Saturated fat and large LDL

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles


For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Comments (44) -

  • Anonymous

    2/16/2010 10:02:36 PM |

    Is there an inexpensive way of finding out which form you have?

  • Anonymous

    2/16/2010 11:02:49 PM |

    is there any truth to the idea that if your trig/HDL ratio is under 2.0 that your LDL type is predominantly large/buoyant?

  • Laura

    2/16/2010 11:37:17 PM |

    Is there a way to determine whether small LDL production is carb- or genetics-caused?

  • Anonymous

    2/16/2010 11:43:41 PM |

    Is this the same for poly/mono unsaturated fatty acids?

  • Anonymous

    2/16/2010 11:46:43 PM |

    Dr. Davis,

    Does the form of saturated fat have any impact on this in the case of genetic predisposition to small LDL formation? For example, does it matter if the fatty acids are lauric acid and stearic acid versus something like palmitic acid?

    Rick Braden

  • Daniel

    2/16/2010 11:50:11 PM |

    Dr. Davis,
    That's very interesting!!  Any chance you could provide the reference?
    Thanks, Dan

  • jtkeith

    2/17/2010 12:26:14 AM |

    This naturally leads to the question about understanding our personal genetic coding.  Without that coding information it seems difficult make an informed decision about the consequences of lowering carbohydrate and increasing fat (and saturated fat) until the consequences are upon you!

  • David

    2/17/2010 12:38:19 AM |

    This definitely needs a follow-up post. I've not seen this distinction until now. If true, Dr. Davis, does it not present a difficult dilemma for those who have both genetic sdLDL and Lp(a)? If saturated fat needs to be restricted for genetically high sdLDL, would this not leave the Lp(a) (which responds best to saturated fat intake) unopposed? What is your proposal to address this?

  • Ellen

    2/17/2010 1:09:25 AM |

    Interesting post, Dr. Davis. How would one find out if they are genetically predisposed to react to saturated fat intake with an increase in small LDL?

  • Harold

    2/17/2010 1:38:12 AM |

    Do you have some specific references for LDLa and saturated fat? Is it essentially congenital hypercholesterolemia that reacts with the sat fat?

  • steve

    2/17/2010 1:49:56 AM |

    this is a long overview discussion. thank you!  What would dietary recommendation be for someone if small LDL is genetic in origin?  Also, wouldn't this pattern possibly require statins to get LDL particle count as low as possible since it is unlikely that diet will do the job?  In my case, i need Lipitor and Zetia; otherwise my particle count mostly small remains high despite Vit D, normal weight,no wheat cornstarch or sugar.  Great post!

  • Anonymous

    2/17/2010 1:50:56 AM |

    Doc -

    Good post but -

    Hard to understand post without the background basis on which the statement is made.

    Is your statement based on clinical observations? Or is it based on opinion only?

  • switters

    2/17/2010 4:44:09 AM |

    Yes, references supporting your premise in this article would be very welcome.

  • Paul

    2/17/2010 9:46:22 AM |

    This post concerns me because as a low carber I find it difficult to maintain a low carb diet without saturated fat sources. Perhaps this is driving the concern and questions from others also.

  • Rabbi HIrsch Meisels

    2/17/2010 2:14:23 PM |

    Count me in those who are waiting to see data where this is coming from.
    Thanks for all your blogs posts.

  • zach

    2/17/2010 3:26:16 PM |

    Yes, I hope this isn't a hit and run post. Many learned people, such as Peter at hyperlipid would probably disagree. Do you have any references?

  • Alfredo E.

    2/17/2010 3:48:38 PM |

    So what do we do if we should not eat but a few carbos and up to certain amount of protein?

    The rest have to be saturated fats, isn't it?

    Please, some more practical information before we all run over the cliff.

  • Anonymous

    2/17/2010 5:48:11 PM |

    Harold, I am also interested in the familial hypercholesterolemia question.  After a quick search, I found this http://www.jlr.org/cgi/reprint/23/8/1196.pdf with a quote: "LDL has been
    found to be cholesterol-enriched and triglyceride-poor
    (5, 6), and in one study, the peak flotation rate of FH LDL
    has been found to be higher than in normals (6),
    implying decreased density, increased size, or both.
    However, these results are difficult to assess, since there
    is considerable heterogeneity of LDL in normal subjects,
    although size, flotation rate, and composition"

    So, FH people may be predisposed to large, fluffy LDL.  However, I do not know whether FHs handle saturated fats better than normals, and this is an important question.  

