Marks Daily Apple
Serving up health and fitness insights (daily, of course) with a side of irreverence.
24 Aug

Does a High-Fat Diet Cause Type 2 Diabetes?

This is a special guest post from Denise Minger (thank you, Denise!). When fear-inducing news headlines hit the papers (and airwaves and iPads…) –  High-Fat Diet Linked to Breast Cancer, Eating Whole Grains Will Help You Live Longer, Fish Oil Linked to Prostate Cancer – she’s the person to go to for an honest and entertaining critique of the research. In the last week I’ve received an untold number of emails from inquiring Mark’s Daily Apple readers about this latest health news “bombshell”. So, naturally, Denise…

It’s that time again. Your inbox is filling up with emails from your low-fat friends. Your mom left four voicemails ordering you to throw away your bacon now (and clean your room while you’re at it). Your diet-savvy coworker left a Yahoo! News article on your desk, weighted in place with a muffin. This just in: High-fat diets cause diabetes—and researchers have proof, doggonit!

At least, that’s what you’d assume from reading headlines like “How Fatty Food Triggers Diabetes” and “Study Reveals How High-Fat Diet Causes Type-2 Diabetes.” It might come as a surprise, then, that this study isn’t really about food at all – it’s about the effect of obesity on gene expression. In mice, no less. This is a classic example of the media spinning an article to help it grab attention, because most people wouldn’t give a flying Fudgsicle if they knew what it was really about.

If you haven’t browsed it already, you can check out the study’s abstract here, officially titled “Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport.” (The full text is securely tucked behind a $32 pay-wall.) Between the jargony bits and focus on mice, it might be tempting to slide this study into the Slush Pile of Unworthiness – but it’s actually pretty interesting. Here’s the lowdown.

The Gist

Basically, the researchers fed a bunch of mice a high-fat diet designed to make them obese, which consequently raised the levels of free fatty acids (FFAs) in their blood. Although we’ve known for a while that FFAs interfere with glucose metabolism, this study uncovered a new piece of the obesity-diabetes puzzle.

In order to gauge your blood sugar and decide how much insulin to secrete, the beta cells in your pancreas have little glucose-sensors hanging out on their surface. Those sensors are maintained by an enzyme called GnT-4a glycosyltransferase (can we call it George for short?). As this study discovered, high levels of FFAs interfere with two of the proteins necessary for producing GnT-4a (er, George), leaving beta cells unable to figure out how much glucose is in your blood. When that happens, those cells can’t release the right amount of insulin to keep your blood sugar in check. Wham, bam, diabetes.

That’s how it works in mice, at least. To clarify the pathway in non-mice, the researchers grabbed some cell samples from humans and cultured them with palmitic acid, a fat sometimes used to simulate the effect of free fatty acids. Lo and behold, the fat interfered with the same two proteins that got goofed up in obese, FFA-ridden mice.

So what does this mean for you and me? Are high-fat diets going to make us obese, fill our blood with free fatty acids, and push us to the brink of diabetes? Should you listen to your mother and feed the bacon to the trashcan?

Mouse Tales

Before we talk diet, let’s talk rodents. In this study, researchers used a popular, inbred mouse strain affectionately referred to as C57BL/6J. Despite their cuteness, the only one who can get away with that kind of name is R2-D2, so let’s use some lab slang and call these mice “black sixes.”

Black-six mice are beloved among researchers, and for good reason. Along with being easy to breed, they’re uber-susceptible to obesity, high blood sugar, insulin resistance, leptin resistance, and all that other fun stuff plaguing modern humans. They’re also genetically predisposed to getting type 2 diabetes, making them particularly useful for the study at hand. And perhaps most importantly, all it takes to send them into a downward spiral of disease is some extra dietary fat. It’s like their kryptonite. Which brings us to…

The Diet of Doom

Although this paper doesn’t give us a detailed description of what the mice were eating, it does reference the product numbers for their formula diets – so we can sleuth out the scoop straight from the manufacturer. Here’s a PDF of what the high-fat diet contained.

Ouch! Where to start?

It’s hard to say which part of this diet sucks the most. The 175 grams of pure sugar? The splash of high omega-6 soybean oil? The suspiciously disease-promoting casein? The main calorie source as hydrogenated coconut oil? The fact that a quarter of the “high fat” diet consists of refined carbohydrates? The complete absence of anything resembling food?

