Insulin Resistance is Real! (Gerald Shulman’s 2018 Banting Lecture on IR Mechanism)


Yeah, even on young thin people, you need
to be looking for insulin resistance. I didn’t get into this part of preventive
medicine too deeply into the past decade. I wish that someone, one of my docs
teaching me had known what I know now and had pushed me to get an OGTT and
insulin levels. Insulin resistance. It definitely does
exist despite what some people might say. It’s an incredibly important
and devastating disease process. There’s a great video that hit the YouTube
community again about a week ago because of Ivor Cummings. We’ll talk about that
in just a minute. It’s a lecture given by Gerald Shulman, June 24th, 2018 I think
when he received the Banting Award for his work at Yale on understanding and
helping us develop the mechanisms for the biochemical mechanisms for insulin
resistance. Dr. Shulman again is it Howard Hughes Medical Institute. He’s
been using a lot of magnetic resonance imaging to find out what’s going on in
terms of gluconeogenesis development of new glucose from the liver glycogen. It’s
development of glycogen and the muscle and the liver and its association
with insulin resistance. I first found that about it by Joe Reilly. Joe Reilly has
mentioned many times. He’s a patient of mine. He’s also a moderator and super
moderator PrevMed community forum channel. It was posted first by Tom, Tom
Deck. I think Tom is also a super moderator for the channel and he’s got
some great points. He said, “Look it’s the best talk I’ve ever heard about insulin
resistance. The long and short of it is that accumulation of fat in
liver and muscle cells.” And he goes on to say that “detailed metabolic
steps get deep but don’t lose interest. Hang in there and maybe
just jump to 31 minutes 39 minutes section where some of the
takeaways are located.” I’m going to go a little bit more into details because
when you start looking at the details, from my perspective, as treating
patients, helping patients, first understand that they have insulin
resistance and then giving them suggestions, giving them opportunities to
to treat this disease process. I think you might get a little bit of a
different perspective on this Shulman lecture.
He said goes on to say, “Don’t get too hung up on Shulman’s affiliation of Big Pharma.” Shulman is working with Big Pharma to develop something that
might help uncouple the mitochondrial activity within the liver cells. That’s
something very interesting neat potential breakthrough for the future
but again this video is not about that. This video is about other things that
Shulman and his community have helped us discover about the disease process of
insulin resistance which we can act on today. How can you find this again? If you
want to go to it, if you want to find it on our forum, you go to the PrevMed website,
click for “more”… excuse me… when you do, you’ll get a dropdown, the first item
on the dropdown, it says “blog and forum,” then you just click on the forum. Once
you get to the forum, you can look for the Shulman talk on insulin resistance
posted by Ivor Cummins. Cummins posted on YouTube by Ivor Cummings and puts it
on the forum by Ted. I mean… excuse me… Tom. Tom,
kudos. Ivor Cummins, as I’ve said many times, he’s somebody that I really
respect. He’s an engineer. He’s got significant interest in insulin
resistance diabetes. His tagline is the Fat Emperor and I’ve wondered if they
had to do with the old story about the emperor that had no clothes obviously by
the banner ad on his page. It does and I must… I don’t know, I’d love
to… I’d love to have a conversation with Ivor to find out exactly what that’s all
about. But here, let’s get to the details for
those of you who just want to hit a quick look for five minutes and then
move on, I’ll give you the five minute summary. Some of the concepts and
learning points and some of the things that we need to do to react to that
are: number one, yes, insulin resistance is real. In fact, for a huge portion of the
research that they’ve done, they used young, thin, otherwise healthy, sedentary
male subjects that had IR (insulin resistance). Most of these male subjects
were offspring of adults that had significant type 2 diabetes. So what can
we get from that? Yeah even on young thin people, you need
to be looking for insulin resistance. I didn’t get into this part of preventive
medicine too deeply into the past decade. I wish that someone, one of my docs
teaching me, had known what I know now and had pushed me to get an OGTT and
insulin levels when I was much much younger. Because one of the things you’ll
find on these studies is that they these young men will have totally normal OGTT
results (oral glucose tolerance results) and if you don’t know what OGTT
or oral glucose tolerance test is, you can look. I’m not going to get into depth
on that right now. It’s just that you’re challenging your body with glucose and
seeing how your body reacts, metabolizes that glucose. One of the
other key… both of these points are key… do the OGTT and do insulin because as I
said, these young, thin, otherwise healthy males, even if you did an OGTT, you would
not have known that they had insulin resistance had you not gotten insulin
levels. And I see that all the time. I probably see that in about ten, maybe
