Ever wondered why sunlight is essential for your health, yet many of us remain vitamin D deficient? In this eye-opening episode, we trace the impacts of urbanization from the Industrial Revolution and how pollution led to widespread vitamin D deficiencies. Uncover the science behind vitamin D synthesis and why even people in sun-drenched areas struggle with low levels. Explore natural food sources rich in this crucial nutrient, from fatty fish to red meats, and learn the critical differences between vitamin D2 and D3. We emphasize the importance of testing your vitamin D levels regularly rather than assuming you're in the clear.
We also demystify the complexities of measuring vitamin D, focusing on why clinicians prefer the 25-hydroxy form over the active 1,25-dihydroxy version for reliable results. Understand the intricate regulation of vitamin D in your body, and why the 25-hydroxy form is the gold standard for assessing your vitamin D stores. Finally, we touch on the principles of functional medicine and how lifestyle modifications can support overall wellness. Remember, our podcast is your guide to health education, but always consult healthcare professionals for personalized advice. Join us for this insightful journey into the world of vitamin D and take control of your health today!
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:02):
Hey everyone, welcome to the Inflammation Nation
podcast.
I'm your host, Dr SteveNoseberg.
Speaker 2 (00:08):
One of the greatest obstacles to crafting health and
wellness is identifying andcontrolling inflammation.
It's at the core of all complexand chronic diseases and it's
the driving mechanism thatunderlies the most common
symptoms that people like youstruggle to overcome.
Join us as we explorecutting-edge science and
research to give you theinformation and tools you need
to create the quality of lifeyou want and deserve.
(00:30):
And now here is the host ofInflammation Nation, dr Stephen
Noseworthy.
Speaker 1 (00:37):
Hey guys, we're back with part two of our discussion
about vitamin D as the nextmiracle molecule in this little
mini-series, and in part one youmight want to go back and
listen to that if you're justjumping into this episode we
talked about, you know, what isa vitamin, what is a hormone?
And is vitamin D a vitamin oris it actually a hormone, like
(00:58):
many people say?
And the answer is it's both.
If you look at the definitionsof those compounds, it's clearly
can be classified as either one, and we talked about some of
the differences between vitaminD2 and vitamin D3.
And we also made a distinctionbetween the 25-hydroxy version,
(01:19):
which is the one that we're allmeasuring or at least we should
be which is actually a precursorhormone, and that has to be
converted into the 125 dihydroxyversion, which is the active
metabolite, and we'll come backto that.
But I want to tell you just alittle bit of history, like we
can go back in what we know, forexample, back in the let's say
(01:43):
it was the advent of theindustrial revolution, say a
couple hundred years ago.
What ended up happening with,with the evolution of industry
and machinery andstandardization of manufacturing
facilities?
Um, what happened was peoplewho lived in the rural, in the
country settings, started in inthe European communities.
(02:05):
They started moving into citiesto get jobs and as more and
more people came into thesecities, the cities built more
houses or housing complexes forthe increasing population.
They also started makingmanufacturing facilities and
plants that used machinery thatburned fuel sources that
(02:27):
increased the level of pollutionin these communities.
And all of these things had theeffect of like, for example,
taller buildings that werecrowded close together with a
pall of smog or pollution in theair basically filtered out the
sun and as a result, shortlyafter the onset of the
(02:49):
Industrial Revolution, there wasa massive increase in vitamin
D-related diseases, particularlyrickets, which is a
bone-related vitamin D diseasewhere calcium doesn't go into
the bones, bones become soft andthey bow under the weight of
someone's body.
So I think it's kind ofimportant to recognize that
(03:11):
number one.
We can make vitamin D from sunexposure, but we need to have
adequate sun exposure.
Now I've been measuring vitaminD with my clients as a routine
part of my initial analysis andsubsequent follow-ups for a
couple of decades now.
It's just part of how I assesssomebody's fundamental
(03:32):
physiology, and I have a lot ofclients in very sunny areas and
they tell me yeah, I spendplenty of time outdoors, but
routinely the only people that Ido my initial vitamin D
assessments on that actuallyhave adequate levels of vitamin
D are people who are takingsupplements, even though they
might live in sunny places andspend what they think is an
(03:52):
adequate amount of time outdoors.
And so I want you to considerthat if you live in a sunny
place and you spend timeoutdoors, you may or may not
have adequate vitamin D levels.
Don't guess, always check.
I mean that's kind of acatchphrase in our levels.
Don't guess, always check.
I mean that's kind of acatchphrase in our world.
It's like, let's test, let'snot guess.
But estimates are that, allother things being equal meaning
(04:14):
say, no interfering factors,that we can or have the
potential to make about 90% ofthe vitamin D that we need just
from the sun.
We also get vitamin D from ourdiet, and so vitamin D occurs
naturally in fatty and oily fishsuch as, say, trout, salmon,
swordfish, sardines, mackerel.
(04:35):
You can also find vitamin D inegg yolks and most of your red
meats, and particularly in organmeats, specifically liver, and
there are plant sources ofvitamin D, but this is mostly
the vitamin D2 version, which isless bioavailable, less
absorbable than the vitamin D3.
