Speaker 1: Brought to you by Toyota. Let's go places. Welcome to
Speaker 1: Forward Thinking. Hey there, and welcome up Forward Thinking, the
Speaker 1: podcast that looks at the future and says, dance with
Speaker 1: me across the sea. I'm Jonathan Strickland and I'm Joe McCormick.
Speaker 1: What is the connection there, doctor doctor, You don't know
Speaker 1: the Thompson twins. Oh my god, Oh my god. I
Speaker 1: was joking in our last episode that I'm too old
Speaker 1: and now I really am too old Thompson twinses, doctor Doctor.
Speaker 1: It's a great song and it has to do with
Speaker 1: the doctor, so medicine. And then we're talking about diabetes
Speaker 1: again in this episode, and that's why. So, guys, this
Speaker 1: is part two of our our series about the future
Speaker 1: of diabetes. In our first episode we talked about what
Speaker 1: the diseases and it's history. It's a long, long, long history,
Speaker 1: the history that dates back more than years. So we
Speaker 1: talked all about that in the last and includes drinking.
Speaker 1: We should, yes, yes, So if you if you missed
Speaker 1: that episode, you clearly want to check it out. Let
Speaker 1: me revise drinking is probably not fair tasting, like a
Speaker 1: wine taste where you're not supposed to swallow us the urine. Yes,
Speaker 1: absolutely true, because diabetes is all about glucose level management
Speaker 1: in the blood but also comes through in the urine,
Speaker 1: and UH, water tasters would be able to detect the
Speaker 1: presence of sugar in patient's urine and thus diagnose them
Speaker 1: with diabetes. Now, of course, our diagnostic and research methods
Speaker 1: have improved significantly since the dark ages with sipping urine UH,
Speaker 1: and in fact, we're learning a lot about diabetes just
Speaker 1: in recent years that really could lead to significant changes
Speaker 1: in understanding what the disease is at its core and
Speaker 1: how to treat it. Now, one thing should say before
Speaker 1: we even go any further is that that there are
Speaker 1: two major types of diabetes. There's type one and type two.
Speaker 1: And as Lauren pointed out in our last episode, type
Speaker 1: one is a type of autoimmune disorder. Type two is different,
Speaker 1: UM it is UH developed in a different way, And
Speaker 1: so some of the stuff we're going to talk about
Speaker 1: is largely focused on on type two. I mean, the
Speaker 1: treatment levels can be for both UH, but there will
Speaker 1: be some stuff on type one as well, right, and so,
Speaker 1: but but just keep that in mind that when we
Speaker 1: talk about diabetes, it's not always universal across both types. Okay, well,
Speaker 1: I thought we we should look at some studies that
Speaker 1: have come out mostly this year here in that have
Speaker 1: detailed interesting developments in diabetes research, a lot of which
Speaker 1: you might not have predicted if you just went a
Speaker 1: few years back. And here here's a really interesting one
Speaker 1: to start with. Now, I would not have expected that
Speaker 1: you would ever disc cover any link between a metabolic
Speaker 1: metabolic disorder like diabetes and air pollution. Yeah, this is
Speaker 1: a very strange correlation that has been found. That that
Speaker 1: is odd. Like, you know, air pollutions one of those
Speaker 1: things where certain conditions you could easily imagine like asthma,
Speaker 1: other you know, respiratory illnesses, um complications and things like
Speaker 1: bronchitis or possibly pneumonia. All of that I could easily
Speaker 1: even heart disease I can think of. But when you
Speaker 1: if you had told me a couple of years ago
Speaker 1: that there was a link between air pollution and diabetes,
Speaker 1: I well, I mean, I'm like, well, small gets into
Speaker 1: your pancreas and then what Yeah, I'm still confused. Specifically,
Speaker 1: what we're looking at here is not not fully diabetes,
Speaker 1: but insulin resistance. So it's a you know, a pre
Speaker 1: precursor related issue here so to diabetes type two, yes, yes,
Speaker 1: So in August, there was a study published in the
Speaker 1: journal Diabetes that looked at the link between long term
Speaker 1: exposure to air pollution and signs of insulin resistance. And
Speaker 1: insulin resistance, of course, it's a condition that often precedes
Speaker 1: type two diabetes. It's influenced by inherited and lifestyle factors
Speaker 1: as well as environmental factors, as we're about to see.
Speaker 1: So the study had a sample size of two thousand,
Speaker 1: nine hundred forty four people in southern Germany between two
Speaker 1: thousand six and two thousand eight, and these people had
Speaker 1: previously they've been participants of a project known as the
Speaker 1: Cooperative Health Research in the region Augsburg and they so
Speaker 1: the researchers looked for links in the data on these
Speaker 1: people between exposure to air pollution at their place of
Speaker 1: residence and the presence of biomarkers that give you a
Speaker 1: sign that the person is probably experiencing insulin resistance, and
Speaker 1: they found a correlation. So, they found a correlation between
Speaker 1: the level of airborne pollutant concentrations at residence sites and
Speaker 1: some biomarkers, particularly those associated with pre diabetes, more so
Speaker 1: than than full diabetes, and so from the press release,
Speaker 1: the lead author Dr Catherine Wolfe said, quote, the results
Speaker 1: revealed that people who already have an impaired glucose metabolism,
Speaker 1: so called pre diabetic individuals, are particularly vulnerable to the
Speaker 1: effects of air pollution. In these individuals, the association between
Speaker 1: increases in their blood marker levels and the increases in
Speaker 1: air pollutant concentrations is particularly significant. Thus, over the long term,
Speaker 1: especially for people with impaired glucose metabolism, air pollution is
Speaker 1: a risk factor for type two diabetes. And that's interesting.
Speaker 1: I mean, I didn't come across any information about what
Speaker 1: the what the link is? Well, and maybe, I mean,
Speaker 1: there are times where one we don't fully understand the mechanism,
Speaker 1: and sometimes it ends up just being that they are correlated,
Speaker 1: but there's not necessarily causal relationship up right. It may
Speaker 1: be that there may be some underlying link that that
Speaker 1: connects the two exactly right. There might be you go
Speaker 1: further back and you realize, oh, well, this one thing
Speaker 1: is affecting both branches. The branches themselves are independent and
Speaker 1: are not necessarily affecting one another, but are both a
Speaker 1: result of this prime source. We don't know, at least
Speaker 1: not based upon the research that we came across for
Speaker 1: this podcast, But it is an interesting thing to look
Speaker 1: at and obviously would be something that if if in fact,
Speaker 1: there is causation there, would guide us to know about
Speaker 1: or or to to look into the possibility of increase
Speaker 1: rates of diabetes in parts of the world where this
Speaker 1: type of air pollution is particularly prevalent. Or it could
Speaker 1: also lead to uh to you know, prevention measures even
Speaker 1: if you recognize this, even without necessarily understanding what the
Speaker 1: cause is yet. Uh. Let's say you develop pre diabetes.
