PUFAs Cause Obesity And Diabetes. Coconut Oil & Fructose Are Protective

Discussion in 'Articles & Scientific Studies' started by Hans, Aug 16, 2018.

  1. Hans

    Hans Member

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    Everyone here knows PUFAs are bad, but I just wanted to post this study, which shows some of the mechanisms how PUFAs and SFAs work. In the study the soybean oil increases bodyfat, inflammation, fatty liver, cancer promoting genes, glucose intolerance, diabetes, etc., whereas the coconut oil has the opposite effect. Soybean oil contains a fair bit of γ-tocopherol, but this was not enough to protect against its harmful effects.

    Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver
    They had 4 groups, and all four ate 40% fat.
    Group 1 (HFD): 36% coconut oil + 4% soybean oil
    Group 2 (F-HFD): same as group 1 + 25.9 kcal% of energy from added fructose
    Group 3 (SO-HFD): 21 kcal% fat calories from coconut oil and 19 kcal% from soybean oil
    Group 4 (F-SO-HFD): same as group 3 + 25.9 kcal% of energy from added fructose

    All groups ate the same amounts of food.
    Core findings:
    "Mice fed SO-HFD gained more weight and at a faster rate than mice fed HFD".

    "Addition of fructose also increased body weight above HFD (Fig 1A right), although not as much as soybean oil (Fig 1B left). SO-HFD mice gained slightly more weight than F-SO-HFD mice, although this difference was significant only between weeks 8 and 16"
    Fructose protects against the obesogenic effect of PUFAs.

    "we found that at 20 weeks the F-HFD did not cause diabetes (fasting blood glucose level > 200 mg/dL) whereas the SO-HFD did (Fig 4A). Furthermore, the F-HFD mice were just barely less tolerant to glucose than the Viv mice while the SO-HFD were extremely intolerant. Interestingly, the addition of fructose to SO-HFD (F-SO-HFD) actually slightly ameliorated the glucose intolerance of SO-HFD. Notably, the diet consisting primarily of coconut oil (HFD) did not show any diabetes or glucose intolerance at 20 weeks."
    Fructose does not cause diabetes and might actually prevent glucose intolerance caused by PUFAs.

    "At 33 weeks, the SO-HFD mice were the most insulin resistant and much more so than F-SO-HFD mice, which were indistinguishable from F-HFD and HFD"
    Fructose restored the insulin resistance caused by PUFAs.

    "SO-HFD livers had very large lipid droplets that were consistently accompanied by severe hepatocyte ballooning, suggesting potential liver damage"

    "the fatty acid translocase Cd36, which aids in free fatty acid (FFAs) uptake and contributes to hepatic steatosis [68] and fatty acid binding protein Fabp4 that helps maintain hepatic metabolic balance and links diet induced obesity to insulin resistance [69,70] was increased in SO-HFD, while fatty acid binding protein 5 (Fabp5), which plays an important role in detoxifying FFAs and preventing lipid dysregulation [71], was decreased three-fold."
    Enzymes that increase fatty acid import into cells are significantly increased, and enzymes that detox fatty acids are decreased. Ray mentioned that PUFAs inhibit it's own detoxification, and looks like inhibiting Fabp5 is one mechanism. PUFAs also cause lipid accumulation in muscles and other organs, and it might be by increasing Cd36 and Fabp4.

    "Similarly, Igfbp1, an important regulator of insulin like growth factor 1 (IGF1) activity, showed an almost five-fold increase in SO-HFD versus HFD livers: increased hepatic expression of Igfbp1 is associated with diabetes [72]. In the inflammation category, Lgals1 (Galectin-1), an important immune response modulator and biomarker for hepatocellular carcinoma (HCC) [7375] was also markedly increased in SO-HFD but not HFD"

    "The most notable gene was Pdk4, which was elevated four-fold in SO-HFD compared to HFD and encodes a mitochondrial gene that plays an important role in the balance between glucose and fatty acid oxidation [76]. In contrast, Hyou1 and Slc25a30 (KMCP1) were expressed at higher levels in HFD compared to both SO-HFD and Viv. Since these genes are considered to be protective against oxidative damage [7780], this suggests that coconut oil may be beneficial but that soybean oil diminishes the effect."
    Pdk4 inhibits the activity of pyruvate dehydrogase (PDH), which is essential for glucose oxidation. Palmitic acid increases PDH. One important thing about this is that, PUFAs increase uncoupling, which reduce ATP, but then also inhibit PDH, so no glucose is able to make up for the loss of ATP. With SFAs, they also increase uncoupling, but also increase glucose oxidation to make up for the reduction in ATP. With PUFAs that inhibit PDH, most of the glucose is going to lactate and not CO2, as lactate dehydrogenase as also elevated in the PUFA group. PUFAs lead to low ATP production and keeps the cells in a low energy state, by also inhibiting many of the complexes in the mitochondrial membrane that's necessary for ATP production.