That comes from the animalsources right, and you can again
(04:57):
, you can get vitamin D fromfungi and algae, but it's just
not as good as the stuff thatyou're going to get from the
animal sources.
A vitamin D is one of fourdifferent fat-soluble vitamins
right, vitamins A, d, e and Kand while vitamin D absorbs
passively from your gut into thebloodstream, it tends to work
(05:17):
better when you take vitamin Dwith fats.
So if you're eating fatty foodsthat have vitamin D in it,
absorption happens very easily.
If you're taking it foods thathave vitamin D in it, absorption
happens very easily.
If you're taking it with asupplement, then it helps to
have it with a fatty meal, forexample.
We'll come back to this towardsthe end of the episode, but the
main way that we get vitamin Dis through adequate sun exposure
.
At least that's the way it'sdesigned to be.
(05:40):
And, again, assuming nointerference, your skin can make
upwards of about 10,000 IUs ofvitamin D every day, and that's
a decent dose, right, but that'swithout any interfering factors
.
For example, if your skin toneis lighter, you will likely make
(06:00):
more vitamin D from the sunthan if you are darker
complected, people with darkercomplexions need more time in
the sun than if you are darkercomplected.
People with darker complexionsneed more time in the sun to get
the same amount of vitamin Dproduction that someone who has
fairer skin.
If you live in a higherlatitude, if you live in more
northern climates, you're goingto make less vitamin D from the
sun.
So if you live near the equator, it's easier to make vitamin D
(06:23):
than if you live, say, in Swedenor Norway.
And also the time of day a sunexposure can make a difference,
like the optimal time to getvitamin D from your skin is
between 10 am and 3 pm, which,of course, is the very time that
dermatologists warn that weshould stay away from the sun.
So how do we actually makevitamin D from the sun?
(06:44):
Well, it's a multi-step processthat requires, number one,
adequate sun exposure.
Number two, adequatecholesterol as a base molecule,
as well as healthy liver andkidney systems.
So here's the process in anutshell when you have adequate
sun exposure, it triggers yourskin cells to trap cholesterol
(07:07):
and then use an enzyme toconvert cholesterol into the
parent vitamin D calledcalciferol.
So the first thing to rememberis that vitamin D number one is
made from cholesterol and stepnumber one happens in the skin
when we expose our skin toadequate sunlight.
Step number two, then, is wherewe take this parent form of
(07:29):
calciferol, the parent vitamin D, and we move that to the liver,
where the liver uses anotherenzyme to convert this parent
calciferol into the pro-hormone,the 25-hydroxyvitamin D Now
remember, this is a pro-hormone.
The 25-hydroxy vitamin D Now,remember, this is a pro-hormone,
it's not biologically activeand it has to be converted in
(07:51):
one more step to the125-dihydroxy version, and this
happens in the kidneys.
So, if you flow through theprocess, here is what you need
to make most of your vitamin D.
Number one adequate sunexposure at key times of the day
, and what is adequate is goingto depend on your skin tone,
where you live relative to theequator, how much time you spend
(08:14):
in the sun, the time of day youspend in the sun, and whether
or not you have enoughcholesterol.
To begin with and this ispotentially a problem with
people on statin drugs, wheretheir cholesterol levels go too
low they start to run out ofmaterial to make vitamin D and
other hormones like cortisol andreproductive hormones.
So adequate sun exposure is key.
(08:36):
Then you need a healthy liverto take that parent cholesterol
compound called calciferol andthen convert that into the
25-hydroxyprohormone.
And while most of your cellshave a small capacity to make
25-hydroxyvitamin D locally, thevast majority of this does come
from the liver.
(08:58):
And once you create this25-hydroxy second product, or
the prohormone, then you need ahealthy kidney system to make
the final end product, which isthe biologically active
125-dihydroxyvitamin D thatbinds to the vitamin D receptors
in your cells.
Now remember, these vitamin Dreceptors live in all of your
(09:22):
cells.
They live inside your cells'nuclei, in the very same place
where you have receptors forthyroid and reproductive
hormones.
And when the active form ofvitamin D binds to the vitamin D
receptor, it turns on and offspecific genes in different
patterns to modulate and controlhow your vitamin D gets
(09:43):
expressed, to modulate andcontrol how your vitamin D gets
expressed.
And so vitamin D functionalityis critical to core cellular
function and to control yourgenetic expression.
And again, this process is sunto skin, to liver, to kidneys.
And then the active form goesinto your cells, binds to the
vitamin D receptor in thenucleus and controls your genes.
(10:04):
That makes the proteins, thatallows your cells to do their
jobs.
And if we want to know what ourvitamin D status is, the best
option is to actually measurethe 25-hydroxy version, the
pro-hormone, which tells us moreabout deficiency or
insufficiency than if we were tomeasure the active
(10:24):
125-dihydroxy version.
We get more information frommeasuring the pro-hormone than
we ever could from actuallymeasuring the active metabolite.
So let's talk about optimallevels and intake.
Since there are two metaboliteforms of vitamin D the 25 and
(10:45):
the 125, there are two tests tomeasure vitamin D status.
So we can either measure the25-hydroxyprohormone or the
active 125-dihydroxyversion, andthere's some disagreement as to
whether to test just one or theother or both, and people have
their favorites.
