We have two really amazing powerhouse, incredible keynote talks today, and this is the first
of them.
I'm really looking forward to this one.
We have Dr. Robert Lufkin, who's going to be talking about, well, the lies that he told
in medical school.
Dr. Lufkin has served as full professor at both UCLA and USC schools of medicine.
He's currently adjunct clinical professor at the USC School of Medicine with an academic
focus on the applied science of longevity.
In addition to being a practicing physician, he is author of over 200 peer reviewed scientific
papers, 14 books available in six languages.
And his most importantly, his two daughters play competitive volleyball, and it is our
great good fortune they do not have a game today.
So we can have him.
Dr. Lufkin, the stage and our attention is yours.
Thanks, Chris.
It's great to be here.
What a great organization this is.
I'm honored to be at this conference and really enjoying all the presentation so far.
And today I get to talk about something near and dear to my heart, the lies that I taught
in medical school.
Before I do, let me make a couple disclosures.
This is not medical advice, as everyone knows, this is for educational purposes only.
What I'm about to tell you does not represent the official opinion of either UCLA or USC
schools of medicine, where I have been or are currently a professor.
And then financial disclosures, you can check my website, I have numerous various health
longevity ventures, and eventually the sales from this book as well.
So now, one of the greatest physicians of all time is shown in this picture on the right.
Sir William Osler famously made one of the greatest quotes about medical education when
he was addressing a school of medical students on their graduation day.
And he said, gentlemen, and at the time, most all medical students were male, if not gentlemen.
He said, gentlemen, I have a confession to make.
Half of what we've just taught you in medical school is wrong.
And furthermore, we don't know which half.
And who's actually right about that, those of you who know medicine and even science
in general know this is the way it is, that it's constantly about learning things and
then figuring out what's wrong and then relearning new things and moving on and on and on.
And that's the way medicine and science moves forward.
So today, what I want to share with you is the half of things that I got wrong and that
I taught that were wrong.
And hopefully, you can learn from them and not make the same mistakes that I made.
And hopefully, you won't harm your life or your health like I did.
Let me start out, first of all, a little bit about my story.
This photograph was taken shortly after the last one.
And this is a picture of my mom and I, where my mom was actually a registered dietitian.
So she was a professional nutritionist and we were raised in a family where we religiously
followed the food pyramid, we ate low fat meals, we assiduously avoided butter because
of the saturated fat and we replaced it with what we thought was a healthy alternative,
which was margarine, which at the time was full of trans fats and industrial seed oils.
We avoided egg yolks and filled our meals, as we're told today, with cereals and grains
and other types of carbohydrates.
Fast forward a few years, I enjoyed her teaching so much about health that I eventually went
to medical school.
And this is a picture of me in medical school.
You can see how long ago it was because color film was still very expensive back then.
And obviously, haircuts weren't invented yet either.
If you look at my expression, it looks like I'm not having a very good time.
But actually, medical school is one of the best times in my life, except for right now.
But I was actually channeling one of my favorite rock stars of the time, which was, anybody
recognize this guy?
Peter Frampton, I think, I think it is anyway.
So I went through medical school, I enjoyed it so much that I eventually, I stayed on
and had a conventional career in academic medicine, which means I got to, I rose to
an academic rank of professor at both of these medical schools, and I still have that rank.
But the academic medicine meant that I got to practice medicine.
I was in the specialty of radiology, I am in the specialty of radiology.
So I got to practice medicine, see patients and teach, and actually one of my teachers
may be in the room today, he said he might be at this conference.
I also got to do scientific research, which meant that I had a laboratory with millions
of dollars in funding, both from the federal government, the National Institutes of Health,
also receive money from drug companies, also from equipment manufacturers.
As everyone did, I authored many, many papers, a peer-reviewed scientific papers, and I was
president of a couple international medical societies and had numerous patents, most
recently in artificial intelligence.
And then the last part, teaching, and those of you who do teaching will hopefully appreciate
this.
The great thing about teaching was that I often usually learn more from my students than
I wound up teaching them because of all the questions that they asked me.
And it was perhaps the most fulfilling part of the experience and continues to be to this
day, teaching healthcare professionals and training residents, et cetera.
And in doing this, I authored many textbooks and then lectured around the world.
So the point is that I'm basically a medical insider, I'm part of the establishment, I'm
not a conspiracy theorist.
I believe there are conspiracies out there, but I'm basically, I represent the establishment
here.
So everything went well, a little bit about my personal life.
These are my two daughters.
I found someone who would marry me, and we had a wonderful family here.
Everything was going great.
And then suddenly, almost at the same time, I was diagnosed with four chronic diseases
that I didn't, you know, I knew a little bit about them, but I went and talked to all the
experts that I could find both at the medical schools and in the community about these diseases
and how to treat them.
And what I learned and what they told me is these diseases were, there were some, some
interrelations, but they were largely unrelated, you know, gout and arthritis is not really
related to dyslipidemia and abnormal blood fats or hypertension, but that they would
take care of me as they did by prescribing certain drugs for these diseases.
And I was prescribed at least one drug for each of these conditions.
I was assured by the physicians taking care of me that these, these drugs would not only
treat the symptoms of the disease, but they would control the progression of it as well.
So that I was in good hands.
I could relax, I would take these drugs.
And then finally, they did mention lifestyle to me.
There were, there were some recommendations about, you know, exercising more, eating right,
whatever that meant.
