April 16, 2025 • 34 mins
A fascinating journey into the world of pulmonary medicine awaits as Dr. Neil Ettinger shares his expertise on the complexities of lung health and disease. With decades of experience as a pulmonologist and researcher, Dr. Ettinger offers valuable insights that could quite literally help you breathe easier.
We dive deep into interstitial lung disease, a condition affecting many older adults where the lungs develop progressive scarring that compromises their ability to function. Dr. Ettinger explains the difference between known causes like autoimmune disorders and occupational exposures versus idiopathic cases where the trigger remains mysterious. His optimism shines through as he discusses recent breakthroughs in treatment options, including two approved medications and a promising new drug that recently succeeded in clinical trials.
The conversation takes a crucial turn toward lung cancer screening, revealing the shocking statistic that only about 6% of eligible Americans participate in these potentially life-saving screenings. Dr. Ettinger outlines who qualifies for the annual low-dose CT scans and why catching lung cancer early makes such a dramatic difference in treatment options and outcomes. For those concerned about lung nodules found on scans, his explanation of benign nodules common in the Midwest provides reassurance about what might be normal findings versus cause for concern.
The future of pulmonary medicine looks increasingly promising as we explore emerging technologies and treatment approaches. From targeted cancer therapies that cause fewer side effects to robotic bronchoscopy systems that navigate the complex airways for precise diagnosis, medicine continues to advance. Dr. Ettinger even touches on how artificial intelligence may soon transform how we detect and diagnose lung conditions, potentially saving countless lives through earlier intervention.
Whether you're concerned about your own lung health, caring for someone with respiratory issues, or simply curious about this vital organ system, this episode offers valuable perspective from the frontlines of pulmonary care. Listen now to gain insights that could help you make better-informed decisions about monitoring and maintaining your respiratory health.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Welcome to Doc Discussions.
This is Jason Edwards, and I'mhere with my good friend, dr
Neil Ettinger.
Neil, how are you doing today?
I'm doing well, jason, good tosee you.
Sir Neil, you're apulmonologist, is that correct?
That's correct, and so tell mea little bit about yourself.
Where are you from originally?
Speaker 2 (00:15):
I grew up in Miami Florida, Really yeah.
Speaker 1 (00:19):
I've known you for a while I never knew that.
Speaker 2 (00:21):
Yeah, you never asked me.
Yeah, so Miami is aninteresting place it was far
more interesting in, you know,the 1960s and 70s, when it was a
new city and it was just beingborn you know, but it's gotten
pretty busy and pretty differentthan when I grew up there.
Speaker 1 (00:40):
Yeah, I was there a few years ago.
One of the things I recognizeit was a third Hispanic, a third
African-American and about athird Caucasian or white Is the
demographics.
Have they changed over theyears?
Speaker 2 (00:52):
I don't know if that's true or not.
I mean, I think it used to behalf, you know, white, half
Hispanic, you know, with a smallsliver of African-American in
there, but it may have changedover the years.
Speaker 1 (01:04):
For sure, yeah, mostly Cuban, right, right, yeah
, and so, yeah, great city forsure, and so, and then, where
did you go for undergrad?
Speaker 2 (01:11):
from Miami, I went to Vanderbilt University, very
good.
So I was there from 75 through79.
So you were a Commodore.
Huh, I was a Commodore, youknow, but it took a while to
adapt to the idea that I was inthat deepest South, you know
place Cause Miami was never feltdeep South, sure, but
Vanderbilt certainly did yeah,miami, it feels like an
(01:38):
international city.
Speaker 1 (01:38):
It does, yeah, it does.
And then um, and then fromVanderbilt, washu med school
Very good, very good, and thenyou stayed there for residency
as well.
Speaker 2 (01:43):
Stay there for residency and then I took a year
off and went to England for ayear studied, did some critical
care at MoBAP for six months andthen six months in London,
england, where I did someresearch on bone marrow
transplant patients with lungcomplications.
Speaker 1 (01:59):
How about that yeah?
Speaker 2 (02:01):
And which?
Hospital was that the RoyalMarsden Hospital in London and
then the Brompton Chest Hospitalin London.
Speaker 1 (02:08):
Yeah, and was their health care system?
Was it different than ours?
Speaker 2 (02:12):
Much different, you know, and it's still the same
today.
I mean, it's a national healthsystem, so long waiting list for
elective procedures.
Speaker 1 (02:20):
Yeah, and you may know this, chris Cronin's
grandfather wrote a book, jackCronin, and they say that that
is kind of the impetus forstarting the NHS.
Oh, really like how theirhealthcare system just wasn't
(02:42):
working well, um and uh, and itkind of became a bestseller, uh,
and then he wrote multiplemovie scripts after that.
Speaker 2 (02:50):
Well, in England they have the Harley street doctors,
which are the equivalent toprivate practice doctors.
If you can afford them or haveinsurance for that, Okay.
Otherwise everybody is in thenational health system and I
don't think that's changed any.
Speaker 1 (03:02):
Okay, yeah, and there's some pluses and minuses
to the socialized health carefor sure, and that's a topic for
a whole other deal.
So now pulmonary.
So after you do your internalmedicine residency, then you do
a palm care residency orfellowship.
Speaker 2 (03:17):
So at the time critical care was not its own
specialty.
I'm that old, I'm that old, soit was pulmonary.
And then you came out with yourcertificate in pulmonary and
critical care.
Later on, critical care becameits own specialty.
So you don't automatically getpulmonary and critical care
(03:39):
these days.
These days you need to do twoseparate fellowships or an extra
year in your pulmonaryfellowship for critical care.
Speaker 1 (03:48):
Okay, I always thought it was the same thing
wrapped up in, but it's theirtwo separate specialties.
Now they are Okay, that makessense.
Speaker 2 (03:56):
I mean you can get certified in pulmonary and
critical care with the extradedicated year to critical care.
Speaker 1 (04:02):
Yeah, and it makes sense that they would go hand in
hand, obviously because a lotof the patients are on
ventilators and things like that.
Speaker 2 (04:09):
Right.
So when I was in training youknow in the 83 to 86 was my
medicine residency I took thatyear off in 87.
So 87 through 89, at that timecritical care started to become
its own specialty and you know,intensive care units started to
(04:29):
take off as dedicated facilities.
So critical care didn't alwayshave the kind of sense of an ICU
that we know today.
You know it kind of thatevolved too.
Speaker 1 (04:40):
Yeah, and you have some are open ICUs and some are
closed.
That's correct.
Speaker 2 (04:44):
Yeah.
Speaker 1 (04:44):
And so, but I think the trend is moving more towards
a closed ICU that's justmanaged by an intensivist.
Speaker 2 (04:49):
The intensivist correct yeah.
Speaker 1 (04:51):
Which seems like a good way to go.
Speaker 2 (04:56):
Maybe, maybe it depends on where you're at.
It depends on you know.
There is a role for specialists, of course, in a closed ICU.
So, as long as the patients getthe best care and there's
interchange of ideas, it's thatinterchange of ideas that makes
a difference between aspectacular ICU and the average
ICU.
(05:16):
You know where when you havedifficult cases you have.
You know people with different,you know approaches to
treatment and diagnosis.
You know all of themcooperating, collaborating on
the same patient.
Speaker 1 (05:30):
Yeah, I would think any ICU should have a strong
relationship with theirpulmonologist, whether they're
managing, you know quote unquotemanaging the patient.
Speaker 2 (05:40):
And I think for the most part we do.
I think you know.
What we don't need to do isduplicate services.
Speaker 1 (05:45):
Yeah, yeah, and especially these days with.
You know most hospitals operateon a very tight margin.
You know we need to beefficient, but maximally
effective as well, and so and sonow, so in your practice, of
course, you and I interact afair amount with patients who
have lung cancer.
Correct, what percentage ofyour practice is you and I
interact a fair amount withpatients who have lung cancer?
(06:06):
What percentage of yourpractice is, you know,
malignancy versus non-malignantpalm issues?
Speaker 2 (06:12):
So you know, I would say malignancy is probably 10 to
15% of my practice.
