Great cholesterol numbers after 4 years on an ultra-strict LCHF diet

Is a strict LCHF diet with unlimited amounts of saturated fat bad for cholesterol levels?

Tommy Runesson has had his blood lipid levels checked four times, including just recently, during his four years on an ultra-strict LCHF diet. The major part of his 200 lb-weight loss (!) occurred before his first blood test, and we don’t know what the numbers were before his weight loss.

The numbers look great. We’re not seeing the significantly elevated total-cholesterol number that a small percentage of individuals show on a strict LCHF diet.

I’d say Runesson’s numbers represent the typical result of a long-term strict LCHF: a normal total cholesterol and LDL, excellent HDL and triglycerides, and a very nice apo-B/apo-A1 ratio. This is what I typically see in most patients that I follow.

Runesson’s results also contradict the strange idea that an LCHF diet may produce good lipid numbers because of ongoing weight loss, but that they would suddenly turn disastrous when weight stabilizes, for some obscure reason. This idea has been put forward by some LCHF skeptics. As far as I know there’s no science to support this idea.

In any case: Runesson has been eating an extremely strict LCHF diet for four years, and has maintained stable weight for the last 2.5 years. And his cholesterol profile is far better than most people’s.

Eat Low Carb High Fat: Cholesterol after 4 years on LCHF

PS: I’m planning another cholesterol checkup myself this fall, after 7 years on an LCHF diet.


New Analysis: LCHF Best For Long-Term Weight and Health Markers

Spectacular Study on Heart Failure and the Supplement CoQ10

Statins May Cause Diabetes

Warnings Against the Atkins Diet “Outdated”

All blog posts on cholesterol, margarine and statins

1 2


  1. Victoria Johnson
    I was diagnosed with T2 diabetes last December; I found this site and started eating LCHF. My weight dropped 25 lbs (down to 120), my cholesterol (taking statin... sigh) dropped to 130. I stopped taking the statin (reports of women and statins... frightening) my cholesterol jumped to 200 (all numbers "just' inside the normal range). I know I need to exercise more; I have a desk job and my after hours is spent playing music. I retire this coming May so hopefully time won't be an issue for that.

    Now, I'm anticipating my next blood check; if these numbers are even higher a battle with the Dr. will ensue. Any feed back on following this diet AND keeping blood numbers in range??

  2. Dawn McVey
    Like you I have no choice but to eat low carb, in 18 mths, I haven't lost a pound. It's a real bummer.
    Reply: #3
  3. Victoria Johnson
    My problem is NOT losing weight. If I keep my glucose normalized, I continue to lose weight. I can stabilize the weight but if I eat TOO much in the way of meat/cheese etc. my blood numbers go up ... I think this is the rock and a hard place. I'm hoping that what I am reading about cholesterol numbers is right, I'm encourage but those reports.
    Reply: #19
  4. charles grashow
    "I’d say Runesson’s numbers represent the typical result of a long-term strict LCHF: a normal total cholesterol and LDL, excellent HDL and triglycerides, and a very nice apo-B/apo-A1 ratio. This is what I typically see in most patients that I follow."

    Then how do you explain Jimmy Moore's horrible lipid panel after a year of a ketogenic VLCHF diet?

    TC - 310
    LDL - 236

    HDL - 66
    Triglycerides - 38

    LDL-P 2730
    Small LDL-P 478

    On 10/25/12 his ApoB was 238

    SO - are these "a normal total cholesterol and LDL"?

    OR - is the HIGH LDL-P AND ApoB a problem??

    Replies: #6, #13
  5. Beth
    Any clue why some people see their cholesterol go up sharply on LCHF? Mine went way up, though they came back down when I added carbs back into my diet. I have not found an explanation for it, so I'm still looking for clues.


