Thanks for a great post, Skot. I was just wondering about the paper linked here (Saito & Kubo); it seems to be saying that EPA and DHA result in less oxidation than expected for a given tissue, according to that tissues "relative peroxidizability index", providing vitamin E is sufficient. This is the first I've heard of the relative peroxidizability index of a tissue, and I'm not sure it's even relevant at any rate, but it seemed like the wrong ref or something. Am I just misunderstanding this?And consumption of fresh, non-oxidized DHA and EPA has been shown to increase markers of oxidative stress in rats.
Is there anything wrong with this college vegan diet?
#31
Posted 25 February 2011 - 03:02 AM
#32
Posted 25 February 2011 - 05:30 AM
....
Notice the clear increase in TBARS (a measure of oxidative damage of the LDL particle) with n-3 fat. It's important to note that this was only a 5-week trial. If it had gone on for longer than that, it's likely the oxidative damage caused by n-3 fats would have been even worse. This isn't surprising if you understand the chemical composition of fats. PUFA are highly vulnerable to oxidative damage because they're the only fatty acids that have two or more double bonds, and it's the carbon that lies between the double bonds that is vulnerable to oxidation (as shown in the figure below):
....
Great post. If you would like to learn more about the chemistry there's this great book I've been working through. Here's a description of the allylic hydrogens from Google Books (here).
#33
Posted 25 February 2011 - 07:41 AM
The RDA for vitamin A (2,600 IU) is inadequate, and even then, over 25% of American consume less than half of the recommended amount. Native populations such as the traditional Inuit – which were free of modern, degenerative disease – got much more vitamin A than the average American. The Greenland Inuit of 1953, prior to much contact with the Western world, got about 35,000 IU of vitamin A per day. It is true that vitamin A is potentially toxic. Some evidence suggests that excess vitamin A increases the risk of osteoporosis. For example,this study showed both low and high serum A carried double risk of fractures as did optimal levels.Word. And why I don't take fish oil pills but am considering small amounts of sardines and/or oysters in my CR profile. Cod liver oil's Vitamin A toxicity: your thoughts? SFA doesn't lead clogged and inflamed blood vessels?
What do you eat, Kismet? What's your typical food day like?
Given that beta-carotene is poorly utilized by many and that vitamin A (retinol) is only found in significant amounts in organ meats, it explains why many Americans don't get enough of it. That said, I believe the claims of vitamin A toxicity are greatly misconstrued. If we dig deeper we find that excess vitamin A only causes problems against a backdrop of vitamin D deficiency. In his excellent article Vitamin A on Trial: Does Vitamin A Cause Osteoporosis, researcher Chris Masterjohn summarizes evidence demonstrating that vitamin D decreases the toxicity of and increases the dietary requirement for vitamin A. Studies show that supplementing with vitamin D radically increases the toxicity threshold of vitamin A. In a hypothetical 160 lb person, vitamin D supplementation increases the toxicity threshold of vitamin A to more than 200,000 IU/d. You'd have to eat 22 ounces of beef liver or take 5 TBS of high vitamin CLO each day to get this amount. Not likely!
The study discussed by Masterjohn:
Vitamin A and retinol intakes and the risk of fractures among participants of the Women's Health Initiative Observational Study
"No association between vitamin A or retinol intake and the risk of hip or total fractures was observed in postmenopausal women. Only a modest increase in total fracture risk with high vitamin A and retinol intakes was observed in the low vitamin D-intake group."
As for saturated fat, I completely disagree that it promotes inflammation. Most of the studies either on low-carb or saturated fat are horribly constructed (like including 14% of calories from trans fat...) or fail to control for confounding factors (such as lifestyle, glycemic load of the diet, or even PUFA). But even with all the bad research, there is still plenty of evidence showing saturated fat to be beneficial and or neutral.. such as the nurses study. I know Kismet hotly disagrees with me on the topic of saturated fat and since I've hashed out my argument for saturated fat countless times on these forums, i'll refrain from repeating myself once again. I will say this... my cholesterol got worse when I cut back dramatically on my fat intake and began consuming a higher carbohydrate, plant based diet. For what it's worth, and I would hate to get someone on a dietary plan that harmed them, my body seems to respond to a low-carb diet rather favorably.