    -Aaron

  • Anonymous

    2/17/2010 5:54:55 PM |

    A question on triglycerides...if high TGs are a trigger for small, dense LDL and should be minimized, are there any ways to reduce area-under-the-curve TGs after a meal (other than the usual low carb, omega-3, etc. recommendations).  Are large, infrequent meals better than small, frequent meals?  Does fiber change the shape of the post-meal TG curve?

    Also, does fasting TG tell the whole story?  Could one have, say, <50 mg/dL fasting TG but have elevated TG throughout the day as a result of large, high-fat meals?  

    -Aaron

  • Anonymous

    2/17/2010 7:04:29 PM |

    Thank you Dr. Davis!  Finally a voice of sanity in this whole sat fat hoopla.

    I for one, although not neurotic about it, do not favor saturated fats and will eat a good non-hydrogenated margarine (like Smart Balance) over butter any day.

    Please keep up this sane blog and give us the WHOLE enchilada, not just what some want to hear.

  • Dr. William Davis

    2/17/2010 7:47:07 PM |

    Search PubMed or Google Scholar and you will find NO data on this issue. To my knowledge, there are none that distinguish genetically -driven small LDL vs. lifestyle-induced.

    This is based on having tested lipoproteins in thousands of people over the past 10+ years.

    Prototypical "genetic small LDL" person: 5 ft 10 inch, 140 lb male who eats low-carb. In other words this person is at ideal weight and does not eat foods that trigger small LDL--yet has 90% small LDL by NMR (e.g., 1200 nmol/L, LDL particle number 1550 nmol/L). Should this person overindulge in saturated fat, small LDL will go up.

  • Scott Miller

    2/17/2010 8:46:27 PM |

    Dr. Davis, how do you know it is saturated fats that are the cause? For example, most low-carbers also have elevated intake of inflammatory polyunsaturated fatty acids, which I would be much more likely to blame.  But, in either case, it seems there are too many uncontrolled variables involved (as far as food intake) to pin any of them to the wall.

    It's very difficult for me to believe saturated fat is the cause, while other possibilities exist.

  • Anonymous

    2/17/2010 9:08:19 PM |

    For everyone worrying about this, just get yourself a VAP or NMR test.  If you have LP(a) or sdLDL, that will show it.  You don't need genetic testing.

  • Anonymous

    2/17/2010 10:27:45 PM |

    What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?

  • Anonymous

    2/17/2010 11:09:09 PM |

    Thanks Dr. Davis for another insightful post from your clinical experience, giving the kind of information that helps elucidate why saturated fat works for some and not for others - and the kind of information you can't get anywhere else.  Ignore the pro saturated fat/anti-polyunsaturated fat zealots, who can't be persuaded by any evidence or logic.

  • Anonymous

    2/17/2010 11:10:11 PM |

    "What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?"

    I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?

  • Kurt G. Harris MD

    2/18/2010 12:56:55 AM |

    Hello Dr. Davis

    You said:

    "Should this person overindulge in saturated fat, small LDL will go up."

    Just to be clear, are you saying you have observed low carb subjects (how low?) that have added saturated fat to their diets and then on subsequent testing you have seen sdLDL rise in absolute and percentage terms?

    If they were truly LC, were they already high sat fat at the time of the NMR or were they high PUFA (South Beach?)

    May I ask how many such cases you have seen?

    You should definitely publish this, or if you don't think it is publishable maybe you could give us all the data in a blog post.

    Thanks, this is very interesting.

  • Dr. William Davis

    2/18/2010 1:52:52 AM |

    In people with presumptive genetically-determined small LDL, HDL can be 70 mg/dl or greater, triglycerides 45 mg/dl or less, yet small LDL persists, usually at 600 nmol/L (NMR).

    I have approximately 100 patients like this. They tend to be very thin with BMI's of 23 or so, yet small LDL persists.

