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  #31   ^
Old Wed, Aug-26-09, 07:55
Rheneas's Avatar
Rheneas Rheneas is offline
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The report is reviewed well here

http://livinlavidalowcarb.com/blog/

Go Jimmy!!
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  #32   ^
Old Wed, Aug-26-09, 09:25
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Kristine Kristine is offline
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Peter from Hyperlipid sums it up pretty nicely here:

Quote:
Cardiologists are impatient people. If they want to study aortic aneurisms they tend to do things like placing a balloon in the aorta via the femoral artery, inflating it and then pulling. Down the aorta, with the balloon inflated. Or they might go in there surgically, cross clamp the aorta in two places, perfuse the isolated section of aorta with some unpleasant chemical, then set all back to normal and try out the latest drug for aneurism treatment on the preparation. The prime requirement is the suspension of disbelief that the "model" has anything to do with human senile dissecting aortic aneurisms. It doesn't.

Obviously the cholesterol fed Syrian hamster is a great model for arteriosclerosis, but it's boring. There's nothing sexy about feeding a herbivore cholesterol. Sexy needs genetically modified mammals to make it happen.

So you want a mouse to get atheroma? Well, they don't. Feed them mouse chow and they get arterial damage and fibrosis all right, but not nice big juicy cholesterol filled plaque. What to do? Delete a gene.

One offspring from the impatience of cardiologists is the apoE-/- mouse. This mouse is a genetic cripple who's ability to process fat has been severely damaged. There are a very, very, very small number of people in the world who are homozygous for defective apoE. They are functionally apoE-/-. Nature does not allow this commonly. Contrast it with FH where there are hundreds of different types of FH, ie breaking your LDL receptor gene is easily done and evolution has not attempted to conserve it particularly highly.

Feeding a high fat diet to apoE-/- mice is bad news for the mice. Until anyone gives us the full text of the paper we'll have no idea of exactly what they fed to the mice but, ultimately, they broke the mice first. Actually, if Dr Murray is anything to go by, even the full text won't tell us much about what they fed the mice!

If you are apoE -/- I wish you luck. Statistically, you're not. Neither is the cardiologist, Dr Rosenzweig, who gave up his LC diet on the basis of this study. But then, he thinks the transgenic apoE-/- mouse is a model for human arteriosclerosis.


Bold mine. To my knowledge, I'm not a genetically-crippled mouse, therefore I'm not sure anything discovered in this study is applicable to me.
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  #33   ^
Old Wed, Aug-26-09, 10:00
pochis40 pochis40 is offline
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Default What do you think about this?

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  #34   ^
Old Wed, Aug-26-09, 10:52
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anadyne anadyne is offline
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Quote:
An article that makes any suggestions about how people should eat, in the course of reporting this mouse experiment, is the kind of journalism we need less of, IMO.


Yeah, well... I don't think we'll ever see the end to that.

I don't necessarily think that it's the researchers who are impatient, but the public, the funding agencies, the politicians, etc. They want sound bites. They want the be-all, end-all, definitive statement of 'fact'.

You take a researcher who insists on making NO broad generalizations pertaining to human health after a mouse experiment, preferring to continue the slow but accurate practice of replicates and good science - and a researcher who puts out a press release to be picked up by bbc news citing the university or lab as a leading research institute (to show credibility) --- and which researcher has a happier boss, a happier institute, maybe even a better chance of getting funded next time?

