For somebody who is considering using anabolics
of any type or PEDs of any type, you need to
do an honest accounting with yourself as to the
level of competition you want to go to and are
willing to invest financially time -wise, et
cetera, to get to. Hi, Luke. It's my pleasure
to have you on Evidence Strong Show. If you could
briefly introduce yourself. Absolutely. My name
is Luke Pelton. I am an assistant professor of
exercise science and the human performance lab
coordinator in the Department of Exercise Science
at Springfield College in Springfield, Massachusetts.
Okay. And the topic of today is anabolic androgenic
steroids. So we need some kind of definition
and explanation what these are. Absolutely. So
anabolic... Androgenic steroids, which for the
purpose of everybody listening and myself talking,
we're going to simply refer to as steroids for
the purpose of this discussion. They are exogenous
synthetic congeners of testosterone or other
androgens. So what that means simply is they
are not things we're producing internally, though
testosterone and other androgens are. These are
kind of facsimiles or copies. that we're making
in a lab. We're synthesizing them to either directly
mimic testosterone or to mimic certain aspects
or augment certain aspects of what androgens
do in the body. So they are chemically derived
versions of usually testosterone and its derivative
dihydrotestosterone. Those are two of the most
prevalent androgens in the body, which do a myriad
of things we associate with performance in strength
and physique sports, muscle tissue, et cetera.
And there are different versions that will be
tweaked chemically out of variety. of capacities
to exert different effects on certain tissues
or certain receptors or certain times, etc. So
that's kind of what we're talking about in this
discussion. Okay. And to have a full background,
we need to know what the function of this externally
supplied steroids would be in the body. And maybe
if you could bring what we know specifically
on the human body and what is known from other
research in animal studies or something. what
they call short considerations. Right. So in
the human body, testosterone and androgens, they're
responsible really truly for a system wide. myriad
of effects. They kind of act as neurotransmitters
in a way in the brain and in our neurology. What
they are most known for probably is for primary
and secondary male secondary sexual characteristics.
So what these include are primary characteristics,
so the spermatogenesis and male fertility, and
then secondary characteristics would be things
that either support reproduction or are kind
of inherently linked. to those pubertal years
so uh things like the thickening of facial hair
and body hair. We could think about deepening
of the voice, enlargement of the vocal cords,
broadening of the shoulder girdle, increased
muscle mass, which is what we're going to spend
a lot of time today talking about, I'm sure,
and other various reproductive linked functions.
So we call a lot of those the androgenic effects.
So that word androgen keeps coming up, come from
the Greek andro meaning male. The counterpart
would be gyno meaning female in the Greek as
well. So, you know, one of those things I mentioned
was that testosterone. and dihydro, testosterone,
other androgens do in the body is they help with
anabolism. They're anabolic as well, which is
where we get the other half of the term anabolic
androgenic steroids. So what they are used for
the most in sport performance and physique is
for building muscle mass. and muscle strength.
Now, I smiled internally at the second part of
your question is what do we know from human studies
and what do we know from sort of everything else?
And the good news is we do know quite a bit from
human trials. The tricky part is we don't know
enough and we know a lot from other animal studies.
Some of the kind of formative research we have.
on the mechanistic side of testosterone, how
it exerts its effects, how it induces anabolism
on certain tissues, etc. A lot of it comes from
the rodent models and a lot comes from chicken
research and cows as well. The reason being certain
compounds were actually developed to improve
muscle mass anabolism, so protein accretion in
livestock animals. So if you can feed an animal
less and have it produce more meat from a capitalist
perspective, that is more beneficial to a degree.
So in a way, we kind of think, oh, I wouldn't
think. that at first, but that does make sense
about what we're trying to do with a person,
which is if we think about a physique athlete
toward the tail end of a bodybuilding prep, they
are consuming fewer calories, but they want to
maintain or build muscle mass during that time
as well. So much of the research comes from that
area. One of the most notorious steroids, Trenbolone,
actually came out of cattle. So it was developed
as a supplement to cattle feed where they could
feed them less, but they would maintain or grow
mean tissue. during that time period, so never
approved for human use. Many of these have been,
so we do have quite a bit of research on things
like oxandrolone, which is known more commonly
as Anovar, on testosterone and its various ester
derivatives and whatnot, where these were used
as medicinal agents and still are for a variety
of purposes. Anovar was developed to combat wasting
diseases in children, so things like muscular
dystrophy, etc. The side effects are very minimal
because of that, because it was meant to be.
