Fish oil, misuse & inflammatory disease - Rob Wolf

Fish Oil

Posted by Robb Wolf on Oct 5, 2011 in Anti inflammatory diet, Autoimmunity, CrossFit, Fitness, General, Paleo Athletes, Paleo Diet Basics, Paleo/Low Carb, Uncategorized | 76 comments

Ahhh…fish oil. A whole industry built around supplying us with something that should be a natural part of our food supply. Prior to the 1970’s meat and dairy in the United states was still grass fed so we received ample amounts of the main constituents of fish oil, EPA and DHA, as part of our normal diet. With the adoption of grain feeding our cattle and the use of seed and vegetable oils heavy in the short omega 6 fat (linoleic acid) we have witnessed a dramatic shift away from the essential fatty acid profile we’d expect to see from an ancestral diet of ~1-1 or 2-1 N-6/N-3 to more than 10-1.

The health implications of this shift have not been great. The N-6 family tends to produce “pro-inflammatory” cellular signaling, while the N-3 family tends to produce “anti-inflammatory” signaling. This is a simplification but it get’s the idea across. More accurately, with excessive N-6 we see cellular signaling profiles that tend to promote pathology including cancer, autoimmunity and glucose dysregulation. I see this more like a band or orchestra playing out of tune than too much of one thing vs another thing, but the fact remains folks likely get too much of the short form of N-6 fats. My early solution (and the solution of many other people including Barry Sears, Charles Poliquin and number of other folks) was to front load the system with large amounts of N-3 fats in the form of fish oil to “balance” the intake of N-6 fats. I mentioned a formula in my book for figuring out your fish oil dose and my pals at Whole9 put up a nifty calculator to help you figure out not only how much fish oil you needed overall, but also how damn many capsules that meant depending upon your product of choice.

These recommendations were born several years ago when I was still working for CrossFit, trying to sneak in as much paleo-pseudoscience as I could between polishing the brass of the magical, 40-30-30 Zone.  Given the relatively low protein recommendation of the Zone, combined with moderate to low carbohydrate levels, the only thing left to recommend to hard charging athletes was to ramp up fat intake, and what better fat to use than nuts and seeds? Portable, cheap, yummy. Also, 36-DD heavy in linoleic acid. No worries I thought, we’ll just “balance” things out with more fish oil. Well, by looking at performance parameters and blood work it became clear we still had inflammatory issues that were far from optimum. Some digging in the literature and review of the basic metabolic pathways showed that linoleic acid intake tends to squash the anti-inflammatory outputs of our EPA/DHA supplementation. Recommendations were tweaked to get fat from sources low(er) in linoleic acid such as coconut and pastured butter and we observed improvements in performance and various blood parameters including C-reactive protein and fasting insulin levels.

Eventually the Zone was canned and folks were told to get protein and carb intake up to levels that matched activity. Things REALLY improved!

But I was still of the opinion that fairly high dose fish oil was beneficial to folks with significant systemic inflammation and health issues. The recommendation was to take a fairly large amount of fish oil for a few weeks, then titrate that down to a maintenance level. The thinking here was that we could send a large “anti-inflammatory” signal to the system and get the Titanic steering away from the proverbial iceberg. Some folks (smarter than myself like Chris Kresser) had different ideas on this. Chris liked limiting linoleic acid and keeping EPA/DHA to low-ish levels, mainly from food, with perhaps a few grams per day of supplemental fish oil. What I had not initially considered is signaling, be it anti or pro-inflammatory is a cell by cell affair, and this is based largely on the make-up of fatty acids in our cell membranes. In an inflamed, sick, standard American diet model, individuals have a significant overabundance of linoleic acid in their cell membranes. The idea of front loading more EPA/DHA to change the fatty acid profile of our cells is great until you run into the brick-wall of our metabolic machinery. Cell fatty acid turnover cannot be “goosed” from behind like shoving a bungee jumper off a bridge. Fatty acid turnover has a rate limiting step that is not “substrate limited.” Or, in non-geek-speak more fish oil will not make the process go faster. Instead we need to limit the intake of linoleic acid, keep a decent intake of EPA/DHA, but we need not, and in fact should not hammer that dosage, as we will see when we look at oxidative stress and free-radical chemistry.

When we talk about “inflammation” we must consider two basic elements:

1-The immune system (in this case mainly the innate, non-adaptive immune system made up of macrophages, leukocytes and neutrophils…we’ll largely ignore (for today) the adaptive immune response which is involved in autoimmunity)

2-The various cell-signaling components that tell the immune system what to do. Now, almost everyone has heard of oxidative damage, free radicals, antioxidants and the like.

In chemistry we characterize reactions in a number of ways, with most synthetic reactions involving the shuffling of an electron pair between one atom or molecule and another atom or molecule. This is like a banjo-playing square-dance! Fun, safe, predictable. Another type of reaction that we must consider in biological systems, particularly the immune system, is free radical chemistry. In this situation we see a single electron running amuck. This is more akin to a mosh-pit at a punk concert. In the technical parlance free radicals can “fuck-shit-up.”

