22 replies to this topic

[zoolander]

well, well, well. What do you blood know!! The latest report of the 2010 Dietary Guidelines Advisory Committee (DGAC) has been criticized for not conforming to using an evidence based approach to formulate it's recommendations.


Check at the coverage @ Science Daily.


Have a read of the source paper (see attached).

Attached Files

•  Nutrition 2010 M.A.T.pdf   495.67KB   208 downloads

[hypnotoad]

No one here is going to be following that crap anyway. A board full of vegans, vegetarians, paleo eaters , CR followers , supplement takers etc. has long since moved past things like the USDA food pyramid.

Generally whatever the government, big agriculture and food companies, and big pharma advises me to do, I do the exact opposite.

Edited by hypnotoad, 04 October 2010 - 11:35 PM.

[Forever21]

No one here is going to be following that crap anyway. A board full of vegans, vegetarians, paleo eaters , CR followers , supplement takers etc. has long since moved past things like the USDA food pyramid.

Generally whatever the government, big agriculture and food companies, and big pharma advises me to do, I do the exact opposite.

You forgot Barry Sears diet

[niner]

Thanks for that, zoo. My congratulations to Hite et al. for saying what needed to be said. About damn time, too. Now we need to blow up the pyramid.

[kismet]

No one here is going to be following that crap anyway. A board full of vegans, vegetarians, paleo eaters , CR followers , supplement takers etc. has long since moved past things like the USDA food pyramid.

Generally whatever the government, big agriculture and food companies, and big pharma advises me to do, I do the exact opposite.

Take off your tinfoil hat. Now to move beyond a priori condemnations.

Thanks for that, zoo. My congratulations to Hite et al. for saying what needed to be said. About damn time, too. Now we need to blow up the pyramid.

To use a literary reference, this paper is full of sound and fury, signifying nothing. In both senses.
Signifying nothing, because most of it is merely criticising the tone and the strength of their recommendations not the direction of their recommendations.
Signifying nothing, because many of us have known the shortcomings of the literature for some time.
Signifying nothing, because it is about public health policy and not life extension.

A few issues..

Low-carbohydrate diets: Science is inaccurately represented
Of course a fair summary is easy: very low CHO diets if not of the eco-atkins type are quite damn toxic.

Dietary fat and health outcomes
The SAFA connection w/ insulin resistance can indeed be criticized. The evidence of an effect on TC/HDL and LDL/TC vs PUFA is basically irrefutable.

But than the author goes off justifying SAFA using corner cases and Jakobsen et al. which, weakly or not, indicts SAFA. That is not an argument for your case.

"The conclusion of the DGAC Report suggests that the replacement of SFA with monounsaturated fatty acids or PUFA creates unequivocally positive cardiovascular risk factor outcomes; this is not the case. Studies cited by the DGAC Report demonstrate increases in atherogenic lipoprotein levels or triacylglycerols, decreases in high-density lipoprotein cholesterol, and varied metabolic responses to lowered dietary SFA in subpopulations"
The evidence in favour of MUFA and surrogates is strong and the evidence in favour of mixed MUFA/PUFA sources is incredibly strong e.g. nuts and EVOO.

Dietary fiber and whole grains: Conclusions do not reflect the quantity and/or quality of science
Justified criticism but ultimately futile: strong evidence suggests that foods rich in fibre are healthy whether because or in spite of fibre is only secondary.

Glycemic load/index: Answers based on an incomplete body of relevant science
This has something of a false dichotomy. Of course, you can and should (in many cases) strive to minimise both GI and GL (via lower total CHO intake: at least when going from 60 to 4x%) to optimise surrogate markers. There is good evidence for both. And again: healthy diets and foods tend to be low GI/GL.

Animal versus plant protein: Recommendations do not reflect limitations and uncertainties of the science
Buhu. The same mistake as in the SAFA-paragraph. The evidence is “moderate, limited, insufficient and inconsistent”; i.e. it is weak -- but not weakly in favour of animal protein weakly against! Public policy: better safe than sorry. Sure, you can criticise their tone but the conclusion still stands, veg. > animal protein even if by a small margin.

