More support for MR's anti-DHA position
#31
Posted 17 June 2006 - 01:27 AM
What I am confused about now is whether it's beneficial to my body or whether it's aging me and oxidizing my cells and mitochondria. Is it a double edged sword?
Who to believe...............?
#32
Posted 17 June 2006 - 02:13 AM
So is fish oil bad for me? I eat fatty fish every other day (mackerel, salmon, sardines). When I take fish oil...I feel better. I feel a better mood (happier) and it's weird, but I sense some sort of sharpness in my brain. It's hard to explain.
What I am confused about now is whether it's beneficial to my body or whether it's aging me and oxidizing my cells and mitochondria. Is it a double edged sword?
Who to believe...............?
Feel free to chime in if anyone disagrees:
1. Fish oil proven benefits.
2. Fish oil theoretic problems with some evidence, but not in humans (which may mean no evidence considering animal evidence often does not transfer to humans).
VS.
3. Flax seed oil which may be fine if you take enough (whatever that is) and are not a pregnant women. I do not believe much/any DHA is synthesized this way...which may be a good or bad thing.
4. ??flax link to prostate ca (there may be similar issue for females).
Sooo fish oil has proven benefits, though it may be a double edged sword, but far from proven.
#33
Posted 17 June 2006 - 04:13 AM
While we don't have the evidence in humans, we do have evidence in more than just mice with their 3-year lifespans. The most convincing evidence is in animals with similar metabolic rates to rodents, yet lifespans 3 to 8 times longer: birds (and bats, if memory serves?). Lifespans over a decade, and in some cases in excess of 20 years, are very hard to dismiss.2. Fish oil theoretic problems with some evidence, but not in humans (which may mean no evidence considering animal evidence often does not transfer to humans).
Of course, this evidence isn't based on the oils in the diet, but the lipids in the mitochondrial membranes. But the evidence is pretty significant.
Edit: I realize this is simplifying, as there are probably multiple factors involved, such as improved nDNA repair/maintenance, increased cancer resistance, etc. But the lipid profiles are pretty telling, and significant in a statistical sense, even if not "ironclad proof".
#34
Posted 17 June 2006 - 04:18 AM
Sorry, I must've glossed over this at some point. Ah, I see, you mentioned it on the first page:4. ??flax link to prostate ca (there may be similar issue for females).
Scott, has this been discussed somewhere on the forum that I could follow up on?Plus no one has mentioned the risk of increased prostate cancer linked with ALA (another discussion but probably needs to be mentioned even if I'm skeptical).
BTW, what's the link with pregnant women? Has that been brought up somewhere in the forum as well?3. Flax seed oil which may be fine if you take enough (whatever that is) and are not a pregnant women. I do not believe much/any DHA is synthesized this way...which may be a good or bad thing.
#35
Posted 17 June 2006 - 04:30 AM
It seems some claims talk as if it were trans-fat, only in the sense of that you shouldnt have ANY.
Currently I am taking the equivalent of 2 servings of fish a week. This is with a fish oil that has higher EPA to DHA than normal, but not a mega EPA pill which I may switch to.
#36
Posted 17 June 2006 - 07:35 AM
I have read the main arguments against DHA supplementation. So the basis of MRs argument is that DHA (as a LCPUFA) is stored in the mitochondrial inner membrane (MIM) and MIM DHA concentration is negatively correlated to maximum life span (MLS). Its is stated that DHA supplementation will increase MIM [DHA] and hence decrease MLS. For this situation, I am going to assume that MLS is the same as mean life span or life expectancy. So essentially MR is saying that DHA supplementation may decrease life expectancy.
Have a look at the diagram I posted above. Is it better to supplement with ALA (omega-3)? Metabolically ALA is converted to EPA (which is also converted to DHA) that are then stored as a membrane phospholipids. So what is the difference between supplementing with ALA and supplementing with DHA/EPA? The end product of their conversion is a membrane phospholipid. I haven't read MRs stand in fine detail but maybe he is saying that when you supplement with fish oil there is a greater amount of DHA stored.
