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Saturated fat and cholesterol good for you

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I don't know. Am I supposed to show you a study that proves it?
So you see, the problem is that you still are not coming to grips with the problem of how you know scientific things. Somehow, you've concluded that mainstream science is wrong for some things, but you didn't reject the mainstream scientific conclusion that arterial stenosis causes TIAs and CVAs. I'm puzzled by the method you're using. I thought perhaps you had located a study that persuaded you of that conclusion (and then I'd want to know what it was about that study that made you accept it, rather than reject it). My first impression was that you were using emotional response to tell you what the conclusion should be, and then evaluating studies based on whether they contradicted you feeling-based conclusion, but I don't think that can be it since you didn't seem to have even thought about the relationship between strokes and stenosis.

Well, anyhow, back to the main issue: what is the physical composition of arterial stenosis? (Clue: "not metalic") Perhaps if you commit to an answer to that, the connection will all be clearer.

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So you see, the problem is that you still are not coming to grips with the problem of how you know scientific things. Somehow, you've concluded that mainstream science is wrong for some things, but you didn't reject the mainstream scientific conclusion that arterial stenosis causes TIAs and CVAs. I'm puzzled by the method you're using. I thought perhaps you had located a study that persuaded you of that conclusion (and then I'd want to know what it was about that study that made you accept it, rather than reject it). My first impression was that you were using emotional response to tell you what the conclusion should be, and then evaluating studies based on whether they contradicted you feeling-based conclusion, but I don't think that can be it since you didn't seem to have even thought about the relationship between strokes and stenosis.

I was basing my conclusion on logic, that since the arteries are more narrow then it would slow or block blood flow. What type of study am I supposed to find?

Well, anyhow, back to the main issue: what is the physical composition of arterial stenosis? (Clue: "not metalic") Perhaps if you commit to an answer to that, the connection will all be clearer.

I knew what the physical nature of arterial stenosis was before, but I didn't want to go any further before figuring out how I know each of these things is true. Otherwise I'll just be repeating what the scientists say without knowing how they know it. I mean, I can tell you that arterial stenosis can be caused by plaque, which consists of fatty substances, cholesterol, cell waste. I don't have any studies if that's what you're expecting though.

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I was basing my conclusion on logic, that since the arteries are more narrow then it would slow or block blood flow. What type of study am I supposed to find?
I think it's a perfectly reasonable leap, but it is a leap. I mostly wanted to know if you had some study in mind that actually proved the conclusion experimentally. I also wanted to know to what extent a priori reaoning played a role in whether you accept or reject conclusions.
I mean, I can tell you that arterial stenosis can be caused by plaque, which consists of fatty substances, cholesterol, cell waste.
At any rate, now you should be able to make the equally reasonable leap that cholesterol and fat can cause heart-related problems (through carotid stenosis and accumulation of plaques in the heart), and so I don't see what your objection to mainstream science is.
Otherwise I'll just be repeating what the scientists say without knowing how they know it.
I would suggest picking something fairly specific and learning about it. For example, maybe pick on the mechanisms for lipoprotein transport in humans, with special attention to atheroma development. (That said, the topic may be too theoretical and model-dependent). What you ultimately should try to do is read a number of clinical studies on a related topic. Just reading the conclusions isn't any good: you have to read the methods part which will tell you how they know. You might be able to identify a flaw of some kind, an uncontrolled variable that they hadn't thought of; then of course, you would want to conduct an experiment to resolve the influence of the putatively confounding variable. In your spare time. I would only waste my time on popular science / health magazine articles as potentially giving you leads to actual clinical studies in real refereed scientific journals.
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I think it's a perfectly reasonable leap, but it is a leap. I mostly wanted to know if you had some study in mind that actually proved the conclusion experimentally.

I agree, it is a big leap. However, finding specific studies isn't exactly easy, espcially a valid one.