They emphasized that lifestyle, you know, it's worth trying, but it didn't really work
and that I should look forward to a life of these drugs for the rest of my life and, you
know, eventually more as the disease has progressed.
Well, this was, this was really, really shocking and hard to take.
And I, it, I began to question all these.
And I started reading about it and talking to other colleagues and realized that there
was a revolution in information that I wasn't aware of.
And actually, some of the physicians I talked to that, that were prescribing these drugs
weren't aware of.
And I began to question and I now believe the fourth, the three things they told me were
incorrect.
And I began to drill down and try and understand some of these things about these diseases.
And I, I began to notice some things.
First of all, I wasn't alone.
For the diabetes, we're, we're in the world's largest diabetes epidemic that we've ever
seen.
It's, it's totally unsustainable.
Type two diabetes, of course, is the largest number and, and it's continuing to grow.
And I knew there was a, I knew there was a problem with obesity because most Americans,
most adult Americans are, if not obese, are overweight, statistically.
So I thought maybe it was related to, to obesity, but I wasn't fat at the time.
I had a dad bod, but I wasn't, I wasn't obese.
I wasn't even overweight by BMI scales.
So, but I realized, looking at some of this data that fully a third of people who get
type two diabetes are not overweight.
So it's not just a matter of getting fat and getting diabetes, although obesity is a risk
factor for, for diabetes, certainly.
The other thing that was a revelation to me that I, that I hadn't known before in that
sort of been getting wrong was that I used to think of diabetes as like a switch.
You either had it or you didn't have it.
It was sort of like, maybe like COVID, you know, you get infected or you don't get infected
or smallpox or it's like an infectious disease.
You either have the infection or you don't.
What I, what I learned is that these chronic diseases like diabetes, like Alzheimer's,
like cardiovascular disease, like cancer, like hypertension, and of course, obesity
are a gradual scale.
And for purposes of, of insurance, maybe we have a cutoff.
And when you cross a certain measure of glucose, fasting glucose, you're called a diabetic
or a pre-diabetic.
What the reality is, we're on a train for these diseases that can last years to decades
before they actually occur.
And this is an interesting study about type two diabetes.
This is, we're actually, this is, these are adult Americans who do not have diabetes.
And the interesting thing is if you look at their hemoglobin A1C marker, which is a surrogate
for, for fasting blood glucose, as you may know, that over time with age, this gets higher
and higher.
So it's almost like for, for many of us, type two diabetes is kind of like gray hair.
In other words, if we live long enough and don't die of something else first, we're on
the path to type, type, type two diabetes.
What does that mean?
We should think about the lifestyle choices we make with this in mind and some of these
other things.
The final wake-up call about, about diabetes and eventually all four of these, these chronic
diseases for me was that do at least the drugs work, right?
You know, that's, that's what we're taught.
And certainly insulin, metformin, these are life-saving drugs.
Insulin is life-saving for, for hyperglycemia in both type one and type two diabetics.
No question about it.
But today, diabetics don't die of, of hyperinsulinemia anymore or diabetic comas.
What diabetics die of is the number one cause of surgical amputations is diabetes.
Of course, the number one cause of renal failure, renal transplants and dialysis is diabetes.
A leading cause of blindness is diabetes.
Cardiovascular disease, strong association with diabetes.
Cancer, strong association with diabetes.
Alzheimer's disease is now so strongly associated with type, with diabetes that some researchers
refer to it as type three diabetes.
So what about these other, these other things?
If I take insulin, if I take metformin, if I'm taking these diabetic drugs, can I at
least rest assured that my disease is being taken care of and controlled?
And the answer, at least from this study and other studies here, is that these are type
two diabetics with intensive blood glucose control with insulin or sulfonylureas.
And what it shows is that they actually, the more intensive the control, the greater
the number of events they have, heart attacks and these other types of events.
So insulin doesn't really cure diabetes.
It just keeps you from dying from hyperinsulin coma.
And actually hyperinsulinemia and insulin resistance, as we're going to see, I believe
is at the, is at the foundation of the metabolic abnormalities that drive not only diabetes
but all chronic diseases that we die of, in effect, as we're going to see aging and longevity
itself.
Well, hypertension, like I said, I was in good company, half of adults almost have hypertension
in America.
I was given the recommendation to avoid salt and lose weight.
I wasn't overweight, so that didn't make a lot of sense.
Salt has been one of the major preservatives of food since the Egyptian times and until
refrigeration came about, people routinely ate huge amounts of salt and hypertension
wasn't that common before.
So something didn't really make sense there.
But there's new research showing that metabolic abnormalities, particularly processing sugar,
particularly the type of sugar known as fructose, is processed, interestingly, unlike glucose
which all our cells use.
Fructose, the only cells that process it are the liver, which is a detoxification organ.
And the liver detoxifies fructose very similar to the way it detoxifies alcohol.
And if you look at the metabolic pathway of fructose shown here, you can see that the
fructose is metabolized in the liver cell, driving inflammation, which is bad, drives
all the chronic diseases, but also creates uric acid, which contributes to the gout arthritis
that I had.
And then also blocks nitric oxide, which is an important chemical that relaxes the endothelium.
It's the way Viagra works.
It lowers blood pressure, nitric oxide, not only works on the vascular endothelium, but
also works on the immune system and the brain.
And who would have thought that fructose can interfere with that?
And then the last thing, and I'll just touch on, this is a complicated issue.
There's a whole chapter of my book on this, but I was given a statin for my blood lipids.
And this paper just came out about 12 months ago, January 23.