be tolerated in a youth population. If you kind
of look through the research, they first started
identifying testosterone as an exogenous agent
back in the 30s. And shortly after that, it was,
oh, performance might be benefited from these
as well. So during that kind of kind of Perry
World War II years from the 30s into the 50s
and beyond, they were readily used by a lot of
Eastern Bloc countries, East Germany, Soviet
Union, etc. And a lot of our kind of additional
knowledge came from that. Obviously not the breadth
nor dosing protocols that we have today. It was
with 1975 when... They were banned from Olympic
use. And then 1990, the United States and various
other places around the world, they were now
illicit illegal compounds. So not even just couldn't
be used in sport, but now could not be possessed
with intent to distribute or use, et cetera,
or sell. So much of the research that we've had
to go off of in the last few decades has been
from rodent models, either rat or mouse. Again,
some of the more kind of livestock driven models
as well. This can make it a little tricky to
then apply directly to a human subject. As many
of the listeners I'm sure know, the difference
between a rodent and a human is substantial.
Mechanistically, maybe not, but it still is not
a direct one -to -one. So if we think about things
like the genomic action of testosterone or other
androgens. So in your cell, you have an androgen
that's going through the blood. And in order
to do anything, it has to interact first and
foremost with an androgen receptor. So it'll
bind to that receptor. It'll translocate. to
the cell nucleus, which is where your DNA is.
It will then bind to specific regions on the
DNA, and that is what drives anabolism. So it'll
cause the manufacture of new proteins, mainly
things like myosin and actin and other contractile
muscle proteins, which will then contribute to
muscle size, strength, et cetera. And you can
apply this to whatever the effects of the androgen
are at any tissue throughout the body. But obviously
we're talking a lot about muscle strength and
mass in this talk here. There's some other non
-genomic actions as well. Some of these could
be through things like the G. protein complex
receptor, which is a complex on the cell membrane,
which initiates a variety of secondary signaling
cascades throughout the cell. And this is where
our knowledge gets a little bit murky. actually.
So we know that we could see an increase in intracellular
calcium levels because of this. And if we think
about a muscle contraction, calcium is going
to be hugely important for the initiation and
continuation of that contraction. So we could
see how a transit increase in calcium levels
would be beneficial for strength. We're not so
sure about what that means for long -term hypertrophic
effects though. So those kind of non -genomic
actions, that's where we're sort of still guessing
in terms of what is the human mechanism responsible
for that. There's a variety of other things like
tissue selectivity. So you have a variety of
tissues in the body. Androgens will have different
effects at different tissues. Many steroids were
manufactured or tweaked in a certain way chemically
to interact preferentially with certain tissues
or without. Would you have an example? Yes. So
I want to think about oral versus injectable.
Steroids is probably the broadest example of
something that the listener might be most familiar
with. So injectable steroids will be the androgen,
possibly with a fatty acid ester attached to
it, so a tail. And the longer that tail is, the
more time it takes to cleave off. And then the
compound is active for longer in the system.
So you could have something, if we see like testosterone
propionate, it's a very, very short tail. Testosterone
suspension actually would have no tail and be
absorbed into the muscle almost immediately.
And then the longer tail, things like sipionate
and enanthate, that would cause it to take longer
to be metabolized and it exerts effects over
a longer time period in the body. Oral steroids,
we usually have something like a methyl group
attached to it where it slows down its metabolism
in the liver. So it exerts its effects much stronger
than a normal drug would. The downside being
now we have liver toxicity, hepatotoxicity to
be concerned about. So a lot of the times, anything
that we're consuming orally. being processed
by the liver, liver toxicity is a concern for
the use of oral steroids. So a lot of these compounds
have been in the last few years, you could, depends
on which way you look at it, it could be considered
a performance enhancing drive or to get around
drug testing, depending on what side of the coin
you're kind of looking at it from. These compounds
have been, designer steroids, been formulated.
to take advantage of how they're metabolized
and used in the body so they can have more potent
effects in strength and performance. So the game
is how to get the compound safely to the tissue
you want and let it act for the time you want
it to be acting. From a purely educational perspective,
yes. And I do want to say broadly, everything
that we're talking about here today is from a
purely educational perspective. I am not condoning
nor giving advice on dosing protocols to any
one individual or parties. I'll make that very
clear to anybody listening in here. But no, you're
exactly correct. And on top of that, the additional...
layer of complication of inter -individual variability
and the genetic factor of whoever happens to
be taking these. If we think about, if we take
10 people off the street, the phenotypic differences,
the external characteristics that make them individual
are going to be huge for the most part. Now,
if we're looking at enteral physiology, those
differences might still be there. So how any
10 people respond to the same dose of the same
compound could be wildly different. Some of the
individuals who colloquially seem to be able
to run these really large cycles and not really
have any ill side effects. Like they might have
a genetic predisposition to being better able
to handle these compounds in the first place
or how they're going to respond. We know with
any medication, you have responders, we have
low responders, we have non -responders. Exercise
is the same way. And it all comes down to whatever
your genetic makeup happens to be. So part of
the paper. That kind of generated this discussion
that we recently published was looking at the
epigenetic factor or trying to look at the epigenetic
factor behind some of these inter -individual
differences or at least training style type differences.
