• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo
- - - - -

Fish and Krill Oils Shorten Life Span of Mice

fish oil krill kril oil lovaza omega-3

  • Please log in to reply
31 replies to this topic

#1 ta5

  • Guest
  • 952 posts
  • 324
  • Location: 

Posted 14 May 2014 - 06:19 PM


This study was referenced in this thread, but wasn't yet published.

 

 

Age (Dordr). 2014 May 10.

Spindler SR1, Mote PL, Flegal JM.
Department of Biochemistry, University of California at Riverside, Riverside, CA, 92521
Marine oils rich in ω-3 polyunsaturated fatty acids have been recommended as a preventive treatment for patients at risk for cardiovascular diseases. These oils also are the third most consumed dietary supplement in the USA. However, evidence for their health benefits is equivocal. We tested the daily, isocaloric administration of krill oil (1.17 g oil/kg diet) and Lovaza (Omacor; 4.40 g/kg diet), a pharmaceutical grade fish oil, beginning at 12 months of age, on the life span and mortality-related pathologies of long-lived, male, B6C3F1 mice. The oils were incorporated into the chemically defined American Institute of Nutrition (AIN)-93 M diet. An equivalent volume of soybean oil was removed. Krill oil was 3 % and Lovaza 11 % of the oil in the diets. When their effects were analyzed together, the marine oils significantly shortened life span by 6.6 % (P = 0.0321; log-rank test) relative to controls. Individually, Lovaza and krill oil non-significantly shortened median life span by 9.8 and 4.7 %, respectively. Lovaza increased the number of enlarged seminal vesicles (7.1-fold). Lovaza and krill oil significantly increased lung tumors (4.1- and 8.2-fold) and hemorrhagic diathesis (3.9- and 3.1-fold). Analysis of serum from treated mice found that Lovaza slightly increased blood urea nitrogen, while krill oil modestly increased bilirubin, triglycerides, and blood glucose levels. Taken together, the results do not support the idea that the consumption of isolated ω-3 fatty acid-rich oils will increase the life span or health of initially healthy individuals.
PMID: 24816553

  • like x 2

#2 tunt01

  • Guest
  • 2,308 posts
  • 414
  • Location:NW

Posted 14 May 2014 - 10:12 PM

When I heard Spindler speak about these unpublished results last year, I think he mentioned specifically that Lovaza was showing lower TG's and that it was a perfect example of how endpoints on most studies are meaningless because the Lovaza ultimately leads to a lower lifespan (in mice).  On the whole, he was pretty negative on fish oil.

 



sponsored ad

  • Advert
Click HERE to rent this advertising spot for SUPPLEMENTS (in thread) to support LongeCity (this will replace the google ad above).

#3 Hebbeh

  • Guest
  • 1,661 posts
  • 570

Posted 15 May 2014 - 02:33 AM

I'm suspecting poor science once again.  Did they administer an oil based antioxidant with the fish such as vitamin E?  Are there any humans consuming fish oil and not supplementing vitamin E?  The first red flag is that if this even remotely represents the real world, then eating fish wouldn't display the positive results that it has shown time and again.  Science in a fish bowl does not represent the real world.  It fails to take the bigger picture into account.

 

edit:  and how fish oil "appears" to affect mice more than likely does not relate to humans.  Mice never evolved eating fish for starters.


Edited by Hebbeh, 15 May 2014 - 02:36 AM.

  • Pointless, Timewasting x 1
  • Agree x 1

#4 mrvontar

  • Guest
  • 40 posts
  • 2
  • Location:Oregon

Posted 15 May 2014 - 02:57 AM

Too much of a good thing is a bad thing. No one would be taking that much fish oil anyways, unless I have the conversions wrong. 


  • like x 1

#5 normalizing

  • Guest
  • 2,692 posts
  • -104
  • Location:Warm Greetings
  • NO

Posted 15 May 2014 - 05:46 AM

i find it interesting how each time there is a study on fish oil that is negative, people rile up to find loop holes and say this or that is flawed. yet, each time a positive study is posted, people come in and go "yeah, nice i like this, ill take my fish oil now" and i cannot recall people riling up then and try to find any of the flaws. not sure if anyone has noticed how bias this is and there is no critisism of this behavior as of yet.


Edited by normalizing, 15 May 2014 - 05:47 AM.

  • dislike x 3
  • like x 2

#6 niner

  • Guest
  • 16,276 posts
  • 2,000
  • Location:Philadelphia

Posted 15 May 2014 - 12:14 PM

Too much of a good thing is a bad thing. No one would be taking that much fish oil anyways, unless I have the conversions wrong.

 
I cringe when I read posts here that talk about taking ten+ grams of fish oil a day.  Some people really do take too much.  Hebbeh pointed out the potential for oxidation, considering that these highly oxidation-prone fatty acids are mixed with the standard chow, and probably get a lot of air exposure.  Finally mice are not people... (I know, shocking...)