A lot of the rest of it ischronic interstitial lung
disease, since that's an areathat I've specialized in and so
I see a lot of patients withinterstitial lung disease and
we're a pulmonary fibrosisfoundation care center here so
(06:35):
we are kind of known for ourexpertise in that.
So I spend maybe half my time.
We have a clinical researchunit called the Lung Research
Center.
That's connected to ourpractice, you know, physically,
and we see we put a lot ofpatients in clinical trials for
new drugs for treatment ofinterstitial lung disease.
Speaker 1 (06:55):
What causes interstitial lung disease?
Speaker 2 (06:57):
Well, there's the group of interstitial lung
diseases, of known causes, andthen the unknown causes, and so
the known causes might beautoimmune disorders or
occupational lung exposures, youknow, drug-induced lung disease
, you know whereas the unknownsmight be, the most common being
idiopathic pulmonary fibrosis.
(07:17):
The idiopathic means we don'tknow what causes it, but the
idiopathic, you know, isprobably the largest group, and
so, for most people, we don'tknow what triggers the
development of pulmonaryfibrosis.
What we do know is it's adisease of aging.
You don't see this in peoplewho are in their 40s or 30s, you
(07:38):
know.
You see this in people who arein their 60s and 70s and 80s.
Speaker 1 (07:42):
What do they think causes it?
Are there any contenders orhypothesis?
Speaker 2 (07:46):
Well, some injury occurs, you know, at the
cellular level that elicits anabnormal response of wound
healing.
So instead of healingcompletely, so that it's
indistinguishable, you know, youhave this constant drive to
form more scar tissue.
Okay, sort of like if you, youknow, are a keloid former and
(08:08):
you cut yourself, you knowordinary non-keloid former
people would heal.
Speaker 1 (08:14):
Yeah.
Speaker 2 (08:14):
And you might not even be able to see the cut down
the road.
You know, but in keloid formersyou get heaped up scar tissue
that develops.
Yeah so what triggers thatexuberant development of scar
tissue?
Well, you see that in the lung,you know, in a patchwork type
quilt inside the, in the lungtissue, where you got normal
areas of lung next to scarred upareas of lung, you know I
(08:35):
actually I treat patients whohave keloids after surgery.
Speaker 1 (08:38):
It's and of course with the keloid it's an
overactivity of the fibroblast,and mostly in African-Americans,
but not exclusively, and thenyou can have excess scar tissue
formation on the palm, which isDupuytren's contracture and a
similar process, and then in thepenis you can have it which
causes Peyronie's disease, butit's probably, I would assume,
in the lung.
(08:59):
It's probably a little bit morecomplex than those processes.
Speaker 2 (09:01):
It's more microscopic , yeah, probably a little bit
more complex than thoseprocesses and it's more
microscopic, you know, and it'shurt, but the lung ultimately
becomes, you know, stiff andsmall and incapable of
exchanging gas.
Yeah, you can't get, you know,oxygen into the system and you
can't get carbon dioxide out atthe end of it.
Speaker 1 (09:18):
You know, when all is said and done, at the end, yeah
, yeah, that delicate tissuethat exchanges the oxygen to the
blood needs to be thin, and ifit has scar tissue it's just not
going to exactly.
Yeah, that that's that'sinteresting.
Um the um.
I recently bought this devicethat I put in my house that
measures particulate matter.
It has like particulate matter2.5, five and 10.
(09:42):
I think it's microns, but I'mnot sure.
And then it measures like um.
It measures like HCHO, which isformaldehyde.
Speaker 2 (09:51):
You want me to come over and help you clean out your
ducts.
Speaker 1 (09:52):
Well, it actually turned out to be pretty good.
The one thing that was high wasformaldehyde oh really, and
they think that can come fromfurniture and things like that.
So I had to get this filter.
It's got like 26 pounds ofcarbon in it, a special type of
carbon to like filter it down.
Speaker 2 (10:12):
Filter the whole house.
Air conditioning yeah.
Speaker 1 (10:15):
And so.
But it just made me kind ofcognizant that like you've got
to kind of be paying attentionto what you're breathing.
Speaker 2 (10:22):
It sounds expensive.
Speaker 1 (10:23):
Yeah, it wasn't cheap , but if I'm breathing every day
, I feel like I should.
There's dumber things to spendyour money on.
Speaker 2 (10:30):
So we're much safer here in the hospital.
I take it.
Speaker 1 (10:33):
Yeah, I think an older building probably just has
cleaner indoor air because theoff-gassing of things whether
it's the materials used to makea house or the carpet, is less
because they've kind ofoff-gassing of things, you know,
whether it's the materials usedto make a house or the carpet
you know is less because they'vekind of off-gassed over time.
And then you know, of course,outdoors is typically the air is
a lot cleaner than indoors.
(10:53):
Yeah, I think that's right.
Does that sound right?
Don't know.
Yeah, yeah, I guess it dependson where you're at Um the um.
To me it seems like St Louis isum very high in allergens.
Um, because the flora and fauna.
Does that play into yourpractice?
People have allergens andasthma.
Speaker 2 (11:13):
It does.
Um, a lot of allergists see theeasy to treat out asthmatics
and the more difficult ones, butum, it seems the pulmonologist
doesn't see the asthmatics quiteas much, unless the way the
patient is presenting ismisleading and you finally
figure out that what theyactually have is asthma.
Speaker 1 (11:33):
Got you.
Speaker 2 (11:34):
You know so, but you know I think the Midwest, and in
the Midwest St Louis isprobably at the top of the list
for allergy, for difficultallergy cities yeah and um, I
think it's always been that wayis that a function of our rivers
meeting here and there's a lotof different flora and fauna?
Don't know don't know, but Isuspect that it does have to do
(11:54):
with the plants that are foundhere and the temperature here
and what's.
You know what spores can livehere in the soil and that sort
of thing and?
Speaker 1 (12:04):
And speaking of things in the soil, you and I
look at a lot of CT scans andsee a lot of benign nodules
Right, and it seems like this iskind of fertile ground for
benign nodules in the lung.
Speaker 2 (12:18):
Is that the fungus that causes that, or Well, as
you know, histoplasmosis kind oflives in the soil here.
And it doesn't take muchdisturbance of the earth to get
the spores.
You know circulating and it iseasy to inhale.
And you know when you inhalehisto you know the body reacts
to it.
You know it turns on itsreaction and kills it where it
(12:42):
sits.
And the nodule is the evidenceof the battle.
Speaker 1 (12:45):
Yeah.
Speaker 2 (12:46):
And it may go on to calcify.
Typically, it will go on tocalcify, which is a good sign.
Speaker 1 (12:50):
You'd rather see a calcified nodule.
Speaker 2 (12:53):
I don't think you've radiated too many calcified
nodules.
Speaker 1 (12:55):
I don't think so and they don't do much.
If you do, I would presume.
I see patients who have ocularmelanoma and a lot of times
we'll get the staging scans forthem and I always try to kind of
give them a heads up.
You know, plenty of people willhave nodules in their lungs in
St Louis that are not cancer,right, and so, and, and you know
, now patients can read their CTscan results before you could
talk to them, and that's anissue.
(13:15):
It is a big issue, right, andit causes a ton of anxiety and
it's a I think it's a federallaw now it is, and so I think
it's probably, in my opinion,done more harm than good.
Do you have any thoughts onthat?
Speaker 2 (13:32):
I mean, I think in some ways it does take the
pressure off that the patientcan be just as informed as you
are.
For sure, I think.
While I don't mind them seeingresults and dealing with the
anxiety that produces, becausethat's a choice that they've
made, at least they have theoption to make that choice.
(13:54):
Yeah, I think what I do mind isthey're being able to read
notes that might have verycandid comments, because you're
trying to be accurate andcommunicate to all the other
doctors and I think sometimespatients may find the ability to
read their own notes disturbing, you know, or upsetting.
Speaker 1 (14:15):
Yeah, yeah for sure, and there's no doubt about it,
it's going to modify thebehavior of the doctor.