twenty percent of my patients where they have normal glucose values all the way
through an OGTT. But once you start getting insulin it’s taking two
times the insulin, sometimes even more, to keep those normal glucose levels. What’s
one of the next things to learn? He mentioned several times about
increasing triglycerides and decreasing HDL. When you start getting into the
liver components of insulin resistance, well, what should we learn from that?
Obviously again, how many videos do I have on the triglyceride-to-HDL ratio?
The triglyceride-to-HDL ratio is something that you can say, “Look, I can’t
afford to go get a two or $300 set of inflammation labs, okay?” But almost every
one of us has a routine cholesterol panel. Look at that routine cholesterol
panel. If your triglyceride over HDL ratio is elevated significantly over one,
you need to be very concerned, be afraid, be very afraid. And then obviously, I’m
being somewhat facetious but you do need to be concerned and you do need to focus
on the potential for having insulin resistance. BMI or RFM. What’s BMI? Body mass
index. RFM – relative fat mass. For those of you who don’t like BMI, he
mentions multiple times in the lecture now covers some screen shots a little
bit later on each of these concepts where he covers them in the lecture and
the impact of these things on insulin
resistance at a biomolecular level. Again what’s the medical
upshot of that? If I’ve said it once, I’ve said it a thousand times to my
patients in videos, there’s nothing more important than the relative fat
mass or your BMI, how much you weigh. I remember talking to a new patient who…
and I get this almost all the time… one of my new patients had a BMI in the
mid 20s and he was saying he thought he maybe needed to gain a little bit of
weight. No, and I typically get patients who have
a BMI close to 30, and they think that is a normal healthy weight. It’s not. The low 20s are much better and see most importantly you get a huge impact on
your biochemistry specific to insulin resistance just by losing a few pounds.
He goes through several episodes of research in that area. The next one is
muscle cell insulin resistance… is DAG – driven… I won’t go into too what DAG is.
But it’s something very much related to fatty acids and what it
creates is lack of transport of glucose. So in other words, it’s not the different
cascades of glycogen development within the muscle or within the liver that is
hampered with insulin resistance. It’s the transport of the glucose across
the cell membrane the muscle cell membrane and the liver cell membrane. Now
why is that an issue? And what can we do with that?
He showed again multiple episodes where simple things like exercise, 45 minute
exercise with the legs, and it almost completely reversed the insulin
resistance process for muscles. Obviously resistance training is a…
we’ve talked about it multiple times on videos. I talked with my patients about
it. One of the reasons I have legs separated out here is that when I talk
about resistance training especially with men, they tend to think about making
big arm muscles, you know our muscles don’t hit. I don’t
care who you are. Your arm muscles usually do just not have the mass that
are going to impact your insulin resistance like your leg muscles ham so
leg muscle work insulin resistant for is critical for insulin resistance. I also
mentioned CGM (continuous glucose monitoring) and CGM directed walks we’ve
mentioned multiple times. Watch how your body reacts to different foods and
especially if you know you’re going to take a carb holiday. It’s okay if you
decide to do that but remember and think. If I take a carb, if I have a pizza and
beer, I don’t usually have that but a lot of people do and that’s the carb holiday
for a lot of folks. If you do that, go out and take a half-hour walk after that and
try to schedule these things and talk to your spouse or whoever you’re having
that dinner with, “Can we go out and walk afterwards because I want to make sure
that I pull that blood glucose back down.” Yes, it did. Talk about meds, there’s
a lot of focus right now on mitochondrial uncoupling within the
liver specifically. He talked about that at the end and that gets a lot of buzz
in terms of a potential breakthrough set of drugs for the future. Yes, that’s great,
it’s wonderful but we also have some drugs now both of which he mentioned
that are critical for insulin resistance management. One is just plain old
metformin. The TAME study (Targeting Aging with Metformin) and old pioglitazone
(Actos). These are medications that have been around forever. They’ve been used
forever and they’re still very good for some resistance. I have a lot of patients
that just don’t want to take any kind of drug whatsoever. I understand that but
again hopefully getting a little bit deeper into the details of these
medications will help help folks begin to maybe take a second look at these
medications, especially if you have significant insulin resistance. Now if
you wanted to get the basics those were the basics I’m gonna give you a little
bit more details though for those of us those of you that want to stay on the
video. The first one is this Banting. Who was Banting? And why were these series of
