0:09

I had the pleasure of sitting down with Kelsey

0:12

Dexter . Now Kelsey is a practicing

0:14

consultant endocrinologist currently

0:17

working in Jackson , tennessee , usa

0:20

, and Kelsey came onto my

0:22

radar as a

0:24

doctor who is really applying

0:26

the light and circadian

0:29

practices to the

0:31

subspecialty of endocrinology

0:33

, which is very , very special

0:35

and very , very interesting . So , kelsey

0:37

, thanks for coming on the podcast .

0:39

It is my great pleasure . I've

0:41

learned so much from you and your guests over

0:44

the last few years , and I'm

0:46

honored to be here .

0:47

Great . Well , let's start with

0:49

your individual story , because

0:51

, as an endocrinologist , I

0:54

think you have such disproportionate power

0:56

in terms of helping to

0:58

educate patients . But , like

1:01

most of us , you had your own journey , so please

1:03

share that with us .

1:04

Yeah , I'd love to . So

1:06

I pretty much knew I wanted to be a

1:08

physician from a tiny age

1:11

and my path led me directly

1:13

there . I didn't take any breaks . But

1:15

my goal in getting

1:18

into medicine was always to help heal people right

1:20

. And when I

1:22

got into medical school and

1:25

sort of realized

1:27

the burden of chronic disease and

1:29

that we were being taught that

1:31

drugs effectively like we are glorified

1:34

pharmacists when we come out of medical school

1:36

in a lot of ways to manage chronic disease processes

1:38

, it was really frustrating to me . I

1:41

actually went to medical

1:43

to be a dermatologist because I was very

1:45

interested in skin and

1:47

skin cancer and I

1:50

was a person who slathered myself

1:52

in sunscreen and avoided the sun at all

1:54

costs and told other people to do that for

1:56

years and years . And I realized

1:58

when I got into medical school that I

2:01

wanted to have

2:03

a bigger impact on metabolic health and

2:05

that led me through internal medicine and

2:07

then endocrinology down

2:09

the road . Metabolism was my

2:12

main interest because we can see the root cause

2:14

of disease in a lot of

2:16

ways in this country , you know , related

2:18

to metabolism and insulin resistance

2:20

. So , interestingly

2:23

, like I've always also been

2:25

interested in integrative health . So I

2:28

back when I was in residency

2:30

there weren't any

2:32

functional programs that

2:34

you didn't have to pay for yourself

2:37

. But I did

2:39

a few rotations in at

2:42

the Osher Center at Vanderbilt

2:44

and was trying to find a pathway

2:46

into more of a bridge

2:49

to functional

2:51

plus traditional medicine . I went

2:53

to the University of Colorado to

2:56

study endocrinology and they have

2:58

a huge obesity research center there

3:00

, so that was part of my background

3:02

. I was the research fellow of my year but

3:11

bench research did not really interest me that much and I was actually working on a

3:13

project in public health looking at community gardens and how

3:16

they impact

3:18

chronic disease

3:20

parameters in people who are new gardeners , which

3:23

was pretty interesting . But let's

3:26

see as far as how

3:28

I ended up on

3:30

the quantum health path

3:32

, it was kind of a crazy

3:35

thing but , if you believe , and

3:37

kind of following golden threads and signs

3:40

, I was working every day

3:42

in this centralized paradigm

3:44

and just feeling the weight of the burden

3:46

of disease and how little impact I

3:48

was making on people's long-term vitality

3:50

and I was

3:52

having chest pain every time

3:54

I walked into the building because

3:57

of this discord . It's the malalignment right

4:00

to the mountains and I was

4:02

hiking through the

4:04

mountains and I

4:06

hear a word in my ear agrimony

4:10

which I've never heard before in

4:12

my mind's ear , and when I got

4:14

to the car and

4:16

I Googled it I realized it was a plant

4:19

. And then I do

4:21

a quick Google search on that

4:23

, this blog post pops

4:25

up describing a man

4:28

who left his corporate

4:30

job and now is sort of a professional

4:32

wild man promoting regenerative

4:35

health practices and things . I ended

4:37

up two years later doing

4:39

a program with him and

4:42

learned all about ancestral

4:45

diets and earth

4:47

connection and that

4:50

was one step toward me

4:52

realizing how much impact

4:54

our disconnection from nature

4:56

has on our

4:59

vitality . So

5:01

since then I've

5:04

done some herbalism training programs

5:06

. I am

5:08

a Reiki attuned practitioner . I

5:10

have a pretty big tool belt

5:12

aside from my Western

5:15

endocrinology training , but

5:17

in the day to day I interact with a lot of

5:19

patients in a centralized paradigm

5:22

, patients

5:28

in a centralized paradigm and I try to figure out how I can

5:30

improve the trajectory of everyone's health . And usually that relates

5:32

back to foundational

5:34

health practices and quantum practices . And

5:37

it's so shocking to me because we're in this

5:39

world where we talk about these things all the time , right

5:42

that it seems common

5:44

sense that being in sunshine

5:46

is good for you , or

5:48

optimizing your sleep , or being

5:50

in contact with the earth , grounding

5:53

and gathering electrons and

5:55

the average person just

5:58

doesn't get it , because

6:00

when you see everyone around you

6:02

living the same way

6:04

, you never question that what

6:06

you're doing is hurting you

6:08

. And I tell patients

6:11

all the time that modern

6:13

life sucks our vitality

6:16

right in a lot of ways and

6:19

if you are sick you

6:21

have to focus on foundational health practices

6:23

to begin to heal , and that has

6:25

nothing to do with Western medicine . So

6:28

yeah , I have

6:30

been . I've

6:35

been sort of pushing

6:37

light as

6:40

light as therapy for

6:43

a couple of years now in

6:45

my patients . And the thing to note

6:47

is people don't come to me to

6:50

talk about quantum and foundational

6:52

health practices . They come to me because they're

6:54

sick and they're on medicine and

6:56

they want medicine management primarily

6:59

. So it's

7:01

a really interesting dynamic when

7:04

I try to fit

7:06

this into every office visit

7:09

and do educating , and

7:11

many patients don't want that , you

7:14

know . So it

7:16

can be a little bit tough , yeah

7:25

, but I see patients all the time that think they have hormone problems , Right , and they want hormone

7:27

testing , and that . That can range from

7:30

. You know , I'm tired all the time . I

7:32

can't lose weight no

7:34

matter what I do , or have

7:38

irregular periods or , you know , transition

7:40

through menopause etc . And I can do

7:42

labs on that person

7:45

and know that they're all going to show up as normal

7:47

, Right . So there

7:50

is relative hormone

7:52

dysfunction just

7:54

in the average American because

7:57

of metabolic issues , and we know that that

8:00

93 percent of Americans

8:02

have metabolic dysfunction , meaning , you

8:04

know , 93%

8:09

of Americans have metabolic dysfunction , meaning we can't efficiently switch between fuel

8:11

sources . We're not fat adapted relative mitochondrial dysfunction

8:14

and that plays a part in pretty much

8:16

every disease process

8:18

that affects Americans today . So

8:21

I , you know , I

8:23

really try

8:25

to think about how what

8:27

kind of actionable steps we can , we

8:30

can engage to move the needle

8:33

slowly but surely in patients that

8:35

don't seem overwhelming . One of the

8:37

biggest battles I have is liquid sugar

8:40

, of course , because you know southern

8:42

sweet tea and soda

8:44

consumption can be staggering . So

8:46

that's one of my general first rules

8:49

is every patient that I see I ask

8:51

them to stop all liquid sugar . And

8:58

we talk about time , restricted eating

9:00

, circadian meal timing , and then we talk about life and

9:09

those are the three first steps

9:11

to getting someone on a healthier path that I generally kind of dip into

9:13

. But I kind of see dysregulated cortisol too and the

9:15

average American living with this

9:17

sympathetic activation that's chronic

9:20

, as a big problem when

9:22

it comes to trying to

9:24

improve metabolism

9:26

, since cortisol makes us insulin resistant

9:28

too right , and we

9:31

need cortisol to

9:33

live . We need it for

9:35

, you know , facing

9:37

stressful events , but

9:40

when it predominates because

9:43

we don't sleep well , we're exposed

9:45

to too much blue light and

9:47

don't have good coping mechanisms , etc . You

9:50

have this imbalance of cortisol in

9:52

relation to melatonin . So too much activation

9:55

, not enough rest and repair . So

9:58

we talk about that

10:00

a lot in my office as well .