The innate immune system makes good use of free radicals when battling bacteria, viruses and parasites. If an immune cell comes in contact with something deemed to be a foreign invader the cell will tend to engulf the item, then release a dose of free-radicals that likely will kill the cell, but will also (hopefully) take out the pathogenic interloper in a Kamikaze style mission. As you recall, inflammation involves not only the immune system but also the cellular signaling components such as prostaglandins, leukotriens and a host of other goodies. In the pro-inflamed state the signaling is effectively “high allert.”

The immune cells are ramped up and just looking for a fight.  As such, there is a tendency for the immune cells to get a little spastic and attack things they should not. As a consequence, we are subjected to an elevated level of oxidative stress. This is to be expected when fighting a cold or bacteria, but it portends doom when it is an outgrowth of endotoxemia (intestinal permeability, bacterial overgrowth) and elevated systemic inflammation from a diet and lifestyle that is throwing too many of the wrong switches. Now, this is a pretty bad scenario as it is, but if we have large amounts of polyunsaturated fats (like those in fish oil, seed and similar oils) in our system things can go from bad to worse.

Polyunsaturated fats are HIGHLY oxidizable. Linseed oil (refined FLAX oil actually…), if added to paper or rags and left open to the air, can get enough reaction going to combust. This is possible because polyunsaturated fats under go what is called a “chain propagative” reaction. Throw one teensy electron into a cell membrane full of polyunsaturated fats and you can witness a mountain of damage. This is why an individual with significant systemic inflammation would do well to limit polyunsaturated fats (particularly linoleic acid) as they are already experiencing oxidative stress. High levels of polyunsaturated fats in the cell membranes will not help things. This oxidative stress issue pops up in other, unlikely spots that can mask problems which otherwise are ascribed a therapeutic effect. Fish oil supplementation has been associated with decreased blood triglyceride levels. Folks savvy to the underpinning of insulin resistance know that elevated triglycerides are an indicator of insulin resistance, so any intervention that lowers triglycerides should be a good thing. Well…in the digestive process all nutrients must be broken down, passed through the gut lining and eventually make their way to the liver.

Fats are released out of the liver in the form of LDL’s, VLDL’s and the like, but they are tested in the liver for oxidative stress potential. If the package is made up of oxidized lipids (lipid peroxides) the batch is scuttled and the liver attempts to degrade the contents of the sample to prevent damage to the rest of the body. The liver is willing to take this hit as it has a large capacity for regeneration, but as with alcoholic cirrhosis, it does take an ass-kicking.  While this chaos ensues in the comfy confines of the liver, our blood triglycerides go down, apparently a good thing, but this is a completely different mechanism of action relative to decreased triglycerides stemming from improved insulin/leptin sensitivity. This is a long-winded way of saying it’s time to revisit our fish-oil recommendations.

 

So, what should I do?

1-LIMIT linoleic acid!! You’d think after I jumped up and down about his for the past 1500 words that it would be obvious, but I just wanted to make sure we are clear on this. Nuts, seeds, corn, safflower, sunflower and similar seed oils are “no bueno.”
 
2-Limit linolenic acid form things like flax, hemp, chia etc. I’d prefer you get the bulk of your N-3’s in the ready made forms of EPA/DHA and your N-6’s as aracidonic acid.  The conversion of linolenic acid to EPA/DHA is inefficient and overall exposes up to a greater oxidative potential as you must consume MORE total polyunsaturated fats to get the goods. I know there are some folks that recommend these short chain fats. Do whatever you like but this is what makes sense to me.

3-Try to get the bulk of your EFA’s (both N-3 and N-6) from grass fed meat, and perhaps pastured dairy in the form of butter. BUT that’s expensive!! I know Buttercup, I know. Do your best. Sardines, mackerel and similar fish are also great sources.

4-Supplement with 2-4 grams of EPA/DHA heavy oils from fish oil, fermented cod liver oil (god help me…that stuff is NASTY, but Chris Kresser loves the stuff) or vegetarian sourced DHA from algae. The DHA can retro-convert to EPA, so no problems there. Which should it be, 2 or 4 grams? If you are “big” take 4. If you are little, take 2. If you do not know if you are big or little, please disavow all knowledge or the paleo diet and adopt veganism. Please.

At the end of the day I think these recommendation support our best understanding of the science and it seems to reflect clinical findings. It also simplifies things to a great degree. Many a client has balked at the high-dose fish oil that has been part of my and other folks recommendations. I think there are some great supplements for specific purposes (adaptogens, creatine and a few other goodies) but where food is concerned, food seems to be best. Shocker. Similarly, there are not shortcuts to health and wellness, just better information and feedback so we can make better decisions.

