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The definitive guide to saturated fat (or how to stop worrying and love butter)

2

Comments

  • #2


    If you believed everything Cordain wrote you'd have nothing left to eat. One of his newsletters focused on the dangers of the toxins in bananas, I mean seriously!

    Academia is all about getting published these days ;)


  • #2


    Cordain may be the father of paelo in some ways but i think his thoughts on saturated fat are more than a little outdated.

    Uffe Ravnskov as been banging on about this for years and to be honest if you have not read or listened to even the smallest amount of his work then your understanding of nutrition is incomplete.

    http://www.ravnskov.nu/cholesterol.htm

    i remember going to a charles poliquin (he gets a bashing from many people but has wayyyy more right than wrong IMO) week long event called the fat loss symposium in which i asked Dr Mark Huston (featured in video below and highly respected doctor) about Uffe and he was in total agreement with Uffe (though still recommend combined use of conventional medicine along with e.g. fish oils etc) and was in constant contact with him.



    It is for this reason that i think doctors who many hold to be givers of health and there some good ones out there, need to get back to re-learning their biochemistry and nutrition so they can help people avoid taking drugs (statins being the primary one!!).

    If more people focused on getting healthy and less on NOT BEING FAT there would be way less struggle with their weight and an explosion in their health.


  • #2


    was very upset and shouting at the telly last night watching supersize vs superskinny. they told the fat lad (and everyone watching) that saturated fats were bad and were increasing his risk of heart disease, and to stop having butter. FFS.


  • #2


    Parsley wrote: »
    was very upset and shouting at the telly last night watching supersize vs superskinny. they told the fat lad (and everyone watching) that saturated fats were bad and were increasing his risk of heart disease, and to stop having butter. FFS.
    yes like butter was what got him that wayyy ,

    go figure ehh


  • #2


    Saturated fat for a failing heart, new study (rats again unfortunately, better than mice though):

    http://ajpheart.physiology.org/content/299/2/H410.abstract


  • #2


    Saturated fat for a failing heart, new study (rats again unfortunately, better than mice though):

    http://ajpheart.physiology.org/content/299/2/H410.abstract

    Im sorry, this may be ignorant but I simply did not have time to read all the posts and at a glance did not see any differentiation of saturated fat type.

    I always recommend at risk patients limit their intake of lauric (C12), myristic (C14) and Palmitc (C16) especially myristic acid, considering these are the most potent cholesterol and insulin rising components.

    Now I dont cut them out, yes there are necessary needs like N-palmitoylation and S-myristylation for post-translational protein modification or monlaurin formation, all necessary in our defences against disease.

    However as a whole where solid fat is wanted, I still recommend a high intake be based upon stearic acid, where insulin levels will not be increased and cholesterol will actually be lowered.


  • #2


    Mellor wrote: »
    Conventional wwisdom, or marketing?
    Seriously, think of the last 5 or 10 times you heard source say, or imply (by saying low in sat fat, or similar). What was the source?
    An scientific paper or an ad for a butter substitute

    Well British Nutrition Foundation says sat fat should not exceed 10% daily energy.

    That's one source


  • #2


    Parsley wrote: »
    was very upset and shouting at the telly last night watching supersize vs superskinny. they told the fat lad (and everyone watching) that saturated fats were bad and were increasing his risk of heart disease, and to stop having butter. FFS.

    What's the problem with that advice?


  • #2


    Compak wrote: »
    Im sorry, this may be ignorant but I simply did not have time to read all the posts and at a glance did not see any differentiation of saturated fat type.

    I always recommend at risk patients limit their intake of lauric (C12), myristic (C14) and Palmitc (C16) especially myristic acid, considering these are the most potent cholesterol and insulin rising components.

    Now I dont cut them out, yes there are necessary needs like N-palmitoylation and S-myristylation for post-translational protein modification or monlaurin formation, all necessary in our defences against disease.

    However as a whole where solid fat is wanted, I still recommend a high intake be based upon stearic acid, where insulin levels will not be increased and cholesterol will actually be lowered.

