Could that Low-Fat Diet Make You Even Fatter?

Could that low-fat diet make you EVEN FATTER, asks Mail Online. Sure it could:

Read the article for some references to recent Food Revolution events in Sweden, the grand experiment of Sam Feltham and some comments by an enlightened cardiologist and a less updated (sadly) dietitian.

Earlier about failed low-fat diets

340 Comments

Top Comments

  1. Bob
    It amuses me when people claim glucose is the preferred energy source of the body.

    Then why doesn't the body have ability to store unlimited supplies of glucose?

    No instead it takes excess glucose and converts it into fat for energy storage. And then it breaks down that fat when needed.

    I wonder: Would we be healthier if we went back to eating fruits and veggies only when they are in season, put on a little weight by fall, and then as the growing season ends switch over to eating exclusively animal products throughout the cold months, losing the excess weight by the time of the next growing season? A seasonal Yo-yo diet so to speak. Hmmm...

    Reply: #8
    Read more →
  2. Martin Levac
    I'm sorry, that's not a good read at all. It's not an experiment, it's an essay. It's not data, it's an opinion. It's not a scientific paper, it's a blog entry. It's not a genuine critique of anything, it's a shameless plug for Colpo's own books. That's the second shameless plug for books you've cited here. First Fumento, now Colpo. That's kind of strange. Do you have anything more serious?
    Read more →
1 2 3 4 5 6 7

All Comments

  1. grinch
    "but the problem (as I see it) IS in the fat-storage mechanism and not in simply how many calories we put in our mouths."

    Since experimentation on humans shows that overfeeding can lead to fat gain on any healthy person, it raises doubt that chronic obesity must be due to a defect in the fat-storage mechanism, but could plausibly be a defect in the regulation of calorie intake. My argument is that there is more evidence in support of this being a defect in regulation of intake over being a defect in fat-storage.

    Replies: #304, #305, #309, #314
  2. grinch
    If you believe that Sam's experiment is legit (which I believe you all do), then there is a massive metabolic advantage to ketogenic diets.
    Replies: #303, #310
  3. FrankG

    If you believe that Sam's experiment is legit (which I believe you all do), then there is a massive metabolic advantage to ketogenic diets.

    Explain your conclusion

  4. FrankG

    ...there is more evidence in support of this being a defect in regulation of intake over being a defect in fat-storage.

    Where? What evidence? What mechanism(s) "regulates intake'? And how does it (they) become defective?

  5. FrankG

    "...there is more evidence in support of this being a defect in regulation of intake over being a defect in fat-storage.

    And does this mean you accept that there IS evidence supporting the fat-defect hypothesis? How is that even possible with your world-view?

    In which case do you still think that MORE evidence is better than BETTER evidence? Somehow quantity makes up for quality -- here we go round in circles again.

    And what exactly do you mean by "evidence"? Do you mean "studies where the researchers reach conclusions that favour your hypothesis"? How well do these studies stand up to scrutiny? Because the studies you have referenced so far do not even stand up to the superficial scrutiny of a "non-scientist (at least according to SG) like myself. Do you have something new which you are holding back on us?

    It's one thing to claim the "weight of evidence", quite another to demonstrate it to a skeptical and free-thinking audience.

    Reply: #306
  6. FrankG

    ...do you still think that MORE evidence is better than BETTER evidence? Somehow quantity makes up for quality -- here we go round in circles again.
    ...

    Seriously, it is amazing that science makes any progress at all. An hypothesis which has been around longer has, as a matter of course, had more research conducted on it, therefor (by default apparently) has the "weight of evidence" and is the de facto theory.

    I for one am very glad that we do not live in a world like that. Instead we can have an Einstein working as a clerk in a Swiss patent office, who in his spare time, can come up with multiple paradigm changing ideas that blew the old theories out of the water.

    If you had your way the Earth would still be the centre of the Universe! Assuming we had even ventured outside our caves, that is :-P

  7. grinch
    "In which case do you still think that MORE evidence is better than BETTER evidence? Somehow quantity makes up for quality -- here we go round in circles again.

    And what exactly do you mean by "evidence"? Do you mean "studies where the researchers reach conclusions that favour your hypothesis"? How well do these studies stand up to scrutiny? Because the studies you have referenced so far do not even stand up to the superficial scrutiny of a "non-scientist (at least according to SG) like myself. Do you have something new which you are holding back on us?"

