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  #1   ^
Old Sun, Oct-15-17, 12:21
RawNut's Avatar
RawNut RawNut is offline
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Default Omega-6 fatty acid biomarkers and incident type 2 diabetes:

Quote:
Background

The metabolic effects of omega-6 polyunsaturated fatty acids (PUFAs) remain contentious, and little evidence is available regarding their potential role in primary prevention of type 2 diabetes. We aimed to assess the associations of linoleic acid and arachidonic acid biomarkers with incident type 2 diabetes.



Methods

We did a pooled analysis of new, harmonised, individual-level analyses for the biomarkers linoleic acid and its metabolite arachidonic acid and incident type 2 diabetes. We analysed data from 20 prospective cohort studies from ten countries (Iceland, the Netherlands, the USA, Taiwan, the UK, Germany, Finland, Australia, Sweden, and France), with biomarkers sampled between 1970 and 2010. Participants included in the analyses were aged 18 years or older and had data available for linoleic acid and arachidonic acid biomarkers at baseline. We excluded participants with type 2 diabetes at baseline. The main outcome was the association between omega-6 PUFA biomarkers and incident type 2 diabetes. We assessed the relative risk of type 2 diabetes prospectively for each cohort and lipid compartment separately using a prespecified analytic plan for exposures, covariates, effect modifiers, and analysis, and the findings were then pooled using inverse-variance weighted meta-analysis.



Findings

Participants were 39 740 adults, aged (range of cohort means) 49–76 years with a BMI (range of cohort means) of 23·3–28·4 kg/m2, who did not have type 2 diabetes at baseline. During a follow-up of 366 073 person-years, we identified 4347 cases of incident type 2 diabetes. In multivariable-adjusted pooled analyses, higher proportions of linoleic acid biomarkers as percentages of total fatty acid were associated with a lower risk of type 2 diabetes overall (risk ratio [RR] per interquintile range 0·65, 95% CI 0·60–0·72, p<0·0001; I2=53·9%, pheterogeneity=0·002). The associations between linoleic acid biomarkers and type 2 diabetes were generally similar in different lipid compartments, including phospholipids, plasma, cholesterol esters, and adipose tissue. Levels of arachidonic acid biomarker were not significantly associated with type 2 diabetes risk overall (RR per interquintile range 0·96, 95% CI 0·88–1·05; p=0·38; I2=63·0%, pheterogeneity<0·0001). The associations between linoleic acid and arachidonic acid biomarkers and the risk of type 2 diabetes were not significantly modified by any prespecified potential sources of heterogeneity (ie, age, BMI, sex, race, aspirin use, omega-3 PUFA levels, or variants of the FADS gene; all pheterogeneity≥0·13).



Interpretation

Findings suggest that linoleic acid has long-term benefits for the prevention of type 2 diabetes and that arachidonic acid is not harmful.





http://www.thelancet.com/journals/l...0307-8/fulltext
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  #2   ^
Old Tue, Oct-17-17, 12:51
HappyLC HappyLC is offline
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Default

I can't believe there are no responses to this yet. I've been watching the topic, hoping somebody smarter than me would have something to say about it, lol.

So I can't wait any longer and I have to know....does this mean Hellman's mayonnaise is okay to eat again?
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  #3   ^
Old Wed, Oct-18-17, 06:01
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RawNut RawNut is offline
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Default

They may have just been eating more fat and fewer carbs. Volek and Phinney's studies have shown that saturated fat in the blood decreases on low carb while Omega 6 increases. The ratio of 06/03 also increases or "worsens" yet inflammation decreases.

Quote:
Abnormal distribution of plasma fatty acids and increased inflammation are prominent features of metabolic syndrome. We tested whether these components of metabolic syndrome, like dyslipidemia and glycemia, are responsive to carbohydrate restriction. Overweight men and women with atherogenic dyslipidemia consumed ad libitum diets very low in carbohydrate (VLCKD) (1504 kcal:%CHO:fatrotein = 12:59:28) or low in fat (LFD) (1478 kcal:%CHO:fatrotein = 56:24:20) for 12 weeks. In comparison to the LFD, the VLCKD resulted in an increased proportion of serum total n-6 PUFA, mainly attributed to a marked increase in arachidonate (20:4n-6), while its biosynthetic metabolic intermediates were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid ratio also increased sharply. Total saturated fatty acids and 16:1n-7 were consistently decreased following the VLCKD. Both diets significantly decreased the concentration of several serum inflammatory markers, but there was an overall greater anti-inflammatory effect associated with the VLCKD, as evidenced by greater decreases in TNF-alpha, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and PAI-1. Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3 are commonly viewed as pro-inflammatory, but unexpectedly were consistently inversely associated with responses in inflammatory proteins. In summary, a very low carbohydrate diet resulted in profound alterations in fatty acid composition and reduced inflammation compared to a low fat diet.