And this is a large study of 60 different studies, almost 300,000 patients that looked
at the effects of not only statins, but PCSK9 inhibitors and azetamide.
These are all insulin lowering drug strategy, I'm sorry, LDL cholesterol lowering drug
strategies.
And what they found was really interesting that the amount of LDL lowering didn't really
correlate with mortality at all.
You would think that if LDL is bad and LDL causes heart disease, that lowering it would
be associated with a greater decrease in mortality for heart disease.
This study didn't find it.
They actually found in some of the patients, or some of the studies within this, that these
LDL lowering drugs didn't actually change overall mortality.
And some of them, they do have a lowering, a small effect on the incidence of heart
attacks and cardiovascular disease on the order of a couple percent.
But this was offset fascinatingly by an increase in other causes of mortality in the population
like suicides and other things.
So there's a lot of complex issues there, but I'll leave that for now.
What happened towards the end of the 20th century, a researcher, Gerald Raven, up in
the Bay Area, came up with a description of a syndrome that he called Syndrome X. He later
renamed it Metabolic Syndrome, where he correlated three of the diseases that I had here that
were all caused by the same metabolic abnormality.
And he began doing research on it.
The problem is this wasn't very well received, because in order to treat this metabolic syndrome
and what he found as a cause of metabolic syndrome was a diet that was high in carbohydrates.
And the problem was the orthodoxy at the time, and still to this day, is that we should be
on a low-fat diet for cardiovascular health.
So this whole idea of metabolic syndrome wasn't very well received and sort of laid dormant,
because it would require everyone to completely change their dietary habits compared to what
the food pyramid and everybody else recommended.
Here's a study from looking at 2009 to 2016 to see how prevalent these metabolic abnormalities
that Gerald Raven described are in the population.
And they found that almost 88% of adult Americans have at least one of these metabolic abnormalities.
And it indicates that we're basically alarmingly ill with metabolic disease, but it's not appreciated,
because these are creeping up.
One person has hypertension, another has dyslipidemia, another has prediabetes.
Well, fast forward to the end of the 20th century, and a new molecule was discovered.
It was arguably the single most important biological switching molecule ever known.
How many people have heard of TOR, this audience?
I see maybe a third of the people, their hands going up.
TOR is fascinating, it's a biological switch that is so important that it's conserved
over billions of years all the way from yeast to human beings.
Every single cell has this switch in it, and yet only a third of people have even heard
of it.
TOR is fascinating, it's a survival switch that tells the cell, it detects nutrients
in the environment, things like glucose and all, and it tells the cell whether to grow
and turn on inflammation and grow, or to turn off when nutrients aren't available and do
things like autophagy and repair and heal.
And over our evolution, both of these are valuable, autophagy is valuable, repair is
valuable, growth is valuable, you don't want to turn TOR either way, you want TOR to be
turned both ways, on and off and on and off.
What's happened though in modern civilization, because of our dietary habits where we're
continually eating and grazing all the time, eating junk food 18 hours a day, TOR is increasingly
turned on to the growth mode.
And there's growing evidence that this consistent hyperactivity in TOR is driving not only the
diseases of metabolic syndrome, but also many of the chronic diseases shown above, like
we've talked about heart disease and stroke, cancer, Alzheimer's disease, and interestingly
even mental illness.
So let's take a look at this and see what we can do.
The best way to deactivate TOR and control the TOR switch and this metabolic disease
switch is with lifestyle, but I want to look at the scientific evidence for what I'm showing
you here and seeing if there's a way we can turn down TOR and see what effects it has,
not only on these diseases, but there's growing evidence that TOR actually drives aging and
not only that longevity itself.
And as it turns out, there's a drug that works on TOR.
As anybody know the name of the drug, a few people do, sure, yeah, it's rapamycin, was
discovered in the 60s in Rapa Nui from the soil there, and there's a wonderful radio
lab story about how that happens.
It's very, very colorful, but rapamycin is a targeted drug that turns TOR off.
In fact, TOR was named as TOR as the target of rapamycin or mTOR, the mechanistic target
of rapamycin.
So rapamycin is a drug that we can give that will turn TOR down and reverse these metabolic
abnormalities, and this is a surrogate for the lifestyle that we're going to talk about
in a minute, but let's look at some studies using rapamycin and what happens.
Let's first look at the phenotypes of aging.
These are the appearances of aging, and then we'll look at the chronic diseases, but the
phenotypes of aging are the obvious ones that anybody can recognize.
Hair changes, loss of hair, gray hair.
This is an animal model for hair loss.
This is a mouse model, and it's interesting, when rapamycin was given to these bald mice,
the hair actually re-grew, and if you look at the graph on the right, the pigmentation
of the hair increased with rapamycin.
What does that mean?
Well, it's reversing gray hair in the animal model, at least.
This is just animals, and it's also increasing the hair growth, which is fascinating.
Why would this M-Tor have anything to do with hair if it weren't a fundamental mechanism
of all aging and longevity and chronic disease itself?
Let's look at something else, skin changes.
This is actually a human study.
It's a small study, but it was a prospective controlled, blinded study.
Individuals rubbed cream on the back of their hands once a day for six months, and then
at the end of the study, these brave souls had punched biopsies of their hands to look
at that, and this is the histology from them.
You can see on one side collagen with the rapamycin, there's actually collagen has
regrown in the basal layers versus the other side, and this is just over six months, and
you can see actually graphic changes in the skin quality from the rapamycin.
Rapamycin is not only affecting gray hair, but also wrinkles and other things.