Of course, some providers willsay that well, since the 125
(11:08):
version is the active metabolite, then that's the one that we
should be looking at, and youknow there's some merit to that
thought.
After all, like when I look atsomeone's thyroid, I want to see
the whole picture, butultimately I want to focus on
what's called free T3, which isthe hormone that acts on the
thyroid receptors inside thenucleus to create thyroid
(11:28):
function.
And I don't mean thyroid glandfunction, I'm thinking cells,
how they function in response tothyroid hormone exposure.
But the problem is in measuringthe active 125, there's some
limitations here.
One of the main issues is thatthis active 125 version has a
much shorter half-life than theprecursor 25 hydroxy version and
(11:53):
, as a general rule, labs liketo measure things that are more
chemically stable, things thathave longer half-lives, which
allows them to give docs like memore accurate and more reliable
assessments, which is what Ilike as a clinician so, and I'm
not going to spend too much timeon this.
But here's a quick list of whymeasuring the active 125 vitamin
(12:14):
D version is perhaps not themost useful thing to do.
Number one the 125-hydroxyversion.
The active metabolite is foundin blood in very, very low
concentrations, which means thatlabs need even more specialized
technology and measurementstrategies to measure them
(12:37):
accurately.
Like if we compare the size ofhow much 25-hydroxy pro-hormone
is circulating in the bloodcompared to the amount of the
125-dihydroxy, the pro-hormonepool is roughly 2,000 times
larger than the size of theactive 125 metabolites.
(12:59):
Than the size of the active 125metabolites, it's simply harder
to measure things that arepresent in only such small
quantities.
So that's a problem, and weknow from studies that different
techniques measuring even thesame blood samples when they're
measuring the 125 version willactually give us different
results and unfortunately, theavailable techniques we have are
(13:21):
known through research tosuffer from poor sensitivity and
specificity.
And, to add insult to injury,we don't even have standardized
reference materials to reallyestablish what we should be
comparing these numbers toanyways.
Another problem and this gets alittle bit more sciencey, but
(13:41):
the 125 biologically activeversion is what we call
lipophilic, meaning it mixeswith fat.
It doesn't mix well with water.
Technically, that makes it moredifficult to measure, and on
top of that, the active 125version has a very short
half-life of only a few hours,versus the 25 hydroxyprohormone,
(14:04):
which has a half-life ofseveral days.
It's just easier to measurethings that hang around longer.
And so, and finally, let mejust kind of put this to rest
here Since the active metabolite, the 125 version, these levels
are very tightly regulated byparathyroid hormone levels,
which in turn is regulated bycalcium and also the parent
(14:28):
vitamin D, calciferol.
The active metabolite, the 125version, the levels that we can
measure actually has little orno relationship to our stores of
vitamin D and therefore wecan't really use the 125 version
as an accurate way to determinewhether or not we have a
(14:50):
vitamin D deficiency,sufficiency, or whether or not
the levels are optimized.
Now, having said that, if you'reinterested in measuring your
125 active vitamin D, there'snothing wrong with that, but you
should never do that withoutalso checking your 25 hydroxy
pro-hormone levels.
(15:10):
It's not an either or do itthis one or that one.
It always starts with measuringthe 25 hydroxy pro-hormone
version, and if you want to thenadd the 125 active metabolite
version, there's nothing wrongwith it.
Here's an illustration of whyit would be wrong to just
measure the 125.
If you measure the active 125version alone and let's say you
(15:35):
decide that you can trust thenumber the lab gives you and the
reference range that they'reusing, you don't know if that
low active level is because theprecursor pool of 25-hydroxy is
too low and you simply don'thave enough of what you should
(15:57):
start with to make what you'remeasuring.
Or you don't know if you'revitamin D sufficient, meaning
you have a lot of 25-hydroxyavailable, but the problem is
with how your kidneys areconverting that into the active
form.
You can't tell if all you'remeasuring is the active
metabolite, and I think that theonly utility in measuring the
125-hydroxy vitamin D is whenyou do it in conjunction with
(16:19):
the 25-hydroxy precursorpro-home version, pro-hormone
version, and, ideally, whenyou're also checking it with
your labs, looking at liverfunction and kidney function,
then, and only then, do I thinkyou start to see the whole
picture.
Now there's one final issue tosort out before we close this
(16:40):
episode, and that is what arethe optimal levels of vitamin D
and how do you get there if yourlevels are too low?
Well, if you compare what mostlabs say or what they define as
vitamin D deficiency, and if youread the medical research, and
then if you ask clinicians whoactually have experience testing
and supporting vitamin D withreal people who have real
(17:03):
problems, you start to see somedisagreement and discordance.
Most labs use the levelsreported in research done many
years ago by a guy named GrantHollick, where he said that
deficiency doesn't happen untilthe 25 hydroxy versions go below
30.
Yet a quick search of PubMedand the National Library of
(17:25):
Medicine will easily show moreupdated research says that
anything below 50 is adeficiency, and most functional
medicine practitioners that Iknow that I consider to be good
clinicians.
As a group we kind of thinkthat optimal levels for the
general population should besomewhere between 70 and 90.
(17:46):
And again, this is the 25hydroxy version being measured
in standard units of nanogramsper milliliter, not metric units
of nanomoles per liter, and youcan count.
