Where Does Insulin Resistance Come From? with Dr. Ben Bikman

00:53:14
https://www.youtube.com/watch?v=O8NJMkrvX4s

Summary

TLDRIn this week's metabolic classroom, the focus is on understanding the origins of insulin resistance, a major global health issue. The discussion categorizes the causes of insulin resistance into primary and secondary causes. Primary causes include inflammation, stress hormones (like cortisol and epinephrine), and chronically elevated insulin levels. These factors are shown to cause insulin resistance in cell, animal, and human models. Secondary causes, such as seed oils and uric acid, may be less direct, often acting through inflammatory pathways. Inflammation leads to insulin resistance by activating pathways within cells, while stress hormones increase blood glucose, prompting insulin resistance. Chronically high insulin levels cause the body to become less responsive to insulin. The role of enlarged fat cells is crucial, as they become insulin resistant to stop growing, establishing a feedback loop of insulin resistance. Starvation, distinct from fasting, also causes insulin resistance through stress responses, but is unique because insulin levels are low. The lecture further explores misconceptions about diet's role, particularly the effect of saturated fats and plant-based diets, in managing or causing insulin resistance. The complex interplay of these factors highlights the challenges in mitigating insulin resistance and underlines the importance of comprehending these causes to improve metabolic health.

Takeaways

  • 📚 Understanding insulin resistance is crucial for global health.
  • 🧪 Primary causes include inflammation, stress hormones, and chronically high insulin.
  • 🔍 Inflammation diminishes cells' response to insulin.
  • 😟 Stress hormones increase blood glucose, leading to resistance.
  • 🍽️ Chronic insulin spikes from diet can cause resistance.
  • 🐀 Animal and cell studies show similar insulin resistance development.
  • 🍭 Uric acid and seed oils are potential secondary causes via inflammation.
  • 🥗 Plant-based versus ketogenic diets are debated for insulin effects.
  • 🧠 High LDL doesn't necessarily mean high heart disease risk in healthy metabolic profiles.
  • 🧪 Experiments reveal unique metabolic effects at cellular levels.

Timeline

  • 00:00:00 - 00:05:00

    The lecturer thanks the audience for participating in this metabolic classroom session, focusing on understanding the origins of insulin resistance. He encourages watching a previous episode defining insulin resistance within metabolic health. Today, the focus is on understanding what drives insulin resistance, drawing attention to a recent study in rats about sugar consumption affecting satiety, hinting at insulin resistance without directly using the term.

  • 00:05:00 - 00:10:00

    Insulin resistance is highlighted as the world's most common health problem, with two categories of causes: primary and secondary. Primary causes are confirmed in cells, rodents, and humans, while secondary causes either lack evidence across all three models or rely on a primary cause. The session proceeds to discuss primary causes: inflammation, stress, and chronically elevated insulin. Each factor is capable of independently causing insulin resistance.

  • 00:10:00 - 00:15:00

    Inflammation is discussed as a primary cause of insulin resistance, affecting nearly all cell types by diminishing their response to insulin. The lecturer describes how the presence of inflammation can be detected clinically via markers like C-reactive protein. The link between inflammation and insulin resistance is demonstrated through experiences in humans and animals.

  • 00:15:00 - 00:20:00

    The discussion shifts to stress as another primary cause of insulin resistance, emphasizing stress hormones like cortisol and epinephrine. It highlights how these hormones elevate blood glucose, requiring insulin to work harder, which contributes to insulin resistance. Causes of stress include sleep deprivation and caffeine consumption, both increasing the body's resistance to insulin as demonstrated in cell and animal studies.

  • 00:20:00 - 00:25:00

    Chronically elevated insulin is presented as the third primary cause, described as particularly pernicious because regular spikes in insulin levels can lead to resistance. Examples include frequent carbohydrate consumption. Unlike other causes, elevated insulin can be swiftly corrected, suggesting dietary changes are an immediate lever to improve insulin sensitivity.

  • 00:25:00 - 00:30:00

    Secondary causes include seed oils, which need more human study to be proven as a primary cause, and uric acid, which causes insulin resistance only through inflammation. The lecturer emphasizes that primary causes like inflammation can cause insulin resistance independently, while secondary causes need another mediator to have an effect.

  • 00:30:00 - 00:35:00

    Starvation is presented uniquely, as it causes insulin resistance through a necessary survival mechanism when the body has no fat to burn, thereby protecting brain function. Unlike other situations, insulin levels are low during starvation-caused resistance. Additional explanations will be explored in future sessions.

  • 00:35:00 - 00:40:00

    The lecturer transitions to discussing creeping insulin resistance beginning with fat cells. As fat cells expand, they may become insulin resistant to avoid overgrowth. Stress and lack of proper nutrient delivery lead to further complications, including inflammation. The importance of adipose tissue and its interaction with insulin is a critical factor. Seed oils are implicated in promoting unhealthy fat cell growth patterns.

  • 00:40:00 - 00:45:00

    The lecture also touches on dietary elements like seed oils contributing to insulin resistance by promoting fat cell growth. He provides a detailed explanation connecting the dietary influences with metabolic health outcomes. There is emphasis on how dietary composition can influence insulin and ultimately health.

  • 00:45:00 - 00:53:14

    In the Q&A session, the lecturer discusses queries related to plant-based diets, diet soda's impact on insulin, and sugar substitutes like allulose. He counters claims on cholesterol and plant-based dietary efficacy, advocating for understanding nutrient needs and physiological impacts rather than following dietary dogma zealously.

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Mind Map

Video Q&A

  • What are primary causes of insulin resistance?

    Primary causes include inflammation, stress hormones (cortisol and epinephrine), and chronically elevated insulin levels.

  • How do stress hormones impact insulin resistance?

    Stress hormones like cortisol and epinephrine raise blood glucose levels, making insulin work harder, which can lead to insulin resistance.

  • What is the role of inflammation in insulin resistance?

    Inflammation activates pathways in cells, causing them to have a diminished response to insulin, contributing to insulin resistance.

  • How does elevated insulin cause insulin resistance?

    Chronically high insulin levels lead to the body becoming less responsive to insulin, hence causing insulin resistance.

  • What are secondary causes of insulin resistance mentioned?

    Secondary causes include factors like uric acid and potentially seed oils, which act through primary causes like inflammation.

  • Can diet soda contribute to insulin resistance?

    Diet soda itself does not cause an insulin spike, but it may increase appetite in some individuals, leading to overeating.

  • How does the fat cell's size contribute to insulin resistance?

    As fat cells enlarge, they may become insulin resistant to stop growing larger, thus contributing to insulin resistance.

  • What is the difference between fasting and starvation in terms of insulin resistance?

    Fasting happens when the body burns fat for energy, whereas starvation occurs when the body runs out of fat and starts using lean mass, causing insulin resistance due to stress hormones.

  • Why is it challenging to address stress and inflammation as causes of insulin resistance?

    Both are influenced by complex factors including lifestyle and genetic predispositions, making them harder to control than dietary influences like insulin.

  • Can elevated uric acid levels cause insulin resistance?

    Yes, uric acid can cause insulin resistance, but it typically acts through inflammatory pathways.