10:03

Yeah , yeah , fantastic

10:05

, and the setting

10:07

or the role that we're practicing in I mean it plays

10:09

a big influence on

10:11

how we eventually

10:14

change or adopt different

10:16

practices . And it sounds like working

10:18

in where you are in Tennessee

10:20

and you mentioned before we started that

10:22

this is the land of the 400-pound

10:25

patient and

10:27

it sounded like you saw

10:30

the worst of the worst , so to speak , and

10:32

that was one of the prompts

10:35

to change

10:37

your approach . And it sounds what

10:39

you're recommending in terms of those foundational

10:42

health practices of time-restricted

10:44

eating , light regulation

10:46

and eliminating liquid

10:49

sugar and refined foods . I mean

10:51

, that's exactly what I teach in my circadian

10:53

reset course and I think that just is

10:55

so , so , so important . But

10:57

describe , paint a picture for us , for the listeners

11:00

, about the environment

11:02

and about the people in

11:04

your area , in your local area . What

11:07

are the factors ? Obviously , we've mentioned the liquid

11:09

sugar , but why and how

11:11

have they gotten to be

11:13

so metabolically sick

11:15

?

11:17

Yeah , I really think that

11:19

primarily this has to do with

11:22

diet culture primarily , and

11:25

I really believe it's dietary

11:27

fructose , because it's just

11:29

so much higher in

11:32

our population whenever you're drinking sugar

11:34

, it just is . So one

11:37

of the issues is when a

11:39

patient's diagnosed with type

11:41

2 diabetes , ok , the manifestations of

11:43

that's the worst manifestation

11:46

of insulin resistance , right ? So

11:48

in the past , our

11:50

medicine options , our options of treatment

11:53

are we decrease

11:55

the glucose load that's going into the body

11:57

so that , you know , the pancreas

12:00

can take care of the amount of glucose that's

12:02

coming in . You can

12:04

decrease the excretion of

12:06

glucose through certain pathways

12:08

, using medications

12:10

, and then you

12:13

can improve insulin sensitivity with

12:16

building muscle by

12:19

taking , you know , metformin or a GLP-1

12:21

agonist , and it decreases the burden

12:24

on the pancreas and

12:26

then you can give insulin and overcome

12:28

the resistance , right . So a lot

12:30

of you know I work in this medicine

12:33

paradigm and those are tools

12:36

in my tool belt and so I

12:38

have been using all of these medicines

12:40

to try to treat type 2

12:42

diabetes for my entire career . And

12:45

older physicians not just

12:48

older , but like less , less um

12:50

the word . So these

12:52

primary care doctors that have been working in

12:54

my area , in these rural areas , um

12:57

, aren't as familiar with new treatment

12:59

guidelines and new medications

13:02

that are not insulin . So the

13:04

worst manifestation of this that I see

13:06

the patient that's 500 pounds typically

13:08

has been diagnosed

13:10

with diabetes put on metformin

13:12

. It was not sufficient . Nobody ever

13:15

talked to that patient about diet

13:18

, exercise , restricted windows

13:20

, anything . And then the next step

13:22

was insulin , right . So when you give someone

13:25

who is already insulin resistant

13:27

more insulin , well

13:29

, insulin is a storage hormone . It's an energy storage hormone

13:32

and it prevents

13:34

the body from being able to break down fat

13:36

stores for fuel . So you

13:38

see weight trend up over

13:40

time in nearly every

13:43

insulin treated patient , trend

13:46

up over time in nearly every insulin treated patient and that makes the patient more

13:48

resistant to insulin . So as the dose of insulin goes up

13:50

and the weight trends up , metabolic

13:53

dysfunction gets worse and worse and

13:55

worse . So whenever

13:57

I am working with patients with type 2

13:59

diabetes , my main goal

14:01

is to use the smallest amount of

14:03

medicine possible . In the

14:05

end that's where we're headed . So sometimes

14:09

I have to use medicine as a bridge

14:11

to get there also , which

14:13

I have seen

14:15

in some individuals to be life-changing

14:17

and as an example , you know

14:20

, if I have a patient who

14:22

is morbidly obese and

14:24

on hundreds of units of insulin a day

14:27

, that patient will not lose weight

14:29

with dietary intervention

14:31

. I am a big fan of metabolic

14:34

resets from a diet standpoint

14:36

, but if a

14:39

person who's taking all this

14:41

exogenous insulin doesn't cut

14:43

carbs down to nothing , they're

14:45

still going to stimulate

14:48

their body's need for insulin

14:50

and it just metabolic dysfunction

14:52

never improves . So

14:54

the average person

14:56

that I interact with is

14:59

not going to do that anyway , even if I tell them

15:01

that this is a path to no medicine . I have to

15:03

meet . Meet an individual

15:05

where they are and what

15:08

is your best effort ? How much can

15:10

you do from a behavior standpoint ? Can I make

15:12

up the difference with

15:14

medication to help you achieve

15:17

goals and help us get your blood sugar down

15:19

, which can help , you know you

15:21

, avoid long term complications ? Yeah

15:24

, so

15:26

yeah , that's kind of my general strategy

15:29

yeah , do ?

15:30

do they ? How ? How ? I mean

15:32

? And I've had this experience too , which is raising

15:35

lifestyle changes with people who

15:37

perhaps didn't come to you for

15:39

specific lifestyle advice , and my

15:41

experience has been that some people will be

15:43

interested , some people won't be interested . Often

15:45

you can't tell who was interested in an

15:47

offhand comment that made

15:50

you know at the end of the consult might be

15:52

enough to stimulate a massive change

15:54

on someone and then spending 20

15:56

minutes with another person and they all they sound

15:58

bought in and they're smiling and nodding , yet they make

16:00

no changes . So what's

16:02

the receptiveness of these messages

16:05

around light , around food

16:07

and obviously you're encouraging to eat

16:09

a lot of meat . If you're

16:11

encouraging basically zero-carb

16:13

or ketogenic diet , so

16:16

tell me how that's received by your patients .

16:18

Most of my patients , when they've had any

16:20

doctor talk to them about diet , have

16:23

heard the common

16:25

narrative watch , don't

16:27

eat red meat , don't eat eggs , don't eat butter

16:29

. And so whenever they say

16:31

, oh , I know I want you , you're going to want

16:33

me to eat healthy , so I'm going to eat more salads

16:35

, right , that's what they all say . I've been

16:37

eating lots of salads , dr Dexter . Well

16:40

, so I have to do a little bit

16:42

of education around , like what's

16:44

nutrient dense and what's appropriate , and

16:46

how our body handles nutrients , et cetera , and

16:49

I think the average person is

16:51

really surprised that

16:54

I recommend that they

16:56

start eating more red meat , eggs and butter , right

16:59

, and I

17:01

fight against the recommendations

17:04

of some of their other providers , because nearly all of

17:06

my patients you know they who have diabetes

17:08

have a cardiologist too who's

17:10

giving them a completely different story

17:13

. I would say that

17:15

most people I interact with end

17:18

up commenting , even if they didn't come

17:20

for any kind of behavioral

17:23

recommendations , that they learned something

17:26

. They always learn something when they come to see me

17:28

. And , yeah , I have seen many

17:31

, many patients make great

17:33

shifts in their overall health over

17:35

the last 10 years of

17:38

working in this field by changing

17:40

their diets . And

17:42

then occasionally I have

17:45

a patient I've seen for five years and I give

17:47

them the same advice every time they come in and

17:50

then one

17:52

day they decide to take it

17:54

and it took me five

17:56

years to get them there and I'm . But

17:59

I walk that road with a

18:01

lot of folks and this

18:03

, this doctor patient relationship

18:06

. We're a team and I

18:08

just keep trying and meeting people where they are

18:11

and doing

18:13

the best I can to let them know how much power

18:15

they have in their own health .

18:17

Yeah , yeah , that's fantastic

18:19

and it is . It's a , it's a partnership

18:21

, and some people might not just have

18:23

the bandwidth or

18:26

space in their life to make radical changes

18:29

, but , yes , it's a progressive

18:31

thing that we can help with over time . Talk

18:34

to how you think about the relative contribution

18:37

of light and food

18:39

to metabolic dysfunction , because

18:42

I liked how you mentioned

18:44

that 93% of Americans

18:46

have one marker of metabolic dysfunction

18:48

and that is something that I talk

18:51

about as well which is we shouldn't

18:53

be waiting for a frank diagnosis

18:55

of type 2 diabetes , but we actually shouldn't

18:57

be waiting for a frank diagnosis of metabolic

19:00

syndrome , which is obviously the five

19:02

markers waist circumference

19:04

, triglycerides , hcl

19:07

, fasting , blood glucose

19:09

and blood pressure . We shouldn't

19:11

be waiting for , um , someone to

19:13

fulfill one of those criteria

19:15

, let alone , um , you know

19:17

, getting all the way to metabolic syndrome , let alone getting

19:19

all the way to to type 2 diabetes

19:21

. So talk about this relative

19:24

metabolic mitochondrial dysfunction

19:26

and and how you think about , maybe

19:28

, what is contributing . Obviously

19:30

, we talked about the liquid sugar , but kind

19:33

of beyond that .

