Friday, December 25, 2009

Rabbits on a High-Saturated Fat Diet Without Added Cholesterol

I just saw another study that supports my previous post Animal Models of Atherosclerosis: LDL. The hypothesis is that in the absence of excessive added dietary cholesterol, saturated fat does not influence LDL or atherosclerosis in animal models, relative to other fats (although omega-6 polyunsaturated oils do lower LDL in some animal models). This appears to be consistent with what we see in humans.

In this study, they fed four groups of rabbits different diets:
  1. Regular low-fat rabbit chow
  2. Regular low-fat rabbit chow plus 0.5 g cholesterol per day
  3. High-fat diet with 30% calories as coconut oil (saturated) and no added cholesterol
  4. High-fat diet with 30% calories as sunflower oil (polyunsaturated) and no added cholesterol
LDL at 6 months was the same in groups 1, 3 and 4, but was increased more than 20-fold in group 2. It's not the fat, it's the fact that they're overloading herbivores with dietary cholesterol!

Total cholesterol was also the same between all groups except the cholesterol-fed group. TBARS, a measure of lipid oxidation in the blood, was elevated in the cholesterol and sunflower oil groups but not in the chow or coconut groups. Oxidation of blood lipids is one of the major factors in atherosclerosis, the vascular disease that narrows arteries and increases the risk of having a heart attack. Serum vitamin C was lower in the cholesterol-fed groups but not the others.

This supports the idea that saturated fat in the absence of excess dietary cholesterol does not necessarily increase LDL, and in fact in most animals it does not.

Merry Christmas!

51 comments:

Inphidel said...

Stefan,

How does this info tie into your first post on the Diet-Heart hypothesis? (http://wholehealthsource.blogspot.com/2009/07/diet-heart-hypothesis-stuck-at-starting.html).

In that post, you showed how excessive dietary cholesterol had little relation to blood cholesterol. However, in today's post, it seems that excessive dietary cholesterol is correlated with high LDL values. How can that be? How excessive is excessive? Is it the case that 7-14 eggs/week is not excessive for humans?

I'm having some trouble reconciling these 2 posts :(

Inphidel said...

And Merry Christmas!

Jim Purdy said...

Stephan, I'm horribly confused.

I know that in your blog you often examine all sides of an issue, in an approach that says "On the one hand ... but on the other hand ..."

Sometimes I think you are saying butter is good, and sometimes I think you're saying butter is bad.

Please make it simple for me. Is butter good, or is it bad?

Or is it bad on Monday, Wednesday and Friday, and good on other days?

Stephan said...

Hi Inphidel,

A natural amount of dietary cholesterol in the diet of an omnivore is one thing, whereas feeding a huge amount to an herbivore is another.

My definition of "excessive" is an amount that exceeds what one can get from food. These are experiments where scientists feed a large amount of purified cholesterol to animals. It has nothing to do with the amount that a human could get from real foods. A natural amount of dietary cholesterol has little or no impact on serum cholesterol in most people.

Hi Jim,

I'm in favor of pastured butter, what makes you think otherwise?

Lisa said...

Hi Stephan,

Merry Christmas and thanks for this and all the other illuminating stuff you've shared so generously over this year.

Tangentially, I can't help but notice that since switching to butter, lard, coconut oil, etc, how my skin is improving - less dry, more glowing - and this at middle age when I could otherwise expect the opposite trend.

Thanks again Stephan, and best wishes for the new year.

switters said...

I posted this elsewhere on this blog, but to address Inphidel and Jim's question:

A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

In the 30% of people who experience an increase, egg consumption increases the proportion of large, buoyant LDL particles that have been shown to be protective against heart disease. Egg consumption also shifts individuals from the LDL pattern B to pattern A. Pattern B indicates a preponderance of small, dense LDL particles (risk factors for heart disease), while pattern A indicates a preponderance of large, buoyant LDL particles (which protect us from heart disease). This is a good thing.

Chris

Inphidel said...

Thank you Stefan

Andy said...

Switters and anyone else who can answer,

Are you sure that large LDL are protective? Do you have a reference for that? I thought all LDL can oxidize, but large ones are less likely to do so. Therefore large LDL are more weakly correlated with heart attack risk. Perhaps your risk will be reduced if small LDL are replaced by big ones, but how can additional large LDL be protective?

I believe I remember that some time ago Randy posted a few references that a bigger count of large LDL is also associated with an increased heart disease risk compared to a lower count of large LDL. Particle count was associated with increased risk even if the LDL was large.

zach said...

Lisa,

Try the Activator X butter oil from green pastures. When I use it, the next morning I definitely notice a "sheen" on my skin. My face almost looks brighter. It sounds quacky, but others i had try it noted similar results. I took it for the supposed vitamin K2 Mk4, and wasn't even looking for skin changes.

Stephan said...

Hi Lisa,

Glad to hear it. I think that's a good sign.

