Speaker 1: Tivy and cook, David Bryan K Patrick Gillespian. It's the
Speaker 1: bloody you project. It's jumbo up the front. Where else
Speaker 1: would I be? We'll start with the lady in the room, height.
Speaker 2: Tiv front and center. You never he stumbled over all
Speaker 2: of those middle names this time.
Speaker 1: Yeah, I don't know. I don't know. He's told me
Speaker 1: I forget. Do you remember now? Do you remember?
Speaker 3: I don't remember them my real one. No, I have
Speaker 3: a real middle name. I remember. It makes that's right.
Speaker 3: See look at Tiffany wow because it makes an embarrassing acronym.
Speaker 1: Yeah, Dad, I thought of that attic as it came
Speaker 1: out of your mouth. Tiff Have you been cookie? How's
Speaker 1: the piano career, the musical career has it taken off?
Speaker 2: It's it's volatile because I go from in a moment yeah,
Speaker 2: because you know, I'm like a little bit impatient and
Speaker 2: I'm like, all right, boring, next, got this mastered, And
Speaker 2: in the moment I'm onto something new, I get frustrated.
Speaker 2: I'm like, why is this doing even had? How could
Speaker 2: they make it make any less sense? Music and reading music?
Speaker 1: Really, I don't know that that's meant to be one
Speaker 1: of the emotional and or psychological outcomes of playing music.
Speaker 1: I feel like it's meant to do the opposite.
Speaker 2: For one, that's where I'm at my best.
Speaker 1: I don't know that you're meant to be competitive when
Speaker 1: you're learning the piano tip.
Speaker 2: I know, but that's how I do everything.
Speaker 1: How's that going?
Speaker 3: Well?
Speaker 1: Really it is it? Could I run you through a.
Speaker 3: Have I dropped in on a psychology session here or something? Ever?
Speaker 1: Sorry? Sorry coming from Australia's leading anti psychology advocate. How
Speaker 1: are you, sir? How's your day going?
Speaker 3: What?
Speaker 1: It's Wednesday? Arbo? What's going on up there? Did you
Speaker 1: go to work today? Did you put on a suit?
Speaker 3: I did go to work. I didn't put on a
Speaker 3: suit because I didn't leave my office to go to work.
Speaker 3: But yeah, I did some work.
Speaker 1: Like an absolute grown up. Well, you wrote a good
Speaker 1: article that I don't know when you write it, but
Speaker 1: it went.
Speaker 3: Up today on finish it this morning. Yes, it's been
Speaker 3: in progress all week.
Speaker 1: So it's on substack everyone. Doctor Gillespie, as many of
Speaker 1: our listeners call you, Doctor Gillespie, who, just to be clear,
Speaker 1: isn't a doctor but could be could be. Doctor Gillespie
Speaker 1: has written an article silencing the food noise, and it's
Speaker 1: basically the once upon a time of ozeenpic. So it's
Speaker 1: now just so it's a g LP one what do
Speaker 1: they call it?
Speaker 3: And yes, yeah, yeah, agonist.
Speaker 1: So it's it's intended purpose Originally, I think I have
Speaker 1: not read the article. I should have. I apologize, but
Speaker 1: it's lower blood sugar. Was that its original intent? In fact,
Speaker 1: why don't you just tell us the story? You should
Speaker 1: read these articles. You know, it's a place I normally do.
Speaker 1: I had a corporate gig, Thesavo, and so I apologize.
Speaker 3: Okay. So it sort of started in the seventies when
Speaker 3: they were first started fiddling around with insulin and its
Speaker 3: counterpart of glucagon. Sorry, not glucagen. It's the They were
Speaker 3: doing it because a brand new disease was starting to occur,
Speaker 3: called type two diabetes. And it might seem odd to
Speaker 3: people today to think of type two diabetes as being
Speaker 3: a brand new disease, but it is. It really really
Speaker 3: wasn't a problem before the early nineteen eighties when we
Speaker 3: started taking health advice from the government and it so
Speaker 3: scientists were tooling around with some of the hormones which
Speaker 3: they knew were in this most particularly insulin. And you know,
Speaker 3: insulin's main job is to move glucose out of the
Speaker 3: bloodstream and into cells that need it. So you know,
Speaker 3: if muscles need energy, then they put receptors up to
Speaker 3: their cell surface, and insulin comes along and unlocks the
Speaker 3: receptor to allow the glucose to enter. Glucose just can't
Speaker 3: really nearly enter any cell in the body. It needs
Speaker 3: insulin to do it. And so insulin is produced in
Speaker 3: response to us eating stuff, and that raises our blood
Speaker 3: sugar level, which then causes insulin to be released, and
Speaker 3: then the insulin helps remove the glucose from the bloodstream.
