Is Low LDL Bad For The Epigenetic Pace of Aging?

Summary

The speaker analyzes correlations between his diet, biomarkers, and epigenetic pace of aging over 12 tests. No foods or nutrients significantly correlate with pace of aging, but DHEA sulfate and LDL cholesterol do, suggesting higher levels correlate with slower aging. The speaker plans to increase LDL levels slightly through more coconut butter to test if it further slows his aging pace, while aiming to remain in the safe range for heart disease risk.

Takeaways

• 😀 The transcript discusses analyzing data on epigenetic pace of aging (DN Pace) to try to slow it down
• 🧪 There were no foods or nutrients significantly correlated with DN Pace, so biomarker correlations were analyzed
• 💉 Four biomarkers were significantly correlated: liver enzymes, platelets and inversely DHEA sulfate and LDL
• 📈 Higher DHEA sulfate was correlated with slower epigenetic aging pace
• ⬇️ Lower LDL was correlated with faster epigenetic aging pace
• ❤️ Moderate LDL levels of 65-120 mg/dL had lowest heart disease mortality risk
• 😕 Very low LDL (<65) or high LDL (>120) increased heart disease mortality risk
• 🥥 Saturated fats like coconut oil can increase LDL levels moderately
• 📅 The goal is to safely raise LDL slightly above 85 mg/dL for the next test on March 4, 2024
• 👍 If successful, this could help validate the correlation between higher LDL and slower epigenetic aging

Q & A

What metric is the speaker using to measure epigenetic pace of aging?

The speaker is using DNA methylation age (DNAm age) and DNA methylation pace (DNAm pace) to measure epigenetic pace of aging.

What is the goal of tracking correlations between biomarkers and diet?

The goal is to find dietary factors that are significantly correlated (p < 0.05) with DNAm age and pace in order to follow those correlations to try to improve the biomarkers.

Which nutrient had the strongest correlation with DNAm age and pace?

Vitamin B6 had the strongest correlation with a p-value of 0.1, but no foods or nutrients met the threshold for statistical significance (p < 0.05).

What biomarker had a significant inverse correlation with DNAm age and pace?

DHEA sulfate had a significant inverse correlation, meaning higher levels were associated with slower epigenetic aging.

How could lowering LDL too much negatively impact health?

The data suggests very low LDL (< 65 mg/dL) is associated with higher risk of heart disease mortality. Lowering LDL too aggressively could potentially negatively impact heart health.

What is the safe target range for LDL based on the presented data?

The data suggests an LDL range of 65-120 mg/dL is associated with lowest risk for heart disease mortality.

What dietary change did the speaker make to try to increase LDL levels?

The speaker increased intake of coconut butter to increase saturated fat intake, as saturated fats are correlated with higher LDL levels.

How many data points did the speaker have relating DNAm metrics to other biomarkers?

The speaker had 9-11 data points relating DNAm age/pace to the other 23 blood biomarkers analyzed.

What technique does the speaker use to precisely track dietary intake?

The speaker uses a food scale to weigh all food, tracks intake in Chronometer, and logs averages over 60 day periods leading up to each blood test.

When is the next DNAm age and pace test scheduled?

The next test is scheduled for March 4, 2024, with results expected in April.

Outlines

00:00

🧬 Author analyzes biomarkers correlated with epigenetic pace of aging

The author explains that he tracked his diet and biomarkers over time to analyze correlations. No foods/nutrients were significantly correlated with epigenetic pace. Analyzing other biomarkers revealed LDL, DHEA sulfate, liver enzymes, and platelets were significantly correlated. The author will try raising LDL slightly to test if it improves epigenetic pace while remaining in the safe range for heart disease mortality risk.

05:02

👴 Lower LDL correlated with faster epigenetic aging pace for author

The data shows a significant inverse correlation between the author's LDL levels and his epigenetic pace of aging. In other words, lower LDL levels correlate with faster epigenetic aging pace. One data point with very low LDL (65 mg/dL) corresponded to his fastest epigenetic aging pace.

10:03

📈 Author aims to safely increase LDL to test correlation

There is a safe LDL range of 65-120 mg/dL associated with lowest heart disease mortality risk based on a large study. To test if higher LDL correlates with slower epigenetic aging pace for him, the author aims to safely raise his LDL from 62-83 mg/dL to 90-95 mg/dL by increasing saturated fat intake from coconut butter.

