126 replies to this topic

[warner]

I am not saying that lp(a) is unimportant. Or that it has not likely improved for you if your ldl improved. But in almost all studies ldl worsens or improves less on a high-fat diet than on a high-carbohydrate diet. The opposite for hdl and triglycerides. Of course, if you have a large weight loss, that is likely far more important than your particular diet. Short term a high-fat or high-protein diet may produce a better weight loss than a high-carbohydrate. Studies (and, yes, anecdotal evidence) suggests this. The question is the long-term effects on weight. I will shortly return to this in a separate thread regarding what the literature says.

So is 7 years not long enough, or is my life being dismissed as "anectodal evidence"?

Theories are of little value that can't explain firsthand human experience. I'm always on the lookout, for example, for cases of people who claim to have addressed their diabetes or prediabetes with a high-carb diet. However, these cases almost always turn out to be those of mild insulin resistance addressed with a switch from higher- to lower-glycemic carbs, plus some calorie reduction, and/or exercise (i.e., it's always about rate of glucose intake and oxidation). If you're truly interested in developing a comprehensive theory about this diet stuff, then sooner or later you'll have to explain any conflicting evidence, and you won't be able to brush it aside by claiming it's just "anectodal evidence".

Having witnessed the "fat causes diabetes as evidenced by rodents" fiasco, I wouldn't put any more faith in "what the literature says" than in what real life subjects and patients are saying about how various nutrients affect their health, especially those with a disease that requires them to closely monitor factors like their blood sugar and nutrient intake.

[Blue]

I am not saying that lp(a) is unimportant. Or that it has not likely improved for you if your ldl improved. But in almost all studies ldl worsens or improves less on a high-fat diet than on a high-carbohydrate diet. The opposite for hdl and triglycerides. Of course, if you have a large weight loss, that is likely far more important than your particular diet. Short term a high-fat or high-protein diet may produce a better weight loss than a high-carbohydrate. Studies (and, yes, anecdotal evidence) suggests this. The question is the long-term effects on weight. I will shortly return to this in a separate thread regarding what the literature says.

So is 7 years not long enough, or is my life being dismissed as "anectodal evidence"?

Theories are of little value that can't explain firsthand human experience. I'm always on the lookout, for example, for cases of people who claim to have addressed their diabetes or prediabetes with a high-carb diet. However, these cases almost always turn out to be those of mild insulin resistance addressed with a switch from higher- to lower-glycemic carbs, plus some calorie reduction, and/or exercise (i.e., it's always about rate of glucose intake and oxidation). If you're truly interested in developing a comprehensive theory about this diet stuff, then sooner or later you'll have to explain any conflicting evidence, and you won't be able to brush it aside by claiming it's just "anectodal evidence".

Having witnessed the "fat causes diabetes as evidenced by rodents" fiasco, I wouldn't put any more faith in "what the literature says" than in what real life subjects and patients are saying about how various nutrients affect their health, especially those with a disease that requires them to closely monitor factors like their blood sugar and nutrient intake.

Yes, personal claims on a web forum is anonymous, anecdotal evidence.

If we should go by anecdotal evidence then homeopathy works. Just read the reviews of homeopathic supplements on iHerb.

Typ II diabetes likely improves greatly if you can achieve and maintain significant weight loss regardless of the diet used. I posted a number of reviews of macro diet and weight loss in another thread. They do not agree, but even those that are positive do not find a dramatically better weight loss on a low-carbohydrate diet. But if it works dramatically in you case, then do continue.

[rwac]

If we should go by anecdotal evidence then homeopathy works. Just read the reviews of homeopathic supplements on iHerb.

The issue there is that "homeopathic" supplements often have non-homeopathic herbal components.
So although the science behind homeopathy is rubbish, certain "homeopathic" remedies can actually work.

[Blue]

If we should go by anecdotal evidence then homeopathy works. Just read the reviews of homeopathic supplements on iHerb.

The issue there is that "homeopathic" supplements often have non-homeopathic herbal components.
So although the science behind homeopathy is rubbish, certain "homeopathic" remedies can actually work.

In some cases, yes. But there are many positive reviews also for those with only homeopathic ingredients.

[JLL]

But in almost all studies ldl worsens or improves less on a high-fat diet than on a high-carbohydrate diet.

I assume that by "LDL worsens or improves less" you mean that LDL either goes up or decreases less than it does on a high-carb diet.

But is higher LDL really worse? As far as I know, the only evidence we have shows that the LDL/HDL ratio positively correlates with CHD, but that's it. This doesn't prove that there isn't some third factor involved. On the contrary, we have some evidence showing that the LDL/HDL ratio by itself is less important than the type of LDL -- that it's the smaller, oxidized form of LDL that causes atherosclerosis.

And while high-fat diets generally do increase LDL, they do not necessarily increase the LDL/HDL ratio -- whereas high-carbohydrates sometimes do -- and that they generally increase the number of large, not small LDL particles. Diets high in carbohydrate, on the other hand, tend to decrease both LDL and HDL, sometimes so that the ratio becomes higher, and the percentage of small LDL particles increases.

All in all, while "a high-fat diet worsens LDL" seems like a simple statement, it's much more complicated than that.

[Blue]

But in almost all studies ldl worsens or improves less on a high-fat diet than on a high-carbohydrate diet.

I assume that by "LDL worsens or improves less" you mean that LDL either goes up or decreases less than it does on a high-carb diet.