« The Paleo Solution – Episode 100 |

About the author

Robb Wolf, author of The Paleo Solution, is a former research biochemist and one of the world’s leading experts in Paleolithic nutrition. Wolf has transformed the lives of tens of thousands of people around the world via his top ranked iTunes podcast and wildly popular seminar series. Read more...

Omega-3 - cooking and oxidation

from comments section of: mega-3 Fats, Angiogenesis, and Cancer: Part I | Perfect Health Diet

woly on 28 Apr 2011 at 1:18 am
I have wondered myself whether cooking fish degrades the omega-3 content. From a quick pubmed search I have come across these 3 abstracts that seem to indicate that the PUFA content of fish does NOT degrade. However, I dont have the full text so I cant make any firm conclusions.

Here are the links:

• Stability of Polyunsaturated Fatty Acids after Microwave Cooking of Fish
• Effects of cooking on the fatty acids of three freshwater fish species
• Stability of polyunsaturated omega-3 fatty acids during deep fat frying of Atlantic mackerel (Scomber scombrus L.)

Ray Peat - evils of unsaturated fatty acids

Ray Peat  - Oils in context

Discusses links between unsaturated fatty acids (UFA) and:

• hypothyroidism
• heart disease
• immunosuppression
• cancer
• brain dysfunction (via UFA peroxidation)
• obesity

Notable mentions:

• nutrition in fish heads
• 600 day half life of dangerous UFA in human tissue
• theory that there is no essential dietary fatty acids for humans

The Bacon Bummer - Whole9

The Bacon Bummer | Whole9 | Let us change your life.
by Whole9

Extract:

The Bummer Part

You see, bacon, however delicious it might be, has some downsides.

First, factory-farmed bacon (approximately 95% of the bacon purchased in the US, according to 2007 data) is, nutritionally speaking, garbage. It’s the fattiest cut of an inhumanely treated, poorly fed, often sickly animal, and it’s loaded with unhealthy (i.e. contaminated) fats, preservatives and additives. We’d venture to call it toxic meat, but then again, we love hyperbole. Nonetheless, we think nobody should eat factory-farmed bacon – ever. 

Even in family farms where the animals are treated well, their diets are not always conducive to our optimal health. Even “pastured” pigs’ diets are often supplemented with corn, grains and soybeans. This makes this kind of pastured pork the equivalent of grain-fed cattle that get to eat a little bit of grass – and we would not designate that meat as optimally healthy for you. Because we believe high-quality, grass-finished, organic meat from ruminants (like beef, lamb and elk) is the most healthy protein source available, promoting lots of lesser quality meats like bacon – even from mostly pastured pork – doesn’t make much sense. (Nonetheless, this is not a case against pork. In a rotation of high-quality meats, 100% pastured, organic pork may have its place.)

So why aren’t we promoting 100% pastured, organic, family-farmed bacon?

Here’s where our experience comes in. Historically, when we give people a nutritional inch, they take a nutritional mile. And like a Paleo version of “telephone”, our message tends to degrade the further it spreads. When we mention that we use 100% egg white powder when we travel, people take that to mean, “It’s okay to drink protein shakes!” We say pastured, organic, clarified butter is a good food choice, they pass along, “Whole9 says eat more butter!” Which is exactly why you’ll never hear us mention bacon.

So if we mentioned 100% pastured, organic, nitrate/nitrite-free , family-farmed bacon in every web article, Facebook post and Twitter tweet, well… readers, followers, and workshop attendees would hear (and tell others), “Whole9 say eat bacon!” And then they’d tell their friends, family members and blog readers to eat more bacon, and then you’ve got a whole group of Paleo newbies buying pounds of Oscar Mayer – and consuming what could, in fact, be the unhealthiest meat product out there (besides Spam) in copious amounts. Oops. So that’s one reason we don’t pimp bacon.

6:3 (You Knew We’d Go There)

Some authors, including the highly-respected Dr. Michael Eades, compare the fatty acid profile of bacon to olive oil and conclude that they are very similar. A few percentage points of monounsaturated fat (MUFA) or saturated fat (SFA) aside, we’ll agree. Furthermore, the total polyunsaturated fat (PUFA) content of bacon fat and olive oil are almost identical. (Weird, right?) So here’s where we come back to having a consistent thought process for our recommendations.

We generally recommend against cooking with olive oil… so why would we champion cooking with bacon?

Here’s the back-story. We (and lots of Smart People like Chris Kresser and Chris Masterjohn ) recommend aggressively limiting your polyunsaturated fat intake because those fragile fats undergo peroxidation most easily (compared to MUFA and SFA). The oxidation process forms damaging free radicals that promote inflammation, contribute to aging, and increase the risk of cancer. Heating these fats and exposing them to air (oxygen) dramatically increases the rate that these fats oxidize. So, logically, we recommend that you avoid heating or cooking with fats (like olive oil) that contain these fragile, prone-to-oxidation PUFAs.

