I’m dr. Chris master John of Chris
master John PhD comm and I’m here with Alex leaf Hey and you are listening to
episode 66 of mastering nutrition where we talk about pantothenic acid part 2
foods lab tests and supplements this is a spring nutrition with Chris master job
take control of your health master the science and apply it like a pro this is
part 2 of our two-part series on pantothenic acid or vitamin b5 where I’m
covering the basic science how much we need from food how to get it from food
how to use lab testing to know if we have enough and alex is covering the
health outcomes and other effects of supplements if you missed part 1 you can
find it at Chris master John PhD comm / 64 and because this is episode 66 you’ll
be able to find the show notes for this episode at Chris master John PhD comm /
66 to catch you up to speed and review the symptoms of signs and symptoms of
vitamin b5 deficiency are fatigue loss of enthusiasm and energy insomnia grumpy
mood cramps including but not limited to in abdominal cramps gut problems like
increased farting feeling nauseated sometimes throwing up getting sick more
often a high pulse in response to minor exertion and potentially neurological
problems causing tingling or numbness in the hands and feet and even stranger
things like an inability to walk on tiptoe and occasionally manifesting in
individuals in inconsistent patterns that might cause constant burning
sensations or constant numbness in the hands or feet and walking funny by
lifting up the foot more than you think you should normally have to when you
walk the forms of vitamin b5 that we use for
enzymatic cofactors to support our metabolism are for phospho panteth een
and coenzyme a when we eat food 85% of the vitamin b5 is found as for Fausto
pantothenic Oh enzyme a coenzyme a is a complicated molecule that takes a while
to digest then a for Fausto panting is all bound to proteins which requires
digesting through the protein to get to it and as a consequence only about 50%
of the vitamin b5 in food is fully digested and absorbed contrary to the
claims of major authoritative reviews we do absorb according to the evidence
significant amounts of forms of b5 from food besides just pantothenic acid so it
is claimed that we digest it all down to pantothenic acid which is found in the
free form in about that’s about 15% of food vitamin b5 is pantothenic acid and
pantothenic acid is not something that we use in the body apart from converting
it to for Fausto Panda theme and coenzyme a in a rather complicated and
very energy intensive and arguably difficult process that involves not just
magnesium and ATP but also involves cysteine which we need vitamin b6 and
glycine to get as well as sufficient protein including the sulfur amino acids
that are more abundant in animal protein than plant protein so it is not a simple
task to make the conversion of pantothenic acid to pour phospho panda
theme and do coenzyme a and in fact there are various genetic defects
causing severe problems in the ability to make those conversions but if you go
back and look at the old literature actually it indicates that we don’t
digest it all down to pantothenic acid but we do absorb for phospho a Panta
theme and pianta theme both of which are more easily converted to coenzyme a or
two for Fausto Penta theme itself which we absorb itself the other major
cofactor that we need when we absorb b5 from food or supplements it does not
stay in our blood for long it’s very quickly transported to our other tissues
it’s known that pantothenic acid is not a major circulating form of vitamin b5
it’s maybe three to eight percent of the total and on till recently we didn’t
really know what the other forms were but there’s recent data suggesting that
the main circulating form delivered to tissues may be four phospho Panda theme
we have very important needs to regulate the amount of coenzyme a that is free
and the amount of coenzyme a that is bound to other molecules and as a result
of that need most likely we break down a small amount every day into pantothenic
acid we don’t know what the total body stores are but they might be about 4.5
grams and we may be excreting in the urine around 4 milligrams or varying
depending on total body status and I’ll make the argument in this episode that
in fact urinary concentrations are very usable reflectors of whole body
nutritional status for vitamin b5 and blood concentrations are not during
adolescence there is probably a markedly increased need for b5 to produce sex
hormones and one hypothesis is that this is why we have an increased risk of acne
during the teenage years during pregnancy and especially in the third
trimester there’s active movement of b5 to the fetus at the mother’s expense and
during lactation there is a movement of significant amounts of pantothenic acid
into the milk at the mother’s expense doses of supplements have been used at
grams per day and they appear to be safe and to be used with high efficiency this
is probably a matter of repleted the whole body stores which as I mentioned
greatly exceed our daily intakes in this episode we talk about what is
the ideal marker for nutritional status what can we do with that to learn how
much we need how do we get that from food do we in fact get any from the
microbiome what are some of the factors that would make us need more what if
anything at all can we say about the prevalence of b5 deficiency Alex goes in
great detail into talking about the differences between panteth thein
pantothenate and dex panteth all he talks about oral and topical uses of b5
supplements he talks about using them for blood lipids for acne and for wound
healing and addresses the question of whether b5 can influence exercise
performance or whether exercise performance influences our need for b5
and whether it can do anything for the greying of hair or for arthritis we
talked about dosages we talked about safety and we talked about how dosages
and safety differ between the different forms and we talked about things like
whether you should take it with food whether you should spread it out over
the day or take it all at once and practical things of that nature again
this is part 2 of a two-part series you can find the other part at Kris master
John PhD dot-com / 64 this is part of a larger series on managing nutritional
status and you can find all the episodes at Kris master John PhD comm / marker
number sign episodes you can get a transcript if you sign up for the CMG
master pass at Chris Masters on PC comm / master pass / mastering nutrition
which that specific URL will give you a 10 % lifetime discount and you can get
all these links in the shown in the description of this episode so let’s dig
right into all the science right after this word from my sponsors this episode is brought to you by
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at checkout mouse models to address it and in the
mouse you don’t have a perfect model because in the human there’s pink one
which is the enzyme that’s dominant in the liver and paint too dominant in the
nervous system and the genetic defect is just in pink too and in Mouse in the
mice it’s not divided the same way their pink one is most abundant in liver but
their pink too is most abundant in their testes rather than their brain so
there’s no specific way to target the defect right into the brain in mice like
there is in humans but as I mentioned it before at the beginning when the pink to
defective mice are given a ketogenic diet they get dramatically worse they
really start like with devastating neurodegeneration and panteth signs
supplementation the form that Alex was talking about can rescue them now in
humans many people have tried a ketogenic diet and know in that no one’s
reporting anything net positive or devastating or harmful from the
ketogenic diet so be basically ketogenic diets so far anecdotally don’t seem to
be doing anything one way or the other for this disorder also in humans there
are a lot of people trying Panta find supplements but it’s not clear whether
they’re working there’s no clinical trials to gauge the progress and there’s
no overwhelming anecdotal support for using pianta thein versus pantothenate
however one thing to note is that panteth thein generates two molecules of
panteth theme when it’s split and Penta theme does have some of the ability to
bypass some of the steps and some of the ATP utilization that the four phospho
Panta theme and the coenzyme a would in food it’s just that panteth thein is not
going to bypass anywhere near as much as you would bypass
by getting four phospho panteth in from food and from the digestion of coenzyme
a in food so researchers have continued to try to find things to do about this
and one of the this was the basis for why in 2015 they found that for Fausto
panda theen was stable in blood and they tried it in mouse models and fruit fly
models of the pantothenic kinase deficiency and it works the problem is
that for Fausto Pinta theme is very difficult to synthesize in high amounts
in high purity to give it to people as a high dose supplement or as a drug
depending on how you would view supplementation with it also it has a
free sulfur group that makes it have a very bad shelf life now if you compare
that to the for Fausto panting in food you don’t have to synthesize it because
the animals and plants are doing it for you and you don’t have to worry about
the stability because it’s bound up in the proteins in that food that protect
it until you digest it so when you’re taught so when you’re talking about food
for Fausto panda thing you don’t have the stability issues that you have with
developing it in pure form so what they did was they developed an acetylated
form of it to protect the sulphur from oxidation and what they found was that
in in human embryonic kidney cells and in fruit fly larvae and in mice when you
made them genetically defective in pentatonic kinase you could completely
rescue the disease by feeding the acetylated form of four phospho Panta
theme remember for phospho Panta theme is one of the major forms in food what’s
the other major form in food coenzyme a what else can rescue fruit flies larvae
live fruit flies mice zebrafish and human cell models of pantothenic kinase
deficiency coenzyme a in every single model preformed coenzyme a
completely rescues the the phenotype the genetic disorder becomes not a genetic
disorder when provided with enough for faso panda theme or coenzyme a which are
the 85% of the beef i found in food and that makes you wonder how what kind of
doses do you need because as we’ll talk about in part two there’s not a lot of
pantothenate in food and really you’re looking at who at nutritional yeast
having the most and liver being a distant second and everything else being
way below that which is funny right because pantothenic acid is named after
the fact that it is everywhere and in everything but it’s not very evenly
distributed in the food supply so i wonder what would happen with
nutritional yeast supplementation and liver eating a lot of liver or you know
at least managed depending on the doses they need you could overdose on the
vitamin a or copper in liver you could overdose on the selenium and nutritional
yeast but I do wonder whether the food forms of vitamin b5 from the foods that
no one eats could have a significant benefit here now there are also genetic
defects in the final steps of Co a cons I’m a synthesis and in some of the ones
in the middle that are more recently discovered and that are more rarer and
for the final steps none of the models have shown any benefit to coenzyme a or
for Fausto Pantha theme and the disease the more the disease manifest is very
similar so there are people with coenzyme a genetic defects who can’t
probably cannot be rescued by the supply of for faso panteth een or or any of
these other things although maybe certain drugs will be developed in order
to help them but where the benefit really is where where it’s very
promising is in people with the for with the pantothenic kinase deficiency and so
this has to make you wonder what if there are polymorphisms that result in a
10 or 20% loss of pantothenic kinase activity could there be many of us out
there who would be completely fine if we had enough
food form vitamin b5 but who would suffer from at least moderate problems
if we didn’t and who would not benefit from taking pantothenic acid supplements
the way we would benefit from food form b5 I think you can make a very
compelling case from this that consuming b5 in food is at least insurance against
the possibility that you could have problems converting the pantothenic acid
in supplements and I think you could make a hypothesis that there may be
polymorphisms out there in the world right now that are making some people
benefit tremendously from eating the foods that are very rich in vitamin b5
so with that this is the end of part 1 but we will come back for part two to
talk about markers of nutritional status how much we need how to get it from food
