that risk by 7%? In this case. I don’t know what that i don’t know what that would be know so.

CL: Yeah, it’s been this. It is often referred to as a study. I’m pretty familiar with myself. The interesting thing about this is that when they originally started the study, they were trying to say that if you look at someone who has a quitter, sick-quitter is the term they use. They say that alcohol looks like it’s healthy only because it’s compared to people who were drinkers but quit because they were unhealthy. And therefore, they’re saying that that is the comparison. It’s people who are already sick.

But this study is very clean in that it took people who are abstainers, and then you also have lifetime non-rankers who know that they’ve never drunk a drop, so it’s not possible they’ve just quit because of some other thing. And they found in this case as well that basically, the people who are infrequent drink occasionally, but maybe once a month or so versus the low volume have a benefit, especially against the people who have never drunk lifetime abstainers. The people who used to drink but quit are the worst, usually because of the reasons that they talk about where they were unhealthy before. The former drinkers versus abstainers is what we see here, right?

But then they shifted again to say. Okay, well, let’s see how about people who drink a moderate amount. How do they compare to people who drink just occasionally? And you’re right? They don’t find that there’s a significant difference, but I would say that basically, you’ve already proved the point that low amounts of alcohol are fine, whether it’s occasionally less than one drink a day or whether it’s one to two drinks a day or less.

Basically, it’s shown that it is beneficial, and they see it in some of the cardiovascular studies and some of the other things. And everyone agrees that once you get over that, and I do that on a semi-regular basis with my friends as well. So, not everything is strawberries all day long.

But it’s part of the normal thing, but it’s something to be aware of because it does seem to have some benefits in that low range, and if it’s something that you enjoy, you should go for it. Harvard has a very good write-up on this that we should link in the post as well. That talks about there are some benefits at a low basis, but clearly not if you’re at any way at risk of going into the higher numbers where all that benefit would be lost, and the damage to the family in your livelihood could be severe.
So, I like this study quite a bit because I think it brings up that clear point in the later studies. Then they do what I call P-washing, where even beyond this, they’ve taken out the lifetime AB lifetime abstainers and shown that there’s a benefit. Then they add in like another six or 13 different categories, and they do something that I call P-washing, which is where you basically reduce your group down so much that the significance is lost. You’re reducing the power of your study, and so at that point, then, you say, Well, there’s no significance, so there’s no benefit. Well, okay. I mean, in some ways.

I say that in the worst case, you could say that moderate drinking is that it’s no better, and so if you really enjoy it then you shouldn’t stop it because you think there’s harm to it at best; this would only be able to show that there’s not direct harm for it as opposed to the poisonous at any dosage kind of things which I think is clearly not the case, and we should save our efforts for places where it’s really going to make a difference in premature death as opposed to something that if you enjoy it and are able to do it within a controlled fashion, is something that you could enjoy as part of your life.

ML: Yeah, no. So that’s a good point that you made that it’s not.
So, at worst, the low volume group is 1.3 to less than 25 grams per day. There’s that it’s not significant, but there is that it’s not significant. It does suggest that it’s clearly not harmful. You don’t have an increased risk, but there is that trend towards a decreased risk. But as you said, if you’ve got you alcoholism or whatever in the family and staying away from the higher intakes because that’s associated with increased all-cause mortality risk, let alone the damage to family, you know. So, actually, alcohol is a potential option on my to-do list, too.

CL: Oka, gonna get you drinking coffee, we’re going to get you have had of beer leave

ML: So DHEA sulfate. So, it declines during aging. And there is some evidence linking alcohol intake to relatively higher levels. Now I don’t know if that’s a good thing or a bad thing because.

But the idea is that it could potentially move the needle towards improving it a little bit. And the reason I raised that is because testosterone is derived from DHEA, which is derived from cholesterol. So my testosterone levels are youthful, total testosterone youthful, so I don’t have. I clearly don’t have a problem in going from cholesterol to DHEA to testosterone. So.
Because to get testosterone, you have to go through DHEA. But my DHEA sulfate is more than half of what it was in my 20’s early 30’s. When I have data, just two data points, but I don’t know if that was with DHEA supplementation or not, but it’s clearly lower. It’s, and it’s 50% lower. Now granted, I’ve maintained it over the past year or so, but knowing that it declines during aging, there is. I do have a window for adding a very small amount. I’m not talking 25 grams per day.

You know, what’s the minimum amount of alcohol that would move the needle in my case where I don’t mess up? Heart rate variability, resting heart rate because, you know, I’m sure, you know, there’s well an abundance of anecdotal data. People are saying. Look at my data, just one drink data, you know. So I don’t want to mess that stuff up, but there may be a small dose, like, you know, less than 100 milliliters per day, far less. I mean, maybe half that, or I’m open to including it to try the experiment.

CL: So, I do follow the moderate on the days when I’m moderate. I just have literally a beer, and I don’t see any impact of it. It’s eyeball, to be clear, but I’ll have full recovery days, according to my whoop, after that. I can’t tell the difference between the days when I have a beer and the days when I don’t.

ML: Is that beer earlier in the day, or is it later in the day? Or does it matter to you?

CL: That’s just dinner, so it’s about seven o’clock or so in the evening, and go to bed at around 10 or 11.

ML: Wow. I mean, any fluid intake at seven o’clock for me is like there’s just a half. There’s no way it’s crazy that you can have any fluid intake and not mess with sleep.

CL: So okay, Yeah, different things. I don’t know that, but I find that that helps me. Actually, if I have the beer, then I tend not to drink a little bit more and then go to bed earlier. So maybe that’s why I’m not seeing the impact- I’m getting a slightly bruised leap from it.

ML: Interesting, interesting, all right.

CL: I’m just going to say, of course, if you once you get to the heavier consumption of alcohol, it’s well known that that will then impair sleep.

ML: Yeah, ye do, so you’ve got the right dose, you know. So that’s the key to finding the dose right.

CL: Yep!

ML: So we covered it all. We covered it today.

CL: I think that’s enough for today. Yep,

ML: Cool, all right, until next time. Criss!

CL: Okay, great to talk to you. Michael.

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