Speaker 3: But you don't want to overshoot, because you know, you
Speaker 3: don't want all that insulin in your bloodstream running around
Speaker 3: releasing all the glucose out, and then you've got no
Speaker 3: glucose left in your bloodstream and you're dropped dead. So
Speaker 3: we have a counterpart to that called gluckagon, which is
Speaker 3: sort of anti insulin, if you like. And so when
Speaker 3: blood sugar levels start to go too low, either because
Speaker 3: you haven't eaten for a while or you've been exercising
Speaker 3: like a nutbag, then your body needs to bring those
Speaker 3: levels back up again, otherwise your brain will stop working
Speaker 3: and other important organs will probably too. And the glugagon
Speaker 3: travels to the liver and instructs the liver to release
Speaker 3: some sugar back into the bloodstream, so bring the sugar
Speaker 3: back up again. So that's what they knew in the
Speaker 3: nineteen seventies, and they, looking at that, thought, oh, maybe
Speaker 3: if we get to fiddle around with these hormones a bit,
Speaker 3: maybe we'll be able to do something about type two diabetes.
Speaker 3: Because type two diabetes is where you essentially have, you know,
Speaker 3: the blood shower is too high, and the body becomes
Speaker 3: effectively insulin resistant, that is, it's no longer listening to
Speaker 3: the signal from insulin telling cells to absorb the glucose
Speaker 3: out of the bloodstream, and having persistently glucose can start
Speaker 3: to do real damage. So they thought, oh, well, what
Speaker 3: if we fiddle around with the glucagon bit of that
Speaker 3: and see if we can, you know, fix that problem
Speaker 3: with a bit of messing about. They weren't terribly successful
Speaker 3: doing that, but they did happen across some other substances
Speaker 3: that were seemed to be part of the equation. They
Speaker 3: weren't quite sure what they did, but they did notice
Speaker 3: that one of them, in particular, one called GLP one
Speaker 3: or glucagon like peptide one, did an interesting thing. It
Speaker 3: seemed to be released around the same time as glucagon,
Speaker 3: and what it did was not only suppress appetite seemingly
Speaker 3: by sending a signal directly to the brain to tell
Speaker 3: us to stop eating, but it also made us feel
Speaker 3: physically full even if we weren't, so it essentially would
Speaker 3: shut us down. It was the biochemical equivalent of I
Speaker 3: don't know, wiring your mouth shut.
Speaker 2: You.
Speaker 3: If you were hit with this stuff, you couldn't eat anymore.
Speaker 3: And so they thought, oh, this is an interesting thing.
Speaker 3: Maybe if we gave people with type two diabetes some
Speaker 3: of this g l P one, then they's they'd eat less,
Speaker 3: but their blood sugar would be lower, and maybe that
Speaker 3: would help their diabetes. So they started doing some trials.
Speaker 3: It actually did, by the way. So the trouble with
Speaker 3: it was that it doesn't last very long in the body.
Speaker 3: So they gave it to people. It normalized their blood
Speaker 3: sugar levels, it made them feel full, but it was
Speaker 3: gone in minutes. It had a half life of minutes
Speaker 3: in the bloodstream. Mostly because we have a thing naturally
Speaker 3: occurring called DPP four, which I'm sure you're all terribly
Speaker 3: interested in, but it's kind of a molecular pac Man
Speaker 3: that goes around eliminating GLP one. Because this is all
Speaker 3: supposed to be being done in real time adjustments minute
Speaker 3: to minute in the human body. You know, you've got
Speaker 3: a bit too much blood sugar adjusted one way, got
Speaker 3: a little too little adjusted the other way, and so
Speaker 3: the body is really good at balancing those things, and
Speaker 3: so pumping us full of one of those hormones, which
Speaker 3: is what they were doing, didn't really work very well
Speaker 3: because the body said, ah, there's too much of that hormone.