    Reply: #20
  6. FrankG
    @CG -- you do know the meaning of the word "typical"... right?
  7. Marco
    Hi all, I have a question that puzzle me since I started LCHF diet a year ago.
    Let's say we have two identical guy; both of them have to eat less than 50 grams of carbs to be in ketosis; one of them eat 49 grams of carbs while the other eat 51 (fat and protein in the same ammount); they virtually have the same diet but one is ketotic and the other is not. What would happen to their cholesterol numbers after months or years? Is ketosis an advantage in this case? Is the "51 grams guy" doing a healty diet anyway? Any idea? Thanks a lot.
    Reply: #10
  8. charles grashow
    @FrankG - Jimmy is as typical as Tommy Runesson is
    Reply: #9
  9. FrankG
    @CG - I disagree and apparently so does Dr Andreas. How many people can you cite whose lipids have become wildly deranged as a result of an LCHF diet? How many, like myself and the many I have conversed with have had their's vastly improve... just like Tommy Runesson? From my perspective that makes Jimmy an "exception".

    To Beth and Victoria I understand that it is common (typical even) to see a rise in LDL-C (as a calculated volume) and Total-C when first starting LCHF. This may be the body re-adjusting to using Fat as the primary fuel as compared to Carbohydrates. In my experience (and that of many others) it usually settles after a few months.

    Reply: #28
  10. robert
    It is just a gut-feeling, but 50g (per day) translates to: practically no junk food (certainly no pizza or pasta, excessive consumption of fizzy drinks...). Most of the work is already done.

    Is the 51g guy doomed? I don't know, but I doubt it. The difference between 49g and 51g is so small, it would be a strong evolutionary disadvantage if that made a difference between healthy living and death. Think about it, 2g of carbs, that's maybe one single grape or one bite of carrot.

    Reply: #12
  11. 1 comment removed
  12. Marco
    "Is the 51g guy doomed? I don't know, but I doubt it. The difference between 49g and 51g is so small, it would be a strong evolutionary disadvantage if that made a difference between healthy living and death."

    Of course he is not doomed.
    My question really was: given the same ammount of food, what difference make being in ketosis or not on blood lipid?

    Reply: #14
  13. Zepp
    Jimmy have a lot of problems.. and have to strugle more then moste peopel!

    For instance he got reactive hypoglycemia.. a typical sign of prediabetes!

    But better late then never.. becuse I think he would have full diabetes by now without low carb?

    And did you know.. his values are not that bad, could be much better.. but you know.. if one have an illnes one should be glad if one can stop the progress of it.

    310/66=4,7.. should be under 6, better if its 5 or lower, great if its 4 or lower!

    Reply: #15
  14. Zepp
    Being in ketosis is mostly a sign.. that you eat litle carbs.. and got low insulin levels!

    If one eat litle carbs and dont get in ketosis, then one have problems.. becuse then one starving.

    Its not if you are in ketosis or not that make the diferens.. its about if you have metabolic syndrome/diabets/hyperinsulinemia.. and revert those to a more normal state that your body get a normal metabolism and after some time even normal values of different risk values.

    Like blood sugar, C-peptid, lipids and inflamaton markers!

  15. charles grashow
    @Zep - you know Jimmy Moore has reactive hypoglycemia because??
    Reply: #16
  16. Zepp
    Becuse he wrote about it and his treatment for it!

    And Reactive hypoglycemia is often by genetic cause, typical for those how got diabetic parents.. or a damaged metabolism.

    Its comes often as the first sign of predibetes/hyperinsulinemia.

  17. FrankG
    Another consideration is that the "normal" lipid values are based largely on populations who are eating the standard american diet (SAD). We don't really know what are the normal or optimal values for those eating LCHF. If indeed cholesterol is even an issue. Certain values may be more of an indicator or symptom of other disorders. Hopefully time will tell but I do know that when I was referred to a Lipidologist he was more impressed by my high HDL-C and low Triglycerides than concerned about my calculated LDL-C volume.

    Why the laser-like focus on Jimmy Moore CG? Do you really think that an exception will discount the value of LCHF to those of us who have clearly benefited; according to every measurable health marker? Are you 100% convinced that his lipids are directly caused by what he eats or do you discount the possibility that something else may be going on there? What it is, I have neither the inclination nor the expertise to speculate. I am not Jimmy Moore's physician. Are you? Why is it your business?

    HDL - 66
    Triglycerides - 38

    Horrible? Really?