Salt: Recommendations do not reflect limitations and uncertainties of the science
A Cochrane review, for example, concluded that “intensive interventions, unsuited to primary care or population prevention programs, provide only minimal reductions in blood pressure during longterm trials”
Plain language summary: yes, it does reduce BP. Which, all else being equal, would save thousands of lives. And we can sustain salt reduction because we are not average joe.

Plus there is outcome data, albeit somewhat inconsistent:
BMJ. 2009 Nov 24;339:b4567. doi: 10.1136/bmj.b4567.
Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies.
Strazzullo et al.
http://www.ncbi.nlm....60/?tool=pubmed

The verdict against salt is clear cut. (although, it may have paradoxical effects on lipid metabolism)

--

Apparently citing the AMA:
"We believe that it would be inappropriate at this time to adopt proposed national dietary goals as set forth in the Report on Dietary Goals for the United States. The evidence for assuming that benefits to be derived from the adoption of such universal dietary goals as set forth in the Report is not conclusive and there is potential for harmful effects from a radical long-term dietary change as would occur through adoption of the proposed national goals."

... this makes clear just how irrelevant this article is to us. We are not public health policy and inertia. We are flexible and will adjust to new evidence, therefore it is almost mandatory to act on the data before the evidence is completely settled. A > B, even if by a small margin, it is still what the best evidence suggests. You go by the preponderance of evidence, not by wishful thinking.

On what grounds would you suggest to act against the evidence? You choose butter over EVOO and nuts? Ok, but it is not science based. GI is irrelevant? The literature disagrees, etc.

Edited by kismet, 05 October 2010 - 03:36 PM.

[Skötkonung]

The evidence of an effect on TC/HDL and LDL/TC vs PUFA is basically irrefutable.

Someone better tell the Kitavans that their diet of starches, saturated fats, and animal proteins is destroying their cardiovascular health. Oh, that's right... they don't have any detectable levels of CVD. From Stephan at WHSource:

"Their blood lipid profile is not what a mainstream cardiologist would expect. In fact, it's "worse" than the Swedish profile in many ways, despite the fact that Swedes are highly prone to CVD. This suggests that blood lipids are not causing CVD, but are simply markers of diet and lifestyle factors. That's very easy for me to swallow because it never made sense to me that our livers would try to kill us by secreting triglycerides and witholding HDL. The blood lipid profile that associates best with CVD and metabolic syndrome in the West (but has no relation to them on Kitava) is one that's consistent with a high carbohydrate intake. Where does carbohydrate come from in the West? Grains and sugar maybe? Kitavans also have very low serum leptin. This may be a keystone to their leanness and health. It suggests that their diet is not interfering with the body's metabolic feedback loops that maintain leanness."

Stephan makes an interesting point that traditional ratings of blood lipids alone may not be relevant depending on constituents of the diet.

http://www.staffanli...itavaStudy.html

The fact that this effect has been observed in several cultures living independently across the globe illustrates the complexity of nutrition and human health. I don't think you can so easily declare that PUFA is superior to SFA as irrefutable in light of these findings. The most one can claim is that in the context of a SAD, PUFA seems to be superior to SFA intake... but even that is debatable at best when one takes into account the Harvard Nurses Study, etc.

Edited by Skötkonung, 05 October 2010 - 06:58 PM.

[hypnotoad]

Take off your tinfoil hat. Now to move beyond a priori condemnations.

No tinfoil hats here, and nothing "a priori" about it. Just going by the empirical evidence.

Of course a fair summary is easy: very low CHO diets if not of the eco-atkins type are quite damn toxic

How so?

Edited by hypnotoad, 05 October 2010 - 11:45 PM.

[zoolander]

No one here is going to be following that crap anyway. A board full of vegans, vegetarians, paleo eaters , CR followers , supplement takers etc. has long since moved past things like the USDA food pyramid.

