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Why we get from insulin resistance

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    [Music]
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    hello everyone and welcome to biohackers
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    lab I'm your host Gary Cohen and on
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    today's episode I have dr. Ben Beckman
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    dr. Pikmin is an associate professor at
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    BYU who conducts research in the
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    laboratory of obesity and metabolism
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    he has also authored the new book coming
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    out in July 2020 called why we get sick
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    and so good to have you back on again
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    hey Gary yeah my pleasure it was so much
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    fun the last time doing it again was
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    inevitable yeah and I mean I I did that
    little introduction
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    about you there but
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    hopefully everyone knows about you
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    because you are the most viewed speaker
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    on the biohackers lab channel on the
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    youtubes so you just everyday there's
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    home does the people that just hit that
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    video and they just want to know more
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    about dr. Ben Beckman and what he's
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    thoughts awesome so I'm glad
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    to have you on again
    oh that's fun I guess I guess
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    people are just something about a shiny
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    bald head that just people just can't
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    can't stay away well don't worry this
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    since views not about shiny bald heads
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    yeah although although all the worse for
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    it it ought to be so I'm gonna my first
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    question for you then is your book why
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    we get sick why is it that we get sick
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    name what's what's the answer to it yeah
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    yeah well thanks thanks for asking
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    thanks for mentioning it this has it was
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    a labor of love really so I let me just
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    do a low background I ended up my
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    University every summer does this event
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    called Education Week where they just
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    have experts from the community and
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    including the university able to teach a
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    week of a class whatever the topic is
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    and there's all kinds of topics so about
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    five years ago I decided to just take
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    some of the the most distilled sort of
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    purist points about insulin resistance
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    that I've ever taught in my class as a
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    professor and and really just tried to
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    present this to the public in a
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    non-academic setting which is and this
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    became the the essence of the book what
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    is insulin
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    why does it matter and that touches on
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    the why we get sick and we can get into
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    that and then what to do about it so
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    sort of three parts and in the over the
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    course of that week five years ago it
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    not only was very well received but so
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    many people said can where can we get
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    your book where can we get your book and
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    I thought maybe I ought to just write a
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    book and it was a wonderful opportunity
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    and challenge to bring it all in to you
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    know a very lucid compilation of
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    thoughts and scientific references so
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    why we get sick I contend that much of
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    chronic disease non-infectious of course
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    is in some way connected to insulin
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    resistance is one single one single
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    problem so you imagine this sort of this
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    this tree of illness and all these
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    different disorders that we focus on by
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    looking at the branches we're looking at
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    hypertension we're looking at
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    infertility we're looking at dementia
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    and migraines in some instances and we
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    would want to conventional medicine
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    would have us just treating each of
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    those separate disorders individually
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    and yet when we can acknowledge that
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    there is to varying degrees a connection
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    with one single disorder with insulin
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    resistance then we can just address the
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    insulin resistance so start taking care
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    of all of the seemingly distinct
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    disorders it's so it's a way to reframe
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    our perspective with regards to modern
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    disease so it's you really can almost
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    just throw a dart at a dartboard of
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    illness in whichever one it hits
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    erectile dysfunction yep that's one of
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    the earliest signs of insulin resistance
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    in many men I've mentioned infertility
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    so polycystic ovarian syndrome and women
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    that is at its core a disease of too
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    much insulin which happens with insulin
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    resistance coming to the ovaries and
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    inhibiting the ovaries ability to make
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    estrogens hypertension I'd mentioned is
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    almost always somehow connected insulin
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    resistance and and many many other
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    disorders and so is that why then
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    lifestyle intervention so the what you
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    eat is such a major part of improving
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    your health yeah that's right that is
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    one of the things I hope people take
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    away from that overall message if
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    someone can appreciate that insulin
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    resistance is a key driver of most
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    diseases then they can lean in to the
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    fact that lifestyle changes really make
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    a powerful change in insulin resistance
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    where there are papers published showing
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    that people who are
    on anti-diabetic medications because
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    their insulin resistance is
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    so bad they have to drop
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    their medications just within just
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    within a matter of a couple weeks the
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    insulin sensitivity gets so better so
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    much better so quickly yeah and
    I guess that is the
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    key thing I'm hearing here
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    too is that you know most of time we
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    just think if I have an instant problem
