vinik interview 412-22-2015 dr ... - diabetes in control · 12/22/2015 · dr. vinik: with the...

Vinik Interview 412-22-2015

Dr. Vinik, Steve Freed, Diabetes in Control

Copyright © 2016 HIPER, LLC February 1, 2016 DiabetesInControl.com 1

Steve: You had mentioned that there is a paradigm shift in treating diabetes. That

protecting the heart may be more important that tight blood glucose

control. Can you explain what you meant by that?

Dr. Vinik: With the advent of the studies, like the diabetes complications trial,

improving glycemic control in type 1 diabetes – they were really showing

that improvement of glycemic control would reduce the microvascular

complications for diabetes. The long-term outcome of the DCCT, the

EDICT study also showed that in people with type 1 diabetes, intensive

glycemic control reduced macrovascular events.

Unfortunately, every attempt to show that glycemic control made the

difference to macrovascular events in type 2 diabetes failed to achieve

success. This all started originally with The United Kingdom Prospective

study. And at the end of the study, they were not able to show that they

were able to reduce cardiovascular events.

As occurred in the DCCT, with the long-term follow up of UKPS

identified a subset of people who were treated with metformin, who did

actually have a reduction of macrovascular events. When it came to

showing that glycemic control, per se could reduce major adverse

cardiovascular events (MACE) the four major studies that were carried out

(ACCORD, ADVANCE, UKPDS and VADT) in a metanalysis of 27049

patients who had 2370 events failed to show that there was a reduction in

cardiovascular events with intensive glycemic control. .

And those studies that people are very familiar with, in particular, were

trying to reduce MACE, (heart attacks, strokes, death, hospitalization and

the need for recanalization of the coronary arteries. only showed a possible

reduction of MI but not cardiac or all cause mortality.

What was even worse was that in the ACCORD study, there was a 22

percent increase in sudden death. And I don’t want to go there because

that’s not what has made the headline right now, but indeed, the fact is

those were not cardiovascular events that killed the people.

What killed the people was related to the autonomic dysfunction and the




fact that they likely died of an autonomic neuropathy complication with

the way you try to intensify glycemic control. But that led to a revisitation

of how important it is for glycemic control.

Should we be glucocentric and totally focused on the glucose alone? And

is it safe to become aggressive in the management of people that have

long-standing diabetes, with coronary calcification, and have carotid

intimal thickness, and have ischemic heart disease, and may have had a

myocardial infarct, or an angina.

All of those people who are at risk for an event, or they’ve had a previous

event, or they’ve had bouts of hypoglycemia, which herald a very bad

outcome if they intensify control. So what’s now slowly becoming

accepted is that this is the era of backing off.

This is the era where the stringent criteria for glycemic control should be

tainted with a note of caution, with people with the appropriate elevation

of risk, we should be accepting lesser targets for glycemic control, lesser

targets for A1c, less stringent control, and less aggression with the

management.

So that’s a very big change in the paradigm of how to look after people,

backing off, relaxing control, not being as aggressive, and also preaching

to your cardiovascular risk status. That’s foreign to a lot of people that are

earnest to evaluate the patient’s likelihood of being alive five years hence,

what their cardiovascular current risk is, and what should be new goals.

You know, we’ve striven to get to an A1c of 6.5 or 7. And now we’re

saying – okay. There are there tiers on which we can manage people, and

those three tiers really say that we can go up to 8 or even higher in the

A1c. And people are now beginning to address the J curve of managing

people who are in this part of the state of susceptibility to a sudden event.

So in the framework of that, they ask the next question which is – well,

with all of these new drugs that we’re getting – the 14 new classes of

drugs that we have now for managing people with diabetes – has anything

emerged that says that what is required is to show that we can impact in a

positive way the cardiovascular events.

So that’s not what has been happening in the major studies, such as the




TE-COS Study. The question that was asked was not, could we improve

on cardiovascular outcomes, but could we not hurt? The ACCORD Study

taught us not to hurt. So all the major new studies that have been done

have primarily looked at non-inferiority, not to hurt, and not to increase

the likelihood of a cardiovascular event.