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  • 00:00:00
    hello everyone thank you so much for
  • 00:00:03
    being a member of the insulin IQ
  • 00:00:05
    community and in particular thank you
  • 00:00:08
    for joining me for this week's metabolic
  • 00:00:11
    classroom that is a title that I've
  • 00:00:13
    always been particularly pleased with
  • 00:00:15
    this idea of me learning and
  • 00:00:20
    teaching all right um thanks again um so
  • 00:00:24
    today uh the focus of the classroom
  • 00:00:27
    today is to help you better understand
  • 00:00:30
    understand the origins of insulin
  • 00:00:32
    resistance um last time and and if you
  • 00:00:34
    haven't make sure you go back and watch
  • 00:00:36
    that episode we discussed what insulin
  • 00:00:37
    resistance is so we really defined it
  • 00:00:40
    particularly in the context of metabolic
  • 00:00:43
    Health uh and different ways of defining
  • 00:00:45
    metabolic Health including metabolic
  • 00:00:47
    syndrome and metabolic flexibility and
  • 00:00:49
    then actually revealing pulling back the
  • 00:00:52
    curtain and showing you that really at
  • 00:00:54
    the heart of both of those problems is
  • 00:00:56
    insulin resistance so we explained the
  • 00:00:57
    scope of the problem and why it matters
  • 00:00:59
    matters and why it matters in particular
  • 00:01:02
    that idea is something we'll focus on
  • 00:01:04
    more next week um so for now uh before
  • 00:01:08
    we get started I I kind of like making
  • 00:01:10
    it a habit of sharing with you guys uh a
  • 00:01:13
    little piece of some newly published
  • 00:01:15
    research there was a paper that was
  • 00:01:17
    published just recently in the journal
  • 00:01:19
    cell reports and what's interesting
  • 00:01:22
    about this is that it shows this to
  • 00:01:25
    invoke a concept of Economics this
  • 00:01:27
    diminishing returns when it comes to
  • 00:01:30
    satiety and our consumption of sweet
  • 00:01:33
    things so the study utilized rats I know
  • 00:01:36
    of no evidence in humans to support or
  • 00:01:40
    refute this so for now we'll assume it's
  • 00:01:42
    relevant in humans until we learn
  • 00:01:44
    otherwise but they fed the the rats a
  • 00:01:47
    diet that had high levels of sugar in
  • 00:01:49
    the water now of course that's how a lot
  • 00:01:52
    of people get sugar right any of these
  • 00:01:54
    sugary sodas or even juice has a lot of
  • 00:01:57
    sugar in it and so they had the animals
  • 00:02:00
    drinking uh the sugar water and then
  • 00:02:02
    they tested the animals response to a
  • 00:02:05
    load of glucose so then gave them a
  • 00:02:07
    bunch of glucose to eat and they found
  • 00:02:10
    that before they had started um this
  • 00:02:13
    high sugar diet the high sucrose uh they
  • 00:02:17
    had a very substantial response to the
  • 00:02:21
    uh glucose and it induced a sense of
  • 00:02:24
    satiety in other words they got the
  • 00:02:26
    glucose load and they felt really full
  • 00:02:28
    however with with this sugar diet with
  • 00:02:31
    the diet that was higher in sugar it
  • 00:02:34
    didn't work as well when they gave the
  • 00:02:35
    animals this load of of carbohydrate
  • 00:02:38
    they didn't have that same degree of
  • 00:02:40
    satiety that signal that sensitivity to
  • 00:02:43
    the carbohydrate load had been
  • 00:02:45
    diminished now they're not using the
  • 00:02:47
    word insulin resistance there and I'm
  • 00:02:49
    not going to either they didn't really
  • 00:02:50
    test it but I will just say they found
  • 00:02:53
    that there was a diminished ability to
  • 00:02:55
    sense the the the the calories or the
  • 00:02:59
    energy coming from from that
  • 00:03:00
    carbohydrate and the animals um would
  • 00:03:02
    have been inclined to just continue to
  • 00:03:04
    eat
  • 00:03:04
    more all right so that's a little bit of
  • 00:03:07
    the science corner of the metabolic
  • 00:03:09
    classroom now let's get into the actual
  • 00:03:11
    meat of the lecture if you will the
  • 00:03:13
    classroom session for today so where
  • 00:03:15
    does insulin resistance come from just
  • 00:03:17
    as a reminder it is insulin resistance
  • 00:03:20
    is the single most common health problem
  • 00:03:22
    worldwide so it is worth talking about
  • 00:03:25
    it is worth devoting a career to
  • 00:03:28
    understanding and and just appreciating
  • 00:03:31
    in in our life and at a global level all
  • 00:03:34
    right so I have
  • 00:03:36
    classified in my understanding in my
  • 00:03:38
    exploration and study of insulin
  • 00:03:40
    resistance really two categories when it
  • 00:03:43
    comes to understanding the causes of
  • 00:03:46
    insulin
  • 00:03:48
    resistance and I use the terms primary
  • 00:03:51
    and secondary now the primary insulin
  • 00:03:54
    resistance is a term that um I use very
  • 00:03:58
    specifically in fact both of these terms
  • 00:03:59
    are very specific with primary I
  • 00:04:02
    consider the cause to meet that to fall
  • 00:04:05
    into that category if it has if it is
  • 00:04:08
    based on Research that has been
  • 00:04:10
    confirmed in all three commonly used
  • 00:04:13
    biomedical research models now what do I
  • 00:04:16
    mean by that as a biomedical
  • 00:04:18
    scientist I will use and have in fact
  • 00:04:21
    published papers on all of this three
  • 00:04:24
    models or three ways of doing
  • 00:04:27
    experiments at the kind of simplest
  • 00:04:30
    um it is just growing cells in a little
  • 00:04:34
    petri dish in in a lab so we have a
  • 00:04:36
    little incubator that will grow cells
  • 00:04:38
    we'll put muscle cells on the petri dish
  • 00:04:39
    or liver cells or neurons or fat cells
  • 00:04:42
    and then we do experiments on those
  • 00:04:45
    cells next you can do experiments in a
  • 00:04:48
    whole organism like in the case of
  • 00:04:51
    laboratory rodents so this is mice or
  • 00:04:53
    rats where you can knock out genes or
  • 00:04:55
    overexpress genes and then you can get
  • 00:04:57
    all of the tissue to study the fat and
  • 00:04:59
    the heart and the Brain stuff that you
  • 00:05:02
    just couldn't get from humans of course
  • 00:05:04
    in a perfectly controlled
  • 00:05:06
    environment in the lab and then next is
  • 00:05:09
    experiments done in humans so these are
  • 00:05:11
    the three commonly used biomedical
  • 00:05:13
    models cells rodents
  • 00:05:15
    humans so the primary causes of insulin
  • 00:05:19
    resistance are those noxious stimuli
  • 00:05:22
    that have been shown to cause insulin
  • 00:05:24
    resistance in all three of those
  • 00:05:26
    models the secondary causes of insulin
  • 00:05:29
    resistance that I'll share with you are
  • 00:05:32
    those that maybe have been shown to
  • 00:05:34
    cause insulin resistance in two of the
  • 00:05:37
    three as we will highlight one
  • 00:05:39
    particular example of that or it is
  • 00:05:43
    actually there's evidence to support all
  • 00:05:45
    three but it does so it causes insulin
  • 00:05:48
    resistance by taking advantage of one of
  • 00:05:51
    the primary causes so it's not
  • 00:05:54
    independent of the primary cause I hope
  • 00:05:56
    that makes sense so that would call it
  • 00:05:58
    Con that would um count it as a
  • 00:06:01
    secondary cause again if it requires the
  • 00:06:03
    involvement of one of the primary causes
  • 00:06:05
    so it's still coming back to the primary
  • 00:06:07
    that if you eliminate the primary then
  • 00:06:09
    you've eliminated the insulin resistance
  • 00:06:12
    but again with the three primary causes
  • 00:06:14
    that I'll talk about in a moment each of
  • 00:06:16
    them is capable of causing insulin
  • 00:06:17
    resistance on their own all right now
  • 00:06:20
    let's go through the three primary
  • 00:06:22
    causes these are the big pillars that
  • 00:06:25
    really contributes to insulin resistance
  • 00:06:28
    in cells rodents and
  • 00:06:31
    humans first one is inflammation this is
  • 00:06:35
    one that I feel pretty strongly about
  • 00:06:38
    and I'm quite familiar with because it
  • 00:06:40
    was largely the focus of my
  • 00:06:42
    post-doctoral fellowship research many
  • 00:06:45
    many years ago and work that I had
  • 00:06:47
    continued and have since then and
  • 00:06:49
    continue to contribute to now so in this
  • 00:06:52
    case of the inflammation it's important
  • 00:06:56
    for you to appreciate that when I say
  • 00:06:58
    inflammation I don't necessarily I don't
  • 00:07:00
    mean an immune response and I don't mean
  • 00:07:04
    an angry red oozing scratch on your arm
  • 00:07:08
    that's gotten
  • 00:07:09
    infected when we when I say inflammation
  • 00:07:12
    I actually just want you to think that
  • 00:07:14
    of of a pathway within virtually every
  • 00:07:17
    cell of the body and that when this
  • 00:07:20
    pathway is activated it it is part of a
  • 00:07:23
    if it were if we were talking about an
  • 00:07:25
    immune cell it would be part of a normal
  • 00:07:26
    immune response but for example muscle
  • 00:07:30
    cells muscle cells have an inflammatory
  • 00:07:32
    pathway or multiple and those aren't
  • 00:07:34
    immune cells fat cells have an
  • 00:07:37
    inflammatory pathway and those aren't
  • 00:07:39
    immune cells those aren't white blood
  • 00:07:41
    cells that are part of an immune
  • 00:07:42
    response to defend the body against
  • 00:07:44
    infection but all of these cells have
  • 00:07:48
    these inflammatory Pathways and what's
  • 00:07:50
    interesting in the muscle for example
  • 00:07:52
    that you activate the inflammatory
  • 00:07:54
    pathway and the muscle isn't going to
  • 00:07:55
    start producing antibodies but it
  • 00:07:58
    actually then show shows this
  • 00:08:00