So we set out to look at the differences between
those trained for powerlifting, bodybuilding,
or strongman competition and those using versus
non -using. But I think what we ended up finding
was that even within those groups, there was
a massive amount of inter -individual variability
in terms of their response and the doses they
were using. using and whatnot. So, you know,
we think about all these things in a vacuum of
what research tells us, but then we're not considering
that if we have, you know, highly competitive
Olympic weightlifters or highly competitive untested
powerlifters or strongmen or IFBB pro bodybuilders,
they are not running lab clinical doses that
were used for medicinal purposes. They're running
many, many, many times beyond that. And it's
going to be specifically engineered and designed
to their needs as an individual. So it's... I
don't want to say it's almost impossible to get
really good human research on the super physiological
doses used by some of these lifters and competitors,
but these are one of the biggest barriers and
challenges that we see, added on top of the fact
that they are illicit for use in many countries
outside of prescribed usage. Therefore, individuals
might be hesitant to come forward and say, oh,
yes, I'm using XYZ at these amounts in my training.
So the part of why a person would like to take
these is pretty clear. They have, let's say,
motivation. if beyond the disease and the need
for it they have the motivation is increased
performance be it strength or power development
and so on and expression of course too yes but
there is another side so they are not researched
that's one thing but from the retrospective research
so looking at the athletes who are known to take
and when they died and what kind of consequences
they developed Of course, because it was not
controlled, we cannot say this is why they died
earlier or this is why they had these issues.
But we expect that there are some issues. So
I think it's important that we bring the other
side too. Yes, this is how they work and what
is the outcome in terms of performance, but there
are costs to that. Because we push the physiology
into producing muscle, producing output, we're
paying for it. So let's go through how the payoff.
comes to be. Sure. That's a very good point.
And one that does deserve to get brought up in
every discussion about steroid usage. We have
this beautiful homeostasis that the body likes
to be at. And if we perturb that too much, we
push too much in one direction, like you said,
something has to give on the other side. So these
most potent compounds we talk about, they tend
to be great for anabolism and strength. They
tend to carry the heaviest side effects with
them as well. I mentioned with the oral steroids,
there's that hepatotoxicity. components of the
liver toxicity, the burden placed on the liver
by having to unduly process more than they should.
for these compounds because they've been chemically
designed to be resistant to being broken down.
You know, this can lead to eventual liver cancer
or just erosion of the tissue itself. It's been
no surprise. And like you mentioned, there've
been a number of notorious high -level competitive
untested athletes within the last five or 10
years who have passed far too young. And if we
look at the root cause, usually it's hypertrophic
cardiomyopathy, some enlargement of the heart,
thickening the heart tissue. The heart is a muscle.
And if we're looking at anabolism system, And
why? That is unfortunately one of the side effects
that can come with long -term heavy steroid use.
So there are cardiovascular risks. On the other
side of that coin, on the cardiovascular system,
skewing of blood lipids. is one of the most prevalent
side effects in steroid usage. So we have an
interference with certain enzymes via the liver,
which are responsible for kind of that mobilization
and usage and uptake and storage, et cetera.
And that can vastly alter the blood lipid profile
of a steroid user. So one of the things we tend
to see is that HDL, so high density. lipoprotein
count will go down. And HDL is what we think
about clearing away. It's called the good cholesterol.
I don't like to ascribe good, bad to cholesterol.
Cholesterol is just doing its job. It's where
it's supposed to be at the time. But HDL tends
to be anti -atherogenic, so better for cardiovascular
health. We tend to see increased LDL and triglyceride
count, sometimes increased BLDL count as well.
And these are things which are going to have
a negative impact on the kind of holistic blood
lipid cardiovascular health. There are negative
side effects with Most of these compounds and
especially past a certain dose threshold, it's
going to be there. Much of the coaching language
surrounding this kind of talk by coaches that
I can't say prescribe, but will suggest usage
for their athletes. It's about harm reduction
or risk reduction. Notice that's not harm prohibition.
