0:00

I'm Joe Graydon. And I'm Terry Graydon.

0:03

Welcome to this podcast of The People's

0:05

Pharmacy. You can find previous podcasts

0:08

and more information on a range

0:10

of health topics at peoplespharmacy.com.

0:14

Americans love easy

0:16

solutions to complex problems. Maybe

0:19

that's why weight loss drugs like Wegovy

0:21

are so popular. This

0:23

is The People's Pharmacy with Terry and

0:26

Joe Graydon.

0:30

GLP-1 agonists like Ozempic, Monjaro, and

0:32

Wegovy help people lose more weight

0:34

than previous medications.

0:37

Are there downsides? Today, part two of our two-part series about the

0:43

benefits

0:43

and risks of medications like

0:45

Wegovy. We've invited

0:48

two medical experts to share

0:50

their different perspectives

0:50

on strategies to overcome obesity.

0:53

Today's guest is author of Metabolical, a the

0:56

lure and the lies of processed

0:58

food, nutrition, and modern medicine. Coming

1:01

up on The People's Pharmacy, a different view on

1:03

medicines

1:04

for obesity. In

1:07

The People's Pharmacy health headlines, COVID-19

1:09

infections can give rise

1:14

to a wide range of conditions that persist long

1:16

after the original infection

1:18

is gone. Researchers wondered

1:21

if using the antiviral medicine Paxlovit

1:23

during the acute phase of COVID would reduce

1:27

the likelihood of post-COVID conditions. To find out, they

1:29

compared the health records of

1:33

patients treated for COVID

1:35

at the Veterans Health Administration

1:37

in 2022. More than 9,500 were treated with Paxlovit. Their

1:40

subsequent health problems were compared to those who did

1:46

not receive Paxlovit, though they were similar in

1:48

other ways. The investigators were disappointed

1:52

to find that Paxlovit reduced the

1:54

chance of only one type of COVID-19 infection.

1:59

complication. Blood clots in

2:02

the legs or in the lungs. Other

2:04

post-COVID problems did not respond.

2:07

The FDA recently issued

2:10

a warning about contaminated eye

2:12

drops. Inspectors found unsanitary

2:15

conditions at a facility that makes 26 different

2:18

types of OTC drops. This

2:20

is not the first time eye drops have posed

2:22

a problem. Last summer, dozens

2:25

of Americans developed eye infections that

2:27

were traced to contaminated eye

2:30

drops. Some people suffered permanent

2:32

loss of vision because of those infections.

2:35

The FDA is now cautioning consumers to

2:37

avoid lubricant eye drops under the brand

2:39

name CBS Health, Leader,

2:42

Rugby, Rite Aid, Target, Walmart,

2:44

and Velocity Pharma. The agency

2:46

warns that using contaminated lubricant

2:49

eye drops could lead to eye infections,

2:51

loss of vision, or even blindness.

2:55

When people have coronary artery disease,

2:57

doctors often prescribe statins to lower

2:59

the likelihood of experiencing heart

3:01

attacks, strokes, or early death.

3:04

But which statin works best? A

3:07

new study called LODESTAR was

3:09

just published in the BMJ. The

3:11

Korean investigators compared a

3:13

torvostatin with rosuvostatin.

3:16

The brand names are Lipitor and Crestor,

3:18

respectively. After three years,

3:21

there was no difference between the two

3:23

groups with respect to their chances of having

3:25

a heart attack or stroke. There

3:27

was, however, a difference with respect

3:30

to side effects. Rosuvostatin,

3:33

which lowered LDL cholesterol

3:35

more than a torvostatin, also

3:38

resulted in a higher risk of type 2

3:40

diabetes and

3:41

cataracts. A very

3:43

old and inexpensive diabetes

3:46

medicine called metformin may have

3:48

an unexpected benefit. A

3:50

study published in JAMA Network Open found

3:53

that people who stopped taking their metformin

3:55

were more likely to develop dementia

3:57

later. Researchers analyzed data

4:00

from electronic health records at Kaiser

4:02

Permanente. More than 12,000

4:05

individuals discontinued metformin

4:08

and were matched to over 29,000 people who continued

4:11

taking their anti-diabetes metformin.

4:15

Those who dropped the drug were 21% more

4:17

likely to be diagnosed with dementia during

4:20

the subsequent five years. One

4:22

conclusion is that metformin may

4:24

be protective against dementia.

4:27

In other research, investigators

4:29

compared two ways of eating to

4:31

see which one worked best to help people

4:33

with type 2 diabetes lose weight.

4:36

They assigned 75 volunteers

4:38

into one of three groups. In

4:41

one group, people ate only between

4:43

noon and 8 p.m. The second

4:46

group paid close attention to counting

4:48

calories and reduced their usual

4:50

intake by A

4:52

third group did not change their eating behavior

4:55

and served as controls. The researchers

4:57

monitored blood sugar levels as well as

4:59

weight and waist circumference during the

5:02

six months of the study. Both

5:04

of the groups who changed their eating patterns

5:06

lowered their HBA1C levels

5:08

during the study. That's a way of measuring

5:11

blood sugar over a number of weeks. Those

5:13

practicing time-restricted eating found

5:15

it easier

5:16

to follow the rules. Their weight

5:18

loss was significant compared to the control

5:20

group. The calorie counters, on the other

5:23

hand, lost a modest amount of weight,

5:25

not significant. When the

5:27

thyroid gland produces too much or

5:29

too little thyroid hormone, it can have

5:32

profound effects on the body. A

5:34

new study reinforces the importance

5:36

of keeping thyroid hormone levels within

5:38

the target range. The authors found

5:40

that older people who had elevated

5:43

levels of thyroid hormone due to hyperthyroidism

5:46

or excessive levothyroxine were

5:48

almost 40% more likely

5:50

to be diagnosed with cognitive impairment.

5:53

And that's the health news from the People's Pharmacy.

5:56

This week.

6:14

Welcome to the People's Pharmacy. I'm

6:16

Terry

6:16

Graydon. And I'm Joe Graydon. Last

6:19

week we spoke with Dr. Jamie Art,

6:21

Professor of Epidemiology and Prevention

6:24

at Wake Forest University School of Medicine.

6:27

She's also President-elect of the

6:29

Obesity Society. Dr.

6:31

Art offered an optimistic view

6:33

of medicines like Otempic, Wegovi

6:36

and Monjaro.