Speaker 3: I'll just go and clean that up, and it did
Speaker 3: so within minutes. So the only real way it could
Speaker 3: be effective was to put someone on a drip where
Speaker 3: they were being continuously infused with it, and yes, then
Speaker 3: it did work. But that's not a particularly practicable, practical,
Speaker 3: or saleable way of managing type two diabetes. So this
Speaker 3: is where the drug companies got involved, In particular, Novo
Speaker 3: Nordisk always get their name wrong. Is Nova Nordisk I
Speaker 3: think it was who said let's have a look at
Speaker 3: this let's see if we can crack this nut about
Speaker 3: not having to have people tended to have dripped the
Speaker 3: whole time just to have this effect. And what they
Speaker 3: did is they managed to engineer a fatty coating to
Speaker 3: the GLT one that stopped it being destroyed by the
Speaker 3: DPP four and it would last thirteen hours rather than
Speaker 3: a minute. So suddenly you've got something that you could
Speaker 3: inject that will last a day effectively because the rest
Speaker 3: of the time you're asleep, And now you've got a
Speaker 3: marketable drug. So that's what they first came out with
Speaker 3: in the nineties I think it was, And from there
Speaker 3: the development took it further and said, hey, all right,
Speaker 3: we're making lots of money from that. What if we
Speaker 3: could do something that didn't have to be injected daily
Speaker 3: because even that's still a big ask, just say to
Speaker 3: someone with type to diabetes where you do have to
Speaker 3: inject this thing every day. And there was the other
Speaker 3: little problem, which is that, rather like GLP one, it
Speaker 3: also tended to make people extremely nauseous to the point
Speaker 3: of vomiting. Remembering that one of the effects of this thing,
Speaker 3: GLP one, is to make us feel full, and if
Speaker 3: you are on a continuous infusion of this. It is
Speaker 3: like you have just eaten the biggest meal of your
Speaker 3: life the entire time, and a lot of people's reaction
Speaker 3: to that is to vomit. So they feel so nauseous
Speaker 3: and so sick from being so full feeling that they vomit.
Speaker 3: So that's a bit of a nasty side effect as well,
Speaker 3: which limited its use. But it was a little bit
Speaker 3: less with the one that they made that had the
Speaker 3: fatty covering and that lasted thirteen hours. Wind forward a
Speaker 3: bit and they eventually cracked the problem, came up with
Speaker 3: a better version of it, one that would last an
Speaker 3: entire week before it was destroyed by the body. And
Speaker 3: that's what we call a zenpic now. And so suddenly
Speaker 3: they'd created all of this time while all this research
Speaker 3: was going on. Of course, diabetes begetting worse and worse
Speaker 3: and worse and worse at an exponential race. So we're
Speaker 3: gone from the nineteen eighties where it barely existed. They're
Speaker 3: doing all this research. By the time we get into
Speaker 3: the early noughties, then there's a market. Then there's a
Speaker 3: real market, and suddenly they've got a license to print money.
Speaker 3: Then they paid close attention to something they had noticed
Speaker 3: in some of the earlier studies, which is, not only
Speaker 3: did it seem to hold people's type two diabetes in check,
Speaker 3: they seem to lose a lot of weight while they
Speaker 3: were consuming it. And I guess that's not unexpected, you know,
Speaker 3: if you're having something that makes you feel full to
Speaker 3: the point where you want to throw up, you've got
Speaker 3: to eat less. So and then suddenly they found out
Speaker 3: that if you increase the dose a bit, you can
Speaker 3: really up that weight loss into the sort of ten
Speaker 3: to fifteen percent range for most people. And that's products
Speaker 3: like Wegovi, for example, which is a higher dose version,
Speaker 3: and it has approval to be sold as a weight
Speaker 3: loss medication, at least in the United States.
Speaker 1: So it.
Speaker 3: That's how we've gotten to today, which is first of all,
Speaker 3: just trying to find a way to do something about
Speaker 3: the hormones and fix type two diabetes, which was then
Speaker 3: not much of a problem but was clearly a growing problem.
Speaker 3: Now we've got an epidemic of type two diabetes and
Speaker 3: it's getting worse by the minute. And we've also got
Speaker 3: an epidemic of obesity, and it's getting worse by the minute.
Speaker 3: And this drug appears to address both of them, at
Speaker 3: least as long as you keep taking the drug. So
Speaker 3: it is unfortunately the case that as soon as you
Speaker 3: stop injecting this stuff, your body goes back to the
Speaker 3: way it was.
