There is this preprint on epigenetic age acceleration and cholesterol: Epigenetic age acceleration is associated with blood lipid levels in a multi-ancestry sample of older U.S. adult, Feb 2024, Lin et al.
This is fantastic data James! "We found that higher epigenetic age acceleration was associated with lower levels of TC, HDL-C, and LDL-C, as well as higher levels of TG"
My guess is that, in the study, low LDL (and TC, HDL) is associated with higher epigenetic age not because of LDL itself but because low LDL could be a marker of malnutrition or nutrient deficiency. For example, to have very low LDL without drugs usually means someone is vegan. And vegans can be at a higher risk of nutrient deficiency. In the study, they also saw stronger associations with females, who are more prone to not eating enough nutrients, such as protein. In the case of Mike, adding eggs may increase LDL (and TC, HDL), but eggs are also super nutrient dense and add a whole lot of other nutrients besides cholesterol. And those other nutrients could benefit the body including DunedinPace. So if LDL is a marker of nutrition status, then how you raise it will affect the DunedinPace outcome. For example, raising LDL by increasing pure saturated fat may not improve DunedinPace because increasing SF doesn’t really improve nutrition. Whereas raising LDL by eating eggs may improve DunedinPace by improving nutrient (macro and micro) intake.
The only evidence based longevity dieter i know who is eating more cholesterol to raise his LDL lmao. this video actually edged me more towards disregarding DunedinPace more than anything else. I was already skeptical about the true effect on longevity of caloric restriction for a healthy whole foods plant based dieter, but seeing that most pace of aging clocks dont correlate with CR, well then, i'll keep on eating my maintenance calories
I'd turn this into a data mining exercise to generate hypotheses myself. I'd suggest three things: 1) run linear models with two dietary variables and rank by p-values, AIC or summed residuals. 2) Assume the LDL correlation holds and run linear models with LDL and one biomarker, ranking by the p value or AIC on the other biomarker. 3) Repeat 2) but use LDL and the dietary variables instead. There would be a large number of models for excel but other programs could handle it easily. We don't care about p
Thanks James, this is great. I think you multivariate linear models? I've used that in the past, but find more value in trying to follow every significant univariate (or sometimes adjusted for BW, calories, or the daily HR) correlation. It's hard to know which way will get closer to the truth, i.e. following all the univariate correlations vs adjusting models for many potential variables, which could exclude potentially important correlations. In terms of AIC or summed residuals, that's beyond my current stats experience...If anyone wants to help crunch those #s, it would be much appreciated!
@@quantifiedmax By most likely I am referring to the selected exploratory modelling approaches, not the outcomes. We could go after more exotic relationships but these would be penalised one way or another. Mike's approach is Bayesian because we aren't sitting in a knowledge vacuum here, we know there are various pathways and epi associations etc and would use those to reason which outcomes/hypothesis are worth pursuing. That's the problem with frequentist approaches to biohacking, here we have more information and we are going to use it after each measurement, which in itself invalidates frequentist assumptions.
@@quantifiedmax I think your omitting the overall approach is to optimise these biomakrers rather than make claims about certain things, such as if they are causative. The optimisation step doesn't operate in traditional statistical approaches in biostatistics (where you are trying to make claims) and its an important consideration here. In the context of traditional biostatistics I agree with most of what you said. If we apply a FDR to the ldl relationship p>0.05 easily so there is nothing to go on. So we are already in an explortory analysis here. Given whatever strength of evidence is derived what happens next? Calorie constraints and knowledge of the literature to choose certain changes are woven in and become priors for the next step (admittedly yes in a non tradtional way). I've said before that presenting CIs would be better but probably less understandable to the audience. I'd be happy to chat some more offline, just send me a message.
What kind of eggs and how prepared? For example, I alternate mine between higher omega 3 content and free range and only eat over easy (as liquid yolk as possible).
Michael, how does the blood based Phenoage (bbPA) compare to these epi clocks in terms of reliability and value? Would be interesting to see how the people who do DunedinPace compare to their bbPA, and the details of what they do (diet etc) and their ages. As an aside, I think optimizing blood parameters organ markers and physical fitness is an excellent strategy independent of all these clocks, even if the optimum values haven't been nailed down in all cases. Thanks!
Hi Peter, I'm not sure-they're likely capturing different aspects of aging, i.e. the molecular (epigenetics) vs proteins (albumin, ALP, AST) and metabolites (creatinine, BUN) as examples. I may cover the full approach in a future video, from the molecular to the whole organism. Definitely agree on BP and function...