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    I'm gonna have a diabetes problem but
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    what you're saying here is if you have
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    an instant problem it's not just
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    diabetes you could actually come up with
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    one of these other conditions before you
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    get classified as diabetic or if you
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    even get classified as diabetic
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    it's right and that is a big if I am most
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    based on just normal statistics that we
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    have available the prevalence of insulin
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    resistance versus type 2
    diabetes it is obvious that
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    most people with insulin resistance
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    will not progress all the way
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    to type 2 diabetes all the more reason
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    to not look at insulin resistance as
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    just a diabetic progression look at it as
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    a progression to multiple diseases
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    and we can focus on it outside the
    context of diabeties
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    you know for example
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    focusing on it in the context of heart
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    disease which is such a main killer even
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    focusing on it in the context of certain
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    cancers like breast and prostate cancers
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    well which appear to be very affected by
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    the insulin resistance status of the
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    individual so yeah if we can remove
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    insulin resistance from just the world
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    of diabetes then we can I would argue
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    start to look earlier in the progression
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    of all you know all the other disorders
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    that insulin resistance is connected to
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    and in your book do you go again into
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    the detail of how
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    lay person can try work with their
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    physician to understand do they have
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    insulin resistance oh yeah yeah
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    absolutely so I mentioned a few tests in
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    the book and give details with regards
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    to the utility of measuring fasting
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    insulin itself which is very rarely done
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    but does have some utility although it's
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    not perfect and then the best of all
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    measuring insulin when possible in the
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    context of a glucose challenge so if the
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    person drinks glucose and if they can
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    just have a couple blood samples and
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    measure insulin from those blood samples
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    at a couple time points then they're
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    really they're really getting some
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    predictive value yeah and I think I saw
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    a tweet from dr. an and she showed how
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    someone had a normal glucose level but
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    if what if he measured the insulin they
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    actually had a massive insulin spike but
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    so they would have just measured their
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    glucose they would have looked normal
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    but the insulin response didn't look
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    normal
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    that's right yep and that is so often
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    just if there's any if there's any one
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    message I hope anyone ever takes away
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    from hearing me talk in any venue it is
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    the the need to look at insulin that we
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    just can't continue to of course in the
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    context of diabetes we always look at
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    glucose that is in fact how we define
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    the disease and I think that's
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    unfortunate but we need to shift the
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    focus to insulin not only for the sake
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    of earlier and better treatment and
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    diagnosis for diabetes but for many
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    other disorders as well yeah and it
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    sounds like here you could do the oral
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    glucose tolerance test not just to say
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    you're diabetic but actually if you have
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    an illness as you mentioned one of these
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    other conditions you could add in the
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    validation with a with this test to show
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    actually I need a major lifestyle
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    intervention because my hypertension my
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    high blood pressure I've got a big
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    problem here I can see it through this
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    day yeah yep that's right and so when
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    the person and hypertension is so common
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    rather than give them an
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    antihypertensive medication that's
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    blocking other hormones or trying to
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    push the the water from the kidneys just
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    then say alright let's lower your
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    insulin and then the healthcare
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    practitioner would know when we lower
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    insulin we can lower aldosterone which
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    is the hormone that's telling the
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    kidneys to hold on to all the water and
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    the salt then rather than take a drug
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    that will block what aldosterone is
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    trying to do
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    which there is just lower aldosterone on
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    its own by allowing insulin to come down
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    and now you're resolving the
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    hypertension so that one's a very strong
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    connection in particular yeah and I mean
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    these are I'm just thinking of common
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    conditions so that everyone's probably
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    heard of and high blood pressures is a
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    simple thing that I think a lot of
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    people have had kidney health too I mean
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    people do suffer chronic kidney disease
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    is insulin related to kidney Hill yeah
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    so insulin does change how kidneys
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    handle urea for example if an insulin
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    resistance the kidneys release less urea
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    into the urine and thus the body is
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    holding on to it and that of course
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    becomes part of the that's an early form
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    of what will become uric acid although
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    that gets us into a different disorder
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    but yeah the kidneys are influenced not
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    only by urea handling with insulin
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    resistance but also the pH an insulin
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    resistance the pH of the urine changed
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    just and actually increases the risk of
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    stone formation which may I hope I never
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    get that's by all accounts is the most
