Are diets high in omega-6 polyunsaturated fatty acids unhealthy?

Yes, so don’t eat ‘em. Thanks for reading.

Whaddya mean you want more of an explanation?  They just are, okay!?

Look, there are plenty of health professionals who tell you to eat or avoid certain things with little in the way of an explanation, so why can’t I?

Tough crowd.

For the vast majority of you, I am preaching to the converted when it comes to warning of the perils of consuming large amounts of vegetable and seed oils, and the many processed foods that contain them, due to their relatively high omega-6 polyunsaturated fatty acid content (herein abbreviated as n6 PUFA).  Specifically, we are talking about the n6 PUFA – linoleic acid (LA).  Others might require a bit more convincing. Here goes…

The main reason we are consuming large amounts of this fat is due to the diet-heart hypothesis (Omega 6 fats, by the way, are the major fat present in the typical Western diet – so when health authorities/researchers point out that we consume too much fat, or are eating high-fat diets, this n6 PUFA is the fat they are referring to… even if they don’t realise it).  This hypothesis states, as we all know, that high cholesterol levels, specifically high LDL (“bad”) cholesterol, is a strong risk factor for cardiovascular disease (*cough*bullshit*cough*). And by reducing our dietary intakes of saturated fat and replacing some of this energy with polyunsaturated fats such as corn oil, soybean oil, safflower oil, and so on, we reduce our total and LDL cholesterol levels and achieve immortality a reduced cardiovascular disease risk.

My last series of posts tackled some of the issues surrounding this hypothesis and the deficiencies that lie within it.  Following on from those, but sticking with a similar theme, I’ve been reading through some papers that look specifically at healthy halo that surrounds n6 PUFA LA-rich vegetable and seed oils and asks whether the biochemistry matches the marketing hype.  We’ll focus, in this post, on a review paper from 2001 published in the European Heart Journal, possibly drawing on a handful of other papers and maybe spilling over into another post – we’ll see how it all goes.

Before we crack into the gems contained within the 2001 paper, let’s set the scene with the abstract from a more recent meta-analysis on this very topic, just so we can firmly establish my confirmation bias from the get go…

n-6 fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials.

Randomised controlled trials (RCT) of mixed n-6 and n-3 PUFA diets, and meta-analyses of their CHD outcomes, have been considered decisive evidence in specifically advising consumption of ‘at least 5-10 % of energy as n-6 PUFA’.

Here we (1) performed an extensive literature search and extracted detailed dietary and outcome data enabling a critical examination of all RCT that increased PUFA and reported relevant CHD outcomes; (2) determined if dietary interventions increased n-6 PUFA with specificity, or increased both n-3 and n-6 PUFA (i.e. mixed n-3/n-6 PUFA diets); (3) compared mixed n-3/n-6 PUFA to n-6 specific PUFA diets on relevant CHD outcomes in meta-analyses; (4) evaluated the potential confounding role of trans-fatty acids (TFA).

n-3 PUFA intakes were increased substantially in four of eight datasets, and the n-6 PUFA linoleic acid was raised with specificity in four datasets. n-3 and n-6 PUFA replaced a combination of TFA and SFA in all eight datasets. For non-fatal myocardial infarction (MI)+CHD death, the pooled risk reduction for mixed n-3/n-6 PUFA diets was 22 % (risk ratio (RR) 0.78; 95 % CI 0.65, 0.93) compared to an increased risk of 13 % for n-6 specific PUFA diets (RR 1.13; 95 % CI 0.84, 1.53).

Risk of non-fatal MI+CHD death was significantly higher in n-6 specific PUFA diets compared to mixed n-3/n-6 PUFA diets (P = 0.02).

RCT that substituted n-6 PUFA for TFA and SFA without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance (RR 1.16; 95 % CI 0.95, 1.42).

Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.

We have a lot going on here.  Firstly, when we review research around any potential benefits of n6 PUFA’s, we also need to be certain that alongside an increased downing of soybean oil, subjects haven’t been barbecuing large lumps of n3-PUFA (omega-3)-rich salmon, and the like, on the side.  And if we are going to be making claims regarding the benefits of n6 PUFA replacing saturated fat (SFA), we need to be sure that they are indeed replacing saturated fat alone and not saturated fat PLUS the infinitely more troublesome trans fatty acids (TFA’s).

