....as discussed in Peat vs. Paleo - The Danny Roddy Weblog - Animal-Based Nutrition
Ray Peat on dietary sucrose:
Paleo advocates recommend lower carb diets. Sisson recommends 150 grams (or less) of carbohydrates a day, while others recommend ketogenic levels (50g or less). This is the greatest departure Ray Peat makes from the typical paleo diet.
He states that sugar (sucrose, fructose) is not an issue when polyunsaturated fats are not in the diet.
Showing posts with label x - unsat fat related. Show all posts
Showing posts with label x - unsat fat related. Show all posts
2.7.11
Ray Peat - evils of unsaturated fatty acids
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
1.7.11
Bacon - 60% PUFA (Wikipedia), and heart disease connection
Bacon - Wikipedia, the free encyclopedia
Researchers from the Harvard School of Public Health found in 2010 that eating processed meats such as bacon, preserved by smoking, curing or salting, or with the addition of chemical preservatives, was associated with an increased risk of both heart disease and diabetes.
The same association was not found for unprocessed meat.[38]
Nutrients
Four 14-gram (0.5 oz) slices of bacon together contain 7.45 grams (0.26 oz) of fat, of which about half is monounsaturated, a third is saturated and a sixth is polyunsaturated, and 7.72 grams (0.27 oz) of protein.[35] Four pieces of bacon can also contain up to 800 mg of sodium, which is roughly equivalent to 1.92 grams of salt. The fat and protein content varies depending on the cut and cooking method.Health concerns
A 2007 study by Columbia University suggests a link between eating cured meats (such as bacon) and chronic obstructive pulmonary disease. The preservative sodium nitrite is the probable cause,[36][37] and bacon made without added nitrites is available. Bacon is usually high in salt and saturated fat; excessive consumption of both is related to a variety of health problems. See the articles on saturated fat and salt for more details.Researchers from the Harvard School of Public Health found in 2010 that eating processed meats such as bacon, preserved by smoking, curing or salting, or with the addition of chemical preservatives, was associated with an increased risk of both heart disease and diabetes.
The same association was not found for unprocessed meat.[38]
Unsaturated vegetable oils toxic - Ray Peat Phd
Coconutoil.com - UNSATURATED VEGETABLE OILS: TOXIC
SUMMARY
- Unsaturated fats cause aging, clotting, inflammation, cancer, and weight gain.
- Avoid foods which contain the polyunsaturated oils, such as corn, soy, safflower, flax, cottonseed, canola, peanut, and sesame oil.
- Mayonnaise, pastries, even candies may contain these oils; check the labels for ingredients.
- Pork is now fed corn and soy beans, so lard is usually as toxic as those oils; use only lean pork
- Fish oils are usually highly unsaturated; "dry" types of fish, and shellfish, used once or twice a week, are good
- Avoid cod liver oil.
- Use vitamin E.
- Use coconut oil, butter, and olive oil
- Unsaturated fats intensify estrogen's harmful effects.
Lard versus olive oil - Paleo forum discussion (...all day everyday?)
bacon all day everyday?
I think they are being very selective about the information they are presenting in that comparison.
In terms of polyunsaturated fats, yes, commercial bacon fat - and in fact all fat from commercial pigs - is similar to olive oil. However, contrary to their scare tactics on polyunsaturated fats, that's because both are fairly low in polyunsaturated fats, and both have reasonable albeit not great omega 3:6 ratios - that's why olive oil is often regarded as the least bad of nonpaleo oils. They also neglect to mention that the fat that actually stays on the bacon is the fat that hasn't gotten hot enough to melt off, so it's far from the temperatures required for oxidation - and if you cook bacon correctly, over low heat, the fat that melts out doesn't get to those temperatures either.
Polyunsaturated fats are only part of the picture, though. Saturated fat is also important, because the saturation of fat is strongly related to cooking stability. The article leaves out the fact that pork fat has about three times the saturated fat of olive oil, a major difference. That's what makes pork fat so much stabler when used as cooking oil, a difference with which I've had plenty of personal experience. They also leave out the smoke points - 370F for lard, 320F for extra virgin olive oil.