  18. FrankG
    You see CG this post was not about Jimmy Moore, it was about someone who has enjoyed measurable success (as defined by the "experts") with a long term LCHF approach, as I have, and as apparently have many others. Sure it is not a panacea. Did anyone claim that it was?
  19. Bob
    I've found cutting out the cheese and reducing the nuts was the key to losing weight on LCHF for me. Maybe the lactose in the cheese is messing with your numbers?

    I have a hard time finding non-cheese foods high enough in fat, but I discovered one that fits the bill perfectly: Beef Brisket. I bought a 10 lb slab of it at Costco at $1.99/lbs., cut it in two, put some spices on the fatty side, wrapped them in foil and placed them on the rack in the turkey pan and slow cooked them for 10 hours at 250°F.

    It was sooooo... good. I ate some cold from the fridge and I tell where cheese gets it flavor. Only this was beef flavored cheese with none of the lactose.

    If you're going to eat a high-fat diet, Beef Brisket should definitely be on your menu. It makes it easy.

    Reply: #32
  20. Bob
    Giver us an example of a typical LCHF diet menu you eat in a day. Maybe a clue can be found in the details?
  21. Mark.
    Whole "packer" brisket with most of the fat intact is great. I bake it for a day at 180F (about 82C). It took a while to get myself to eat the fat: I always wanted to eat the fat on corned beef brisket as a boy, and decades later I still feel disobedient. With good seasoning the fat is nicely flavorful.
  22. Exceptionally Brash
  23. Alex
    I also think I read that Jimmy Moore has had his last couple of cardiac calcium scores come in at zero. I personally have never had a lipid panel done (maybe they did one with the volume of blood the OB took during my final pregnancy but results were not shared with me.) I don't know if there really is any compelling reason to do these tests when I have eaten a very clean low carb paleo diet for years now.
  24. daniel b ferreira
    I have been ok keto for the past 2 yrs.
    Im lean and muscular. Cholesterol perfect by my docs standard. And when I told him I eat 20 eggs a day, he called me a genetic freak bc my cholesterol was better than everyone he sses daily.

    Excuses I hear bc of my awsome cholesterol
    1. You are young
    2. You work out
    3. Genetic freak
    4. Your doc is lying

    Point is , there is no point. If you want to belive that being on ketosis is like being on starvation mode you are obviously naive. How can you starve and eat calories?

  25. Wade Henderson
    Well apparently there are some people who can have great lipid panels on a LCHF diet just as there are on a HCLF diet. The anecdotal reports give us many examples.

    I wouldn't be surprised if Tommy Runesson had gone on a HCLF diet and not only lost a similar amount of weight, but also had a similar lipid panel outcome.

    Which method would provide the best long term health is unknown for any one individual.

    People looking for better health should experiment. See which path is best for them.

  26. Andrew
    Eat an avocado once in a dang while, Heck if you like them eat one everyday. No problem and watch those numbers plummet.

    I thought the whole cholesterol = CPD had been shown to be hogwash.

    Reply: #27
  27. sten
    Total cholesterol = Hogwash ? Yes indeed, but trying to manipulate it can also be dangerous.

    General consensus is that HDL is credit and LDL is debit. Not even very creative accountants have suggested to add debit and credit together and drawing conclusions of financial health from the rendered total. Yet medical science is above here, or at least different; there seems to be few boundaries on creativity when it comes to increase statin sales, even though risk of hemorrhagic stroke can increase in some circumstances, in a select few statin can also be beneficial. That no across the board increase/decrease of CVD risks have been found to be associated with low or high totalt cholesterol should consequently not come as a surprise for anyone initiated and most of us assume our doctors are initiated professionals, not statin sales agents.

    Reply: #29
  28. Chupo
    Another one with "normal" cholesterol here. I've been doing this for five years. My cholesterol is:

    TC 177
    TG 68
    HDL 77
    LDL Calc 86

    What happens is that the few people whose numebers jump way up the are the ones who get noticed and are remembered.

  29. FrankG
    Yes sten I never did get the focus on Total -C...

    as you point out HDL-C is deemed "good" so more = "better"

    BUT HDL-C is part of what makes up Total-C

    ...where somehow more HDL-C = higher Total-C = "BAD!"