Anyhow.....MRs hypothesis is strong and makes sense but.......
What is more important? How many years we live or the quality of the years that we live?
Fish oil supplementation has been show to minimise the risk of many chronic diseases. Chronic diseases that could have you spending the last decade of your life with chronic pain and discomfort.
What are the consequences of increased lipid peroxidation as a result of high levels of DHA in the MIM? Decreased MLS? Why is the MLS decreased? Are we just putting of an age-related death i.e slowing the aging process, or are we minimising the risk of chronic disease that would subsequently result in a decrease in MLS.
The study that looks at how mitochondrial membrane peroxidizability is inversely related to MLS in mammals (1)
doesn't really tell you how the mammals died. Maybe the younger animals died healthy albeit prematurely. Prematurely compared to the oldest mammals in the study group.
I am not overly concerned about dying "prematurely" so to speak. Its all the same to me. If I die 'naturally' at age 80 and someone else beside me dies 'naturally' at age 100, from a health view point, what is the difference? Yeah maybe the guy in the next bed who is 100 will be pointing at the scoreboard but I don't give a flying you know what about the score. My main concerns are with chronic debilitating diseases.
You decide whats best for you.
#37
Posted 17 June 2006 - 10:37 AM
I think it's important to realize that what it's not such a leap of faith here with MR's postion as it might seem i.e something might be harmful despite positive SHORT TERM human studies. We know that cellular apostosis could be considered a similar double-edged sword (see for example work by Campisi): if we could make a drug that drastically increased cellular apoptosis in case of even miniscule DNA damage, that would in short term prove to superior cancer fighteing drug. However, in the long run the increased cellular turnover would probably decrease life-span (due probably to Hayflick limit), as has been noticed in mice.
In fact, the antagonist pleiotrophy theory, one of the most succesful evolutionary theories on aging, predicts (on genetical level, but probably could be extended here) that some interventions that are superior enhancing sexual selection, might prove harmful in the long run.
#38
Posted 17 June 2006 - 11:21 AM
Growing fetuses (sp?) need DHA for optimum brain development.
There is also this which is pretty tentative, but still
http://www.imminst.o...25&hl=doctor&s=
"While we don't have the evidence in humans, we do have evidence in more than just mice with their 3-year lifespans. The most convincing evidence is in animals with similar metabolic rates to rodents, yet lifespans 3 to 8 times longer: birds (and bats, if memory serves?). Lifespans over a decade, and in some cases in excess of 20 years, are very hard to dismiss."
It has nothing to do with lifespan. What works in rats don't always work in people because of differing biochemical pathways. So differing animals ain't proof. No matter what animal data you get it may not be the same in people and ain't as solid evidence of human studies on fish oil in people (not saying it is not worth looking at, but human data is human data).
Jay no I have not discussed the ALA prostate cancer link on the forum anywhere. The link I gather comes from epidemiology studies so it is not by an y means definitive, but I thought at least should be mentioned.
I'm with zoolander:
"What is more important? How many years we live or the quality of the years that we live?" (if indeed this is the choice).
And has anyone mentioned that if "increased mitochondrial membrane peroxidizability" is true, perhaps mitochondrial antioxidants (I"m out on a limb here I realize since I don't know if these work in that part of the mitochondria) e.g. NAC, lipoic acid, and the other ones people are feeding their rats i.e. spin traps might be of use?
#39
Posted 17 June 2006 - 11:23 AM
http://www.omega-res...?ID=279&catid=1
AJP - DHA helps to reduce cellular impairment in insulin-resistant and insulin-deficient induced rat, findings reported
Ovide-Bordeaux S, Grynberg A. Docosahexaenoic acid affects insulin deficiency- and insulin resistance-induced alterations in cardiac mitochondria. Am J Physiol Regul Integr Comp Physiol, 2004; 286: R519-R527.
The effect of docosahexaenoic acid (DHA) intake on cardiac mitochondrial function was evaluated in permeabilized fibers in insulin deficiency and insulin resistance in rats.