6:37

This is the second in a two-part

6:39

series giving you the lowdown

6:41

on new medicines

6:42

for treating obesity. Our guest today

6:45

is Dr. Robert Lustig, Professor

6:47

Emeritus of Pediatrics in the Division

6:49

of Endocrinology at the University

6:51

of California San Francisco. He

6:53

specializes in the field of neuroendocrinology

6:57

with an emphasis on the regulation of energy

6:59

balance by the central nervous system. Dr.

7:02

Lustig is the author of several books including

7:05

his most recent, Metabolical,

7:07

The Lure and the Lies

7:09

of Processed Food, Nutrition and

7:12

Modern Medicine.

7:14

Welcome back to the People's Pharmacy.

7:17

Dr. Rob Lustig.

7:18

Thank you so much, Terry and

7:20

Joe, for having me back yet again. Dr.

7:23

Lustig, during your career, which

7:26

is long and distinguished,

7:28

you have treated people, especially children,

7:31

who have had obesity. What

7:34

are the consequences of

7:37

excess weight for both

7:39

children and adults? Okay,

7:42

well now we're getting down into

7:45

the weeds when you say excess weight.

7:48

Obviously, obesity is

7:50

excess weight, but obesity

7:54

is not actually the problem.

7:56

Metabolic dysfunction

7:59

is the

7:59

problem.

7:59

problem. So let's take that

8:02

apart. And this is actually very important for

8:05

the rest of this discussion. There

8:07

are actually three fat depots we

8:09

need to be concerned about. Three

8:11

places where the body stores fat. Now,

8:14

the first one, the big one,

8:17

the one everybody notices, the

8:19

one that doesn't look so good in the bathing suit,

8:21

that's called subcutaneous fat. Or

8:24

if you want big butt fat,

8:26

as in, does this bathing suit make me look

8:29

fat? Fat, that

8:33

fat. That is actually

8:36

metabolically protective.

8:38

That's where your body wants to

8:41

put excess energy. So

8:44

while it may be cosmetically undesirable,

8:46

from a metabolic standpoint, it's actually

8:49

inert. It's what your body wants

8:51

to do with fat. Now,

8:53

how many pounds

8:57

of excess big butt fat

8:59

do you have to gain before

9:01

you start developing metabolic

9:04

problems? About 22, about 10 kilos

9:06

or 22 pounds. So

9:09

you can put on a fair amount of

9:12

weight

9:13

before you will show signs

9:15

of metabolic decompensation.

9:18

And of course, those metabolic decompensations,

9:20

you know, can result in type two diabetes

9:23

and cardiovascular disease and fatty

9:25

liver disease and ultimately put you

9:27

at risk for cancer and dementia and

9:30

many, many other different problems.

9:34

The second fat depot

9:36

is called visceral or

9:38

big belly fat.

9:40

Now, that fat is much more metabolically

9:42

active. And that's fat you don't

9:44

want. But what causes

9:47

that fat is stress. That fat is

9:49

not due to calories or diet.

9:52

That fat is due to stress. And the reason

9:54

we know that is because people who are clinically

9:56

depressed, who are losing weight

9:58

because they think they're going to lose weight. don't want to eat

10:01

because they are anhedonic, that

10:03

they don't have any interest in eating

10:05

because they're even suicidal and have

10:07

to sometimes be admitted to the hospital to save

10:10

them from themselves. When you stick them

10:12

in an MRI scanner, they actually have increased

10:15

visceral fat. They're losing subcutaneous

10:17

fat and they're gaining visceral fat.

10:21

Now, how many pounds of visceral fat

10:23

do you have to gain before you become

10:26

metabolically unhealthy? About

10:29

five. So 22 pounds

10:32

for the subcutaneous fat, only about

10:34

five pounds for the visceral

10:36

fat. And then finally, the third fat

10:38

depot and perhaps the most important fat

10:40

depot, the

10:41

liver,

10:42

liver fat. Now, the liver's

10:44

not supposed to store fat, but

10:47

now today 45% of the entire US population

10:51

has fatty liver disease. When

10:53

that fatty liver is actually

10:56

causing all sorts of hormonal

10:59

imbalances, it is the primary

11:01

reason for type 2 diabetes. Because

11:04

when your liver stores fat, the

11:06

insulin that comes from your pancreas

11:09

can't do its job. When your

11:11

insulin can't do its job, then your blood glucose

11:13

rises and you have type 2 diabetes.

11:16

Now, how many pounds

11:18

of liver fat can you store

11:21

before you become metabolically ill?

11:24

A half a pound. So 22

11:26

pounds for subcutaneous

11:28

fat, five pounds for visceral fat, a

11:30

half a pound for liver fat, and

11:33

everyone in America today has the liver

11:35

fat.

11:36

So

11:37

when you say, what does excess

11:39

weight do, you have to qualify

11:42

it as to

11:43

which weight are we talking about?

11:46

So I think

11:48

that's really important for people to understand.

11:52

And I think in the three

11:54

minutes we have before the break, we

11:57

need to understand what are the health

11:59

conditions.

11:59

consequences when somebody

12:02

has more than five pounds

12:05

of liver fat and No,

12:07

no more than half a pound of liver fat When

12:10

someone has more than half a pound of liver

12:12

fat and more than five pounds

12:14

of visceral fat. Health consequences,

12:16

please

12:17

Yes, absolutely. So that's where

12:20

the metabolic dysfunction comes in.

12:22

So when you

12:24

have either liver or visceral fat

12:26

You have this phenomenon called insulin

12:29

resistance Insulin of course

12:31

is the energy storage hormone Insulin

12:34

is the driver of energy into

12:36

fat cells in the first place. No

12:38

insulin no fat more insulin

12:41

More fat ask any type 1 diabetic

12:43

who starts taking insulin shots what

12:45

happens to their weight and what happens to

12:48

their fat depots so Insulin

12:51

is the driver turns out insulin

12:53

is also the bad guy in terms

12:55

of metabolic dysfunction Because insulin

12:58

causes growth when it should

13:00

it causes growth of coronary arteries

13:03

Leading you to risk for heart attack. It causes

13:05

growth of various glandular tissues Which

13:08

can lead to prostate and breast cancer or pancreatic

13:10

cancer. It can cause changes

13:13

in the vascular Tree

13:15

in the brain ultimately leading to

13:17

dementia It can specifically

13:20

drive the changes in the neurons

13:23

that lead to Alzheimer's disease. It

13:26

can cause numerous

13:29

problems that we are now

13:31

suffering from as a country

13:34

and really globally across

13:36

the world in a big

13:38

way and it's because of this

13:40

phenomenon called insulin resistance

13:43

and Yes, obesity is related

13:45

to insulin resistance. Of course, that's

13:47

true But there are plenty of obese

13:49

people who are insulin sensitive and

13:51

there are plenty of normal weight people who are insulin

13:54

resistant So while obesity

13:57

is a risk factor for all of these chronic

14:00

metabolic diseases, it's not the

14:02

cause.