    Some logic there escapes me but then I am not in the business of selling statins :-)


    and @WH "I wouldn't be surprised if Tommy Runesson had gone on a HCLF diet and not only lost a similar amount of weight, but also had a similar lipid panel outcome."

    I would have been very surprised if that had happened. The evidence that it doesn't happen is all around us. Not to mention the studies which Dr Andreas has listed here which showing more favourable lipid panels on an LCHF diet.

    Reply: #30
  30. sten
    Agree. Statin sales is for the ones on HCLF diet, the standard diet, but low carbers are often feeling a pinch especially soon after starting.
    When changing to a low carb diet the LDL weight goes up due to larger LDL particle sizes
    Most people that go LCHF can be assumed to have health issues, the reason they started LCHF.
    Start off with many small LDL particles and no surprise that they initially get bigger. Not until most of the High Carb (high blood sugar peaks-) driven inflammations have petered out the also LDL weights reduce.
    In between start measure the numbers that reflect the real risk for cardiac arrest in ALL populations segments: the Apo-Quotient (AQ). It distinguishes between high risk small LDL and low risk larger particles.
    I had AQ 0.63 after a year on strict LCHF. Normal is 0.7-0.9. Before I don't know what it was but I suffered from stentable angina pectoris for 6 years before LCHF so I guess I would have been way over 0.9.
    Double the AQ value means double the number of heart attacks measured on over 30,000 heart attacks worldwide through the Inter Heart study from 2006.
    That's real figures, not figures to flog statins.
    Reply: #31
  31. murray
    sten, how is the Apo-Quotient determined?
    Replies: #33, #34
  32. murray
    Bob, cheese has very little or no lactose. Lactose is what the bacteria feed on during fermentation. Some people report blood sugar response to milk products such as cheese and butter. I don't. I measured myself and don't seem to respond this way. Indeed, my lowest body fat I ever measured was arriving home after a two-week vacation in Italy that was for the most part a cheese tour, during which I ate a lot of cheese. There are fantastic local cheeses in Italy, as one might expect.
  33. Zepp
    Its a test there they count every APOb and APOa1.. then they now how many one have.

    ApoB is LDL, APOa1 is HDL.. and there are only one of those apolipoproteins in every LDL and HDL.

    Reply: #38
  34. sten
    Zepp is right.
    The number of LDL and HDL particles are being accounted for via the lipoproteins, then #LDL/ #HDL. Google "Inter Heart Study" for the risks!
    Diet doctor is very clear here, but in Swedish....!
    Don't ask me why not translated yet...
    The last (?) section not yet translated?
  35. murray
    Got it, re Apo-quotient. Thanks.

    Thomas Dayspring argues (based on statistics) that it is only LDL-P that matters, for which apo-B is a surrogate, and not LDL particle size. I didn't find the numbers overwhelming (Peter Attia reproduces the argument on his blog). Dayspring notes that some people in ketosis with high sat fat get high LDL-P. He acknowledges there is no data for this group regarding heart disease risk and that projecting from SAD high LDL-P data to LCHF might be invalid, but he is of course cautionary in the absence of data showing low risk.

    I note that the Apo-quotient does not directly account for LDL-P particle size, but presumably this would be accounted for in the apo-A number, on the assumption that more HDL particles is indicative of a diet that makes the LDL-P larger.

    It is unclear to me whether high HDL is actually causative to lower CVD risk, or is merely indicative of a diet and lifestyle that is low risk. Dayspring notes HDL serves numerous functions transporting cholesterol in the body, so there is no simple direct metabolic explanation.

    Are there studies that show apo-B/apo-A is a better predictor than LDL-P? A better predictor than TRG:HDL-C ratio?

    Replies: #36, #37
  36. Zepp
    APOb/APOa1 is the new golden standard in Sweden.. to predict risk of CVD from lipids!

    And if one take the standard lipid panel in the same time.. there are a good corelation to find out if one have a lot of small LDL.

    I think it was Interheart studie that fund that there are a clear link betwen high HDL and lower risk of CVD.

    But.. some drug companys tryed to develop drugs that rise ones HDL.. and they did.. but it didnt alter the risk of CVD!