And of course, all that neglects the fundamental argument for paleo: it protects us against the problems we don't know about, not just the problems we do know about. Pigs on the hoof are delicious and were eaten by paleolithic humans.
Now, is grass finished beef tallow even better for cooking? In terms of omega 3:6 ratios, it's certainly better than commercial pork fat. On the other hand, I've found even grass finished beef tallow to be a little too saturated to be ideal for some cooking applications.
Extract:
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.
I think they are being very selective about the information they are presenting in that comparison.
In terms of polyunsaturated fats, yes, commercial bacon fat - and in fact all fat from commercial pigs - is similar to olive oil. However, contrary to their scare tactics on polyunsaturated fats, that's because both are fairly low in polyunsaturated fats, and both have reasonable albeit not great omega 3:6 ratios - that's why olive oil is often regarded as the least bad of nonpaleo oils. They also neglect to mention that the fat that actually stays on the bacon is the fat that hasn't gotten hot enough to melt off, so it's far from the temperatures required for oxidation - and if you cook bacon correctly, over low heat, the fat that melts out doesn't get to those temperatures either.
Polyunsaturated fats are only part of the picture, though. Saturated fat is also important, because the saturation of fat is strongly related to cooking stability. The article leaves out the fact that pork fat has about three times the saturated fat of olive oil, a major difference. That's what makes pork fat so much stabler when used as cooking oil, a difference with which I've had plenty of personal experience. They also leave out the smoke points - 370F for lard, 320F for extra virgin olive oil.
And of course, all that neglects the fundamental argument for paleo: it protects us against the problems we don't know about, not just the problems we do know about. Pigs on the hoof are delicious and were eaten by paleolithic humans.
Now, is grass finished beef tallow even better for cooking? In terms of omega 3:6 ratios, it's certainly better than commercial pork fat. On the other hand, I've found even grass finished beef tallow to be a little too saturated to be ideal for some cooking applications.
30.6.11
Omega 6 bad, omega 3 good - major (2010) study
Food and Behaviour Research: Ramsden CE et al 2010 - n-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials
Web URL: View this and other related abstracts on PubMed here
Lay Summary:
Web URL: View this and other related abstracts on PubMed here
Lay Summary:
NON-TECHNICAL SUMMARY
These findings indicate that dietary advice to consume more 'polyunsaturated fats' (PUFA) by using vegetable oils to replace solid fats like butter, lard or hard margarines may actually increase the risk of heart disease if the vegetable oils only contain omega-6 PUFA.
Previous studies relating dietary fat intake to heart health have failed to consider the very different effects of omega-6 versus omega-3 PUFA. (Broadly speaking, omega-6 PUFA tend to promote inflammation and blood clots, whereas omega-3 PUFA have the opposite effects).
These findings, published in the British Journal of Nutrition, are based on a detailed re-analysis of results from placebo-controlled treatment trials involving over 11,000 people in total. This time, the scientists carefully separated the studies in which the dietary treatments contained omega-6 PUFA only, or a mixture of omega-3 and omega-6 PUFA.
Only the 'mixed omega-3 and omega-6 PUFA' trials showed any benefits in reducing heart disease risk. By contrast, the use of omega-6 PUFA alone was associated with slightly worse heart disease outcomes.
Omega-3 PUFA have repeatedly been shown to have benefits for heart health, but it is the longer-chain forms (EPA and DHA) - found in oily fish and seafood - which are the most valuable for heart health (as well as for the brain and immune system). Only a few vegetable oils (such as flaxseed oil, rapeseed oil, or soybean oil) contain any omega-3 PUFA - although this is in a shorter-chain form (alpha-linolenic acid) that is not as beneficial to human health as EPA and DHA. Many of the most commonly used vegetable oils (such as corn oil, sunflower oil or safflower oil) are high in omega 6 PUFA, and contain no omega-3 PUFA at all.
| Abstract: 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. |
28.6.11
Eskimo study - high omega-3 reduces obesity-related disease risk
Eskimo study suggests high consumption of omega-3s in fish-rich diet reduces obesity-related disease risk
"Because Yup'ik Eskimos have a traditional diet that includes large amounts of fatty fish and have a prevalence of overweight or obesity that is similar to that of the general U.S. population, this offered a unique opportunity to study whether omega-3 fats change the association between obesity and chronic disease risk," said lead author Zeina Makhoul, Ph.D., a postdoctoral researcher in the Cancer Prevention Program of the Public Health Sciences Division at the Hutchinson Center.