Hi Andy,

The question is still controversial. I think Dr. Ronald Krauss makes a good case, based on his research and others, that large LDL are not a major contributor to heart disease. But I don't think any academics are arguing that they're actually protective, to my knowledge.

Hi Zach,

Green Pastures butter oil makes my skin look nice too. I think it's the butyric acid and possibly the K2 as well.

Helen said...

Here are some articles that suggest that large, buoyant LDL may be protective.

ACCUMULATION OF CHOLESTEROL IN LARGE LDL PARTICLES IS ASSOCIATED WITH A REDUCED RISK OF ISCHEMIC HEART DISEASE IN MEN
AC St-Pierre, B Cantin, GR Dagenais, J-P Despr├ęs, B Lamarche
“CONCLUSIONS: These results suggest that a preferential accumulation of cholesterol in large LDL particles may be protective against the risk of IHD in men, even among those with elevated plasma LDL cholesterol concentrations.”
http://www.pulsus.com/ccc2003/abs/a880.htm


Slides from “Lipids Online” show that only 26% of patients who had had a “coronary event” had large, buoyant LDLs. Patients with a small, dense LDL pattern had 3-4 times the risk of having a coronary event compared with the large LDL group. (See bottom two slides.)

http://www.lipidsonline.org/slides/slide01.cfm?tk=70&pg=2

Another article states that large LDL seems to be inversely proportionate to vLDL, though this was in the context of another topic, and when I looked at the reference, the abstract was not illuminating. Still, if this is true, I think it would be safe to say that large LDL is protective, or at least having the large LDL being the predominant type is protective, which leaves open the question of whether having a higher overall LDL is protective, or if it is simply protective if it replaces vLDL.

http://www.jci.org/articles/view/21637/version/1#B12

Stephan said...

Hi Helen,

I see. I suppose there is some evidence for that then. Although the large LDL were associated with high HDL and low trigs ("pattern A"), so it's not clear that the LDL itself was protective.

Honestly though, I'm not sure how useful it is to mathematically "control for" other lipoproteins when looking at associations between LDL and CHD. In other words, I don't know how useful it is to say "at a given level of HDL, how does large LDL affect CHD risk"? These things all come together in patterns, I think it's best just to look at the patterns. After all, these studies are mostly good for determining diagnostic criteria rather than cause-and-effect relationships. Small LDL, low HDL, and high trigs travel together and associate with high risk.

randy said...

Hi Stephan and Helen.

BTW Helen - Thanks for the info on Dr. Davis last week. Appreciate it.

Stephan Wrote:
"I see. I suppose there is some evidence for that then. Although the large LDL were associated with high HDL and low trigs ("pattern A"), so it's not clear that the LDL itself was protective."

Reply
In fact that's exactly what happened. The study did not account for trigs.
As discussed in this paper, http://www.athero.org/commentaries/comm564.pdf, these and other measurement/confounders have distorted the issue. When these "details" are properly accounted for Ldl size becomes insignifcant in most studies, but total paticle number is a strong predictor.

In fact some of the "proper" studies have shown large Ldl to be less harmfull.
See: http://www.ncbi.nlm.nih.gov/pubmed/11572739, http://jcem.endojournals.org/cgi/reprint/88/10/4525.pdf, http://www.athero.org/commentaries/comm564.pdf

A recent review of the best studies concluded that only particle number is determinent, not particle size.
See: http://www.ncbi.nlm.nih.gov/pubmed/19349632

Stephan Wrote:
"I'm not sure how useful it is to mathematically "control for" other lipoproteins when looking at associations between LDL and CHD. In other words, I don't know how useful it is to say "at a given level of HDL, how does large LDL affect CHD risk"? These things all come together in patterns, I think it's best just to look at the patterns."

Reply:
This has got to be done if we want to find out if there is a differnce between Ldl particle sizes and CVD. Some believe that the large particles are harmless/helpfull. The only way we can make a determination is by anylazing the data and allowing for confounders the best we can.

Regards
Randy

Lisa said...

Zach, thanks for the butter oil tip. Can't get that where I live unfortunately, but the added anecdotal evidence for the correlation between skin improvements and butter is very interesting.

kilton9 said...

FYI, a newer egg study from the folks who did the hypo/hyper-responders study: http://jn.nutrition.org/cgi/content/full/138/2/272

The eggs appeared to raise HDL-C significantly. The increases in LDL-C were apparently non-significant.

randy said...

Hello Stephan,

Here's a recent paper (1)that claims 1 year reductions in Ldl via decreasing SFA & Trans and increasing PUFAs and MUFAs.

Another study claims childern on high SFA diets show increased chllesterol (actually apo b) at 6month/1 year/ 2year periods (2).

