Speaker 1: This particular illness started in late December twenty fifteen, and
Speaker 1: the first thing I noticed was some unexplained weight loss,
Speaker 1: which I only noticed because I had had any illness
Speaker 1: about six years prior. That also started with some weight loss,
Speaker 1: and so I was a little bit worried. But I
Speaker 1: felt fine so far. But then a few days after that,
Speaker 1: I started getting really really thirsty. And it started with
Speaker 1: just a really dry throat, but before long it became
Speaker 1: a really deep thirst and I just returned from a
Speaker 1: family visit. So one friend suggested that maybe I was
Speaker 1: dehydrated from being on the plane. But it didn't go
Speaker 1: away no matter how much I drank, and I started
Speaker 1: keeping track of how much I drank, and for the
Speaker 1: next little while it was just between one and two
Speaker 1: gallons of water every day. I just could not get
Speaker 1: enough water. After a while, I also started craving salt.
Speaker 1: I wanted chips, pickles, everything salty that I could get,
Speaker 1: which was a little bit unusual, which was probably due
Speaker 1: to all the water I was drinking. So as things
Speaker 1: went along, things just started adding to that. You know,
Speaker 1: with all the water drinking, I had some bathroom trips.
Speaker 1: It was hard to concentrate my head felt really heavy,
Speaker 1: I was sleepy. My sleep actually was all over the place.
Speaker 1: Sometimes I had insomnia and sometimes I couldn't get enough sleep,
Speaker 1: but no matter how much I slept, it didn't help.
Speaker 1: Eventually I started developing I think they're called hipnick jerks,
Speaker 1: which is if you've had this, you'll know right as
Speaker 1: you're falling asleep, all your muscles just jerk. It kind
Speaker 1: of feels like you're falling. And that started happening almost
Speaker 1: every time I went to sleep. I just felt really
Speaker 1: unwell all the time, and I could not get energy
Speaker 1: no matter what I did, And eventually it got to
Speaker 1: the point where it was hard to stand for more
Speaker 1: than about fifteen minutes. It just felt like my legs
Speaker 1: were going to give up. They wouldn't support me anymore.
Speaker 1: If I didn't sit down right away, I would have
Speaker 1: staring spells because just my mind couldn't get enough energy
Speaker 1: to figure out the steps for the tasks. One time,
Speaker 1: it took me almost half an hour to figure out
Speaker 1: how to make a salad. And by make a salad,
Speaker 1: I mean getting a bag of salad out of the
Speaker 1: fridge and pouring it into a bowl and putting dressing
Speaker 1: on it. And eating it. Eating was really hard. Sometimes
Speaker 1: I didn't feel like it. I had no appetite. Sometimes
Speaker 1: I forgot Sometimes, like with the salad example, I just
Speaker 1: couldn't get enough energy. I couldn't figure it out. And
Speaker 1: then there were other times where I would have bursts
Speaker 1: of hunger and I just would eat everything I could
Speaker 1: get to. I had to nap in my car after
Speaker 1: work after I got home, before I went into the house.
Speaker 1: Sometimes I had to completely stay home from work and
Speaker 1: just rest. Sometimes on the way home from work, I
Speaker 1: would be in tears just from how tired I was.
Speaker 1: I think the worst night I remember it was towards
Speaker 1: the end of January and I was with some friends
Speaker 1: and getting ready to go home, and I just suddenly
Speaker 1: lost all my energy. I had to sit down because
Speaker 1: my legs were giving out. One of my friends helped
Speaker 1: me walk because I couldn't walk into straight line, and
Speaker 1: we took an elevator down. Still had to rest, sit
Speaker 1: down on sidewalk and rest on the way to the
Speaker 1: parking lot. And I stayed at their house that night.
Speaker 1: And that was the first time I had muscle spasms
Speaker 1: and they were in my chest and.
Speaker 2: That was scary. But we figured out.
Speaker 1: It was just muscle spasms. The worst part was that
Speaker 1: I didn't know what was going on. It was scary.
Speaker 1: It felt like my body was going to start shutting
Speaker 1: down and I didn't know why, and that was the
Speaker 1: worst part. The fatigue was just bone deep weariness. One day,
Speaker 1: I caught myself in the mirror as I was walking by.
Speaker 1: And I was in my thirties at this point, but
Speaker 1: I looked at myself in the mirror and I was
Speaker 1: walking hunched over and slow, as if I were really old.
Speaker 1: I had to take the stairs one at a time
Speaker 1: with both feet like a toddler. I started wondering if
Speaker 1: I would eventually get to the point where I wasn't
Speaker 1: able to function at all and had to have full
Speaker 1: time care or something. And I was starting to wonder
Speaker 1: about what kind of plans I would have to make,
Speaker 1: like if I would have to move, who would take
Speaker 1: care of me, what my life would be like if
Speaker 1: it changed that drastically. Emotionally, I was a wreck from
Speaker 1: the fear and not knowing it was just physical and
Speaker 1: emotional exhaustion. All in all, I was sick for about
Speaker 1: three months, but in the beginning of January, probably about
Speaker 1: a week or two into feeling sick, I had gone
Speaker 1: to the doctor and they did a basic blood test.
Speaker 1: It came back and everything was normal except for low
Speaker 1: vitamin D and low sodium, and because low sodium is
Speaker 1: life threatening, the doctor rightfully concentrated on that, and I
Speaker 1: think it was because of all the water had been drinking.
Speaker 1: I just flushed all the sodium out, so the doctor
Speaker 1: put me on a water restriction. I could only drink
Speaker 1: about I think it was about eighty ounces of water
Speaker 1: a day, and that added to the emotional toll because
Speaker 1: I was still very thirsty. But because of the low
Speaker 1: so sodium, the doctor didn't tell me anything about the
Speaker 1: vitamin D. Eventually I changed doctors about a month later
Speaker 1: this so this was about the middle of February. By
Speaker 1: this point, that doctor didn't have any answers, but did
Speaker 1: notice the low vitamin D test results from before and
Speaker 1: gave me a prescription. That doctor also sent me to
Speaker 1: a neurologist where I got tested for everything from vitamin
Speaker 1: B deficiency to multiple sclerosis. Every single test came back normal.
Speaker 1: But while I was having all this testing, I had
Speaker 1: started the vitamin D prescription, and within one day I
Speaker 1: noticed a difference and started feeling better after all of
Speaker 1: the testing came back normal, but because I was feeling better,
Speaker 1: they just decided that that must have been the issue.
Speaker 1: And I have just been really careful about my vitamin
Speaker 1: D levels up things have been okay since then. I
Speaker 1: should mention your vitamin D should be at about thirty
Speaker 1: and on that first blood test in January, my levels
Speaker 1: were eleven. So it took a while to get things
Speaker 1: up to where they were supposed to be again, but
Speaker 1: everything just immediately started getting better and things turned round
Speaker 1: after that. And so, like I said, I've been really
Speaker 1: careful to make sure that I take vitamin D and
Speaker 1: try to get some sunlight because I had never been
Speaker 1: so miserable before or since, and I am never going
Speaker 1: to let that happen ever again if I can control
Speaker 1: anything in my life.
Speaker 3: Wow, I mean, I honestly had no idea how many
Speaker 3: things vitamin D could affect. So thank you, Brittany for
Speaker 3: sharing your story with us.
Speaker 2: Yeah, thank you, thank you for having to relive.
Speaker 3: That awful Hi.
Speaker 2: I'm Aaron Welsh and I'm Aaron Oman Dyke.
Speaker 3: And this is this podcast will kill you.
Speaker 2: Welcome to Vitamin D Yes.
Speaker 3: The Sunshine neest of all the vita. Yeah, makes no sense.
Speaker 3: I'm not good at improv Aron, That's okay. Yeah, this
Speaker 3: is our first vitamin or vitamin deficiency topic of the season,
Speaker 3: and I always like doing these topics because I think
Speaker 3: it gets us to think about health and the history
Speaker 3: of discovery in different ways than we normally do.
Speaker 2: Agreed. I also had so many thoughts about like the
Speaker 2: evolutionary context of this hormone slash vitamin that I don't
Speaker 2: think that we'll have answers too, but I'm hoping that
Speaker 2: we can at least chat about them.
Speaker 3: Yeah, there is definitely going to be a lot to
Speaker 3: chat about. I am. I can't wait to hear what
Speaker 3: you have to say for the supplementation guidelines and whatnot.
Speaker 2: Yeah. A reminder that this is not a medical advice podcast.
Speaker 2: You're not your doctors. We're going to talk a lot
Speaker 2: about what other people have to say about supplementation. It's
Speaker 2: going to be really fun.
Speaker 3: It is. But first, should we get started.
Speaker 2: With quarantiny time?
Speaker 3: Yes, yep, yep, we should.
Speaker 2: We should. Today we're drinking Vitamin Delicious.
Speaker 3: I'm glad that you liked that one.
Speaker 2: I actually laughed out loud when you sent it.
Speaker 3: I was in my head pronouncing it vitamin delicious.
Speaker 2: Oh, that's cuter.
Speaker 3: And we had to include some source of vitamin D
Speaker 3: in this quarantiny, and I thought we should maybe stay
Speaker 3: away from things like fish liver oils and stuff like that.
Speaker 2: You didn't want to use some delicious cod liver oil
Speaker 2: in our the much higher grade of or like, you know,
Speaker 2: higher concentration of and D.
Speaker 3: I feel like it. There's a trade off there between
Speaker 3: taste and vitamin D levels, so we went with milk
Speaker 3: or cream. Vitamin delicious is basically a white.
Speaker 2: Russian fantastic delicious.
Speaker 3: Delicious, which, if you need a reminder, is cream Kalua
Speaker 3: vodka simple Delicious.
Speaker 2: We'll post the full recipe for that quarantini, as well
Speaker 2: as our non alcoholic plusy Breta on our website, This
Speaker 2: podcast will Kill You dot com and our social media channels.
Speaker 3: On our website, you can find a whole host of things.
Speaker 3: Check it out. Yeah, that's all I'm gonna say.
Speaker 2: That's fine. We're episode We're three episodes into the season.
Speaker 2: I think we're done telling people.
Speaker 3: We're already just going it.
Speaker 2: Oh, I do.
Speaker 3: I do want to point out that there is a
Speaker 3: submit your first hand account form that is new on
Speaker 3: the website that I have mentioned before. But if you
Speaker 3: need a reminder it is there, just go to this
Speaker 3: podcast will Kill You dot com.
Speaker 2: Okay, should we get started with the actual meat of
Speaker 2: this episode?
Speaker 4: I think think we should right after this break.
Speaker 2: So, vitamin D, which goes by a whole bunch of
Speaker 2: names which I'll get into in just a second, is
Speaker 2: a secosteroid or a pechosteroid. I tried really hard to
Speaker 2: figure out which the pronunciation was, and I couldn't.
Speaker 3: I like them both.
Speaker 2: I like secosteroid it feels correct, which basically just means
Speaker 2: this is a molecule that is derived from a steroid.
