ah the science keeps marching on...

it's been claimed in this forum that athletes on low carb diets lose muscle mass. the author of this article disagrees, and has the studies to back up his assertions.

http://www.nutritionandmetabolism.com/content/pdf/1743-7075-3-9.pdf

Conclusion

Although more long-term studies are needed before a firm conclusion can be drawn, it
appears, from most literature studied, that a VLCARB is, if anything, protective against
muscle protein catabolism during energy restriction, provided that it contains adequate
amounts of protein.

you know, brown rice has almost as many carbs as white rice...

I think you mean to say it has almost as much amylopectin. Or at least, brown long-grain vs. white long-grain are comparable in their starch content (though the former has more fiber and vitamins as well as a slightly lower GI). Basmati and other "dry" varieties are higher in amylose, decreasing their glycemic index (though they are still in the intermediate range and are not really low-GI foods).

(I eat brown Basmati, in meals with lower-GI foods, for a moderate glycemic load.)

HTH!

I think you mean to say it has almost as much amylopectin. Or at least, brown long-grain vs. white long-grain are comparable in their starch content (though the former has more fiber and vitamins as well as a slightly lower GI). Basmati and other "dry" varieties are higher in amylose, decreasing their glycemic index (though they are still in the intermediate range and are not really low-GI foods).

(I eat brown Basmati, in meals with lower-GI foods, for a moderate glycemic load.)

HTH!

amylpectin?

ah the science keeps marching on...

it's been claimed in this forum that athletes on low carb diets lose muscle mass. the author of this article disagrees, and has the studies to back up his assertions.

http://www.nutritionandmetabolism.com/content/pdf/1743-7075-3-9.pdf

Dammit. My browser ate my post.

So. Some guy from Finland sees an article in the quack journal that claims that "DEXA data indicated both the VLCARB and VLF diets resulted in significantly more lean mass loss as a proportion of weight loss (32% and 31%) compared to the HUF diet (21%) (P<0.05)". (Oh, and by the way, HUF or high unsaturated fat is actually a "balanced diet with good fats", 50% carbo/30% fat/20% protein with low sat fat!)

So he up and shoots off a "letter to the editor" -- the SAME DAY as the original publication no less -- in which he claims that he feels that the protein sparing effects of very low carb (<10 g CHO, that's not even applicable to YOUR diet, mrfreddy!) couldn't possibly be overruled in this study of 67 people. His proof? DEXA (http://www2.gsu.edu/~wwwfit/bodycomp.html#DEXA) is inaccurate!

Then he goes on to blab about maybe 3 or 4 studies that were pretty unrelated to the one he's evaluating, that support his personal notions.

How is that science?

amylpectin?

Amylopectin and amylose are the two forms of starch in grains. Amylose is less readily digested, so it affects the blood sugar less immediately. I believe this is because amylopectin is more branched, providing more surface area for digestion. Amylopectin is the starch that makes sticky rice sticky and arborio gooey. High-amylose forms of rice, those that are light and fluffy and dry, have only a fraction of the GI of high-amylopectin, low-amylose species.

Dammit. My browser ate my post.

So. Some guy from Finland sees an article in the quack journal that claims that "DEXA data indicated both the VLCARB and VLF diets resulted in significantly more lean mass loss as a proportion of weight loss (32% and 31%) compared to the HUF diet (21%) (P<0.05)". (Oh, and by the way, HUF or high unsaturated fat is actually a "balanced diet with good fats", 50% carbo/30% fat/20% protein with low sat fat!)

So he up and shoots off a "letter to the editor" -- the SAME DAY as the original publication no less -- in which he claims that he feels that the protein sparing effects of very low carb (<10 g CHO, that's not even applicable to YOUR diet, mrfreddy!) couldn't possibly be overruled in this study of 67 people. His proof? DEXA (http://www2.gsu.edu/~wwwfit/bodycomp.html#DEXA) is inaccurate!

Then he goes on to blab about maybe 3 or 4 studies that were pretty unrelated to the one he's evaluating, that support his personal notions.

How is that science?


ah, you're just nitpicking!

"some guy from finland!!" did you really mean to insult the entire country of Finland? :>

you're right, my diet includes more carbs, maybe I should cut some more out, hahaaa.... seriously tho, I dont see how you can discount the study just based on that little fact.

where are the studies supporting the opposite arguement? haven't seen one yet telling me that an athlete who has had time to adapt to a high fat diet suffers from impaired aerobic performance or muscle loss or any of the numerous other claims made here.

Amylopectin and amylose are the two forms of starch in grains. Amylose is less readily digested, so it affects the blood sugar less immediately. I believe this is because amylopectin is more branched, providing more surface area for digestion. Amylopectin is the starch that makes sticky rice sticky and arborio gooey. High-amylose forms of rice, those that are light and fluffy and dry, have only a fraction of the GI of high-amylopectin, low-amylose species.


at full risk of getting abused again by the j person, let me say this about that: if choosing good carbs over bad is a good idea, because they effect blood sugar more slowly, then it only follows that choosing foods that effect blood sugar even more slowly (meats, fish, low starch veg., low sugar fruit), must be a much better idea. Unless of course you're getting some nutritional value from those "good carb" foods that cannot be found elsewhere, and of course, that ain't the case.

just my opinion, of course.