(On a side note about the Harvard study... Even Walter Willett and his team of Harvard researchers failed to make this distinction between saturated and trans-saturated fat until the 1990s. Once they took trans fats into account, they discovered that trans fats are often the real culprits in causing heart disease, cancer, diabetes, obseity and other modern, degenerative diseases. Working with the refined data, Walter Willett confirmed, in the Nurses Health Study II, that nurses with higher rates of cancer were those who consumed more margarine and vegetable shortenings – not those who ate butter, eggs, cheese and meat. Funny how that works... )
Edited by Skötkonung, 25 February 2011 - 07:46 AM.
#34
Posted 25 February 2011 - 07:43 AM
I'll see if I can grab you the full study to clarify for you!Thanks for a great post, Skot. I was just wondering about the paper linked here (Saito & Kubo); it seems to be saying that EPA and DHA result in less oxidation than expected for a given tissue, according to that tissues "relative peroxidizability index", providing vitamin E is sufficient. This is the first I've heard of the relative peroxidizability index of a tissue, and I'm not sure it's even relevant at any rate, but it seemed like the wrong ref or something. Am I just misunderstanding this?And consumption of fresh, non-oxidized DHA and EPA has been shown to increase markers of oxidative stress in rats.
Much appreciated.....
Notice the clear increase in TBARS (a measure of oxidative damage of the LDL particle) with n-3 fat. It's important to note that this was only a 5-week trial. If it had gone on for longer than that, it's likely the oxidative damage caused by n-3 fats would have been even worse. This isn't surprising if you understand the chemical composition of fats. PUFA are highly vulnerable to oxidative damage because they're the only fatty acids that have two or more double bonds, and it's the carbon that lies between the double bonds that is vulnerable to oxidation (as shown in the figure below):
....
Great post. If you would like to learn more about the chemistry there's this great book I've been working through. Here's a description of the allylic hydrogens from Google Books (here).
Edited by Skötkonung, 25 February 2011 - 07:44 AM.
#35
Posted 25 February 2011 - 05:19 PM
Regarding saturated fat, I know this issue is in hot debate and have seen quite a few noisy blogs. Until more is learned, the American Heart Association recommends <10% of Calories from SFA - being vegan it hasn't been one of my own particular worries.
Aside, it's possible to eat a relatively low carb vegan diet by eliminating grains, starchy vegetables, added sugars, fruit drinks, etc. Maybe not low carb to Paleo standards, but nevertheless lower carb.
#36
Posted 25 February 2011 - 08:38 PM
Most of the evidence indicates that retinol (vitamin A) and vitamin D act synergistically.Hmmm, so many voices, studies conflicting tangles. Thanks for all staying chill and civil. I thought the issue with cod liver oil was that vitamin A (preformed retinols) can be present in liver tissue in high concentrations (eg, don't eat polar bear guts). Dosing preformed retinols may cause bone toxicity? I see your D3 statements. Yet high retinol intake may thwart the protective effect of vitamin D on distal colorectal adenoma?
As you noted, "vitamin A" from plants is quite different from retinol. Actually, vitamin A in plants isn't vitamin A at all... it's beta-carotene. New research (which I linked to in my previous post) is indicating that upwards of half the population can't process beta-carotene into retinol at all, so despite your high intake of beta-carotene, you may actually be deficient in vitamin A. If you plan on maintaining a vegan lifestyle, I would get a "RBP-EIA" (retinol-binding protein-enzyme immunoassay) to test for deficiency. You should also be taking carnitine, taurine, carnosine, biotin, as deficiencies in these nutrients have shown to cause vegans higher levels of plasma AGEs / glycation. Furthermore, these micronutrient deficies (likely in combination with a high PUFA intake) are contributing to increased readings of glycated LDL particles. Not good for longevity...My intake of "Vitamin A" is now at such high levels due to leafy green eating (collards, kale, mustard greens, chard) that I often get, according to COM, more than 100,000 IU. But my understanding is that plant sources are comprised of different component levels than concentrated animal retinol sources.
