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Palm Oil: maybe not such a good idea after all

There are two things that you can be certain of when it comes to palm oil: 1) business is booming and 2) orangutans hate palm oil (if they could speak to us, I’m confident that’s what they would say). We can now add another certainty to that: palm oil causes low-grade inflammation that is linked to insulin resistance, obesity and other metabolic diseases that are partially mediated by our resident gut microbes.

Palm oil is touted as a panacea for everything ranging from a route out of poverty for small-scale farmers, a sustainable biofuel, and for its powerful nutritional virtues. However, palm oil plantations are linked to unsustainable deforestation throughout the world – that aside from the obvious biosphere issues – is reducing livable habitat for orangutans to the point that some are calling it genocide.

Palm-oil

Source: FAO

Consumer demand – or maybe that should be manufacturer demand – for palm oil has resulted in palm oil in one of every two packaged products in the super market! You can find it in baked goods, cereals, crisps, sweets, margarine and popular soaps and cosmetics – to name a few.  Often listed under a dizzying number of names, like palmate and Sodium Lauryl Sulphate, it’s not always easy to spot.  Red palm oil has become very popular among the more affluent, both for its taste, cool red color, and superior antioxidant load. The Red palm oil is derived from the fleshy part of the fruit – hence its red color – while the clear stuff comes from the whitish kernel in the center. Or you can refine Red palm oil down to a clear version (but in the process, you lose some of the goodness).

I have discussed elsewhere (here and here) the potential impact of a high-fat diet and changes in your gut microbial ecosystem that can (does) lead to low-grade inflammation that furthers leads to insulin resistance, obesity and other issues. In short, high-fat intake shifts the gut microbiota and increases the translocation of lipopolysaccharides (LPS) or endotoxins from your gut into your blood, which then triggers inflammation – and then the cascade of problems start.

palm oil fruitThese “high-fat-increases-endotoxin-load-in-serum” studies used varying amounts and types of fat – with no particular emphasis on the type of fat being used. These researchers also, due to the nature of the research and the questions being asked, used what some might consider unrealistic levels of fat in the mouse or human diet being tested. Levels you would not see in a free-living human population. This research reality is simply a function of the researchers exploring cause and effect and in order to do so, need to “dial it up” a bit to get any meaningful shifts in the data. In either case, the outcomes are still informative.

Researchers in France decided to address both of these issues in a recent study among mice fed proportional and realistic levels of fat and tested oils with differing fatty acid composition (albeit in mice). The fats/oils tested included milk fat, palm oil, rapeseed (canola) oil, or sunflower oil.

Regardless of which fat the mice received, fat content as a percentage of diet was maintained at 22.4% (or, 38% of the energy of the diet). Mice were randomly divided into five groups (8 mice per group), and fed one of the five diets (one was a control – i.e., normal mice chow not spiked with fat). Fast forwarding a bit, the researchers found that depending on which oil the mice received, it could change the levels of endotoxins in serum (impaired gut) and increase markers of inflammation (not so good).

orangutanTurns out, that compared to a high-fat diet formulated with either milk fat, rapeseed oil, or sunflower oil, one that includes palm oil resulted in higher inflammation in “plasma and adipose tissue” as measured by a number of markers. Interestingly, rapeseed oil resulted in much lower inflammation. (Would encourage folks that are interested in the subject to read the detailed study themselves, and related).

In this study, researchers used refined non-hydrogenated palm oil, not oil from the kernel. That is, Red palm oil without the red. If you are concerned about low-grade inflammation, then you might want to think twice about forking out the extra money for the fancy palm oil and might want to check the ingredient labels a little closer as well. Or maybe it doesn’t matter at all. Maybe the differences between the inflammation triggered by one fatty acid over the other is insignificant. Maybe they should have used more mice, or heated the oil. Maybe mouse studies don’t matter. More studies are needed.

In either case, thinking twice about Palm oil might please the orangutans.

29 Comments

  1. Ahh, experiements with mice are always representative of humans. Their lab diet is too. It’s primarily sucrose (e.g. crap in a bag). Attributing any deleterious change to the fat is a stretch when so much sucrose is consumed.