    Beef fat is mostly stearic acid FWIW.

    But I don't get the fear of the other fats, why would our body convert all excess carbohydrate to palmitic acid if it was so toxic to us? In fact the majority of palmitic acid in the bloodstream is derived from carbohydrate. Dietary palmitic acid has very little influence on serum palmitic acid beyond initial post-prandial levels.

    Lauric acid is largely the reason why coconut oil has such a great health reputation, it's anti-bacterial, anti-fungal and anti-viral as well as increasing HDL cholesterol.

    Can I see the ref where sat fat raises insulin? Preferably fasting insulin as post-prandial insulin release doesn't really have a negative effect. (In a healthy person, barring hyperinsulemia or something like that)


  • #2


    Compak wrote: »
    What's the problem with that advice?

    Doctor, I strongly suggest you read this thread from start to finish.


  • #2


    Beef fat is mostly stearic acid FWIW.

    But I don't get the fear of the other fats, why would our body convert all excess carbohydrate to palmitic acid if it was so toxic to us? In fact the majority of palmitic acid in the bloodstream is derived from carbohydrate. Dietary palmitic acid has very little influence on serum palmitic acid beyond initial post-prandial levels.

    Lauric acid is largely the reason why coconut oil has such a great health reputation, it's anti-bacterial, anti-fungal and anti-viral as well as increasing HDL cholesterol.

    Can I see the ref where sat fat raises insulin? Preferably fasting insulin as post-prandial insulin release doesn't really have a negative effect. (In a healthy person, barring hyperinsulemia or something like that)

    Sorry whats FWIW?

    Never start with "why would our bodies", it straight away creates a bias.
    Plus we know excess carbs especially when introduced to replace fat raise serum triglycerides and supress HDL.

    I know Lauric acid is anti-infective, it is why we need limited amounts for monlaurin production

    here is a ref for sat fat raising insulin and also points out it is a lack of comprehension to dismiss carbon chain length in determining the biological effects of your fat.

    J Surg Res. 1992 Apr;52(4):328-33.
    Insulinotropic potency of lauric acid: a metabolic rationale for medium chain fatty acids (MCF) in TPN formulation.
    Garfinkel M, Lee S, Opara EC, Akwari OE.


  • #2


    Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease - 12566134

    "When saturated or trans unsaturated fats are replaced with monounsaturated or n-6 polyunsaturated fats from vegetable oils, primarily low-density lipoprotein (LDL) cholesterol decreases. The LDL to high-density lipoprotein (HDL) cholesterol ratio decreases. When carbohydrates are used to replace saturated fats, in a low-fat diet, LDL and HDL decrease similarly, and the ratio is not improved; triglycerides increase as well when carbohydrate increases, except when low glycemic index foods are used."

    Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. 20351774

    "These findings provide evidence that consuming PUFA in place of SFA reduces CHD events in RCTs. This suggests that rather than trying to lower PUFA consumption, a shift toward greater population PUFA consumption in place of SFA would significantly reduce rates of CHD."


  • #2


    Tremelo wrote: »
    Doctor, I strongly suggest you read this thread from start to finish.

    True, but let me say I once believed the same as you about sat fats.
    Its not all one big conspiracy theory. There is some proof required by agencies when they set recommendations.

    The max recommendations as I have them

    -Australia, sat fat max 8%
    - Germany and surroundings - 10%
    -Northern Europe - 10%
    -France -8%
    -Netherlands -10%
    -Uk -11%
    -USA - 7%

    WHO - 10% and 7% in high risk patients

    They do have experts with some type of aptitude and base their careers in this area.