The AHA diet is one of the WORST diets to follow for heart health. Come on... they put their label of juices fortified with corn syrup and sugary cereals made with processed flour. But don't take my word for it.. when researchers actually put monkeys on the AHA diet their health actually declined... and they got fat.Regarding saturated fat, I know this issue is in hot debate and have seen quite a few noisy blogs. Until more is learned, the American Heart Association recommends <10% of Calories from SFA - being vegan it hasn't been one of my own particular worries.
In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:
"Still, about 40 percent do not put on a lot of weight. Barbara C. Hansen of the University of South Florida said calories, but not high fat, were important. “To suggest that humans and monkeys get fat because of a high-fat diet is not a good suggestion,” she said."
"'It wasn't until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."
"Fat Albert, one of her monkeys who she said was at one time the world's heaviest rhesus, at 70 pounds, ate "nothing but American Heart Association-recommended diet," she said."
Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?
Edited by Skötkonung, 25 February 2011 - 09:01 PM.
#37
Posted 25 February 2011 - 11:38 PM
Thanks for the supplement advice! I agree with you: taurine, carnosine, carnotine are parts of my quiet vegan life. Biotin, I don't know.
As far as the AHA goes, I'm pretty anti-establishment, too, and I'm basically a street corner hippie at this point in my life. Yet I wonder when I see:
"A recent study by the Harvard School of Public Health has produced the first conclusive evidence that reducing saturated fat with polyunsaturated fat substitution reduces CHD risk by 19%. The meta-analyses of 8 randomized trials revealed that for every 5% increase in polyunsaturated fat consumed, the risk of CVD decreased by 10%. The Institute of Medicine recommends that 5%–10% of energy intake should come from polyunsaturated fats. Other trials have advised an intake of 15%."
Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Medicine. 2010;7(3) Article ID e1000252.
Yes, I read the Times' monkey article, too. I suppose I question Dr. Hansen's notion that the couch potato macaques were getting an AHA sanctioned diet.
Does the AHA really support HFCS sugary junk drinks? Does the it encourage sedentary lifestyles with calorically dense diets like those imposed on our monkey captive friends? Or is this hyperbolic anti-government bashing? I honestly haven't bothered to check - it would be really stupid if they do.
Also in that same piece (I love the NYT!) the paragraph preceding the one you quoted reads: "They also drink a fruit-flavored punch with the fructose equivalent of about a can of soda a day. In all, they might consume about twice as many calories as a normal-weight monkey. Dr. Grove and researchers at some other centers say the high-fructose corn syrup appears to accelerate the development of obesity and diabetes."
Maybe the AHA says a can of poison a day is okay, I really should check. I appreciate the banter.
#38
Posted 25 February 2011 - 11:54 PM
"As part of a healthy diet, an adult consuming 2,000 calories daily should aim for:
• Fruits and vegetables: At least 4.5 cups a day
• Fish (preferably oily fish): At least two 3.5-ounce servings a week
• Fiber-rich whole grains: At least three 1-ounce-equivalent servings a day
• Sodium: Less than 1,500 mg a day
• Sugar-sweetened beverages: No more than 450 calories (36 ounces) a week
Other Dietary Measures:
• Nuts, legumes and seeds: At least 4 servings a week
• Processed meats: No more than 2 servings a week
• Saturated fat: Less than 7% of total energy intake
The American Heart Association recommends that you eat a wide variety of nutritious foods daily. Remember, even simple, small changes can make a big difference in living a better life."
http://www.heart.org...SubHomePage.jsp
#39
Posted 26 February 2011 - 03:45 PM
Edited by kismet, 26 February 2011 - 03:46 PM.
#40
Posted 26 February 2011 - 05:35 PM
upwards of half the population can't process beta-carotene into retinol at all,
can you post this study or pmid? i had read the study out of england where ~50% had a reduced rate of conversion, but have never seen any studies showing NO conversion.