    "Genes in the cancer category showed a definite predominance of pro-proliferation genes upregulated in SO-HFD while anti-proliferative genes tended to be upregulated in HFD but not SO-HFD."

    "Both capric and lauric acid have been shown to cause a decrease in adiposity, increased insulin secretion and improved serum lipid profile"

    "Interestingly, the pro-inflammatory eicosanoid 12-HETE (an AA metabolite) and the marker of lipid peroxidation 13-HODE+9-HODE (LA metabolite) [9193] were significantly decreased in HFD versus Viv at both 16 and 35 weeks, suggesting that coconut oil may be protective against inflammation. The lower levels of these metabolites could be due to decreased expression of Cyp2c54 (Fig 9B), which is known to metabolize AA and LA to HETEs and HODEs"

    This is a very good study in my opinion showing how and why coconut oil/saturated fat are good and PUFAs are bad. Longer chain saturated fat, such as stearic acid, will have its own set of benefits not discussed in this study, because coconut oil doesn't have lots of stearic acid.
    They also show that fructose protects against the harm of PUFAs.

    But this is just a rat study, so should be carefully extrapolated to humans, but still it shows some good points. I advise to read to whole study.
     
  2. lollipop

    lollipop Guest

    Bump. Interesting.
     
  3. Jon

    Jon Member

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    @Salmonamb good stuff. Recently I was chatting with @Travis and he was schooling me in all things biochem, and he happened to mention the proven necessity of dha in the prevention of cholesterol deposition of cell membranes. More specifically he pointed to the possibility that the dha precursor; α-linolenic (18∶3ω−3) is the real hero here, and that things like grassfed beef, dairy, and leafy greens have minute amounts that seem to be stable enough to not cause damage and quite possibly be beneficial.

    The homie, @Amazoniac also pointed out to me that pufa depletion to the point of meadic acid synthesis is most likely going to cause stress, and that pufa is in all food to some extent for a reason.

    It's really making me rethink the whole pufas are pure evil thing. Though omega 6 doesn't really seem to have any redeemable qualities unless one considers MAYBE it exists purely to stimulate some sort of systemic defense to promote immunological processes. I dunno though lol.

    (Sorry for the shameless name dropping)
     
  4. OP
    Hans

    Hans Member

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    Travis knows all about the harmful effects of omega 6 and he is avoiding it like the plague. ALA does seem to have that benefit as he has pointed out in a few posts. I bet he is so PUFA depleted he is making mead acid, which I believe he thinks is beneficial. I'm not trying to speak for him and he can correct me if I'm wrong.
    Haiduts' mead acid is above the upper range, and I'm not sure his body is feeling stressed because of it.
    I don't think making mead acid is stressful. I think if someone is unable to produce enough mead acid when pufa depleted, it could be stressful.

    PUFAs are in almost everything edible and impossible to avoid. We only have animal studies on pufa depleted diets, and animals are different from humans. The only human example we have is William Brown, but he only did a PUFA free diet for 6 months, so we don't know what effect a long term pufa depleted diet would have in humans.

    And everyone is different. One guy does exceptionally good on 10-15g of fat a day and another does best while eating 100g of fat a day. So even if we do have some human evidence on a pufa depleted/fat free diet, it will still not work for everyone despite the evidence.

    PUFA avoidance is not something that Peat has made up, it's got some solid evidence behind it. I think it's a good idea to keep it as low as possible, and then find the proper amount of saturated fat that your body requires and stick to that.
     
  5. Jon

    Jon Member

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    Well stated. I'm definitely not trying to make a case for TRYING to ingest them, more so just questioning how beneficial it actually may be to avoid Even ALA (in tiny amounts)

    I don't know if he still does this but Travis once wrote he was regularly ingesting almonds because of their superior Ratio of omega 3:eek:mega 6. I understand they fight for absorbency, so would this still being able to deplete pufa over time?
     