Actually, rapamycin, as you may know, is an FDA approved drug for certain indications.
It was originally approved for renal transplant, immune suppression, which is a scary thing.
That's why many physicians are afraid of it, but I think we don't have to be afraid of
it.
In fact, the FDA just approved skin cream a few months ago for rapamycin, not to get
rid of wrinkles like these people did, but for lymph angiomatosis for another indication.
People are using the skin cream off-label now for their wrinkles and this sort of thing.
That's gray hair and wrinkles, a big deal.
What are some other things in aging?
Peridonal disease, old people lose their teeth.
This is an animal model of periodontal disease.
You can actually see the absorption of the teeth right here.
This is the periodontal disease where this is the control, and then with rapamycin it
actually gets less.
These are young mice.
You can measure the resorption.
It's relatively small.
Adult mice, it gets larger, and then old mice, it gets huge as their teeth falls out.
When these mice get rapamycin orally, it actually reverses periodontal disease.
Rapamycin toothpaste may be in our future, and there's actually people have patented
that already.
Hearing loss, even if you manage to avoid those Led Zeppelin concerts in your youth,
60% or 50% of 60-year-olds have some degree of hearing impairment related to age, and
it gets worse over there.
Gets worse after that.
This is a study, again, an animal study with mice, but it shows the cochlear hair cells,
which are the measurements of damage to the cochlea, the hearing organ.
The number of hairs actually increase when these animals are put on rapamycin, and there's
some basic levels of hearing that actually improve when they're on rapamycin.
This is crazy.
It's improving all these phenotypes of aging.
What are other phenotypes of aging?
Here's one that only affects 50% of the population, but every single one of this population gets
it if they live long enough, and that's ovarian failure.
Menopause is an age-related condition.
It's aging.
If rapamycin and turning down mTOR is a master switch for longevity and aging, it should
affect menopause, too.
Let's see what the data shows.
This is an animal model for aging in the mouse model.
When the mice are given rapamycin here on the left graph, you can see that the number
of pups in their litter increases, and the age of mice at menopause gets greater.
In other words, it increases their fertility, and it delays the onset of menopause.
In fact, human studies are now underway using rapamycin to turn down mTOR for this particular
condition.
But wait a minute.
You're saying, hey, nobody dies of baldness or gray hair.
Nobody dies of menopause, even.
What about longevity, right?
What do we die of?
Well, it's actually a very simple question.
All of us in this room, statistically, most of us will die of one of the diseases on this
list.
In fact, most of us are going to die of heart disease, and slightly fewer of us will die
of cancer, and then it'll go down the list, including Alzheimer's disease and stroke.
If turning down mTOR in this metabolic pathway is a universal effector in aging and longevity,
it's not enough just to turn near hair, get rid of gray hair and wrinkles, but it should
affect these diseases of aging, right?
I mean, because this is what determines our longevity.
Let's take a look at these.
Heart disease, everybody knows in this audience, when we say heart disease and stroke, it's
atherosclerosis primarily, which is hyperplasia of the intima of the blood vessels, which
cause narrowing of the blood vessels, right?
If I get a heart attack today, the treatment, in most cases, all will get a stent, which
is a mechanical device that opens up the blood vessel.
It's inserted endovascularly, and it opens up the narrowing of the blood vessel.
Many people, when they have stents, they go, oh, I had a heart attack, but I got my stent,
so it's taken care of.
Well, getting a stent for a heart attack is sort of like getting insulin in a hyperglycemic
reaction.
It takes care of the acute event, but it doesn't change anything to do with the underlying
cardiovascular disease.
In other words, the rest of my blood vessels are going to continue to narrow.
In fact, the area of the stent is even going to narrow and clot off again, and that's what
happens with stents.
So what does turning down mTOR do with cardiovascular disease?
The graph on the right shows patients, the cumulative frequency here, and then the stenosis,
the narrowing of the vessels, and you can see that people immediately, when the stent
is placed, and then after six months, the stents quickly narrow down again, but the
point here is rapamycin delays, prevents this narrowing of the stent.
It prevents the atherosclerosis or dramatically slows it.
In fact, so much so that the FDA has now approved rapamycin turning down mTOR as an indication
for stent coding, and the best stent coding treatments are with serolimus or a rapamycin
type drug, and people are even, there are studies now looking at oral rapamycin to slow
down cardiovascular disease in all the blood vessels there.
So that's cardiovascular disease, but what about cancer?
How can rapamycin affect cancer, you know, turning down mTOR?
If it is truly fundamental in all these chronic diseases, it should affect cancer also.
Well, in cancer, there's a very powerful human model of cancer in transplant patients.
I didn't know this, but actually for heart transplant patients, the number one cause
of death within the first five years following transplants is not transplant rejection, which
is what I would have thought, but instead, it's a malignancy occurring due to the immune
suppression and everything, a number of factors.
So these studies here are looking at time from transplant in years and patient survival
and malignancy-free survival, and the graph at the top is patients who had rapamycin for
their immune suppression, for their treatment for the transplant, versus other types of
immune suppression, which did not include mTOR suppressors like rapamycin, and they're
shown down below at the bottom.
So it's a 38% versus a 70% difference in cancer rates with mTOR turning down in these patients.
And no surprise, the FDA has now approved rapamycin for eight indications for cancer,
including things like metastatic renal cell carcinoma, which is the most common renal malignancy
there.
So interestingly, turning down mTOR in these metabolic pathways actually works on the second
killer of all of us, which is cancer and the second determinant of longevity.