 

Here's a discussion of the results from human trials looking at omega 3 fatty acids in CVD.  The gist of it is that the well-powered studies with adequate followup show benefits.  There are some recent studies that were relatively underpowered, used questionable dosage forms (like omega 3-spiked margarine, for godsake), and shorter followups that were equivocal. 

 

I'll continue with my current dose of a gram of fish oil a day.  Based on this study, I will refrain from mixing it with dry foods, baking it into cookies, or taking way more than I do now.


  • like x 2

#7 Dolph

  • Guest
  • 512 posts
  • 122
  • Location:Germany

Posted 15 May 2014 - 12:19 PM

  Based on this study, I will refrain [...] baking it into cookies,[...].

 

 

Damn, I think you just identified a huge market niche. Is "Krilleos" already a registered TM?


  • like x 2
  • Cheerful x 1

#8 Galaxyshock

  • Guest
  • 1,470 posts
  • 180
  • Location:Finland

Posted 15 May 2014 - 12:36 PM

Alright I won't feed a mouse with fish oils if I see one


  • like x 2
  • Cheerful x 1

#9 normalizing

  • Guest
  • 2,692 posts
  • -104
  • Location:Warm Greetings
  • NO

Posted 15 May 2014 - 07:42 PM

niner, the only noticable effect of fish oil against depression and other more serious neurological problems is actually high doses. now, you and others who have no problems and its questionable why you even take fish oil (assuming you are one of those just wanting to live forever), you cant possibly understand how vital high dose is for some people. such studies just go to show, if you cant take something in high dose based on its actual proven benfit for some people, then you might have to rely on future medications. sad as it is.


  • dislike x 1

#10 tunt01

  • Guest
  • 2,308 posts
  • 414
  • Location:NW

Posted 15 May 2014 - 07:57 PM

niner, the only noticable effect of fish oil against depression and other more serious neurological problems is actually high doses. now, you and others who have no problems and its questionable why you even take fish oil (assuming you are one of those just wanting to live forever), you cant possibly understand how vital high dose is for some people. such studies just go to show, if you cant take something in high dose based on its actual proven benfit for some people, then you might have to rely on future medications. sad as it is.

 

For those individuals suffering serious neurological problems, they may have to make a trade-off between longevity and improved functionality.  It's not as uncommon a choice as one might think, and quite honestly it's a trade-off/choice that is made every day whether consciously or not.


  • like x 1

#11 Mr.Orange

  • Guest
  • 12 posts
  • 5
  • Location:Germany

Posted 15 May 2014 - 09:02 PM

I'm suspecting poor science once again.  Did they administer an oil based antioxidant with the fish such as vitamin E?  Are there any humans consuming fish oil and not supplementing vitamin E?  The first red flag is that if this even remotely represents the real world, then eating fish wouldn't display the positive results that it has shown time and again.  Science in a fish bowl does not represent the real world.  It fails to take the bigger picture into account.

 

edit:  and how fish oil "appears" to affect mice more than likely does not relate to humans.  Mice never evolved eating fish for starters.

 

That's not really making sense, does it? Fish is a combination of all sorts of substances. That, of course, can have a very different effect. Furthermore: try to eat ~250 gram fish oil by eating real fish - you'll end up eating at least 5 Kg fish... but that's a different aspect.


Edited by Mr.Orange, 15 May 2014 - 09:11 PM.

  • like x 1

#12 Mr.Orange

  • Guest
  • 12 posts
  • 5
  • Location:Germany

Posted 15 May 2014 - 09:05 PM

Too much of a good thing is a bad thing. No one would be taking that much fish oil anyways, unless I have the conversions wrong. 

 

Totally. What were they thinking submitting 4,4g/Kg?? That's about 286 gram FISH OIL PER DAY for a normal human being (65 Kg). WTH?? Anyone got an explanation?



#13 normalizing

  • Guest
  • 2,692 posts
  • -104
  • Location:Warm Greetings
  • NO

Posted 16 May 2014 - 12:24 AM

^ people seem to forget rats have unique very rapid metabolism compared to humans. so it makes logic to put much more mg per kg for rats than humans. in a way, for humans this might translate at i dunno maybe 20 grams or so which is still a lot but possible to occur.

also all studies done on rats have used megadoses of stuff like curcumin, green tea etc how come nobody ever questioned the huge amount comparable in humans? reason being, it satisfies everyone. easy and cheap to obtain, supposed health benefits, win win who cares.



#14 Hebbeh

  • Guest
  • 1,661 posts
  • 570

Posted 16 May 2014 - 12:38 AM

^ Scientists seem to have overlooked the fact that, unlike humans, mice have a very poorly developed endogenous antioxidant system which would have difficulty keeping all that omega-3 from oxidizing.  That is the whole point.  Not alone that in spite of a well developed endogenous antioxidant system, humans would also be consuming additional lipid antioxidants such as vitamin E.  Quite honestly, worthless research as far as the real world in respect to humans.