Speaker 1: You know a doctor who if this research is validated,
Speaker 1: if it's replicated and shown multiple times, the doctor might
Speaker 1: want to say, if you want to avoid progression into
Speaker 1: full type two diabetes, you you know, depending on where
Speaker 1: you live, you might want to move right And for
Speaker 1: some people that might be a possibility. Some people, of course,
Speaker 1: that may not be an option. UM. You could also
Speaker 1: argue that this is one more reason out of the
Speaker 1: thousands that we have often listed on this show too
Speaker 1: clean that stuff up man of our carbon emissions. We've
Speaker 1: got plenty of reasons for that already, but adding another
Speaker 1: one is yet another argument to say, look like, if
Speaker 1: you add up all the even from an economic standpoint,
Speaker 1: if you just add up all the negative impact from
Speaker 1: pollution and you assigned a dollar amount, it makes financial
Speaker 1: sense to get to to make a transition, not just
Speaker 1: you know, yeah, it's gonna be hard. It's not. It's
Speaker 1: not an easy thing. It's not a convenient thing, but
Speaker 1: it ultimately is the best thing, not just for people's health,
Speaker 1: for the environment, but for the wallet and so and
Speaker 1: thus we can excuse Ferngully to capitalism, and and it
Speaker 1: will be a terrific movie that is beloved by future
Speaker 1: generations of children. Um, there was a fern gully too,
Speaker 1: wasn't there? Oh? I'm pretty sure there was. Was there? Really?
Speaker 1: I think there was? And I is there a rapping
Speaker 1: bat in it? I don't know that there's a rapping
Speaker 1: Probably not. I was about to say, Bruce Willis, where
Speaker 1: did that come from, Robert Williams. Yeah, you're turning into
Speaker 1: me Lauren where I just will take names and then
Speaker 1: if there's a name that is even remotely similar, I'm like, Nope,
Speaker 1: that's the name I wanted. You know what. There was
Speaker 1: a lot of infern gully Flora, there was oh and
Speaker 1: that's a great transition to our next one. This is
Speaker 1: actually my favorite one because gut flora is my new
Speaker 1: favorite topic. I love. I love how much the bacteria
Speaker 1: that overpopulate um or don't don't overpopulate, but but but
Speaker 1: massively overwhelmed the amount of cells of you that there
Speaker 1: are in your body have so much to do also
Speaker 1: all of your health. Gut Flora is also a great
Speaker 1: name for a future Bruce Willis movie. I'm just going
Speaker 1: to throw that out there before we get too far
Speaker 1: away from Bruce Willis. We're never too far away from
Speaker 1: Bruce Willis, but do continue well, So so let's talk
Speaker 1: about this. So what is the influence of gut flora
Speaker 1: on diabetes? Well, this one is perhaps a little more
Speaker 1: intuitive than than a possible correlation between air pollution and diabetes.
Speaker 1: So this was based on a sixteen study in the
Speaker 1: American Journal of Pathology that reported on effects of a
Speaker 1: type of gastric bypass surgery on mice with a with
Speaker 1: a model condition designed to sort of replicate the effects
Speaker 1: of type two diabetes. And it has been observed that
Speaker 1: gastric bypass surgery, so a surgery that that sort of
Speaker 1: reroutes part of the digestive process can cause remission of
Speaker 1: type two diabetes in humans and in mice. So you
Speaker 1: think that this might be because gastric bypass leads to
Speaker 1: weight loss. Right, that's probably good, and weight gain is
Speaker 1: is one of the comorbidities, what one of the co
Speaker 1: signs of diabetes. Right but right, But medical researchers conclude
Speaker 1: that the remission can't be explained by weight loss alone.
Speaker 1: There's something else going on here. And so after the surgery,
Speaker 1: subjects show improvements in both insulin sensitivity and glucose tolerance.
Speaker 1: So what's going on here And what they found in
Speaker 1: this study was there was an examination of gut micro
Speaker 1: organisms before and after the bypass surgery that showed a
Speaker 1: decrease in pathogenic bacteria and an increase in other micro
Speaker 1: organisms in the gut that are considered beneficial old for
Speaker 1: gut health. And these changes seem to coincide with improvements
Speaker 1: in metabolic and glycemic regulation. So the researchers, again, this
Speaker 1: is one of these things where they've just found an
Speaker 1: early interesting result and they're recommending more direct research into
Speaker 1: the subject. But essentially, what we need to figure out
Speaker 1: is how changes in gut micro biota influenced diabetes and
Speaker 1: metabolism in general. Mm hmm, that is really I mean,
Speaker 1: the more I learn about gut flora, the more I
Speaker 1: am pretty convinced that I'm not in charge of myself. Yeah,
Speaker 1: you're you're a you're a hybrid organism. Well, you know,
Speaker 1: I like to think of myself as an involved being.
Speaker 1: There's a book out about that that I've actually been
Speaker 1: meaning to read. I haven't read it yet, but it's
Speaker 1: by the science writer Ed Young, who I like. In
Speaker 1: the book is called I Contain Multitudes, and it's about
Speaker 1: that title. It's about microbiota. It came out either this
Speaker 1: year of the year before, and keep meaning to read it.
Speaker 1: I've heard it's very good. Wow. Cool. All right. So
Speaker 1: uh again, more understanding of that could lead to a
Speaker 1: greater understanding of how to to manage diabetes. But the
Speaker 1: picture is about to get even more complicated. So yet
Speaker 1: another study came out this year in and Diabete a
Speaker 1: logica diabeto logica, however you pronounced. That study found that
Speaker 1: people who have an abundance of healthy fat stem cells
Speaker 1: in their body were more resistant to developing diabetes, even
Speaker 1: in equally obese patients. Um, so people with obesity that
Speaker 1: have the presence of the certain adipose cells fat stem
Speaker 1: cells makes their organs more more better, more efficient at
Speaker 1: storing fat in a way that is not ultimately detrimental
Speaker 1: to the body and leading to conditions that are associated
Speaker 1: with obesity, like cardiovascular disease and diabetes. And so they
Speaker 1: the researchers concluded that understanding the molecular mechanisms that underlie
Speaker 1: this difference between obese patients with healthy fat stem cells
Speaker 1: and obese patients without them could help us develop new
Speaker 1: therapies to prevent insulin resistance in type two diabetes. But man,
Speaker 1: we're starting to get a really complicated picture of all
Speaker 1: the different influences that might work themselves out in the body.
Speaker 1: To me, this is a continuation of that story that
Speaker 1: we explored in the first episode about the history of
Speaker 1: our understanding of diabetes, which not a big surprise, but
Speaker 1: over time becomes more complex and involved. Uh. I mean, obviously,
Speaker 1: anytime you're looking at a really complicated subject, that progression
Speaker 1: is going to go in that direction. Right. We're not
Speaker 1: gonna suddenly have a huge understanding and then go backward
Speaker 1: unless we have another dark ages. But I'm just sure,
Speaker 1: but yeah, no, it's just interesting to think that, like
Speaker 1: the same way that people in the nine twenties might
Speaker 1: have been looking back at previous centuries and millennia of
Speaker 1: researchers going like, you thought it had to do with
Speaker 1: the kidneys, you idiots, But now we're like, oh, it
Speaker 1: has to do with the bacteria and stem cells. And yeah,
Speaker 1: one really more brief note to complicate it even more,
Speaker 1: there was also there was also a study this year
Speaker 1: in the journal psycho neuro into Chronology that essentially identified
Speaker 1: a pathway from psychological state two diabetes, and the pathway
Speaker 1: was from a type of executive function known as low inhibition.
