Tim Ferriss on Ketosis, Microbiome, Lyme Disease, and Biomarkers

Tim Ferriss on Ketosis, Microbiome, Lyme Disease, and Biomarkers

July 26, 2019 100 By William Morgan


All right.
Dr. Rhonda Patrick here.
Today I’m very excited to be sitting here
with my friend Tim Ferriss, a notorious self-experimenter,
a three-time New York Times bestselling author,
an angel investor, startup advisor, and much,
much, much more.
So before we start, I really just want to
say that I really enjoyed the last time you
had and I had a conversation.
Me too.
It was about a year ago, I think, on your
podcast.
Oh my gosh.
Time flies.
Micronutrients, aging, epigenetics, stem cells,
all that stuff, super fun.
So I’m very excited to have the opportunity
to interview you on my podcast.
Yeah.
I’m intimidated.
But I’m looking forward to it.
Great.
I kind of want to start off with the self-experimentation.
Sure.
We were actually just having this interesting
conversation that we’ve stopped so that we
can continue it live and that has to do with
a little bit about the night you just had
and what you’re doing to recover from that
night.
Do you want to talk a little bit about that?
So I had, like a lot of people on Saturday
nights, a little more booze than intended
or anticipated.
We were talking about mineral excretion.
I was talking about some of my pregame tactics,
whether that’s consuming carbohydrates.
I tend to drink the most booze on cheat days
for that reason because I’m retaining whatever
it is, I guess 4 grams of water per gram of
carbohydrates, something like that.
So it helps to counteract the effects of inhibition
of vasopressin because vasopressin is an anti-diuretic
hormone, which means it prevents you from
peeing or minimizes peeing.
So it’s used in children who bed wet past
a certain age.
I think they use desmopressin.
I became, jumping around a little bit, but
I became interested in vasopressin first because
when I was in college, I was reading up on
the smart drug literature at the time and
it was purported for being very effective
for boosting short-term memory.
So you would take hits in each nostril, study
whatever you had to study and then quickly
scurry off to the test before it evaporated.
Right.
But then you had some very interesting comments
on vasopressin.
Yes.
So I did use vasopressin for a period of time,
found the headaches and side effects ultimately
not worth it for me the way that I was using
it.
But it is something that’s kind of stuck with
me when someone says, “Oh my god.
I was at the bar and then all of a sudden
I time traveled and I was at Denny’s.”
I’m like, “Aha, it might have something to
do with vasopressin because you just gave
yourself sort of a reverse smart drug.”
Very interesting.
Yeah.
I’m familiar with vasopressin because it’s
also a hormone.
It’s a social hormone.
And it’s particularly important.
It’s kind of like the counter, or not the
counter, it’s the male version of oxytocin.
So in females, oxytocin is this notorious
love hormone.
When you produce oxytocin, you feel good,
you bond, social bonding, things like that.
Well, in males, vasopressin serves a similar
role to oxytocin in females.
Vasopressin is associated with pair bonding
and specifically with monogamy.
So they’ve done studies in prairie voles where
they actually genetically engineer them to
not be able to respond to vasopressin.
So they like engineer their vasopressin receptor
to be non-responsive.
And these prairie voles, which are monogamous
become polygamous like that.
So it’s very interesting.
Also, they’ve done human studies where they’ve
looked at gene polymorphisms which are just
variations in the sequence of DNA of a gene
that changes the function.
We all have various polymorphisms.
You’re familiar with that.
So there’s a particular variety of this polymorphism
in the vasopressin receptors that males have
that make them less responsive to vasopressin.
These males are more likely to be either divorced
or never been married, whereas males that
don’t have this polymorphism are more likely
to be happily married.
Surprise, surprise.
So yeah, alcohol, there may be actually a
mechanism through vasopressin that leads to
polygamy or being more promiscuous, I guess.
I wonder if that’s in the water in San Francisco.
It’s sort of ground zero for all the polyamorous
flag wavers.
So on the self-experimentation topic, you’ve
been self-experimenting for many years and
I was wondering if throughout your years of
experimentation if there are three or four
biomarkers . . . so, you typically measure
blood biomarkers routinely.
If there are three or four really important
ones that you think are important that you
routinely measure and if they have anything
to do with performance or mental acuity or
perhaps aging.
Yeah.
There are a few . . . well, there are many
blood markers that I look at.
I had a fun conversation with Pete Attia on
the podcast not too long ago about this.
But my markers, the markers that I’m following
right now are number one, my millimolar concentration
of ketones.
So I have a device just on the counter over
there, a Precision Xtra device by Abbott Labs
that allows me to use both glucose strips
and ketone strips.
So I can look at my fasting or waking fasting
glucose level and then ketone level and monitor
that after certain types of, say, exercise
when the ketone level can drop and so on and
so forth.
Because I’ve identified for myself, part of
the reason I have fat in my tea, is I operated
best mentally at around 1.1 to 1.7 millimolars
and I only figured that out by tracking.
Very interesting.
Some people, for instance, perform much better
the higher concentration.
The higher the concentration of ketones, the
better they feel.
I don’t fall in that camp.
I was having a conversation with a scientist
a few days ago about this.
He said, “Well, really,” and this is not a
new observation, “But your blood level of
ketones can be gained or increased in many
different ways.”
So you can just eat a meal that’s full of
medium chain triglycerides or eat a meal that’s
just full of fat in general and you can spike
your ketone level.
That’s not necessarily indicative of an endogenous
production of ketones or you could be fasting
and like deep fasting after five or six or
seven days.
In my particular case, I think you also want
to look at–and this is true, a lot of very
smart people like Pete Attia, Dom D’Agostino,
very, very smart guy, Dominic–would say likely
that it also could be some people utilize
ketones better than others.
Yes.
So just because you have a high level of ketones,
doesn’t mean you’re necessarily doing a lot
with it.
So in my case, a high level of ketones, my
hypothesis is well maybe past a certain point,
my kind of machinery gets very inefficient
or gets damaged.
So between 1.1 and 1.7, my brain operates
functions at a level reminiscent of pre-Lyme.
That’s a whole separate thing.
I kind of knocked out normal cognitive function
for nine months due to severe Lyme disease.
But when I am focused on at least a nominal
amount of ketones, I feel like my old self.
So that’s one.
Other things that I focus on or look at . . . there
are some esoteric things that I play with
every once in a while.
But if you’re looking at the routine levels,
I’m going to look at obviously the sex hormones,
look at free testosterone.
I’ll look at free testosterone as relative
to sex hormone binding globulin, for instance.
I’m not convinced that higher sex hormone
binding globulin is always a bad thing.
That’s a whole separate.
Because my testosterone in experimenting with
high fat, total testosterone has gone from
650 to 950 in a span of nine months.
It’s a non-trivial increase.
Now, sex hormone binding globulin has also
increased over time.
But I’ve gained so much lean muscle tissue
that I have other ideas.
I was talking to Steven Phinney about this–scientist,
very well known for looking at the ketogenic
diet–and what he was saying is independent
of insulin levels, insulin made very anabolic
. . . sorry, we’re getting into the weeds
here.
It’s possible that my lean mass gains can
be account for by decreased degradation of
branch chain amino acids.
I was like, “That’s really interesting.”
Maybe that explains by fasting plus chemotherapy
is very, very effective, for instance.
People can recover faster from chemotherapy.
So you have the ketones.
You have the sex hormones.
Hemoglobin A1c, sort of like your running
three-month average of glucose levels just
as an insurance policy to ensure that I’m
not skewing towards pre-diabetic in any way.
And then a laundry list of like five or six
different pages of stuff.
So your biomarkers tend to be a lot of performance-related
biomarkers.