14:04

Dr. Lustig, I'm

14:07

thinking about the statistic

14:09

you just gave us that 45% of the U.S. population

14:14

has fatty liver disease.

14:16

Presumably most of that is non-alcoholic

14:19

fatty liver disease. Correct.

14:22

I'm thinking about the fact that that hasn't

14:24

always been the case. So

14:28

I'm also thinking about

14:30

the previous conversations you and

14:33

we have had about the problems

14:35

with sugar.

14:38

Is that the reason why there's

14:41

been such an alarming increase

14:43

in metabolic dysfunction since 1975?

14:47

Exactly right, Terry. So the

14:50

question is, if the fat,

14:52

if the liver is not supposed to store

14:54

fat, how did the fat get there?

14:57

Yeah. The uninitiated, the

15:00

novices would say, well, it's

15:03

the fat you eat. Actually, it's not

15:06

the fat you eat. The fat you eat

15:08

passes through the liver just fine.

15:11

It gets turned into a

15:14

molecule that you've heard about a zillion

15:17

times. It's called LDL. Now,

15:20

LDL is not completely benign. LDL

15:23

can be a harbinger of

15:25

cardiovascular disease. I don't argue

15:27

that. People with very high LDL

15:30

levels need to see their doctor. Slightly,

15:34

they will get put on a statin in

15:37

order to lower their LDL levels

15:39

in order to prevent heart disease. Well,

15:42

the fat you eat ends

15:44

up as LDL. That is not

15:46

the fat in the liver.

15:48

The fat in the liver

15:51

is triglyceride. The fat

15:53

in the liver is VLDL,

15:57

or very low density lipoproteins.

16:00

and it is primarily triglyceride. Now,

16:02

the question is, how

16:04

did the triglyceride get there? Did

16:07

that come from your food? It turns

16:09

out not at all. That fat,

16:12

that triglyceride, was actually

16:14

made in the liver

16:16

directly.

16:18

The liver actually turned something

16:21

into fat, and that

16:23

something is either one of

16:26

two items, alcohol, and

16:29

that's what, if you had fatty liver before 1980,

16:33

that was the reason. If you saw fat

16:36

in the liver on a microscopic

16:38

slide, from a liver biopsy, that

16:41

was an alcoholic, up to 1980. And

16:44

then, in 1980, we discovered that

16:46

there was this new version,

16:49

and we called it non-alcoholic

16:51

fatty liver disease. Well, for

16:53

the last 40 years, we've been chasing that

16:55

down to try to figure out what is the source,

16:58

what is the cause of that fat?

17:00

And the answer is sugar.

17:03

Sugar

17:04

gets turned into fat in

17:06

the liver, and it gets turned specifically

17:08

into that triglyceride. Now, some

17:11

of that,

17:12

the LDL

17:13

that the triglyceride makes will

17:15

make it out, and that could ultimately

17:18

be a substrate for obesity and heart disease too,

17:21

but a lot of it will precipitate right there in

17:23

the liver, and now you've got fatty

17:25

liver disease, now you've got insulin

17:27

resistance, now you've got metabolic

17:29

dysfunction, now you've got

17:32

risk for all of those chronic

17:34

metabolic diseases we talked about at the beginning.

17:37

You're listening to Dr. Robert Lustig,

17:40

Professor Emeritus of Pediatrics in

17:42

the Division of Endocrinology at the University

17:44

of California, San Francisco. His

17:47

research and clinical practice has focused

17:49

on childhood obesity and diabetes.

17:52

Dr. Lustig is the author of several books, including

17:55

the most recent, Metabolical,

17:57

The Lure and the Lies of Processed Food.

19:51

Last

20:00

week we focused on the benefits of Wegovi

20:03

and Manjaro.

20:04

This week our guest has a different

20:06

perspective. Dr. Robert Lustig

20:09

is Professor Emeritus of Pediatrics

20:12

in the Division of Endocrinology at

20:14

the University of California San Francisco.

20:17

His most recent book is Metabolical,

20:20

The Lure and the Lies of Processed

20:22

Food, Nutrition, and Modern

20:25

Medicine.

20:27

So Dr. Lustig, the

20:29

pharmaceutical industry now

20:32

believes, and a great many

20:34

of your colleagues seem to agree, that

20:36

they've come up with the solution,

20:39

the answer to the problem. These

20:42

new drugs, you

20:45

can tell people what a GLP-1

20:47

receptor agonist is, glucagon...

20:53

Like... Like... Like...

20:56

That's right. And so these drugs are

20:59

being hailed as the

21:02

answer to obesity. And

21:05

not only that, they can control blood

21:08

sugar, they can reduce cardiovascular

21:11

risk, they may limit cravings

21:13

for cigarettes or alcohol. It's

21:16

like the miracle medicine

21:18

of all time. The only downside

21:21

is they're kind of pricey, like about $1,200

21:23

a month.

21:24

Well it really sounds like you're good to be true.

21:27

It is true, it is

21:30

true that GLP-1 receptor

21:32

analogs

21:33

are a big step forward.

21:36

And I don't argue that. I actually

21:38

applaud that. It is really,

21:41

for the first time, something that actually

21:44

works. And I'm not downgrading

21:47

it, but like everything,

21:49

like everything in medicine that comes

21:51

with a downside, okay? There

21:53

is a lot of baggage

21:56

here that we have to peace out and

21:58

dissect in order for your... audience

22:00

to be able to understand exactly what

22:03

these medicines do, what

22:05

they don't do, what they put

22:07

you at risk for, and

22:10

whether or not these are actually a good

22:12

idea for you.

22:14

Not necessarily for

22:16

someone else, but for you. And I need to

22:18

say, we are talking about semaglutide.