Speaker 1: Essentially that is correlated with the state that's known as
Speaker 1: anxious arousal emotional anxiety, and then correlated to inflammation, which
Speaker 1: is then correlated to diabetes, which is that actually also
Speaker 1: correlated to gut bacteria, the so so all of these
Speaker 1: things so so anyway, but this becomes a self fulfilling
Speaker 1: prophecy because knowing this is making me anxious, which is
Speaker 1: therefore eat a yogurt you'll be fine. So yeah, this
Speaker 1: is even possible. I mean, this is one of these
Speaker 1: things that's making me think that there have got to
Speaker 1: be a lot of false trails here. I mean, I'm
Speaker 1: sure all these different areas of research or turning up
Speaker 1: some things that are going to turn out to not
Speaker 1: really be primary causes. Right. They may be may be
Speaker 1: a factor that influences but perhaps not is is you know,
Speaker 1: definitive in causing, or or it could be an indicator
Speaker 1: that this other thing is happening and not not a
Speaker 1: cause of right. Right, But anyway, I mean, I feel like, nevertheless,
Speaker 1: our picture of the cause and effect relationship with whole
Speaker 1: body state versus metabolic regulation is getting very complicated. Yeah,
Speaker 1: seems likely based upon the last few stories you've shared
Speaker 1: with us, Joe. But then, of course there is another one.
Speaker 1: This one has more to do with type one diabetes. Okay,
Speaker 1: this is uh. There was a study that came out
Speaker 1: in called hotspot Autoimmune T cell receptor binding underlies pathogen
Speaker 1: and insulin peptide cross reactivity explicable. Let's let's let's break
Speaker 1: that one down just a little bit. This was in
Speaker 1: the Journal of Clinical Investigation. All these have been sixteen studies.
Speaker 1: This one is um Uh. It found something pretty interesting
Speaker 1: the presence of pathogens germs maybe the cause or a
Speaker 1: cause of type one diabetes. So how how would you
Speaker 1: figure that? Well, here's how it goes. There are these
Speaker 1: insulin producing cells that we talked about in the previous episode,
Speaker 1: known as pancreatic beta cells, and in type one diabetes,
Speaker 1: immune system cells known as T cells. White blood cells
Speaker 1: attack these beta cells and destroy the body's ability to
Speaker 1: produce insulin. But what causes the autoimmune response? Like, why
Speaker 1: do the T cells attack the beta cell? They didn't
Speaker 1: like the cut of their jib because they're dumb as
Speaker 1: a bag of hammers. They are pretty dumb. They don't
Speaker 1: even have brains. You wouldn't believe it. I well, as
Speaker 1: someone who suffers massive all allergic reactions, I am not
Speaker 1: a big fan of the way my my body's immune
Speaker 1: system will misidentify certain allergens and then go into yeah,
Speaker 1: you know exactly then, Jonathan, how how strange, how poorly
Speaker 1: understood states within the body at the cell level of
Speaker 1: cell function um can cause complex systemic reactions that are
Speaker 1: not necessarily what your body intended intended in quotes, you know,
Speaker 1: as we said, the cells don't have brains, but they
Speaker 1: do have a sort of programmatic function. They're supposed to
Speaker 1: be attacking pathogens to keep them out. But the study
Speaker 1: here found that these T cells were cross reactive in
Speaker 1: a particular way, and that means they react to a
Speaker 1: complex set of conditions that determine their behavior. And these conditions,
Speaker 1: the study found, could be brought on by the presence
Speaker 1: of particular pathogens. Uh. A quote from the study abstract
Speaker 1: is T cell cross reactivity with pathogen derived antigens might
Speaker 1: break self tolerance, which that that's a great term self tolerance.
Speaker 1: I assume that means the immune system not attacking your body.
Speaker 1: I've got very low self tolerance. But that's something else, yeah, yeah,
Speaker 1: in the end to induce autoimmune disease. So it demonstrates
Speaker 1: the value in looking at the various ways external influences
Speaker 1: such as germs and other pressures might alter T cell
Speaker 1: function to cause autoimmunity. Autoimmunity being not a good thing
Speaker 1: when the immune system attacks you, and that would include
Speaker 1: type one diabetes. So there can be certain there can
Speaker 1: probably be certain germs present in your body in certain
Speaker 1: ways that can trigger this chain reaction of autoimmune response
Speaker 1: against your betas holes. So that's heavy stuff you've laid
Speaker 1: down on us. Joe, it's really fascinating learning more about
Speaker 1: this disease that we keep thinking we've got, like or
Speaker 1: at least the indication I always felt this was that
Speaker 1: we had a pretty good handle on it, but it
Speaker 1: turns out that it's far more complicated than I had anticipated. Well,
Speaker 1: I think we do understand a lot of the basics.
Speaker 1: Sure well, sure, yeah, but it's just that our pictures
Speaker 1: becoming and you know, the broader picture is becoming more
Speaker 1: and more complicated, right, right, But we also have a
Speaker 1: lot of research into the practical means of how we
Speaker 1: could uh improve the treatment for diabetes. And I've got
Speaker 1: one more little bit of of research that I found
Speaker 1: that that that could potentially help lead to better understanding
Speaker 1: and better therapies in the future. Um. There was a
Speaker 1: recent study that was published in the Journal of Clinical
Speaker 1: Investigation that looked into those early stages of type two
Speaker 1: diabetes that you were talking about a minute ago, UM
Speaker 1: that that that insulin resistance. UM. The authors of this
Speaker 1: study were investigating whether there's a link between the processes
Speaker 1: processes that lead to accumulated fat in muscle tissue, which
Speaker 1: again obesity being a common alongside to insulin resistance. Um
Speaker 1: the others of this one. We're looking specifically at UM
Speaker 1: whether there's a link between accumulated accumulated fat and muscle
Speaker 1: tissue that that that obesity kind of issue that we
Speaker 1: were talking about earlier, and the decreased glucose uptake that
Speaker 1: is one of those early indicators of insulin resistance and
Speaker 1: therefore of type two diabetes. And there is UM. There's
Speaker 1: this protein that's called mondo A that is a link
Speaker 1: between accumulated fat and muscle tissue and decreased glucose uptake UM.
Speaker 1: And this protein, the single protein appears to regulate genes
Speaker 1: that control both fat synthesis and insulin signals. They think
Speaker 1: that this protein might be what's telling your cells to
Speaker 1: stop taking in glucose and instead convert it into fact um.
Speaker 1: But they think that when the protein is activated too often,
Speaker 1: when there's just so much glucose in your blood, that
Speaker 1: that that this protein is being triggered constantly, it could
Speaker 1: make your cells permanently resistant to insulin instead of just
Speaker 1: temporarily resistant to glucose UM. So, you know, but potentially
Speaker 1: in the future, this this could lead to treatments that
Speaker 1: could target and inhibit mondo A. Maybe hopefully, um. I mean,
Speaker 1: the researchers think that it could even help people manage
Speaker 1: their overall metabolism and body weight by managing the function
Speaker 1: of the single protein. That's cool. And so it's important
Speaker 1: to also uh reiterate that a lot of these areas
Speaker 1: of research may ultimately not uh not result in a
Speaker 1: useful treatment, but there's a lot of potential out there,
Speaker 1: and there's so many different avenues of exploration that there's
Speaker 1: a lot of hope that we can find much more
Speaker 1: effective ways of either preventing type two diabetes from forming,
Speaker 1: or even type one in the case of the possibility
Speaker 1: that germs play an important role in the development of
Speaker 1: that type of diabetes, or the management making management more
Speaker 1: less of a pain, both literally and figuratively. Uh. And
Speaker 1: to that end, there's a lot of different approaches that
Speaker 1: people have been looking into on one aspect of diabetes management,
Speaker 1: and that is monitoring your glucose levels in the first place,
Speaker 1: because we mentioned like the original tests were all about
Speaker 1: testing the sugar levels and urine, which are not necessarily
Speaker 1: as precise as you would want as reading of your
Speaker 1: blood glucose levels. That's more of a relevant measurement. But
Speaker 1: blood glucose. The way you measure that typically is that
Speaker 1: you have to prick a finger or some other part
Speaker 1: of your body and uh get a blood sample and
Speaker 1: then use a device to analyze it. So it's invasive
Speaker 1: by definition, right, you have to get at the blood.