  • like x 2
  • Needs references x 1
  • Agree x 1

#15 niner

  • Guest
  • 16,276 posts
  • 2,000
  • Location:Philadelphia

Posted 16 May 2014 - 12:43 AM

 

Too much of a good thing is a bad thing. No one would be taking that much fish oil anyways, unless I have the conversions wrong. 

 

Totally. What were they thinking submitting 4,4g/Kg?? That's about 286 gram FISH OIL PER DAY for a normal human being (65 Kg). WTH?? Anyone got an explanation?

 

It was 4.4g/Kg of their food, not their body weight.  I imagine that mice eat more food relative to their body weight than humans do, so that probably covers the scaling that normalizing was complaining about in the previous post.  A typical mouse is in the ballpark of 25g, and eats 2-3g/day or so.  That would be like a human eating ~15lbs of food a day?  So this probably covers the faster metabolism argument.



#16 tunt01

  • Guest
  • 2,308 posts
  • 414
  • Location:NW

Posted 16 May 2014 - 02:47 AM

I listened to a discussion from Spindler before these results were made public.  FWIW, his comments at the time were as follows:

 

 

 

With Krill oil and highly purified lovaza (has methylmercury removed), even more potently decreased lifespan (a significant degree of the mice).  We weren’t oiling them up to a ridiculous level.  We just removed some of the corn oil in the diet and replaced it with Krill or the Lovaza, so it’s not like the whole diet was high fat/high fish oil.  It was just a little bit.  And that was certainly not beneficial and in fact was harmful.

 

As you can see, he did not remark upon exact g/kg figures, but his view was that the fish oil wasn't overdone in the diet.  He covered many of his individual studies in mice, so we spent just a few moments of time on the fish/krill oil.  

 

I think Hebbeh makes some excellent points -- that mice are probably not the best model for fish oil consumption and humans are very different.

 

 

 

 


Edited by prophets, 16 May 2014 - 02:48 AM.

  • like x 1

#17 Mr.Orange

  • Guest
  • 12 posts
  • 5
  • Location:Germany

Posted 16 May 2014 - 05:57 AM

 

 

Too much of a good thing is a bad thing. No one would be taking that much fish oil anyways, unless I have the conversions wrong. 

 

Totally. What were they thinking submitting 4,4g/Kg?? That's about 286 gram FISH OIL PER DAY for a normal human being (65 Kg). WTH?? Anyone got an explanation?

 

It was 4.4g/Kg of their food, not their body weight.  I imagine that mice eat more food relative to their body weight than humans do, so that probably covers the scaling that normalizing was complaining about in the previous post.  A typical mouse is in the ballpark of 25g, and eats 2-3g/day or so.  That would be like a human eating ~15lbs of food a day?  So this probably covers the faster metabolism argument.

 

 

Thanks, it makes sense then! How important it is to understand these "little" details... :)
 



#18 normalizing

  • Guest
  • 2,692 posts
  • -104
  • Location:Warm Greetings
  • NO

Posted 16 May 2014 - 07:29 PM

the funny bit reading this is few people saying "oh well fish oil doesnt compare in rats as well as it does in humans" and it makes me ask what study in rats ever compares well to humans....


  • dislike x 3

#19 ta5

  • Topic Starter
  • Guest
  • 952 posts
  • 324
  • Location: 

Posted 17 May 2014 - 12:57 PM

From the full text Discussion:

 

Of the pathologies found upon necropsy, hemorrhagic diathesis seems likely to be responsible for a significant proportion of the early mortality of the treated mice. It was substantially and significantly elevated in both the Lovaza- and krill oil-treated mice (Table 1). It is a probable consequence of the anticoagulant effects of dietary marine oils observed in both rodents and humans (Calder and Yaqoob 2012; Sano et al. 2003). The increase in lung tumors in the Lovaza- and krill oil-treated mice also may have contributed to their early mortality. Recent evidence suggests that a diet containing fish oil promotes tumor growth by suppressing CD8+ activation in mice (Xia et al. 2014). Thus, the anti-inflammatory effects of marine oils may have negative as well as positive consequences. A fish oil-containing diet significantly decreased the number of CD8+ T cells in the lungs of influenza virus-infected mice, leading to elevated rates of morbidity and mortality (Schwerbrock et al. 2009).

 



#20 Deep Thought

  • Guest
  • 224 posts
  • 30
  • Location:Reykjavík, Ísland

Posted 17 May 2014 - 01:21 PM

Isn't it well known that one must consume a wide variety of fatty acids, and not just a single kind of fatty acid in massive amounts?

 

I wonder how many percent of the mices' total fatty acid intake consists of fish oil. If it's in the range of 50%+, then I'm not really surprised that the mice were harmed by it.