You can go online and justconvert them between the two.
But very simply, you can gofrom US units to metric units by
multiplying by two and a half.
(18:06):
So, for example, if yourvitamin E level is 10, your
metric versions would be 25.
If it's 100, it would be 250.
Or you can go the otherdirection you can take your
metric units and divide it bytwo and a half and you'll get
the US standard units.
But this guideline of vitamin Dbeing between 70 and 90 changes
(18:28):
when someone has an activeautoimmune issue or if they're
chronically ill, chronicallyinflamed.
In those cases, I and otherlike-minded docs like to see the
25-hydroxyvitamin D versioncloser to 100.
And listen, it's okay if yourlevels go above that, as long as
your calcium levels stay normal.
(18:49):
And in fact, let me addressthis crazy notion that if your
vitamin D is like 103 or if it'sbarely just a smidge above the
lab range, that your vitamin Dtoxic and you need to stop
taking it or else something badis going to happen.
Like my personal coachingclients hear this nonsense from
their medical doctors all thetime and it just tells me that
(19:11):
these MDs don't understandvitamin D at all.
So let me be very clear.
What is vitamin D toxicity?
It is hypercalcemia period,like anyone who takes way too
much vitamin D and ends up inthe ER because they've had some
kind of a toxic reaction.
It's because massive amounts ofvitamin D can cause calcium to
(19:31):
go too high, which won't killyou, but you're going to feel
like you're dying and you'regoing to call 911 and end up in
the ER.
And the ER will either tell youjust simply stop taking vitamin
C, drink plenty of water andyou're going to be fine, or, if
your calcium is high enough,then they'll give you some
medications to bring it downfurther and faster until you
(19:52):
stabilize.
And in fact, there are ahandful of case reports in the
medical literature that addressthis and in every single case
report, people who are quoteunquote vitamin D toxic were
taking millions of IUs ofvitamin D because of a product
mislabeling.
And that's what got them intotrouble, because they were
(20:13):
taking like literally millionsof IUs of vitamin D when the RDA
is like 400 IUs.
These people were takingmillions every day and in every
case they were hypercalcemic,their calcium went too high and
their symptoms resolved oncetheir calcium levels came back
to normal.
So unless you're buying yourvitamin D from a spurious or a
(20:38):
non-trusted source, and as longas your intake isn't in the sky
high range and, most importantly, as long as your calcium levels
are normal, then you're notvitamin D toxic, even if your
lab says that your 25 hydroxy isabove the lab range.
It's just that simple, all right, two final points.
(20:59):
First, I mentioned this earlier.
Since vitamin D is afat-soluble vitamin, we know
that its absorption is enhancedeither by taking a vitamin D
supplement with a fatty meal or,perhaps better yet, using a
supplement where the vitamin Dis in some kind of a fat or an
oil base.
The one that I use with mypersonal coaching clients is in
(21:22):
a base of MCT oil, which isderived from coconuts.
In this case, I also like touse a liquid form that can be
used sublingually under thetongue, and the combination of
vitamin D in a base of healthyfat like MCT oil and being held
under the tongue beforeswallowed, will typically help
improve vitamin D status morethan a poorly formulated product
(21:46):
and not taking it with somekind of a fat.
So how much do you need?
Well, honestly, it depends, andI'm sure you probably knew I
would say that, but I can't giveyou a vitamin D dose that's
going to work for everyone.
In fact, I can have two clientsstarting with the same low
level of vitamin D.
Give them the same dose of thesame formula and measure their
vitamin D levels eight weekslater, and one will have their
(22:11):
vitamin D levels improvedramatically and the others will
have barely moved.
And so proper dosing depends onwhere you're starting from.
How low is your starting pointdepends on what your target is,
of course, combined with otherfactors like how much you might
store in body fat or how activeyour immune system is.
(22:35):
So it's easier to raise vitaminD levels in leaner people, who
have less body fat, who havemore stable immune systems, who
are less inflamed, as comparedto someone, say, with
Hashimoto's or any otherautoimmune reactivity, who has
more body fat and is moreimmunologically unstable, who's
(22:56):
always getting flared up andthey're always inflamed.
Immunologically unstable who'salways getting flared up and
they're always inflamed.
Those people are going to havetwo very different responses to
the same dose of the samesupplement, but I'll say that as
a general rule, once you getyour vitamin D levels to where
you want them to be.
You can generally keep themthere with a daily intake of
anywhere from 6,000 to 10,000IUs per day.
(23:17):
Again, it just depends on theirmetabolic state and other
factors.
Some people we can keep theirlevels normal or optimal with
6,000.
Others they have to go to 10.
Everyone's a little bitdifferent.
And ignore the 400 IU RDA.
That's ridiculous.
In fact, we often joke that RDAstands for the ridiculously
(23:42):
dumb amount and maybe I'll do aseparate podcast on that someday
.
All right, that's it forvitamin D.
I'll be back soon with our nextmiracle molecule, right here on
the Information Nation podcast.
This podcast is for generalinformational and educational
purposes only and does notconstitute the practice of
medicine in any form or capacity.
(24:04):
No doctor-patient relationshipis formed.