Generally whatever the government, big agriculture and food companies, and big pharma advises me to do, I do the exact opposite.

I do understand this however one of the main issues here is that once these guidelines are set it becomes increasingly difficult to modify the guideline. It makes it difficult to get research grants when individuals in the study are placed on to diets that do not conform to the guidelines, it makes it difficult to develop diet programs to be accredited when they don't conform to the guidelines and so on on.

[JLL]

Low-carbohydrate diets: Science is inaccurately represented
Of course a fair summary is easy: very low CHO diets if not of the eco-atkins type are quite damn toxic.

Toxic in what way?

Dietary fat and health outcomes
The SAFA connection w/ insulin resistance can indeed be criticized. The evidence of an effect on TC/HDL and LDL/TC vs PUFA is basically irrefutable.

And that effect is what? Are you saying SAFA lowers the HDL/LDL ratio? What about PUFA increasing ox-LDL and Lp(a), which are much stronger risk factors of CVD than even TC/HDL?

Who cares what SAFA does to TC -- the whole premise of TC causing heart disease is false.

But than the author goes off justifying SAFA using corner cases and Jakobsen et al. which, weakly or not, indicts SAFA. That is not an argument for your case.

"The conclusion of the DGAC Report suggests that the replacement of SFA with monounsaturated fatty acids or PUFA creates unequivocally positive cardiovascular risk factor outcomes; this is not the case. Studies cited by the DGAC Report demonstrate increases in atherogenic lipoprotein levels or triacylglycerols, decreases in high-density lipoprotein cholesterol, and varied metabolic responses to lowered dietary SFA in subpopulations"
The evidence in favour of MUFA and surrogates is strong and the evidence in favour of mixed MUFA/PUFA sources is incredibly strong e.g. nuts and EVOO.

In favour of MUFA or in favour of olive oil polyphenols?

Dietary fiber and whole grains: Conclusions do not reflect the quantity and/or quality of science
Justified criticism but ultimately futile: strong evidence suggests that foods rich in fibre are healthy whether because or in spite of fibre is only secondary.

Wrong, because you're essentially talking about vegetables and fruits, while the fiber theory is used to promote whole-grain wheat products. And where is the evidence whole grain wheat is healthy?

Animal versus plant protein: Recommendations do not reflect limitations and uncertainties of the science
Buhu. The same mistake as in the SAFA-paragraph. The evidence is “moderate, limited, insufficient and inconsistent”; i.e. it is weak -- but not weakly in favour of animal protein weakly against! Public policy: better safe than sorry. Sure, you can criticise their tone but the conclusion still stands, veg. > animal protein even if by a small margin.

Where is the evidence showing that vegetable protein is better than animal protein? Show me the proper studies -- not the ones that compare SAD vs. vegetarians etc. because those are not related to the question at hand. Better in what way? Sure it's not better from an amino acid profile perspective. Better maybe if you're striving for a low-protein diet, but then why not just cut back on protein in general?

... this makes clear just how irrelevant this article is to us. We are not public health policy and inertia. We are flexible and will adjust to new evidence, therefore it is almost mandatory to act on the data before the evidence is completely settled. A > B, even if by a small margin, it is still what the best evidence suggests. You go by the preponderance of evidence, not by wishful thinking.

On what grounds would you suggest to act against the evidence? You choose butter over EVOO and nuts? Ok, but it is not science based. GI is irrelevant? The literature disagrees, etc.

But your "evidence" is not the kind of evidence that supports your case in any relevant way. But if you do have proper evidence then by all means hit me up with some links.

[hypnotoad]

No one here is going to be following that crap anyway. A board full of vegans, vegetarians, paleo eaters , CR followers , supplement takers etc. has long since moved past things like the USDA food pyramid.

Generally whatever the government, big agriculture and food companies, and big pharma advises me to do, I do the exact opposite.