Hey @NmlssNmlss, the goal is to identify the food pattern within my own diet that pushes DunedinPACE towards it's lowest value as a primary strategy, If that faills (after many attempts), then trying something else. For your list, I already average ~245g of mushrooms/d, 60g of fresh parsley/d, To include any others, I'd have to take stuff out, and the goal is to not blow up the system (see Quantifying Biological Age, Test #2 in 2024), but to make minor changes.
@@conqueragingordietrying123 Thanks for responding! Of course, I totally understand. I only shared because I thought you might be interested in experimenting with some of these.
@@conqueragingordietrying123 Oh, I forgot an even more interesting one (which may or may not be on your radar already): wakame , a type of brown seaweed (e.g., Wel Pac wakame is available on Amazon and takes a few minutes to make). It's a source of fucoidains (the best activator of SIRT6), fucoxanthin, and has a number of other interesting properties.
You are not the only one. Siim Land should be #1 and they are also blocking him from the leaderboard. Shame on the project and their head: Brian Johnson!
@@conqueragingordietrying123 I think that there are so many slow aging people already tested that, if they updated, Brian Johnson may be out of the leaderboard and they don't want that. So they are waiting for Brian to gain their desired position before updating.
@@espinosalexis That's possible I suppose. From what I can tell from Bryan's protocol, it seems he has a problem with glucose spiking, with his cgm numbers not being particularly amazing, even though he was on CR, eating mostly vegetables and taking metformin and acarbose. And I wouldn't be surprised if he had hard to move epigenetic phenotype, perhaps his LDL is too low? However credit to him for the work done so far and for publishing data and his protocol.
Mike, great video as always 👍💪😎 They tell us that saturated fat is inflammatory. Let us know if you see an increase in inflammation markers with your increase in saturated fat.
Byran Johnson, just announced 0.64, let's see if the Olympics are updated and if he publishes the likely reasons. Did you have any further leads on lowering DunedinPACE Mike?
Hey James, that's great news for Bryan-did he document how? Outside of the LDL-DP correlation, nothing is significant diet-wise. I'm waiting on results form the 4/29 test, new correlations (and hopefully leads) after that...
@@conqueragingordietrying123 No specific documentation yet. But I noticed he reduced protein intake, reduced iron intake and removed chlorella. But there are other interventions, with the follistatin gene therapy and potentially increased muscle mass being a possibility. Hopefully he'll publish the candidates.
Mike, morning. Thank you for the video as always. Do you know which of these tests are commercially available, and how would you recommend in terms of the top 2-3 priorities for getting tested with these methods?
Hi David, DunedinPACE is commercially available... In terms of priorities, I may specifically focus on it in a video, but the goal (at least mine) is to optimize biomarkers from the small scale (molecular, metabolites, proteins, cells), to the large (physical function and body composition) In terms of getting tested, epigenetics (Horvath, DunedinPACE), metabolomics, and standard chemistry panel +CBC and hsCRP cover a lot of these bases...
Hey Tony, I have 3 testosterone tests from October 2023 to Jan 2024-LDL wasn't on the low side of my range for any of the 3 tests (78, 83, 80), whereas total T was 746, 895, 971.
Hi @diamond_s, which supplements? Afaik, only the TRIM trial saw a reduction for epigenetic age, and if I remember correctly, Bryan Johnson (anecdotally) used GH and it wasn't good for his DunedinPACE
CA-AKG was claimed to reduce epigenetic age by several years in some types of tests. Another study using resveratrol enriched wine also claimed epigenetic rejuvenation by several years
Why didn't you return the coconut oil back to what it was previously when you added the eggs, as the coconut oil did not do anything and it is extra calories that will subtract from other foods? Also, do you get any C15 (pentadecanoic acid) in your diet? It is supposed to work wonders. Somehow I doubt that, but it would be nice if we could see what an increase in that would do in someone so well tracked and so close to optimum health.
Hey @ChessMasterNate, not coconut oil, but coconut butter-they're different products... The goal is to increase LDL, and for a couple of recent tests, SFA were relatively low, but I added eggs (4d/week), which didn't increase LDL above my range (62-83). Similarly, higher SFA alone (without eggs) didn't raise LDL, although it was at the high end of my range, too. Both are significantly correlated with LDL in my data, so I'm doing the experiment to see if their combination will push LDL a bit higher relative to either alone. C15 can be produced by the gut microbiome, but outside of that, I'm not sure, as iollo's kit doesn't currently measure it in blood.