But is higher LDL really worse? As far as I know, the only evidence we have shows that the LDL/HDL ratio positively correlates with CHD, but that's it. This doesn't prove that there isn't some third factor involved. On the contrary, we have some evidence showing that the LDL/HDL ratio by itself is less important than the type of LDL -- that it's the smaller, oxidized form of LDL that causes atherosclerosis.

And while high-fat diets generally do increase LDL, they do not necessarily increase the LDL/HDL ratio -- whereas high-carbohydrates sometimes do -- and that they generally increase the number of large, not small LDL particles. Diets high in carbohydrate, on the other hand, tend to decrease both LDL and HDL, sometimes so that the ratio becomes higher, and the percentage of small LDL particles increases.

All in all, while "a high-fat diet worsens LDL" seems like a simple statement, it's much more complicated than that.

The standard claims from the paleo blogs. Which as mentioned earlier do not reflect the scientific evidence.

Regarding what blood lipid variables do are important see this Consenus Report From the American Diabetes Association and the American College of Cardiology Foundation
http://content.onlin...acc.2008.02.034

"A large body of research, ranging from molecular to population studies, indicates that elevated LDL cholesterol is a major predictor of CVD, including in populations with CMR or diabetes... ....In addition to the robust data indicating the usefulness of LDL cholesterol as a predictor of CVD in individuals with diabetes, there are a number of large randomized controlled trials that have established that lowering LDL cholesterol in individuals with diabetes or with multiple cardiovascular risk factors lowers CVD event rates for both primary and secondary prevention."

"The size of LDL particles can also be measured. As small dense LDL particles seem to be particularly atherogenic, assessment of particle size has intuitive appeal. Both LDL particle concentration and LDL size are important predictors of CVD. However, the Multi-Ethnic Study of Atherosclerosis suggested that on multivariate analyses, both small and large LDL were strongly associated with carotid intima-media thickness , while the Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial (VA-HIT) showed that both were significantly related to coronary heart disease (CHD) events. The association of small LDL and CVD may simply reflect the increased number of LDL particles in patients with small LDL. Hence, it is unclear whether LDL particle size measurements add value to measurement of LDL particle concentration."

Edited by Blue, 29 November 2009 - 12:14 PM.

[JLL]

Well, a quote that says "a large body of research -- indicates that elevated LDL cholesterol is a major predictor of CVD", consensus report or not, does not prove anything by itself. What exactly are the studies that show LDL causes CVD?

That some claim appears in a paleo blog does not mean it's false (nor does it mean it's true).

EDIT: And the statin studies don't prove that lowering LDL is the key; it may, again, be that LDL is only a surrogate marker for another, more profound effect.

Edited by JLL, 29 November 2009 - 03:48 PM.

[Blue]

Well, a quote that says "a large body of research -- indicates that elevated LDL cholesterol is a major predictor of CVD", consensus report or not, does not prove anything by itself. What exactly are the studies that show LDL causes CVD?

That some claim appears in a paleo blog does not mean it's false (nor does it mean it's true).

EDIT: And the statin studies don't prove that lowering LDL is the key; it may, again, be that LDL is only a surrogate marker for another, more profound effect.

There are lots of other studies mentioned in the sections "Central Role of LDL in Atherogenesis" and "LDL cholesterol".

[oehaut]

Isn't it weird that in somes studies with fish oil, LDL goes up and motality goes down? http://www.ncbi.nlm....mp;ordinalpos=6


I have not reviewed the litterature on the subject, and I have not yet read the paper that you cited Blue, but i'm at least aware of that study which found a good relation between small LDL and CVD.

I think it's more important to concentrate on the Pattern B than on small LDL per se. But it seems like ppl with small LDL have usually low HDL and high TG. That is obviously a disaster.

I'm just wondering. If LDL were that much of a great risk marker, and if saturated fat were that bad, they would always end up with making things worst. Yet in many studies the link is far from being evident. (just look at the some i've posted before, ok they might not be all that good quality papers, and yes there can be some confounding facters, but c'mon, let's stop trying to find excuses)

I think it's just normal to be skeptic when the results are not clearly pointing at them as risk factor.

I think telling someone to eat margarine instead of butter because of the sat fat content is not helping him. I don't think telling someone to avoid high-quality meat because of the sat fat content and to replace that with lentille is not helping them, at least not ppl with insulin resistance issue and weight probleme.

I really don't think that under a calorie control diet, with regular physical activity, tonz of vegetable, sat fat per se can be bad. I think people should worry much more about how much they eat before worrying about how much sat fat they eat.

When the basic are setttle, then I think it really come down to be pretty individual. We know that there are high-fat phenotype and high-carbs phenotype. Try something, have your blood test done, if everything is fine I think you have the answer.

I'm really far from being done reviewing most of the studies out there, but i'm doing it slowly. So far I can't seems to be convince that sat fat are bad and that LDL-C is that much of a great risk markers.

Since about everybody now consider CVD as an inflammatory response, I'm hoping they will spend more time looking at inflammatory markers than lipids marker, or at least both. It seems pretty rare that someone has is CRP levels tested.

Here are my points to consider :

1. There's population eating a lot of sat fat that don't have much CVD (ok this might not be a very strong argument)
2. We have primary controlled trial which didn't find any benefits from cutting sat fat.
3. We have prospective cohort studies which didnt find any benefits from cutting sat fat.
4. We know that mother's milk is full of sat fat - just makes one wonders.
5. When on a very high-carb, the body starts making palmitic acid out of it - just makes one wonder.
6. Stearic acid shows and inverse relationship with CVD.