#21 Hebbeh

  • Guest
  • 1,661 posts
  • 570

Posted 17 May 2014 - 08:25 PM

From the full text Discussion:

 

Of the pathologies found upon necropsy, hemorrhagic diathesis seems likely to be responsible for a significant proportion of the early mortality of the treated mice. It was substantially and significantly elevated in both the Lovaza- and krill oil-treated mice (Table 1). It is a probable consequence of the anticoagulant effects of dietary marine oils observed in both rodents and humans (Calder and Yaqoob 2012; Sano et al. 2003). The increase in lung tumors in the Lovaza- and krill oil-treated mice also may have contributed to their early mortality. Recent evidence suggests that a diet containing fish oil promotes tumor growth by suppressing CD8+ activation in mice (Xia et al. 2014). Thus, the anti-inflammatory effects of marine oils may have negative as well as positive consequences. A fish oil-containing diet significantly decreased the number of CD8+ T cells in the lungs of influenza virus-infected mice, leading to elevated rates of morbidity and mortality (Schwerbrock et al. 2009).

 

 

This is the exact reason why I use and will continue to use fish oil.  The ONLY genetic red flag I received from my 23andMe results was an extremely elevated genetic risk for "deep vein thrombosis" which is blood clots leading to strokes and other problems.....and which didn't surprise me since deep vein thrombosis induced stroke is what killed my father and his father before him.  My father spent the final years of his life on warfarin but it was too little too late for him.  I'll take my chances with fish oil and aspirin which I have been using for at least the past 15 years and I'm 57.

 

And in spite of fish oil and aspirin, I don't bleed or bruise and clot like a normal person.  With respect to the immune suppression via CD8+ suppression, all I can say is I haven't had so much as a sniffle in probably the past 10 years...in spite of everybody else in the office sick and hacking with every single bug that comes along.  I'm the one that NEVER gets sick....knock on wood.

 

edit...just wanted to add that probably more people are eventually at risk for some degree of elevated clotting and stroke risk than not.  Probably like everything else, the only way to know how much supplements such as fish oil and aspirin will be beneficial is through genetic risk testing and medical evaluation. 


Edited by Hebbeh, 17 May 2014 - 08:30 PM.

  • like x 1
  • Needs references x 1

#22 Michael

  • Advisor, Moderator
  • 1,293 posts
  • 1,792
  • Location:Location Location

Posted 17 May 2014 - 11:10 PM

I'm suspecting poor science once again.  Did they administer an oil based antioxidant with the fish such as vitamin E?  Are there any humans consuming fish oil and not supplementing vitamin E?


The krill oil comes with significant vitamin E (and, as its vendors like to scream, astaxanthin and other antioxidants) in it; "Dietary supplementation of krill oil attenuates inflammation and oxidative stress in experimental ulcerative colitis in rats; there is a small amount of E added to Lovaza capsules; standard rodent chow contains a generous supply of vitamin E, which is more than can be said for the general population; and there's no evidence of long-term benefit to vitamin E supplementation in man or mouse.
 

One hundred thirteen subjects with normal or slightly elevated total blood cholesterol and/or triglyceride levels were randomized into three groups and given either six capsules of krill oil (N = 36; 3.0 g/day, EPA + DHA = 543 mg) or three capsules of fish oil (N = 40; 1.8 g/day, EPA + DHA = 864 mg) daily for 7 weeks. A third group did not receive any supplementation and served as controls (N = 37).  ... No statistically significant differences in changes in any of the serum lipids or the markers of oxidative stress and inflammation between the study groups were observed.

 
Additionally, (a) others have already quoted some reasonable mechanistic hypotheses for the excess of deaths, which relate to EPA's (and to a lesser extent DHA's) established effects on inflammation, platelet aggregation, and immune function, not oxidative streess; and (b) to the extent that oxidative stress really might affect lifespan in a normally-aging man or mouse, absent involvement in major pathology or metabolic disease (which were clearly not present in these mice), it would be in the mitochondria, where pharmacological doses of vitamin E (or nearly anything else) do not reach.
 

edit:  and how fish oil "appears" to affect mice more than likely does not relate to humans.  Mice never evolved eating fish for starters.

 
Fish oil ain't fish: the Lovaza, in particular, is a very highly-purified EPA/DHA supplement, and even most "fish oil" supplements are essentially just fat. The 'fish' thing really falls out of it.
 

Isn't it well known that one must consume a wide variety of fatty acids, and not just a single kind of fatty acid in massive amounts?


I would agree. But while the population at large is consuming one set of fats in massive amounts (omega-6 oils and saturated fats, and decreasingly but still excessively trans-fats), many people in the health-nut community are per contra grossly overconsuming EPA+DHA. If you don't have hypertriglyceridemia, specific diseases (rheumatoid arthritis, possibly depression, or established, clinical cardiovascular disease), the dose of EPA+DHA that is justified for preventive purposes is the equivalent of two fatty fish meals a week); I know many, many health-nutty folk who are consuming more than two fatty fish meals a week, and taking 300-1500 mg of supplemental EPA+DHA a day.
 

I wonder how many percent of the mices' total fatty acid intake consists of fish oil. If it's in the range of 50%+, then I'm not really surprised that the mice were harmed by it.