  • Stephen

    2/18/2010 3:11:53 AM |

    Hi Dr. Davis,

    This post really intrigues me. I am a first year medical student (24 yo) with familial hypercholesterolemia. I am on a low carb paleo diet, taking omega 3, vit D and just recently added magnesium to the mix as well. I went off Lipitor two months ago just an experiment to go along with this new eating plan, and received blood work only a few days ago. Numbers about 450 on total and 285 for LDL. My CT scan already showed plaque buildup in the coronary arteries, aorta, and one valve. While I am not looking for medical advice per se (since I know you prefer not to give it over your blog) I was just curious as to how your track the plaque plan and recommendations are effected with this type of genetic disorder. My cardiologist says if I dont go on drugs immediately I'll have a cardiac event at 40 years of age. I could use some advice and direction to persue. Is it impossible to avoid genetics, and the use of drugs are unavoidable? Thanks. Really appreciate it.

  • Anonymous

    2/18/2010 3:15:38 AM |

    How do you know how much small LDL you have?

  • Bonnie

    2/18/2010 3:53:00 AM |

    ""I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?""

    Well - just speaking for myself, I have high HDL and low trigs, and always had a mix of small/large (A/B) pattern LDL.  When I stopped eating wheat, my LDL all became large.  

    I also have high Lp(a), which was uneffected by my eliminating wheat.

    You can drive yourself crazy figuring out what's OK to eat and what's not.  I don't worry about it anymore.  I rarely eat wheat because I've seen results from Not eating it, try not to overdo the sugar and fruit, get plenty of veggies and protein.  

    I get my VAP test once or twice a year to make sure everything is where it should be, more or less.

    I'm just not going to worry about it beyond that.  

    Bonnie

  • LeenaS

    2/18/2010 4:12:28 AM |

    Dr. Harris:

    Are these customers of yours lean lowcarbers eating plenty of LA or very, very much protein in their diet? If not, then what do they eat?

    With regards,
    LeenaS

  • Mike

    2/18/2010 4:26:28 AM |

    Interesting, and concerning, since I fit that description:

    Chol: 6.35mmol/L
    HDL: 1.88
    LDL: 4.2
    Triglycerides: 0.66
    Chol/HDL ratio: 3.4
    American Values:  TG 58.47 LDL 162.54 HDL 72.75
    Triglyceride/HDL ratio: 0.8
    Hieght: 6'0
    Wieght: 165lbs
    BF 8%

    I've had other opinions on these numbers; should I be pursuing more accurate particle numbers?  I go out of my way to consume large amounts of red meat, coconut oil, butter, and eggs.  I'm fitter and healthier (subjectively) than I ever have been at 36 than I was in my 20's.  I find it disconcerting than I could potentially be doing something detrimental.

  • Kurt G. Harris MD

    2/18/2010 4:43:49 AM |

    Hi Dr. Davis

    In the original post you said:

    "saturated fat will increase small LDL.  In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL."

    So, if I follow this correctly, you are saying that these 100 patients all had increases in their sdLDL after documented increases in saturated fat in their diets? In other words you had two data points for each subject, correct?

    If the subjects did not all have documented increases in sLDL then by "persist", do you mean their sdLDL went down with LC eating (like 800 to 600, say) or do you just mean that they had a single high value and it was only measured once, but it was high?

    If it is the latter, I could see how it's fair to say that some LC eaters have a higher sdLDL than we might predict (for whatever reason) but it seems like a non sequiter to conclude that the sdLDL would be made higher with more sat fat consumption.

    I just want to make sure I get this straight so I understand it correctly.

  • Paul

    2/18/2010 6:19:52 AM |

    Thin. Nice. I'm less concerned. lol

  • Anonymous

    2/18/2010 1:22:06 PM |

    Does this group of people also have elevated blood sugar, as might be predicted by another of your blog postings?

    http://heartscanblog.blogspot.com/2009/12/to-track-small-ldl-track-blood-sugar.html

  • David

    2/19/2010 3:10:43 AM |

    Dr. Davis,

    I concur with Dr. Harris in that more details would be nice to better understand exactly what you're saying.

    Are other variables accounted for? Were many, most, or all of these patients on statin drugs, which could have prevented a shift in particle size if triglycerides were low and insulin sensitivity was high?