    So it sems that high HDL is only a sign of a good and healty lipid metabolism.. if it comes the natural way!

  37. sten
    Don't know about LDL-P but here is a direct link to an original diagram from the Inter Heart study showing AQ and heart attack risk. Risk from about 1x to 4x when AQ from 0.4 to 1.28 .

    Since it would take longer time to get an heartattack with a better AQ, even a rather good AQ could result in one, but I guess at much higher age! Would like to see the diagram age adjusted, which could be 4 graphs one for each age group.

    Otherwise we now know -or think we know - that high blood sugar is main culprit not only causing injury to blood vessels walls but also directly through these injuries prompting requirement for increased LDL-production, the sole repair material used to heal the injuries.

    The formation of plaque I see like a renewed injury to an injury, before healed out or old scab fallen off. On a high a carb diet small injuries can be often be inflicted at least once a day, damage increasing with meal size and accelerated by reduced blood sugar control. Dr Davies of trackyourplaque has found plaque to increase exponentially without intervention, and reduced by normalizing blood sugar especially after meals (1 hour values). The reduction to take place by deselecting/reducing implicated foods.

  38. Francois
    Zepp, a few precisions on cholesterol. HDL is HDL and has nothing to do with either apo-A or apo-B. They are different things.

    Cholesterol is not a fat but a sterol (something similar to a wax). Cholesterol is an essential component of our makeup and is an essential component of our cell walls and the basic building block for all our sex hormones, amongst other things. If we don't eat cholesterol, our liver will make some. We need it: it is essential.

    Cholesterol has to be coupled to a protein to be able to circulate in our blood vessels. When it leaves the liver to go to all the cells of the body, it is carried by LDL (low density lipoprotein). When all cells have been repaired, cholesterol is brought back to the liver by HDL to be reprocessed and sent back via LDL to the tissues in periphery.

    People have accused cholesterol of "causing" heart disease because there is cholesterol in each and every plaque (this is an observation, and cannot imply causation. Most physicians and epidemiologists have forgotten that fact. To try reducing plaque and the incidence of heart and vascular disease by decreasing cholesterol levels is like trying to reduce the number of fires in a city by getting rid of firefighters, who are always there when there is a fire... If you don't treat the cause, you won't resolve the issue (as statin drugs have some anti-inflammatory properties, this may explain why statins do reduce the incidence of cardiovascular disease in males over the age of 50 and below 65 who have already suffered from a heart attack). But marketing is so strong, data so manipulated and deceitful that 75% of statin prescriptions are given in primary prevention, where they have no effect whatsoever to reduce cardiovascular events.

    Cholesterol is not the cause of heart disease: inflammation is: inflammation is caused by chronically elevated blood sugars or by an excess of omega-6 or the mere presence of any trans fats.

    When this happens, LDL-cholesterol becomes inflamed and oxidized (the apo-B LDL-C). Apo-B is extremely sticky and will attach to any raw surface on the inside of the blood vessel.

    So what you want is high HDL, relatively high cholesterol (there is a J curve for people over 60 where the lowest risk of death is when the total cholesterol is at 7"ish". The risk increases as cholesterol decreases and increases quite rapidly as cholesterol gets over 7). As far as LDL-chol, you want apo-A, not apo-B.

    How do you know? Your doctor could ask for a LDL particle size evaluation, but this is rather expensive and in the US and in my country (Canada), most general practitioners don't have a clue of what you are speaking about. But there is an easy way out: when triglycerides (another component of the lipid panel) are elevated, you are in trouble, as the LDL is probably apo-B. When triglycerides are low, then the LDL-C is probably the heart-neutral apo-A. And of course, triglycerides will increase with alcohol AND Carbs. The higher the carbs intake, the higher the triglycerides. So stick to LCHF.

    Reply: #39
  39. Zepp
    Strange.. becuse APOa is in HDL.. and APOb is in LDL!

    Its a way to count those, becuse there are only one in each.

    Otherwise.. I agree with you.. but I didnt thougt I needed to explain everything?

    And as you say.. numbers of APOb is important.. peticuly numbers of small ones.. but I dont know anybody doing that test outside some scienetific laboratories.