Indeed, even if you believe high-fat diets can be healthy, it’s hard to find any redeeming qualities in this one. For starters, the primary fat is a hydrogenated oil, which doesn’t belong in the body of any living organism, whether two-legged or four. As far as obesity goes, rodents have dramatically different responses to the types of fat they eat—with rats, for instance, getting tubby from lard but slimming down with marine oils. And hydrogenation aside, some mice strains gain different amounts of weight when their high-fat diet consists of unsaturated fats rather than saturated fat. So can we extrapolate the effects of this diet to high-fat diets in general? No way. Not for mice, and certainly not for humans.

And let’s remember that we’re dealing with a particularly fat-sensitive creature here. Although most mice turn into metabolically deranged messes when they eat too much fat (which makes sense, considering their natural diet is mostly grains), not all of them succumb to the same fate. Black sixes are one of the unlucky types that get rapidly obese on high-fat diets, but some other strains remain lean on the same cuisine and are far more resistant to diabetes.

When “High Fat” Isn’t High Fat

This brings us to a major problem with rodent studies in general. As this paper explains, there’s literally no standard for what “high fat” means, and rodent researchers have thrown everything from 20%-fat diets to 60%-fat diets under the same “high fat” umbrella. Usually those diets contain a hefty portion of sugar, too. Not only does this make the rodent literature hard to navigate, but it also gives an incomplete picture of the effect of diet on obesity – because something special happens when mice get a truly high-fat menu.

Case in point: this study on ketogenic diets in rodents. As we might expect, researchers found that mice eating a moderately high-fat diet became obese, leptin resistant, and insulin resistant – but when they dropped the sugar and increased fat to around 78% of calories, the mice “lost all excess body weight, improved glucose tolerance, and increased energy expenditure” without even reducing calorie intake. In other words, a high-fat diet undid the damage of a moderately high-fat diet.

Lessons For Non-Rodents

So what can we learn from all this? Does this study – or rodent research in general – have much relevance for those of us who lack tails, fuzzy ears, and adorable pink noses?

The answer is an equivocal “yes and no.” One reason mice are a favored lab animal is that they share so many genes with humans – 15,187 of them, to be exact. Heck, it was only 90 million years ago that we split from a common ancestor. I’ve met Okinawans older than that!

But that doesn’t mean gene expression always works the same, or that the causes and progression of disease are identical across species. Even when high-fat diets catapult mice towards diabetes, for instance, their markers for disease don’t always resemble ours. Unlike metabolically damaged humans, who tend to have rock-bottom HDL cholesterol and rising triglycerides, some mice experience higher HDL and unchanged (or reduced!) triglycerides when eating the diets that make them diseased (PDF). This points to some clear differences between how humans and mice experience diet-induced metabolic problems.

And that includes the diabetes pathway in this study. We have enough high-fat, low-carb research at this point to know that such a diet won’t cause an unstoppable snowball towards obesity in humans like it does in some mice. If anything, its impact on diabetes is beneficial. So even if weight gain (and the associated increase in free fatty acids) sets us down Diabetes Avenue, a high-fat diet isn’t necessarily the instigator in humans. Especially not a high-fat diet that’s based on real food instead of hydrogenated coconut oil.

Bottom line: Mice are actually useful little suckers when it comes to studying genes and biochemical processes – but only when we clearly understand the limitations. Disney-themed costume parties aside, you are not, and never will be, a mouse. Nor will a mouse ever be you. So when it comes to studies like this one, white out the headline, read with an open but critical mind, and then invite Mother Dearest over for a bacon brunch.

You want comments? We got comments:

Imagine you’re George Clooney. Take a moment to admire your grooming and wit. Okay, now imagine someone walks up to you and asks, “What’s your name?” You say, “I’m George Clooney.” Or maybe you say, “I’m the Clooninator!” You don’t say “I’m George of George Clooney Sells Movies Blog” and you certainly don’t say, “I’m Clooney Weight Loss Plan”. So while spam is technically meat, it ain’t anywhere near Primal. Please nickname yourself something your friends would call you.

  1. Great analysis of the science of the article. I also find it interesting that they don’t give the exact composition of the diet even though it’s an article about the _effects_ of diet. Kinda vital piece of information, there…

    But I’m also commenting because a couple of the lines in here made me laugh hard:
    “weighted in place with a muffin.”
    “I’ve met Okinawans older than that!”

    Jen wrote on August 24th, 2011
  2. Denise, you are the bomb. You are invaluable. But there is something you wrote that just makes me crazy, because so many people follow this line of thinking:

    This is a classic example of the media spinning an article to help it grab attention, because most people wouldn’t give a flying Fudgsicle if they knew what it was really about.