Speaker 1: So there's been a lot of look into the possibility
Speaker 1: of developing non invasive means of measuring blood glue close levels,
Speaker 1: which would remove at least one of those barriers. And
Speaker 1: one of those frustrations that people UM encounter when it
Speaker 1: comes to diabetes, could you do a breath a wizer,
Speaker 1: one would hope, And that was not one of the
Speaker 1: ones that I read about. There was a paper published
Speaker 1: in the National Institutes of Health back in two thousand
Speaker 1: twelve that was sort of a review of various processes
Speaker 1: that had been UM experimented with. In some cases even
Speaker 1: products were brought to market, but ultimately uh spoiler alert
Speaker 1: did not perform very well, and uh they wanted to.
Speaker 1: It was specifically looking at these noninvasive appre which is like,
Speaker 1: are there any that are on a level that is promising,
Speaker 1: if not as good as monitoring glucose levels through actually
Speaker 1: analyzing blood directly. So here's some of the ones that
Speaker 1: they looked at, they looked at UH bio impedence spectroscopy.
Speaker 1: So this is measuring the resistance to electric current flowing
Speaker 1: through tissue impedence UM. So this is not that different
Speaker 1: from things that use like capacitis touch screens, that kind
Speaker 1: of stuff. I mean, our bodies we've talked about many times. UH,
Speaker 1: we conduct electricity. We also have stuff in us that
Speaker 1: impedes the conductance of electricity, and that changes depending on
Speaker 1: our body chemistry. So the key here is that there
Speaker 1: are variations in glucose concentrations that change the number of
Speaker 1: sodium id ions and potassium ion concentrations in our blood.
Speaker 1: So typically sodium ion concentration goes down, potassium ion concentration
Speaker 1: goes up. This changes our resistance to electricity. UM. So
Speaker 1: if you were able to measure that in a meaningful way,
Speaker 1: you would be able to make some UH, you would
Speaker 1: be able to to figure out what the gluecoast levels
Speaker 1: of blood were. However, all of these different approaches I'm
Speaker 1: going to talk about have different drawbacks. The one for
Speaker 1: this one is that it's not as reliable as other
Speaker 1: methods of checking blood glucost levels, and at the time
Speaker 1: the paper was written in two thousand twelve. It also
Speaker 1: required the diabetic person to rest for sixty minutes before
Speaker 1: taking any measurements. So yeah, you have to be at
Speaker 1: rest for an hour before you could take a measurement. Obviously,
Speaker 1: that's not practical for a lot of people, particularly people
Speaker 1: who are suffering type two diabetes. And it maybe it's
Speaker 1: not a very severe case, but it's enough for them
Speaker 1: to have to monitor their glucose levels. Uh, they might
Speaker 1: have a fairly active lifestyle, which is part of the
Speaker 1: way to help treat or manage diabetes. Um. So yeah,
Speaker 1: that is a little bit. That's it's not ideal, right,
Speaker 1: so are other ones to electromagnetic sensing similar It's also
Speaker 1: reliant upon the dielectric properties of tissue, but in this
Speaker 1: case you're talking about electromagnetic frequencies, not passing an electric
Speaker 1: current through tissue. They use two different inductors to sense
Speaker 1: any variation of dielectric parameters of the body and glucose
Speaker 1: levels would affect those parameters. Also, this approach has drawbacks. Uh,
Speaker 1: it's very sensitive to temperature for one thing, so there
Speaker 1: are optimal frequencies you would want to use based upon
Speaker 1: the temperature and that means that if you haven't set
Speaker 1: your inductors properly, then you're gonna get erroneous readings. And
Speaker 1: since those depend upon temperature and it's very sensitive, that
Speaker 1: is a level of ambiguity that is problematic when it
Speaker 1: comes especially when it comes to something that you would
Speaker 1: want in a home uh kit, write something that a
Speaker 1: diabetic person could use on their own without having to
Speaker 1: go to a professional to have this. I mean, if
Speaker 1: you if you're gonna have to go to a professional,
Speaker 1: I think most people just a like I hate having
Speaker 1: to prick my finger, but it's better than having to
Speaker 1: go multiple times a day to somebody else. Um, then
Speaker 1: you have reverse ion toe fesis. I was about to say,
Speaker 1: do you have anything in the in the electrical end
Speaker 1: that's more difficult to pronounce? I to foresis is probably
Speaker 1: up there, and I'm certain I am mispronouncing it. Uh.
Speaker 1: That's a fancy way of saying. You measure the flow
Speaker 1: of low electrical current between an anode and a cathode
Speaker 1: that would both be placed on a on the skin's surface.
Speaker 1: Now this one, I'm gonna be straight up with you, guys.
Speaker 1: I do not fully understand the mechanism here because I
Speaker 1: read the I read the whole paper, and I read
Speaker 1: the section, and even after I read it three times,
Speaker 1: I was like, I'm still not sure what's going on here.
Speaker 1: But the way they described it was that you would
Speaker 1: put the electrodes on the skin and it would rely
Speaker 1: on quote a physiologically relevant fluid sample end quote. Don't
Speaker 1: know what that means. Physiologically relevant would obviously means something
Speaker 1: that would also have glucose in it and would be
Speaker 1: relevant to the blood glucose levels. But since it's not invasive,
Speaker 1: it's not the blood itself, because you're not putting the
Speaker 1: electrodes in you, You're just putting them on the skin surface.
Speaker 1: Do you have to cry to use this? You do?
Speaker 1: For another one? You do for another one. You get
Speaker 1: in ahead of me because that's next. Um. But the
Speaker 1: product there wasn't Probably that was actually brought to market
Speaker 1: using this particular approach, but it was discontinued after numerous
Speaker 1: issues became apparent, largely that well, one thing, the electrodes
Speaker 1: would tend to irritate the skin, and also you had
Speaker 1: to have them in place for an hour before you
Speaker 1: could take a reading similar to the previous one. I
Speaker 1: talked about. So not only do they irritate the skin,
Speaker 1: you had to wear them for a long time before
Speaker 1: you could even get your blood glucose level reading. Also,
Speaker 1: sweating would throw off the accuracy of the measurements. So, uh,
Speaker 1: if you started sweating during that hour while you're waiting
Speaker 1: to get your blood glucose level measurement, you would throw
Speaker 1: things off. So not ideal. But now we're getting into
Speaker 1: tears and crying. Yeah, fluorescence technology. Fluorescence is exactly what
Speaker 1: you think it is. It's using an enzyme of some
Speaker 1: sort that would cause, uh, in this case, your tears
Speaker 1: to fluoresce when exposed to a particular type of light,
Speaker 1: and you measure that fluorescence, and uh, the level of
Speaker 1: fluorescence and the type of fluorescence would depend upon the
Speaker 1: levels of glucose found in your tears, which according to
Speaker 1: a study, uh that this particular paper cited. I am sorry,
Speaker 1: I didn't write down the name of the other paper,
Speaker 1: but they cited a study that suggested that glucose levels
Speaker 1: and the tears correlate with glucose levels in the blood. Um.