"some guy from finland!!" did you really mean to insult the entire country of Finland? :>

He listed his affiliation as "Advanced Research Press" and his email at "luukku.com"! (Only by further investigation did I discover that is is or was on the faculty of Physiology at a Finnish university.) Those credentials don't give him any more weight than any other guy from Iowa or Italy. He's just a guy.

where are the studies supporting the opposite arguement? haven't seen one yet telling me that an athlete who has had time to adapt to a high fat diet suffers from impaired aerobic performance or muscle loss or any of the numerous other claims made here.

We're not even talking athletes or adaptation here! This discussion is about a 12 week trial of giving different people the same number of calories with different macronutrient distributions. They had about the same adherence to the diet, and they lost about the same amount of weight (a calorie is a calorie, which dear Manninen also disagrees with), but the ones on a balanced diet lost less lean mass vs. the ones on low-fat and low-carb diets.

Anyway. About carbo. I eat grain foods because I can use the calorically dense boost. I came home last night after a hard spinning class (avg HR 178!) and was I ever glad for my ~4 oz. of al dente pasta! But you're right, fruits and veggies are a superior way to get carbo, especially if you are watching your intake, because they are jammed full of nutritional benefits and are low in caloric density. Last year I would have said that a diet based on grain (which has a reasonable protein content, some fiber and minerals, and digestible caloric energy) was great. I've moved away from that because of my conviction that phytonutrients and essential fats need to be emphasized more.

We're not even talking athletes or adaptation here! This discussion is about a 12 week trial of giving different people the same number of calories with different macronutrient distributions. They had about the same adherence to the diet, and they lost about the same amount of weight (a calorie is a calorie, which dear Manninen also disagrees with), but the ones on a balanced diet lost less lean mass vs. the ones on low-fat and low-carb diets.

Anyway. About carbo. I eat grain foods because I can use the calorically dense boost. I came home last night after a hard spinning class (avg HR 178!) and was I ever glad for my ~4 oz. of al dente pasta! But you're right, fruits and veggies are a superior way to get carbo, especially if you are watching your intake, because they are jammed full of nutritional benefits and are low in caloric density. Last year I would have said that a diet based on grain (which has a reasonable protein content, some fiber and minerals, and digestible caloric energy) was great. I've moved away from that because of my conviction that phytonutrients and essential fats need to be emphasized more.

hmm, I just re-read it, kinda quickly since I'm at work and supposed to be doing other things, hahaa but it seemed to me that he was raising valid criticisms of the study you mentioned, and then pointing out a few studies that, tho not perfect, have clearly pointed in the other direction. he concedes more need to be learned, but the weight of the evidence does not support the conclusions of the first study mentioned.

and when I'm hungry after a hard workout, I reach for a calorie dense steak! or if I want a snack, some cashews or some cheese. but then again, I dont need to restock carbos...

and when I'm hungry after a hard workout, I reach for a calorie dense steak! or if I want a snack, some cashews or some cheese. but then again, I dont need to restock carbos...

Not many overweight couch potatoes do

and when I'm hungry after a hard workout, I reach for a calorie dense steak! or if I want a snack, some cashews or some cheese. but then again, I dont need to restock carbos...

I actually wasn't hungry. I redlined my HR during that workout, and was belchy and all kinds of ick. But I knew from experience that if I don't get glycogen replenishing foods during the post-workout window, my recovery takes days. Today I have only a slight, pleasant DOMS. Mmm. ;)

I actually wasn't hungry. I redlined my HR during that workout, and was belchy and all kinds of ick. But I knew from experience that if I don't get glycogen replenishing foods during the post-workout window, my recovery takes days. Today I have only a slight, pleasant DOMS. Mmm. ;)

ok, I'll go out on a limb here... it could be that your recovery takes days because you are relying on glucose to fuel your workouts. glucose turns into lactic acid causing achy muscles. when you burn fatty acids instead, carbon dioxide and water are the by-products, and are very easily excreted (according to Barry Groves anyway...).

In my case, I only started working out seriously four weeks ago, and I can already work out six days a week, seven if I wanted to, without a problem. sometimes my muscles ache a bit but they are always back in form and ready to go by the next day.


DOMS??

it could be that your recovery takes days because you are relying on glucose to fuel your workouts.

Do you really think that at non-ketogenic carbo intake, you're completely bypassing glycolysis for high-intensity work (~90% MHR)?

Here's a fun site about the role of lactate in exercise. http://www.pponline.co.uk/encyc/0175.htm

DOMS??

Delayed Onset Muscle Soreness. Microtears in the muscles. Proof that you worked out. :)

Do you really think that at non-ketogenic carbo intake, you're completely bypassing glycolysis for high-intensity work (~90% MHR)?

I honestly don't know. I know that I don't eat a lot of carbs, so there can't be much glucose in my system to burn. I did just have half a banana tho!

I do know that I'm not at 90% MHR, except when I did a few sprints the other day in the pool. my best guess is that I'm working out at 77% MHR these days.

Not many overweight couch potatoes do


How do I put this guy on my "ignore list" so I no longer see his BS posts?

Mike

How do I put this guy on my "ignore list" so I no longer see his BS posts?