Modify the behavior of thedoctor.
Like to give the listener anexample.
If somebody is very obese, thatcan play into their breathing,
it can play into a lot ofdifferent health issues.
(14:35):
But I'm probably going to beless inclined to say a patient
is very obese in their note, ifI know they're reading their
note, you know and it's, andmaybe that's bad on me, but but
or I'm just saying the doctor,the generic doctor, would be
less inclined to say somethingthat's true, but maybe reflects
poorly on the patient and isWell a good example for for me,
(14:57):
would be somebody who complainsof shortness of breath and
you've done a complete workupand they're in the end you
suspect it may be due to obesityor deconditioning, or it may be
related to anxiety or stress.
Speaker 2 (15:12):
But you cannot reach that conclusion without having
done the work to be sure it'snot the heart or not the lungs.
Um, people don't sometimes feeldismissed when they're they're
asked about anxiety or stress ordepression, but it's a
necessary question when you havesymptoms of shortness of breath
that aren't obviously explainedby something else.
(15:33):
Yeah, because it is a true,bona fide cause of of these
symptoms.
No, no, no doubt about it.
Same thing with obesity anddeconditioning.
You know it is sometimesdifficult to say well, you know
you're overweight, you're out ofshape, you're deconditioned and
the heart's good, the lungs aregood, everything we've checked
is good.
But sometimes people feeldismissed by that.
(15:56):
You know, by reaching thatconclusion.
So reading it in the absence ofbeing able to discuss it at
that moment with the doctor canbe, I think, hard to handle
sometimes.
Speaker 1 (16:07):
Yeah, and kind of in both situations there's a lack
of context and nuance that youcould in a face-to-face
conversation you can seesomebody's not trying to hurt
your feelings, they're justtrying to be as honest and as
accurate as possible.
And yeah, yeah for sure.
So it's made medicine and thepractice of medicine, which is
already complex, kind of morecomplex.
(16:28):
True, and so a lot of thepatients that I end up seeing
ultimately for lung cancer havegone through our lung screening
CT program and, and I think wedo a really good job of that
Lola Brand is awesome.
One of our nurses who helps withthat and there's some pluses
(16:52):
and minuses of every screeningprogram.
You can have some falsepositives and can you talk a
little bit about the screeningprogram and kind of what
patients qualify for that?
Speaker 2 (17:08):
Well, patients from like age 55 through 77 qualify.
If they have stopped, they canstill be smokers.
If they've quit smoking, itcan't be for more than 15 years
and if they've smoked up to Iguess, 20 or 30 pack years I
can't remember the precisecriteria there and if they meet
(17:32):
those criterias they can thenenter into an annual low-dose
CAT scan screening program.
And low-dose radiation is whatwe're talking about.
And because by the time you seean abnormality on a chest X-ray
, most of the time that may bemore than a stage 1 cancer.
Yeah, and you know, metastasesare common when you're waiting
(17:56):
to see something pop up on afilm.
So chest X-rays have neverreally saved any lives, but CAT
scans have been shown to save asignificant number of lives by
finding cancers when they'remore treatable.
When you're annually screeningsomebody, you have a very good
chance of getting something whenit's an early stage cancer.
Speaker 1 (18:17):
And you know lung cancer more than you know other
more common cancers like breast,prostate and even colon cancer.
It can really go from stage oneto stage four pretty quickly.
It does, and the outcomesdifference between a stage one
and a stage four cancer are justnight and day, and so it's not
(18:39):
surprising I think that thesurvival benefit that came from
this trial was stronger than theother screening programs, and
it's kind of not surprising forthat reason.
But it's the minority of peoplewho actually would qualify for
it who actually get screened.
Is that right?
Speaker 2 (18:59):
Say that again the minority of people.
Speaker 1 (19:01):
The minority.
So the amount of people outthere who are eligible to
undergo screening for lungcancer, you know, is much larger
than those that actually getscreened.
Yeah, yeah, it's just very few.
Speaker 2 (19:14):
Well, it helps.
That's why it's helpful to havea coherent program.
Speaker 1 (19:18):
Yeah.
Speaker 2 (19:19):
But recognizing that the patient, the new patient
that you're seeing in front ofyou, who has an internist and a
you know endocrinologist and arheumatologist, and you know
who's going to remember to orderthe lung cancer screening.
It's nothing is made automatic.
Somebody has to remember toorder it Once you're in a
program and most centers andhospitals have a program rather
(19:41):
than just randomly offer a CATscan.
Or, in hospitals, have aprogram rather than just
randomly offer a CAT scan butonce you are in a program, then
annually someone's going to bereaching out to you or notice
that you didn't show up ordidn't have a screen.
Speaker 1 (19:52):
Yeah.
Speaker 2 (19:53):
And so I think having a real bona fide program is key
.
No doubt about it, because allthose people that are not being
reached are sometimes fallingthrough the cracks in their own
physician's office and in theirpulmonologist's office.
Speaker 1 (20:09):
Yeah, and I feel very fortunate to have a great
program here.
The number I have is that onlyabout 6% of eligible US adults
get screened, which is just youknow.
Speaker 2 (20:22):
Think of how many lives we could save.
It leaves a lot of room forimprovement.
Speaker 1 (20:24):
It was 80 or 90%?
Oh yeah, for sure.
And it's the newest screeningprogram too.
I mean mammograms andcolonoscopies have been out and
prostate PSA checks have beenout there for a long time and
the lung cancer screening isrelatively new.
I think it was maybe 2010 orsomething like that that the
trial was actually published.
(20:47):
But I think you know, if we'relooking to save lives, that's
certainly an area of opportunityand if a listener's interested,
you can call St Luke's and getright into the program.
Usually, if you meet thecriteria, it's not an issue at
all and it's very well run andwe've saved a lot of lives
through our hospital with thesepatients.
(21:09):
If it's a stage one lung cancer, the patients are typically
seen by Ryan Reedy or JeremyLeidenfrost and they have a
lobectomy or a wedge resectionor seen by me, and we treat them
with a short course ofradiation.
Lobectomy or a wedge resectionor seen by me, and we treat them
with a short course ofradiation.
So of course, the majority ofpatients who have lung cancer it
(21:33):
comes from tobacco cigaretteuse, but there are some patients
who do have a lung cancerthat's not from smoking.
Is that right?
That is correct, and do theyknow what causes that?
Speaker 2 (21:43):
Well, you know there may be.
You know other things likeradon gas in a household yeah,
you know it might be.
You know chemicals in the homeenvironment or in the food
supply, you know.
So there's lots of angles bywhich you know people can
develop lung cancer.
You know across the world it's.
You know indoor cooking lungcancer, you know in across the
(22:06):
world it's.
You know indoor cooking, youknow with.
You know when you have yourburning charcoal or your burning
wood.
You know to cook and to eat.
You know people get lungcancers and emphysema from those
exposures.
Speaker 1 (22:16):
Yeah.
Speaker 2 (22:16):
You know.
So, yeah, there's, you know,absolutely you know, a role for
non-cigarette, non-tobaccocauses of lung cancer, although
you know tobacco is the firstthing we think of when we think
of lung cancer.
Speaker 1 (22:30):
Yeah, if I recall it was like 95% are from cigarettes
.
Now, sometimes, and especiallyin Missouri, radon is a real
issue and that's why if you getby a house, you have to, you
know, see if you need amitigation system in your
basement.
It's.
And we actually use radium totreat cancer.
(22:51):
You know radium 226 and radium223.
And radon is just an offproduct of that and so it can.
It's, you know, it'sradioactive.
Right.
So it's a big deal.
And then sometimes whenpatients especially if they're a
nonsmoker have a lung cancer,they have what they call a
(23:12):
driver mutation, as you know,and there's some targeted
chemotherapy.
Speaker 2 (23:18):
That's just a pill that you take and patients can
do really well, even if theyhave metastatic cancer, and so
um, so what you're saying isthat the that in non-smokers who
get lung cancer, they may bemore amenable to some of the new
targeted therapies that we haveyeah, absolutely that many
(23:38):
smoking related lung cancerpatients are not um they they
not benefit.