What we can’t have is omega-3 fatty acids replacing trans fatty acids and then claim that substituting out your butter for margarine is doing your cardiovascular system any favours. Because clearly it’s not.  And in fact, based on the above meta-analysis, replacing SFA and TFA with n6 PUFA actually leads to an increased CVD risk.  But selling the opposite message has obvious financial benefits for stakeholder companies if the public and their guiding health authorities are sucked in by it all.

Almost a decade prior to this meta-analysis, we have questions being asked in a review by Elliot M. Berry from the Department of Human Nutrition at the Hebrew University Hadassah Medical School, Israel.  He writes;

However, in spite of the widespread enthusiasm for increasing PUFAs in the diet some 20 years ago, more recent studies from a variety of disciplines suggest possible deleterious effects of a high consumption of LA.

Israel has one of the highest dietary polyunsaturated/saturated fat (P/S) ratios in the world; the population consumes some 8% more omega-6 PUFAs than in the U.S.A., and some 10–12% more than in most European countries. Israeli Jews may be regarded as a population-based dietary experiment of the effect of a high omega-6 PUFA diet on disease, one which, until recently, was widely recommended. Despite such national habits, paradoxically there is a high prevalence of cardiovascular diseases, hypertension, non-insulin dependent diabetes mellitus (NIDDM) and obesity—all diseases which are associated with hyperinsulinaemia and insulin resistance.

Berry touches on what is commonly known as the Israeli Paradox, with paradox being code for “these bastards aren’t doing what they are supposed to when eating foods that we recommend they do or don’t eat and they are making us look quite silly”.  A prime example is the French – they eat a fair amount of saturated fat and yet the buggers just won’t die of heart disease like they are supposed to.  Because we all know that saturated fat is artery clogging, yet the French don’t generally have clogged arteries to the same degree as other countries eating less arterycloggingsaturatedfat, we call that a paradox (and we make a big deal of it, suck up some research money over it, and generally look for all sorts of explanations for it other than the patently obvious one that saturated fat doesn’t actually clog arteries).

Conversely, the Israeli’s eat seemingly large amounts of hearthealthyvegetableoils – way more than the recommendations, yet they are having cardiac events left, right, and centre.  Now of course the argument could potentially be made that, despite the high number of events, their mortality rates are quite low.  Israeli men, at least, are ranked very high in terms of lifespan.  They tend to live a good length if they survive the high rates of heart disease, cancer and diabetes and this likely is more reflective of Israeli doctors have good success in treating these diseases than any protective effect of vegetable oils.

Here is a study on exactly this paradoxical phenomenon…

Diet and disease–the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet.

Israel has one of the highest dietary polyunsaturated/saturated fat ratios in the world; the consumption of omega-6 polyunsaturated fatty acids (PUFA) is about 8% higher than in the USA, and 10-12% higher than in most European countries. In fact, Israeli Jews may be regarded as a population-based dietary experiment of the effect of a high omega-6 PUFA diet, a diet that until recently was widely recommended. Despite such national habits, there is paradoxically a high prevalence of cardiovascular diseases, hypertension, non-insulin-dependent diabetes mellitus and obesity-all diseases that are associated with hyperinsulinemia (HI) and insulin resistance (IR), and grouped together as the insulin resistance syndrome or syndrome X. There is also an increased cancer incidence and mortality rate, especially in women, compared with western countries. Studies suggest that high omega-6 linoleic acid consumption might aggravate HI and IR, in addition to being a substrate for lipid peroxidation and free radical formation. Thus, rather than being beneficial, high omega-6 PUFA diets may have some long-term side effects, within the cluster of hyperinsulinemia, atherosclerosis and tumorigenesis.

There are a number of ways in which excess linoleic acid may adversely affect metabolic pathways.  Omega-6 and omega-3 fatty acids compete for the same enzymes involved in their conversion to the main fatty acids used within the body (AA on the omega-6 side of things, and EPA and DHA on the omega-3 side of the ledger).  Each of these fatty acids are involved in the production of eicosanoids – signalling compounds involved primarily in inflammatory and immune function pathways.  The omega-3-derived eicosanoids generally tend to drive anti-inflammatory pathways, whilst the omega-6-derived eicosanoids are inflammatory (keeping in mind that a degree of inflammation is needed for healthy functioning).