Speaker 2: And vitamin D happens to be both a hormone which
Speaker 2: we make ourselves. A hormone is something that gets transported
Speaker 2: in our blood to a different site of action in
Speaker 2: like a different organ and has various regulatory functions which
Speaker 2: we will get into, I promise. But vitamin D is
Speaker 2: also a vitamin, which means it's a micronutrient that is
Speaker 2: essential in our diet because we in general as a
Speaker 2: rule can't make enough of it, which I find so fun.
Speaker 2: Right off the bat, there are multiple forms of this vitamin,
Speaker 2: and all of them have to be activated prior to
Speaker 2: being hormonally active. So there's vitamin D two or ergo calciferol,
Speaker 2: which is found in plants and some fungi, and vitamin
Speaker 2: D three or cola calcipherol, which is found in animals
Speaker 2: sources like fish liver oils, for example, and is used
Speaker 2: for a lot of fortification like in our milk, and
Speaker 2: is the type of vitamin D that we make in
Speaker 2: our skin.
Speaker 3: Right off the bat. Okay, are you going to tell
Speaker 3: me the difference between these two functionally or is there
Speaker 3: a functional difference?
Speaker 2: Excellent question. There may or may not be differences, but
Speaker 2: since we're focusing on broad strokes on this podcast, practically
Speaker 2: there's not that big of a difference because both of
Speaker 2: these if we ingest or make D three or ingest
Speaker 2: D three or D two in either case, these forms
Speaker 2: both have to make it either from our guts or
Speaker 2: from our skin to our liver, where they then have
Speaker 2: to be hydroxylated into something called twenty five H vitamin D.
Speaker 2: Then they have to travel to our kidney to be
Speaker 2: converted yet again into the active metabolite, which is one
Speaker 2: twenty five die hydroxy vitamin D three aka calcid trial
Speaker 2: and that is the actual active form. So yes, there
Speaker 2: are differences between D two and D three, and there's
Speaker 2: a lot of debate in the literature as to whether, like,
Speaker 2: is it better to supplement with D two or D three,
Speaker 2: And there's not a hard and fast rule as of yet,
Speaker 2: but in general they both have to be converted by
Speaker 2: a pretty similar, if not exactly the same process, and
Speaker 2: so really not a huge difference.
Speaker 3: Okay, okay, interesting.
Speaker 2: Because no matter what, whether we're making vitamin D or
Speaker 2: ingesting it in various forms, we have to process it
Speaker 2: both in our liver and our kidney for it to
Speaker 2: be active. What is this activity of this hormone, vitamin D.
Speaker 3: That's an easy question to answer, right, so easy.
Speaker 2: It's just like really simple and straightforward. One of the
Speaker 2: most well known and important functions of calcitrial or active
Speaker 2: vitamin D. Realistically, for this episode, I'm just gonna say
Speaker 2: vitamin D one of the major functions in our bodies
Speaker 2: is its involvement in ensuring that calcium levels in our
Speaker 2: blood are maintained, and calcium, most everyone probably knows, is
Speaker 2: critical to the health of our bones. So how does
Speaker 2: this work. Vitamin D calcitrial specifically travels to our guts
Speaker 2: from our kidneys to our guts, where it promotes the
Speaker 2: absorption of calcium and phosphorus, both of these are really
Speaker 2: important minerals for calcification of our bones. It also works
Speaker 2: in our kidneys where it's actually made to increase the
Speaker 2: amount of calcium that gets reabsorbed so that we're not
Speaker 2: peeing out as much calcium, we lose less in our
Speaker 2: p And then it does this weird slightly counter into
Speaker 2: it a thing where it also stimulates our bone cells,
Speaker 2: specifically osteoclasts, which are responsible for breaking down bone to
Speaker 2: release calcium, and that seems counterintuitive, but what it ends
Speaker 2: up doing is in the long run, resulting in more
Speaker 2: calcium being available to then be deposited into our bones
Speaker 2: to build strong bones.
Speaker 3: Kind of like bone renovation or bone remodeling, I guess
Speaker 3: would be the I will really.
Speaker 2: Really like renovations. I like that a lot better. Just
Speaker 2: a little bone renovation going on, just a little bit
Speaker 2: going on, exactly like that. So, in short, without vitamin D,
Speaker 2: we can't absorb enough calcium or phosphorus. Both of these
Speaker 2: minerals are essential for bone ossification. So what we end
Speaker 2: up with if we are deficient with vitamin D is
Speaker 2: deficiencies of both calcium and phosphorus. So unsurprisingly then one
Speaker 2: of the biggest concerns when it comes to especially severe
Speaker 2: vitamin D deficiency is osteomalasia or soft bones, and this
Speaker 2: can increase the risk of fractures. In children. This results
Speaker 2: in what is known as rickets. So in kids, their
Speaker 2: bones are still growing right, so they're not fully mineralized
Speaker 2: to begin with. So what happens in a child, infant
Speaker 2: or a young child who ends up with a vitamin
Speaker 2: D deficiency is that their bones are never able to mineralize.
Speaker 2: So what we see in terms of both symptoms as
Speaker 2: well as signs that we look at like radiographically and
Speaker 2: on X rays and things, is that their growth plates,
Speaker 2: like the plates where your long bones and things are
Speaker 2: still growing, become really widened, and then we see evidence
Speaker 2: of bones that are not strong, they're not well ossified.
Speaker 2: What this results in is slowed growth. So on a
Speaker 2: growth curve, these kids will be either slowing down in
Speaker 2: their linear growth like their height growth, or they might
Speaker 2: fall off of their growth curve that we look at.
Speaker 2: How they're growing okay. You can also see really commonly
Speaker 2: a boeing deformity, especially of the legs if the kid
Speaker 2: is old enough to be walking already, because those long
Speaker 2: bones like your femur, are so weak that it just
Speaker 2: can't support the weight of the rest of the body,
Speaker 2: so you get this boeing at the knees. You can
Speaker 2: also see, especially in very young kids, delayed closure of
Speaker 2: the bones of the skull. Babies are born with skull
Speaker 2: bones that are not fused, and this fusion can take
Speaker 2: longer in the case of rickets because because you don't
Speaker 2: have enough calcium and phosphorus to be able to mineralize
Speaker 2: that bone. And then what's interesting is that you can
Speaker 2: see this excessive growth of cartilage in the places where
Speaker 2: our bones and our cartilage meet, especially in our chest
Speaker 2: wall or in the wrists. So this results in these
Speaker 2: kind of characteristic findings that they're often called like beads
Speaker 2: on a rosary. It looks like kind of knobby beads
Speaker 2: along the center of the chest wall. Huh, because the
Speaker 2: cartilage is like you can almost think of it as
Speaker 2: like trying to compensate.
Speaker 3: Yeah, yeah, trying to bridge the gaps of like yeah,
Speaker 3: there's no calcium, okay, And.
Speaker 2: Then the same thing you can see at the wrist,
Speaker 2: so you can see actually these wrists that look wider
Speaker 2: and larger, but in fact it's because the bones underneath
Speaker 2: are so weak and small. And then you can also
Speaker 2: see delayed dentitions, since our teeth are also made of calcium.
Speaker 3: Right, a lot of things.
Speaker 2: A lot of things that I'm not even done. If
Speaker 2: it's very severe, if rickets becomes very, very severe, then
Speaker 2: what you can see is hypocalcemia, so calcium levels in
Speaker 2: our blood that are so low that you have additional
Speaker 2: signs that are extra skeletal. So not just looking at bones,
Speaker 2: but you can have muscle spasms that are called tetany
Speaker 2: where if you like tap in certain places, you'll see
Speaker 2: a spasm of the muscles or even this can progress
Speaker 2: to seizures, and in worst case scenario, it can actually
Speaker 2: result in cardiac failure. Because calcium is also really important
Speaker 2: in stabilizing the cells of our heart. So when your
Speaker 2: electrolytes become so out of whack because you're not able
Speaker 2: to absorb enough calcium and phosphorus, then the electrical system
Speaker 2: of your heart can start to fail and that's all
Speaker 2: just under the umbrella of rickets.
Speaker 3: Whoa I know. Okay, so historically I had read about
Speaker 3: mortality rates due to rickets, but I had no idea
Speaker 3: how what actually happened. That sounds horrible, I know. I
Speaker 3: have a couple questions. Great, okay, tetany I'm assuming comes
Speaker 3: from tetanus.
Speaker 2: Oh, that's a good question. I never thought about it,
Speaker 2: but probably.
Speaker 3: And then my other questions are about well, one is
Speaker 3: about timing, not of rickets, but of vitamin D and calcium.
Speaker 3: So you need to have vitamin D present in order
Speaker 3: to absorb calcium, right, So what is the timing of that?
Speaker 3: Like how long does calcium stay in your guts or
Speaker 3: how long you know what I mean? Like, yeah, what's
Speaker 3: the timing?
Speaker 2: That's a good question. I'm not going to give you
Speaker 2: like an actual answer, like fifteen minutes post whatever. But
Speaker 2: one thing that is important to note is that the
Speaker 2: active form of vitamin D, how's the trial, the kind
Speaker 2: that's made in our kidneys, does have a very short
Speaker 2: half life on the matter of hours. Oh wow, okay,
Speaker 2: so we have to continually make active vitamin D and
Speaker 2: what circulates in our body and what we measure to
Speaker 2: see if somebody is sufficient or deficient in vitamin D.
Speaker 2: Is that second form the twenty five oh vitamin D
Speaker 2: that we make in our liver. Okay, So that is
Speaker 2: kind of an important point, is that you have to
Speaker 2: first make that liver form, which then we can detect
Speaker 2: and is kind of floating around in your body in
Speaker 2: theory or is stored in our fat cells, which is
Speaker 2: important and we'll talk more about that later. But then
Speaker 2: it has to be converted by our kidneys to actually
Speaker 2: be active, and that active form doesn't last that long.
Speaker 2: This is all very tightly controlled in conjunction with another
Speaker 2: hormone called parathyroid hormone and controlled by our calcium levels.
Speaker 2: So it all works in like very complex hormonal loops
Speaker 2: that I'm not going to get into. But yeah, So
Speaker 2: like if you, for example, our milk that we drink
Speaker 2: in the US, at least milk has very high amounts
Speaker 2: of calcium. We fortify milk with vitamin D, but that
Speaker 2: doesn't mean that the vitamin D that you're drinking in
Speaker 2: that milk is helping you absorb that calcium in that
Speaker 2: particular glass of milk.
Speaker 3: Fascinating, I know, it's kind of fun, right, whoa, Okay.
Speaker 3: My other question is about rickets interventions, so which I
Speaker 3: assume is primarily through supplementation with vitamin D and calcium yep.
Speaker 3: How does that work and how well does that work?
Speaker 2: Yeah? Great question, It definitely works. I don't think I
Speaker 2: can give you exact statistics on like, depending on how
Speaker 2: sick a kid got, like how severe their rickets was
Speaker 2: to begin with, at what point do you need to intervene?