Keywords

💡epigenetic pace of aging

This refers to the rate at which a person's epigenome changes over time. The video discusses measuring the epigenetic pace of aging using DNA methylation data. A slower pace means the epigenome is changing more slowly, suggesting slower biological aging.

💡DNA methylation

DNA methylation is an epigenetic mechanism that regulates gene expression. The level of DNA methylation at specific sites on genes can be used to estimate biological age and the epigenetic pace of aging.

💡biomarkers

Biomarkers are measurable indicators of biological processes or disease state. The video analyzes correlations between the epigenetic pace of aging and various other biomarkers like LDL, platelets, etc.

💡LDL cholesterol

LDL (low-density lipoprotein) is considered bad cholesterol, but the video found higher LDL levels correlated with slower epigenetic aging pace. However, very high or very low LDL increased heart disease mortality risk.

💡DHEA sulfate

Dehydroepiandrosterone (DHEA) sulfate is a hormone that declines with age. The video's data shows significantly higher DHEA sulfate correlates with slower epigenetic aging.

💡nicotinic acid

Nicotinic acid (niacin) is a B vitamin. The video hypothesizes that high-dose nicotinic acid supplementation may have increased NAD+ to high levels, negatively impacting epigenetic aging pace.

💡biological aging

Biological aging refers to the time-dependent biological changes that accumulate overtime, causing gradual decrease in an organism's ability to resist stress and damage. The video discusses measuring and trying to slow down biological aging.

💡aging

Aging is the process of becoming older. It involves molecular and cellular changes overtime throughout the body leading to an increased risk of disease. The video is about measuring biological aging and attempting to slow it down.

💡longevity

Longevity refers to how long people live on average or maximum lifespan. The video discusses techniques for measuring biological aging with the ultimate goal of increasing healthy longevity.

💡biohacking

Biohacking refers to biological experimentation done by individuals outside of professional science. The video discusses the author's self-experiments in measuring biomarkers, testing diets and supplements for anti-aging effects.

Highlights

I have 12 tests currently done for DHEAA and Pace to track epigenetic aging

No foods or nutrients significantly correlated with DHEAA and Pace

Looked at correlations between DHEAA/Pace and 23 other biomarkers

Higher DHEA sulfate significantly correlated with slower epigenetic aging pace

Higher LDL significantly correlated with slower epigenetic aging pace

Lower LDL correlated with faster epigenetic aging pace

Increasing LDL may improve epigenetic aging pace without increasing heart disease risk