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    you know painful thing you can have
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    happen interesting so if someone suffers
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    kidney stones then it could it could be
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    here that that is one of those disorders
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    where I'm not at all attempting to say
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    it's only insulin resistance no there
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    could be many other variables but that
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    is one yeah but yeah as a simplicity
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    test it sounds like again oral glucose
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    tolerance test with and with added
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    insulin testing is so good as a baseline
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    not only for diabetes but just all these
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    other types of conditions you know yeah
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    like for example Alzheimer's disease
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    that is one of those diseases that
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    really terrifies me and the the evidence
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    suggesting that insulin resistance is an
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    early indicator and and that is altering
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    the way the brain accesses glucose and
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    so there's this very early detectable
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    change in brain glucose use in people
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    before they have any diagnosed
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    Alzheimer's disease that later becomes
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    Alzheimer's hmm and I think I like that
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    because Alzheimer's and I'm guessing
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    even age-related dementia just basic
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    brain health
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    if you want to see how well your brain
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    is aging you could see how well do you
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    have insulin resistance so as you're
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    aging if brain health is a important
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    factor for you
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    which I think most people is doing a
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    basic weight test to see if you got
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    insulin resistance is another key signal
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    to say yeah your brain is is a is only a
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    good part as we age yeah yeah so there
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    was a study that found that for every I
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    think it was of every 10 years someone
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    had type 2 diabetes which as we know is
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    at its core insulin resistance the brain
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    was 2 years older than it should have
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    been compared to the you know the same
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    age person without the disease so this
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    insulin resistance state is prematurely
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    aging the brain or it's accelerating the
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    aging yeah yeah and I get you know I
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    could think of other neurology I mean
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    the brain is one mass but could be so
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    many other things so that it gives me
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    thinking cause we're gonna move on into
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    diet stuff here now which everyone loves
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    because they can this action what they
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    can do it yeah and we're speaking
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    currently in January which is well
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    carnival month and I've had a lot of
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    questions of people asking ok can you
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    ask dr. Beckmann about the whole insulin
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    and protein thing again yes you know
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    they they want to know hey I'm doing all
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    this and it looks like I'm getting
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    healthy and I'm seeing all these success
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    stories while people going carnivore but
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    protein you know a lot of protein can
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    cause an insulin response any thought
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    yet on on that on the carnivore diet and
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    in general assistance yeah I sure do so
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    a lot of I made that an effort of of
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    research a few years ago and it was not
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    my findings these were I was relying on
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    the findings of earlier scientists so
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    these these were questions that had been
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    asked and answered and although my lab
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    is just starting up a slightly altered
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    version of that study which we can come
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    back to in a moment but the the some of
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    the data was that if you load the body
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    with amino acids so protein because it's
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    the amino acid that's going to have the
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    insulin effect or not so if you if the
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    blood is enriched with amino acids and
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    the glucose level is elevated then the
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    insulin spike from the glucose is
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    amplify
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    significantly with the cart with the
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    protein so the protein combined with
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    with carbohydrate is is insulin and
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    genic that will spike the insulin level
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    higher in contrast if it is a protein
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    spike or an amino acid load without a
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    glucose load then there is no
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    significant spike in insulin there's a
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    little hiccup of the as the amino acids
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    come past the pancreas and but it's not
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    it's nothing like what you had in the
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    hyperglycemic state and a part of this
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    is really the the likely reason for this
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    if we try to find the rational reason
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    which is fun to try to do why is the
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    body working that way we know that it
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    does and then we ask well why we go one
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    step further to try to see the design or
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    the reason for it in that case when
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    someone is eating glucose they can have
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    glucose with protein there it makes
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    sense to stimulate insulin to try to say
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    hey we are loaded with nutrient in the
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    blood let's get this out let's push it
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    into all the tissues and that really is
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    what insulin is facilitating among many
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    other things it is at its core anabolic
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    and and it wants to is so it needs
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    material to be pushed into the cells and
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    and an insulin will facilitate that
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    process thus giving some reason for
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    insulin being even higher when there's
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    high glucose and high amino acid in
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    contrast if there's high amino acid but
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    low glucose in the diet then the liver
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    is very busily making glucose through
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    this process of gluconeogenesis and
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    that's healthy it needs to happen in
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    order to maintain normal glycemia which
