How Fat Can Harm Your Brain

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    Mar 05, 2014 4:09 PM GMT
    It’s been known for some time that obesity can alter cognition in animals. Past experiments with lab rodents, for instance, have shown that obese animals display poor memory and learning skills compared to their normal-weight peers. They don’t recognize familiar objects or recall the location of the exit in mazes that they’ve negotiated multiple times.

    Many thought the brain, though, should be insulated from those harmful effects. It contains no fat cells and sits behind the protective blood-brain barrier that usually blocks the entry of undesirable molecules.

    However, recent disquieting studies in animals indicate that obesity weakens that barrier, leaving it leaky and permeable. In obese animals, substances released by fat cells can ooze past the barrier and into the brain.

    http://well.blogs.nytimes.com/2014/03/05/how-fat-may-harm-the-brain-and-how-exercise-may-help/?hp
  • Destinharbor

    Posts: 4435

    Mar 05, 2014 5:01 PM GMT
    And you have to bring this up on Lobster and baked potato night?
  • DiverScience

    Posts: 1426

    Mar 05, 2014 5:32 PM GMT
    So... yes and no.

    First, it doesn't make the blood brain barrier "leaky." I don't know where the hell they came up with that bull. Cytokines, including interleukin, have transport mechanisms for crossing the blood brain barrier, we've known that for decades.

    So don't worry, your fat friends' brains aren't leaking.

    Second, the fat mice don't "accumulate more fat cells." That's not how fat cells work, they get bigger, they don't multiply.

    Now, the meat of the actual study.

    Conceptually, they've vaguely got the idea right. Very fat mice have some cognitive deficits, especially in formation of long term memory.

    Very fat mice also release higher levels of IL-1 (Interleukin-1) a cytokine related to inflammation, among other things. In the brain, IL-1 causes "microgliosis" meaning expansion and proliferation of glial cells (the cells that protect your neurons and ensure fast neural transmission).

    Under normal conditions, this isn't actually bad. Proliferation of glial cells helps protect your neurons, reduces inflammation, promotes healing.

    Under non-normal situations like extreme obesity, there's no injury to heal, and no end "healed wound" to signal an end to the IL-1 secretion. The constantly increased IL-1 results in continued microgliosis, and while that's fine for an injury, it also slows the formation of new axonal connections. New axonal connections are needed for many memory functions.

    So, they've determined that IL-1 is bad for your formation of long term memories (hippocampal function). But interestingly, exercise blocks the effect even if the mice were fat.

    It's also worth noting that there are many other sources for IL-1, as it's a major component of your immune response.

    So. IL-1 is bad for long term memory in mice. Exercise seems to block this effect, as does something that directly binds the IL-1. Fat is one source of IL-1.
  • frogman89

    Posts: 418

    Mar 05, 2014 5:46 PM GMT
    DiverScience saidSo... yes and no.

    First, it doesn't make the blood brain barrier "leaky." I don't know where the hell they came up with that bull. Cytokines, including interleukin, have transport mechanisms for crossing the blood brain barrier, we've known that for decades.

    So don't worry, your fat friends' brains aren't leaking.

    Second, the fat mice don't "accumulate more fat cells." That's not how fat cells work, they get bigger, they don't multiply.

    Now, the meat of the actual study.

    Conceptually, they've vaguely got the idea right. Very fat mice have some cognitive deficits, especially in formation of long term memory.

    Very fat mice also release higher levels of IL-1 (Interleukin-1) a cytokine related to inflammation, among other things. In the brain, IL-1 causes "microgliosis" meaning expansion and proliferation of glial cells (the cells that protect your neurons and ensure fast neural transmission).

    Under normal conditions, this isn't actually bad. Proliferation of glial cells helps protect your neurons, reduces inflammation, promotes healing.

    Under non-normal situations like extreme obesity, there's no injury to heal, and no end "healed wound" to signal an end to the IL-1 secretion. The constantly increased IL-1 results in continued microgliosis, and while that's fine for an injury, it also slows the formation of new axonal connections. New axonal connections are needed for many memory functions.

    So, they've determined that IL-1 is bad for your formation of long term memories (hippocampal function). But interestingly, exercise blocks the effect even if the mice were fat.

    It's also worth noting that there are many other sources for IL-1, as it's a major component of your immune response.

    So. IL-1 is bad for long term memory in mice. Exercise seems to block this effect, as does something that directly binds the IL-1. Fat is one source of IL-1.
    Thanks for this detailed insight.