Speaker 1 (23:43):
Yeah, it just kind of happens, you know, to be like
that, and so the outcome ofsomebody who's a non-smoker with
a lung cancer compared to asmoker is better, and it's the
same with head and neck cancerstoo for a different reason, but
it's because those are driventypically by HPV and not smoking
(24:05):
.
Speaker 2 (24:06):
Do you foresee the demise of standard chemotherapy
at some point?
Speaker 1 (24:14):
I think that it will be utilized less, but I think we
will always use it to somecapacity.
But the targeted therapy andthe immune therapies have really
made a lot of headway.
And then now you have theemergence of CAR T-cell therapy,
which is kind of just on thecusp, mainly used in lymphoma
(24:35):
where you used the patient's ownT cells to attack the cancer.
So there's some exciting, youknow totally new classes of
drugs, you know in the pipelineand you know Mark Fessler here,
right, super smart guy.
Speaker 2 (24:54):
And super exciting work.
Speaker 1 (24:56):
Who's doing some really great clinical trials.
You know he's working with alot of that and it's just
totally cutting edge stuff and,to be you know, I'm somewhat
familiar with it, but he cancertainly speak about that much
more intelligently than I can.
So, but you know, so you canget to a point where those don't
(25:18):
work anymore.
You know the cancer outsmartsit because you've not only got
to kill every cancer cell butthere's different clones of
cancer cells, and so you cankill the majority of them or
keep the majority of them at bayfor a while, but it's hard to
take out everyone.
You know if somebody hasmetastatic disease and so.
But I do think that that's thetrend will continue where we
utilize those much more than theother medication.
(25:40):
You know the old schoolchemotherapy drugs like
cisplatin and Taxol and thingslike that, and the nice thing
about that is the targetedtherapies and the
immunotherapies have much lessside effects typically, you know
, compared to the standardchemotherapies, although they've
gotten a lot better at managingthe side effects from the
standard chemotherapies as well.
And so, yeah, I think you knowhearing about all this kind of
(26:05):
stuff it's it's it's daunting,you know, especially with you
know, when you're havingbreathing issues.
Of course, anxiety and breathingissues go hand in hand If you
come in, you can't breathe,you're going to be anxious, I
promise and it's dauntingthinking about this, but it's
also coupled with someexcitement looking into the
future that hopefully,especially if they can use AI
(26:27):
with research, you know they canaccelerate of treatment
strategies can change prognosisfor pancreatic cancer, for
glioblastoma, for some of theuntouchable cancers that seem
not to have a really goodresponse to treatment, that are
(26:50):
almost inevitably fatal.
Speaker 2 (26:52):
If we can change the conversation in those tumors,
that would be awesome.
Speaker 1 (26:57):
Yeah, and you know something that I haven't seen a
lot of but I think is, you know,maybe on the forefront too, is
cancer metabolism.
As far as, like, the things youcan do as a person, is there an
optimal diet that may work withan optimal therapy?
I think there's a lot to bekind of learned in that and
that's still pretty wide open.
(27:17):
I mean, there's not a ton ofrecommendations, you know, on
that kind of stuff.
You know they thought does aketo diet help with?
you know, um, and that's not,you know, ready for prime time
yet, but you know that's anotherquestion that can be answered.
Um, in fact I had a patient whowas on.
She was on on TPN for anotherreason, but she had a pretty bad
(27:39):
lung cancer and we treated itand she kind of did surprisingly
well for a long time and itjust, you know, it's it's a one
of one situation, so you don'tknow, but it's like she's on TPN
, it's.
Does that have something to dowith it or not?
I don't know, but it alwaysjust made me think, you know, is
(28:01):
there something we can do?
You know, on the other end, andhopefully with ai analysis of
patient outcomes, you know, wecan maybe detect some of these
trends a little bit better.
That would, kind of point,point us in the right way to
generate a good hypothesis totest um well, ai is going to
change things for everybody,including in lung, lung nodule
detection.
Speaker 2 (28:19):
I'm sure you know that we will see a higher yield,
you know, and um, and maybeeven more accurate diagnosis
with the use of AI.
Speaker 1 (28:29):
Yeah, yeah, I think there's plenty of room for
excitement and it's something weshould embrace, um and so, but
you know it's something weshould embrace, and so you know
it's good to be skeptical.
Good scientists should beskeptical, so we should embrace
it with some skepticism but alsoembrace it, you know in
aggregate as well.
So are there any new thingsthat you see on the horizon with
(28:51):
pulmonary care, any newmedications coming out?
Speaker 2 (28:57):
Well, we have in the field that I am active in in
interstitial lung disease.
We've had two drugs approved in2014 that are almost identical
in effectiveness both Ofev andEspriate and we have a new drug,
naramandelast, which is a brandnew antifibrotic drug that just
(29:18):
met the criteria for success inthe clinical trial, so we'll
have a third drug now to starthopefully designing some
combination treatment trials toget better results than we are
Right now.
we're adding two or three yearsto the people's lifespans and
we're, you know, we are findingthe disease you know still
(29:40):
inevitably fatal you know.
So we don't have a drug thatwill stop it, but we, hopefully,
will have combinations of drugsthat will stop progression.
Speaker 1 (29:49):
Yeah.
Speaker 2 (29:49):
You know we can slow it down, but we can't stop it
yet.
Speaker 1 (29:52):
Well, it's exciting to see that we're making some
headway in that we are, so we'regetting better in the world.
Speaker 2 (29:57):
There's a lot of attention in clinical trials for
, you know, finding drugs forpulmonary fibrosis, both the
idiopathic versions of it aswell as the autoimmune versions
of fibrotic lung disease.
Speaker 1 (30:09):
Yeah.
Speaker 2 (30:10):
You know, so we are getting better at managing these
patients.
Speaker 1 (30:14):
And, as you well know , I mean there's.
The truth of the matter isthere are many ways a person's
life can come to an end, andsome are much worse than others,
and I would think kind ofslowly suffocating would be a
bad one, and so yeah, so that'sexciting to see that we're maybe
(30:36):
making some progress with somenew drugs, and I'm sure there's
many other drugs in the pipeline.
Some of them will work out andsome of them won't in the
clinical trials, but hopefullywe have an exciting future here
in developing some newmedications.
Speaker 2 (30:50):
And then there may be new delivery systems,
delivering using interventionaltechniques.
You know chemotherapy tonodules, you know.
Whether we have the technologyto ensure accuracy and to allow
that kind of risk is stilldebatable, but that's something
on the horizon that I think is agoal.
(31:10):
Yeah, you know.
So.
I think you know we haverobotics.
You know now in interventionalpulmonary Probably the yield is
probably a little bit better,you know, than the navigation
systems that we use now.
But you know down the roadwhether we can actually use it
(31:33):
both to diagnose and to treat.
That's a really importantquestion to answer.
Speaker 1 (31:38):
And you're talking about actually going down the
throat through the trachea andgetting to the lung nodule.
Speaker 2 (31:43):
That's correct and navigating to that nodule using
either robotics, you know, orGPS for the lung, so to speak.
Speaker 1 (31:52):
Yeah, and it's tougher than you know.
Probably most people wouldinitially think, because you
don't get to pick exactly whereyou go.
You have to follow thewindpipes.
Speaker 2 (32:02):
You have to be following the airway that you're
given.
Yeah, you know the ones thatGod made for you, and sometimes
things may be behind a wall youknow, and you, you know you have
to still be able to deliver andto both diagnose and to treat.
Speaker 1 (32:15):
And then on top of that, the lung is.
The whole lung is moving up anddown and the nodules moving up
and down.
That's correct, and so it's.
It's some fancy dancing to getthere, Right.
Speaker 2 (32:25):
And it's usually an hour and a half procedure,
whereas a typical bronchoscopymight be 20 minutes.
So it does take a lot of timeto to navigate to these, these
lesions, yeah.
Speaker 1 (32:36):
And I think I may have told you this once before,
but Don Busick once said thisabout you.
He said if you really want toget a good biopsy and get a good
piece of it, call Neil Ettinger.