Regards
Randy

1.
Dietary intervention to lower serum cholesterol.
Clifton P, Colquhoun D, Hewat C, Jones P, Litt J, Noakes M, O'Brien R, Shrapnel B, Skeaff M.
CSIRO Division of Human Nutrition, Adelaide, South Australia. peter.clifton@csiro.au

PMID: 19521587 [PubMed - indexed for MEDLINE]


2.
Effect of a high-fat ketogenic diet on plasma levels of lipids, lipoproteins, and apolipoproteins in children.
Kwiterovich PO Jr, Vining EP, Pyzik P, Skolasky R Jr, Freeman JM.

PMID: 12928468

Stephan said...

Randy, come on man, the point is to find a study where PUFAs were kept the same! I agree 100% that PUFAs lower LDL and TC. But that doesn't answer the question of long-term effects of SFA on cholesterol.

Helen said...

Or the long-term effects of PUFAs on cardiovascular health.

randy said...

Hello Stephan,

Stephan Wrote:
Randy, come on man, the point is to find a study where PUFAs were kept the same! I agree 100% that PUFAs lower LDL and TC. But that doesn't answer the question of long-term effects of SFA on cholesterol.

Reply:
It does answer the question that TC and Ldl are raised long term when fat content is constant but shifted for greater SFA and lower PUFA.

Here's a study that keeps PUFA and Total Fats the same but varies SFA and MUFA. The results are the same, TC, LDL, TC/HDL are all significantly increased.

http://www.ajcn.org/cgi/reprint/70/6/1009

As I've mentioned before the data from metabolic ward feeding studies
is massive. These guys have tested all permutation and SFA (some more than others, some not at all) increase TC under all sorts of variation (PUFA constant).

Here's one paper dealing with this:

http://www.ajcn.org/cgi/content/abstract/65/5/1628S

Regards
Randy

Stephan said...

Randy. Seriously. The diet periods in that study only lasted 24 days. 24 days.

You have not provided a single study showing that SFA increase serum TC or LDL on timescales of 1 year or more, independent of PUFA. I've provided several references to support my contention that SFA are irrelevant to TC and LDL in the long run.

You keep presenting studies that are either short term or changed PUFA. You're wasting my time and yours.

randy said...

Hello Stephan,

Stephan Wrote:
You have not provided a single study showing that SFA increase serum TC or LDL on timescales of 1 year or more, independent of PUFA.

Reply:
Just because long term studies with your criteria haven't been done (or I haven't been able to find), there is no reason to think the results would be different.

The TC raising ability of > SFA/PUFA has been demonstrated in both short term and long term studies. MUFA/SFA acts the same way short term, I think it is Unreasonable (until we have long term info)to Assume the situation would be different long term.

Your argument is like claiming that smoking is not harmfull if you keep your eyes closed. I say that absurb. You say showing of study of smoking standing on one leg.

Regards
Randy

Stephan said...

Randy, we know there's a difference between the (modest) short-term effects of SFA and the (nonexistent) long-term effects, because the studies have already been done. I've provided you with several references, so are you just disagreeing for the sport of it?

Typically when someone disagrees as persistently as you do, they have some kind of data to back up their claims. But it's clear that you have none. I'm done with this "debate".

LeenaS said...

To randy:
We have a human experiment on the go. Our healthty son (now in early twnties) has been on lowish carbs since year 2000. Furtherrmore, he has been on high butter and high animal fats for the latest few years. Blood lipids?

His HDL is 1.4 mmol/l, LDL 1.6 mmol/l, trigs 0.5 mmol/l. And this happens without supplements, and in spite that we live in a countrly quite inadequate in vitamin D from sun for most of the year. Ant there is not much fish on the menu, either.

Us adults, on similar diet, have higher LDL's (but as good HDL's and trigs) - yet we were not that healthy at the start on 2000, after decades on the recommended diet low in animal fats. Pity. But we have been exceptionally much better since then.

So, while waiting for controlled studies we'll get by on our own experiments. And yes, I do think more and more that the reason foru our good health may lay mainly in excessive use butter and restriction of grains.

With regards,
LeenaS

Andy said...

It seems there is some confusion about whether there are long term studies about the effects of saturated fats on cholesterol levels while keeping PUFA's the same, so I'll quote Stephan from the post "The Diet-Heart Hypothesis: Stuck at the Starting Gate"

"The long-term data are also not kind to the diet-heart hypothesis. Reducing saturated fat while greatly increasing LA does lower blood cholesterol substantially. This was the finding in the well-controlled Minnesota Coronary Survey trial, for example (14% reduction). But in other cases where LA intake changed less, such as MRFIT, the Women's Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, reducing saturated fat intake had little or no effect on total cholesterol or LDL (0-3% reduction). This generally dumbfounded the investigators. The small changes that did occur could easily have been due to other factors, such as increased fiber and phytosterols, since these were multiple-factor interventions."

randy said...

Hello Stephan,

Stephan Wrote:
Typically when someone disagrees as persistently as you do, they have some kind of data to back up their claims. But it's clear that you have none. I'm done with this "debate".

Reply:
Your statment is untrue. I always supply references and the logic to tie them together.
I'm going to review the arugment down to its basics so anyone thats fair can see how unreasonable you are being.