Safe LDL range is 65-120 mg/dL for lowest heart disease mortality risk

Increased coconut butter intake to raise LDL for next test

Next blood test scheduled for March 4, 2024 to validate correlation

Detailed correlation data available on Patreon

Discounts available for epigenetic testing, blood testing, diet tracking

Attempting to biohack aging through testing correlations

Significant correlations guide interventions to improve biomarkers

Following correlations to conquer aging or die trying

Transcripts

who has the slowest epigenetic pace of

Aging we can see that data here this is

the top 15 for the Rejuvenation Olympics

and if you notice I'm not on the list so

with that in mind what's my data so I

have 12 tests currently for done and

pace and to get on this test to get on

the leaderboard you need an average of

three done and Pace measurements over 6

months so my last test was in January of

2024 6 months prior would be June of

2023 now I don't have three tests over

that time span I have six tests so I

don't know how they'll rank that but I

think what makes the most sense is

taking the average over that 6-month

period which in my case is

0.81 0.81 would put me at 14th Place

which isn't bad but the goal is

obviously to move up now there is hope

for optimism as two of those six tests

two of the most recent six tests were

relatively lower 75 and 74 which would

put me into a tie for eighth place so in

order to more consistently see my best

data I need to know which factors are

significantly correlated with the and

pace so let's start off with

correlations for diet with the and pace

and for those who are unfamiliar with

the approach since 2015 I weighed all my

food using a food scale I then entered

those daily food amounts into

chronometer and if you want to track

your own diet there's a discount link

for chronometer in the video's

description and then I manually log that

data into a spreadsheet so then each

blood test has a corresponding average

dietary intake in other words for a

given 60-day period in between blood

tests because I'm tracking diet every

day I can take the 60-day average which

then lines up with the latter blood test

so every blood test has a corresponding

average dietary intake and then with

many blood tests and many dietary

intakes that correspond I can calculate

correlations and after calculating

correlations with the goal of improving

uh biomarkers I I follow or I try to

follow as many of the significant

correlations as possible with a p Val uh

P value less than 0.05 being the measure

of statistical significance all right so

with that in mind I then looked at 97

comparisons for den and past with Foods

macro and micronutrients and this is a

12 test analysis and we can see the D

that data for what data is closest to

the being significantly associated with

daita Pace here so on the left we've got

the food or nutrient and in the middle

we've got the correlation and then on

the right we've got the P value and

notice though that there are no Foods or

nutrients that are significantly

correlated at a P value less than 0.05

with DED and Pace as the best hit the

best correlation is vitamin B6 with a P

value of 0.1 which is outside of

significance so at this point I have two

options one just keep testing and gather

more data and I'm going to do that

anyway so that's not really an option or

two I decided to take a deeper dive and

this isn't the first time I've done this

this I've done biomarker versus

biomarker analyses before but in order

to get potentially gain more insight

into mechanisms that may impact Don need

and Pace I then decided to look at

correlations for D and Pace with other

biomarkers and we can see that full list

here correlations for D and Pace with

other biomarkers more specifically 23

biomarkers that I commonly track as

shown here with the full list on the

left and then I on the same day as done

and pay testing I also measured other

bio biomarkers versus ven venopuncture

so going to the lab and having them pull

it pull it out of my vein and then when

I got home I did the uh blood test

finger prick for done and pace so I have

9 to 11 tests that correspond for

standard Blood biomarkers on the same

day of testing as D and Pace almost all

of the tests as you can see with the N

which is the number of samples almost

all of them are 11 so 11 tests that

match up with the KN and Pace with the

exception of DHEA sulfate which I

currently have nine data points that

overlap and then aging a where I have 10

but aging. a has been unfortunately

discontinued so that'll always be 10

unless that's uh restored and then again

in the middle we've got the correlation

and then the P value so now we've got

four of these biomarkers that are

significantly correlated with Don and

Pace the liver enzymes a plus alt

platelets but then where the story

starts to get interesting at least for

me is DHEA sulfate which is

significantly inversely correlated with

Don and paast in other words a

relatively higher D DHE sulfate in my

data is significally correlated with a

slower epigenetic pace of aging and why

that's interesting is because my DHEA

sulfate is currently one of the

weaknesses in my data it's close to age

expected and not youthful I've had

values that are um about 2 and a half

times higher in my early 30s and I just

didn't track it for a very long time and

they declined over the past uh 15 years

or so so getting them back to you for

levels without supplementation is a part

of the one of the current goals but then

where the story gets most interesting at

least for me is LDL and there too is a

significant inverse correlation so let's

take a deeper look at that

correlation so it's 11 tests for Don and

Pace versus LDL and then we can see with

Donita Pace on the y- axis plotted

against the LDL concentration on the X

we can see that significant inverse

correlation for LDL against D Pace in

other words relatively higher LDL in my

data is significantly correlated with a

slower epen pace of Aging conversely

lower LDL is significant correlated with

a faster epigenetic pace of Aging but

note that these data just to highlight

the range in my case at this current uh

point in time is from 62 to 83 Mig per

deciliter I I'm not trying to make any

extrapolations for people who have LDL