  6. OP
    Hans

    Hans Member

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    I have also thought a lot about these things, and then I come back to the conclusion that one cannot avoid PUFAs completely and if PUFAs were indeed necessary, that small amount in foods will probably be enough.
    I don't think he eats almonds anymore as he mentioned it a while back that he quit. So not sure if he started eating them again.
    ALA inhibits the conversion of linoleic acid to arachidonic acid, but linoleic acid also inhibits the conversion of ALA to DHA, so it would be good to keep linoleic acid as low as possible imo.
     
  7. Jon

    Jon Member

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    I see, good explanation. Just FYI after our chats on other boards I've been toying with the idea of lowering my fat a bit lol you've painted a pretty appealing picture of what benefits it may have. I haven't pulled the trigger yet just because I want to make sure I've thought about all the angles so I don't end up hurting my newly increased testosterone. Was was able to increase it 200ng/dl in about a years time, but now I'm wondering if the next step to take is maybe lower my fat a bit. My goal is to get over the clinical range of 916ng/dl (currently in 818ng/dl) so I've been trying to find ways to eek out that last 100ng/dl. What do you think? My micros are very balanced, I keep pufa at 4g/day or less, and I'm wondering if because I've been able to increase test that maybe I'm less pufa ridden and may be able to handle/benefit from low fat?
     
  8. OP
    Hans

    Hans Member

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    Lowering your PUFA by a gram or three might not really have that big of an impact on your testosterone levels, although, some studies show that mice on a fat free diet had double the testosterone than the control group. So maybe it's worth a try. However I have not seen a study of fat free vs hydrogenated coconut oil on testosterone levels in rats. Saturated fat are androgenic, so maybe it would work better to lower PUFAs more, but try to keep saturated fat high. Another ex member here, visionofstrength, did a diet where his fat intake was like 130g daily, with less that 2g PUFA. I don't know how it impacted his testosterone levels, but just sharing that it is possible to eat high fat and not high PUFA at the same time.
    In regards to the study I shared above, eating coconut oil will not affect glucose tolerance and will actually lower inflammation, which is good.
    So maybe keeping some saturated fat in the diet vs a vlfd will be more beneficial. But anyway, its worth experimenting with to find your personal 'sweet-spot'.
    Other ways to increase testosterone that might have a bigger impact than a little PUFA will be to keep serotonin, cortisol and prolactin as low as possible.
     
  9. Terma

    Terma Member

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    This is still rats (there are irreconcilable differences pointed out somewhere I can't remember), but the fructose is less extreme.

    The problem is still is goes from nearly 0% fructose to 30-40% or something (in weight I means).

    The glucose regulation benefits from fructose are already well-known, so you get no idea of a curve by going from ~0% to 30-40%. It still caused lipid accumulation and problems so it's not as if fructose was "healthy" in that context. It was just "much less bad", and not compensated sufficiently by the choline/other nutrient content.

    The ~0% could be seen more as a case of fructose deficiency than anything. (Evolutionarily, when did humans or rats eat starch without fructose? Even tubers contained some) Why the extremes all the time?
     
  10. Terma

    Terma Member

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    What would be the % in weight anyway? They write maltodextrin + corn starch + fructose is 120 + 125 + 355 grams, so fructose is 355/600 of 53% weight = 31% weight? I'm getting drunk now so I'm not too sure about maltodextrin, why they feed that to rats anyway.
    journal.pone.0132672.t001.PNG
     
  11. Cirion

    Cirion Member

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    So why did the mice fed fructose alongside the "healthy" fat diet (High coconut oil) gain noticeably more weight than the group with just high fat?

    The other results suggests fructose is "Better" than the PUFAs for energy, but the results seem to suggest SFA's are superior to fructose, or am I missing something?

    My takeaway from this is:

    SFA > Fructose > PUFA

    Is that true or did I miss a key takeaway from this?

    And from what I've seen here by the way in response to a conversation above, I believe that with people with damaged metabolisms (those starting off RP) are going to do better with a good amount of SFA's in the diet (I know I do). I don't know of ANY person here who did good (if there are any, I don't know any) who have done well on a very low / zero fat diet starting off. I think only otherwise healthy people can tolerate that. Most here still eat a respectable amount of fats. Which, the results of this study are good in that context (40% fat is pretty high, and that's actually often close to what I aim for, something like 40% fat 40% carb 20% protein, although I don't count macros/calories anymore)
     
  12. Cirion

    Cirion Member

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    You noted the same thing as me. I wonder if there is an ideal point somewhere between the 0% and 30%.