    intersection of the immune system or the
  • 00:08:03
    inflammatory system and the metabolic
  • 00:08:06
    system so anytime you activate
  • 00:08:10
    inflammatory Pathways within a cell you
  • 00:08:13
    cause that cell to have a diminished
  • 00:08:15
    response to insulin resistance so at
  • 00:08:18
    cell at a cell level you can just
  • 00:08:21
    incubate cells with an inflammatory
  • 00:08:23
    protein like for example C reactive
  • 00:08:25
    protein have you heard of that does that
  • 00:08:27
    one sound familiar CR P or C reactive
  • 00:08:30
    protein is a protein that has been
  • 00:08:32
    increasingly measured in clinical tests
  • 00:08:35
    because it's such a good marker of
  • 00:08:37
    inflammation and just overall cardi
  • 00:08:39
    metabolic health so if I have muscle
  • 00:08:42
    cells or fat cells or liver cells or
  • 00:08:44
    brain cells and I put C reactive protein
  • 00:08:47
    in that little culture bath with the
  • 00:08:49
    cells and then I test how the cells
  • 00:08:52
    respond to insulin it will be diminished
  • 00:08:55
    the insulin response will be turned down
  • 00:08:58
    same thing goes for animals
  • 00:08:59
    if you induce an inflammatory response
  • 00:09:01
    in animals they become demonstrably
  • 00:09:03
    insulin resistant and the same thing
  • 00:09:05
    happens in humans in fact it has been
  • 00:09:07
    fascinating for me to notice during this
  • 00:09:11
    period of time over the last few years
  • 00:09:12
    where everyone's much more mindful of
  • 00:09:15
    their immune Health that people and at
  • 00:09:18
    the same time people are wearing more
  • 00:09:19
    continuous glucose monitors it's been
  • 00:09:22
    interesting to see how people can almost
  • 00:09:24
    predict that they have a cold or a flu
  • 00:09:27
    coming on because they know notice that
  • 00:09:29
    their blood glucose levels start to
  • 00:09:31
    climb and get more variable a general
  • 00:09:34
    sign of insulin resistance and indeed
  • 00:09:37
    that is the case in humans if you induce
  • 00:09:39
    an immune response the body will become
  • 00:09:42
    more insulin resistant if you activate
  • 00:09:44
    those inflammatory Pathways in in fact
  • 00:09:46
    there's some fascinating Publications
  • 00:09:48
    that have touched on this before that
  • 00:09:50
    have looked at rheumatoid
  • 00:09:53
    arthritis like every autoimmune disease
  • 00:09:56
    rheumatoid arthritis has an EB and a
  • 00:09:59
    flow to it it will it will have periods
  • 00:10:01
    of time where it's really active and
  • 00:10:03
    aggressive and painful and other periods
  • 00:10:05
    of time where it starts to retreat and
  • 00:10:07
    settles down a little bit you can
  • 00:10:09
    actually track the insulin resistance
  • 00:10:11
    that goes with it that as the body is
  • 00:10:13
    activating an immune response inflam or
  • 00:10:16
    insulin resistance goes with it so to
  • 00:10:18
    sum all of that up inflammation is we
  • 00:10:21
    could call that the first primary cause
  • 00:10:23
    of insulin resistance now unrelated to
  • 00:10:26
    insulin
  • 00:10:27
    resistance is
  • 00:10:29
    stress now stress is a big term it's a
  • 00:10:33
    kind of blanket term that within pop
  • 00:10:35
    culture has taken on a lot of
  • 00:10:38
    Dimensions that uh that are sometimes
  • 00:10:41
    used inappropriately and other times uh
  • 00:10:44
    precisely so with stress this is when I
  • 00:10:48
    say stress I really mean the stress
  • 00:10:50
    hormones I can't help but think about
  • 00:10:52
    stress as a hormone response or an
  • 00:10:55
    endocrine in situation and specifically
  • 00:10:58
    there are two primary stress hormones in
  • 00:11:01
    the body cortisol and epinephrine also
  • 00:11:04
    known as adrenaline I'll call it
  • 00:11:06
    epinephrine that's the more technical
  • 00:11:08
    term that's used so cortisol and
  • 00:11:11
    epinephrine these hormones are actually
  • 00:11:14
    totally unre unrelated they are produced
  • 00:11:17
    in different cell types they are moved
  • 00:11:20
    through the they're produced very
  • 00:11:22
    differently they're very different types
  • 00:11:23
    of hormones they move through the blood
  • 00:11:25
    in different ways they actually act on
  • 00:11:28
    different cells throughout the body in
  • 00:11:30
    different ways and have different
  • 00:11:31
    effects throughout the body the one
  • 00:11:33
    thing they have in common is that they
  • 00:11:36
    both want to increase blood glucose and
  • 00:11:39
    so if you have these stress hormones
  • 00:11:41
    that are trying to push glucose up
  • 00:11:43
    there's another hormone that now has to
  • 00:11:45
    work even harder to bring the glucose
  • 00:11:47
    down and of course that's insulin and so
  • 00:11:50
    it's no surprise then that if these
  • 00:11:51
    stress hormones are continually pushing
  • 00:11:54
    up the glucose the body's becoming more
  • 00:11:57
    insulin resistant
  • 00:12:00
    now what are some of the causes of
  • 00:12:01
    stress uh this can be something as
  • 00:12:03
    benign as sleep deprivation and insomnia
  • 00:12:07
    one bad night of sleep will
  • 00:12:09
    significantly increase cortisol the next
  • 00:12:11
    day which causes insulin resistance that
  • 00:12:13
    next day now thankfully one good night
  • 00:12:15
    of sleep wipes that all out but sleep
  • 00:12:18
    deprivation is a simple and very common
  • 00:12:20
    cause of stress on the body which has a
  • 00:12:22
    metabolic consequence
  • 00:12:25
    similarly um for example if we drink
  • 00:12:27
    there are even more seemingly benign
  • 00:12:30
    things but tragic when you couple it
  • 00:12:32
    with poor sleep which is excessive
  • 00:12:34
    caffeine consumption that if someone's
  • 00:12:36
    taking in too much caffeine perhaps to
  • 00:12:38
    try to make up for their or to feel
  • 00:12:40
    better with the lack of sleep then that
  • 00:12:42
    increases the other stress hormone the
  • 00:12:45
    epinephrine and when epinephrine goes up
  • 00:12:47
    now it's trying to push up glucose which
  • 00:12:50
    then makes insulin work harder and so
  • 00:12:52
    it's easy to see how a person can fall
  • 00:12:54
    into this vicious cycle of sleeping
  • 00:12:57
    poorly taking caffeine to make up for it
  • 00:12:59
    which just continues to drive this
  • 00:13:02
    insulin resistance and again this is
  • 00:13:04
    something that happens in humans you
  • 00:13:06
    give humans a load of of cortisol or or
  • 00:13:09
    cortisol like molecule give them
  • 00:13:11
    epinephrine and then try to treat them
  • 00:13:13
    with insulin they'll need much more
  • 00:13:15
    insulin to bring their glucose down to
  • 00:13:17
    what would have been just a nor a modest
  • 00:13:19
    amount of insulin prior to the
  • 00:13:21
    introduction of the stress hormones same
  • 00:13:23
    with animals and same with cells having
  • 00:13:26
    done those experiments myself you treat
  • 00:13:28
    the cells with those molecules and they
  • 00:13:30
    become insulin
  • 00:13:32
    resistant now the third and final of the
  • 00:13:35
    primary causes I leave in the final pole
  • 00:13:39
    position if you will um in order to uh
  • 00:13:42
    just really emphasize it because it's
  • 00:13:44
    the one that I believe is over time
  • 00:13:47
    chronically the most relevant of all of
  • 00:13:49
    them and that is chronically elevated
  • 00:13:52
    insulin now let me just introduce a
  • 00:13:56
    brief tangent where some people
  • 00:13:59
    will say or they'll want to think that
  • 00:14:02
    I'm saying any insulin spike is bad and
  • 00:14:05
    should be avoided at all costs that's
  • 00:14:07
    not what I'm saying but I want someone
  • 00:14:09
    to appreciate the impact of multiple
  • 00:14:12
    insulin spikes that are stacked together
  • 00:14:15
    now to to elaborate on that if someone
  • 00:14:17
    eats a load of carbohydrate because
  • 00:14:19
    protein and fat are generally going to
  • 00:14:21
    have no uh elicit no insulin response if
  • 00:14:23
    someone eats pure carbohydrate insulin
  • 00:14:25
    will come up and the insulin will take
  • 00:14:27
    usually about 2 hours hours to come back
  • 00:14:29
    down in an insulin sensitive person
  • 00:14:31
    maybe you know between two and three
  • 00:14:33
    hours until the insulin comes back down
  • 00:14:34
    to
  • 00:14:35
    normal now remember the reason I'm
  • 00:14:37
    talking about this is because too much
  • 00:14:39
    insulin causes insulin resistance you
  • 00:14:42
    can do this in humans you can do this in
  • 00:14:44
    rodents and in cells and I've done it in
  • 00:14:47
    not in humans but others have give
  • 00:14:49
    humans an infusion of insulin and then
  • 00:14:52
    give them a few hours and the insulin
  • 00:14:53
    starts working worse and worse and worse
  • 00:14:56
    so it's increasingly resistant the body
  • 00:14:58
    is to to it so you have the person who
  • 00:15:01
    gets an insulin response to a
  • 00:15:02
    carbohydrate load unfortunately the
  • 00:15:05
    average person not only eats a very
  • 00:15:08
    starchy sugary breakfast but they do the
  • 00:15:10
    same thing with a midm morning snack and
  • 00:15:12
    so right around the time insulin's about
  • 00:15:14
    to come back down to its fasted levels
  • 00:15:17
    we have a culture of incessant snacking
  • 00:15:19
    and eating they spike it right back up
  • 00:15:21
    then they spike it right back up and
  • 00:15:23
    they do it again they do it for lunch
  • 00:15:24
    they do it for an afternoon snack they
  • 00:15:26
    do it for U dinner they do it for
  • 00:15:28
    evening snack so every waking moment is
  • 00:15:31
    spent in a state of elevated insulin
  • 00:15:34
    elevated insulin causes insulin
  • 00:15:37
    resistance the nice thing about all