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    happens in world carnivore month if
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    someone's eating zero carbohydrate
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    they'll notice that their blood glucose
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    levels are perfectly normal
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    that's because of the livers ability to
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    pull almost it's almost totally from
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    lactate importantly it's not it's very
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    rarely from amino acids but the liver
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    will pull in lactate and convert that
  • 15:24 - 15:27
    lactate into glucose but that can't
  • 15:27 - 15:33
    happen unless insulin is low and so too
  • 15:33 - 15:35
    wrap this idea up if gluco if dietary
  • 15:35 - 15:37
    glucose is low but dietary protein is
  • 15:37 - 15:40
    elevated we cannot afford to have
  • 15:40 - 15:42
    insulin being spiked because that would
  • 15:42 - 15:44
    prevent the livers ability in this low
  • 15:44 - 15:46
    dietary glucose state from making
  • 15:46 - 15:49
    glucose because insulin turns that off
  • 15:49 - 15:52
    so we have separated that that event so
  • 15:52 - 15:55
    if protein is high but glucose is or
  • 15:55 - 15:58
    carbohydrate is low insulin stays low so
  • 15:58 - 16:00
    that the liver can continue to make
  • 16:00 - 16:03
    glucose from lactate and other precursor
  • 16:03 - 16:06
    molecules but mostly lactate okay so
  • 16:06 - 16:09
    someone who does have insulin resistance
  • 16:09 - 16:12
    if they go on on something like that
  • 16:12 - 16:14
    carnivore diet experiment it's actually
  • 16:14 - 16:16
    not a bad thing because it could help
  • 16:16 - 16:20
    them try to get more insulin sensitivity
  • 16:20 - 16:22
    I would suspect that would be the case
  • 16:22 - 16:24
    very strongly yes now of course I'm not
  • 16:24 - 16:27
    their doctor you neither of us is but
  • 16:27 - 16:29
    yes I would suspect if someone has
  • 16:29 - 16:31
    insulin resistance and they adopted a
  • 16:31 - 16:33
    zero carbohydrate diet and again I'm not
  • 16:33 - 16:36
    telling anyone to do it but I imagine
  • 16:36 - 16:37
    they would have pretty profound
  • 16:37 - 16:39
    improvements and insulin resistance
  • 16:39 - 16:40
    quite quite quickly
  • 16:40 - 16:44
    yeah so yeah because I guess I mean we
  • 16:44 - 16:45
    talked about that in our last interview
  • 16:45 - 16:47
    and how a low carbohydrate diet seems to
  • 16:47 - 16:50
    be the the more sustainable diet when it
  • 16:50 - 16:52
    comes to managing your instant of it
  • 16:52 - 16:55
    over time carnivore diets just another
  • 16:55 - 16:58
    x4 more extreme version of a low
  • 16:58 - 17:00
    carbohydrate diets it is yeah yeah and
  • 17:00 - 17:03
    one thing I will say in defense of a
  • 17:03 - 17:06
    carnivore diet to defend it but not
  • 17:06 - 17:09
    advocate it it is that there's something
  • 17:09 - 17:13
    wonderfully just pure about it there you
  • 17:13 - 17:15
    are not eating any processed food
  • 17:15 - 17:18
    everything you're eating is just real
  • 17:18 - 17:21
    substantial food there's a real part of
  • 17:21 - 17:24
    me that appreciates that part of the
  • 17:24 - 17:26
    diet that there's nothing fake about it
  • 17:26 - 17:28
    but yeah for the for the sake of the
  • 17:28 - 17:31
    average individual a low carbohydrate
  • 17:31 - 17:36
    diet is far more realistic achievable I
  • 17:36 - 17:38
    can say attempting to adhere to a
  • 17:38 - 17:41
    carnivore diet in a family with a wife
  • 17:41 - 17:42
    and little kids that that is a challenge
  • 17:42 - 17:46
    in and of itself that that's so I if I'm
  • 17:46 - 17:47
    projecting that
  • 17:47 - 17:49
    the average individual whose
  • 17:49 - 17:50
    insulin-resistant and wanting to try
  • 17:50 - 17:53
    things I as powerful as the carnivore
  • 17:53 - 17:56
    diet could be and very very likely is
  • 17:56 - 17:59
    you don't have to go that far we know
  • 17:59 - 18:02
    from earlier publications that if you
  • 18:02 - 18:05
    put people on a low-carb versus a
  • 18:05 - 18:08
    low-fat diet and the low-carb diet can
  • 18:08 - 18:10
    be calorie unrestricted their insulin
  • 18:10 - 18:11
    levels will come down four times more
  • 18:11 - 18:14
    than the insulin drop you have in the
  • 18:14 - 18:15
    low-fat diet
  • 18:15 - 18:18
    so just low-carb is extremely powerful
  • 18:18 - 18:21
    for lowering insulin which itself is
  • 18:21 - 18:23
    evidence of the body becoming more
  • 18:23 - 18:25
    insulin sensitive it just doesn't need
  • 18:25 - 18:27
    as much insulin to get the job done and
  • 18:27 - 18:30
    that is powerful mm-hmm and then another
  • 18:30 - 18:32
    question that people want me to ask was
  • 18:32 - 18:33
    about ketone levels when you're
  • 18:33 - 18:36
    carnivore to because some people don't
  • 18:36 - 18:38
    have high ketone levels when they're
  • 18:38 - 18:40
    carnivore but now they're wondering is
  • 18:40 - 18:42
    it because because we talked about keep
  • 18:42 - 18:45
    your levels or ketones and recently
  • 18:45 - 18:49
    using it as a surrogate marker yes so if
  • 18:49 - 18:51
    I if I'm eating a strict carnivore diet
  • 18:51 - 18:53
    but I don't have high ketone levels is
  • 18:53 - 18:55
    what do you think's happening with my
  • 18:55 - 18:56
    insulin level yeah yeah that's a good
  • 18:56 - 18:58
    question what I suspect happens in the
  • 18:58 - 19:01
    person is that their ketone levels are
  • 19:01 - 19:02
    probably quite high at the beginning of
  • 19:02 - 19:04
    the carnivore experiment and then they
  • 19:04 - 19:06
    start to steadily go down almost this
  • 19:06 - 19:10
    sort of diminishing returns that also
  • 19:10 - 19:14
    reflects the diminishing utility in
  • 19:14 - 19:16
    using ketones themselves as an inverse
  • 19:16 - 19:18
    indicator of insulin so one of the
  • 19:18 - 19:21
    problems is the person is just adapting
  • 19:21 - 19:24
    to using their ketones better so a high
  • 19:24 - 19:25
    level of ketone in the blood simply
  • 19:25 - 19:27
    means you're making more ketone than
  • 19:27 - 19:31
    you're using that's not optimal over
  • 19:31 - 19:35
    time accordingly the body being
  • 19:35 - 19:37
    abhorring anything that's not optimal
  • 19:37 - 19:40
    starts to use more of this nutrient
  • 19:40 - 19:42
    that's being produced namely the ketones
  • 19:42 - 19:44
    so the fact that ketones I suspect
  • 19:44 - 19:46
    strongly would be higher at the
  • 19:46 - 19:47
    beginning of the experiment and within
  • 19:47 - 19:48
    maybe a couple weeks
  • 19:48 - 19:50
    they're now lower and the person's
  • 19:50 - 19:52
    having a hard time achieving that same
  • 19:52 - 19:54
    level of ketosis I would say that's not
  • 19:54 - 19:58
    the protein inhibiting ketogenesis is
  • 19:58 - 20:00
    rather an enhanced
  • 20:00 - 20:02
    utilization of the ketones themselves
  • 20:02 - 20:05
    okay so so you don't have to be at the
  • 20:05 - 20:08
    1.5 mil Imola and nutritional ketosis
  • 20:08 - 20:10
    level yeah it's actually you're probably
  • 20:10 - 20:13
    at either low to the low point
  • 20:13 - 20:15
    something's and that's a healthy state
  • 20:15 - 20:18
    oh I would absolutely say it is yeah
  • 20:18 - 20:19
    okay
  • 20:19 - 20:21
    and then I want to get into the fat
  • 20:21 - 20:24
    because I know you what you you have a
  • 20:24 - 20:26
    few ideas around fat but the first part
  • 20:26 - 20:29
    of fat I want to get into is I got since
  • 20:29 - 20:31
    view Brad Marshall recently around his
  • 20:31 - 20:33
    croissant diet and how he was adding
  • 20:33 - 20:36
    stearic acids to croissants and making
  • 20:36 - 20:39
    them very fatty what are your thoughts
  • 20:39 - 20:41
    there from a insulin response and what
  • 20:41 - 20:43
    what could happen there by adding all
  • 20:43 - 20:45
    these saturated fats and pacifically
  • 20:45 - 20:47
    stearic acid along with carbohydrate and
  • 20:47 - 20:50
    what it's doing to the body yeah now I
  • 20:50 - 20:52
    not knowing any of the details of his of
  • 20:52 - 20:56
    his blood biochemistry although I heard
  • 20:56 - 20:58
    about that experiment stearic acid is an
  • 20:58 - 21:02
    interesting fatty acid it's particularly
  • 21:02 - 21:05
    enriched in chocolate or cocoa beans and
  • 21:05 - 21:09
    it has a higher oxidative priority than
  • 21:09 - 21:12
    than palmitate which is the most common
  • 21:12 - 21:15
    saturated fat that we eat by that I mean
  • 21:15 - 21:19
    when a person eats long-chain fats all
  • 21:19 - 21:23
    the way from like omega-6 and omega-3 or
  • 21:23 - 21:26
    or or longer than that I should say as
  • 21:26 - 21:29
    they start going down to two stearic
  • 21:29 - 21:33
    acid which is 18 carbons and so to our
  • 21:33 - 21:36
    alpha linolenic acid which is an omega-3
  • 21:36 - 21:38
    and linoleic acid which is an omega-6
  • 21:38 - 21:40
    and then you go on shorter to or you
  • 21:40 - 21:43
    start to break off the unsaturation so
  • 21:43 - 21:45
    you take the 18 carbon polyunsaturated
  • 21:45 - 21:48
    fat and then you turn it into the purely
  • 21:48 - 21:50
    saturated fat 18 carbon which is stearic
  • 21:50 - 21:54
    acid alpha linolenic acid I promise I'll
  • 21:54 - 21:57
    make this relevant and clear so if we
  • 21:57 - 21:59
    look at when a person eats a diet of
  • 21:59 - 22:01
    mixed fats which we do all the time
  • 22:01 - 22:04
    certain fats are burned more readily
  • 22:04 - 22:06
    than other fats whereas other fats are
  • 22:06 - 22:09
    stored more readily than they are burned
  • 22:09 - 22:12
    palmitate is a fat that the body likes
  • 22:12 - 22:13
    to store
  • 22:13 - 22:17
    stearic acid is a and thus if you look
  • 22:17 - 22:19
    at the long-chain fats palmitate is the
  • 22:19 - 22:23
    one that is the least burned so the body
  • 22:23 - 22:25
    will burn it last if you will if you eat
  • 22:25 - 22:27
    the all these mixed fats and they're all
  • 22:27 - 22:29
    kind of lining up and forming a queue to
  • 22:29 - 22:32
    get on the fat-burning bus palmitate
  • 22:32 - 22:34
    will be at the back ahead of that will
  • 22:34 - 22:36
    be stearic acid so this is a fact that
  • 22:36 - 22:38
    is more preferentially burned than
  • 22:38 - 22:40
    palmitate or pull medic acid is
  • 22:40 - 22:43
    interestingly the alpha linolenic acid
  • 22:43 - 22:46
    from from like flaxseed is the most
  • 22:46 - 22:48
    burned of all of them the body has a
  • 22:48 - 22:51
    very high preference to burn that but
  • 22:51 - 22:52
    that's kind of beside the point
  • 22:52 - 22:55
    so I I wonder whether some of his
  • 22:55 - 22:58
    improvements come from the body being
  • 22:58 - 23:01
    forced to burn a fat now that it didn't
  • 23:01 - 23:03
    have to before and that is a necessary
  • 23:03 - 23:06
    part of someone becoming fat adapted