And so I thought that was areal compliment.
Well, that was nice of Don tosay that.
Well, neil, thanks so much fornot only joining me today, but
all of the work that you do withour mutual patients and all the
(33:00):
work that you're doing withinterstitial lung disease and
trying to prolong the length ofpatients' lives and improve the
quality of their lives.
Speaker 2 (33:08):
Well, thank you, jason, and I do want to say that
the same goes for you, becausewhen we're making a diagnosis of
lung cancer in somebody, to beable to pick up the phone and
know that they're going to betreated with the care you
provide them, the emotionalsupport that you give them and
(33:28):
the high-quality medicine thatyou practice with them, you know
that really, you know, means alot to those of us that work
with you and take care of thesepatients.
Speaker 1 (33:37):
Oh, thank you, sir, I appreciate it.
Speaker 2 (33:39):
Thank you yeah.
Welcome to Doc Discussions.
This is Jason Edwards, and I'mhere with my good friend, dr
Neil Ettinger.
Neil, how are you doing today?
I'm doing well, jason, good tosee you.
Sir Neil, you're apulmonologist, is that correct?
That's correct, and so tell mea little bit about yourself.
Where are you from originally?
Speaker 2 (00:15):
I grew up in Miami Florida, Really yeah.
Speaker 1 (00:19):
I've known you for a while I never knew that.
Speaker 2 (00:21):
Yeah, you never asked me.
Yeah, so Miami is aninteresting place it was far
more interesting in, you know,the 1960s and 70s, when it was a
new city and it was just beingborn you know, but it's gotten
pretty busy and pretty differentthan when I grew up there.
Speaker 1 (00:40):
Yeah, I was there a few years ago.
One of the things I recognizeit was a third Hispanic, a third
African-American and about athird Caucasian or white Is the
demographics.
Have they changed over theyears?
Speaker 2 (00:52):
I don't know if that's true or not.
I mean, I think it used to behalf, you know, white, half
Hispanic, you know, with a smallsliver of African-American in
there, but it may have changedover the years.
Speaker 1 (01:04):
For sure, yeah, mostly Cuban, right, right, yeah
, and so, yeah, great city forsure, and so, and then, where
did you go for undergrad?
Speaker 2 (01:11):
from Miami, I went to Vanderbilt University, very
good.
So I was there from 75 through79.
So you were a Commodore.
Huh, I was a Commodore, youknow, but it took a while to
adapt to the idea that I was inthat deepest South, you know
place Cause Miami was never feltdeep South, sure, but
Vanderbilt certainly did yeah,miami, it feels like an
(01:38):
international city.
Speaker 1 (01:38):
It does, yeah, it does.
And then um, and then fromVanderbilt, washu med school
Very good, very good, and thenyou stayed there for residency
as well.
Speaker 2 (01:43):
Stay there for residency and then I took a year
off and went to England for ayear studied, did some critical
care at MoBAP for six months andthen six months in London,
england, where I did someresearch on bone marrow
transplant patients with lungcomplications.
Speaker 1 (01:59):
How about that yeah?
Speaker 2 (02:01):
And which?
Hospital was that the RoyalMarsden Hospital in London and
then the Brompton Chest Hospitalin London.
Speaker 1 (02:08):
Yeah, and was their health care system?
Was it different than ours?
Speaker 2 (02:12):
Much different, you know, and it's still the same
today.
I mean, it's a national healthsystem, so long waiting list for
elective procedures.
Speaker 1 (02:20):
Yeah, and you may know this, chris Cronin's
grandfather wrote a book, jackCronin, and they say that that
is kind of the impetus forstarting the NHS.
Oh, really like how theirhealthcare system just wasn't
(02:42):
working well, um and uh, and itkind of became a bestseller, uh,
and then he wrote multiplemovie scripts after that.
Speaker 2 (02:50):
Well, in England they have the Harley street doctors,
which are the equivalent toprivate practice doctors.
If you can afford them or haveinsurance for that, Okay.
Otherwise everybody is in thenational health system and I
don't think that's changed any.
Speaker 1 (03:02):
Okay, yeah, and there's some pluses and minuses
to the socialized health carefor sure, and that's a topic for
a whole other deal.
So now pulmonary.
So after you do your internalmedicine residency, then you do
a palm care residency orfellowship.
Speaker 2 (03:17):
So at the time critical care was not its own
specialty.
I'm that old, I'm that old, soit was pulmonary.
And then you came out with yourcertificate in pulmonary and
critical care.
Later on, critical care becameits own specialty.
So you don't automatically getpulmonary and critical care
(03:39):
these days.
These days you need to do twoseparate fellowships or an extra
year in your pulmonaryfellowship for critical care.
Speaker 1 (03:48):
Okay, I always thought it was the same thing
wrapped up in, but it's theirtwo separate specialties.
Now they are Okay, that makessense.
Speaker 2 (03:56):
I mean you can get certified in pulmonary and
critical care with the extradedicated year to critical care.
Speaker 1 (04:02):
Yeah, and it makes sense that they would go hand in
hand, obviously because a lotof the patients are on
ventilators and things like that.
Speaker 2 (04:09):
Right.
So when I was in training youknow in the 83 to 86 was my
medicine residency I took thatyear off in 87.
So 87 through 89, at that timecritical care started to become
its own specialty and you know,intensive care units started to
(04:29):
take off as dedicated facilities.
So critical care didn't alwayshave the kind of sense of an ICU
that we know today.
You know it kind of thatevolved too.
Speaker 1 (04:40):
Yeah, and you have some are open ICUs and some are
closed.
That's correct.
Speaker 2 (04:44):
Yeah.
Speaker 1 (04:44):
And so, but I think the trend is moving more towards
a closed ICU that's justmanaged by an intensivist.
Speaker 2 (04:49):
The intensivist correct yeah.
Speaker 1 (04:51):
Which seems like a good way to go.
Speaker 2 (04:56):
Maybe, maybe it depends on where you're at.
It depends on you know.
There is a role for specialists, of course, in a closed ICU.
So, as long as the patients getthe best care and there's
interchange of ideas, it's thatinterchange of ideas that makes
a difference between aspectacular ICU and the average
ICU.
(05:16):
You know where when you havedifficult cases you have.
You know people with different,you know approaches to
treatment and diagnosis.
You know all of themcooperating, collaborating on
the same patient.
Speaker 1 (05:30):
Yeah, I would think any ICU should have a strong
relationship with theirpulmonologist, whether they're
managing, you know quote unquotemanaging the patient.
Speaker 2 (05:40):
And I think for the most part we do.
I think you know.
What we don't need to do isduplicate services.
Speaker 1 (05:45):
Yeah, yeah, and especially these days with.
You know most hospitals operateon a very tight margin.
You know we need to beefficient, but maximally
effective as well, and so and sonow, so in your practice, of
course, you and I interact afair amount with patients who
have lung cancer.
Correct, what percentage ofyour practice is you and I
interact a fair amount withpatients who have lung cancer?
(06:06):
What percentage of yourpractice is, you know,
malignancy versus non-malignantpalm issues?
Speaker 2 (06:12):
So you know, I would say malignancy is probably 10 to
15% of my practice.
A lot of the rest of it ischronic interstitial lung
disease, since that's an areathat I've specialized in and so
I see a lot of patients withinterstitial lung disease and
we're a pulmonary fibrosisfoundation care center here so
(06:35):
we are kind of known for ourexpertise in that.
So I spend maybe half my time.
We have a clinical researchunit called the Lung Research
Center.
That's connected to ourpractice, you know, physically,
and we see we put a lot ofpatients in clinical trials for
new drugs for treatment ofinterstitial lung disease.
Speaker 1 (06:55):
What causes interstitial lung disease?
Speaker 2 (06:57):
Well, there's the group of interstitial lung
diseases, of known causes, andthen the unknown causes, and so
the known causes might beautoimmune disorders or
occupational lung exposures, youknow, drug-induced lung disease
, you know whereas the unknownsmight be, the most common being
idiopathic pulmonary fibrosis.