Yeah.
And I’ve done the genetic stuff.
So I know, let’s just say that I’m a poor
methylator, the motherfucker gene, as they
say.
Yes, MTHFR.
Yeah.
I’m not in an ideal spot.
So taking, say, l-methylfolate could be a
good option for me and I’ve experimented with
that in the past, looking at how that can
lower homocysteine or things like that.
Have you noticed any differences after experimented
with 5-methylfolate, L-5-methylfolate, methylcobalamin?
Yeah.
I haven’t noticed many changes in blood markers
and I haven’t noticed subjective changes in,
say, performance or clarity or anything like
that.
Yeah.
It doesn’t mean it isn’t doing things.
Yeah.
I have an anecdotal story.
So I’m very into looking at different gene
polymorphisms.
23andMe is a great service that can do that.
So my friends, family, etc., I’m telling everyone
to do it.
So my mother-in-law got genotyped and we found
out that she is homozygous for MTHFR, meaning
that her MTHFR enzyme only is working at about
10 to 20% efficiency.
She’s always had really high blood pressure,
to the point where doctors were wanting to
get her on medicine for it and she’s always
refused.
Nothing she did . . . she’s done various diets,
lots of exercise, lots of things she’s tried,
nothing has gotten her into a normal range
until we identified she had MTHFR, got her
supplementing with 5-methylfolate and methylcobalamin.
But she’s been taking pretty high doses of
it.
But now her blood pressure for the first time
is in like a normal range.
So I was kind of curious if you had ever . . .
I have very consistently what you would consider
excellent blood pressure.
So I haven’t looked closely at that.
The question that comes to mind for me always
because I’ve noticed . . . so, I’m a big fan
of Richard Feynman.
Richard Feynman, and I’m not saying this is
the case with your, you said mother-in-law?
Yes.
But the importance of not tricking yourself
because you’re the easiest person to fool,
basically, is what he would say.
I know that what I have initially thought
were sort of causal relationships with high
correlative value . . . for instance, I’ve
talked to people who have gone on fill in
the blank diet.
They’re like, “This thing changed.
I’m so glad I found this diet.”
I’m like, “So you haven’t changed anything
else?”
“No, no, no.
I started running in the morning.
I started doing this.
I started doing that.”
I’m like, “Hell yeah” . . . because like one,
it’s so hard.
That’s where the observational data gets so
challenging, when you look at, say anything,
whether it’s the China study or whatever.
We don’t need to get into that one.
That’s a sensitive one.
But any observational self-reporting and so
on, the data is almost always so flawed because
humans almost never change just one thing.
Yeah.
I think that’s why it’s so important when
you’re looking at epi studies that are associative
that are not a clinical, randomizable trial,
coupling that data with mechanistic data done
on animal models or lower organisms, I think
coupling the two is very important because
then you go, “Oh, okay.
We’ve noticed this observational data and
here we’ve done X, Y or Z to manipulate it
in a worm or in a fly or a mouse.”
Right.
So you have a plausible mechanism.
Right.
So you have a mechanism.
That’s where I think looking comprehensibly
at the whole . . .
At the intersection.
Yeah, scientific is very important.
Totally agree.
It’s interesting.
You mentioned the ketone thing.
I just want to briefly give you my story.
Yeah.
So I’ve never noticed, really, any extreme
mental benefits or mental acuity changing
when I consume large amounts of MCT on empty
stomach, on whatever.
I found out that I have one ApoE4 allele.
And of course, at that point, I became terrified
of Alzheimer’s because it increases the risk
for Alzheimer’s by two-fold and I’m writing
an academic paper on this right now and getting
into all the mechanisms–diet, lifestyle,
things like that.
But what I found really interesting are the
studies that they’ve done where they give,
for example, people who have dementia or people
in the early stages of Alzheimer’s, they give
them beta-hydroxybutyrate, which is a ketone
body.
And there’s improvement.
I have some synthetic jet fuel in the freezer
if you want to try it.
We’ll probably both vomit on my couch.
So let’s do it later.
Yeah.
I’ve heard it’s disgusting.
So people who were ApoE3 responded very well.
So they had improvements in learning and memory.
With a supplemental MCT?
With beta-hydroxybutyrate.
They gave them beta-hydroxybutyrate.
But what was interesting to me and also very
discouraging was that people with ApoE4 allele
did not have those benefits.
If you look at Alzheimer’s, people with Alzheimer’s,
between 65 and 80% of all people who have
Alzheimer’s have one allele of ApoE4.
Oh, well I bet I have that on both sides of
my family, then because I have Alzheimer’s
on both sides.
Yeah.
I wanted to ask you, so you mentioned that
you have Alzheimer’s and Parkinson’s on both
sides of your family.
So I’m curious.
Has this changed your diet, your lifestyle?
Oh, definitely.
How so?
Well, the Parkinson’s maybe a bit less so.
But on the Alzheimer’s side, I have just looked
at it like some scientists look at it, which
is as brain diabetes.
I think that’s a helpful, simplified way of
looking at it.
You I’m sure know much more about this than
I do.
But there’s the prevalent theory of why I
say Alzheimer’s has the effects it has on
cognitive performance or, in this case, degradation
or otherwise.
For a long time, I was like, “It’s the plaques,
kind of like, plaques, it’s this, it’s that.”
And it turns out to be more complicated than
that because you have people who have massive
tangles of plaques but they seem asymptomatic.
They’re 100 and x years old but they still
play the piano every day or whatever it may
be.
Great movie called “The Lady and Number Six”
as a side note, 109 year old piano player.
It doesn’t get into Alzheimer’s.
But where it has led me is just to be more
cognizant of insulin, things that are related
to and/or affect insulin.
To look at not only ketosis but fasting, to
look at cyclical ketogenic diets and so on,
targeted ketogenic diets where you’re timing
carbohydrate intake near workouts, which a
lot of endurance athletes do so they can consume
like 300 or 400 grams of carbohydrates in
a day and still say in ketosis, pretty wild
stuff.
Wow.
But what I start wondering, for instance in
the case . . . because if I take supplemental
MCTs or even beta-hydroxybutyrate, and there
are tasty ways to do it now.
I think it’s Patrick Arnold and Prototype
Nutrition.
They have a . . . well, people say KetoCaNa,
C-A-N-A, but it tastes like Gatorade, basically
and it’s beta-hydroxybutyrate.
If I take that when I’m not, say, above 0.6
millimolars ketones, I don’t feel much.
But when my body has shifted into that fat-adapted
state, I do feel it.
Off hand, I don’t know what my status is from
the genetic standpoint.
But what’s been very interesting say for me
when I’m thinking about it from the standpoint
of brain diabetes is it’s not just enough
. . . and this comes back to how people, if
they focus solely on the millimolar concentration,
they can fool themselves because you can be
in non-nutritional ketosis but consuming a
lot of supplemental beta-hydroxybutyrate and
be like, “Oh, I’m killing it.
I’m at two millimolars concentration.”
Whereas I’m also taking my glucometer readings
precisely because I don’t want to be running
at 120 glucose and dismiss that.
If I wake up and I’m fasting 120 glucose each
morning, something funny is going on that
I need to pay attention to.
Whereas if I drop into nutritional ketosis
and let’s just say I’m at 74, 80, even lower
and I have high millimolar, my response to
at that point supplemental beta-hydroxybutyrate
is totally different.
That’s interesting.
Anyway, I’m still kind of a novice in this
space, but it’s interesting stuff.
So the cyclical ketogenic diet is something
that you do now practicing.
And that’s, you think, as a consequence of
thinking of Alzheimer’s like type 2 diabetes.