In general, eicosanoids formed from the omega-3 fatty acids are much less potent in causing biological responses than those formed from the omega-6 fatty acids, including such adverse reactions as the stimulation of cytokine production and inflammatory responses.

So to give omega-3′s a fighting chance, they have to be within cooee of omega-6 concentrations.  Within the modern diet, however, this ratio is heavily weighted in favour of omega-6.  And most health authorities want to make this worse.

This image is a nice summary of the specific essential fatty acid pathways and their influencers.

Lets get into specific health endpoints with regard to omega-6 fats.  From Berry, again;


Omega-6 PUFAs increase the susceptibility of lowdensity lipoprotein (LDL) to oxidative modifications and, perhaps because of this, the risk for acute myocardial infarction and coronary thrombosis. LA consumption may reduce the level of high density lipoprotein (HDL) cholesterol, increasing the risk for coronary heart disease (CHD) mortality. Lipid peroxidation mediated by free radicals and/or hydroxy radicals is considered associated with the activation of radical scavengers, initiation and development of atherosclerosis…

…LA and LA hydroperoxides reduce the activity of prostacyclins in the vascular wall, alter the production of thromboxane B2 and the tendency for platelet aggregation.

Translation: Linoleic acid and its oxidised metabolites make your blood vessels more constricted and drives your blood toward clotting.  If you want a heart attack, those are a good couple of ingredients to start with.


The metabolites of arachidonic acid (20:4n-6) derived from LA via the cyclooxygenase reactions may be arrhythmogenic.

Arachidonic acid (AA) can be considered an animal fat and as such can get itself into trouble (think “animal fats cause inflammation”).  However, as it is also derived from linoleic acid, lots of linoleic acid can increase arachidonic acid levels markedly.  Those people who suffer arrhythmia may be advised to cut down on animal fats in order to reduce AA, with little to no attention paid to the intake of LA chemically derived from animal fats.


Some reports suggest that LA potentiates tumourigenesis by providing structurally and functionally essential fatty acids for the growth of dividing cells, and by serving as precursor for eicosanoid metabolites of arachidonic acid (AA). Leukotrienes C4 and D4 might act as tumour-enhancing agents, and PGE2 in turn may be involved in tumour development, promotion and immunosuppression. This reduces macrophage tumouricidal activity and inhibits interleukin-2 production, which activates the natural killer cell and cytotoxic T cell activity.

…higher linoleate to arachidonate concentrations were found in gynaecological tumours, perhaps indicating decreased insulin sensitivity.

Insulin resistance

Omega-6 fatty acids may increase the secretion of insulin, and/or reduce insulin catabolism, causing impaired insulin action and leading progressively to insulin resistance, which determines accelerated atherosclerosis. Insulin activates the enzyme phospholipase A2, which hydrolyses membrane phospholipids to generate free PUFA. These are substrates for eicosanoid formation via the cyclo-oxygenase and lipoxygenase pathways, during which processes free radical are generated which may enhance lipid peroxidation.

The same relationships hold for eicosanoids formed from dietary omega-6 lipids affecting thrombosis, vasospasm, arrhythmia and chronic inflammatory processes. In the absence of adequate insulin activity there is a relative decrease in the conversion of LA to AA.

Studies have shown that AA is inversely related to both HbA1c concentrations, as well as to the degree of diabetic complications. There is also a correlation between AA and insulin sensitivity in muscle biopsies.

In summary, there appears to be a reciprocal relationship between insulin and the omega-6 fatty acid pathway; these fatty acids impair insulin activity which in turn regulates their metabolic conversions.

The inverse relationship between AA and HbA1c (consider this a rolling average of your blood sugar levels and an indicator of how well your blood sugar is being controlled), is particularly interesting given that AA (preformed) is derived from animal foods, suggesting that such foods may improve insulin sensitivity.