What about Alzheimer's disease?
Alzheimer's disease, if you think about it, represents the ultimate failure of our medical
research establishment, right?
We've had decades of time, and really when you think about it, unlimited financial resources
for drug companies to come up with pharmaceuticals that effectively slow down Alzheimer's or
have any effect on it.
And to this day, there's no drug that really works to significantly slow down the progression
of Alzheimer's disease.
And that may be a number of reasons, and we go to detail it in the book, it may be that
the beta amyloid model is flawed, and that's probably true.
But back to point here, if turning down mTOR is fundamental, what does mTOR have to do
with Alzheimer's disease?
What if we give rapamycin to Alzheimer's models?
And these are mice models for Alzheimer's disease on the left, and these are mice that
are engineered mouse-heimer models, if you will, where they actually get cognitive impairment.
And you can test the cognitive impairment on the mice reliably, and you can see that
this is the wild-type mice here, and then these are the mice with Alzheimer's disease.
They have a decreased contextual memory test, but interestingly, when rapamycin is given
to these mice, their cognitive functions return almost to the level of normals.
And this is, there are some other experiments on the right with Alzheimer's disease, also
in animal models, showing mTOR suppression having significant effects on there.
Bottom line is, this is extremely promising, and to the point where the University of Texas
now has a human study, a multi-million dollar human study for Alzheimer's disease with patients
giving rapamycin as well as other metabolic therapies there.
Well these are, it's all great to have this effect on these chronic diseases, but just
out of curiosity, what about longevity itself?
Does this translate into longevity?
In other words, if we do these lifestyle changes that turn down mTOR that fix our metabolic
disease, do we live longer?
Is there any evidence for that?
Well, for humans, unfortunately not, just because humans live, you know, a hundred years
and it's not practical to do long-term longevity studies in humans, but there is a gold standard
longevity mechanism, testing mechanism, that was set up about twenty years ago by the federal
government.
It's called the Interventions Testing Program from the National Institutes of Aging.
It's a great model.
They take mice that are wild-type mice, they're not lab mice, but they're bred to be heterogeneous
mice, and they take these mice and they divide them into two groups.
Mice only live about three years, so they let one group live their normal life, and then
the other group, they give them a drug, and then they see if there's any difference, and
then they graph survival versus age there, as you can see on this picture here, and the
untreated mice live here and live this age, and then if the intervention is successful
and it improves longevity, it'll show an increase in survival, like we see here on the yellow
curve there.
So the great thing about this test is you can all write in and recommend things to be
tested, because it's a federal program, they accept recommendations from the public.
So over the years, things like resveratrol, MCT oil, curcumin, methylene blue, statins
have been tested, NAD supplements, ashwagandha, green tea extract, metformin, all these things
have been tried, and what were the results?
None of them worked, there was no significant difference from any of these.
Now, there's a caveat here, of course, when a drug fails the intervention's testing program,
it just means it didn't work at that particular dose.
In other words, as we all know, if I have pneumonia and I take an antibiotic from the
pneumonia and I take the wrong dose, or it's too low a dose, it won't work.
So if a drug fails the ITP, it means it just fails at that dose.
So it may work at another dose, we just don't know.
Well, you might ask, did anything work?
Are there any drugs that actually make animals live longer?
And yeah, here are some successes.
Small amounts, things like aspirin, only males.
Acarbose is a diabetes drug that blocks carbohydrate absorption, it actually increased longevity
in both males and females, a small amount.
If you have any, if you're still on the fence about a low carb diet, this is a drug
that blocks carbohydrates in your gut and you actually live longer from it, so think
about that.
A couple other drugs there, small effects.
Well, what about blocking mTOR?
This is what we're talking about, right?
The ultimate metabolic pathway.
If we block mTOR, what does that do to survival?
This is rapamycin from the ITP, a dramatic effect in survival.
The interesting thing, and this rapamycin produces dramatic longevity, survival effects
in every animal system it's been tested in.
It's tested in yeast, it's tested in flatworms, it's tested in fruit flies, and it's even
tested in dogs.
So the interesting thing about this particular study with rapamycin is most of these ITP
studies, the animals are given the drugs their entire life, you know, from birth till death,
this get the effect.
And that's not really realistic for all of us sitting in the room here, right?
Well, in this study with rapamycin and these mice, there was a mix up on the formulation
of the food.
So the animals didn't get the rapamycin until they were the equivalent of 60 to 70 years
old in humans age, until near the end of their life.
And the point is that even beginning rapamycin late in life in this particular animal model
resulted in a dramatic improvement in longevity.
So then the question is, okay, here's a drug that turns down mTOR, why don't we just take
this drug and maybe a few others throw in a carbose or something, and we'll just all
live longer, we won't get these chronic diseases as soon.
Is that the answer?
Probably not.
Why not?
Well, we really, really don't understand these drugs.
We don't understand mTOR.
It's linked with many other longevity pathways like AMP kinase and insulin like growth factor
and many different things.
There are surprises constantly happening in 2016 when they combined metformin plus rapamycin.
Rapamycin has no effect on longevity in the ITP.
When they combined it with rapamycin, they got actually a greater effect than either
one of those individually.
And then in 2022, just a few months ago, they published when they combined rapamycin and
a carbose, they got an even greater effect on longevity.
So something is going on there.
And ultimately, the greatest effectors of the greatest way to turn down mTOR is with
lifestyle and these basic effects there.
Now, should you take rapamycin?