19:33

It's definitely a multifactorial issue

19:36

, right ? What I think is interesting

19:39

in the grand scope of things is

19:41

our ancestors were

19:43

outside all the time , right

19:45

, so the light environment wasn't an issue , but they

19:48

were also looking

19:50

for food to support survival , so

19:52

more likely to be hungry than

19:54

fed , and the choice of

19:56

food was limited to what was available

19:59

or able to be killed or caught or gathered

20:01

. And now we live in

20:03

an environment where nutritional energy

20:05

is abundant and we

20:08

can eat essentially any

20:10

food that we can think of . I

20:13

mean , maybe there's

20:15

some nuance with that in regard to , like

20:18

, food deserts and transportation

20:20

and accessibility in certain populations

20:22

, and we can talk about that too . But now

20:25

we are trying to figure out how we

20:27

can limit the excess

20:30

, right . What do I think about

20:32

? Whether diet or light

20:34

plays a bigger part , what relative part

20:36

? I do know that the rate

20:38

of obesity and metabolic

20:41

dysfunction is progressively getting worse and

20:43

worse , and it's really skyrocketed in

20:45

the last 15 years . And

20:47

I think about when I was

20:49

young and I grew up in this area

20:51

, to you know , the rate of childhood obesity

20:54

and the incidence of type

20:56

2 diabetes in children was very

20:58

low and we still

21:01

had sweet tea and soda and

21:03

Pop-Tarts and the diet was

21:05

effectively the same . Some

21:08

would argue that the

21:14

same . Some would argue that over the years , high fructose corn syrup has sort of infiltrated

21:16

all processed foods to a greater degree and there

21:18

are people that think about

21:20

how they can make this particular

21:22

processed food more addictive by

21:24

changing the sugar and salt content . So a lot

21:27

of that goes on in the background and that kind

21:29

of gets worse when it comes

21:31

to processed food , adulteration

21:33

of fructose . But what really

21:35

shifted about 15 years ago

21:37

was our light environment and you

21:40

know we've moved from incandescent light

21:42

bulbs , which emit red

21:45

and infrared light , to LED lights

21:47

that are mostly

21:49

blue light emitting . In our homes

21:52

Our screens have all shifted to LED

21:54

, which is

21:56

blue light , and then every person

21:58

has a device in their

22:00

face all day long shining

22:03

blue light into their eyes . And

22:05

you know I go

22:08

out and see kids all the time

22:10

on tablets in restaurants while

22:12

they're eating . I have

22:14

I think Dr Cruz posted a

22:17

study looking at bumblebees and

22:19

feeding bees under

22:21

red light versus blue light and the prandial

22:24

glucose excursion being about 50 percent higher

22:26

, percent

22:31

higher . And you know , we know the mechanism

22:34

by which blue light increases blood sugar and

22:36

increases insulin by CLIP right . So

22:38

I know that this is a

22:40

big part of what's going on in

22:42

chronic disease . And also

22:45

, you know , hormones

22:47

, all hormones , chemical

22:49

messengers in the body have a

22:52

circadian drive . They all do . Every

22:54

cell pretty much does Right . And

22:56

whenever we

22:58

alter our light environment and

23:00

we're crushing our melatonin release

23:03

when we should be resting

23:05

, sleep gets disrupted

23:07

and that dysregulates

23:10

all hormones downstream . So

23:14

cortisol in particular has

23:16

a it's very circadian

23:18

driven with this diurnal release and

23:22

it's very easy to dysregulate

23:24

cortisol . And

23:26

dysregulating sleep on its own

23:29

will dysregulate cortisol , which

23:31

increases insulin resistance

23:34

. And then whenever you add

23:36

blue light's independent mechanism

23:39

to increase insulin by clip

23:41

, it's just a tangled web

23:43

overall . Yeah

23:46

, I really think that

23:48

your food diet and your light

23:50

diet are probably equally important .

23:53

Yeah , I love that , kelsey , because you

23:56

are as I said this

23:58

before , you're probably the world's first

24:00

decentralized endocrinologist who is actively

24:03

talking about the effect of light on

24:05

metabolism and metabolic disease . And

24:09

, yeah , no one as far as I've talked

24:11

about in terms of endocrinologists are really acknowledging

24:13

this . And we're really two

24:16

steps removed from the standard of care

24:18

here because and obviously the

24:20

standard of care is not even advising

24:22

patients of , or earnestly

24:25

of , these dietary changes like

24:27

getting rid of processed foods . This

24:29

base layer is simply , you know , here's

24:31

the insulin prescription , here's your

24:33

GLP-1 agonist prescription , here's

24:36

your metformin prescription . You know , go off , do

24:38

your thing . The next level is the metabolic-focused

24:41

doctors , the low-carb carnivore

24:43

practitioners , who are doing fantastic work

24:45

and looking at this at a

24:47

food-centric point of view , again having

24:50

fantastic results , still helping

24:52

to reverse chronic disease , get

24:54

people off insulin , reverse their

24:56

diabetes . But really I

24:58

don't think they're getting the whole picture here and the

25:00

metabolic story , as you've just alluded to

25:02

, is so much

25:05

a circadian story because all those

25:07

metabolic hormones and leptin

25:10

, even insulin itself , insulin

25:12

sensitivity , has a diurnal circadian

25:14

influenced secretion

25:17

and effect . The

25:19

fact is that

25:21

we really , in my opinion

25:23

and your opinion too , we need to really

25:26

encourage and recognize

25:28

the role of light in affecting glucose

25:30

sensitivity , blood glucose levels , insulin

25:32

sensitivity , and all this and

25:34

the paper that I think you might be . There was another

25:36

paper that was actually

25:38

published in January and they used

25:41

red light and they had a

25:43

. I'll quickly read out the results

25:45

. They found that 15-minute

25:49

exposure to 670 nanometer

25:51

light so that's in the visible red range reduced

25:54

the degree of blood glucose elevation following

25:56

glucose intake by 27.7%

25:59

, integrated over two hours after

26:01

the glucose challenge , and maximum glucose

26:03

spiking was reduced by seven . So what

26:06

they said is that photobiomodulation

26:08

with 670 nanometer light

26:11

can be used to reduce blood glucose spikes following

26:13

meals . So that is the evidence

26:16

. I think that provides so much great

26:18

evidence that it's the light environment that is essentially

26:20

modulating the effect of food

26:24

on our blood glucose . Maybe

26:26

talk now a bit about the

26:29

kind of approach that you have

26:31

to someone with metabolic syndrome

26:34

and insulin resistance , particularly

26:36

with regard to leptin

26:38

, because a lot of people have talked about

26:41

leptin and how

26:44

that can make . Basically , leptin resistance

26:46

can influence our ability to lose weight

26:48

. So do you measure leptin in

26:50

your practice or do you talk about leptin

26:52

to your patients and how do you think about leptin

26:55

in this picture ?