    Funny thing about rapeseed oil is that stroke-prone, spontaneously hypertensive rats are fed a variety of deadly fats, the rats fed Canola oil die soonest and the rats fed coconut oil live the longest.

    • Note the mice in the study were not fed sucrose.

  2. But how can you extrapolate to _all_ fat (i.e. a “high-fat diet” leads “to low-grade inflammation that furthers leads to insulin resistance, obesity and other issues), when the mice were fed predominantly vegetable and also refined and processed fats? These are different from natural fat that would be consumed as part of a healthy human diet. Some of the healthiest high-fat traditional diets were based on fatty (pastured) animal foods, nothing like refined sunflower oil–something our ancestors probably never consumed in large quantities!

    • thanks for the comment. i’m not extrapolating – just referencing the published research. agree on the veg oils – novel to human biology – no matter what the source.

  3. Jeff, why do you keep writing these articles that make it sound like high fat is bad? I read the comments in the first article you linked to and you mentioned many times that you wanted to focus on the lack of fiber rather than the fat…but it seems like this article contracts those comments.

    Not to mention that any study done on mice fed unhealthy diets (and very likely not organic) that they would never eat in the wild doesn’t provide valuable information to humans! Are you really suggesting humans not eat palm oil because of this completely unrelated study?

    • Thanks for the comments. Good ones I might add. I don’t have a horse in this race. Just writing about the published work – which is all over the place as you know. And I don’t cherry pick what I write about – other than focusing on studies that deal with microbes. But, again, as you know, more to the story than just microbes. But an emerging theme is that elevated fat in the diet (whatever the source), increases the likelihood that endotoxins will make their way into serum which can contribute to an inflammatory state. But importantly, this is “exactly” what is supposed to happen. The inflammation more than likely is a an evolutionary-conserved strategy to trigger insulin resistance to conserve glucose. Gotta remember, when our ancestors consumed meat and thus fat (from organs etc) carbs and thus glucose in the diet dropped. Either for hours, days, or months. In order to conserve glucose – which is a primary fuel for brain and reproduction – insulin resistance brought on via low-grade inflammation is a survival strategy that was positively selected. However, today, we have a steady supply of fat – on a daily basis. This “constant” daily availability is out of sink with our evolutionary reality. Meat and fat were important, but were not necessarily a daily or even weekly input. keep the questions coming. I think just chatting about it is important. I’m not an expert on the subject, nor is anyone else.

      • What I find most interesting is that the palm oil was refined, which removed the potent antioxidants (primarily vitamin E and beta carotenes) Who knows how the results would have differed had the whole oil been used. Additionally (and others have pointed this out), mice are not humans. They do not eat fatty diets in the wild. How those results can be extrapolated as meaningful to humans is beyond me. But a randomized, controlled feeding trial of humans is expensive and difficult to execute so in the mean time we are stuck with this nonsense.

        • Oops I meant carotenoids not beta carotenes.

        • Thanks for the comments. Though I don’t know for sure, I don’t think the refining had an impact on the fatty acid composition – which was the issue. And yes, mice are not humans. But do not dismiss it because of that. The mechanisms that are being assessed are the same. As for being nonsense, ppl can take away from the published research what they like – its there for anyone to read.

      • Great reply, Jeff. I really liked this response and it was thought provoking. I think there is something to be said for how constant any diet is and how that compares to evolutionary principles. But the next question is how to get around it or whether it is advantageous to deliberately created abundances and shortages of certain macronutrients, vitamins and mindrals and shake things up from time to time? I don’t really have a strong opinion on it either, but it is interesting to ponder.

        • That’s a great question. Don’t know. And yes, interesting to ponder. Better to absorb this kind of info rather than filter. Thanks for great comments.

