Are YOU Aware That The Saturated Fat is Bad For You MYTH IS DISCREDITED BY 18 CLINICAL DOUBLE BLINDED TRIALS?

Question

Are you


Here are all 18

http://answers.yahoo.com/question/index;ylt=AoT2g3IHBUiCV6cxLq2UDQvfxQt.?qid=20070313174717AADeaME

Answer 1

Just because some rogue "scientists" say that a trial found "X", that doesn't make it true.

Are you BLINDLY accepting what Colpo et. al. say? No matter WHO says something, it's a bad idea to blindly accept it.

Here's a thought, is Razwell/Mike/Ashley, etc actually one of the people he adores?

Razwell, you need to learn, as I've pointed out before, that you can't call others "fools". That's considered a viollation of community guidelines and gets you reported.

Take a deep breath, relax, and try to come up with someone else besides your two idols to quote. If their point is that solid, you can surely find other, more reputable people to quote.

Answer 2

YOU KNOW WHY THE LINK DOESN'T WORK?

BECAUSE YOU, YOU had it removed because it was DAMNING EVIDENCE TOWARD YOUR MENTAL ACROBATICS DO DEFEND A FALSE PREMISE






Studies in ANIMALS DO NOT MATTER

Monkeys have a VERY DIFFERENT REACTION TO POLYUNSATURATED FATS THEN HUMANS


THIS IS ADDRESSED IN BOTH RAVNSKOV AND COLPOS BOOK THOROUGHLY


ALL YOUR STUDIES DO IS PROVE THAT LDL IS RAISED


BUT GUESS WHAT LDL REDUCTION IS UNFOUNDED AND LDL HAS NEVER BEEN SHOWN TO BE ATHEROHGENIC



I HAVE POSTED RANDOMIZED DOUBLE BLINDED CLINICAL TRIALS

MY LINK WORKS IN THE OTHER ARTICLES I WROTE LOOK THEM UP YOU WILL SEE ALL 18


YOU have been EXPOSED and YOU must no thave learnd much because

HUMANS DO NOT REACT WELL TO POYUNSATURATED FATS AS PROVEN IN THE 18 CLINICAL DIETRAY INTERVENTION TRIALS TO DATE


THE MOST WELL CONTROLLED



AGAIN AS ADDRESSED IN COLPOS AND RAVNSKOV BOOK POLYUNSATURATED FAT IS GOOD FOR MONKEYS BYT BAD FOR HUMANS


REACTION IS NOT THE SAME

Answer 3

Hey Mikey, eh Razzy, or is it Ashley today?

Your link is broken - so sorry.
(I have nothing to do with your broken link. Keep in mind that if you violate the terms of this forum, call people names, fail to ask questions, answer your own questions, or a violate a variety of other conventions - anyone can report the violation and your blather will be removed. I have no interest in suppressing your speech, only that you play nice - which you almost never do.)

The problem is double blinding adults in what they are eating, getting them to adher to, and then testing them to determine if there is atherogenic evidence...like performing repeated cardiac catheterizations - is that it is near impossible to do.

Fortunately we have animal studies.
You always want me to read your studies. Try mine:

Current Atherosclerosis Reports, November 2006, pp 466-471.

Dr. Denke writes:
All saturated fatty acids, with the notable exception of stearic acid (C18:0), raise low-density lipoprotein (LDL) cholesterol levels. A few less ubiquitous fatty acids also have LDL cholesterol effects. Trans-monounsaturated fatty acids, at equivalent doses of saturated fatty acids, raise LDL cholesterol. Polyunsaturated fatty acids, at three times the dose of saturated fatty acids, lower LDL cholesterol. Higher intakes of most fatty acids raise high-density lipoprotein (HDL) cholesterol, with the notable exception of trans-monounsaturated fatty acids, which lower HDL cholesterol to the same extent as carbohydrate when either is substituted for other dietary fatty acids.

Denke concludes:
Although dietary composition remains an important, modifiable predictor of dyslipidemia, overconsumption of any form of dietary energy may replace overconsumption of saturated fat as the primary factor that increases lipid and lipoprotein levels.

So if you overeat - regardless of the food type, it negates the positive affects of eating polyunsaturated fats. Interesting...maybe that's where your studies went wrong.