22:22

We are talking about osempic.

22:25

We are talking about wegovi. Now

22:28

osempic was approved for diabetes, type 2

22:30

diabetes. Wegovi was approved

22:32

for obesity, and there are others

22:35

as well.

22:36

In the same category,

22:38

we have terzepatide, which is called

22:40

Mount

22:40

Jaro. And that's about

22:42

to get approval from the FDA for

22:44

obesity as well. So tell us,

22:48

the pros and the cons of

22:50

these now hard

22:52

to get drugs, because they are in short

22:54

supply.

22:55

They are very

22:57

expensive, and right now

22:59

there is a tremendous social

23:02

disparity, because everyone

23:04

in Hollywood can get them, because they can afford

23:07

them, and no one else can. And

23:09

that seems a little bit preposterous,

23:12

but there we are. They cost

23:15

about $1,300 a month right now. So

23:19

if everyone in America who

23:22

qualified for any one

23:24

of these three drugs actually got

23:27

them, that would be $2.1 trillion

23:30

to our healthcare system. Well our

23:32

healthcare system is $4.1 trillion, so

23:34

that would be a 50% increase. We

23:36

can't afford the healthcare system we

23:39

have now. How are we going to afford a 50%

23:42

surcharge on top of that? Having

23:45

said that, money is not the only

23:48

problem here.

23:49

So let's

23:50

discuss exactly what do

23:53

these medicines do.

23:55

Well

23:56

they do two things. The first thing they

23:58

do is they go to... the pancreas

24:00

and they cause the pancreas to kick out

24:02

a little extra insulin and

24:05

that will lower blood glucose. And

24:07

that's why ozempic is a

24:09

treatment for diabetes.

24:12

The other thing that it does which seems to be

24:14

even more relevant is

24:17

it goes to the brain

24:18

and it binds to receptors

24:21

in the brain stem and

24:24

basically what that information

24:27

tells the brain is, hey I've

24:29

eaten, I

24:30

don't need to eat again.

24:32

It's part of the satiety signal. Now

24:35

this is a normal phenomenon

24:37

that occurs regularly in

24:39

everyone.

24:40

You

24:41

eat, you're tested, makes GLP1

24:45

and it goes into the bloodstream, goes to your

24:47

pancreas, makes it kick out some more insulin,

24:49

goes to the brain and tells your

24:51

brain, okay I'm full,

24:53

it's part of the satiety signal. But clearly

24:56

some people don't get

24:58

that signal as well as others. Now

25:00

we've looked for people with GLP1

25:02

deficiency, haven't found them. So

25:06

that's, we're not treating a deficiency

25:08

here.

25:09

But

25:10

giving extra GLP1 analog

25:13

can make people think

25:16

that they've eaten and so

25:19

they will slow down and

25:21

reduce their food intake. Now that

25:23

sounds like a great thing

25:25

and it will ultimately

25:29

predispose to weight loss. And

25:32

people who are on Ozempicum or the week

25:34

and lose up to 16% of

25:36

their weight and that is significant

25:39

and it's really the first time we've been able to

25:41

do that. So again I applaud

25:43

these drugs, I'm not against them.

25:46

However

25:47

let's think about what that 16% of weight

25:49

loss is. When

25:52

you stick people into the DEXA scanner

25:55

to look at body composition analysis,

25:58

you have lost as much money. muscle

26:01

as you have fat. In

26:03

other words,

26:04

Ozempek and Mugovi and Munjaro are

26:06

working

26:07

by inducing starvation. In

26:10

starvation, you lose equal amounts of fat

26:13

and muscle. The goal is not to

26:15

lose muscle. The goal is to lose

26:17

fat. In fact, that's one

26:19

of the reasons why we say exercise is

26:22

to maintain your muscle, especially

26:25

while you're losing weight.

26:26

Ask any little old lady

26:29

if she would like a little extra muscle

26:32

just before she breaks her hip. And

26:35

if you've read numerous

26:38

articles and reports, and if you read Peter Atia's

26:40

book Outlive, you will know that maintaining

26:43

your muscle mass is extraordinarily

26:46

important for longevity. Well, these

26:49

drugs don't do it. These

26:51

drugs actually make

26:54

you lose muscle mass. This

26:56

is not necessarily a good thing.

26:59

So there's a little robbing Peter to pay Paul

27:01

here. You can't dissociate

27:05

the satiety effect from the

27:07

starvation effect and the starvation

27:09

effect from the loss of muscle mass.

27:11

That's not great. So

27:14

that's one problem. Second

27:16

problem, these medicines

27:19

also work by

27:21

slowing gastric emptying.

27:23

So

27:24

if your stomach isn't emptying

27:27

as fast, then it seems

27:29

full longer. So you seem

27:31

less hungry. Now, that sounds

27:34

like a good idea too,

27:36

except

27:37

that numerous people have

27:39

actually had significant

27:42

GI complications. And I

27:44

have just read an article about a case

27:46

study of patients with gastroparesis.

27:50

That is, that their stomach doesn't

27:52

move at all. And

27:55

it's not just because of the medicine.

27:58

You take a medicine away. And

28:00

it's

28:01

still there.

28:02

Six to twelve months later, you

28:04

still have gastroparesis. Now,

28:08

we don't know

28:09

who's at risk for that. We don't know

28:11

whether any individual patient would

28:13

get that or not. But

28:15

that is a really bad complication.

28:19

It also causes nausea. It

28:21

causes vomiting. As if

28:23

you basically overstuffed someone

28:26

who'd already eaten, that's

28:29

how it works. It can

28:31

cause pancreatitis. An

28:33

earlier version of a GLP-1 analog

28:35

called Exenatide was linked with

28:37

pancreatic cancer. We haven't had

28:40

these drugs long enough to be able to see that

28:42

signal yet. So this

28:45

is not exactly a completely

28:47

benign drug. It's not like, oh,

28:50

this is the magic bullet, weight loss, and

28:52

you're done.

28:53

There's stuff going on. And one more

28:55

thing.

28:56

Yes. When you stop these drugs,

28:59

what happens? The weight comes

29:01

rushing back. And the reason is because

29:03

you actually haven't fixed the problem.