Speaker 1: Not exactly like on a you know, it's not saying
Speaker 1: that the level that you find in your tears is
Speaker 1: the same as in your blood. But yes, and that
Speaker 1: if you know one, you can you can uh, exactly,
Speaker 1: thank you. How many times a day do you have
Speaker 1: to watch the end of Homeward Bound? Uh? Well, the
Speaker 1: pends you can. You can change it up, right, like
Speaker 1: you can watch Brian's game, or you can rouge. Yeah.
Speaker 1: I cry whenever anyone suggest turning on Mulan Rouge. Um.
Speaker 1: Not not the actual movie, just the thought of having
Speaker 1: to watch it again. Okay, look I'm not saying it
Speaker 1: is no fern Gully to the Magical Rescue? Is that
Speaker 1: the actual name of fair Gully too? It is. I
Speaker 1: looked it up while you guys were talking. Um. So,
Speaker 1: so this this method would involve using this enzyme in
Speaker 1: your tears and then analyzing the tears to find the
Speaker 1: blood glucose level. So it's not invasive. However, the enzymes
Speaker 1: have a short lifespan, and there's some questions about biocompatibility,
Speaker 1: which is obviously something you want any kind of medical process.
Speaker 1: You don't want to find out it's non compatible with
Speaker 1: your biology. Yeah, that's what we call bad. Yeah, toxic
Speaker 1: is probably one of those things you want to stay
Speaker 1: far away from, right so then you had infrared spectroscopy.
Speaker 1: Both mid infrared and near infrared uses of this technology.
Speaker 1: Obviously they're using different frequencies on the infrared spectrum. UH.
Speaker 1: This would involve measuring absorption rates, really the reflective rates, UH,
Speaker 1: the the amount of light that comes back after you
Speaker 1: would expose an area where you're you know it's tissue
Speaker 1: area to get an idea of blood glucose levels. Right,
Speaker 1: and this is this is a method that they're using
Speaker 1: to to certainly take pulses, not invasively and mechanically right
Speaker 1: and so electronically. Rather you're looking at reflection because uh,
Speaker 1: infrared does not penetrate very far into tissue, so you're
Speaker 1: not gonna like shine and infrared light through It's not
Speaker 1: like an X ray, it's not going through your body.
Speaker 1: So you're looking at the reflective reflection of those um,
Speaker 1: those infrared rays, those that infrared light, and then you're
Speaker 1: being able to to extrapolate from that what the glucose
Speaker 1: levels and the blood are. But these also have issues. UM.
Speaker 1: For one thing, there are other elements that can affect
Speaker 1: the absorption of the infrared rays, like water content in
Speaker 1: your blood, so you might get a false reading because
Speaker 1: of the water content, not the glucose levels in your bloodstream. Obviously,
Speaker 1: if you're looking at medicating, that is a problem if
Speaker 1: you're going on a false reading. Also, with near infrared spectroscopy,
Speaker 1: you have to exert a great deal of scanning pressure.
Speaker 1: In other words, you have to really dig in there. Yeah,
Speaker 1: you can't just you can't just lay the device against
Speaker 1: your skin in that case, there's other methods ultrasonic approaches.
Speaker 1: In the report that I was reading, the researcher actually
Speaker 1: noted that very little research had gone into using ultrasound itself,
Speaker 1: but a variation on ultrasound called photoacoustic spectroscopy had been
Speaker 1: experimented with, and it's kind of a funky approach. So
Speaker 1: here's here's how it works. And when I read this,
Speaker 1: I was like, wow, now we're getting into some who
Speaker 1: thought of this. At what point did someone say, hey,
Speaker 1: I got an idea again. So you use a laser
Speaker 1: to excite fluid within tissue. So you're using the laser
Speaker 1: to essentially heat stuff up essentially, and then you listen
Speaker 1: to that tissue. You actually listen to the excitement of
Speaker 1: the tissue. Yeah, you you put a microphone up to
Speaker 1: that tissue and you're like, go crazy, guys. And then
Speaker 1: you analyze the sound that comes from the tissue from
Speaker 1: thermal expansion and you measure, you analyze it, measuring it
Speaker 1: peak to peak, and this will give you enough information
Speaker 1: to figure out the blood glucose levels tissue. I think
Speaker 1: they were watching the scene and Ghostbusters too with the
Speaker 1: Pink Goo where they play the music for it and
Speaker 1: it starts dancing when you play your love is Yeah,
Speaker 1: it's lifted to hire. Yeah. Uh so, yeah, it's um maybe.
Speaker 1: But apparently they can analyze the peak to peak value
Speaker 1: of the acoustic signal and determine the glucose levels from that.
Speaker 1: But like the other methods I've mentioned, this one also
Speaker 1: has limitations. Changes in temperature and pressure in particular or
Speaker 1: cause problems with precision and accuracy using this methodology, as
Speaker 1: well as proximity to Vigo the Carpathian Yes, yeah, and
Speaker 1: those giant portraits. Uh so. They also looked at a
Speaker 1: lot of other different scanning technologies, similar to some of
Speaker 1: the spectroscopy I had mentioned already. I didn't want to
Speaker 1: go into all of them, but they across the board.
Speaker 1: The conclusion was that the demand for non invasive glucose
Speaker 1: monitoring is very high for multiple reasons, right as a
Speaker 1: quality of life issue, as a means to to remove
Speaker 1: that barrier from people who are afraid of getting UH
Speaker 1: diagnosed because they don't want to deal with that reality.
Speaker 1: And some people are very UH do have phobios of
Speaker 1: of of skin pricks and absolutely so being able to
Speaker 1: remove that, there's obviously a demand for it. However, according
Speaker 1: to the research, there's we're just not there yet. None
Speaker 1: of these technologies had reached a level of maturity where
Speaker 1: it could be as dependable as the accepted methodology. So
Speaker 1: without that, it's you can't really recommend people switch over. Sure,
Speaker 1: speaking of technology that isn't quite there yet, Um, yeah,
Speaker 1: there's one in development. Yeah, yeah, I found I found
Speaker 1: I found a food sensor. Yeah, I looked into this,
Speaker 1: So you're you found a company called tell Spec T
Speaker 1: E L L S P e C. And it's a
Speaker 1: sensor that you used to and to find out what
Speaker 1: ingredients are in the food at a molecular level. You
Speaker 1: like pointed at a food and it tells you the
Speaker 1: entire nutritional content. I think we've actually talked about this
Speaker 1: device on the podcast before. We may have. I think
Speaker 1: we have. It sounds really familiar, well, and there are
Speaker 1: forgotten way more than I've said. There's some related topics
Speaker 1: as well, Like there was a Kickstarter campaign for a
Speaker 1: type of mug that was supposed to give you a
Speaker 1: readoubt of the specific stuff that was in the mug
Speaker 1: um and then ultimately I think what the Kickstarter campaign
Speaker 1: delivered was just a mug like like like they downgraded
Speaker 1: their their promise from this will tell you the ingredients
Speaker 1: of the stuff that's in here in this too. This
Speaker 1: will hold liquid um, a fluid will take the shape
Speaker 1: of the mug itself, just like any other container. Uh
Speaker 1: But the idea was I just thought of a great idea.