We're not stopping the harm, but we can mitigate
it a little bit. So we'll see a lot of ancillary
compounds, things like milk thistle or Tudka
for. liver health, where they'll kind of give
a boost to these processes or act as antioxidants
to stop the degradation of these enzymes, we'll
see things like... fish oil, high dose EPA, DHA
blends that will kind of help balance out those
high triglyceride levels that we'll often see
from the skewed blood lipid panels. And it's
also one of the reasons that many IFBB pro bodybuilders
do a high amount of steady state, low intensity
cardiovascular exercise. It's not some, it is
a bit for a core expenditure, but a lot of it
is just for keeping your heart and cardiovascular
system functioning, especially at these very,
very high doses. Would diet, changing the diet
and avoiding, would that have any influence?
To extend. Absolutely. So the chicken and broccoli
is the art of that? They were right all along.
In a way, yes. I don't know. I want to backtrack.
I think they might have stumbled upon that being
a good side effect of it. If you go back and
you watch Pumping Iron, the Arnold documentary
he made back in the 70s, and even interviews,
he talks about having lots of fatty meats like
steaks and things like that. They were not carb
consumers usually. So if you think about it,
almost like... keto style diet, like that might
be one of the worst things to have if you are
using AAS just because of like, we're already
risking that kind of cardiovascular health, high
saturated fat, stragglers rides, LDL, etc. So
yeah, it's a very controllable diet is going
to be the best one that has a balance of fatty
acid types. So saturated, polyunsaturated, monounsaturated,
usually the rule of threes. So one third of your
fats should be monounsaturated, polyunsaturated,
and no more than a third should be saturated,
especially for users here. We've seen from some
research that dietary cholesterol is not necessarily
a driver of blood lipid changes. But again, as
soon as you have high dose AAS here, a lot of
that research goes out the window because we're
dealing with a very, very different physiology
than that of a normal inactive person, especially.
Yeah, a lot of the very strict controlled diet,
it's not just for the aesthetic purposes, but
it is from a health perspective as well. So,
yeah, we do tend to see that being one of the
side effects from that. Any other negative effects
we know about? Yeah, and some of these might
be negative in context, person to person, but
they are non -performance side effects. Maybe
we'll say that. They're not goal -oriented side
effects. Fertility issues and sexual function
is going to be one of the most prevalent as well.
Steroids are... sex hormones in the body i mean
very truly that we they are i mean testosterone
estrogen progesterone like these are all in the
family of reproductive linked hormones across
the sex spectrum so if we think about we have
somebody who is injecting any amount of exogenous
hormone into their body we'll say testosterone
because that's what you know the most basic form
would be testosterone is going to exert its effects.
It's also going to be converted to a few things
in the body. So I mentioned dihydrotestosterone
or DHT earlier. So the enzyme 5 -alpha reductase
will turn testosterone into DHT. DHT is very
androgenic. So a lot of the male pattern hair
loss and baldness, that's DHT derived, but also
beard growth, facial hair growth is DHT derived.
So there's a kid's toy from back in the day,
Wooly Willy, and have like a magnet with thought
metal shavings. You could make hair or a beard.
So I joke when I talk about this, it's like you're
just dragging the hair down the face because
it thins on top and it grows down here. So that's
kind of the effect we have there. But DHT is
heavily linked with feelings of well -being and
sexual function, especially in males. Testosterone
could also be aromatized to estrogen. So the
aromatase enzyme will convert testosterone to
estrogen. This is how males really have estrogen
in the body. And males do need estrogen. Estrogen
is hugely important. It's cardioprotective. It's
neuroprotective. It's osteoprotective. If we
think about postmenopausal females with osteoporosis,
it's from that precipitous drop in estrogen,
which a lot of that is actually where my research
has gone in the last few years. But we can talk
about that later. But estrogen has a separate
hypertrophy modulation pathway, the MAPK enzyme.
So. Estrogen is very important for everybody,
males included. It used to be thought, oh, when
you go on your steroid cycle, you take an aromatase
inhibitor because you don't want estrogen. That
is not true. Very often, a lot of the negative
side effects we see with steroid use are kind
of balanced out by having the proper estrogen
ratio within a certain boundary as a result of
that. Estrogen in too high amounts can lead to
things like water retention and bloating, mood
swings, and other ill side effects. But if it
gets too low, it's also very, very, very bad.