  • 00:15:39
    three of those primary causes and this
  • 00:15:42
    is an upcoming topic before the end of
  • 00:15:45
    the month of about how to resolve
  • 00:15:46
    insulin resistance but I'm sort of
  • 00:15:48
    getting a little bit ahead of myself it
  • 00:15:50
    is that of all three of these primary
  • 00:15:52
    causes again inflammation stress and
  • 00:15:54
    elevated insulin it's the elevated
  • 00:15:56
    insulin that can be corrected so quickly
  • 00:15:59
    for example if you had someone who you
  • 00:16:01
    were a clinician or you're talking to a
  • 00:16:02
    loved one and you found out that they
  • 00:16:04
    had all of those things high stress High
  • 00:16:06
    inflammation High insulin you would say
  • 00:16:09
    hey your stress is high you need to
  • 00:16:11
    lower your stress hormones well you
  • 00:16:13
    don't know exactly how they're doing it
  • 00:16:15
    or maybe you know that they're sleeping
  • 00:16:16
    poorly and you say I know you're
  • 00:16:18
    Insomniac you have insomnia um you're
  • 00:16:20
    not sleeping well you need to sleep
  • 00:16:22
    better and they're going to say oh
  • 00:16:23
    thanks now I'm going to be stressed even
  • 00:16:25
    more than I was before about my lack of
  • 00:16:27
    sleep and so it's difficult to really
  • 00:16:29
    get a firm grasp on stress to turn it
  • 00:16:32
    down same same with inflammation that if
  • 00:16:35
    someone has an elevated C reactive
  • 00:16:37
    protein for
  • 00:16:38
    example uh knowing how to reduce that
  • 00:16:41
    can be a little tricky they might not
  • 00:16:44
    know it might not be something that
  • 00:16:45
    they're even doing in their lifestyle it
  • 00:16:47
    could be a result of their fat cells
  • 00:16:49
    which I'll get to in just a moment but
  • 00:16:51
    insulin we know what spikes insulin and
  • 00:16:54
    so it becomes a lever that we can grab
  • 00:16:56
    whereas the other two are slippery and
  • 00:16:58
    it's difficult ult to grab them this one
  • 00:17:00
    we can grab it and immediately start
  • 00:17:02
    pulling it down within a day improving
  • 00:17:04
    insulin resistance as a
  • 00:17:06
    result so those are the three primary
  • 00:17:09
    causes now let's go on where again just
  • 00:17:11
    to reiterate we have evidence multiple
  • 00:17:15
    Publications across all three commonly
  • 00:17:17
    used biomedical models that these are
  • 00:17:19
    all on their own capable of causing
  • 00:17:20
    insulin resistance now some of you may
  • 00:17:23
    be thinking that there are some
  • 00:17:25
    conspicuously absent causes here for
  • 00:17:27
    example why haven't I mentioned seed
  • 00:17:29
    oils well now I will let's transition
  • 00:17:32
    from the primary causes to the secondary
  • 00:17:34
    causes and I speak about seed oils with
  • 00:17:36
    enormous respect in all sincerity um the
  • 00:17:39
    the amount of papers I've now been
  • 00:17:41
    introduced to despite not being an
  • 00:17:42
    expert on seed oils is is remarkable and
  • 00:17:45
    these are definitely contributing to
  • 00:17:46
    diseases across the
  • 00:17:48
    board I just of course focus on my area
  • 00:17:51
    of expertise namely insulin resistance
  • 00:17:53
    there is evidence in cell cultures that
  • 00:17:56
    linolic acid the primary omega-6
  • 00:17:59
    polyunsaturated fatty acid that
  • 00:18:00
    constitutes linolic a that constitutes
  • 00:18:02
    soybean oil and the other refined seed
  • 00:18:04
    oils that in cells it can cause insulin
  • 00:18:09
    resistance kind of there's mixed
  • 00:18:12
    evidence there um next in animals if you
  • 00:18:15
    have an animal eat a high uh animals
  • 00:18:17
    will eat a high soybean oil diet as
  • 00:18:19
    opposed to say coconut oil the soybean
  • 00:18:22
    oil diet consumers will get um more
  • 00:18:26
    insulin resistant than the coconut oil
  • 00:18:28
    so there's something more uniquely
  • 00:18:30
    pathogenic but in humans I've just never
  • 00:18:33
    seen a study in humans where you have
  • 00:18:35
    the person eat soybean oil specifically
  • 00:18:37
    independent of any other types of fats
  • 00:18:40
    and then they become insulin resistant
  • 00:18:42
    that's why I haven't quite been able to
  • 00:18:44
    graduate seed oils into the primary
  • 00:18:46
    cause I I believe it's contributing in
  • 00:18:49
    fact I'll mention a reason that it might
  • 00:18:50
    be a bit indirect in in a moment with
  • 00:18:53
    regards to fat cells but um the direct
  • 00:18:56
    effect of just eating the linolic acid
  • 00:18:59
    do you get it um do you get the insulin
  • 00:19:03
    resistance uh no no I've not seen the
  • 00:19:06
    studies on that but again I'll revisit
  • 00:19:09
    that in just a
  • 00:19:10
    moment all right now the other secondary
  • 00:19:12
    cause of just two that I'm going to
  • 00:19:14
    mention and then I'll mention the last
  • 00:19:16
    one which is very unique is uric acid um
  • 00:19:21
    thanks in large part to my good friend
  • 00:19:23
    Rick Johnson at the University of
  • 00:19:25
    Colorado the world has really woken up
  • 00:19:27
    to the dangers of your acid and just as
  • 00:19:29
    a reminder as much as the world has
  • 00:19:32
    focused on meat as a sole cause of uric
  • 00:19:34
    acid because of some of the unique um
  • 00:19:38
    molecules within it fructose will
  • 00:19:40
    increase uric acid far more than any
  • 00:19:44
    amount of meat will and that's primarily
  • 00:19:46
    what Rick has focused on this fructose
  • 00:19:48
    um every time you metabolize a molecule
  • 00:19:50
    of fructose you're producing some uric
  • 00:19:53
    acid so it's a heavy heavy contributor
  • 00:19:55
    now interestingly uric acid has been
  • 00:19:58
    shown to cause insulin resistance in all
  • 00:20:00
    three biomedical models you treat cells
  • 00:20:02
    with uric acid they become insulin
  • 00:20:04
    resistant you increase the uric acid in
  • 00:20:06
    the animals they become insulin
  • 00:20:07
    resistant if you block uric acid
  • 00:20:09
    production they don't become insulin
  • 00:20:11
    resistant and the exact same thing is
  • 00:20:13
    seen with humans more uric acid as you
  • 00:20:16
    spike it up more insulin resistance you
  • 00:20:18
    block uric acid production insulin
  • 00:20:20
    resistance gets better it's pretty
  • 00:20:22
    robust evidence now why don't I put it
  • 00:20:24
    in the category of primary because if
  • 00:20:27
    you block the influx
  • 00:20:29
    effect of the uric acid there's no
  • 00:20:31
    insulin resistance or you wipe it out
  • 00:20:34
    and so this is the case that I alluded
  • 00:20:36
    to earlier where you have a trigger a
  • 00:20:38
    stimulus but it is acting through
  • 00:20:41
    another mediator and that if you take
  • 00:20:43
    away this mediator so it's dependent on
  • 00:20:46
    specifically inflammation and in the
  • 00:20:48
    absence of inflammation there's no
  • 00:20:50
    insulin resistance so it's dependent so
  • 00:20:53
    uric acid causes insulin resistance
  • 00:20:55
    dependent on its ability to increase
  • 00:20:58
    increase inflammation or activate these
  • 00:21:00
    immune path these inflammatory Pathways
  • 00:21:02
    that's why I put it in the secondary
  • 00:21:04
    realm because remember with the primary
  • 00:21:06
    all of those are capable of causing
  • 00:21:08
    insulin resistance on their own in the
  • 00:21:10
    absence of any other signal they're not
  • 00:21:12
    dependent on anything but
  • 00:21:15
    themselves now in all of these what all
  • 00:21:18
    of these have in common is that they
  • 00:21:21
    will manifest with class all the signs
  • 00:21:24
    of insulin resistance and remember there
  • 00:21:26
    are two real aspects it's the
  • 00:21:29
    analogy where you will have cells that
  • 00:21:31
    aren't responding well to insulin and in
  • 00:21:33
    the whole body insulin levels will be
  • 00:21:36
    elevated which makes the elevated
  • 00:21:38
    insulin cause of insulin resistance
  • 00:21:40
    particularly vicious because if elevated
  • 00:21:43
    insulin is a cause of insulin resistance
  • 00:21:46
    which is then causing more elevated
  • 00:21:48
    insulin which then contributes to
  • 00:21:50
    further insulin resistance you can see
  • 00:21:51
    how this becomes a positive feedback and
  • 00:21:53
    a vicious cycle so the last one that is
  • 00:21:56
    totally unique is
  • 00:21:58
    starvation now I need to Define that
  • 00:22:01
    term because too often people will think
  • 00:22:03
    of starvation as just fasting no there's
  • 00:22:07
    a big divide between fasting and
  • 00:22:10
    starvation in fact that divide is
  • 00:22:12
    something we can pinch and jiggle namely
  • 00:22:14
    our body fat that if you have body fat
  • 00:22:17
    to burn this is a topic for another time
  • 00:22:19
    so I'll be a little sparse on it then
  • 00:22:21
    you're fasting the moment you are
  • 00:22:24
    restricting calories and you've run out
  • 00:22:26
    of fat now you're burning your lean mass
  • 00:22:29
    you're burning muscle for energy in
  • 00:22:31
    particular and even bone and everything
  • 00:22:32
    else you'll start eating away at your
  • 00:22:34
    body to just continue to make enough
  • 00:22:37
    energy for the brain to survive and in
  • 00:22:40
    that state the body becomes very insulin
  • 00:22:43
    resistant which is primarily
  • 00:22:45
    interestingly a stress response but it's
  • 00:22:48
    unlike the earlier stress response that
  • 00:22:50
    I spoke about because in this instance
  • 00:22:52
    where the body is wasting away you are
  • 00:22:54
    insulin resistant but insulin levels are
  • 00:22:57
    low
  • 00:22:58
    the body can't afford to keep insulin
  • 00:23:00
    High because if insulin's High then the