Point 1.
I presented evidence that long term diets that vary SFA and PUFAs do result in significant increases/decreases in TC and LDL.

Ref:
Finish Mental Health Study
Minnesota Mental Health Study
Dietary intervention to lower serum cholesterol. http://www.ncbi.nlm.nih.gov/pubmed/19521587
Effect of a high-fat ketogenic diet on plasma levels of lipids, lipoproteins, and apolipoproteins in children. http://www.ncbi.nlm.nih.gov/pubmed/12928468

Point 2:
Your response to the above was:
"Randy, come on man, the point is to find a study where PUFAs were kept the same! I agree 100% that PUFAs lower LDL and TC."

So you agree that adjusting SFA/PUFA levels do effect in the long term.

You then stated:
"the point is to find a study where PUFAs were kept the same! "

Point 3:
Here the studies I presented that show that keeping PUFAS constant but varing SFA increase TC and Ldl.

Ref:
High–monounsaturated fatty acid diets lower both plasma
cholesterol and triacylglycerol concentrations1–3
http://www.ajcn.org/cgi/reprint/70/6/1009

Individual fatty acid effects on plasma lipids and lipoproteins: human studies
http://www.ajcn.org/cgi/content/abstract/65/5/1628S

Effects of Reducing Dietary Saturated Fatty Acids on Plasma Lipids and Lipoproteins in Healthy Subjects
http://atvb.ahajournals.org/cgi/content/full/18/3/441

Point 4:
Your response was:
"Randy. Seriously. The diet periods in that study only lasted 24 days. 24 days. "

That's only true for the first study the other 2 were for >=56 days.

But you haven't answered why we should think the long term results would be any different long term.
You've aleady agreed that varying SFA/PUFA results in long term changes (>=1year), why should MUFA be any different??

There have not been any long term studies done with this particular permuation, but you haven't presented any evidence of why this should not be true long term.

Stephan, this is not rocket science and you not a dumb guy, but you don't want to have a reasonable conversation - That's unfortuneate.

Regards
Randy

randy said...

@Andy,

The counter examples you cited were all free living studies where the only check on subjects diets is what they report.

These are notoriously unreliable.

The diets in the studies I reported were either totally controlled or cross checked.

This descreptency has been noted and studied. You just can't trust what people tell you they've been eating.

Regards
Randy

randy said...

@LeenaS,

I do not discount your experince Leena.

My argument is not that many many folks don't feel and function much better on high SFA paleo diets.

Also I don't discount the high relevance of "how you feel" to make dietary decisions.

My arugment is when objective data is twisted or ignored to justify a dietary philosphy.

I have no problem with "I don't care what the science says, I feel great and going to continue with this diet".

What I get riled about is distorting the evidence to support a particulare view.

What will go along way settling this issue are imaging studies, sonagrams of the carotid artery, Angograms, calcium scans.

Regards
Randy

Anna said...

Randy,

You are asking for coronary artery calcium scores in relation to individual high SFA intake and lipid test trends. Here's mine:

My coronary calcium scan last Dec 08 was *0* on a high SFA LC diet.

Here is the context:
I've been eating LC since January 2004 (GF since January 08) increasing the naturally saturated fats as well as avoiding industrial veg oils, reducing industrially processed food, reducing grain-fed animal foods, in favor of mostly seasonal local produce and pastured or wild caught/game animal foods, especially the past 2-3 years.

My TC has been slowly rising from low TC since age 30, along with a TSH that crept up. I'm going by memory but I think my last lipid panel was TC in the 240s, HDL went from low 40s to at least 60, & LDL has risen, too. My Trigs declined to well under 100 with LC eating and remain fairly steady. I'm quite sure I was Vit D deficient after a basal cell carcinoma removal and much sun avoidance - now I get some some prudent sun exposure, supplement with 5000iU Vit D most days , and my 25 (OH)D averages about 65-75 ng/dL. I'm about average in activity level. FBG averages about 100, but will go up if I don't watch my CHO intake. I'm definitely at least borderline diabetic (1st phase insulin response is weak or gone, second phase is still robust, I think - fasting insulin was only 5 about 2 years ago but the lab neglected to test insulin insulin levels for the rest of the 3 hr GTT !@#$%^&* - which is why I was there because I can't self-test insulin so I don't know how it responds to rising glucose).

Don't take any OTC meds except NSAIDs maybe 2xYR, some supplements. My Rx meds are natural desiccated thyroid hormone and bioidentical progesterone. No diabetes meds to date.

There is significant CVD in my maternal family health history, and now diabetes in my generation and my mother's generation, so I take my risk level seriously.

Last year my 11 yo son and I have tested positive (Enterolab tests, Dr. Kenneth Fine) for IgA gliadin antibodies, anti-tissue transglutaminase, and we each carry two HLA genes that predispose to gluten sensitivity and/or celiac, so we are gluten-free now. Son now reacts to gluten exposure with canker sores, GI symptoms are far more subtle.