Estrogen and testosterone, when they're in the
body, The body senses that, and the production
of sex steroid hormones in the human body kind
of acts on what we call the classical negative
feedback loop. So the body senses a presence
of a certain level of these hormones, goes up
to the hypothalamus, to the pituitary, which
is where the hormone production starts, and it
kind of sends a signal saying, we have enough.
We don't need to release. The kind of precursor,
which is gonadotropin -releasing hormone, goes
from the hypothalamus to the pituitary, and then
luteinizing hormone, LH. and follicle -stimulating
hormone, FSH, are released. They go to the gonads,
even testes in biological males, the ovaries
in biological females. And then from there, they
act on the cells to produce your testosterone,
estrogen, et cetera. So for blocking the signal
there, we're not getting the releasers, which
then are initiating the release of hormones from
the gonads. So you suppress your natural production
of in -males testosterone. So if a male is deep
into a steroid cycle, they're likely to see a
null sperm count if they were to do a sperm analysis.
Coming off of a cycle, it can take anywhere from
three to six months for that process. to kind
of restart. There are certain compounds like
inconafine, citrate, DHEA, which will help kind
of boost that system as we get back in. Also,
you can take synthetic congeners of LH and FSH,
so human chorionic anatotropin or human menopausal
anatotropin, so they kind of act like LHFSH,
so they can restart the production of endogenous
hormones from the gonads, even during a cycle.
So again, there are ways to kind of mitigate
this, but it's all about... risk reward and also
how much money you have to spend because a lot
of people talk about many of the things are very
very expensive and i'm not willing to get into
a price point on anything here but these can
definitely add up so anybody who's considering
using for i want to put this out here for the
listeners anybody who's considering using there
are two questions you need to ask yourself one
is am i looking to go or am i currently at an
incredibly high competitive level if not if it's
just for recreational purposes i wouldn't recommend
it i don't think the juice is worth the squeeze.
The other thing is, if I am a high -level competitor,
how much am I willing to monetarily and from
a health -wise invest and kind of give up in
pursuit of this goal? To back to the fertility
thing here, if somebody is considering going
on, if you're a male, I would consider If children
are something you want in the future, then I
would maybe do, you know, semen analysis and
maybe freeze a sample just so you have security,
peace of mind. Obviously, if you're a female
competitor looking to use these compounds, doing
an egg retrieval cycle, again, if this is something
that you are at all considering in the future,
it's peace of mind, you know, because some of
these things may be irreversible. I will say,
unfortunately. The male reproductive system is
much more robust to kind of bouncing back over
time than the female system. The effects of steroids
on female reproductive physiology sometimes are
irreversible past a certain point. In males,
you need many, many years of very high doses
with very little time off to really see any kind
of lasting permanent effects. Again, this will
differ person to person, but that is some of
the big changes we see in reproductive health.
Usually when people are on a steroid cycle, they
feel great. I mean, strength is to the roof and
physique probably is improved. Libido is going
to be very, very high. It's the coming off or
it's the mismatch of the internal hormone balance
because of what you're using that is likely to
kind of give some of those negative side effects.
If we look at, again, talking about female steroid
users, deeply virilizing, masculinizing side
effects. So deepening of the voice, facial hair,
body hair, thinning of the scalp follicles, acne.
you know, heavy sebaceous gland oil production,
things like that. And again, many of these are
irreversible in female competitors or users there.
Those are some of the major symptoms we think
about. There's a variety of other smaller side
effects that might differ person to person. I
did mention it before and I'll kind of... close
on this is the neurotoxic side effects of certain
compounds more than others. So like I said, androgens,
the brain uses them for a variety of compounds,
excuse me, for a variety of reasons. And certain
compounds tend to have more neurotoxic effects
than others, specifically the family called 19NORs.