It’s really interesting, that connection between
insulin resistance and type 2 diabetes.
I don’t know if you measure any blood biomarkers
or if you’re aware of this, but there is a
biomarker that is present in blood that’s
called insulin-like receptor 1, IRS1 and it’s
recently, very, very recently been shown to
be a diagnostic for Alzheimer’s 10 years in
advance with 100% accuracy.
[inaudible 00:19:13]
So I don’t think it’s like something that
. . . well, you can modulate.
So 10 years in advance is a long to change.
Just by the way, you are fucked.
You’re screwed.
Good luck with that.
Yeah.
It’s inactive.
IRS1 using [inaudible 00:19:32]
Yes.
What’s interesting to me is I typically think
of the connection between type 2 diabetes
and insulin resistance and Alzheimer’s as
the connection between inflammation and a
nerve degenerative disease because inflammation,
we’ve now recently found that the lymphatic
system connects directly to the brain.
The lymphatic system is what carries blood
cells, cytokines, inflammatory molecules and
inflammation is a major, major downstream
consequence of being insulin resistance.
Inflammation causes reactive oxygen species,
things that damage all sorts of cells.
But the inflammatory molecules get into the
brain and they do start causing all sorts
of immune type reactions and aggregation of
more amyloid beta plaques and all that stuff
starts to happen more quickly.
So I think that the inflammation . . . because
if you look at people, type 2 diabetics, being
type 2 diabetic, you have a two-fold roughly
increased chance of getting Alzheimer’s.
But if you look at people with Alzheimer’s,
a small percentage of them have type 2 diabetes.
So I think that it’s not just the insulin
resistance.
I think there are the consequences, the byproducts,
the indirect things that are associated with
. . .
100%
. . . type 2 diabetes that lead to Alzheimer’s.
Yeah.
It’s rarely, if ever, just one thing.
I think humans strive for simplicity and in
sort of a sea of noise, especially if you’re
not a trained scientist, it’s like, “God,
thank goodness somebody gave me a definitive
answer.
Now I know A causes B.” It’s like, okay, maybe
as a temporary holding bay, we can use that
answer.
But it’s probably not right.
But on the inflammation side, I’ve been thinking
a lot about this recently because number one,
and this is not that uncommon, but I’ve noticed
that if I consume carbohydrates, cycling carbohydrates
and I’ll do a cheat day like yesterday where
I’m eating an entire pound cake by myself,
this kind of thing, and then even several
hours later, I get acupuncture and that’s
a whole separate conversation, but I will
bleed more.
I will bleed much more than if I am, say in
a ketotic state.
But then I have all these questions that come
to mind.
For instance, I’m consuming like turmeric
with ground pepper.
I always read it.
I never say it, piperine?
Yeah, piperine.
There we go.
So to increase the bioavailability and absorption.
So that’s pretty old school.
You’ve got turmeric, curcumin pills or whatever.
There are a million ways to go about it.
But I’ve tried to whenever possible . . . so,
you have like L-methylfolate, let’s say.
Very interesting to me.
But unless I’m mistaken, pretty new kid on
the block.
It’s a relatively new addition to the supplement
arsenal.
Whereas like turmeric, it’s like, Ayurvedic
medicine, they’ve been doing that for thousands
of years.
I feel pretty comfortable bringing in turmeric
tea with some ginger and black pepper to counteract
unnecessary inflammation.
At the same time I’m like inflammation . . . this
is where maybe you can help me gain some clarity,
but I’m like inflammation also serves some
really important purposes, right?
If, for instance, you have people go do a
weight training workout, there’s a fair amount
of empirical data, I don’t know if there’s
research data to support this, where athletes
will be like, “Oh my god, I don’t want to
be so sort out of my workout.
I’ll take like NSAIDs, Advil, Ibuprofen, whatever,
to facilitate recovery.”
In fact, then they have less hypertrophy and
they have less muscle growth as a result.
So it’s like what is the inflammation that
we want to not interfere with versus the inflammation
that we should try to prevent.
Yes.
I think that it’s something I’ve been thinking
about in a similar way with inflammation and
also antioxidants because I think that the
type that you want to interfere with is the
colonic inflammation, the kind that’s coming
from your gut, that’s leaking endotoxin, which
is released from like dead bacteria and it
causes all sorts of damage because it binds
to cholesterol.
Anyways, I can get into this whole conversation.
But it’s the bad stuff.
The inflammation that’s causing that chronic
reactive oxygen species which damages DNA,
proteins, lipids in your cells which gets
into the brain and stops serotonin from being
released, so it causes depression and things
like that.
Sounds like a bad cycle.
Yes.
Very viscous cycle too because then you start
to activate more inflammatory molecules.
I think the good type of inflammation, the
good type of damage, the good type of stress
is when you exercise, is when you’re doing
that type of exercise or heat stress or cold
stress or that type of transient stress on
the body that induces all these, the expression
of genes that deal with stress so you’re increasing
the expression of all these good genes that
deal with inflammation expressed.
Having that inflammation, having that stress
is critical to do that.
That’s how turmeric works and curcumin.
One of the ways it works is it’s actually
slightly toxic to us.
Because it’s slightly toxic to us, our body
goes, “Oh wait a minute, I need to increase
the expression of all these genes so they
make more of the gene to do all this good
stuff, to fight inflammation, to fight reactive
oxygen species, all that bad stuff.
So I think it’s sort of like . . .
It’s like what Dread Private Roberts did in
“Princess Bride” with iocane powder.
Yes.
A little bit every day.
Yes.
But it’s like the chronic versus acute, good
type of stress.
So that’s what I think about.
I also have been thinking about it in regards
to supplemental antioxidants.
I used to take a lot of vitamin C, supplemental
vitamin C. And there were studies that we’re
showing taking two grams of supplemental vitamin
C a day with lower C-reactive protein and
there are all these reasons why I was taking
it.
But then, studies started to come out where
if you take the supplemental vitamin C like
after a workout, the half life is like an
hour in a half in the plasma or something.
Then, when you work out, you create oxidated
stress and you want that.
That’s what induces mitochondrial biogenesis.
That stress is what signals to the mitochondria
to make more mitochondria.
But if you dampen that by like sequestering
that stress with an antioxidant, we’re not
going to get those benefits.
There are studies now showing this both in
humans and mouse animals.
So now I’m kind of a little more cautious
about supplemental antioxidants specifically
because they can sequester some of that good
stress that you want from things like exercise
or intermittent fasting, for example, things
like that.
Wow.
Interesting.
So you think antioxidants could negate some
of the benefits of, say, intermittent fasting.
Yes.
They can.
And it’s been shown that that can.
That’s good to know.
Supplemental antioxidants, because when you’re
intermittent fasting, a lot of things are
going on, but it is a type of stress.
When you’re stressing your cells, you’re creating
reactive oxygen species.
That’s what happens.
And part of that, there’s a hermetic effect.
So when you create these reactive oxygen species
. . . and this is the good type of stress.
Creating the good type of species because
you’re chronically inflamed because you’re
eating processed carbohydrates and you’re
poking holes in your gut leading to inflammation
and blah, blah, blah, that’s not the good
type.
You don’t want that constant reactive oxygen
species being made every day.
But when you’re intermittent fasting or you’re
exercising, that burst of it, which is much
more powerful, so it’s not like a little bit
each day, it’s like, “Boom, here I am.”
It’s enough to signal to your genes, to other
cells, “Make more of this gene that deals
with inflammation.
Make more of this gene that deals with stress.
Make more mitochondria.”
It’s just enough to do that.
You want.
Some of the benefits of intermittent fasting
and exercise rely on that.