and how to get it from supplements alright so let’s talk about vitamin b5
and what we know about how much we need first we need to understand what we
should be using as markers for nutritional status I will make the case
that the best marker of in fact the only legitimate marker of nutritional status
is urine concentrations and that blood concentrations are not a useful marker
of nutritional status in fact I’m not sure exactly what I’m gonna do for my
testing nutritional status the ultimate cheat sheet I am going to have to remove
the recommendation to use blood levels of pantothenic acid that are offered by
lab core but the only the only lab that offers urine testing for pantothenic
acid is the Great Plains organic acids test and you have to order the whole
test for a lot of money in order to get that so I think what I will do is
suggest that people who have signs and symptoms that seem like they could be b5
deficiency should use the Great Plains test instead of the Genova test when
doing comprehensive nutritional screening but that people with financial
limitations should just try because of its safety ways of
increasing vitamin b5 intake through foods and supplements if they believe
that they might be deficient so let’s let’s lay out that case that that urine
and not blood is where you want to measure it in the study by Peggy Frey in
1976 that I mentioned at the beginning of the last episode where concentration
where people were put on nine weeks of either a pantothenic acid efficient
synthetic diet or a pantothenic acid replete synthetic diet they looked at
the urinary excretion and the blood concentrations over many periods in this
study and what do you find is that in the urine the the pantothenic acid in
the deficient group dropped each week of the study getting worse and worse and
worse by the end of the study dropping 74 percent in the replete group they
were actually getting better pantothenate than what was in their diet
because their diet was you know probably mediocre and then now they’re getting a
synthetic diet with 10 milligrams per day and the supplement is actually
probably absorbed better than what whatever was in the diet because
supplements are probably absorbed at low doses with close to a hundred percent
efficiency and diet is absorbed with about fifty percent so they have better
pantothenate status than they came into the study and their urine concentration
goes up each week of the study by the end of it going up 47 percent now
contrast this with what happened in the blood in the blood in the deficient
group it dropped by 28 percent but then it started recovering so instead of
getting worse and worse and worse through the course of the study after an
initial drop it started getting better and better and better by the end of the
study in the replete group even though they were getting better pantothenic
acid status they actually dropped 12 percent at first and then fully
recovered by the end so part of the drop in pantothenic acid early in the study
in the the deficient group was something about
the synthetic diet that they put them on because it happened in the control group
as well and what you find in both cases is that the blood tends to recover over
time what if they had put these people on a deficient diet for 18 weeks
probably the blood would have gone back up to what had been in the first place
so in dramatic contrast to the blood results the urine results faithfully
reflect the degree of deficiency and the length of time that you’ve been
deficient for another thing that’s really interesting is that they took
both groups at the end of the study and they said okay one group has been
deficient for nine weeks the other groups that has been really good status
for nine weeks by taking ten milligrams a day now let’s give you all 100
milligrams per day what happened in the we then the group that had been getting
10 milligrams per day for the nine weeks the control group they immediately shot
up to from from 5.8 milligrams of pantothenic pantothenic acid in their
urine per day to 52 and then to 62 so they shot up very fast in the deficient
group they shot up fast but only to 36 it took them a whole week to get up to
59 so after one week of taking a hundred milligrams a day everyone gets up to
around 60 but the group that had been deficient in the past took a lot longer
to get their urine concentrations up that high then they let everybody else I
mean excuse me everybody just start eating what they usually eat so I went
back to regular diets that were mediocre the deficient group the group that had
been deficient this is now over a week since they had been in the deficiency
group right they so these people they nine weeks of deficiency one week of a
hundred milligrams a day and now they go back to their to their regular diet for
a week so it’s been two weeks since they were part of the deficiency group
their urinary concentrations go down from 6213 but in the sufficient group
we’ve been getting good pantothenate dosing all along they went up to 100
milligrams a day for a week they drop down to their usual diet for a week they
only went down to 20 so so the past experience of sufficiency led to 20%
higher urine values at the very end of the study compared to the past
experience of deficiency so what’s going on in this I believe that you lose a a
some certain percentage of your total body stores of pantothenic acid on a
daily basis and this is because you’re trying very hard to conserve your
coenzyme a and your for Fausto Panta theme but if you need to if you need to
regulate the acetyl co a to free Co a ratio or you need to concert if you need
to regulate the total Co a pool you’re going to wind up degrading some of it
and because you’re always going through a fasting feeding cycle you’re always
shifting around the co way needs of more you know more need in the liver during
the during the fasting state for example where the liver is acting as a metabolic
hub to support the energy needs of the rest of the body by making glucose and
by making ketones so as you’re always cycling through the fasting feeding
cycle you’re shifting the co e needs around at the different tissues and
they’re always gonna have some that’s being degraded as a result of that
that’s the model that I’m using to understand why you’re losing this little
bit in the urine everyday but just like say creatine you you will you have 120
grams of creatine in your body and you lose about 2 grams a day which is 1.6
percent and in that case it’s because the creatine gets just randomly damaged
it’s not a controlled process but if you look at the excretion of creatinine in
the urine which is down product of creatine it’s
proportional to the total creatine stores of your body so if you increase
your muscle mass your urinary creatinine is gonna go up if you start taking
creatine and increase the amount of creatine stored in your muscles your
urinary creatinine is gonna go up I believe that urinary pantothenic acid
is very much the same thing if you increase your your whole body stores
then there’s some small percentage of the whole body stores that will be
degraded and that is what is reflected in the urine that’s why urine faithfully
goes up when your status gets better and better
urine faithfully goes down when your status gets worse and worse and that’s
why when you see piggie fries study in 1976 that I was just describing why the
past history of deficiency or sufficiency is reflected so clearly in
the urine stores and by contrast what is what is blood reflecting ninety percent
is in is in the erythrocytes to red blood cells and what is it serving it’s
serving the metabolic needs of the erythrocytes and so it the erythrocytes
their needs don’t change because you’re deficient their needs don’t change
because you’re sufficient their needs don’t change because you’re mega dosing
and so they’re their needs as long as you’re not pushing the system to
dramatic levels one way or the other their needs are gonna stay pretty
constant the blood values are gonna stay pretty regulated now it gets a little
worse so Eisenstaedt in 1986 looked at blood levels and urine levels and intake
and they found that intake correlated 14 percent with the levels in blood and 36
percent in the urine so at first you look at this and you say okay it
correlates three times better with urine than with blood but there’s another
important point the urine didn’t correlate with the blood at all the
correlation between urine and blood was zero and so what that means is that you
have to pick one if both of them were offering some information about status
then whatever this that information about status is that’s contributing to
either of them would make blood and urine correlate but
if if they don’t correlate at all only one of them can be telling us about
status and if only one of them is telling us about status we have to pick
one and if we pick one we have to take the thing that reform that we know
reflects long-term status that we know faithfully gets worse when you get worse
that faithfully gets better when you get better and that one is not blood it’s
urine in further support of this fox and lynx Weller in 1961 took women on an
average diet and put them on three doses of pantothenic there were doses that
were lower and doses that were higher than what they were usually taking in in
the low dose were they dropped to a lower pantothenate intake they were
eating 2.8 milligrams per day and they were losing somewhere between 3.2 and 4
milligrams per day in their urine if urine was going to reflect acute intake
that would be impossible they’re not urinating out the excess over what
they’re taking in their urinating out something that’s reflecting their full
body stores that’s why they’re urinating out more than what they took in because
they were only recently put on the deficient diet and their body stores are
intermediate or maybe even pretty decent and so the amount that they lose in
their urine has nothing to do with this new deficient diet they’re on it has
everything to do with their full body stores in further support in late
pregnancy pantothenate levels drop in blood but they don’t drop in urine and
milk correlates with diet and with urine but not blood supplementation in
pregnancy raises milk levels fivefold but not blood in further support in
pregnant women the blood concentration to drop as the pantothenate moves
towards the fetus in through the umbilical cord
but the urine doesn’t drop and that’s because the
if they are well nourished during pregnancy still have good whole body
stores their urine reflects their whole body stores and their blood drops
reflecting the what they are doing with it right now because they are
transporting it from their blood into the umbilical cord blood and then in
lactating mothers the milk correlates very well with diet and with urine but
not with blood this reflects the fact that you’re putting pantothenate into
the milk in reflections of your ability to do so which are reflected in your
whole body stores and that your urine is a faithful reflection of your whole body
stores but you don’t see the correlation in blood
because what you’re immediately doing is using your blood to transport the
pantothenate into the milk so the blood is reflecting very acute events of where
things are going where and it’s reflecting the the needs of the
erythrocytes whereas the urine as long as you’re not currently taking a mega
dose I believe will faithfully reflect the whole body stores if you take a mega
dose of a supplement some portion of that that’s not retained does go in the
urine but when you go off that supplement for a day your urine goes
back to reflecting your whole body stores so can we use this to determine
how much we need in the 1998 DRI report they used the fact that in 19 to 50 year
old adults urinary excretion equaled intake at four milligrams per day and
they basically use the idea that you want to maintain pentatonic status
balance you don’t want to urinate out more than you’re taking in so they
looked at data and they said okay the point at which your intake equals your
excretion is that four milligrams per day so let’s say that five milligrams
per day is enough to make sure that you’re not losing pantothenate over time
and then they extrapolated downwards for all the children based on body
weight values for infants 0 to 6 months they took the average amount that what
they were taking in from milk and for pregnant women they rounded the data the
average consumption among pregnant women up to 6 milligrams and because there’s
an extra 1 point 7 milligrams put into the milk they increased the adequate
intake to 7 milligrams for nursing mothers let’s come back to this idea of
pantothenic acid balance how much can we trust the concept of not wanting to take
in less pantothenic acid than were than we are excreting in the urine for that
Alex I know you’ve done a lot of research in using nitrogen balance as a
marker of protein needs which is a very similar idea can you comment on you know