So they are formulated differently at one of
the alpha carbon, the carbon positions, steroid
rings, and the way that they interact with brain
chemistry is potentially devastating. So if we
have somebody who is prone to mood imbalances,
mood swings, depressive anxiety, paranoia symptoms,
anything like that, even to a small degree, the
use of that steroid might heighten that. I think,
and I might be shooting from the hip a little
bit here, but when we think about somebody having
a roid rage, which I don't believe is a blanket
concept across the board, there are certain compounds
which I'm willing to believe might be the result
of that if the person already has a tendencies
in the first place. So a lot of these compounds
will heighten the kind of brain neurochemistry
that you are predisposed to. I don't think they
introduce something new. out of nowhere but again
we do not have a lot of research on that because
no ethics board is going to approve a study with
super physiological doses specifically to see
if they elicit neurodegenerative side effects
it's not but unfortunately so you know when we
talk about to wrap up talking about side effects
and harm reduction this is where i think the
research could be a little more robust because
if people are going to be using steroids i think
we deserve to give them the best evidence -based
backing of how they best can keep themselves
healthy and alive All right. I want to give you
an opportunity to talk about your study. So you
mentioned it a little bit. Could we just quickly
go through the setup? How did you design the
study? Who have you recruited? And then we will
go to the results. Absolutely. So this project
actually was my doctoral dissertation. And so
this would have been back about 2022, 2023. And
the purpose of this was. To identify any differences,
again, like I said, between training styles and
competitive strength and physique athletes. So
powerlifters, bodybuilders, and strongmen. Unfortunately,
no Olympic weightlifters in this study. When
I saw your email come through originally, I was
like, I wish I had Olympic weightlifters in this
study for your audience. We did have some powerlifters,
as you mentioned, though. And to see... differences
specifically in the expression of certain myogenic
growth factors in humans. So this had come out
of a systematic review, which I'd also done as
part of my doctoral work. And it was looking
at, again, the effects of steroids across both
rodent and human models. Obviously not athletes,
because we're looking at rodents here, but how
they affected the genetic expression or the mRNA
expression of any gene related to muscle that
they looked at in these studies. And I actually
made a giant word cloud when I was doing my proposal.
And there were, I want to say, 40 or 50 plus
different genes that they looked at. And that's
a small number. There are many, many pathways
that are doing anything in muscle at any given
moment in time. But the three most common growth
factors that were looked at across studies and
that were increased by administration of steroids
were myogenin, so myo -G, myoblast, differentiation
factor one. And so my OD and IGF -1. And so my
growth factor one. So IGF -1 is the growth factor
in the body. It is across any tissue, probably
the most prevalent and important thing responsible
for analysis. So growing tissues. And this is
in utero through adulthood and beyond. If we
think about growth hormone, human growth hormone,
its primary role is to cause the release of IGF
-1. So that's how important IGF -1 is. So any
tissue that we're expecting to be growing. we
would expect to see heightened IGF -1 levels
because of that. Myogenin and MyoD1, these are
hugely responsible for the muscle tissue cycle
of proliferation, differentiation, and integration.
So, you know, very briefly, you, as our understanding
says right now, hang in, this is where we're
kind of at the what do we know, what don't we
know level of research. We don't gain more muscle
sets. We make them thicker and we add more nuclei
to them. So again, the nucleus is where DNA is
housed. It's the brain of the cell. So if we
could have more nuclei in a muscle cell, those
are more factories, so to speak, where we're
manufacturing proteins. So if we think about
the kind of genomic effects of Android administration,
we're going to see the more nuclei there are,
the more protein can be made, et cetera, et cetera.
Where do those nuclei come from? They come from
something called satellite cells. And satellite
cells, very simply, are stem cells that are specific
to muscle. The stem cell, the satellite cells
are quiescent, so kind of like resting and waiting.
When they're kind of called upon, they proliferate,
they differentiate, and they are taken up into
mature myotunes and myoblasts, and they add their
nuclei to the muscle cell. That is kind of what
we see happening and what we are understanding
in theory of how muscle anabolism works really
truly. So that's kind of what Myogen and MyoD.
one do and the cool thing about myogenin is it's
self -activating so it can boost itself on a
loop it's linked directly with myo g1 and in
the the manuscript which we'll definitely make
sure we can link to your listeners if they want
to go and read it i have a diagram kind of showing
how these growth factors work in congruence with
other signaling proteins, androgens, the G protein
couple receptor, as I mentioned before, et cetera.
So that's kind of what we see happening here.
So these tend to go up or down together. They
go hand in hand in hand, so to speak. So that's
why we chose to look at those three genes specifically.
We'd expect to see them boosted in, A, those
who are maybe trained with higher volumes, right,
more of a hypertrophic stimulus, and those who
are using steroids, because we definitely expect
that to be more. of a hypertrophic studio. So
that was kind of what we set out to do. We recruited
from a sample, again, of competitive powerlifters,
bodybuilders, and strongmen. We wanted competitive
athletes. One of the limitations of much research,
as we've kind of alluded to, is the fact that
We are limited in terms of sampling methods and
who we can actually get to participate in our
study, humans or otherwise. So the issue with
taking already competitive athletes is that you
can't really standardize their training because
they're going to say, I have a training program
that I've been doing for years. It works for
me. It's custom built by my coach. I'm not going
to do a program that's exactly right. So and
you mentioned it before, a lot of this is retrospective.