I do understand this however one of the main issues here is that once these guidelines are set it becomes increasingly difficult to modify the guideline. It makes it difficult to get research grants when individuals in the study are placed on to diets that do not conform to the guidelines, it makes it difficult to develop diet programs to be accredited when they don't conform to the guidelines and so on on.

I completely agree.. and now we will end up with yet another generation of increasingly sick people who eat the wrong things in the wrong amounts and believe they are going to be healthy because that's what the government tells them to do. They will continue to follow government sponsored high-carb low fat diets that make them fatter and sicker. They will go on statins and insulin, suffer serious side effects (but still die early) because that's what their doctors tell them to do.

I suppose the recommendations are better than promoting guzzling down endless HFCS drinks and eating the SAD, but the people who are going to ignore it completely aren't going to change their diet regardless of what the guidelines say. They are a "lost cause" anyway.

Edited by hypnotoad, 06 October 2010 - 09:40 AM.

[kismet]

But your "evidence" is not the kind of evidence that supports your case in any relevant way. But if you do have proper evidence then by all means hit me up with some links.

I know I have been imprecise w/ some of my statements* to keep it short, nonetheless I am sorry to say that many of your answers read like misrepresentation of what I say and not just misunderstanding (I hope to be wrong). Because many of your arguments have been addressed and refuted (or at least shown implausible compared to the consensus view) here, on the CR-list and in the scientific literature I will respond some other day. For now, the burden of proof lies on you to show your boldest statements to be true (e.g. the incredibly bold TC unrelated to CVD).

*oh darn that, for instance, was outright wrong and should read "The evidence of an effect on TC/HDL vs PUFA & MUFA (and at least in the short- to mid-term) is basically irrefutable."

edit: corrected correction.

Edited by kismet, 06 October 2010 - 06:28 PM.

[hypnotoad]

Toxic in what way?

Yea I'd like an answer for that one as well..

And that effect is what? Are you saying SAFA lowers the HDL/LDL ratio? What about PUFA increasing ox-LDL and Lp(a), which are much stronger risk factors of CVD than even TC/HDL?

Who cares what SAFA does to TC -- the whole premise of TC causing heart disease is false.

That's my understanding as well. Total cholesterol is of limited value compared to individual values of trig/HDL/LDL (+ LDL particle size breakdown)

Cardiologist William Davis sums it up well on his blog:

How often does someone develop coronary heart disease from high cholesterol alone?

Believe drug industry propaganda and you'd think that everyone does. Physicians have bought into this concept also, driving the $27 billion annual sales in statin cholesterol drugs.

In my experience, I can count the number of people who develop coronary disease from high cholesterol alone on one hand. It happens--but rarely.

That's not to say that cholesterol is not an issue. That rant populates many of the kook websites and conversations on the internet that argue that high cholesterol is a surrogate for some other health issue, or that it is part of a medical conspiracy.

The problem with conventional measurement of cholesterol is that it ignores the particle size issue: whether particles are large or small. Small LDL are flagrant causes of coronary atherosclerotic plaque. Large LDL is a rather meager cause. Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

Conventional total and LDL cholesterol do not distinguish between large and small particles, nor reveal the presence of other hidden patterns. An LDL cholesterol of 150 mg/dl, for instance, may contain 100% large LDL--a relatively good situation that by itself is unlikely to cause heart disease, or it might contain 100% small LDL--a very bad situation that is likely to cause heart disease. Just knowing that LDL is 150 mg/dl tells you almost nothing. In 2008, most people have some mixture of the two, particularly with the proliferation of "healthy whole grains" in the American diet, foods that trigger formation of small LDL.

The imprecision and uncertainty of conventional total and LDL cholesterol has provided ammunition for some to discount the entire cholesterol concept. And they are right to a degree: cholesterol by itself is indeed a lousy predictor of heart disease. But small LDL is a very reliable predictor of potential for heart disease. Dismissing the entire concept because the standard measurement stinks is not right, either.