#41
Posted 06 March 2011 - 10:33 AM
http://www.ncbi.nlm.nih.gov/pubmed/21116022Abstract
The aim of this investigation was to assess the effects of 6 wk of eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) supplementation on resting and exercise-induced lipid peroxidation and antioxidant status in judoists. Subjects were randomly assigned to receive a placebo or a capsule of polyunsaturated fatty acids (PUFAs; 600 mg EPA and 400 mg DHA). Blood samples were collected in preexercise and postexercise conditions (judo-training session), both before and after the supplementation period. The following parameters were analyzed: α-tocopherol, retinol, lag phase , maximum rate of oxidation (Rmax) during the propagating chain reaction, maximum amount of conjugated dienes (CDmax) accumulated after the propagation phase, nitric oxide (NO) and malondyaldehide (MDA) concentrations, salivary glutathione peroxidase activity, and the lipid profile. Dietary data were collected using a 7-day dietary record. A significant interaction effect between supplementation and time (p < .01) on triglycerides was noted, with values significantly lower in the n-3 long-chain-PUFA (LCPUFA) group after supplementation than in the placebo group. Significant interaction effects between supplementation and time on resting MDA concentrations and Rmax were found (p = .03 and p = .04, respectively), with elevated values in the n-3 LCPUFA group after supplementation and no change in the placebo group's levels. The authors observed a significantly greater NO and oxidative-stress increase with exercise (MDA, Rmax, CDmax, and NO) in the n-3 LCPUFA group than with placebo. No main or interaction effects were found for retinol and α-tocopherol. These results indicate that supplementation with n-3 LCPUFAs significantly increased oxidative stress at rest and after a judo-training session.
I was getting amazing results with 12g/day of fish oil... I will have to buy some Idebenone, synthetic analog of CoQ10 with reduced oxidant generating properties.
'' CoQ10 inhibits lipid peroxidation by preventing the production of lipid peroxyl radicals (LOO). ''
Edited by Ichoose2live, 06 March 2011 - 11:27 AM.
#42
Posted 06 March 2011 - 05:03 PM
#43
Posted 06 March 2011 - 05:59 PM
#44
Posted 06 March 2011 - 07:24 PM
Yes - I'm fascinated - what would have lead one to take in 12g/day of fish oil pills? I mean c'mon - I aint being critical and mean - just really curious. Some small amounts of oily fish every now and then might be healthy but 12g/day of fish oil would seem like a poisonous overshot of the good. What kinds of amazing results were you getting?
The order of my results with high-dose of fish oil is constant euphoria (hypomania?) greater than attention & focus greater than clarity of thoughts and greater than anxiolytic & confidence. Plus I assume it is synergic with Piracetam through improving membrane fluidity. >>>> http://www.longecity...post__p__450747
Right, I have reduced my dosage to 4g/day... let's wait if I see any change.
Edited by Ichoose2live, 06 March 2011 - 07:27 PM.
#45
Posted 06 March 2011 - 07:41 PM
#46
Posted 06 March 2011 - 08:14 PM
Ok, I get it. But how do you know the good mood and focus wasn't caused by a good night's sleep or maybe a nice conversation you had or a really bright cup of coffee? And why spend such cash on any amount of fish pillage that may be harmful to you?
Simply because I have no social life, sleep problems and I only drink water and non-fat milk.
Edited by Ichoose2live, 06 March 2011 - 08:14 PM.
#47
Posted 06 March 2011 - 09:22 PM
1. Toss a coin and get heads 100 times in a row and use superstistics to conclude that the next toss is more likely to be tails than heads.
2. A well known superstistics conclusion: "The outcome of Washington Redskins home football games has correctly predicted the winner of every U.S. presidential election since 1936." (snopes)
#48
Posted 08 March 2011 - 01:29 AM
http://www.ncbi.nlm.nih.gov/pubmed/15061297 It is contradictor to the recent post ---->>> http://www.longecity...post__p__454434Effect of fish oil on oxidative stress, lipid profile and renal function in IgA nephropathy.