lectures named after him? It’s an award that’s given each year by the American
Diabetes Association. Frederick Banting… he and his supervisor at University of
Toronto received a… and a couple of other guys on this team received a Nobel Prize
for medicine in 1923. What they did was they just they as well as several other
people began to realize that there was something in the pancreas and maybe
specifically even in the Islets of Langerhans that had to do with keeping
blood sugar down and treating or keeping people from having diabetes. They took
isolates from cow and pig pancreas that was you know cows and pigs that were
being slaughtered for sale and this is the dog. There was a fella named Best
that was working with him. This is a picture on top of the roof at the
University of Toronto. There are a few dogs that… they were about a dozen I
think… that they took the pancreas out of and then gave them this isolate, this
substance they isolated from the pancreas of the pigs and the cows. The
first few times, the first ten dogs died but Marjorie lived at least a few months.
Now then, you go on to say, “Was that real?” or “Did they leave some of Marjorie’s
pancreas in there?” That actually dive infection you know there’s
just a bunch of other critical stories but the bottom line was that team won
the Nobel Prize for discovery of insulin. I first thought that they were referring
to William Banting. Those of you who have read the books a couple of Gary Taubes’
books. “Good Calories, Bad Calories or why would get fat and what to do about it.”
May have thought of William Banting. The books start out just describing uh an
undertaker who was born in 1796, died in 1878. He was obese and based on the
advice of a Scottish doc, he decided to just cut all carbs out of his diet. He
lost weight. He wrote this up and that became the first popular publication on
the low-carb diet. So it’s still even a term today. People will ask, “Are you
Banting?” When they do, they mean, “Are you doing low-carb diet?” It turns out… at
least Wikipedia says… William was actually a distant relative of Frederick.
Now let’s go back into some of the details on that Banting lecture
and what we can see in terms of medicine today just dreams for metaphor
medications for tomorrow. First again, insulin resistance is real. Dietary carbs
are problems. Triglyceride over HDL ratio is a big big deal. And it’s something
then, after watching this lecture, you begin to understand why you see that on
your labs. It is very much associated with ectopic fat. What is “ectopic” mean? It
just means something that’s not where it should be, that’s all. And the ectopic fat
that we’re talking about here is fat in the muscle tissue,
liver tissue. Those are both very much associated with insulin resistance. Now
he mentioned several times that fatty acids inhibit insulin-stimulated glucose
transport activity. In other words, what they did was they actually incubated and
you can demonstrate this by incubating skeletal muscle in fatty
acids. It begins to shut down insulin response. Now the question that obviously
comes up is, “Well, is there a way that you can decrease exposure to fatty acids?” I
don’t think that’s ever gonna be practical. The body burns fatty acids. You
get to the question about, “Well, should I quit taking exogenous ketones? Are those
bad for me?” I don’t think so. Again, I think this is just something for us to
be aware of who something may come up with it in the future. But for right now,
fatty acids are just part of our metabolism. You cannot eat oils and stay
them or fats and stay the same weight and never have your body exposed to
fatty acids. Now some people could theoretically get into, “Well, that’s the
problem with the low-carb diet. There are much bigger problems with high carb
diets.” That’s again I think most folks watching this channel will understand
that. As we mentioned before, they’ve done research showing that just a single bout
of exercise can reverse the abnormal pattern of carbohydrate storage in
insulin resistance individuals. So again, as you see, that is a temporary that
albeit temporarily temporary, it is an effective reversal of insulin resistance.
So exercise, exercise, exercise. That’s one of the comments that Tom Deck put
originally in the comments that he left on the
forum. This information is critical to helping us understand why exercise is so
important. Fat transport normalizes in muscle and
liver. Fat transplant normalizes this process. Now fat transplants come in to
the same place that exposure to fatty acids comes. You don’t see us doing
significant fat transplants, they did them on mice, and they actually reversed
this problem. Now how about being thin and having insulin resistance? This is a
picture of a 17-year-old girl that has lipodystrophy. Lipo meaning
fat or oil, and dystrophy meaning inappropriately formed. In fact, you see
little or no fat around her body but she’s got a protruding abdomen. That
abdomens protruding the cause of a grossly overgrown liver and is grossly
over gone through ground because of fat. They’re using leptin therapy and got a
huge improvement. So again that raises another potential. Well is leptin therapy
something for our future? Again that’s something that’s a little bit beyond the
scope of this video. Something that’s not beyond the scope of this video and it’s