You know, just as another random side note,
this could be the alcohol that I was fed by
Polish people yesterday, but you said reactive
oxygen species, ROSs, sounds a lot like ROUS,
rodents of unusual size, also from “Princess
Bride.”
I’m wondering how much biochemistry you can
teach using metaphors from “The Princess Bride.”
But that’s a whole separate conversation probably
not worth having.
But the one thing that I’ve been pondering,
I’m not an expert in this area, but vitamin
C, if you look at protocols being used at,
say, the University of Kansas for antiviral
purposes or anti-cancer purposes, the vitamin
C is thought of when it’s delivered intravenously
as a pro-oxidant.
So then I’m wondering could you use vitamin
C in a pro-oxidant capacity, or I guess it’s
being converted into like hydrogen peroxide,
to not mitigate but exaggerate the benefits
you want of, say, intermittent fasting.
That’s interesting.
Yeah.
If you were doing not even necessarily intermittent.
Let’s say you do a seven-day water fast.
Could you do like 50 to 75 grams of vitamin
C each day?
Would that end up nullifying a lot of the
effects or dramatically enhancing the effects?
So here are my thoughts.
I’m speculating here.
Intravenous vitamin C, you get much higher,
up to millimolar concentrations of vitamin
C in your blood.
So vitamin C is constantly going through the
cycle of being reduced and oxidized and reduced
and oxidized.
When it’s oxidized, it can act as a pro-oxidant.
That’s part of the way it kills cancer cells
because cancer cells, they’re ready to die
but they’ve found a way around death by increasing
all these genes that stop them from dying.
But all they need is a little push.
That little push is like reactive oxygen species
or a pro-oxidant like vitamin C. It just pops
them, pushes them to death.
So intermittent fasting, for example, one
of the benefits of intermittent fasting is
that your autophagy occurs.
Your body is clearing out all these damaged
cells.
So that would, in theory, if you’ve got damaged
cells . . . so, the problem is with damaged
cells, if they don’t die, they become senescent.
When they’re senescent, they sit around and
they secrete pro-inflammatory cytokines.
So then they damage nearby cells because the
inflammatory cytokines.
So it’s like this vicious cycle and it’s why
you need to get them back.
You need to get the cellular Zamboni to clear
that stuff.
That’s a funny analogy.
I used to be an ice skater.
That’s my ring name.
Oh, really?
For many, many years I was a competitive ice
skater, both freestyle and drills team.
So you want to clear them out.
I would think that if you have this senescent
cell, that would help get rid of it.
So very, very interesting observation.
I’ve been thinking about it also because cancer
generally . . . by the time you’re 40, we
all have pre-cancerous little cells.
But the question is do they grow?
Do they then metastasize or become a problem,
or do they just remain these little mutations
that don’t cause any particular harm among
other things obviously?
For me, I’ve become also interested in . . . I’d
love to get your opinion on metformin.
There are people who’d say, “Well, if you
want to try to dodge that cancer bullet, we
know that cancer cells, they love sustaining
themselves anaerobically . . . or let me rephrase
that, with glucose.
They love glucose.
So if we can dramatically lower, whether it’s
storage of glycogen, plasma, glucose, whatever
it might be, then in theory, we should be
able to lower the risk of cancer and limit
cancer growth, cancer cell growth.
What are your thoughts on metformin and why
are you taking it or not taking it?
I’m not taking it.
The reason I’m not taking it . . . I think
it has been shown, like you said, it can possibly
prophylactically prevent cancer so far.
I think the studies that have shown that have
been pretty short-term.
My concern with metformin is the feedback
mechanisms that happen when you’re taking
this drug.
How is that going to affect other cells and
how they respond to glucose and things like
that over the long-term, like 15 years down
the line?
I think that limiting your sugar intake is
probably . . . if you haven’t damaged yourself
by eating a bunch of crap, a bunch of processed
sugars and carbohydrates and things like that,
then I think limiting your sugar intake is
probably good, good enough.
To a certain component, there’s a certain
component of cancer that there is a genetic
component.
What I mean by that is not that you’re born
with it but . . . so, downstream of a cell
that’s glycolytic, that’s only using glucose
to make ATP through this glycolysis pathway
is inflammation again.
I come back to it because it’s just downstream
of everything.
And inflammation damages DNA and eventually
you get it in the right gene that’s saying,
“Oh, this gene usually protects,” whenever
there’s any damage, it kills a cell.
It’s called a tumor suppressor gene.
You get it in that tumor suppressor gene,
you’re screwed.
Now any time you get damaged, that pathway
isn’t activated to go, “Whoa, wait a minute,
this is not good.
I’m going to die.
And it just keeps living.”
Yeah.
If you look at, for example, our lymphocytes,
our lymphocytes are glycolytic and they’re
not cancer.
So it’s not as simple as a glycolytic cell
is going to give you cancer.
No, no.
But definitely starving . . . I think before
you get to the point where you’re starving
a cancer cell, you can kill the damaged cell
before it becomes to that point where it’s
shifted its metabolism.
What do the lymphocytes do in a ketotic state?
I don’t know.
Do they derive glucose form lactate or something?
Yes.
They do get it from lactate.
Lactate is something that they do use.
Yeah.
Cool.
It’s interesting because lactate also is much
like ketone bodies, energetically thermodynamically
favorable.
So it takes less energy to make energy.
Yeah.
So you’re consuming less oxygen because you
don’t need as many ATP molecules to make ATP.
But back on the ketones since we’re back on
the ketone, I do want to get to the Lyme disease
because it’s a topic that I avoid.
I’ve never talked about it.
It’s one I avoid too.
I always have this knee jerk reaction because
the signal to noise ratio is so small.
I feel like there’s just a lot of confusion.
So much nonsense.
But I’d be really interested because you’re
a very analytical person.
I try to be.
So obviously it’s a real disease.
People suffer from it.
You can observe spirochetes under a microscope.
So it’s definitely real.
It’s just a lot of craziness that seems to
be associated with it.
But maybe you can talk a little bit about
. . . because you mentioned going on the ketogenic
diet to treat your Lyme disease.
Can you talk a little bit about what you found
in terms of your experience with Lyme disease
and how you got to treating it with ketogenesis?
Yeah.
I can talk about it.
So where to begin with this . . . First of
all, I’d just like to agree with you and sort
of emphasize for everybody that the amount
of nonsense and charlatanism out there surrounding
Lyme is just beyond belief.
There are so many fraudulent companies and
practitioners who are just printing money
by either misdiagnosing people with Lyme or
treating Lyme in the quackiest of quackery.
Why Lyme?
So here’s my thinking.
So I contracted Lyme on Easter in Long Island.
If you look at the CDC map, the Center for
Disease Control heat map for Lyme disease,
that is ground zero.
That’s where the bomb went off.
Lyme is named after Lyme, Connecticut.
So it really has historically focused on that
Northeastern area–Pennsylvania, Upstate New
York, Hudson Valley.
I think Lyme has become this popular topic
of conversation for a few reasons.
Number one, it’s poorly understood on a lot
of levels.
So there are ample opportunities for non-scientists
and quacks to sort of invent stories around
it.
That makes sense.
Number one.
Number two, it’s scary.
It involves a bug biting you and you catch
this disease, so the media loves it.
The media loves it.
The media writes about it.
Then the media sometimes correctly, often
incorrectly lists the symptoms of Lyme disease–joint
pain, depression, fatigue–it’s like, “Well,
that’s one out of every two people in the
United States at some point every year.”
And then people go, “Oh, my god.
I’ve had my . . . ” I got an email from a
friend of mine who says, “My shoulder has
been bothering me for a couple weeks and two
of my friends said it might be Lyme.”
I’m like, Oh, god.