Speaker 2: I mean, obviously the earlier the better, But supplementation or
Speaker 2: fortification to kind of prevent rickets is effective, and we
Speaker 2: have seen that kind of epidemiologically as well. Importantly, vitamin
Speaker 2: D deficiency isn't the pure and only cause of rickets.
Speaker 2: There are a various other genetic or enzyme related disorders
Speaker 2: that can cause rickets or can cause severe vitamin D deficiency,
Speaker 2: even apart from like a nutritional deficiency, if that makes sense,
Speaker 2: but those tend to be more rare. So the most
Speaker 2: common cause of rickets overall is nutritional deficiency of vitamin
Speaker 2: D and or calcium calcium because of vitamin D, if
Speaker 2: that makes sense. Now when it comes to adults, because
Speaker 2: we can also be deficient in vitamin D severe vitamin
Speaker 2: D deficiency results in osteomilasia, which I mentioned already. This
Speaker 2: is a process of demineralization of the bone. Importantly, this
Speaker 2: is not the same thing as osteoporosis, which more people
Speaker 2: have probably we heard of. Osteoporosis. Now, the risk of
Speaker 2: osteoporosis may also be increased with vitamin D deficiency, but
Speaker 2: osteomylasia is a process that's actually interfering with the bone
Speaker 2: mineralization itself, So that means that in osteomilasia we see
Speaker 2: a change in the amount of mineralized ossified calcified bone
Speaker 2: compared to the amount of bone matrix or non calcified bone.
Speaker 2: Whereas osteoporosis, which can happen from calcium deficiency that's not
Speaker 2: related to vitamin D as well as vitamin D deficiency
Speaker 2: and other things like just aging. Osteoporosis is probably a
Speaker 2: whole episode in and of itself, but this is a
Speaker 2: decrease in overall bone mass, but with normal ratios of
Speaker 2: mineralized to bone matrix bone, that makes sense.
Speaker 3: Yes, okay, both of.
Speaker 2: These things, osteoporosis and osteomolasia can increase the risk of fractures.
Speaker 2: They both can coexist as well, so fun. But osteomylasia,
Speaker 2: you can think of, at least the way that I've
Speaker 2: been thinking of it, is kind of like the same
Speaker 2: process as rickets in kids, but with bones that have
Speaker 2: already been formed. So it's not just the growth that's
Speaker 2: being affected, but it's the remodeling of the larger, especially
Speaker 2: large and long bones that tends to be the most affected.
Speaker 2: So in terms of symptoms, what we can see with
Speaker 2: osteomylasia is actually a lot of bone pain. Osteoporosis is
Speaker 2: a painless process. Osteomylasia can be quite painful, and vitamin
Speaker 2: D deficiency in osteomolasia can also cause a lot of
Speaker 2: muscle pain and muscle weakness because our skeletal muscles also
Speaker 2: have vitamin D receptors, and those two things together can
Speaker 2: increase the risk of and therefore fractures. Wow, I know.
Speaker 3: Okay, And that's that's still just like one part of
Speaker 3: the vitamin D story.
Speaker 2: Yeah. That My next sentence is we're not done yet. Yeah,
Speaker 2: we're not, because that's just the skeletal manifestations. Yeah, Vitamin
Speaker 2: D receptors are found in our brain, in the prostate,
Speaker 2: in the breast tissue, colon tissue, immune cells, calcitrial. The
Speaker 2: active form of vitamin D has effects on more than
Speaker 2: two hundred genes that are involved in everything from cellular
Speaker 2: proliferation to apoptosis and angiogenesis that's blood vessel formation. It
Speaker 2: is an immune modulator. Like the list goes on and
Speaker 2: on and on, and we are really still learning the
Speaker 2: extent to which vitamin D has extraskeletal effects. So when
Speaker 2: it comes to severe, especially severe vitamin D deficiency, rickets
Speaker 2: and osteomylasia historically have been the two biggest diseases that
Speaker 2: we see. But when it comes to deficiency or what
Speaker 2: some people call insufficiency, we actually have a lot of
Speaker 2: epidemiological evidence that vitamin D deficiency or insufficiency is also associated.
Speaker 2: I can see your face and I can't wait to
Speaker 2: talk about it. But it's also associated with an increased
Speaker 2: risk of various cancers, potentially with higher overall mortality. It's
Speaker 2: associated with various autoimmune diseases, including MS type one diabetes.
Speaker 2: The risk of cardiovascular disease is increased with vitamin D deficiency,
Speaker 2: not to mention things like chronic fatigue syndrome and fibermyalgia
Speaker 2: that we still just don't understand there are a lot
Speaker 2: of things that epidemiologically are associated with vitamin D deficiency
Speaker 2: or with having low levels of vitamin D, but that
Speaker 2: doesn't mean that we have the slightest clue yet if
Speaker 2: these relationships are causal, or if they might be consequential,
Speaker 2: like is vitamin D just a consequence of these various diseases, disorders, conditions,
Speaker 2: or what any of the mechanisms actually are, or.
Speaker 3: If it's not mechanistic but just an indicator of something
Speaker 3: else right right, or many other things. Yeah, yep, Yeah,
Speaker 3: there's a lot that we could get into in that
Speaker 3: realm of things, and I think it's a little bit
Speaker 3: frustrating sometimes. I think to see these studies that look
Speaker 3: at vitamin D one measure of one thing, and then
Speaker 3: something cardiovascular disease, as if vitamin D will hold all
Speaker 3: the answers to all of the things. And vitamin D
Speaker 3: is clearly very important, but I feel like we are
Speaker 3: still so far from understanding not the individual role that
Speaker 3: it plays in different tissues or in different organs, but
Speaker 3: how that fits into the bigger picture of health and disease.
Speaker 2: A thousand percent I agree.
Speaker 3: I have a couple of questions.
Speaker 2: Okay, great.
Speaker 3: The first one is about insufficiency versus deficiency.
Speaker 2: Ooh versus severe deficiency versus sufficient versus oh my gosh.
Speaker 3: Arin, Yeah, yeah.
Speaker 2: Listen, I have questions too. It's like you would think
Speaker 2: it's not that difficult, but it is in fact that
Speaker 2: difficult to answer that question. And the exact I'm going
Speaker 2: to give you some numbers here, so don't worry, but
Speaker 2: the exact numbers that you choose to use to define
Speaker 2: sufficient in vitamin D versus deficient versus severe deficiency. And
Speaker 2: it seems like some groups like to say insufficient versus deficient,
Speaker 2: and some groups say like sufficient deficient severely deficient. And
Speaker 2: depending on which paper you read or which consensus statement
Speaker 2: you read, the laboratory values are going to vary just
Speaker 2: a little bit, but we at least have some like
Speaker 2: generalities here. Many groups define sufficient like you have enough
Speaker 2: vitamin D. And remember that we are measuring twenty five
Speaker 2: oh vitamin D, which is the one that is made
Speaker 2: in our liver, regardless of whether the initial vitamin D
Speaker 2: came from a plant or your milk or a supplement
Speaker 2: or your skin that you made. Okay, and it's not
Speaker 2: the active form that's made in our kidneys, so sufficient
Speaker 2: most places define it as greater than twenty nanograms per
Speaker 2: mili leader or fifty animals per leader. Then they would
Speaker 2: define insufficient as between twelve and twenty nanograms per mil
Speaker 2: or thirty to fifty animals per leader. Some places, instead
Speaker 2: of saying insufficient, say deficient for that category, and then
Speaker 2: they would say deficiency or severe deficiency as less than
Speaker 2: twelve nanograms per mil or thirty animals per leader. The
Speaker 2: lab where I work, and some consensus statements and some
Speaker 2: societies flag anything less than twenty nanograms per mil as deficient.
Speaker 2: So it's like a higher threshold for calling something deficient
Speaker 2: and anything between twenty one and thirty nanograms per mil insufficient.
Speaker 2: So basically it's raising it saying that you should have
Speaker 2: at least thirty nanograms per mil or seventy five animals
Speaker 2: per leader to act be sufficient in vitamin D. Okay,
Speaker 2: I know those numbers, like, well, okay, I have.
Speaker 3: I have two more questions, okay, follow ups. Now, So,
Speaker 3: so you mentioned that when we measure vitamin D levels,
Speaker 3: we are measuring the one that has a longer half
Speaker 3: life in the body. It lasts longer in the body.
Speaker 2: Yeah.
Speaker 3: So let's say I go in and my vitamin D
Speaker 3: level is twenty. How long has it been twenty?
Speaker 2: Ooh, that's a really good question. I don't know, okay,
Speaker 2: but it definitely does like fade with time. For example,
Speaker 2: if you measure a population at the end of winter,
Speaker 2: inevitably their vitamin D levels are going to be significantly
Speaker 2: lower than that same exact population with no changes at
Speaker 2: the end of summer. Right, But I don't have an
Speaker 2: exact timeline for you.
Speaker 3: And then my other question is, and maybe this is
Speaker 3: too big of a question, but how were these categories established?
Speaker 3: Like how was baseline? How is thirty decided to be
Speaker 3: the cutoff point for good versus bad levels of vitamin D?
Speaker 2: That is a spicy question, man, Yeah, I think that
Speaker 2: it might be. I can tell you that twelve, that
Speaker 2: that number that is often cited as like deficient or
Speaker 2: severely deficient, that's based on rickets and osteomilaysia. Okay, So
Speaker 2: that's based on risk specifically for rickets and osteomilaysia. Above that,
Speaker 2: there's not I don't think great data, and that is
Speaker 2: why there is still controversy. Is it twenty Is it thirty,
Speaker 2: is it fifty? Is it seventy five? Like it? There
Speaker 2: is a lot of debate still. There's also some societies
Speaker 2: that say, no, it actually needs to be even higher. Yeah.
Speaker 3: So yeah, Well, speaking of that, we've talked so far
Speaker 3: about vitamin D deficiency. Is there such thing as the
Speaker 3: opposite of deficiency? I'm blanking on the word toxicity?
Speaker 1: There?
Speaker 2: We go absolutely erin there, certainly is. In terms of
Speaker 2: lab values, we would categorize it as greater than one
Speaker 2: hundred to one hundred and fifty nanograms per mil. That's
Speaker 2: usually that somewhere in that range, depending on the lab
Speaker 2: is what's considered toxic or at risk of toxicity. What
Speaker 2: does that mean? I don't know what does it look
Speaker 2: like if you have vitamin D toxicity. I will say
Speaker 2: that toxicity of vitamin D is exceedingly rare. Interestingly, even
Speaker 2: though this is a fat soluble vitamin, which means that
Speaker 2: we can potentially store quite a bit of it in
Speaker 2: our fat cells, Vitamin D toxicity is generally associated with
Speaker 2: extremely high supplementation rates, like taking a whole bunch of
Speaker 2: vitamin D supplements, or, in rare cases, genetic mutations that
Speaker 2: lead to changes in the metabolism of those various phases
Speaker 2: of vitamin D. So when you have too much vitamin D,
Speaker 2: it can lead to the opposite problem logically, and that
Speaker 2: is hyper calcemia, too much calcium in your blood, which
Speaker 2: can then go on to affect primarily the kidney and
Speaker 2: lead to a lot of kidney problems. Okay, so once
Speaker 2: we know what our lab values are supposed to look like,
Speaker 2: the natural next question is like, how do we get
Speaker 2: enough vitamin D or how do we make enough vitamin D?