So observational research, ex post facto saying,
what are you already doing? Can we kind of account?
for that? And then what do we see going forward
based on what we're looking at? So we gathered
their usage of steroids or not, and we had them
do a seven -day training log of the seven days
preceding when we took the salivary sample. I'm
going to touch on that again in... a second.
So from there, we were able to calculate volumes
for the different athletes, just simply reps
and sets. We didn't do tonnage, which would have
accounted for training intensity as well. One
of the interesting things that we found was that
more athletes than you'd expect did not keep
a very strict log of the certain weights that
they utilized in their training, which as a meticulous
note taker, that blew my mind. I first came across
that. It's like, how do you know if you're getting
better? We were simply calculating volume, so
it was okay. And from those who identified anonymously
as steroid users, we gathered their doses of
whatever compounds they were using. So the previous
systematic review that I had done, I want to
say there were about over 18 different steroid
compounds that were identified. It probably is
more than that as well. We think about designer
compounds and things not get in research, etc.
So we gave them the opportunity to identify any
of those and then other. Was there anything that
wasn't on this list that you were taking? I think
there's only one compound that was identified
as such. So we have them identify all that, how
much they were using, etc. And all the information
also is in the paper. There's a nice table on.
the descriptive characteristics of the doses
that were reported by participants. They weren't
as high as you may expect. I think the highest
was about 600 milligrams total per week across
all compounds, and the lowest was 50 to 100,
something like that. So, you know, if you think
about the variety in dose size and frequency,
et cetera. There was a very small sample of steroid
users already. So we could see how that high
amount of within -group variability is going
to have a massive statistical impact on can we
actually get anything from this? So we gathered
all this information and analyzed it, had all
of the salivary samples analyzed for the three
genes. You know, there's a lot of debate within
the review process about whether salivary samples
were appropriate for this kind of analysis. And
I definitely think there is credence to call
them into question. There is evidence suggesting
And kind of finding that IDF1 and other similar
growth factors can be found in meaningful quantities
in saliva. Doing something like a biopsy probably
would have been better. So doing a proteomic
analysis alongside this genomic analysis from
a muscle specific biopsy that, you know, that
likely would be something to improve upon this
design in the future. But that is, that is what
we did. And we had them analyzed. We found really
no difference to any combination of spork or
steroid use. across any of the three growth factors.
And I was fine with that. I am not somebody who
needs to find significant results from a paper.
I think non -significant findings are still,
they're still findings and they're still relevant.
They still tell us maybe what does not work so
that future researchers building upon this lineage
can say, well, we don't have to try this again.
It's already been tried. Or maybe we can tweak
this design, et cetera. We needed a larger sample
size. I mean, that is probably one of the first
things I would address. We need a larger sample
size, more balanced groups. We had a bit more
power afters than either of the other two. And
then steroid users to non -users. Again, I think
it might be challenging for steroid users to
be willing to come forward and say, I'm willing
to disclose, even though on the informed consent,
obviously we're saying all of this is de -identified.
It's anonymous and confidential. No one's going
to be looking at this. The social desirability
bias and like when you're doing a survey, even
if no one's going to know it's you, you don't
want to come. crosses as being a bad person and
not that steroid use makes you a bad person,
but these are the fears that can kind of come
to people's minds when they're going to self
-disclose this kind of information. So those
are some of the issues that we ran into. Again,
doing a robust tissue analysis opposed to a salivary
sample analysis. It can also be challenging to
get a muscle biopsy from individuals, especially
if you have people who you're training heavily
saying, oh, we're going to take a right of right
size, yeah, bit of muscle from your quad and
you have to squat heavily this week. That's not
going to go over very well. well for the most
part the other some of the other limitations
you know like i said we weren't controlling their
training so there's a lot of inter -individual
variability in terms of what movements they were
doing volume intensities etc we there was a standardized
dosing protocol or use of compounds and i think
just with the narrow range of people that we
had to pull from, a lot of these differences
just weren't able to manifest based on those
limitations. So, you know, be it as it may, it
was a good kind of, I think, look into this process.
Nothing like that had been done on athletes of
that level before. From the systematic review
that we did before, I think there were 29 studies
we identified and only three of them had human
participants. The rest were all mouse or rat.
And that was after cutting out other non -human
or rodent. Because rodent, again, it still gets
some pretty decent mechanistic carryover. There
were a few cattle studies. There were many studies
in zebrafish. Zebrafish, there's a lot of steroid
research in zebrafish for some reason, which
is fascinating. But I'm not a zoologist, so I
can't speak into that. So yeah, only three studies
on humans. None of them were an athletic population.