So if we believe olive oil should not be heated, and bacon and olive oil have almost the same PUFA content, why would we portray bacon as a healthy choice, given that no one eats their bacon carpaccio-style? Bacon is generally cooked in the open air at fairly high temperatures until “well done”, which smells like oxidized PUFA to us. (And given that their PUFA profile is practically identical, it also doesn’t make sense for us to recommend against cooking with olive oil, but then to give cooking with bacon fat the green light.)

The kicker is that the amount of total fat (and thus PUFA, as a percentage of the total) in a manly-sized serving of bacon is much greater than you’d get from a tablespoon-sized serving of olive oil. (Remember, it’s not just about the ratio of 6:3 in any given food or meal – it’s more about the total dose.) So dissing EVOO for cooking but crispifying a pound of bacon every morning – or frying all your food in bacon fat – just doesn’t add up to us.

Delicous Isn’t Good Enough.

Our concern is not just with the amount of – or 6:3 ratio of – pastured vs. conventional bacon – it’s not just about the fat. (And we don’t really want to debate the potential harm of nitrates/nitrites that are commonly used to preserve bacon. That smacks of justification.) The final reason we don’t promote bacon is because even if you buy the uncured, organic, 100% pastured, nitrate-free stuff, it’s still not your best protein choice. (It doesn’t even make our Top Ten, in fact.) Amy Kubal, RD, says “Many consider bacon a quality source of protein, but this is not necessarily the case compared to beef or chicken. In fact, bacon is often just as much fat as protein.

Bacon is delicious – don’t get me wrong. It’s my favorite ‘condiment’ and should be treated as just that – a condiment. A slice or two every now and then is great, but as an everyday protein option, you can do better.”

Jake 23 May, 2011 at 10:50 am # 

Cook bacon in the microwave between 4 sheets of paper towels. PUFAs have a very low melting point and they flow out to be absorbed by the paper towels. The saturated fat stays in the bacon.

PUFA essential nutrient, or toxic? - by Ray Peat Phd

Unsaturated fatty acids: Nutritionally essential, or toxic?

A R T I C L E
by Ray Peat Phd

Unsaturated fatty acids: Nutritionally essential, or toxic?

In 1929 George and Mildred Burr published a paper claiming that unsaturated fats, and specifically linoleic acid, were essential to prevent a particular disease involving dandruff, dermatitis, slowed growth, sterility, and fatal kidney degeneration.

In 1929, most of the B vitamins and essential trace minerals were unknown to nutritionists. The symptoms the Burrs saw are easily produced by deficiencies of the vitamins and minerals that they didn't know about.

 

What really happens to animals when the "essential fatty acids" are lacking, in an otherwise adequate diet?

Fish oil - "more is not better", Chris Kresser

When it comes to fish oil, more is not better

October 25, 2010 in Food & Nutrition, Heart Disease | 95 comments

By Chris Kresser - The Health Sceptic

Article summary

• The benefits of fish oil supplementation have been grossly overstated
  
• Most of the studies showing fish oil benefits are short-term, lasting less than one year
• The only fish oil study lasting more than four years showed an increase in heart disease and sudden death
• Fish oil is highly unstable and vulnerable to oxidative damage
• There’s no evidence that healthy people benefit from fish oil supplementation
• Taking several grams of fish oil per day may be hazardous to your health

A new study was recently published showing that 3g/d of fish oil in patients with metabolic syndrome increased LDL levels and insulin resistance.

Too much fish oil can wreak havoc in your body

Omega-3 fatty acids are highly vulnerable to oxidative damage. When fat particles oxidize, they break down into smaller compounds, like malondialdehyde (MDA), that are dangerous because they damage proteins, DNA, and other important cellular structures.

PUFA phobia - Matt Sone explains Ray Peat

180 Degree Health: Ray Peat - PUFA

Extract:

If you know anything about Peat, know that he has a vendetta against polyunsaturated fat – which could very well be his greatest scientific contribution because of the numerous negative actions that excessive polyunsaturated fat intake exerts on human tissues, organs, and glands like the wondrous thyroid.

Omega-3 - Angiogenesis & Cancer

Omega-3s, Angiogenesis and Cancer: Part II | Perfect Health Diet
Omega-3 - Angiogenesis & Cancer

Conclusion

It looks like we have a recipe for angiogenesis:

DHA + retinyl + oxidative stress = angiogenesis
This recipe is invoked normally and properly during wound healing. But it is also invoked excessively in pathological contexts – notably in cancers and age-related macular degeneration, probably also in other angiogenesis-associated diseases such as arthritis, rosacea, obesity, psoriasis, endometriosis, dementia, and multiple sclerosis.
In the case of cancer, DHA oxidation to CEP might transform miniscule, harmless cancers to high-grade, life-threatening cancers.
Should this possibility affect our dietary omega-3 recommendations? Well, we need to know the relative importance of the three ingredients on the left side of the above equation in producing angiogenesis. Chris Kresser wondered in the comments Tuesday whether oxidation may be the key factor:

I question whether DHA supplementation would truly play a causative role in the absence of a *pro-oxidative environment*.
In other words, perhaps in someone eating a SAD, not exercising, under a lot of stress, etc. DHA is more easily oxidized and thus potentially carcinogenic.
But in someone that is keeping all other oxidative risk factors low (i.e. they’re avoiding n-6, exercising, managing stress, reducing exposure to chemical toxins, etc.) I tend to doubt that supplementing with DHA could cause significant harm.