  • #2


    Ah looking at papers past 12am, its like the good old study days

    An independent association of saturated fat intake with CVD risk has not been consistently shown in prospective epidemiologic studies, although some have provided evidence of an increased risk in young individuals and in women. Replacement of saturated fat by polyunsaturated or monounsaturated fat lowers both LDL and HDL cholesterol. However, replacement with a higher carbohydrate intake, particularly refined carbohydrate, can exacerbate the atherogenic dyslipidemia associated with insulin resistance and obesity that includes increased triglycerides, small LDL particles, and reduced HDL cholesterol. In summary, although substitution of dietary polyunsaturated fat for saturated fat has been shown to lower CVD risk, there are few epidemiologic or clinical trial data to support a benefit of replacing saturated fat with carbohydrate.

    Furthermore, particularly given the differential effects of dietary saturated fats and carbohydrates on concentrations of larger and smaller LDL particles, respectively, dietary efforts to improve the increasing burden of CVD risk associated with atherogenic dyslipidemia should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.


  • #2


    Compak wrote: »
    True, but let me say I once believed the same as you about sat fats.
    Its not all one big conspiracy theory. There is some proof required by agencies when they set recommendations.

    The max recommendations as I have them

    -Australia, sat fat max 8%
    - Germany and surroundings - 10%
    -Northern Europe - 10%
    -France -8%
    -Netherlands -10%
    -Uk -11%
    -USA - 7%

    WHO - 10% and 7% in high risk patients

    They do have experts with some type of aptitude and base their careers in this area.

    My diet is around 60% fat (approx. 40% saturated fat) for well over a year. I've lost approximately 30kg of excess bodyfat eating this way, and my cholesterol levels have fallen markedly. Just some anecdotal evidence. I certainly won't be lowering my butter and meat intake any time soon ;)


  • #2


    Diet-heart: a problematic revisit

    Extracts of a critical review of a meta analysis which showed sat fat was associated with 1.07 risk of CVD (non significant)

    "Of 15 studies that unequivocally concern the SFA-CHD relation, 4 did not
    include other dietary lipids or serum lipids among covariates. Their CHD relative risks (RRs) ranged from 1.22 to 2.77"

    "As to item 3, the meta-analysis did not compare SFA–fatal CHD and SFA–total CHD outcomes (total CHD is undefined). This merits exploration. My calculations, from data for 16 CHD studies (meta-analysis tables), with RRs weighted by person-years of exposure, yielded contrasting CHD risks: for “hard” fatal CHD (11 studies), the RR was 1.32; for “soft” total CHD (5 studies), the RR was 0.99; and for all 16 studies, the RR was 1.09 (compared with the meta-analysis RR estimate of 1.07). "

    "the meta-analysis (2) reported its findings as independent of a quality score including diet assessment. Of the 16 CHD studies, 4 relied on one 24-h dietary recall; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Five used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids (2). These facts, which were unnoted in the meta-analysis (2), prompt the question: Did low-level reliability (reproducibility) of dietary SFA data drive RR values toward 1.00 (the regression-dilution bias problem)? No data on SFA reliability are given."

    "Trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits.” The investigators concluded that “more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk” (5). This inference is concordant with extensive data that show CHD rates lower by 90% and life expectancy years longer for the small minority of adult Americans with favorable levels of the 4 readily measured diet-dependent major CHD risk factors [total cholesterol, BP, body mass index (BMI), glycemia/diabetes] and nonsmoking status"


  • #2


    Tremelo wrote: »
    My diet is around 60% fat (approx. 40% saturated fat) for well over a year. I've lost approximately 30kg of excess bodyfat eating this way, and my cholesterol levels have fallen markedly. Just some anecdotal evidence. I certainly won't be lowering my butter and meat intake any time soon ;)

    My cholesterol was 2.8 5 years ago. Do I win?

    Im sorry Im just kidding, Im not anti anti fat or sat fat. Indeed I see full merits of atkins like diets.

    Truth is sat fat as a group and for a population will likely not be a massive risk, especially if as and Im just guessing you've lowered your carbs significantly especially refined carbs.

    I also have to ask if you incorporated/increased exercise in this regieme change.