    I do believe that it is also a psychological effect that the scientists might have disregarded. Fat mice spend a lot more time focussing on food than other things. Their learning processes are different from healthy mice.
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    Mar 05, 2014 5:54 PM GMT
    The study continues:

    The consequences of that seepage became the subject of new neurological experiments conducted by researchers at Georgia Regents University in Augusta and published last month in The Journal of Neuroscience. For the studies, the scientists gathered mice bred to overeat and grow obese, which, after a few weeks of sitting quietly in their cages and eating at will, the animals had obligingly accomplished. As they grew rotund and accumulated more fat cells, the researchers found, their blood showed increasingly hefty doses of a substance called interleukin 1 that is created by fat cells and known to cause inflammation.

    In these mice, as interleukin 1 migrated to the head, it passed the blood-brain barrier and entered areas such as the hippocampus, a part of the brain critical for learning and memory. There, it essentially gummed up the works, the researchers found when they examined tissue from the animals’ brains, which had high levels of interleukin 1 together with widespread markers of inflammation. While inflammation can represent a healthy response to invading molecules, it hurts cells if it persists.
  • frogman89

    Posts: 418

    Mar 05, 2014 6:15 PM GMT
    woodsmen saidThe study continues:

    The consequences of that seepage became the subject of new neurological experiments conducted by researchers at Georgia Regents University in Augusta and published last month in The Journal of Neuroscience. For the studies, the scientists gathered mice bred to overeat and grow obese, which, after a few weeks of sitting quietly in their cages and eating at will, the animals had obligingly accomplished. As they grew rotund and accumulated more fat cells, the researchers found, their blood showed increasingly hefty doses of a substance called interleukin 1 that is created by fat cells and known to cause inflammation.

    In these mice, as interleukin 1 migrated to the head, it passed the blood-brain barrier and entered areas such as the hippocampus, a part of the brain critical for learning and memory. There, it essentially gummed up the works, the researchers found when they examined tissue from the animals’ brains, which had high levels of interleukin 1 together with widespread markers of inflammation. While inflammation can represent a healthy response to invading molecules, it hurts cells if it persists.

    See? That's not a mouse's natural behavior. They are modified to eat at will and grow obese. They have a completely different psychological profile as normal mice. How can they compare these two groups?
    They had the mice grow fat in a few weeks. Imagine you sit your flat eating day in and day out. This is your only activity. Your intellectual skills would decrease immensely, too.

    Plus, the radical increase of weight and fat is also a factor. If the growth is too fast, it equals an inflammatory process that the body has to accomodate to first. It really is no surprise that IL-1 is high in those mice.
  • 1AlanZSky

    Posts: 1505

    Mar 05, 2014 6:53 PM GMT
    The brain is mostly fat, girls.
  • DiverScience

    Posts: 1426

    Mar 05, 2014 10:18 PM GMT
    Incidentally, my comments after the "meat of the actual study" comment, come from the actual published study in the journal. Before that, I was commenting on the linked NYTimes article. I.e. as usual, the newpaper decided it would embellish the original science, and make it more "shiny" for the masses.

    AlanZSky: Yes, they are largely fat at 60+ percent. However, that is not the same as fat cells. In fact, most of the fat in your brain is from membrane, which is approximately the same fat as is in the membrane of every cell. You just have a LOT of membrane in your brain (layered membrane is the key to our fast transmitting neurons).

    And yes, it's also worth noting as Frogman points out, that these are db/db mice. At least largely. I'm not sure if the final lipectomy and fat transplantation were also in db/db mice. Those should have been done on WT mice (normal mice) as a control, but I'm away from home and can't as easily access J Neuro the way I usually can so I can't check the methods section.
  • Posted by a hidden member.
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    Mar 05, 2014 10:25 PM GMT
    DiverScience, Thank you for illuminating the NYT article.
  • thadjock

    Posts: 2183

    Mar 06, 2014 3:20 AM GMT
    MuchMoreThanMuscle saidIt doesn't pay to be a FATTY!


    but u can't train skinny girls to do cool tricks:

    fat-girl-loves-cookies-300x219.jpg

    d340f1_8e02216a8353e7918817218227cff25f.
  • Posted by a hidden member.
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    Mar 06, 2014 3:32 PM GMT
    DiverScience saidSo... yes and no.

    First, it doesn't make the blood brain barrier "leaky." I don't know where the hell they came up with that bull. Cytokines, including interleukin, have transport mechanisms for crossing the blood brain barrier, we've known that for decades.

    So don't worry, your fat friends' brains aren't leaking.

    Second, the fat mice don't "accumulate more fat cells." That's not how fat cells work, they get bigger, they don't multiply.

    Now, the meat of the actual study.

    Conceptually, they've vaguely got the idea right. Very fat mice have some cognitive deficits, especially in formation of long term memory.