I suppose I could site studies all day long at a population-based, which show at higher LDL is strongly correlated with heart disease. Of course there are a few diseases such as cancer that result in lower LDL but if an Individual is healthy with higher LDL, he may simply be an outlier. I think deliberately increasing LDL it’s a dangerous game because you don’t know whether you are that outlier or not.
Hi @paulcohen6727, I'm not proposing a crazy high LDL increase, just pushing the high end of my recent range from < 85 to < 95, to test the DunedinPACE hypothesis.
Are you keeping the higher saturated fat for the next test as well? Are you adding eggs in addition to your diet for the last test or are you reducing calories somewhere else to offset the eggs so that total calories/macros stay the same?
Hey @justsaying7065, yep, average total fat intake is 90g/d, up from 81g/d two tests ago (1/15), and 84g/d for the last test (3/4), with the increase exclusively from coconut butter. 5 eggs/week, with the removal of dates on those days to stay close to eucaloric (or less).
I would be very interested in your average daily Total Calories vs burned Calories. What's your average exercise like? You inspired me to start eating set meals, for the first time. It makes counting calories so much easier. Now i'm trying to tweak that against my average exercise expenditure. That's tough to work out. How do you do it?
I'm not sure about avg vs burned, but I track BW and intake daily, so I know what my BW maintenance calories are, which is ~2100. Two 90-minute, full body workouts/week with light cardio (walking) on the other days.
@@conqueragingordietrying123 thanks. I'm trying to be on a small deficit and your numbers are close to mine. I think avg 2000 or less and workout about 7 hours a week.
Please excuse my ignorance, but can’t you find what the blood levels would need to be to get a 0.6 Dunedinpace from them? Isn’t it just a calculation based on your age and your blood markers measured at that time?
@@conqueragingordietrying123 I’ll need to look into this more. I just assumed it was a bunch of blood bio-markers. My bad. I’ll be going down a hole of DunedinPace now.
Hyperbaric is on the list, but I'd need to do it often to see an effect, which isn't practical atm I've experimented with melatonin in the past, haven't taken it in a long time.
Coconut is also a fat known to improve nutrient absorption, I wonder if the relationship is indirect; higher SFA -> better nutrient absorption -> lower DunedinPACE, with LDL increase being coincidental.
You need to make a tutorial on how to have basic tracking on health data variables, calculating correlations with excel, standardizing blood tests every time etc.. it would be really good for humanity... at least for those who care ;)
Dave Pascoe has a very low DunedinPACE, but I wonder how much of that is genetics given his long lived family. But I noted he was taking SAMe. So I wonder if there was some magic supplement in that supplement stack.
@@conqueragingordietrying123 If you do Mike, maybe you could ask him what changed to reduce his DunedinPACE to those low levels, as I couldn't quite pinpoint what the timeline/changes were from his website.
@@conqueragingordietrying123 No one has the slowest epigenetic Pace Of aging. You are misleading everyone that is gullible and naive, of course. These tests do not measure every aspect of epigenetic age - that is, every CpG site. You may have what the test particularly measures as younger, but for you or anyone else to make a bold claim that they have the full spectrum of biological or epigenetic markers as being younger is pure hubris. Biological age tests, especially those based on epigenetics, attempt to measure a wide spectrum of biological age by assessing DNA methylation patterns, which are influenced by an individual's lifestyle, environment, and genetics. These tests provide a snapshot of how well or poorly your body is aging compared to your chronological age. However, while epigenetic tests are a powerful tool for gauging biological age, they don't capture every aspect of it. Biological age can be influenced by various factors including: Body composition (e.g., muscle mass, fat distribution) Cardiovascular health Metabolic function Neurological health Immune system function Each of these factors could be aging at a different rate within the same individual. Therefore, although epigenetic tests offer valuable insights, they are part of a broader assessment that might also need to include clinical evaluations, lifestyle assessments, and other biomarkers to fully capture the "full spectrum" of biological aging. With all due respect, if your goal is to live to 150 and beyond, how will any of this help you break the maximal lifespan ceiling? Very misleading, what you say
Apart from maintaining CRP, fasting Insulin and apoB as low as possible I've been fascinated with homocysteine recently. I try to look for biomarkers that have a strong and linear relationship with all cause mortality. It seems that the methylation cycle is critical piece of the puzzle for lifespan. Mutants with upregulated transsulfuration have increased lifespan. Increasing the products of transsulfuration (glutathione, hydrogen sulfide, taurine) all increase lifespan. Decreasing the reactants (protein, methionine) increases lifespan. And in humans homocysteine is right in the middle of this. Unfortunately it seems that how to achieve this metabolic profile seems species specific, in some cases SAM increases lifespan and in others decreases. I stick to trying to minimise homocysteine which has robust positive relationship with mortality starting at 0
I'm glad you are committed to following the path of experimentation where it takes you. But I've just got to say, intentionally attempting to raise LDL cholesterol, in the face of numerous gold-standard studies showing that higher ldl-c indicates higher APO(b), is a bridge too far for me. Put plainly: What if you 'win' your little longevity Olympics there, but end up clogging your blood vessels with extra plaque in the process? Pyrrhic victory, if you asked me.