That's up to you and your doctor.
I mean, I take it, but I also do lifestyle.
And if I had to give up one, I'd give up the rapamycin because lifestyle is most important.
So what happened to me?
After doing all this reading and research and everything, I dramatically changed my lifestyle.
I got rid of junk food and it was not easy because I'm a recovering junk food addict.
It was not an easy task to give up junk food.
I stopped eating all the time.
So I now eat one meal a day with my kids at dinner time and I've never felt better.
It's not like I'm fasting or giving up.
I just feel better.
I don't get brain fog in the middle of the day and it's wonderful.
But I give up carbohydrates, refined carbohydrates.
I give up seed oils and I give up grains.
For me, that's what works.
I looked at my sleep.
I also looked at exercise.
I looked at stress.
And the question is, did it work?
What happened?
Well, I went in after doing this and it was actually a fairly short amount of time.
In the order of months, I went into my doctor's office and they couldn't believe it.
They thought the lab tests were an error and they wanted me to repeat the tests.
They couldn't believe it.
All my lab values had returned to normal and I had no more symptoms and I was off all medications.
And to this day, that was, hey, thank you.
No one's ever applauded before, but I'll take it.
Thank you.
Yeah, and to this day, I'm still following that lifestyle.
It's not a diet.
It's just the way I live now and I've never felt better and it's working for me.
So I began to think, I think this is great.
A lot of people don't know this.
A lot of my colleagues don't know that.
And they're even teaching wrong things to people in the profession.
So I wanted to reach out and instead of writing textbooks that nobody reads, I try and reach
out in social media and other ways of getting the message out to the general public.
So after never having tweeted or really done Facebook or anything, I dove headfirst into
social media.
I just passed 100,000 followers on Twitter.
I've got 250,000 total with Instagram.
I'm not on TikTok yet, but my teenage daughters are pressuring me.
So that may be coming there as well.
So I began reaching out.
This book is going to be published in the spring from Ben Bella Press,
which is Penguin Random House Imprint.
And then I get a lot of speaking engagements.
My hero growing up was William Shatner in Star Trek.
And, you know, my dream was someday to be on a program with him.
And sure enough, next month in Miami, Mr. Shatner and I are going
to be speaking at a longevity biohacking conference.
And I have to say at 92, almost 93,
he knows a lot more about longevity than I do.
So I'm really looking forward to what he has to say.
Also, I just came back from Costa Rica.
We filmed a television series there on how people can understand metabolism,
how they can turn down mTOR with their lifestyle and other factors,
and how they can actually do all the things we're talking about here,
change the phenotypes of aging, reverse the chronic diseases,
and actually live longer.
And the show has just been picked up by PBS, and it'll be
on the Discovery Channel in about six months to a year when it's coming out.
So.
But I had to be honest enough with myself that, you know,
this is all just sort of flash.
And if you really want to move the needle on medicine and research
and science, you have to do the science
and actually do something with it.
So the next step what I did was got together with several colleagues
in Los Angeles, and we've purchased a,
essentially 120,000 member managed care organization in Los Angeles.
And this is an underserved group with Medicare, Medicaid patients
in a socioeconomically poor area.
They get poor health care.
They don't get access to cutting-edge health care.
They have poor longevity.
They have poor metabolic health, and it's our mission to change all of that.
We have 200 physicians, primary care physicians, 600 specialists.
And the great thing about a managed care organization like this is,
unlike an insurance company where you basically make money
by denying claims, sadly, with a managed care organization,
it's really up to us.
We can choose whatever we want that works
to make the patients live longer and live healthier.
And the healthier they are, the more successful the managed care organization is.
What that means is that we can do any sort of interventions we want.
We can do red light therapy.
We can do massage.
We can do meditation.
We can even give away movie theater tickets to people who go to the gym or whatever.
So this may be a fun collaboration with FLCC and some of your innovations
and some of your programs.
We'd love to get them started in this population of underserved patients.
On top of this, we're putting together an innovation lab.
So we can take new companies that come in in an incubator style,
like Y Combinator type incubators.
And we will help them test new medical interventions,
new strategies, thinking out of the box, thinking different ways on this population.
And if they work, then we'll scale it with this whole population
and even a greater number there.
And we hope to set up a venture studio fund so that the companies can be funded as well
and really take off there.
So we're really excited about this.
But again, at the end of the day, we realize this really wasn't enough.
If you really, really want to change the needle and really, really change the future,
you have to reach the people, the new generation,
the new people who are being trained now, the new students.
And to that, we've just formed a new graduate medical education program
in Southern California at a hospital there
where we have accredited graduate medical education programs.
Thank you in family medicine, psychiatry, transitional care medicine.
We're adding radiology this summer.
And we're even in discussions with the state of California
about possibly adding on undergraduate and making it a whole medical school.
But the idea is these people will be trained with a view of the new medicine,
the way of seeing how these things can really make a difference in these patients.
So this is a great time to be in health care.
I mean, I'm excited about the longevity things,
especially as the older I get out of self-interest.
But longevity progress means that all the chronic diseases are being addressed.
That's what longevity means.
And there's really been a revolution in longevity, in our understanding.
Literally in the last 10 years, all of these things have happened.
This is a maximum lifespan on a C. elegans model, which is the flatworm model.
But you can see caloric restriction or lifestyle is one of the most powerful,
strongest ones, but rapamycin's right up there.
And then there's a whole list of other ones that are being developed
and new ones are coming forward every day.