just everyday practical blocking and tackling. If you’re a doc or if you’re a
patient, you should be thinking about a patient with insulin resistance. “Is
metformin really that bad for me?” And again this helps you understand exactly
how that metformin works. There’s been several studies a group called Madiraju
with the principal author have published a couple of times in Nature magazine. He
mentioned a Nature magazine article in 2014 and I’ve got a
follow-up article coming up in just a minute.
Basically what they’re showing is that up until these articles, it really wasn’t
that clear what metformin does. It does a lot of things. For example, it does impact
the gut biome. However, what these guys think now is that it may be mostly due
to inhibition of gluconeogenesis through a redox reaction…. reduction impact
within the cells of the liver. I personally am skeptical… not so much…
that there’s a major redox mechanism going on or oxidation-reduction
mechanism. I also think it’s got more than one mechanism. And I think, for
example, that gut biome mechanism, it’s probably helpful now multiple times in
this lecture. He mentions Bach so one TNF-alpha and IL-6 interleukin 6. TNF
stands for tumor necrosis factor. He mentions those a lot. Basically, I think
the takeaway from that on this lecture is basically he goes into
liver-targeted mitochondrial uncoupling. Again, that’s exciting, that’s
something that they may develop in terms of a whole new category of drugs for
treatment of insulin resistance for the future. But as I mentioned here again,
this is exciting but this lecture is not just about the future. It’s about
understanding what’s going on in our body now and doing some basic blocking
and tackling. Like keeping our weight at where it should be, decreasing a relative
fat mass, decreasing carbs, managing our carb intake, understanding the
importance of muscle activity, understanding the importance of looking
for something simple like triglycerides over HDL and against
very basic medications. Speaking of BMI or RFM, if you look at this chart, but
basically what you see is for folks that have BMI 30 or greater, they have huge
amounts of fat in their liver. This reminds me of a patient that I have. He’s a
doc and we just we helped him discover his aunt’s significant insulin
resistance. And one of the things he’s pointing out is that he thinks there’s a
lot more to non-alcoholic fatty liver disease. And that’s what you hear
multiple times in this, like very strong association with non-alcoholic fatty
liver disease. And you can see it here, looking at just this simple graph for
folks that have a BMI 30 or greater, they tend to have a lot of fat in their liver
cells. That’s what that means in the second side. The first side is these guys
with the yellow bar, the second side is a padded lipid content or liver fat cell
content. Again, very elevated. Just a couple of more slides and we’re about
done. We mentioned metformin. We didn’t mention pioglitazone yet. The pioglitazone,
these are medicines that have been around for a while. They were very
popular about a decade ago. Actos, you may remember that. And then he
he goes in to show the exact mechanism. Basically, one of the things that they
calles aimed ions decreasing that ectopic fat that you
find in the liver and muscle cells and redirecting that fat back to
subcutaneous fat. Subcutaneous fat by the way is not the problem, does not cause
insulin resistance. It’s where you get that spillover of subcutaneous fat into
muscles. So again pardon me, if it’s been a long video. It
was a great lecture. I can’t help but thank Ivor Cummins again for his
discovery of this video. You know, I went and looked I found the video on his
channel after Tom Deck posted it. You know, went to look to see how he
discovered that video and I still don’t understand how he did. There’s a lot of
information on the web about the Banting awards and the Banting lectures.
But again my kudos to Mr. Cummins for finding out in that specific lecture. It
was a great one. If you’ve made it this far, thank you so much for your interest.
So I’m very excited to announce we now have a membership page. Now what is that?
That’s the one place where you can go and access all of our digital products.
It starts off with a few free things, like a lot of infographics which help
you understand the basics of insulin resistance, cardiovascular inflammation,
and other key concepts on how to prevent heart attack and stroke. The next free
item is the intro and first chapter of the book that we’re writing on plaque and
the standards of medicine just aren’t doing very well right now in terms of
the number one killer and disabler plaque. We don’t do a good job of
measuring it, we don’t do a good job of monitoring it, and there are better ways.
So that’s what this book is all about. Again, go in and get a free look at the
intro and in the first chapter. And if you’ve purchased the cardiovascular
inflammation and IR courses, thank you so much for
that. You purchased those at a time before we had them totally cleaned up
and we’ve cleaned them up now and they’re available for you right there on
the membership page. Hit the link below, register and go in, and take a look. Look
forward to seeing you there. Thank you.