Hi @mkvalor, as mentioned in the video, moving up the RO leaderboard is important, but more important is slowing the epigenitic pace of aging to its lowest value, and keeping it there,. There's published data in large studies showing that an LDL of 65-120 is associated with lowest CHD mortality risk-I'm not talking about anything crazy, but instead moving it from my ~80 mg/dL average to 95, to see if the correlation is real.
Hello @Sam-gs7yb, I'm all about biomarkers. If more improve than not on FMD, then go for it. Long-term fasting beyond 16-18h/d (which is already part of the approach) isn't something I'm interested in...
Have you done any extended fasts (3+ day water fast) to turn on autophagy? I’ve seen videos of Dr. Ron Rosedale stating that during autophagy the body goes into a state of recycling and repair. Maybe you are still consuming too many calories. Didn’t those Blue Zone folks on Okinawa survive on just sweet potatoes and seaweed. Not saying anyone should try and reproduce a harsh dietary scenario like that. But, it seems like the body rewards it’s owner for eating much less than the average person usually does. I’m the same height as you but I weight 160 lbs. How many grams of protein do you consume each day? And in how many feedings? I’m doing about 45 grams twice a day and within a keto diet of less than 50 grams of carbs a day.
@@conqueragingordietrying123 Gotcha. I can only do extended fasting when I’m on a vacation from work. If you’ve done 3+ day fasts you know the mood swings and variable energy levels are best experienced in a low stress environment. But, I would have to say I have an incredibly other level healthy energy after a three day water fast.
Thanks. Not saying much but, I eat 1 or 2 eggs every morning and my LDL is just shy of 84 mg /dL (2.17 mmol/L) so it may take at least an egg a day for a signif change depending on how your body manages LDL.
Eggs are great, providing so many nutrients. The only issue is that they don’t just provide cholesterol, they also provide protein, fat, vitamins and minerals. With so many variables, if your DunedinPace changes with eggs, how do you know which nutrients are actually making the difference?
I don't-I'm more interested in the end result-if DunedinPACE improves (and the net effect is not negative on all the other biomarkers), then that's good enough (for me). I could spend a year or two trying to prove causation, that's not the primary focus.
![DDG & G Herbo - Nosey [Official Video]](http://i.ytimg.com/vi/I9Ra0Zc2NlQ/mqdefault.jpg)
It’s a shame they haven’t updated the Rejuvenation Leaderboard in over a year. Would be nice to know the latest info.
There is this preprint on epigenetic age acceleration and cholesterol: Epigenetic age acceleration is associated with blood lipid levels in a multi-ancestry sample of older U.S. adult, Feb 2024, Lin et al.
This is fantastic data James!
"We found that higher epigenetic age acceleration was associated with lower levels of TC, HDL-C, and LDL-C, as well as higher levels of TG"
@@conqueragingordietrying123 Yes there was a negative sign on the association, indicating epidemiological evidence for what your finding here.
My guess is that, in the study, low LDL (and TC, HDL) is associated with higher epigenetic age not because of LDL itself but because low LDL could be a marker of malnutrition or nutrient deficiency.
For example, to have very low LDL without drugs usually means someone is vegan. And vegans can be at a higher risk of nutrient deficiency.
In the study, they also saw stronger associations with females, who are more prone to not eating enough nutrients, such as protein.
In the case of Mike, adding eggs may increase LDL (and TC, HDL), but eggs are also super nutrient dense and add a whole lot of other nutrients besides cholesterol. And those other nutrients could benefit the body including DunedinPace.
So if LDL is a marker of nutrition status, then how you raise it will affect the DunedinPace outcome. For example, raising LDL by increasing pure saturated fat may not improve DunedinPace because increasing SF doesn’t really improve nutrition. Whereas raising LDL by eating eggs may improve DunedinPace by improving nutrient (macro and micro) intake.
I think it's a dangerous game to play...