    Again, if there is such a phenomenon going on, is the "genetic sdLDL" clearly atherogenic in the same way that "environmental sdLDL" seems to be?

    If so, I ask again, what is the solution for someone who is afflicted by both Lp(a) and genetic sdLDL? The "profile" for genetic sdLDL is similar to the profile for those with Lp(a), and there is probably a lot of crossover. Saturated fat lowers Lp(a), but (presumably) raises genetic sdLDL. This is a fierce dilemma! Would not the better choice be to choose the diet that opposes the more vicious of the two, which is Lp(a)? What is the priority?

    Has a high SFA diet only increased sdLDL per NMR, or has it also clearly been shown to increase CAC scores? In other words, does it clearly progress the disease itself?

    David

  • pmpctek

    3/7/2010 5:50:15 PM |

    Saturated fats not linked to heart disease: Meta-analysis - American Society for Clinical Nutrition (January 13, 2010). doi:10.3945/ajcn.2009.27725 © 2010

    It would really be interesting to know what the primary sources of saturated fat are for these "100 patients".  There may be a single (widely available) common source of sat fat that these specific patients are consuming, do we even know that?  I agree, by what has been revealed, that there are too many variables to know conclusively that saturated fat is the cause of their persistently elevated small LDL.

    Mark me down as someone who is not convinced that CLA, n3 rich organic, free range, and wild animal sources of fat could possibly in any way be detrimental to anyone.

  • Anonymous

    4/19/2010 1:45:33 PM |

    When will people stop worrying about cholesterol numbers? They really don't mean anything.

    Until someone explains a plausible mechanism through which lipoproteins directly kill me I will ignore it any suggestion that they do. This is what a good scientist would do.

  • buy jeans

    11/3/2010 6:44:37 PM |

    If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

  • Chris Kresser

    11/3/2010 6:55:04 PM |

    buy jeans: I'd love to see clinical evidence supporting that claim.

  • gastric bypass surgery Los Angeles

    2/28/2011 2:33:52 PM |

    Heart diseases are a major matter of concern these days therefore all that can be done to correct the diet and make it benefit good health should be taken to.

Loading
Man walks after removing wheat

Man walks after removing wheat

No, this isn't some National Enquirer headline like "Woman delivers alien baby."

Tom is a 26-year old man with a complex medical condition, a malformation he was born with and has had reconstructed. Aside from this, he leads a normal life: works, is married, and is, in fact, quite intelligent.

He came to me for an opinion regarding his overall health. Tom was worried that his congenital condition would impair his long-term health and longevity prospects, so he wanted to optimize all other aspects of his health.

But, when I examined Tom, he could barely get himself up on the exam table without wincing in pain. When I asked him to walk, he hobbled a few steps, again clearly in pain. When I asked him what hurt, he said "everything." He said that all his joints hurt just to move.

He told me that his several doctors over the years didn't know why he was in such pain: It wasn't rheumatoid arthritis, gout, pseudogout, or any of the other inflammatory joint diseases that might account for virtually incapacitating this 26-year old man. Even the rheumatologists were stumped. It was also unrelated to his repaired congenital condition. So Tom went on with his life, barely able to even go for a walk with his wife without pain, slowing him down to the pace of an 80-year old.

So I suggested that he eliminate all wheat products. "I don't know for a fact whether it will work, Tom. But the only way to find out is to give it a try. Why not try a 4-week period of meticulously avoiding wheat? Nothing bad will come of it."

He and his wife look perplexed, but were so desperate for a solution that they agreed to give it a try.

Tom returned 6 weeks later. He walked into the room briskly, then bounded up on the exam table. He told me that, within days, all his joint pains had completely disappeared. He could walk, stretch, do all the normal physical things with none of the pain he had suffered previously.

Tom told me, "I didn't think it could be true. I thought it was just a coincidence. So I had a sandwich about 2 weeks into it. In about 5 minutes, I got about half my pains back."

Tom now remains wheat-free and pain-free, thankfully with no discernible joint impairment.

So, yes, Tom walked freely and without pain simply by eliminating wheat from his life.

Is it an immune phenomenon? Does wheat gluten trigger some inflammatory reaction in some people? There is surely something like this underlying experiences like Tom.