    But for certain groups especially genetic hypercholesterolemia sat fat is a major cholesterol production inducer and broad sweeping statements by some people not to worry about fat because an observation study of a population -open to massive bias- showed a trend but failed to reach significance really just are unfair on these people


  • #2


    Another pro paper

    Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study. 2010

    SFA intake was inversely associated with mortality from total stroke, including intraparenchymal hemorrhage and ischemic stroke subtypes, in this Japanese cohor


  • #2


    Yes, you win. But give me another year ;)
    Compak wrote: »
    I also have to ask if you incorporated/increased exercise in this regieme change.

    I did. But calorically, the vast majority of my excess weight was lost in the kitchen, not the gym.


  • #2


    Ok last one since its so late and Im prob talkign to myself

    This is a nice one to finish on as its a 2010 review from an expert panel in Denmark

    "Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2–3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives."

    Just my own additional points


    One, they say insufficient evidence exists for a benefit for replacing with MUFAs, true but what does exist is quite positive

    Two, the bit I made bold is so important and what I tried to bring up. I know it got dismissed and I realize that people here are likely not biochemists academics in nutrition etc and so distinguishing effects of fat group type is difficult enough without breaking them down further.

    But lets say for now sat fats are totally neutral on cholesterol. Well if I know that stearic acid -which is abundant in the typical sat fat found in the diet-lowers cholesterol, well surely by simple math there is another fatty acid raising it back up to give a net of 0.

    So just like I can manipulate the effects of omega 3s by what fatty acid chain is positioned in the sn2 position I can also influence the effects of the fatty acids by determining what type of ones I take.

    This why you will often hear that dairy is the worst for raising cholesterol levels in susceptible people


  • #2


    Tremelo wrote: »
    Yes, you win. But give me another year ;)



    I did. But calorically, the vast majority of my excess weight was lost in the kitchen, not the gym.

    ha ha actually Im up to 3.4 now, so I fear another year :)

    Do you understand though that your n=1 study would be thrown out academically? As regardless of your source of weight loss -though exercise is a big plus- weight loss alone dramatically reduces your risk of CV disease and all indicating factors. The inflammation reduction alone from 30kg of fat loss -congrats btw-is just huge.


  • #2


    Compak wrote: »
    Do you understand though that your n=1 study would be thrown out academically?

    You do understand he wasn't suggesting it was a study but rather anecdotal?
    Are you aware that there have been study with significant numbers of participants, they have been accepted, published and show the same results?


  • #2


    Compak wrote: »
    Sorry whats FWIW?

    Never start with "why would our bodies", it straight away creates a bias.
    Plus we know excess carbs especially when introduced to replace fat raise serum triglycerides and supress HDL.

    I know Lauric acid is anti-infective, it is why we need limited amounts for monlaurin production

    here is a ref for sat fat raising insulin and also points out it is a lack of comprehension to dismiss carbon chain length in determining the biological effects of your fat.

    J Surg Res. 1992 Apr;52(4):328-33.
    Insulinotropic potency of lauric acid: a metabolic rationale for medium chain fatty acids (MCF) in TPN formulation.
    Garfinkel M, Lee S, Opara EC, Akwari OE.

    FWIW, For what it's worth. :)

    That paper is post-prandial levels, and in mice. I'd have to see something for fasting insulin to be remotely concerned. Post-prandial insulin is not the bogeyman we once thought it was. Physiological =/= pathological.

    Plus last time I checked we don't eat fatty acids in isolation, and it's misleading to extrapolate these very reductive studies to a human population without an controlled human trial. For example if you feed isolated fructose to mice their triglycerides rise, but feed those mice fructose in the context of honey and we don't observe the same effect.

    Re: LDL, review papers in this area are based on short-term feeding studies, which as saturated fat enhances the clearing of fat from the liver, this is a temporary effect. Long term studies show no association between chol and sat fat intake.

    Also, PUFA lowers cholesterol, but not in a good way, it lowers the total volume but increases the proportion of small-dense LDL.

