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  #1   ^
Old Thu, Sep-27-18, 23:57
Grav Grav is offline
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Default Openheart/BMJ: Omega-6 vegetable oils as a driver of coronary heart disease

https://openheart.bmj.com/content/o...000898.full.pdf

Quote:
SUMMARY

The consumption of the omega-6 polyunsaturated fat linoleic acid has dramatically increased in the western world primarily in the form of vegetable oils. OxLDL is thought to play an important role in atherosclerosis formation; however, it is the oxidised linoleic acid contained in LDL that leads to harmful OXLAMs (oxidised linoleic acid metabolites), which induces atherosclerosis and CHD. Thus, reducing the amount of dietary linoleic acid, mainly from industrial vegetable/seed oils, will reduce the amount of linoleic acid in LDL and likely reduce oxLDL as well as the risk for CHD coronary heart disease.

In summary, numerous lines of evidence show that the omega-6 polyunsaturated fat linoleic acid promotes oxidative stress, oxidised LDL, chronic low-grade inflammation and atherosclerosis, and is likely a major dietary culprit for causing CHD, especially when consumed in the form of industrial seed oils commonly referred to as ‘vegetable oils’.

There's much more in the PDF but it's a pain to re-format here, so basically, "here's 29 reasons why too much O6 is probably bad for you, and nowhere near as many reasons why it might be good."
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  #2   ^
Old Fri, Sep-28-18, 06:03
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Ms Arielle Ms Arielle is online now
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We dropped the usual oils from our diet this year. I do keep one small bottle. like a security blanket. Otherwise lots of olive oils, in ddifferent flavors, coconut oilsin refined and unrefined, BUTTER. Butter is mostly organic, or grassfed. Very hard to get grassfed. And exoensive. BUT I think about what is the cost of CHD as the alternative.

Still looking at beef fat as we consume this on a regular basis. Very concerned that the omega 6 is far too high in relation to omega 3. No amount of fish oil will rebalance this. The beef fat is easy to come by and cheap as it is trimmings from conventional beef.

Grass fed beef would be ideal.

Perhaps beef tallow is a reasonable substitute for the vegetable oils.

This is one study, thought I cannot say if it is a good study or not.

https://academic.oup.com/jn/article/136/1/88/4664179

Last edited by Ms Arielle : Fri, Sep-28-18 at 06:14.
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  #3   ^
Old Fri, Sep-28-18, 07:18
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teaser teaser is offline
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Beef is low in polyunsaturated fat, 3 or 6. I don't worry about it. Same with butter.
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  #4   ^
Old Fri, Sep-28-18, 08:28
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https://www.ncbi.nlm.nih.gov/pubmed/10556987

Quote:
Dietary habits affect the susceptibility of low-density lipoprotein to oxidation.
Korpela R1, Seppo L, Laakso J, Lilja J, Karjala K, Lähteenmäki T, Solatunturi E, Vapaatalo H, Tikkanen MJ.
Author information
Abstract
OBJECTIVE:
To study, if there are differences in the fatty acid composition of low-density lipoprotein (LDL) in people eating three different long-standing habitual diets: vegetarian, high fish intake, or high saturated fat (milk fat) diet as a control group, and to study if these differences influence the oxidation susceptibility of LDL.

DESIGN:
Cross-sectional study using blood samples and a validated dietary frequency questionnaire with illustrations.

SETTING:
Helsinki University Central Hospital, Finland.

SUBJECTS:
The effect of three different types of long-standing diets of different fatty acid content (a strict vegetarian diet, n=11; a high fish intake diet, n=9; and a high saturated fat (milk fat) diet, controls, n=7) on the serum and LDL fatty acid content, and on the susceptibility of LDL to oxidation in vitro, was studied in healthy normocholesterolemic volunteers who had been on these diets for years. Oxidation of LDL was carried out by using CuSO4 as a pro-oxidant.

RESULTS:
There were no statistically significant differences in the serum lipids or lipoproteins, though the vegetarian group exhibited lowest mean values of total, high-density lipoprotein (HDL) and LDL cholesterol levels. Both the serum and LDL eicosapentaenoic, docosapentaenoic and docosahexaenoic acid proportions were highest in the fish and lowest in the vegetarian groups. Linoleic acid was highest among the vegetarians. In the fish group, the vitamin A concentration in serum was higher than in vegetarians and controls and beta-carotene lower than in controls, but in alpha-tocopherol, or lycopene concentrations there were no statistically significant differences. The lag phase of LDL oxidation was shortest (116 min) in the fish group and longest (165 min) in the vegetarian group, and the control group was between them (129 min). The mean oxidation percentage after 2.5 h of copper-induced oxidation was highest (44%) in the fish group and lowest (22%) in the vegetarian group and intermediate (31%) in the control group.