26:56

Well , the vast majority of people I see

26:58

, I know , are leptin resistant right , because

27:00

leptin resistant pretty much precedes insulin

27:03

resistance or accompanies it at

27:05

the very least . And I

27:09

talk to a lot of patients about leptin

27:11

, my lab actually has no

27:13

option to measure leptin , which

27:15

is insane to me . So

27:19

I am not accustomed to actually

27:21

looking at objective levels . I

27:24

just make an assumption that dysregulation

27:26

is an issue , and

27:28

usually I'm talking to women

27:31

who say my periods

27:33

are irregular , I can't lose

27:35

weight , I'm barely eating anything , I'm

27:38

tired , help me . And I think leptin and

27:40

regulating leptin really has so

27:43

much to do with circadian

27:46

health , less to do , maybe

27:48

, with the diet , more to do with the light , or

27:50

you can't have one without the other to get

27:53

it regulated . So I encourage

27:55

every patient who comes in with that

27:58

sort of constellation of complaints to

28:00

work on their light

28:02

first . This is what we always talk about

28:04

, I think , actually , when patients

28:06

find working on their light environment

28:08

to be less intimidating than working on their food

28:10

, and so I really like

28:12

to get the light environment

28:15

right before I try to talk a patient

28:17

into a very low carb

28:19

, ketogenic diet , and

28:22

both at the same time can be a little bit overwhelming , but

28:24

in the average patient

28:26

who's working on leptin sensitivity with

28:28

me . I encourage them to

28:31

see the sunrise with naked eyes

28:33

every day and start that circadian

28:36

signal to improve

28:39

their melatonin production

28:41

and secretion effectively

28:46

. Keto breakfast within

28:48

an hour of waking up

28:50

to send that meal

28:52

timing , safety , satiety

28:54

signal to the brain . Blocking

28:57

artificial light at night not just

28:59

blue light , but trying to . I talk

29:01

to every patient about strategies to decrease

29:04

their blue light toxicity and

29:06

that's sort of the first bridge

29:08

overall that we cross . I really

29:10

believe . As far as low

29:13

carb diets , you know the average

29:15

person that I deal with with pretty

29:17

profound insulin resistance . If I ask

29:20

that person to go straight to carnivore

29:22

, the body's not fat adapted right

29:24

. So as glucose in

29:27

the bloodstream starts to fall with

29:29

that low-carb diet , the

29:31

brain is going to get a signal that

29:34

the patient needs to eat carbs . And

29:37

because that pathway

29:39

to flip fuel

29:41

sources has not really been triggered

29:43

in maybe decades , the

29:46

blood sugar tends to get pretty low in

29:48

patients who are on low carb diets . And

29:51

whenever glycogen stores

29:53

are released and

29:56

glycogen is extended and we get to the point

29:58

where the body's asking

30:00

for fuel , it's not really efficient at

30:02

using ketones for fuel and that person

30:05

will feel awful weak

30:07

muscles , low sugar , shaking

30:09

, sweating and will give

30:12

up after , you know , a few days

30:14

. So I

30:16

do think that diets

30:18

have to be really individualized with patients

30:20

. And one thing that bothers me a

30:22

lot , just sort of in the health

30:24

community is all

30:26

this nutritional dogma right

30:29

. So carnivores and plant-based

30:31

folks fight out all the time

30:33

about which is better and what's the

30:35

optimal way to eat , and different

30:37

bodies need different balances

30:40

of macronutrients depending

30:43

on health , disease and goals

30:45

. But in general for

30:48

metabolic dysfunction , I really

30:50

don't believe anything works better than

30:52

a low carb diet for a metabolic

30:54

reset . So

30:56

I tend to take patients meal by meal

30:58

into , like slowly into

31:00

ketosis after we work on their

31:02

lights . So we

31:05

start with the high

31:08

protein , high fat breakfast

31:10

and leptin reset and we

31:12

might do that for a couple weeks and be really consistent

31:15

with that behavior . And then we

31:17

start working on lunch and

31:20

making cutting out the carbs at lunch

31:22

and then eventually less

31:24

than 30 grams of carb a day is what I recommend

31:26

to sort of as

31:29

a dietary strategy to work on reprogramming

31:32

metabolism , and

31:35

I don't expect patients

31:37

to eat very low

31:39

carb long term and I don't know that

31:41

that's good for every person . I think our

31:43

body has to be adept

31:46

at using glucose

31:48

for fuel and using

31:50

ketones for fuel . You know , when you eat a

31:52

long-term ketogenic diet , the metabolism

31:55

accommodates that and you can get relative insulin

31:58

resistance and

32:00

when you have carbs , have really high glucose

32:02

excursions if you've been in long-term ketosis

32:05

. So I do really like the idea of

32:07

long-term cycling of

32:10

carbs .

32:11

Yeah , yeah , that's something

32:13

that I've thought myself , which is it

32:16

is seasonally appropriate

32:18

to be cycling in

32:20

and out of a fat-burning metabolism

32:23

. And you know , unless we're living

32:25

in the Arctic Circle where there's only

32:27

seal , blubber and caribou

32:29

available for food , then it

32:32

doesn't make really much sense to be

32:34

in that burning mode the

32:37

whole year round . So that

32:39

is a nuance that I

32:42

like to make , and especially that

32:44

allowance is permitted when people have healed

32:46

their metabolic dysfunction and

32:48

when they've got all those

32:50

markers under control . In

32:53

terms of , I also really

32:55

like your approach of gradually introducing

32:58

or reducing the carb amount

33:00

and I imagine for the patients that

33:02

you work with , that is definitely

33:04

necessary . Tell us about helping

33:06

people come off these heroic doses

33:09

of insulin , and

33:11

my approach too , which

33:13

I think maybe Dr Bernstein kind

33:15

of pioneered in his treatment

33:17

or recommendation for type 1 diabetics , is trying

33:20

to be using the minimum amount of insulin necessary

33:22

. Obviously they don't have working

33:25

pancreatic islet cells , but in

33:28

type 2 diabetics , who are on massive

33:30

amounts of insulin , how do you think

33:32

about getting them off what is

33:34

essentially quite a dangerous

33:37

drug and medication ?

33:38

Oh , yeah , well , I talk

33:41

to every patient about the fact

33:43

that the more insulin it takes to

33:45

control your blood sugar , the higher your risk of chronic

33:47

disease , right ? So we know

33:49

it's not the blood sugar per se , it's

33:52

the insulin level , insulin resistance

33:54

that's associated with the

33:56

diseases that kill Americans

33:58

type 2 diabetes and complications , cardiovascular

34:01

disease and complications , alzheimer's and cancer

34:03

. And so when I lay that

34:05

out to a patient and say hey , you're

34:08

on , you know , 200

34:10

units of insulin a day , I need

34:12

to get this down to the lowest amount possible

34:14

. And can you help me ? I

34:17

can motivate some pretty significant

34:19

behavioral shifts . But

34:21

, like I alluded to before

34:23

, I do often use insulin

34:25

sensitizing drugs , in this

34:27

case to decrease

34:29

the burden of insulin , because if I can get

34:31

the insulin level down , the patient can start

34:33

to lose weight independent

34:36

of the effect the weight loss effect

34:38

of a GLP-1 agonist

34:40

like Ozempic or Manjaro , right ? So

34:42

if a patient starts to lose weight

34:44

and insulin sensitivity improves , I can

34:46

just progressively drop the

34:49

insulin and

34:57

the goal in the end , as long as a pancreas is still making some insulin enough

34:59

to manage glucose levels at baseline , then we try to come off of all insulin

35:01

or medicines that increase insulin , because

35:04

that provides the best long-term health benefit

35:06

for that patient and that's the way you

35:08

reverse metabolic disease right

35:11

.

35:11

Love it .

35:13

I have had , and in regard to type

35:15

1 , I think , in

35:17

the past . Patients who have type 1

35:19

diabetes don't

35:21

make insulin from

35:24

their beta cells so we have to have insulin

35:26

to survive and insulin

35:28

has gone through many iterations and

35:31

evolution in the last few years and

35:33

it's been a really exciting time to

35:36

be in endocrinology because

35:38

our options for treating type 1

35:40

diabetes have broadened

35:42

so much . In the past if

35:44

a person was insulin deficient

35:51

they would be on a long-acting insulin

35:54

for basal coverage that

35:56

works either six

35:59

hours , eight hours , ten hours , and

36:01

then over the years these

36:03

long-acting insulins have improved so

36:05

that you give one injection and you get

36:07

a 24-hour coverage of needs

36:09

. But what we do on injection

36:11

therapy is we try to estimate

36:13

the best median

36:17

need of insulin right

36:19

. So when you have a fixed dose of

36:21

basal insulin in a patient

36:23

who is dynamically using glucose

36:25

, there are going to be days

36:28

when that dose is perfect

36:30

, optimal days when they've been more

36:33

active , eaten less , different

36:36

cycle time for women , et cetera , when

36:38

it's going to be a little bit too much . And

36:40

then there are going to be days when they're stressed

36:42

, sick , not moving

36:44

whatever , where that basal need is going to be

36:47

higher . So in general

36:49

there's been a tendency to

36:52

cover mealtime

36:55

insulin needs with

36:57

a basal insulin in the background . Even

36:59

in patients who have type 1

37:01

, doctors tend to

37:03

slightly overshoot the

37:06

basal dose requirement to try to prevent

37:08

the blood sugar from going too high

37:10

when the patient eats , and that causes

37:13

the patient to have to eat to maintain

37:16

their maintain

37:18

normal blood sugars . And the higher

37:21

the insulin dose in the background , the

37:23

more likely a person is to gain

37:26

weight , since insulin inhibits

37:28

lipogenesis , lipolysis

37:32

.

37:33

Lipolysis .