Mike


User Control Panel (top right corner of this page) then Buddy/Ignore lists bottom left... works like a charm.

Adding my two cents...

I was a competitive long distance runner for years and years. As is the norm for endurance sports, I was on a low-fat/high carb eating regimen. I thought I was healthy. Turns out, I was in the worst nutritional shape of my life, I just didn't know it, until I had something else to compare it to. Honestly, out of spite to prove someone wrong, I tried the Zone eating plan for a week. After day one, I felt an immediate and huge difference: Workouts were easier, I recovered faster, I wasn't as sore after tough workouts, I had boundless energy during the day when I wasn't working out... Everything seemed really easy.

Then, I took up mountain biking, and had to literally double my caloric intake. ;)

I don't adhere strictly to the Zone or any other eating plan, but I do know, for me personally, the low-fat/high-carb diet is something I'll *never* go back to. I had no idea just what kind of roadblocks I was putting in front of myself that prevented me from building more muscle, keeping that muscle, and giving my body the fuel it needed to recover. For me, high-carb doesn't work. Now I eat plenty of protein, plenty of fat, and carbs are an afterthought (I just try to eat plenty of fruits & veggies).

I'm adding my two cents in because, really, had I not tried a low-carb plan for that week, I never would have believed it could work. But I guess it all depends on what works for you individually.

Now I eat plenty of protein, plenty of fat, and carbs are an afterthought (I just try to eat plenty of fruits & veggies).

Let's get some more concrete measures in here. What's your macronutrient breakdown in percentages? For example, I tend to hit 50/30/20 (CHO/fat/protein) on the nose when I'm "eating clean". The "Zone" diet, at 40/30/30 is not that far from me. I also don't believe that's low-carb per this discussion, but I am open to being corrected. :)

Well, the Zone is low-carb compared with the high-carb way I was eating before. (I was in the bagels/pasta/rice/fat-free yogurt crowd.)

I'm afraid I'm not the measuring, exacting type. I haven't really put any concrete measures to anything for a few years now. The key for me is to just not hold back on stuff I used to hold back on. I go heavy on the mayo now, for example. I don't balk at cheese, or guacamole, or ground beef. I eat a (probably large, compared with some folks) serving of protein (and by that I mean meat, fish or eggs) at every meal. If I don't, I pay for it in the energy department.

EDIT: Adding to my reply... when I first started on the Zone, I was very exacting, and ate 40-30-30.

Interesting. If you get a chance, you might just pop a "typical" day's intake into FitDay.com. I go ape**** if I try to track every morsel, every day, but throwing a single day's worth in every so often keeps me kind of on track and aware of how my changing diet affects my performance. :)

I'm not a huge friend to meat, but I do try to get a "good protein source" (usually legume) at every meal, I eat a moderate amount of cheese, and while I'm not a mayo fan you had better believe I'll have ranch dressing on my buffalo chicken salad tonight. ;)

It's funny, I tried to really pump the animal protein for a few days last year, and ended up without enough appetite to get the calories I needed for my workouts! This eating style works well for me. :)

Yeah! Funny you should mention that. I don't get hungry like I used to on my old high-carb plan. I can tell when my body needs food, but I actually feel satiated after eating, and for a longer time. Which is cool.

FitDay.com... I'll check it out. Does it calculate your macronutrient ratios for you?

FitDay.com... I'll check it out. Does it calculate your macronutrient ratios for you?

yup!

User Control Panel (top right corner of this page) then Buddy/Ignore lists bottom left... works like a charm.


Oh wow... I wish I knew about this feture before!!!!! much nicer place now!

Oh wow... I wish I knew about this feture before!!!!! much nicer place now!


yes, I know, I know.

Heres the Nurse’s Study findings. Probably the largest study on nutrition ever done.

http://content.nejm.org/cgi/content/short/337/21/1491

Results Each increase of 5 percent of energy intake from saturated fat, as compared with equivalent energy intake from carbohydrates, was associated with a 17 percent increase in the risk of coronary disease (relative risk, 1.17; 95 percent confidence interval, 0.97 to 1.41; P = 0.10). As compared with equivalent energy from carbohydrates, the relative risk for a 2 percent increment in energy intake from trans unsaturated fat was 1.93 (95 percent confidence interval, 1.43 to 2.61; P<0.001); that for a 5 percent increment in energy from monounsaturated fat was 0.81 (95 percent confidence interval, 0.65 to 1.00; P = 0.05); and that for a 5 percent increment in energy from polyunsaturated fat was 0.62 (95 percent confidence interval, 0.46 to 0.85; P = 0.003). Total fat intake was not significantly related to the risk of coronary disease (for a 5 percent increase in energy from fat, the relative risk was 1.02; 95 percent confidence interval, 0.97 to 1.07; P = 0.55). We estimated that the replacement of 5 percent of energy from saturated fat with energy from unsaturated fats would reduce risk by 42 percent (95 percent confidence interval, 23 to 56; P<0.001) and that the replacement of 2 percent of energy from trans fat with energy from unhydrogenated, unsaturated fats would reduce risk by 53 percent (95 percent confidence interval, 34 to 67; P<0.001).
Conclusions Our findings suggest that replacing saturated and trans unsaturated fats with unhydrogenated monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease in women than reducing overall fat intake.


http://www.health.gov/dietaryguidelines/dga2005/minutes01_2829_2004.htm

These are the minutes of the dietary guidlines committee.
In there, even the Weston Price Foundation recommends grains.