So, with all those contradiction, isn't normal to be in doubt?

[Blue]

Isn't it weird that in somes studies with fish oil, LDL goes up and motality goes down? http://www.ncbi.nlm....mp;ordinalpos=6


I have not reviewed the litterature on the subject, and I have not yet read the paper that you cited Blue, but i'm at least aware of that study which found a good relation between small LDL and CVD.

No mention of LDL in the first link.

As stated in the consensus paper, the association between LDL size and CVD likely is incorrect. Small LDL particles likely is not more dangerous than large LDL particles. However, small LDL may often be associated with increased numbers of LDL particles which may be what is dangerous. If anyone know a study regarding if a high-fat diet will increase or decrease LDL number, then please post a link.

Regarding saturated fats, see
http://www.imminst.o...o...=33878&st=0
http://www.imminst.o...o...st&p=357858

Edited by Blue, 29 November 2009 - 05:42 PM.

[Blue]

To sum up blood lipid changes from a low carbohydrate diets they include lower triglycerides and higher HDL which is good. There is also a tendency compared to high carbohydrate diet towards higher LDL (weight per volume). On the other hand LDL particle size may be higher so how LDL particle number per volume, which may be the most important LDL variable, will actually change is unclear. If LDL number does not change then the other lipid changes would advocate for a low carbohydrate diet.

Edited by Blue, 29 November 2009 - 05:52 PM.

[oehaut]

Isn't it weird that in somes studies with fish oil, LDL goes up and motality goes down? http://www.ncbi.nlm....mp;ordinalpos=6


I have not reviewed the litterature on the subject, and I have not yet read the paper that you cited Blue, but i'm at least aware of that study which found a good relation between small LDL and CVD.

No mention of LDL in the first link.

As stated in the consensus paper, the association between LDL size and CVD likely is incorrect. Small LDL particles likely is not more dangerous than large LDL particles. However, small LDL may often be associated with increased numbers of LDL particles which may be what is dangerous. If anyone know a study regarding if a high-fat diet will increase or decrease LDL number, then please post a link.

Regarding saturated fats, see
http://www.imminst.o...o...=33878&st=0
http://www.imminst.o...o...st&p=357858

BACKGROUND: Epidemiologic studies, studies of mechanisms of action, and many animal studies indicate that dietary intake of omega-3 fatty acids has antiatherosclerotic potential. Few trials in humans have examined this potential. OBJECTIVE: To determine the effect of dietary intake of omega-3 fatty acids on the course of coronary artery atherosclerosis in humans. DESIGN: Randomized, double-blind, placebo-controlled, clinically controlled trial. SETTING: University preventive cardiology unit. PATIENTS: 223 patients with angiographically proven coronary artery disease. INTERVENTION: Fish oil concentrate (55% eicosapentaenoic and docosahexaenoic acids) or a placebo with a fatty acid composition resembling that of the average European diet, 6 g/d for 3 months and then 3 g/d for 21 months. MEASUREMENTS: The results of standardized coronary angiography, done before and after 2 years of treatment, were evaluated by an expert panel (primary end point) and by quantitative coronary angiography. Patients were followed for clinical and laboratory status. RESULTS: Pairs of angiograms (one taken at baseline and one taken at 2 years) were evaluated for 80 of 112 placebo recipients and 82 of 111 fish oil recipients. At the end of treatment, 48 coronary segments in the placebo group showed changes (36 showed mild progression, 5 showed moderate progression, and 7 showed mild regression) and 55 coronary segments in the fish oil group showed changes (35 showed mild progression, 4 showed moderate progression, 14 showed mild regression, and 2 showed moderate regression) (P = 0.041). Loss in minimal luminal diameter, as assessed by quantitative coronary angiography, was somewhat less in the fish oil group (P > 0.1). Fish oil recipients had fewer cardiovascular events (P = 0.10); other clinical variables did not differ between the study groups. Low-density lipoprotein cholesterol levels tended to be greater in the fish oil group. CONCLUSION: Dietary intake of omega-3 fatty acids modestly mitigates the course of coronary atherosclerosis in humans.

[Blue]

Isn't it weird that in somes studies with fish oil, LDL goes up and motality goes down? http://www.ncbi.nlm....mp;ordinalpos=6


I have not reviewed the litterature on the subject, and I have not yet read the paper that you cited Blue, but i'm at least aware of that study which found a good relation between small LDL and CVD.

No mention of LDL in the first link.

As stated in the consensus paper, the association between LDL size and CVD likely is incorrect. Small LDL particles likely is not more dangerous than large LDL particles. However, small LDL may often be associated with increased numbers of LDL particles which may be what is dangerous. If anyone know a study regarding if a high-fat diet will increase or decrease LDL number, then please post a link.