what you’ve learned about the limitations of using nitrogen balance
for protein as an analogy yeah it all comes back to the body being smart and
adaptable and not trying to actively kill itself so with nitrogen balance in
protein studies the issue is that they’re waiting for the body to
establish an equilibrium at various intake levels of protein and this
requires being on for example a low protein diet for one to two weeks but
the body is smart and that’s adequate time for it to start down regulating
important processes that are not essential for survival but that do
contribute to overall health such as immune function and muscle protein
synthesis and so nitrogen balance studies are inherently flawed because
they provide a lower limit of what’s necessary for survival but not what’s
necessary to maximize health over the long term if we’re going to bring
back to pantothenic acid and then we can presume it would be similar where the
urinary excretion would be the body could adapt and therefore reach an
equilibrium based on survival needs rather than optimal health needs yeah so
the first idea here is that the is that there is no rationale in the DRI report
for using the balanced approach and as Alex pointed out we know we know very
well that the body engages in all kinds of compensations to try to preserve
itself when you go on low intakes of something but there’s a bigger problem
here which is that if there’s a math problem here if dietary pantothenate is
50% bioavailable then the people who are consuming 4 milligrams a day are
absorbing 2 milligrams a day and if an intake of 4 milligrams a day equals a
urinary excretion of 4 milligrams a day then they’re actually absorbing 2
milligrams a day and losing 4 so they’re losing 2 milligrams a day now we don’t
know how big the co the the b5 pool is in humans
I made a rough guesstimate based on rat data adjusting for size of organ weights
that it would be 4.5 grams and Alex I cited some disgusting study in episode 1
suggesting that we can actually retain 5.6 grams of a megadose so we don’t we
don’t know exactly what the pool is and we don’t know how variable it is but if
we just slap some numbers on this if you’re if you’re consuming 4 milligrams
a day you’re absorbing 2 milligrams a day and you’re losing 4 you have a net
loss of 2 milligrams a day you would run out of your whole body stores in 6 years
if your whole body stores are 4.5 grams obviously that’s not going to happen and
you’re gonna engage in all kinds of compensations to preserve the b5 pool
including urinating less out of it but that doesn’t mean that your
getting very far away from your optimal health level and I think it’s very very
interesting to take this back to the original studies of deficiency in the
1950s they were giving the people a pantothenic acid deficient diet and an
antagonist and six weeks through the study they are several weeks through the
study they had to increase the dose of the antagonist because the people were
adapting and conserving and stuff but they were still clearly not that healthy
and and we you know we can also say from the Peggy Fry’s 1319 in the 1970s that
nine weeks per just produced fatigue and loss of enthusiasm and didn’t produce
the worst neurological effects well why because over those nine weeks
what happened to the urinary pantothenic acid it shot down because they were
conserving their stores right so so it seems very it seems like at four
milligrams a day we’re probably not even in pantothenic acid balance and we can
be pretty sure that that’s actually deficient but we don’t really know you
know what is the potential to what what is the potential to optimize health with
higher intakes and one thing that’s that’s that I think is worth asking is
if we just use our imagination for a moment I’d like to think about how much
might we be able to improve our pantothenic acid pools over time with a
very good diet from the average and we don’t have data on that but Alex can you
come in and talk about as an analogy with muscle mass you know there’s
there’s an average that we have from just doing normal life what is our
potential to expand that pool of muscle protein so if we go back to the
reference man that was put together in 1975 weighing 70 kilograms or about 154
pounds they have 40% of their body weight as
muscle mass which is about 62 pounds and when we look at estimates of how
much muscle you can put on with consistent resistance training as we
work towards our maximum genetic potential we can see that you can put on
20 to 25 pounds in about one year which corresponds to two pounds per month
after two years after that one year during the second year that rate slows
by about half and it slows by another half during the third year of consistent
proper training but overall over a three year period of consistent proper
resistance training you can expect for that reference man was 62 pounds of
muscle he could expect to double his muscle mass before it begins slowing
down to you know being only about 2 to 3 pounds of muscle per year if that um
where someone would be considered a very advanced training but as we discussed in
part 1 of this podcast with most of the pantothenic acid being stored in
skeletal muscle tissue 30 to 40 percent of it then and we can expect from all of
the studies and humans that these are done in being just lightly active
certainly not regularly resistance training people that they could double
their biggest storage site of pantothenic acid so there is a lot of
potential to expand this pool yeah I mean that’s that’s pretty fascinating
because if you double your your muscle mass you almost certainly need a lot
more pantothenic acid because just to maintain the normal concentrations in
that muscle pool but if we take the if we take it also as an analogy of how
much can you expand that I guess another analogy is with creatine even even in
over the short term in a month where
we do not gain muscle except whatever water comes from that creatine we’re
able to expand the creatine pool what thirty or forty percent somewhere around
that and so and so you can imagine for vitamin b5 we don’t know what it is but
look we can guesstimate that based on my rack data I guess they made four and a
half grams based on the short-term studies of a hundred milligrams a day
for a week sixty percent of that dose is retained based on a forty five milligram
injection sixty percent of that is retained based on the studies that alex
cited in the last episode or in the last episode in this series five point six
grams of mega-doses of Panta fine might be retained so we can imagine that our
total body storage is grams and that probably we can improve our store by
grams and without putting more detail on it than that so if if we put if we if we
put some numbers on this and we imagine that the total body stores of an average
person of an average adult weight are four point five grams what we lose in
the urine would be about 0.1% of our total body stores well no wonder nine
weeks of zero intake only produce fatigue and obvious loss of enthusiasm
no no wonder because what do you lose on a zero B five diet for nine weeks about
six percent of your total body stores and if you’re thinking of big doses a
hundred milligrams would only be two percent of your total body stores if
your capacity was to increase your total body stores by double or by thirty
percent even then taking doses far above what
you could get from food would be able to be effectively retained for quite some
time also think about if it takes this long of a moderate deficiency to
drain total body stores many of us may have been walking around for years of
consuming something where we’re just losing 1 milligram a day out of her
total body stores and we have a very long history that has set us up to at
least over the course of weeks or months benefit from supplementation with much
higher doses than we would expect to get from food so one thing that’s difficult
to say about any of the studies on on how much we should be consuming is that
many of us might not be expected to just need maintenance doses from food we may
have had a history of deficits that we need to make up from with that said if
we look at some of the studies that have been done one thing that I would want to
see is is there any indication that something changes about the relationship
between your intake and your urinary excretion at some level of intake for
example is there a level of intake at 10 milligrams a day or 15 milligrams a day
where all the sudden your excreting the overwhelming proportion of the dose and
in all the studies that have been done looking at that none of them found any
such change over the range of 1 to 10 to 12 milligrams per day of intake so
knowing that at 4 milligrams per day you’re probably losing pantothenic acid
every day and looking at what you could get possibly get from food then I’m
inclined to say that we probably want something on the order of 10 to 15
milligrams per day and if we do get that two things number one if you do measure
your urinary pantothenic acid that would probably correspond to about five
milligrams per gram creatinine and then number two going forward to looking at
how we get pantothenic acid from food one of the targets that we’ll look at is
how to get the Institute medicines adequate intake of 5
milligrams a day and also how to get what I think is a reasonably higher
target of 10 milligrams a day I think that we know a lot less than we would
like to know about pantothenic acid requirements and probably less than for
any other B vitamin but we can say a few things at the AI of 5 milligrams a day
for most adults 6 milligrams per day for pregnancy and 7 milligrams per day for
lactation that’s probably consistent with that’s probably just under what’s
consistent with long term protection against frank deficiency you probably
want at least a little bit more than that given the lack of evidence for
extrapolations to children if you’re gonna favor the AI of 5 milligrams a day
for adults or my idea of 10 milligrams per day for adults I would consider this
to be based on a 2,000 calorie diet so for a child if you want to if you want
to decrease the amount you could say alright we want to point 5 milligrams
per thousand calories following the AI or we want 5 milligrams per thousand
calories following my recommendations keeping in mind that the only data that
we have suggest that children and adolescents because they’re growing
actually need more pantothenic acid not less and so it might be the case that
you really want to focus on getting as much as you can from food in a child I also think that because there’s such
dramatic uncertainty about number one what are the maintenance needs and then
number two what is the potential requirement to correct years of
suboptimal intake then I think it makes sense to say look I don’t have $800 to
run an organic acids test and and yet I am eating 10 milligrams a day and yet I
have fatigue I have mood problems I’ve insomnia or I have tingling in my hands
and feet or I have gut problems or I have cramps
if I think if you have signs and symptoms of pantothenic acid deficiency
giving the complete lack of evidence for any toxicity syndrome then I think it
does make sense to use high doses to see if they help and those doses could be
hundreds of milligrams per day I always think that you should start low and work
your way up it’s something it’s better to start with something on the order of
10 milligrams per day or to go to 100 milligrams per day before you go to a
gram per day but I do think it’s safe to experiment with higher doses so how
would we get any of these targets from diet first we have to consider some
general considerations for diet so the bioavailability of pantothenate from
food is probably 50% and that’s based on canned foods that were homogenized into
a goop but in the study that made that estimation they did analyze the b5
contents after the food was canned and homogenized into a goop and so the
results are probably pretty accurate now there seems to be pretty dramatic losses
of b5 with various types of processing in foods there was a study in 1971 that
was not a controlled study and we can’t place high confidence in the details of
the numbers but they took over 700 foods that were published in the USDA database
and they compared the fresh foods to the frozen foods and canned foods and they
found that for fish and shellfish the thwart the frozen foods had 20% less
than the fresh foods for canning there was 20% less as well for meat and
poultry they didn’t have freezing numbers but they had canning numbers and
there was 26% less in a canned meat for dairy products there was 35% less in the
canned milk for corn there was 50% less when it was canned and 19% less when it
was frozen for root vegetables there was 46% less when it was canned for potatoes
37 percent less in frozen for legumes 78% less in canned 78% 57%
less in frozen very strong argument for dr legumes here for vegetables 56% less