Speaker 1: But I just ask, and so is the weight loss
Speaker 1: mechanism is essentially just because people are consuming less calories,
Speaker 1: so still energy in and out is the I.
Speaker 3: Mean it's to do. It does have an effect on
Speaker 3: the brain's appetite control system a little as well, but
Speaker 3: it's a transient effect. The primary effect of it is
Speaker 3: that you feel so full that you couldn't eat anything anyway.
Speaker 1: So I guess it messes also with grellin and you know,
Speaker 1: the hunger hormone, and I think it's leptin, the society
Speaker 1: hormone or whatever like, so people.
Speaker 3: Part of that matrix of the hormones of appetite.
Speaker 1: Yes, and then so people, I mean, what unless I'm
Speaker 1: missing something and I don't know. So this is a
Speaker 1: legit question because I've done this is my first real
Speaker 1: lesson in ozen pic Like, I had a vague idea
Speaker 1: and I knew that it was originally designed for blood
Speaker 1: sugar regulation or flurering. You know, blood sugar blah blah blah.
Speaker 1: But and for type two diabetics, which is, as you said,
Speaker 1: is basically a new new condition. But like, ultimately the
Speaker 1: weight loss is still coming because or it's still a
Speaker 1: byproduct of people just consuming less food.
Speaker 3: Correct, Yeah, it's the it's the biochemical equivalent of stomach stapeling.
Speaker 1: So you know that.
Speaker 3: You could be just as a active by wiring people's
Speaker 3: mouth shut. It's the same essential principle, except you're doing
Speaker 3: it with drugs rather than physical impairments. So it's that's
Speaker 3: the principle of it, and it's effective for as long
Speaker 3: as you keep taking it or can tolerate it, remembering
Speaker 3: that the nausea thing is still there and some people
Speaker 3: can't tolerate that. Think.
Speaker 1: I think the lie though, is, oh, this drug makes
Speaker 1: you lose weight. Well, well, this drug makes you less hungry,
Speaker 1: and what makes you lose weight is the fact that
Speaker 1: you're fucking eating less, Like you're consuming less calories because
Speaker 1: you feel somewhere between full and sick and nauseous. And
Speaker 1: I'm reading the side effects here constipated, fatigued. Fuck. You know,
Speaker 1: it's like like the real reason that you're losing weight
Speaker 1: is just because you're reducing your calories, which and I
Speaker 1: know people will jump up and down, but you can
Speaker 1: kind of do that without these drugs.
Speaker 3: Yeah, And in fact, you can do it with weight
Speaker 3: loss shakes for example, for as long as you can
Speaker 3: tolerate that. I'm not believing, I'm not advocating for them.
Speaker 3: I'm just saying that they're the same essential principle, which
Speaker 3: is you just drastically reduce what you're consuming and then
Speaker 3: you will lose weight. There is another way to lose weight,
Speaker 3: which is stop consuming things which mess up your appetite
Speaker 3: control system, like fructose, and this doesn't help that at all.
Speaker 3: You can still you know, if the three grams of
Speaker 3: stuff that you can tolerate is fructose, then you're not
Speaker 3: changing anything about what you're consuming. You'll still lose weight
Speaker 3: because how much you can consume will be controlled. But
Speaker 3: the damage that's being done in there by the sugar
Speaker 3: a you know, which is you know, fatty, liver disease,
Speaker 3: kidney disease, hypertension, disease, all of those good things that
Speaker 3: sugar brings to us are all still there, but it's
Speaker 3: being masked by this drug which is hiding the obvious symptom,
Speaker 3: which is that you look fat or that you've got
Speaker 3: type two diabetes. So masking those symptoms is not very helpful.
Speaker 3: You're still doing the damage, you're just hiding it. And
Speaker 3: that's I guess the point of the article I wrote,
Speaker 3: which is to say, let's understand that this is like
Speaker 3: having a boat with a leak in it and then
Speaker 3: putting a pump in, and so the boat still keeps
Speaker 3: working for as long as the pump keeps working because
Speaker 3: it doesn't fill with water and sink to the bottom.