 
This is given in the paper's abstract, quoted in the first post:

 

The oils were incorporated into the chemically defined American Institute of Nutrition (AIN)-93 M diet. An equivalent volume of soybean oil was removed. Krill oil was 3% and Lovaza 11% of the oil in the diets.

 

11% of the oil, NB — not 115 of Calories or 11% of diet by weight. Further, more detailed analysis is given in the free full text, explaining the incorporation of metabolic scaling to account for differences in species mass-specific metabolic rate:

 

 

The American Institute of Nutrition (AIN)-93 M diet contains 40 g soybean oil per kg diet... The krill oil brand used is 23 % EPA and 6.5% DHA by weight, while Lovaza is 55% EPA and 45 % DHA by weight. ... The recommended dose [of prescription Lovaza] in humans is 4.0 g/day, which would provide 50 mg/kg bw/day for an 80-kg adult. The cross-species scaling factors used to adjust dosages between animals and humans suggest that mice should receive 8 to 12 times the effective human dosage of a drug to account for species-specific pharmacodynamic and pharmacokinetic differences (reviewed in Spindler 2012).

 

This is consistent with what he's done in all of these studies: taken the standard recommended dose of a drug or supplement in humans, and scaled it down using standard methods to a metabolically equivalent dose in mice.

 


Edited by Michael, 17 May 2014 - 11:11 PM.

  • like x 1

#23 Hebbeh

  • Guest
  • 1,661 posts
  • 570

Posted 17 May 2014 - 11:47 PM

 

I'm suspecting poor science once again.  Did they administer an oil based antioxidant with the fish such as vitamin E?  Are there any humans consuming fish oil and not supplementing vitamin E?


The krill oil comes with significant vitamin E (and, as its vendors like to scream, astaxanthin and other antioxidants) in it; "Dietary supplementation of krill oil attenuates inflammation and oxidative stress in experimental ulcerative colitis in rats; there is a small amount of E added to Lovaza capsules; standard rodent chow contains a generous supply of vitamin E, which is more than can be said for the general population; and there's no evidence of long-term benefit to vitamin E supplementation in man or mouse.
 

 

 

 

My comment was in relation to the major opponents argument against fish oil of the risk of omega-3 tissue lipid per-oxidation (which I've always felt was over blown).  Regardless, Ta5's post #19 sums up the papers argument of the possible causes of early mortality.  And I stand by my post #21 in my response to those concerns,   And perhaps mice are not prone to deep vein thrombosis and accompanying disorders and if so, would not only gain no advantage from those benefits but would only suffer adverse side effects as the paper suggests, once again demonstrating that mice aren't men.


  • Pointless, Timewasting x 1

#24 Deep Thought

  • Guest
  • 224 posts
  • 30
  • Location:Reykjavík, Ísland

Posted 18 May 2014 - 07:10 AM


 I would agree. But while the population at large is consuming one set of fats in massive amounts (omega-6 oils and saturated fats, and decreasingly but still excessively trans-fats), many people in the health-nut community are per contra grossly overconsuming EPA+DHA. If you don't have hypertriglyceridemia, specific diseases (rheumatoid arthritis, possibly depression, or established, clinical cardiovascular disease), the dose of EPA+DHA that is justified for preventive purposes is the equivalent of two fatty fish meals a week); I know many, many health-nutty folk who are consuming more than two fatty fish meals a week, and taking 300-1500 mg of supplemental EPA+DHA a day.

 

 

Are two fatty fish meals a week all it takes? I thought the goverments dietary recommendation was bollocks.



#25 Mind

  • Life Member, Director, Moderator, Treasurer
  • 19,054 posts
  • 2,002
  • Location:Wausau, WI

Posted 18 May 2014 - 12:54 PM

the funny bit reading this is few people saying "oh well fish oil doesnt compare in rats as well as it does in humans" and it makes me ask what study in rats ever compares well to humans....

 

From following such results for over a decade, it seems to me that mouse and rat studies rarely translate into anything actionable for human longevity.


  • like x 2

#26 Michael

  • Advisor, Moderator
  • 1,293 posts
  • 1,792
  • Location:Location Location

Posted 18 May 2014 - 05:22 PM

All:
 

 

 

I'm suspecting poor science once again.  Did they administer an oil based antioxidant with the fish such as vitamin E?  Are there any humans consuming fish oil and not supplementing vitamin E?


The krill oil comes with significant vitamin E (and, as its vendors like to scream, astaxanthin and other antioxidants) in it; "Dietary supplementation of krill oil attenuates inflammation and oxidative stress in experimental ulcerative colitis in rats; there is a small amount of E added to Lovaza capsules; standard rodent chow contains a generous supply of vitamin E, which is more than can be said for the general population; and there's no evidence of long-term benefit to vitamin E supplementation in man or mouse.

 

 
My comment was in relation to the major opponents argument against fish oil of the risk of omega-3 tissue lipid per-oxidation (which I've always felt was over blown).

 

 
Hm. Your comment seemed to be saying the opposite: that the study would be flawed if it did not administer antioxidants.
 