    Maybe this could help explain why a lot of people new to RP still have health issues? Fruit is a good food, but if you eat it to the point that fructose is 30% of your caloric intake, that just seems like a lot (most fruit is roughly 1:1 glucose/fructose, so 30% fructose in diet means a whopping 60% of calories in diet from fruit basically, that's bordering on the "Banana Girl" diet/fruitarian), and it can be tempting to dive head-first into the RP pool and eat fruit for all your carbohydrate needs (especially when so many of the anti-starchers are out there saying that starch is the devil, further increasing fructose intakes). I did that when I first started RP'ing and I can say that for me, this actually increased my stress hormones no matter how much fruit I ate. There's definitely a thing as too much fruit.

    I am trying to get around half of my carb intake from starch now, so maybe at most my sucrose intake is 20-30% (which means my fructose intake is roughly 10-15%). with the other half from straight glucose (aka starch).
     
  13. Jon

    Jon Member

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    @Salmonamb has explained this well, but the reason for the quicker weight gain on fructose+sfa is most likely because the metabolism is saving mitochondria from being flooded and killed by excess energy. Sfa is easily excluded from entering a cell in times of energy surplus thus leading to rapid fat gain whereas cells can not as easily exclude pufa because of how they are oxidized down the electron transport chain (essentially skipping the step that otherwise would prevent them from entering a cell). In this way, the rapid fat gain you see from sfa+fructose is a form of protection from systemic damage.
     
  14. Cirion

    Cirion Member

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    Still confused... you say it saves the mitochondria from "excess energy". How is it excess if each grouping has the same amount of calories? And you say SFA is excluded from entering a cell in times of energy surplus, wouldn't that lead to less gain not more in that case? Did you mean to say that fructose is not excluded therefore because SFA is, most of the fructose gets stored as bodyfat (and not the SFA)?

    Wouldn't this then mean that just because something doesn't make you fat, doesn't mean it is good for you? Is that a correct interpretation? If that's true, then that makes the whole obesity + health connection that more complicated?

    I thought that something not getting stored as bodyfat was generally a good thing? Just about everyone would say being lean is a marker of good health (ie, not storing bodyfat)

    I was under the impression that SFA's are a good thing (and if you consider that the high SFA group is the leanest, if you count leanness as the good thing, then that's exactly what this study says)

    This raises more questions to me than answers! Maybe I'm just dense haha
     
  15. Jon

    Jon Member

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    lol I understand your confusion. Unfortunately where health is concerned, not all sources of calories are metabolized equally. For instance, fructose is not metabolized in the small intestine, it's metabolized in the liver. This is why fructose can cause insulin resistance rather rapidly since when the body sees an excess of it (surplus energy) it will store the energy in adiposites within the vicinity of the site of metabolism. This is also why starch tends not to cause much of any visceral fat accumulation, but does cause subcutaneous fat gain being that it's mostly utilized for energy by muscles and so onelce they've had their fill and there's an excess, it gets stored in near by fat cells.

    I should have clarified when I said "is excluded from cells" I mean lean tissue. It still will make you fat but will take a bit longer, which you would think is a good thing it isn't as this case signifies that once you start getting fat off pufa it's likely because it's causing to some extent permanent insulin resistance (by destroying cells, where sfa insulin resistance is basically 100% reversible since it doesn't kill cells (lean tissues) by feeding them to death.
     
  16. Cirion

    Cirion Member

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    Ok that makes more sense. That means fructose is a double edged sword then and care should be avoided not to intake it in excess (i.e., don't get 100% of your carbs from fruit), which like I mentioned previously, corresponds to some of my experiences with too much fructose. Of course, you can make the same argument against anything in excess generally speaking, so that just makes logical sense. That said, SFA's in excess is far better than PUFA in excess, because storing SFA's is not nearly as unhealthy as stored PUFA. Right?

    All that said, it seems like it is impossible to avoid some amount of bodyfat gain while starting this process, and it takes many people as long as several years to become PUFA free and (healthfully) lose the body fat and as long as body fat that is gained during the process is from SFA and not PUFA it's not too bad. This is where I struggled the first time I tried RP and quit, because I gained fat and called it a failure, but I think some fat gain is inevitable, temporarily at least and if I make sure PUFA is very low I should be good over the long term.
     