  • 23:06 - 23:10
    which itself is a part of something that
  • 23:10 - 23:13
    we refer to as metabolic flexibility and
  • 23:13 - 23:16
    at the risk of introducing you know
  • 23:16 - 23:20
    another idea into this answer one of the
  • 23:20 - 23:22
    problems in the modern world especially
  • 23:22 - 23:24
    in someone with insulin resistance is
  • 23:24 - 23:25
    that they are losing their metabolic
  • 23:25 - 23:27
    flexibility the body is very much a
  • 23:27 - 23:29
    hybrid engine burning fat in
  • 23:29 - 23:32
    carbohydrate as the person starts to
  • 23:32 - 23:34
    have a higher intensity of an activity
  • 23:34 - 23:37
    the body will burn more and more fat in
  • 23:37 - 23:39
    contrast or sorry more and more glucose
  • 23:39 - 23:41
    in contrast as intensity starts to
  • 23:41 - 23:43
    subside like you and I sitting here the
  • 23:43 - 23:45
    body is predominantly burning fat and
  • 23:45 - 23:47
    the ability to shift between these fuels
  • 23:47 - 23:50
    as intensity is going up using glucose
  • 23:50 - 23:53
    or down using fat is metabolic
  • 23:53 - 23:56
    flexibility in contrast the person with
  • 23:56 - 23:59
    insulin resistance and Beyond they're
  • 23:59 - 24:01
    stuck in what I say sugar burning mode
  • 24:01 - 24:03
    they're stuck in glucose burning mode so
  • 24:03 - 24:05
    even if they were to sit down like us
  • 24:05 - 24:08
    and talk whereas our metabolic fuel
  • 24:08 - 24:09
    starts to shift more towards fat they're
  • 24:09 - 24:13
    stuck burning burning glucose a part of
  • 24:13 - 24:16
    that could just be an inability of well
  • 24:16 - 24:19
    at the risk of oversimplifying it
  • 24:19 - 24:22
    mitochondria that are just reluctant to
  • 24:22 - 24:24
    burn fat the fact that stearic acid
  • 24:24 - 24:26
    demands
  • 24:26 - 24:29
    be to be burned more than palmitic acid
  • 24:29 - 24:31
    does which is the conventionally
  • 24:31 - 24:33
    predominant saturated fat in our diet it
  • 24:33 - 24:35
    could that then could lead to the the
  • 24:35 - 24:38
    mitochondria in the body and I would say
  • 24:38 - 24:41
    particularly the muscle cells getting
  • 24:41 - 24:43
    the signal hey there's a fat coming in
  • 24:43 - 24:45
    now that we have to burn let's build up
  • 24:45 - 24:48
    all the metabolic machinery to burn this
  • 24:48 - 24:50
    fat more so activate the production of
  • 24:50 - 24:53
    more mitochondria put in place more of
  • 24:53 - 24:56
    the enzymes involved in in the burning
  • 24:56 - 25:00
    of the fat ultimately okay so what you
  • 25:00 - 25:02
    were just mentioning did is it a good
  • 25:02 - 25:05
    thing that we're exposed to a variety of
  • 25:05 - 25:08
    fats then to maintain maintain the
  • 25:08 - 25:10
    health oh yeah yes that's a great
  • 25:10 - 25:12
    question I'm glad you brought it up yes
  • 25:12 - 25:14
    I argue that it is absolutely healthy
  • 25:14 - 25:19
    our diet has shrunk almost completely to
  • 25:19 - 25:21
    long-chain fats and that's kind of
  • 25:21 - 25:24
    palmitate and to lesser degrees theory
  • 25:24 - 25:28
    or stearic acid what we what those in
  • 25:28 - 25:30
    the low-carb community have started
  • 25:30 - 25:32
    eating more medium chain fats and that's
  • 25:32 - 25:34
    when you have like twelve carbons to
  • 25:34 - 25:38
    around six carbons or so and those are
  • 25:38 - 25:40
    in a medium chain triglycerides or MCT
  • 25:40 - 25:43
    but in the diet conventionally they're
  • 25:43 - 25:45
    not too prevalent unless you're seeking
  • 25:45 - 25:46
    them out coconut oil
  • 25:46 - 25:50
    however is a very good source of medium
  • 25:50 - 25:52
    chain fats and then lastly we have
  • 25:52 - 25:55
    almost a completely forgotten family or
  • 25:55 - 25:58
    you know kid the third you know the the
  • 25:58 - 26:00
    third kid in the family the short chain
  • 26:00 - 26:03
    fats those used to be much more
  • 26:03 - 26:04
    prevalent because we get those from
  • 26:04 - 26:07
    bacteria now interestingly there's two
  • 26:07 - 26:11
    sources of these in the body one is that
  • 26:11 - 26:13
    our gut bacteria make them so our gut
  • 26:13 - 26:16
    bacteria can take fiber particularly
  • 26:16 - 26:19
    soluble fiber and and turn it into short
  • 26:19 - 26:21
    chain fats and then we those can get
  • 26:21 - 26:23
    absorbed into the bloodstream and
  • 26:23 - 26:25
    they're very beneficial they increase
  • 26:25 - 26:26
    some things I just mentioned
  • 26:26 - 26:28
    mitochondrial biogenesis they're very
  • 26:28 - 26:32
    ketogenic so the the the bacteria in our
  • 26:32 - 26:34
    guts can make them now I can't tell you
  • 26:34 - 26:37
    which family of bacteria in the millions
  • 26:37 - 26:38
    they're all it seems like there always
  • 26:38 - 26:39
    are
  • 26:39 - 26:41
    um and I would encourage anyone
  • 26:41 - 26:43
    listening to this anytime someone
  • 26:43 - 26:45
    speaking about gut bacteria with too
  • 26:45 - 26:49
    much certainty be very skeptical because
  • 26:49 - 26:51
    the more I learn about the gut bacteria
  • 26:51 - 26:53
    the more I think we just don't really
  • 26:53 - 26:54
    know much yet I'm not saying they're not
  • 26:54 - 26:55
    important
  • 26:55 - 26:57
    but I don't think we I don't think we've
  • 26:57 - 26:59
    cracked that code yet but nevertheless
  • 26:59 - 27:02
    short chain fats can come from dietary
  • 27:02 - 27:04
    fiber that is metabolized now second and
  • 27:04 - 27:07
    what I believe is the last part of the
  • 27:07 - 27:09
    diet it is that we don't have any
  • 27:09 - 27:11
    fermented foods in our in our diet
  • 27:11 - 27:13
    anymore it's very very rarely our our
  • 27:13 - 27:15
    early ancestors would have certainly
  • 27:15 - 27:19
    fermented and whatever they could and
  • 27:19 - 27:23
    even things like like wine itself that's
  • 27:23 - 27:25
    a fermented food vinegar apple cider
  • 27:25 - 27:27
    vinegar is you know when wine has been
  • 27:27 - 27:29
    even one step further fermented and I'm
  • 27:29 - 27:31
    a huge advocate of apple cider vinegar
  • 27:31 - 27:34
    it has demonstrable improvements on
  • 27:34 - 27:37
    insulin sensitivity in in in people with
  • 27:37 - 27:39
    type 2 diabetes you can just give them a
  • 27:39 - 27:41
    couple tablespoons a day and do nothing
  • 27:41 - 27:43
    else and their insulin sensitivity
  • 27:43 - 27:46
    starts to get better so incorporating
  • 27:46 - 27:49
    those short chain fats into the diet I
  • 27:49 - 27:53
    believe is very important and the medium
  • 27:53 - 27:55
    chain fats which again in the low carb
  • 27:55 - 27:59
    ketogenic diet er more appreciated but
  • 27:59 - 28:00
    but finding ways to incorporate those
  • 28:00 - 28:02
    and then the long-chain fats will always
  • 28:02 - 28:04
    get and then earlier I'd mentioned the
  • 28:04 - 28:07
    kind of oxidative priority queue line
  • 28:07 - 28:10
    getting on the fat burning bus these
  • 28:10 - 28:13
    short chain fats there's no I'm unaware
  • 28:13 - 28:16
    of any capacity in the body to store
  • 28:16 - 28:18
    those so when we eat short chain fats we
  • 28:18 - 28:20
    get them into our blood we have to burn
  • 28:20 - 28:22
    them and that might be part of the
  • 28:22 - 28:25
    reason why the liver and other tissues
  • 28:25 - 28:26
    start to develop so many more
  • 28:26 - 28:28
    mitochondria it's because of their
  • 28:28 - 28:29
    seeing a lot of those short chain fats
  • 28:29 - 28:31
    the body's not going to store them
  • 28:31 - 28:33
    they're going to burn they're going to
  • 28:33 - 28:35
    burn them medium chain fats can be
  • 28:35 - 28:38
    stored a little but they're far more
  • 28:38 - 28:40
    preferentially oxidized and there also
  • 28:40 - 28:43
    isn't a rate limiter on either of these
  • 28:43 - 28:45
    the short or the medium chain if they
  • 28:45 - 28:46
    come into the cell which they do very
  • 28:46 - 28:47
    readily
  • 28:47 - 28:48
    they also very readily move right into
  • 28:48 - 28:50
    the mitochondria they don't need an
  • 28:50 - 28:52
    escort to get from the
  • 28:52 - 28:54
    outside the mitochondria in the
  • 28:54 - 28:56
    mitochondria to be burned in stark
  • 28:56 - 28:58
    contrast to the long-chain fats there is
  • 28:58 - 29:02
    an escort there's a molecule that waits
  • 29:02 - 29:04
    for them essentially at the surface of
  • 29:04 - 29:05
    them out of country and then we'll bring
  • 29:05 - 29:07
    them in so they have to be escorted in
  • 29:07 - 29:09
    and so the rate at which you're burning
  • 29:09 - 29:12
    those is going to be less than what
  • 29:12 - 29:13
    you're burning this with which you're
  • 29:13 - 29:15
    burning the short and medium because the
  • 29:15 - 29:16
    short meeting will just come in as
  • 29:16 - 29:18
    quickly as they want the long-chain
  • 29:18 - 29:20
    there it's kind of throttled by this
  • 29:20 - 29:23
    this transporter that that will be
  • 29:23 - 29:24
    bringing them in to be burned you know
  • 29:24 - 29:28
    very orderly mm-hmm and then so when it
  • 29:28 - 29:31
    comes to vegetable oils which everyone
  • 29:31 - 29:33
    also tries to avoid and talks about so
  • 29:33 - 29:35
    much in the community where do they form
  • 29:35 - 29:39
    into this picture yeah yeah so invoking
  • 29:39 - 29:42
    vegetable oils means we discuss linoleic
  • 29:42 - 29:46
    acid that is the it's again an eighteen
  • 29:46 - 29:49
    carbon like stearic acid is but this is
  • 29:49 - 29:54
    a polyunsaturated omega-6 it is
  • 29:54 - 29:56
    essential in the diet so just to make
  • 29:56 - 29:57
    that clear
  • 29:57 - 30:00
    we do need omega-6 fats just like we
  • 30:00 - 30:02
    need omega-3 and and so it's a good
  • 30:02 - 30:05
    thing then they're everywhere any fat
  • 30:05 - 30:08
    you eat from a natural source like an
  • 30:08 - 30:10
    animal source is going to have linoleic
  • 30:10 - 30:12
    acid in it and of course those are fats
  • 30:12 - 30:14
    that we've eaten since the beginning of
  • 30:14 - 30:17
    time as a species so we're going to get
  • 30:17 - 30:19
    enough we don't need a lot we're going
  • 30:19 - 30:22
    to get enough the problem now is that at
  • 30:22 - 30:24
    least in the US and I'm sure it's
  • 30:24 - 30:27
    similar around the the Western diet
  • 30:27 - 30:28
    eating world which is far beyond the
  • 30:28 - 30:31
    west these days as I've spoken
  • 30:31 - 30:33
    throughout Asia and the Middle East but
  • 30:33 - 30:38
    the linoleic acid from soybean oil
  • 30:38 - 30:40
    soybean oil itself has become the single
  • 30:40 - 30:43
    most consumed fat in in the human diet
  • 30:43 - 30:45
    it went from nothing 100 years ago and I
  • 30:45 - 30:47
    mean it there's some pretty compelling
  • 30:47 - 30:49
    there's one compelling figure that I'm
  • 30:49 - 30:51
    thinking of right now looking at US
  • 30:51 - 30:54
    dietary consumption where this fat went
  • 30:54 - 30:58
    from just zero in around 1910 1920
  • 30:58 - 31:00
    started to climb climb climb climb
  • 31:00 - 31:02
    climbing now it beats out any other
  • 31:02 - 31:04