Many of them were of elderly population, right?
So if we think about the benefits of this research,
it might not even be looking at athletes. It
might be looking at geriatric populations or
hypogonads. genetic populations, you know, those
who on these medications were prescribed, were
developed in or prescription for in the first
place. But yeah, that was kind of our main finding
from this. Unfortunately, not much to go off
here. It doesn't seem that those three genes
specifically impacted much, but due to the reasons
that I mentioned before, that might give credence
as to why. Did you ask your participants how
long have they been using for? Because I expect
that there is one of the elements will be how
long you... have to be using to actually become
a different person to the person who is not using
metabolically and then physiologically. Right.
We had defined it as use of at least six months
prior to the time of the study. And I think the
information we gathered was within the five weeks
preceding the tissue sample gathering. So again,
like six months, not really a long time. Something
could have started right before this. like six
months before and say, oh, I'm a steroid user.
Somebody who's been doing this for 16 years,
right? That's going to be, like you said, it's
vastly different. You're 100 % correct. These
are things that could have given us a more robust
design. The issue is the more arms of analysis
you add, the number of people you need to detect
meaningful changes goes through the roof. I'm
not saying that that can't be done or that's
a reason not to do it, but that definitely gives
some insight into maybe why this was not able
to really detect any meaningful differences between
these groups. I think that's another study that
should be run between teams and between countries
and so on where the researchers pull the data
together and... Because otherwise it's impossible
to get a study running for long enough and controlled
enough to get enough people. Basically that's
where it comes down to. Yeah. Multi -site data
collection is a trend that is being seen more
and more in exercise and sports science specifically,
which is great because we've been played with
small sample sizes since this field really became
a thing. Let's bring it all together. What would
be your advice on the base of your knowledge
and your study for athletes and coaches? I definitely
want to hearken back to what I said earlier about
for somebody who is considering using anabolics
of any type or PEDs of any type. You need to
do an honest accounting with yourself as to the
level of competition you want to go to and are
willing to invest financially, time -wise, et
cetera, to get to. I truly believe that 99 .9
% of individuals could do an audit of lifestyle,
nutrition, sleep, everything else that we can
control for and probably make quite a bit more
progress if that's something they truly care
about. I don't think they're a viable shortcut
method for those not looking to really compete
in the highest echelons of competition. And for
those who are, as they say, it's a marathon,
not a sprint. So we want to think about longevity
being the name of the game, you know, time that
you can spend training healthily and not just
make a big splash then disappear because you've
seriously injured yourself. So, and that comes
to coaches too. For coaches out there, if you
are working with athletes and you are suggesting
use or asking use of PEDs of any type, anabolic
steroids or otherwise, you need to be doing your
due diligence to educate yourself. first of all,
on what these things actually do in the body,
the myriad of side effects, desirable or otherwise,
that come with them. And you need to be considering
minimal effective dose, so getting the most out
of the least, and proper harm reduction and mitigation
protocols that can be used. And at all times,
you need to remember that these are people you
are working with. They are not science experiments.
They are not lab rats. These are individuals
and humans. And if we looked at it from a research
perspective, things about respect for persons,
do no harm, we need to be doing the same as coaches.
as well is the risk or is the reward worth the
risk you're willing to put this person through
and you need to be upright and honest with your
athletes if you are asking this of them. That's
what I would, my advice I would give. Thank you.
Two short questions to finish. The first one
is, what is your favorite lift? The barbell bash
press. Why is that? It's the one that I think
I've had to put the most work into over the years.
So there's a bit of rewarding aspect there. And
as I get older, it's the one that causes me the
least trouble that I can still have fun with.
Yes, I'd say for those reasons. Very nice. And
the last question is, where people can find you
if they want to... Follow your work or see what
you're up to or maybe ask a question. Absolutely.
So there's a few ways. Social media wise, I'm
really just on Instagram. I don't do anything
else, unfortunately. So my handle is at doctor
underscore Lukey underscore lifts. And I'm sure
we can put that in the show notes for the listeners
if they want to find that. I am on ResearchGate.
So if you type Luke Pelton into ResearchGate,
I should pop up. I have my faculty and research
profile. So Luke Pelton Springfield College.
I should come up there as. well. And my email
should be readily accessible from all of those.
Feel free to send me a DM. I would genuinely
love to talk with anybody who's interested. I
truly mean that. Thank you so much, Luke. It
was a pleasure. Absolutely. Thank you, Alex.