Eskimo Study Suggests High Consumption of Omega-3s in Fish-Rich Diet Reduces Obesity-Related Disease Risk
ScienceDaily (Mar. 25, 2011) — A study of Yup'ik Eskimos in Alaska, who on average consume 20 times more omega-3 fats from fish than people in the lower 48 states, suggests that a high intake of these fats helps prevent obesity-related chronic diseases such as diabetes and heart disease.
The study, led by researchers at Fred Hutchinson Cancer Research Center and conducted in collaboration with the Center for Alaska Native Health Research at the University of Alaska-Fairbanks, was published online March 23 in the European Journal of Clinical Nutrition."Because Yup'ik Eskimos have a traditional diet that includes large amounts of fatty fish and have a prevalence of overweight or obesity that is similar to that of the general U.S. population, this offered a unique opportunity to study whether omega-3 fats change the association between obesity and chronic disease risk," said lead author Zeina Makhoul, Ph.D., a postdoctoral researcher in the Cancer Prevention Program of the Public Health Sciences Division at the Hutchinson Center.
27.6.11
EFA deficiency, immune function - study audit on Ray Peat position
180 Degree Health: Ray Peat - PUFA
- john Do you know of any studies that actually manage to induce clinical symptoms of EFA deficiency in humans (ie dermatitis etc)? I've only seen one, conducted in infants who received a completely fat-free diet, and very few studies seem to actually investigate whether the symptoms could rather be due to depletion of some nutrient due to the increased metabolism. I went through some of the literature on EFA-deficient mice, and its really true as Peat says that EFA-deficiency seems to be highly protective against many different toxins and auto-immune diseases. There's half a dozen papers on how EFA-deficienct mice are immune against streptozotocin and cyclosporin-induced diabetes, EFA-deficiency prevents autoimmune diabetes, toxin-induced renal failure and autoimmune kidney disease, makes mice strongly resistant to endotoxic shock, infectious disease and almost completely eliminates the edema associated with arthritis. Seeing as how the main purported role of PUFAs is to modulate the immune system, if they were truly essential, it just seems very odd to me that EFA-deficient animals actually show many signs of having superior immune function. Some refs: Diabetes http://www.ncbi.nlm.nih.gov/pubmed/3045812 http://www.ncbi.nlm.nih.gov/pubmed/7667243 http://www.ncbi.nlm.nih.gov/pubmed/9389417 http://www.ncbi.nlm.nih.gov/pubmed/7579534 http://www.ncbi.nlm.nih.gov/pubmed/2307932 Arthritis http://www.ncbi.nlm.nih.gov/pubmed/2307932 Endotoxic shock http://www.ncbi.nlm.nih.gov/pubmed/394879 Kidney disease http://www.ncbi.nlm.nih.gov/pubmed/2212002 http://www.ncbi.nlm.nih.gov/pubmed/2809195 Trypanosoma infection http://www.ncbi.nlm.nih.gov/pubmed/1342611 Antimicrobial activity http://www.ncbi.nlm.nih.gov/pubmed/2649598 http://www.ncbi.nlm.nih.gov/pubmed/9119445
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?
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?
Omega-6 & 3 Consumption over the Last Century
Whole Health Source: US Omega-6 and Omega-3 Fat Consumption over the Last Century
by Stephan Guyenet Whole Health Source
Drs. Chris Ramsden and Joseph Hibbeln worked on this paper (the first author was Dr. Tanya Blasbalg and the senior author was Dr. Robert Rawlings)-- they were the first and second authors of a different review article I reviewed recently (2). Their new paper is a great reference that I'm sure I'll cite many times. I'm going to briefly review it and highlight a few key points.