    This is where so many people simply write off the media as simply “trying to be sensationalistic” and “grab headlines to get ratings/sell copy.”


    Our corporate owned media tells we the sheeple precisely what their corporate sponsors want them to tell us.

    Journalists go to journalism school, where the only thing they learn about “science” is that scientists are the authority that must not be questioned. At best, these self-important buffoons read an abstract or conclusion of a study that often misleads or downright lies about what the study actually proved (as you’re so adept at dissecting and explaining to we laymen), and than write their own sensationalistic headlines or cover stories with the belief that it’s been “proven” by the holy priesthood of SCIENCE.

    This deliberate deception is done on purpose. We live in a society for which a certain segment purposely misleads and confuses the masses to deliberately create sick people. They profit off the “food” they create that makes everyone sick, than the sick people go to the medical industrial complex for treatments that mostly don’t cure, but simply “manage” the symptoms, all at tremendous profit.

    And yet, whenever anyone tries to point out that the status quo is something done ON PURPOSE, most people simply shrug off “conspiracy theory” as crazy talk only loonies ever contemplate.

    Keoni Galt wrote on August 24th, 2011
  3. Awesome! and Necessary! Thanks Mark and thanks Denise for all your work.

    Damn the money-and-fame-hungry researchers and damn the stupid media, who just takes the press releases and prints them without question, while most people still take the published word as gospel. Damn them all to hell!

    By the way, can Denise look into the study published recently – something to the effect that being fat is okay as long as you are, um, healthy!?

    That one was heavily debated on the forum, but all regular readers of MDA should know better than to conveniently pick-and-choose which study they believe at face value and which they do not.

    HillsideGina wrote on August 24th, 2011
  4. I sure do love reading Denise’s posts. When the world begins to understand that there are differences between fats, the health news will be less dumb.

    A quick refutation of the notion that high-fat (I call them High-fat mouse-murder diets) diets cause insulin resistance in rodents is to point out the delicate balance between omega-3 and omega-6 fats that tends to determine how animals react to inflammation, which strongly influences insulin sensitivity. Too little omega 3 in the cells causes excessive inflammation and too much omega-6 or too little omega-3 causes that deficiency. Excessive inflammation is a strong contributor to insulin resistance.

    When you give them some omega-3 they do not become insulin-resistant Most of these high-fat mouse-murder diets don’t even supply omega-3, and they supply too much omega-6 to even have a good omega-3 index with some omega-3 in the diet. This is beyond proven in the scientific literature and it would behoove health journalists to understand it. (the discussion is well-referenced and explains)

    Stabby wrote on August 24th, 2011
  5. Hi Denise,

    Great analysis. Here’s a little additional background on inbred mice:

    I used to run a breeding colony of C57Bl/6y — an inbred strain derived from the C57Bl/6j — the “J” means that the animal is derived from the Jackson Labs breeding stock. Black-sixes (we called them that, too) are an old inbred strain. Probably around since the 50s or 60s (I don’t have my reference library here, or I’d check exactly when they were officially inbred.) It takes 20 generations of brotherxsister matings to achieve official inbred status. Most strains die off prior to that from fatal gene expression. Black-sixes are pretty hardy, breed fairly well and are mostly fat. And with a conservative 4 generations of animals per year, they are now probably over 200 generation of brotherxsister inbreeding!

    They weren’t developed for diabetes research — they just turned out that way. Inbred strains are used in research because all animals in the strain are basically identical (give or take and X or Y chromosome.) It is useful, as it eliminates genetic variation influences on the experimental outcome. But is it natural? No. Not at all.

    Black- sixes are fat mice (not all inbred strains are fat.) They also tend to be surly. Their normal lab diet is Purina Mouse Chow, or something similar. Chow is a pressed, extruded cube that the mice can gnaw on. They don’t eat normally for mice, haven’t ever eaten normally for mice. No inbred mouse eats normally compared to a wild mouse. (BTW — they are inbred from the european house mouse, mus musculus — no real relation to the field mice you see in the US.)

    Inbred mice, and studies on them, can be very useful. But extreme caution must be exercised when comparing any study using these “highly processed” animals that compares them to humans (or dogs, or whatever.)

    I will also add that research animals are treated very humanely today. They are kept in clean cages, fed a reasonable diet (probably comparable to the typical SAD diet.) Even mice are given enrichment — toys to play with, bits of wood to gnaw, nesting materials, etc. The people who work directly with the animals in the animal care industry today are some of the most caring and careful individuals I know.