    Its funny that you keep bringing this up, because you've cited what a few free-living studies demonstrating that people can lose weight without counting calories by reducing their carbohydrate intake (which nobody is denying), and that is supposed to prove that obesity is a defect of fat metabolism, or that is supposed to prove that carboyhydrates are the primary cause?

    Replies: #308, #312
  8. FrankG

    ...there is more evidence in support of this being a defect in regulation of intake over being a defect in fat-storage.

    Where? What evidence? What mechanism(s) "regulates intake'? And how does it (they) become defective?

  9. Martin Levac

    "but the problem (as I see it) IS in the fat-storage mechanism and not in simply how many calories we put in our mouths."Since experimentation on humans shows that overfeeding can lead to fat gain on any healthy person, it raises doubt that chronic obesity must be due to a defect in the fat-storage mechanism, but could plausibly be a defect in the regulation of calorie intake. My argument is that there is more evidence in support of this being a defect in regulation of intake over being a defect in fat-storage.

    The validity of evidence has little to do with its quantity. We could even argue that when we finally have strong enough evidence to confirm or refute a hypothesis, then few new experiments will be done on it, if only to teach young scientists how to do proper science. This means if we confirm or refute a hypothesis by experiment early in its development, we will end up with little evidence, but just as valid. This is the case for example with the Bellevue all-meat trial, where the experiment and its results are quite reliable.

    I think it would be more appropriate if you said instead that the evidence in favor of CICO is stronger than the evidence in favor of the carbohydrate hypothesis. At least, that's how I would say it. But then, I wouldn't say that anyway because I disagree and instead I say that the evidence in favor of the carbohydrate hypothesis is stronger.

  10. Martin Levac

    If you believe that Sam's experiment is legit (which I believe you all do), then there is a massive metabolic advantage to ketogenic diets.

    I can't say whether Sam's experiment is legit or not. In fact, I doubt anybody can say that, except Sam himself. That's because only Sam knows all the facts. So we can only take his word for it. However, previous experiments have produced similar results, and so Sam's experiments can be considered likely. So, if Sam's experiments are likely, then so do ketogenic diets likely have a metabolic advantage. In order to confirm or refute this likelihood, we'd have to repeat Sam's experiments properly with multiple subjects and multiple observers.

  11. Martin Levac
    Here's an interesting potential effect of finally getting strong enough evidence.

    When we finally have strong enough evidence - because we've refined both our hypothesis and the experiments - we can then use this as a reference, i.e. it becomes reliable. This is very useful to test new research tools for example, as any variation in the results can be used to refine those tools, and subsequently obtain even more reliable results. All the while this is happening, we're repeating the same experiments many times over, such that we end up with a ton of evidence.

  12. FrankG

    Its funny that you keep bringing this up ... that is supposed to prove that [carbohydrates] are the primary cause?

    Easy enough to take carbohydrates right off the table. Simply list me "foods which people tend to consistently overeat" (in your FR way of thinking) but contain NO sugar or refined starches. I know how you bleat about carbs being necessary for palatability and somehow it is the added fat which really does the damage (all those calories or something) but until you can list these foods you can not legitimately dismiss the carbohydrate hypothesis.

    Meantime the food most commonly recognised as first on the list of those associated with obesity, by researchers from pretty much every school of thought (except those who represent the soft drinks industry) is soda... basically ALL sugar and refined starches, with NO added fat!

    Funny indeed...

  13. grinch
    You guys love to pay lip service to good scientific principles, but then you use free-living studies with confounders (uncontrolled calories, uncontrolled protein, uncontrolled palatability) as your so-called quality evidence that lowed carbs and hence lowered insulin is what causes the weight loss (or causes the reduction in calories resulting in weight loss, depending on where the goal posts are currently positioned).
    Replies: #316, #317
  14. Martin Levac

    Since experimentation on humans shows that overfeeding can lead to fat gain on any healthy person, it raises doubt that chronic obesity must be due to a defect in the fat-storage mechanism, but could plausibly be a defect in the regulation of calorie intake.

    I forgot to address your point above.

    The doubt that is raised is due to your argument that when obesity is created intentionally, then it is not a growth disorder. Now that I think about it, we could explain it another way. Instead of saying intentionally, we could say exogenously. This way, the difference is exogenous vs endogenous. Another way of saying that is environmental vs genetic.