Speaker 1: You could sell something that will guarantee that whatever liquid
Speaker 1: you put in it has a ten percent increase in
Speaker 1: lead content. Not not something I'm gonna market anytime soon, Joe,
Speaker 1: But I appreciate your MOXI. Uh so. So tell Spec
Speaker 1: is working on a product that, as far as I
Speaker 1: can tell, is not yet at UM brought to market.
Speaker 1: It's still in the prototyping stage where it will use
Speaker 1: near infrared spectroscopy and bioinformatics to measure the ingredients of
Speaker 1: food on a molecular level. And uh, what you would
Speaker 1: do is you'd use the small device. It would pair
Speaker 1: with a small art phone. You scan the food you
Speaker 1: want to eat with the device. The device would send
Speaker 1: the data collects up to the cloud for analysis. That
Speaker 1: analysis would then be beamed down to your smartphone and
Speaker 1: an easy to read format on an app. And then
Speaker 1: you would be able to see what what what is
Speaker 1: made up of the food you're about to eat. And
Speaker 1: this could help diabetics plan out their insulin dosage is right,
Speaker 1: Like if they realize, oh, there are a lot of
Speaker 1: carbohydrates in this that I didn't anticipate when I ordered it,
Speaker 1: that would impact how they would, uh manage their insulin
Speaker 1: throughout the day. So it could allow people who have
Speaker 1: diabetes a better understanding of what they are eating and
Speaker 1: thus be able to manage their treatment on a more
Speaker 1: granular level. Yeah, and this this is a very common
Speaker 1: I mean, I'm sure that that most human people at
Speaker 1: this point in in the universe have an experience of
Speaker 1: like looking at a food label, trying to decide whether
Speaker 1: the food that you're about to eat is terrible or okay,
Speaker 1: and having no idea right in some cases, you're like, Okay,
Speaker 1: I got it. If I'm going to eat a deep
Speaker 1: fried onion, that's bad. That's obviously not the best. But
Speaker 1: I think it's the most not the best, at least
Speaker 1: a few years ago. I think it was something like
Speaker 1: what if it's awesome? Well, so many jokes, but I'm
Speaker 1: gonna avoid I don't let me just say that. I
Speaker 1: think I read something where it was like the highest
Speaker 1: caloric intake of any regular menu. I don't. Well, first
Speaker 1: of all, if you're eating an entire awesome blossom, I'm
Speaker 1: not sure. I'm not, but I watch your entire blooming onion.
Speaker 1: I will put that away. But they're okay, do not
Speaker 1: tell me they are the same thing. You will have words, Okay,
Speaker 1: I really don't know. The breading okay. Also the just
Speaker 1: the way they cut the onion, it's different. I didn't
Speaker 1: know you had a real opinion. I thought you were playing.
Speaker 1: I haven't add one in many, many years because I
Speaker 1: realized how bad they were for me. But there are
Speaker 1: the craving is always there, like a vampire. I always
Speaker 1: craved the bluemen onion. Yeah, I I just lived my
Speaker 1: life denying myself that. But but point point being yes,
Speaker 1: UH nutrition is difficult, and making anything that you can
Speaker 1: do to make this kind of thing easier for people
Speaker 1: good news. Yeah. I think if they're really worry a
Speaker 1: device that gave you really solid, complex nutritional information with
Speaker 1: this sort of non invasive scan of your food, that
Speaker 1: would be cool. I'm I don't know, I'm kind of
Speaker 1: skeptical of this device. Yeah, And we've seen we've seen,
Speaker 1: um the approach from the providers side, like from the
Speaker 1: actual like the food vendor side. We've seen that change
Speaker 1: over time, right, more and more places require UH restaurants
Speaker 1: to include nutritional information about their menu items. It's not
Speaker 1: that yeah, yeah, I would love to see a broader
Speaker 1: adoption of that policy across all regions. It's not like
Speaker 1: it's everywhere, but you might notice that if you go
Speaker 1: to certain restaurants, like a fast even fast food restaurants,
Speaker 1: you can look up and get at least some basic
Speaker 1: idea of the nutritional value of food. And often it's
Speaker 1: not very you know, it doesn't go very deep. But
Speaker 1: then if you go to the website you might get
Speaker 1: more information. This gets a little more complicated when you're
Speaker 1: talking about like a mom and pop place, not not
Speaker 1: a chain you know. Then you're like, well, this is
Speaker 1: that's when a little handheld device would really come in handy,
Speaker 1: because chances are you don't have like a website that
Speaker 1: gives you deep nutritional information about all those different dishes
Speaker 1: or make um easy to use mass spectrometers available to
Speaker 1: everyone and as profitable as it is to mark up
Speaker 1: drugs in the market. Yeah, yeah, well let's talk about
Speaker 1: something else. It's a totally different So you have to
Speaker 1: atomize your food before you eat it, you know, just
Speaker 1: you know the mom and pop shop. You know, it
Speaker 1: gets gets there, they're they're kick back, atomizes a plate
Speaker 1: of that and then you know the past the nutritional
Speaker 1: data savings onto you. Yeah, definitely, Well how about alt
Speaker 1: we switched gears for a second. I want to talk
Speaker 1: about cell transplants. This was another another piece that was
Speaker 1: that we we had in our notes and then I
Speaker 1: started research again. It's it's really fascinating and there there
Speaker 1: have been several cell transplant procedures and in different ways,
Speaker 1: and I'm going to go through some of them, but
Speaker 1: the one I really wanted to talk about was one
Speaker 1: that happened last year the Diabetes Research Institute at the
Speaker 1: University of Miami Health System developed a transplant procedure in
Speaker 1: which they took insulin producing islet cells, or those beta cells,
Speaker 1: and they implanted them into a layer of fat in
Speaker 1: a recipient's abdomen uh, and they submit them into place
Speaker 1: using a sticky gel like substance so that that holds
Speaker 1: them so that they are able to um to to
Speaker 1: to produce insulin and move it into the bloodstream where
Speaker 1: it's needed. I think actually did use ghack, wasn't it ghack?
Speaker 1: It was not. Oh, I just remember the smell of
Speaker 1: that stuff. You guys are you guys are killing me
Speaker 1: here with your young references. I know what gag is,
Speaker 1: but that's after my time. It smells like petroleum in
Speaker 1: my head. Now. Well. They they performed this procedure on
Speaker 1: a diabetic patient named Windy Peacock who uh said that
Speaker 1: within a month, actually the doctor said that within a month, Uh,
Speaker 1: those cells were producing insulin the way a healthy pancreas went,
Speaker 1: and they were responding to glucose levels. Naturally, they would
Speaker 1: produce more insulin if the glucose levels increased, and produced
Speaker 1: less when they went down. She was still taking doses
Speaker 1: of insulin as a supplement in order really in order
Speaker 1: to not put too hard a strain on these cells
Speaker 1: immediately out of the gate, right to have kind of
Speaker 1: an onboarding process where the cells could get up to speed. Uh.