    single source of fat in the diet so we
  • 31:04 - 31:06
    eat more soybean oil
  • 31:06 - 31:09
    more fat as soybean oil than any other
  • 31:09 - 31:11
    fat in in the Western diet and that is
  • 31:11 - 31:13
    it ought to be shocking
  • 31:13 - 31:16
    particularly when we appreciate that
  • 31:16 - 31:18
    this fat linoleic acid is also
  • 31:18 - 31:21
    exceedingly well I'm gonna use the word
  • 31:21 - 31:24
    I have before in this conversation but I
  • 31:24 - 31:25
    mean use it differently it's exceedingly
  • 31:25 - 31:27
    well oxidized now when I said oxidized
  • 31:27 - 31:30
    earlier about burning a fat to be clear
  • 31:30 - 31:32
    I should have said beta oxidized so beta
  • 31:32 - 31:35
    oxidation is the process of taking a fat
  • 31:35 - 31:37
    and breaking it down to burn it in
  • 31:37 - 31:39
    contrast when you have a fed that it's
  • 31:39 - 31:41
    just purely oxidized by that I mean it
  • 31:41 - 31:43
    has bumped into a reactive oxygen
  • 31:43 - 31:46
    molecule like oxidative stress molecules
  • 31:46 - 31:48
    and this oxidative stress molecule has
  • 31:48 - 31:51
    now kind of conveyed that oxidative
  • 31:51 - 31:54
    stress onto the fat and linoleic acid is
  • 31:54 - 31:58
    very well oxidized which is not a good
  • 31:58 - 32:01
    thing it means it becomes pathogenic and
  • 32:01 - 32:03
    dangerous very quickly and it becomes
  • 32:03 - 32:06
    this molecule called four hydroxy non
  • 32:06 - 32:11
    enol for H and E and among other things
  • 32:11 - 32:14
    for H and E will make fat cells very
  • 32:14 - 32:18
    sick and and force them to grow through
  • 32:18 - 32:20
    a manner of hypertrophy so people will
  • 32:20 - 32:22
    talk about the personal fat threshold
  • 32:22 - 32:25
    and I think rightly so where it's this
  • 32:25 - 32:27
    idea that a person's body has a certain
  • 32:27 - 32:30
    fat level beyond which it now starts to
  • 32:30 - 32:32
    become metabolically sick namely insulin
  • 32:32 - 32:34
    resistance I believe we can look at that
  • 32:34 - 32:36
    personal fat threshold at the level of
  • 32:36 - 32:40
    the fat cell and essentially if a fat
  • 32:40 - 32:41
    cell is growing through hypertrophy
  • 32:41 - 32:44
    rather than the fat tissue growing
  • 32:44 - 32:46
    through hyperplasia so making more fat
  • 32:46 - 32:49
    cells that is bad hypertrophy is a sick
  • 32:49 - 32:52
    hypertrophic fat cells a sick fat cell
  • 32:52 - 32:53
    hyperplasia
  • 32:53 - 32:55
    fat cells are healthy they might be the
  • 32:55 - 32:57
    person may be fatter than they want to
  • 32:57 - 32:58
    be but they're going to be very insulin
  • 32:58 - 33:00
    sensitive and metabolically fine
  • 33:00 - 33:04
    linoleic acid once it's oxidized to for
  • 33:04 - 33:07
    H and E and we have that product of for
  • 33:07 - 33:09
    H and E it pushes the fat cells to
  • 33:09 - 33:11
    hypertrophic growth and blocks the
  • 33:11 - 33:13
    hyperplastic growth so if someone's
  • 33:13 - 33:15
    eating a diet that's wanting their fat
  • 33:15 - 33:17
    cells to get big so they have ample
  • 33:17 - 33:18
    calories and they have insulin being
  • 33:18 - 33:20
    elevated the
  • 33:20 - 33:22
    tissue is going to want to grow to store
  • 33:22 - 33:23
    that energy and insulin tells the body
  • 33:23 - 33:27
    to store energy if for H and E is high
  • 33:27 - 33:29
    because of high say soybean oil
  • 33:29 - 33:31
    consumption it's going to push that fat
  • 33:31 - 33:33
    grow through hypertrophy which is
  • 33:33 - 33:35
    decidedly unhealthy
  • 33:35 - 33:37
    in contrast the person who's avoiding
  • 33:37 - 33:40
    seed oils but still eating foods that
  • 33:40 - 33:42
    are going to keep their insulin too high
  • 33:42 - 33:45
    in calories that are too I then they're
  • 33:45 - 33:47
    an ample calories to support their
  • 33:47 - 33:48
    growth the fat cells will more likely
  • 33:48 - 33:51
    grow through hyperplastic expansion
  • 33:51 - 33:55
    interesting so taking us back to the the
  • 33:55 - 33:59
    bakery if you've got baked goods and
  • 33:59 - 34:02
    there's all these oxidized badly
  • 34:02 - 34:05
    oxidized vegetables made in the process
  • 34:05 - 34:07
    there plus you're getting all this
  • 34:07 - 34:08
    carbohydrate and you're going to get an
  • 34:08 - 34:11
    insulin lift you're getting a double
  • 34:11 - 34:12
    whammy because you're going to be
  • 34:12 - 34:13
    slicing through the carbohydrate plus
  • 34:13 - 34:16
    the way the food is made has got these
  • 34:16 - 34:19
    oxidize oils and as you're saying that's
  • 34:19 - 34:21
    actually causing individual fat cells to
  • 34:21 - 34:23
    want to grow bigger versus growing more
  • 34:23 - 34:25
    fat cells for the hypertrophy scenario
  • 34:25 - 34:28
    and that's just like a combination
  • 34:28 - 34:29
    that's just not good for us oh yeah I'd
  • 34:29 - 34:31
    say it's a perfect storm but you made me
  • 34:31 - 34:33
    think of another idea if I were to get
  • 34:33 - 34:36
    croissants here in the US I guarantee
  • 34:36 - 34:37
    the main fat is probably going to be
  • 34:37 - 34:40
    some soybean oil or some form corn oil
  • 34:40 - 34:43
    or something some seed oil as opposed to
  • 34:43 - 34:45
    that guy's experiment where he is
  • 34:45 - 34:47
    deliberately enriching the croissants
  • 34:47 - 34:50
    with the non seed oil fat with stearic
  • 34:50 - 34:54
    acid not only is it not eliciting that
  • 34:54 - 34:57
    same disastrous effect on the fat cells
  • 34:57 - 35:01
    but it also is again so readily burned
  • 35:01 - 35:03
    that could be a part of another part of
  • 35:03 - 35:04
    the magic that he saw
  • 35:04 - 35:07
    yeah and bread also talks about that
  • 35:07 - 35:08
    because he's a he's been a pig farmer
  • 35:08 - 35:11
    and how the the feed to the pigs has
  • 35:11 - 35:13
    changed so much and the quality of the
  • 35:13 - 35:16
    fats the difference between European
  • 35:16 - 35:19
    pigs and American pigs but usually what
  • 35:19 - 35:22
    something else I remember is that it's
  • 35:22 - 35:23
    meant to be that if you've got someone
  • 35:23 - 35:26
    who's got a big tummy like a fat tummy
  • 35:26 - 35:28
    if you product if it's a soft tummy
  • 35:28 - 35:30
    that's a better indicator than if it's a
  • 35:30 - 35:33
    hard oh yeah honey so hard fat versus
  • 35:33 - 35:33
    our software
  • 35:33 - 35:34
    is that what's it tied into this
  • 35:34 - 35:37
    hyperplasia hypertrophy yeah actually
  • 35:37 - 35:39
    that's actually a different situation
  • 35:39 - 35:41
    where if it's if it's I always joked
  • 35:41 - 35:43
    that if it jiggles it's good and that's
  • 35:43 - 35:44
    what kind of what you're talking about
  • 35:44 - 35:46
    with regards to is it polka ball or is
  • 35:46 - 35:50
    it not that's generally going to be a
  • 35:50 - 35:53
    difference of is it is it subcutaneous
  • 35:53 - 35:55
    fat or is it visceral fat so the person
  • 35:55 - 35:57
    who's fat is jiggly and squishy
  • 35:57 - 35:59
    that is subcutaneous that's right
  • 35:59 - 36:02
    beneath the skin that generally is
  • 36:02 - 36:04
    healthier in a number of ways it has
  • 36:04 - 36:06
    less macrophage invasion so it's less
  • 36:06 - 36:09
    inflammatory typically it produces more
  • 36:09 - 36:11
    leptin which is itself a metabolically
  • 36:11 - 36:13
    beneficial hormone and then in contrast
  • 36:13 - 36:15
    if we look at the visceral fat that is a
  • 36:15 - 36:19
    person whose stomach has fat at one
  • 36:19 - 36:21
    layer deeper in the body and then it has
  • 36:21 - 36:24
    the muscle over top of it so the fat is
  • 36:24 - 36:27
    accumulating beneath the muscle layer so
  • 36:27 - 36:29
    if you poked that person's belly you're
  • 36:29 - 36:32
    feeling that muscle of the abs and even
  • 36:32 - 36:33
    it might feel even harder than normal
  • 36:33 - 36:34
    because it's being pushed out and
  • 36:34 - 36:36
    somewhat distended so that muscle is
  • 36:36 - 36:38
    stretched and of course as a muscle is
  • 36:38 - 36:40
    stretched it is more firm so in the
  • 36:40 - 36:42
    person who has a big round belly that's
  • 36:42 - 36:45
    hard and you slap it that's likely
  • 36:45 - 36:46
    assigned them of them having more
  • 36:46 - 36:51
    visceral fat hmm okay and just also
  • 36:51 - 36:53
    bringing this into context here because
  • 36:53 - 36:54
    we're talking all about insulin
  • 36:54 - 36:56
    resistance so someone who's on a
  • 36:56 - 37:00
    high-fat diet the the type of fats that
  • 37:00 - 37:02
    used to eat is important too from an
  • 37:02 - 37:03
    insulin response
  • 37:03 - 37:06
    point is it yeah yeah that's a good
  • 37:06 - 37:10
    question um probably I I would argue
  • 37:10 - 37:13
    that if someone is you know I have to
  • 37:13 - 37:15
    I'm speculating a bit Gary it's a good
  • 37:15 - 37:16
    that's an astute question I don't have a
  • 37:16 - 37:18
    great answer for it because you've
  • 37:18 - 37:21
    mentioned the insulin spiking effects of
  • 37:21 - 37:25
    the fat right mmm yeah so dietary fat
  • 37:25 - 37:29
    alone does not increase insulin so the
  • 37:29 - 37:31
    person well their insulin whatever it is
  • 37:31 - 37:32
    before they take the fat the insulin
  • 37:32 - 37:34
    just hums along as normal there's no
  • 37:34 - 37:38
    significant bump from insulin alone and
  • 37:38 - 37:41
    some people have shared studies looking
  • 37:41 - 37:43
    at adding fat to an oil adding sorry
  • 37:43 - 37:46
    adding oil to a coffee and there was a
  • 37:46 - 37:47
    little hiccup
  • 37:47 - 37:48
    of insulin but was not statistically
  • 37:48 - 37:51
    significant and thus we can't say there
  • 37:51 - 37:53
    was an effect I mean it was so slight
  • 37:53 - 37:55
    and indeed it did not reach statistical
  • 37:55 - 37:57
    significance in fact it wasn't it wasn't
  • 37:57 - 37:59
    even close
  • 37:59 - 38:02
    so we we can't answer say that was that
  • 38:02 - 38:06
    there were difference so eating fat
  • 38:06 - 38:09
    alone does not change insulin now we
  • 38:09 - 38:11
    don't often just eat fat alone now those
  • 38:11 - 38:13
    in the low-carb Orkut especially I
  • 38:13 - 38:14
    should say keto community they do they
  • 38:14 - 38:17
    may directly add fat to things and I
  • 38:17 - 38:18
    would just say that if someone's trying
  • 38:18 - 38:19
    to lose weight through low carb diet
  • 38:19 - 38:21
    then not to do that
  • 38:21 - 38:23
    just eat fat as it comes with the real
  • 38:23 - 38:25
    foods you're eating indeed I often just
  • 38:25 - 38:27
    say eat fat as it comes with the protein
  • 38:27 - 38:29
    that you're prioritizing in your diet
  • 38:29 - 38:32
    but but nevertheless the fat alone won't
  • 38:32 - 38:37
    have an effect and I would say that if
  • 38:37 - 38:39
    someone is eating a fat with an insulin
  • 38:39 - 38:43
    spike in carbohydrate palmitate which is
  • 38:43 - 38:45
    the most common of the saturated fats it
  • 38:45 - 38:47
    may be one to avoid but that's almost a
  • 38:47 - 38:49
    whole other topic that I don't know if
  • 38:49 - 38:51