  • 00:23:03
    body is attempting to store energy which
  • 00:23:06
    would deprive the brain because the
  • 00:23:07
    brain can't handle a state if energy is
  • 00:23:10
    just being stored stored stored because
  • 00:23:12
    it doesn't store energy it needs to be
  • 00:23:14
    pulling it from the blood we'll talk
  • 00:23:16
    we'll revisit this idea when we talk
  • 00:23:18
    about the metabolic origins of
  • 00:23:19
    Alzheimer's disease in in up in an
  • 00:23:21
    upcoming lesson but
  • 00:23:23
    nevertheless just to reiterate this
  • 00:23:26
    unique metabolic state starvation is
  • 00:23:29
    insulin resistance through stress
  • 00:23:31
    hormones but it's Unique because insulin
  • 00:23:34
    levels are low and any other instance of
  • 00:23:37
    insulin resistance that I'm aware of and
  • 00:23:38
    I think I'm aware of all of them insulin
  • 00:23:40
    will be elevated if the body has insulin
  • 00:23:45
    resistance including physiological
  • 00:23:48
    insulin resistance and we'll we can talk
  • 00:23:49
    about we'll talk about that at a future
  • 00:23:51
    time all right now let's move on um to a
  • 00:23:57
    next sort of segment as I wind up the
  • 00:23:59
    lecture classroom part of this before we
  • 00:24:00
    do some
  • 00:24:01
    Q&A all of these stimuli that I've
  • 00:24:04
    talked about are Direct effects if you
  • 00:24:06
    directly increase inflammation due to
  • 00:24:08
    illness for example or a food
  • 00:24:10
    sensitivity the body becomes insulin
  • 00:24:12
    resistant but if you remove that
  • 00:24:14
    stimulus they're insulin sensitive same
  • 00:24:16
    with stress same with elevated insulin
  • 00:24:18
    so these are Direct effects direct
  • 00:24:20
    noxious stimuli causing insulin
  • 00:24:22
    resistance but there's a more creeping
  • 00:24:25
    version of insulin resistance which now
  • 00:24:28
    brings us back to the fat cell there are
  • 00:24:31
    multiple theories of which tissue of the
  • 00:24:34
    body becomes insulin resistant first
  • 00:24:37
    some will say that it is the muscle that
  • 00:24:39
    becomes insulin resistant first some
  • 00:24:41
    will say that it's the liver others will
  • 00:24:43
    say that it's the fat cells um anyone
  • 00:24:46
    who says it's other than the fat cells
  • 00:24:47
    is totally wrong now I expect it say the
  • 00:24:50
    same thing about me but I'm right fat
  • 00:24:52
    cells are the beginning that is the
  • 00:24:54
    first Domino to fall you know probably
  • 00:24:57
    by now of my affection for alliteration
  • 00:24:59
    fat Falls first when it comes to insulin
  • 00:25:03
    resistance and the now so what makes the
  • 00:25:05
    fat cell get big this is actually a
  • 00:25:08
    topic that I just spoke at um at a
  • 00:25:10
    recent meeting a low carb meeting in the
  • 00:25:12
    upcoming metabolic Health Summit uh at
  • 00:25:14
    the time I'm recording this and I will
  • 00:25:16
    post this lecture um at a future point
  • 00:25:20
    on the insulin IQ site but it's
  • 00:25:22
    basically the name of that is shrinking
  • 00:25:24
    fat cells energy versus insulin and so
  • 00:25:27
    when a fat cell is uh when a fat cell
  • 00:25:29
    starts to grow that's that's a process
  • 00:25:32
    called hypertrophy and as the fat cell
  • 00:25:34
    continues to grow it it starts to
  • 00:25:37
    experience two problems first it can't
  • 00:25:39
    grow anymore it's actually reaching the
  • 00:25:42
    limit that the cell membrane can hold
  • 00:25:44
    together it's like a water balloon
  • 00:25:46
    that's getting so full that it's about
  • 00:25:48
    to burst it's going to pop and then
  • 00:25:51
    everyone gets messy and we get water all
  • 00:25:52
    over the house now one solution let's
  • 00:25:55
    just stick with the the analogy
  • 00:25:57
    comparing the fat cell to the to a water
  • 00:25:59
    balloon if we can't disconnect the
  • 00:26:02
    balloon to the tap that is filling the
  • 00:26:04
    balloon what if we could just poke a
  • 00:26:07
    small little hole in the balloon without
  • 00:26:09
    popping the whole balloon now it's
  • 00:26:11
    starting to leak out some of the water
  • 00:26:14
    to match the fat that's coming in that's
  • 00:26:16
    really analogous to what's happening
  • 00:26:18
    with the fat cell is it gets too big
  • 00:26:20
    insulin is continually telling it to
  • 00:26:22
    grow mostly by inhibiting its ability to
  • 00:26:25
    release the fat but but also by force
  • 00:26:28
    feeding it and so the fat cell basically
  • 00:26:32
    says insulin you're not letting me break
  • 00:26:34
    down this fat I'm not listening to you
  • 00:26:36
    anymore and so I'm going to become
  • 00:26:37
    insulin resistant and so it becomes
  • 00:26:40
    insulin resistant to stop growing this
  • 00:26:43
    this is why people on average can't
  • 00:26:45
    limitlessly get fat there is this point
  • 00:26:48
    Beyond which they can't get any fatter
  • 00:26:50
    now there are some exceptions where some
  • 00:26:51
    people genetically have the ability to
  • 00:26:53
    make new fat cells they can multiply
  • 00:26:55
    their fat cells those are people who
  • 00:26:57
    continue who can continue to get fat but
  • 00:26:59
    that's uncommon so the big fat fat cell
  • 00:27:03
    the hypertrophic fat cell becomes
  • 00:27:04
    insulin resistant to stop future
  • 00:27:07
    growth second as it gets so big it
  • 00:27:10
    starts to get pushed further and further
  • 00:27:12
    away from capillaries which is the
  • 00:27:14
    essential blood vessel where a cell gets
  • 00:27:17
    all of its oxygen and all of its
  • 00:27:19
    nutrients and then dumps all of its
  • 00:27:21
    waste products into the blood to be
  • 00:27:22
    eliminated from the body through the
  • 00:27:24
    kidneys or the liver or the breath in
  • 00:27:26
    some instances like CO2 so it's the
  • 00:27:29
    capillary and so the fat cell that's
  • 00:27:31
    getting so big is getting pushed too far
  • 00:27:34
    from the capillary and that becomes
  • 00:27:36
    what's called hypoxic in other words
  • 00:27:38
    it's running out of oxygen in one
  • 00:27:40
    response to that the fat cell is saying
  • 00:27:43
    hey I'm suffocating here it will start
  • 00:27:45
    releasing pro-inflammatory
  • 00:27:48
    proteins what are called cyto now
  • 00:27:51
    through the body this begins to turn on
  • 00:27:54
    all of those inflammatory Pathways that
  • 00:27:55
    will then cause insulin resistance
  • 00:27:58
    but at the level of the fat cell one
  • 00:28:00
    effect of one of these pro-inflammatory
  • 00:28:03
    proteins will be to tell the capillaries
  • 00:28:05
    to start making new capillaries so it
  • 00:28:08
    will increase the vascular the
  • 00:28:10
    vascularization of the fat cell helping
  • 00:28:13
    it start to breathe better it can get
  • 00:28:14
    oxygen again but again a consequence is
  • 00:28:18
    that it's spilling the inflammatory
  • 00:28:19
    proteins throughout the body now what is
  • 00:28:22
    it that makes the fat cell get
  • 00:28:24
    big there are two essential elements to
  • 00:28:27
    this you cannot have one without the
  • 00:28:30
    other in the whole body it is impossible
  • 00:28:33
    and again you'll have to watch the talk
  • 00:28:34
    in the future um in order to in order to
  • 00:28:37
    understand it so you must have an
  • 00:28:40
    elevated insulin level to signal to the
  • 00:28:44
    fat cell that it needs to grow that's
  • 00:28:46
    the stimulus telling the fat cell grow
  • 00:28:49
    and then you must have sufficient energy
  • 00:28:52
    or enough calories available to fuel
  • 00:28:55
    that growth I hope that you can
  • 00:28:57
    appreciate the difference a fat cell
  • 00:29:00
    that is swimming in a sea of calories in
  • 00:29:02
    the absence of insulin will not store
  • 00:29:04
    any of those calories it is totally
  • 00:29:08
    completely physically impossible for a
  • 00:29:11
    fat cell to not only grow but even stay
  • 00:29:14
    big if insulin is low it cannot hold on
  • 00:29:17
    to its
  • 00:29:18
    energy so you need an insulin stimulus
  • 00:29:21
    and you need sufficient energy to fuel
  • 00:29:24
    that stimulus to grow now you have a
  • 00:29:26
    hypertrophy or fat fat cell and then you
  • 00:29:29
    have this kind of more in creeping
  • 00:29:32
    Insidious version of insulin resistance
  • 00:29:34
    that you know that's sort of settling in
  • 00:29:36
    over time as the person's gaining this
  • 00:29:38
    weight in a unique Way by making the fat
  • 00:29:40
    cells get big so that is the sort of
  • 00:29:43
    final sentiment here now one other point
  • 00:29:47
    where I mentioned I would bring back the
  • 00:29:48
    soybean oil or the linolic
  • 00:29:51
    acid linolic acid contributes to insulin
  • 00:29:54
    resistance in part through this fat cell
  • 00:29:57
    effect because linolic acid will inhibit
  • 00:30:01
    the fat cell's ability to multiply and
  • 00:30:04
    so as a fat as the fat tissue elevated
  • 00:30:06
    insulin sufficient energy is being told
  • 00:30:09
    and fueled to grow if there's linolic
  • 00:30:12
    acid coming in it accumulates in the fat
  • 00:30:14
    cell converts becomes this other
  • 00:30:17
    molecule called 4 h& for hydroxy nonanol
  • 00:30:20
    4 h& and 4 h& will basically dictate to
  • 00:30:24
    the fat tissue and say fat tissue you've
  • 00:30:27
    been told to grow I'm going to tell you
  • 00:30:30
    how to grow and that's specifically
  • 00:30:32
    through hypertrophy now insulin does
  • 00:30:33
    that too um insulin will also
  • 00:30:36
    selectively promote hypertrophy but
  • 00:30:38
    linolic acid contributes to that so this
  • 00:30:40
    is another unique mechanism whereby it
  • 00:30:43
    contributes to insulin resistance by
  • 00:30:46
    selectively influencing the way the body
  • 00:30:49