    Having said that, does this suggest a difference in the mechanism through which obesity is created? I don't believe so. The cause could be different, but the mechanism must be the same. So, whether it's environmental or genetic for example, either cause must still act on the same hormones and enzymes that regulate fat tissue in order to create obesity. This is true with diabetes type 1 for example, where one lacks an essential element of this mechanism, i.e. insulin.

  15. FrankG
    It strikes me that FR ought o be easy enough to test. It has been shown that we can deceive our taste and perception of foods with various sensory tricks such as changing the colour of the food, or the lighting, plugging up the nose, or even playing sounds (crisps can be made be denied their crunch) when eating that do not match the food. In this way we could change the external perception of that food without altering its makeup

    Would a pukey-green, soggy pringle (as perceived) still keep you coming back for more... and if it did (or didn't) what if anything, would that say about FR vs. the Carbohydrate hypothesis?

    Easy enough that I wonder why such tests have not already been carried out?

  16. Martin Levac

    You guys love to pay lip service to good scientific principles, but then you use free-living studies with confounders (uncontrolled calories, uncontrolled protein, uncontrolled palatability) as your so-called quality evidence that lowed carbs and hence lowered insulin is what causes the weight loss (or causes the reduction in calories resulting in weight loss, depending on where the goal posts are currently positioned).

    Ah no, we don't move the goalposts in that particular fashion. The argument that since low-carb causes a spontaneous reduction of food intake, then it must be this reduction of food intake that causes weight loss, is used by opponents of the carbohydrate hypothesis, not its adherents.

  17. FrankG

    You guys love to pay lip service to good scientific principles, but then you use free-living studies with confounders (uncontrolled calories, uncontrolled protein, uncontrolled palatability) as your so-called quality evidence that lowed carbs and hence lowered insulin is what causes the weight loss (or causes the reduction in calories resulting in weight loss, depending on where the goal posts are currently positioned).

    Even if I had NO evidence at all, that still does not prove your position

    You don't win by default in science! LOL

    YOU are the one claiming the weight of evidence, not me... so where is it? Put up or shut up! as they say.

  18. grinch
    Frank,

    So no burden of proof lies with your position?

    Reply: #320
  19. Martin Levac
    Besides food, we can create obesity, or make somebody leaner, with other agents. On this web page, we find quite a few examples, with references: http://www.why-low-carb-diets-work.com/unexplained-weight-loss.html

    Assuming the evidence is reliable, then it suggests that when food creates obesity, it does so through the same mechanisms as those non-food agents.

  20. FrankG
    I have a credible hypothesis that successfully predicted not jut mine but the [significant] health improvements in many others with which I have conversed on this topic. I have basic biochemistry, well established: such as the functions of insulin. I have your inability to list any "foods which people tend to consistently overeat" (in your FR way of thinking) but contain NO sugar or refined starches.

    This is a recently emerged (re-emerged) hypothesis which as yet has not been sufficiently studied to have conclusive research -- do you think that means it must be wrong? Guilty before a trail even? Is that how your World works? This is what NuSI is all about... because apparently "real scientists" are too scared of losing their tenured positions to risk upsetting the food and drug manufacturers which support them.

    You, on the other hand have a vague, ill-defined (if even definable) hypothesis that as best I can determine was cooked, up by SG when he was put in his place by Gary Taubes. The key principle of which seems to be denying the role of insulin at all costs. As a result he and you flounder around, unsuccessfully trying to fit square pegs into round holes -- which is why you keep contradicting yourself with your incoherent babbling -- it's all about excess calories and not macros.. oh except protein blah blah blah ... I don't believe in simple CICO but it's still all about calories blah blah blah etc... etc... ad nauseum

    Even if I had NO evidence at all, that still does not prove your position

    You don't win by default in science! LOL

    YOU are the one claiming the weight of evidence, not me... so where is it? Put up or shut up! as they say.

  21. grinch
    If there does not exist a consistently overeaten food that has no sugar or refined starches, what exactly does that prove? Correlation now equals causation, except when it applies to saturated fat, right?