At any rate, now you should be able to make the equally reasonable leap that cholesterol and fat can cause heart-related problems (through carotid stenosis and accumulation of plaques in the heart), and so I don't see what your objection to mainstream science is.

Because it's too vague. For cholesterol, is it HDL or LDL? What type of HDL or LDL? Ingested cholesterol or self-produced? When eaten with sugar? For fat, I don't know if it's poly, mono, saturated, unsaturated, trans, or just triglycerides which doesn't necessarily have to do with eating fat. Etc, etc...

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Because it's too vague. For cholesterol, is it HDL or LDL? What type of HDL or LDL? Ingested cholesterol or self-produced? When eaten with sugar? For fat, I don't know if it's poly, mono, saturated, unsaturated, trans, or just triglycerides which doesn't necessarily have to do with eating fat.
Those are fair distinctions to worry about. What makes you think that mainstream science is too vague on the matter? Or are you saying that the popular science reports are too vague? That's something that's pandemic with pop-science reporting, even when you read the NY Times Science section which has a pretty good pop-sci section. Now I don't really blame them, since the sound-bite approach is much more interesting to a wider range of people, and after all, their goal is to sell copy, not publish cutting edge scientific research.
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I meant that even though it's known that fat and cholesterol clog arteries, that doesn't necessarily mean it's from eating fat and cholesterol, and also that the statement doesn't clarify specifics. This would be a good time for you to pull out the study(s) that you know of that shows eating saturated fat and/or cholesterol contributes significantly to plaque or a disease.

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This would be a good time for you to pull out the study(s) that you know of that shows eating saturated fat and/or cholesterol contributes significantly to plaque or a disease.
It is your responsibility to pull out a mainstream study which you claim makes erroneous claims to support your attack on science. It is not my job to do your research for you. I will only respond to an actual scientific study they you have objections to. No links, no pop-sci magazine articles. References to reviewed science.
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It is your responsibility to pull out a mainstream study which you claim makes erroneous claims to support your attack on science. It is not my job to do your research for you. I will only respond to an actual scientific study they you have objections to. No links, no pop-sci magazine articles. References to reviewed science.

So you're saying instead of finding studies that prove that the mainstream scientists are right on the issue, I have to find studies that prove them wrong? Forget I said anything about mainstream scientists and lets stick to the specific issue of saturated fat and cholesterol. Is their proof that they cause heart disease? Or are you just saying they do because that's what is generally accepted by the main health organizations?

Also, I have access to hardly any actual studies, like most people..

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It is your responsibility to pull out a mainstream study which you claim makes erroneous claims to support your attack on science.

J Am Coll Cardiol. 2006 Aug 15;48(4):715-20. Epub 2006 Jul 24. Nicholls is one of the authors.

This is a study that tried to prove that eating just one high saturated fat meal "reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function," which is what their conclusion came to be after the study. The problem with their method was that in the high saturated fat meals carrot cake and a milk shake were the foods eaten. Both of them are filled with a high amount of sugar which could possibly be the main influence to the conclusion they came to. There are other factors that could be involved as well, such hydrogenated oils in the cake. They made a huge assumption just so they could write the conclusion they wanted.

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Finally you're aimed in the right direction, although your emotional psychologisation -- "They made a huge assumption just so they could write the conclusion they wanted" -- is an instance of you making a huge assumption just so you could write the conclusion you wanted. Your criticism comes down to saying that they failed to distinguish between two conclusions, both consistent with the data. The first is the one that they drew, and the second is "when combined with __ amounts of sugar" (the foods did not have "high" levels of sugar; note that this was an isocaloric meal); and in fact there are other hypotheses to consider, for example "when in the presence of protein". While you could not deny the harmfulness of saturated fats in foods containing sugar, you might not be certain whether that carries over to sugar-free foods. Thus you would conduct a follow-up study to test that hypothesis, by controlling that variable.