I am also hypothyroid, probably have been to some degree since age 30, but only officially diagnosed and treated since mid 2006 when I had increased soy and gluten exposure. Wasn't tested for thyroid antibodies until recently (neg) so don't think it is autoimmune.

I'll be 48yoa in just over a week and haven't yet passed menopause though definitely perimenopausal (I'm aware that menopause might make a difference in my CAC score in the future. Bone density is good. BP is good, even lowish. My BMI is about 22-22.5, so not very overweight (<10 lbs) as long as I restrict CHO.

CVD is significant in my maternal family health history since mid-century (diabetes is popping up in the last 12 years, too), but I've not seen any health benefit for older family members who have long-followed the AHA/ADA guidelines, in fact I'd argue it's made their health worse (no MIs lately, but now they get diabetes and double bypass surgery despite all the "prevention").

Hope that isn't TMI.

randy said...

Hello Anna,

Thanks for the info and congrats on the excellent numbers.

This is the kind of data that's needed on a large scale to really resolve the issue.

Your TC/HDL (the older best lipid marker for CVD) is fairly good.

I'm impressed with your low BMI. I wish I could report those numbers.

Couple of comments:

1. I think a Carotid Imt test might be a better indicator can take calcium some years to build up after plaque is being depositied

2. Do you have any idea how many calories you eat daily and how much SFA?

My concern, Anna is not for folks like your self that are intelligent, and monitor their condition.

My critism is for the folks that really jack up their SFA and have TC and Ldl level that are in the stratashpere and think their safe because of one sided views presented on this and simular blogs.

It might be true the super high Ldl levels don't matter in the context of Paleo High SFA diet, but this has not been established in a scientific manner. I open to the possiblitiy but there is not enough data

What I find particularly galling is when data is distorted to support a dietary philosophy.

Thanks again for your input.

Regards
Randy

LeenaS said...

To randy: As long as you accept the Finnish mental study as hard data, I will doubt your ability to read sceincen critically. With the known weaknesses, no sincere researcher should take that as a proof of anything. Sorry.

And as for my personal experience, by now I know dozens of butter eaters in the Scandinavian low carb movements, who report lipid value changes similar to us.

We might have better milk products up here (less grains in cow feed), but essentially it is still only mass produced butter that gives these shining results - and has done so even before Keys's times... Our problems started when sugar, margarines and mass produced grain products found a poor and stressed nation, right after a war much too big for it - and this is shown in the national statistics timeline. Which, b.t.w. also show that the reason was NOT in The North Karelia Project.

Stephan said...

Hi Randy,

"What I find particularly galling is when data is distorted to support a dietary philosophy."

For once we agree. You're trying to provoke me, and I'm about a millimeter away from taking the bait and kicking you off the blog. The only reason I hesitate is that I like having alternative perspectives around I'm hoping that at some point you will use your knowledge to bring something useful to the blog.

What I've mostly seen from you so far is this: you regurgitate references and I have to waste time pointing out that you misquoted them or that they're irrelevant. Then, in response, you regurgitate the same references again as if I hadn't written anything. Repeat ad nauseam. Have you seen the movie "Memento"?

Consider this your final warning. I'm not going to tolerate one more post where you attempt to cloud the debate by misquoting studies or flooding us with irrelevant references. It's "information pollution" and there's no room for it in a serious discussion of diet and health.

randy said...

Hi LeenaS,

LeenaS Wrote:
"As long as you accept the Finnish mental study as hard data, I will doubt your ability to read sceincen critically. With the known weaknesses, no sincere researcher should take that as a proof of anything. Sorry"

Reply:
My reference to the Finnish Study was was the data that showed TC levels were reduced Long Term when PUFAs were in increased and SFAs decreased.

Stehpan has agreed to this.

I was not referring to any reduction in CVD.

Regards
Randy

randy said...

Hello Stephan,

Once again you respond in generic terms without dealing with the specifics of our technical disagreement.

To review again:

Stephan Wrote:
"So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. This turns out to be largely a myth"

Reply:
I responded with data to show this wasn't true in both long term and short term controlled diet studies.

YOu seem to agree but repharsed your contention by saying this was only true when PUFAS were exchanged with SFAs.

I then presented studies that showed this was also true when PUFAs were kept constant but SFA were reduced. Your response was that these studies were not long term.

I then asked you why I should think the results would be any different in long term studies and have not received a response.

Just because long term studies have not been done with this permutation(or I haven't found them yet) doesn't mean its not true. Unless, that is, you provide that information which I haven't seen yet.

The counter studies you provided all free living studies where we have to depend on what the subjects are reporting. Its when we look at the controlled studies, where we have more certainty on what the subjects are eating that we find consistent results.

Also, I'm a little miffed at why you have to get "personal" when this is a straight forward technical discussion.

I have been very clear and specific, Stephan. If you could do the same we could put an end to this. Even if we "agree to disagree".

Regards
Randy

Stephan said...