      • You may not cherry-pick, but that in itself is a form of selection — for example, just about any study funded or promoted by the sugar industry should be discounted. They’ve been trying to blame insulin problems on fats for ages, when even small doses of sugars can cause all the measures of heart risk (from triglycerides to HDL/LDL ratio) to shoot into the red, and they’re trying to obscure that. Another few decades and our misunderstanding of healthy fats versus sugars and starches will look like the disinformation cloud surrounding smoking in the 1950s…

  4. Jeff wrote:

    “However, today, we have a steady supply of fat – on a daily basis. This ‘constant’ daily availability is out of sink with our evolutionary reality. Meat and fat were important, but were not necessarily a daily or even weekly input.”

    But I don’t think that is true, at least not across the board. Certainly some traditional eaters had access to meat/animal foods on a daily basis, and had enviable good health.

    It’s just too bad that so many studies lump “fats” all together, rather than differentiating between them. That’s like saying: eating carbs from kale is the same as a twinkie is same as a potato, which we generally agree is not true–or at the very least, that such reductionist “science” doesn’t provide much useful information. If anyone is going to _become_ an expert on human/microbe metabolism etc., it seems useful to cherry pick the most scientific science to reference…

    Just saying. :)

    • Good points. However, dietary fat and animal protein throughout human evolution was sporadic and seasonal. I’m talking about seal hunters in the northern latitudes, I’m talking about those parts of the world where humans and our immediate predecessors spent much of their time developing. It’s important to note that access does equal intake. For example, the Hadza in Tanzania today will focus on honey during the peak of the rainy season – which is also the time of year when game is the most dispersed and harder to acquire. Honey doesn’t run very fast. So, during this period honey dominates the diet and meat (and ipso facto fat from organs etc) drops off significantly. It’s simply not a priority. However, during the dry season when game aggregates around ever shrinking water holes, ambush hunting goes up and thus animal fat and protein go up as well. Fatty nuts are seasonal as well. Just saying :)

  5. This looks like poor science to me. I’m not impressed with how impressed you are with this study. You note the objections pointed out (mice, eating crap food that’s not their natural diet, extrapolating this to humans) but don’t seem to take any of it in. If the fat choices are milk fat, rapeseed oil or sunflower oil, that doesn’t tell me a thing about my diet, which includes liberal use of pastured butter, pastured lard (rendered by me), extra-virgin olive oil (eaten raw, not cooked), coconut oil, among other things like ample vegetables, some fruits and nuts, and moderate meat and egg intake, no grains (which makes it fairly anti-inflammatory). Rapeseed oil? Is that meant to be canola oil, or is this normal high-erucic acid rapeseed? Sunflower oil, isn’t that high in Omega 6 fatty acids? It is no doubt processed under heat, light and pressure, which are all damaging. I haven’t eating palm oil in years, myself, because I don’t like the taste.

    This is just not believable according to everything I have read about dietary fats and healthy gut flora from a variety of reputable sources.

    As to sustainability, if that’s the issue, that alone is good reason to forgo palm oil, but I’m not convinced that all of it is farmed unsustainably.

    • Eaten, haven’t eaten palm oil in years, gah!

    • Hi Jeanmarie. The published research is available for anyone to read and interpret. If you are interested in the subject, I would recommend doing a PubMed search for the terms, “endotoxins, LPS, endotoxemia”. The facts/studies – whether in mice or human studies – are simple: 1) increasing fat in diet increases endotoxin producing bacteria in the gut; 2) endotoxins translocate into serum via several mechanisms such lipoprotein particles like chylomicrons; 3) increased endotoxin load in serum is associated with low-grade inflammation and 4) this inflammation is exacerbated in subjects with existed and higher levels of adipose tissue. It’s also important to point out that increased endotoxin load in the gut does not mean you will have higher levels in serum. However, the composition of your gut microbiota does coorelate with serum loads of endotoxin. People can decide to like the research or not. It’s there for anyone to read.

      • Hi Jeff,

        You wrote: “The facts/studies – whether in mice or human studies – are simple: 1) increasing fat in diet increases endotoxin producing bacteria in the gut; 2) endotoxins translocate into serum via several mechanisms such lipoprotein particles like chylomicrons; 3) increased endotoxin load in serum is associated with low-grade inflammation and 4) this inflammation is exacerbated in subjects with existed and higher levels of adipose tissue.”