in canned 48% less in frozen for fruit and fruit juice 51% less in canned 7.2
percent less in frozen in refining of grains the refining process removes half
the pantothenate but pantothenate is not one of the nutrients that is added to
enriched flour so refined grains even if they are enriched are a major risk
factor for having low pantothenate status now this paper was not a
controlled study and we don’t know to what degree its canning and freezing
versus other factors in the production of those foods but there are some
controlled studies they show that freezing is not that important as as
freezing itself so in breast milk over long-term storage
there’s 14% loss of B 5 over 3 months when it’s slow frozen and there is very
good stability over time when it’s quick frozen so quick freezing is better but
the thing with frozen vegetables is it’s the blanching loss that kills them when
frozen when vegetables are frozen they are blanched first and they can lose up
to 50% of the b5 during blanching for example soybeans when they are blanched
lose 50% of their b5 in in spinach they lose 64% in water blanching but only 13%
in steam blanching broccoli loses 62% in water blanching
and 45% in steam blanching once the vegetables are frozen long-term storage
they lose a smaller amount so the the blanched broccoli for example it lost
62% and then it lost another 24% when it was under 60 days of frozen story
after that the loss leveled off now it depends on the food though so for
example in in sweet potatoes boiling them didn’t destroy any b5 but baking
them at a higher temperature destroyed 23% whereas in peanuts boiling them for
40 minutes caused a 25% loss roasting them at 180 degrees Celsius destroyed
all of the be five but roasting them at 160 degrees Celsius only destroyed 25%
so rather than trying to memorize all these numbers and actually I should
point out one more thing for for fava beans sprouting them even though it
increases some nutrients dramatically it reduces the b5 by 19%
so rather than like memorizing all these numbers are trying to make rules out of
it the rule that we derive from this is that because the effect of processing is
so incredibly strong when we’re looking at databases we absolutely cannot use
data for raw foods and assume that there will be a similar amount of b5 in the
cooked food we have to look at data where it’s actually been measured from
the cooked food the way that we are cooking it so with that said using only
foods that have been cooked the way people usually consume them I look I
analyze the data from the USDA database and came up with five tiers of how to
get b5 from food Tier one yields 10 milligrams in one serving the only food
in tier one is two heaping teaspoons of unfortified nutritional yeast
now fortified nutritional yeast I’m not including here because I’m just looking
at natural foods in tier two these are foods that yield 10 milligrams in two
servings here we have the liver of chicken beef lamb or veal and we have
sunflower seeds that’s it in tiers 3 these are foods where 3
servings would yield 10 milligrams here we have beef pancreas and beef kidney G
toasts to cheese I don’t know if I’m pronouncing that right black and red
coffee the kidney from Lam imported from New
Zealand not the kidney from other van pork liver and most products made from
pork liver shiitake mushrooms and canned grape leaves in Tier four we jumped down
a lot we give up on trying to get ten milligrams and we say okay I want to get
the RDA I five milligrams a day recommended by the Institute of Medicine
food and nutrition board in five servings per day on this list we have
some things that a lot of people eat we have canned chili peanuts peanut butter
cashews mushroom in the case of white mushrooms and portobello mushrooms raw
avocado salmon trout if they’re fresh eggs and then we start moving into
things that most people don’t eat we have duck and goose we have pate we
have beef thymus and heart poor kidney and brain emu meat and the giblets and
heart of chickens and turkeys many cuts of steak and other fresh meats do go
into tier four but many don’t and the data is very messy tier five is you have
a good chance of hitting the AI of five milligrams
if you eat four pounds of these foods in total in other words if you eat four
pounds of food a day like the average American and all of it is these foods
you will hit the AI this food has most cuts of fresh meat that are not in Tier
four and as Whole Grains most natural dairy products besides butter most
seafood that is not canned most beans that are not canned roasted almonds raw
coconut most other nuts and seeds but not all most processed meats most spices
and many vegetables are in tier five but many are not and the data is very messy
the foods is that you know are going to make you not hit the AI for B five if
you don’t eat any of the foods in the top three tiers
which is basically liver some organs and nutritional yeast if you if you eat any
of these foods and you don’t eat the super foods you will not meet the AI we
have sugar we have fat added fat refined flour many canned goods many heavily
cooked goods and heavily processed foods right these are the foods where if if we
do not eat the super foods and we do not take a supplement we do not take a
multivitamin and we eat a meaningful amount of those foods sugar fat refined
flour canned heavily cooked heavily processed foods you will probably not
meet the AI for vitamin b5 now we come to the question of the intestinal
bacteria this is the first time where I really questioned whether the intestinal
bacteria may be a major source of vitamin b5 and I still don’t know the
answer but I think compared to every other B vitamin that I’ve looked into
this is the one where the case is most compelling so let’s review the case in
2016 gomen Act published a paper that laid out the case for the microbiome
being a major supplier of pantothenic in his case he was using high-dose vitamin
D defects sleeping problems in a case of a thousand neurology patients and their
sleep problems came back after a while of being on the vitamin D supplement he
speculated that the d may have disturbed their microbiome and he added a B
complex and this made the sleep better and so he you know looking at his data
he’s this is a hypothesis paper in medical hypotheses he doesn’t have a
strong case from his data but he hypothesized that maybe what was
happening was the the the microbiome that should be making B vitamins needed
because it was killed off in these patients they needed extra B vitamins to
jumpstart their intestinal microbiome so I think from his doubt of the cases a
week but he cites some interesting evidence so his claim is that in modern
life where we’re living indoor lifestyles we have a pandemic of vitamin
D deficient and the wrong microbiome and he argues
that maybe gut microbes are needed to help us digest coenzyme a in foods that
guy gut microbes might might require vitamin b5 such as lactobacillus and may
steal b5 from us if we’re engaging in probiotic supplementation unwisely or
that microbial synthesis is supplying us with b5 and when I read this paper I’m
I’m not too convinced because I think his dad are very compatible with just
vitamin D and B vitamins helped sleep and that’s it but I do think it’s
interesting that gut microbes could steal b5 and they could make b5 I also
think that the hypothesis is interesting that you may need exogenous B vitamins
to affect your intestinal ecology in a way that promotes B vitamins synthesis
and I’ll come back to that after I talk about one more paper so sipping and
Strauss in 2016 made a stronger case for this they pointed out that the lacto
Bulgaria’s factor that was known out about in the early 20th century turned
out to be panteth i’m this was a factor that lactobacillus bulgaricus was
producing in large amounts to feed other lactic acid bacteria and so the form of
supplementation that Alex was talking about pianta thein is produced by lacto
bulgaricus in very large amounts and it is used to supply b5 to other lactic
acid bacteria that cannot make it themselves and so this this is an
example of where if your B vitamin producing microbiome gets killed off
then you might need to supply those B vitamins to get those other lactic acid
bacteria actually produced because you have an ecological Network where even
though we net they are b5 producers for you there are so many members of that
Network that depend on this central hub in
lactobacillus bulgaricus where if it’s not there the whole ecology suffers and
your net B vitamin production just gets destroyed in your gut because of the
lack of that ecology there are other microbes that might produce panteth on
such as ecoli a number of human pathogens and symbiotes cannot make
their own b5 and may be net stealers of b5 the bacterium that causes syphilis
may be a net stealer of b5 Garner Ella vaginalis which causes bacteria yeast
infections may steal b5 some mycoplasma and bifidobacteria and chlamydia steal
b5 and Bifidobacterium considered good bacteria but if you don’t have
lactobacillus bulgaricus in your gut and you don’t have a lactobacillus community
which in fact I found out through you biome is exactly what my gut looks like
and do you have Bifidobacterium which is steal b5 which I have three times more
than the average person my gut bacteria looks like it’s a net stealer of b5
because I have so much Bifidobacterium I don’t have a lock toe bacillus community
now the one study that seemed compelling at first that Simon and Strauss cite is
that mice on b5 deficient diets only develop severe problems when given
antibiotics now one of the things you have to keep in mind whenever you’re
trying to generalize from mice and rats about the microbiome is that mice and
rats eat their own feces so if you go back to this paper they say that they
put the mice in a wire mesh cage so that the feces would drop between the wire
meshing and the mice would eat less of their own feces they don’t say they did
that so they won’t eat their own feces they say they did that so they’d eat
less and when you look at why they gave the antibiotic the reason that they gave
is that they knew the animals were eating their own feces and so they
wanted to read they wanted to eliminate the beef
the vitamin b5 that would be produced in the feces that the animals would eat so
I looked up you know how do mice eat their own feces
well there are videotaped examples of how each species eats its own feces so
for example rats will they will poop into their hand the excuse me they will
bend around and poop right into their mouths to eat their feces in mice they
they can’t reach with their mouths but they put their forelimbs they’re like
our hands right they put their forelimbs right up to their anus and they take the
feces then they bring the feces back to their mouth and they eat it so you put
them on wire mesh cages and they can’t eat the feces that falls between the
wire meshing but they can eat the but they eat 50 to 60 percent of their feces
right by taking it from their anus and then on top of that they will eat the
feces that sticks to the wire machine and when you put mice on be vitamin
deficient diets this was studied in the case of b12 put them on a b12 deficient
diet they double how much feces they eat so I’m sure they do when you put them on
a b5 deficient diet in fact the only way to prevent a mouse from eating its own
feces is to is to make them wear a plastic tube that prevents them from
bending their torso so they can’t reach around to their anus and even then they
will still eat the feces that falls in the wire mesh caging so you have to make
the wire meshing very big so that very little falls on it so if we come back to
the mouse study it’s it’s not convincing that they developed b5 deficiency only
when given antibiotics but there are some elements of the evidence that are
very compelling so number one gut bacteria can make pantothenic acid and
some of them secrete it for use by other bacteria if they were just making it for
their own use maybe you wouldn’t absorb it at all but if lactobacillus
bulgaricus makes it for other bacteria then it’s it’s freeing the b5 into the
environment and it should be available for absorption
gut bacteria also may scavenge b5 and steal it from you so
both those things are true makes sense that your gut microbiome is gonna affect
your b5 status I would add other evidence to this cells in the colon do
possess a sodium dependent transporter that transports vitamin b5 now some
other things that made me think that the microbiome might be important is that in
the in the deficiency cases they had to use an antagonist to produce severe
deficiency in an experimentally controlled setting and so I thought you
know why is this well maybe that what that antagonist is doing is preventing
them from from activating b5 that’s produced by their microbiome why is it
so hard to produce a deficiency with just dietary restriction alone and then
there are these studies that used very high doses that Alex will talk about to