    So what incentive do scientists have for denying the insulin hypothesis? And don't even mention the lipid hypothesis, because there are plenty of people who reject that hypothesis but still reject the insulin hypothesis as well, not for political reasons, but because that is what the evidence seems to demonstrate to them.

    As SG once pointed out, if you look up "food reward" and obesity in google scholar there are thousands of papers on the subject. He did not make this stuff up. Here is one example:

    http://www.jneurosci.org/content/30/39/13105.short

  22. FrankG
    Here's a thought -- I believe you like to suggest that LCHF works "by accident" because it happens to result in avoiding "highly palatable foods", resulting in bland, boring food which we will naturally eat less of thus, resulting in less CI?

    Now I don't actually buy any of that reasoning because it does not fit my experiences at all (my food is far from bland and boring) but nonetheless...

    What is your response to the suggestion that FR works "by accident" because it happens to result in your avoiding foods high in sugar and or refined starches?

    In other words FR is a subset of the Carbohydrate Hypothesis just as Martin has been telling you -- I suggest it is the sugars and refined starches which make the food "palatable" and keep us coming back for more (despite having just eaten) due in large part to the action of insulin, primarily on the fat cells... and unless you can suggest "foods which people tend to consistently overeat" (in your FR way of thinking) but contain NO sugar or refined starches. you are in no position to claim otherwise.

    And NO potatoes are NOT high in sugar or refined starches. If you really don't know what I mean by "refined starches" try looking up maltodextrin as an example. Modern processed food has gone many levels above the refinement attained with polished white rice!

  23. grinch
    I don't buy into this "insulin primarily on fat cells" because people can have problems with overeating even when their metabolic health markers are perfectly healthy. I just don't see how it explains all the observations.

    If this is really how it worked, then any source of sugar should cause me or anyone else to start overeating and all sugar should be palatable to us. There are very few foods high in sugar and/or refined starches but low in fat that cause me any problems. Every food I can think of at the top of my head is both high in fat and sugar. I've already posted links to studies where palatability per se caused increased intake independent of composition that you've shrugged off as useless since they are short term.

    Replies: #324, #327, #330, #331, #332
  24. FrankG
    Yes so you keep saying... this is why I insist on "foods which people tend to consistently overeat". I'm not looking for your personal preferences here. I also don't like the taste of foods high in sugar or refined starches.. way too sickly sweet for me these days.. so what?

    The simple fact is that if sugar or refined starches were really not the problem here you could readily name me "foods which people tend to consistently overeat" which did not have ANY. And you CAN"T!

    It is NOT the fat alone but it can be (your claimed personal tastes aside) sugar alone.

    So moving on with your clear assent (based on your inability to respond), that leaves the question, what is it about sugar and/or refined starches which make us overeat?

    And enough already with the pathetic strawman "but if I drink a soda why don't I immediately become ravenously hungry!" Are you really that dense? This is NOT a one-off short-term effect but something which builds slowly and insidiously over many weeks, months and years. Something which SG also likes to conveniently forget, so he can present a seven day trial on an handful of rodents as somehow equivalent.. just like you and your soda.

  25. Paul the rat
    @ grinch

    "...I just don't see how it explains all the observations…"

    grinch, there is no such thing in any sciences like - "explains all observations", especially in biological sciences. Gauss curve applies to everything - but you know that, don't you. Yet statements like this one cited, makes me think that it is something amiss with the way you reason or, more likely, you are just having fun. Overall, you are not consistent and go in circles - like my rats in a treadmill.

  26. Galina L.
    Not all scientists deny the insulin hypothesis. Do you remember, guys, the brief period when Dr.JJ decided to pay a visit to a nutritional part of a blogosphere because he studied the issue at that time? I saved some of his posts, may be , if you re-visit his comments, it will settle down the dispute a little bit.
    JJ - " There are many types of human obesity, and obviously to me, many causes. I see hyperinsulinemia as a requirement, but I don't see it as sufficient, especially at all ranges of insulin."
    Reply: #328
  27. FrankG

    There are very few foods high in sugar and/or refined starches but low in fat that cause me any problems. Every food I can think of at the top of my head is both high in fat and sugar.

    http://wholehealthsource.blogspot.ca/2013/08/food-reward-friday_9.html

  28. FrankG

    Not all scientists deny the insulin hypothesis.

    I certainly didn't mean to imply this was the case Galina. NuSI as just one example has some very reputable researchers involved.