So within that framework here, the major new drugs, such as the DPP-4

inhibitors, but most recently, the SGLT2 inhibitors are probing the

cardiovascular safety not superiority. The SGLT2 agents act to target the

kidney to increase glucose passing through the kidney, a mechanism that

is antithetic to what nature has designed.

Because nature has designed that the kidney will not give up all of its

glucose to the urine. It is very avid for reabsorbing the glucose to utilize it

for other purposes. So it has a very efficient transport mechanism. And in

people with diabetes, strangely enough, that mechanism is virtually better

than normal, nondiabetic people.

So it is antithetic then to paralyze that mechanism, to enhance glucose

disposal by the kidney because we all don’t like the notion that we pee

glucose, and peeing glucose ultimately increases your likelihood of

urinary tract infections in both males and females. But, lo and behold, if

you do that in a very large population of people, two major things emerge.

That there is a very significant reduction in cardiovascular events. There is

a very significant reduction in mortality, and a reduction in coronary artery

episodes, and even more so, a reduction in cardiac failure as has been

shown in EMPA-REG

Steve Freed: Okay. So what you’re saying is that we can be more aggressive with these

new treatments?

Dr. Vinik: No. I’m not saying that, Steve. What I’m saying is if we use an alternative

approach – to trying to get glycemic control, it isn’t the glycemic control

that’s achieved with an SGLT2. Oh, no. That’s not the factor that is

changing anything. Nobody really understands the mechanism of

cardioprotection but there is much speculation. .

But the mechanism whereby you reduce the intravascular volume, you

decrease the after load on the heart. You decrease the work the heart has to




do, is associated with, a reduction in cardiovascular events, and a

reduction in congestive heart failure, so that lo and behold, what sounds as

if you going after aggressive therapy by choosing a drug that will lower

glucose, quite by accident, is doing what people have stopped trying to

achieve.

You know the study I quoted were – intensive of glycemic control, getting

to know there were some things. So it’s not the glycemic control. It’s

something that’s associated with what you’re doing to the kidney to

change its mechanism of reabsorption of glucose into the circulation.

That has lots of wonderful consequences, incidentally. The consequences

are, the body defends itself furiously, aggressively, angrily, and says – you

don’t want to do that to me. I’ve put this in place for your benefit, and now

what you’re doing is – you’re poisoning it. And, lo and behold, out of this

comes this incredible data, which was never before. This was bigger news

than the other thing and a prospective study top boot. It was bigger news

than the DCCT. And this is only one compound, in a class of compounds,

for which there are now several that have the capability of doing this.

But that’s not as easy as it looks, and we can talk about that. I don’t know,

Steve. Have I declared that it’s not the glycemic control that’s made this

difference; it’s approaching an organ that we were a little frivolous about,

in terms of, how much it contributed to diabetes and the complications of

diabetes.

And, lo and behold, with this study that was designed primarily as a non-

inferiority study comes up with superiority, for the first time.

Steve Freed: So what are your recommendations in the treatment of patients with type 2

diabetes, with elevated blood sugars?

Dr. Vinik: If you have any of the risk factors I spoke about before, however, you

target lesser influence for glycemia because it’s less glycemic control that

matters. It’s not in most people, what is going to hurt them or kill them,

and it’s not going to get them the benefit.

If they’ve got a longevity of not even five years expected and they have

minimal complications, because they’ll target the old dogs, if they have a

longevity anticipated that’s less than that and they’ve already had any




events, like cardiovascular events, then it behooves us to adopt a much

gentler approach.

And I think now, I’m beginning to be convinced that people are hearing

that, and they’re listening. But there is another element that has arrived on

the scene. And that element is, if I can protect your heart, and I can offload

your heart, and decrease the pressure that your heart has to pump against,

and you’re a person that’s a candidate for going into a hospital for heart

failure, or your have an ambulatory tendency to heart failure, I have

another tool.

It’s like the days of the foxglove, Steve, when we did still have a digitalis,

and we could get people out of failure with the foxglove. Here we can take

people, and get them out of failure, because we offload their hearts. And

so, don’t try and promulgate or promote the notion that this is glycemic

control.