29:06

You have band-aided the problem. You have bypassed

29:09

the problem. The problem,

29:12

the metabolic dysfunction is actually

29:14

still there. And so when the

29:17

drugs stop, all the

29:19

weight comes rushing back, and in some

29:21

cases, plus some. You

29:24

might have to be on these medicines the rest of your

29:26

life at $1,300 a month. Now,

29:30

that's

29:30

not such a good deal either.

29:33

And then lastly,

29:34

you mentioned, Joe, that

29:36

some people are actually taking

29:39

these drugs and are finding that

29:41

their addictions are getting better.

29:44

Their cravings for alcohol and

29:46

for street drugs are getting better. And

29:49

this is extraordinarily interesting

29:51

and absolutely needs to be researched,

29:53

evaluated, and perhaps this will

29:56

end up being a significant

29:58

addition to the... addiction medicine

30:01

armamentarium. And again, I'm

30:03

not against it. I'm for it. However,

30:06

there

30:06

have been now

30:08

numerous case studies and now

30:10

a cohort of study that

30:12

shows that patients on these medicines,

30:15

because of the change

30:18

in the reward system, can develop

30:20

severe depression and suicidal

30:23

ideation. Now, I

30:25

don't know if you guys

30:28

can remember back to 2006. So 17

30:30

years ago, there

30:34

was a drug that was approved in

30:36

Europe.

30:37

The drug was named Ramanobant.

30:39

The trade name was Accomplia. And

30:42

it was a huge

30:44

weight loss giant. And

30:47

everybody wanted it. And what it

30:50

was, was it was an anti

30:52

marijuana drug. It bound

30:54

to the endocannabinoid receptor in

30:57

the brain. And what it did was it reduced

31:00

interest in food.

31:02

Well,

31:03

it also reduced interest in everything.

31:06

These patients became severely depressed.

31:08

And there were numerous cases of suicide.

31:11

And ultimately, the

31:12

European Food Safety Administration,

31:14

the European Drug Administration had to pull the

31:16

drug. It never got approved here

31:19

in the United States. So playing

31:21

with the reward system sounds

31:24

like a good idea, but it can have

31:26

really disastrous consequences. So

31:29

we need to know a lot more about

31:31

what these drugs do and in home before

31:34

we can just sort of apportion them

31:36

out willy-nilly.

31:38

Dr. Lustig, we

31:40

have spoken with you before. And

31:42

when we have, you have suggested

31:45

that we all need to pay much

31:47

more attention to eating real

31:50

food. Can you tell

31:53

us how that

31:55

would affect metabolic dysfunction?

31:58

Indeed, I would be delight it.

32:02

So,

32:03

what is real food? So,

32:06

let's define it. That is food

32:08

that came out of the ground or animals that ate

32:10

the food that came out of the ground. That's real

32:13

food. If it went to a plant,

32:16

okay, it's not real

32:19

food. If it has a label

32:22

on it, that means that something's

32:24

been done to it. Now, by a plant,

32:27

you mean a factory. I mean a factory,

32:29

that's right. Okay. Yes, let's

32:31

be clear. If it went

32:34

to a food manufacturing

32:36

plant, it's not real food. All

32:39

real food is

32:42

naked. It doesn't have a label. Okay,

32:45

if it has a label, it's a warning label. It

32:47

means something's been done to it. And

32:49

so, you need to understand that that's what

32:52

we're talking about here.

32:53

So,

32:54

what does ultra-processed

32:57

food

32:58

do?

32:59

By the way, 73% of the

33:00

items in the grocery

33:02

store

33:04

are ultra-processed food. 57%

33:07

of the

33:09

food that we eat is ultra-processed

33:11

food. Chris Van Tulliken

33:14

in Europe just published a book called Ultra-Processed

33:17

People. Indeed, that's what we are. So,

33:20

the question is, what does that do?

33:23

The answer is, it is the

33:25

driver

33:26

of this chronic metabolic disease. And

33:29

the reason is because it interferes

33:32

with the function

33:33

of the mitochondria.

33:36

Now, the mitochondria, for those of you who

33:38

don't remember your 10th grade biology, they

33:40

have the little powerhouses of

33:42

each cell that generate the chemical

33:45

energy that the cell runs on

33:47

to do its job. When the energy

33:50

runs out, the cell dies. So, those

33:52

mitochondria are pretty important. Well,

33:55

turns out those mitochondria are actually

33:57

very fragile, and there are different compounds

34:01

that can interfere

34:03

with that mitochondrial functioning. Some

34:05

of it's in the food, some of

34:07

it's in the food packaging, some

34:09

of it's in the air, some of it's

34:12

in the water, some of it's in the

34:14

plastics, some of it's in the cosmetics,

34:17

some of it's in the hair dye

34:19

you use. The bottom line

34:21

is we have

34:23

a

34:24

metabolic

34:26

catastrophe because

34:28

our mitochondria are

34:30

under assault non-stop.

34:34

Now how do you fix

34:36

that?

34:37

Well

34:38

a lot of the things are baked into the cake. Like

34:41

for instance, I'll give you an example of a compound

34:44

that's baked into the cake. Yes,

34:48

polyfluoride alkylated

34:50

substances, the most common

34:53

of which, the one that you all remember

34:55

very well, Teflon.

34:57

Go see the movie Dark Waters. You

34:59

will learn everything you need to know about Teflon.

35:02

Well Teflon turns out to have been a mitochondrial

35:04

toxin.

35:06

Teflon is still around

35:08

even though it's been

35:10

removed from all cooking

35:12

surfaces.

35:13

It is still around because it is a forever chemical.

35:17

We will never get rid of it.

35:19

Same with DDT. DDT was

35:21

the first insecticide.

35:23

We stopped using DDT in 1972

35:27

but you can measure the metabolite

35:29

of DDT called DDE in

35:32

the urine of pregnant women and

35:34

that level correlates with

35:36

obesity in their offspring

35:40

at age 5 and age 10.

35:42

So

35:43

these we can't do anything

35:45

about. They're with us. But

35:47

the big one, the big thing that causes

35:50

mitochondrial dysfunction,

35:52

the thing we could do something about, the thing

35:54

that is in all of our food,

35:58

sugar,

35:59

is a direct

36:00

mitochondrial toxin. Sugar

36:03

causes three separate enzymes

36:06

in the mitochondria to be dysfunctional.

36:09

I can name them. Your audience can

36:11

look them up. One is called AMP

36:14

kinase, which is the fuel gauge on the liver cell.

36:16

The second one is called ethyl-CoA dehydrogenase

36:19

flowing chain or ICAD-L.