    Re: epidemiology, did you look at the graph I posted of consumption in Europe? How can you pull a positive correlation out of that? If anything there's a slight negative correlation. Also the pacific islanders who eat 50% of their diet of lauric acid rich coconut oil and have little to no heart disease.

    In any case, I'd need a controlled trial where they made one group reduce sat fat and it reduced coronary events.

    I'm aware of the Lyon Diet-heart trial, which reduced PUFA below 4%.

    Then there's the Finnish Mental Hospital trial which had a flawed design as well as issues with the control group taking more drugs known to increase the risk of CHD.

    Then you have the Corn oil trial that increased PUFA for sat fat and increased heart attacks.

    I'm dashing off to work but I'll update later.

    TLDR: Show me controlled studies in humans where any type of sat fat increased coronary events.


  • #2


    Compak wrote: »
    Ah looking at papers past 12am, its like the good old study days

    An independent association of saturated fat intake with CVD risk has not been consistently shown in prospective epidemiologic studies, although some have provided evidence of an increased risk in young individuals and in women.

    No it hasn't, 25 trials, only 4 showed an association. That's pretty much the opposite of consistent.


  • #2


    No it hasn't, 25 trials, only 4 showed an association. That's pretty much the opposite of consistent.

    Write a critique to the peer reviewed study and get it published, its not my quote.


    We will agree to disagree you can't post a nutritional study in the world that I cant flaw, its nutrition, so seriously its a mute issue.

    the simple fact you tried to critique the well known fact that increasing PUFAs will lower CHD by using an n6 only study shows you will not be deterred even if you try and pulll the wool over peoples eyes.

    Where are your RCTs? why is the onus on me to prove every world authority right and you as an internet poster who has the backing of other posters start off as infallible. Observationals studies at most are a possiblity.

    Fact is I personally don't care, last time I checked I did nt have stocks or financial interest in saturated fats. I know what I see in clinical practice.

    You dont even have the balance to give a simple recommendation of to try your 'theory' put and get bloods done a few months later.


  • #2


    Compak wrote: »
    Write a critique to the peer reviewed study and get it published, its not my quote.


    We will agree to disagree you can't post a nutritional study in the world that I cant flaw, its nutrition, so seriously its a mute issue.

    the simple fact you tried to critique the well known fact that increasing PUFAs will lower CHD by using an n6 only study shows you will not be deterred even if you try and pulll the wool over peoples eyes.

    Where are your RCTs? why is the onus on me to prove every world authority right and you as an internet poster who has the backing of other posters start off as infallible. Observationals studies at most are a possiblity.

    Fact is I personally don't care, last time I checked I did nt have stocks or financial interest in saturated fats. I know what I see in clinical practice.

    You dont even have the balance to give a simple recommendation of to try your 'theory' put and get bloods done a few months later.

    Lets say that no one had ever said that saturated fat increased heart disease, and someone presented you with the evidence you've presented us. Would you describe that evidence as weak or strong in support of that hypothesis? Be honest.

    I don't need to write the review article, it has already been done by a renowned Harvard lipid researcher.

    I don't need RCT's to prove no association, if there's no proof, there's no proof. I've pretty much reviewed all the available evidence for the theory and seen it to be flawed, weak and inconsistent.

    The fact that many public health authorities recommend it is merely an appeal to authority, given that the evidence they based that decision on was flawed I think their opinion is largely irrelevant. There are lots of public health recommendations that are based on very little evidence. If the public health case is SO strong then how come one little anonymous internet poster can demolish is with no formal training in medicine or biochemistry?

    We have nothing but a few observational studies and RCTs, pretty much all have been listed on this thread or in attached links. You make a great point about how flawed most nutrition science is (the lack of inability to blind is a huge issue for example) but yet you think this flawed evidence is good enough to make a blanket recommendation. If I replaced 'reduce saturated fat' with 'take this drug' would you accept that level of contradictory evidence?

    And yet as weak as this evidence is, the totality of it points to saturated fat being beneficial, not harmful.

    Also, check out my first post with my cholesterol results. I've been eating this way for four years. I don't have a baseline but if it was any lower than that my all cause mortality risk would begin to rise.