The use of the information inthis podcast or any materials
associated with or linked to thepodcast is at the listener's
own risk.
The content of this podcast isnot intended to be a substitute
for professional andpersonalized medical advice,
diagnosis or treatment, andlisteners should not disregard
(24:27):
or delay obtaining propermedical advice when a health
condition exists and warns them.
And finally, functionalmedicine is not intended or
designed to treat disease, butrather is a natural approach to
support restoring health andwellness.
The use of diet and lifestylemodifications and nutritional
supplementation is supportivefor adjunctive care.
Hey everyone, welcome to the Inflammation Nation
podcast.
I'm your host, Dr SteveNoseberg.
Speaker 2 (00:08):
One of the greatest obstacles to crafting health and
wellness is identifying andcontrolling inflammation.
It's at the core of all complexand chronic diseases and it's
the driving mechanism thatunderlies the most common
symptoms that people like youstruggle to overcome.
Join us as we explorecutting-edge science and
research to give you theinformation and tools you need
to create the quality of lifeyou want and deserve.
(00:30):
And now here is the host ofInflammation Nation, dr Stephen
Noseworthy.
Speaker 1 (00:37):
Hey guys, we're back with part two of our discussion
about vitamin D as the nextmiracle molecule in this little
mini-series, and in part one youmight want to go back and
listen to that if you're justjumping into this episode we
talked about, you know, what isa vitamin, what is a hormone?
And is vitamin D a vitamin oris it actually a hormone, like
(00:58):
many people say?
And the answer is it's both.
If you look at the definitionsof those compounds, it's clearly
can be classified as either one, and we talked about some of
the differences between vitaminD2 and vitamin D3.
And we also made a distinctionbetween the 25-hydroxy version,
(01:19):
which is the one that we're allmeasuring or at least we should
be which is actually a precursorhormone, and that has to be
converted into the 125 dihydroxyversion, which is the active
metabolite, and we'll come backto that.
But I want to tell you just alittle bit of history, like we
can go back in what we know, forexample, back in the let's say
(01:43):
it was the advent of theindustrial revolution, say a
couple hundred years ago.
What ended up happening with,with the evolution of industry
and machinery andstandardization of manufacturing
facilities?
Um, what happened was peoplewho lived in the rural, in the
country settings, started in inthe European communities.
(02:05):
They started moving into citiesto get jobs and as more and
more people came into thesecities, the cities built more
houses or housing complexes forthe increasing population.
They also started makingmanufacturing facilities and
plants that used machinery thatburned fuel sources that
(02:27):
increased the level of pollutionin these communities.
And all of these things had theeffect of like, for example,
taller buildings that werecrowded close together with a
pall of smog or pollution in theair basically filtered out the
sun and as a result, shortlyafter the onset of the
(02:49):
Industrial Revolution, there wasa massive increase in vitamin
D-related diseases, particularlyrickets, which is a
bone-related vitamin D diseasewhere calcium doesn't go into
the bones, bones become soft andthey bow under the weight of
someone's body.
So I think it's kind ofimportant to recognize that
(03:11):
number one.
We can make vitamin D from sunexposure, but we need to have
adequate sun exposure.
Now I've been measuring vitaminD with my clients as a routine
part of my initial analysis andsubsequent follow-ups for a
couple of decades now.
It's just part of how I assesssomebody's fundamental
(03:32):
physiology, and I have a lot ofclients in very sunny areas and
they tell me yeah, I spendplenty of time outdoors, but
routinely the only people that Ido my initial vitamin D
assessments on that actuallyhave adequate levels of vitamin
D are people who are takingsupplements, even though they
might live in sunny places andspend what they think is an
(03:52):
adequate amount of time outdoors.
And so I want you to considerthat if you live in a sunny
place and you spend timeoutdoors, you may or may not
have adequate vitamin D levels.
Don't guess, always check.
I mean that's kind of acatchphrase in our levels.
Don't guess, always check.
I mean that's kind of acatchphrase in our world.
It's like, let's test, let'snot guess.
But estimates are that, allother things being equal meaning
(04:14):
say, no interfering factors,that we can or have the
potential to make about 90% ofthe vitamin D that we need just
from the sun.
We also get vitamin D from ourdiet, and so vitamin D occurs
naturally in fatty and oily fishsuch as, say, trout, salmon,
swordfish, sardines, mackerel.
(04:35):
You can also find vitamin D inegg yolks and most of your red
meats, and particularly in organmeats, specifically liver, and
there are plant sources ofvitamin D, but this is mostly
the vitamin D2 version, which isless bioavailable, less
absorbable than the vitamin D3.
That comes from the animalsources right, and you can again
(04:57):
, you can get vitamin D fromfungi and algae, but it's just
not as good as the stuff thatyou're going to get from the
animal sources.
A vitamin D is one of fourdifferent fat-soluble vitamins
right, vitamins A, d, e and Kand while vitamin D absorbs
passively from your gut into thebloodstream, it tends to work
(05:17):
better when you take vitamin Dwith fats.
So if you're eating fatty foodsthat have vitamin D in it,
absorption happens very easily.
If you're taking it foods thathave vitamin D in it, absorption
happens very easily.