Wheat contains far more than gluten. Modern wheat is a collection of hundreds of different proteins, though gluten is the most plentiful, the one that confers the "viscoelasticity" of dough. But there's plenty more to wheat than gluten or celiac disease.

Comments (27) -

  • loco

    5/9/2010 2:04:43 PM |

    Maybe Monsato knows what causes it.

  • Nancy

    5/9/2010 2:04:43 PM |

    This is similar to what happened to me, although it took a lot longer.  I was diagnosed with Ankylosing Spondylitis and had pain in almost every joint.  Removing gluten from my diet and in about a year my AS went into remission and I am feeling so much better.

  • loco

    5/9/2010 2:06:50 PM |

    Scratch that.  Amazingly wheat is one of the few product "monsanto" doesn't touch.

  • Lori Miller

    5/9/2010 2:40:44 PM |

    After cutting way, way back on the carbs (and eliminating wheat), my little aches and pains, sinus headaches and fatigue disappeared. My skin is better, too. Oh, and I'm back to what I weighed in high school. I'm so happy with my new diet that it's hard not to proselytize.

  • Darrin

    5/9/2010 4:43:35 PM |

    It's interesting how little attention is paid to gluten intolerance, and more generally grain intolerances, in humans.

    In contrast, it is quite easy to find statistics on the amount of the world's population that is lactose intolerant and which populations are most susceptible.

    Quite the eye-opening post.

  • Mike Turco

    5/9/2010 8:27:19 PM |

    I have a story that is somewhat similar. I've had chronic neck and back pain for years. Nothing debilitating but it was "there" every day, sometimes for many hours. I was taking way too much ibuprofen to manage the discomfort.

    Anyways, I read an article in the news somewhere about how "we" all sit in chairs too much, that the human body wasn't meant to do that kind of thing, and that doing so could lead to chronic neck and back pain! The suggestion was to use a standing desk.

    Being a bit of a cheapskate, I setup a shelving unit about two weeks ago, put my computer and so forth up on the shelf, and gave it a shot.

    Literally, the next day my back and neck pain was gone. Just gone. Hasn't come back. In addition, my weight loss efforts seem to be doing a little better. Hey, its not much exercise, but its certainly a better "workout" than sitting on my duff all day.

    Granted, I've only been at this for two weeks and its too early to tell whether any of the affects are real or just coincidental. Still, though, I'd recommend to just about anybody that they give a shot at standing up throughout their workday instead of sitting down. It can't hurt anything, I think, and its worth a try.

    Mike

  • Anonymous

    5/10/2010 11:57:24 AM |

    Apparently, nobody cares about wheat. It's been this way for 15 years. It's like trying to convince people that earth is round rather than flat. We have a long way to go. Frustrating when we have Federal Government promoting low fat, high carbs diet.

  • scall0way

    5/10/2010 1:56:05 PM |

    I believe it. Most of my aches and pains went away when I eliminated wheat also. I used to almost have to crawl out of bed in the morning, which I attributed to "getting old". Yet not one single doctor ever once suggested my diet could have anything to do with the problem.

  • Fred Hahn

    5/11/2010 12:05:31 AM |

    Bill -

    You should send this story to Oprah!

  • WheatFreeNow

    5/11/2010 5:28:19 AM |

    Not surprising at all! :0  It's going to become more and more common to see results like this - and yes - I agree with your point about the problem being SO MUCH more to do with the gluten issue - it's more about the over commercialized, genetically modified wheat that has entered our diet which is probably causing the problem.

  • Dr. William Davis

    5/11/2010 11:45:28 AM |

    Hi, Fred!

    I was so impressed when I heard you talk that you mentioned the grain-rheumatoid arthritis connection. That's a pretty obscure relationship, but one I, too, am convinced is real.

  • Ned Kock

    5/11/2010 2:47:31 PM |

    This type of case must be very rewarding for a doctor.

    Not only did you save this person's life with your advice, his quality of life improved dramatically.

  • monte

    5/11/2010 5:13:34 PM |

    I also was diagnosed with Ankylosing Spondylitis when I was 20 years old. I'm now 42 and have had both of my hips replaced. I read another article about the dangers of gluten:
    http://www.huffingtonpost.com/dr-mark-hyman/gluten-what-you-dont-know_b_379089.html

    I've been off wheat now for about 4 months and the inflammation is almost completely gone. When I started I could only walk about 3 blocks but I'm up to a mile now and without the extreme pain in my joints. I still have a lot of therapy to do but I'm actually hopeful about my health for the first time in years.