CONCLUSION:
Long-term dietary habits predict the fatty acid composition of serum and LDL, and influence the susceptibility of LDL to oxidation. In the fish group with the highest content of omega-3 fatty acids in LDL, the oxidation susceptibility of LDL was highest. In the vegetarian group with less omega-3 fatty acids in LDL, the LDL was more resistant to oxidation.



https://www.ncbi.nlm.nih.gov/pubmed/10556987

Quote:
Omega-6 fats for the primary and secondary prevention of cardiovascular disease.

Abstract
BACKGROUND:
Omega-6 fats are polyunsaturated fats vital for many physiological functions, but their effect on cardiovascular disease (CVD) risk is debated.

OBJECTIVES:
To assess effects of increasing omega-6 fats (linoleic acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (AA)) on CVD and all-cause mortality.

SEARCH METHODS:
We searched CENTRAL, MEDLINE and Embase to May 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews.

SELECTION CRITERIA:
We included randomised controlled trials (RCTs) comparing higher versus lower omega-6 fat intake in adults with or without CVD, assessing effects over at least 12 months. We included full texts, abstracts, trials registry entries and unpublished studies. Outcomes were all-cause mortality, CVD mortality, CVD events, risk factors (blood lipids, adiposity, blood pressure), and potential adverse events. We excluded trials where we could not separate omega-6 fat effects from those of other dietary, lifestyle or medication interventions.

DATA COLLECTION AND ANALYSIS:
Two authors independently screened titles/abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias of included trials. We wrote to authors of included studies. Meta-analyses used random-effects analysis, while sensitivity analyses used fixed-effects and limited analyses to trials at low summary risk of bias. We assessed GRADE quality of evidence for 'Summary of findings' tables.

MAIN RESULTS:
We included 19 RCTs in 6461 participants who were followed for one to eight years. Seven trials assessed the effects of supplemental GLA and 12 of LA, none DGLA or AA; the omega-6 fats usually displaced dietary saturated or monounsaturated fats. We assessed three RCTs as being at low summary risk of bias.Primary outcomes: we found low-quality evidence that increased intake of omega-6 fats may make little or no difference to all-cause mortality (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.88 to 1.12, 740 deaths, 4506 randomised, 10 trials) or CVD events (RR 0.97, 95% CI 0.81 to 1.15, 1404 people experienced events of 4962 randomised, 7 trials). We are uncertain whether increasing omega-6 fats affects CVD mortality (RR 1.09, 95% CI 0.76 to 1.55, 472 deaths, 4019 randomised, 7 trials), coronary heart disease events (RR 0.88, 95% CI 0.66 to 1.17, 1059 people with events of 3997 randomised, 7 trials), major adverse cardiac and cerebrovascular events (RR 0.84, 95% CI 0.59 to 1.20, 817 events, 2879 participants, 2 trials) or stroke (RR 1.36, 95% CI 0.45 to 4.11, 54 events, 3730 participants, 4 trials), as we assessed the evidence as being of very low quality. We found no evidence of dose-response or duration effects for any primary outcome, but there was a suggestion of greater protection in participants with lower baseline omega-6 intake across outcomes.Additional key outcomes: we found increased intake of omega-6 fats may reduce myocardial infarction (MI) risk (RR 0.88, 95% CI 0.76 to 1.02, 609 events, 4606 participants, 7 trials, low-quality evidence). High-quality evidence suggests increasing omega-6 fats reduces total serum cholesterol a little in the long term (mean difference (MD) -0.33 mmol/L, 95% CI -0.50 to -0.16, I2 = 81%; heterogeneity partially explained by dose, 4280 participants, 10 trials). Increasing omega-6 fats probably has little or no effect on adiposity (body mass index (BMI) MD -0.20 kg/m2, 95% CI -0.56 to 0.16, 371 participants, 1 trial, moderate-quality evidence). It may make little or no difference to serum triglycerides (MD -0.01 mmol/L, 95% CI -0.23 to 0.21, 834 participants, 5 trials), HDL (MD -0.01 mmol/L, 95% CI -0.03 to 0.02, 1995 participants, 4 trials) or low-density lipoprotein (MD -0.04 mmol/L, 95% CI -0.21 to 0.14, 244 participants, 2 trials, low-quality evidence).

AUTHORS' CONCLUSIONS:
This is the most extensive systematic assessment of effects of omega-6 fats on cardiovascular health, mortality, lipids and adiposity to date, using previously unpublished data. We found no evidence that increasing omega-6 fats reduces cardiovascular outcomes other than MI, where 53 people may need to increase omega-6 fat intake to prevent 1 person from experiencing MI. Although benefits of omega-6 fats remain to be proven, increasing omega-6 fats may be of benefit in people at high risk of MI. Increased omega-6 fats reduce serum total cholesterol but not other blood fat fractions or adiposity.