Often you hear people complain about the amount of time it takes for a cure, an answer, anything substantial to be publicized about a disease or cure or health issue. They are impatient with the time it takes to get to human testing and the amount of variability inherent in the population, muddying the waters and hindering that definite statement of fact. They want answers tomorrow, not in 2012. Now the first stage experiments are picked up by the news media and sensationalized. What used to be one small brick in a large, well-built wall becomes a story in and of itself and it gives people a skewed impression of science and of the discovery process.
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  #35   ^
Old Wed, Aug-26-09, 14:17
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Judynyc Judynyc is offline
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Quote:
Originally Posted by pochis40

Quote:
How reliable are the findings?
The trouble with studies in mice is that we don't know whether or not the results will also apply to people. These particular mice were bred with a high genetic chance of developing arterial disease for the study. They were given food specially prepared to mimic either a low-carbohydrate diet or a typical 'Western' diet – but neither of these is the type of diet a mouse would usually eat. So it's hard to know whether we can rely on this study to tell us how low-carbohydrate diets affect humans.

^above from your link...which states what others have been saying in this thread.
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  #36   ^
Old Wed, Aug-26-09, 16:08
Bexicon Bexicon is offline
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Quote:
Originally Posted by anadyne
I don't necessarily think that it's the researchers who are impatient, but the public, the funding agencies, the politicians, etc. They want sound bites. They want the be-all, end-all, definitive statement of 'fact'.

You take a researcher who insists on making NO broad generalizations pertaining to human health after a mouse experiment, preferring to continue the slow but accurate practice of replicates and good science - and a researcher who puts out a press release to be picked up by bbc news citing the university or lab as a leading research institute (to show credibility) --- and which researcher has a happier boss, a happier institute, maybe even a better chance of getting funded next time?

Often you hear people complain about the amount of time it takes for a cure, an answer, anything substantial to be publicized about a disease or cure or health issue. They are impatient with the time it takes to get to human testing and the amount of variability inherent in the population, muddying the waters and hindering that definite statement of fact. They want answers tomorrow, not in 2012. Now the first stage experiments are picked up by the news media and sensationalized. What used to be one small brick in a large, well-built wall becomes a story in and of itself and it gives people a skewed impression of science and of the discovery process.

Yes, I know why it's happening; Gary Taubes describes the process in detail regarding the cholesterol thing in GCBC... it's just sort of a sad comment on society. The public demanding cures and answers is the same public complaining they're given conflicting advice every time they turn on the news, but they've engineered that situation by gobbling up any half-assed conclusion tacked onto studies like these.

The nice thing, though, is that you're only a victim of misinformation if you want to be; it's not so hard to unearth more information or background about things... it's just a matter of having enough interest to do so. I wouldn't be bothered too much if the whole world believed something I didn't about what I eat... I'm free to eat however I like, don't explain myself to people, and have little interest in converting anyone
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  #37   ^
Old Thu, Aug-27-09, 09:06
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Nancy LC Nancy LC is offline
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Quote:
Nutrition & Metabolism founder and editor Dr. Richard Feinman responded to this discrepancy by noting “the scientifically correct title of this study should be ‘Vascular effects of a low-carbohydrate high-protein diet in ApoE mice’ because that is what it is about.”

Noted Milwaukee, WI-based cardiologist Dr. William Davis added another wrinkle to this study by revealing to Livin’ La Vida Low-Carb that “there are three forms of ApoE mice (2,3,4), each of which responds differently to different diets. For example, apoE2 people (and mice) respond to low-fat diets differently than apoE4 people.” Now this is getting really interesting. So which mice did Dr. Rosenzweig and his team use? It’s anyone’s guess!

Good Calories, Bad Calories author Gary Taubes explained to Livin’ La Vida Low-Carb that this study using mice actually contradicts a great preponderance of the evidence that we’ve already seen in human studies, including how an Atkins low-carb diet improves cholesterol panels, reduces inflammation, lowers blood pressure and more. So why are mice a better model for the development of atherosclerosis in humans than humans? Excellent question, Gary!

http://www.examiner.com/x-867-LowCa...-not-for-humans
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  #38   ^
Old Thu, Aug-27-09, 10:03
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Nancy LC Nancy LC is offline
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Another gem, from Hyperlipid:
Low carbohydrate, high protein and ApoE-/- mice
Quote:
And here's the press release from 2009, I've put the text up on my odds and sods blog as press releases don't last for ever on the net. The paragraphs are a bit chewed up but you can get the gist OK.