benefit certain things why would you need high doses that are a hundred
milligrams to actual Gram amounts how why would you need those to have
benefits if food doses are 5 to 10 milligrams unless the microbiome is a
major producer so these things did make me think but most of them are not that
convincing so you could easily explain the difficulty of inducing a deficiency
over the short period of time when you have such massive body stores that alone
can explain almost all of those things and if we know that we could have years
of deficiency and high doses can make up for that
then even doses of Gram amounts might be correcting years and years and years of
suboptimal status still the convincing parts are back to gut bacteria can make
b5 gut bacteria can still be five and we do have b5 transporters in the colon
still there’s a very powerful argument to me against the microbiome being a
major source in own basically everyone that’s ever been studied in the last 100
years and that is that normal urine concentrations are around 3 to 4
milligrams per day and they dropped a 0.8 in response to
nine weeks of consuming no b5 at all they almost double in response to 10
milligrams if the microbiome is the major supplier
of b5 why is it that the urinary concentration drops 80% over the course
of weeks of no dietary b5 and why is it the case that something like 5 or 10
milligrams to make such a huge difference in your urinary
concentrations this indicates to me that in the last hundred years of people have
been studied that the microbiome makes maybe a minor contribution to b5 status
on the order of 10 to 20 percent now it’s possible that if everyone over the
last hundred years has had the wrong microbiome because of modern lifestyles
and industrialization that there could be a quote unquote lost microbiome of
ancestral days that none of us have that we should have and that our bodies are
designed to live on the high amounts of b5 produced by this lost microbiome but
there’s no evidence of that and that’s very speculative so what I think is yes
the microbiome probably contributes 10 to 20 percent of a person’s b5 status a
bad microbiome may make things a lot worse by not giving you that 10 or 20%
and by stealing b5 from you so the microbiome is relevant but I think it’s
very very very hypothetical to suggest that maybe we all just have the wrong
microbiome and in and in some some faraway microbiome of times past that
the b5 produced in the micro in the gut was the major b5 if that’s true it has
not been the major b5 over the last hundred years
so what might be causes of suboptimal status or deficiency well remember we
don’t know that much because our assumption our working assumption of the
last 100 years has been that no one develops natural deficiency and so it’s
very under researched but some things that we do know ethanol is an inhibitor
of pantothenic kinase it seems that in alcoholics they have adaptations that
prevent them from having serious problems but ethanol does act as the
antagonist used in the 1950s to produce clinical deficiency or as the genetic
defect that I discussed in the last that the last episode in the series
pantothenic kinase deficiency ethanol does mimic that to some degree there’s
an old paper showing that firemen and riboflavin increased pantothenate levels
in the urine there were no statistics in this paper I don’t know how much we can
trust it probably those people were had very mediocre status of all these
nutrients based on the urine concentrations but that gives proof of
principle that you might have your pantothenate status hurt by deficiencies
of other B vitamins that makes sense in a couple ways what is that all the steps
in activating pantothenic acid are or most of them are dependent on ATP you
need the other B vitamins to make your ATP this comes back to what we talked
about a nice and in riboflavin where we said things that hurt your ATP status
like hypothyroidism insulin problems under eating that use of metformin or
Berber and these could theoretically compromise your pantothenate status
because you can’t activate it as effectively the math suggests that
high-fat diets would slightly increase b5 needs because you use 20% more b5
when you burn fat compared to carbs the mouse study that I cited in the last
episode in this series where in a model of the genetic defect in pantothenic
kinase they had very slight neuro degeneration on a normal diet but
devastating neuro degeneration on a ketogenic diet suggests that if you have
very bad b5 status or you have an impairment in b5 metabolism that perhaps
a high-fat diet be more harmful than that 20% math
should suggest finally there are many inborn errors of metabolism that cause
backups in metabolism that hog the co a pool
these don’t cause b5 deficiency but they effectively cause a functional b5
deficiency because they deplete you of CO II available for the reactions that
you need it for and the most commonly these are disorders of fatty acid
metabolism or amino acid metabolism what happens is let’s say you’re burning a
fatty acid you burn that fatty acid partway you’ve you’ve attached the fatty
acid to Co way to make a fatty acyl Co a you’ve started chopping off acetyl co
way from it to enter into the rest of metabolism and you’re stuck with these
fatty acyl Koei’s where you hit a metabolic block and you can’t go any
further the fatty acyl Koei’s accumulate and now there’s no freako way left to
continue those reactions and that causes all sorts of effects that would be very
much like the effects of vitamin b5 deficiency in a very severe way because
you’ve depleted yourself of the ability to use coenzyme a most of those
disorders are are helped a lot by avoiding fasting and feeding high
carbohydrate diets and that’s because you use less koay there’s less stress on
the co a pool and you have more roundabout ways of getting your energy
when you use carbs then when you use that in addition to genetic defects all
of which incidentally are very rare individually but are substantial
collectively apart from the genetic defects deficiencies of Byatt biotin
will elevate levels of prep ional Co a which is derived from the amino acids
methionine threonine or the branched chain amino acids if your propyne ilka
way goes up your your Co a pool gets hog because it’s all sequestered as propyne
you’ll collect if you are b12 deficient you will elevate methylmalonyl coenzyme
which is derived from prop I Anil Cohen and if methylmalonyl coenzyme m film
ellen yoko a and you become deficient in the co a needed for all the other
reactions if you are riboflavin deficient then the amino acids lysine
and tryptophan can lead to elevations of glue t’rul co a because they can’t be
fully broken down and because riboflavin is so important for fatty acid oxidation
you can have fatty acyl Co ways that elevate because they can’t be broken
down those co those acyl khloe’s accumulate and you’re left without
freako a to engage in the metabolic reactions that you need and so even
though these disorders and severe nutrient deficiencies are not super
common they are they will at least be rare cases of functional b5 deficiency
but also my suspicion is that a lot of people may have some cap on their
metabolic pathway like you may only be so good at metabolizing branch chain
amino acids but because you’re reading a very high protein diet or your downing
weight you know tons and tons of whey protein for some people you may surpass
your metabolic capacity in a way that causes a very moderate problem of this
nature and effectively induces a vitamin b5 deficiency a functional vitamin b5
deficiency unfortunately nothing can really be said about the prevalence of
suboptimal status because in all these studies that were that we’re looking at
like when I talk about they put they looked at dietary intake versus urinary
excretion none of those studies reported surveys
of fatigue or loss of enthusiasm or gut problems or cramping or any of the signs
of vitamin b5 deficiency so I think it’s a very open question of whether there
exists natural suboptimal status and my suspicion is that there does so with
that said I’ll conclude my contribution to this by saying I think
supplementation with high doses is warranted even if even if you don’t have
data and even if your diet looks fine if you have
any of these signs and symptoms fatigue feeling down in the dumps low-energy
insomnia grumpy mood cramps got problems if you if you any of those things I
think are reasons to say you know what maybe I should try some higher dose b5
and see if it helps and so with that on the topic of supplementation I’ll bring
it over to Alex Alex what can you tell us about some of the benefits besides
fixing deficiency what are some of the benefits that we might get from
supplementing with pantothenic acid or its derivatives
yeah so when I was looking around at what pantothenic acid is used for for
supplementation there isn’t a lot out there and what is available is heavily
concentrated in two areas the first being as a therapeutic for elevated
blood lipids and this is specific towards the form of pantothenic acid
called panteth I which is basically to pants Athene molecules bonded together
by a chemical bond between two sulfur molecules and this does contribute
bioavailable pantothenic acid to the body but pantothenic acid itself doesn’t
appear to have the same effects so what caught my attention with this first and
foremost was a review article in 2005 that looked at 28 clinical trials in
patients with dis lipedema and it reported that using panteth in
supplements reduced LDL cholesterol content by 10 to 20 percent and reduced
triglycerides by 14 the 33% and increased HDL cholesterol by 6 to 8
percent and it was an interesting review because the studies that it included
were all published within an eleven year period began
in 1981 and going through 1992 and there wasn’t any clinical trials published in
the 12 years up to the publication of this 2005 review article and of these 28
studies 25 of them were conducted in Italy which is again strange because
panteth ein was first approved for lowering blood lipids in Japan not Italy
but only three of the trials were in Japan and the other 25 were in Italy
so overall the studies lasted three to 48 weeks with an average duration of 12
weeks and they used 600 to 1200 milligrams of panteth on the most common
dosage was 300 milligrams taken three times per day with meals and there
weren’t any severe adverse reactions as we discussed in part one the adverse
effect rate was about 1.4 percent with the most commonly reported reactions
simply being mild heartburn itchiness and some diarrhea and the effects don’t
occur with pantothenic acid because when the researchers started to investigate
the mechanisms of this it was found that there the effects are likely mediated by
system eeen which is the molecule that is binding
the pantothenic acid molecules together so the way pant Athene works is going to
be similar to a statin in that it ultimately inhibits hmg-coa reductase
however the actual point of inhibition of pants Athene is not at that is not at
that location in cholesterol synthesis it’s further downstream somewhere
between somewhere within the 19 steps of cholesterol synthesis between lana
sterile and cholesterol and what happens is the inhibition leads to a accumulation of oxy sterols that then
inhibit hmg-coa reductase as a negative feedback loop and panteth on also
appears to inhibit acyl Co a carboxylase which is used to provide the Malon elko
a substrate for the biosynthesis of fatty acids which decreases fatty acid
synthesis and can help explain the triglyceride lowering effect in addition
to the cholesterol lowering effect and i mentioned that it was similar to statins
but there is one key difference in that when we look at the adverse effects of
panteth 9 add ministration we don’t see changes in serum levels of coenzyme q10
like we do in statins which are known to deplete the coenzyme q-10 pool in
individuals and therefore requires supplementation to help offset the
adverse effects of that and so the mechanisms through which panteth ioan
work are similar but they don’t appear to be of the same magnitude as a statin
and the off stream adverse effects don’t occur there are you know no indication
that it increases the risk of diabetes or muscle pain or other things that you
might see with a statin now of course the effect isn’t as large but it’s also
not negligible so again in people who have elevated blood lipids it suggests
that over a four month period using an average of 900 milligrams 300 milligrams
three times per day you will see reductions in LDL cholesterol that
average 20% average increases in HDL cholesterol of eight percent and average
reductions in triglycerides of 33% now since all of these studies were
published throughout the 80s there have been two more randomized control trials
in North America the first being published in 2011 that basically saw all