Speaker 2: Or who is that risk for not having enough vitamin
Speaker 2: D for having low levels of vitamin D Vitamin D
Speaker 2: deficiency And we're going to get into a lot of
Speaker 2: this in the epidemiology section. It has been on the
Speaker 2: rise for decades now across the globe. There are a
Speaker 2: number of different things that can contribute to this risk
Speaker 2: of deficiency, however specific number you define it. Number one
Speaker 2: is lack of sun exposure, because we primarily are making
Speaker 2: this in our skin from exposure to UVB radiation. So
Speaker 2: lack of sun exposure can look like a lot of
Speaker 2: different things. It can look like living at northern latitudes
Speaker 2: where half the year there is simply not enough sun
Speaker 2: and specifically not enough UVB radiation to physically make enough
Speaker 2: vitamin D for like half the year or potentially more.
Speaker 2: That's one way you cannot get enough sun. It also
Speaker 2: can mean wearing sunscreen all the time, or covering your
Speaker 2: body in clothing to protect it from the sun, or
Speaker 2: for whatever reason that we wear clothing. And I just
Speaker 2: want to say that that's important because skin cancer is
Speaker 2: also very real. Yes, it could also mean more pigmentation
Speaker 2: in the skin. Melanin is protective to a certain degree
Speaker 2: against UV rays and so it reduces the amount of
Speaker 2: UVB that's available to cause the reaction to make vitamin D.
Speaker 2: So that's another way you can have less vitamin D available.
Speaker 2: It also can just be not being outdoors very much
Speaker 2: at all and being exposed to the sun, even in
Speaker 2: places that have adequate sunlight for most of the year.
Speaker 2: But besides sunlight, this is also a micronutrient. It's a
Speaker 2: vitamin and it turns out that we get very little
Speaker 2: vitamin D in our diets, especially as we eat not
Speaker 2: a lot of fish and fatty fish oils, which I
Speaker 2: don't know, maybe like people used to eat more.
Speaker 3: Of those, well, not even just fish oils, but specifically
Speaker 3: fish liver.
Speaker 2: Liver oils, yeah, but fatty fish in general, fatty fish yeaheah.
Speaker 2: There are also certain medical conditions that can increase your
Speaker 2: risk of vitamin D deficiency. Things that result in the
Speaker 2: lack of absorption in general like IBD, or after a
Speaker 2: gastric bypass, or from other conditions that might make it
Speaker 2: difficult for us to convert to active vitamin D, like,
Speaker 2: for example, chronic kidney disease.
Speaker 3: Okay.
Speaker 2: And then another important and very interesting aspect of risk
Speaker 2: of vitamin D deficiency is higher body fat mass. So
Speaker 2: vitamin D is a fat soluble vitamin, which means that
Speaker 2: it is stored in our fat. It gets distributed into
Speaker 2: our fat tissue. In the case of having higher fat mass,
Speaker 2: higher adipose tissue, this vitamin D gets so well distributed
Speaker 2: into that tissue it's not actually very readily available for
Speaker 2: use in our bodies. So you can see a relative
Speaker 2: vitamin D deficiency in those cases, which I think is
Speaker 2: very interesting. So there are a lot of different things
Speaker 2: that can contribute to the risk of vitamin D deficiency.
Speaker 2: It's almost never just one thing.
Speaker 3: It's this story is just the most simple thing in
Speaker 3: the world's very clear, very clear. Yeah, yeah, complex at all.
Speaker 2: Another thing that's really clear is recommended daily allowances.
Speaker 3: Oh yeah, super clear.
Speaker 2: I'm not even gonna mention what they are because they're
Speaker 2: so varied, Arren, They're so varied.
Speaker 3: Everyone has has a different opinion on it.
Speaker 2: Huh. Yeah. And like you asked the question of how
Speaker 2: did we determine that this level is adequate, in this
Speaker 2: level is insufficient or deficient, I don't think that we
Speaker 2: really have strong data to say that this is the
Speaker 2: necessary recommended daily intake. So nonetheless, you can find it
Speaker 2: on your public health website of choice for your country.
Speaker 2: So that is is pretty much what I have for
Speaker 2: the biology of vitamin D. I mean it's a lot.
Speaker 3: I learned a lot.
Speaker 2: Oh good, Yeah, I mad you learned something I didn't
Speaker 2: know I did.
Speaker 3: I I mean, vitamin D it is so astonishing, Yeah,
Speaker 3: for how much it is involved in different processes. But
Speaker 3: we don't understand all of it.
Speaker 2: I totally understand why people get really excited about the
Speaker 2: idea of vitamin D being this like maybe not cure all,
Speaker 2: but like this thing that's like so important. We've been
Speaker 2: overlooking it for so long. Like I get that because
Speaker 2: it's fascinating and it's interesting and it's cool. And depending
Speaker 2: on the way that you look at data, you could
Speaker 2: convince yourself that that might be true. But if you
Speaker 2: look at it another way, you might not.
Speaker 3: If you design a study to look for vitamin D
Speaker 3: differences and as it relates to whatever your disease of
Speaker 3: choice is, and you have a big enough sample size,
Speaker 3: you're probably going to find something. Is that meaningful? Is
Speaker 3: that a good study? These are good questions to ask.
Speaker 2: Oh, Aaron, I feel like you're gonna have some more,
Speaker 2: some more vitamin tea to.
Speaker 3: Spill vidim and tea. I love it, just a little
Speaker 3: bit more of a soapbox.
Speaker 2: Yeah, I can't wait, can't wait? Can we get into it?
Speaker 2: Where did this come from?
Speaker 1: Like?
Speaker 2: What what's the deal? Evolution? Why do we make it?
Speaker 2: Why do we still have to eat it?
Speaker 3: So glad you asked. I will attempt to answer right
Speaker 3: after this break. One of the things you asked is
Speaker 3: where did this thing come from? Yeah, it's a great question,
Speaker 3: and answering that question will take us back further in
Speaker 3: time than we've ever gone before. I'm pretty sure.
Speaker 2: I feel like that was like an intro to Star.
Speaker 3: Trek because to trace the origins of vitamin D or
Speaker 3: when organisms first began to use or produce vitamin D,
Speaker 3: we have to go back not millions of years, but
Speaker 3: billions of years billions with a B. Yeah, vitamin D
Speaker 3: has been produced or utilized by plants and animals basically
Speaker 3: since life began. And one paper I read suggested that
Speaker 3: vitamins D two in D three could be as old
Speaker 3: as one point two billion years.
Speaker 4: Wow.
Speaker 3: Yes, isn't that amazing? Yeah, they are thought to be
Speaker 3: this old because the transformation of pre vitamin D two
Speaker 3: or pre vitamin D three into D two and D
Speaker 3: three via UVB radiation that does not require enzymes, right, transformation.
Speaker 2: That's amazing, you know, I know I didn't mention that,
Speaker 2: but it's non ensmatic reactions.
Speaker 3: Quay cool, It's mind blowing. Yeah. And nearly every paper
Speaker 3: examining the history or evolutionary history of vitamin D mentions
Speaker 3: at the top that phytoplankton have been producing vitamin D
Speaker 3: for at least seven hundred and fifty million years. Wow,
Speaker 3: which is just Yeah. Speaking of phytoplankton, we talked about
Speaker 3: how cod liver oil is a great source of vitamin
Speaker 3: D well, it's likely that cod liver is packed full
Speaker 3: of vitamin D because of phytoplankton, which produced tons of
Speaker 3: vitamin D and then the concentration of it in the
Speaker 3: food chain and so on.
Speaker 2: Oh, because the cod or eating little fytle LinkedIn.
Speaker 3: Or eating things that I don't really know. The the
Speaker 3: fish diet of cod.
Speaker 2: Brings me back to my marine biology days. I should know.
Speaker 3: I mean, I've taken an ichthyology class. I have never
Speaker 3: taken an entomology class, but I remember nothing. It was
Speaker 3: a great class. But anyway, we usually think of vitamin
Speaker 3: D in terms of calcium absorption and bone remodeling or renovation.
Speaker 3: But the phytoplankton and other organisms producing vitamin D seven
Speaker 3: hundred and fifty million years ago, they weren't using it
Speaker 3: to create skeletons bony skeletons. So what was it used for.
Speaker 3: Some researchers hypothesize that vitamin D two and D three
Speaker 3: largely served to protect DNA and proteins from damage due
Speaker 3: to UVB radiation ooh, and that it was only later on,
Speaker 3: millions of years later on that the endocrine function and
Speaker 3: immune function of vitamin D evolved. And then about three
Speaker 3: hundred and eighty five million years ago, water dwelling species
Speaker 3: began moving on to land, but they encountered a problem
Speaker 3: that they didn't have to deal with as much in
Speaker 3: the water. Gravity gravity. Yes, moving around was a much
Speaker 3: different ballgame on land than it wasn't water, and some
Speaker 3: land dwellers underwent changes in their bony skeletons to better
Speaker 3: support their movement in these new environments, which is where
Speaker 3: vitamin d's role in calcium absorption came into play.
Speaker 2: I can't express to you how excited I am by
Speaker 2: this story right now, Like I I love it.
Speaker 3: It's I do too. I love a deep time evolutionary story.
Speaker 2: It's so good it is.
Speaker 3: It was very fun to read this. I was also
Speaker 3: very I was like, whoa, this is not an era
Speaker 3: of time that I'm used to thinking in what's going on?
Speaker 3: Soup right off? And calcium, of course, was important also
Speaker 3: for the bony fishes that already existed in aquatic environments,
Speaker 3: but calcium was more abundant in the water and so
Speaker 3: it wasn't as much of a limiting factor.
Speaker 2: Ooh okay.
Speaker 3: Given this incredibly deep evolutionary history of vitamin D and
Speaker 3: how early it emerged, it makes complete sense that it's
Speaker 3: essential for so many organisms, that it serves so very
Speaker 3: many purposes and is involved in so many different pathways.