Speaker 3: But as soon as you turn the pump off, you've
Speaker 3: still got a boat with a leak in it. And
Speaker 3: that's what's going on here, only it's worse in that
Speaker 3: the pump is also hiding some other things that are occurring,
Speaker 3: which woul whether you were on this stuff or not,
Speaker 3: if you continue to consume the seed, oils or sugar
Speaker 3: that are causing the underlying metabolic conditions. Remembering that we're
Speaker 3: talking about a condition type two diabetes and obesity, both
Speaker 3: conditions that barely existed prior to nineteen eighty barely existed,
Speaker 3: and I know that for all of us living now,
Speaker 3: it seems like they've been there forever, but they really haven't.
Speaker 3: And the fact that that's the case stops us looking
Speaker 3: for the solution to the problem, stops us looking at
Speaker 3: the cause, stops us trying to repair the hole in
Speaker 3: the boat that's causing the leak, and diverts us to
Speaker 3: investing in better and better pumps to disguise it. Yeah.
Speaker 1: Yeah, And I think also it's worth noting that when
Speaker 1: people lose weight quickly, like a lot of weight the
Speaker 1: short time, generally what they're losing in order is water, muscle,
Speaker 1: and fat in that order. And then when they regain it,
Speaker 1: which is not inevitable but common, they regain water, fat, muscle.
Speaker 1: And so somebody who's gone through rapid weight loss, whatever
Speaker 1: the means of the rapid weight loss was, that you
Speaker 1: can find, for example, you know, somebody might start it.
Speaker 1: Let's just say one hundred kilos. They lose twenty kilos
Speaker 1: in eight weeks, which is two and a half kilos
Speaker 1: a week, which is too quick. Generally, they lose a
Speaker 1: lot of weight, and a fair percentage of that is
Speaker 1: lane tissue, is muscle, and then they regain the weight
Speaker 1: because the wedding's over, or the school reunion or the
Speaker 1: whatever is over and then they end up back at
Speaker 1: one hundred kilos, but now they've got a higher body
Speaker 1: fat percentage at the same weight because in this yo
Speaker 1: yoing cycle they've lost lane tissue and that as well.
Speaker 3: It's because you're not, once again not addressing the fundamental
Speaker 3: reason why you needed to lose weight in the first place,
Speaker 3: which is that something is malfunctioning in your environment that's
Speaker 3: causing you to eat more than you should. Something is
Speaker 3: interfering with your appetite control system. And believe it or not,
Speaker 3: we have a perfectly functional appetite control system. It's all
Speaker 3: controlled by hormones. It's all perfectly well regulated. As long
Speaker 3: as we don't mess with it, we will stop eating
Speaker 3: when we've had enough. We will know exactly how many
Speaker 3: calories is enough because our appetite control system will shut
Speaker 3: us down. The only time that doesn't happen is when
Speaker 3: we do something that breaks our appetite control system. So
Speaker 3: that's the fundamental thing, and it's a problem also even
Speaker 3: with most dietary prescriptions these days, whether it's will go
Speaker 3: over you or anything else, which is there's this fundamental
Speaker 3: thing assumption that what you've got to do to lose
Speaker 3: weight is get in there and manually start counting calories,
Speaker 3: which is idiotic because you don't do it when you're
Speaker 3: wanting to put on height. So when you're growing, you know,
Speaker 3: you didn't start out, you know, the fabular six foot
Speaker 3: five you are. You started out significantly smaller than that,
Speaker 3: and your body automatically allocated calories and resources to get
Speaker 3: you to the height that your hormones programmed you to be.
Speaker 3: But somehow when we and nobody would argue with me
Speaker 3: there if I said that to them. But for somehow,
Speaker 3: when we're talking about growing vertical, of growing horizontally rather
Speaker 3: than vertically, suddenly it willpower is required. It's like, in
Speaker 3: order to be six foot five, you had to will
Speaker 3: yourself to that height, and that's nonsense. You are that
Speaker 3: height because hormones made you that height, and the same
Speaker 3: goes for diet. There's this building in assumption that fault
Speaker 3: is involved, that in some way you are a weak person.
Speaker 3: If you're overweight that you are, you know you have
Speaker 3: some sort of moral fault, And bizarrely, it's a moral
Speaker 3: fault that's really only occurred in the population in the
Speaker 3: last fifty years. Prior to that, no one even gave
Speaker 3: it a moment's thought because prior to that, there was
Speaker 3: no significant corruption of our appetite control system, and our
Speaker 3: bodies did what they did, which is, they allowed us
Speaker 3: to eat when we needed to eat, and they stopped
Speaker 3: us eating when we'd had enough, and no one knew
Speaker 3: how to counter calorie and never needed to.