I would bet $1,000 it’s not Lyme disease.
Given where you live, given the likelihood
of having contracted it, it’s just so unlikely
for most people.
Now, all of that having been said, Lyme is
a real thing.
Like you said, you can observe the spirochetes
under a microscope.
I think another reason it’s popular to talk
about is people love saying the word “spirochete.”
I’m not kidding.
They love saying spirochetes.
They imagine this screwdriver, this horribly
evil like Maleficent like spiral bug that
like digs into your body and like the antibiotics
come in and they’re like, “Oh no, we’re going
to hide from the antibiotics.”
It’s not that sentient.
My husband’s grandmother says spirochetes
like at least every conversation that I have
with her.
People love saying spirochetes.
So you get it.
Yes.
So for all these reasons it’s popular to talk
about.
I think primarily because the symptoms overlap
with a million other conditions.
What I came to realize for myself is like
yes, it’s a real thing.
It’s almost certain after Western blot tests
and ELISA tests and looking at all the diagnostics,
which are really primitive, it’s very likely
that I already had Lyme disease at some point
because I’ve been bitten by ticks hundreds
of times.
Almost everyone in my immediate family has
had Lyme disease.
On Long Island, it’s just kind of like, “Suck
it up.
Take some antibiotics.
You’re fine.
Move on with life.”
It’s not viewed as like a huge crisis by everyone
who gets it on Eastern Long Island because
it’s so common.
So I shrugged it off.
I took three or four deer ticks that were
embedded off of me in the span of two or three
weeks.
It historically hadn’t been a big deal.
So I was like, “That sucks.”
Pick it off, make sure the head is not in
there, move on.
I did not develop what’s thought of as the
trademark bullseye rash.
So I ignored progressively worsening symptoms
for eight weeks where my joints started getting
very sore, swollen.
I had trouble getting out of bed in the morning.
I started getting slow cognitively and had
trouble recalling friends’ names and just
really common words and eventually got to
a point where my assistant was like, “I’ve
seen you sick.
I’ve seen you tired.
I’ve seen you burning the candle at both ends.
This is none of those things.
You need to see a doctor.”
It sounds like dementia, like not remembering
friends’ names.
Yeah.
Things are really funny.
If you look at the advanced symptoms of severe
Lyme, it takes on dementia-like qualities,
even cerebral palsy in some cases, really
scary stuff.
So long story short, then I get diagnosed
with Lyme.
When I walk into the clinic on Long Island,
to give you an idea of how common it is, so
this walk-in emergency clinic open on the
weekend, they had a poster up that was like,
“Hey, allow us to send your blood sample to
such and such lab, Upstate New York, to do
research on Lyme,” and there’s a picture of
a tick, “And we’ll give you a free $50 Amazon
gift card.”
It’s that common.
But then the question was, “Okay, I have Lyme.”
I’m taking doxycycline.
I do that for eight weeks or 12 weeks, whatever
it was.
I still feel really shitty.
Now what?
That’s a long antibiotic course.
Yeah.
Some people take antibiotic for years, which
I think is not the thing to do.
This is where I am and I’ll try to sum it
up because this can be a very long conversation.
I think that there are very, very credible
scientists and infectious disease specialists
who do not believe that chronic Lyme exists.
Their position would be there’s no evidence
that the whatever it is, the borrelia spirochete
cannot be eradicated with broad spectrum antibiotics
like a doxycycline or something else.
There’s no evidence to suggest that they burrow
away and hide and come back, hide in biofilm
or whatever.
Yeah, right.
Right.
Then you have people, and there aren’t that
many, but a handful of people who are like,
“Well, it is possible that this Lyme could
behave something like herpes simplex,” where
it’s like a recurring infection essentially
and maybe it takes root in the nervous system
somehow and only comes back out in times of
stress.
There are people, credible doctors who have
been like, “It’s not completely beyond the
realm of possibility that is has some recurring
nature.”
Okay.
Still, kind of descriptive, not prescriptive,
what do we do?
Right?
Then the theory that I kind of came up with,
and I’m sure other people have come up with
it, but I haven’t read it, I was like, “Well,
let’s look at the symptoms of Lyme.
You have like depression, fatigue.
What are other potential causes after a long
course of antibiotics?
Well, maybe you just completely scorched earth
your microbiome among other things.
So one of my theories is that what people
perceive as chronic Lyme is in fact a collection
of similar symptoms caused by the long course
of antibiotics.
So you should focus on prebiotics, probiotics.
I have had a tremendous amount of difficulty,
at least as measured in common stool testing
and so on, in repopulating my gut diversity.
It’s been extremely hard.
I have consumed just about every type of pre
and probiotic imaginable.
I’ve also tweaked my diet to be more favorable
for certain types of gut repopulation.
It’s been really tough.
I did like a three-month intense protocol
of all sorts of stuff.
So I’d love your thoughts.
I did a follow-up stool sample analysis and
it was still like, “No, you’re fucked.”
I was like, “Wow . . . ” depressing.
So you’re talking about measuring your fecal
bacteria population using uBiome?
Yeah.
UBiome or there are others, like Rocky Mountain
blah, blah, blah doctors data, whatever it
was.
Okay.
There are other ones.
Yeah.
UBiome has a slightly different approach,
but along those lines.
I agree with you for one.
First of all, I heard a podcast that you did
with Jessica Richman from uBiome and I think
you had talked about this and that’s how I
became first aware the link between . . . when
you mentioned having this hypothesis that
you thought possibly some of these symptoms
of Lyme disease were a symptom of complete
gut disbiosis where you’re taking several
rounds of antibiotics and you are obliterating
your gut bacteria, a lot of the good ones
are going away.
If you don’t take a very strong probiotic
immediately after antibiotics, it repopulates
with all the bad stuff and it’s really hard
to get because they occupy space.
They’re sitting in what’s called the mucin
in the gut.
They have to stick in the mucin to stay, otherwise
anything you take will kind of just flow through.
It’s kind of like the flow through.
So it’s really hard to repopulate.
I’ve been doing a lot of self-experimentation.
I’ve been using uBiome to track my gut bacteria
genotypes.
But have you tried VSL3?
I have it in the refrigerator right now.
Do you?
Yeah.
Okay.
So the sachets are what I recommend because
. . .
Yeah.
I have the capsules.
The sachets have 450 billion, which is more
than what the capsules have.
450 billion is ten times more than what most
probiotics have.
The thing about VSL3, very interesting, so
it’s the probiotic that I take.
I’m taking it because I’ve had some gut issues
that started in graduate school because I
got MRSA.
Yeah.
That’s not fun.
Antibiotics were the prescription and I had
several courses of strong ones.
Finally, it kept coming back and I was like
fed up.
How do you get MRSA?
I don’t really know.
I worked in a hospital.
Is that methicillin-resistant Staph?
Yes.
Aureus.
Staphylococcus aureus.
Staphylococcus aureus, yeah.
So I worked at a children’s hospital.
That’s a good place to get it.
They’re everywhere in hospitals.
Who knows where I got it?
The point is I got it and it sucked.
Finally after like, I don’t know, three or
four rounds of antibiotics, I would take it
and it would go away and then a month later
it would come back again and again.
I was like, “I can’t do this.”
So I read the literature, with the help of
my husband Dan, that garlic and grapefruit
seed extract, a concoction of things, I applied
both topically and made a cream and I orally
took and within 24 hours I got this thing
to come to a head, pus out, it never came
back.
Interesting.
But as a consequence of antibiotic use, I
had serious gut issues, led to IBD.
I’ve finally been able to recover.
IBD, irritable bowel disorder.
Inflammatory bowel, yeah.
Inflammatory bowel disorder.