    But it is an unfortunate fact that too many now answer more to their paymasters than any unbiased scientific method. Even those that don't, may find themselves constrained as to how their study is designed, what methodology is used and how the data is presented, based on who is paying for it... even if it gets accepted for study or published at all. There is clear bias shown to publishing only favourable reports (while withholding negative ones) for certain drugs for example. SG has made it clear that his ultimate aim is a pharmaceutical solution. Cha Ching! Again there are studies republished with the lists of authors or title changed enough to appear as a different trial... great way to skew meta-analyses of the data in your favour. And all good money for the publications which can generate even more revenue by printing out glossies of the favourable articles to circulate to Doctors etc... They might be portrayed as science but are little more than adverts for a product. Also cases of "ghost writing" where an article is penned by a big-pharma (or big-food) employee and then an established "scientist" is paid to put his name as the author to add credibility. Sure SG and grinch have the "weight of the evidence" alright LOL

  29. Galina L.
    I know. Was it not an enjoyable reading of dialogs between JJ and SG? Poor youngster was flapping like a fish taken from the water. I am not saying that everything is clear, black and white, there are friends and enemies, but an arrogance could be annoying.
  30. FrankG

    I've already posted links to studies where palatability per se caused increased intake independent of composition that you've shrugged off as useless since they are short term.

    Is this meant as your response to my "put up or shut up" challenge? If so then surely you are simply adding to the postilion that quantity does not make up for quality -- which by the way does not necessarily mean I am claiming I have quality studies but you proffering poor quality ones does not prove your point... sorry did you think the rules were different for you? And meantime how many of "our" studies have you "shrugged off as useless" for your own reasons? "Free-living" seems to be the main one... everybody lies....right? Except that most of the people I know dealing with overweight/obesity and related metabolic issues _are_ actually "free-living" and not locked up. Again did you think the rules were different for you?

    So once again I take your lack of response as assent... you do NOT have the weight of evidence... you do not have any strong evidence... in fact you have offered NOTHING substantial to support your position other than a great deal of hot air, hype and occasional buzzwords.. just like SG in fact!

  31. Martin Levac

    I don't buy into this "insulin primarily on fat cells" because people can have problems with overeating even when their metabolic health markers are perfectly healthy. I just don't see how it explains all the observations.If this is really how it worked, then any source of sugar should cause me or anyone else to start overeating and all sugar should be palatable to us. There are very few foods high in sugar and/or refined starches but low in fat that cause me any problems. Every food I can think of at the top of my head is both high in fat and sugar. I've already posted links to studies where palatability per se caused increased intake independent of composition that you've shrugged off as useless since they are short term.

    Do you mean to say there's a relationship between health markers and insulin, or health markers and fat tissue? If that is the case, then in your argument we must assume these health markers are accurate measures of health.

    I noticed that you often use your personal experience to support your opinion. May I offer a suggestion? Don't do that. Just like with Sam's experiment, nobody can be sure of your personal experience, except yourself of course. Because you are the only one who knows all the facts about your personal experience. Therefore, we can only take your word for it. Just as with Sam's experiment, for any of your experience that you relate to us, if we wanted to confirm or refute it, we'd have to do a proper experiment with multiple subjects and multiple observers.

    This begs the question. When you say "explains all the observations", are you referring to your personal observations? Then that's not "all observations", is it. What you really want here is strong enough evidence that explains your personal observations. That's fine. That's what I want for myself too.

  32. Martin Levac

    If this is really how it worked, then any source of sugar should cause me or anyone else to start overeating and all sugar should be palatable to us. There are very few foods high in sugar and/or refined starches but low in fat that cause me any problems. Every food I can think of at the top of my head is both high in fat and sugar. I've already posted links to studies where palatability per se caused increased intake independent of composition that you've shrugged off as useless since they are short term.

    You know, I forgot to address your point here as well.

    If I understand your argument correctly, you're saying composition changes palatability, and then palatability changes food intake. Do I understand your argument correctly? If I do, then why do you also say the effect is independent of composition?

    I'm just trying to understand how we can first establish that composition has an effect on palatability, but then when we look at the effect of palatability on food intake, we suddenly ignore how we achieved this palatability in the first place.