This is a new discovery – a new direction – quite by accident. We were

looking for another one of Ralph DeFronzo’s octets, which is the kidney,

to say – well, we should target the kidney like we’re targeting many other

tissues right now and at least eight and maybe 10 or more that we target

right now, to try and avoid the rampant vascular disease that accompanies

diabetes.

So if I’ve got people like that – yes. Whereas, I prescribe these drugs. I

warn people about the urinary tract infections. I tell people, if they’ve had

that type of problem before, no. I’m not going to use this drug. If you’ve

had a tendency to falls and fractures, I’m not going to use this drug.

It can be unsafe for you. It produces hypotension, with a contraction of the

plasma volume, with a bit of dizziness, fainting, and a predisposition to

falls. I’m not going to use this drug. And, once more, the newest kid on

the block is the euglycemia ketoacidotic syndrome. So if you do not feel

well test your urine for ketones and do not reduce your insulin dose.

So this drug has given us another lease on life of discovering new

physiologies and pathophysiology. I dug up a paper I wrote in 1968, and it

was comparing diabetic ketoacidosis and diabetic non-ketotic

hyperosmolar syndrome. And at that point in time, we didn’t have the

tools.




We couldn’t measure insulin, glucagon, GLP-1, and all these other things

that we postulated, that they were very different mechanism, at the

disposal of glucose that differentiated these syndromes. And one of them

is associated with the release of fatty acids from adipose tissue with

markedly elevated ketone production but the sugar was low and spilling

through the urine!.

And the second was, there was very little release of fatty acids from fatty

tissue, so the blood sugar went up, and you became hyperglycemic

hyperosmolar and non-ketotic. Now we’ve gone to the other extreme. The

other extreme is we have a syndrome that your blood sugar doesn’t have

to go very high and you are severely ketoacidotic.

Blood sugar is 200 to 250 mg/dL, yet you can go into ketoacidotic coma,

or stupor. We had one case or two case reports, and then nine case reports,

and then 19. And then now that it’s become on the FDA radar, more than

100 cases have been reported and the FDA has now issued a warning!

So we’re learning about new mechanisms for producing ketoacidotic

coma, euglycemic coma. And some people are excited because glucagon

levels go up if you allow sugar to escape from the urine, and glucagon

may be a contributor. But I think there are other mechanisms related to

activation of the autonomic nervous system, by contraction of the plasma

volume, and creating another form of stress.

Steve Freed: So you’re kind of upbeat with the SGLT2 compounds?

Dr. Vinik: I’m in reversal of being downbeat.

Steve Freed: Okay. So let’s change the subject for a second. I remember the first thing

that got me in contact with you was some research, which was being

called the INGAP research, and you were responsible for that research.

You were the head of the research, and I actually thought it was the cure

for diabetes and regenerating beta cells.

And, to me, that was exciting. And I know a lot of things have happened

since then. So maybe you can kind of tell us – where is that research right

now?




Dr. Vinik: Okay. Thanks very much for asking about this because, the truth of the

matter is, I appreciate you noting the work and recognizing the

contributions that have been made over the years. But when we started

doing this, the belief was that the pancreatic beta cell, like a beta cell in

your brain, does not have the ability to regenerate.

And then working at the University of Michigan with a surgical fellow,

Lawrence Rosenberg, from McGill University, we started wrapping

pancreases to see if we could induce pancreatitis because were intrigued

with the observation that if you initiated the problem of pancreatitis, and it

kept going, you couldn’t stop it.

And that went on until the pancreas was destroyed. So we wanted an

animal model that would do that, and then we could study the mechanisms

whereby an initial assault on the pancreas heralded a continuous process

of self-destruction. Well, we spent months trying to develop this model of

wrapping the pancreases in Saran, and it didn’t do that.

But what it did do was stimulate the growth of new islets, and we got very

taken with that. So as people have heard before, when you come to a fork

in the road take it. We did. We said – no more pancreatitis. We’re

creating new islets here. But people didn’t want to believe that.

They said how do stones regenerate? But we showed them that they did.