If you're taking it with asupplement, then it helps to
have it with a fatty meal, forexample.
We'll come back to this towardsthe end of the episode, but the
main way that we get vitamin Dis through adequate sun exposure
.
At least that's the way it'sdesigned to be.
(05:40):
And, again, assuming nointerference, your skin can make
upwards of about 10,000 IUs ofvitamin D every day, and that's
a decent dose, right, but that'swithout any interfering factors
.
For example, if your skin toneis lighter, you will likely make
(06:00):
more vitamin D from the sunthan if you are darker
complected, people with darkercomplexions need more time in
the sun than if you are darkercomplected.
People with darker complexionsneed more time in the sun to get
the same amount of vitamin Dproduction that someone who has
fairer skin.
If you live in a higherlatitude, if you live in more
northern climates, you're goingto make less vitamin D from the
sun.
So if you live near the equator, it's easier to make vitamin D
(06:23):
than if you live, say, in Swedenor Norway.
And also the time of day a sunexposure can make a difference,
like the optimal time to getvitamin D from your skin is
between 10 am and 3 pm, which,of course, is the very time that
dermatologists warn that weshould stay away from the sun.
So how do we actually makevitamin D from the sun?
(06:44):
Well, it's a multi-step processthat requires, number one,
adequate sun exposure.
Number two, adequatecholesterol as a base molecule,
as well as healthy liver andkidney systems.
So here's the process in anutshell when you have adequate
sun exposure, it triggers yourskin cells to trap cholesterol
(07:07):
and then use an enzyme toconvert cholesterol into the
parent vitamin D calledcalciferol.
So the first thing to rememberis that vitamin D number one is
made from cholesterol and stepnumber one happens in the skin
when we expose our skin toadequate sunlight.
Step number two, then, is wherewe take this parent form of
(07:29):
calciferol, the parent vitamin D, and we move that to the liver,
where the liver uses anotherenzyme to convert this parent
calciferol into the pro-hormone,the 25-hydroxyvitamin D Now
remember, this is a pro-hormone.
The 25-hydroxy vitamin D Now,remember, this is a pro-hormone,
it's not biologically activeand it has to be converted in
(07:51):
one more step to the125-dihydroxy version, and this
happens in the kidneys.
So, if you flow through theprocess, here is what you need
to make most of your vitamin D.
Number one adequate sunexposure at key times of the day
, and what is adequate is goingto depend on your skin tone,
where you live relative to theequator, how much time you spend
(08:14):
in the sun, the time of day youspend in the sun, and whether
or not you have enoughcholesterol.
To begin with and this ispotentially a problem with
people on statin drugs, wheretheir cholesterol levels go too
low they start to run out ofmaterial to make vitamin D and
other hormones like cortisol andreproductive hormones.
So adequate sun exposure is key.
(08:36):
Then you need a healthy liverto take that parent cholesterol
compound called calciferol andthen convert that into the
25-hydroxyprohormone.
And while most of your cellshave a small capacity to make
25-hydroxyvitamin D locally, thevast majority of this does come
from the liver.
(08:58):
And once you create this25-hydroxy second product, or
the prohormone, then you need ahealthy kidney system to make
the final end product, which isthe biologically active
125-dihydroxyvitamin D thatbinds to the vitamin D receptors
in your cells.
Now remember, these vitamin Dreceptors live in all of your
(09:22):
cells.
They live inside your cells'nuclei, in the very same place
where you have receptors forthyroid and reproductive
hormones.
And when the active form ofvitamin D binds to the vitamin D
receptor, it turns on and offspecific genes in different
patterns to modulate and controlhow your vitamin D gets
(09:43):
expressed, to modulate andcontrol how your vitamin D gets
expressed.
And so vitamin D functionalityis critical to core cellular
function and to control yourgenetic expression.
And again, this process is sunto skin, to liver, to kidneys.
And then the active form goesinto your cells, binds to the
vitamin D receptor in thenucleus and controls your genes.
(10:04):
That makes the proteins, thatallows your cells to do their
jobs.
And if we want to know what ourvitamin D status is, the best
option is to actually measurethe 25-hydroxy version, the
pro-hormone, which tells us moreabout deficiency or
insufficiency than if we were tomeasure the active
(10:24):
125-dihydroxy version.
We get more information frommeasuring the pro-hormone than
we ever could from actuallymeasuring the active metabolite.
So let's talk about optimallevels and intake.
Since there are two metaboliteforms of vitamin D the 25 and
(10:45):
the 125, there are two tests tomeasure vitamin D status.
So we can either measure the25-hydroxyprohormone or the
active 125-dihydroxyversion, andthere's some disagreement as to
whether to test just one or theother or both, and people have
their favorites.
Of course, some providers willsay that well, since the 125
(11:08):
version is the active metabolite, then that's the one that we
should be looking at, and youknow there's some merit to that
thought.
After all, like when I look atsomeone's thyroid, I want to see
the whole picture, butultimately I want to focus on
what's called free T3, which isthe hormone that acts on the
thyroid receptors inside thenucleus to create thyroid
(11:28):
function.
And I don't mean thyroid glandfunction, I'm thinking cells,
how they function in response tothyroid hormone exposure.
But the problem is in measuringthe active 125, there's some
limitations here.