(07:17):
The idiopathic means we don'tknow what causes it, but the
idiopathic, you know, isprobably the largest group, and
so, for most people, we don'tknow what triggers the
development of pulmonaryfibrosis.
What we do know is it's adisease of aging.
You don't see this in peoplewho are in their 40s or 30s, you
(07:38):
know.
You see this in people who arein their 60s and 70s and 80s.
Speaker 1 (07:42):
What do they think causes it?
Are there any contenders orhypothesis?
Speaker 2 (07:46):
Well, some injury occurs, you know, at the
cellular level that elicits anabnormal response of wound
healing.
So instead of healingcompletely, so that it's
indistinguishable, you know, youhave this constant drive to
form more scar tissue.
Okay, sort of like if you, youknow, are a keloid former and
(08:08):
you cut yourself, you knowordinary non-keloid former
people would heal.
Speaker 1 (08:14):
Yeah.
Speaker 2 (08:14):
And you might not even be able to see the cut down
the road.
You know, but in keloid formersyou get heaped up scar tissue
that develops.
Yeah so what triggers thatexuberant development of scar
tissue?
Well, you see that in the lung,you know, in a patchwork type
quilt inside the, in the lungtissue, where you got normal
areas of lung next to scarred upareas of lung, you know I
(08:35):
actually I treat patients whohave keloids after surgery.
Speaker 1 (08:38):
It's and of course with the keloid it's an
overactivity of the fibroblast,and mostly in African-Americans,
but not exclusively, and thenyou can have excess scar tissue
formation on the palm, which isDupuytren's contracture and a
similar process, and then in thepenis you can have it which
causes Peyronie's disease, butit's probably, I would assume,
in the lung.
(08:59):
It's probably a little bit morecomplex than those processes.
Speaker 2 (09:01):
It's more microscopic , yeah, probably a little bit
more complex than thoseprocesses and it's more
microscopic, you know, and it'shurt, but the lung ultimately
becomes, you know, stiff andsmall and incapable of
exchanging gas.
Yeah, you can't get, you know,oxygen into the system and you
can't get carbon dioxide out atthe end of it.
Speaker 1 (09:18):
You know, when all is said and done, at the end, yeah
, yeah, that delicate tissuethat exchanges the oxygen to the
blood needs to be thin, and ifit has scar tissue it's just not
going to exactly.
Yeah, that that's that'sinteresting.
Um the um.
I recently bought this devicethat I put in my house that
measures particulate matter.
It has like particulate matter2.5, five and 10.
(09:42):
I think it's microns, but I'mnot sure.
And then it measures like um.
It measures like HCHO, which isformaldehyde.
Speaker 2 (09:51):
You want me to come over and help you clean out your
ducts.
Speaker 1 (09:52):
Well, it actually turned out to be pretty good.
The one thing that was high wasformaldehyde oh really, and
they think that can come fromfurniture and things like that.
So I had to get this filter.
It's got like 26 pounds ofcarbon in it, a special type of
carbon to like filter it down.
Speaker 2 (10:12):
Filter the whole house.
Air conditioning yeah.
Speaker 1 (10:15):
And so.
But it just made me kind ofcognizant that like you've got
to kind of be paying attentionto what you're breathing.
Speaker 2 (10:22):
It sounds expensive.
Speaker 1 (10:23):
Yeah, it wasn't cheap , but if I'm breathing every day
, I feel like I should.
There's dumber things to spendyour money on.
Speaker 2 (10:30):
So we're much safer here in the hospital.
I take it.
Speaker 1 (10:33):
Yeah, I think an older building probably just has
cleaner indoor air because theoff-gassing of things whether
it's the materials used to makea house or the carpet, is less
because they've kind ofoff-gassing of things, you know,
whether it's the materials usedto make a house or the carpet
you know is less because they'vekind of off-gassed over time.
And then you know, of course,outdoors is typically the air is
a lot cleaner than indoors.
(10:53):
Yeah, I think that's right.
Does that sound right?
Don't know.
Yeah, yeah, I guess it dependson where you're at Um the um.
To me it seems like St Louis isum very high in allergens.
Um, because the flora and fauna.
Does that play into yourpractice?
People have allergens andasthma.
Speaker 2 (11:13):
It does.
Um, a lot of allergists see theeasy to treat out asthmatics
and the more difficult ones, butum, it seems the pulmonologist
doesn't see the asthmatics quiteas much, unless the way the
patient is presenting ismisleading and you finally
figure out that what theyactually have is asthma.
Speaker 1 (11:33):
Got you.
Speaker 2 (11:34):
You know so, but you know I think the Midwest, and in
the Midwest St Louis isprobably at the top of the list
for allergy, for difficultallergy cities yeah and um, I
think it's always been that wayis that a function of our rivers
meeting here and there's a lotof different flora and fauna?
Don't know don't know, but Isuspect that it does have to do
(11:54):
with the plants that are foundhere and the temperature here
and what's.
You know what spores can livehere in the soil and that sort
of thing and?
Speaker 1 (12:04):
And speaking of things in the soil, you and I
look at a lot of CT scans andsee a lot of benign nodules
Right, and it seems like this iskind of fertile ground for
benign nodules in the lung.
Speaker 2 (12:18):
Is that the fungus that causes that, or Well, as
you know, histoplasmosis kind oflives in the soil here.
And it doesn't take muchdisturbance of the earth to get
the spores.
You know circulating and it iseasy to inhale.
And you know when you inhalehisto you know the body reacts
to it.
You know it turns on itsreaction and kills it where it
(12:42):
sits.
And the nodule is the evidenceof the battle.
Speaker 1 (12:45):
Yeah.
Speaker 2 (12:46):
And it may go on to calcify.
Typically, it will go on tocalcify, which is a good sign.
Speaker 1 (12:50):
You'd rather see a calcified nodule.
Speaker 2 (12:53):
I don't think you've radiated too many calcified
nodules.
Speaker 1 (12:55):
I don't think so and they don't do much.
If you do, I would presume.
I see patients who have ocularmelanoma and a lot of times
we'll get the staging scans forthem and I always try to kind of
give them a heads up.
You know, plenty of people willhave nodules in their lungs in
St Louis that are not cancer,right, and so, and, and you know
, now patients can read their CTscan results before you could
talk to them, and that's anissue.
(13:15):
It is a big issue, right, andit causes a ton of anxiety and
it's a I think it's a federallaw now it is, and so I think
it's probably, in my opinion,done more harm than good.
Do you have any thoughts onthat?
Speaker 2 (13:32):
I mean, I think in some ways it does take the
pressure off that the patientcan be just as informed as you
are.
For sure, I think.
While I don't mind them seeingresults and dealing with the
anxiety that produces, becausethat's a choice that they've
made, at least they have theoption to make that choice.
(13:54):
Yeah, I think what I do mind isthey're being able to read
notes that might have verycandid comments, because you're
trying to be accurate andcommunicate to all the other
doctors and I think sometimespatients may find the ability to
read their own notes disturbing, you know, or upsetting.
Speaker 1 (14:15):
Yeah, yeah for sure, and there's no doubt about it,
it's going to modify thebehavior of the doctor.
Modify the behavior of thedoctor.
Like to give the listener anexample.
If somebody is very obese, thatcan play into their breathing,
it can play into a lot ofdifferent health issues.
(14:35):
But I'm probably going to beless inclined to say a patient
is very obese in their note, ifI know they're reading their
note, you know and it's, andmaybe that's bad on me, but but
or I'm just saying the doctor,the generic doctor, would be
less inclined to say somethingthat's true, but maybe reflects
poorly on the patient and isWell a good example for for me,
(14:57):
would be somebody who complainsof shortness of breath and
you've done a complete workupand they're in the end you
suspect it may be due to obesityor deconditioning, or it may be
related to anxiety or stress.
Speaker 2 (15:12):
But you cannot reach that conclusion without having
done the work to be sure it'snot the heart or not the lungs.
Um, people don't sometimes feeldismissed when they're they're
asked about anxiety or stress ordepression, but it's a
necessary question when you havesymptoms of shortness of breath
that aren't obviously explainedby something else.