    That said — it is an industry. It is big business. It is closely allied with agribusiness (ConAgra springs to mind!). Like milk cows and standard, corn-fed beef, they suffer from living far from their natural habitat and diet. For inbred mice, it is a very far distance indeed.

    A final comment on the High-fat diet they were fed. AWFUL! And the fact that the actual content of the diet was not included in the research article (only a reference to be tracked down) is appalling.

    But as we Primal-types know, we are what we eat.

    Diane wrote on August 24th, 2011
  6. Its worth noting also that the palmitic acid they used to reduce insulin secretion in human cells is the same fatty acid manufactured by the liver (de novo lipogenesis) from excess carbohydrate. Eat too much carbohydrate, especially refined and you increase palmitic acid, which could affect GnT-4a (George).

    David Fisher wrote on August 24th, 2011
  7. “Your diet-savvy coworker left a Yahoo! News article on your desk, weighted in place with a muffin.”

    LOL! Love the quality of yahoo news articles…

    Jon wrote on August 24th, 2011
    • If on faceplant/down, it wouldv’e been some type of cheese sandwich . .. ;0

      Lucy wrote on August 24th, 2011
  8. Can we also point out that mice are primarily carb-ivores – they are BUILT to eat grains. So really, why should it surprise us if/when their wee bodies freak out when given what would be just dandy for a human?

    Sure we share many genes with them but not our dietary ones. Humans = fat good/grains bad. Mice = grains good/fat bad.

    Danielle Meitiv wrote on August 24th, 2011
    • This reminds me of the cholesterol myth. Those tests were done on rabbits by some russian guy. On rabbits!!!
      Uh, aren’t those herbivores…

      Arty wrote on August 24th, 2011
  9. Excellent work Denise, as usual.

    I loved seeing Robb Wolf and Denise Minger back to back. Who’s up tomorrow to complete Murderers Row?

    BW wrote on August 24th, 2011
    • Peter @ HyperLipid ?

      He was my first .. 😉

      Lucy wrote on August 24th, 2011
  10. The media is full of crap, plain and simple. I wouldn’t trust the media for dietary advice anymore than I would trust them for financial advice.

    Chris Johnson wrote on August 24th, 2011
  11. If it isn’t about mice, then it’s about cats:

    I am a diabetic, type 1 (so I didn’t eat my way into diabetes!) and I use the PB lifestyle to maintain a near normal A1C value.

    My endocrinologists say it’s only a matter of time before my honeymoon is done, but with the PB lifestyle, I hope to extend it for as long as I can.

    Jason Sandeman wrote on August 24th, 2011
  12. I watched Dr Oz on Oprha yesterday ,with interest being a Type ! diabetic for 11 years-the whole program was about diabetes- my jaw hung agape for the whole hour as we were fed the usual diabetic healthy diet ??????
    I have been Primal for 2 yrs now and for the last 10 days been totally insulin free I do not require even a basel rate on my pump …I can only guess that the 2yrs on Primal has recovered my pancreas enough to drop that rate..I know I am not cured as ANY carb /sugar I would have to take insulin… but being pump free is enough incentive !!!
    Cant wait to see my next bloods- I have decided not to tell my Dr by the way- for reasons I dont have to explain- I just want to watch his face with my HB1C results in…lol

    Sue wrote on August 24th, 2011
    • That is so awesome. Good for you! Our son is a type 1 diabetic and although he can’t ever be cured by a primal diet it sure has cut his insulin needs in half and brought his sugars much more in line.

      Tim wrote on August 25th, 2011
  13. After reading this critique, I went and found the article in question.

    Too me, using those fats does make sense. A. Despite their unhealthiness, many people in the west eat them. I assume much of the fats the human donors ate would have been junk fats as well (unfortunately the donors were cadavers so could not tell us their diets). B. there is greater consistency with the processed diet they used. Consistency is one of the mantras of science. Using natural unprocessed fats would be better in a follow-up study were the resulting variation could be better dealt with. After reading the article, I definitely agree with Denise over the type of fats used + other ingredients in the feed can affect the results. It would have only taken them 1 sentence to tell us what types of fats were used. Often researchers in other fields often reference techniques or ingredients, but all it would have taken them is one sentence!. I also hate when journal editors put the methods section at the back where people are less likely to find and read it! (I’m used to ecology and entomology articles where methods are rarely pushed to the end and you can easily review them PRIOR to reviewing the results)