And then we showed, in many different models, that we could induce this

regeneration. And it took us some years to find initially, Ilotropin, which

was a protein that we identified was released by the wrapped pancreas,

which was capable of stimulating growth and proliferation of beta cells,

from pancreatic ductal or pancreatic cells, from a pro-differentiated stem

cell that was present there.

The problem with Ilotropin, the initial protein, was that it was a mixture of

many proteins. It was very much like the initial insulin preparations that

had at least 100 different proteins, before the advent of purification and

synthetic production of insulins.

Well this came to pass when we cloned and sequenced the Ingap gene, and

then showed that we could take a portion of the Ingap gene islet,

neogenesis associated peptide, a portion, just 15 minor acids, and it would

do what Ilotropin did before – stimulate growth and proliferation of




diabetes insulin cells, with a complete islet, with all the constituents of the

islet – the glucagon, somatostatin, pancreatic polypeptide, etc., that would

grow.

So that was neo-islet (new islet) formation, and just by this little peptide.

So new studies were started. And the compound Ingap was licensed to

several different companies sequentially, to show that it could possibly

cure diabetes. And it did very well in the initial trials.

Both type 1 diabetes and type 2 diabetes were found to restore in part, beta

cell function, increasing C-peptide, which is now the classic measure of

showing that you’ve improved beta cell function. But, lo and behold, when

you created these new islets, the process in type 1 diabetes was not abated.

It went on. And as soon as the new islets were formed, they were

destroyed by the endogenous (within the body) autoimmune destructor

process, and that was a little disheartening. And the good news was that if

you used an anti-inflammatory agent, in combination with Ingap, in the

animal models, you could actually get 75 percent remission of the

diabetes.

So it sounded like it would be a piece of cake and we would go into

human studies, with a combination of Ingap and an anti-inflammatory

agent. So this was done indeed with an antagonist of IL-1, which had been

tried on its own, for the potential for a cure of diabetes.

And this did not enhance the response to Encap, so it was very

disappointing that, that combination did not work. At the time that this

was happening, Dr. Jerry Nadler up at the University of Virginia, who had

been looking at anti-inflammatory agents, and his particular area of

interest was the role of IL-12 and IL-5 lipoxygenases, which generated

inflammatory compounds – a cascade of inflammatory compounds, that

were capable of destroying beta cells.

So he had antagonists of his inflammatory molecules, and he combined

those in an animal model that’s Ingap plus an antagonist inflammatory

molecule, generated by this cascade. And the answer to that was, he got 75

percent remission, if not higher. And so that generated a lot of excitement,

and it has led to further developments in the area of trying to find

compounds that will work certainly on IL-12 and work on this pathway.




The good news that has emerged – there was a newspaper announcement

about a month ago – I think you probably came across it – which said that

there’s been the initiation of a new study looked at the combination of

Ingap with with a new anti-inflammatory agent- Ustekinumab-based upon

the work that now had been done in Virginia, of combining Ingap and an

anti-inflammatory agent in an animal model, and taking it to the human

situation. The anti-inflammatory agent has been shown to be effective in

treating psoriasis!

And that trial has just gone viral in Canada. It’s already done here. I think

I’ve explained that before, being the discoverer of Ingap, and having had it

licensed to different compounds, even though, albeit, through the school

over here. It’s a conflict of interest for me to do.

So I’m excited that this has made headline news. They had a little

notification on the Inverness Magazine that this study was launched, and it

got the public’s attention.

Steve Freed: Yes, so this can actually be a benefit for not just type 1s but for type 2s

also?

Dr. Vinik: Absolutely. The interesting thing is that once we initiated new growth of

islets in type 2, even the person with type 2 has the ability to destroy those

islets.

Steve Freed: I’ve always thought the fact that type 1 diabetes, you had no control over,

but type 2 diabetes, there’s the inference there that it’s the patient fault.

They’ve overeaten. They haven’t exercised. Can there really be a possible

cure for type 2 diabetes for the person who continues to overeat, and not

be physically active?