far higher that's a story for a

different day now also note that for one

of these tests highd do nicotinic acid

uh on this on the where I had a 0.98

which which is my worst Donan Pace yet

to date LDL on that date was 65 now in

earlier videos I've hypothesized that

highd dose nasin 600 milligrams per day

May raise Ned too high and that may have

been what messed up Don pce sending it

to my worst value to date but these data

would suggest that maybe going uh maybe

highd do nasin nicotinic acid reduces

LDL to a level where it may be too low

negatively impacting epigenetic pace of

Aging so note that there are only two

data points on the far left side of 65

mg per decer so there is some

extrapolation on this graph so instead

of testing that hypothesis by reducing

my LDL as low as it can go and seeing if

my the need and Pace gets even worse

conversely I think testing the other

side of that curve or the other side of

that that uh

slope in other words if I increase LDL

will I see my best DNE and Pace I think

that makes more sense sense but what

about coronary heart disease risk right

if we increase LDL wouldn't that

increase heart disease

risk so let's take a look at what the

data has to show so on the y-axis we've

got the hazard ratio for coronary heart

disease CHD

mortality plotted against serum levels

of LDL and there are two main reasons

why I like this study first it has a

very large sample size this is about 4.5

million people that were included in

this study and then second is that there

are three curves and as we'll see the

fully adjusted model included almost

every comorbidity that could potentially

impact the association for LDL with

heart disease risk and unfortunately

most studies at least the ones that I've

come across don't adjust for all

comorbidities that can impact that

Association so it's somewhat part of the

picture not the full picture whereas I

think this study is closer to the full

picture and for those who who disagree

please leave a comment we can debate

that there so in terms of What's

significant we put up our red line at a

hazard ratio of one remember where the

Shaded region for any of these three

colored lines is completely above one or

completely above below one we have a

significant

Association so for the first Model Model

one this is the minimally adjusted model

in blue they adjusted for age sex race

and smoking status and just using an LDL

of 120 as an example that was

significantly associated with a about a

20% reduced heart disease mortality risk

but then when including stattin use BMI

hypertension and diabetes into the model

that same 120 for LDL was now only

associated with a 10% reduced risk of

heart disease mortality risk what about

the fully adjusted model so that's shown

in green and as I mentioned they

adjusted for basically every comorbidity

that you can think of in addition to

removing data for a 2-year lag so people

who died within the first two years was

removed so basically these are very sick

people who died within 2 years they

didn't want that to skew their results

and then they also adjusted for HDL

pre-existing coronary artery artery

disease atrial fibrillation pre-existing

heart failure stroke anemia liver

disease kidney disease lung disease

cancer depression and dementia in other

words almost every comorbidity that can

impact the association for LDL with

heart disease mortality risk and when

looking at the data for model 3 now we

can see that an LDL of 120 is not

significantly associated with a reduced

risk for heart disease mortality in

contrast when LDL is greater than 120

that's associated with a significantly

increased heart disease mortality risk

but that's only half the story the other

half of that story is when LDL was less

than 65 Mig per deciliter that too was

associated with an increased heart

disease mortality risk now if you

remember the data on the right hyos

nasin reduced my LDL to 65 MGS per

deciliter which is right on that edge of

an increased heart disease mortality

risk so is it possible that in my case

for whatever reason Reon going too low

for LDL may not be good for epigenetic

uh the epigenetic pace of Aging but also

potentially bad for heart disease

mortality risk at least based on what

this published data

shows so with that in mind there is a

relatively safe range based on this plot

for 65 to 120 for LDL being associated

with lowest risk for heart disease

mortality so I do have room for

improvement in my LDL current LDL data

to go a bit higher and to do it safely

so that in mind that's the goal for the

next test to raise LDL to greater than

85 Mig per deciliter I'm not talking

about anything outrageous like 170 even

just a small increase to 90 to 95 to do

that I've increased total fat intake

which is significantly correlated with

LDL in my data those correlations are in

the correlation tier on patreon so if

you're interested in that check it out

but even within total fat where do you

go from there so subdividing that

saturated fat as expected that's

significant correlated with LDL in my

data but that doesn't tell you from what

also coconut butter is significantly

correlated which is the major source of

my saturated fat intake so for the next

test I've increased coconut butter

intake for the past week or so so I'll

have about two plus weeks of data with a

relatively higher saturated fatty acid

content from coconut butter and we'll

see if I can push my LDL just a bit

higher to test this correlation with the

need and Pace will it work test number

two in 2024 is scheduled for March 4th

so that up video will be coming sometime

in April all right that's all for now if

you're interested in more about my

attempts to biohack aging check us out

on patreon and before you go we've got a

whole whole bunch of discount links that

you may be interested in including

discount links for D and pace and

epigenetic testing or microbiome

composition Ned quantification at home

metabolomics at home blood testing with

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diet tracking with chronometer or if

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that link and all the other links will

be in the video's description thanks for

watching hope that you enjoyed the video

have a great

day