It's important to understand the mechanism...why would LDL do anything
The only evidence based longevity dieter i know who is eating more cholesterol to raise his LDL lmao.
this video actually edged me more towards disregarding DunedinPace more than anything else. I was already skeptical about the true effect on longevity of caloric restriction for a healthy whole foods plant based dieter, but seeing that most pace of aging clocks dont correlate with CR, well then, i'll keep on eating my maintenance calories
*a small LDL increase, nothing crazy
What in the video leads you to discount DunedinPACE's importance?
Right, CR for someone with a 30% bodyfat would be very different than for someone less than 10% bf and not getting enough nutrition from diet
I'd turn this into a data mining exercise to generate hypotheses myself. I'd suggest three things: 1) run linear models with two dietary variables and rank by p-values, AIC or summed residuals. 2) Assume the LDL correlation holds and run linear models with LDL and one biomarker, ranking by the p value or AIC on the other biomarker. 3) Repeat 2) but use LDL and the dietary variables instead. There would be a large number of models for excel but other programs could handle it easily. We don't care about p
Thanks James, this is great. I think you multivariate linear models? I've used that in the past, but find more value in trying to follow every significant univariate (or sometimes adjusted for BW, calories, or the daily HR) correlation. It's hard to know which way will get closer to the truth, i.e. following all the univariate correlations vs adjusting models for many potential variables, which could exclude potentially important correlations.
In terms of AIC or summed residuals, that's beyond my current stats experience...If anyone wants to help crunch those #s, it would be much appreciated!
@@quantifiedmax By most likely I am referring to the selected exploratory modelling approaches, not the outcomes. We could go after more exotic relationships but these would be penalised one way or another. Mike's approach is Bayesian because we aren't sitting in a knowledge vacuum here, we know there are various pathways and epi associations etc and would use those to reason which outcomes/hypothesis are worth pursuing. That's the problem with frequentist approaches to biohacking, here we have more information and we are going to use it after each measurement, which in itself invalidates frequentist assumptions.
@@quantifiedmax I think your omitting the overall approach is to optimise these biomakrers rather than make claims about certain things, such as if they are causative. The optimisation step doesn't operate in traditional statistical approaches in biostatistics (where you are trying to make claims) and its an important consideration here. In the context of traditional biostatistics I agree with most of what you said. If we apply a FDR to the ldl relationship p>0.05 easily so there is nothing to go on. So we are already in an explortory analysis here.
Given whatever strength of evidence is derived what happens next? Calorie constraints and knowledge of the literature to choose certain changes are woven in and become priors for the next step (admittedly yes in a non tradtional way). I've said before that presenting CIs would be better but probably less understandable to the audience.
I'd be happy to chat some more offline, just send me a message.
What kind of eggs and how prepared? For example, I alternate mine between higher omega 3 content and free range and only eat over easy (as liquid yolk as possible).
Free range, microwaved or hard boiled. Not specific to a higher O3 content, at least not yet
Michael, how does the blood based Phenoage (bbPA) compare to these epi clocks in terms of reliability and value? Would be interesting to see how the people who do DunedinPace compare to their bbPA, and the details of what they do (diet etc) and their ages. As an aside, I think optimizing blood parameters organ markers and physical fitness is an excellent strategy independent of all these clocks, even if the optimum values haven't been nailed down in all cases. Thanks!
Hi Peter, I'm not sure-they're likely capturing different aspects of aging, i.e. the molecular (epigenetics) vs proteins (albumin, ALP, AST) and metabolites (creatinine, BUN) as examples. I may cover the full approach in a future video, from the molecular to the whole organism.
Definitely agree on BP and function...
Here some ideas for foods you might want to introduce and check correlations (Dunedin and other tests) for:
- kefir and Greek yogurt (probiotics)
- natto (PQQ, spermidine, K2, etc)
- buckwheat and capers (quercetin)
- herbs: parsley and oregano/rosemary/sage (CD38, apigenin, rosmarinic acid, luteolin, ursolic acid, etc)
- hibiscus tea and black rice (anthocyanins)
- blueberries
- aged cheddar/gouda (K2, spermidine, etc)
- more mushrooms (lion’s mane, maitake, or shiitake - ergothioneine, spermidine, beta glucans, etc)
Hey @NmlssNmlss, the goal is to identify the food pattern within my own diet that pushes DunedinPACE towards it's lowest value as a primary strategy, If that faills (after many attempts), then trying something else.
For your list, I already average ~245g of mushrooms/d, 60g of fresh parsley/d, To include any others, I'd have to take stuff out, and the goal is to not blow up the system (see Quantifying Biological Age, Test #2 in 2024), but to make minor changes.
@@conqueragingordietrying123 Thanks for responding!
Of course, I totally understand. I only shared because I thought you might be interested in experimenting with some of these.