of these studies and asked why don’t we have any studies in North America
looking at this and so the researchers wanted to see what the effect was the
difference being that these people didn’t have dis lipedema they weren’t at
risk for cardiovascular disease they were middle-aged adults that were
considered to be at a very low risk of cardiovascular disease in that for
example their average LDL cholesterol when they started this thing was around
a hundred milligrams per deciliter and even in these people supplementing with
900 milligrams of panteth I in a lowered their LDL cholesterol by 4% their apoB
containing particle counts by 5% and their triglycerides by 12% keeping in
mind that in absolute terms these weren’t very large reductions right 4%
corresponds to only four milligrams per deciliter but it’s still notable
considering that their levels were already considered optimal by current
cholesterol treatment guidelines and in the study again they observed no effects
on blood pressure no effects on inflammation liver enzymes or coenzyme
q-10 values and there was no difference from the placebo group for adverse
events it was basically small benefit towards blood lipids without any known
bad effects and so in a follow-up study by the same research lab three years
later they did take people who were at risk for cardiovascular disease and
these were people who were candidates for statin therapy their LDL cholesterol
was around 170 to 180 when they started the intervention and it was the exact
same intervention over 12 weeks but they saw more pronounced reductions they saw
an Everage 11% reduction in LDL cholesterol
and 8% reduction in apob containing particles in the blood which corresponds
to 20 and 10 milligrams per deciliter respectively and again no other effects
on blood chemistry other in this case minor reductions in liver enzymes and
CRP a marker of inflammation with no adverse events reported and so while the
studies are largely constricted to Italy with a handful in Japan and then now we
have two studies in North America overall they suggest that pant Athene is
a dietary source of pantothenic acid that is effective at reducing LDL
cholesterol and apoB by about 4% in people with already low levels of blood
lipids and 10 to 20 percent in people who have disappeared mao it also seems
to reduce triglycerides and increase HDL cholesterol exclusively in people with
disabilities these tasks by inhibiting cholesterol synthesis and liver and
fatty acid synthesis with minimal side effects or adverse effects so Alex
having researched this and niacin will would be your B vitamin of choice to use
as a drug to liver lipids I think this one I think that niacin
hat would have a more pronounced effect but nice and also carries with it the
higher risk profile we there’s literally we don’t know of any risks with this and
then as we talked in the other episode about the toxicology of pantothenic acid
supplementation it’s basically non-existent and so
especially at these doses which were well below some of the doses that were
being tested upwards of 30 grams per day and here we’re talking less than one
gram per day yeah – just to give some perspective
here the the required amount of niacin is on the order of 15 16 milligrams and
the lowest case the lowest dose used in case reports of liver failure or
modestly like usually it’s 3 to 9 grams a day but it’s been 300 milligram as low
as 300 milligrams a day has been the lowest case report
whereas pantothenic acid the adequate intake is 5 milligrams I’m recommending
10 but we have studies going up to like 15 to 30 grams of it so the the safe the
ratio of zero effect that those extraordinary doses compared to how much
is the minimal requirement like the window between the minimal requirement
and the dose that does cause harm in niacin verses the dose that has no event
so Harman pantothenic acid just it just seems like a pantothenic acid is just
dramatically more safe it seems at high doses yeah definitely and it has an
effect in people who are already healthy for blood lipids you know so it’s really
kind of seems to be a default choice for anyone who just wants to ensure optimal
cardiovascular health there don’t there doesn’t seem to be a downside to doing
it at least not one that we know of so with that the other most widely
researched use of pantothenic acid is for acne and general skin health and
wound healing and these studies use primarily topical application except in
the case of acne so with regards to skin health and wound healing there is a
compound called Dex panthenol which is basically an alcoholic analogue of
pantothenic acid that was first introduced as a skin ointment in 1944
called bepanthen and today you can find a variety of Dex panthenol preparations
available creams emollients gels lotions oils and so forth
but when applied topically decks panthenol is readily absorbed in the
skin and converted to pantothenic acid which is then available to produce co a
and this is important because the skin depends on a mixture of sphingo lipids
cholesterol and fatty acids to maintain its integrity and that water barrier and
in particular the creation of sphingo lipids depends highly on the
concentration of co a being available to condense Pama till co a with sarin and
so with this provides the kind of basis for why this was investigated in the
first place is because this cream is absorbed very effectively into the skin
and it provides the necessary substrate to maintain skin barrier integrity and
so we do see that in clinical trials looking at its effects on overall skin
health we know that Dex panthenol acts like a
moist moisturizer with skin barrier improving properties and it may go above
and beyond that to also facilitate wound healing so there have been studies
showing that its application increases the expression of genes that are
involved in skin proliferation inflammation and tissue repair and it’s
been shown when you apply it to like rashes and the such on the face that
it’s beneficial in reducing inflammation both that type that’s caused by a like
toxic external chemical that causes an irritation on the skin and also signs
are types of inflammation that come about endogenously from like a nutrient
excess or deficiency such as shal itis which is inflammation around the lips
and even when we when we apply so there when we apply it on the inside of the
mouth as well using a Lawsons where we take it we take the Lawson’s we suck
on it we let that decks panthenol kind of coat the inside of the mouth and the
throat we see that it accelerates mucosal healing aft and reduces throat
pain after tonsillectomy in children and it can also help facilitate the healing
after tattoos so the studies we have are scattered and they’re kind of random
frankly right you go from tonsillectomy to tattoo removal to chemical induced
like burns but they all point in a consistent direction that topical
application of dex panthenol facilitates the healing process and reduces pain and
sensitivity in the area which might be secondary just to its effectiveness as a
moisturizer now the other thing I mentioned was acne and it’s been
hypothesized that pantothenic acid deficiency is related to acne and the
rationale is basically that puberty results in a greater demand for Co a and
any shortage of dietary pantothenic acid would result in a less than efficient
rate of fatty acid metabolism that would give rise to the deposition of fat
droplets in the sebaceous glands of their your hair follicle ducts which
would result in acne and so we have a handful of studies for example the one
that came up with the hypothesis to begin with after generating the
hypothesis they took a hundred Chinese kids and they reported near immediate
and I mean within one to two days reductions in sebum secretion on the
face with reduced acne and a regression of lesions within one to two weeks and
complete control of acne within eight weeks using ten grams per day of oral
pantothenic acid taken in four divided doses
Plus using the Dex panthenol cream applying it to their face four to six
times per day and over an 18-month follow-up period they found that the
acne remained under control as long as the students maintained a dose of 1 to 5
grams of pantothenic acid every day with higher doses required for those who
started with more severe acne and so the study got followed up with two other
trials and one was first a pilot trial in people with mild to moderate acne
that did eight weeks of supplementing was something called Pantheon which
provided 2.2 grams of pantothenic acid along with other B vitamins and a small
amount of L carnitine and they found that in the small group of people after
eight weeks of supplementation the average number of skin lesions present
on their face were reduced from 20 down to 11 which came with subjective
improvements in quality of life so these researchers conducted a larger study to
follow up on that one over a 12-week period and in these in this study they
recruited people with moderate acne that had more than 50 non inflammatory
lesions and up to 50 inflammatory ones and they reported using that same
panther chin supplement regime that overall skin lesions were reduced by 68%
so again minimal studies here but they all point in a consistent direction
where pantothenic acid supplementation appears to benefit individuals with acne
when supplemented in relatively high doses of 2 to 10 grams per day and a
topical application of Dex panthenol cream seems to benefit skin health and
may accelerate wound healing and the Dex panthenol creams for those of you
interested were about 5% Dex panthenol so a couple other areas where
pantothenic acid has been investigated but where things have not panned out
would be an exercise performance so pantothenic acid has been investigated
for its role in sports performance since it’s required for the production of
coenzyme a which is required among other things to transport fatty acyl xin to
the mitochondria so that fats can be used for energy production and it’s been
proposed that a reduced availability of situs taluk freako a could be a rate
limiting step for fat oxidation during exercise and we only have three studies
using one to one point eight grams per day of pantothenic acid for one to two
weeks and all of them failed to no performance improvements in a cohort of
recreationally active men a cohort of trained cyclists and a cohort of trained
distance runners using tests such as a 50 kilometer submaximal cycling a 2,000
meter time trial and cycling to exhaustion had 75 percent of vo2 max
plus power output there were also no changes in blood chemistry including
respiratory exchange ratios which would give an indication of how much they’re
relying on fatty acids and there were no changes in perceived exertion or freak
away levels in skeletal muscle one of the studies actually took muscle
biopsies and there was no change in freako a levels within the skeletal
muscle so what lemon did daddy we do have
suggest that supplementation with pantothenic acid will not benefit
endurance exercise performance this seems fairly analogous to riboflavin
right so like riboflavin the evidence was very pretty you know pretty much
indicated that there wasn’t really an effect on performance but yet where we
had a very good marker of riboflavin status and we had very good cut-offs
that were well established from a lot of research in the field we were able to
see things like when you do cardio – six days a week your riboflavin requirement
goes up 60% and when you lose weight it goes up 60% when you do both it doubles
and things like that and so it seems like in this case we have this century
of baggage of believing that natural pantothenic acid deficiency doesn’t
exist so we have no idea how to go about saying well well you may not need this
for performance but did you performing increase your requirement in other ways
you know for example like I don’t know if I don’t know if this is plausible or
if there is data but maybe in some subset of the population you the
teenagers get acne more when they’re involved in certain sports because
they’re because look your your body is is your body’s not going to poison
itself by limiting the supply of Koh a42 to be able to handle the influx of fatty
acids that’s what happens in fatty acid oxidation disorders and that’s why
people that have that often don’t survive bouts of fasting and exercise
you know you’re like the the limit of having a limitation of the KO a pool is
poisonous to your metabolism for reasons that I won’t go into now and explained
in the episode 1 of this two-part series but it makes total sense that your body
would and also there are studies where you can the heart for example and I
believe this is probably true in skeletal muscle has a very large reserve
of pantothenic acid that’s just they’re waiting to be turned into kauai
and the heart can boom like make that ko a real fast if it needs it and so I
think that what that what we’re seeing here is that when you engage in exercise