        Here’s the thing: your point #1 (upon which your other points are based) _is_ an extrapolation from evidence that is inconclusive. That is: “increasing fat in diet” is NOT what the studies you reference were actually studying. They were looking at the effects of increasing certain TYPES of fat, but they did not, in general, study “fat” in its unrefined, unprocessed state, and they also didn’t acknowledge that they WERE studying a sub-group of (processed, refined, primarily vegetable-source) lipid types at all.

        So, I think it’s a bad idea to extrapolate in this case from studies that feed refined vegetable/dairy fats (or even studies that look at so-called “good” fats in addition to these in combination), and conclude that increased “fat” intake causes inflammation. That is so similar to the line we were fed for years, about how saturated fats (“including trans fats”) were terrible. Now it turns out that human-produced trans fats are probably worse than we ever thought, while saturated fats–possibly simply because they were studied _in combination_ with trans–may have been unfairly vilified.

        So what I’m really saying is: it seems tempting to read fascinating studies like the one you quoted, and come up with gripping headlines concerning what we should and shouldn’t eat. But I guess I’d encourage conservatism with the extrapolations, and ask for more focus on the questions. (I appreciate how folks like Gary Taubes are trying to understand how future studies can be conducted more effectively so that we don’t spend decades trying to make sense of study results based upon meaningless groupings of foods such as “those containing saturated and trans fats”.)

        By the way, I definitely agree with your point that seasonal availability must have played a key role in human food consumption/metabolism in the past. I’m thinking that I’ll go sit in front of our picture window and watch the snow fall while I eat some organic imported coconut. :)

        • Thanks for your comments. However, the role of fat and other substrates on microbial composition is not inconclusive as you state. There is a considerable amount of research on this. Patrice Cani did some of the initial work, which triggered a great many other studies. A simple PubMed search on the subject will provide plenty to read on the subject. For some reason, people assume I’m a vegetarian or some kind of anti-fat crusader. Which is bizarre as I pretty much follow a Paleo/Primal diet and consume – by many standards – a high fat diet. There is no need to be conservative as you indicate. It’s very simple: fat in diet is linked to endotoxin translocation from the gut into serum (dozens and dozens of published research indicates this). It’s not a theory nor is it debated among researchers. What debate there is, revolves around the various mechanisms at play. Either way, good points and thanks for the spirited exchange. This is how we both learn.

          • Hi Jeff,

            You wrote:

            “…However, the role of fat and other substrates on microbial composition is not inconclusive as you state. There is a considerable amount of research on this. Patrice Cani did some of the initial work, which triggered a great many other studies. A simple PubMed search on the subject will provide plenty to read on the subject.”

            Okay, I think I get what you’re saying. (I still think it was a mistake for you to use this particular (with its flawed methodology) study to illustrate your point–but I already noted that in my previous comments.)

            So now the question is, as you ask: what benefit does this apparently increased-low-grade-inflammation-when-consuming-a-high-fat-diet confer to an eater? And, if part of the benefit in bygone times was, as you posit, increased sensitivity to glucose during periods when carbs were scarce…what does that mean for us?

            It’s interesting to ponder whether a primarily-high-fat diet would be actually more damaging if lots of carbs were ALSO consumed…and whether the low grade inflammation in that fatty diet would be pretty much beneficial UNTIL the carbs came on the scene.