@@conqueragingordietrying123 Oh, I forgot an even more interesting one (which may or may not be on your radar already): wakame , a type of brown seaweed (e.g., Wel Pac wakame is available on Amazon and takes a few minutes to make). It's a source of fucoidains (the best activator of SIRT6), fucoxanthin, and has a number of other interesting properties.
You are not the only one. Siim Land should be #1 and they are also blocking him from the leaderboard. Shame on the project and their head: Brian Johnson!
I'm not sure if it's purposeful or that they have other issues to handle, but yep, Siim should be close to the top for the next update.
@@conqueragingordietrying123 I think that there are so many slow aging people already tested that, if they updated, Brian Johnson may be out of the leaderboard and they don't want that. So they are waiting for Brian to gain their desired position before updating.
@@espinosalexis That's possible I suppose. From what I can tell from Bryan's protocol, it seems he has a problem with glucose spiking, with his cgm numbers not being particularly amazing, even though he was on CR, eating mostly vegetables and taking metformin and acarbose. And I wouldn't be surprised if he had hard to move epigenetic phenotype, perhaps his LDL is too low? However credit to him for the work done so far and for publishing data and his protocol.
I'm curious why you do not use Glycan age clock?
It's promising, but I'm waiting for more data to be published.
Mike, great video as always 👍💪😎
They tell us that saturated fat is inflammatory. Let us know if you see an increase in inflammation markers with your increase in saturated fat.
Thanks Steve. It's likely context dependent-in my case, hsCRP has been below the limit of detection (< 0.3 mg/L) for 16 tests in a row.
Byran Johnson, just announced 0.64, let's see if the Olympics are updated and if he publishes the likely reasons. Did you have any further leads on lowering DunedinPACE Mike?
Hey James, that's great news for Bryan-did he document how?
Outside of the LDL-DP correlation, nothing is significant diet-wise. I'm waiting on results form the 4/29 test, new correlations (and hopefully leads) after that...
@@conqueragingordietrying123 No specific documentation yet. But I noticed he reduced protein intake, reduced iron intake and removed chlorella. But there are other interventions, with the follistatin gene therapy and potentially increased muscle mass being a possibility. Hopefully he'll publish the candidates.
Thanks again.
How about increasing your intake of nuts to bump up your LDL? Tastes better than eggs.
SFA and cholesterol intake are the strongest correlations for higher LDL in my data, not nuts...
Is DHEA-S still correlated with DunedinPace?
Nope, r=-0.49, p=0.15
Mike, morning. Thank you for the video as always. Do you know which of these tests are commercially available, and how would you recommend in terms of the top 2-3 priorities for getting tested with these methods?
Hi David, DunedinPACE is commercially available...
In terms of priorities, I may specifically focus on it in a video, but the goal (at least mine) is to optimize biomarkers from the small scale (molecular, metabolites, proteins, cells), to the large (physical function and body composition)
In terms of getting tested, epigenetics (Horvath, DunedinPACE), metabolomics, and standard chemistry panel +CBC and hsCRP cover a lot of these bases...
@@conqueragingordietrying123 Thank you!
Really interesting this LDL correlation, hopefully you find the goldilocks zone! Did you test your testosterone levels when LDL was at its lowest?
Hey Tony, I have 3 testosterone tests from October 2023 to Jan 2024-LDL wasn't on the low side of my range for any of the 3 tests (78, 83, 80), whereas total T was 746, 895, 971.
My problem is there are supplements that have been hinted at reversing epigenetic age by several years. That is below zero pace of epigenetic aging.
Hi @diamond_s, which supplements? Afaik, only the TRIM trial saw a reduction for epigenetic age, and if I remember correctly, Bryan Johnson (anecdotally) used GH and it wasn't good for his DunedinPACE
CA-AKG was claimed to reduce epigenetic age by several years in some types of tests. Another study using resveratrol enriched wine also claimed epigenetic rejuvenation by several years
As a side note from self-experiments on a forum, simple AAKG has worked too.
if the human is not eating ( CR) then his bile not release so the cholesterol will backup to high levels found in the blood ? hypothesis
Why didn't you return the coconut oil back to what it was previously when you added the eggs, as the coconut oil did not do anything and it is extra calories that will subtract from other foods?
Also, do you get any C15 (pentadecanoic acid) in your diet? It is supposed to work wonders. Somehow I doubt that, but it would be nice if we could see what an increase in that would do in someone so well tracked and so close to optimum health.
Hey @ChessMasterNate, not coconut oil, but coconut butter-they're different products...