https://www.ncbi.nlm.nih.gov/pubmed/18046594
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  #4   ^
Old Wed, Oct-18-17, 07:39
Zei Zei is offline
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Good point, RawNut. The study didn't look at how much omega 6 fats people ate, just biomarker levels of the stuff in the bloodstream. Therefore their conclusion that these fats are okay or healthy to eat isn't supported by their research because they're assuming having it exist in the bloodstream from whatever cause is the same thing as sticking it in your mouth and swallowing it. Not a good assumption because a lot of things don't work that way when swallowed into the digestive tract.
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  #5   ^
Old Wed, Oct-18-17, 08:19
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GRB5111 GRB5111 is offline
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Thanks for the links, RawNut.

Quote:
Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3 are commonly viewed as pro-inflammatory, but unexpectedly were consistently inversely associated with responses in inflammatory proteins. In summary, a very low carbohydrate diet resulted in profound alterations in fatty acid composition and reduced inflammation compared to a low fat diet.

I believe Dave Feldman's research supports this dynamic as well: http://cholesterolcode.com/

Determining the effects of fatty acid composition in the diet is important to be able to select the healthy fats and truly understand the recommended combination of sat fats and PUFAs for humans with the goal of minimizing inflammation. Feldman doesn't get into this detail at the moment.
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  #6   ^
Old Wed, Oct-18-17, 09:32
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RawNut RawNut is offline
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O6 may only be harmful if it's allowed to oxidize. Here's a post detailing all the nasty OxLAMs it turns into: http://breaknutrition.com/omega-6-f...s-civilization/

But, what if 06 is protected from oxidation on a low carb diet? Here's a thread about corn oil reducing inflammation, and extending health and longevity of mice: http://forum.lowcarber.org/showthre...13&page=1&pp=15

I still wouldn't consume highly processed vegetable oils though. I do eat a lot of nuts, avocado and olive oil however.


I love Dave's research! He's doing a carb experiment now and plans on a vegan experiment in the future.

Last edited by RawNut : Wed, Oct-18-17 at 09:37.
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  #7   ^
Old Wed, Oct-18-17, 12:02
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teaser teaser is offline
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There are mechanisms by which omega 6 fatty acids might be inflammatory, and an association with the modern diet of omega 6 fatty acids also came with increases in inflammation... when it comes down to it, it's just as easy to make linoleic acid look like a dietary villain as it is to make saturated fat look bad. And maybe just as warranted.

There are some studies showing that extreme avoidance of omega fatty acids can be anti-inflammatory, but this is at a level of avoidance that it's very hard to achieve, especially on a high fat diet, we're talking taking barely enough to avoid essential fatty acid deficiencies. Inflammation happens for a reason, and it's not simply that the body had enough materials to drive the inflammatory process.

One study I was looking at the other day gave rats endotoxin to initiate inflammation. This illustrates what I'm talking about, they fed hydrogenated coconut oil as the fat source to deny the animals enough omega 6 to have a normal reaction, and endotoxin resulted in less inflammation. Those endotoxins signal the body that there are pathogenic bacteria present, this is what the immune response/inflammation are intended to protect against.

On the other hand, I think whatever contributes to donuts, pizza, and potato chips also contributes to modern diseases. Walnuts might be a wonderful food, but if they make me more likely to eat high-sugar ice cream, that can be a problem.

Quote:
Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats.

Ling PR1, Malkan A, Le HD, Puder M, Bistrian BR.
Author information
Abstract
This study examined fatty acid profiles, triene-tetraene ratios (20:3n9/20:4n6), and nutritional and inflammatory markers in rats fed an essential fatty acid-deficient (EFAD) diet provided as 2% hydrogenated coconut oil (HCO) alone for 2 weeks or with 1.3 mg of arachidonic acid (AA) and 3.3 mg of docosahexaenoic acid (DHA) (AA + DHA) added to achieve 2% fat. Healthy controls were fed an AIN 93M diet (AIN) with 2% soybean oil. The HCO and AA + DHA diets led to significant reductions of linoleic acid, α-linolenic acid, and AA (20:4n6) and increases in Mead acid (20:3n9) in plasma and liver compared with the AIN diet; but the triene-tetraene levels remained well within normal. However, levels of 20:3n9 and 20:4n6 were lower in liver phospholipids in the AA + DHA than in HCO group, suggesting reduced elongation and desaturation in ω-9 and -6 pathways. The AA + DHA group also had significantly lower levels of 18:1n9 and 16:1n7 as well as 18:1n9/18:0 and 16:1n7/16:0 than the HCO group, suggesting inhibition of stearyl-Co A desaturase-1 activity. In response to lipopolysaccharide, the levels of tumor necrosis factor and interleukin-6 were significantly lower with HCO, reflecting reduced inflammation. The AA + DHA group had higher levels of IL-6 and C-reactive protein than the HCO group but significantly lower than the AIN group. However, in response to endotoxin, interleukin-6 was higher with AA + DHA than with AIN. Feeding an EFAD diet reduces baseline inflammation and inflammatory response to endotoxin long before the development of EFAD, and added AA + DHA modifies this response.