The insulin-deficient state was obtained by streptozotocin injection 2 mo before investigations. Insulin resistance was obtained by feeding a 62% fructose diet for 3 mo.
DHA was incorporated in the diet to modify the fatty acid composition of cardiac membranes, including mitochondria.
Insulin deficiency decreased mitochondrial creatine kinase (mi-CK) activity and mitochondrial sensitivity to ADP.
DHA intake prevented these alterations. Moreover, the insulin-deficient state significantly decreased n-3 polyunsaturated fatty acids (PUFA) and slightly increased n-6 PUFA in both cardiac and mitochondrial membranes, inducing a significant increase in the n-6-to-n-3 ratio.
DHA intake maintained high myocardial and mitochondrial DHA content.
Insulin deficiency also decreased glutamate- and palmitoylcarnitine-supported mitochondrial respiration, but DHA intake did not prevent these effects.
In contrast, insulin resistance did not affect mi-CK activity or sensitivity to ADP.
However, insulin resistance influenced the myocardial fatty acid composition with decreased n-6 and n-3 PUFA contents and increased monounsaturated fatty acid content.
Only slight alterations were observed in mitochondrial fatty acid composition, and they were corrected by DHA intake. Moreover, insulin resistance decreased the glutamate-supported respiration, and DHA intake did not influence this effect.
In conclusion, the impairment of cardiac mitochondrial function was more pronounced in the insulin-deficient state than in insulin resistance. The modification of fatty acid composition of cardiac and mitochondrial membranes by DHA partially prevented the mitochondrial alterations induced in the two models.
nordic naturals has a whole website with EPA/DHA references I'll look later for more DHA ones.
#40
Posted 19 June 2006 - 04:40 PM
#41
Posted 19 June 2006 - 04:45 PM
Right, human data is human data, but data from multiple phyla and varying lifespans (1 year up to 25 or so years) and metabolic rates provides much stronger evidence than mouse data alone. In the absense of human data, it provides a second leg of evidence for the DHA claims to stand on."While we don't have the evidence in humans, we do have evidence in more than just mice with their 3-year lifespans. The most convincing evidence is in animals with similar metabolic rates to rodents, yet lifespans 3 to 8 times longer: birds (and bats, if memory serves?). Lifespans over a decade, and in some cases in excess of 20 years, are very hard to dismiss."
It has nothing to do with lifespan. What works in rats don't always work in people because of differing biochemical pathways. So differing animals ain't proof. No matter what animal data you get it may not be the same in people and ain't as solid evidence of human studies on fish oil in people (not saying it is not worth looking at, but human data is human data).
#42
Posted 19 June 2006 - 04:55 PM
It is certainly important for people to know about your/Michael's position so they can make they own informed decision.
And I'm still waiting for someone to tell me why even if you are right, taking increased mitocondrial antioxidants can't compensate.
#43
Posted 19 June 2006 - 05:01 PM
I believe that was one of MRs arguments as well. It is the basis for my taking 2 servings of fish worth of the oil, when I dont get adaquate seafood in my diet.
"And I'm still waiting for someone to tell me why even if you are right, taking increased mitocondrial antioxidants can't compensate."
Yes, I was thinking the same thing. That is why I am curious on the disease prevention benefits of a mega-dose.
#44
Posted 19 June 2006 - 05:02 PM
I'll think about it, but for now I'll still have to defer to proven benefits and increased mitichondrial antioxidants.
#45
Posted 19 June 2006 - 05:04 PM
#46
Posted 19 June 2006 - 05:05 PM
#47
Posted 19 June 2006 - 05:07 PM
That's like asking why improving the volumetric efficiency of a car's engine can't be used to "compensate" for poor aerodynamics. You can do both. One doesn't actually "compensate" for the other, in that doing both would have cumulative benefits.And I'm still waiting for someone to tell me why even if you are right, taking increased mitocondrial antioxidants can't compensate.