1. The intake of omega-6 linoleic acid has increased quite a bit since 1909. It would have been roughly 2.3% of calories in 1909, while in 1999 it was 7.2%. That represents an increase of 213%. Linoleic acid is the form of omega-6 that predominates in seed oils.
2. The intake of omega-3 alpha-linolenic acid has also increased, for reasons that I'll explain below. It changed from 0.35% of calories to 0.72%, an increase of 109%.
3. The intake of long-chain omega-6 and omega-3 fats have decreased. These are the highly bioactive fats for which linoleic acid and alpha-linolenic acid are precursors. Arachidonic acid, DHA, DPA and EPA intakes have declined. This mostly has to do with changing husbandry practices and the replacement of animal fats with seed oils in the diet.
4. The ratio of omega-6 to omega-3 fats has increased. There is still quite a bit of debate over whether the ratios matter, or simply the absolute amount of each. I maintain that there is enough evidence from highly controlled animal studies and the basic biochemistry of PUFAs to tentatively conclude that the ratio is important. At a minimum, we know that excess linoleic acid inhibits omega-3 metabolism (3, 4, 5, 6). The omega-6:3 ratio increased from 5.4:1 to 9.6:1 between 1909 and 2009, a 78% increase.
5. The biggest factor in both linoleic acid and alpha-linolenic acid intake changes was the astonishing rise in soybean oil consumption. Soybean oil consumption increased from virtually nothing to 7.4% of total calories, eclipsing all sources of calories besides sugar, dairy and grains! That's because processed food is stuffed with it. It's essentially a byproduct of defatted soybean meal-- the second most important animal feed after corn. Check out this graph from the paper:
I think this paper is an important piece of the puzzle as we try to figure out what happened to nutrition and health in the US over the last century.
by Stephan Guyenet Whole Health Source
US Omega-6 and Omega-3 Fat Consumption over the Last Century
Omega-6 and omega-3 polyunsaturated fats (PUFA) are essential nutrients that play many important roles in the body. They are highly bioactive, and so any deviation from ancestral intake norms should probably be viewed with suspicion. I've expressed my opinion many times on this blog that omega-6 consumption is currently too high due to our high intake of refined seed oils (corn, soybean, sunflower, etc.) in industrial nations. Although it's clear that the quantity of omega-6 and omega-3 polyunsaturated fat have changed over the last century, no one had ever published a paper that attempted to systematically quantify it until last month (1).Drs. Chris Ramsden and Joseph Hibbeln worked on this paper (the first author was Dr. Tanya Blasbalg and the senior author was Dr. Robert Rawlings)-- they were the first and second authors of a different review article I reviewed recently (2). Their new paper is a great reference that I'm sure I'll cite many times. I'm going to briefly review it and highlight a few key points.
1. The intake of omega-6 linoleic acid has increased quite a bit since 1909. It would have been roughly 2.3% of calories in 1909, while in 1999 it was 7.2%. That represents an increase of 213%. Linoleic acid is the form of omega-6 that predominates in seed oils.
2. The intake of omega-3 alpha-linolenic acid has also increased, for reasons that I'll explain below. It changed from 0.35% of calories to 0.72%, an increase of 109%.
3. The intake of long-chain omega-6 and omega-3 fats have decreased. These are the highly bioactive fats for which linoleic acid and alpha-linolenic acid are precursors. Arachidonic acid, DHA, DPA and EPA intakes have declined. This mostly has to do with changing husbandry practices and the replacement of animal fats with seed oils in the diet.
4. The ratio of omega-6 to omega-3 fats has increased. There is still quite a bit of debate over whether the ratios matter, or simply the absolute amount of each. I maintain that there is enough evidence from highly controlled animal studies and the basic biochemistry of PUFAs to tentatively conclude that the ratio is important. At a minimum, we know that excess linoleic acid inhibits omega-3 metabolism (3, 4, 5, 6). The omega-6:3 ratio increased from 5.4:1 to 9.6:1 between 1909 and 2009, a 78% increase.