37:34

Yeah , lipolysis , lipolysis , lipolysis

37:37

, yeah , lipolysis . And

37:43

so in many patients with type 1 diabetes , when they're started on insulin therapy , they immediately

37:45

start to gain weight , and the more weight that's gained , the

37:48

more insulin resistance . And they

37:50

don't have the option really to

37:52

suppress insulin , which

37:55

is what's required to burn fat stores

37:57

right , because

38:04

they have this constant injected dose . That's the same

38:06

all the time . Patients with

38:08

type 1 are also taught to be scared of ketosis because we have a life-threatening complication

38:11

of DKA . So patients try

38:13

really hard to avoid ketones in general

38:15

whenever they have type 1 diabetes

38:17

. And when you

38:19

eat to support your insulin dose

38:21

, you're consistently gaining weight and you're

38:24

never in ketosis that creates

38:26

metabolic disease . So

38:29

I'm really , really excited

38:31

about the landscape

38:34

of type 1 diabetes treatment

38:37

now because you know , as

38:39

far as insulin delivery , our gold standard

38:41

is hybrid closed-loop insulin

38:43

pumps and whenever you

38:45

have a glucose monitor that

38:48

can communicate with

38:50

an insulin delivery device , you

38:53

can program that

38:55

system to turn off whenever

38:58

glucose levels fall . So for the first

39:00

time , patients who

39:02

have type 1 diabetes have

39:05

this option to only get insulin

39:07

when they need it , right , and that

39:09

opens up this pathway

39:11

to improve metabolic health

39:13

dramatically in that population . Improve

39:16

metabolic health dramatically in that population and you know I've

39:18

got I really I

39:26

argue with insurance companies about this all the time

39:28

but I really believe that type one and type two diabetes coexist . Frequently

39:30

I have patients who have known

39:33

pancreatic islet destruction

39:35

. Our insulin deficient have gained

39:38

, you know , 150 , 200

39:40

pounds over the years and

39:42

I know that if their pancreas were functional

39:45

it wouldn't be making 200

39:48

units of insulin a day . It

39:50

wouldn't be able to . So they would

39:52

effectively have type 2 diabetes if

39:54

they had a functional pancreas based on their insulin

39:56

requirement . And I

40:01

have used medications

40:04

like GLP-1

40:07

agonists , like Ozempic and Majaro

40:09

, in patients sort of off-label

40:11

, who have type 1 diabetes , to decrease

40:14

the insulin burden and

40:16

I've seen incredible

40:19

improvements in metabolic health over

40:21

time , which has been really rewarding

40:23

. So you know , I've got

40:26

a patient I can think of offhand who was

40:28

using about 250 units of insulin a day

40:30

to control his blood sugar and now

40:32

he's down to 20

40:35

units a day and he's lost 100

40:38

pounds . And then

40:40

, once we restore metabolic

40:42

health , I try to wean patients off of the

40:44

GLP-1s and

40:47

usually if we have been working on

40:50

light environment diet

40:52

, changing behavior and they're

40:55

educated , they know like the

40:57

more insulin they need , the faster

41:00

like this metabolic disease can

41:02

come back . You know they tend to do really

41:04

really well . So

41:07

I've had many

41:09

patients with type 1 , you

41:11

know that are incredibly

41:14

insulin resistant who have benefited from all

41:16

these practices as well . But we try really

41:19

hard . Every

41:21

patient that's taking insulin I want them to take

41:23

the least amount possible

41:25

, yeah .

41:27

Yeah , I love it , kelsey . There's

41:29

so much gold there for what you

41:31

just said , for family doctors

41:33

and for other endocrinologists , and I want to summarize

41:36

a little bit of it , and specifically

41:38

around the nuance of these GLP-1

41:41

agonist drugs like Ozempic , and

41:47

what I think is that it's a completely different kettle of fish for people who are sick and the ones

41:49

that we're talking about on a clinical point of view is not

41:51

the same as the person who's trying to

41:53

lose five kilos has nothing

41:56

wrong with them and is using his to

41:58

lose weight . That's completely

42:00

a different story , and what I think you're really showing

42:03

us is that these GLP-1 agonists

42:05

can be used very judiciously to

42:07

help people regain

42:09

insulin sensitivity and therefore bootstrap

42:12

this whole process of resolving

42:14

their metabolic disease and improving their

42:16

metabolic disease , because it allows us to

42:19

get that total exogenous

42:21

insulin dose down quicker . And

42:24

, as you said , for people who

42:26

aren't aware , the larger the insulin dose

42:29

, the more risk of a hypoglycemic event

42:31

, the more risk of a hypoglycemic

42:33

coma and something very , very bad

42:35

. So I really like that nuance

42:37

there and that's the reason why anyone who is taking

42:39

medications really needs to see a

42:42

metabolically trained doctor , because

42:44

there's all these nuances around drug

42:46

weaning that we have to go

42:48

through to make sure that this

42:50

whole process can happen safely . So

42:52

that's a great point . The

42:54

other point is that loop of carbohydrate

42:57

consumption in those with type 1 diabetes . The other point is that loop of carbohydrate consumption in those with type

42:59

1 diabetes and this is something that you

43:01

see not only in type 1

43:03

diabetics , who have remember

43:05

for the listener an autoimmune destruction

43:07

of their body's ability to make insulin

43:09

it's not

43:12

only them , but it's also gestational diabetics

43:14

. So late in pregnancy we see people

43:16

become quite insulin resistant and women

43:19

often get prescribed insulin to

43:21

again maintain their blood

43:23

glucose lower . But

43:26

what we commonly see is that people get put on

43:28

a high dose

43:30

of carbs because they're on insulin and there's

43:32

this drug loop of

43:34

glucose and insulin . They're both drugs

43:36

. People are taking a high insulin dose

43:38

because they're eating carbs

43:40

and therefore it's a vicious

43:43

cycle that escalates upwards and upwards

43:46

and from thinking from first principles . I

43:48

mean , I'm not an endocrinologist , but it's obvious

43:50

to me that that is not

43:52

a winning strategy if we're trying to optimize

43:55

people's health in the long term and

43:57

maintain the insulin sensitivity , reduce

43:59

their total lifetime . Insulin

44:01

signaling in the body .

44:04

Yeah , I think this is sort of the

44:06

old diabetes

44:08

education framework , right ? If you have a

44:11

fixed dose of insulin that you're giving someone

44:13

multiple times a day , you need a

44:15

fixed amount of carb to be

44:17

eaten with that insulin

44:20

, or else you have low blood sugar

44:22

. So I think that's kind of where it came from right

44:24

, this recommendation to eat what I

44:27

think it's like 50 grams of carb per

44:29

meal , which is insane . That's what

44:31

the average patient who's had diabetes education

44:33

comes in and tells me . I said , well , I'm eating

44:36

50 grams of carb a meal like I'm supposed

44:38

to , but anyway , we

44:40

just have to learn better and do better

44:42

.

44:42

Yeah , it's my hobby horse because I think

44:45

there's so much harm being done by these high-carb

44:47

dietary recommendations for type 1 diabetics and

44:49

gestational diabetics

44:51

. If they're eating a meat-based

44:55

diet , a lot less carbohydrates

44:57

, then the whole body's demand

45:00

for exogenous insulin goes down and

45:02

the whole process is much more

45:05

. The body is healthier . I

45:08

want to talk about a topic that you just

45:10

alluded to , which is a

45:12

disease called latent onset

45:14

diabetes of adulthood , which is essentially

45:16

this coexistence of both

45:19

type 1 and type 2 diabetes

45:21

, and it is something that we

45:23

can see sometimes in someone

45:26

who's perhaps gained weight , but

45:28

they're essentially not only insulin

45:30

resistant but they become insulin

45:33

deficient too . So talk about

45:35

that and why it's a very important

45:37

diagnosis for any doctors listening to

45:39

consider when they have someone

45:41

who is perhaps

45:44

making a new diagnosis of diabetes .