Abstract
The omega-3 polyunsaturated fatty acids in fish oil have been shown to produce beneficial effects, such as a reduction in blood pressure, proteinuria, lipid levels and inflammation. Aggregated immunoglobulin A obtained from IgA nephropathy patients induced greater oxygen free radicals in polymorphonuclear leukocytes than other glomerulopathy. All of which may affect the course of IgA nephropathy. Twenty-three adult patients with biopsy proven IgA nephropathy, with proteinuria more than 1 g/day, serum creatinine less than 3 mg/dl and blood pressure control less than 130/80 mmHg were given omega-3 polyunsaturated fatty acids (PUFA) in the form of an Omacor capsule 4 g/day equivalent to eicosapentaenoic acid (EPA) 1.88 g and docosahexaenoic acid (DHA) 1.48 g for 6 months. A 3 to 6 month follow-up was planned, with monthly evaluations of the patients. By six months, the serum triglyceride was significantly reduced (143.45 +/- 62.65 vs 91 +/- 42.89 mg/dl, p = 0.002), serum cholesterol was also reduced but not statistically significant (234.16 +/- 56.29 vs 219.76 +/- 51.25 mg/dl, p = 0.07). There was a trend of increased serum high density lipoprotein (HDL)-cholesterol (39.26 +/- 10.56 vs 42.72 +/- 8.37 mg/dl, p = 0.056). Urine beta-2-microglobulin was elevated in IgA patients and decreased statistically significant after 3 months (453 +/- 580 vs 308 +/- 274 microg/24 h, p < 0.001) and 6 months of fish oil therapy (453 +/- 580 vs 142 +/- 182, p < 0.03) while urine N-acetyl-glucosaminidase (NAG) was of no significant difference both before and after fish oil administration (21 +/- 10 vs 22 +/- 10 and 21 +/- 9 U/24 h, p = 0.08). Plasma malondialdehyde (MDA), the end product of oxidative stress was statistically, significantly decreased (1.09 +/- 0.51 vs 0.89 +/- 0.49 nmol/L, p = 0.003). The study did not show any change in blood pressure, proteinuria, or serum creatinine. The authors conclude from the results of this study that patients with idiopathic IgA nephropathy with proteinuria and mildly reduced GFR did not benefit from short-term treatment with 4 g per day of omega-3 PUFA regarding the total protein excretion and glomerular filtration rate (GFR), but the advantage was the improvement in tubular dysfunction, lipid profiles, and oxidative stress.
The results of this study were summarized in the Perfect Health Diet, by Paul and Shou-Ching Jaminet:
I see nothing wrong with that, the level was already high at the beginning. Is this company specialised in research of nutrition?? I don't think we should rely on this study. The Japanese civilisation eat over 20 grams/day of Fatty acids and guess what??? They have the highest life expectancy on Earth!!
FUTHERMORE!
http://www.ncbi.nlm.nih.gov/pubmed/14559317Decreased oxidative stress in patients with ulcerative colitis supplemented with fish oil omega-3 fatty acids.
Abstract
OBJECTIVE: The potential pathogenicity of free radicals may have a pivotal role in ulcerative colitis. Fish oil omega-3 fatty acids exert anti-inflammatory effects on patients with ulcerative colitis (UC), but the precise mechanism of the action of fish oil on oxidative stress is still controversial. The aim of the present work was to verify the blood oxidative stress in patients with UC and determine whether the association of sulfasalazine to fish oil omega-3 fatty acids is more effective than isolated use of sulfasalazine to reduce the oxidative stress.
METHODS: Nine patients (seven female and two male; mean age = 40 +/- 11 y) with mild or moderate active UC were studied in a randomized crossover design. In addition to their usual medication (2 g/d of sulfasalazine), they received fish oil omega-3 fatty acids (4.5 g/d) or placebo for 2-mo treatment periods that were separated by 2 mo, when they only received sulfasalazine. Nine healthy individuals served as control subjects to study the oxidative stress status. Disease activity was assessed by laboratory indicators (C-reactive protein, alpha1-acid glycoprotein, alpha1-antitrypsin, erythrocyte sedimentation rate, albumin, hemoglobin, and platelet count), sigmoidoscopy, and histology scores. Analysis of oxidative stress was assessed by plasma chemiluminescence and erythrocyte lipid peroxidation, both induced by tert butyl hydroperoxide (t-BuOOH) and by plasma malondialdehyde. Antioxidant status was assayed by total plasma antioxidant capacity (TRAP) and microsomal lipid peroxidation inhibition (LPI). Superoxide dismutase (SOD) and catalase erythrocyte enzymatic activities were also determined.