5. The biggest factor in both linoleic acid and alpha-linolenic acid intake changes was the astonishing rise in soybean oil consumption. Soybean oil consumption increased from virtually nothing to 7.4% of total calories, eclipsing all sources of calories besides sugar, dairy and grains! That's because processed food is stuffed with it. It's essentially a byproduct of defatted soybean meal-- the second most important animal feed after corn. Check out this graph from the paper:
I think this paper is an important piece of the puzzle as we try to figure out what happened to nutrition and health in the US over the last century.
Omega 6 & 3 in nuts, oils etc - harm from too much
Omega 6 and 3 in nuts, oils, meat and fish. Tools to get it right. | Julianne's Paleo & Zone Nutrition Blog
One of the ways our diets have changed dramatically from the diets of our ancestors and even the very recent past is the ratio of Omega 6 to Omega 3 polyunsaturated fatty acids in the food we eat. A huge amount has been written about this subject, dozens of studies have been published. I’m not going into detail, the object here is to provide tools to help you get this balance right. At the end of the page – I’ve posted some links to other interesting blog posts and articles.
Omega 6 and 3 in nuts, oils, meat and fish. Tools to get it right.
You are strict paleo, you eat nothing but meat, seafood, fruit and veggies, nuts and seeds. Your snacks are mainly a handful of almonds. Did you know just 60 grams of almonds gives you all the omega 6 you need – and more may be detrimental?One of the ways our diets have changed dramatically from the diets of our ancestors and even the very recent past is the ratio of Omega 6 to Omega 3 polyunsaturated fatty acids in the food we eat. A huge amount has been written about this subject, dozens of studies have been published. I’m not going into detail, the object here is to provide tools to help you get this balance right. At the end of the page – I’ve posted some links to other interesting blog posts and articles.
Fish oil - "more is not better", Chris Kresser
When it comes to fish oil, more is not better
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
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.
Extract:
Potatoes or Omega-6 makes you fat? | Hunt.Gather.Love.
Potatoes Make You Fat? Or Omega-6 makes you fat? | Hunt.Gather.Love.
No, it's not about potatoes, but about potato products:
Potatoes Make You Fat? Or Omega-6 makes you fat?
This morning I clicked on this headline at Grub Street "It's official: Potatoes make you fat. Which still explains nothing about why the French are not obese. [WSJ]"No, it's not about potatoes, but about potato products:
Eating more potato chips and French fries is likely to lead to a bigger weight gain over the years than the weight change associated with eating more of other foods, new research indicates.Apparently these are worst than cakes and sugary foods
Marion Nestle, New York University professor of nutrition and public health, expressed surprise that potato products were linked with more weight gain than desserts like cake, cookies and doughnuts, which contribute the most calories to the American diet, other research shows. She says she suspects people who eat potato chips and fries also tend to eat too much in general, making these foods markers for a diet leading to weight gain.
26.6.11
Omega-3 - DHA reduces Alzheimer's disease risk
Omega-3 fatty acid docosahexaenoic acid increases ... [J Neurosci. 2007] - PubMed result
Omega-3 fatty acid docosahexaenoic acid increases SorLA/LR11, a sorting protein with reduced expression in sporadic Alzheimer's disease (AD): relevance to AD prevention.
Source
Department of Medicine, University of California, Los Angeles, California 90095, USA.