    we want to get into but but in general I
  • 38:51 - 38:53
    guess it's easy enough just to say in
  • 38:53 - 38:55
    general you don't want to be spiking
  • 38:55 - 39:00
    insulin and eating fat so you know
  • 39:00 - 39:01
    something like typically like a
  • 39:01 - 39:03
    croissant it would be something to be
  • 39:03 - 39:04
    very careful with a bagel you know
  • 39:04 - 39:07
    that's where it's or a doughnut high fat
  • 39:07 - 39:09
    and high carbohydrate that's not an
  • 39:09 - 39:11
    optimal mix mm-hmm it's like throwing a
  • 39:11 - 39:13
    grenade and your body is it yeah yeah
  • 39:13 - 39:17
    yeah metabolic grenade that's right
  • 39:17 - 39:19
    I want to ask you about frequency of
  • 39:19 - 39:21
    eating because bringing us back into the
  • 39:21 - 39:24
    carnival-themed where I've noticed a lot
  • 39:24 - 39:26
    of people when they go very strict
  • 39:26 - 39:28
    carnivore they also tend to go Oh mad
  • 39:28 - 39:31
    so one meal a day does do you think then
  • 39:31 - 39:34
    a lot of the benefit is coming from
  • 39:34 - 39:37
    reducing your eating window so we're
  • 39:37 - 39:40
    having a three thousand calorie meal or
  • 39:40 - 39:43
    even bigger and so for some people one
  • 39:43 - 39:45
    very small window what that's doing for
  • 39:45 - 39:47
    an insulin response point of view oh
  • 39:47 - 39:50
    yeah I am if someone is wanting to
  • 39:50 - 39:53
    improve insulin sensitivity or maintain
  • 39:53 - 39:56
    it I strongly contend that an optimal
  • 39:56 - 39:58
    way and ideal way of doing that is to
  • 39:58 - 40:00
    eat less
  • 40:00 - 40:04
    frequently the longer a person can go
  • 40:04 - 40:07
    through the day with low insulin I
  • 40:07 - 40:11
    believe the better that will be if if
  • 40:11 - 40:12
    for example you look at someone who's
  • 40:12 - 40:14
    just woke waking up in the morning their
  • 40:14 - 40:16
    insulin levels have had time to lower
  • 40:16 - 40:17
    throughout the night and indeed when
  • 40:17 - 40:19
    they wake up in the morning insulin is
  • 40:19 - 40:23
    going to be low and how unfortunate and
  • 40:23 - 40:25
    they are burning more fat than than they
  • 40:25 - 40:27
    would have otherwise been burning and
  • 40:27 - 40:29
    and that may be evident in some people
  • 40:29 - 40:32
    being in a mild very mild low level of
  • 40:32 - 40:35
    ketosis maybe point three point four
  • 40:35 - 40:37
    you know millimolar that can happen that
  • 40:37 - 40:42
    is evidence of fat burning and how
  • 40:42 - 40:44
    unfortunate then that they immediately
  • 40:44 - 40:45
    stopped that fat burning and go right to
  • 40:45 - 40:48
    sugar burning mode by eating a starchy
  • 40:48 - 40:50
    sugary breakfast as so many people do
  • 40:50 - 40:55
    around the world and then if specially
  • 40:55 - 40:56
    if their insulin resistance their
  • 40:56 - 40:58
    insulin levels have spiked around two to
  • 40:58 - 41:01
    three hours later if their insulin
  • 41:01 - 41:04
    resistant and most adults are then they
  • 41:04 - 41:06
    will have a rebound very commonly a
  • 41:06 - 41:08
    rebound hypoglycemia even though they're
  • 41:08 - 41:11
    not clinically hypoglycemic it may just
  • 41:11 - 41:13
    they're normally burning their normal
  • 41:13 - 41:15
    glucose I'm not going to know this a
  • 41:15 - 41:17
    milli molar for any of the Commonwealth
  • 41:17 - 41:19
    listeners so I'm sorry I can't I have to
  • 41:19 - 41:20
    lean into the American in me now
  • 41:20 - 41:22
    although I'm from Canada so I'm ashamed
  • 41:22 - 41:26
    that I can't do this I'm ashamed so well
  • 41:26 - 41:28
    if I all speak in just general terms so
  • 41:28 - 41:29
    their their their glucose levels are
  • 41:29 - 41:33
    normal they under state over shoot I
  • 41:33 - 41:35
    mean the insulin release was was not
  • 41:35 - 41:36
    commensurate with the glucose spike and
  • 41:36 - 41:39
    so now they have over the under they go
  • 41:39 - 41:41
    on below their glucose levels that
  • 41:41 - 41:43
    period can be sensed as an immediate
  • 41:43 - 41:46
    hunger that'll happen two to three hours
  • 41:46 - 41:47
    in so what do they do they go have a
  • 41:47 - 41:49
    snack and that immediately bums seeing
  • 41:49 - 41:51
    slim back up and then three or so hours
  • 41:51 - 41:53
    later is the insolence trying to come
  • 41:53 - 41:55
    back down they they sense that little
  • 41:55 - 41:59
    relative hypoglycemia again they bump it
  • 41:59 - 42:00
    up again they bump it up again so
  • 42:00 - 42:03
    they're eating six times a day and
  • 42:03 - 42:05
    there's not a single hint of fat burning
  • 42:05 - 42:08
    for coal parts of the day and insulin
  • 42:08 - 42:11
    elevated and this I believe not only
  • 42:11 - 42:12
    does this have impact with insulin
  • 42:12 - 42:14
    doesn't itself that
  • 42:14 - 42:16
    faithfulness elevated all day in inflam
  • 42:16 - 42:20
    itself and create resistance to itself
  • 42:20 - 42:22
    too much insulin causes influence isn't
  • 42:22 - 42:25
    but it also is dangerous I believe for
  • 42:25 - 42:29
    brain disorders where there is this
  • 42:29 - 42:31
    phenomenon that I mentioned earlier of
  • 42:31 - 42:33
    glucose hypometabolism many neurological
  • 42:33 - 42:36
    disorders Alzheimer's disease has a
  • 42:36 - 42:37
    detectable reduction in brain glucose
  • 42:37 - 42:39
    use people who suffer from migraines
  • 42:39 - 42:41
    have a technical reduction in brain
  • 42:41 - 42:44
    glucose a Parkinson's disease if those
  • 42:44 - 42:47
    instances are at least partly driven by
  • 42:47 - 42:49
    the brain not being able to get all of
  • 42:49 - 42:51
    its energy through there's only one
  • 42:51 - 42:53
    other fuel the brain can use and that's
  • 42:53 - 42:56
    ketone and yet if insulin is elevated
  • 42:56 - 42:59
    every moment of the day the brain just
  • 42:59 - 43:02
    forced to go without an alternative fuel
  • 43:02 - 43:04
    that it was very desperately hoping in
  • 43:04 - 43:07
    bed and get a Tanz on eating every three
  • 43:07 - 43:10
    hours we ensure especially if it's
  • 43:10 - 43:14
    conventional high our meals and snacks
  • 43:14 - 43:18
    we ensure the brain gets no whiff of
  • 43:18 - 43:20
    ketone and ensure that we are in sugar
  • 43:20 - 43:22
    burning mode all day and if someone's
  • 43:22 - 43:24
    trying to lose weight and you don't
  • 43:24 - 43:25
    wanna do it sugar you're not going to do
  • 43:25 - 43:29
    it to not to get into fat-burning let me
  • 43:29 - 43:32
    come down so I strongly so make it to
  • 43:32 - 43:34
    make that clear I am a strong advocate
  • 43:34 - 43:37
    eating less frequently the person at
  • 43:37 - 43:41
    most e to the three meals per day and I
  • 43:41 - 43:43
    would argue that many would thrive on
  • 43:43 - 43:46
    simply eating too and it seems like that
  • 43:46 - 43:48
    seems a natural progression and the
  • 43:48 - 43:50
    success stories that I hear that people
  • 43:50 - 43:54
    fall into that too sometimes one big one
  • 43:54 - 43:57
    yeah very very seldomly three meals in a
  • 43:57 - 44:00
    day so the one challenge I'll say in one
  • 44:00 - 44:02
    meal a day is I've experimented as well
  • 44:02 - 44:05
    um just because I my priority in life as
  • 44:05 - 44:07
    husband and father so family matters
  • 44:07 - 44:08
    more than anything
  • 44:08 - 44:10
    that means dinnertime is important that
  • 44:10 - 44:13
    social time although my family is such
  • 44:13 - 44:15
    an early morning family the breakfast is
  • 44:15 - 44:18
    always social as well but if I didn't
  • 44:18 - 44:20
    eat dinner with my family it would be
  • 44:20 - 44:22
    weird as we're all sitting there and
  • 44:22 - 44:24
    then I'll be looking at daddy not eating
  • 44:24 - 44:26
    but if I don't eat breakfast no one
  • 44:26 - 44:27
    notices it all there's always
  • 44:27 - 44:29
    just enough of a fuss just getting ready
  • 44:29 - 44:32
    for the day I always make breakfast for
  • 44:32 - 44:34
    the family in the mornings and like this
  • 44:34 - 44:35
    morning it was some little egg cheese
  • 44:35 - 44:38
    bacon muffins but I was fasting this
  • 44:38 - 44:40
    morning they don't they don't notice a
  • 44:40 - 44:42
    bit no one notices I'm talking with them
  • 44:42 - 44:44
    we're all being very social it's no one
  • 44:44 - 44:46
    notices so if I try one meal a day my
  • 44:46 - 44:49
    point the ends up being dinner it's a
  • 44:49 - 44:51
    meal that I eat it is so difficult for
  • 44:51 - 44:55
    me not to overeat to the point that it's
  • 44:55 - 44:57
    going to affect my sleep I say that is
  • 44:57 - 45:00
    someone who I'm a terrible sleeper and I
  • 45:00 - 45:04
    have found without any ambiguity I have
  • 45:04 - 45:08
    my best night's sleep I'm not even close
  • 45:08 - 45:12
    to full I'm just no so now I guess my
  • 45:12 - 45:14
    point is I tend to eat a big lunch and
  • 45:14 - 45:19
    then I eat a mild small dinner whatever
  • 45:19 - 45:21
    the family is eating for dinner um if I
  • 45:21 - 45:24
    can make it for me low carb easily then
  • 45:24 - 45:27
    I will but if it's the meals and we have
  • 45:27 - 45:30
    to deny our carb I am NOT gonna skip
  • 45:30 - 45:33
    dinner as my family I nevertheless I try
  • 45:33 - 45:36
    to control the portion sizes and that is
  • 45:36 - 45:38
    really easy for me to do if I've had a
  • 45:38 - 45:41
    big lunch it's easy to keep small dinner
  • 45:41 - 45:44
    and make my bed with a relatively your
  • 45:44 - 45:47
    stomach since I sleep so much better not
  • 45:47 - 45:50
    quantifiably matter is I finally bought
  • 45:50 - 45:53
    a little sleep tracker ring I absolutely
  • 45:53 - 45:55
    you know I have the data to validate
  • 45:55 - 45:57
    what I long suspected yeah interesting
  • 45:57 - 45:59
    so again that personalization in your
  • 45:59 - 46:02
    case where you know what time of day you
  • 46:02 - 46:04
    eat even affects the quality of your
  • 46:04 - 46:06
    sleep yeah now I would say someone
  • 46:06 - 46:07
    listening to this could just be shaking
  • 46:07 - 46:09
    their head saying no no no no I just do
  • 46:09 - 46:09
    better
  • 46:09 - 46:12
    eating dinner hey awesome I I'm not at
  • 46:12 - 46:14
    all claiming that my way is the way to
  • 46:14 - 46:14
    do it
  • 46:14 - 46:16
    I just find I have a hard time
  • 46:16 - 46:19
    controlling my appetite if I'm waiting
  • 46:19 - 46:20
    if everything goes into dinner now I
  • 46:20 - 46:22
    haven't been able to do it sometimes
  • 46:22 - 46:26
    well but often I get hungry to the point
  • 46:26 - 46:32
    that I overeat I'm asleep and moving
  • 46:32 - 46:34
    away from eating frequency then some
  • 46:34 - 46:37
    actually that gets me thinking you talks
  • 46:37 - 46:40
    about the apple cider vinegar
  • 46:40 - 46:42
    is that something that someone can do if
  • 46:42 - 46:44
    they're gonna what you mentioned that if
  • 46:44 - 46:46
    you happen to be in a family setting and
  • 46:46 - 46:48
    they eating a higher carb situation if
  • 46:48 - 46:50