    Reply: #40
  40. Francois
    Sorry to be a pest, but HDL is HDL (the transport back to the liver) and LDL (the transport to the periphery) can either be non oxidized (apo-A LDL) or oxidized (atherogenic) (apo-B LDL.

    You need HDL AND LDL, but you want the LDL to be apo-A. If you did not have LDL, you could not bring back your cholesterol to the liver.

    As for the total deaths versus total cholesterol curve I was referring to, please see this blog entry by Stephan Guyenet - specifically the graph from the Mr Fit data. Total mortality decreases significantly until blood cholesterol hits 7.0. Then, it increases again. Too bad we do not have data on HDL and LDL (apo-A and apo-B). Would have been interesting.

    If you have access to full articles of the Lancet, go take a look at the following article: truly fascinating! Forette B, Tortrat D, Wolmark Y, “Cholesterol as a risk factor for mortality
    in elderly women”, The Lancet, April 22, 1989, 868-870

    Reply: #42
  41. Chupo

    You are confusing pattern A and pattern B LDL with ApoA-I and ApoB. ApoA-I is only found in HDL.

  42. sten
    This is what or dietdoctor writes. My translation of first paragraph from:

    As discussed above, it is a problem that most dangerous blood fats - small dense LDL, is not shown in a normal LDL sample. Luckily there is a very good solution to this problem. Each LDL contains an edition of a protein called apolipoprotein B. Each HDL on the other hand, contains an edition of a protein called apolipoprotein A1.

    One can measure the amount of these which represents the NUMBER of LDL particles.
    In this way, the dangerous small, dense LDL become proportionally well represented.


  43. murray
    Francois, it seems there is some lack of consensus on these points, or perhaps difference in terminology or abbreviations. Dr. Thomas Dayspring refers to cholesterol binding to apo-A1 and apo-A2 proteins to make various forms of HDL. He also notes the multi-facted roles of HDL. One of these includes transferring cholesterol into LDL particles (through cholesterol ester transfer proteins). I saw a report that found people with reduced CETP activity tended to higher cardiovascular disease. This suggests a protective function of HDL may be to keep LDL particles large and fluffy and keep them from circulating as small dense LDL particles. (Just my hypothesis.) In any event, the following summative paragraph from a Dayspring manuscript indicates we don't really know why HDL may or may not have positive effect.

    "We have to redefine our HDL terminology. As with all lipoproteins, HDL particles are
    involved with vascular cholesterol transport (moving it in several directions). HDL
    acquires UC mostly from the liver and small intestine but also from peripheral tissues and
    esterifies it. The CE is trafficked to the periphery (steroidogenic tissues, adipocytes) or
    directly back to the liver or intestine (TICE) or transfers it to apoB particles (LDLs).
    HDL participates in both direct and indirect RCT, although only a minor amount of the
    CE in HDL derives from what is termed MRCT (delipidation arterial wall macrophages).
    Thus HDL particles participate in both forward and reverse cholesterol transport. If one
    looks at the overall efficient flux process of peripheral cholesterol transport, where HDL
    particles are formed, lipidated, exchange lipids, and then delipidated one can understand
    that the overall process will not affect the total HDL-C level in a predictable fashion, as
    there is constant remodeling or shifting of HDL particle size and cholesterol content.
    Despite what has been taught for decades, a serum HDL-C has no relationship to the
    apoA-I lipid trafficking process (review the next graphic). Indeed there is no available
    blood test (e.g. HDL sizes, HDL-P, HDL subfraction-cholesterol) that a clinician can use
    to assay exactly what HDLs are doing in a given individual."

  44. FrankG
    For me the take-away from all this discussion is that: "cholesterol" is NOT as simple and straightforward a concept as we have been led to believe for the last few decades.

    Heck we still have some "experts" talking in terms of it clogging up the arteries like the build up in the water pipes in your house!

    The days are long gone when I will accept a "oh your cholesterol is high, you need to avoid saturated animal fats and take a statin" ...and yet sadly (potentially dangerously in my view) that message is still being promoted!

  45. Zepp
    There are different apolipoproteins in different lipid fractions.. APOb100 is in LDL, VLDL and IDL.

    APOb48 is found in chylomicrons.