RESULTS: No significant changes were observed in any laboratory indicator or in the sigmoidoscopy or histology scores, with the exception of erythrocyte sedimentation rate, which decreased with both treatments. Oxidative stress was demonstrated by significant decreases in TRAP and LPI levels, increased chemiluminescence induced by t-BuOOH, and higher SOD activity in patients with UC. Treatment with fish oil omega-3 fatty acids reverted the chemiluminescence induced by t-BuOOH and LPI to baseline levels but that did not occur when patients received only sulfasalazine. Levels of plasma malondialdehyde, erythrocyte lipid peroxidation, and catalase were not different from those in the control group.
CONCLUSIONS: The results indicated that plasma oxidative stress occurs in patients with UC, and there was a significant decrease when the patients used sulfasalazine plus fish oil omega-3 fatty acids. However, there was no improvement in most laboratory indicators, sigmoidoscopy, and histology scores. The results suggested that omega-3 fatty acids may act as free radical scavengers protecting the patients against the overall effect of oxidative stress.
Edited by Ichoose2live, 08 March 2011 - 01:43 AM.
#49
Posted 08 March 2011 - 05:15 AM
One diff between you and them, though, is you're taking pills and they're eating food. I'd be happier for you if you ate a few cans a day of sardines rather than your current course of action. Might save you money, too.
#50
Posted 08 March 2011 - 05:28 AM
http://www.impactagi...ull/100288.html
#51
Posted 08 March 2011 - 05:38 AM
#52
Posted 10 March 2011 - 05:22 PM
ALOX5 gene variants affect eicosanoid production and response to fish oil supplementation.
Stephensen CB, Armstrong P, Newman JW, Pedersen TL, Legault J, Schuster GU, Kelley D, Vikman S, Hartiala J, Nassir R, Seldin MF, Allayee H.J Lipid Res. 2011 Feb 4. [Epub ahead of print]
PMID: 21296957 [PubMed - as supplied by publisher] Free Article
http://www.jlr.org/c...lr.P012864.long
http://www.jlr.org/c...012864.full.pdf
Abstract
The objective was to determine if 5-lipoxygenase gene (ALOX5) variants. associated with cardiovascular disease affect eicosanoid production by monocytes.
The study was a randomized, double-masked, parallel intervention trial with fish oil (5.0 g fish oil daily containing 2.0 g eicosapentaenoic acid [EPA] and 1.0 g docosahexaenoic acid [DHA]) or placebo oil (5.0 g of a corn/soy mix).
116 subjects (68% female, 20 - 59 yr) of African American ancestry enrolled and 98 completed the study.
Neither ALOX5 protein nor arachidonic acid (AA)-derived LTB4, LTD4 and LTE4 varied by genotype but 5-hydroxy eicosatetraenoate (5-HETE), 6 trans-LTB4, 5-oxo-ETE, 15-HETE and 5,15-DiHETE were higher in subjects homozygous for
the ALOX5 promoter allele containing 5 Sp1-element tandem repeats (55 genotype) than in subjects with one deletion (3 or 4 repeats) and one common allele (d5) or with two deletion alleles (dd). The EPA-derived metabolites 5-HEPE and 15-HEPE and the DHA-derived metabolite 17-HDoHE had similar associations with genotype and increased with supplementation; 5-HEPE and 15-HEPE increased and 5-oxo-ETE decreased to a greater degree in the 55 than in the other genotypes.
This differential eicosanoid response is consistent with the previously observed interaction of these variants with dietary intake of omega-3 fatty acids in predicting cardiovascular disease risk.
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