Abstract
Environmental and genetic factors, notably ApoE4, contribute to the etiology of late-onset Alzheimer's disease (LOAD). Reduced mRNA and protein for an apolipoprotein E (ApoE) receptor family member, SorLA (LR11) has been found in LOAD but not early-onset AD, suggesting that LR11 loss is not secondary to pathology. LR11 is a neuronal sorting protein that reduces amyloid precursor protein (APP) trafficking to secretases that generate beta-amyloid (Abeta). Genetic polymorphisms that reduce LR11 expression are associated with increased AD risk. However these polymorphisms account for only a fraction of cases with LR11 deficits, suggesting involvement of environmental factors. Because lipoprotein receptors are typically lipid-regulated, we postulated that LR11 is regulated by docosahexaenoic acid (DHA), an essential omega-3 fatty acid related to reduced AD risk and reduced Abeta accumulation. In this study, we report that DHA significantly increases LR11 in multiple systems, including primary rat neurons, aged non-Tg mice and an aged DHA-depleted APPsw AD mouse model. DHA also increased LR11 in a human neuronal line. In vivo elevation of LR11 was also observed with dietary fish oil in young rats with insulin resistance, a model for type II diabetes, another AD risk factor. These data argue that DHA induction of LR11 does not require DHA-depleting diets and is not age dependent. Because reduced LR11 is known to increase Abeta production and may be a significant genetic cause of LOAD, our results indicate that DHA increases in SorLA/LR11 levels may play an important role in preventing LOAD.
Omega 3: various studies - links (nto fr 50k)
Omega 3: What is good for the heart may not be good for the prostate, study suggests
Altering Fatty Acid Levels In Diet May Reduce Prostate Cancer Growth Rate
Omega-3 Fatty Acids May Help Slow Prostate Cancer Growth
Omega Fatty Acid Balance Can Alter Immunity And Gene Expression
Altering Fatty Acid Levels In Diet May Reduce Prostate Cancer Growth Rate
Omega-3 Fatty Acids May Help Slow Prostate Cancer Growth
Omega Fatty Acid Balance Can Alter Immunity And Gene Expression
Omega-3 - New Paper: Linked to Cancer Progression
Omega-3 Fats, Angiogenesis, and Cancer: Part I | Perfect Health Diet
New Paper: DHA Linked to Cancer Progression
A new paper, just published yesterday, from “the largest study ever to examine the association of dietary fats and prostate cancer risk” has linked blood DHA levels to cancer risk. Specifically:
Docosahexaenoic acid was positively associated with high-grade disease (quartile 4 vs. 1: odds ratio (OR) = 2.50, 95% confidence interval (CI): 1.34, 4.65) … [4]
This is a large effect: the highest quartile had 2.5-fold higher risk than the lowest-quartile.
That it was the omega-3 DHA specifically, and not polyunsaturated fats generally, that caused the problem, is supported by the fact that (note: edited to correct error in original post – PJ) omega-6 linoleic acid had no effect, and 18:1 and 18:2 trans-fats which are mostly obtained from partially hydrogenated vegetable oils were associated with protection against cancer:
TFA 18:1 and TFA 18:2 were linearly and inversely associated with risk of high-grade prostate cancer (quartile 4 vs. 1: TFA 18:1, OR = 0.55, 95% CI: 0.30, 0.98; TFA 18:2, OR = 0.48, 95% CI: 0.27, 0.84). [4]
People in the top trans-fat quartile had only half the risk of people in the lowest omega-6 quartile. This makes it looks like omega-6-derived trans-fats were protective.
This result conflicts with the idea that the only influence of omega-3 fats is through regulation of inflammation; if so the anti-inflammatory omega-3 would have suppressed cancer. As lead study author Theodore Brasky said in the press release:
“We were stunned to see these results and we spent a lot of time making sure the analyses were correct,” said Brasky, a postdoctoral research fellow in the Hutchinson Center’s Cancer Prevention Program. “Our findings turn what we know — or rather what we think we know — about diet, inflammation and the development of prostate cancer on its head and shine a light on the complexity of studying the association between nutrition and the risk of various chronic diseases.”
Angiogenesis A Possible Pathway
Angiogenesis is very important for cancer progression. Cancers need to form angiogenic vessels if the tumor is to be able to grow beyond about 0.5 mm (0.02 inch) in diameter.
Indeed, angiogenesis seems to be a controlling factor for cancer mortality risk. It is believed that 50% of adults over age 40, and 100% of adults over age 70, have microscopic cancers. However, most tumors never develop an ability to induce angiogenesis and thus the tumors never grow beyond 0.5 mm and cause no observable disease.
Dietary factors that promote angiogenesis favor cancer progression, and anti-angiogenic factors tend to prevent cancer progression. Diet seems to be crucial for cancer prevention. Here is a TED video by Dr. William Li discussing the link between angiogenesis, dietary influences upon angiogenesis, and cancer.