    gains
  • 00:30:50
    fat all right that is
  • 00:30:54
    it let's now thanks for listening
  • 00:30:57
    hopefully you took some notes and again
  • 00:30:59
    that talk that I referred to shrinking
  • 00:31:01
    the fat cells insulin versus energy um
  • 00:31:03
    that's one that will'll get posted here
  • 00:31:05
    soon and you will really enjoy it you'll
  • 00:31:08
    like it it's really me diving into these
  • 00:31:10
    last points that I was just talking
  • 00:31:12
    about namely taking the big fat cell and
  • 00:31:14
    shrinking it all right let's move over
  • 00:31:17
    to the
  • 00:31:18
    Q&A and thank you for those who have
  • 00:31:20
    joined live and those who watch later I
  • 00:31:23
    hope you come to another session with
  • 00:31:25
    some of your questions um but those who
  • 00:31:27
    are here live um Rich uh thanks for
  • 00:31:31
    tuning in Ben so glad you're talking
  • 00:31:33
    about insulin resistance an old but new
  • 00:31:35
    Theory out in the plant-based world is
  • 00:31:37
    that fat actually is a cause of insulin
  • 00:31:39
    resistance they're trying to show that
  • 00:31:40
    plant-based diets are more effective
  • 00:31:43
    yeah yeah so a common um refrain in the
  • 00:31:47
    plant-based Community is that fat causes
  • 00:31:50
    in well specifically saturated fat in
  • 00:31:53
    fact they will use these really
  • 00:31:54
    scientific terms like gum up or clogs up
  • 00:31:58
    the insulin
  • 00:32:00
    receptor which is just silly um but
  • 00:32:03
    there's a there's an oun there's a speck
  • 00:32:05
    of Truth in what they've found and and
  • 00:32:08
    in fact I've contributed to this so
  • 00:32:10
    whether they know it or not in some
  • 00:32:12
    instances they're actually invoking my
  • 00:32:14
    own work um from my earlier research
  • 00:32:16
    during my post-doctoral time so if you
  • 00:32:19
    take cells or you infuse treat them with
  • 00:32:23
    saturated fats or you infuse them with
  • 00:32:27
    or you infuse an animal rather with
  • 00:32:29
    saturated fat they will become insulin
  • 00:32:31
    resistant that's not the case if you say
  • 00:32:35
    um treat the cells or Infuse the animals
  • 00:32:37
    with oleic acid the monounsaturated fat
  • 00:32:40
    and then it's kind of varying responses
  • 00:32:43
    in the case of the omega-6
  • 00:32:45
    polyunsaturated fat linolic acid from
  • 00:32:48
    soy oil for example or any refined seed
  • 00:32:51
    oils um so in this case the there is
  • 00:32:53
    some evidence um but remember INF using
  • 00:32:57
    saturated fat you know me having Rich
  • 00:32:59
    you come into my lab and we stick an IV
  • 00:33:01
    in you and Infuse some palmitate that is
  • 00:33:03
    not the same as you eating palmitate and
  • 00:33:06
    so now we go to the human studies like
  • 00:33:08
    some of the work from Jeff volik at the
  • 00:33:10
    University at the Ohio State University
  • 00:33:12
    and he has found that in his work you
  • 00:33:15
    can have a a low carb group that is
  • 00:33:17
    eating multiples more saturated fat than
  • 00:33:21
    a low fat group and they not only have a
  • 00:33:24
    greater reduction in inflamm
  • 00:33:27
    but they have this significant
  • 00:33:29
    Improvement in insulin resistance so at
  • 00:33:31
    the level of what goes into your mouth
  • 00:33:34
    which is where we should care um where
  • 00:33:37
    this
  • 00:33:37
    happens um especially if carbohydrates
  • 00:33:40
    are restricted the saturated fat is not
  • 00:33:42
    causing insulin resistance now to
  • 00:33:45
    complicate it a little bit if you have
  • 00:33:48
    someone eating a high carb diet and then
  • 00:33:51
    you add to that high carb diet saturated
  • 00:33:53
    fat or monounsaturated fat the SAT
  • 00:33:56
    saturated fat does have cause greater
  • 00:33:59
    insulin resistance um but of course
  • 00:34:02
    that's in the context of a high carb
  • 00:34:04
    diet which does not apply of course to a
  • 00:34:06
    ketogenic diet that's the opposite of a
  • 00:34:08
    ketogenic diet so these plant-based
  • 00:34:11
    plant-based Advocates that are vilifying
  • 00:34:12
    saturated fat they're just selectively
  • 00:34:15
    taking some lines of evidence and
  • 00:34:16
    applying it to fit their ideas now what
  • 00:34:19
    happens when you take a plant-based diet
  • 00:34:22
    and compare it to a ketogenic diet um
  • 00:34:26
    which generally is to be on the opposite
  • 00:34:28
    end of saturated fat
  • 00:34:29
    consumption there is not a single study
  • 00:34:32
    to show that a plant-based diet
  • 00:34:33
    outperforms um the ketogenic diet now
  • 00:34:36
    that is not the same as like the
  • 00:34:37
    Stanford twin study that was just
  • 00:34:38
    published that was not ketogenic they
  • 00:34:40
    had a plant-based group and then they
  • 00:34:42
    had an omnivore Group which was eating
  • 00:34:44
    lasagna and hamburgers you know all
  • 00:34:47
    kinds of stuff not not ketogenic
  • 00:34:49
    whatsoever so it was heavily heavily
  • 00:34:51
    skewed to find the result that they
  • 00:34:53
    wanted to that they wanted to get and of
  • 00:34:56
    course immediately Netflix made a
  • 00:34:58
    documentary about it I can highlight
  • 00:35:00
    that study in the future metabolic
  • 00:35:02
    classroom just specific to that report
  • 00:35:05
    um which which I will do from time to
  • 00:35:07
    time we'll just do uh metabolic
  • 00:35:09
    classroom that's based on just analyzing
  • 00:35:10
    a popularly published manuscript and
  • 00:35:12
    that would fit the bill so anyway um the
  • 00:35:15
    plant-based diets only improve insulin
  • 00:35:18
    resistance because they restrict energy
  • 00:35:21
    um because you just start to have a
  • 00:35:23
    calorie restriction as you only eat
  • 00:35:25
    plants um and so that's how it works if
  • 00:35:28
    you try to put them on a higher calorie
  • 00:35:30
    version of it they won't have any
  • 00:35:31
    Improvement um in fact some of the
  • 00:35:33
    studies that have compared plant-based
  • 00:35:35
    diets to just normal standard American
  • 00:35:37
    diet show modest improvements or no
  • 00:35:39
    improvements whatsoever if you're not
  • 00:35:41
    make forcing them to go into a low
  • 00:35:43
    calorie state but remember the fat cell
  • 00:35:46
    if it's really really big or one thing I
  • 00:35:48
    didn't talk about but I do in this talk
  • 00:35:50
    that I will direct everyone to once it
  • 00:35:52
    gets once I share it on insulin IQ if
  • 00:35:55
    you start restricting energy in the diet
  • 00:35:57
    as you do so every single study that's
  • 00:35:59
    ever looked at a plant-based diet has
  • 00:36:01
    taken people from their standard
  • 00:36:04
    American diet that they were eating
  • 00:36:05
    which is high carb high calorie and then
  • 00:36:08
    lowered the calories and put them on a
  • 00:36:10
    plant-based diet even lowering the total
  • 00:36:12
    amount of carbs they're eating which
  • 00:36:15
    sounds crazy and so any of these studies
  • 00:36:18
    that look at lowfat plant-based diets if
  • 00:36:19
    you actually look at the insulin it goes
  • 00:36:22
    down because you're taking them from
  • 00:36:24
    this high calorie standard American into
  • 00:36:27
    the plant-base you do anything to those
  • 00:36:29
    people and they're going to get better
  • 00:36:31
    including a plant-based diet the problem
  • 00:36:34
    the more your plant-based diet the more
  • 00:36:36
    nutrient deficient you become so this
  • 00:36:38
    this Stanford twin study for example
  • 00:36:41
    even after just a couple weeks the
  • 00:36:42
    people were getting low and nearly
  • 00:36:44
    deficient in vitamin
  • 00:36:46
    B12 uh so uh that's that's a problem of
  • 00:36:49
    course um where B12 is essential
  • 00:36:51
    throughout the body all right Rich
  • 00:36:53
    hopefully that helps um Carly thanks for
  • 00:36:56
    joining Lindsay this may be a dumb
  • 00:36:58
    question but will you see
  • 00:36:59
    hyperinsulinemia when the underlying CL
  • 00:37:01
    causes inflammation or stress yep yep so
  • 00:37:03
    I I mentioned that uh with those primary
  • 00:37:06
    causes well of course with insulin
  • 00:37:08
    that's one that one's obvious but yes if
  • 00:37:10
    you induce insulin resistance through
  • 00:37:12
    stress response or an inflammatory
  • 00:37:14
    response as the body becomes insulin
  • 00:37:16
    resistant elevated insulin is soon to
  • 00:37:18
    follow in that case in that instance
  • 00:37:20
    it's a consequence of the insulin
  • 00:37:22
    resistance but it is an Inseparable
  • 00:37:25
    consequence there's no splitting that
  • 00:37:29
    apart Carol thanks for tuning in yes to
  • 00:37:32
    ask more about Rich's comment from the
  • 00:37:34
    mastering diabetes perspective they
  • 00:37:35
    promote a no Animal product and no fat
  • 00:37:37
    diet the claim is that this is the
  • 00:37:38
    method to lower IR yeah again Carol you
  • 00:37:41
    note this further down anytime you start
  • 00:37:44
    depriving the body of energy insulin
  • 00:37:46
    comes down and thus it's no surprise
  • 00:37:49
    that the body will become insulin
  • 00:37:50
    resistant my counter to that is how long
  • 00:37:53
    can you continue to restrict the energy
  • 00:37:56
    and how long can you afford to deprive
  • 00:37:58
    yourself of essential nutrition like ham
  • 00:38:00
    iron or vitamin B12 for example or
  • 00:38:03
    omega-3 fatty acids the essential ones
  • 00:38:06
    that you cannot get from plants so the
  • 00:38:08
    more I have very strong feelings about
  • 00:38:10
    the plant-based diet because I just
  • 00:38:12
    generally view it as an anti-human view
  • 00:38:15
    that the more you try to force humans to
  • 00:38:17
    only eat plants the more you are