Hoped for protective effects of omega 6 fatty acids haven't really panned out. But the studies designed to look for protective effects haven't shown much in the way of deleterious effect, either.

I do see a problem in intervention in this, though. I've looked for data on the lipid profile of fat stores. What we oxidize in a day, at least on a mixed diet, is generally estimated to be half from storage, half from the diet. Studies in the sixties typically show low single digit percentages of any polyunsaturated fat in human fat cells. In modern studies, it's not uncommon to see levels of 25 or 30 percent. Also the average human fat stores are given a half-life of around 600 days, at that point half of the fat stores will have been replaced by whatever the diet's fat sources have been over that time. So if you want to see the effect of linoleic acid, good or bad, it makes sense to take into account this massive source most of us carry around these days.
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  #5   ^
Old Fri, Sep-28-18, 09:40
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GRB5111 GRB5111 is offline
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And . . . from 4 years ago, here's the alternative view of the healthfulness of vegetable oils from our friends at Harvard's T.H. Chan School of Public Menace er umm, Health:
https://www.hsph.harvard.edu/nutrit...-heart-disease/
Quote:
Dietary linoleic acid and risk of coronary heart disease
Swapping saturated fat and carbohydrates for linoleic acid – the main polyunsaturated fat found in vegetable oil, nuts, and seeds – lowers risk of coronary heart disease, according to a new study by Harvard School of Public Health researchers.

We talked to lead author Maryam Farvid, a visiting scientist and Takemi fellow in the Department of Nutrition, about the study to find out more.

1. Your research shows that by reducing the amount of saturated fat and carbohydrates we eat, and replacing those calories with foods rich in linoleic acid – such as vegetable oil, nuts, and seeds – we can reduce our risk of developing coronary heart disease. What’s so special about linoleic acid? And should consumers focus on reducing saturated fat and carbohydrates equally, or should we reduce one more than the other?

Replacing either saturated fat or carbohydrate with vegetable oils and seeing significant benefits indicates that reduction in saturated fat or carbohydrate is not the only reason for the beneficial effects of linoleic acid. Instead, linoleic acid itself plays a special role in support of heart health. Randomized clinical trials have shown that replacing saturated fat with linoleic acid reduces total and LDL cholesterol. There is also some evidence that linoleic acid improves insulin sensitivity and blood pressure.

2. Lately there’s been a lot of talk about healthy and unhealthy fats, with saturated fat being debated in the media. What can readers learn from your research about polyunsaturated versus saturated fats?

Our data provide strong support that substituting vegetable oils rich in polyunsaturated fat for saturated fat is beneficial for the prevention of coronary heart disease. The current debate about the role saturated fat misses an important point: the replacement nutrient. If saturated fat is replaced by carbohydrates (typically refined carbohydrates), there will be no benefit on heart disease. This is why many epidemiologic studies have failed to observe a significant association between saturated fat and risk of CHD as carbohydrates were typically used as a comparator. However, if saturated fat is replaced by polyunsaturated fat, then there is a clear benefit for heart disease prevention.

3. Is there a certain amount of linoleic acid consumers should aim to eat each day? What are the best sources?

Consistent with the American Heart Association guidelines, our data continue to support consumption of 5-10% energy intake from linoleic acid* to decrease CHD risk. Linoleic acid is the predominant n-6 polyunsaturated fatty acid (PUFA) in the Western diet and we can obtain it from vegetable oils such as sunflower, safflower, soybean, corn, and canola oils as well as nuts and seeds. A table spoon of soybean or corn oil contains about 7-8 g of linoleic acid, and 7 shelled walnuts provide about 11 g of linoleic acid. It should be noted that important sources of linoleic acid such as soybean and canola oils and walnuts also contain substantial amounts of alpha-linolenic acid, a plant-based omega-3 fatty acid.

*For example, for a 2,000 calorie diet that would equal 100-200 calories from linoleic acid.

4. Your study also addresses claims that linoleic acid is pro-inflammatory. Can you explain what you found when you researched this?

Concerns have been raised about higher linoleic acid consumption being harmful for heart health because of potential pro-inflammatory and thrombogenic properties. Linoleic acid can be elongated to arachidonic acid and subsequently synthesized to a variety of pro-inflammatory eicosanoids, which may increase CHD risk. But this speculation is not supported by randomized controlled feeding studies, in which dietary intake of linoleic acid was not found to increase plasma levels of arachidonic acid or inflammatory markers. On the contrary, some studies have found anti-inflammatory effects of diets higher in linoleic acid compared to those higher in saturated fat.