Regardless, Ta5's post #19 sums up the papers argument of the possible causes of early mortality. And I stand by my post #21 in my response to those concerns

 
 

 

From the full text Discussion:
 

Of the pathologies found upon necropsy, hemorrhagic diathesis seems likely to be responsible for a significant proportion of the early mortality of the treated mice. It was substantially and significantly elevated in both the Lovaza- and krill oil-treated mice (Table 1). It is a probable consequence of the anticoagulant effects of dietary marine oils observed in both rodents and humans (Calder and Yaqoob 2012; Sano et al. 2003). The increase in lung tumors in the Lovaza- and krill oil-treated mice also may have contributed to their early mortality. Recent evidence suggests that a diet containing fish oil promotes tumor growth by suppressing CD8+ activation in mice (Xia et al. 2014). Thus, the anti-inflammatory effects of marine oils may have negative as well as positive consequences. A fish oil-containing diet significantly decreased the number of CD8+ T cells in the lungs of influenza virus-infected mice, leading to elevated rates of morbidity and mortality (Schwerbrock et al. 2009).

 

 
This is the exact reason why I use and will continue to use fish oil.  The ONLY genetic red flag I received from my 23andMe results was an extremely elevated genetic risk for "deep vein thrombosis" which is blood clots leading to strokes and other problems.....and which didn't surprise me since deep vein thrombosis induced stroke is what killed my father and his father before him.  My father spent the final years of his life on warfarin but it was too little too late for him.  I'll take my chances with fish oil and aspirin which I have been using for at least the past 15 years and I'm 57.
 
And in spite of fish oil and aspirin, I don't bleed or bruise and clot like a normal person.  With respect to the immune suppression via CD8+ suppression, all I can say is I haven't had so much as a sniffle in probably the past 10 years...in spite of everybody else in the office sick and hacking with every single bug that comes along.  I'm the one that NEVER gets sick....knock on wood.
 
edit...just wanted to add that probably more people are eventually at risk for some degree of elevated clotting and stroke risk than not.  Probably like everything else, the only way to know how much supplements such as fish oil and aspirin will be beneficial is through genetic risk testing and medical evaluation.

 

 
First, I would put a lot of salt substitute on your 23andMe report: if it's your only reason to think you're at elevated risk, I would suggest you either get professional guidance from a specialist or a genetic councilor or both. When the GAO looked into direct-to-consumer personal genetics services, they found wide variations (including some opposite risk assessments) in the risk predictions given by different companies to the same people's spit, even amongst the more professional companies (23andMe, deCODEme, Pathway Genomics, Navigenics ). We are still in the very early days of genetic association studies, with lots of convincing-looking findings being contradicted in subsequent studies, or suggestions of specificity to particular populations, or just lack of replication: there are a few very solid gene-disease-risk links (ApoE haplotype, BRCA1 mutations), but the significance of the vast majority of SNP associations are dubious.
 
Second, even if you really are at high genetic risk, that risk is relative: if you're not yet collecting Social Security and are not at risk for other reasons (smoking, obesity, sedentary lifestyle), your absolute risk of DVT is low. Third, there are plenty of other things one can do to reduce the risk of DVT. Fourth, no matter what your DVT risk is, aspirin is not indicated, and I would drop it unless you have some other, strong reason to be on it: aspirin is an antiplatelet medication, and useful for thrombi formed at atherosclerotic lesion sites (which is why it's useful in persons who've had heart attacks or strokes) and other places where the blood vessels have been injured (like after a cut), but DVT happens in otherwise-healthy veins and is managed with anticoagulants like heparin and warfarin. (Antiplatelet vs anticoagulant agents). And finally, even if you develop DVT, most cases can be managed post facto: lung collapse stories are dramatic, but rare.

With all of that said: the evidence supporting fish oil for DVT is inconsistent (perhaps in part because fish oil has weak but nontrivial effects on elements of both the platelet and the coagulant pathways), but favorable enough (notably this recent study) that I would say that if you really are at elevated risk, taking a bit more fish oil than is justified in the average bear might be sensible, granted the relatively low risk of the supplement. But that's a far cry from the widespread, lifelong use of megadose long-chain omega-3 that is widespread amongst the health-conscious community.
 

And perhaps mice are not prone to deep vein thrombosis and accompanying disorders and if so, would not only gain no advantage from those benefits but would only suffer adverse side effects as the paper suggests, once again demonstrating that mice aren't men.

 
Most humans are not at meaningful risk of DVT either. Again, in the general human population, the available evidence supports consumption of the equivalent of two fatty fish meals a week, and not more. This rodent study suggests the risks of long-term overconsumption, and certainly is evidence against the very many health claims made for such supplementation.
 

 

If you don't have hypertriglyceridemia, specific diseases (rheumatoid arthritis, possibly depression, or established, clinical cardiovascular disease), the dose of EPA+DHA that is justified for preventive purposes is the equivalent of two fatty fish meals a week); I know many, many health-nutty folk who are consuming more than two fatty fish meals a week, and taking 300-1500 mg of supplemental EPA+DHA a day.