Regarding saturated fats, see
http://www.imminst.o...o...=33878&st=0
http://www.imminst.o...o...st&p=357858

BACKGROUND: Epidemiologic studies, studies of mechanisms of action, and many animal studies indicate that dietary intake of omega-3 fatty acids has antiatherosclerotic potential. Few trials in humans have examined this potential. OBJECTIVE: To determine the effect of dietary intake of omega-3 fatty acids on the course of coronary artery atherosclerosis in humans. DESIGN: Randomized, double-blind, placebo-controlled, clinically controlled trial. SETTING: University preventive cardiology unit. PATIENTS: 223 patients with angiographically proven coronary artery disease. INTERVENTION: Fish oil concentrate (55% eicosapentaenoic and docosahexaenoic acids) or a placebo with a fatty acid composition resembling that of the average European diet, 6 g/d for 3 months and then 3 g/d for 21 months. MEASUREMENTS: The results of standardized coronary angiography, done before and after 2 years of treatment, were evaluated by an expert panel (primary end point) and by quantitative coronary angiography. Patients were followed for clinical and laboratory status. RESULTS: Pairs of angiograms (one taken at baseline and one taken at 2 years) were evaluated for 80 of 112 placebo recipients and 82 of 111 fish oil recipients. At the end of treatment, 48 coronary segments in the placebo group showed changes (36 showed mild progression, 5 showed moderate progression, and 7 showed mild regression) and 55 coronary segments in the fish oil group showed changes (35 showed mild progression, 4 showed moderate progression, 14 showed mild regression, and 2 showed moderate regression) (P = 0.041). Loss in minimal luminal diameter, as assessed by quantitative coronary angiography, was somewhat less in the fish oil group (P > 0.1). Fish oil recipients had fewer cardiovascular events (P = 0.10); other clinical variables did not differ between the study groups. Low-density lipoprotein cholesterol levels tended to be greater in the fish oil group. CONCLUSION: Dietary intake of omega-3 fatty acids modestly mitigates the course of coronary atherosclerosis in humans.

Missed that. Note that the change in cardiovascular events was not statistically significant. The results can interpreted in several ways. Those advocating for that LDL is important may argue that it was the rise in LDL that caused the fish oil supplementation to not be beneficial because the higher blood omega-3 was offset by the higher blood LDL.

Edited by Blue, 29 November 2009 - 06:04 PM.

[oehaut]

Isn't it weird that in somes studies with fish oil, LDL goes up and motality goes down? http://www.ncbi.nlm....mp;ordinalpos=6


I have not reviewed the litterature on the subject, and I have not yet read the paper that you cited Blue, but i'm at least aware of that study which found a good relation between small LDL and CVD.

No mention of LDL in the first link.

As stated in the consensus paper, the association between LDL size and CVD likely is incorrect. Small LDL particles likely is not more dangerous than large LDL particles. However, small LDL may often be associated with increased numbers of LDL particles which may be what is dangerous. If anyone know a study regarding if a high-fat diet will increase or decrease LDL number, then please post a link.

Regarding saturated fats, see
http://www.imminst.o...o...=33878&st=0
http://www.imminst.o...o...st&p=357858

BACKGROUND: Epidemiologic studies, studies of mechanisms of action, and many animal studies indicate that dietary intake of omega-3 fatty acids has antiatherosclerotic potential. Few trials in humans have examined this potential. OBJECTIVE: To determine the effect of dietary intake of omega-3 fatty acids on the course of coronary artery atherosclerosis in humans. DESIGN: Randomized, double-blind, placebo-controlled, clinically controlled trial. SETTING: University preventive cardiology unit. PATIENTS: 223 patients with angiographically proven coronary artery disease. INTERVENTION: Fish oil concentrate (55% eicosapentaenoic and docosahexaenoic acids) or a placebo with a fatty acid composition resembling that of the average European diet, 6 g/d for 3 months and then 3 g/d for 21 months. MEASUREMENTS: The results of standardized coronary angiography, done before and after 2 years of treatment, were evaluated by an expert panel (primary end point) and by quantitative coronary angiography. Patients were followed for clinical and laboratory status. RESULTS: Pairs of angiograms (one taken at baseline and one taken at 2 years) were evaluated for 80 of 112 placebo recipients and 82 of 111 fish oil recipients. At the end of treatment, 48 coronary segments in the placebo group showed changes (36 showed mild progression, 5 showed moderate progression, and 7 showed mild regression) and 55 coronary segments in the fish oil group showed changes (35 showed mild progression, 4 showed moderate progression, 14 showed mild regression, and 2 showed moderate regression) (P = 0.041). Loss in minimal luminal diameter, as assessed by quantitative coronary angiography, was somewhat less in the fish oil group (P > 0.1). Fish oil recipients had fewer cardiovascular events (P = 0.10); other clinical variables did not differ between the study groups. Low-density lipoprotein cholesterol levels tended to be greater in the fish oil group. CONCLUSION: Dietary intake of omega-3 fatty acids modestly mitigates the course of coronary atherosclerosis in humans.

Missed that. Note that the change in cardiovascular events was not statistically significant. The results can interpreted in several ways. Those advocating for that LDL is important may argue that it was the rise in LDL that caused the fish oil supplementation to not be beneficial because the higher blood omega-3 was offset by the higher blood LDL.

That's an intresting way of seeing it. Still, in the paper, the authors stated:

Levels of LDL cholesterol were, at
times, significantly greater in the fish oil group than
in the placebo group (Table 3). On average, fish oil
increases LDL cholesterol levels by 4% in healthy
persons and 7% in hypertriglyceridemic patients
(33). Unlike findings in all other similar studies
(26), this finding clearly implies mechanisms of action
other than LDL cholesterol lowering.

So, if the fish oil raise LDL and decrease CVD, there as to be another mechanism at work, as they say. And that put a question mark on the role of LDL-C in CVD.