It has everyones point of view, but the majority still recomend limiting sat fats.

"Saturated fats raise cholesterol levels and the risk of heart disease. They come primarily from animal sources such as fatty meats, whole fat dairy products, lard, and shortening. These are the kinds of fats you need to avoid for good heart health.

In the health professional follow-up study, men who ate the most saturated fat (15 percent of calories) had 1.72 times as many fatal heart attacks as men eating the least (five percent of calories from saturated fat). Women in the Nurses' Health Study had similar results with a 38 percent increase in mortality. Eating less saturated fat is obviously important to heart health! "

Heres the Nurse’s Study findings. Probably the largest study on nutrition ever done.

http://content.nejm.org/cgi/content/short/337/21/1491



http://www.health.gov/dietaryguidelines/dga2005/minutes01_2829_2004.htm

These are the minutes of the dietary guidlines committee.
In there, even the Weston Price Foundation recommends grains.

It has everyones point of view, but the majority still recomend limiting sat fats.

"Saturated fats raise cholesterol levels and the risk of heart disease. They come primarily from animal sources such as fatty meats, whole fat dairy products, lard, and shortening. These are the kinds of fats you need to avoid for good heart health.



Well I had to bite with the Weston A Price Foundation reference.

True the WAPF is not nessecarily against grains. From a traditionalist point of view they have a long history as part of the human diet. Now the catch is that the WAPF only reccomends TRADITIONALY prepared grains through long soaking or long fermentation. It's realy hard to buy the properly prepared grain products and the knowledge of how to do it at home has almost been lost so the point is a little mute.

As to the nurses study, from memory this is a poorly controlled study that relies on a lot of guess work and its not all its cracked up to be. I think they fail to control for smokers and other such things.

Regards, Anthony

That one link I found interesting mainly because it has what seems like every viewpoint expressed in one long (real long) page. I wasnt making any claims that any one part was true and others were false, mainly that a majority of the different groups attending adhere to the 'limiting sat fats'. Good to see the 'low fat' craze is pretty much discounted by all who attended.

I tried to search for weston price and nurses studie, or weston price and Dr Hu who conducted it, but couldnt find much reference to both. I figured you might respond Anthony because you know the WP site the best, in my limited time on it, I couldnt find much reference to it. Odd that the single largest study saying sat fat is bad isnt referenced, or discounted, more on there.

If you google 'sat fat bad' most places that subscribe to that theory, refer to the nurses study as the main relevent one. The nurses study is 84,000 people over 14 years, conducted by harvard, so it was quite extensive, but like all studies involving humans and diet over time, hard to pinpoint exact evidence since there are so many variables that are not controlled.

I agree that zero processing is better than high processing for sure. Unfortunate that less refined goods still are not prevalent in city supermarkets.

But I'll continue with my 50/30/20 diet, low gl carbs, low sat fat, least trans fat as possible, style diet, combined with 2.5 hours of 70-90 % mhr exercise a day, untill such time as the mainstream places advise me otherwise :).

But all info is good info, and even if I dont follow everything on weston price site (i do beleive some) its all food for thought.

Well I found this on Dr Mercola's site about the nurses study which points to saturated fat being helpful, http://www.mercola.com/2001/mar/17/saturated_fat_stroke.htm so I may have to retract some of what I've said about the nurses health study!

I'll keep looking. I've read so many references to the Nurses health study that I don't know where to look. You know it may be one of those cases where the study say's one thing but someone writes something completely different in the executive sumary and that's all people pay attention to.

Regards, Anthony

Yes.
What the mecola site doesnt say, is what the numbers are, just the increase percentage. It might have been .01 % to .02 % and he is correct, in that its an increase of double, but going from 1 to 2 out of 100,000 still wouldnt mean much.

Thats where studies and how people pick data from them , although they dont lie, can be cherry picked to show any viewpoint your tring to get across.

""The Iowa Women's Health Study examined the relationship between dietary fatty acids and Type II diabetes in a cohort of over 35,000 nondiabetic women (ages 55-69). The study showed that women with the highest intake of vegetable fat had a 22% lower risk of developing diabetes during the 11-year follow-up. Substituting polyunsaturated fats for saturated fats reduced the incidence of diabetes by an average of 16%, regardless of fiber intake, magnesium levels, obesity, physical exercise, or smoking status (Meyer et al. 2001; LEF 2001).""

Like that. Says there is a 22% lower risk, but not what the overall risk of both groups were.

I'll keep looking. I've read so many references to the Nurses health study that I don't know where to look. You know it may be one of those cases where the study say's one thing but someone writes something completely different in the executive sumary and that's all people pay attention to.