Berry includes a section within his review which can be applied to all areas of human nutrition and how it relates to disease, but particularly with regard to studying the effect of dietary fat on health and disease…

Translating these animal and experimental studies into the clinical situation requires knowledge of the long-term habitual diet. The evidence required to link diet and disease may be assessed at a number of different levels. Work in cell culture (in vitro ‘feeding’) and animals may suggest possible biological mechanisms for findings from epidemiological/geographical studies. However, these relationships suggest association rather than causality, which is also the limitation of case control retrospective studies. Cohort studies are prospective and more reliable. However, dietary studies are notoriously difficult to evaluate because of the extended time-scale of the exposure and the lack of suitable instruments for assessing the long-term habitual dietary intake in the absence of objective biomarkers.

An example of such confusion is provided in the field of carcinoma of the breast, where most animal and case control studies suggest a relationship between fat and cancer, while cohort studies (meta-analysis) fail to do so. An answer, therefore, has to await a long-term dietary intervention randomized control trials with all their difficulties of compliance. However, work on animals suggests an alternative explanation, in that it is total energy intake which is of more relevance than the type or quantity of fat ingested.

Much is made of the ratio between omega-6 to omega-3 fatty acids in the diet.  And for a while there, in the paleosphere, this lead to the recommendation of taking enormous doses of fish oil capsules in order to rebalance this ratio.  However, in recent years there has been more focus on the absolute amounts rather than the ratio between the two (though it pays to keep the two in reasonable balance even if consuming them in relatively small amounts).

Berry makes a good point when considering the plant-derived precursors to AA (omega-6) and EPA (omega-3), and how we interpret any research that uses these plant derived fatty acids…

The competition between the two pathways of essential fatty acids is very difficult to untangle biologically. Thus it is not known with any confidence in what proportions C20 [AA] and C22 [EPA] long-chain fatty acids will be produced from a given mixture of linoleic and alpha-linolenic acids fed to any animal.

I’ll cap this post off with one last comment from Berry.  This time in reference to the perception that omega-6 vegetable oils are a suitable and heart-healthy replacement for saturated fats in the diet…

The above considerations suggest that a reductionist (single nutrient) approach to nutritional recommendations may not be appropriate when considering fatty acids. They have to be considered in terms of their biological function in relation to other nutrients (integrationist approach)…

…attention to lifestyle and the quantities eaten are of far more importance than the type of fatty acid consumed.

To be continued…**

**If some of my sentences seem to slur a bit more than usual, it is because of the two glasses of Pinot I had whilst completing this post.  And yes, I’m a cheap date when it comes to alcohol.

29 thoughts on “Are diets high in omega-6 polyunsaturated fatty acids unhealthy?

    • But it does not trump absolute amounts. Let’s say we really only need 10g per day each of omega 6 & 3 fats (I’m picking illustrative numbers), in a 1:1 ratio. If we then take in 100g each of 6 & 3, the ratio is still 1:1 yet we are now getting 10 times more than we need, with deleterious effects. I get the argument when most people have a degree of imbalance between n6 & n3, that their ratio is stuffed. But if the issue is excess LA, we don’t correct this by simply throwing more EPA/DHA, or worse, ALA, into the system. You would knock the LA intake out, reducing the absolute amount being taken in, and then maybe undertake a period of time taking in additional omega 3′s if required. The ratio is secondary to the absolute amounts in my book.

  1. I’m convinced that excess LA impairs conversion of ALA to EPA and DHA, and also that excess LA impairs conversion of LA to DGLA and GLA, but not so much that excess LA is antagonistic to DHA/EPA when derived from foods. Like in this study with rats, omega-6 didn’t make a different to omega-3 incorporation into cardiac muscle

    However I have seen one where a deficiency in omega-6 causing increases brain DHA, but I’m not sure if that can be applied to a normal diet. What do you think about omega-6 and its effects on the incorporation and utilization (I know nothing of utilization) of DHA from dietary sources?

    Of course there is a world else wrong with high omega-6 diets so my intake is staying right where it is regardless.

    • Stabby, just at a quick glance, I would agree – LA can interfere with the conversion pathways whilst the function and utilisation of preformed n3′s like EPA & DHA is relatively preserved. That is, put the end-product that your body desires in the tank and your body will use it for exactly what it needs it for. With these preformed end-products, LA seemingly can’t competitively inhibit enzymes for desaturation and elongation – there is no need. Where I do think LA could have an influence is in the triggering of lipid peroxidation reactions. The likes of EPA & DHA are very prone to oxidation due to their highly desaturated nature. If the body lacks the capacity to protect excessive amounts of LA finding its way into our bodies from oxidation, then we can have problems with all polyunsaturated fats.