Conclusion
So far, we’ve set the stage. On Thursday I’ll discuss a mechanism by which excessive DHA intake may promote angiogenesis. If this mechanism is important, then excessive fish oil or DHA supplementation may act as a major cancer-promoting food.
UPDATE: The next post in this series: Omega-3s, Angiogenesis and Cancer: Part II
References
[1] Nanji AA et al. Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. Gastroenterology. 1995 Aug;109(2):547-54. http://pmid.us/7615205.
[2] Church MW et al. Excess omega-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring. Neurotoxicol Teratol. 2010 March – April;32(2):171-181. http://pmid.us/19818397.
[3] Szymczak M et al. Modulation of angiogenesis by omega-3 polyunsaturated fatty acids is mediated by cyclooxygenases. Blood. 2008 Apr 1;111(7):3514-21. http://pmid.us/18216296.
[4] 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.)
Omega-3 - Angiogenesis & Cancer
Omega-3s, Angiogenesis and Cancer: Part II | Perfect Health Diet
Omega-3 - Angiogenesis & Cancer
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*.That’s the last piece of the puzzle: how do we minimize the level of oxidized DHA?
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.
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.
Omega-3 - Angiogenesis, excess & Cancer
Omega-3 Fats, Angiogenesis, and Cancer: Part I | Perfect Health Diet
Some Known Consequences of Omega-3 Excess
What are the likely consequences of omega-3 toxicity?
The obvious dangers are those related to oxidative stress from lipid peroxidation. The concern with omega-3 fats is not direct toxicity, but toxicity from their oxidation products. Omega-3 fats have a lot of fragile carbon double bonds which are easily oxidized: EPA has 5 double bonds and DHA 6. These are therefore among the most fragile lipids in the human body.
We would expect such problems to show up primarily in the liver and in the nervous system, where EPA and DHA levels are highest.
Indeed, they do. In mice, high dietary omega-3, in conjunction with alcohol or sugar, induces fatty liver disease. [1] In pregnant rats, excessive doses of omega-3 fats cause offspring to have shortened life span and neural degeneration. The authors concluded, “both over- and under-supplementation with omega-3 FA can harm offspring development.” [2]
However, there are associations of high omega-3 intake with disease in other tissues. In particular, emerging work is linking high omega-3 intake to diseases of pathological angiogenesis.
Angiogenesis is the creation of new blood vessels in mature tissue. (Vasculogenesis is the creation of vessels in a developing embryo.) It is a normal part of wound healing, but over a dozen diseases feature inappropriate angiogenesis.
Omega-3 Intake Is Usually Anti-Angiogenic
Before I go further, let me emphasize that nothing I am saying here repudiates the idea that it is desirable to bring tissue omega-6 and omega-3 fats into proper balance.
There are many studies showing that when tissue omega-6 to omega-3 ratios are too high, as on the standard American diet (SAD), additional omega-3 DHA and EPA can improve the omega-6 to omega-3 balance, reduce inflammatory signaling, and through reduced inflammation exercise an anti-angiogenic effect.
The mechanisms linking the anti-angiogenic effects of omega-3 to a condition of omega-6 excess are fairly well understood. Here is one description of the mechanism:
Here, we demonstrate that omega-6 PUFAs stimulate and omega-3 PUFAs inhibit major proangiogenic processes in human endothelial cells, including the induction of angiopoietin-2 (Ang2) and matrix metalloprotease-9, endothelial invasion, and tube formation, that are usually activated by the major omega-6 PUFA arachidonic acid. The cyclooxygenase (COX)-mediated conversion of PUFAs to prostanoid derivatives participated in modulation of the expression of Ang2. Thus, the omega-6 PUFA-derived prostaglandin E2 augmented, whereas the omega-3 PUFA-derived prostaglandin E3 suppressed the induction of Ang2 by growth factors. Our findings are consistent with the suggestion that PUFAs undergo biotransformation by COX-2 to lipid mediators that modulate tumor angiogenesis, which provides new insight into the beneficial effects of omega-3 PUFAs. [3]
So the question at issue is not whether omega-6 and omega-3 balance needs to be achieved. Rather, two points are at issue:
(a) At what level of polyunsaturated (and omega-3) fat intake should balance be achieved – high or low?