            I wonder what this means those of us whose dietary pendulums have swung from low-fat-high-carb to high-fat-low-carb and then over to high-fat-high-carb…

            Regards,
            Sarabeth

          • Thanks. However, not sure how you think the palm oil study was flawed? But, you can agree to not like or think the study was flawed. Again, I have no horse in this race. Just think the mechanisms associated with the role of endotoxins and microbiota in low-grade inflammation is an interesting subject and worth following – as I do. Some see this as an attack on fat – which is beyond me. As type this as I chomp down slices of bacon this morning, topped with scrambled eggs and olive oil, with a fat-rich avocado on the side. As for your second point, I think the greatest misconception about paleo/primal diet as it pertains to fat, is the incorrect assumption that our genome (and metagenome) was selected on a daily consumption of fat that hovered between 30-70% of calories. In othe words, that it was somehow a constant. This ignores basic ecology and seasonality. And, it does zero good to drag into the conservation those more recent populations in northern latitudes. We need to stay focused on those mid latitudes and the organisms that inhabited over the last 5-7M years.

  6. Wait, did I just read about a RODENT study on the HUMAN food project? Aren’t we aware by now that one animal’s medicine is another animal’s poison? That we can’t generalize the effects on one animal to the potential effects on another? It would be like koala’s running a study on eucalyptus leaves on humans and then announcing that eucalyptus is toxic to koalas. Ridiculous. Where do little mice even get fat in their natural diet? Not really very much to be found, is there? Come on you guys, you can do better.

    • wow. i don’t know how to even respond to that comment. or where to begin. so i will let it sit!

  7. Hi Jeff- Great article and very interesting. Where can I find more info on this subject? I tried a google search and all the big name food guru’s are all promoting palm oil as a great anti-inflammatory supplement. I’m with you though. If you look at humans as an evolutionary animal, I can’t imagine us in the old days that taking the time to squeeze the oil out of olives or palm.

    • check out the link to the original peer-review articled – linked in post.

  8. how tacky that you wouldn’t be man enough to post my comment correcting your word.. You should have answered, wow, thx, Val, for that correction.. That would have said a lot about you. tsk tsk

    • Hi Val. Not sure what comment you are talking about. This is the only comment from a “Val” that I see. In the future, keep the comments civil. No need to be nasty.

  9. Hi Jeff,

    interesting article, and responses. I follow a few specific people who talk about high fat diets. Everyone I’ve read says that saturated fats are good, and polyunsaturated fats lead to massive inflammation. The pufa’s cause inflammation either because they got damaged via heat processing and will cause a big free radical cascade when consumed, or because they add to the bad omega 3 to omega 6 ratio which should be 1:6, not 1:20. Sometimes the author even includes a summary of the chemistry behind the reactions.

    So to read that palm oil, which “Practical Paleo” lists at 54% saturated and 42% monounsaturated, may be causing inflammation on the same level as the evil vegetable oils surprises me. It seems that some readers are contending that butter and tallow are better because grass fed cows produce better stuff. And I’ve read information along the same lines. But I thought that was because grass fed butter has more butyric acid and no antibiotics, which isn’t the same as the structural argument.

    Does this mean that I need to care about how the palm tree was grown? Could it be that in an area willing to do awful things to orangutans, the soil is full of something like pesticides, and this causes inflammation?

    I read a blog article by a phD who tore apart that French gmo study, saying the mice were given water out of BPA leaching plastic bottles. And the plastic alone would have given the mice all those tumors. I am totally not capable of digging into a study in that way–probably not in any way, really.

    I read one of your previous articles about eating more starches. It went against everything I thought I’d read. But I’ve been mulling things over and reading more. I tend to pay more attention to information geared at people with chronic health problems. And the groups and doctors talking to those populations are saying high fat and high protein–for healing. It doesn’t sound like most paleo/primal/Weston Price people who haven’t had chronic health problems eat 70% fat diets. And I look like the Kitavan people I found on google. So I probably need to do better at feeding bacteria that produce fat from vegetable starches in addition to considering how to deal with health problems. At the very least, I’ll stop worrying about hitting that 70% fat marker.

  10. The trouble with Paleo diets is that our knowledge of what Paleo people ate is limited, but we know enough to prove that they don’t reflect what we probably did eat back then, and besides, we’ve evolved since–as have the foods we eat, with human intervention. In other words, Paleo diets as practiced have been debunked:

    http://www.salon.com/2013/03/10/paleofantasy_stone_age_delusions/

    http://www.youtube.com/user/PrimitiveNutrition