      • I agree with that. Lack of vitamin e and other nutrients worsens omega-3 status, so tons and tons of omega-6 could do the same because it increases the need for those nutrients and oxidized the heck out of stuff.

        • I recently read a hellaciously complex paper proposing that bucketsful of omega6 fatty acids actually decreased inflammation via downregulation of the ecosanoids… it’s all very effed up.

          • But I have to say that at the Harvard law 2011 TEDx talk with Walter Willet and Ludwig and whatnot they were fairly laissez-faire regarding the omega 6 fatty acids. Meaning that their precious epidemiological groups seemed to fair better on a diet of corn oil and broccoli and beans so anyone on the other side had better prove some bad news on the omega 6 front.

        • The AHA’s 2009 “pro omega-6″ paper is one of the most misleading position papers I’ve ever seen.

          There are several interesting things about this paper, but some of the most humorous include…

          1. Lead author William Harris disclosed at the end his research grant from…Monsanto! Penny Kris-Etherton is on the advisory board at the California Walnut Commission. I wonder why they would want to write a position paper that is pro omega-6? :)

          2. The paper setup is ludicrous, for such a large group of well-versed authors. They start by essentially saying “there have been some concerns about omega-6, so we did this review.” Then they proceed to cherrypick studies from this quite large field of literature, not even pretending to make their methods transparent or comprehensive.

          3. The wise Greek doctor gives a more logical view, which naturally made the paper authors displeased…
          “But Dr Artemis Simopoulos (Center for Genetics, Nutrition, and Health, Washington, DC), a leading proponent of reducing omega-6 intake, disputes the AHA advisory, arguing to heartwire that US and other Western diets include far too much omega-6 PUFAs, in levels far higher than intake of omega-3s (a ratio of 16:1, she says). “The studies that have been done very clearly show that [eicosapentaenoic acid] EPA and [docosahexaenoic acid] DHA are very potent anti-inflammatory agents, whereas linoleic and arachidonic acids are only slightly so. And when you have them in high amounts as they exist in Western diets, they interfere with the incorporation and the elongation and saturation going from alpha-linolenic acid to EPA and DHA,” she said. “Second, it’s important to think in terms of evolution and evolutionary biology. We evolved on a diet that was never, until 150 years ago and in particular the past 50 years, so high in omega-6 fatty acids. This is an artificial way and a general experiment, being done without any scientific evidence.”

  2. In May 31, 2010, there was a famous ISSFAL dinner debate about the omega-6 “healthy” fats, which is described in this paper: According to a portuguese friend who was there, Prof. William Harris pro-omega6 arguments were destroyed by Dr. Chris Ramsden. For the record, this was a comment left in my extinct blog on this issue: “(…) This meta-analysis published by Chris Ramsden (a young physiatrist, who does research at the NIH on Omega 6 and chronic pain, under the umbrella of Joe Hibbeln, a psychiatrist who studies the role of n-6 and n-3 in neuropsychiatric diseases) came after a dinner debate in the last congress of ISSFAL in Maastricht. In this debate, Chris Ramsden faced the heavyweight William Harris (co-creator of the Omega-3 Index), which was the main researcher / author of the position stand of the American Heart Association on omega 6 (which recommends increasing the consumption of these fatty acids). This debate was at least unprecedented since Chris Ramsden (who still has few publications and 20 years less than Dr . Harris) destroyed all the arguments of Dr. Harris, leaving him speechless and causing 90% (this number is accurate because there was voting at the end) of researchers who were in the audience to vote against the recommendation to increase consumption of Omega-6. Regards, PB.”

  3. Hi Jamie,

    Nice post. However, I think the evidence is scarce regarding the negative effects of omega-6. I think excess o-6 from vegetable oils are not healthy, but if we look at the study you mentioned:

    “For non-fatal myocardial infarction (MI)+CHD death, the pooled risk reduction for mixed n-3/n-6 PUFA diets was 22 % (risk ratio (RR) 0.78; 95 % CI 0.65, 0.93) compared to an increased risk of 13 % for n-6 specific PUFA diets (RR 1.13; 95 % CI 0.84, 1.53).”