Randy, you're again ignoring the fact that I referenced numerous studies showing that SFA has no effect on TC or LDL in long-term studies when PUFA are kept the same. I warned you. Sionara, buddy.

Anna said...

Sigh.

I've been reading this blog a long time, possibly longer than most of the current frequent commenters. The level of discussion is now often far above my ability to contribute, so I remain in lurk mode more often, but I get a *lot* out of reading the comments nonetheless.

I've got to agree with Stephan on Randy's participation in the comments. There has always been a congenial exchange of ideas at this blog, with plenty of room for musing, questions from new and longtime readers, and friendly debate of ideas.

But Randy, I'm going to be blunt: whenever you join the discussion, the tone eventually changes like a fast moving cloud obscuring the sun, casting a chill over the air. I can't speak for other readers (but I suspect I'm not alone), but I don't like it and I agree with Stephan 100%. The *way* you harass Stephan with nit-picky challenges detracts from the discussion, it disturbs the friendly nature of this blog, and it takes up too much of Stephan's time.

Please reconsider your approach in the comments. Perhaps that's too vague: mind your manners and try to remember you are a guest on someone else's turf. If you can't manage to rein in your "fencing style", you should find another forum that is more suited to your combative style, perhaps your own blog.

Jim Purdy said...

Having been kicked off more than a few forums and blogs myself, I've learned the hard way that it's usually not WHAT you say that offends people, it's HOW you say it.

Forums and blogs are kind of one-dimensional, not allowing for nuances of face-to-face discussions, like tone of voice, facial expressions, hand gestures, and body language.

For example, all my doctors call me non-compliant, but a few of them say it in a friendly way, with a smile, which makes me much more likely to pay attention.

Let's all make a New Year's resolution to be more friendly.

I promise to make a little smily face the next time I argue with Stephan.

:)

LeenaS said...

Randy said:
My reference to the Finnish Study was was the data that showed TC levels were reduced Long Term when PUFAs were in increased and SFAs decreased.

Why reference that at all, since it was not a valid study. The long term effect is not well known in that study, since the experimental groups were not really controlled (with all newcomers included and with all those who left ignored in data)? And, b.t.w., you know that, by now, since it was discussed too in Stpehans answer.

Besides, in real, controlled studies (several of which has been discussed with your prescence) a real TC reduction due to Pufas has been shown to be due to shrinking of the LDL particles into ozidised, more artherogenic phopholipids... as well as in decrease in HDL.

It is good to be critical, but real discussions evolve as information is gained on both sides. This is not it.

Andy said...

Stephan,

I respect your decision to end this conversation with Randy, but I would appreciate it if you could comment and help clarify some of his arguments for me, as they are somewhat confusing and I probably cant figure this out by myself.

One of them is that the data from metabolic ward studies is massive and consistent that SFA increase TC and LDL under all sorts of conditions, even when PUFA's are the same. However, these are short-term.

Then the argument that there is no reason to believe LDL will fall after a year or so.

And he says all the long-term studies you have provided demonstrating no effect of SFA on LDL when PUFA kept the same are done in free-living subjects who report what they eat, and that this is notoriously unreliable and has been studied and documented, yet on the other hand the more controlled studies are consistent but short term.

skepticaldoc said...

I think Randy definitely makes significant, cogent remarks. I am a board certified lipidologist with a pretty good grasp of the lipid literature so I was very disappointed to see that you booted him.

Stephan said...

Hi Andy,

Have you read my post "The Diet-Heart Hypothesis: Suck at the Starting Gate"? I laid out the whole argument there.

It's true that studies in free-living subjects are not perfect, but that doesn't make them useless. In the Lyon trial (omega 3:6 modification, among other things) for example, there was a roughly 75% difference in heart attack incidence between groups. That indicates that they were complying with the diet advice, otherwise there would have been no difference between groups, let alone a massive one. LDL was the same in both groups despite a substantial difference in SFA consumption.

In the Physician's health study, there was no difference in TC over a 2-fold difference in SFA consumption.

Then there's the data from the Masai and Tokelau, who both have low TC despite eating more SFA than any other cultures on the planet. The Masai in particular have extremely low TC, which is lowest during the period of their lives when they're restricted to fatty milk, meat and blood.

Then there's this study, that showed that a low-carb diet rich in SFA caused a slight and non-significant increase in LDL at 6 months that disappeared at one year and actually went lower than baseline at 24 months:

http://content.nejm.org/cgi/content/full/359/3/229

The difference in LDL between the low-fat group and low-carb group was not significant at 24 months (p=0.94!), despite a 28% difference in SFA consumption.

The same thing has been seen in animal studies under 100% controlled conditions. In this study, feeding rabbits coconut oil without added cholesterol caused a transient increase in TC that disappeared at 6 months.

http://circres.ahajournals.org/cgi/content/abstract/20/6/658

This study also found a transient increase in rabbits fed coconut oil without added cholesterol compared to low-fat chow, which resolved at 6 months, although the transient increase was not statistically significant.

http://www.ncbi.nlm.nih.gov/pubmed/20032571

I've pointed all this out to Randy but he ignored it.