45:46

Yeah , so you know , in the past

45:48

we called type one diabetes juvenile

45:50

diabetes because it tends to occur

45:52

in kids , and

45:55

there's a known autoimmune

45:57

pathway that involves the

45:59

destruction of beta cells that produce insulin

46:02

. That result in an insulin deficient

46:04

state there , and then most

46:06

often patients with type 2 diabetes

46:08

get there through an insulin resistance pathway

46:11

, so the pancreas

46:13

can't make enough insulin to overcome

46:16

the body's resistance , which causes

46:18

blood sugars to rise , and

46:21

then so it's not a disorder

46:23

of insulin deficiency , it's

46:25

you need to improve insulin resistance

46:28

to help the blood sugar come down . So

46:30

completely different conditions

46:32

. Then we know now that

46:34

type 2 diabetes can occur in

46:36

children , right , because of severe

46:39

insulin resistance that we see , which is likely

46:41

, as we said , related to light environment

46:43

in young kids , and

46:46

we also know that the iPad in the

46:48

mountain I had yes , in the mountain

46:50

at the same time . And

46:52

then we know that autoimmune

46:55

type 1 diabetes can occur in adults

46:57

, and I don't really think about LADA

46:59

latent autoimmune diabetes

47:02

of the adult right

47:04

as being a type 2

47:06

variant . It's a type 1 variant . The

47:10

average person I see that comes in

47:12

with LADA has been treated as

47:14

a type 2 by a primary

47:16

care doctor for , you know , five

47:19

or 10 years with an A1C of

47:21

about eight and on four different

47:23

medicines for type two diabetes and isn't

47:25

getting better . And so then I check

47:27

that patient's endogenous

47:30

insulin reserves and

47:32

screen for type one antibodies

47:35

and they are not making much insulin

47:37

. They're making some , but not much , and then they have positive

47:39

antibodies . So I call that patient a

47:42

lot , but

47:48

when you consider that the average American is insulin resistant already , right , you

47:50

have these patients that end up with type 1 who still have maybe

47:52

a little bit of insulin , and so

47:56

it's this area

47:58

where we're dealing . They're really two

48:00

independent pathophysiologies

48:04

that can coincide

48:06

in any patient , and

48:09

so the average person

48:11

that I have with type one or LADA

48:13

is also insulin resistant and

48:16

they can benefit from both types of therapies

48:18

, you know have to take insulin

48:21

but also have to work

48:23

on the resistance pathways .

48:24

Yeah , yeah , and I think that if there's

48:27

been the way I think about it , if there's been a sudden

48:29

, relatively sudden

48:31

, maybe over a year kind of decline

48:33

in blood glucose control or increase

48:36

in the HbA1c , despite someone being

48:38

pretty adherent to a good lifestyle

48:40

, then that's my kind of prompt

48:42

to check the C-peptide , check

48:44

the islet autoantibodies

48:47

, to make sure that we're not also dealing with a

48:49

concurrent insulin deficiency process which would

48:51

necessitate even a little

48:53

bit of exogenous insulin . But that

48:56

is really helpful and I think it's important for

48:58

doctors to think about because , like

49:00

you said , they're coexistence and if

49:03

we tie in the light environment

49:05

and we're thinking about how dysfunctional

49:07

people's light environment is , how vitamin

49:09

D deficient they are , so we know

49:12

that immune function is so intrinsically

49:15

linked to our sunlight exposure

49:17

and therefore our vitamin D levels that

49:19

not only does

49:21

infectious disease susceptibility , but also

49:24

autoimmune disease is

49:26

going to be going hand in hand . So if the patient

49:28

is guzzling the Mountain Dew and

49:30

on the iPad in front of

49:32

the TV for decades

49:35

and they're vitamin D

49:37

deficient because they never go outside , it makes a

49:39

lot of sense to me that they would be at risk

49:41

of this autoimmune process in addition

49:44

to the insulin resistance

49:46

process .

49:48

And yeah . So there's

49:50

quite an overlap in

49:53

endocrinology and sort of autoimmune

49:57

disease etiology of

49:59

glandular diseases . So I think about this a lot

50:01

too because I have , you know , many

50:03

, many patients with Hashimoto's and Graves'

50:05

disease , which are autoimmune diseases

50:07

of the thyroid , and then Addison's

50:10

disease , which is autoimmune destruction of

50:12

the adrenal glands . Autoimmune diseases

50:14

in general are increasing

50:17

pretty dramatically and

50:19

I really believe that our

50:21

altered light environment has played a big

50:23

part in that . And vitamin D deficiency

50:25

right . So every I check

50:27

vitamin D in every patient that I see and

50:30

unless a patient is actively

50:33

supplementing consistently

50:35

, they are going to be low every

50:38

time . And I

50:40

talk to patients a lot about the

50:43

benefit of making

50:45

your own D from cholesterol right

50:47

in response to sunshine . And I view

50:50

vitamin D deficiency as

50:52

a surrogate marker of light deficiency , natural

50:54

light deficiency of

51:01

light deficiency , natural light deficiency . So I really don't like high dose prescription vitamin

51:03

D supplements . I don't think that giving huge

51:06

doses of once weekly

51:08

vitamin D which is really the only prescription

51:10

version of vitamin D that's

51:13

available so that tends to be what

51:15

physicians give patients I

51:18

don't think that that's probably the optimal

51:20

way to replace severely deficient

51:23

bulbs too In

51:26

the wintertime . You know , supporting vitamin

51:28

D levels . If you didn't get your vitamin

51:30

D level to a robust place

51:32

by the end of the summer through sunlight exposure is

51:34

probably important . I really try

51:37

to recommend that patients do

51:39

daily D3 instead

51:41

of weekly D2

51:44

. So anyway , but

51:46

I see some

51:48

patients that you know I end up getting

51:50

a lot of malabsorption syndromes

51:53

that have

51:55

low calcium . Patients that have low

51:57

calcium from either gastric bypass or they've

51:59

had parathyroid surgery

52:01

and now have chronically low calcium and

52:04

there is no way

52:06

for me to supplement

52:09

their D and get their level to

52:11

a perfect place . It just cannot

52:14

happen . And for those patients

52:16

we talk so much about

52:18

UVB exposure

52:21

and building a solar callus

52:23

early in the springtime and

52:25

I have seen

52:27

miraculous improvements

52:30

in these malabsorptive

52:34

, low calcium patients who have actually

52:36

taken this on and and

52:39

made a commitment to get intentional

52:41

uh low intensity sun

52:43

exposure it's , it's so pivotal .

52:45

This the light story . And and tying

52:48

it into endocrinology , is this

52:50

this marker that we measure um

52:52

25 hydroxy vitamin d is basically a proxy

52:55

. That's how I think about it too . It's

52:57

basically a rough proxy of

52:59

the solar yield that that patient has

53:01

had and deficiency

53:04

, which is . In Australia it's

53:06

defined as essentially

53:08

above or below 50 nanomoles

53:10

per liter . But that kind

53:12

of target was set

53:15

as avoiding any of the frank bone

53:17

complications . That's mild

53:19

deficiency and then more severe

53:21

is under 30 . And I know you guys use

53:23

nanograms per deciliter , but

53:26

when you look at the other roles

53:28

that vitamin D plays in the body processes

53:31

, especially to do with the immune system

53:33

, getting it above 75

53:36

is much more

53:38

reasonable still too low in my opinion . And

53:40

then if you look at these traditional hunter-gatherer peoples

53:43

and outdoor workers , it looks like a

53:45

natural vitamin D level is hovering

53:47

above 100 , around 120 nanomoles

53:49

per liter

53:51

. So do you target any particular number or

53:54

what do you do in terms of target

53:59

any particular number or what ? What do you do in terms ?

54:00

of um aiming to to get people's vitamin d2 . Oh , I would love to see vitamin d is

54:02

over 80 um , but

54:04

in general um , my treatment

54:06

goal is over 60 , if

54:09

we can get it there . Yeah , um

54:11

, in our standard labs

54:14

we consider less

54:16

than 30 to be deficient , but you

54:18

know , I think about 40

54:20

as being probably deficient . It's

54:23

definitely not optimal . So

54:25

I have so much overlap with other providers

54:27

and I , you know , see lots of patients

54:30

come on and off these high-dose vitamin D

54:32

supplements . They'll get their vitamin

54:34

D replete to 35 , and

54:36

someone will stop their replacement in the middle

54:38

of winter and then they

54:40

can't maintain it , etc . So

54:43

, yeah , I pay a lot of attention

54:45

to vitamin D and , like I said

54:47

, we try to keep patients

54:49

over 60 if possible and

54:51

get that through sun exposure when possible .

54:54

Yeah , and that's the solar callus

54:56

concept too , which I think could

54:58

be one of the most important facets

55:01

of this whole lifestyle change that could

55:03

potentially alleviate so much metabolic

55:05

disease as well as cardiovascular

55:08

disease and cancer . And my interview

55:10

with Richard Weller , which will be released by the time

55:12

this goes out his data

55:14

has shown that people who have

55:16

higher UV exposure are living

55:19

longer and they've

55:21

got less cardiovascular mortality , less cancer

55:23

mortality . So we're really kind

55:25

of up against these skin

55:27

cancer narratives when we're

55:29

trying to encourage people to build a solar callus , but

55:31

in terms of the weight of benefit

55:33

and risk , I think it's undoubtedly clear

55:36

that people need to be getting more

55:38

progressive UVB and

55:40

full-spectrum sunlight exposure .