Note that i'm not denying LDL-C as a risk factor, i'm just wondering if it's causative or a by product of something else.

Could it be that high LDL-C is dangerous if you're in a pro-oxidant environment?

What if you have high LDL-C but it doesnt get oxidized?

What if you have low LDL-C but it gets oxidized?

Wouldn't that explain the fact that some ppl have low LDL and still get CVD, while some have high LDL and dont have it?

[warner]

Regarding what blood lipid variables do are important see this Consenus Report From the American Diabetes Association

The first thing many diabetics figure out is that the American Diabetes Association (ADA) has a pro-low-fat, high-carb point of view, and cannot be trusted to give sound advice, or to present an objective view of research results.

A great example of this is their wacko contention that because diabetics on high-carb diets maintain slightly greater insulin sensitivity than those on low-carb diets, that this means that high-carb diets are preferred. This is wacko since it misses the point that diabetics on high-carb diets have much higher blood glucose levels to deal with, meaning any advantange they have in being slightly more insulin sensitive is overwhelmed by all the damage done by the higher blood sugar levels. (There's also speculation now that the slightly lower insulin sensitivity on a low-carb diet is simply the body's way of preserving blood glucose for the brain when on a low-carb diet.)

There are endless stories out there of diabetics getting screwed (i.e., poor blood sugar control) by the ADA.

Edited by warner, 29 November 2009 - 06:57 PM.

[oehaut]

Regarding what blood lipid variables do are important see this Consenus Report From the American Diabetes Association

The first thing many diabetics figure out is that the American Diabetes Association (ADA) has a pro-low-fat, high-carb point of view, and cannot be trusted to give sound advice, or to present an objective view of research results.

A great example of this is their wacko contention that because diabetics on high-carb diets maintain slightly greater insulin sensitivity than those on low-carb diets, that this means that high-carb diets are preferred. This is wacko since it misses the point that diabetics on high-carb diets have much higher blood glucose levels to deal with, meaning any advantange they have in being slightly more insulin sensitive is overwhelmed by all the damage done by the higher blood sugar levels. (There's also speculation now that the slightly lower insulin sensitivity on a low-carb diet is simply the body's way of preserving blood glucose for the brain when on a low-carb diet.)

There are endless stories out there of diabetics getting screwed (i.e., poor blood sugar control) by the ADA.

Seeing these ADA financial partners, it's not hard to understand that they are pro low-fat, high carbs.

Damn, Pepsi, Coca-cola and Kellog's! Wow, how healthy is that?

http://www.beveragei.....08~ Final.pdf

CHICAGO–The American Dietetic Association, the nation’s largest organization of food and nutrition professionals, announced March 1 that The Coca-Cola Company has become an ADA Partner in the Association’s corporate relations sponsorship program.The program provides Partners a national platform via ADA events and programs with prominent access to key influencers, thought leaders and decision makers in the food and nutrition market place.

So coca-cola has now prominent access to key influencers, thought leader and decision makers in the food and nutrition market place thanks to the ADA!

Not that the ADA should not be trust, but I think everything they say should be consier in the light of their financial ties.

Edited by oehaut, 29 November 2009 - 07:10 PM.

[warner]

Yes, personal claims on a web forum is anonymous, anecdotal evidence.
If we should go by anecdotal evidence then homeopathy works. Just read the reviews of homeopathic supplements on iHerb.

You won't find salvation in the "literature" (or "experts", or groups of experts, etc.). Both the literature and first-hand accounts need to be examined for authenticity, honesty, hidden agendas, etc. If I'm talking to a close friend about his diet, for example, I would put much higher faith in that than any published literature (unless I witnessed the research first-hand). Personal accounts on the internet must be judged like any other evidence. For example, I trust the long-term posters on the Bernstein Forum based on my prolonged interaction with them, and the agreement of their accounts with a wide range of other sources of information. But I don't have much to say about the accounts of homeopathy.

I don't automatically discard any sources of info, and expect that any compreshensive theory of diet/metabolism would be able to address all the individual cases out there. If it didn't, then that would be the definition of an inadequate theory.

[Blue]

Isn't it weird that in somes studies with fish oil, LDL goes up and motality goes down? http://www.ncbi.nlm....mp;ordinalpos=6


I have not reviewed the litterature on the subject, and I have not yet read the paper that you cited Blue, but i'm at least aware of that study which found a good relation between small LDL and CVD.

No mention of LDL in the first link.

As stated in the consensus paper, the association between LDL size and CVD likely is incorrect. Small LDL particles likely is not more dangerous than large LDL particles. However, small LDL may often be associated with increased numbers of LDL particles which may be what is dangerous. If anyone know a study regarding if a high-fat diet will increase or decrease LDL number, then please post a link.