Regards, Anthony

bingo! you hit the nail on the head. this happens a lot, where the studiers do their best to bend the results to fit their pre-conceived notions, or perhaps to fit the notions of whoever is funding the study. Which was one of Gary Taubes main points in his "big fat liar" articles, that there is a lot of really really bad science going on in this field.

here's a good read on the history of the cholestoral hypothesis...

it's too long to quote here, but here's the link and a few choice snippets.

http://www.spiked-online.com/Articles/0000000CAE78.htm


Dr. Malcolm Kendrick

..The cholesterol hypothesis can be likened to a cathedral built on a bog. Rather than admit they made a horrible mistake and let it sink, the builders decided to try and keep the cathedral afloat at all costs...

...Although direct contradictions to the cholesterol hypothesis repeatedly appear, nobody dares to say 'okay, this isn't working, time to build again from scratch'. That decision has become just too painful, especially now that massive industries, Nobel prizes, and glittering scientific careers, have grown on the back of the cholesterol hypothesis. The statin market alone is worth more than £20billion each year...


...In fact, no clinical trial on reducing saturated fat intake has ever shown a reduction in heart disease. Some have shown the exact opposite...


...no trial has ever demonstrated benefits from reducing dietary saturated fat...


...In 1988, the surgeon general's office in the USA decided to silence the nay sayers by putting together the definitive report proving a causal link. Eleven years later the project was abandoned...



... in order to find out what makes LDL levels rise, we must surely find out, firstly, what makes VLDL levels go up; and what makes VLDL levels go up, primarily, is eating excess carbohydrates. What makes them go down is eating fat!...


...In truth, the current ideas on plaque formation used to keep the cholesterol hypothesis afloat are complex nonsense...


...To those who have studied the hypothesis with a critical eye, it seems unbelievable that it can possibly still be standing. Dr George Mann pronounced it dead in an editorial in the New England Journal of Medicine in 1977, referring to it as the 'Greatest scam in the history of medicine'. Yet this hypothesis has never had more followers than today...

Saturated fats raise cholesterol levels and the risk of heart disease. They come primarily from animal sources such as fatty meats, whole fat dairy products, lard, and shortening. These are the kinds of fats you need to avoid for good heart health."

Saturated fats aren't the only thing that raises cholesterol, though. There's a myth that if you don't eat sat fats and don't eat choloesterol, then your own cholesterol levels can't possibly raise. It's simply not true. I don't have time to look up stats on that right now, but you can raise your choloesterol by eating certain fat-free, cholesterol-free foods.

The key is moderation and listening to your own body. I think everyone knows by now that spending every meal at a drive-thru, or ignorning fruits and vegetables, or cutting an entire food group out of your diet is probably not a good idea. The rest is just personal preference and common sense.

...In fact, no clinical trial on reducing saturated fat intake has ever shown a reduction in heart disease. Some have shown the exact opposite...


...no trial has ever demonstrated benefits from reducing dietary saturated fat...


Dr. Malcolm Kendrick

Nurse's study, and mens study, and their two follow up studies. Links already provided.
But keep sticking your fingers in your ears and ignoring it since it doesnt give the results your looking for.

Looking thru Mercola's site. He actually does talk about the nurse's study and saturated fat.

http://www.mercola.com/1997/archive/dietary_fat_linked_to_heart_disease.htm

He doesnt dispute that saturated fat caused 17% increase in heart disease. " It is my belief that the risk is secondary to other factors." is his response. He agrees it shows increased heart disease, but his belief is that the benefits of sat fat outweigh its bad points.

And he emphasises that trans fat are so much more evil that they should be concentrated on reducing.

Edit : one last quote from Dr Mercola "some people tend to believe that saturated fat is a great evil. It certainly is not healthy in the large quantities that many people consume it."

But, in the future you can refrain from these type of comments now:

Saturated fats ARE the healthy fats despite everything you've heard or read. If anyone has any real science to dispute this I would like to see it because to this date it doesn't exist.


Where are your studies proving that saturated fats are unhealthy? They just don't exist

The scientific theory that saturated fats are harmfull is a flawed one with no scientific evidence in existence to back it but we have believed it for soo long and we have taken it so deeply into our culture that it's just too embarrasing to admit we were wrong.


Everyone can make their own conclusion and either pig out on sat fat or limit it to the recomended 10% based on their own research. But telling people there is no researxch supporting anti sat fat is just wrong.

Regarding the nurses study, theres a link to critisisms of this study right at the top of the page. Going through some of them in no paticular order and in no great detail.

The results aren't controled for Body Mass Index. Those who exercised the most usualy ate the least fat and had the lowest BMI. Those who exercised least consumed the most fat and had the highest BMI. You can draw your own conclusions from this but high BMI is a known risk factor and it wasn't controlled for which is a serious problem. What they needed to do was compare the high fat and low fat diets with the same exercise levels but they didn't do this.

Another valid critisism is that even the nurses with the worst results were better than the overall population by a significant margin so again some statistical shenanigans is going on. ALL of them were in the highest category in relation to the overall population.

Even by this study's own figures a 5% reduction in Saturated fat has a significantly smaller reduction than a 2% reduction in Transfat. There's some statistical shenanigans.

There are also questions about the validity of the "Food diary" method of estimating calorie consumption. The sample wasn't that large either and so errors are multiplied.

Overal its a study that could be useful but its open to abuse and it doesn't address the important question of "cause and effect".