  33. grinch
    "I noticed that you often use your personal experience to support your opinion. May I offer a suggestion? Don't do that. Just like with Sam's experiment, nobody can be sure of your personal experience, except yourself of course. Because you are the only one who knows all the facts about your personal experience. Therefore, we can only take your word for it. Just as with Sam's experiment, for any of your experience that you relate to us, if we wanted to confirm or refute it, we'd have to do a proper experiment with multiple subjects and multiple observers."

    Since the current body of the scientific literature has been insufficient to disprove the insulin hypothesis according to your opinions here (however that same literature certain't hasn't confirmed it either), all I have left is my personal experience. Since it would appear my personal experience is more supportive of the FR hypothesis, why should I put my faith in the insulin hypothesis? I could listen to the experiences of others out there, but unfortunately all the low carbers who testify they can't lose weight by restricting calories are invalidated by the fact that underreporting of calorie intake is correlated with BMI according to scientific research.
    -----

    "If I understand your argument correctly, you're saying composition changes palatability, and then palatability changes food intake. Do I understand your argument correctly? If I do, then why do you also say the effect is independent of composition?

    I'm just trying to understand how we can first establish that composition has an effect on palatability, but then when we look at the effect of palatability on food intake, we suddenly ignore how we achieved this palatability in the first place."

    Yes composition changes palatability, but that's not what I said there. I said I posted links to studies where composition (macronutrients) is the same, but palatability is increased, leading to higher ad lib intake.

    Replies: #334, #335
  34. Martin Levac
    Actually, total evidence either way is insufficient, hence why NuSI was formed.

    As for your personal experience, let me illustrate what I mean.

    Could I use _your_ personal experience to support _my_ opinion?

  35. FrankG
    Further rationale against you accepting your own personal experience was in one of your many comments discounting Sam's n=1 experiment...

    Didn't you suggest that: despite his diligent efforts at recording everything he ate, he could still be [unconsciously] under/over-reporting due to some effect of his cognitive bias?

    Are you so sure you are not similarly under the thrall of your own (very evident) cognitive bias?

    And why did you fail to raise these same concerns when you constantly harped on about the Fit2Fat2Fart guy, after he did a very similar n=1 to Sam's?

  36. Martin Levac
    Earlier (comments #144-145), I said that I'd like to turn around the idea that we could use Sam's experiment as evidence to support a hypothesis, and instead use a hypothesis to see if it could predict Sam's experiment, which I proceeded to do using several papers from which I extracted this hypothesis.

    Here, I invite others to do the same with their own personal experience, i.e. see if the hypothesis can predict what you see. Another way of saying this is to see if the hypothesis can _explain_ what you see. Here are the papers I used, and the corresponding hypothesis:

    Thermal efficiency: http://jama.jamanetwork.com/article.aspx?articleid=1199154
    Hormonal regulation: http://www.nejm.org/doi/full/10.1056/NEJMoa1105816
    A-TO-Z study: http://www.ncbi.nlm.nih.gov/pubmed/17341711

    The hypothesis: The diet most likely to cause weight gain is the one that produces least increase in Eout, and greatest increase in Ein.

    Now how do we figure out what's going on with Eout or Ein, if we don't actually get into a metabolic chamber to measure these things? Well for example, if Eout goes up, then we should feel this as an increase in energy, or a better ability to remain alert during the day. On the other hand, if Ein goes up, then we can easily measure the amount of food we eat. Now this won't prove anything to anybody else, but for each of us who do this, it might give us some reliable measure of what to expect when we eat or don't eat certain foods. Finally, we could always get on a scale, and see the final result.

    It's possible that several hypotheses could explain the same facts, so here we have to see which hypothesis can _best_ explain those facts, or at least explain them without being forced to ignore certain facts along the way.

    Reply: #337
  37. FrankG

    ...or at least explain them without being forced to ignore certain facts along the way.

    True dat!

  38. vkool
    My answer is no. Low-fat diet will help prevent us from being overweight. Having low-fat diet is good for our heart and arteries. Controlling the eating habit is good but not enough to keep us from being fat. The most important thing is exercising. We have to exercise every day if we are not doing manual work.
    Reply: #340
  39. FrankG
    Two steps forward and one step back.
  40. Paul the rat
    Good by good people, I wish you all good health.
1 2 3 4 5 6 7

Leave a reply

Reply to comment #0 by

Older posts