Cardiologists are impatient people. If they want to study aortic aneurisms they tend to do things like placing a balloon in the aorta via the femoral artery, inflating it and then pulling. Down the aorta, with the balloon inflated. Or they might go in there surgically, cross clamp the aorta in two places, perfuse the isolated section of aorta with some unpleasant chemical, then set all back to normal and try out the latest drug for aneurism treatment on the preparation. The prime requirement is the suspension of disbelief that the "model" has anything to do with human senile dissecting aortic aneurisms. It doesn't.

Obviously the cholesterol fed Syrian hamster is a great model for arteriosclerosis, but it's boring. There's nothing sexy about feeding a herbivore cholesterol. Sexy needs genetically modified mammals to make it happen.

So you want a mouse to get atheroma? Well, they don't. Feed them mouse chow and they get arterial damage and fibrosis all right, but not nice big juicy cholesterol filled plaque. What to do? Delete a gene.

One offspring from the impatience of cardiologists is the apoE-/- mouse. This mouse is a genetic cripple who's ability to process fat has been severely damaged. There are a very, very, very small number of people in the world who are homozygous for defective apoE. They are functionally apoE-/-. Nature does not allow this commonly. Contrast it with FH where there are hundreds of different types of FH, ie breaking your LDL receptor gene is easily done and evolution has not attempted to conserve it particularly highly.

Feeding a high fat diet to apoE-/- mice is bad news for the mice. Until anyone gives us the full text of the paper we'll have no idea of exactly what they fed to the mice but, ultimately, they broke the mice first. Actually, if Dr Murray is anything to go by, even the full text won't tell us much about what they fed the mice!

If you are apoE -/- I wish you luck. Statistically, you're not. Neither is the cardiologist, Dr Rosenzweig, who gave up his LC diet on the basis of this study. But then, he thinks the transgenic apoE-/- mouse is a model for human arteriosclerosis.

Peter

EDIT: OK, I now have the full text (thanks H) and here is the total information supplied in the methods section about the diets:

"Male pups were placed on one of the three study diets 1 week after weaning: standard chow diet (Harlan Teklad #2018 rodent chow), high-fat ‘Western’ diet (Harlan Teklad # 88137) and a custom-ordered low-carbohydrate diet manufactured to our specifications (Harlan Teklad)."

That's it. It is traditional to give enough information in the methods section to allow another group to repeat your protocol. If the problems in these mice are NOT from being apoE-/- then Foo et all are to be congratulated on developing a diet to produce more problems than the Western or Cafeteria diet, but they ain't telling anyone how to do it! No answer from Murray on the same query.

Prompt reply from Dr Rosenzweig with the table of diet compostion, just asking now about the Ca modification and if it involves PO4 changes
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  #39   ^
Old Fri, Aug-28-09, 06:36
tomsey tomsey is offline
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Quote:
Good Calories, Bad Calories author Gary Taubes explained to Livin’ La Vida Low-Carb that this study using mice actually contradicts a great preponderance of the evidence that we’ve already seen in human studies, including how an Atkins low-carb diet improves cholesterol panels, reduces inflammation, lowers blood pressure and more. So why are mice a better model for the development of atherosclerosis in humans than humans? Excellent question, Gary!



Actually, the study found their cholesterol levels, level of inflammation etc were all fine. It was their blood vessels that were not. So there is no contradiction, more like a confirmation and possible explanation. I think that it is the most interesting part of the study - there were no telling markers ... everything looked good and actually "improved".

It is well known for example that many people have good blood work but still die suddenly of heart disease, have arterial blockages etc.