55:42

I recommend sun exposure

55:44

to generally every patient that I see

55:46

. For these reasons , these

55:48

myriad of benefits and the number

55:51

of patients that tell me that they cannot

55:54

tolerate the sun and argue with

55:56

me on this is significant , significant . I'm allergic , tolerate the sun and argue with

55:58

me on this is significant , significant . I'm allergic to the sun

56:00

. I get rashes and hives in

56:02

the sun , I can't sweat so

56:05

I can't go outside , et cetera . And

56:08

my personal anecdote okay

56:11

, I was a big-time

56:14

sunscreen lover , like

56:16

I said , my entire life . I had a reputation

56:18

for being the palest person

56:21

around , especially

56:23

my family , and I always thought

56:25

that I was sun sensitive right

56:28

, because I had no innate

56:30

protection . And I walked out in the sun in the middle

56:32

of July , got burned in five seconds , so I thought

56:34

I had fair skin and was sun sensitive

56:36

. July and got burned in five seconds , so I thought

56:38

I had fair skin and was sun sensitive . And then , whenever I started , I had my own

56:40

health issues . That got me

56:42

on this journey to it really started with

56:45

with vitamin D and the sun in

56:47

relationship to the benefit , um

56:49

, to the neurologic system , right

56:51

. So I decided I was going

56:53

to be my own experiment

56:56

and I started a couple

56:58

years ago in March with

57:00

the D-Minder app , outside

57:02

in the mornings in the

57:05

low intensity light , and by

57:07

the time I got to summer , with

57:09

no sunscreen , I could , you

57:12

know , lay out at solar noon

57:14

for an hour and a half and

57:16

not get a sunburn . And

57:18

so I proved it to myself as

57:21

a person who always thought she

57:23

was sun sensitive , and

57:25

I've since done the

57:27

same thing with my kids . Right , and

57:29

people around me are sort of amazed at

57:32

this . So I really , I

57:34

really believe that anyone

57:36

can tolerate some sun . Right

57:38

, we are designed to

57:41

be receptacles for

57:43

sunlight Like this is . This is our physiology

57:46

. It's all wrapped up in this light story and

57:48

every person can get some

57:50

exposure safely . Start

57:52

with low intensity and

57:54

let the skin

57:57

be exposed to beneficial protective

58:00

frequencies in the light spectrum

58:02

red light and infrared light , right to help mitigate

58:04

damage , and over time

58:06

, there's clear benefit to

58:09

everybody that tries it . I think .

58:11

Yeah , I couldn't agree more and it's

58:13

a misconception that people with Fitzpatrick

58:15

even one uh skin need

58:18

to , you know , avoid the the sun . And

58:20

based on what we know about the benefits

58:22

of sunlight for health and , as you mentioned

58:24

, we are receptacles for uh

58:28

sunlight and our body has evolved these mechanisms

58:30

to harness ultraviolet

58:32

light through melanin , um to harness

58:34

infrared light through things

58:36

like the cerebrospinal fluid and the work

58:39

of Scott Zimmerman . So it's

58:42

so key and that's why I've released a solar

58:44

callus course so people can check that out if

58:46

they want to get all the information

58:48

they need to safely get sun exposure

58:50

. Can you talk now about thyroid

58:52

disease , and

58:54

particularly in the context of both insulin

58:56

resistance and maybe leptin resistance

58:59

, because so often I see

59:01

women who are

59:03

having problems with their hormones . They're having problems with

59:05

their sleep , frequent snap

59:08

or being hungry , frequently stubborn

59:10

weight , they're pale

59:12

and they have

59:15

some degree of thyroid dysfunction . So

59:17

can you explain to us and the listener how

59:19

do you conceive about the thyroid within

59:22

the context of the things that we've talked about ?

59:24

So the average person that comes

59:26

to me with that constellation

59:28

of symptoms assumes that they have a thyroid

59:30

problem , right ? So the

59:33

collective narrative is if

59:35

you're having trouble losing weight

59:38

and you're tired all the time , it's

59:40

probably your thyroid . And so

59:42

I did a lot of

59:44

just general thyroid screening to

59:47

look for thyroid disease , primary

59:49

thyroid disease , and for me

59:51

that's pretty extensive . In my clinic I think I

59:54

probably do more

59:56

testing than the average endocrinologist

59:58

and screening antibodies , thyroid

1:00:01

antibodies in every person that comes in and

1:00:03

a full thyroid panel

1:00:05

. And often

1:00:07

in that patient there is no

1:00:09

thyroid dysfunction or perhaps

1:00:12

there is a very like

1:00:14

. The thyroid levels are slightly

1:00:16

suboptimal but still in the normal

1:00:18

range . And then the question

1:00:21

always is you know that patient

1:00:23

has been reading , it says information

1:00:26

is everywhere . So patients come in very

1:00:28

well informed and will say to me

1:00:30

you know that PSH is

1:00:33

not optimal and why . And

1:00:36

then we have to talk about the

1:00:38

interface between leptin

1:00:42

, leptin resistance and how this

1:00:44

has an impact on

1:00:46

overall thyroid function . But

1:00:48

the issue itself is

1:00:51

not the primary thyroid dysfunction

1:00:54

, it's leptin resistance , which

1:00:56

is a really common

1:00:58

issue , and

1:01:01

so you know . Then again we're

1:01:03

talking about low carb diets

1:01:05

and light diets in

1:01:07

those patients .

1:01:08

Yeah , yeah , no , that's great

1:01:10

advice and

1:01:13

it's become so simple often

1:01:16

, but it's also a process

1:01:18

of education and helping people understand that

1:01:21

they need those light signals to essentially

1:01:23

kick off the whole hypothalamic

1:01:26

pituitary thyroid axis and

1:01:28

we need those morning light signals to get the

1:01:30

party started . From a thyroid

1:01:33

point of view , and maybe

1:01:36

because you're a consultant endocrinologist

1:01:38

and this is kind of these couple more nuanced

1:01:41

topics , can you talk about things

1:01:43

like something like

1:01:45

Addison's disease or maybe some other

1:01:47

more traditional endocrine

1:01:49

pathology that you

1:01:51

see that might be related

1:01:54

to or contributed to by lifestyle

1:01:56

and light ?

1:02:04

So autoimmune disease is a little bit nebulous in general

1:02:06

, right , because Western medicine says we don't really know why immune systems

1:02:09

turn on bodies and there are a lot

1:02:11

of theories that have to do with gut

1:02:14

dysfunction , leaky gut , post-viral

1:02:17

syndromes etc . And

1:02:20

I don't really

1:02:23

know about

1:02:25

a direct relationship in

1:02:27

literature

1:02:29

or understanding with light

1:02:32

, environment and autoimmune

1:02:34

diseases . But there is , like

1:02:37

you said , a direct impact

1:02:39

of vitamin D deficiency

1:02:42

on decreased immune function and I'm

1:02:44

not sure if that's the primary mechanism by

1:02:47

which this interfaces , but it could

1:02:49

be . I do think that because

1:02:51

our light signaling

1:02:54

has such a profound

1:02:56

impact on every

1:02:58

body system , if you are trying

1:03:01

to heal autoimmune disease , you

1:03:04

have to get your light right , and

1:03:06

we know that there's a direct relationship

1:03:09

between D deficiency and multiple

1:03:11

sclerosis , which is

1:03:13

an autoimmune disease of the nervous system , and

1:03:15

we just supporting

1:03:18

the body on a foundational level involves

1:03:21

getting these

1:03:23

factors optimized

1:03:26

right . So we get

1:03:29

our light environment right , we drink

1:03:31

clean water , we eat healthy , nutrient-dense

1:03:33

food that's relatively low carb . They're just like

1:03:36

it's part of the package to

1:03:38

encourage healing in any kind

1:03:40

of autoimmune disease , I think .

1:03:43

Yeah , yeah , I agree with that totally

1:03:45

. Maybe we could finish on a

1:03:47

couple more kind of lifestyle

1:03:50

practices or aspects that

1:03:52

you think people could include

1:03:54

to improve their their

1:03:56

blood glucose , and we obviously we've talked a lot about

1:03:58

light , um , and I mentioned that study about

1:04:00

the effect of red light 670 nanometer

1:04:03

, which is essentially you can get from from the morning

1:04:05

sunrise and , and the evening

1:04:07

, um , sunset , um , but and

1:04:09

we've obviously talked about a lower carb diet

1:04:11

, but tell us

1:04:13

how you think about things like cold

1:04:16

exercise and maybe

1:04:18

stress in terms of that

1:04:21

blood glucose , and maybe what people might

1:04:23

even measure on something like a continuous glucose

1:04:25

monitor .