Here's another variable that they didn't control: the color of the shirt that the patient wore on the day in question. One good reason why that variable is not controlled and reported is that we know enough about human physiology to know that that would be irrelevant. Since I'm not a cardiologist, I don't know whether it's reasonable to think that the effect would only be present when sugars are also consumed, so we'll have to leave that up in the air, until an actual expert can weigh in. If it would be unreasonable, given our knowledge of human physiology, to expect sugar content to be relevant, then it would be unreasonable to demand that separate tests be conducted to test the effect of sugar (that is, scientific tests don't procede by pairing all 100 imaginable variables and looking at the power set of factors). For now, I will accept that there is some chance that the effect is due to an interaction between sugar and saturated fat, which might require a refinement of the conclusion, when some facts are presented to support the claim. You should test your hypothesis by eliminating the sugar content and otherwise replicating the test -- but you do have to come up with a palatable food, i.e. shoving a cup of coconut oil vs. safflower oil down someone's throat will not be tolerated. At any rate, you might try to sell your idea to someone who runs medical experiments for a living.

A different kind of error is reported in a reply by Christopher Masterjohn in JACC 49,17: 1825 who observes that “safflower oil contains 77 times the alpha-tocopherol, more than 100 times the gammatocopherol, and 73 times the total tocopherol". That is a more telling criticism, because he notes the known relationship between Vitamin E and ICAM-1 and VCAM-1; he rightfully calls for control of this contribution.

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A different kind of error is reported in a reply by Christopher Masterjohn in JACC 49,17: 1825 who observes that “safflower oil contains 77 times the alpha-tocopherol, more than 100 times the gammatocopherol, and 73 times the total tocopherol". That is a more telling criticism, because he notes the known relationship between Vitamin E and ICAM-1 and VCAM-1; he rightfully calls for control of this contribution.

I just read his article and it's very good. Masterjohn also pointed out that besides a higher amount of vitamin E in safflower oil than coconut oil(which you seem to agree could be a main contributor to anti-inflammation), that the high saturated fat group actually had less impaired flow-mediated dilation than the lower saturated fat group after their meals, based on the regression of the mean concept. However, the numbers he provides on flow-mediated dilation(33% higher at baseline for CO, 9% higher, 29% higher) I think means the CO group decreased more but they started off much higher, which could affect the results.

Thanks for responding.

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Am J Clin Nutr. 2005 Nov;82(5):957-63; quiz 1145-6. One author: Lefevre.

I found a study that shows the effects of fat intake on cholesterol levels. All variables seemed to be controlled, except it doesn't mention exercise amounts(just "free-living"). The results show that the only group with noticeable improvements in total cholesterol/HDL ratio was the highest fat group, while the other two lower fat groups stayed the same. I calculated the total cholesterol/HDL ratios to be: AAD- 4.63 to 4.50, Step 1- 4.63 to 4.63, Step 2- 4.63 to 4.62. Another stat is how the diets effected triglyceride levels: AAD- 96.57 to 93.91, Step 1- 96.57 to 106.32, Step 2- 96.57 to 108.09.

Edited by progressiveman1
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Am J Clin Nutr. 2005 Nov;82(5):957-63; quiz 1145-6. One author: Lefevre.

I found a study that shows the effects of fat intake on cholesterol levels. All variables seemed to be controlled, except it doesn't mention exercise amounts(just "free-living"). The results show that the only group with noticeable improvements in total cholesterol/HDL ratio was the highest fat group, while the other two lower fat groups stayed the same. I calculated the total cholesterol/HDL ratios to be: AAD- 4.63 to 4.50, Step 1- 4.63 to 4.63, Step 2- 4.63 to 4.62. Another stat is how the diets effected triglyceride levels: AAD- 96.57 to 93.91, Step 1- 96.57 to 106.32, Step 2- 96.57 to 108.09.