Speaker 1: And it seemed to be working. Uh. There had been
Speaker 1: other cell transplant procedures before this, most of them involved
Speaker 1: transplanting islet cells onto the liver. Now this works, but
Speaker 1: it also was somewhat limited uh and and slightly less
Speaker 1: successful than this other approach, which was less invasive as well,
Speaker 1: uh than the liver surgery. But the long term effects
Speaker 1: are still being studied. So with the liveral approach, typically
Speaker 1: you see a five year lifespan for those cells and
Speaker 1: then you would need another procedure after that. Uh. They
Speaker 1: tend to produce insulin properly for about five years before
Speaker 1: they die off. They don't know as much about the
Speaker 1: experimental process where they did it in the layer of
Speaker 1: fat on the abdomen because it was only last year
Speaker 1: when the procedure was done, So we don't know if
Speaker 1: the cells will last longer or if they won't last
Speaker 1: as long. Uh. That remains to be seen. So that's
Speaker 1: part that's part of the ongoing study. AH. But there
Speaker 1: is a massive trade off to the cell trans approach.
Speaker 1: It's not something that is automatically a cure that is
Speaker 1: going to make people feel better for the rest of
Speaker 1: their lives. UH. That massive trade off is that you
Speaker 1: have to take um immune suppressing medications for the rest
Speaker 1: of your life because because you are taking some something
Speaker 1: else that sells into your body. Yeah, yeah, you've got
Speaker 1: you've got essentially foreign cells. And if you want to
Speaker 1: make sure that your body does not identify those cells
Speaker 1: as hostile and thus go into attack mode. Similar to
Speaker 1: what we talked about with the type one diabetes, you
Speaker 1: have to take immune suppressing medications, and that of course
Speaker 1: has its own suite of risks. Obviously, you have a
Speaker 1: higher risk of infection, particularly UH the month or so
Speaker 1: after you've undergone a surgical procedure. UH. For this reason,
Speaker 1: the procedures for cell transplants are typically reserved just for
Speaker 1: people with type one diabetes and and those who have
Speaker 1: severe hypoglycemia that low blood sugar. UH. If they have
Speaker 1: episodes that are really severe and come with little to
Speaker 1: no warning, then they are candidates for this kind of
Speaker 1: cell transplant surgery because the trade off of having to
Speaker 1: go on immune suppressing drugs for the rest of your life.
Speaker 1: Is still better than having to deal with type one
Speaker 1: diabetes where you're constantly having to to administer insulin in
Speaker 1: some form, either you're doing shots or you've got an
Speaker 1: insulin and that even on your very best days when
Speaker 1: you're keeping up with it, you still you still have
Speaker 1: a pretty high risk for form going into seizure comma. Yeah, yeah, exactly,
Speaker 1: not the good times. But there's some research that I
Speaker 1: was looking into that might might help mitigate this autoimmune
Speaker 1: response to transplant itself. Um because like like kind of
Speaker 1: in this case, all you have to do is figure
Speaker 1: out a way to protect the cells. All that's all
Speaker 1: you have to do is simple. Um, So enter some
Speaker 1: fun materials science. Um. There was a team headed up
Speaker 1: by researchers out of m I T and the Boston
Speaker 1: Children's Hospital, and they were working with materials that have
Speaker 1: been derived from brown algae. Uh. These alginate, yes, alginate
Speaker 1: gels can encapsulate the beta cells and you know, protect
Speaker 1: them while still allowing materials some molecules like like sugar
Speaker 1: and proteins to to go in and out, so allowing
Speaker 1: the cells to remain living. If you encapsulate cells so
Speaker 1: that they're perfectly safe. But they all die, then you're
Speaker 1: not really doing much good. Um. So, so when you
Speaker 1: implant cells that are encapsulated with these alginate gels in
Speaker 1: primates and humans, they tend to cause scar tissue to develop, however,
Speaker 1: which is bad news. You know. It indicates that another,
Speaker 1: although slightly less troublesome, immune response is happening. So so
Speaker 1: they created like eight hundred chemical derivatives of these alginate
Speaker 1: gels um each with like we little molecular changes to
Speaker 1: see if they could get one of them to just
Speaker 1: slip under the immune systems, right, and uh, and they
Speaker 1: did so far it works in mice um and there
Speaker 1: that their next step is planning a non human primate trials.
Speaker 1: So it's moving along and uh, you know it might
Speaker 1: be it might be a while before they get it right,
Speaker 1: but it could give it could give this this transplant
Speaker 1: of cells concept of a new breath of life. Yeah,
Speaker 1: that'd be great to see a reduction in that necessity. Right,
Speaker 1: and also too because if that happens, if in fact
Speaker 1: you can reduce the risk of essentially the body's rejection
Speaker 1: of those cells, you open up the potential of applying
Speaker 1: that strategy to a broader range of diabetic patients. First,
Speaker 1: you would assume that you would apply it to more
Speaker 1: type ones, but who have less or fewer hypoglycemic episodes
Speaker 1: or or they tend to come with enough of a
Speaker 1: warning so that you can you can preemptively avoid it. Uh.
Speaker 1: And then possibly, if it's an effective enough treatment, you
Speaker 1: could start discussing the idea of looking at type two.
Speaker 1: I think that would be far less likely. Yeah, yeah,
Speaker 1: you'd have to you have to figure out whether or
Speaker 1: not the you know, what type of therapies are more
Speaker 1: effective for for type two diabetes, and whether it really
Speaker 1: whether you could just start replacing those insulin creating cells
Speaker 1: in the pancreas, or whether it would be more effective
Speaker 1: to to look at the sugar the glucose re uptake
Speaker 1: right right, because remember with type two you are still
Speaker 1: producing insulin, you're just not doing it necessarily as well.
Speaker 1: And yeah, so it's it's a different different beasts than
Speaker 1: type one. So one other interesting study that came out
Speaker 1: this year that I thought was worth looking at was
Speaker 1: about a new research approach for the understanding the function
Speaker 1: of beta cells, which could actually lead to the creation
Speaker 1: of regenerative medicine therapies for diabetes. So of course regenerative medicine,
Speaker 1: what is that that that's dealing with the cell level,
Speaker 1: being able to re engineer, regrow, or replace cells that
Speaker 1: that are having problems within the body. They're dysfunctional or
Speaker 1: they've been damaged or destroyed. And so what did this
Speaker 1: study in Nature find, Well, they identified a protein known
Speaker 1: as f l t P or flat top, that's really
Speaker 1: what they called it, flat top, and it's a marker
Speaker 1: that helps divide pancreatic beta cells into groups. So you've
Speaker 1: got these two different types of beta cells. One group
Speaker 1: does the work there the workhorses of the beta cell brigade.