The goal is to increase LDL, and for a couple of recent tests, SFA were relatively low, but I added eggs (4d/week), which didn't increase LDL above my range (62-83). Similarly, higher SFA alone (without eggs) didn't raise LDL, although it was at the high end of my range, too. Both are significantly correlated with LDL in my data, so I'm doing the experiment to see if their combination will push LDL a bit higher relative to either alone.
C15 can be produced by the gut microbiome, but outside of that, I'm not sure, as iollo's kit doesn't currently measure it in blood.
I suppose I could site studies all day long at a population-based, which show at higher LDL is strongly correlated with heart disease. Of course there are a few diseases such as cancer that result in lower LDL but if an Individual is healthy with higher LDL, he may simply be an outlier. I think deliberately increasing LDL it’s a dangerous game because you don’t know whether you are that outlier or not.
Hi @paulcohen6727, I'm not proposing a crazy high LDL increase, just pushing the high end of my recent range from < 85 to < 95, to test the DunedinPACE hypothesis.
Is your practice in the NYC area and are you accepting new patients. I’m in Brooklyn. Thank you.
Hi @paulfiedler6820, I offer consults on Zoom, which may be of interest: www.patreon.com/michaellustgartenphd/membership
Are you keeping the higher saturated fat for the next test as well? Are you adding eggs in addition to your diet for the last test or are you reducing calories somewhere else to offset the eggs so that total calories/macros stay the same?
Hey @justsaying7065, yep, average total fat intake is 90g/d, up from 81g/d two tests ago (1/15), and 84g/d for the last test (3/4), with the increase exclusively from coconut butter. 5 eggs/week, with the removal of dates on those days to stay close to eucaloric (or less).
I would be very interested in your average daily Total Calories vs burned Calories. What's your average exercise like? You inspired me to start eating set meals, for the first time. It makes counting calories so much easier. Now i'm trying to tweak that against my average exercise expenditure. That's tough to work out. How do you do it?
I'm not sure about avg vs burned, but I track BW and intake daily, so I know what my BW maintenance calories are, which is ~2100. Two 90-minute, full body workouts/week with light cardio (walking) on the other days.
@@conqueragingordietrying123 thanks. I'm trying to be on a small deficit and your numbers are close to mine. I think avg 2000 or less and workout about 7 hours a week.
Please excuse my ignorance, but can’t you find what the blood levels would need to be to get a 0.6 Dunedinpace from them? Isn’t it just a calculation based on your age and your blood markers measured at that time?
Hi @LandonPark, DunedinPACE is a stand-alone test, afaik it's not based on a compilation of multiple biomarkers
@@conqueragingordietrying123 I’ll need to look into this more. I just assumed it was a bunch of blood bio-markers. My bad. I’ll be going down a hole of DunedinPace now.
Interesting. Would love to know if hyperbaric oxygen or melatonin supplementation have a positive effect.
Hyperbaric is on the list, but I'd need to do it often to see an effect, which isn't practical atm
I've experimented with melatonin in the past, haven't taken it in a long time.
Coconut is also a fat known to improve nutrient absorption, I wonder if the relationship is indirect; higher SFA -> better nutrient absorption -> lower DunedinPACE, with LDL increase being coincidental.
That would be easily testable at least with Mike's data by running an analysis for mediation with SFA/coconut.
Thanks Michael. May be LDL is U shaped curve with optimum is 100 as you mentioned in another video. Surprising no mention about Apo B?
Thanks @barasra8847, I haven't measured ApoB since 2022, so I don't have correlations with DunedinPACE
You need to make a tutorial on how to have basic tracking on health data variables, calculating correlations with excel, standardizing blood tests every time etc.. it would be really good for humanity... at least for those who care ;)
Yes @asijdhoahndouahd, the plan is sooner than later, I have a video in mind!
Dave Pascoe has a very low DunedinPACE, but I wonder how much of that is genetics given his long lived family. But I noted he was taking SAMe. So I wonder if there was some magic supplement in that supplement stack.
I've considered taking SAMe, it's a possible option. I'm looking to interview Dave on the channel, maybe sooner vs later!
@@conqueragingordietrying123 If you do Mike, maybe you could ask him what changed to reduce his DunedinPACE to those low levels, as I couldn't quite pinpoint what the timeline/changes were from his website.
@@conqueragingordietrying123 No one has the slowest epigenetic Pace Of aging. You are misleading everyone that is gullible and naive, of course. These tests do not measure every aspect of epigenetic age - that is, every CpG site.
You may have what the test particularly measures as younger, but for you or anyone else to make a bold claim that they have the full spectrum of biological or epigenetic markers as being younger is pure hubris.