That’s the last piece of the puzzle: how do we minimize the level of oxidized DHA?
As I replied to Chris in the comments, low-carb Paleo dieters are not out of the woods in regard to oxidative stress. Oxidative stress is generated normally during metabolism, immune function – and by cancers. If anti-oxidant minerals like zinc, copper, and selenium and vitamins like vitamin C are deficient, then oxidative stress can be very high on a low-carb Paleo diet.
At the moment, I think it’s prudent to eat no more than 1 pound of salmon or similar cold-water fish per week, to avoid further EPA/DHA supplements, and to avoid low-fat diets which tend to elevate membrane DHA levels. Moderate omega-3 consumption is especially important for those suffering from diseases of pathological angiogenesis – especially cancer. DHA is essential for good health – but in excess, it is probably dangerous.

References

[1] Brasky TM et al. Serum Phospholipid Fatty Acids and Prostate Cancer Risk: Results From the Prostate Cancer Prevention Trial. Am. J. Epidemiol. April 24, 2011 DOI: 10.1093/aje/kwr027 (Will be at http://pmid.us/21518693.)
[2] Raatz SK et al. Total fat intake modifies plasma fatty acid composition in humans. J Nutr. 2001 Feb;131(2):231-4. http://pmid.us/11160538.
[3] MacLean CH, Newberry SJ, Mojica WA, et al. Effects of Omega-3 Fatty Acids on Cancer. Summary, Evidence Report/Technology Assessment: Number 113. AHRQ Publication Number 05-E010-1, February 2005. Agency for Healthcare Research and Quality, Rockville, MD. http://www.ahrq.gov/clinic/epcsums/o3cansum.htm.
[4] Harris RE. Cyclooxygenase-2 (cox-2) and the inflammogenesis of cancer. Subcell Biochem. 2007;42:93-126. http://pmid.us/17612047.
[5] Gu X et al. Carboxyethylpyrrole protein adducts and autoantibodies, biomarkers for age-related macular degeneration. J Biol Chem. 2003 Oct 24;278(43):42027-35. http://pmid.us/12923198.
[6] Hollyfield JG et al. A hapten generated from an oxidation fragment of docosahexaenoic acid is sufficient to initiate age-related macular degeneration. Mol Neurobiol. 2010 Jun;41(2-3):290-8. http://pmid.us/20221855.
[7] West XZ et al. Oxidative stress induces angiogenesis by activating TLR2 with novel endogenous ligands. Nature. 2010 Oct 21;467(7318):972-6. http://pmid.us/20927103.
[8] Amann PM et al. Vitamin A metabolism in benign and malignant melanocytic skin cells: Importance of lecithin/retinol acyltransferase and RPE65. J Cell Physiol. 2011 Apr 4. doi: 10.1002/jcp.22779. [Epub ahead of print] http://pmid.us/21465477.

PUFA 23 times worse for glycation that carbs - Ray Peat

180 Degree Health: Ray Peat - PUFA


"The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do (Fu, et al., 1996). And the oxidation of fats rather than glucose means that the proteins won't have as much protective carbon dioxide combined with their reactive nitrogen atoms, so the real difference in the organism is likely to be greater than that seen by Fu, et al."

Lipid peroxidation - Wikipedia, the free encyclopedia

Lipid peroxidation - Wikipedia, the free encyclopedia

Lipid peroxidation

From Wikipedia, the free encyclopedia

Mechanism of lipid peroxidation.

Lipid peroxidation refers to the oxidative degradation of lipids. It is the process in which free radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage. This process proceeds by a free radical chain reaction mechanism. It most often affects polyunsaturated fatty acids, because they contain multiple double bonds in between which lie methylene -CH2- groups that possess especially reactive hydrogens. As with any radical reaction, the reaction consists of three major steps: initiation, propagation, and termination.