    Rats may not be ideal, but it’s the best we have to work with due to the nature of the experiment. If I was doing this study, I would have chosen the rats who are more suseptable to diabetes too, as I would be assured results. If I couldn’t get rats to have diabetes, I couldn’t see the pathway that was causing it; I could see what genes, their alleles, and their expression were part of the problem. Then you can compare them to less suseptable mice; if you attempt to indice diabetes in them by the same method, both results, diabetes or not, would tell you something about diabetes in “average” rats. I would do the same with humans if I ethially could. However, Denise hits it on the mark when she talks about the dietary sources of diabetes in rats and humans; differences between our natural diets is likely were the trouble in using rats lies. Is there an animal that is more dietary relevant to us that can be practically researched? (exclusing humans ourselves; leave us for clinical experimentation!)

    I think that most of the problem here with this study is how the media picked it up, because after reading it, I agree with Denise that this is about gene pathways. I am a little upset by some of the general comments against processes in science as I am in that line of work. I’ve been a part of the review process, and I think it’s all about the journals you submit your to. Most scientists do think and care about their work. In the context of this study, i think this article was fine. Now it’s time to watch for the follow-up work to see if they (or others) differentiate between the kinds of fats in the high fat diets.

    Despite some of my disagreements, I due enjoy reading Denise’s critiques as it is nice to see someone who is comfortable with stats and analysis.

    Erin wrote on August 24th, 2011
    • bravo!

      scott wrote on August 28th, 2011
  14. Great article. I was type 2 for 11 years. On 4/15/2011 weighing 250 lbs and 5′ 10″, bf=34% a1c came back 7.8(very diabetic). Was on ActosPlus and doctor came back and said next time I see you we will add another pill. I stared looking and thank the gods found MDA. Following Mark, I did an a1c self-test and on 8-20-2011 it was 5.7(non-diabetic) weight 210 lbs and the way to 170. Thanks Mark, I will keep eating fat and eggs and can’t wait to see doctor next week.

    Richard wrote on August 24th, 2011
  15. Awesome article, and I don’t think I’ve ever read a takedown of a scientific study that was so fun to read.

    Kris wrote on August 24th, 2011
  16. Great article.

    I don’t believe any of the big-news health headlines, ever. It’s almost always a case of “garbage in, garbage out.”

    DFH wrote on August 24th, 2011
  17. It’s so incredibly fantastic having people like Denise who can look at these studies with a critical eye. I’ve decided it’s best to ignore detractors who try to PubMed you to death with these types of bunk science experiments. I don’t all out ignore the data, I just use my own data – blood tests, blood glucose readings, my weight, body fat measurements and athletic PRs – to confirm my diet is healthier than the SAD. Perfect acronym really.

    Dave wrote on August 24th, 2011
  18. For anyone interested in reading the full text of the journal article, I’ve got it up in Google docs and linked to it in this post on this study:

    If you’re eating a SAD, fatTENING, diet, this paper elucidates yet another mechanism by which the excess circulating free fatty acids (NEFA) associated with excess fat and adipose IR contributes to beta cell dysfunction.

    Evelyn wrote on August 24th, 2011
  19. Well, they could repeat the study using [i]actual food[/i] if they are so sure they are right. Which they won’t. Because they know they are wrong, but are being funded to say otherwise. This research = corruption, and the media has only made it worse by misinterpreting it.

    knifegill wrote on August 24th, 2011
  20. What happens to a mouse when it goes paleo?

    Erik wrote on August 24th, 2011
    • huevos grande?

      PrimalGrandma wrote on August 24th, 2011
  21. This is going to help many many people out there. And this crap is coming from Nature…

    Still I don’t ump on any bandwagons. If people can help people with low fat diets cure diabetes, we can’t adopt this mob mentality. Not all diabetics do well on high-fat, some do very well on low fat high starch

    Avishek Saha wrote on August 24th, 2011
    • Death doesn’t count, I’m afraid . .. sry

      Lucy wrote on August 24th, 2011
  22. So basically . . . researchers just proved how awful the everyday American diet of hydrogenated oils and high sugar foods is. You WILL develop diabetes if you eat this diet. Thanks a lot for the new info researchers. I think the study backfired if you read between the lines.

    Josh wrote on August 24th, 2011
  23. My cat was just diagnosed with type II diabetes. I want to get him off insulin as quickly as possible so I did a little internet research and guess what?? A high protein, low carbohydrate diet (the opposite of what most cat foods are–even the expensive “science” brands) is what has been proven to cure diabetes in cats!!