  17. OP
    Hans

    Hans Member

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    Saturated fats are oxidized at a slower rate than PUFAs: Octanoic acid (5x faster than oleic acid) > Lauric acid = Oleic acid > linolenic acid (α/γ) > linoleic > arachidonic > palmitic acid > stearic acid. PUFAs also stimulate lipolysis, whereas saturated fat inhibits it. So eating mostly PUFAs will elevate free fatty acids, make you more insulin resistant, and also interfering with the oxidation of glucose and causing hyperglycemia.
    Glucose enters cells via GLUT4, which is rate limited, but fructose transport isn't rate limited.
    Fructose also doesn't increase insulin as much as glucose, which inhibits lipolysis to a lesser degree, thus you have higher free fatty acids present at the same time with all your fructose. That is why studies show that fructose "stimulates" de novo lipogenesis, but actually, fructose doesn't inhibit lipolysis as much as glucose, hence the elevated free fatty acids.
    But in the real world, fructose is always present with glucose. There is a study which shows that the addition of about 450cal+ fruits to the diet doesn't affect blood lipids or insulin signaling. 450cal isn't much, but it's something. I don't know much about fruititarians, but I don't think they have fatty livers. Correct me if I'm wrong.
    Studies actually show PUFAs are "better" for fat loss than saturated fat, because it stimulates lipolysis. But I think the major thing about getting fat on a Peat diet, is because of caloric excess, and not necessarily stored PUFA. I also think a lot of people don't think calories matter anymore when they go on a Peat diet, because it's supposed to stimulate the metabolism right... "eat eat eat to recover your metabolism".
     
  18. Cirion

    Cirion Member

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    Well I think we all agree PUFA's are not good to have, in the long run at least. I agree with your overall thinking, the problem is that a metabolism that is chronically damaged from under-nourishment, that the last thing you need to do is count calories or restrict them artificially. If the body is giving hunger signals, they need to be met, if healing is to occur. You can't provide the building blocks to heal otherwise, and further dieting will only serve to cause even further stress. I know this all too well, being a chronic yo-yo dieter myself. In fact I'd venture a guess that at least 80% of people here before finding RP were yo-yo dieters. Health must be obtained before optimal weight is achieved (all the success stories I've seen here, this is how it occurred, in that order, not weight and then health).

    I'd be curious to hear your strategy to heal without gaining (some) body fat, because I don't see how it is possible. I have blood sugar crashes, mood swings, and all sorts of fun things if I even remotely try to restrict food intakes, it ALWAYS backfires on me, no matter how "healthy" my food intake is.

    I in fact am a recovering orthorexic, and I refuse to ever restrict food ever again, if that means getting fatter then so be it. I have come to terms with that now I think.

    Feeling good & maybe a little fat > being lean and moody any day. I understand your snarky remark about "eat eat eat" but this premise is true to an extent, you must eat to bring your resting temps and pulses to a good level (plus your mood, which usually follows a good temp/pulse).

    If I sound a little argumentative sorry about that, but the age old "calories in calories out" argument really leaves me cold, given that CICO has effectively ruined 5 years of my life (5 years of chronic dieting) following that old garbage. Reality is so much more complicated than simple CICO. I mean, you post here a lot, I don't need to tell you that.
     
  19. Jon

    Jon Member

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    Not speaking for @Salmonamb at all, this is my opinion; you should only have to overeat for about 4 days, mostly on carbs, very little fat, minute amounts of fructose, mostly starchy carbs. 3 days of overeating on starch pretty much recovers all leptin sensitivity and so you should no longer feel ravenous and should be able to go to a maintenance calorie level and not gain any fat. The caveats of course are that you need to not be doing physical activity that over stresses you, you must be getting as much sleep as possible, and you must be eating the proper foods.

    In my personal experience this holds true as I can eat "intuitively" with out any fat gain after a 4 day carb refeed even after extensive periods of fat loss.
     
  20. OP
    Hans

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    No I wasn't suggesting calorie restriction, merely not overeating too much. Yes you should eat to food cravings, but keep in mind that adding fat with everything, because saturated fat and sugar tastes so good, will have you overeating real fast without being very full at the end of the day. Maybe eating more protein and limit fat intake to ~60g and using vit E will help to keep hunger under control, limit fat gain and lipid peroxidation. Someone can easily consume 250ml+ cream and other fats with 100+ sugar just as snacks. And this excludes the main meals. Eating more protein and lean satiating foods can help limit fat gain.
     
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