Controls ate 2 percent soybean oil, if you manage to get your omega 6 intake that low while eating a high fat diet, you are working very hard to do so.

I think intervention studies might be a problem for this stuff. I've seen studies from the sixties where body fat was maybe 4 percent linoleic acid. And more recent studies where human body fat was more like 25 percent linoleic acid. You could see that really interfering with finding out whether getting linoleic acid levels right down there would benefit people with inflammatory disease, the figure I've seen put out for body fat half life for people at a stable body weight is around 600 days.
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  #8   ^
Old Thu, Oct-19-17, 10:56
HappyLC HappyLC is offline
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Thank you smart people! So that's a definite maybe/maybe not on the Hellman's, lol.
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  #9   ^
Old Fri, Oct-20-17, 05:03
Zei Zei is offline
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DIY avocado oil mayo. Small batch in a bullet blender is pretty easy. It often doesn't thicken the first whirl, but refrigerated and then reblended it does. Problem with the commercial products is the omega 6 oils are damaged by the heavy refining they go through. Yuck.
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  #10   ^
Old Sat, Oct-21-17, 06:10
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WereBear WereBear is offline
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I found my own inflammation subsided when I laid off the Omega 6 oils.
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  #11   ^
Old Sat, Oct-21-17, 07:02
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teaser teaser is offline
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I've never found it to have any obvious effect. Repeatable n=1 results are certainly useful to the individual. When you look at mechanisms--saying that it doesn't seem to be generally true that linoleic acid intake determines arachidonic acid/inflammatory metabolites of arachidonic acid levels in people isn't the same as saying that it's impossible for this to be true in individuals. Arachidonic acid from linoleic acid is usually limited, for the same reason dha from alpha linolenic acid is limited, the same enzymes are involved, just as some people can produce enough dha from flaxseed that they might not need it preformed in the diet, the same could be true of arachidonic acid.

edited; typed linoleic instead of linolenic.

Last edited by teaser : Sun, Oct-22-17 at 06:24.
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  #12   ^
Old Sat, Oct-21-17, 12:58
HappyLC HappyLC is offline
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Quote:
Originally Posted by Zei
DIY avocado oil mayo. Small batch in a bullet blender is pretty easy. It often doesn't thicken the first whirl, but refrigerated and then reblended it does. Problem with the commercial products is the omega 6 oils are damaged by the heavy refining they go through. Yuck.


Thanks, Zei. I tried making my own with extra light-tasting olive oil and didn't like it at all. Then I bought a bottle of avocado oil and all I have to remind me of it is the stain it left on my front walk where the bottle smashed when the supermarket bag broke! There's $15 I'll never get back, lol. I've been using commercial avocado oil mayo. I've tried Sir Kensington and Choice Foods. They're both okay. Not great. I just really love the taste of Hellman's. I grew up on it.
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  #13   ^
Old Sat, Oct-21-17, 13:00
HappyLC HappyLC is offline
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Quote:
Originally Posted by WereBear
I found my own inflammation subsided when I laid off the Omega 6 oils.


I don't know if I've ever gone off omega sixes long enough to see a difference. Probably a good idea.
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  #14   ^
Old Sat, Oct-21-17, 13:07
HappyLC HappyLC is offline
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Quote:
Originally Posted by teaser
I've never found it to have any obvious effect. Repeatable n=1 results are certainly useful to the individual.


Probably worth giving it up long enough to see if it makes a difference. Thanks.
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  #15   ^
Old Sun, Oct-22-17, 06:03
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WereBear WereBear is offline
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I get the Paleo Mayo from the market at Mark's Daily Apple. YUUUUUMMMMMMMM.

I eat a lot of canned seafood, and this is the perfect partner.
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