Vegetable Oils and Heart Disease : A Closer Look

Precious Yet Perilous
Written by Chris Masterjohn Phd

Vegetable Oils and Heart Disease : A Closer Look
 
Six randomized, controlled trials specifically testing the effect of the substitution of polyunsaturated vegetable oils for animal fats on heart disease have been published.^64-69

The first randomized, controlled trial of dietary fat substitution was published in 1965. Substitution of corn oil for animal fat and carbohydrate doubled the number of major cardiac events. The results were not quite statistically significant, meaning there was a slight possibility they were due to chance. The researchers concluded “that under the circumstances of this trial corn oil cannot be recommended as a treatment of ischaemic heart disease. It is most unlikely to be beneficial, and it is possibly harmful.”⁶⁴
A second trial found that replacing animal fats with polyunsaturated vegetable oils increased mortality by 39 percent. Rather than considering the possibility that the lipid hypothesis might be false, the investigators concluded that “men who have had myocardial infarction are not a good choice for testing the lipid hypothesis.”⁶⁶

Three other such trials found either no effect,^{65, 67} or a small increase in mortality in the group consuming vegetable oil, which was not statistically significant.⁶⁸

The longest study on the effect of vegetable oil ever conducted was the Wadsworth Veterans Administration Hospital Study.⁶⁹ The researchers randomized over four hundred men who were long-term inpatients to one of two dining halls. One hall used butter and the other used a mix of vegetable oils. The study was double-blinded and lasted over eight years. The researchers took care not to reuse the vegetable oil after cooking but took no such precautions with the butter, resulting in butter that was very deficient in vitamin E.⁷⁴ There were also twice as many heavy smokers and 60 percent more moderate smokers in the butter group. The group consuming butter had 50 percent more cardiovascular deaths. The group consuming vegetable oil, however, had more atherosclerosis than the control group and in the last few years of the study began experiencing a marked increase in the risk of cancer. Total mortality was slightly higher among those consuming vegetable oil, but the difference was not statistically significant.

There are two remarkable findings about this study. Even though cardiovascular deaths were lower in the vegetable oil group, atherosclerosis slightly increased. This clearly disproves the hypothesis that vegetable oils decrease the accumulation of atherosclerotic plaque by decreasing cholesterol levels. It further suggests that had there been an equal distribution of smokers between groups and had the control group received adequate vitamin E, vegetable oil may have proven to markedly increase the accumulation of atherosclerotic plaque as well as the risk of cardiovascular mortality. The fact that cancer began rising in the vegetable oil group in the last few years of the study—again, despite the heavy rate of smoking and deficient intake of vitamin E in the control group—suggests that the full extent of the ravages of oxidative stress and inflammation caused by vegetable oils takes at least five years to develop. A longer study may have shown a much greater risk of mortality in the vegetable oil group. These six studies clearly show that vegetable oils are not capable of reducing total mortality and strongly suggest that they may raise the risk of heart disease and cancer.

The Perils of PUFA: Oxidative Stress (broken glass analogy)

Precious Yet Perilous
Written by Chris Masterjohn Phd
September 22 2010 15:02

The Perils of PUFA: Oxidative Stress

In 1985, the lipid researcher Hugh Sinclair gave a pre-banquet speech on his seventy-fifth birthday before the Second International Congress on Essential Fatty Acids, Prostaglandins and Leukotrienes in London, in which he described the deleterious effects of one hundred days on an “Eskimo diet” of seal blubber and undeodorized mackerel oil. He went on the diet to measure his bleeding time because the weather during a recent trip with several colleagues to northwestern Greenland had curtailed him from measuring the bleeding times of real Eskimos. Despite a daily supplement of vitamin E, his blood and urine levels of malondialdehyde (MDA)—a product of the oxidative destruction of PUFA (see Figure 3d)—rose to fifty times the normal level. Although MDA causes birth defects, Sinclair was not worried about having “misshapen offspring” because his sperm had disappeared.³¹
Sinclair’s experience illustrates one of the unique dangers of all essential fatty acids, regardless of their class—their vulnerability to oxidative stress.

---

Figure 3. Oxidative Stress and the Shattering of Delicate PUFAs
Compounds with unpaired electrons, called free radicals, are capable of
stealing electrons from, or “oxidizing,” PUFAs. PUFAs are uniquely vulnerable
to oxidation because they are the only fatty acids with two or more double
bonds, and it is the carbon that lies directly between two double bonds that
is vulnerable to oxidation at physiological temperatures. In the figure, a lipid
peroxyl radical (LOO) steals an electron and a hydrogen atom from a PUFA.
b. Having stolen the electron and hydrogen atom, the lipid peroxyl radical becomes
a lipid peroxide (LOOH). The addition of oxygen to the oxidized fatty
acid forms a new lipid peroxyl radical that can oxidize another PUFA (LH).
c. There are now two lipid peroxides, one shown in its chemical structure and
one abbreviated as LOOH. The newly oxidized fatty acid (L•) can now continue
the chain reaction.
d. Many of these oxidized fatty acids will continue to degenerate into smaller
compounds, like a glass that shatters into many pieces. One such compound,
malondialdehyde (MDA), is shown in the figure. MDA is particularly dangerous
because it can leave the membrane and damage proteins, DNA, and
other important cellular structures. This process can be likened to the shattering
of delicate glass, which results in a mess of dangerous shards that must be
properly cleaned up.