    Thanks for getting this info out to people!

  • Anne

    5/11/2010 7:12:09 PM |

    My knee pain was the first thing that disappeared when I stopped eating gluten. That was 7 yrs ago and still doing well. I wake up in the morning with no joint pain. Not bad for 67 yrs.

  • Anonymous

    5/11/2010 8:06:08 PM |

    Yup, my mother-in-law was diagnosed with rheumatoid arthritis back in the '70s.  I convinced her to give up wheat a year ago and all her pains went away.  

    I'm convinced many "diseases" are actually symptoms of various food intolerances, with wheat being the most likely suspect.

  • Professor Tom

    5/12/2010 2:14:50 PM |

    Are you claiming that everyone should eliminate wheat from their diet?

    What about the recent attacks on sodium from the UN in the form of Codex Alimentarius? Personally, I think it's more about control as I documented here

  • DrStrange

    5/12/2010 2:56:39 PM |

    "I'm convinced many "diseases" are actually symptoms of various food intolerances, with wheat being the most likely suspect."

    More specifically gluten, so we need to include rye, barley, tritcale, spelt, kamut, in that.  Also dairy #2.  If it does not bother your individual body, it does not.  But for so many one or both of there are disasters.

    The hardest part, second after the addiction/cultural promotion of them as good, healthy foods, is that it can take many days of zero intake before improvement is really noticeable.  People are so emotionally attached to what they eat they fight tooth and nail against giving something up for that long "just to see." That is of course, unless/until they are truly desperate!

  • TedHutchinson

    5/13/2010 10:44:10 AM |

    Dr Dr Davis
    I think I may have mistakenly posted a link to an review on Resolution of Adipose Tissue Inflammation that I intended as a reply to a different blog.
    Although it's an interesting paper confirming the importance of the role of omega 3, it is off topic for this particular thread. I'd be pleased if you could delete it.Many thanks Ted

  • Anonymous

    5/13/2010 5:05:29 PM |

    I used to have severe menstrual cramps from the time I hit menarche. And miraculously they went away last year after I gave up wheat.

    MB

  • Neonomide

    5/15/2010 12:55:01 AM |

    Loren Cordain has written a paper on the role of dietary lectins in rheumatoid arthritis:

    http://www.thepaleodiet.com/articles/Arthritis%20PDF.pdf

  • Neonomide

    5/15/2010 2:23:45 AM |

    How convenient - this brand new Cordain's Paleo newsletter has some information on the subject as well:



    Q: Could you suggest recent scientific articles on the topic of dietary lectins and rheumatoid arthritis?

    Many thanks,
    Allena

    A: Dear Allena,

    To my knowledge, there are no recent studies addressing the role of a paleolithic diet and its implications in rheumatoid arthritis, except from that of Dr. Cordain. On his DVD How to Treat Multiple Sclerosis with Diet, Dr. Cordain thoroughly explains the dietary mechanisms of autoimmunity in MS which are almost the same for all autoimmune diseases, including RA. These include: increased intestinal permeability, increased passage of luminal antigens into peripheral circulation, molecular mimicry and genetic susceptibility (genes encoding for the HLA system), among other factors.

    In recent years, new substances have been discovered which might be responsible for increased intestinal permeability - namely saponins - found in legumes, potatoes, soya, quinoa, amaranth, alfalfa sprouts or tomatoes. If you've seen Dr. Cordain's scientific paper entitled "Modulation of immune function by dietary lectins in rheumatoid arthritis", I am sure you are aware of the role lectins play in autoimmunity.

    Adjuvants are used by immunologists in order to boost the immune system and induce immune response. It turns out that certain foods possess bioactive compounds that have adjuvant-like activity. This is the case for tomatoes or quillaja (a foaming agent used in beers and soft drinks).

    Gliadin is a prolamine found in wheat which has been shown to increase intestinal permeability, and hence the risk of suffering from an autoimmune disease. While several clinical trials conducted have shown promising results, unfortunately they have used a gluten-free diet or vegan diet instead of a whole paleolithic diet, which we think is superior.