 
Are two fatty fish meals a week all it takes? I thought the goverments dietary recommendation was bollocks.

 

 
I used to think so too, until I actually started reading the reports underlying them ;) . The actual gov't dietary recommendations are very cautious and hedged in by conflicts between the USDA's twin missions of nourishing the country and supporting the ag industry, but the Insitute of Medicine reports that lie at their foundation (the Dietary Reference Intakes manuals) are solid expert assessments made on strict, thorough methodological assessment of all available evidence; one is often baffled by the critics of their conclusions after actually reading their assessments. Indeed, I am in many cases forced to conclude that the critics either haven't read the reports, or have and are hoping that when they issue their silly rebuttals (whose objections are covered in the original reports), their customers will just take their criticism at face value and won't bother to read the reports themselves.
 
IAC, I came to the conclusion that going beyond 2 fish meals a week was of no further benefit (in average, basically-healthy people) and possibly harmful long before the IOM came out with a recommendation consistent with that conclusion, based on evaluation of the epidemiological evidence. Again, I am not saying that there are not people for whom higher doses may be sensible, such as those with existing heart disease, hypertriglyceridemia, a range of autoimmune disorders, and other specific indications (which might include a real, near-term risk of DVT).
 

 

the funny bit reading this is few people saying "oh well fish oil doesnt compare in rats as well as it does in humans" and it makes me ask what study in rats ever compares well to humans....

 
From following such results for over a decade, it seems to me that mouse and rat studies rarely translate into anything actionable for human longevity.

 


Of course, whether or not a positive finding from rodent studies translates from mouse to human is one thing; people's insistence on doing this for which there isn't even support in rodent studies, or that is contraindicated from the rodent studies is another.



#27 Hebbeh

  • Guest
  • 1,661 posts
  • 570

Posted 18 May 2014 - 07:03 PM

 

First, I would put a lot of salt substitute on your 23andMe report: if it's your only reason to think you're at elevated risk,

 

Perhaps you missed this part...

 

and which didn't surprise me since deep vein thrombosis induced stroke is what killed my father and his father before him.  My father spent the final years of his life on warfarin but it was too little too late for him.

 

 

I would just as soon not repeat family history.  23andMe was spot on.

 

 

but DVT happens in otherwise-healthy veins and is managed with anticoagulants like heparin and warfarin

 

 

I can assure you don't want to be on warfarin.

 

Fourth, no matter what your DVT risk is, aspirin is not indicated, and I would drop it unless you have some other, strong reason to be on it: aspirin is an antiplatelet medication, and useful for thrombi formed at atherosclerotic lesion sites (which is why it's useful in persons who've had heart attacks or strokes) and other places where the blood vessels have been injured (like after a cut), but DVT happens in otherwise-healthy veins and is managed with anticoagulants like heparin and warfarin. (Antiplatelet vs anticoagulant agents). And finally, even if you develop DVT, most cases can be managed post facto: lung collapse stories are dramatic, but rare.

 

 

Not according to the American Heart Association....you may want to read up...

 

http://www.strokeass...452_Article.jsp

 

Antiplatelet agents, including aspirin work by inhibiting the production of thromboxane. Aspirin is highly recommended for preventing a first stroke, but it and other antiplatelets also have an important role in preventing recurrent strokes.

According to a statement by the American Heart Association, taking aspirin within two days of an ischemic stroke reduces the severity of the stroke. In some cases, it prevents death

 


Edited by Hebbeh, 18 May 2014 - 07:07 PM.

  • Pointless, Timewasting x 1

#28 Hebbeh

  • Guest
  • 1,661 posts
  • 570

Posted 18 May 2014 - 07:24 PM

 

Most humans are not at meaningful risk of DVT either.

 

I couldn't help but respond to this too.  Your entire post was misleading at best and full of misinformation.

 

http://www.cdc.gov/stroke/facts.htm

 

Stroke in the United States
  • Stroke kills almost 130,000 Americans each year—that’s 1 out of every 19 deaths.1
  • On average, one American dies from stroke every 4 minutes.2

  • Ill informed x 1

#29 Michael

  • Advisor, Moderator
  • 1,293 posts
  • 1,792
  • Location:Location Location

Posted 18 May 2014 - 07:34 PM

All (but mostly Hebbeh, of course):
 

 

First, I would put a lot of salt substitute on your 23andMe report: if it's your only reason to think you're at elevated risk

 
Perhaps you missed this part...
 

and which didn't surprise me since deep vein thrombosis induced stroke is what killed my father and his father before him.  My father spent the final years of his life on warfarin but it was too little too late for him.

 
I would just as soon not repeat family history.  23andMe was spot on.

 

 
Hang on. Your dad and grandfather died of stroke (I'm sorry, and yes that's scary, and yes you should manage your own risk). However, while stroke is known to increase the risk of DVT, the data are inconsistent on whether DVT increase the risk of stroke. What makes you confident that your ancestors' strokes were in any way related to DVT?
 