I should point out that since this studys' objective wasn't to measure the effects of saturated fat specifically, the difference in fat for each group is going to be with multiple fat types such as poly, mono, and saturated fat as well. I understand this studys' objective wasn't to focus solely on SF, but if it was then they should have controlled total fat, carb, and protein intake and just varied SF in each group.

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JAMA, Nov 1995; 274: 1450 - 1455

I found another solid study, which focuses on high fat/cholesterol vs low fat/cholesterol diet. The subjects started the study by eating a high fat/cholesterol diet and then switched to a low fat/cholesterol diet. When switched to the low fat/cholesterol diet, their total cholesterol/HDL ratio increased by 14.6% and triglyceride levels increased by a staggering 47%. This was during weight maintenance.

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Arteriosclerosis, Thrombosis, and Vascular Biology. 1998;18:441-449. One author: Ginsberg.

Time for the nail in the coffin, so to speak. All variables controlled in this study, with the only difference in each controlled group is saturated fat intake. The results are consistent with the two previous studies I just mentioned. Total cholesterol:HDL ratio increased in correlation with lower saturated fat intake. Meaning, the less saturated fat one ate, the more their TC:HDL ratio increased. Triglycerides also increased noticeably more on the low saturated fat diets. Lp(a) significantly rose as well on the low saturated fat diets.

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Does anyone know how accurate the results are from several year long studies, such as this one(citation at bottom) when they just do checkups every few years? It seems like there would be a large room for error. And also in that study, they predict the effects of a certain variable after making an adjustment from other risk factors. Can that be an accurate way of measuring effects of that variable? For example, they say "adjustment for smoking, glucose intolerance, bmi... did not materially change the results."

JAMA. Vol. 278 No. 24, December 24, 1997

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Greetings from Argentina!

I think it is interesting to note that my own doctor has told me that diet can, at best, lower your cholesterol by 10%. I hope to find a source or support for that. I believe the Atkins people say that as well.

My father who is turning 74 this January, is a lifelong carnivore and saturated fat junky. As ranchers in Canada our main source of protein was beef, but we also ate a lot of pork which we also raised. My dad is famous for eating the drippings from beef sausages and bacon out of the pan after dinner with some homemade bread. He has only developed a slight case of cholesterol since retiring a few years ago, and probably it is due to his much more sedentary lifestyle.

As far as high fat, low carb diets go, there is a book that really deserves much more attention. It is called "The Ketogenic Diet". You can read more about it here. The author, Lyle McDonald, studied hundreds of medical journals and diet experiments around the world and this book is the result. For those of you looking for support for your claims, this would obviously be a great place to start.

http://ketogenicdiet.lylemcdonald.com/

When I was living on a high protein/high fat diet with minimal carbohydrate intake, my blood cholesterol and blood sugars went down. I have known this to be the case with almost everyone who has gone on such an eating plan for either slimming or healther reasons.

Keep searching for good information, but especially, enjoy eating and being alive!

Michael

(borodinalex)

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He has only developed a slight case of cholesterol since retiring a few years ago, and probably it is due to his much more sedentary lifestyle.
I think this very likely is the hammer meeting the proverbial nail-head straight on, and is probably the most significant under-controlled variable in all of these studies.
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I found a study that contradicts the results from the last 3 studies I provided. The lowest saturated fat diet reduced TC:HDL the most. However, similar effects were seen in HDL, LDL, total cholesterol, triglycerides- they were just to different extents. These studies show that a diet high in saturated fat raises HDL and LDL stays the same or goes up slightly. Low fat intake relates with lowering of both HDL and LDL.

Now it's up to me to figure out why these numbers differed to extents. It appears to me at this point that these 4 studies control variables in a similar fashion, so possibilities for the difference may not be related to diet unless I just haven't picked up on the specific factor. Individual reactions may also be the cause of the difference.

Journal of Lipid Research, Vol 29, 963-969, Copyright © 1988 by Lipid Research, Inc

Edited by progressiveman1
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