    APOa1 is found only in HDL!

    Those Apolipoproteins have a function.. they are keys that attatch to different receptors.

    Its overkill to know about it.. one only need to know how they do the tests.. and they measure APOb 100 and APOa1.. to count the numbers of LDL and HDL!

    The thing is.. that APOb100 counts for one VLDL, LDL, IDL or LDLremnant.. and APOa1 is one HDL!

  46. Z.M.
    I don't buy the "response to retention" hypothesis pushed by people like Dayspring and Attia. IMO modified ldl/oxidative stress is far more important. The body seems to want to prevent these changes as much as possible given that there are antioxidants within LDL. Also, HDL transports vitamin E, has antioxidant properties and inhibits LDL oxidation.
    Reply: #47
  47. sten
    Re antioxidants....
    There are other factors like dietary omega 6 that clearly predated our new found(?) need for lots of "antioxidants". Could it be that part of the inflammatory action ascribed to omega 6 fats are consequences of that the those fats - when taken in excess as often today - simply will not survive as long in our bodies as the more difficult to oxidize monounsaturated and saturated fats will?

    Some Americans heavy in omega 6 consumption can be found with over 70% HUFAs ( omega 6 and other highly unsaturated fats) in their BODY FAT TISSUES, by tissue fat composition analysis.
    At the same time CVD mortality as per graph (appr. 3 pages from top) is over 4 x higher than those with only 30% tissues made up of omega 6 fats.
    Swedish surgeons have had fat composition in arterial plaque analyzed and found omega 6 to be the most prevalent fat in such plaque.

    Is it possible that LDL (and HDL) in part can be made up of omega 6 fats due to dietary excess of such fats (or shortage of the other fats), resulting in an easy oxidized LDL variety ? Any related research on composition of LDL and oxidized LDL ?

    Reply: #48
  48. sten
    Here is a study supporting the problem of PUFAs in LDL:
    "....we found that the major fatty acid oxidation product was esterified hydroperoxyoctadecadienoic acid (HPODE), the oxidized product of the most abundant polyunsaturated fatty acid in human LDL, linoleic acid..." From:
    (Paper from 1994.)
    Combined with the strong association of heart disease with high tissue HUFA content the evidence against the "heart healthy fats" being real culprits start to look credible.

    Here a link to a study abstract where effectiveness of reservatrol protecting PUFA s from oxidation is investigated.
    Is it so easy that monounsaturated and saturated fats don't need to be investigated while easy to oxidize omega HUFAs like linolenic, linoleic and arachidonic fatty acids.

    Finally Stephan Guyenet wrote about this alread 2009 !

    One take home is that Unilevers Becel (Benecol?) reduces cholesterol very well but the same fats also enable the production of LDL rich in PUFAs which are easy to oxidize.
    OxLDL has been shown to predict heart disease 2- 4 times better than conventional tests, according to Stephan. Unilever has restricted its claims to lower choleserol.

    Did Unilever really never check prevalence of heart disease in the regular customer base to try to widen the sales scope to also cover heart disease in general ?

  49. Jennifer - Yummylowcarb
    I am about to book my cholesterol check and am really excited to see what LCHF and intermittent fasting has done for my levels (don't think I have ever had high cholesterol but still interesting to check!).

    PS. Follow my instagram for LCHF recipes and inspiration - @yummylowcarb

  50. Z.M.
    Sten, I believe excess omega-6 to be a problem also.

    Unfortunately we have no trials testing current omega-6 intakes to very low intakes. The Lyon Diet Heart Trial achieved the best n-6:n-3 ratios and had the best result of any diet trial despite no differences in cholesterol levels between the groups. So it is consistent with the idea that low intakes of n-6 fats are desirable.

    The data comparing different fats with regard to the oxidation of LDL are in-vitro and short term studies. Not reliable! Oxidative stress/modified ldl is a very complicated phenomena which is why researchers are still trying to develop biomarkers to measure it accurately. Also, there may be non-oxidative mechanisms that contribute to disease also, so I don't mean to imply that this is the only issue.

    I suggest to take a look at my thoughts here -

1 2

Leave a reply

Reply to comment #0 by

Older posts