Stephan said...

Hi Skepticaldoc,

Sorry you feel that way. I want to be perfectly clear that I didn't kick Randy off for disagreeing with me. I kicked him off because he consistently distorted the data and ignored contradictory points. I have zero tolerance for science abuse. You may not have been around long enough to witness some of our other discussions, but here are a few specific instances:

-He wouldn't accept the fact that the Anti-Coronary Club trial had many more deaths in the intervention than the control group, and he cherry-picked data from a specific age group to support his claim that mortality was the same, despite the fact that he had the paper right in front of him.

-He stubbornly insisted that the Finnish Mental Hospital trial was blinded, when the paper states it wasn't. He had the paper. He also made the claim that the Finnish trial is universally accepted by researchers, and that there were no critical editorials, which is ludicrous, but he had to back down when I cited editorials critical of it.

-In the current discussion, he dropped references that were irrelevant to the debate at hand, over and over again, as if they were supportive. This is typical of nearly every discussion we had.

-In nearly every discussion we had, he stubbornly refused to acknowledge data that disagreed with his ideas. He typically did this by simply ignoring it, and regurgitating or quoting from the same refs he had already posted earlier in the thread.

The "mistakes" he made in citing the lit were always in favor of his argument, never against it. I realized a few months ago that I was dealing with someone who was not discussing to arrive at accurate information, but simply to justify his own beliefs. You may have noticed that nothing we discussed over the past year plus changed his beliefs one iota. Whereas I've had my mind changed in the comments section a number of times.

Yet I still felt a responsibility to debate with him, so that other readers could be informed of the holes in his arguments. This was quite a burden because I'd have to make a point 3-4 times before he'd even acknowledge it, if he acknowledged it at all. I ended up getting fed up, and when he began provoking me (I admit I wasn't very nice either), that was the last straw. I gave him one last chance to salvage the situation, and he took the opportunity to launch a parting salvo, so that was that.

I actually like having people around who disagree with me, as long as they can support their views without having to resort to science abuse. The only other person I've kicked off, Bris, was also a science abuser. Whenever you followed his references, they were generally not supportive of his claims. Plus he was a bully. If you thought Randy was making some good points, and you think what I'm saying is incorrect or shaky, then I invite you to share your perspective.

skepticaldoc said...

For openers:

Am J Clin Nutr. 2009 Jul;90(1):23-32. Epub 2009 May 13.
Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo.

Brinkworth GD, Noakes M, Buckley JD, Keogh JB, Clifton PM.

Preventative Health National Research Flagship, Commonwealth Scientific and Industrial Research Organization-Human Nutrition, Adelaide, SA, Australia. grant.brinkworth@csiro.au

BACKGROUND: Long-term weight loss and cardiometabolic effects of a very-low-carbohydrate, high-saturated-fat diet (LC) and a high-carbohydrate, low-fat diet (LF) have not been evaluated under isocaloric conditions. OBJECTIVE: The objective was to compare an energy-controlled LC diet with an LF diet at 1 y. DESIGN: Men and women (n = 118) with abdominal obesity and at least one additional metabolic syndrome risk factor were randomly assigned to either an energy-restricted (approximately 6-7 MJ) LC diet (4%, 35%, and 61% of energy as carbohydrate, protein, and fat, respectively) or an isocaloric LF diet (46%, 24%, and 30% of energy as carbohydrate, protein, and fat, respectively) for 1 y. Weight, body composition, and cardiometabolic risk markers were assessed. RESULTS: Sixty-nine participants (59%) completed the trial: 33 in the LC group and 36 in the LF group. Both groups lost similar amounts of weight (LC: -14.5 +/- 1.7 kg; LF: -11.5 +/- 1.2 kg; P = 0.14, time x diet) and body fat (LC: -11.3 +/- 1.5 kg; LF: -9.4 +/- 1.2 kg; P = 0.30). Blood pressure, fasting glucose, insulin, insulin resistance, and C-reactive protein decreased independently of diet composition. Compared with the LF group, the LC group had greater decreases in triglycerides (-0.36 +/- 0.15 mmol/L; 95% CI: -0.67, -0.05 mmol/L; P = 0.011), increases in HDL cholesterol (0.23 +/- 0.09 mmol/L; 95% CI: 0.06, 0.40 mmol/L; P = 0.018) and LDL cholesterol (0.6 +/- 0.2 mmol/L; 95% CI: 0.2, 1.0 mmol/L; P = 0.001), and a greater but nonsignificant increase in apolipoprotein B (0.08 +/- 0.04 g/L; 95% CI: -0.004, 0.171 g/L; P = 0.17). CONCLUSIONS: Under planned isoenergetic conditions, as expected, both dietary patterns resulted in similar weight loss and changes in body composition. The LC diet may offer clinical benefits to obese persons with insulin resistance. However, the increase in LDL cholesterol with the LC diet suggests that this measure should be monitored.