But it’s been a really, really long journey
in tweaking my diet.
Doctors, of course, I went to see doctors
and they were just like, “Here, take an SSRI,
it helps with the pain.”
I’m like, “I’m not going to take an SSRI.
Yeah.
No thanks.
I walked out of that doctor, like, “You’re
insane.”
This was like a pelvic pain specialist doctor.
So I’ve just had terrible experiences with
doctors.
Finally, I’m like, “Why aren’t you asking
me about my diet, fiber, things like that?”
So I tweaked my diet and did lots of things.
But VSL3 . . .
With the uBiome testing, have you seen . . . I
haven’t done a follow-up test in a few months,
but I have been taking VSL3, so now I’m optimistic
hopefully.
So I did a 30-day VSL3 course with the sachets,
which are 450 billion and did a stool test.
I’m still waiting for those results.
My husband and I both, Dan, he’s done a recent
course of antibiotics.
So I had him do his baseline and then right
after, literally the day he stopped taking
antibiotics, did a sample for uBiome.
I got that data back, so I’ve been looking
at that.
So I’m going to talk about all that.
It’s really complicated and things in the
literature are confusing and some people think
some things and they’re actually not true.
So I’ve been looking at other people’s uBiomes.
I’m going to be doing a series of talks on
this.
Cool.
I’m pretty excited.
I’ll check them out.
May I add just a little bit of color on the
ketosis?
Yes.
The color there is I began looking at fasting
as a tool for many, many different reasons.
And whether that be related to, say, longevity
or the reason I was excited about it is I
was looking at it as a reboot of the immune
system, even shorter fasts, three days.
I began playing around with fasting.
Then, of course, you fast long enough and
you go into pretty deep ketosis.
Correct.
So it was almost an accidental discovery for
me whereby I had not been in nutritional ketosis
for 10 years, 15 years.
I did a lot of experimentation with the cyclical
ketogenic diet when I was in college and competing
as an athlete.
Then I just stopped because it was kind of
a pain in the ass and it was really boring.
But then I did this fasting to help reboot
my immune system.
I’ll keep it simple.
So rebooting my immune system kicked over
into deep ketosis and it just felt amazing.
My cognitive function just went through the
roof compared to what I had felt up that point
after Lyme disease.
I was like, “Well, this is very interesting,
isn’t it?”
I said, “Well, I don’t have to fast to be
in nutritional ketosis.
So let me now play around with ketosis and
see what I can discover just by tracking and
logging a lot of data.”
So I have my pet hypothesis about the gut
biome and the antibiotics leading to symptoms
that appear to be Lyme when in fact they’re
caused by something else.
Another hypothesis, and the reason I’d like
to dig into this, but I haven’t come up with
a great plausible explanation for this, is
that Lyme or the antibiotics or both somehow
interfere with carbohydrate metabolism.
That’s just a starting point.
But because I’ve been public about the Lyme
stuff because I was incapacitated, I had to
tell people.
I was like, “Sorry, I’m not going to reply
to your email.
I’m archiving 2,000 emails.
Sorry.”
“Why?”
“Lyme.”
And then people started coming out of the
woodwork to be like, “Hey, my wife has Lyme.
She’s been debilitated.
What should we do?
What have you learned?”
And the only advice that I gave a few people
was like, “Look, there’s a lot of BS out there.”
So number one is put your thinking cap on
and be a good scientist to the extent possible.
Number two is try a carb-restricted diet.
Ideally, go into ketosis.
All of the people who have gone into ketosis
have had the same experience I have.
Now, it’s a handful of people.
So the sample size is really small.
These are people that like, “Cannot function,
had to quit my job,” serious cases, go into
ketosis, “Wow, I feel like my old self.”
Have you measured any changes in gut bacteria
after going into ketosis or after doing the
ketogenic diet?
I haven’t.
That is also a very interesting topic of discussion.
So what effect does ketosis have on the gut
biome or the repopulation, the rate or the
diversity of repopulation?
The short answer is I don’t know.
Part of it is, and this is where maybe I’m
not being a thorough scientist.
But I felt it worked so well to me that I’m
so excited to get back to building things
and creating things and being my old self
that I haven’t taken the time to dissect it
to the extent I probably should.
Your carbohydrate . . . I have this interesting
hypothesis that sort of is related.
People that have a severe imbalance of gut
bacteria, let’s say they have a lot less of
the commensal bacteria which is making short
chain fatty acids and metabolites like lactate
that are feeding other good bacteria, they’re
feeding your gut cells.
So you have less of those and you have more
of the bacteria that are methane or hydrogen
sulfate producing, so you get bloated, more
of the more pathogenic type of bacteria.
So you have this overgrowth of bad bacteria.
The thing is let’s say you eat something that’s
typically supposed to be good.
You eat something that has a lot of fiber
or like vegetables.
So you’re getting this fiber that’s supposed
to be not digested, but the bacteria can digest
it and make it into this good stuff.
Well, bad bacteria can digest that as well.
So you’re feeding this bacteria substrates
to keep going and to make more of the bad
bacteria.
Right.
Now, the interesting thing that I don’t know
is there are certain species of bacteria.
There’s phyla, class, species, it’s incredibly
complicated, but certain species only metabolize
fat and I don’t know which ones those are
and if they’re good or bad.
It sounds like you’ve had a positive experience.
But that would be really interesting to measure
in general.
But I’m glad you’re feeling better.
Yeah.
The ketogenic diet is something that I’m interested
in diving into and understanding more about.
I’d like to talk to Peter.
Peter is a smart guy.
I’ve listened to the podcast.
I don’t know if he’s done more than one podcast,
but I listened to one he’s been on.
Yeah.
He did one with me which was our conversation
and then he did a follow-up with me which
was answering the 10 most popular questions
submitted.
Okay.
I listened to the conversation and I heard
him and I was like, “I want to talk to this
guy.
He’s a scientist.
He thinks like a scientist.
I respect what he’s saying and I think that
he and I have a lot of interesting overlap.”
He’s also compulsively performance driven.
And he walks the talk.
What I like about Peter is that he’s not an
academic who takes his breaks at the hospital
like going outside and smoking cigarettes
and has like a paunch.
He’s a competitive athlete.
I say that because I literally saw a bunch
of people standing outside of a hospital in
their scrubs like smoking cigarettes on break.
I can’t believe people smoke still.
It’s crazy.
Oh, my god.
But Peter on the other hand is still a very
competitive, driven athlete.
So he just has a unique perspective on all
this stuff.
So on the athletic side, I have a question
for you.
In “The 4-Hour Body,” you talk about the minimal
effective dose.
You mention high intensity interval training
and how you can get long lasting effects with
less effort, basically.
At first I was like, “Hmm . . . ” and then
you went on to talk about biomarkers and studies
that have shown high intensity interval training
increases mitochondrial biogenesis as much
if not more than, let’s say, like an hour
and a half or something of cardio.
And then you went on to the brain.
That was my real concern.
I was like, “Well, fine, if you’re going to
get the same amount of muscle mass or more
by doing this, but what about the brain benefits?”
Because I’m interested in staving off Alzheimer’s.
Like I mentioned, I’ve got an increased risk.
So exercise has been shown to people with
ApoE4 allele are much, much less likely to
get Alzheimer’s if they exercise, the more
intensely the better.
Part of that is your BDNF, your increasing
neurotrophic factors that are growing your
neurons because you need to repair a lot of
that damage that’s going on in the brain.
So I’m interested in whether or not you are
still engaging in high intensity interval
training and what, if anything, you measure
to know that minimal effective dose is working.
Yeah.
That’s a good question.