#48
Posted 19 June 2006 - 05:21 PM
#49
Posted 19 June 2006 - 05:58 PM
#50
Posted 19 June 2006 - 06:10 PM
Yes, some people can eat a diet that, statistically speaking, will usually remove decades from the average lifespan, and yet live decades longer than the average. It doesn't really have any significance. Irrational and weak minds are often and easily swayed by such evidence, but just because it's easy to fall for, that doesn't make it any more significant.
#51
Posted 19 June 2006 - 06:28 PM
Oh and talk of number of servings of fish/week is silly without knowing which fish and EPA/DHA content.
Here is what I use as a guide
http://www.aafp.org/...040701/133.html
Two to three grams of epa/dha is the general range for a serving of fish, I think. Unfortunately many studies for prevention of disease have used servings of fish, instead of oil amount.
#52
Posted 19 June 2006 - 06:30 PM
That's like asking why improving the volumetric efficiency of a car's engine can't be used to "compensate" for poor aerodynamics. You can do both. One doesn't actually "compensate" for the other, in that doing both would have cumulative benefits.
Yes, but if there is prevention of disease with a mega-dose, then it is worth the possible negative if taking mita antioxidants, IMO.
#53
Posted 19 June 2006 - 06:36 PM
Heh, don't get me wrong, I'm not advocating that we stop all DHA dietary intake altogether. I myself eat fish from time to time (once every 1-2 weeks on average, but not very consistent).Yes, but if there is prevention of disease with a mega-dose, then it is worth the possible negative if taking mita antioxidants, IMO.
But I think eating fish >2-3 times per week is overkill, considering diminishing returns on short-term health benefits, and increasing likelihood of the problems Michael Rae brings up.
#54
Posted 19 June 2006 - 06:49 PM
#55
Posted 19 June 2006 - 07:38 PM
My grandfather died at 89 last year, eating fried chicken, mashed potatoes, and all the other glorious Alabama food, and being overweight and technically diabetic. What does that mean? Not much.
I probably should have added that they were healthy and had a good quality of life. Sure genetics is a factor, but my grandparents weren't sick, diabetic, etc (at least not known).
But you missed my point, they didn't have a diet with an appreciative amount of DHA/EPA and didn't die of a deficiency. I think this entire DHA/EPA thing is all hype and blown out of proportion.
#56
Posted 19 June 2006 - 07:45 PM
Based on what? Your grandparents?I think this entire DHA/EPA thing is all hype and blown out of proportion.
#57
Posted 19 June 2006 - 08:55 PM
Based on what? Your grandparents?
No, based on all the info that I have read regarding its pro-oxidant effects as well as all other polyunsat's. I see the omega hype everywhere now from eggs to ridiculous claims of grass fed beef. I don't think it's something that we need in significant quantities (if at all) and taking doses of 1 or more teaspoons of fish oil is giving a large dose of EPA/DHA. I think a healthy person doesn't need to supplement with this product. If you don't eat fish or have other ailments then chose to do so at your own risk, but this product hasn't been tested long term.
Overall, I think i'm starting to side more with Dr. Peat and Dr. Groves that polyunsaturates should be limited as much as possible. It's hard to believe anything anymore these days but I wouldn't exactly be surprised if omega 3 and omega 6 weren't exactly "essential". It's all a bunch of BS these days so I believe that sticking to whole food is the best way to go.
#58
Posted 19 June 2006 - 08:58 PM
#59
Posted 19 June 2006 - 09:17 PM
Paleo will you please start backing up your statements rather than simply saying "you read something somewhere at sometime". This is a very scientifically minded community, without references you're position will be considered baseless.
I'm not trying to convince anyone of anything. If whoever wants to follow up with the research they can look it up for their own interest...I provided names of the doctors. Regardless, i'm not fighting for "my position" and couldn't really care what anyone else thinks.
#60
Posted 19 June 2006 - 09:57 PM
There's a huge difference between trying to avoid the latest fad and stick to whole foods, and trying to maximize saturated fat intake (especially animal saturated fats). Talk about a fad (and a poorly backed one, scientifically speaking).It's all a bunch of BS these days so I believe that sticking to whole food is the best way to go.
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