It is therefore an unfortunate oversimplification to say that high cholesterol causes heart disease or that it doesn't. It can--but not always, depending on size and other factors. In my view, it is therefore irreponsible to treat total or LDL cholesterol without knowledge of particle size. I've seen this play out many times: Someone with an LDL cholesterol of 150 mg/dl but all large still gets prescribed a statin drug by his/her doctor. Or someone with an LDL of 100 mg/dl--generally "favorable" by most standards--is not treated but it is all small and the person is truly at high risk. (Also, knowledge that all LDL particles are small does not mean that statins are the preferred agent. In my view, they are not.)

I've also seen in various places on the web that fasting insulin, CRP , calcium score etc. are far more stronger indicators of CVD risk than simple TC.

But I think the focus on TC is a red herring anyway, the underlying issue with the food pyramid that I think is erroneous is the implication that SAFA should be minimized vs PUFA. Not talking about fish oils, but the premise that chemically extracted seed oils (an invention only about 75 years old) are preferable to sat animal fat. The little "oil" image on the pyramid is a Wesson Corn oil bottle. This is clearly wrong, for many reasons, and the end result of the food pyramid are that all vegetables = good (grains, seed oils) and meat = bad. I could not disagree more based on the evidence I've seen.

I have no quibble with the food pyramid promoting fruits and classic food vegetables. But I laugh at putting meat and beans in the same categories, and I'm disgusted that breads, cereals, and pasta are so heavily pushed along with the previous mentioned PUFA heavy vegetable oils. I think the food pyramid is one big advertising billboard for farmers and the agriculture business. It would be nice is they promoted wild/pastured/grass fed meat and fish as well not only for health reasons (3:6) but for ethical and environmental reasons. Such subtleties would be lost on most people I assume, but it would still be a nice addition.

The carbohydrate heavy food pyramid has been a disaster for decades and this is hardly much better than the old version.

Edited by hypnotoad, 06 October 2010 - 10:47 PM.

[hypnotoad]

Wrong, because you're essentially talking about vegetables and fruits, while the fiber theory is used to promote whole-grain wheat products. And where is the evidence whole grain wheat is healthy?

This is another interesting topic. The more I learn, the more convinced I am that excessive soluble fiber is harmful to the body and only small to moderate amounts of insoluble fiber from veggies is needed. Of course that goes against the conventional wisdom we have all been pushed our whole lives. But I think that like just the lipid hypothesis and the "grains are good for you" camp, it's a bunch of half-truths, bad science, and marketing propaganda.

The fact that traditional Inuits and the Muran-period Masai didn't consume any appreciable fiber and don't suffer any ill effects blows holes in the notion that without fiber we'll all drop dead from cancer or constipation or heart disease or whatever else the grain industry is pushing. Of course the occasional paper like this doesn't help the case for bran either: http://www.ncbi.nlm....0?dopt=Abstract

Aside from the various scientific/medical reasons for my changing beliefs, there is the simple fact that whole grains and fiber give my wife raging IBS symptoms (and to me as well to a lesser extent) Since eliminating grains, bran, oats etc. from her diet her IBS has cleared up completely. That's all the evidence I need. We do get some fiber from broccoli, cauliflower etc. so it's not like we are on an Inuit fiber free diet, but if she needed to go that extreme to avoid symptoms I wouldn't worry for her health anymore like I used to.

As with many aspects of food and nutrition, I guess fiber is a "your mileage may vary" sort of subject.

Edited by hypnotoad, 06 October 2010 - 11:12 PM.

[zoolander]

It's great to see this topic getting some discussion.

Obviously, there is quite a bit of disagreement about what is the right diet. This disagreement exist here bit also exists in the research.

In actuality, it's hard to come by strong research when it comes to diet and nutrition. This may be the result of a number of limiting factors.