(b) Does overshooting toward an omega-3 excess generate significant or insignificant dangers?
If omega-3 toxicity is significant, then it will be important to achieve balance at low intakes of both omega-6 and omega-3, and to be careful to avoid overshooting to an omega-3 excess.
New Paper: DHA Linked to Cancer Progression
A new paper, just published yesterday, from “the largest study ever to examine the association of dietary fats and prostate cancer risk” has linked blood DHA levels to cancer risk. Specifically:
Docosahexaenoic acid was positively associated with high-grade disease (quartile 4 vs. 1: odds ratio (OR) = 2.50, 95% confidence interval (CI): 1.34, 4.65) … [4]
This is a large effect: the highest quartile had 2.5-fold higher risk than the lowest-quartile.
That it was the omega-3 DHA specifically, and not polyunsaturated fats generally, that caused the problem, is supported by the fact that (note: edited to correct error in original post – PJ) omega-6 linoleic acid had no effect, and 18:1 and 18:2 trans-fats which are mostly obtained from partially hydrogenated vegetable oils were associated with protection against cancer:
TFA 18:1 and TFA 18:2 were linearly and inversely associated with risk of high-grade prostate cancer (quartile 4 vs. 1: TFA 18:1, OR = 0.55, 95% CI: 0.30, 0.98; TFA 18:2, OR = 0.48, 95% CI: 0.27, 0.84). [4]
People in the top trans-fat quartile had only half the risk of people in the lowest omega-6 quartile. This makes it looks like omega-6-derived trans-fats were protective.
This result conflicts with the idea that the only influence of omega-3 fats is through regulation of inflammation; if so the anti-inflammatory omega-3 would have suppressed cancer. As lead study author Theodore Brasky said in the press release:
“We were stunned to see these results and we spent a lot of time making sure the analyses were correct,” said Brasky, a postdoctoral research fellow in the Hutchinson Center’s Cancer Prevention Program. “Our findings turn what we know — or rather what we think we know — about diet, inflammation and the development of prostate cancer on its head and shine a light on the complexity of studying the association between nutrition and the risk of various chronic diseases.”
Angiogenesis A Possible Pathway
Angiogenesis is very important for cancer progression. Cancers need to form angiogenic vessels if the tumor is to be able to grow beyond about 0.5 mm (0.02 inch) in diameter.
Indeed, angiogenesis seems to be a controlling factor for cancer mortality risk. It is believed that 50% of adults over age 40, and 100% of adults over age 70, have microscopic cancers. However, most tumors never develop an ability to induce angiogenesis and thus the tumors never grow beyond 0.5 mm and cause no observable disease.
Dietary factors that promote angiogenesis favor cancer progression, and anti-angiogenic factors tend to prevent cancer progression. Diet seems to be crucial for cancer prevention. Here is a TED video by Dr. William Li discussing the link between angiogenesis, dietary influences upon angiogenesis, and cancer.
Conclusion
So far, we’ve set the stage. On Thursday I’ll discuss a mechanism by which excessive DHA intake may promote angiogenesis. If this mechanism is important, then excessive fish oil or DHA supplementation may act as a major cancer-promoting food.
UPDATE: The next post in this series: Omega-3s, Angiogenesis and Cancer: Part II
References
[1] Nanji AA et al. Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. Gastroenterology. 1995 Aug;109(2):547-54. http://pmid.us/7615205.
[2] Church MW et al. Excess omega-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring. Neurotoxicol Teratol. 2010 March – April;32(2):171-181. http://pmid.us/19818397.
[3] Szymczak M et al. Modulation of angiogenesis by omega-3 polyunsaturated fatty acids is mediated by cyclooxygenases. Blood. 2008 Apr 1;111(7):3514-21. http://pmid.us/18216296.
[4] 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.)
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