Regarding saturated fats, see
http://www.imminst.o...o...=33878&st=0
http://www.imminst.o...o...st&p=357858

BACKGROUND: Epidemiologic studies, studies of mechanisms of action, and many animal studies indicate that dietary intake of omega-3 fatty acids has antiatherosclerotic potential. Few trials in humans have examined this potential. OBJECTIVE: To determine the effect of dietary intake of omega-3 fatty acids on the course of coronary artery atherosclerosis in humans. DESIGN: Randomized, double-blind, placebo-controlled, clinically controlled trial. SETTING: University preventive cardiology unit. PATIENTS: 223 patients with angiographically proven coronary artery disease. INTERVENTION: Fish oil concentrate (55% eicosapentaenoic and docosahexaenoic acids) or a placebo with a fatty acid composition resembling that of the average European diet, 6 g/d for 3 months and then 3 g/d for 21 months. MEASUREMENTS: The results of standardized coronary angiography, done before and after 2 years of treatment, were evaluated by an expert panel (primary end point) and by quantitative coronary angiography. Patients were followed for clinical and laboratory status. RESULTS: Pairs of angiograms (one taken at baseline and one taken at 2 years) were evaluated for 80 of 112 placebo recipients and 82 of 111 fish oil recipients. At the end of treatment, 48 coronary segments in the placebo group showed changes (36 showed mild progression, 5 showed moderate progression, and 7 showed mild regression) and 55 coronary segments in the fish oil group showed changes (35 showed mild progression, 4 showed moderate progression, 14 showed mild regression, and 2 showed moderate regression) (P = 0.041). Loss in minimal luminal diameter, as assessed by quantitative coronary angiography, was somewhat less in the fish oil group (P > 0.1). Fish oil recipients had fewer cardiovascular events (P = 0.10); other clinical variables did not differ between the study groups. Low-density lipoprotein cholesterol levels tended to be greater in the fish oil group. CONCLUSION: Dietary intake of omega-3 fatty acids modestly mitigates the course of coronary atherosclerosis in humans.

Missed that. Note that the change in cardiovascular events was not statistically significant. The results can interpreted in several ways. Those advocating for that LDL is important may argue that it was the rise in LDL that caused the fish oil supplementation to not be beneficial because the higher blood omega-3 was offset by the higher blood LDL.

That's an intresting way of seeing it. Still, in the paper, the authors stated:

Levels of LDL cholesterol were, at
times, significantly greater in the fish oil group than
in the placebo group (Table 3). On average, fish oil
increases LDL cholesterol levels by 4% in healthy
persons and 7% in hypertriglyceridemic patients
(33). Unlike findings in all other similar studies
(26), this finding clearly implies mechanisms of action
other than LDL cholesterol lowering.

So, if the fish oil raise LDL and decrease CVD, there as to be another mechanism at work, as they say. And that put a question mark on the role of LDL-C in CVD.

Note that i'm not denying LDL-C as a risk factor, i'm just wondering if it's causative or a by product of something else.

Could it be that high LDL-C is dangerous if you're in a pro-oxidant environment?

What if you have high LDL-C but it doesnt get oxidized?

What if you have low LDL-C but it gets oxidized?

Wouldn't that explain the fact that some ppl have low LDL and still get CVD, while some have high LDL and dont have it?

Again, in this study fish oil caused at most a weak, usually not significant, effect on CVD. Fish oil is known to have many other "mechanisms", such as decreasing triglycerides, and omega-3 fats are likely has an anti-inflammatory effect. So why was not the anti-CVD effect greater? Maybe because the bad LDL offset the good other effects. So this study certainly does not mean that LDL is proved not be harmful.

You seem to misunderstand what a risk factor means. It means increased risk of disease, not that you must get a disease.

Edited by Blue, 30 November 2009 - 03:39 PM.

[Blue]

Yes, personal claims on a web forum is anonymous, anecdotal evidence.
If we should go by anecdotal evidence then homeopathy works. Just read the reviews of homeopathic supplements on iHerb.

You won't find salvation in the "literature" (or "experts", or groups of experts, etc.). Both the literature and first-hand accounts need to be examined for authenticity, honesty, hidden agendas, etc. If I'm talking to a close friend about his diet, for example, I would put much higher faith in that than any published literature (unless I witnessed the research first-hand). Personal accounts on the internet must be judged like any other evidence. For example, I trust the long-term posters on the Bernstein Forum based on my prolonged interaction with them, and the agreement of their accounts with a wide range of other sources of information. But I don't have much to say about the accounts of homeopathy.

I don't automatically discard any sources of info, and expect that any compreshensive theory of diet/metabolism would be able to address all the individual cases out there. If it didn't, then that would be the definition of an inadequate theory.

If trusting anonymous web stories above published research, then further discussion is likely pointless. Why bother discussing here if you already know THE TRUTH and contrary scientific research is irrelevant/falsified/part of a conspiracy?

[oehaut]

Isn't it weird that in somes studies with fish oil, LDL goes up and motality goes down? http://www.ncbi.nlm....mp;ordinalpos=6


I have not reviewed the litterature on the subject, and I have not yet read the paper that you cited Blue, but i'm at least aware of that study which found a good relation between small LDL and CVD.

No mention of LDL in the first link.

As stated in the consensus paper, the association between LDL size and CVD likely is incorrect. Small LDL particles likely is not more dangerous than large LDL particles. However, small LDL may often be associated with increased numbers of LDL particles which may be what is dangerous. If anyone know a study regarding if a high-fat diet will increase or decrease LDL number, then please post a link.