your body is going to prioritize fulfilling the requirements of that
exercise and it’s probably coming up the expense of something but because we have
so much less research here on the requirement than riboflavin we just
don’t have the tools we need to figure out what that is yeah definitely um and
it is certainly possible that exercise would increase requirements not just for
from an energy metabolism standpoint but simply because a secondary effective
exercise would be more muscle tissue and if you have more muscle then you’re
going to need more koay to maintain it um but something else to keep in mind as
well with the very very limited pool of studies we have on exercise is that
every single performance outcome they were testing was primarily glycolic
right when you’re doing a 2,000 meter time trial or cycling to exhaustion at
75% of vo2 max or even competing like actually competing for a 50 kilometer
cycling you’re going to be relying primarily on glucose as an energy source
that is the only energy source you know notwithstanding proof ATP and creatine
phosphate but that’s the only energy source that can maintain high levels of
exercise intensity and so if the entire hypothesis but so I think that your your
level of intensity is gonna be super dependent on glucose but you are still
gonna burn a ton of extra fatty acid than a marathon right yes yes on a
hundred percent you’re always going to be burning some fat but the point is is
that your body will preferentially the more that you push yourself rely on
glucose and in fact it’s a reliance on glucose that lets you push
to higher intensities if you didn’t have any glucose available then your
perceived high intensity effort would not be as actual high intensity as if
you did have glucose available yeah and I think this kind of relates to
something that I a point that I made at the beginning of the of part one in here
which was when the b5 pool is limiting if you have enough carbohydrate you can
just run anaerobic glycolysis and say I don’t care about my coway levels but if
you don’t have the carbohydrate then then you can be in trouble
and so in the mouse study that I cited twice in the course of this two-part
series it was a where they had a genetic defect in pantothenic kinase and their
neuro degeneration was not that bad on a regular diet and then they went on a
keto diet and all the sudden it was devastating and so you know it’s it’s
because even though even even the it’s because the when you are put under
conditions where you are under a lot of stress if you have carbohydrate where
you can derive energy quickly without using koay at all the stress of having a
limited Co a pool just isn’t that stressful it’s you know what would
happen if they repeated those studies on a ketogenic diet then then the b5 may
have proved to be limiting yeah and so the whole point I brought up the high
intensity glucose thing it was simply that the entire hypothesis of
pantothenic acid supplementation was to improve fatty acid oxidation during
exercise but all of their tests weren’t stressing the fatty acid pool they were
all using glucose and so it is possible that supplementation could benefit
performance at lower intensities or in people doing events like ultra marathons
but we simply don’t have that data available and so we can’t do much more
than you know logically speculate so another area if we come back to kind
of the aesthetic realm with skin another areas hair and pantothenic acid
deficiency in rats was shown to cause graying of the hair since at least 1946
and we don’t have any human data available but other than the fact that
the elimination of pantothenic acid in the urine doesn’t seem to differ between
people with normal hair and people who have graying hair or hair loss the only relatively modern evidence for
pantothenic acid on hair Health involves one study that measured hair variables
after they put product in their hair and let it sit there and dry which you know
is difficult because it’s neither really an oral supplement nor a form of shampoo
it’s like you get out of the shower and then you put this project on your hair
and then you just let sit there for the rest of the day and the project
contained pantothenic acid along with some other nutrients and it showed that
hair fiber diameter increased along with its flexibility and break stress but it
was we can’t really draw any conclusions about the role of pantothenic acid
because it also had things like caffeine nicotine amide dimethicone and an
acrylamide polymer so it’s like okay maybe but we can’t form any conclusions
there and finally is the last thing that’s been investigated for is
arthritis and the first report I could find was published in 1953 titled the
therapeutic advantages of the addition of calcium pantothenate to sallow Sates
in the oral treatment of rheumatoid arthritis and the final report I could
find was published in 1980 titled calcium pantothenate in arthritic
conditions a report from the general practitioner Research Group I couldn’t
locate the full text of and since then this research has pretty
much dropped off the map and there’s good reason for that so an article in
The Lancet in 1963 found that arthritic patients had low whole blood levels of
total pantothenic acid that’s including free and bound forms and it didn’t
matter what type of diet the arthritic patient was on whether they were
vegetarian or omnivore compared to omnivores and vegetarians with our
arthritis they had lower levels and within this article they mentioned a
study where daily injections of 50 milligrams of calcium D pantothenate
alleviated symptoms of rheumatoid arthritis after a week of treatment with
no further improvement after three weeks and all blood levels rose from the
levels that they observed in their arthritic patients up to the levels they
observed in the omnivores and vegetarians and the levels fell after
they stopped supplementing and the symptoms severity returned to baseline
now in response to this article a physician in communication published
that he had been successfully treating patients with osteoarthritis using 12
and 1/2 milligrams of oral pantothenic acid in the morning and evening for 25
milligrams per day and that the benefits usually took one to two weeks to
manifest but disappear when they stopped supplementing and he mentions studies in
rats that gave him this idea that showed joint changes resembling osteoarthritis
when they suffered pantothenic acid deficiency and he suggests to the
original article author that you know it might not be the rheumatoid component of
the arthritis it might be the osteoarthritic component since osteo
since rheumatoid arthritis has components of osteoarthritis in it in
terms of joint degeneration and bone on bone contact
but it could also just be a placebo effect and the reason I say that is
because somebody finally decided to conduct a double-blind controlled trial
in 1971 involving 40 patients in their mid 60’s with osteoarthritis of the knee
and they gave one group 25 milligrams of calcium D pantothenate each day and
compared it to placebo for 12 weeks and they assessed symptoms both by a
physician as well as the self-reported symptoms of the patients themselves and
there was no difference between groups at any time point and so the authors how
do those doses compared to the ones that are effective for acne these are much lower doses so yes a
limitation that I will get to but the authors suggest that if low levels of
pantothenic acid is confirmed that the deficiency appears to be a result of the
disease rather than causing the disease but like you just brought up these are
really low doses granted they’re like five times greater than the current
adequate intake but still really low compared to using 900 milligrams per day
of panteth on or you know 2 to 10 grams per day for the treatment of acne so I
think one of the huge limitations here that we have in even trying to
understand what the dose means is the fact that the total body pool is so
large and that what might be relevant is the repletion of the total body pool in
other words these high gram doses may it’s very possible based on what we both
reviewed that most of those doses are actually effectively repeating the whole
body pool like of those gram doses you might have Grim’s that are replete in
the whole body pool and so if you take someone whose whole body pool is
depleted 5% from what it should and you supplement them with 10 milligrams you
may see an effect but you could take the same exact problem and take a group of
people who have been depleted they’ve been losing 5 milligrams a day of
pentatonic acid for the last 20 years and their pool is like grams under what
it should be and over the course of a short term your your 20 milligram dose
seems really high it seems that’s four times the AI and yet what is it in
relation to the total body pool and that’s the thing that I think is like
it’s the giant elephant in all these studies is that your intake is sort of
like totally irrelevant almost it’s to what degree is your total body pool
compromised and to what you know what kind of dosa do you need to get it back
to normal yeah I agree completely
um and I mean you know one of the other recurring themes of this two-part
podcast is simply that research on pantothenic acid is very scarce compared
to other vitamins in general um and so it is just a kind of a giant gray area
from the supplementation standpoint you know what we can say with relative
certainty is that taking gram dosas is going to restore your body pools pretty
quickly and taking these gram dosas is probably going to benefit your blood
lipids if you use panteth ein again it’s not seen with regular pantothenic acid
and it could benefit if you suffer from acne it could benefit your acne if you
apply Dex panthenol to your skin it can also help with skin repair wound healing
and hydration and overall integrity uh so I would say that from a
supplementation standpoint those are kind of the big three panteth on for
blood lipids pantothenic acid for acne and dex panthenol for topical wound
healing cool so while i’ll add a couple things on to
that so i made the case that for some people and these are these are
navigation around very very grey grey areas but for some people the food
sources of coenzyme a and for phospho panda theme are probably the best
sources that would apply if there’s any limitation in your energy status because
you don’t even have to have a defective pantothenate kinase you just have to
have low ATP levels or low magnesium levels to make it hard for you to
activate that maybe there are genetic polymorphisms
that we don’t know about that mimic the genetic mutations that cause severe
diseases that we do know about that cause you know moderate impairments and
the ability to get that if you compare that to what’s in supplements panteth
thein is going to have some of the properties of being more easily
converted to co a but not not like coenzyme a and for Fausto panting from
food would panteth thine may be an important part of the gut microbiome
production if lactobacillus bulgaricus is a major producer b5 in the humans
that have high lactobacilli in their intestines then there’s probably a lot
of humans getting a significant amount of panteth 9 so that’s interesting from
that perspective I think on the horizon we’re going to see the development of
acetylated for phospho panteth een produced for the genetic defects in
pantothenate kinase i do not know whether that’s going to be available as
a supplement like acetyl glutathione and a siena steel cysteine or if that’s
going to be patented and distributed as a drug at extremely high prices because
of the disease treatment possibilities but if if that in the future if an
acetylated for Fausto Panta theme comes out on the market that’s probably the
one way that you could get food based b5 or or something that mimics the the
benefits of food based b5 as a high dose supplement because as it stands you can
only get high doses of coenzyme a and phospho panda theme from nutritional
yeast and from liver and as it stands you would probably overdose on selenium
from the yeast and on vitamin A and copper from the liver if you were to try
to achieve very high doses of that so I think that’s interesting
the pantothenic acid it seems like is is there any reason to use pantothenic acid
specifically or it’s it is the studied form with acne right calcium kappa yeah
yeah that’s the that’s the form used with acne but the mechanism is real
– the actual pantothenic acid whereas for example with blood lipids the
mechanisms are likely related to the sulfur groups that are attached to the
pantothenic acid which is why you need to use pants Athene so I would probably
argue that just using pant assigned in general would be a better form although
these studies with panteth thein for adverse effects have only gone up to
1200 milligrams per day and so there is a possibility that pushing higher gram
doses that you might need for acne control could lead to more complications