(15:33):
Yeah, because it is a true,bona fide cause of of these
symptoms.
No, no, no doubt about it.
Same thing with obesity anddeconditioning.
You know it is sometimesdifficult to say well, you know
you're overweight, you're out ofshape, you're deconditioned and
the heart's good, the lungs aregood, everything we've checked
is good.
But sometimes people feeldismissed by that.
(15:56):
You know, by reaching thatconclusion.
So reading it in the absence ofbeing able to discuss it at
that moment with the doctor canbe, I think, hard to handle
sometimes.
Speaker 1 (16:07):
Yeah, and kind of in both situations there's a lack
of context and nuance that youcould in a face-to-face
conversation you can seesomebody's not trying to hurt
your feelings, they're justtrying to be as honest and as
accurate as possible.
And yeah, yeah for sure.
So it's made medicine and thepractice of medicine, which is
already complex, kind of morecomplex.
(16:28):
True, and so a lot of thepatients that I end up seeing
ultimately for lung cancer havegone through our lung screening
CT program and, and I think wedo a really good job of that
Lola Brand is awesome.
One of our nurses who helps withthat and there's some pluses
(16:52):
and minuses of every screeningprogram.
You can have some falsepositives and can you talk a
little bit about the screeningprogram and kind of what
patients qualify for that?
Speaker 2 (17:08):
Well, patients from like age 55 through 77 qualify.
If they have stopped, they canstill be smokers.
If they've quit smoking, itcan't be for more than 15 years
and if they've smoked up to Iguess, 20 or 30 pack years I
can't remember the precisecriteria there and if they meet
(17:32):
those criterias they can thenenter into an annual low-dose
CAT scan screening program.
And low-dose radiation is whatwe're talking about.
And because by the time you seean abnormality on a chest X-ray
, most of the time that may bemore than a stage 1 cancer.
Yeah, and you know, metastasesare common when you're waiting
(17:56):
to see something pop up on afilm.
So chest X-rays have neverreally saved any lives, but CAT
scans have been shown to save asignificant number of lives by
finding cancers when they'remore treatable.
When you're annually screeningsomebody, you have a very good
chance of getting something whenit's an early stage cancer.
Speaker 1 (18:17):
And you know lung cancer more than you know other
more common cancers like breast,prostate and even colon cancer.
It can really go from stage oneto stage four pretty quickly.
It does, and the outcomesdifference between a stage one
and a stage four cancer are justnight and day, and so it's not
(18:39):
surprising I think that thesurvival benefit that came from
this trial was stronger than theother screening programs, and
it's kind of not surprising forthat reason.
But it's the minority of peoplewho actually would qualify for
it who actually get screened.
Is that right?
Speaker 2 (18:59):
Say that again the minority of people.
Speaker 1 (19:01):
The minority.
So the amount of people outthere who are eligible to
undergo screening for lungcancer, you know, is much larger
than those that actually getscreened.
Yeah, yeah, it's just very few.
Speaker 2 (19:14):
Well, it helps.
That's why it's helpful to havea coherent program.
Speaker 1 (19:18):
Yeah.
Speaker 2 (19:19):
But recognizing that the patient, the new patient
that you're seeing in front ofyou, who has an internist and a
you know endocrinologist and arheumatologist, and you know
who's going to remember to orderthe lung cancer screening.
It's nothing is made automatic.
Somebody has to remember toorder it Once you're in a
program and most centers andhospitals have a program rather
(19:41):
than just randomly offer a CATscan.
Or, in hospitals, have aprogram rather than just
randomly offer a CAT scan butonce you are in a program, then
annually someone's going to bereaching out to you or notice
that you didn't show up ordidn't have a screen.
Speaker 1 (19:52):
Yeah.
Speaker 2 (19:53):
And so I think having a real bona fide program is key
.
No doubt about it, because allthose people that are not being
reached are sometimes fallingthrough the cracks in their own
physician's office and in theirpulmonologist's office.
Speaker 1 (20:09):
Yeah, and I feel very fortunate to have a great
program here.
The number I have is that onlyabout 6% of eligible US adults
get screened, which is just youknow.
Speaker 2 (20:22):
Think of how many lives we could save.
It leaves a lot of room forimprovement.
Speaker 1 (20:24):
It was 80 or 90%?
Oh yeah, for sure.
And it's the newest screeningprogram too.
I mean mammograms andcolonoscopies have been out and
prostate PSA checks have beenout there for a long time and
the lung cancer screening isrelatively new.
I think it was maybe 2010 orsomething like that that the
trial was actually published.
(20:47):
But I think you know, if we'relooking to save lives, that's
certainly an area of opportunityand if a listener's interested,
you can call St Luke's and getright into the program.
Usually, if you meet thecriteria, it's not an issue at
all and it's very well run andwe've saved a lot of lives
through our hospital with thesepatients.
(21:09):
If it's a stage one lung cancer, the patients are typically
seen by Ryan Reedy or JeremyLeidenfrost and they have a
lobectomy or a wedge resectionor seen by me, and we treat them
with a short course ofradiation.
Lobectomy or a wedge resectionor seen by me, and we treat them
with a short course ofradiation.
So of course, the majority ofpatients who have lung cancer it
(21:33):
comes from tobacco cigaretteuse, but there are some patients
who do have a lung cancerthat's not from smoking.
Is that right?
That is correct, and do theyknow what causes that?
Speaker 2 (21:43):
Well, you know there may be.
You know other things likeradon gas in a household yeah,
you know it might be.
You know chemicals in the homeenvironment or in the food
supply, you know.
So there's lots of angles bywhich you know people can
develop lung cancer.
You know across the world it's.
You know indoor cooking lungcancer, you know in across the
(22:06):
world it's.
You know indoor cooking, youknow with.
You know when you have yourburning charcoal or your burning
wood.
You know to cook and to eat.
You know people get lungcancers and emphysema from those
exposures.
Speaker 1 (22:16):
Yeah.
Speaker 2 (22:16):
You know.
So, yeah, there's, you know,absolutely you know, a role for
non-cigarette, non-tobaccocauses of lung cancer, although
you know tobacco is the firstthing we think of when we think
of lung cancer.
Speaker 1 (22:30):
Yeah, if I recall it was like 95% are from cigarettes
.
Now, sometimes, and especiallyin Missouri, radon is a real
issue and that's why if you getby a house, you have to, you
know, see if you need amitigation system in your
basement.
It's.
And we actually use radium totreat cancer.
(22:51):
You know radium 226 and radium223.
And radon is just an offproduct of that and so it can.
It's, you know, it'sradioactive.
Right.
So it's a big deal.
And then sometimes whenpatients especially if they're a
nonsmoker have a lung cancer,they have what they call a
(23:12):
driver mutation, as you know,and there's some targeted
chemotherapy.
Speaker 2 (23:18):
That's just a pill that you take and patients can
do really well, even if theyhave metastatic cancer, and so
um, so what you're saying isthat the that in non-smokers who
get lung cancer, they may bemore amenable to some of the new
targeted therapies that we haveyeah, absolutely that many
(23:38):
smoking related lung cancerpatients are not um they they
not benefit.
Speaker 1 (23:43):
Yeah, it just kind of happens, you know, to be like
that, and so the outcome ofsomebody who's a non-smoker with
a lung cancer compared to asmoker is better, and it's the
same with head and neck cancerstoo for a different reason, but
it's because those are driventypically by HPV and not smoking
(24:05):
.
Speaker 2 (24:06):
Do you foresee the demise of standard chemotherapy
at some point?
Speaker 1 (24:14):
I think that it will be utilized less, but I think we
will always use it to somecapacity.
But the targeted therapy andthe immune therapies have really
made a lot of headway.
And then now you have theemergence of CAR T-cell therapy,
which is kind of just on thecusp, mainly used in lymphoma
(24:35):
where you used the patient's ownT cells to attack the cancer.
So there's some exciting, youknow totally new classes of
drugs, you know in the pipelineand you know Mark Fessler here,
right, super smart guy.