So I am coming off of and rehabbing some very
serious leg, knee and ankle injuries that
inflicted on myself doing the crazy parkour
episode for my TV show.
So I’m not doing a lot of interval training
that would be recognizable as, let’s just
call it tabata training or some type of sprint
training because it’s too high impact.
So I have concluded yes I am still practicing
the minimal or minimum effective dose in a
lot of facets of exercise.
I think that most people do as much as possible,
not as little as is needed.
You can land somewhere in the middle.
But the higher the level of athletics, generally
speaking, the more coaches work on holding
their athletes back and not pushing their
athletes.
I think this is a very poorly understood idea.
But at the highest level, pushing the athletes
is not the problem.
With some team sports it’s different, like
even in the NFL.
But if we’re talking about, say, track and
field, the coaches spend more time pulling
their athletes back.
So in my case, for instance, most people go
to the gym one hour a day, five days a week
if they’re trying to change body composition
would get better results by doing two or three
sets of kettlebell swings per weeks.
I’ve seen this hundreds of thousands of times
in readers already.
For me, with mental performance, and there’s
the book “Spark” that talks about a lot of
this stuff and like you said, the brain drive
neurotrophic factors and so on, from a subjective
standpoint, I’ve seen as good results if not
better results in terms of cognitive performance
from resistance training of almost any type
when compared to, say, steady state or even
higher intensity interval training that could
be thought of as cardio, like sprinting or
cycling or what not.
Mechanistically, I don’t have specific before
and after biomarkers that I’m tracking.
But I am looking at, say, pages per day output,
quality of writing, which can get very subjective.
But I think that as these studies hopefully
get funded, we will see that resistance training,
if you think about it, weight training is
very effective cardio.
Yes, if you push it.
Either way.
If you’re using, and Doug McGuff has talked
about this quite a bit, if you’re utilizing
musculature to move your body through space,
particularly with resistance, your heart has
to work really hard generally to supply all
the necessary nutrients and so on to get that
job done.
So I think that on top of that, if you’re
looking to prevent age-related cognitive end
physical decline, one of the key correlates
with all the bad stuff is sarcopenia, so loss
of muscle mass, to which I would say targeted
resistance training, much more effective bang
for the book in not only preventing lean muscle
tissue loss but increasing muscle gain than
say most types of internal training, even
if you’re temporarily spiking certain hormones.
But that’s also because I hate doing endurance
work.
Yeah.
I really hate doing metabolic conditioning.
I find it miserable.
I usually avoid it.
But I do think if you were to just do two,
three sets.
I really focus these days personally in my
exercise regimen on high intensity very brief
duration or very, very long duration, typically
walks, like two to four hour walks.
I have a bar bell approach.
So it’s kind of like my investing approach.
But my physical training approach is very
barbell-oriented.
So it’s either like these sprint-like demands,
which could be, say, overhead squats are really
fantastic for a whole host of reasons for
preventing a lot of the physical maladies
that plague people as they get older and then
long two to four hour walks.
Awesome.
Humans have made a lot of evolutionary tradeoffs
to be able to walk long distances.
So I feel like maybe that’s something we need
to do more of.
We’ve made so many compromises to be able
to walk long distances.
I find quality of life suggestively assessed
a lot higher when you’re doing long, steady-state
walking.
And it’s also the meditative aspect of it.
That’s something that you get from walking
long distances.
For sure.
Especially if you’re in a calm and peaceful
environment.
Yeah.
A lot of parks out there.
Get outside.
I’m interested to know.
You do talk about meditation a lot and being
mindful and how that’s important for a lot
of things and it’s been shown to improve learning,
memory, things like that.
Have you ever tried floatation tank?
I have.
You have?
I have.
I’ve tried flotation tanks.
I like floatation tanks.
There is a new location, actually, in the
city that I have not been to.
Reboot Spa or something, I think is . . .
Yeah, Reboot Spa, maybe Float Lab.
I’m not sure exactly what the name is.
I think it’s Reboot.
The only location that I had available to
me beforehand was a real pain to get to from
where I am kind of in the Noe Valley are.
As a result, I went a handful of times, but
could never make it a regular trek or didn’t
want to make a regular trek.
But I could see using floatation tank for
all sorts of different experiments, including
potentially incorporating microdosing of various
types.
But do you use floatation tanks?
I’m actually going to try it for the first
time next week.
So this new floatation tank place reached
out to me, I think it’s Reboot, and gave me
some free passes and I’m like, “You know what?
I’ll do it.
Let’s get it a go.”
So I’m going to go next week.
Cool.
Don’t shave the day before.
Oh, okay.
Yeah.
You’re basically in the Dead Sea.
It’s all salt.
So you will be really unhappy.
I’m excited.
I wouldn’t shave for a couple days beforehand.
Just a couple not particularly health-related
questions I just wanted to ask you before
we close.
Sure.
One is in your books and also on your TV show,
“The Tim Ferriss Experiment,” you talk about
doing some silly things that help people push
past anxiety, like laying on the floor of
a crowded place or going and ordering a cup
of coffee and asking for a discount arbitrarily.
So what do you think some of the positive
benefits that can be reaped from that are
and are there any specific fear-inducing things
that you’ve engaged in that have given you
benefits in your life?
So I think the benefits of practicing discomfort
is realizing repeatedly that the worst case
is just isn’t that bad.
So becoming comfortable with increasing levels
of discomfort, especially something that’s
ridiculous and has no real tangible downside
other than embarrassment . . . and this comes
back to my obsession with stoic philosophy.
But if you were to look at, for instance,
Cato, who is considered the perfect stoic
for a period of time, he would wear a tunic
that was an unusual color to train himself
because he would get ridiculed for it, to
train himself to be embarrassed about only
those things which are truly worth being embarrassed
about, clothing not being one of them.
So going into, say, Starbucks or whatever
and just kind of calmly sitting down and laying
down on the floor for ten seconds, super awkward,
people are going to think it’s weird.
Some people might take five steps back and
kind of freak out.
Then you get back up and be like, “I’m fine.”
It’s a small way of inoculating yourself against
succumbing to peer pressure about stupid things
or holding off on making important decisions
or having uncomfortable conversations because
of this irrational fear of this massive downside
that you’ve never actually thought about.
So something like laying down, asking for
a free coffee or asking for a discount is
really just rehearsal for the things that
happen outside of your control or the more
important conversations so that you have a
certain level of calmness and have repeatedly
had the realization that the worst case scenario
you’re imagining is almost never that bad.
So those are just training mechanisms.
Yeah.
So you’re basically dealing with stress.
You’re inducing stress to deal with it better
for the next time when there actually is a
stressful situation.
You’re more calm.
Yeah.
Right.
If you want to negotiate a raise with your
boss, probably not the best to practice your
negotiating in that first conversation.
You should go to a state fair and like learn
how to haggle.
Take $100 and that’s your tuition, that’s
your MBA in haggling.
Don’t be a jerk and negotiate with everybody
and not buy anything.
But it’s like all right, you have $100 to
spend.
Your job is to get $300 worth of stuff for
like $100 at a state fair.
It’s like go practice.
That’s a great suggestion.
I’ve actually overcome . . . I had a lot of
fear of public speaking.
I would go into the mall and tell jokes to
random people.
I am not a comedian.
I’m a scientist.
I’ve been in a lab most of my life reading
books.
Social interaction is a little anxiety inducing
for me.
So I would do this and most of the time, people
would laugh at my bad jokes and look at me
like I’m insane.
I’d still get that.
I did get over that anxiety of having people
think I’m crazy or just like that awkwardness
of like talking to someone.
Now I’m communicating science to people.
So it worked for me.
Yeah.