    Re: your clinical experience. I severely doubt you saw a long term drop in cholesterol from reducing sat fat without weight loss, reduction in trans fats, reduction in deep fried food, increase in exercise, fish consumption, fruit and vegetable intake and smoking cessation. After all a physician will normally recommend doing these things in tandem and people normally do a number of different things when embarking on a healthier lifestyle.


  • #2


    Sorry to lower the erudition of this thread once more, but El Dangeroso? You know the way you said to love butter? Does that go for cream too? Because today I hit 62.5kg (down from a high of 92) after a year and a half of high fat eating. So I just cracked open a 250ml carton of Avonmore Fresh Cream, whipped it all up, mixed it with strawberries and devoured every last bit of it. Between that and my 250g of ground beef and my 300g of veg drizzled in butter, I won't need to eat for another 24 hours at least. Onwards to 60kg :D


  • #2


    Lets say that no one had ever said that saturated fat increased heart disease, and someone presented you with the evidence you've presented us. Would you describe that evidence as weak or strong in support of that hypothesis? Be honest.

    I don't need to write the review article, it has already been done by a renowned Harvard lipid researcher.

    I don't need RCT's to prove no association, if there's no proof, there's no proof. I've pretty much reviewed all the available evidence for the theory and seen it to be flawed, weak and inconsistent.

    The fact that many public health authorities recommend it is merely an appeal to authority, given that the evidence they based that decision on was flawed I think their opinion is largely irrelevant. There are lots of public health recommendations that are based on very little evidence. If the public health case is SO strong then how come one little anonymous internet poster can demolish is with no formal training in medicine or biochemistry?

    We have nothing but a few observational studies and RCTs, pretty much all have been listed on this thread or in attached links. You make a great point about how flawed most nutrition science is (the lack of inability to blind is a huge issue for example) but yet you think this flawed evidence is good enough to make a blanket recommendation. If I replaced 'reduce saturated fat' with 'take this drug' would you accept that level of contradictory evidence?

    And yet as weak as this evidence is, the totality of it points to saturated fat being beneficial, not harmful.

    Also, check out my first post with my cholesterol results. I've been eating this way for four years. I don't have a baseline but if it was any lower than that my all cause mortality risk would begin to rise.

    Re: your clinical experience. I severely doubt you saw a long term drop in cholesterol from reducing sat fat without weight loss, reduction in trans fats, reduction in deep fried food, increase in exercise, fish consumption, fruit and vegetable intake and smoking cessation. After all a physician will normally recommend doing these things in tandem and people normally do a number of different things when embarking on a healthier lifestyle.

    Look we will have to agree to diagree. I for one can't stay posting and arguing, I spend enough time all day doing it and get paid well for it, without going over the same things time and time again outside hours.

    I see it in academia all the time, thats nutrition there will never ever be unanimous consensus.

    I for one already admitted as a whole, saturated fatty acids are not a major deal, dep on the rest of the diet, if you are n3 deficient and replace some sat fats with them big plus, replace with carbs especially refined big minus. Off course it appears you won't even accept this


    I tried to add another aspect to the thread, the individual properties of the fatty acid, how this a big factor and manipluation of such can promote the biggest metabolic effect.

    In essence you are not interested. I do not expect most people here to take an interest in them, its big enough chore to check the sat fat content of a food without trying to find out the individual makeup. However considering your initial posts I believed you had a general scientific interest in this field and this would help inform you. However, I see you are not grasping what I am putting across or simply do not care.

    Can I suggest though, considering the fundamental flaws in dietary analysis, recall, questionnaires etc, it is of great use to look at the actual biochemical happenings as discovered by lab tests and animal studies.

    You ignore clinical practice of many I know where sat fat is a no no for familial hypercholesterolemia types, its easy to hide behind a username on a forum, others of us have to deal with litigation issues and Ive not met many in the public to make a claim for any person of any genetic type to eat sat fat as they like.