    Tammy Spanley wrote on August 24th, 2011
    • My old cat, had MAJOR colon problems, poor thing! An old vet told me to NEVER feed anything in a bag, NEVER.

      He said that although the canned wasn’t the best, it was preferred to get an animal to health.. he did as he said, and she lived many more years! Now I can take care of myself, as well as a cat or canine.

      Lucy wrote on August 24th, 2011
  24. If you are looking for real world research in actual humans then check out some of the research being done by Dr David Jenkins and colleagues in Canada (University of Toronto). They have published a load of studies looking at the effects of increasing levels of monounsaturated fats in the diet. I will just mention 3
    1. Published in CMAJ 2010 showed a diet with increased MUFA actually decreased LDL, triglycerides, ApoB and CRP
    2. Published in JAMA 2011 assessed a low saturated fat diet against a diet with increased amounts of plant sterols, soy protein, nuts and viscous fibres and showed that the diet higher in fats actually reduced LDL
    3. In Diabetes Care 2011 they replaced a muffin with two ounces of nuts daily and showed improved glycemic control and serum lipids (LDL) and this is specifically in diabetics!!

    Now I don’t agree with a lot of the food choices from some of their studies and they definitely aren’t primal (soy milk, sunflower oil etc) but they all point to the same thing, increasing fats in the diet in place of sugar improves health parameters.

    Brad wrote on August 24th, 2011
  25. Some of this stuff is heavily industry sponsored as well (take a look at the competing interests and funding sections) but some of the results would still appear valid.

    Brad wrote on August 24th, 2011
  26. Thank you Denise for this great review! I first saw this “high fat cause diabetes”-article in a swedish evening paper… I’m so tired of journalists with little to no knowledge about nutrition who throws these provoking headlines in the faces of their readers.

    Simon wrote on August 24th, 2011
  27. I LOVE the sensibility of this artcle…LOVE the “Black-six mice are beloved among researchers, and for good reason. Along with being easy to breed, they’re uber-susceptible to obesity, high blood sugar, insulin resistance, leptin resistance, and all that other fun stuff plaguing modern humans. They’re also genetically predisposed to getting type 2 diabetes, making them particularly useful for the study at hand. And perhaps most importantly, all it takes to send them into a downward spiral of disease is some extra dietary fat. It’s like their kryptonite.” kind of says it all…

    zwhocansee wrote on August 24th, 2011
    • I thought that perhaps our western diet is to attack TPTB/elites.
      Inbreed, surly, fatties, that control the industries of death by diet, may have backfired? hummm.

      Something about 170 dead Microbiologists, really. Health ‘scares’ be damned!

      Lucy wrote on August 25th, 2011
  28. Thank you for this fantastic article! You make the science in the studies digestible for the rest of us. Please do more..we need you..

    Marli wrote on August 25th, 2011
  29. Great article, great info! Thanks for a wonderful read :)

    Amy wrote on August 25th, 2011
  30. As a scientist myself, seeing how much legitimate science was behind the paleo lifestyle was what initially drew me to it. I have been on and off the band wagon for a while, currently on it… I have never felt better than when I am on it. I loved this article and the indepth criticism of the study. THAT is what pushes science forward. Hopefully sometime soon, those criticisms will reach the lab and someone will do a study on a truly paleo diet. Not me though… I’m a geologist.

    Jess wrote on August 25th, 2011
  31. Great article!

    One poster said this and I will elaborate: maltodextrin = a type of sugar that comes from corn = bad for us & diabetes promoting. Next time you are at a diner or cafe look at the little packets of Equal. They contain maltodextrin. Sneaky way to say it’s sugarless when biochemically it is not!

    Also, rats to my knowledge are herbivores not carnivores, so the amount of fat they would eat in their normal environment, compared for example to a wolf, would be only whatever came from certain seeds. So any research study that feeds them a diet not natural for them (on top of their being bred genetically predisposed to get disease) is really a crock of Fudgesicle.

    Grok on!

    PrimalAlex wrote on August 25th, 2011
  32. Except its proven in humans too. Do you guys ever tell the wholentruth? Dnise Minger? You guys are so wrongnyou should feel ashamed. I will never return, this is unredeemable

    martinella wrote on August 25th, 2011
    • Do tell – proven in humans where? What are you doing here in the first place?

      HillsideGina wrote on August 25th, 2011

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