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Oxidative stress, or lipid peroxidation, shown in Figure 3, can be thought of as the destruction of structurally and functionally important molecules within the body, beginning with the shattering of PUFAs. PUFAs, in this sense, are like delicate glass. Glass performs many useful functions: we use it to protect ourselves and our property from the assaults of raging storms, for the utensils from which we eat and drink, to see when our vision fails, to examine complex specimens whose details we cannot otherwise distinguish with the naked eye, and in many other more sophisticated examples of modern technology. At the same time, glass is delicate and can shatter. When glass shatters, it invariably leaves behind a mess of dangerous shards. Anyone who breaks a glass on their kitchen floor knows to clean up the shards immediately, lest they or their family cut their feet by walking on them. Likewise, when PUFAs shatter they leave behind shards such as MDA, which are capable of damaging proteins, DNA and other structurally and functionally important components of our cells.
The best way to avoid shattering glass is to be careful with how one uses, cleans and stores it. Nevertheless, the danger of breaking glass will increase simply by having too much of it around. Likewise, the consumption of excess PUFAs increases oxidative stress even when the oils are fresh and properly cared for. Consumption of fresh, non-oxidized DHA, EPA or omega-3-rich perilla oil increases markers of oxidative stress in rats.⁵⁸ Rats fed 30 percent of their diet as corn oil have double the rate of lipid peroxidation, half the aerobic capacity, and 42 percent lower glycogen stores in their heart tissue compared to rats fed an equal amount of coconut oil.⁵⁹ A randomized, doubleblind, placebo-controlled trial likewise showed that six grams per day of fish oil increased lipid peroxides and MDA in healthy men, regardless of whether they were supplemented with 900 IU of vitamin E (see Figure 4).⁶⁰
Sinclair might have better replicated the “Eskimo diet” had he sought the guidance of an Eskimo. Arachidonic acid is necessary for sperm production, and the liberal consumption of glands and other organs rich in arachidonic acid may protect the Inuit and Aleut peoples from the high levels of EPA they obtain from fatty fish and marine oils.³¹ There may be other components of their traditional diets that limit the vulnerability of PUFAs to oxidative stress, such as antioxidants like coenzyme Q10, lipoic acid, and preformed vitamin A found abundantly in organ meats, or other unknown factors. Human studies have generally used alpha-tocopherol, a form of vitamin E, to protect against the oxidation of fish oils within the body, but supplements of pure alpha-tocopherol suppress levels of gamma-tocopherol, a different form of vitamin E with a unique spectrum of antioxidant protection. Some of the main oxidants in human blood, moreover, are water-soluble so PUFAs require water-soluble antioxidants such as vitamin C for protection. Exactly which components of the traditional Inuit diet best protected them from their high intake of fish oils is unclear, but Sinclair’s experience demonstrates the danger of attempting to replicate a particular peculiarity of one group’s traditional diet without replicating the diet as a whole.

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Figure 4. Fish Oil Increased in Lipid Peroxides and MDA in Humans While Vitamin E Had No Effect
A double-blind, randomized, placebocontrolled trial compared six weeks of supplementation with six grams per day of omega-3 fatty acids from menhaden fish oil to supplementation with six grams per day of olive oil, with or without 900 IU per day of vitamin E as synthetic alpha-tocopherol, in healthy men. For each group, the bar on the left represents the change in lipid peroxides, and the bar on the right represents the change in MDA. Asterisks indicate a statistically significant increase over the course of the six weeks. Fish oil supplementation caused a significant increase in lipid peroxides while MDA and vitamin E had no effect. Adapted from the data in reference 60.

The Great Fish Oil Experiment - Ray Peat

The Great Fish Oil Experiment

Flax, shun it - Rancid Fats and Anti-Nutrients

Integrated Supplements Blog: From Rancid Fats to Anti-Nutrients - More Reasons to Avoid Flax

With flax, it seems that (as is so often the case in the marketing of health foods) we’ve only been given the part of the story which sells products, and not the part of the story we need to make a truly informed decision.

In the previous Integrated Supplements Blog post, we began to take a look at some of the potential problems associated with the regular consumption of flax–based products. We showed you a study which revealed that people consuming flaxseed meal suffered significantly reduced antioxidant status – possibly a result of the nearly unavoidable presence of rancid, oxidized fats found in almost all flaxseed–containing items.

Related Articles:

• Some Reasons to Avoid Flaxseeds - Study Finds Flaxseeds Weaken Antioxidant Defenses
• Rancid Fats and Oxidative Stress - Strategies To Reverse Aging - Part 1
• Combating Oxidative Stress - Strategies to Reverse Aging - Part 2
• The Anti-Aging Diet Part 1 - Can Some Foods Accelerate Aging?