And the baby steps that seem so ridiculous,
like the telling of the jokes or asking for
a free coffee, it’s hard for some people to
realize how much those experiences transfer
because they’re like, “When am I ever going
to have to ask for free coffee?”
It’s like you’re missing the point.
The point is to subject yourself to the same
types of fear and discomfort that you will
experience in a million other circumstances
and to overcome that in a very sort of rehearsed
way.
For instance, for me, in the dating episode,
the dating game episode of the TV show, Neil
Strauss, who wrote “The Game,” forced me to
do cold approaches at the Ferry Building here
in San Francisco, which was like my ultimate
nightmare.
It brought back like every stressful sweaty
palm miserable situation from like eighth
and ninth grade.
It’s giving me sweaty palms thinking about
it.
Yeah, I mean it’s just so bad.
But I enjoy like every week, it’s like plan
something out that is going to force you to
do something potentially funny, right, that
is going to be stress-inducing.
Just figure out what that is and go do it.
Maybe it’s getting a milk crate and a hat
and going out and try to busk without getting
arrested, but trying to busk and be a shitty
dancer and make $5.
That’s your goal.
You have an hour to make $5 being a shitty
dancer or being a terrible mime or whatever
it is.
The more you practice that type of thing . . . I’m
going to disappear from camera for a second.
I have this.
I don’t even know how to pronounce his name,
which I’m embarrassed by, but this quote is,
“Life shrinks or expands in proportion to
one’s courage.”
If you can pronounce that, you’ve got me beat,
A-N-A-I-S, with a umlaut over the I, N-I-N.
So this is something that I have reminders
like this in front of me constantly so that
I realize that very rarely are the things
we’re afraid of worth being afraid of.
To overcome that, you just have to practice.
Most of the time we’re not.
It’s very hard to think your way out of something
you didn’t think your way into.
So if you’re afraid of asking for a discount
on coffee, that’s not really a rational fear.
It’s just not.
The way you overcome that is not by sitting
down and drawing out a decision tree, although
that stuff can help, like fear setting, this
exercise I do a lot can be very helpful.
You go out and just try it.
That’s how you overcome these irrational reptilian
fears.
Absolutely.
Like you said, next time you have that fear,
you’re more calm, you’re thinking more clearly.
I’m sure if they were to do MRIs of people
before they do the sort of microdosing themselves
to this type of fear, then after when they’re
in a difficult situation, they may see that
their amygdala isn’t as hyperactive or something
like that where you’re really training your
brain.
The mediation, you mentioned that, the meditation
helps a lot.
The meditation helps you to not overreact.
I’m a very like aggressive, bull in a china
shop kind of guy.
So the mediation is particularly helpful for
me.
Let’s say you ask for a discount on the coffee
and the guy is like, “Who the fuck do you
think you are?”
My instinct would be like, “Who the fuck . . . ” and
instead to be like, “Hmm . . . that’s a good
question.
Give me a second.”
And then to calmly respond, get a laugh, and
then the guy gives you the discount.
Like having that composure to have a delay
between the immediate like . . .
That impulse.
. . . is really, really helpful in almost
every circumstance.
And if people are looking to get started with
mediation, it can be a super nebulous . . . people
can get very sanctimonious about their meditative
stuff.
Just think about it as bringing your attention
back to one thing.
Get distracted, you bring it back .You get
distracted, you bring it back to any number
of things.
That translates a lot to productivity and
being effective throughout the day so you’re
not like, “Oh my god, I just spent two hours
on Facebook.
What the hell happened?” to avoid that kind
of experience.
Just get an app like Calm or Headspace and
start doing like 10 minutes a day.
Headspace, all right.
I’m going to try it.
I’d like to get more into the mediation.
It’s super, super helpful.
It just trains you to be able to calmly kind
of come back to what you’re supposed to be
doing or what you want to be doing.
You do that 10 minutes a day.
Especially when you get like five or seven
days straight, it’s amazing how something
that neurologically or cognitively just clicks.
After five or seven days of doing it consistently,
I do it first thing in the morning.
You do Headspace?
I do transcendental meditation.
Transcendental.
So I just kind of sit there and focus on my
breathing.
Like I did that before you guys got here.
How long?
If you do that every morning for five to seven
days, it’s really profound how much more calmly
effective you are.
And I’ve never been a big woo-woo meditation
guys.
I’m just like, “Eh . . . I’ll just have a
cup of coffee.
It will do me twice as good.”
Not true.
Ten minutes in the morning will make you calmly
efficient.
You’ll get 50% more done if you do that every
day for a week.
Ten minutes is not a lot of time.
It’s not a lot.
My magic number for me is 20 minutes.
But don’t start there because it’s too much
to start with.
Start with whatever you’re going to do, baby
steps.
Start with whatever you’re going to actually
do.
If it’s three minutes, make it’s three minutes.
If it’s 30 seconds, then make it 30 seconds.
But use an app like Headspace with guided
mediation makes it a lot easier.
Just commit to doing it for a week or two.
Then it becomes self-perpetuating.
You’ll see the positive effects.
But yeah, I think mediation, sometimes mindfulness
practice plus practicing humiliation, super
potent, valuable combination.
Quite frankly, the practicing humiliation,
and nine times out of 10 you don’t end up
being humiliated, it’s just fun.
It’s a good way to get laughs.
You can do it with your friends too.
Exactly.
Well, Tim, this has been great.
I’ve got one last question I’m dying to ask
you and then we’ll close.
So I did read on, I think it was your Reddit
Ask Me Anything, you talked about how you
were interested in recruiting Hollywood talent,
whether it’s directors or actors, etc. coupled
with your interest in fiction writing, it
leads me to believe that you’re writing the
next “Matrix” or something cool, totally hoping
to blow your cover here.
Are you writing a cool . . . ? Is this . . . ?
I am working on some screenplay stuff.
Yeah.
Awesome.
I hope it’s science fiction.
Yeah.
Whether it will be cool or not is to be determined.
One of the main reasons I’m spending more
time in Hollywood and spending more time with
people who are good at, whether it’s screenwriting,
directing, fill in the blank is because I
want to start to absorb the gestalt understand
of how that whole machine and ecosystem functions
but I also want to get to know people who
are like the good guys and the good gals,
the people who are not only really good at
what they do, but the cool people I can be
friends with for 10-15 years.
So I’m spending more time down there.
I’m not in a rush.
I’d rather do it right than do it quickly.
That doesn’t surprise me.
Yeah.
So I’m taking time.
Honestly, for screenwriting, for books, for
blogs, for podcasting, whatever, the power,
for those people who have a direct audience
is growing by the day.
So making a movie the way I would like to
make a movie I think will just get easier.
Six months from now it will be easier than
it is today.
A year from now it will be much easier than
it is today.
Two year from now it will be even easier than
it is today.
That’s very exciting.
Just like science.
Just like science.
Very exciting, Tim.
I really enjoy talking to you as always.
Likewise.
Thanks a lot for coming on the podcast.
My pleasure.
Most people know where to find you.
You’re pretty famous.
But for those that don’t, where can they find
you?
They can find me at FourHourWorkWeek.com all
spelled out and there are a million ways to
misspell that, which is like in retrospect,
oops on me.
But four as in the number four, hour, H-hour,
not O-U-R, FourHourWorkWeek.com.
On Twitter, @TFerriss with two R’s and two
S’s.
Facebook, I put up a lot of videos, like Q&As
and stuff on Facebook.
That’s just Facebook.com/TimFerriss, two R’s
and two S’s.
Awesome, Tim.
Yeah.
Thanks a lot for doing this.
My pleasure.
Thanks for having me.
I look forward to talking to you again.
Yeah.
Until next time.
All right.
Awesome.