Regards, Anthony

Regarding the nurses study, theres a link to critisisms of this study right at the top of the page. Going through some of them in no paticular order and in no great detail.

The results aren't controled for Body Mass Index. Those who exercised the most usualy ate the least fat and had the lowest BMI. Those who exercised least consumed the most fat and had the highest BMI. You can draw your own conclusions from this but high BMI is a known risk factor and it wasn't controlled for which is a serious problem. What they needed to do was compare the high fat and low fat diets with the same exercise levels but they didn't do this.

Another valid critisism is that even the nurses with the worst results were better than the overall population by a significant margin so again some statistical shenanigans is going on. ALL of them were in the highest category in relation to the overall population.

Even by this study's own figures a 5% reduction in Saturated fat has a significantly smaller reduction than a 2% reduction in Transfat. There's some statistical shenanigans.

There are also questions about the validity of the "Food diary" method of estimating calorie consumption. The sample wasn't that large either and so errors are multiplied.

Overal its a study that could be useful but its open to abuse and it doesn't address the important question of "cause and effect".

Regards, Anthony


well put. according to people who devote a lot time studying this subject, there are still no well controlled, double blind, randomized studies that show any benefit to reducing sat. fat in the diet. and a lot of studies showing the opposite.

I'm no scientist, but it seems to me that a large study like the nurse's study is only useful for suggesting areas that could be studied further. due the large number of uncontrolled variables, and unreliable data collection, etc. etc. no conclusions should be drawn from these things. Unless of course they coincide with your preconceived notions, that is, ha haa..

You asked for a study, there it is.
Even your frequently referenced Dr Mercola doesnt dispute it.

Spin it all you want.

Edit : one last quote from Dr Mercola "some people tend to believe that saturated fat is a great evil. It certainly is not healthy in the large quantities that many people consume it."



I'd be interested in knowing where that quote atributed to Dr Mercola comes from. Dr Mercola is NOT against Saturated fat and infact he's also on, or was on the WAPF board. You've got to be careful with some of Dr Mercola's posted articles because he isn't reponsible for all of them and he certainly doesn't concur with all of them. He has a practice of posting new studies and then commenting on them afterwards.

Regards, Anthony

I'm no scientist, but it seems to me that a large study like the nurse's study is only useful for suggesting areas that could be studied further. due the large number of uncontrolled variables, and unreliable data collection, etc. etc. no conclusions should be drawn from these things. Unless of course they coincide with your preconceived notions, that is, ha haa..

Remember Danno's Harvard link?

"Though time-consuming and expensive, cohort studies generally provide more reliable information than case-control studies because they don't rely on information from the past. Cohort studies gather the information all along and before anyone develops the disease being studied. As a group, these types of studies have provided valuable information about the link between lifestyle factors and disease. Two of the largest and longest-running cohort studies of diet are the Harvard-based Nurses' Health Study and Health Professionals Follow-up Study."

The correlations found in such studies aren't causative. But if they're strong enough, they are a sound basis from which to make an educated decision. It's like the connection between BMI and disease. BMI over 35 is strongly correlated with a battery of health problems and with increased mortality. Does that mean being heavy for your height is explicitly the cause of all those woes? Are you going to drop dead when your BMI hits that level? No, but chances are if you decrease your weight you're less likely to get those problems. And it's probably smart to do so. For another example, smoking is so strongly correlated with lung cancer that we take their causative effect to be a given. We can't do the study that randomizes whether people get real cigarettes or fake ones, and then look to see if they get cancer -- it wouldn't be ethical.

Similarly, saturated fat intake is pretty well correlated with heart disease. One might not be able to prove conclusively that there's a causative element involve, but nonetheless, I'd rather be in the lower-risk group, thanks!

I'd be interested in knowing where that quote atributed to Dr Mercola comes from. Dr Mercola is NOT against Saturated fat and infact he's also on, or was on the WAPF board. You've got to be careful with some of Dr Mercola's posted articles because he isn't reponsible for all of them and he certainly doesn't concur with all of them. He has a practice of posting new studies and then commenting on them afterwards.

Regards, Anthony

http://www.mercola.com/2001/jul/21/trans_fat.htm

Its from his comments, not a posted article.

http://www.mercola.com/2001/jul/21/trans_fat.htm

Its from his comments, not a posted article.

OK, the article is old. Something that you have to admire Dr Mercola for is that he's not afraid to admit mistakes and change his reccomendations. He's changed his advice regarding saturated fats since this article was posted.

Regards, Anthony

Remember Danno's Harvard link?

"Though time-consuming and expensive, cohort studies generally provide more reliable information than case-control studies because they don't rely on information from the past. Cohort studies gather the information all along and before anyone develops the disease being studied. As a group, these types of studies have provided valuable information about the link between lifestyle factors and disease. Two of the largest and longest-running cohort studies of diet are the Harvard-based Nurses' Health Study and Health Professionals Follow-up Study."

The correlations found in such studies aren't causative. But if they're strong enough, they are a sound basis from which to make an educated decision. It's like the connection between BMI and disease. BMI over 35 is strongly correlated with a battery of health problems and with increased mortality. Does that mean being heavy for your height is explicitly the cause of all those woes? Are you going to drop dead when your BMI hits that level? No, but chances are if you decrease your weight you're less likely to get those problems. And it's probably smart to do so. For another example, smoking is so strongly correlated with lung cancer that we take their causative effect to be a given. We can't do the study that randomizes whether people get real cigarettes or fake ones, and then look to see if they get cancer -- it wouldn't be ethical.