Biological age tests, especially those based on epigenetics, attempt to measure a wide spectrum of biological age by assessing DNA methylation patterns, which are influenced by an individual's lifestyle, environment, and genetics. These tests provide a snapshot of how well or poorly your body is aging compared to your chronological age.
However, while epigenetic tests are a powerful tool for gauging biological age, they don't capture every aspect of it. Biological age can be influenced by various factors including:
Body composition (e.g., muscle mass, fat distribution)
Cardiovascular health
Metabolic function
Neurological health
Immune system function
Each of these factors could be aging at a different rate within the same individual. Therefore, although epigenetic tests offer valuable insights, they are part of a broader assessment that might also need to include clinical evaluations, lifestyle assessments, and other biomarkers to fully capture the "full spectrum" of biological aging.
With all due respect, if your goal is to live to 150 and beyond, how will any of this help you break the maximal lifespan ceiling? Very misleading, what you say
@@conqueragingordietrying123 This would be a stellar interview.
Apart from maintaining CRP, fasting Insulin and apoB as low as possible I've been fascinated with homocysteine recently. I try to look for biomarkers that have a strong and linear relationship with all cause mortality.
It seems that the methylation cycle is critical piece of the puzzle for lifespan. Mutants with upregulated transsulfuration have increased lifespan. Increasing the products of transsulfuration (glutathione, hydrogen sulfide, taurine) all increase lifespan. Decreasing the reactants (protein, methionine) increases lifespan.
And in humans homocysteine is right in the middle of this. Unfortunately it seems that how to achieve this metabolic profile seems species specific, in some cases SAM increases lifespan and in others decreases.
I stick to trying to minimise homocysteine which has robust positive relationship with mortality starting at 0
Thanks for the cool study; greetings from Japan😀
I'm glad you are committed to following the path of experimentation where it takes you. But I've just got to say, intentionally attempting to raise LDL cholesterol, in the face of numerous gold-standard studies showing that higher ldl-c indicates higher APO(b), is a bridge too far for me.
Put plainly: What if you 'win' your little longevity Olympics there, but end up clogging your blood vessels with extra plaque in the process? Pyrrhic victory, if you asked me.
Hi @mkvalor, as mentioned in the video, moving up the RO leaderboard is important, but more important is slowing the epigenitic pace of aging to its lowest value, and keeping it there,.
There's published data in large studies showing that an LDL of 65-120 is associated with lowest CHD mortality risk-I'm not talking about anything crazy, but instead moving it from my ~80 mg/dL average to 95, to see if the correlation is real.
Hello. What is your take on Valter Longo studies. And his FMD really interested to hear your opinion and if you considered trying it.
Hello @Sam-gs7yb, I'm all about biomarkers. If more improve than not on FMD, then go for it.
Long-term fasting beyond 16-18h/d (which is already part of the approach) isn't something I'm interested in...
Have you done any extended fasts (3+ day water fast) to turn on autophagy? I’ve seen videos of Dr. Ron Rosedale stating that during autophagy the body goes into a state of recycling and repair. Maybe you are still consuming too many calories. Didn’t those Blue Zone folks on Okinawa survive on just sweet potatoes and seaweed. Not saying anyone should try and reproduce a harsh dietary scenario like that. But, it seems like the body rewards it’s owner for eating much less than the average person usually does.
I’m the same height as you but I weight 160 lbs. How many grams of protein do you consume each day? And in how many feedings? I’m doing about 45 grams twice a day and within a keto diet of less than 50 grams of carbs a day.
Nope on the extended fasts, as it messes with my mental and physical health. Daily fasting, though, ~16h/d, sometimes longer.
@@conqueragingordietrying123 Gotcha. I can only do extended fasting when I’m on a vacation from work. If you’ve done 3+ day fasts you know the mood swings and variable energy levels are best experienced in a low stress environment. But, I would have to say I have an incredibly other level healthy energy after a three day water fast.
Thanks. Not saying much but, I eat 1 or 2 eggs every morning and my LDL is just shy of 84 mg /dL (2.17 mmol/L) so it may take at least an egg a day for a signif change depending on how your body manages LDL.
Eggs are great, providing so many nutrients. The only issue is that they don’t just provide cholesterol, they also provide protein, fat, vitamins and minerals. With so many variables, if your DunedinPace changes with eggs, how do you know which nutrients are actually making the difference?
I don't-I'm more interested in the end result-if DunedinPACE improves (and the net effect is not negative on all the other biomarkers), then that's good enough (for me). I could spend a year or two trying to prove causation, that's not the primary focus.