It is easier to deal with mice because you can then kill them and easily look at their blood vessels plus the process can be sped up. Hopefully, this study will lead to human studies. Of course, this is not the first time a study/event has suggested low carb/heart related issues.

http://ang.sagepub.com/cgi/content/abstract/51/10/817

From July 2009:

Development of Symptomatic Cardiovascular Disease after Self-Reported Adherence to the Atkins Diet
Ted D. Barnett, Neal D. Barnard, Tim L. Radak
Journal of the American Dietetic Association


I thought the lead doc made an interesting comment in terms of him seeing many low carbers for heart disease.

And this is why mice are generally used in experiments btw:
http://www.vetmed.ucdavis.edu/anima...ves/whymice.htm

Last edited by tomsey : Fri, Aug-28-09 at 07:27.
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  #40   ^
Old Fri, Aug-28-09, 07:34
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mahout mahout is offline
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Are you ever worried that government would one day be able to somehow "force" high carb diet onto people?
I mean - like someday in the future it will be hard / impossible to get foods like proper red meats, animal fats or full fat dairy and so on?

It probably sounds silly, but sometimes, when I read stupid bogus studies like this I am worried.

What happened with eg smoking (not that it´s a bad thing it is restricted or forbiden in some countries), but obviously government took steps when study after study showed its effects on lungs and cancer etc.

With all these "studies" showing lowcarb/high fat is "unhealthy" and with studies which prove otherwise getting ignored...
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  #41   ^
Old Fri, Aug-28-09, 08:13
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Merpig Merpig is offline
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Quote:
Originally Posted by tomsey
Of course, this is not the first time a study/event has suggested low carb/heart related issues.
http://ang.sagepub.com/cgi/content/abstract/51/10/817


Actually, in reading the abstract of that article, it does not suggest a relationship between heart issues and low carb. It suggests a relationship between heart issues and *high protein* - just as the mouse study did.

But as has been mentioned here and in many other places, the diet most of us follow is not *high protein* at all. In fact I'd say I probably eat less protein now than I did when I was following the SAD. My protein intake is usually about 15-20% of my daily total. I don't think that would be considered "high". What virtually all low carbers do is eat a *high fat* diet - which didn't at all seem to be what the above study actually studied.

Last edited by Merpig : Fri, Aug-28-09 at 10:53.
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  #42   ^
Old Fri, Aug-28-09, 10:45
tomsey tomsey is offline
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If that is what all low carbers do then they are not following the suggestions of atkins (30%-35%), zone 30% and probably not protein power. I do see people talking about increasing their fat and lowering their protein lately.

Most of the people I know who low carb eat a lot of protein, meat three times a day.
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  #43   ^
Old Fri, Aug-28-09, 10:57
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Merpig Merpig is offline
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Quote:
Originally Posted by tomsey
If that is what all low carbers do then they are not following the suggestions of atkins (30%-35%), zone 30% and probably not protein power. I do see people talking about increasing their fat and lowering their protein lately.Most of the people I know who low carb eat a lot of protein, meat three times a day.


I lost 80 pounds on the Protein Power plan at one time. I followed it very closely, eating the amount of protein they suggested, and my protein still never exceeded about 25% of my calories. Of course others will eat differently, but you've made me curious enough now to think about starting another thread, and asking people about their protein intake. I think even the people who eat mostly meat eat the fattier cuts, as historically it's been shown that people get sick if their food intake is primarily only lean protein. I'm curious now to see what others think about their own eating plans.
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  #44   ^
Old Fri, Aug-28-09, 11:05
tomsey tomsey is offline
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The paleo diets have a protein emphasis too I believe.
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  #45   ^
Old Fri, Aug-28-09, 11:10
HappyLC HappyLC is offline
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Quote:
Originally Posted by tomsey
If that is what all low carbers do then they are not following the suggestions of atkins (30%-35%), zone 30% and probably not protein power. I do see people talking about increasing their fat and lowering their protein lately.

Most of the people I know who low carb eat a lot of protein, meat three times a day.


Atkins is still a high fat diet, not high protein.
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