Dr. Vinik: That’s a lovely question. You see, what people forget about is that, no

matter how much you over eat and no matter how resistant you are to the

action of insulin, no matter how obese you are, no matter how thick you

think your waist circumference is – you will never become a diabetic if

your pancreatic beta cells can cope. Never.

Now people in early years counted upon this notion because everybody

was tuned to resistance of the action of insulin, being at the core, and we




doing it to ourselves. But most recently, studies by Ralph DeFronzo, in

Texas, and Ele Ferrannini, in Italy – they’ve gone back to say – let us look

at newly diagnosed type 2s and see when we do our sophisticated time

studies, that we now get a good measure of pancreatic beta cell function.

That’s been the worst and most difficult thing to do for all of us, is to

actually get a good handle on the beta cell mass, and how well the beta

cell is functioning, in contrast to what we can do in animal models. Where

it’s very easy today to gauge a beta cell mass, and it’s very easy to get a

measure of how well a beta cell is secreting.

Based upon those things, we’ve learned that the day you become a type 2

diabetic, you’ve incubated things that have been ongoing since you

immerged from your mother’s womb, over 30 or 40 years, what has been

an attack on the pancreatic beta cell.

And in all that time – now you go from day zero, just when you’re born, to

the time that you become diabetic – you’ve got a steady six to 10 percent

reduction in the pancreatic beta cell capacity for the secretion of insulin

and for the islet mass, which is steadily pouring all the time.

And then you hit day zero – the day that you become a diabetic. At that

time, there’s 50 percent loss of beta cells. Now that 50 percent may be

even more. The data from Italy says it may be even as high as 90 percent,

almost like a type 1 diabetic, but it’s much higher than we thought. And

you will not become a diabetic unless you have lost beta cells or have

impairment of their function.

Then and thereon, from that day on, you continue to do six to 10 percent

here, and there’s a mechanism for during that piece that’s different from

what happens in the type 1 diabetic. In the type 1 diabetic, you have

autonomic destruction of the pancreatic beta cells.

In the type 2 diabetics, you also have beta cell destruction, but the major

mechanism is the infiltration of amyloid and amyloid-induced beta cell

apoptosis, and heart attack, or death. So there can be a second approach to

this as to try and stop this type of killing. As long as you can stop the

killing, we should be able to overcome that and get you back up that curve

of the six to 10 percent loss of beta cells per year, get back up that curve,

and get you to where you can cope with the degree of insulin resistance




that you have.

And that actually is a very nice thought that doing that, either by

increasing beta cell growth, or improving beta cell function, we will take

people with type 2 diabetes and will cure them just as well as we would a

type 1 diabetic. So that time and longevity of the beta cell is compromised

in type 2 diabetes and the type 2 diabetic becomes to look like a type 1.

And then you’re treating the same thing. You’re treating the loss of beta

cell mass and beta cell function by addressing the pancreatic beta cells. So

I’m not condoning the things about eating like a pig. I’m not condoning

slothfulness or laziness. I’m not condoning all of that. I’m not condoning

smoking and having a big, thick waist.

I’m not condoning that. But I’m saying, in answer to your question – yes.

And approach to “curing diabetes” will be restoring beta cell function to

where it can cope with the demands made of it. And that’s an important

point. If a person was relatively lean and athletic and exercising regularly,

and had developed type 2 diabetes later in life, the amount of restoration

of the beta cell function and mass is much smaller than what I have to do

if I’m a big, obese person with insulin resistance.

So we’re asking it to do a lot more in those people but, of course, it can be

done.

Steve Freed: That’s kind of good news because I always thought that for type 1, we’ll

have a cure with a short period of time because there’s so much research

going on in the bionic pancreas, etc., etc., Ingap and so many other studies

going on that, type 1 is almost an easy cure with the knowledge that we

have today.

Type 2 – I always thought that’s a little bit more difficult task and keeping

those beta cells alive. But from what you’re saying is, if we can do that –

they’re not going to die from the diabetes complications. They’ll die from

something else most likely, and we’ll find out what that is, and then we

can go ahead and treat that.