Or how about Journal of Lipid Research in October of 1990, pp. 1873-1882. Dr. Rudel et. al state:

The present study was carried out in a primate model, the African green monkey, to evaluate the effects of dietary monounsaturated fat on plasma lipoprotein cholesterol endpoints. All diets contained 35% of calories as fat.

For the group fed the diet enriched in monounsaturated fat compared to saturated fat, whole plasma and LDL cholesterol concentrations were significantly lower while high density lipoprotein (HDL) cholesterol concentrations were not affected.

For the group fed the diet enriched in polyunsaturated fat compared to saturated fat, both LDL and HDL cholesterol concentrations were significantly lower than in the group fed saturated fat.

Since effects on plasma lipoproteins similar to those seen in humans were identified in this primate model, relevant mechanisms for the effects of dietary fatty acids on lipoprotein endpoints related to coronary artery atherosclerosis, per se, can subsequently be examined.

Then Dr. Rudell et al went on to test whether there was any affect on atherosclerosis. His results are published in Arteriosclerosis, Thrombosis, and Vascular Biology in December of 1995, pp. 2101 - 2110.

He writes:

Atherogenic diets enriched in saturated, n-6 polyunsaturated, and monounsaturated fatty acids were fed to African green monkeys for 5 years to define effects on plasma lipoproteins and coronary artery atherosclerosis. The monkeys fed polyunsaturated and monounsaturated fat had similar plasma concentrations of LDL cholesterol, and these values were significantly lower than for LDL in the animals fed saturated fat.

Coronary artery atherosclerosis as measured by intimal area was less in the polyunsaturated fat compared with the saturated fat groups, was less in the animals fed polyunsaturated fat compared with the monounsaturated fat-fed animals, but did not differ between the monounsaturated and saturated fat groups.

In sum, the monkeys fed monounsaturated fat developed equivalent amounts of coronary artery atherosclerosis as those fed saturated fat, but monkeys fed polyunsaturated fat developed less. Dietary polyunsaturated fat appears to result in the least amount of coronary artery atherosclerosis because it prevents cholesteryl oleate accumulation in LDL and the coronary arteries in these primates.

WHAT HAVE WE LEARNED?

To conclude, we have learned that polyunsaturated fat consumption results in lower levels of LDL. Additionally we find that over consumption of ANY food type negates these positive affects.

We also learned that the African Green Monkey behaves similiarly to humans in terms of response to saturated fats. Those monkeys that were fed polyunsaturated fats have less coronary artery atherosclerosis than those monkeys fed saturated and mono-unsaturated fats.

It seems that eating a diet rich in polyunsaturated fats and limiting caloric intake results in less coronary arterosclerosis -which seems to contradict your assertions - who knew?

LDL's elevation have absolutely been associated with arteriosclerosis (see above even!) in both animal and human models. And arteriosclerosis is of course implicated in occlusive coronary heart disease.

WHY ITS USELESS TO DEBATE WITH YOU

You want me to go to medical libraries and dig out material from 1966 and read your full articles...when you fail to even read my full response - written right here for your convenience! (For if you had you would have known the relationship between arteriosclerosis and LDL)

Animal studies are absolutely relevant if established as a similar model...and the Green monkeys have been. In fact you can be very specific with your controls with animal studies and perform repeated studies on them that would not be possible with humans...unless you are Hitler.

I too have provided you with compelling epidemiologic evidence and you don't accept it...you have stated it is not strong enough evidence...well it is the only way to test these matters. We are not dealing with physics or chemistry in search of natural laws. All variables can not be accounted for and/or controlled - these are complex biologic beings.

By the way, epidemiologic evidence "is considered a cornerstone methodology of public health research, and is highly regarded in evidence-based medicine for identifying risk factors for disease and determining optimal treatment approaches to clinical practice." So even if you don't regard it, the rest of the world does.

I know that no matter how specific, compelling, and relevant my evidence, you will not stop for minute to CONSIDER it in your crusade against cholesterol lowering efforts - which makes you a waste of time.

So if you do not want to engage in an exchange of ideas - then what is your purpose? Perhaps you should just take out advertising or publish your own journal articles if you think you have the material to support it.

Good luck to you.