Speaker 2 (24:54):
And super exciting work.
Speaker 1 (24:56):
Who's doing some really great clinical trials.
You know he's working with alot of that and it's just
totally cutting edge stuff and,to be you know, I'm somewhat
familiar with it, but he cancertainly speak about that much
more intelligently than I can.
So, but you know, so you canget to a point where those don't
(25:18):
work anymore.
You know the cancer outsmartsit because you've not only got
to kill every cancer cell butthere's different clones of
cancer cells, and so you cankill the majority of them or
keep the majority of them at bayfor a while, but it's hard to
take out everyone.
You know if somebody hasmetastatic disease and so.
But I do think that that's thetrend will continue where we
utilize those much more than theother medication.
(25:40):
You know the old schoolchemotherapy drugs like
cisplatin and Taxol and thingslike that, and the nice thing
about that is the targetedtherapies and the
immunotherapies have much lessside effects typically, you know
, compared to the standardchemotherapies, although they've
gotten a lot better at managingthe side effects from the
standard chemotherapies as well.
And so, yeah, I think you knowhearing about all this kind of
(26:05):
stuff it's it's it's daunting,you know, especially with you
know, when you're havingbreathing issues.
Of course, anxiety and breathingissues go hand in hand If you
come in, you can't breathe,you're going to be anxious, I
promise and it's dauntingthinking about this, but it's
also coupled with someexcitement looking into the
future that hopefully,especially if they can use AI
(26:27):
with research, you know they canaccelerate of treatment
strategies can change prognosisfor pancreatic cancer, for
glioblastoma, for some of theuntouchable cancers that seem
not to have a really goodresponse to treatment, that are
(26:50):
almost inevitably fatal.
Speaker 2 (26:52):
If we can change the conversation in those tumors,
that would be awesome.
Speaker 1 (26:57):
Yeah, and you know something that I haven't seen a
lot of but I think is, you know,maybe on the forefront too, is
cancer metabolism.
As far as, like, the things youcan do as a person, is there an
optimal diet that may work withan optimal therapy?
I think there's a lot to bekind of learned in that and
that's still pretty wide open.
(27:17):
I mean, there's not a ton ofrecommendations, you know, on
that kind of stuff.
You know they thought does aketo diet help with?
you know, um, and that's not,you know, ready for prime time
yet, but you know that's anotherquestion that can be answered.
Um, in fact I had a patient whowas on.
She was on on TPN for anotherreason, but she had a pretty bad
(27:39):
lung cancer and we treated itand she kind of did surprisingly
well for a long time and itjust, you know, it's it's a one
of one situation, so you don'tknow, but it's like she's on TPN
, it's.
Does that have something to dowith it or not?
I don't know, but it alwaysjust made me think, you know, is
(28:01):
there something we can do?
You know, on the other end, andhopefully with ai analysis of
patient outcomes, you know, wecan maybe detect some of these
trends a little bit better.
That would, kind of point,point us in the right way to
generate a good hypothesis totest um well, ai is going to
change things for everybody,including in lung, lung nodule
detection.
Speaker 2 (28:19):
I'm sure you know that we will see a higher yield,
you know, and um, and maybeeven more accurate diagnosis
with the use of AI.
Speaker 1 (28:29):
Yeah, yeah, I think there's plenty of room for
excitement and it's something weshould embrace, um and so, but
you know it's something weshould embrace, and so you know
it's good to be skeptical.
Good scientists should beskeptical, so we should embrace
it with some skepticism but alsoembrace it, you know in
aggregate as well.
So are there any new thingsthat you see on the horizon with
(28:51):
pulmonary care, any newmedications coming out?
Speaker 2 (28:57):
Well, we have in the field that I am active in in
interstitial lung disease.
We've had two drugs approved in2014 that are almost identical
in effectiveness both Ofev andEspriate and we have a new drug,
naramandelast, which is a brandnew antifibrotic drug that just
(29:18):
met the criteria for success inthe clinical trial, so we'll
have a third drug now to starthopefully designing some
combination treatment trials toget better results than we are
Right now.
we're adding two or three yearsto the people's lifespans and
we're, you know, we are findingthe disease you know still
(29:40):
inevitably fatal you know.
So we don't have a drug thatwill stop it, but we, hopefully,
will have combinations of drugsthat will stop progression.
Speaker 1 (29:49):
Yeah.
Speaker 2 (29:49):
You know we can slow it down, but we can't stop it
yet.
Speaker 1 (29:52):
Well, it's exciting to see that we're making some
headway in that we are, so we'regetting better in the world.
Speaker 2 (29:57):
There's a lot of attention in clinical trials for
, you know, finding drugs forpulmonary fibrosis, both the
idiopathic versions of it aswell as the autoimmune versions
of fibrotic lung disease.
Speaker 1 (30:09):
Yeah.
Speaker 2 (30:10):
You know, so we are getting better at managing these
patients.
Speaker 1 (30:14):
And, as you well know , I mean there's.
The truth of the matter isthere are many ways a person's
life can come to an end, andsome are much worse than others,
and I would think kind ofslowly suffocating would be a
bad one, and so yeah, so that'sexciting to see that we're maybe
(30:36):
making some progress with somenew drugs, and I'm sure there's
many other drugs in the pipeline.
Some of them will work out andsome of them won't in the
clinical trials, but hopefullywe have an exciting future here
in developing some newmedications.
Speaker 2 (30:50):
And then there may be new delivery systems,
delivering using interventionaltechniques.
You know chemotherapy tonodules, you know.
Whether we have the technologyto ensure accuracy and to allow
that kind of risk is stilldebatable, but that's something
on the horizon that I think is agoal.
(31:10):
Yeah, you know.
So.
I think you know we haverobotics.
You know now in interventionalpulmonary Probably the yield is
probably a little bit better,you know, than the navigation
systems that we use now.
But you know down the roadwhether we can actually use it
(31:33):
both to diagnose and to treat.
That's a really importantquestion to answer.
Speaker 1 (31:38):
And you're talking about actually going down the
throat through the trachea andgetting to the lung nodule.
Speaker 2 (31:43):
That's correct and navigating to that nodule using
either robotics, you know, orGPS for the lung, so to speak.
Speaker 1 (31:52):
Yeah, and it's tougher than you know.
Probably most people wouldinitially think, because you
don't get to pick exactly whereyou go.
You have to follow thewindpipes.
Speaker 2 (32:02):
You have to be following the airway that you're
given.
Yeah, you know the ones thatGod made for you, and sometimes
things may be behind a wall youknow, and you, you know you have
to still be able to deliver andto both diagnose and to treat.
Speaker 1 (32:15):
And then on top of that, the lung is.
The whole lung is moving up anddown and the nodules moving up
and down.
That's correct, and so it's.
It's some fancy dancing to getthere, Right.
Speaker 2 (32:25):
And it's usually an hour and a half procedure,
whereas a typical bronchoscopymight be 20 minutes.
So it does take a lot of timeto to navigate to these, these
lesions, yeah.
Speaker 1 (32:36):
And I think I may have told you this once before,
but Don Busick once said thisabout you.
He said if you really want toget a good biopsy and get a good
piece of it, call Neil Ettinger.
And so I thought that was areal compliment.
Well, that was nice of Don tosay that.
Well, neil, thanks so much fornot only joining me today, but
all of the work that you do withour mutual patients and all the
(33:00):
work that you're doing withinterstitial lung disease and
trying to prolong the length ofpatients' lives and improve the
quality of their lives.
Speaker 2 (33:08):
Well, thank you, jason, and I do want to say that
the same goes for you, becausewhen we're making a diagnosis of
lung cancer in somebody, to beable to pick up the phone and
know that they're going to betreated with the care you
provide them, the emotionalsupport that you give them and
(33:28):
the high-quality medicine thatyou practice with them, you know
that really, you know, means alot to those of us that work
with you and take care of thesepatients.
Speaker 1 (33:37):
Oh, thank you, sir, I appreciate it.
Speaker 2 (33:39):
Thank you yeah.
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