Regarding saturated fats, see
http://www.imminst.o...o...=33878&st=0
http://www.imminst.o...o...st&p=357858

BACKGROUND: Epidemiologic studies, studies of mechanisms of action, and many animal studies indicate that dietary intake of omega-3 fatty acids has antiatherosclerotic potential. Few trials in humans have examined this potential. OBJECTIVE: To determine the effect of dietary intake of omega-3 fatty acids on the course of coronary artery atherosclerosis in humans. DESIGN: Randomized, double-blind, placebo-controlled, clinically controlled trial. SETTING: University preventive cardiology unit. PATIENTS: 223 patients with angiographically proven coronary artery disease. INTERVENTION: Fish oil concentrate (55% eicosapentaenoic and docosahexaenoic acids) or a placebo with a fatty acid composition resembling that of the average European diet, 6 g/d for 3 months and then 3 g/d for 21 months. MEASUREMENTS: The results of standardized coronary angiography, done before and after 2 years of treatment, were evaluated by an expert panel (primary end point) and by quantitative coronary angiography. Patients were followed for clinical and laboratory status. RESULTS: Pairs of angiograms (one taken at baseline and one taken at 2 years) were evaluated for 80 of 112 placebo recipients and 82 of 111 fish oil recipients. At the end of treatment, 48 coronary segments in the placebo group showed changes (36 showed mild progression, 5 showed moderate progression, and 7 showed mild regression) and 55 coronary segments in the fish oil group showed changes (35 showed mild progression, 4 showed moderate progression, 14 showed mild regression, and 2 showed moderate regression) (P = 0.041). Loss in minimal luminal diameter, as assessed by quantitative coronary angiography, was somewhat less in the fish oil group (P > 0.1). Fish oil recipients had fewer cardiovascular events (P = 0.10); other clinical variables did not differ between the study groups. Low-density lipoprotein cholesterol levels tended to be greater in the fish oil group. CONCLUSION: Dietary intake of omega-3 fatty acids modestly mitigates the course of coronary atherosclerosis in humans.

Missed that. Note that the change in cardiovascular events was not statistically significant. The results can interpreted in several ways. Those advocating for that LDL is important may argue that it was the rise in LDL that caused the fish oil supplementation to not be beneficial because the higher blood omega-3 was offset by the higher blood LDL.

That's an intresting way of seeing it. Still, in the paper, the authors stated:

Levels of LDL cholesterol were, at
times, significantly greater in the fish oil group than
in the placebo group (Table 3). On average, fish oil
increases LDL cholesterol levels by 4% in healthy
persons and 7% in hypertriglyceridemic patients
(33). Unlike findings in all other similar studies
(26), this finding clearly implies mechanisms of action
other than LDL cholesterol lowering.

So, if the fish oil raise LDL and decrease CVD, there as to be another mechanism at work, as they say. And that put a question mark on the role of LDL-C in CVD.

Note that i'm not denying LDL-C as a risk factor, i'm just wondering if it's causative or a by product of something else.

Could it be that high LDL-C is dangerous if you're in a pro-oxidant environment?

What if you have high LDL-C but it doesnt get oxidized?

What if you have low LDL-C but it gets oxidized?

Wouldn't that explain the fact that some ppl have low LDL and still get CVD, while some have high LDL and dont have it?

Again, in this study fish oil caused at most a weak, usually not significant, effect on CVD. Fish oil is known to have many other "mechanisms", such as decreasing triglycerides, and omega-3 fats are likely has an anti-inflammatory effect. So why was not the anti-CVD effect greater? Maybe because the bad LDL offset the good other effects. So this study certainly does not mean that LDL is proved not be harmful.

You seem to misunderstand what a risk factor means. It means increased risk of disease, not that you must get a disease.

I think that you are right. Tho I didn't post it to show that LDL was not a concern, simply because it was a weird observation to see an increase in LDL and a decrease in mortality. But you're right, the mortality decrease might have been bigger if LDL had not been high at all. We can't say for sure tho.

May I ask you what you think of the hypothesis of ox-LDL? Wouldn't that make more sens than simply LDL as being the problem?

Obviously if you have high LDL it has more chance of being ox so that would be a logical connection here.

Because I have never read any mechanistic paper on how LDL by itself could be a problem. It always implicate some modification of it, ox-LDL being the most frequent.

[HaloTeK]

When Cordain was researching HG cholesterol levels, most of them were in the 100 to 150 range. Are we just going to dismiss his work?

Here's the paper: http://www.thepaleod...C LDL Final.pdf

Many high fat (and saturated) paleo types or Atkins-types have cholesterol in the 200-280 range. I've seen people with 100+ HDL and 180 LDL and they proclaim themselves heart-attack proof <------ how about BULLS**T!

Even if some HG groups ate a decent amount of saturated fat, something in their diet or infection (or otherwise) was causing their TC to dip to low ranges. Maybe this alone was why most HG groups did not have heart disease. We sure know they weren't dying of cancer/depression etc from the low TC.

There are HG groups with high inflammation in South America with low TC that don't get heart disease -- so we know TC is a factor all on its own.

Until we know otherwise -- I'd view high LDL with high HDL as suspect.

Monounsaturates still seem pretty neutral in my opinion.

Edited by HaloTeK, 30 November 2009 - 09:13 PM.

[Sillewater]

Could it be the fasting that lowers TC. Why do people who do CRON have such low cholesterol?

[JLL]

Could it be the fasting that lowers TC. Why do people who do CRON have such low cholesterol?

If you're on any kind of serious CRON, you can't eat much saturated fat. Too dense in calories.

[Highlander]

Could it be the fasting that lowers TC. Why do people who do CRON have such low cholesterol?

It sounds corresponding at least to my experience: I was surprised to discover my TC on 280 level after 1 year on Atkins(low-carb, high proteins) type of diet...now I have managed to decrease it dramatically only after lowering proteins (more fruits) + intermittent fasting. Though no doubt that Atkins performs well in weight loss task...