  • 00:38:20
    weakening them and even killing them for
  • 00:38:23
    example and ruining the species if you
  • 00:38:25
    put men on a lowfat diet guess what
  • 00:38:28
    happens to their testosterone guess what
  • 00:38:30
    happens to their sperm production and
  • 00:38:33
    motility down and the more a woman is
  • 00:38:36
    deprived of vitamin B12 the more
  • 00:38:38
    incapable she is of carrying a fetus
  • 00:38:40
    carrying a baby fullterm so you
  • 00:38:42
    literally start to kill the human
  • 00:38:44
    species and that to me is pretty telling
  • 00:38:48
    all right Jerry alosis touted as not
  • 00:38:50
    causing a glucose response but does it
  • 00:38:52
    raise insulin wonderful question it does
  • 00:38:54
    not in fact we are sick 6 weeks into an
  • 00:38:57
    animal study on alilo and we're just
  • 00:38:59
    about to start a human study so anyone
  • 00:39:01
    living in Utah Valley if you're wanting
  • 00:39:04
    to participate I'll be making an
  • 00:39:05
    announcement soon about that but no
  • 00:39:08
    there is no insulin response to alose at
  • 00:39:10
    all one of the other reasons I'm a
  • 00:39:12
    little enthusiastic about allulose is
  • 00:39:16
    that it's more than just a replacement
  • 00:39:18
    for sugar like every other sweetener is
  • 00:39:20
    whether it's Stevia or rral and those
  • 00:39:21
    are fine um monk fruit extract they're
  • 00:39:25
    all fine in my book uh but they just act
  • 00:39:29
    by replacing sugar the thing about alos
  • 00:39:31
    is it also replaces table sugar as a
  • 00:39:34
    rare sugar itself but it increases
  • 00:39:37
    glp1 um and glp1 helps not only keep
  • 00:39:41
    keep glucagon in check which is why it's
  • 00:39:43
    likely so helpful with people with type
  • 00:39:44
    1 diabetes but it also delays gastric
  • 00:39:47
    emptying making you feel Fuller for
  • 00:39:50
    longer which is of course very
  • 00:39:53
    beneficial all right jack um Shar 's a
  • 00:39:56
    question from a follower um Ben from one
  • 00:39:59
    of our followers I heard Dr Vickman
  • 00:40:01
    talking about diet soda he sounded like
  • 00:40:02
    he was saying people overeat from
  • 00:40:04
    drinking diet soda because it makes one
  • 00:40:07
    Hungry Jack let me see if I can expand
  • 00:40:09
    that okay I think that's the end of the
  • 00:40:11
    question oh I believe some weight
  • 00:40:12
    gainers are not overeating due to the
  • 00:40:14
    soda it's the insulin effect alone so no
  • 00:40:17
    there is uh diet soda alone the
  • 00:40:20
    aspartame in the diet soda will not
  • 00:40:22
    cause an insulin Spike I have I've
  • 00:40:24
    really looked into that to because I
  • 00:40:27
    know it's such a commonly enjoyed
  • 00:40:30
    sweetener because of its presence in in
  • 00:40:32
    diet sodas there is no insulin
  • 00:40:35
    effect however there is something that's
  • 00:40:38
    referred to as the calic effect where
  • 00:40:41
    you taste something sweet and then the
  • 00:40:44
    body is expecting the calories from that
  • 00:40:48
    sweetness um and that's understandable
  • 00:40:51
    especially from carbohydrate it wants a
  • 00:40:53
    glucose load because in nature there is
  • 00:40:55
    nothing that is sweet unless it is a
  • 00:40:58
    carbohydrate there's no sweet fats
  • 00:41:00
    there's no sweet proteins it's only
  • 00:41:02
    carbohydrate and so the body's expecting
  • 00:41:04
    a glucose load because of that and so
  • 00:41:08
    but not everyone appears to feel this so
  • 00:41:11
    my general sentiment on diet soda is if
  • 00:41:14
    you are in your most honest moment
  • 00:41:18
    capable of enjoying a diet soda and you
  • 00:41:23
    don't start snacking you don't have this
  • 00:41:25
    kind of per iive effect on the back end
  • 00:41:27
    of it then it's fine what do I mean by
  • 00:41:29
    that if you're sipping on a diet soda
  • 00:41:34
    and then you feel I'm gonna get the
  • 00:41:35
    fries too and I'm gonna get this big
  • 00:41:37
    hamburger and I'm gonna eat the bun you
  • 00:41:38
    know whatever um because I have the diet
  • 00:41:41
    soda or you you feel like you need to
  • 00:41:44
    eat just because it makes you hungry
  • 00:41:46
    then it's a problem and I think you
  • 00:41:48
    should wean yourself off of diet soda if
  • 00:41:50
    you're able to enjoy a diet soda and it
  • 00:41:52
    stops with the diet soda and mind you
  • 00:41:54
    that's not something that necessarily
  • 00:41:55
    happens hour an hour after it could be
  • 00:41:58
    that you have the diet soda at noon and
  • 00:42:00
    maybe you're getting really snacky and
  • 00:42:02
    hungry in the evening um then you need
  • 00:42:05
    to monitor your consumption more but
  • 00:42:07
    again just to confirm there or reiterate
  • 00:42:10
    there is no direct effect to the
  • 00:42:12
    aspartame increasing insulin which is
  • 00:42:14
    inre increasing fat gain it's a it's a
  • 00:42:17
    consequential effect BEC uh in some
  • 00:42:20
    people if they start to eat more or
  • 00:42:22
    indulge more
  • 00:42:24
    after all right Right Carly on a hangout
  • 00:42:28
    yesterday we talked about alos and the
  • 00:42:29
    source matters since some sources come
  • 00:42:31
    from corn anything you can add to this
  • 00:42:33
    conversation yeah yeah as far as I know
  • 00:42:36
    there's no difference um whether it
  • 00:42:38
    comes from figs or corn it is allulose
  • 00:42:42
    and not in any other way
  • 00:42:44
    adulterated um I'm pretty confident on
  • 00:42:47
    that as I've become more familiar with
  • 00:42:49
    alos I'm unaware of any evidence fact
  • 00:42:51
    this I can state conclusively I'm
  • 00:42:53
    unaware of any evidence but you may say
  • 00:42:54
    well that's just because you're ignorant
  • 00:42:55
    I'm pretty pretty sure there's nothing
  • 00:42:57
    out there um that suggests the source is
  • 00:42:59
    going to
  • 00:43:01
    matter um Joseph one of my clients
  • 00:43:03
    mentioned how every time their blood
  • 00:43:05
    sugar goes up she gets knee pains could
  • 00:43:07
    this be the inflammation you talked
  • 00:43:09
    about
  • 00:43:10
    um it could be Joseph it could be it
  • 00:43:14
    could be inflammation but it's difficult
  • 00:43:16
    I always try to be careful in the order
  • 00:43:18
    of events when I talk about these things
  • 00:43:21
    and the way I spoke about inflammation
  • 00:43:23
    in the context of metabolic Health was
  • 00:43:25
    from the position of inflammation then
  • 00:43:29
    creating the metabolic problem not the
  • 00:43:32
    metabolic problem creating the
  • 00:43:34
    inflammation if that makes sense so in
  • 00:43:36
    this case of the knee pain I actually
  • 00:43:38
    would be more
  • 00:43:40
    inclined to think of the a
  • 00:43:44
    possible this I might be really kind of
  • 00:43:47
    getting a little kooky here but it was
  • 00:43:49
    the first thought that came to mind so
  • 00:43:50
    I'll go with it it might be a systemic
  • 00:43:53
    vasil constriction and a relative blood
  • 00:43:55
    flow restri restriction so one of the
  • 00:43:57
    interesting things about the knee and
  • 00:43:59
    these joints is that um they they
  • 00:44:02
    generally have very little blood flow
  • 00:44:04
    and so if you compromise the blood flow
  • 00:44:06
    even a little more they go from Little
  • 00:44:08
    to almost nothing and if you eat a big
  • 00:44:12
    spike you get a big spike of glucose
  • 00:44:14
    that that activates your sympathetic
  • 00:44:15
    nervous system um this is one of the
  • 00:44:18
    reasons why many people sleep so poorly
  • 00:44:20
    it's because they indulge on glucose
  • 00:44:23
    spiking starches and sugars in the
  • 00:44:25
    evening and they go to bed hyperglycemic
  • 00:44:27
    wondering why they're anxious well
  • 00:44:28
    you're not anxious you've just activated
  • 00:44:30
    your sympathetic nervous system so
  • 00:44:31
    you're hot you're sweaty your heart is
  • 00:44:33
    beating hard but another effect related
  • 00:44:36
    to the heart beating is that you get
  • 00:44:38
    what's referred to as a systemic Vaso
  • 00:44:40
    constriction so in the sympathetic
  • 00:44:42
    nervous system is turned on it starts to
  • 00:44:44
    restrict the blood vessels um and that
  • 00:44:47
    might be what is contributing if I had
  • 00:44:50
    to guess that's actually where I think
  • 00:44:51
    it would fall Joseph I think it would be
  • 00:44:53
    more on this acute response to the hyper
  • 00:44:56
    glycemia and the restricted blood
  • 00:44:58
    flow Rich Ben the plant-based diets also
  • 00:45:01
    tout that it lowers cholesterol is there
  • 00:45:02
    a benefit in lowering cholestrol no I do
  • 00:45:05
    not believe there is in fact many many
  • 00:45:07
    lines of um admittedly correlational
  • 00:45:11
    evidence which is the only kind there is
  • 00:45:12
    when it comes to longevity show that the
  • 00:45:14
    longest lived people typically have high
  • 00:45:17
    cholesterol levels now a lot of these
  • 00:45:19
    plant-based people will of course invoke
  • 00:45:20
    the idea of blue zones and we'll address
  • 00:45:22
    that in a future classroom but I firmly
  • 00:45:25
    believe the whole Blue Zone phenomenon
  • 00:45:27
    is based on fraudulent uh it's all a
  • 00:45:30
    fraud actually there's some pretty
  • 00:45:32
    convincing evidence the only the only
  • 00:45:34
    evidence that exists that in every one
  • 00:45:36
    of these so-called Blue zone areas
  • 00:45:38
    whether it's Okinawa or whether it's
  • 00:45:40
    Sardinia they actually paradoxically on
  • 00:45:43
    average have among the lowest life
  • 00:45:45
    expectancies and among the lowest
  • 00:45:47
    literacy rates within their respective
  • 00:45:49
    countries and what this person has
  • 00:45:51