1:04:27

Oh yeah , so

1:04:29

I love objective measurements of

1:04:31

blood sugar to try to help people determine

1:04:34

how they can get better control of

1:04:36

their glycemic health and

1:04:38

use this a lot . But I

1:04:41

generally think about metabolic

1:04:43

health as being this

1:04:45

ability to bounce in and out of

1:04:47

fat metabolism easily

1:04:50

right

1:04:58

easily and cold thermogenesis . Of course , when you have the ability to make heat in your

1:05:00

brown fat from your fat stores , it improves insulin sensitivity

1:05:03

, and I've I've done some experimentation

1:05:05

with this on myself , where I put on a continuous

1:05:07

glucose monitor and get in a cold plunge for three

1:05:09

minutes and I can see my blood sugar

1:05:11

fall from , you know , 90

1:05:14

to 55 within

1:05:16

just a short

1:05:19

, short amount of cold therapy

1:05:21

. So that's pretty exciting overall

1:05:23

and I talked to a lot of patients about

1:05:25

getting cold

1:05:27

air exposure like just underdressing

1:05:30

for the weather , because that's a good gateway

1:05:33

into cold therapy for most people and

1:05:35

it's not very intimidating and many

1:05:37

, many patients are very receptive to

1:05:39

that when we're talking about improving

1:05:42

insulin sensitivity and helping metabolism

1:05:44

, our muscles hold

1:05:46

our primary stored

1:05:49

form of glucose right , so muscles

1:05:51

are the biggest source

1:05:53

of glycogen that we have in our bodies

1:05:55

. We hold about 500 grams

1:05:57

of glycogen in muscles on average and then about

1:06:00

80 in the liver . So

1:06:02

whenever our blood sugar falls in fasting

1:06:04

state or we're using energy , glycogen

1:06:06

is the first thing to be mobilized and

1:06:09

so the bigger reserve

1:06:11

you have for holding glycogen

1:06:13

, the less glucose

1:06:16

will be shuttled into fat

1:06:18

stores whenever you have a blood

1:06:21

sugar rise . So improving

1:06:24

muscle mass , increasing

1:06:26

muscle tone and strength is a great strategy

1:06:29

to improve insulin sensitivity strategy

1:06:37

. To improve insulin sensitivity and I really think you know there are

1:06:39

lots of health influencers that tell the general

1:06:41

public that you know , you know I eat

1:06:43

rice three times a day and

1:06:45

I have metabolically flexible

1:06:47

and you can , you can eat carbs

1:06:50

and still lose weight , et cetera

1:06:52

. And that completely

1:06:54

has to do with how

1:06:56

insulin resistant a person is , how much muscle

1:06:59

mass they have , how much they move every day

1:07:01

, right . So for the average person

1:07:03

that I see who doesn't

1:07:05

exercise or can't because of chronic

1:07:08

pain or issues with very

1:07:10

low muscle mass

1:07:12

reserve and very low activity

1:07:15

, that person

1:07:17

is going to benefit from

1:07:19

carb restriction , trying

1:07:22

to get cold and any amount

1:07:24

of activity they

1:07:26

can muster . But you have to lean

1:07:28

more heavily into diet

1:07:31

and light when you can't move and build muscle

1:07:33

right , and so it's a stepwise approach

1:07:35

. You get a little bit healthier

1:07:37

when you can't move and build muscle right . So it's a stepwise approach you

1:07:42

get a little bit healthier , you can move more and then you can integrate

1:07:44

eventually more carbs into your diet if you improve the metabolic

1:07:46

issue and then are able to build some

1:07:48

muscle et cetera , and get healthier

1:07:50

.

1:07:52

Yeah , no , I know what you're saying . You read posts

1:07:55

by guys like Carnivore Aurelius about

1:07:58

eating carbs , croissants and

1:08:00

orange juice and all this

1:08:02

kind of thing , but really they're talking to that 7%

1:08:05

of people who are metabolically healthy in

1:08:07

society and that advice is just

1:08:09

completely inappropriate for someone who is

1:08:11

spending 93% of their time indoors

1:08:13

. You know on the Mountain Dew

1:08:15

and you know TV blue light diet

1:08:18

. It's not appropriate

1:08:20

and it's not transferable

1:08:23

in any way . I agree

1:08:25

that we have to fix this underlying

1:08:27

insulin resistance and metabolic dysfunction before

1:08:30

you can earn back

1:08:32

the right to eat

1:08:34

things like seasonal carbs . The

1:08:37

points that you made about the cold are

1:08:40

very , very well taken , great advice , and

1:08:42

I interviewed Thomas Seeger and I really encourage

1:08:44

people to check out my episode with that and he

1:08:47

noticed the same thing that if he decided

1:08:49

to eat a cake or something like this , he could

1:08:51

simply pop in his cold

1:08:53

plunge , his ice bath and essentially

1:08:55

suck the glucose out of the system . And that

1:08:58

is the power of the brown fat and the cold

1:09:00

adaption . So rather than chasing

1:09:02

carbs with insulin , maybe we need

1:09:04

to be chasing carbs with cold plunge

1:09:06

, because that's a much better way of

1:09:09

getting the glucose out of the system . The other

1:09:11

point is this concept has actually got a diagnosis

1:09:14

, which is sarcopenic obesity

1:09:16

, which is the confluence

1:09:18

of both sarcopenia so

1:09:20

low muscle mass and obesity

1:09:24

. So that is something that we see in nursing

1:09:26

homes so commonly , which

1:09:28

is that really bad

1:09:30

combination of having no muscle , very low muscle

1:09:32

mass , and being insulin , being insulin resistant and metabolically

1:09:34

sick . And you know the antidote to that

1:09:37

, I mean , I think sarcopenia , obesity , the

1:09:39

reason why people get it is because they're so profoundly

1:09:41

disconnected from an ancestral

1:09:43

lifestyle and basically everything

1:09:45

that we've talked about you know in this past

1:09:47

hour , good thing to be aware of . And

1:09:50

if you see someone , you know they're

1:09:52

sitting in a chair , frozen essentially

1:09:54

in a chair frozen essentially in a nursing home , not

1:09:56

moving , and all these endocrine

1:09:58

systems are completely you

1:10:01

know they're going wrong . They're leptin resistant

1:10:03

, insulin resistant . So maybe

1:10:05

, yeah , just fixing it

1:10:07

starts with doing everything

1:10:09

we talked about , but

1:10:20

particularly the light and the food , because you don't have to necessarily be physically active

1:10:22

to start those two . Fantastic . Kelsey , did you have any other kind of thoughts that you wanted to

1:10:24

share with everyone ? Maybe to colleagues , because we've talked a lot about some

1:10:26

of the technical ins and outs of

1:10:28

treating insulin resistance . Maybe

1:10:31

you have some message from some medical or doctor

1:10:33

colleagues who are listening .

1:10:34

I think primarily

1:10:36

we have to understand that pharmaceutical

1:10:40

medicine is not going

1:10:42

to be the answer to heal

1:10:44

metabolic issues

1:10:47

and we can't just lean

1:10:49

on that toolbox . We

1:10:51

have to get interested in

1:10:53

physiology again , right

1:10:55

, and how our body

1:10:58

works , and I found that leaning

1:11:01

well , learning from

1:11:04

other colleagues , being humble and

1:11:06

open-minded is probably

1:11:08

the most important

1:11:11

part of growth as

1:11:13

a provider and a healer . And

1:11:15

we don't know everything

1:11:17

in Western medicine . There's so

1:11:20

much we don't know and I

1:11:23

have learned and changed

1:11:25

my mind and changed my approach on

1:11:27

treatment options so much over the

1:11:29

last 10 years and we have to

1:11:31

get back to foundational

1:11:34

health practices and supporting

1:11:37

vital functions in patients and

1:11:39

letting the body heal itself

1:11:41

, because it's very

1:11:43

capable in many cases of restoring

1:11:46

balance when the right inputs are

1:11:48

received . Yeah

1:11:50

, Amazing .

1:11:52

Well , dr Kelsey Dexter , thank you so much for

1:11:54

talking to me and I

1:11:56

think your message is so , so well received . So how

1:11:59

can people get in touch with you if they want

1:12:01

to send your message or

1:12:03

or have a chat or what , or , basically

1:12:06

, or see you as a as a patient ?

1:12:07

well , I , you know , see patients in

1:12:09

Jackson , Tennessee and on telehealth

1:12:12

, Um . But I

1:12:14

I have a a social

1:12:16

media presence , um on Instagram

1:12:19

. I am sort

1:12:21

of active there , not really , but I'm open

1:12:23

to getting any kind of messages through

1:12:25

that platform too .

1:12:27

Cool , great , all right . Thank you very much .