especially since its mechanisms of action are similar to that of a statin
yeah I think that’s a really good point so I the way that I would view the
safety profile is don’t use the form at higher doses than it’s been used so
panteth fine you could argue is if you don’t have one
reason to know one way or the other it’s definitely gonna be better for blood
lipids and maybe it’s just as good or better for acne and there’s no just acne
right there’s no world though stinging effects on wound healing
it’s a dex panthenol and dex panthenol creams are used topically for wound
healing and and acne together with the oral dosing if you’re going to go to a
gram gram gram amounts as in the case of the acne doses you probably want to use
calcium pantothenate just because that’s what we know it has calcium or sodium
pantothenic because that’s what we know has the highest high safety yeah and i
mean you can always combine them too so if you want to treat acne walls so
managing blood lipids you could take you know 900 milligrams of pants Athene per
day plus another one to two grams of just regular pantothenic acid yeah that
makes sense so some rapid-fire questions that are
sort of standard – supplements does it matter if we take divided doses or if we
take it all at once uh well the dosing schedule in all of
these why shouldn’t say all but in the limited studies we have hasn’t been
investigated but they consistently are the most frequent mode of application at
least when came to blood lipids which is where we have the most research
available was three times per day with meals some studies went two times per
day for example 600 milligrams twice a day to get 1200 milligrams total but
most used 300 milligrams three times per day so I would say 2 to 3 times per day
is probably your best bet for the acne studies those use it at 4 times per day
keeping in mind too that the higher dose you use in a single like acute bolus the
more likely you are to get a side effect like diarrhea yeah so I I guess there
the jury is out because there’s no head-to-head studies of different dosing
schedules but what we have uses divided doses and I think from a physiological
standpoint I think it’s less important than four nice and in riboflavin where
metabolic trapping may be meaning the ATP level to just keep it in the
intestinal cell available for further metabolism is super important I think
the evidence is very clear that you can absorb like massive doses of this right
but still there has to be a maximal rate of coenzyme a synthesis per hour right
and although you can store a lot of free pantothenic acid in your tissues there’s
got to be some limit to how much you will store in a given point so if I had
to place my bets on it I would say that you want to spread it out just to have a
more probability that you are never hitting the the thresholds where you’ve
saturated your ability to do something with it in which case that you’re
obviously going to pee out what you can’t do anything with from what you’ve
seen does it matter if you take it with food again we don’t know the actual answer
here but most studies do take it with food and that could also potentially be
one reason why the report of side-effects are so minimal um it does
make sense with for example diarrhea that if you take a gram of pantothenic
acid on an empty stomach you’re more likely to have some GI distress than if
you take it with a meal yeah that makes sense and I think that the principle is
is kind of similar like I don’t think it matters as much as for nice and in
riboflavin in terms of retaining it with the meal because you know you like
everything we looked at has high retention but apart from the the
possibility that you’d minimize digestive concerns it it does if it
matters it’s probably better to take it with food from again from the
perspective of retaining it through doing something with it it probably
doesn’t matter that much it probably does matter more at higher doses but if
but there’s no there’s no rational basis for doing the opposite there’s no
there’s no argument for doing it on an empty stomach and I also think for most
people it’s probably going to be more convenient if their supplements are
taking with meals just because as you go to the kitchen that’s where the food is
that’s where the cabinet is and so on yeah I think that pretty much covers the
the practical applications there so I want to end with two quotes from papers
that I thought were really interesting that I encountered while doing the
research for this so the first one is from a 2016 paper by sipping and Strauss
where they are talking about how the dogma has been all through the 20th
century that there is one way you make coenzyme a you start with pantothenic
acid and you proceed in five steps and you you don’t you don’t ever start from
anything but pantothenic acid and this has been overturned by the need to over
turn it in pantothenate kinase deficiency disorders and so in a paper
about the multiple routes of CO a synthesis he says now a series of recent
articles demonstrate that cells and some microorganisms in fact have several
strategies to obtain Co a in retrospect such evidence is present in older
literature but the implications were largely overlooked in the absence of our
current knowledge of the myriad roles of Co a I think this is a super important
philosophical framework for understanding research the when when
researchers do something a hundred years ago they may have found twenty things
and been able to interpret two of them and so eighteen got lost as loose
threads and now if we go back to that we may have the tools we need to understand
nine of those eighteen that were lost but if we don’t go back to that old
research we will never know about the threads that were lost and in going back
to the old research in the in the one of the original papers in the 1950s on
inducing vitamin b5 deficiency with an antagonist there was a wonderful quote
about the individuality of requirements they said and the foundation for this
paragraph is the background for it is they’re talking about how the different
people seem to have different manifestations of the disease with
different severa teas they said experiments such as these long as
originally confining tests but short in man’s lifespan impress upon us the wide
range of variation even in subjects chosen to conform to a standard what
Williams has emphasized as biochemical individuality and Medawar as the
uniqueness of the individual we see in the personal quirks and inconsistent
biochemical patterns which bedevil the framers of human nutritional experiments
and make exasperated the necessarily unsatisfactory solution of the problems
of controls of the problem of controls we have no doubt that some of the
discordant results among our experiments or within a single test run come from
ignorance and poor planning but the wide variations in normal
persons can easily frustrate the best experimental design if the requirement
for pantothenic acid should very many fold in a small group of subjects I
think this was incredibly insightful long before the days of now where we are
just in our infancy of starting to unravel all of the genetic and other
variations in our metabolism and our requirements and I think the first
sentence is is worth repeating experiments such as these long as
rigidly confining tests but short in man’s lifespan no matter how long our
randomized controlled trial is it impresses us as scientific researchers
when it’s longer than the longest randomized controlled trial but it’s
still so much shorter than man’s life and we can directly apply this to the
claim that pantothenic acid from the Greek bond dose everywhere everything
that you cannot become naturally deficient in because it’s everywhere and
in everything we can directly apply this to the study of Peggy Frey in the 1970s
where people were put on a pantothenic acid deficient diet zero pantothenate
for nine weeks and all that it produced was complaints of fatigue and an
apparent loss of energy and enthusiasm nothing more impressive than that well
that study was very impressive in the length of keeping people on a rigidly
controlled synthetic diet particularly within the field of vitamin b5 where we
don’t have longer experiments than that it’s impressive in that way but it’s not
very impressive with respect to man’s life nine weeks is not very long to give
someone to become deficient in vitamin b5 when their total
body stores might take six years to deplete at the level that you lose every
day in the urine and when there are so many compensations that we have to
prevent us from ever getting anywhere near that point pantothenate is
everywhere and in everything but there are tremendously higher concentrations
of pantothenate in nutritional yeast than there are in liver and there are
tremendously higher concentrations in liver than in most other foods
pantothenate is in everything but it’s not evenly distributed in the food
supply pantothenate is everywhere but is fatigue nowhere is apathy nowhere is
discomfort uneasiness and pain nowhere pantothenic acid is everywhere but is
quarrelsome NIST’s and sullenness and childishness and spending the whole day
in bed nowhere pantothenic acid is everywhere
but is numbness and tingling in the hands and feet nowhere pantothenic acid
is everywhere but is insomnia know where our muscle cramps nausea abdominal
cramps nowhere is farting nowhere pantothenic acid should not be known as
the B vitamin that you are least likely to become deficient in it should be
known as the B vitamin that we know the least about this episode is brought to you by ample
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it’s always best to sit down and take your time eating a home-cooked meal from
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on-the-go the coconut oil provides some medium chain fats to keep my energy
levels up to the carbs the vitamins in the minerals
all come exclusively from food sources like sweet potatoes bananas cocoa powder
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ancestral supplements traditional people’s Native Americans and early
ancestral healers believed that eating the organs from a healthy animal would
strengthen and support the health of the corresponding organ of the individual
for example the traditional way of treating a person with a weak heart was
to feed the person the heart of the healthy animal modern science makes
sensitise heart is uniquely rich in coenzyme q-10 which supports heart
health the importance of eating organs though is much broader than simply
matching the organ you eat to the organ you want to nourish for example natives
the Arctic had very limited access to plant foods and got their vitamin C from
adrenal glands if vitamin C is important to far more parts of your body than
simply your adrenals in his epic work nutrition and physical degeneration
Weston Price recorded a story of natives who cured blindness using eyeballs which
are very rich in vitamin A but now that we understand vitamin A we know that we
can get even more vitamin A by eating liver making liver good for your eyes
our ancestors made liberal use of organ meats both to be economical and to
utilize their healing and nourishing properties animals in the wild do the
same Weston Price had also recorded a story of how the zoos in his era were
capturing lions tigers and leopards oh my only to watch them become infertile
in captivity researchers then observed what the Lions did when they killed
zebras in the wild what they did was they went straight for the organs and
bone marrow leaving the muscle meat behind for the birds but even the birds
took what they could of the organs in bone marrow Pryce reported that once the
zookeeper started feeding the animals organ meats boom their fertility
returned the problem I often encountered though is that many people just don’t
like eating organ YZ let’s face it if you weren’t raised on them it can be
very hard to acquire a taste for them that is where ancestral comes in
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episode you

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Methew Wade

7 thoughts on “Pantothenic Acid, Part 2 (Testing, Food, and Supplements) | Mastering Nutrition #66”

  1. Any ideas on why pantothenic acid would be sky-high on urinary organic acids test? (Great plains and genova nutreval)

  2. Chris, why ceruloplazmin×3 can be higher than serum copper? As I know, free copper = ceruloplazmin×3 – serum copper, and my free copper is -2,2
    Serum – 107mcg/dl
    Ceruloplazmin – 36,4mcg/dl
    Is it infection? Or just copper defficiency? My white blood cells and platelets are low too.

  3. What is actually the nutritional yeast Chris is talking about? I use flakes and cronometer reports 1,27mg of B5 per 20g, not 10mg (Red Star, Nutritional Yeast)

  4. Dr. Gominack is “her,” but a Masterjohn/Gominack podcast on sleep and nutritional status would be highly encouraged!!!

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