So let’s change the subject. I really appreciate the time, so friend, this

won’t take much time. I’m working on a study and I mentioned it to you

before – not so much a study, but a new diagnostics screening tool for




kidney disease. And we know that microalbumin plays an important role

in testing for kidney failure or kidney disease, congestive heart failure,

etc., inflammation, and so forth, and it plays a major role.

And I’m working to develop a microalbumin test, not so much like a color

dot where you stick a stick into the urine and it changes colors – that’s

approved for doctors’ offices. I’m working on something that I want to get

approved for home use. There is no home use FDA approved test now for

microalbumin.

And this test basically looks like a pregnancy test. It’s a little container

with a strip in there. And you put a couple of drops of urine into it, or pee

into it. And if a red line appears, then you’ve got at least 20 micrograms

per milliliter of microalbumin.

Now, I know there’s a lot of different things that can cause microalbumin.

It could be a temperature or a fever. It could be a medication you’re

taking. So there’s going to be some false negatives. No question about it.

And the whole purpose is to basically have the patient, if they get a red

stripe, to contact their physician, or to contact an 800 number.

This information will all come with the test, and that information will also

be not only be to educate the patient what this might possibly be and, like I

said, it’s only a screening tool. It’s not diagnostic for anything. But there’s

$30 billion being spent on kidney failure.

There’s 10 percent of the population that have some kind of kidney failure

that will probably go to dialysis. The cost for dialysis is $250,000.00 per a

person’s lifetime. And if there was a way to screen – and even if you get

20 or 30 percent false positives – if they go to their doctor, and their

doctor does the other test, and a letter will go with that to the doctor, and

some suggestions – I can’t imagine that we couldn’t prevent a large

number, or at least 10 percent to 20 percent of the people, to go to kidney

failure and go into dialysis.

Going on dialysis, people just don’t have a clue. I know what dialysis is

like. You know what dialysis is like. Three days a week you’re in the

clinic, and then three days a week, you have to rest up because it knocks

the hell out of you. So basically, people on dialysis have one day to live,

and that’s on Sunday.




And that’s true for everybody on dialysis. So if there’s a way where we

can save billions of dollars – and I’ve talked to other physicians, and they

say – you know what, you need to do three tests. If they get a positive on

one, you do another test. And if they get a positive on two, then they

contact their physician.

If they get a positive and a negative on the two tests, then they need to do

a third test. That will cut down on the positives and negatives that you get.

So I’m trying to come up with a test that’s very inexpensive, that could be

sent out to hundreds of thousands of people for managed care, and find

those people.

And all I’m saying is, they need to contact their physician and have them

do other tests, if needed, and just to talk to their doctor about this. You

know, years ago, they tried to do this and the cost was prohibitive. But

now, I think I can get the costs down to less than a dollar to do this.

Dr. Vinik: That’s a good place to be.

Steve Freed: What are your thoughts? Do you think it’s worth going forward or is it a

waste of time?

Dr. Vinik: So Steve, you and I have spoken about this, and I’ve written you a fairly

lengthy opinion about it, and gone through some of the details. I have no

doubt that using microalbumin as a marker or a biomarker for when

damages occur into the kidney, and also damages that occur into the

endothelium of blood vessels throughout the body, and the

microalbuminuria reflects what is happening to blood vessels universally.

It’s not only a marker of what is happening in the kidney. But I think

microalbumin over there is a really good biomarker for just about any one

of the major macro and micro complications of diabetes. So it’s nice.

People were looking at A1cs a couple of decades ago.

That really is saying – okay. I can use an A1c to detect your diabetes and

use it as a biomarker, and we now know, years later, about all the fallacies.

But it hasn’t gone to a stage where we can’t use it at all. It’s gone to the

stage where we now know, when you start getting erroneous

measurements with different A1cs for different reasons.




So we’ve got to learn all of that as we measure because we originally

thought that proteinuria, microalbuminuria, meant destruction of the

glomeruli. We then started treating people with ACES and ARBs and

reducing the microalbuminuria and, lo and behold, when you went off the

ACE and the ARB, the proteinuria came back again.