Speaker 1: They regulate glucose metabolism, and the other group is marked
Speaker 1: as immature cells that undergo accelerated cell division, meaning they
Speaker 1: multiply more frequently. And how can you tell the difference. Well,
Speaker 1: when the protein flat top is present, the cells assumed
Speaker 1: their mature cell function, meaning that that is the mark
Speaker 1: the mark of a mature beta cell that's doing the
Speaker 1: jaw but that it's meant to do regulating glucose in
Speaker 1: the surroundings and releasing insulin. But beta cells without flat
Speaker 1: top that they're the breeding cells the rabbit cells. Basically
Speaker 1: they proliferated four times as much as cells without flat
Speaker 1: top and UH. And the question one of the questions
Speaker 1: the researchers were wondering about, as well, can we be
Speaker 1: sure that these rapidly proliferating cells in the pancreas or
Speaker 1: pancreatic cells eventually do turn into mature beta cells that
Speaker 1: are going to be doing the work that that a
Speaker 1: diabetic would need done, you know, releasing, or that anyone
Speaker 1: would need done, especially that you have lost function of
Speaker 1: if you have diabetes. And the researchers found yes, they
Speaker 1: use this technique that's known as lineage tracing, so they
Speaker 1: made all the cells go on too ancestry dot com. No,
Speaker 1: they use color coded genes. That these genes have different
Speaker 1: color signals that activate when a gene is being expressed,
Speaker 1: and you can use that to trace the life cycle
Speaker 1: of an individual cell. And all this means that hopefully
Speaker 1: through research based on these new findings about the division
Speaker 1: of cells of pancreatic beta cells, we might be able
Speaker 1: to better understand how to regenerate beta cells to replace
Speaker 1: the ones that have been damaged to destroyed through diabetes.
Speaker 1: Now that we know this about these about the relationship
Speaker 1: between these immature proliferating rabbit cells and the mature cells
Speaker 1: that do the work. Oh, that's fascinating. And then we
Speaker 1: have the concept of the artificial pancreas. There are three
Speaker 1: essentially three main approaches to this, UH, one of which
Speaker 1: is actually called the artificial pancreas so UH. In two
Speaker 1: thousand and six there was a project launch called Artificial Pancreas.
Speaker 1: This was essentially the technological approach to creating a device
Speaker 1: that does a lot of the functions of the pancreas
Speaker 1: um at least as far as monitoring and responding to
Speaker 1: lucost levels is concerned. It couldn't actually produce insulin. You
Speaker 1: would have to ah feed it insulin essentially. But what
Speaker 1: it boils down to is what I talked about in
Speaker 1: that last episode with the wireless insulin pumps. It's a
Speaker 1: more sophisticated approach to that, where you have a glucose
Speaker 1: monitor that is connected to a wireless pump that is
Speaker 1: automamatically responding to changes in the blood glucose level as
Speaker 1: indicated by the monitor, so that people can live, you know,
Speaker 1: relatively unimpeded lives. They don't have to put thought into it.
Speaker 1: They don't have to actually monitor the pump or make
Speaker 1: any modifications to it. It all has taken care of
Speaker 1: and can increase a person's quality of life dramatically as
Speaker 1: a result. Ah. So it's kind of a wireless pump
Speaker 1: on overdrive. At least that's the the the goal, and
Speaker 1: it's a project that's still going on today. Are people
Speaker 1: who have had the basic level of technology. UM, They've
Speaker 1: been part of pilot programs and they the reports I've
Speaker 1: seen have said that it is a very positive experience
Speaker 1: compared to what they were coming from. UH. But ultimately, again,
Speaker 1: this is a technology that will really monitor and glucose
Speaker 1: levels and deliver insulin. It doesn't it doesn't replace a pancreas.
Speaker 1: It's not like a robo pancreas that you have in
Speaker 1: your body that does the work of producing insulin and
Speaker 1: distributing it properly. That being said, there are other alternatives
Speaker 1: that also fall into the artificial pancreas category, one of
Speaker 1: which is the bioengineering approach. This is essentially that cell
Speaker 1: transplant UH strategy I was talking about earlier, where you
Speaker 1: would create a bio artificial pancreas using the cells that
Speaker 1: produce insulin. But as we mentioned in that previous section,
Speaker 1: this can have pretty drastic consequences. It's not meant for
Speaker 1: every person who suffers from diabetes, at least not in
Speaker 1: the implementation that we have right now. And then there's
Speaker 1: the gene therapy approach. There are some researchers who are
Speaker 1: looking into using gene therapy to transform cells within the
Speaker 1: digestive tract essentially within the intestines themselves, into insulin producing cells,
Speaker 1: so that you would uh repurpose some cells in the
Speaker 1: body to take on the job of producing an insulin
Speaker 1: and releasing it into the bloodstream in in response to
Speaker 1: glucose levels in the blood. So these are all possibilities
Speaker 1: that we could see. Where it's not so much I
Speaker 1: don't know so that's so much a cure as it
Speaker 1: is an automated management system for diabetes. It's hard to
Speaker 1: mention it be like it's not like you no longer
Speaker 1: have the disease, but rather that you have systems within
Speaker 1: your body that can manage the disease. So it is
Speaker 1: almost as if you do not have it. Um it's
Speaker 1: a little you know, It's not the same thing as saying, Wow,
Speaker 1: I used to have diabetes, but now I know I'm
Speaker 1: diabetes free, right right? Well, and and really, I mean,
Speaker 1: I I love I love doing these episodes where we
Speaker 1: look into something that I think that I know things about,
Speaker 1: and then by the end of it, I'm like, oh,
Speaker 1: not only do I have no idea how it works,
Speaker 1: but literally no one has any idea how it works.
Speaker 1: Like there's like, like, we we know the basic mechanisms
Speaker 1: by which diabetes works, and we've been talking about a
Speaker 1: lot of the new research that's that's gone into it.
Speaker 1: But um but but really, like like on a inter
Speaker 1: cellular molecular level, we're still not sure what's going on.
Speaker 1: And so it's it's so great that all of this,
Speaker 1: all of this is being done and under and within
Speaker 1: so many different avenues to to look for potential, if
Speaker 1: not cures, at least um much more effective and less
Speaker 1: invasive treatment options. Yeah. And uh, I mean the incentive
Speaker 1: to do so is clear that we covered that in
Speaker 1: our first episode really extensively. The millions of people that
Speaker 1: this would benefit, not to mention the financial impact it
Speaker 1: would have. Um, there there is every incentive to continue
Speaker 1: this kind of of line of of of research and
Speaker 1: experimentation and uh advances in various forms of management and
Speaker 1: treatment and diagnosis as well. So I feel like I
Speaker 1: learned a ton um Like, I didn't know about anything
Speaker 1: from three thousand years ago with a relation to diabetes
Speaker 1: until we did this episode, and now I feel like
Speaker 1: pub trivia, I'm ready for it. So assuming that they
Speaker 1: have just an entire section on diabetes, who knows that
Speaker 1: is a very very popular pub trivia night. Yeah nothing, nothing,
Speaker 1: Nothing gets the party going like talking about a terrible
Speaker 1: disease that millions of people have. Um. That being said,
Speaker 1: I know some pub trivia masters who probably would have
Speaker 1: done at least a question, if not around on the
Speaker 1: subject because of their their particular sensibilities. I'm not passing judgment.
Speaker 1: I'm merely making an observation. Guys, if you have any
Speaker 1: suggestions for future episodes of Forward Thinking, Maybe it's a
Speaker 1: big broad topic that you want us to do a
Speaker 1: deep dive on, or maybe it's just something you know
Speaker 1: that you're just curious about. Maybe there's a technology or
Speaker 1: or scientific development that you've heard about and you want
Speaker 1: to you want to learn more about. Send it our way.
Speaker 1: We'll take a look. You can do that by sending
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