5. Based on this new study, what are some simple steps consumers can take to improve their diet?

Instead of using butter, cream, lard, and other animal fat as the primary source of culinary fat, one should use liquid vegetable oils like soybean, corn, olive, and canola oils for cooking, on salad and at the table. Although olive oil contains little linoleic acid, many studies have shown health benefits of Mediterranean diets rich in olive oil. Nuts and seeds are also excellent sources of healthy fats.

References

1. Farvid MS, Ding M, Pan A, Sun Q, Chiuve SE, Steffen LM, Willett WC, Hu FB. Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies. Circulation. 2014

There's a reason why we're in the dark ages in our understanding of how fats and seed oils impact our health. Agendas influenced by the funding and grants from food manufacturers is the major confounder. There's also a reason why many have started a WOE that flies in the face of these claims using our own improved health outcomes (N=1s) as being more credible than the claims that are likely influenced by the manufacturers of these products. My take? Favor healthy saturated fats, omega 3s, and monounsaturated fats. There are always polyunsaturates in combination in many foods, but for processed seed and vegetable oils, I make an extra effort to avoid them. When I can't control my ingredients in a meal is when I'm eating at a restaurant. Many places will serve canola or soy oil as olive oil. We need to understand that minimizing this consumption serves us better, but it's not completely avoidable.
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  #6   ^
Old Fri, Sep-28-18, 10:12
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Ms Arielle Ms Arielle is online now
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SAD.

Harvard could self fund this research and be completely independent if it wanted to be. It sits on billions.
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Old Sat, Sep-29-18, 11:51
Zei Zei is offline
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The difference in the findings from the different kinds of studies above illustrates IMO why you can't rely on prospective or epidemiological/association studies so much like the "gold standard" of randomized controlled trials. The very first analysis quoted looked specifically at RTC's only, while the Harvard report was based only on prospective and epidemiologically-observed associations. So randomly controlled "gold standard" type studies show no health benefit to linoleic acid. But the Harvard professor reports positive associations between health and linoleic acid. Associations only, remember, that kind of studies can't ever prove causation. So how to explain the differences in findings between the two types of studies? Here comes my opinion: for one thing, certain professors at that particular institution seem to have had a strong bias for some time against saturated fat, so yes. Your biases, your own paradigm of things, will affect what you look for and what you find. Believing is seeing, etc. But a bigger factor, again IMO here, could be the healthy user effect. People for decades are told don't eat "bad" saturated fat; linoleic acid-rich polyunsaturated omega 6 seed oil is "good" for you. So who's listening and following this advice? Right. People concerned about their health, doing all kinds of other things to improve it, not the guy dining at Mickey D's. Same type of people as the women who were healthier while taking HRT for so many years until a real RTC showed it was bad. My take? I'm putting my eggs (and meat, butter and coconut oil ) in the saturated fat basket and avoiding those linoleic acid-rich industrial seed oils.
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Old Sat, Sep-29-18, 12:10
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Quote:
My take? I'm putting my eggs (and meat, butter and coconut oil ) in the saturated fat basket and avoiding those linoleic acid-rich industrial seed oils.


I'm with her ^^^ Bacon fat too!!!
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  #9   ^
Old Mon, Oct-08-18, 16:36
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amergin amergin is offline
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Quote:
Originally Posted by GRB5111
And . . . from 4 years ago, here's the alternative view of the healthfulness of vegetable oils from our friends at Harvard's T.H. Chan School of Public Menace er umm, Health:
https://www.hsph.harvard.edu/nutrit...-heart-disease/

...Replacing either saturated fat or carbohydrate with vegetable oils and seeing significant benefits indicates that reduction in saturated fat or carbohydrate is not the only reason for the beneficial effects of linoleic acid. Instead, linoleic acid itself plays a special role in support of heart health. Randomized clinical trials have shown that replacing saturated fat with linoleic acid reduces total and LDL cholesterol. There is also some evidence that linoleic acid improves insulin sensitivity and blood pressure...


The argument made for Omega6 by Maryam I find completely unconvincing. The foundation appears to be that Saturated Fat increases cholesterol and therefore "risk of heart disease". It seems to be the fallback argument when actual endpoints are being avoided, or not measured, in favor of surrogate markers such as total Chol.
Also the language used is vague and lacks rigor, such as "On the contrary, some studies have found anti-inflammatory effects of diets higher in linoleic acid compared to those higher in saturated fat." (My bolds).
"Some" studies say this. Presumably then other studies don't.
But let's just ignore them because they don't support my p.o.v.
Chipping away the statements not backed by hard evidence leaves mostly a statement of opinion. And an unconvincing one at that.
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