36:21

It is the enzyme that

36:23

cleaves fats into two carbon

36:25

fragments so that they can be burned to make

36:28

ATP. And the third one

36:30

is called CPT-1 or carnitine

36:32

palmitole transferase 1, which is the shuttle

36:35

mechanism to get fats

36:37

into the mitochondria in the first place. So

36:39

if you have defective

36:42

mitochondria,

36:43

number one,

36:44

you're not making energy. Your cells are

36:46

starving. You're going to eat more in

36:49

an attempt to try to

36:50

undo that. And

36:52

second, you're going to make fat. And you're

36:54

going to make fat in places you shouldn't, like

36:56

your liver. And now you've got chronic

36:59

metabolic disease. So

37:01

our current

37:03

environment is driving

37:06

this phenomenon. How

37:08

can you undo that? Well,

37:11

real food. Because ultra-processed

37:13

food

37:14

is very high sugar

37:17

and very low fiber. And fiber

37:19

actually is necessary to reduce

37:21

the inflammation

37:23

that would occur because

37:25

the bacteria in your gut are

37:28

unhappy with the food that you ate because

37:30

that's the food they eat too.

37:33

You're listening to Dr. Robert Lustig,

37:36

author of Metabolical, The Lure

37:38

and the Lies of Processed Food, Nutrition

37:41

and Modern

37:41

Medicine. After the break, we'll

37:43

explore the implications of real

37:46

food.

37:46

Does that put all the responsibility

37:48

on the consumer?

37:49

What about people in food deserts?

37:51

They could have a hard time getting real food.

37:54

We do worry about some of the side effects

37:56

of GLP-1 agonists.

37:58

also

38:00

addresses drug effectiveness.

38:11

You're listening to The People's

38:15

Pharmacy with Joe and Terry Graden. This

38:18

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39:23

Welcome back to The People's Pharmacy,

39:25

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39:27

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39:47

It's estimated that more than 40%

39:50

of Americans are officially obese.

39:53

No wonder then that drugs to help people lose

39:55

weight have become very popular. Last

39:58

week we focused on the benefits of

40:00

medications like Ozempic, Wigovi,

40:03

and Monjaro. Today, we're

40:05

looking at some of the downsides.

40:06

Our guest is Dr. Robert

40:09

Lustig, Professor Emeritus of

40:11

Pediatrics in the Division of Endocrinology

40:14

at the University of California, San Francisco.

40:17

His most recent book is Metabolical,

40:20

The Lure and the Lies of Processed

40:22

Food, Nutrition, and Modern

40:25

Medicine.

40:26

Dr. Lustig, I get

40:28

the idea of real food. Carrots

40:30

and apples, you know, chicken

40:33

and fish, that's real food.

40:36

But what I'm wondering is

40:39

when we say eat real food, it

40:41

sounds as though we're telling people this

40:43

is your responsibility. And I'm

40:45

wondering how people can do

40:47

that if they live in a food desert

40:50

where the nearest place that they

40:52

have to buy food

40:56

has nothing but ultra-processed

40:59

food in it.

41:00

Terry, I couldn't agree with you more,

41:03

all right? And I will tell you that

41:05

this is what I have devoted my retirement

41:08

to,

41:08

is fixing the food supply for

41:11

just this reason. So I

41:13

don't disagree with you. You're exactly

41:15

right. And you have to put your finger on the

41:18

single biggest problem we have

41:20

in America, okay? The social

41:23

disparity of food

41:25

availability and procurement. I don't

41:27

disagree. I am with you. I

41:30

am totally there. In fact,

41:32

we have started a nonprofit

41:34

called Eat Real to get real

41:36

food into K-12 in all

41:40

public schools in

41:42

the United States. Now, right

41:44

now, if you go into any schoolroom

41:47

cafeteria,

41:48

what are they serving? They're serving pizza.

41:51

They're serving chicken nuggets. And those were

41:54

frozen bags delivered by Cisco

41:56

or Guggenheim or McDonald's itself. And

41:59

that's it.

41:59

what they call lunch. Take

42:02

a look at the National School Breakfast Program.

42:05

What is a National School Breakfast Program

42:07

breakfast look like? It's a bowl

42:09

of fruit loops and a glass of orange juice. That's 41

42:13

grams of sugar. The

42:15

American Heart Association says the

42:17

maximum for children should be 12 grams

42:20

of sugar per day. That's 41

42:24

grams of sugar for breakfast

42:28

and you still have the whole day left. So

42:31

think about what that's doing to your mitochondria.

42:34

Think about what that's doing to your metabolism.

42:37

Think what that's doing to your brain.

42:40

We have to solve that. Now how

42:42

do we solve that? Well we

42:44

are working on that. We have developed a business

42:47

model that actually works to be able to

42:49

do this for K to 12. Now how

42:51

do we do that for supermarkets? Well

42:55

one thing we have to do is we have to educate the public

42:57

which we're doing right now as to why this

42:59

is important because if people

43:02

think that ultra-processed food is somehow

43:04

better because it's cheaper because

43:07

price matters more than food

43:10

quality you know then we'll never get

43:12

it solved because after all why

43:14

would a supermarket stock real

43:17

food if nobody would buy it because

43:19

they're addicted to the

43:22

ultra-processed food because after all

43:24

sugar is addictive. So this

43:27

is a very large topic

43:30

with a lot of twists and turns and

43:32

what we have to do is we have to bring all stakeholders

43:35

to the table all at once and

43:38

the only group that can do that is Congress

43:41

and unfortunately they have been completely

43:44

silent and absent

43:47

on this issue.

43:48

Dr. Lustig you have stated

43:51

fix the food first.

43:55

Let's see if these drugs and now we're

43:57

talking about the GLP-1 agon. Let's

44:00

see if these drugs are actually better

44:04

or even comparable to real

44:07

food. That study hasn't

44:09

been done yet.

44:10

No it hasn't. I'm not sure

44:12

it ever will be done, but it needs to be done. So

44:16

here's the question. Ozempic

44:19

with Ovi Manjaro, okay? Yes,

44:21

they cause you to eat less. They

44:24

cause you to eat less of whatever it is you're eating.

44:26

They cause you to eat less ultra-processed

44:29

food. But ultra-processed food

44:31

is a mitochondrial toxin, so you

44:33

still got the problem.