    you put more vinegar on the food will
  • 46:50 - 46:52
    that have a blunter effect oh yeah
  • 46:52 - 46:54
    insulin response that you're gonna guess
  • 46:54 - 46:56
    it sure will it sure will yeah so
  • 46:56 - 46:57
    remember vinegar is a short chain fat
  • 46:57 - 47:00
    and in fat does mitigate some of the
  • 47:00 - 47:01
    insulin effect of a carbohydrate that
  • 47:01 - 47:05
    that is real so yes if someone is eating
  • 47:05 - 47:06
    a salad or they have the opportunity of
  • 47:06 - 47:08
    adding more oil and vinegar do it
  • 47:08 - 47:11
    alternatively what I love to do I will I
  • 47:11 - 47:14
    drink a lot of club soda I love just
  • 47:14 - 47:18
    just sparkling water and I will add a
  • 47:18 - 47:21
    shot of apple cider vinegar to that and
  • 47:21 - 47:23
    that'll be what I'm drinking during the
  • 47:23 - 47:27
    meal now also in addition to a little
  • 47:27 - 47:28
    bit of cider vinegar
  • 47:28 - 47:32
    we still or sparkling water or some can
  • 47:32 - 47:34
    put the carbohydrates at the end of the
  • 47:34 - 47:37
    meal that has it the even if they eat
  • 47:37 - 47:39
    the same amount same grams of
  • 47:39 - 47:40
    carbohydrate and everything else is the
  • 47:40 - 47:40
    same
  • 47:40 - 47:43
    there's some study not long ago
  • 47:43 - 47:45
    published it finds if you put the
  • 47:45 - 47:47
    carbohydrate at the end of the meal the
  • 47:47 - 47:48
    insulin effect of the overall meal is
  • 47:48 - 47:50
    significantly lower than this carb dirt
  • 47:50 - 47:54
    upfront okay good tip there another one
  • 47:54 - 47:56
    then you mentioned about the snacking
  • 47:56 - 47:59
    and how this I mentioned I was going to
  • 47:59 - 48:00
    bring about frequency I just thought of
  • 48:00 - 48:04
    it now but so try to avoid snacking but
  • 48:04 - 48:06
    then when someone's going from a place
  • 48:06 - 48:08
    where they're just they it's their
  • 48:08 - 48:09
    hunger problem they're just being hungry
  • 48:09 - 48:11
    all the time and now they're going
  • 48:11 - 48:14
    carnival or ketogenic whatever it
  • 48:14 - 48:15
    happens to be to try to get the better
  • 48:15 - 48:17
    response but they're looking for just
  • 48:17 - 48:19
    things to help them break up the hunger
  • 48:19 - 48:21
    in between what's your thoughts in on
  • 48:21 - 48:25
    these on high-fat meal replacements yeah
  • 48:25 - 48:28
    yeah I think that a a high-fat meal
  • 48:28 - 48:31
    replacement shake which ideally is also
  • 48:31 - 48:33
    going to be high protein I'll emphasize
  • 48:33 - 48:34
    that if it's just pure fat I don't think
  • 48:34 - 48:37
    that does satiating so a higher fat
  • 48:37 - 48:44
    higher protein can be very effective and
  • 48:44 - 48:47
    we looked at as a meal not as a snack
  • 48:47 - 48:49
    and the last thing to do is to have that
  • 48:49 - 48:51
    be a drink that someone's eating with a
  • 48:51 - 48:53
    meal that is not how those are commute a
  • 48:53 - 48:56
    full disclosure in the next few months I
  • 48:56 - 49:00
    have a shake coming out that I've helped
  • 49:00 - 49:03
    make someone you that'll be available
  • 49:03 - 49:07
    online helps HLT eight but what we've
  • 49:07 - 49:10
    liberally tried to do is put it in a
  • 49:10 - 49:13
    ratio of a one to one fat to protein by
  • 49:13 - 49:17
    mass I'm with in significant number of
  • 49:17 - 49:21
    carbs net carbs like two grams but a one
  • 49:21 - 49:23
    to one that I believe I'd oak with a
  • 49:23 - 49:26
    divine ratio that we see that in eggs we
  • 49:26 - 49:27
    see that in mistake
  • 49:27 - 49:30
    I consider the most nutritious foods on
  • 49:30 - 49:33
    the planet by mass this one the one of
  • 49:33 - 49:39
    fat protein that's that again can use
  • 49:39 - 49:41
    very effectively it is an easy way to
  • 49:41 - 49:44
    get good nourishment but it shouldn't be
  • 49:44 - 49:47
    used as a snack and never coupled with a
  • 49:47 - 49:48
    normal meal it's not a shake that you're
  • 49:48 - 49:51
    drinking with your fries and hamburger
  • 49:51 - 49:53
    that is not a low calorie food a meal
  • 49:53 - 49:55
    and in themself it should be looked at
  • 49:55 - 49:59
    it ok so again people who are not doing
  • 49:59 - 50:01
    carnival this month but they're doing
  • 50:01 - 50:04
    ketogenic then and I know the keto
  • 50:04 - 50:08
    shakes are quite popular it sounds like
  • 50:08 - 50:10
    juice frequency window eating maybe have
  • 50:10 - 50:13
    the shake to start today as you said but
  • 50:13 - 50:14
    then later in the day you can have your
  • 50:14 - 50:17
    bigger real food meal and hopefully
  • 50:17 - 50:18
    there you're not going to get to meet
  • 50:18 - 50:21
    too many insulin responses yes yeah yeah
  • 50:21 - 50:23
    that's right so the power of say
  • 50:23 - 50:25
    starting the morning if someone likes to
  • 50:25 - 50:26
    eat something for breakfast which I
  • 50:26 - 50:29
    totally understand focus on protein and
  • 50:29 - 50:31
    fat not only are those the two essential
  • 50:31 - 50:33
    macronutrients in the human diet
  • 50:33 - 50:36
    carbohydrates are not essential to focus
  • 50:36 - 50:38
    on what's essential is essential fat is
  • 50:38 - 50:40
    essential amino acid you also meet in
  • 50:40 - 50:42
    the two macros that have the least or no
  • 50:42 - 50:45
    effect on insulin that's a great way to
  • 50:45 - 50:47
    keep the body burning fat and help it
  • 50:47 - 50:49
    maintain that high degree of metabolic
  • 50:49 - 50:52
    flexibility yeah otherwise yeah lots of
  • 50:52 - 50:54
    scrambled eggs right absolutely
  • 50:54 - 50:57
    absolutely scrambled eggs and butter yes
  • 50:57 - 50:58
    that's an easy one
  • 50:58 - 51:01
    yes it sure is great I'm just trying to
  • 51:01 - 51:04
    think I mean I got so many questions
  • 51:04 - 51:06
    that people want to ask you I'm just
  • 51:06 - 51:07
    trying to think of a lot of hands
  • 51:07 - 51:09
    hopefully I've I've covered most of them
  • 51:09 - 51:11
    I've covered all the big topics I
  • 51:11 - 51:14
    believe is there anything else that's
  • 51:14 - 51:16
    come out around insulin resistance that
  • 51:16 - 51:18
    we haven't visited since our last talk
  • 51:18 - 51:23
    um yell probably there are in fact one
  • 51:23 - 51:25
    study comes right to my mind
  • 51:25 - 51:29
    as much as we talk about glucose and the
  • 51:29 - 51:33
    insulin spike a lot of there is a really
  • 51:33 - 51:34
    there's more and more evidence another
  • 51:34 - 51:35
    study just published finding that
  • 51:35 - 51:38
    fructose itself pure fructose like fruit
  • 51:38 - 51:42
    juice is really unhealthy for the fur
  • 51:42 - 51:44
    and it promotes liver fat accumulation
  • 51:44 - 51:47
    and then and then liver insulin
  • 51:47 - 51:48
    resistance and when the liver becomes
  • 51:48 - 51:50
    insulin resistant it starts releasing
  • 51:50 - 51:53
    fat and glucose and in that of course
  • 51:53 - 51:55
    the high glucose is driving the insulin
  • 51:55 - 51:57
    even higher and that's just feeding the
  • 51:57 - 51:59
    whole systemic insulin resistance
  • 51:59 - 52:02
    so another encouragement if we didn't
  • 52:02 - 52:05
    talk about last time don't drink fruit
  • 52:05 - 52:09
    if you want fruit eat it in controlled
  • 52:09 - 52:12
    amounts don't don't drink it ever good
  • 52:12 - 52:14
    points yeah perfect
  • 52:14 - 52:17
    well Ben that was again a fascinating
  • 52:17 - 52:19
    talk I learned so much from you every
  • 52:19 - 52:22
    time and hopefully I've added value to
  • 52:22 - 52:24
    other people have also listened to your
  • 52:24 - 52:27
    first interview just a treasure trove of
  • 52:27 - 52:29
    information every time well I love the
  • 52:29 - 52:31
    opportunity I really do as an academic
  • 52:31 - 52:34
    there's one of the most frustrating
  • 52:34 - 52:35
    things about it is you feel like you're
  • 52:35 - 52:37
    learning a lot answering really neat
  • 52:37 - 52:40
    questions and if you just published them
  • 52:40 - 52:40
    in paper
  • 52:40 - 52:42
    no one ever exceeds it and so the
  • 52:42 - 52:43
    opportunity to come on something like
  • 52:43 - 52:46
    that's like you're doing here is such a
  • 52:46 - 52:49
    fun way to convey the little bits these
  • 52:49 - 52:52
    little pearls of wisdom that I've been
  • 52:52 - 52:56
    able to gather my own and others yeah
  • 52:56 - 52:57
    and that's why I enjoy you know good
  • 52:57 - 52:58
    because you are you're on the cutting
  • 52:58 - 52:59
    edge you're in the lab you're
  • 52:59 - 53:01
    discovering things and then you're
  • 53:01 - 53:03
    breeding other papers and so people like
  • 53:03 - 53:06
    me need PhDs like you to be able to read
  • 53:06 - 53:07
    these things and then say hey this is
  • 53:07 - 53:09
    what science is finding and it's up to
  • 53:09 - 53:11
    you to decide what you want to do so yep
  • 53:11 - 53:14
    yeah well speaking of which from my lab
  • 53:14 - 53:16
    we got some really neat papers that were
  • 53:16 - 53:18
    in the process of preparing so we'll
  • 53:18 - 53:20
    have some data looking at how ketones
  • 53:20 - 53:22
    accelerate metabolic rate from that
  • 53:22 - 53:27
    issue and people will harden for we have
  • 53:27 - 53:29
    data showing how ketones enhance memory
  • 53:29 - 53:32
    and learning in the brain through a
  • 53:32 - 53:34
    novel mechanism so something that's not
  • 53:34 - 53:37
    before we have another paper anyway we
  • 53:37 - 53:38
    have we have some cool stuff coming out
  • 53:38 - 53:41
    all the time that's us it ends yeah this
  • 53:41 - 53:43
    is the time when I want you to share how
  • 53:43 - 53:44
    people can follow you and keep up to
  • 53:44 - 53:46
    date with all these papers that you can
  • 53:46 - 53:49
    be sharing right yes thank you yeah so I
  • 53:49 - 53:52
    on Twitter and Instagram I regularly
  • 53:52 - 53:56
    share the latest research through those
  • 53:56 - 54:00
    accounts that's been Whitman AMA and
  • 54:00 - 54:04
    we'll see Instagram then Facebook I have
  • 54:04 - 54:06
    a public profile page which is just
  • 54:06 - 54:10
    Benjamin but um I think maybe Benjamin
  • 54:10 - 54:13
    bhp and I've been trying to get Facebook
  • 54:13 - 54:14
    a little more time
  • 54:14 - 54:18
    fine I give it a little bit like
  • 54:18 - 54:20
    sometimes it's a little too much we're
  • 54:20 - 54:23
    trying to work that some water yeah well
  • 54:23 - 54:24
    I'll link to all those in the show notes
  • 54:24 - 54:26
    for everyone but again Ben I just want
  • 54:26 - 54:27
    to say thank you again for sure
  • 54:27 - 54:29
    a pose of wisdom well thanks so much
  • 54:29 - 54:31
    Gary what a fun opportunity
Title:
Why we get from insulin resistance
Description:

In today's interview I get to speak with associate professor doctor and bitmap about how insulin resistance make a Sikh causing more than just diabetics he is also back to answer some of your commonly asked questions

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Video Language:
English
Duration:
54:38

English, British subtitles

Revisions