Speaker 3: It also then makes sense that most animals can experience
Speaker 3: vitamin D deficiency dogs, as we'll hear later on in
Speaker 3: the history, other mammals, amphibians, reptiles, birds. Vitamin D is
Speaker 3: fundamental to so much of life on this planet, and
Speaker 3: it's this vital nature of vitamin D that has led
Speaker 3: many people to explore its possible role in human evolution,
Speaker 3: particularly in terms of skin color. Right off the bat,
Speaker 3: I want to say that I am not familiar enough
Speaker 3: with the literature of this topic to make any assessments
Speaker 3: about what is known or commonly accepted about the drivers
Speaker 3: of skin pigmentation in humans. But one popular hypothesis that
Speaker 3: you may have heard of is known as the vitamin
Speaker 3: D hypothesis or the vitamin D folate hypothesis. This hypothesis
Speaker 3: states basically that more melanin i e. Darker skin pigmentation
Speaker 3: was selected for when humans evolved around three hundred thousand
Speaker 3: years ago in Africa in tropical latitudes, and it evolved
Speaker 3: to protect from harmful exposure to UV radiation. Then The
Speaker 3: hypothesis continues when humans begin to migrate out of Africa
Speaker 3: around seventy to ninety thousand years ago, those that move
Speaker 3: to higher latitudes eventually lost melanin to better absorb vitamin
Speaker 3: D now that UVB levels were lower. This is a
Speaker 3: common narrative, a very common hypothesis that I saw repeated
Speaker 3: in nearly every paper that I read about vitamin D.
Speaker 3: And again, I haven't read enough of this literature to
Speaker 3: be able to tell you all the bits of evidence
Speaker 3: there are to support or refute this hypothesis. I did
Speaker 3: read a paper, a recent paper from twenty twenty two,
Speaker 3: that discussed how people residing in Western Europe had darker
Speaker 3: skin pigmentation from around forty thousand years ago when they arrived,
Speaker 3: until around eight thousand years or so ago, and that's
Speaker 3: when lighter skin became more common. So for that really
Speaker 3: long chunk of time, about thirty two thousand years, humans
Speaker 3: residing in northern and western Europe had darker skin. And
Speaker 3: the proposed reason for this more recent change in terms
Speaker 3: of skin pigmentation in that part of the world is
Speaker 3: that that's around when diet would have shifted to rely
Speaker 3: more on grain. Basically, the shift from hunting and gathering
Speaker 3: to agriculture, so the beginning of the agricultural revolution. But
Speaker 3: bones from that time and earlier don't, as far as
Speaker 3: I read, show signs of vitamin D deficiency, which you
Speaker 3: might expect to see if vitamin D deficiency was such
Speaker 3: a strong driver. Only after so more recent the past
Speaker 3: few thousand years, our skeletal remains found that indicate vitamin
Speaker 3: D deficiency, And of course this could be that we
Speaker 3: just haven't found many remains from earlier times. I don't know.
Speaker 3: There is some evidence showing that variations in particular parts
Speaker 3: of some genes are associated with vitamin D synthesis, but
Speaker 3: these variations don't seem to be linked to skin pigmentation
Speaker 3: variation or skin pigmentation overall mechanistically. And again, there's way
Speaker 3: more to this field of study if you want to
Speaker 3: read more. But the reason that I wanted to bring
Speaker 3: it up was to talk not about variation in vitamin
Speaker 3: D production and humans, but how we talk about that variation.
Speaker 3: If vitamin D was a strong driver, if skin pigmentation
Speaker 3: over human evolutionary history, that does not necessarily mean that
Speaker 3: it can explain everything about health today, particularly health disparities.
Speaker 3: What do I mean by that? I mean that many
Speaker 3: medical studies will look at whether a certain outcome like
Speaker 3: infection with COVID maybe, or cardiovascular disease or cancer or
Speaker 3: what have you, is associated with vitamin D levels and
Speaker 3: race presumably, though not necessarily explicitly stated as a proxy
Speaker 3: for skin pigmentation, which is I think a problem in
Speaker 3: and of itself.
Speaker 2: Like that, that's absolutely like literally entire books have been written,
Speaker 2: yeah about the problem with that. Yeah, And we.
Speaker 3: Saw countless of these types of studies during COVID I
Speaker 3: remember seeing so many headlines about what role vitamin D
Speaker 3: may play in susceptibility to infection or infection severity. And
Speaker 3: if you look on Google scholar you can find peer
Speaker 3: reviewed article after peer reviewed article suggesting that racial disparities
Speaker 3: in COVID infection or COVID mortality could be attributable to
Speaker 3: vitamin D levels. It's like, not not accounting for structural
Speaker 3: inequalities or even discussing it, not institutionalized racism, nothing, just
Speaker 3: vitamin D.
Speaker 2: Yeah, it's like so problematic.
Speaker 3: It's yeah, And you know, of course, it is very
Speaker 3: possible that vitamin D does play a role in COVID infection.
Speaker 3: We know that it's involved in immune function. But the
Speaker 3: problem that I have with these studies is that, at
Speaker 3: the least, the conclusions drawn are overly simplistic and fail
Speaker 3: to take into account the myriad of factors that play
Speaker 3: a role in COVID severity or heart disease. And at
Speaker 3: the worst, they're not far off from victim blaming. They
Speaker 3: tell you that you got COVID because your skin color,
Speaker 3: or because your diet doesn't get you enough vitamin D,
Speaker 3: or because you don't spend enough time in the sun,
Speaker 3: or because you have too much body fat. It places
Speaker 3: the burden solely on the individual rather than on the
Speaker 3: systems that perpetuate these health disparities in medicine today. This
Speaker 3: isn't to say that we shouldn't look at vitamin D
Speaker 3: in health. We absolutely should, but maybe just take a
Speaker 3: more thoughtful approach to study design as well as interpretation
Speaker 3: of results. And this also goes to popular media taking
Speaker 3: these scientific articles and making a headline that's like, vitamin
Speaker 3: D will prevent you from dyeing, Like I don't know.
Speaker 2: I saw that was like an actual headline in the
Speaker 2: New York Times.
Speaker 3: We see the vitamin D is vitamin D the key
Speaker 3: to immortality.
Speaker 2: Yeah, oh, well, how did we not mention it in
Speaker 2: our episode?
Speaker 1: Yeah?
Speaker 3: Wow, how about that?
Speaker 1: Uh?
Speaker 3: But yeah, I mean, keep studying vitamin D, but I
Speaker 3: think it just needs to be more thinking about why
Speaker 3: and what we're actually measuring about vitamin D. But looking
Speaker 3: at vitamin D is important because, like I said at
Speaker 3: the top, and like we learned in the biology section
Speaker 3: just now, it is a vital part of life. And
Speaker 3: so when did humans first recognize it as such?
Speaker 2: Ooh tell me?
Speaker 3: The first thing they recognized, of course, was not vitamin
Speaker 3: D itself, but rather the absence of it, and earliest
Speaker 3: descriptions date back to ancient Greece around one hundred and
Speaker 3: ten to one hundred and thirty CE, as well as
Speaker 3: ancient China close to the same period. The first writing's
Speaker 3: generally agreed upon to be about rickets come from Serrano
Speaker 3: of Ephesus quote, when the infant attempts to sit and
Speaker 3: to stand, one should help in its movements, For if
Speaker 3: it is eager to sit up too early and for
Speaker 3: too long a period, it becomes hunchbacked. If moreover, it
Speaker 3: is too prone to stand up and desirous of walking,
Speaker 3: the legs may become distorted in the regions of the
Speaker 3: thighs end.
Speaker 4: Quote.
Speaker 3: After this early description, we have to wait around fourteen
Speaker 3: hundred years for the next one, which is when in
Speaker 3: fifteen fifty four Theodosius of Bologna wrote about a child
Speaker 3: quote that could not move or sit, indeed hardly hold
Speaker 3: its head erect, and which showed in the lower dorsal
Speaker 3: region both a gibbus and a marked lateral curvature. Quote.
Speaker 3: This long silence in medical texts about rickets doesn't mean
Speaker 3: that people weren't experiencing vitamin D deficiency rickets during that time,
Speaker 3: and we have archaeological evidence backing that up. Skeletal remains
Speaker 3: have been found from ancient Rome around the fourth century,
Speaker 3: in France, sixteenth century Italy, and parts of what is
Speaker 3: now the UK, and these remains show signs of things
Speaker 3: like childhood rickets or adult osteomalaysia. I don't know if
Speaker 3: enough of these remains have been found or analyzed to
Speaker 3: give any sort of prevalence estimate during this time, but
Speaker 3: that changes as we head into the seventeenth century, and
Speaker 3: this is when ricketts really begins to pick up steam
Speaker 3: and doesn't slow down until the twentieth century. The word
Speaker 3: rickets is either said to have an unknown origin, come
Speaker 3: from the German or Old English word ricken, meaning twisted
Speaker 3: or to twist, or have its roots in the Greek
Speaker 3: word racus, meaning spine, which gave rise to the more
Speaker 3: medical term rachitis rickittis. Wherever it came from, the word
Speaker 3: ricketts first appeared in a sixteen thirty two receipt book
Speaker 3: containing cures for quote rickets and children, and then just
Speaker 3: a couple of years after, in sixteen thirty four, it
Speaker 3: makes an appearance on the London Annual Bill of Mortality.
Speaker 3: That year, fourteen deaths were attributed to rickets out of
Speaker 3: ten thy nine hundred deaths total for a population of
Speaker 3: around two hundred thousand.
Speaker 2: Wow.
Speaker 3: Okay, yeah yeah. These London Annual Bills of Mortality are
Speaker 3: actually quite useful over the next decades in tracing the
Speaker 3: rise of rickets, especially going into the Industrial Revolution. Scientific
Speaker 3: and medical writings focusing on rickets paralleled this increase in
Speaker 3: incidents of the condition in the British Isles. For instance,
Speaker 3: a sixteen forty publication listing botanical cures includes a reference
Speaker 3: to what maybe rickets in the thistle section quote Galen
Speaker 3: saith that the root and leaves hereo are of healing
Speaker 3: quality and good for such persons that have their bodies
Speaker 3: drawn together by some spasm or convulsion, or by some
Speaker 3: other infirmity, which disease is truly to be called. The rickets,
Speaker 3: which happening sometimes to children, doeth so buying them in
Speaker 3: their nerves, ligaments, and whole structure of their body, that
Speaker 3: it suffereth not to grow or prosper, either in height, strength,
Speaker 3: or alacrity.
Speaker 2: That was like a whole Shakespeare situation. I know.
Speaker 3: That's honestly why I included so many of these quotes.
Speaker 3: I get to say, uh, do beginneth, suffereth doeth. But
Speaker 3: most researchers attribute the first clear and controvertible descriptions of
Speaker 3: Ricketts to either Daniel Whistler, who published a monograph in
Speaker 3: sixteen forty five while in medical school titled Quote Inaugural
Speaker 3: Medical Disputation on the Disease of English Children, which is
Speaker 3: popularly termed Rickets, or Francis Glisten, an English physician who
Speaker 3: in sixteen fifty published a treat on Ricketts based on
Speaker 3: clinical and post mortem experience. Like Whistler, g Listen described
Speaker 3: the signs and symptoms of the disease pretty well, including
Speaker 3: the characteristic age of onset, and the suggested treatments that
Speaker 3: Glisten gave were simple, really, I mean compared to some
Speaker 3: of the other things that we've talked about on the podcast,
Speaker 3: incisions to draw bad humors, oh dear, blistring, or tying
Speaker 3: soft wool around limbs to prevent blood flow.