20 thoughts on “Insulin Resistance is Real! (Gerald Shulman’s 2018 Banting Lecture on IR Mechanism)

  1. Ive been using a glucose monitor for about a month (thanks to your suggestion) and i seem to have a pretty strong insulin response.
    I think fasting has really helped. Got my BMI down to 21.
    How do i get insulin values?

  2. I'm curious as to why IR is the term given for all of this rather than hyperinsulinemia. Blood insulin levels can reach over 10 times their normal level and can be monitored. If my my blood insulin levels are ten times too high, my goal should be to decrease them to normal by having a blood test every few months until they are normal. I don't know how to keep track of my 'insulin resistance', but I can measure my fasting blood insulin levels. Once my fasting blood insulin levels are normal, other reducing carbs to zero, I know of no other better treatment. All the metformin, bererine, even chromium do is SHOVE the sugar into the most delicate tissues that will eventually rot them. I don't understand why they are pushed so much. Faithful, consistent OMAD or longer fasting and low to zero carb are the 2 biggest consistent things people can do to affect their hyperinsulinemia/IR/Blood glucose. If the masses are going to understand this, they will understand it better through high blood insulin levels regardless of age, weight or apparent fitness. A low resting pulse below 60, a waistline that is less than 50% of a person's height, blood pressure at or beow 120/80, the ability to be able to run an 8 minute mile or less, and normal blood insulin levels are the biggest indictators of health.

    Second, I'm curious as to why everyone advocates 'paying' for a carb holiday afterward by walking for a half hour. How about doing glute/ham/quad/calf excercises for an hour BEFORE you have that 'carb holiday' and EARN IT by draining the glycogen out the muscles to handle the carb intake initially and then 'pay' for it as well by walking off most of the rest. I keep promising my self I'm going to have a carb holicay but in 21 months I have not had the nerve to do it. I feel I need a bigger health reserve and I may never get there. I had a CT scan of heart 13 years ago and it was over 1300. I didn't know what to do about until 21 months ago so I'm pretty sure that score doubled or more because my diet became worse after that.

    I use a Walmart plastic $8 folding 12 inch stool next to a indoor dorway as a poor man's stepping/calf/step machine. I do step ups that focus on glutes/hams/quads, and hang my heels over the edge for a calf/stepping machine. I do them at all times of the day, especially when listening to lectures like this and kill 2 birds with one stone. I use the doorway trim as handles to hold onto. I also use the powerblock dumbells to do dumbell deadlifts. 100lbs of dumbells is enough because they are closer to floor than a barbell making a longer moment arm. Using your elbows slightly in front of knees when loading accents the glutes/hams/ having your elbows. alongside or slightly behind the knees accents the quads. I do up to 10 sets of 15 every other day and do other exercises on the other day. I walk for 2 hours everyday. I do other other excercises for my arms shoulds and back, like bent over rows. But the powerblocks and the little stool is the best home gym workout center I ever had, and I've had everthing. And it takes up the space of about 2 large loaves of bread with the stool folded.

  3. Extremely interesting video Dr. Brewer! I forwarded this video to my cousin who also was an ER Doc & is now concentrating on what he terms "Hidden Heart Disease". Like me, he had 2 stents after an acute MI. To bad that you guys couldn't hook up. Anyway, keep up the great work. BTW, I had included a link to his face book page in a recent video of yours. He is located in NJ…………. Thanks!

  4. Dr. Brewer – superb!. I've had a TG/HDL of >10 – to -1 for decades (sometimes even higher). Tricor + Omega3 (>2mg EPA/ DHA per day) help a lot. Pre-diabetic for 9 years now, so Met x2 day really helps too. Both conditions related, for sure.

  5. Some time ago had a free (new French-made ultrasound machine) liver test done and came out as having fatty liver. Tried to get accepted into a Stage 1 trial for new fatty liver treatment (seems many Big Pharma companies are into this epidemic condition). Got rejected as my liver function panel was not off the standard parameters. Anyway, read somewhere that Berberine may help fatty liver…any thoughts?