44:36

What if

44:37

you instead didn't consume

44:40

a mitochondrial toxin?

44:43

What if you consumed real food?

44:45

What if your mitochondria actually made

44:48

enough ATP? Maybe

44:51

just maybe you would reduce

44:53

your total food intake. And

44:55

in fact, we already know the answer to that.

44:58

It would.

44:59

And if you reduced your total food intake,

45:02

maybe then you would lose fat

45:05

and not muscle

45:06

because you were eating real food and

45:09

you were getting enough protein in order

45:11

to be able to do it.

45:13

And maybe you could

45:15

solve this without medicine, without $1,300

45:18

a month, and actually solve your

45:23

metabolic health issue. And

45:25

let's say the entire country

45:27

did that because they actually reduced

45:30

their total sugar consumption down

45:32

to USDA guidelines. So

45:35

instead of paying $2.1 trillion a year for these drugs, we

45:37

would save $4 trillion a

45:46

year in healthcare costs. Now,

45:50

which

45:51

is a better deal?

45:53

Well, I go for real food.

45:56

It's a better deal just on the

45:58

basis of dollars and cents. but also

46:00

on the basis of

46:03

overall health.

46:05

So as long as people think that

46:07

ultra-processed food is food,

46:11

we're not gonna solve this problem.

46:13

So that is the question, is ultra-processed

46:15

food food? Is it?

46:17

Well,

46:18

if you go to the dictionary and you look

46:20

up the word food, here's

46:23

what you find. This is the direct quote

46:25

from the dictionary. Substrate

46:27

that contributes either to growth or burning

46:29

of an organism. 100% agree,

46:33

that is a perfect definition.

46:35

Growth or burning? Okay,

46:37

does ultra-processed food contribute to burning?

46:40

I've already told you, it inhibits mitochondrial

46:42

function.

46:43

So it inhibits burning.

46:45

Does it

46:46

contribute to growth?

46:48

My colleague, Dr. Afroat-Mansonego

46:52

Ornan at Hebrew University Jerusalem

46:55

did this study, and she actually showed

46:57

that ultra-processed food inhibits

47:01

bone growth, it inhibits cortical

47:03

bone growth, it inhibits trabecular bone growth,

47:06

it inhibits organ growth. What

47:10

it does do is it hijacks

47:12

growth for cancer cells and

47:15

actually helps promote cancer formation.

47:19

So in both cases, ultra-processed

47:21

food neither

47:23

promotes growth nor burning.

47:26

In fact, it actually does the opposite. So

47:29

is ultra-processed food?

47:31

Food.

47:33

Answer?

47:35

No, if

47:35

it's not food,

47:37

it's poison.

47:39

Dr. Lustig, you mentioned that the

47:41

GLP1 agonists, the

47:45

drugs like osempic and wigovia and mongoro

47:49

can cause gastroparesis. We

47:52

would just call that stomach paralysis. That's

47:56

a good word. This is a big...

47:59

big issue

48:01

for anesthesiologists and

48:03

surgeons. Tell us why.

48:06

Well, if you have

48:09

a paralyzed stomach and

48:11

the food doesn't go down

48:14

into the next part of the intestine

48:16

called the duodenum,

48:17

then

48:19

when you try to put someone to sleep,

48:21

they will vomit and

48:24

they will aspirate into their lungs.

48:27

And there's a really good chance that they'll end

48:29

up in the ICU or possibly even death.

48:32

Not a good thing to do.

48:34

The last time we talked with you, Dr.

48:36

Lustig, you said that drug

48:39

effectiveness in general is

48:42

much lower than I think most people

48:44

realize. So we talked about statins

48:47

and the number needed to treat. We

48:50

talked about diabetes drugs.

48:52

And I remember, I'm so old, I remember

48:54

the UGDP trial

48:57

of tolebutamide. But nobody

48:59

else remembers that. Yes, nobody else remembers that.

49:01

But maybe you do. It was the UKPDS

49:04

study, the UK Prospective Diabetes study.

49:06

Right, that was the other study. And so

49:09

I just want your big picture

49:11

view of our medications

49:14

and the fact that a surprising

49:16

number of them, especially some of the really

49:19

pricey ones, are not as

49:21

effective as most people think. So

49:24

Joe, Terry, read

49:26

my lips. You

49:30

can't. We're on radio.

49:35

The medications that we have for chronic

49:38

metabolic disease are

49:41

treating the symptoms, not

49:44

the disease.

49:47

They're treating the symptoms, not

49:49

the disease. So let's

49:52

take that apart.

49:55

Statins. Statins treat LDL. The

49:58

LDL is not the disease. the LDL

50:00

as the symptom of the disease. The disease

50:03

is the metabolic dysfunction

50:05

in the liver that's driving the triglycerides.

50:08

You're treating the LDL, the

50:10

wrong target. So,

50:15

primary prevention

50:17

for heart disease with statins, you

50:20

get a total increase in longevity

50:22

of four days. Now,

50:24

secondary prevention,

50:26

so if you've already had a heart attack and you're now on

50:29

a statin to prevent a second heart attack,

50:31

there, statins are actually working because

50:34

you have actually chosen a select

50:38

group. You have

50:41

found the appropriate selection

50:44

criteria for

50:46

treating with statin.

50:47

But for primary prevention across the board,

50:49

four days. Okay, let's take

50:52

number two. Oral

50:54

hypoglycemics.

50:56

Okay, they treat blood glucose.

50:59

The glucose goes down. The high

51:02

glucose is the symptom of the problem.

51:04

It is not the problem.

51:06

What is the problem? The problem is

51:09

the insulin resistance and

51:11

the oral hypoglycemics do not treat

51:13

that.

51:14

In fact, the insulin stays high

51:16

and because that insulin is growing, your

51:19

cardiovascular tree, increasing

51:22

vascular smooth muscle proliferation and your

51:24

coronary arteries and also increasing

51:27

glandular growth, you're

51:29

at risk for heart disease and cancer anyway

51:32

and you die just the same

51:36

and that's what the UKPDS showed

51:38

is you can do intensive therapy for

51:40

diabetes and you'll still die

51:42

at the same time. Let's

51:44

take number three.