Speaker 2: Oh gosh. Okay.
Speaker 3: Suspension was also thrown into the mix, particularly for infants. Well,
Speaker 3: I'm sorry what suspension? Like, you didn't suspend them?
Speaker 2: What does that mean?
Speaker 3: You would just suspend them? You fold in the cheese?
Speaker 2: I literally, I can't understand what that means.
Speaker 3: Okay, I imagine it's like one of those things that
Speaker 3: I don't know if people still use them, but you
Speaker 3: like put a kid in like a doorway, and it's
Speaker 3: like one of those suspend.
Speaker 2: Things, a bouncy.
Speaker 3: Thing so they don't have to put weight on their
Speaker 3: on their limbs. I assume. Is so, except like you've
Speaker 3: got things to do, you need to create a contraption
Speaker 3: for suspending your baby.
Speaker 2: I can't.
Speaker 3: Dissension, okay, cool? Yeah. Yeah. With this incredible rise in
Speaker 3: Rickett's cases, people must have been wondering what on earth
Speaker 3: caused it, but again the explanations are fairly mundane. According
Speaker 3: to Glisten, it was neither heritable nor contagious, but that
Speaker 3: it was caused by quote cold distemper that is moist
Speaker 3: and consisting of penury or paucity of and stupefaction of spirits. Yeah,
Speaker 3: that's logical, that's I mean, that's the way things were.
Speaker 3: The world would have to wait another two hundred and
Speaker 3: fifty years to learn what ultimately caused rickets, and in
Speaker 3: the meantime, prevalence of this condition would grow and grow
Speaker 3: and grow, especially in North America and Northern Europe, particularly
Speaker 3: Great Britain, to the point where it earned the nickname
Speaker 3: the English disease. And to what do we owe this
Speaker 3: massive increase in vitamin D deficiency the Industrial Revolution? From
Speaker 3: around the mid eighteenth century to the mid nineteenth century,
Speaker 3: people in North America, Europe, and Great Britain began moving
Speaker 3: in large numbers from the rural countryside to cities, often
Speaker 3: with bad air pollution, where many of them lived in
Speaker 3: crowded conditions. The increase in specialized labor and growth of
Speaker 3: factories meant that people were spending their days indoors working,
Speaker 3: and that, combined with the change in diet, bread taking
Speaker 3: the place of the dairy and the reduction in air quality,
Speaker 3: led to lower calcium intake, lower vitamin D production via
Speaker 3: both diet, and lower exposure to UVB, and thus higher
Speaker 3: cases of rickets and overall vitamin D deficiency. No one
Speaker 3: during the Industrial Revolution was completely exempt from this drop
Speaker 3: in vitamin D levels, but rickets did tend to happen
Speaker 3: more commonly in cities and among those earning lower incomes.
Speaker 3: Over this period, ricketts cases grew to unimaginable levels. A
Speaker 3: physician published a report of infants aged eighteen months or
Speaker 3: less that had died in nineteen oh nine. I don't
Speaker 3: know how many were in this report, but he reported
Speaker 3: that ninety six percent of those infants had rickets at autopsy. Wow.
Speaker 3: Ninety six percent.
Speaker 2: Right, So even if it wasn't that rickets is why
Speaker 2: they died, Like every kid had rickets to some degree.
Speaker 3: Yes. Yeah. Despite the incredibly high prevalence of this disease
Speaker 3: late nineteenth century, physicians still couldn't explain why it happened
Speaker 3: and to whom. But they wouldn't have to wait too
Speaker 3: much longer, as research into diet and micronutrients began to
Speaker 3: transform our understanding of what exactly was in the food
Speaker 3: that we ate and how those components sustained life. By
Speaker 3: the late eighteen hundreds, scientists had started digging into the
Speaker 3: question of what a diet should contain in order to
Speaker 3: maintain health, and many experiments were carried out to see
Speaker 3: what proportion of carbohydrates, fats, proteins, and salts were needed
Speaker 3: for animals to survive and thrive. Importantly, but what these
Speaker 3: scientists were often finding in these experiments using very restricted
Speaker 3: diets was that even though the caloric needs of these
Speaker 3: animals were being met, the animals were still dying or
Speaker 3: failing to thrive. Something was clearly missing, and so researchers
Speaker 3: set out to find that missing piece of the puzzle,
Speaker 3: which of course turned out to be not one piece
Speaker 3: but many. And I feel like I've said that exact
Speaker 3: phrase on the podcast before. It is now ringing, like
Speaker 3: I'm experiencing deja vu.
Speaker 2: But yep, maybe it was in full eight.
Speaker 3: It could have been in full It could have been
Speaker 3: vitamin C could have been yep. Over the next decades
Speaker 3: into the early nineteen hundreds, researchers began linking diet with
Speaker 3: human diseases. Barry Berry cured by including the wholes of rice,
Speaker 3: scurvy by adding citrus or sauerkraut, zeriphthalmia by incorporating butterfat
Speaker 3: or cod liver oil. This pattern where certain diseases were
Speaker 3: cured by certain foods suggested to scientists that these foods
Speaker 3: contained some sort of micronutrient whose deficiency was behind the
Speaker 3: signs and symptoms that they observed, and that given the
Speaker 3: wide array of signs and symptoms, and that different foods
Speaker 3: cured different diseases, there were likely many micronutrients. I know
Speaker 3: we've talked about this before on the podcast, but I
Speaker 3: just think this history of discovery is so fascinating.
Speaker 2: It's so fun. It's so fun it is.
Speaker 3: And one by one, researchers were finding these vitamins and
Speaker 3: they were given names starting with A in nineteen thirteen,
Speaker 3: and researchers began to uncover more about their biochemistry. Side note,
Speaker 3: I know that someday we'll probably do a Vitamin A episode,
Speaker 3: but I just wanted to include in here so that
Speaker 3: I don't forget that I have always read that it
Speaker 3: was a researcher named McCollum who started this alphabetical naming system,
Speaker 3: but it was actually his master's student, Cornelia Kennedy who
Speaker 3: first used A and B. Love that love it yep. Anyway,
Speaker 3: research into vitamin discovery was well underway by the night
Speaker 3: eighteen tens when Sir Edward Mellonbee decided that he might
Speaker 3: like to dip his toe into the vitamin waters. In
Speaker 3: nineteen eighteen, he set out to induce rickets experimentally in
Speaker 3: his chosen study, animal puppies. He took puppies between the
Speaker 3: ages of five and eight weeks old and exposed them
Speaker 3: to one of four limited diets diets like only milk, rice,
Speaker 3: oatmeal and salt, or just milk and bread. He reportedly
Speaker 3: based these diets off of what was commonly consumed by
Speaker 3: people earning lower income in Great Britain, and these diets
Speaker 3: were maybe thought to contribute to the high prevalence of rickets.
Speaker 3: He also crucially kept the puppies indoors the entire time,
Speaker 3: unsurprisingly I think to us anyway, from this perspective, in
Speaker 3: the future, the puppies developed rickets, and melon Bee began
Speaker 3: experimenting with food to see if any particular item could
Speaker 3: effectively treat it. Among the foods he tried were cod liver, oil, butter,
Speaker 3: and whole milk, things that we know today are good
Speaker 3: sources of vitamin D, but at the time were known
Speaker 3: to be rich in fat soluble vitamin A, which had
Speaker 3: already been found by that point. These foods appeared to
Speaker 3: relieve the symptoms of rickets, which led Melanbie to conclude
Speaker 3: that quote it therefore seems probable that the cause of
Speaker 3: rickets is a diminished intake of an anti rikittic factor,
Speaker 3: which is either fat soluble A or has a somewhat
Speaker 3: similar distribution to fat soluble A pretty pretty good conclusion,
Speaker 3: and this experiment marked a pretty big step forward for
Speaker 3: ricketts research Number one because it showed that rickets was
Speaker 3: likely caused by a dietary deficiency or at least could
Speaker 3: be treated by diet. And number two, it demonstrated how
Speaker 3: rickets could be intentionally induced for scientific study purposes. But
Speaker 3: there were still at least two big things to be
Speaker 3: figured out, detangling vitamins A and D and understanding the
Speaker 3: role of ultraviolet light. Before I get into that, though,
Speaker 3: I want to take a step back in time, because
Speaker 3: Melanbee didn't come up with these ideas all on his own. Where,
Speaker 3: for instance, did he get the idea to treat rickets
Speaker 3: with cod liver oil? As I mentioned, it had been
Speaker 3: used successfully to treat xerophthalmia caused by vitamin A deficiency,
Speaker 3: so maybe he got it from there, Or maybe he
Speaker 3: got it from d Shoot, who in eighteen twenty four
Speaker 3: recommended it for treatment of rickets.
Speaker 2: Sorry, did you say Dwight? Dwight? True?
Speaker 3: Or maybe he got it from Bland Sutton, who in
Speaker 3: eighteen eighty nine used it along with crushed bone dust
Speaker 3: to treat lion cubs with rickets at the London Zoo,
Speaker 3: or from Casimir Funk, who wrote in nineteen fourteen, five
Speaker 3: years before melon Bee's experiment that quote. It is very
Speaker 3: probable that rickets occurs only while certain substances in the
Speaker 3: diet essential for normal metabolism are lacking or are supplied
Speaker 3: in insufficient amounts. The substances occur in good breast milk
Speaker 3: also in cod liver oil, but are lacking in sterilized
Speaker 3: milk and cereals. Or perhaps melon Bee and probably most
Speaker 3: of the people I just listed, got the idea because
Speaker 3: cod liver oil had long been a folk remedy for rickets,
Speaker 3: like for a very long time, especially for those living
Speaker 3: along the coast in Great Britain, which I kind of
Speaker 3: love when like this thing that is like, oh, take
Speaker 3: cod liver oil, it will cure your whatever, it will
Speaker 3: cure your you know, and then it's like, oh no,
Speaker 3: but it does actually does.
Speaker 2: Yeah, it has an incredible amount of vitamin D. Yeah,
Speaker 2: but also like who caught what's up with cod liver oil?
Speaker 2: Like whoa who made it in the first place, and
Speaker 2: why were they? Like let me take this in my mouth.
Speaker 3: I mean, yeah, the whole history of cod liver oil.
Speaker 3: I have a paper on it that I will I
Speaker 3: will post, but it goes back to ancient Greece. I
Speaker 3: think Hippocrates wrote about dolphin liver oil, which I don't
Speaker 3: know the content of vitamin D Okay, but it's been
Speaker 3: for I mean like really for hundreds, if not thousands
Speaker 3: of years. It's been a very common, how interesting medicinal thing. Yeah,
Speaker 3: I think it was also used for many other purposes,
Speaker 3: not just like medically. Oh yeah too.
Speaker 2: Yeah.