Similarly, saturated fat intake is pretty well correlated with heart disease. One might not be able to prove conclusively that there's a causative element involve, but nonetheless, I'd rather be in the lower-risk group, thanks!


only that there are dozens of better controlled studies showing that sat. fat is NOT correlated with heart disease.

only that there are dozens of better controlled studies showing that sat. fat is NOT correlated with heart disease.

And we come full circle. :rolleyes:

Look! Monkeys! http://atvb.ahajournals.org/cgi/content/abstract/15/12/2101

And I'll just come full circle and say, I've got enough on my plate (har har) with maximizing my plant foods and "good fats". Everything I can find that suggests that it's probably not removing sat fat that decreases risk, proposes that instead it's adding n-3, vit E, and antioxidants that does the trick. So I'll do the latter and not worry about the former.

Oh, and here's the bleeding edge of cholesterol research!

"Low-density lipoproteins (LDL) are detergent-like globules which transport cholesterol and other lipids in blood. Their outer hydrophilic shell is composed mainly of phospholipids, free cholesterol, and a protein (apoB-100), while their lipophilic core contains cholesterol esters, and triglycerides. During the oxidation of LDL polyunsaturated fatty esters are transformed into reactive oxidized lipids, many of which attach themselves to the LDL protein. The resulting oxidatively modified (ox) LDL is recognized by specialized receptors on the surface of macrophage cells. Receptor recognition promotes unregulated uptake (endocytosis) of the oxLDL by the cells. Partial digestion of the damaged LDL leads to the accumulation of large quantities of cholesterol esters that coalesce into droplets giving the cells the appearance of being foam-filled. The resulting "foam cells" accumulate in the subendothelial space of artery walls leading to the formation of fatty streaks, the earliest form of atherosclerotic plaques.

Our discovery that the level of isoLG-derived modification of blood proteins is closely correlated with cardiovascular disease is consistent with a seminal role for lipid-based oxidative protein modifications in the development of atherosclerosis. Our more recent observations indicate that certain oxidized lipids themselves are also recognized and endocytized through macrophage receptors."

You'll like this, from Molecular Nutrition & Food Research Volume: 49, Issue: 11, November 2005. pp. 1050 - 1062.:

"If oxidative injury contributes to the progression of AS, lowering levels of total cholesterol may not be suff icient to prevent further oxidative injury. Iso[4]LGE2-protein adduct levels appear to signal an independent defect which results in an abnormally high level of oxidative injury that is tightly associated with AS but not with total cholesterol levels. Therapeutic interventions that specifically lower levels of iso[4]LGE2-protein adducts, e. g., antioxidants, may be beneficial."

And we come full circle. :rolleyes:

Look! Monkeys! http://atvb.ahajournals.org/cgi/content/abstract/15/12/2101

And I'll just come full circle and say, I've got enough on my plate (har har) with maximizing my plant foods and "good fats". Everything I can find that suggests that it's probably not removing sat fat that decreases risk, proposes that instead it's adding n-3, vit E, and antioxidants that does the trick. So I'll do the latter and not worry about the former.

Oh, and here's the bleeding edge of cholesterol research!

"Low-density lipoproteins (LDL) are detergent-like globules which transport cholesterol and other lipids in blood. Their outer hydrophilic shell is composed mainly of phospholipids, free cholesterol, and a protein (apoB-100), while their lipophilic core contains cholesterol esters, and triglycerides. During the oxidation of LDL polyunsaturated fatty esters are transformed into reactive oxidized lipids, many of which attach themselves to the LDL protein. The resulting oxidatively modified (ox) LDL is recognized by specialized receptors on the surface of macrophage cells. Receptor recognition promotes unregulated uptake (endocytosis) of the oxLDL by the cells. Partial digestion of the damaged LDL leads to the accumulation of large quantities of cholesterol esters that coalesce into droplets giving the cells the appearance of being foam-filled. The resulting "foam cells" accumulate in the subendothelial space of artery walls leading to the formation of fatty streaks, the earliest form of atherosclerotic plaques.

Our discovery that the level of isoLG-derived modification of blood proteins is closely correlated with cardiovascular disease is consistent with a seminal role for lipid-based oxidative protein modifications in the development of atherosclerosis. Our more recent observations indicate that certain oxidized lipids themselves are also recognized and endocytized through macrophage receptors."

You'll like this, from Molecular Nutrition & Food Research Volume: 49, Issue: 11, November 2005. pp. 1050 - 1062.:

"If oxidative injury contributes to the progression of AS, lowering levels of total cholesterol may not be suff icient to prevent further oxidative injury. Iso[4]LGE2-protein adduct levels appear to signal an independent defect which results in an abnormally high level of oxidative injury that is tightly associated with AS but not with total cholesterol levels. Therapeutic interventions that specifically lower levels of iso[4]LGE2-protein adducts, e. g., antioxidants, may be beneficial."

Actualy I'm not in disagreement of that article. It points the finger of blame at oxidised, POLYUNSATUTATED LDL.