In fact, Ray Kurzweil is a person who, a scientist,
who talks about escape velocity and longevity.
He's saying that as more and more of these longevity innovations in our age,
our life expectancy keeps increasing, increasing, increasing.
At a certain point, you're going to exceed the rate of increases
so that basically people live indefinitely.
You know, I don't know about that, but it's an interesting aspiration
and an interesting idea for hope for people.
So we're really in a remarkable time today.
I mean, 2024, who would have thought that, you know,
an 80-something-year-old woman would be on the cover as a model
for the sports-illustrated swimsuit issue, no less?
And of course, our friends there, Mick and Keith, are touring now in their 80s
with Rolling Stones, filling up stadiums with tens of thousands of people.
And because this is not a political conference,
I'm not going to have their pictures there, but I'm sure you know the two
leading candidates from the political parties will be in their 80s when they do this.
So this is an exciting time.
I think the message is metabolic illness is something we need to pay attention to.
I think it's fundamental in all these chronic diseases
that ultimately determine our longevity.
And while rapamycin is a great drug and it does a lot of things,
really the way to change metabolic disease and change longevity is
by changing our lifestyle.
The great thing about lifestyle is it puts the power back in our hands.
Every morning when I get up, I get to make a decision about what foods I eat,
when I eat, I get to make a decision about do I exercise, what I do with my life.
And I'm suddenly in control of my life, and it's a big deal.
I think this is a revolution, and hopefully the best is yet to come.
This is a, thank you.
All in here, this is a book here.
If you want a sample chapter of my book, please just email that and just put lies
in the subject line, and we'll mail you the first chapter of the book.
You can check it out.
It's not going to be out until June, but hopefully you'll enjoy it.
Buy it, or get it from your library.
Anyway, thanks so much, and have a great day.
Chris, did you want to take questions or two, or we're?
We're going to have a few questions.
Okay.
We're going to have, so why don't you grab a seat over here?
Okay.
Anyone, pick one.
Very quickly, if the Wi-Fi is still not up,
and you want to ask a Slido question, you just turn your Wi-Fi off.
I've been informed, and it works across cellular.
We're going to burn your plans up to get your questions in.
Otherwise, if that doesn't work, we will also have some microphones.
So, we just want to make sure we get all the questions in.
I see some have come up here on this.
So, first question.
Robert, when you walk around, you just look at people and say, man,
that dude needs some mTOR suppression.
No judgment.
I've got my own set of imperfections.
We're all on this journey together.
All right, can you, Abigail Hemkin is asking,
can you address the black box warning on rapamycin?
Yeah, great question.
I think the black box warning is related to immune suppression.
I think, if I'm not mistaken.
And rapamycin, like I said, was FDA approved for immune suppression
for renal cell transplant and other things.
That's given on a daily dose.
And when rapamycin is given once a week,
it actually improves immune function in humans
as Joan Manek showed in a 2016 study.
It was a small study.
It was a prospective study.
It improves immune function.
And that is the dosing regimen that people take for metabolic health
for longevity and to turn down mTOR.
It's once a week.
And that black box warning is, how serious is it?
Well, you don't want to take it daily to turn down immune function.
So, you definitely want to take it once a week.
Rapamycin is very safe drug.
There are relatively few side effects from it.
The only thing people ever really significantly report are mouth ulcers,
but those go away.
And there's a report in the literature someone tried
to overdose on rapamycin.
They took about 5 to 10 times the normal dose, went to an emergency room,
and basically nothing happened.
They, you know, punt their stomach, they went home,
and there wasn't any problem with it.
So, it seems to be otherwise a very same safe drug.
As far as side effects, despite the dramatic effects, as we've seen,
at least with obviously cherry-picked literature that I showed you,
but it showed some very tantalizing promising effects
on phenotypes of aging and chronic disease.
Excellent. So, we have a question from Anonymous here.
Is there a natural source of rapamycin?
Yeah, rapamycin is from nature.
It's from a bacteria that was isolated, as I mentioned briefly,
in the talk from the soil from Easter Island or Rapa Nui.
And so, it can be grown from the bacteria.
So, if the bottom of the food pyramid now should be dirt,
that's what I'm going to say.
That's right.
Sounds like it.
You know, I've already looked in.
Jen Reel is asking, any data comparing rapamycin
to caloric restriction?
Yeah, that's a great question.
Cleric restriction is the longest-standing
and by far the most consistent improvement in longevity.
It's been known for decades.
And the way rapamycin works, it's believed, is obviously
by turning down mTOR, which means that the cells,
since there are no nutrients there.
So, you're sort of fooling the body into thinking
that you're fasting.
So, those mechanisms seem to be very similar there.
Now, one could argue, and it's still not known,
and this is the argument that I make,
that turning down mTOR with rapamycin may not be the same
as fasting.
It mimics one aspect of it, but just because we don't know,
I would still recommend lifestyle strategies
such as time-restricted feeding, fasting,
and watching other things as well.
Well, we have another question around that,
which is what dose of rapamycin may help
for premature ovarian insufficiency?
I'm seeing more young women post-jab suffering from POI.
No medical advice here.
I have no idea on the dose for that.
I think if you look at the literature,
if you, the one article is referenced on my slides,
and if you download the chapter,
I'll have the references on there as well.
But you can check.
I suspect it would be similar to the longevity strategy,
which is 6 to 10 milligrams once a week.
Great, thank you.
But there are studies underway, so if you Google it
or PubMed it, you can get some more information on that.