Speaker 3: However, Melanbee got the idea though cod liver oil and
Speaker 3: milk seemed to work wonders for rickets, and this was
Speaker 3: clearly shown in humans in a nineteen twenty two landmark
Speaker 3: investigation by Harriet Chick and co authors who used these
Speaker 3: to treat malnourished children with rickets and a clinic in
Speaker 3: post World War One. Vienna. Chick will come back into
Speaker 3: the story later, but first let's get back into the
Speaker 3: steps of vitamin D discovery, starting with detangling A and
Speaker 3: D to test whether rickets was caused by vitamin A
Speaker 3: deficiency or something else. In cod liver oil, McCollum, who
Speaker 3: was the person who first discovered vitamin A, and his
Speaker 3: colleagues destroyed vitamin A in cod liver oil through like
Speaker 3: heating or aeration, and then they use the resulting substance
Speaker 3: to treat rickets, and sure enough it worked, and so
Speaker 3: they concluded that this was a new vitamin, the fourth
Speaker 3: to be discovered, hence vitamin D, and that it was
Speaker 3: likely involved in bone growth. And around this time other
Speaker 3: researchers began to shine a light on the roll of light,
Speaker 3: particularly sunlight I couldn't resist as a treatment for rickets.
Speaker 3: Harriet Chick noticed that rickets seemed to be seasonal, appearing
Speaker 3: mostly in the winter, months and wondered if uv irradiation
Speaker 3: via lamps and sunlight could work as treatment and prevention
Speaker 3: for rickets. It certainly did, and was as effective as
Speaker 3: cod liver oil. Ooh, you know, this is actually I'm
Speaker 3: thinking of this now. So one of the things that
Speaker 3: I didn't include in here was the importance of the
Speaker 3: development of X rays in terms of diagnosing and understanding
Speaker 3: the extent to which people had vitamin D deficiencies. Some
Speaker 3: to look at their bones exactly, and that kind of
Speaker 3: like really helped understanding the scope of the problem. But
Speaker 3: as we talked about in our radiation episode, people thought
Speaker 3: radiation was also this like huge healing thing around that time,
Speaker 3: and so they were like drink uranium whatever, And so
Speaker 3: I wonder if uv irradiation and vitamin D like that
Speaker 3: was that hype around radiation contributed to that in any way.
Speaker 2: I don't know, that's interesting to think about.
Speaker 3: Ooh yeah. But I will say that people had long
Speaker 3: believed that sunlight could treat rickets, but this study done
Speaker 3: by Chick was one of the first scientific studies to
Speaker 3: demonstrate it clearly. And at nearly the same time that
Speaker 3: Chick was employing those uv lamps, a researcher named Holchinsky
Speaker 3: was also working in Vienna and demonstrated the same thing.
Speaker 3: And I can't help but think of how strange this
Speaker 3: would have seemed, right like to it blew my mind
Speaker 3: when I learned, I don't know how when that we
Speaker 3: make vitamin D from sun.
Speaker 2: I know, I know, it's just it's still as.
Speaker 3: Amazing to me. And so it must have been really
Speaker 3: strange to think, like, wait a second, so here's this thing,
Speaker 3: this vitamin that we find in incredible amounts in cod
Speaker 3: liver oil. But then also sunlight can help us make
Speaker 3: it Like what is what is going on here? And
Speaker 3: this question drew the attention of several researchers, Harry Goldblatt
Speaker 3: and Catherine Solmes at the Lister Institute and Harry Steinbach
Speaker 3: at the University of Wisconsin. Goldblatt and Solmes carried out
Speaker 3: what sounds like a fairly gruesome experiment. First, they fed
Speaker 3: rats on a diet that made them develop rickets. Okay.
Speaker 3: Then they killed those rats, took out their livers, and
Speaker 3: irradiated them. Still okay. Then they ground up those livers
Speaker 3: and fed them to other rats with rickets. That seems
Speaker 3: that's yeah, that's the part yeah, but hey, no more rickets?
Speaker 3: What uh huh? Okay okay, I know that was exact
Speaker 3: my reaction, and Steinbach did something similar, minus the forced cannibalism.
Speaker 3: So previously, he had worked with goats that showed calcium
Speaker 3: loss when living indoors in the winter without much sunlight,
Speaker 3: and so he wondered if that same lack of sunlight
Speaker 3: could be causing the skeletal changes in rats with rickets
Speaker 3: via vitamin D deficiency. To test this, he irradiated the rats,
Speaker 3: their food and the air in their cages to see
Speaker 3: if there was any improvement. There wasn't with the irradiated air,
Speaker 3: but definitely there was when the food or the rats
Speaker 3: themselves were irradiated. Hesse and Weinstock followed up these experiments
Speaker 3: by Goldblatt, Somes, and Steambock with yet another grizzly experiment.
Speaker 3: They induced rickets and rats, irradiated some of their skin
Speaker 3: but left other parts untouched, and then fed that skin
Speaker 3: to other rats with rickets. Those that were fed the
Speaker 3: irradiated skin of their brethren got back better, but those
Speaker 3: that were fed the non irradiated skin did not.
Speaker 2: It's just so weirdly specific.
Speaker 3: I have nothing well, but I think it's kind of
Speaker 3: amazing in that it showed the importance of skin in
Speaker 3: vitamin D production and skin as an organ rather than
Speaker 3: just a mirror protective covering quote unquote is the phrase
Speaker 3: that they had used, and that's like I think at
Speaker 3: that time maybe what it was largely thought to be right,
Speaker 3: But skin is doing something, doing something, so I don't know,
Speaker 3: I think that's kind of cool. I mean, not the
Speaker 3: forest cannibalism part again, but like skin. Once the roll
Speaker 3: of sunlight and vitamin D production became clear, all that
Speaker 3: was left to do was characterize the nature of vitamin D,
Speaker 3: what its chemical structure was, how it functioned, the physiological
Speaker 3: processes it was involved in, just the simple stuff. And
Speaker 3: throughout the nineteen thirties and nineteen forties, researchers filled in
Speaker 3: these knowledge gaps about vitamin D, differentiating D two and
Speaker 3: D three describing their chemical structures. Nobel Prize winner Adolph
Speaker 3: Windhaus played a large role in this, showing that cod
Speaker 3: liver oil contained D three, that vitamin D was a steroid,
Speaker 3: and revealing the detailed structure of vitamin D three via
Speaker 3: X ray crystallography, which was done in nineteen forty eight
Speaker 3: by doctor Dorothy Crowfoot Hodgkin Nobel Prize winner in chemistry,
Speaker 3: whom we've mentioned more than months on this podcast. We
Speaker 3: love actra crystallography. The rest of the twentieth century was
Speaker 3: filled with further important developments in our understanding of vitamin D,
Speaker 3: but for public health officials, the big chunks of knowledge
Speaker 3: were already there in the early decades of the nineteen
Speaker 3: hundreds that allowed them to enact measures reducing vitamin D deficiency,
Speaker 3: namely vitamin D supplementation through food or sunlight to help
Speaker 3: treat and prevent rickets and the consequences of vitamin D deficiency.
Speaker 3: Many programs supplementing children's diets with vitamin D had been
Speaker 3: underway since the late nineteen tens, and the widespread fortification
Speaker 3: of food with vitamin D, especially in milk and infant formula,
Speaker 3: led to ricketts nearly being eliminated in many places. But
Speaker 3: nearly is not the same thing as completely, and rickets
Speaker 3: is just one aspect of vitamin D deficiency. And I
Speaker 3: think that, as you mentioned erin, we are kind of
Speaker 3: increasingly becoming more vitamin D deficient. And so I'll turn
Speaker 3: it over to you now to tell me a little
Speaker 3: bit more about that.
Speaker 2: Ooh, I can't wait to Let's take a quick break
Speaker 2: and then I'll get into it really quick. Before I
Speaker 2: jump into the epidemiology, I wanted to just mention because
Speaker 2: I thought of it as you were mentioning that they
Speaker 2: used milk in these historical studies to treat rickets. As
Speaker 2: a couple of things, one is that milk is actually
Speaker 2: not high in vitamin D, but it is fortified with
Speaker 2: vitamin D in the US and in a lot of
Speaker 2: countries in Europe, though I'm pretty sure not in the
Speaker 2: UK currently. It's a whole other thing. And human breast
Speaker 2: milk is also very low in vitamin D. It has
Speaker 2: very poor transfer into breast milk in human breast milk,
Speaker 2: and so breastfed babies are actually at high risk in
Speaker 2: vitamin D deficiency, which I didn't mention when I was
Speaker 2: mentioning all the other ways that you can become vitamin
Speaker 2: D deficient.
Speaker 3: That's very interesting.
Speaker 2: It's especially when you think about it evolutionarily. But you know,
Speaker 2: if we just we're exposed to a lot more sunlight
Speaker 2: usually yeah, makes sense.
Speaker 3: So anyways, Oh, that was actually a question that I
Speaker 3: was going to ask in biology, and then I forgot,
Speaker 3: how quickly do we make vitamin D from sun exposure?
Speaker 2: Oh, that's such a fun question. I have some numbers
Speaker 2: on that. Actually, there's some estimates that for example, and
Speaker 2: this of course will depend on like the day and
Speaker 2: the season and the latitude and et cetera, But exposure
Speaker 2: of your arms and legs for five to thirty minutes
Speaker 2: between ten am and three pm twice a week usually
Speaker 2: makes enough that people don't become deficient. That was one
Speaker 2: estimate I saw. Another one is that exposure to where
Speaker 2: your skin gets just a little bit red not recommended
Speaker 2: skin cancer, et cetera, while wearing only a bathing suit
Speaker 2: is the equivalent of ingesting about twenty thousand international units
Speaker 2: of vitamin D. WHOA, I know, isn't that interesting?
Speaker 3: Wow?
Speaker 2: Yeah? So yeah, so it can kind of vary, but yeah, okay, anyways,
Speaker 2: this is supposed to be the epidemiology section. Let me
Speaker 2: tell you since, like I laid out in the biology section,
Speaker 2: the definitions that you use for deficiency and insufficiency are
Speaker 2: going to vary, and so unsurprisingly are estimates for population
Speaker 2: level numbers of deficiency or insufficiency. They vary. Okay, they're
Speaker 2: not great, But I do actually have a lot of
Speaker 2: numbers for you. Looking at deficiency as defined as less
Speaker 2: than twenty nanograms per mill or fifty animals per leader,
Speaker 2: which is kind of the most common definition. Rates of
Speaker 2: vitamin D deficiency are as high as twenty four percent
Speaker 2: in the US, thirty seven percent in Canada, and forty
Speaker 2: percent in Europe, depending on what paper you look at.
