Is Low LDL Bad For The Epigenetic Pace of Aging?
Summary
TLDRThe 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
🧬 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.
👴 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.
📈 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.
Mindmap
Keywords
💡epigenetic pace of aging
💡DNA methylation
💡biomarkers
💡LDL cholesterol
💡DHEA sulfate
💡nicotinic acid
💡biological aging
💡aging
💡longevity
💡biohacking
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
sciox health which includes apob green t
diet tracking with chronometer or if
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can do that with the website buy me a
coffee we've also got merch so if you're
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or die trying brand as I've got on here
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
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