    Very fat mice also release higher levels of IL-1 (Interleukin-1) a cytokine related to inflammation, among other things. In the brain, IL-1 causes "microgliosis" meaning expansion and proliferation of glial cells (the cells that protect your neurons and ensure fast neural transmission).

    Under normal conditions, this isn't actually bad. Proliferation of glial cells helps protect your neurons, reduces inflammation, promotes healing.

    Under non-normal situations like extreme obesity, there's no injury to heal, and no end "healed wound" to signal an end to the IL-1 secretion. The constantly increased IL-1 results in continued microgliosis, and while that's fine for an injury, it also slows the formation of new axonal connections. New axonal connections are needed for many memory functions.

    So, they've determined that IL-1 is bad for your formation of long term memories (hippocampal function). But interestingly, exercise blocks the effect even if the mice were fat.

    It's also worth noting that there are many other sources for IL-1, as it's a major component of your immune response.

    So. IL-1 is bad for long term memory in mice. Exercise seems to block this effect, as does something that directly binds the IL-1. Fat is one source of IL-1.
    +1 also the growth in number of glial cells makes the mouse predisposed to brain tumors as they form from these kind of cells...
  • Posted by a hidden member.
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    Mar 06, 2014 3:35 PM GMT
    frogman89 said
    woodsmen saidThe study continues:

    The consequences of that seepage became the subject of new neurological experiments conducted by researchers at Georgia Regents University in Augusta and published last month in The Journal of Neuroscience. For the studies, the scientists gathered mice bred to overeat and grow obese, which, after a few weeks of sitting quietly in their cages and eating at will, the animals had obligingly accomplished. As they grew rotund and accumulated more fat cells, the researchers found, their blood showed increasingly hefty doses of a substance called interleukin 1 that is created by fat cells and known to cause inflammation.

    In these mice, as interleukin 1 migrated to the head, it passed the blood-brain barrier and entered areas such as the hippocampus, a part of the brain critical for learning and memory. There, it essentially gummed up the works, the researchers found when they examined tissue from the animals’ brains, which had high levels of interleukin 1 together with widespread markers of inflammation. While inflammation can represent a healthy response to invading molecules, it hurts cells if it persists.

    See? That's not a mouse's natural behavior. They are modified to eat at will and grow obese. They have a completely different psychological profile as normal mice. How can they compare these two groups?
    They had the mice grow fat in a few weeks. Imagine you sit your flat eating day in and day out. This is your only activity. Your intellectual skills would decrease immensely, too.

    Plus, the radical increase of weight and fat is also a factor. If the growth is too fast, it equals an inflammatory process that the body has to accommodate to first. It really is no surprise that IL-1 is high in those mice.
    cutie...there are people who eat nonstop...there are obese people...animals are not used to large amounts of foods and they have more active activities then humans....they tired to make them be more like most of the sedentary people out there who suffer from obesity
  • frogman89

    Posts: 418

    Mar 06, 2014 5:14 PM GMT
    ChrisMD said
    frogman89 said
    woodsmen saidThe study continues:

    The consequences of that seepage became the subject of new neurological experiments conducted by researchers at Georgia Regents University in Augusta and published last month in The Journal of Neuroscience. For the studies, the scientists gathered mice bred to overeat and grow obese, which, after a few weeks of sitting quietly in their cages and eating at will, the animals had obligingly accomplished. As they grew rotund and accumulated more fat cells, the researchers found, their blood showed increasingly hefty doses of a substance called interleukin 1 that is created by fat cells and known to cause inflammation.

    In these mice, as interleukin 1 migrated to the head, it passed the blood-brain barrier and entered areas such as the hippocampus, a part of the brain critical for learning and memory. There, it essentially gummed up the works, the researchers found when they examined tissue from the animals’ brains, which had high levels of interleukin 1 together with widespread markers of inflammation. While inflammation can represent a healthy response to invading molecules, it hurts cells if it persists.

    See? That's not a mouse's natural behavior. They are modified to eat at will and grow obese. They have a completely different psychological profile as normal mice. How can they compare these two groups?
    They had the mice grow fat in a few weeks. Imagine you sit your flat eating day in and day out. This is your only activity. Your intellectual skills would decrease immensely, too.

    Plus, the radical increase of weight and fat is also a factor. If the growth is too fast, it equals an inflammatory process that the body has to accommodate to first. It really is no surprise that IL-1 is high in those mice.
    cutie...there are people who eat nonstop...there are obese people...animals are not used to large amounts of foods and they have more active activities then humans....they tired to make them be more like most of the sedentary people out there who suffer from obesity

    Exactly. That's why you can't compare these two groups of mice.

    "There are people who eat nonstop" - That's true, but that's a minority even among obese people.