    concluded this was an Australian
  • 00:45:53
    scientist it is that um this these are
  • 00:45:56
    people who are fraudulent in reporting
  • 00:45:59
    their birth dates and they can because
  • 00:46:01
    of poor recordkeeping the areas are very
  • 00:46:03
    generally a little more impoverished but
  • 00:46:05
    they're doing this to um get um
  • 00:46:08
    retirement benefits earlier and so I I
  • 00:46:12
    actually think that's all pretty
  • 00:46:13
    validated because the evidence is so
  • 00:46:14
    hard to reconcile these are areas with
  • 00:46:16
    poor literacy overall lower mortality
  • 00:46:20
    rates in the rest of the country so on
  • 00:46:21
    average people are dying more and then
  • 00:46:23
    we're expected to believe that there are
  • 00:46:24
    these paradoxical anomalies in their
  • 00:46:26
    midst where they're suddenly living to
  • 00:46:28
    well over a 100 I think it's all based
  • 00:46:30
    on fraud indeed they're poor which is
  • 00:46:33
    why they aren't eating a lot of meat um
  • 00:46:36
    and then in fact in some of the longest
  • 00:46:37
    lived countries on on the planet like
  • 00:46:39
    Hong Kong they have the highest per
  • 00:46:42
    capita consumption of meat so that
  • 00:46:44
    doesn't quite work with that idea um and
  • 00:46:48
    again high cholesterol might be part of
  • 00:46:49
    the benefit um interestingly a paper was
  • 00:46:53
    just published and I'm going to do a
  • 00:46:54
    little Instagram post on this in a bit
  • 00:46:57
    where just today where they found that
  • 00:46:59
    um people who adopt a ketogenic diet
  • 00:47:01
    there's this big concern you eat all
  • 00:47:03
    that saturated fat and your cholesterol
  • 00:47:04
    is going to go through the roof what
  • 00:47:06
    this group found was that this is a
  • 00:47:07
    phenomenon that only happens in people
  • 00:47:10
    who are already fairly lean this is part
  • 00:47:13
    of the lean mass hyperr phenomenon that
  • 00:47:16
    Dave Feldman has really posited and now
  • 00:47:18
    continues to grow in attention and
  • 00:47:20
    evidence that if someone is
  • 00:47:23
    overweight they don't appear to have
  • 00:47:25
    have this LDL increased effect in
  • 00:47:28
    response to the ketogenic
  • 00:47:30
    diet all right Mindy um do you know
  • 00:47:34
    anything about a sugar called treos that
  • 00:47:36
    you can share with us that's a great
  • 00:47:39
    question um I am familiar with
  • 00:47:43
    treos um that it's a it's a very
  • 00:47:47
    uncommon sugar and I just am going to
  • 00:47:49
    kind of look up how what it gets
  • 00:47:51
    digested into and I think it's just too
  • 00:47:54
    I think it's a
  • 00:47:56
    it's a basically a starch or a glucose
  • 00:48:00
    molecule bound together with a What's
  • 00:48:02
    called the glycos two glucoses bound
  • 00:48:04
    together with a glycosidic bond that the
  • 00:48:06
    body has a hard time digesting um that
  • 00:48:09
    we don't split that Bond very well we
  • 00:48:11
    have an amalay enzyme that can split
  • 00:48:13
    lots of other glucose bonds um taking
  • 00:48:16
    that bread that polymer of starches and
  • 00:48:18
    turning it into a lot of glucose but
  • 00:48:20
    with Tre hos we don't split that very
  • 00:48:21
    well now I'm speculating a little um I
  • 00:48:24
    can't totally remember it even though
  • 00:48:26
    I've become I've been familiar with it
  • 00:48:28
    in the past but I believe that's how it
  • 00:48:29
    acts we basically don't digest it very
  • 00:48:31
    well and thus we taste the sweetness as
  • 00:48:35
    it hits our mouth and yet we don't have
  • 00:48:36
    any um glucose impact but I'm kind of
  • 00:48:40
    speculating there Mindy I'm sorry that
  • 00:48:41
    I'm not more familiar with it I'll I'll
  • 00:48:43
    bone up on that um all right another one
  • 00:48:46
    Tanya how does Hong Kong Stack Up on the
  • 00:48:48
    rates of heart disease yeah yeah super
  • 00:48:50
    low um you can look up the incidence and
  • 00:48:53
    mortality especially mortality of heart
  • 00:48:55
    disease and Longevity and it's one of
  • 00:48:57
    the longest lived countries on the
  • 00:49:00
    planet so that's pretty impactful but
  • 00:49:03
    also you guys just as a just as a
  • 00:49:05
    counter to that whole narrative that
  • 00:49:06
    meat is causing these diseases of
  • 00:49:09
    civilization or what I call the plagues
  • 00:49:10
    of prosperity look at what has happened
  • 00:49:13
    to red meat consumption in the last 120
  • 00:49:16
    years in the United States it went down
  • 00:49:19
    a lot from the early 1900s through the
  • 00:49:22
    1960s 1970s um what was up up up up and
  • 00:49:26
    then it plummeted in the 1970s and it's
  • 00:49:28
    come back a little bit and then
  • 00:49:30
    flatlined and it's been flatlined for
  • 00:49:32
    about 20 30 years so we're not eating
  • 00:49:35
    more and more meat every year but what
  • 00:49:37
    is happening during the same time span
  • 00:49:39
    with heart disease with Cancers with
  • 00:49:41
    diabetes they're all skyrocketing they
  • 00:49:44
    continue to go higher and higher so just
  • 00:49:46
    at this Global superficial 10,000 foot
  • 00:49:50
    view the whole thing falls
  • 00:49:52
    apart I hope that anyone who listens to
  • 00:49:55
    this so those tuned in now can be honest
  • 00:49:59
    in looking at this that way that if you
  • 00:50:02
    again if you look at meat consumption
  • 00:50:04
    red meat consumption it has gone down
  • 00:50:07
    since 120 years ago per person and
  • 00:50:11
    during the same span heart disease and
  • 00:50:13
    diabetes in particular have just
  • 00:50:15
    skyrocketed and continued to climb red
  • 00:50:18
    meat does not continue to climb so again
  • 00:50:21
    even at just the simplest glance this
  • 00:50:24
    whole story starts to fall
  • 00:50:26
    apart Jackie we'll say this is the last
  • 00:50:29
    question for today and please join me
  • 00:50:31
    next week so I'm overweight and my LDL
  • 00:50:33
    is Skyhigh but low triglycerides and
  • 00:50:35
    high LDL and Insulin below three so
  • 00:50:38
    Jackie interestingly you are probably
  • 00:50:41
    among those few people who have what's
  • 00:50:43
    called hyperplastic fat growth so this
  • 00:50:47
    is the process whereby fat cells
  • 00:50:49
    multiply so when there's elevated
  • 00:50:51
    insulin and sufficient energy to fuel
  • 00:50:53
    the growth that insulin stimulating
  • 00:50:56
    rather than each individual fat cell
  • 00:50:57
    getting bigger and bigger and bigger
  • 00:50:59
    there are people who have this ability
  • 00:51:02
    to make a new fat cell so before this
  • 00:51:05
    fat cell gets too big we have a new one
  • 00:51:07
    that can start to carry some of that
  • 00:51:09
    metabolic burden and so none of the fat
  • 00:51:11
    cells ever end up getting too big and
  • 00:51:14
    thus they prevent the insulin resistance
  • 00:51:16
    and thus they prevent the
  • 00:51:18
    inflammation so the fact that you are
  • 00:51:20
    overweight now and just as a reminder
  • 00:51:22
    women naturally have more fat than men
  • 00:51:24
    as a consequence sex hormones it's
  • 00:51:26
    natural it's by Design and it's
  • 00:51:28
    healthier for women because of how women
  • 00:51:30
    store fat including a little more
  • 00:51:33
    hyperplasia a little more multiplication
  • 00:51:35
    of fat cells at the butt and hips areas
  • 00:51:38
    those are areas that can get bigger by
  • 00:51:40
    making new fat cells which helps the
  • 00:51:41
    woman stay more insulin sensitive
  • 00:51:43
    despite the fat Mass Jackie in your
  • 00:51:46
    instance it could be what's that's
  • 00:51:48
    what's happening you have this ability
  • 00:51:50
    to make fat cells so you have more fat
  • 00:51:53
    cells but they're smaller and so you're
  • 00:51:56
    insulin sensitive the fact that your
  • 00:51:57
    triglyceride to HDL ratio is so low to
  • 00:52:00
    me matters way more than your LDL and
  • 00:52:02
    this is supported in published research
  • 00:52:05
    that LDL doesn't predict the heart
  • 00:52:07
    disease um risk but triglyceride to HDL
  • 00:52:10
    ratio does much much better than LDL um
  • 00:52:15
    there's in fact one particular study
  • 00:52:16
    that highlights this looking at
  • 00:52:17
    triglyceride to HDL ratio and LDL and
  • 00:52:20
    plotting them on this kind of
  • 00:52:21
    threedimensional curve or or plot
  • 00:52:24
    finding that across all of the LDL
  • 00:52:26
    levels if triglyceride to HDL ratio is
  • 00:52:28
    low there's no increase in heart disease
  • 00:52:30
    risk but the moment you look at the
  • 00:52:32
    triglyceride to HDL ratio going up now
  • 00:52:34
    all of a sudden heart disease risk goes
  • 00:52:36
    up regardless of whether LDL is high or
  • 00:52:39
    low and the fact that your insulin is
  • 00:52:41
    below three suggests in combination with
  • 00:52:43
    the triglyceride to HDL ratio that your
  • 00:52:45
    body is very insulin sensitive and of
  • 00:52:47
    course as a reminder never giving
  • 00:52:49
    medical advice just your friendly
  • 00:52:50
    neighborhood scientist you guys thanks
  • 00:52:52
    for tuning in I hope that you feel that
  • 00:52:55
    you are much more familiar with the
  • 00:52:57
    causes the origins of insulin resistance
  • 00:52:59
    primary secondary and the unique ones
  • 00:53:01
    and the contributing role of the fat
  • 00:53:03
    cell and I look forward to you tuning in
  • 00:53:06
    next week where we'll discuss more about
  • 00:53:08
    the consequences of insulin resistance I
  • 00:53:11
    will see you
  • 00:53:13
    then
Tags
  • insulin resistance
  • metabolic health
  • primary causes
  • inflammation
  • stress hormones
  • elevated insulin
  • fat cells
  • starvation
  • diet
  • metabolic flexibility