Thats one of the reasons for saturated fats being BENIFICIAL. They don't oxidise the way polyunsaturated fats do.

Also on a personal level I get lots of antioxidants in my diet. Raw animal foods and homemade sauerkraut are loaded with antioxidants.

Regards, Anthony

Actualy I'm not in disagreement of that article. It points the finger of blame at oxidised, POLYUNSATUTATED LDL.

Thats one of the reasons for saturated fats being BENIFICIAL. They don't oxidise the way polyunsaturated fats do.

Also on a personal level I get lots of antioxidants in my diet. Raw animal foods and homemade sauerkraut are loaded with antioxidants.

Regards, Anthony


raw animal foods? hope you kill your own or you have a close personal relationship with your butcher...

"Low-density lipoproteins (LDL) are detergent-like globules which transport cholesterol and other lipids in blood. Their outer hydrophilic shell is composed mainly of phospholipids, free cholesterol, and a protein (apoB-100), while their lipophilic core contains cholesterol esters, and triglycerides. During the oxidation of LDL polyunsaturated fatty esters are transformed into reactive oxidized lipids, many of which attach themselves to the LDL protein. The resulting oxidatively modified (ox) LDL is recognized by specialized receptors on the surface of macrophage cells. Receptor recognition promotes unregulated uptake (endocytosis) of the oxLDL by the cells. Partial digestion of the damaged LDL leads to the accumulation of large quantities of cholesterol esters that coalesce into droplets giving the cells the appearance of being foam-filled. The resulting "foam cells" accumulate in the subendothelial space of artery walls leading to the formation of fatty streaks, the earliest form of atherosclerotic plaques.

this is way more sciencey speak than my poor brain can handle on Friday afternoon, but isn't this the sort of contorted guesswork Malcom Kendrick was referring to? The lipid hypthesis doesn't stand on its own, so let reach and come up with ever more complicated explanations to hold it up... this is a sample of the flying buttresses on the cathederal built on the bog!

let me appl another of Malcom's points: if "foam cells" lead to atherosclerotic plaques, why don't they lead to plaques in other places in your body? it's the same tissue type, etc. etc. perhaps there are intelligent heart seaking cholestoral bombs lurking in my juicy steaks?

raw animal foods? hope you kill your own or you have a close personal relationship with your butcher...

Yes I buy from an organic butcher that I know. I'm also in Australia so a lot of grass fed beef is around even in conventional butcher stores. Valid question though as I would be concerned about the state of factory fed meat in America.

Regaring that study reference. It is pointing the finger at OXIDISED, POLYUNSATURATED lipids which is inline with the WAPF point of view. EDIT: ie, rancid, oxidised, refined polyunsaturated cooking oils are the bad fats and saturated animal fats are the good fats because they resist oxidative damage.

Regards, Anthony

Yes I buy from an organic butcher that I know. I'm also in Australia so a lot of grass fed beef is around even in conventional butcher stores. Valid question though as I would be concerned about the state of factory fed meat in America.

Regaring that study reference. It is pointing the finger at OXIDISED, POLYUNSATURATED lipids which is inline with the WAPF point of view. EDIT: ie, rancid, oxidised, refined polyunsaturated cooking oils are the bad fats and saturated animal fats are the good fats because they resist oxidative damage.

Regards, Anthony


I buy frozen grass fed beef via the internet, it gets shipped from Missouri to NYC... It's a lot safer, cleaner, more humane, etc. than feed-lot beef, but I still wouldn't eat it raw... my hat's off to ya!

r

if "foam cells" lead to atherosclerotic plaques, why don't they lead to plaques in other places in your body? it's the same tissue type, etc. etc. perhaps there are intelligent heart seaking cholestoral bombs lurking in my juicy steaks?

They do. Atherosclerosis can occur anywhere in the body. When is occurs in coronary arteries, a heart attack can result. In the brain or carotid arteries can result in a stroke. Anywhere else (i.e. legs, arms) results in some level of pain.

The lipid hypthesis doesn't stand on its own, so let reach and come up with ever more complicated explanations to hold it up... this is a sample of the flying buttresses on the cathederal built on the bog!

Kind of. More like, let's see how oxidizing lipids contribute to human disease. Oh, look, lipoprotein (as in HDL and LDL) has something to do with oxidizing lipids. Oh, look, there's this extraordinarily reactive oxidated lipid. It's so reactive, that when it reacts with low density lipoprotein, bad things happen. Like "The levels of isoLG-protein adducts present in the blood from patients with atherosclerosis are approximately double those found in healthy individuals". (Turns out you can test for heart disease pretty well by looking for those isoLG-protein adducts. And they stick around in people on cholesterol-lowering drugs too.)

So LDL is bad. And here's why. And focusing solely on lowering cholesterol (or raising HDL) might not be enough. We've got to target that oxidative species with...antioxidants.

'Least that's how I read it.

EDIT: Point being, it's mostly scientific mumbo-jumbo to me. Best I can do is recognize that there's a lot of great minds working on this subject. I don't have enough specialized medical knowledge to stay ahead of the curve on this one. All's I can do is follow the best, most commonsensical information from the most valid sources, and listen to my body.