Omega-6 Fat Research News & Commentary - blog

......dormant blog with great omega 3/6 resources/links:

from Omega-6 Fat News & Commentary Research News by Evelyn Tribole, MS, RD -

Mission:

"The balancing act between omega-6 and omega-3 fats is an important detail often missed in the headline research news and even by the scientists themselves! This site/blog focuses on the omega-6 fat issue, by offering brief summaries of recently published studies and an occasional commentary from me. It is written for health professionals and individuals who are interested in the science of omega-6 fats and their impact on health."

Background:

Type 3 Diabetes - Brain Diabetes?

USPharmacist.com > Type 3 Diabetes: Brain Diabetes?

Type 3 Diabetes: Brain Diabetes?

A relationship between diabetes mellitus (DM) and dementia is undeniable, with numerous studies concluding that DM increases the risk of cognitive decline and dementia, including Alzheimer’s disease (AD).^1-5 Not only does DM increase the risk of dementia, it actually increases the rate of dementia development two- to threefold.³

The mechanism of this impairment is not fully understood, but it is hypothesized that hyperglycemia, insulin resistance, oxidative stress, advanced glycation end products, and inflammatory cytokines collectively lead to cognitive dysfunction.⁵

In fact, diabetes was described as a “special kind of accelerated aging” in 1976 owing to its many associated complications.⁵

The apparent overlap between DM and dementia has led to the suggestion that AD is not solely a neurologic disorder, but rather a neuroendocrine disorder, with Steen et al coining the term type 3 diabetes to describe this hybrid disease.⁶

Omega-3 - Harvard School of Public Health

notable: some leading researchers/commentators are in disagreement with some of the Harvard SPH conclusions below, or present a position that appears far more nuanced, including for example on:

• the quality of the omega 3 and 6 oils
• the harmful impact of all supplemented (ie not ingested as part of whole food) omega 6 oils
• the oxidation of omega 3 and 6 oils, causes and effect on disease
• the typical over consumption of omega 6 and its impact on omega 3 effectiveness
• the potential toxic, or unhelpful side effects of too much and/or bad omega 3

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Ask the Expert: Omega-3 Fatty Acids - Your Nutrition Questions Answered - The Nutrition Source - Harvard School of Public Health

1. What are omega-3 fatty acids, and why should I make sure to include them in my diet?

α-linolenic acid (omega 3) and heart disease - references

α-linolenic acid and reduction of cardiac deaths
StephenC Cunnane a b, Dennis McIntosh a b, Peter Marckmann c d, Jo̸rgen Jespersen c d
The Lancet, Volume 344, Issue 8922, Page 622, 27 August 1994

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doi:10.1016/S0140-6736(94)92012-5Cite or Link Using DOI

References

Dolecek TA.. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the Multiple Risk Factor Intervention Trial. Proc Soc Exp Biol Med 1992; 200: 177-182. PubMed

Flaxseed oil - baking/storage, Flax Council of Canada

Baking/storage_99/2000 (Page 1) - Flax Council of Canada

Baking effects:

ALA in whole and milled flaxseed also appears to be stable to heat equal or greater than the temperatures involved in baking batters and doughs such as muffins and yeast bread. Thermal stability was shown in 1992 by the absence of significant changes in peroxide values and fatty acid composition when both forms of flaxseed were heated for 60 minutes at either 100°C (212°F) or 350°C (662°F).

Stability of omega-3 fatty acids - deep fat frying mackerel

Stability of polyunsaturated omega-3 fatty acids during deep fat frying of Atlantic mackerel (Scomber scombrus L.)
 

J.L. Sebedio^a, W.M.N. Ratnayake^{, b, *}, R.G. Ackman^b and J. Prevost^a

INRA, Station de Recherches sur la Qualité des Aliments de l'Homme, Unité de Nutrition Lipidique, 17 rue Sully, BV 1540, 21034 Dijon, France
Technical University of Nova Scotia, CIFT, PO Box 1000, Halifax, Nova Scotia, Canada B3J 2X4

Received 24 July 1992; 

Accepted 2 November 1992. 

Available online 22 September 2003.

Abstract

Fall-caught Atlantic mackerel (Scomber scomburus L.) were cut transversely into steak sections and deep fat fried for 7 min in canola oil at 180°C. A total of 20 batches, each consisting of 10 randomized steak sections with approximately 12%, total fat, was fried over 10 days.

The longer-chain omega-3 polyunsaturated fatty acid content of the mackerel was not affected by deep frying. Only small quantities of polar components, polymers and geometrical fatty acid isomers of the long chain highly polyunsaturated fatty acids were formed during deep frying.

Examination of the fatty acid composition of the frying medium, the fish skin, and the meat showed extensive lipid exchanges between the fish and the frying medium. Of the major isomers of eicosapentaenoic acid formed by thermal action 20:5Δ5c,8t,11c,14t, 17c was less then 0·1% of the total 20:5 recovered from the used canola oil.

Keywords: heated fat; omega-3 fatty acids; polymers; polar components; gas liquid chromatography; eicosapentaenoic acid; eicosapentaenoic acid geometrical isomers

The work was executed at both INRA and CIFT.