    The RR is only 1.13, and the CI includes 1. This means that its equally probable that there were no differences between those eating more PUFAs and those who doesnt.

    “RCT that substituted n-6 PUFA for TFA and SFA without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance (RR 1.16; 95 % CI 0.95, 1.42).”

    Same as above, the CI, in my opinion, is too close to 1 to make strong assumptions.

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  6. re: ‘ drives your blood toward clotting.’

    What about clotting role in saturated fats: “Saturated fats can also cause blood platelets to stick together and form blood clots that can cause a heart attack or stroke.”
    Transcend, Ray Kurzweil and Terry Grossman MD

    So far I’ve read Minger say about stearic fatty acid: “This study examined the effects of two unsaturated fats (oleic and linoleic acids) and a saturated fat (stearic acid) on thrombotic—or blood-clotting—tendency. Long story short:

    In conclusion, our results do not suggest that stearic acid is highly thrombogenic compared with oleic and linoleic acids.” 14% of the fat in beef tallow of stearic, but what about the 26% palmitic fatty acid?

    • Lance,

      We do need a degree of clotting, and with all other things being equal, SFA may well be involved with this at a physiological rather than a pathological level. However, in the context of how people eat in the real world, there is going to be a large difference between the clotting potential of any fat consumed against the backdrop of a standard Western diet (high carb, low protein, low n-3, multiple nutrient deficiencies, etc.) and that which is consumed against the backdrop of a low-carb, high-protein, high omega-3, nutrient-rich diet.


  7. better watch out for those omega 3′s too

    Dietary supplementation with n-3 fatty acids may impair glucose homeostasis in patients with non-insulin-dependent diabetes mellitus.-
    “The blood glucose concentration tended to increase during MaxEPA treatment, and to decrease during the placebo period, the changes under the two regimes being significantly different (P less than 0.01). In addition, the rate constant for glucose disappearance (k value) for the intravenous insulin-tolerance test, which reflected the peripheral insulin sensitivity, tended to decrease during MaxEPA treatment and increase during administration of the placebo, there being a significant difference (P less than 0.03) between the changes during the two treatments.”

    O3 deteoriates glycemic response-
    “Average blood glucose concentrations during the third week were significantly higher fasting (+ 15%, p < 0.01), and during the day at 1100 h (+18%, p < 0.001) and 1500 h (+ 17%, p=0.002) on PUFA than on the saturated fat diet."

    Acceleration of experimental diabetic retinopathy in the rat by omega-3 fatty acids-
    Despite these biochemical changes, diabetes-associated pericyte loss remained unaffected and the formation of acellular, occluded capillaries was increased by 75% in the fish oil treated diabetic group (115.1 +/- 26.8; untreated diabetic 65.2 +/- 15.0 acellular capillary segments/mm2 of retinal area). We conclude from this study that dietary fish oil supplementation may be harmful for the diabetic microvasculature in the retina.

    Other various studies on AA/LA-

    Role of arachidonic acid and other free fatty acids in mitochondrial dysfunction in brain ischemia.-
    There was a significant increase in arachidonic (20:4), stearic (18:0), palmitic (16:0), and docosahexaenoic (22:6) acid during ischemia. BSA treatment removed all 20:4 and reduced the amount of 18:0 and 16:0, but had no significant effect on 22:6. The main conclusions were 1)
    that 20:4, 18:0, and 16.0 were responsible for the partial uncoupling (increase in state 4 respiration) of mitochondrial respiration during ischemia, 2) that the inhibition of state 3 respiration caused by ischemia could only partly be attributed to an effect of FFAs, and 3) that the ischemia-induced mitochondrial dysfunction was caused by a combination of factors including 20:4.