  6. Exercise isn't everything, though. I exercised a LOT – and had an MI at mile 10 of my 11 mile bike ride. ( my diet, however, was pitiful )

  7. Thank you for this video. My father was diagnosed with type 1 diabetes in 1929 at the age of ten, not long after the discovery of insulin therapy. He lived to be 70. He never was diagnosed as such but in retrospect I think he probably developed type 2 as well in his later years. My mother was a type 2 in her later years and died at 67. My older sister 65 who is mentally slow also has type 2 along with bad kidney problems from it I assume. I am 57 and have been athletic and healthy all my life. I am 5' 6" and I weigh 162 pounds and have noticed recently that my fating glucose levels have been between 100 and 120 fairly consistently so I have started eating a keto diet. I am continuing my HIIT exercise as well as some strength training.

  8. Thank you doc- as you know- this whole topic of Triglycerides to HDL is very near and dear to my heart. I beg anyone, especially men, to really take this seriously- and wives- stay in your husband about it- you will be glad you did.

  9. When I watched this video a couple weeks ago I was really impressed. I hope you picked up the part of how metformin works.

  10. I think it might explain why fasting makes in improving insulin resistance than just keto. The cells.may be forced to burn the fats internal to the cell and unblock GLUT4. Also, kind of debunks the idea that the cells are just to full to allow more glucose in.
    I watched 3 times so far and probably will again.

  11. I’ve learned so much from your videos Dr. Brewer. Thanks a lot.
    About fasting insulin levels…my labs normal range is 2.6 to 24.9 uU/ml…..according to you what is an optimal fasting insulin level.
    Secondly, I live in Singapore and Malaysia….haven’t been able to find a cardiologist that is willing to listen to any of the information I have gathered through videos like yours. Very frustrating …..

  12. WOWOW, doc, your Chinese fans here. You covered so much in this video and I think a lot of them deserve a episode or two.
    First, "get in the gym" a lot trainers lack of medical knowlodge how to help with a IR patient, and a lot of doctors just lost their way in gym. We need a hyperbreed to deal with these new situation.

    Second, "leptin treatment" Once again, for those bodybuilder and Dr. Ford who like to play with hormons. It almost bring tears into my eyes you realize there is value in hormon on weight lossing. noradrenaline, leptin, thyroxin, even androgen There are papers you can look into, they all help your fat cell release fat into your blood stream, so you lose fat in this catabolic effect.

    Third. “Gluconeogensis” Look into whats the global control signal in your body to turn on or off gluconeogensis. It is Insulin! so for those with IR or desfunctioning pancreas. Your liver or kidney just keep pumping glucos into your blood. Yeah, I read the same paper you refer to in this video. People dont realize how powerful your internal glucos making machine is, fasting for a week and your blood suger is still on the level, think about it., thats your liver and kidney pumping sugar into your body. No wonders metformin help with blood sugar control. Everybody is talking about insulin but no one talking about glucagon. Hey, they both come out the pancreas.

  13. I thank you for focusing my attention on prediabetes. Even with a fasting glucose under 90, an HbA1c of 5.3%, a fasting insulin of 7, a HOMA-IR under 2, a TRG/HDL under 1 my OGTT has my glucose spiking to 200 before returning to the initial level by 2 hrs and remaining there. I suspected that I have type 2 prediabetes, my doctors do not want to hear of this and consider me a bit of a hypochondriac.
    I have been wearing an Abbot CGM from which I have learned a lot about how I react to particular foods.
    My most pleasant surprise was how well I manage ice cream, a food I have written off my diet.
    The most dramatic discovery is how different a reaction I have to certain foods on an empty stomach as contrasted to having the same food after a meal
    Certain fruits raise my glucose from 90 to 180 when consumed on an empty stomach while they do not seem to have any significant effect when I enjoy them post meal
    Yesterday I enjoyed something like a baked pretzel covered with sesame seeeds. I could hardly believe that my glucose shot up to 215 – I only consumed less than 50g!
    The Glycemic Index is useful but it is based on an average of many responses, only the CGM can identify the foods that affect you most.
    The CGM has also enabled me to identify patterns, such as the importance of having dessert/fruit only after a meal and the incredibly beneficial effect of postprandial walks

  14. Thanks again for the VDO, very well explained! Can you please help me understand the following: You as well as Gerald Shulman indicates that Exercise is very very important to prevent IR. If I remember well you have exercised the most part of your life, e.g. doing Marathons. How can it be that you have developed IR??

  15. What TG/HDL ratio would you classify as "significantly" over one. My fasting TG are 62 and HDL is 44 which equals a ratio of 1.4 HbA1c of 4.9, i am also rather young ( in my 20s). Would you consider that a problem?

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