    We all know sat fat is required and beneficial, the quantity is the point of contention, and this is not proven on either end, so I dont know how you can make such claims.

    Science is about enlightening people and allowing them to make decisions yet it seems to me certain people here just like to go against the norm as contrarian is in trend.

    All I ask is people who up their sat fat after listening to you get baseline bloods done and then bloods done a few months later. I wonder how many would actually do it,despite the supposed want for knowledge. A boards own study, how intriguing that would be.

    Anyway I've said my piece, good luck with your work/ research. Im sure ill see more writings as I mange to pop in every two weeks or so to have a look.


  • #2


    Compak wrote: »
    All I ask is people who up their sat fat after listening to you get baseline bloods done and then bloods done a few months later. I wonder how many would actually do it,despite the supposed want for knowledge. A boards own study, how intriguing that would be.

    You're dead right about this. I didn't embrace high sat fat from El Dangeroso though; I got it from Mark Sisson's Primal Blueprint. And last week I had blood tests done and a full health check. My doctor said I "have a heart like a stag" and that I was one of the healthiest people to walk through his door in six months. This week, I had a DEXA scan done by Prof Phil Jakeman at the University of Limerick who said my body composition is perfectly fine for a male my age and height, though I have a fat mass of 15kg which I will get down to 10kg without problems.

    Now, suppose I had gone for the conventional advice of eat little sat fat, etc. I'd still be on a weight-loss/weight-gain roller coaster. I know that because I've been there. The reality is that I have never in my whole life been healthier than I am now. My case won't stand up academically, but there's no arguing that my health and well-being shot up dramatically when I embraced high fat eating. My success can't be put down to exercise - the sums just don't add up. I lost 80% of my weight, and my cholesterol plummeted, when I started eating a fat-heavy diet. It's incontestable.


  • #2


    Compak,

    Forgive me if I see your post as somewhat of a copout.

    As flawed as observational science is, you seem to be saying that we need to instead rely on in vitro studies and clinical experience, which as you know are lesser forms of evidence. There is no biological plausibility for the same substance that fuels us in our sleep is somehow toxic in dietary form. Lab studies are useful, but only to determine the biological mechanisms of things we already know or to generate hypotheses. You really cannot rely on them as proof of anything. If anything, due to the 'healthy user' and recall biases from 30 years of advice to reduce saturated fat, the observational evidence should indict saturated fat, but it doesn't even come close.

    For example, If I were to rely solely on biochemical rationisations then I would come to the conclusion that too many apples will cause eventual failure of the liver due to the fructose, but as we eat real food and not isolated chemicals, it is unwise to make biological predictions on the basis of a very reductionist viewpoint. This is where the entire saturated fat investigation went wrong.

    Re: Familial hypercholesterolmia, total strawman argument but I'll entertain it. Again I'll ask for long term evidence that saturated fat increases LDL. Short term feeding studies show it does but this effect levels off over time.

    You sound exasperated at the fact that I am not willing to accept weak and inconsistent human evidence, well I'm sorry, but I work in clinical research and have seen countless fabulous looking compounds that bring mice and rats back from the brink of death do absolutely nothing (or worse) to humans. So it's human evidence or no evidence, in this case, no evidence.

    I accept increasing n-3 decreases the risk of CHD (at least in the short term), I don't however agree that carbohydrate is intrinsically atherogenic. We have too many high-carbohydrate eating cultures without overt heart disease for that.

    I'm not interested in the break down of various fatty acids no, why? Because as long as we get enough food we can desaturate or saturate whatever we need. If one was supposedly toxic (and I've never seen a shred of credible evidence that it is), the body can quickly convert it to a non-toxic form.

    It's a bit of name-calling to just say I'm contrarian for the sake of it. I agree with a lot of mainstream nutritional recommendations, but some turned out to be wrong.

    Why are you clinging on to the idea of saturated fat being harmful based on such poor evidence. Again, I ask you if this level of evidence was presented as a drug treatment, would you accept it?


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