Speaker 1: Yeah. I saw a photo the other day of I
Speaker 1: don't know if you've seen that you too, I don't know.
Speaker 1: I don't know whether it was doctored, but it looked legit.
Speaker 1: It was like a photo of a bunch of ossies
Speaker 1: on the beach in nineteen sixty three. It was like
Speaker 1: hundreds of people.
Speaker 3: Yeah, I've seen the phone.
Speaker 1: Ever, Yeah, everyone in shape.
Speaker 3: Yep, you know, not necessarily in shape.
Speaker 1: I mean, well, what I mean is there was they
Speaker 1: won't overweight, no apparent obedity, is what I'm saying.
Speaker 3: And you don't need photos to see that. There's very
Speaker 3: good statistics on it. So the reality is that our
Speaker 3: current environment and our current population, this is the first
Speaker 3: time in human history that we've had any more than
Speaker 3: about ten percent of the human population overweight or obese.
Speaker 3: But we're up around seventy percent, and that's not ringing
Speaker 3: alarm bells, people looking at that and saying, oh, well,
Speaker 3: there must be some sort of moral turpitude, there must
Speaker 3: be some sort of fault, a lack of willpower. These
Speaker 3: are obviously weak willed individuals, And that's nonsense. It were
Speaker 3: this anything other than something that you could look down
Speaker 3: upon people about, were this growing an extra arm or whatever,
Speaker 3: we'd be trying to solve it. We'd actually be looking
Speaker 3: at the real causes and we'd be sorting it out.
Speaker 3: But for some reason, when it's something that you can
Speaker 3: sneer at people about and have a judgment about, suddenly, oh,
Speaker 3: well that's just because they're weak willed.
Speaker 1: Yeah. Interesting, Wow, it's that kind of you know, the
Speaker 1: inability to feel satisfied. You know that some people like
Speaker 1: where some people eat and it's like it's never enough,
Speaker 1: not because as you said, they're weak willed or they've
Speaker 1: got some psychological issue, but because that satiety they don't
Speaker 1: experience it.
Speaker 3: No, that doesn't because they have a malfunctioning appetite control system.
Speaker 3: And you can actually make this happen, like in animal experience,
Speaker 3: you can make it happen. You can disable the part
Speaker 3: of the brain that does control the appetite and they
Speaker 3: can't stop. Anyone who's ever owned a laborador knows this.
Speaker 3: You know, they're unable to be satisfied until they finished
Speaker 3: eating your socks and all the pebbles in the garden
Speaker 3: and half your car. You know. It's it's an actual
Speaker 3: malfunction in the human brain, and you can make it happen,
Speaker 3: and we are making it happen. We know we can
Speaker 3: make it happen just by giving humans fructose, which is
Speaker 3: half of sugar, and there's forty grams of it in
Speaker 3: everyone's you know, sorry, not forty grams, forty tea spoons
Speaker 3: of it in everyone's diet today. So giving some giving
Speaker 3: everybody forty tea spoons a day of something that we
Speaker 3: know in affects appetite control, you should not be surprised,
Speaker 3: so that we would then have an appetite control problem.
Speaker 1: Forty tea spoons of sugar a day, So a tea
Speaker 1: spoon is five grams. That's two hundred grams of sugar
Speaker 1: a day.
Speaker 3: Four grams, yeah, so four sixty yeah, and people will have.
Speaker 1: One hundred and sixty grams in a month.
Speaker 3: Yeah. But people will say that sort of thing to
Speaker 3: me when I give that statistic and if I point
Speaker 3: a couple of things out, So for example, if you
Speaker 3: sat down to breakfast of a Heart foundation to prove
Speaker 3: breakfast cereal, say something like a Sultana brand and a
Speaker 3: glass of orange juice, you're at twenty tea spoons right there.
Speaker 3: That's before you go near a Mars bar or a
Speaker 3: coke or pushback on the breakfast table. Okay, So it
Speaker 3: is very easy to get there on healthy food.
Speaker 1: Okay. So and again everyone, we're not recommending, we're not.