Speaker 2: Some studies even say that up to one hundred percent
Speaker 2: of elderly adults might be deficient. That seems excessive. WHOA
Speaker 2: if we look at severe deficiency or what in some
Speaker 2: cases is just defined as deficiency. If the other version
Speaker 2: is just insufficiency, and that is less than twelve nanograms
Speaker 2: per mill or thirty animals per leader, that's estimated to
Speaker 2: be at around six percent in the US, seven point
Speaker 2: four percent in Canada, and thirteen percent in Europe. And
Speaker 2: now these are all very big places, and these are
Speaker 2: all very big populations, and that's not even including so
Speaker 2: much of the rest of the world. I do have
Speaker 2: numbers as well for India, Tunisia, Afghanistan. These just happen
Speaker 2: to be some places that have data in the papers
Speaker 2: that I read there, those estimates tend to be around
Speaker 2: twenty percent or more of the population that may be deficient,
Speaker 2: and I don't have numbers for severely deficient globally. What
Speaker 2: this adds up to is that it's estimated that one
Speaker 2: billion people worldwide have vitamin D deficiency or insufficiency, that
Speaker 2: less than twenty number, and of course this is going
Speaker 2: to be higher in certain subpopulations as well, like kidney
Speaker 2: failure or with severe liver disease. When it comes to
Speaker 2: looking at the diseases that we know are caused by
Speaker 2: vitamin D deficiency, specifically rickets, the numbers are thankfully much
Speaker 2: less dire than they once were. In a twenty seventeen
Speaker 2: review looking at rickets, the case rates were estimated at
Speaker 2: between three and twenty seven cases per one hundred thousand
Speaker 2: individuals in the US and in Europe.
Speaker 3: That's higher than I thought.
Speaker 2: It's higher, but it's a decrease from an estimated prevalence
Speaker 2: as high as twenty five percent or like you even
Speaker 2: saw you're in ninety six percent of kids who died
Speaker 2: and twenty five percent of kids overall in the late
Speaker 2: eighteen hundreds. Yeah, so that's massive. A lot of that
Speaker 2: in the US and Europe is likely in part due
Speaker 2: to fortification programs like you mentioned with formula and milk,
Speaker 2: all milks in the US, including plant based milks and
Speaker 2: orange juice. Weirdly, yeah, is fortified with vitamin D as
Speaker 2: well as supplementation. The recommendation for supplementation in like breast
Speaker 2: fed infants and things like that. So we know that
Speaker 2: those kind of programs can improve this risk of severe
Speaker 2: vitamin D deficiency can reduce the prevalence of things like
Speaker 2: rickets osteomolasia in adults. I had a really hard time
Speaker 2: finding data on probably because it's just widely underrecognized in general.
Speaker 2: Despite all of that, like good news, we still know
Speaker 2: that those numbers of overall deficiency are pretty high.
Speaker 3: Yeah, they are like.
Speaker 2: Twenty to forty percent. Like that's really high numbers. So
Speaker 2: then this is where things get a little weird.
Speaker 3: It's kind of fun, Okay, my favorite two adjectives put together.
Speaker 2: Because we know that deficiency, whatever specific number you choose
Speaker 2: to use to define it, is a problem. We know
Speaker 2: that there's epidemiological data to suggest that it's associated with
Speaker 2: a lot of risky, scary sounding things cancers, cardiovascular disease,
Speaker 2: et cetera, et cetera. There's these associations because of this,
Speaker 2: Because of those two things, there are a lot of spheres,
Speaker 2: especially on the interwebs.
Speaker 3: Oh, the interests.
Speaker 2: Say that everyone needs to be supplementing, we all need
Speaker 2: to be taking supplements, every one of us. And the
Speaker 2: thing is a lot of studies have looked at this,
Speaker 2: a lot of studies in the recent ten years or so,
Speaker 2: since about twenty eleven, when a big Institute of Medicine
Speaker 2: report came out that said, here's the recommend did daily intakes,
Speaker 2: Here's how much vitamin D we need to be getting
Speaker 2: to hit these thresholds of twenty nanograms per mil you know,
Speaker 2: across the board. They were also like, hey, we also
Speaker 2: need a lot of better research to figure out do
Speaker 2: we need supplementation widespread or are we doing okay with
Speaker 2: just our diets and the fortification programs that exist. So
Speaker 2: a lot of studies have come out since that twenty
Speaker 2: eleven paper that have tried to look at this, specifically
Speaker 2: looking at widespread supplementation with vitamin D supplements at various
Speaker 2: levels one thousand a day, two thousand a day, four
Speaker 2: hundred a day, whatever, without checking first if someone is
Speaker 2: deficient or not for them to be in the study. Okay,
Speaker 2: let's take a group. Yeah, let's take a group of people.
Speaker 2: Let's give them vitamin D and see what happens. And
Speaker 2: most all of that data, whether in individual studies or
Speaker 2: in meta analyzes, does not improve outcomes. So there is
Speaker 2: data to suggest that this widespread supplementation without checking if
Speaker 2: people are deficient before they're in the study, does not
Speaker 2: reduce the risk of fractures, does not reduce the risk
Speaker 2: of low bone mass or osteoporosis. Those are just the
Speaker 2: skeletal things. It also doesn't have any evidence for prevention
Speaker 2: of cardiovascular disease, prevention of falls, improvement in cognitive function,
Speaker 2: prevention of stroke, prevention of all cause mortality, or cardiovascular mortality.
Speaker 2: And this is all super fascinating to me.
Speaker 3: Ugh, I mean it is. It's interesting. I don't know
Speaker 3: if I love that they didn't test people's baseline vitamin
Speaker 3: D levels, but that.
Speaker 2: Is kind of part of the questions, right is its
Speaker 2: do we need widespread supplementation?
Speaker 3: Yeah?
Speaker 2: Well, and where it gets even more interesting is that
Speaker 2: there's also been a really big push in the literature
Speaker 2: when it comes to even screening for vitamin D deficiency.
Speaker 2: Essentially looking at the costs to healthcare systems to test
Speaker 2: everybody for vitamin D deficiency, either annually or on some frequency,
Speaker 2: just as a routine lab with no real indication, like
Speaker 2: no symptom that you're worried about, no specific risk factor
Speaker 2: like kidney disease or whatever, but just like check it
Speaker 2: on everybody. That happens in a lot of places as
Speaker 2: a matter of routine, and there's not a lot of
Speaker 2: data to suggest that it's beneficial, especially when you look
Speaker 2: at what the supplementation studies also show that, like widespread
Speaker 2: supplementation also isn't helpful. And yet at the same time
Speaker 2: we know that deficiency is probably underestimated. So it's just
Speaker 2: it's really interesting.
Speaker 3: We do not have it figured out.
Speaker 2: No, we don't. And I do think that part of
Speaker 2: this comes back to what I mentioned when I said
Speaker 2: that while we have a lot of these epidemiological associations
Speaker 2: between low vitamin D status and all these various diseases
Speaker 2: or outcomes, we do not have evidence of these relationships
Speaker 2: being causal. And if they're not causal, then there isn't
Speaker 2: a reason why supplementation would improve any of those outcomes.
Speaker 2: We wouldn't expect it, so are they. A consequence is
Speaker 2: vitamin D deficiency some kind of early or easily identified
Speaker 2: consequence of various diseases, disorders, conditions.
Speaker 3: I love this, It's really it's really good food for thought.
Speaker 3: It is what does vitamin D mean beyond vitamin D?
Speaker 2: Yeah, And it's so fun to read about because the
Speaker 2: drama when you read some of these articles, Oh gosh,
Speaker 2: you know what it felt like, Aaron, this is very niche,
Speaker 2: but it felt like the dilution effects.
Speaker 3: Oh, which just easy.
Speaker 2: Conscious people are just like so passionate everyone Like people
Speaker 2: are like, we're everyone is defficient. You need to be
Speaker 2: supplementing with everything, and people are like, no, never take
Speaker 2: a supplement.
Speaker 3: Like it's just a very strong feelings about this.
Speaker 2: Such strong feelings, which I feel like always tells you something,
Speaker 2: you know, when people are so steadfast and like this
Speaker 2: is the one and only way, Like, eh.
Speaker 3: It probably means that the truth lies somewhere in that
Speaker 3: at all, exactly.
Speaker 2: I think that that what it means is that the
Speaker 2: truth lies somewhere in. Vitamin D is an important substance
Speaker 2: that is necessary to human life and function and a
Speaker 2: lot of our different human functions, and we need to
Speaker 2: know more about it, and there's a lot of people
Speaker 2: in the world who probably aren't getting enough of it,
Speaker 2: either they're not making enough of it or they're not
Speaker 2: getting enough of it in their diet or some combination thereof.
Speaker 3: Yeah, sums it up.
Speaker 2: But that's that's vitamin D. There's a lot more there.
Speaker 2: There's cool stuff like you mentioned the vitamin D and COVID.
Speaker 2: There's a lot of really interesting research being done on
Speaker 2: vitamin D and like severe illness and sepsis, severe infection
Speaker 2: in general, super interesting stuff. No answers, of course, not
Speaker 2: but really interesting.
Speaker 3: And speaking of really interesting things. In case you want
Speaker 3: to read more, should we do sources?
Speaker 2: Yeah, we absolutely need to.
Speaker 3: Okay, I have many, and I just want to shout
Speaker 3: out too in particular. All the rest will be on
Speaker 3: our website. One is by Carlberg from twenty twenty two
Speaker 3: called Vitamin D in the context of evolution and then
Speaker 3: in terms of the history of vitamin D. One paper.
Speaker 3: There were many, but one paper I really liked was
Speaker 3: by Roja Kumar from two thousand and three called Vitamin D,
Speaker 3: cod liver oil, sunlight and rickets excellent.
Speaker 2: I also had a number of for this episode. A
Speaker 2: few of my favorites just about the biology and kind
Speaker 2: of current epidemiology of vitamin D. One was just called
Speaker 2: Vitamin D Deficiency in the New England Journal of Medicine.
Speaker 2: That was a very useful one. Another was the Diagnosis
Speaker 2: and Management of Vitamin D Deficiency that was published in
Speaker 2: BMJ back in twenty ten, a little older. And then
Speaker 2: of course there's those really fun papers looking at vitamin
Speaker 2: D supplementation and all of the various things. Some of
Speaker 2: those are coming from the Vital Study VIL. We will
Speaker 2: post the list of all of our sources from this
Speaker 2: episode and every one of our episodes on our website.
Speaker 2: This podcast will kill you dot com.
Speaker 3: We sure will. A big thank you again to Brittany
Speaker 3: for sharing your first hand account. Thanks so much for
Speaker 3: being willing to do that.
Speaker 2: Yeah, thank you. Thank you also to Leona Scuilacci for
Speaker 2: your amazing audio mixinc.
Speaker 3: And speaking of audio, thank you to Bloodmobile for providing
Speaker 3: the music for this episode and all of our episodes.
Speaker 2: Thank you to the Exactly Right Network, and.
Speaker 3: Thank you to you listeners. We hope that you liked
Speaker 3: this A deep dive into vitamin D. Who knew it
Speaker 3: would be so very deep.
Speaker 2: Tell us if you're really mad at our, If you're
Speaker 2: like closure's the truth. And of course a special shout
Speaker 2: out to our patrons. Thank you so so much for
Speaker 2: your support. We love it. It means the most, it
Speaker 2: really does.
Speaker 3: Thank you. Okay, well, until next time, wash your hands,
Speaker 3: you filthy animals. O