 

DVT happens in otherwise-healthy veins and is managed withanticoagulants like heparin and warfarin

 
I can assure you don't want to be on warfarin.

 


Sure -- unless you have to be. I'm not suggesting that you do (see rest of post).
 

 

Fourth, no matter what your DVT risk is, aspirin is not indicated, and I would drop it unless you have some other, strong reason to be on it: aspirin is an antiplatelet medication, and useful for thrombi formed at atherosclerotic lesion sites (which is why it's useful in persons who've had heart attacks or strokes) and other places where the blood vessels have been injured (like after a cut), but DVT happens in otherwise-healthy veins and is managed with anticoagulantslike heparin and warfarin. (Antiplatelet vs anticoagulant agents). And finally, even if you develop DVT, most cases can be managed post facto: lung collapse stories are dramatic, but rare.

 
Not according to the American Heart Association....you may want to read up...
 
http://www.strokeass...452_Article.jsp
 

Antiplatelet agents, including aspirin work by inhibiting the production of thromboxane. Aspirin is highly recommended for preventing a first stroke, but it and other antiplatelets also have an important role in preventing recurrent strokes. According to a statement by the American Heart Association, taking aspirin within two days of an ischemic stroke reduces the severity of the stroke. In some cases, it prevents death

 

First, this is a general guide to prevention of stroke -- again, not for the management of DVT. I come back again to why you think your ancestors' strokes were DVT-related.

 

As to aspirin for the primary prevention of stroke: in fact, the evidence only supports aspirin use in high-risk patients and for secondary prevention in people who've already had an MI or stroke . The largest meta-analysis of trials finds "aspirin decreased the risk for CV events and nonfatal MI, but there were no significant differences in the incidences of stroke, CV mortality , all-cause mortality and total coronary heart disease."(1)

 

This is broadly consistent with the earlier report from 2009 from the U.S. Preventive Services Task Force (tho' it was favorable on total (fatal plus nonfatal) CV events and stroke): "Men in these studies experienced fewer myocardial infarctions and women experienced fewer ischemic strokes. Aspirin does not seem to affect CVD mortality or all-cause mortality in either men or women. The use of aspirin for primary prevention increases the risk for major bleeding events, primarily gastrointestinal bleeding events, in both men and women. Men have an increased risk for hemorrhagic strokes with aspirin use [but women apparently don't]"(2) Evidently, more evidence became available in the ensuing two years.

 

Again: with your family history, you may well be at high risk of stroke, so this general-population evidence may be less relevant to you -- but that's about stroke per se, not about DVT.

 

References

1.  Bartolucci AA, Tendera M, Howard G. Meta-analysis of multiple primary prevention trials of cardiovascular events using aspirin. Am J Cardiol. 2011 Jun 15;107(12):1796-801. Epub 2011 Apr 8. Erratum in: Am J Cardiol. 2011 Aug 15;108(4):615. PubMed PMID: 21481826.

 

2: Wolff T, Miller T, Ko S. Aspirin for the primary prevention of cardiovascular events: an update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2009 Mar 17;150(6):405-10. Review. PubMed PMID: 19293073. 



sponsored ad

  • Advert
Click HERE to rent this advertising spot for SUPPLEMENTS (in thread) to support LongeCity (this will replace the google ad above).

#30 Hebbeh

  • Guest
  • 1,661 posts
  • 570

Posted 18 May 2014 - 08:11 PM

 

What makes you confident that your ancestors' strokes were in any way related to DVT?

 

 

That's what my dad was diagnosed with and why he was prescribed warfarin....to control the clots.  Although I don't have a bonafide diagnosis for my grandfather from 1954, it is my understanding he had all the same symptoms and if I was a betting man, the odds are the diagnoses would be the same.  And to give 23andMe their due...family history would indicate they are spot on.  Again, if I'm a betting man, with the multi-generational family history (and I don't know any family medical history beyond my grandfather...that goes back way too many years) backed up by the apparently spot on 23andMe flag, I would have to assume that It would be prudent to take precautions. DVT (clots) and stroke can not be diagnosed until it's too late.  Prevention is the best medicine.

 

First, this is a general guide to prevention of stroke -- again, not for the management of DVT

 

 

Your comment makes no sense.  You can't prevent the stroke without management of the clots (DVT).  The clots are what cause the stroke.

 

As to aspirin for the primary prevention of stroke: in fact, the evidence only supports aspirin use in high-risk patients and for secondary prevention in people who've already had an MI or stroke 

 

 

As my previous reference to the American Heart Association (among other sources)

 

 Aspirin is highly recommended for preventing a first stroke

 

 

Initial prevention is extremely key.  After the first stroke, if you survive (due to the miracle of modern medicine) it's all down hill from there.


  • Needs references x 1





Also tagged with one or more of these keywords: fish oil, krill, kril oil, lovaza, omega-3

1 user(s) are reading this topic

0 members, 0 guests, 0 anonymous users


    Bing (1)