Speaker 1: So can you give us a snapshot of somebody for
Speaker 1: somebody who's listening to this, who is resonating with what
Speaker 1: you're saying. And I haven't actually asked you your opinion
Speaker 1: of ozeenpic, but is there Do you have a pros
Speaker 1: and cons list of a zempic of people using it
Speaker 1: or are you just like no.
Speaker 3: No, it's good for what it was invented for, which
Speaker 3: is it is. When you can compare it to most
Speaker 3: of the drugs which are available for controlling type two diabetes,
Speaker 3: it is significantly more effective than most of them. But
Speaker 3: you have to go in with your eyes open and
Speaker 3: understand it's not fixing anything. It's controlling and the methodology
Speaker 3: for actually fixing type two diabetes is to change what
Speaker 3: you're eating. Yeah, So as a holding pattern, it's clearly
Speaker 3: good science. It clearly does what's advertised in the box.
Speaker 3: I'm less keen on it as a weight loss solution
Speaker 3: because it's not a solution to anything. It's a masking.
Speaker 3: It's like, and I don't know if we've talked about
Speaker 3: this another time, and if not, we can do it
Speaker 3: another time. It's exactly the same as putting teenage girls
Speaker 3: on the pill and then missing and then missing some
Speaker 3: fairly significant medical problems because you've masked so many of
Speaker 3: the symptoms.
Speaker 1: Yeah, if do you know anyone? Obviously, without mentioning names
Speaker 1: who you uses it.
Speaker 2: I have been told of people that have tried it
Speaker 2: for a short period of time. I'm not a fan.
Speaker 1: I've stopped using it.
Speaker 2: Yeah, she needs I just had to get myself down
Speaker 2: into a respectable weight category. David.
Speaker 3: Yeah, I see. Craig hasn't stopped using and he's still
Speaker 3: going yeah. Yeah, you're waste away, Craig. If you if
Speaker 3: you can't using that.
Speaker 1: Stuff, you know, well, I think I think Tiff is
Speaker 1: the labrador in this cruise so definitely if anyone, well,
Speaker 1: you definitely don't need it because you do eat a lot,
Speaker 1: but you don't you don't gain weight, do you per se?
Speaker 3: No?
Speaker 2: Not not so much like I. I just have a Yeah,
Speaker 2: I'm a I'm a feeder. I eat a lot, I
Speaker 2: ate a lot of.
Speaker 3: That could be a combination of two things. Firstly, you
Speaker 3: know lumber lumberjacks have fifty eight hundred day calorie diets
Speaker 3: right because they do may do a lot of exercise,
Speaker 3: and Tiffany may well be in that category. And she
Speaker 3: just may be genetically blessed too, where she's just really
Speaker 3: inefficient with her calories and has to eat a lot
Speaker 3: or can't maintain a reasonable body weight.
Speaker 1: Isn't it funny to think that somebody that gains weight easily,
Speaker 1: they could survive in the bush longer than you, tiff
Speaker 1: like you and me.
Speaker 2: Because I'd be so hungry that I would go away
Speaker 2: with them just through.
Speaker 1: You'd eat them. If I got up to twenty percent
Speaker 1: body fat and you got up to twenty percent body
Speaker 1: fat and we went and got lost bloody hiking, you'd
Speaker 1: die before me.
Speaker 2: I'd have to drive to go and find food.
Speaker 1: And imagine all the energy you'd expend doing it, that's true.
Speaker 3: Well after she'd eaten you, she'd then move on to
Speaker 3: finding other stuff to eat. So you know that show alone.
Speaker 3: I think the third series of it, I think starts
Speaker 3: this week on SBS. It's I think, yeah, the one,
Speaker 3: the one who wins is the one who put on
Speaker 3: the more weight before they started. Usually you know they're
Speaker 3: the one of going in carrying forty extra kilos because
Speaker 3: it seems to be mostly a starvation contest.
Speaker 1: Have you seen that show? Tip? No, No, it's brutal.
Speaker 1: It's brutal. They absolutely yeh. Always good to chat, sir.
Speaker 1: Where can people find all of your stuff? If they
Speaker 1: want to go and have a little bit of a
Speaker 1: read of your fine work.
Speaker 3: Go look for me on substack. The thing is called
Speaker 3: raisin Hell, but you could also just find me on
Speaker 3: Facebook and there's links to it there.
Speaker 1: Perfect. We'll say goodbye, fair but once again, thank you sir.
Speaker 3: See you next time, solute pleasure, See you next time.