51:46

The hypertensives for blood pressure,

51:49

you are not treating the symptom,

51:53

not the cause. Yes, it

51:55

is true that blood pressure is

51:58

a problem. Okay, and it is. is

52:00

necessary to get blood pressure down. But

52:02

what is the cause of that blood pressure? It is

52:04

endothelial dysfunction. So

52:07

you can vasodilate. You can reduce

52:09

that blood pressure. But the endothelial dysfunction

52:12

is still there. And so you're still going

52:14

to end up with

52:16

chronic vascular tree disease.

52:19

So

52:19

in each case, we are

52:22

targeting the wrong pathology.

52:25

So in order to fix

52:28

these big

52:30

metabolic disease problems, we

52:32

have to fix the cause, not

52:35

the result. We

52:37

have to go upstream. We have

52:39

to find the root cause. And we are

52:41

not doing that.

52:43

The root cause of all of these

52:45

is the metabolic dysfunction associated

52:48

with metabolic syndrome, associated with insulin

52:50

resistance, associated with fatty liver disease.

52:53

And the only way to fix that, there is no medicine.

52:56

Only way to fix that is real food. Dr.

52:58

Rob Lustig, thank you so much

53:01

for talking with us on The People's Pharmacy

53:03

today.

53:04

Oh, it is my pleasure always, Joanne

53:06

Terry. You've been listening to

53:09

Dr. Robert Lustig, Professor

53:11

Emeritus of Pediatrics in the Division

53:13

of Endocrinology at the University of

53:15

California, San Francisco. Dr.

53:18

Lustig is the author of several books, including

53:20

his most recent, Metabolical,

53:23

The Lure and the Lies of Processed

53:25

Food, Nutrition, and Modern

53:28

Medicine.

53:29

This is the second of a two-part

53:31

series on recent medications prescribed

53:33

to treat obesity. Last week, we

53:36

explored this same topic with a physician

53:38

who has a different perspective on these drugs.

53:41

You can listen to the entire interview on your

53:43

preferred podcast app or at peoplespharmacy.com.

53:45

Right

53:48

now, we offer you a little sample

53:50

from last week's show. Dr.

53:52

Jamie Yard is Professor of Epidemiology

53:55

and Prevention at Wake Forest University

53:57

School of Medicine. He is also present.

54:01

of the obesity society.

54:04

Dr. Rard, I am wondering if you can

54:06

give us a quick rundown

54:08

on the pros and the cons

54:10

of these medicines because we

54:12

do understand that any medicine is going

54:14

to have some potential side effects.

54:17

Sure. So the pros,

54:20

let's start there.

54:22

I think the main benefits

54:25

that people notice are the

54:28

process of losing weight is

54:30

much easier. They feel

54:32

less consumed by food. They

54:35

feel more in control of food.

54:38

The sense of fullness,

54:40

that signal is much stronger. So a lot

54:42

of my patients would say it felt like a suggestion

54:45

before maybe to stop eating.

54:47

Now it's a very clear emphatic.

54:50

Yeah, I'm done.

54:51

So it really is a benefit

54:54

in terms of helping people reset

54:57

how they interact

54:58

with food from that perspective.

55:02

I think the other benefit that we're starting to

55:04

see in some of the newer data, newer trials,

55:06

is that this is,

55:08

for example, the top line results.

55:10

We don't have the full peer review results of the

55:13

cardiovascular outcome trial from somaglutide,

55:16

but

55:16

it showed that treating people with known

55:19

heart disease

55:20

had led to a reduction of 20% in

55:24

major adverse cardiovascular events. That's

55:26

life-saving. That's what that means. So

55:29

we're starting to see the potential for

55:32

treating obesity as being a primary way

55:35

to help improve longevity,

55:38

decrease adverse cardiovascular

55:41

outcomes. So more to

55:43

come on that area. Now on the cons,

55:46

I think the side effects of any drug

55:48

are going to be important for people to understand.

55:52

And these drugs certainly have a

55:54

well-documented side effect profile

55:57

that typically includes GI

55:59

related. So by that

56:01

I mean related to the stomach and intestines

56:03

and the gut. And so most commonly

56:06

people will experience nausea.

56:08

So I tell patients, most of my patients

56:11

will experience nausea probably eight

56:13

out of ten. It's usually mild

56:15

and transient. And as we gradually

56:17

increase the dose, people tend

56:19

to be able to manage

56:22

that nausea and their body

56:24

sort of gets accustomed to that. I think the

56:26

other main side effects are related

56:28

to diarrhea or constipation.

56:31

Some people will experience that and again

56:34

that may be dose dependent. But

56:36

there are ways to mitigate all of these types

56:38

of side effects. Some people just won't tolerate

56:41

the medication and just won't

56:43

be able to take it. And that's okay.

56:46

We have other anti-obesity medications

56:48

that can be useful and part of a treatment

56:50

plan.

56:51

I think the other big con for most

56:54

people is cost in

56:56

access to these medications. While

56:59

they can be incredibly helpful, they're

57:02

only helpful to the extent that people can get them.

57:05

That was Dr. Jamie Ard of Wake

57:07

Forest University School of Medicine. He's

57:09

President-elect of the Obesity Society.

57:11

We urge you to listen

57:14

to both experts so you and

57:16

your doctor can weigh the pros and

57:18

cons together. Lynn Siegel

57:20

produced today's show. Al Wadarski engineered.

57:23

Dave Graydon edits our interviews.

57:25

B.J. Liederman composed our theme music.

57:28

This show is a co-production of North Carolina

57:30

Public Radio, WUNC,

57:33

with The People's

57:33

Pharmacy. Today's show is

57:35

number 1,362. You

57:38

can find it online at peoplespharmacy.com.

57:41

That's where you can share your comments about today's

57:43

interview. You can always email us, radio,

57:47

at peoplespharmacy.com.

57:49

Our interviews are available through your favorite

57:51

podcast provider. You'll find the show

57:53

on our website on Monday morning.

57:55

At peoplespharmacy.com, you

57:57

can sign up for our free online

57:59

newsletter. to get the latest news about

58:01

important health stories. When you subscribe,

58:04

you also have regular access to information

58:07

about our weekly podcast, so you can

58:09

find out ahead of time what topics

58:11

we'll be covering. In Durham, North

58:13

Carolina, I'm Joe Graden. And I'm

58:16

Terri Graden.

58:16

Thank you for listening. Please join

58:18

us again next week. Thank

58:45

you for listening to the People's Pharmacy podcast.

58:48

It's an honor and a pleasure to bring

58:50

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