    LA diet-
    "Fasting blood glucose and insulin levels were significantly higher on the linoleic acid diet compared with the oleic acid diet (P < 0.01 and P < 0.002, respectively). Plasma cholesterol and LDL cholesterol levels were also significantly higher on the linoleic acid diet (P < 0.001). Likewise, fasting chylomicron apo B48 and apo B100 (P < 0.05) and postprandial chylomicron and VLDL apo B48 and B100 (P < 0.05) were also higher on the linoleic acid diet. "

    Fatty acid tissue composition and diabetes-
    "The FA composition of serum phospholipids (S-PL) measured by gas liquid chromatography and insulin action during a 2-step hyperinsulinemic isoglycemic clamp (1 and 10 mU/kg. min) were determined in 21 newly diagnosed DM2 subjects (DMN), in groups of long-term DM2 patients treated with hypoglycemic agents (DMH; n = 21) or diet alone (DMD; n = 11), and in 24 healthy subjects (HS)….Increased contents of highly unsaturated n-6 family FA (P <.01), arachidonic acid in particular, were found in all groups of diabetics compared with HS."

  8. Here are two studies on polyunsaturated fats vs monounsaturated fats vs saturated fats.

    Thyroid hormone metabolism may depend on dietary fat

    Thyroid hormone metabolism may depend on dietary fat

    Dietary fat type and level affect thyroid hormone plasma concentrations in rats

    The rats which were fed palm oil had the highest metabolic rate. The rats which were fed rapeseed oil had the second highest metabolic rate. The sunflower oil fed mice had the worst metabolic rate. Also, the weights of the rats were the highest when polyunsaturated fats were the highest.

    Allthough the rats eating the palm oil probably had have a higher metablic rate than those eating rapeseed and sunflower oil, the various tests (TPO, T3, T4, rT3) indicate no difference and some of them even indicate that the animals eating more PUFA had better thyroid function.

    Thyroid signaling is dynamic. If PUFA suppresses some thyroid enzymes, the thyroid would compensate by secreting extra thyroid hormone, or lowering the amount of thyroxine binding globulins. This is called “thyroid resistance”, similar to “insulin resistance.” Therapeutic usage aside, supplementing with thyroid hormone is a lot like giving a diabetic extra shots of insulin.

    Research has shown that the type of fat affect the sensitivity of thyroid receptors.[29,30,31] However, the two studies I mentioned didn’t measure that.[27,28] It seems plausible that those rats have a case of “thyroid resistance.” Hence, the thyroid adjusts itself in the face of consequences.

    Thyroid stimulating hormone (TSH) should rise the most in the sunflower oil group, followed by the rape seed oil group.

    Evidence that the thyroid adjusts itself: The first one is anecdotal. Colldén and Lillea suddenly experienced massive energy increases. It might due to a fluctuation of serum PUFA concentration, speeding up thyroid activity. However, because it takes time for their thyroids to adjust to the sudden lack of PUFA, they experienced temporary hyperthyroidism.

    Another piece of evidence: Suppose a hypothyroid person consumes half as much oxygen as a euthyroid person. But PUFA suppress thyroid activity in many ways, including thyroid hormone release, thyroid hormone circulation, and thyroid receptor sensitivity. Following this logic, PUFA should suppress oxygen consumption by ten times.

    If PUFA suppresses thyroid function by ten times, then why does a hypothyroid person consume half as much oxygen as a euthyroid person? Wouldn’t he/she only consume a tenth as much oxygen? He/she doesn’t because the thyroid adjusts itself by increasing it by five times. One-tenth multiplied by five is one-half. So that person has half the metabolic rate, rather than a tenth, due to thyroid re-adjustment.

    If it wasn’t for the thyroid to re-adjust itself in the presence of PUFA, then we would all be dead.

    A corollary is that the typical markers of thyroid function are inaccurate. It only measures the risk factors associated with hypothyroid symptoms within the American population, with the possible exception of thyroid-stimulating hormone (if the pituitary gland isn’t “exhausted”). It’s a lot like reading cholesterol levels.

  9. “The main reason we are consuming large amounts of this fat is due to the diet-heart hypothesis…”

    Actually, it’s because they’re cheaper than animal fats. The answer to the old Economics 101 question, “Guns or Butter?” was seed oils… That was well before the Diet Heart Hypothesis…

    • Right! They produced it just like they overproduce everything that’s a commodity (with gov’t subsidies and all that), THEN they had to find a use for it….hmmmm. Well, we already put it in cars and in floor polish…..Eureka, we could make people eat it! Brilliant!

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