    In the vegan diets, authors often claim that the benefits cited might be due to the lack of meat, but we think the positive effect relies on the lack of diary proteins and gluten. Meat has historically been seen as the "bad guy" of inflammation, but the data to support that notion is not sufficiently compelling.

    Listed below are some references that may be helpful.

    Cordially,
    Maelán Fontes

    References:

    1: Modulation of immune function by dietary lectins in rheumatoid arthritis. Cordain L, Toohey L, Smith MJ, Hickey MS. Brit J Nutr 2000, 83:207-217.

    2: Gluten-free vegan diet induces decreased LDL and oxidized LDL levels and raised atheroprotective natural antibodies against phosphorylcholine in patients with rheumatoid arthritis: a randomized study. Elkan AC, Sjöberg B, Kolsrud B, Ringertz B, Hafström I, Frostegård J. Arthritis Res Ther. 2008;10(2):R34. Epub 2008 Mar 18.

    3:A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Hafström I, Ringertz B, Spångberg A, von Zweigbergk L, Brannemark S, Nylander I, Rönnelid J, Laasonen L, Klareskog L. Rheumatology (Oxford). 2001 Oct;40(10):1175-9.


    So gliadin in wheat seems to be an important bad guy, eh ?


    PS: Thank you so much Dr Davis for bringing information on wheat havoc  to the masses. It's very much appreciated!

  • Felix Olschewski

    5/21/2010 7:13:12 AM |

    Dr. Davis,
    I hope you don't mind that I have (kind of) translated this post into German and published it on my Blog. You can find it on http://www.urgeschmack.de/schmerzfrei-getreideverzicht/

  • Carrie

    6/23/2010 12:03:56 PM |

    With a few exceptions, I have found those who comment on this blog to be very well informed, adding wonderful references, insights and experiences to the conversation.

    @Professor Tom; even a rudimentary glance of Dr. Davis' blog would reveal that he does not think EVERYONE should stop eating wheat, but for his heart patients, patients with pain and inflammation, patients with neurological disorders, and patients with weight, blood sugar and hormonal imbalances, or other serious and chronic health conditions he advises them to TRY 4 weeks of completely avoiding all wheat/gluten and see if it makes a difference, and in 70% of people it does.  

    It is not some kind of mind control conspiracy theory to make us into docile sheep.  It is the opposite in fact.  He is helping people regain their health by bucking convention; opting out of the wheat based culture and freeing ourselves from dependence on pharmaceuticals.  

    I have seen miraculous health results of going totally grain free for 3 members of my family.  Personally, I only experienced weight loss and increased immunity but that is still worth it.

  • Neonomide

    6/23/2010 1:57:19 PM |

    Carrie,

    I've had a different impression. I understand that Dr Davis does not consider wheat to be human food at all and as a paleo scholar, I completely agree.

    I also acknowledge that all wheat is not equal - here in Finland I think wheat elimination alone will not show as dramatic effects as in US. Different genome, in both humans and wheat itself.

    In energy versus nutrient equations wheat loses anyway and added salt further unbalances the essential sodium/potassium ratio that is very important in BP control and kidney health. Antinutrient in wheat are a great way to weaken your micronutrient status. The greens and berries own wheat every time.

    IMHO, playing risk game with not-yet-sick people with catastrophe food like wheat is simply stupid. When wheat derived autoimmune disease starts to take it's toll, it may not be reversed anymore. As for sdLDL, it may not cause symptoms at all before the first MI. Then you're dead or in the risk risk of sudden death for the rest of your life. Not fun.

  • hernia surgery Los Angeles

    12/22/2010 10:27:24 AM |

    That is amazing if you could detect something so smoothly and it worked...it's like a miracle or a magic.Why is gluten bad and for all joint pains?

  • Geoffrey Levens

    12/22/2010 3:52:33 PM |

    I would not say that gluten is bad!  What is bad or damaging is many individuals (NOT all) physiological reaction to it.  If you are reactive to gluten, then it is systemically inflammatory.  If you have poor blood sugar regulation, then wheat (maybe its the gluten?) can dramatically raise blood sugar and elevated blood sugar is also inflammatory.

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