I'm sorry, I just don't know off the top of my head.
Yeah, interesting.
Sebastian McGee, important question, gets right to the heart
of your talk, is someone applying to medical school now,
how can I most readily distinguish between truth
and non-truth in medical education?
If you know the answer to that, come on up here,
and I'm going to sit down.
That's a great question.
And everything is evolving.
And, you know, as somebody pointed out, the book I'm writing
about lies I told in medical school, well,
the stuff that people are teaching now, they're still,
you know, half of it is going to be wrong, you know,
20 years from now or 10 years from now.
So it's a very good question, but it's very difficult to answer.
I think we look at the best evidence we have
which are, you know, controlled clinical studies
which show causality rather than just epidemiological studies
which show correlation.
And we, you know, all we can do is we use our minds
and use our best judgment to analyze them and just be humble
and accepting that, you know, half of what we know is probably
wrong.
Well, how about the stuff that you learn about nutrition
in medical school?
Can we just take that and throw that right out the window?
Yeah, I mean, to this day, most medical education is very
light on nutrition.
You know, it's a matter of a couple hours, typically.
And so it's, most doctors get very little training
on nutrition.
Yeah.
And it's usually by the nutritional institutions
like the American Dietetic Association or it has a new name
now that my mom was a member of.
But it was funded, it was founded by a religious group
that happens to have a very vegetarian agenda.
I have nothing against vegetarians.
I was a vegetarian for a few years.
But anytime you have either a religious group
or a specific agenda driving nutritional choices,
that can be very bad.
In fact, the Longevity Blue Zones brand was just purchased
by the same religious group with the vegetarian agenda.
So that will probably influencing the messaging
on that as well, which is not good.
Fascinating.
Brad is asking, physicians are often defensive
when patients present non-traditional approaches.
How do you suggest the conversation should begin?
That's a great idea.
I mean, it's all about patients taking control
of their own lives and the most powerful thing,
the most powerful medical tools we have
for chronic diseases at least, not necessarily a fracture
or a contusion, but for chronic diseases are,
in my opinion, the lifestyle factors.
So it needs to be a back and forth conversation
with your physician on that.
And if your physician is not in agreement with you,
then you're probably not going to convince them necessarily,
although you can try.
But the ultimate option is just to find another physician.
Good. Well, let's see.
Anonymous asking, what is the name
of your new graduate medical program and contact information?
Yeah, if you want, just contact me on my website.
It's at a small hospital in Southern California
in the Los Angeles area.
And what track would you take to begin to wake,
I guess wake up a California nurse who graduated shortly
before the COVID moment, work through that,
but who doesn't see the corruption yet anonymous question?
I bet there's a name attached to this question.
That's a great question.
You know, it's just getting into dialogue with people
and, you know, having honest, humble conversations
and, you know, doing your best.
I don't have any particular insight on that, unfortunately.
Interesting. Well, I mean, you've been certainly up
against that pushing against all of this.
I love your disclaimers, right?
Hey, my views, my views alone, you know, all of that.
Is that a stay employed sort of a strategy?
Well, they actually, they like all their speakers to do that.
So it's not necessarily that my stuff is particularly
off the rails, although it is more on the edge
than many of their people talk about.
Yeah. Fascinating.
If there are more questions, they're not appearing.
I have one here, old school Slido.
Not sure about this word. Ever try, is that pregnesolone?
Pregnesolone precursor of 154 hormones was drug of choice
to cure arthritis and lower cholesterol.
Pregnenolone. No, I haven't tried it.
All right. Diane, registered nurse, is asking,
how is it that USC and UCLA supporting Dr. Lufkin
with the research he's doing and wanting to change
what is being taught seems to go against the narrative?
Okay. Well, to be clear, the laboratory I had at UCLA
was funded by drug companies and pharmaceutical
and device companies and the government.
I was researching things in radiology and all.
I wasn't researching this.
After I got these diseases and went on this personal journey,
that's when I've changed and I'm no longer doing research
myself in the lab, which is both good and bad
for a number of reasons.
I'm now reaching out, doing things like this
and on social media and all the things
that I talked about there.
So they are, my lab is no longer running at UCLA
and they're minimally supporting me on this.
Yep. Well, I noticed that you said,
wow, I did these four simple things.
I mean, their lifestyle changes
will not always be experienced as simple,
but you did these things, they worked.
We would think in an evidence-based society
that that would get picked up and replicated.
What's, is that really gotten traction
or do you feel like your colleagues sort of look at you and?
Well, the things I did in these lifestyle changes,
they're simple, but they're not easy
and that's an important difference to make.
Our medical system today is designed
both on the physician side and the patient side.
Everybody wants a pill.
The patient want, they come in,
they want a pill for something
and the doctor gives them a pill.
In seven minutes, you don't have time
to explain a low carbohydrate diet
or these lifestyle changes, they take a lot of time.
Furthermore, it's not enough just to educate the people
that sugar is bad for you and causes heart disease.
There are addictions things at play.
Like I said, I was a junk food addict,
I am a junk food addict.
So I know that for some people,
they need to have coaching programs
or they need to have intensive addiction help.
In fact, we're doing low-dose naltrexone
for some junk food addiction,
which is a drug that's used for other types
of physical addictions.
And as it turns out, it's fascinating.
Low-dose naltrexone is actually a longevity drug too,
which leads to increased longevity
for all sorts of reasons
that you can hypothesize and imagine.
Well, very good.
Well, thank you very much for your talk.
Thanks, Chris.