So you hadn’t changed the natural history of the disease. We’ve still got a

biomarker of what about – this is something bad happening in that person

and I must do something about it. And the best time to do it is before

there’s gross structural damage.

And who are the people I would like to see come onboard with your new

in-house test, are the people who are the greatest candidates, of the highest

risk. In other words, family members or people with type 2 diabetes. I

think it’s hard to find a family that doesn’t have a family member anymore

with type 2 diabetes.

And then the other bedfellow also to run with that metabolic syndrome

criteria – hypotension itself. Every second diabetic is hypertensive,

dyslipidemic with elevated triglycerides, and a reduction in HDL. Those

are the people that constitute the larger population that are at risk.

By that I mean – we know we have 30 million people with diabetes in the

United States. We have about 80 million people with this pre-diabetes. So

here you’ve got a large captured population of people, captured because of

the susceptibility criteria that I’ve mentioned earlier.

And if you look at that population and you can save 10 percent of the

people/15 percent of the people, progressing to diabetes, and its

complications, and, in particular, using it for damage to any portion of the

cardiovascular system, and about the micro and the macro – that’s a good

place to be.

If I had a family history of diabetes, if I was hypertensive, If I was

dyslipidemic, if I had the features of metabolic syndrome and I could do a

dollar a day test, or if I used the test maybe once a month or whatever it

was, and it cost me a dollar a time over there, and I’d find out whether or

not I was really causing damage – I’d like to know that at a time that I can

do something about it. And that’s the time.




Steve Freed: Well, I want to thank you for your time. I’m always interested in talking to

you. You have some things that you’ve been involved with that have made

some major differences, especially at your university. And I just want to

thank you again, and I hope to see you at ACE. I know that, that’s a part of

your blood that you will be at ACE, and you’ll be at AEA, and I hope to

see you there and certainly take you out for dinner, along with your wife,

Etta.

By the way, how is Etta doing?

Dr. Vinik: Oh, she’s doing fine. She’s putting together a conference on turning the

tide against diabetes again. She’s resumed activity in that regard on March

19th, 2016.

Steve Freed: One of the things that I’ve been asked to do is to do a web cast for AADE,

the diabetes educators. And they want me to talk about the future of

diabetes education. So I may ask for your help on that or Etta’s help, as far

as, where is the future of diabetes education going?

Because I personally think that with 100 million or 80 million people with

pre-diabetes – and just in this people, 30 million people with diabetes, that

number one, doctors don’t have the time to do it, and they can’t get paid to

do it, so forget about doctors.

Then if you go to diabetes educators, there’s not enough educators and

hospital programs to educate all of those people, and people don’t like to

go to hospitals. So I personally feel that the future of diabetes education

has got to be answered with technology. I think that’s where the future

will hold itself and now with one-on-one treatments, and educations and

things.

It’s got to be done in such a way where you can hit 100 million just in this

country alone, and if we move to the other English speaking countries or

the Spanish speaking countries, you’re talking about billions, if not. How

do you get to them? And it certainly isn’t going to be one-on-one

education.

That’s for sure. There’s just no way we can do that. So I’m going to ask

for your thoughts on that because I know whatever you can come up with




would be great. So I will be back in touch with you. So start thinking

about it now.

Dr. Vinik: Well, thanks for the warning.

Steve Freed: Okay. And, by the way, if you have any slide decks that you want to share,

because I know you must have a million of them that are maybe a little

outdated – if you want to share those, send them to me. And you sent me

about eight slides, but I’m looking to get a large number of slides or slide

decks or something that we can share with other medical professionals that

you’re not using any more. Certainly, I’ll give you credit for it. But if you

have any of those, feel free to send them to me, or put them in a drop box,

or whatever, so I can upload them.

Dr. Vinik: I’ll go scrounge around in Pandora’s Box.

Steve Freed: Okay. I appreciate it. You have a great day, and have a happy holiday and

a healthy one.

Dr. Vinik: Have a happy holiday and a Happy New Year, and I look forward to

working with you some more in the new year.

Steve Freed: Okay. Thanks. Take Care. Bye.

Dr. Vinik: Bye.

[End of Audio]

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