One of the main issues is thatthis active 125 version has a
much shorter half-life than theprecursor 25 hydroxy version and
(11:53):
, as a general rule, labs liketo measure things that are more
chemically stable, things thathave longer half-lives, which
allows them to give docs like memore accurate and more reliable
assessments, which is what Ilike as a clinician so, and I'm
not going to spend too much timeon this.
But here's a quick list of whymeasuring the active 125 vitamin
(12:14):
D version is perhaps not themost useful thing to do.
Number one the 125-hydroxyversion.
The active metabolite is foundin blood in very, very low
concentrations, which means thatlabs need even more specialized
technology and measurementstrategies to measure them
(12:37):
accurately.
Like if we compare the size ofhow much 25-hydroxy pro-hormone
is circulating in the bloodcompared to the amount of the
125-dihydroxy, the pro-hormonepool is roughly 2,000 times
larger than the size of theactive 125 metabolites.
(12:59):
Than the size of the active 125metabolites, it's simply harder
to measure things that arepresent in only such small
quantities.
So that's a problem, and weknow from studies that different
techniques measuring even thesame blood samples when they're
measuring the 125 version willactually give us different
results and unfortunately, theavailable techniques we have are
(13:21):
known through research tosuffer from poor sensitivity and
specificity.
And, to add insult to injury,we don't even have standardized
reference materials to reallyestablish what we should be
comparing these numbers toanyways.
Another problem and this gets alittle bit more sciencey, but
(13:41):
the 125 biologically activeversion is what we call
lipophilic, meaning it mixeswith fat.
It doesn't mix well with water.
Technically, that makes it moredifficult to measure, and on
top of that, the active 125version has a very short
half-life of only a few hours,versus the 25 hydroxyprohormone,
(14:04):
which has a half-life ofseveral days.
It's just easier to measurethings that hang around longer.
And so, and finally, let mejust kind of put this to rest
here Since the active metabolite, the 125 version, these levels
are very tightly regulated byparathyroid hormone levels,
which in turn is regulated bycalcium and also the parent
(14:28):
vitamin D, calciferol.
The active metabolite, the 125version, the levels that we can
measure actually has little orno relationship to our stores of
vitamin D and therefore wecan't really use the 125 version
as an accurate way to determinewhether or not we have a
(14:50):
vitamin D deficiency,sufficiency, or whether or not
the levels are optimized.
Now, having said that, if you'reinterested in measuring your
125 active vitamin D, there'snothing wrong with that, but you
should never do that withoutalso checking your 25 hydroxy
pro-hormone levels.
(15:10):
It's not an either or do itthis one or that one.
It always starts with measuringthe 25 hydroxy pro-hormone
version, and if you want to thenadd the 125 active metabolite
version, there's nothing wrongwith it.
Here's an illustration of whyit would be wrong to just
measure the 125.
If you measure the active 125version alone and let's say you
(15:35):
decide that you can trust thenumber the lab gives you and the
reference range that they'reusing, you don't know if that
low active level is because theprecursor pool of 25-hydroxy is
too low and you simply don'thave enough of what you should
(15:57):
start with to make what you'remeasuring.
Or you don't know if you'revitamin D sufficient, meaning
you have a lot of 25-hydroxyavailable, but the problem is
with how your kidneys areconverting that into the active
form.
You can't tell if all you'remeasuring is the active
metabolite, and I think that theonly utility in measuring the
125-hydroxy vitamin D is whenyou do it in conjunction with
(16:19):
the 25-hydroxy precursorpro-home version, pro-hormone
version, and, ideally, whenyou're also checking it with
your labs, looking at liverfunction and kidney function,
then, and only then, do I thinkyou start to see the whole
picture.
Now there's one final issue tosort out before we close this
(16:40):
episode, and that is what arethe optimal levels of vitamin D
and how do you get there if yourlevels are too low?
Well, if you compare what mostlabs say or what they define as
vitamin D deficiency, and if youread the medical research, and
then if you ask clinicians whoactually have experience testing
and supporting vitamin D withreal people who have real
(17:03):
problems, you start to see somedisagreement and discordance.
Most labs use the levelsreported in research done many
years ago by a guy named GrantHollick, where he said that
deficiency doesn't happen untilthe 25 hydroxy versions go below
30.
Yet a quick search of PubMedand the National Library of
(17:25):
Medicine will easily show moreupdated research says that
anything below 50 is adeficiency, and most functional
medicine practitioners that Iknow that I consider to be good
clinicians.
As a group we kind of thinkthat optimal levels for the
general population should besomewhere between 70 and 90.
(17:46):
And again, this is the 25hydroxy version being measured
in standard units of nanogramsper milliliter, not metric units
of nanomoles per liter, and youcan count.
You can go online and justconvert them between the two.
But very simply, you can gofrom US units to metric units by
multiplying by two and a half.
(18:06):
So, for example, if yourvitamin E level is 10, your
metric versions would be 25.
If it's 100, it would be 250.
Or you can go the otherdirection you can take your
metric units and divide it bytwo and a half and you'll get
the US standard units.
But this guideline of vitamin Dbeing between 70 and 90 changes
(18:28):
when someone has an activeautoimmune issue or if they're
chronically ill, chronicallyinflamed.