Stephan said...

Hi Skepticaldoc,

Thanks for your response. Here is the problem I perceive with using that reference as evidence that saturated fat increases LDL over a long timescale. The low-carb diet was a ketogenic diet, as pointed out in fig 2. The LC dieters ate 19-32 g of carb per day (5-9 % of energy). I acknowledge that diets with extreme compositions like that can raise LDL in some people, sometimes dramatically. But in my opinion this study does not imply that saturated fat was responsible for the effect.

Despite an extreme diet composition and a saturated fat intake that differed by four-fold, the difference in LDL-c between diets was only about 15% at one year. The LDL particle number didn't change from baseline and was not significantly different from the high-carb diet at one year (table 4). That indicates that the small change in LDL that did occur was due to an increase in LDL size rather than particle number.

skepticaldoc said...
This comment has been removed by the author.
skepticaldoc said...

I thought we were talking about "LDL", not LDL particle size or particle number. Large LDL is less atherogenic than small LDL, but atherogenic none the less. 15% increase in LDL in face of significant weight loss, which usually lowers LDL, is an impressive and significant increase in LDL, IMO.

Stephan said...

Hi Skepticaldoc,

Yes, we are talking about LDL-c, but the question is, what effect does SFA have on it. In my opinion, that study does not tell us about the effect of SFA on LDL-c because the macronutrient composition is so extreme.

LDL-c is basically a crude, and more easily measured, proxy for LDL particle number. The fact that LDL particle number didn't increase, HDL increased, and trigs decreased on the VLC diet indicates to me that the lipid changes were not "atherogenic" by the mainstream conception of blood lipids. Don't get me wrong, I don't recommend eating like that except in the case of diabetes. But these changes would not be expected to promote atherosclerosis according to the mainstream scientific view.

Robert Andrew Brown said...

Skepticaldoc,

Interesting trial. Thank you for sharing.

Do you have a breakdown of the fats type of saturates etc.

Cab.consumer said...

Stephan,

thank you for the good work you do on this blog. I have had similar experiences with people who remain fixed to their viewpoints and it can not only be immensely frustrating but it can derail an usefulness of an inquiry for everyone. I respect your decision to have booted him.

It is extremely useful for me to have someone out there writing what you do; I rarely have the time to read dietary studies (I read one on the side effects of my immunosuppressive drugs instead!), but I am pretty convinced of the benefits of a paleolithic approach.

I have been taking the Green Pastures Cod Liver and Butter Oil for a while and I've noticed the great effects on my skin and wellbeing also.

Please keep up the good work Stephan.

Carl.

Daniel said...

Hi Stephan,

Haven't read the full paper yet so I don't know about the rigidity of the study; but you might want to check this one:

Eggs distinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet

The Journal of Nutritional Biochemistry
Volume 21, Issue 4, April 2010, Pages 261-267

http://dx.doi.org/10.1016/j.jnutbio.2008.12.011

trinkwasser said...

"My arugment is when objective data is twisted or ignored to justify a dietary philosphy.

What I get riled about is distorting the evidence to support a particulare view.

What I find particularly galling is when data is distorted to support a dietary philosophy."

Randy is now back at his day job, telling the denizens of newsgroup alt.support.diabetes to eat more carbs and less fat, and still totally unaware of the irony of his above comments.

He came here because Alan

http://www.loraldiabetes.blogspot.com/

listed a bunch of useful blogs, and he and some others decided to invade these blogs. One of his colleagues was banned much more promptly from several.

I don't recognise Bris as an individual but I recognise the way he also worked to disrupt discussion using interpersonal manipulation techniques.

Among their techniques are claims that all anecdotal evidence is lies, that all people who claim that low fat high carb diets fail are secretly eating too much fat, that the likes of Jeff Volek are financed by Atkins, that Atkins was hugely fat and died of heart disease, that all blogs are written by amateurs including the likes of Michael Eades who is not actually a doctor, that you are an amateur who shouldn't have got a PhD . . .

. . . the point they completely miss is that IF they and their Authorities were correct then blogs and forums like this simply wouldn't need to exist as everyone would already be cured. Let alone that dietary researchers wouldn't need to furiously cook their results to "prove" things that simply don't occur in the Real World.

I consider your work important enough that I'm re-reading your blog and many of the references you and your contributors provide.

Which will probably make you a target for future invasions.

grubinski said...

Stephan,

For something *really* interesting, google "Rabbit Cholesterol Iodine". I found this coincidentally after my sky-high total cholesterol numbers came down from 595 !! to 378. There are 3 things I changed in this period... I started standing all day at my desk, I drank a little more bourbon (HDL went from 64 -> 79), and I started supplementing with 36x RDA of Iodine in the form of 2 Iosol drops/day. If the Iodine in the rabbit studies eliminated atherosclerotic lesions, perhaps it did so by reducing LDL?