Edited by Highlander, 01 December 2009 - 10:01 AM.

[warner]

If trusting anonymous web stories above published research, then further discussion is likely pointless. Why bother discussing here if you already know THE TRUTH and contrary scientific research is irrelevant/falsified/part of a conspiracy?

I didn't say anything about "irrelevant/falsified/part of a conspiracy" or about knowing "THE TRUTH" or about trusting "anonymous web stories".

It's just extemely naive on your part to be so trusting of a scientific abstract, while so untrusting of all first-hand accounts, esp. from people who have proven themselves to be trustworthy.

The ideal of science is one thing, the practice is another. Peer-reviewed science performed by scientists attempting to follow the scientific method is extremely valuable, but isn't the only source of "truth", nor can it easily escape our non-scientific tendencies. The reporting of corporate-based science, for example, is often compromised by corporate interests, while academics are typically caught spending much of their time chasing funding. And people are doing science for a lot of non-scientific reasons: fame, money, etc. So what comes out of all that needs to be met with a healthy dose of skepticism, which is the scientific thing to do.

But you're right about one thing, it's probably a waste of time discussing this with you.

[TheFountain]

Could it be the fasting that lowers TC. Why do people who do CRON have such low cholesterol?

If you're on any kind of serious CRON, you can't eat much saturated fat. Too dense in calories.

I thought lowering total cholesterol didn't mean as much as lowering the LDL to HDL ratio. So what is the current consensus on total cholesterol vs LDL?

[Skötkonung]

Could it be the fasting that lowers TC. Why do people who do CRON have such low cholesterol?

If you're on any kind of serious CRON, you can't eat much saturated fat. Too dense in calories.

I thought lowering total cholesterol didn't mean as much as lowering the LDL to HDL ratio. So what is the current consensus on total cholesterol vs LDL?

I'm of the impression that lowering total cholesterol is just as important as changing the ratio.

Simplistically speaking, cholesterol is sent to areas damaged by inflammation because it is a major component of our cellular structures and is needed for repair. LDL brings the cholesterol to the damage site and HDL retrieves it. If you have more LDL as compared to HDL, you will be leaving more lipid at the damage site to become oxidized and create plaque. If you have high cholesterol, even if your HDL is high in respect to your LDL, it is still an indicator of inflammation. Same with LDL particle size.

At least that is my understanding of the situation.

Edited by Skotkonung, 01 December 2009 - 09:20 PM.

[kismet]

It's just extemely naive on your part to be so trusting of a scientific abstract, while so untrusting of all first-hand accounts, esp. from people who have proven themselves to be trustworthy.

While you are right that it is naive, or maybe more exactly, intelectually dishonest to use abstracts (and not full papers or better yet the totality of evidence) to arrive at a strong conclusion you should forget first-hand accounts. There is no such thing like a reliable first hand account. Everyone is subject to cognitive and statistical bias. Everyone is subject to the placebo effect. Everyone is human. And we're all slaves to statistics (do you think the bull curve, including the SD, applies to everyone but you and your measurements?).

Thus even well-controlled case-reports, i.e. a level of evidence much higher than anecdotes, are inherently unreliable. Sometimes we're forced to use such weak evidence, but preferably, no.

Edited by kismet, 01 December 2009 - 10:26 PM.

[JLL]

I'm of the impression that lowering total cholesterol is just as important as changing the ratio.

Simplistically speaking, cholesterol is sent to areas damaged by inflammation because it is a major component of our cellular structures and is needed for repair. LDL brings the cholesterol to the damage site and HDL retrieves it. If you have more LDL as compared to HDL, you will be leaving more lipid at the damage site to become oxidized and create plaque. If you have high cholesterol, even if your HDL is high in respect to your LDL, it is still an indicator of inflammation. Same with LDL particle size.

At least that is my understanding of the situation.

I disagree with this view. If the above were true, then LDL/HDL ratio would not be more strongly associated with CVD than LDL. And not all lipids are oxidized at the same rate.

[Skötkonung]

I'm of the impression that lowering total cholesterol is just as important as changing the ratio.

Simplistically speaking, cholesterol is sent to areas damaged by inflammation because it is a major component of our cellular structures and is needed for repair. LDL brings the cholesterol to the damage site and HDL retrieves it. If you have more LDL as compared to HDL, you will be leaving more lipid at the damage site to become oxidized and create plaque. If you have high cholesterol, even if your HDL is high in respect to your LDL, it is still an indicator of inflammation. Same with LDL particle size.

At least that is my understanding of the situation.

I disagree with this view. If the above were true, then LDL/HDL ratio would not be more strongly associated with CVD than LDL. And not all lipids are oxidized at the same rate.

There has also been noted a correspondence between higher triglyceride levels and higher levels of smaller, denser LDL particles and alternately lower triglyceride levels and higher levels of the larger, less dense LDL.

Small LDL and its clinical importance as a new CAD risk factor: a female case study.

Estimating low-density lipoprotein cholesterol by the Friedewald equation is adequate for classifying patients on the basis of nationally recommended cutpoints.

It seems adventageous to have total triglycerides within "safe" range, favorable LDL/HDL ratio and subtype. That is the only sure way to reduce CVD risk, everything else is a gamble IMO. Especially considering the role that LDL/HDL play in the body, high total triglycerides is indicative of trouble regardless of particle subtype or ratio.