In those cases, I and otherlike-minded docs like to see the
25-hydroxyvitamin D versioncloser to 100.
And listen, it's okay if yourlevels go above that, as long as
your calcium levels stay normal.
(18:49):
And in fact, let me addressthis crazy notion that if your
vitamin D is like 103 or if it'sbarely just a smidge above the
lab range, that your vitamin Dtoxic and you need to stop
taking it or else something badis going to happen.
Like my personal coachingclients hear this nonsense from
their medical doctors all thetime and it just tells me that
(19:11):
these MDs don't understandvitamin D at all.
So let me be very clear.
What is vitamin D toxicity?
It is hypercalcemia period,like anyone who takes way too
much vitamin D and ends up inthe ER because they've had some
kind of a toxic reaction.
It's because massive amounts ofvitamin D can cause calcium to
(19:31):
go too high, which won't killyou, but you're going to feel
like you're dying and you'regoing to call 911 and end up in
the ER.
And the ER will either tell youjust simply stop taking vitamin
C, drink plenty of water andyou're going to be fine, or, if
your calcium is high enough,then they'll give you some
medications to bring it downfurther and faster until you
(19:52):
stabilize.
And in fact, there are ahandful of case reports in the
medical literature that addressthis and in every single case
report, people who are quoteunquote vitamin D toxic were
taking millions of IUs ofvitamin D because of a product
mislabeling.
And that's what got them intotrouble, because they were
(20:13):
taking like literally millionsof IUs of vitamin D when the RDA
is like 400 IUs.
These people were takingmillions every day and in every
case they were hypercalcemic,their calcium went too high and
their symptoms resolved oncetheir calcium levels came back
to normal.
So unless you're buying yourvitamin D from a spurious or a
(20:38):
non-trusted source, and as longas your intake isn't in the sky
high range and, most importantly, as long as your calcium levels
are normal, then you're notvitamin D toxic, even if your
lab says that your 25 hydroxy isabove the lab range.
It's just that simple, all right, two final points.
(20:59):
First, I mentioned this earlier.
Since vitamin D is afat-soluble vitamin, we know
that its absorption is enhancedeither by taking a vitamin D
supplement with a fatty meal or,perhaps better yet, using a
supplement where the vitamin Dis in some kind of a fat or an
oil base.
The one that I use with mypersonal coaching clients is in
(21:22):
a base of MCT oil, which isderived from coconuts.
In this case, I also like touse a liquid form that can be
used sublingually under thetongue, and the combination of
vitamin D in a base of healthyfat like MCT oil and being held
under the tongue beforeswallowed, will typically help
improve vitamin D status morethan a poorly formulated product
(21:46):
and not taking it with somekind of a fat.
So how much do you need?
Well, honestly, it depends, andI'm sure you probably knew I
would say that, but I can't giveyou a vitamin D dose that's
going to work for everyone.
In fact, I can have two clientsstarting with the same low
level of vitamin D.
Give them the same dose of thesame formula and measure their
vitamin D levels eight weekslater, and one will have their
(22:11):
vitamin D levels improvedramatically and the others will
have barely moved.
And so proper dosing depends onwhere you're starting from.
How low is your starting pointdepends on what your target is,
of course, combined with otherfactors like how much you might
store in body fat or how activeyour immune system is.
(22:35):
So it's easier to raise vitaminD levels in leaner people, who
have less body fat, who havemore stable immune systems, who
are less inflamed, as comparedto someone, say, with
Hashimoto's or any otherautoimmune reactivity, who has
more body fat and is moreimmunologically unstable, who's
(22:56):
always getting flared up andthey're always inflamed.
Immunologically unstable who'salways getting flared up and
they're always inflamed.
Those people are going to havetwo very different responses to
the same dose of the samesupplement, but I'll say that as
a general rule, once you getyour vitamin D levels to where
you want them to be.
You can generally keep themthere with a daily intake of
anywhere from 6,000 to 10,000IUs per day.
(23:17):
Again, it just depends on theirmetabolic state and other
factors.
Some people we can keep theirlevels normal or optimal with
6,000.
Others they have to go to 10.
Everyone's a little bitdifferent.
And ignore the 400 IU RDA.
That's ridiculous.
In fact, we often joke that RDAstands for the ridiculously
(23:42):
dumb amount and maybe I'll do aseparate podcast on that someday
.
All right, that's it forvitamin D.
I'll be back soon with our nextmiracle molecule, right here on
the Information Nation podcast.
This podcast is for generalinformational and educational
purposes only and does notconstitute the practice of
medicine in any form or capacity.
(24:04):
No doctor-patient relationshipis formed.
The use of the information inthis podcast or any materials
associated with or linked to thepodcast is at the listener's
own risk.
The content of this podcast isnot intended to be a substitute
for professional andpersonalized medical advice,
diagnosis or treatment, andlisteners should not disregard
(24:27):
or delay obtaining propermedical advice when a health
condition exists and warns them.
And finally, functionalmedicine is not intended or
designed to treat disease, butrather is a natural approach to
support restoring health andwellness.
The use of diet and lifestylemodifications and nutritional
supplementation is supportivefor adjunctive care.
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