1) Monitoring diet is not easy. In most studies subjects are consuming their diet in a free living environment and information about diet and the various components of the diet are collected using food frequency questionnaires (FFQs) which are well know for underestimating actual intakes. A more reliable way to measure intakes is to prepare meals and to collect information in a more controlled environment however, in the real world, this is not realistic and it's near impossible to conduct a study with greater than 100 subjects (i.e. well powered) over extended periods of time (e.g. 3 months/12months/24months). So we are left with FFQ's.

2) There is a great deal of interindividual variation in the way we respond to diet and this is largely the result of genetics. This of course makes it even harder to conduct a well-powered study because if you stratify groups based on genotype and then randomly assign subjects to treatment groups the number of subjects you need for the study increases. This is especially the case if you are measuring something that is effected by a gene or gene variations that are present at low frequency in the population you are measuring (which needs to be of the one type if considering genetics or you need further stratifacation). Let's say a particular genotype effects the way we respond to diet and the effect size for this genotype is large (i.e. explains a large proportion of the interindividual difference in response [not often the case]) however, the number of individuals with this variation/polymorphism in the population is small but still clinically valid (eg. 5%). This means if you recruit 100 people, you might only get 5 people with that particular variation. An n of 5 is not enough in most situations. It get's even more complicated if you consider that often there are a number of variations involved (common and rare). Take type 2 diabetes for example. Meta-analyses of genome wide association studies (GWAS) looking at the association between single nucleotide polymorphisms (SNPs) and type 2 diabetes reveal a number of associations (Zeggini,Scott et al. 2008). Most of the SNPs in these studies are associated with insulin secretion and production and thus glycemic control. Another recent GWAS also showed a strong association between genotype and fasting blood glucose (Dupuis,Langenberg et al. 2010). Hence, from this, considering the effect genotype on phenotype (i.e glycemic control) one might conclude that modifying carbohydrate quantity and quality of the diet, based on genotype might be able decrease the risk of type 2 diabetes. I am aware of one study that demonstrated that carbohydrate quality and quantity modified risk of T2D associated with TCF7L2 genotype (Cornelis, Qiet al. 2009). The same could also be said for modifying dietary lipid intake (MUFA vs. PUFA vs. SFA) and the ApoE4 genotype which has been shown on many occasions to be modulated by diet and other lifestyle factors [see Ordovas (2008) for review].

So, with all that said, it's complicated and I've probably only scraped the surface in regards to the many compounding factors in dietary research. We'll be arguing about what is right and what is not right for sometime I think. Genetics has really added another dimension to it and nutrigenetic/genomic research is in it's infancy. Whilst there is quite a bit of research out there looking at SNPs, researching looking at effect of copy number variation (CNV) and rare gene variants on response to diet is hard to come by. Come to think of it there is not a lot of research looking at the effect of SNPs or SNP combinations in response to diet. Most of the research with SNPs looks at disease associations and not response to diet. Finally, might as well through epigenetics in there to complicate the situation even further.

Meh!



References

Cornelis, M. C., L. Qi, et al.(2009). "TCF7L2, dietary carbohydrate, and risk of type 2 diabetes in USwomen." The American journal of clinical nutrition 89(4): 1256-1262.

Dupuis, J., C. Langenberg, et al. (2010)."New genetic loci implicated in fasting glucose homeostasis and theirimpact on type 2 diabetes risk." Nat Genet 42(2): 105-116.

Ordovas, J. M. (2008)."Genotype-phenotype associations: modulation by diet and obesity." Obesity(Silver Spring) 16 Suppl 3:S40-46.

Zeggini, E., L. J. Scott, et al. (2008)."Meta-analysis of genome-wide association data and large-scale replicationidentifies additional susceptibility loci for type 2 diabetes." NatGenet 40(5): 638-645.

Edited by zoolander, 07 October 2010 - 01:50 AM.

[charliesrp]

Very timely article as I am trying to lose weight before the holidays so that I can look my best when I visit my relatives. These tips are sure to come in hand.

Edited by charliesrp, 08 October 2010 - 04:30 AM.

[Dmitri]

Take off your tinfoil hat. Now to move beyond a priori condemnations.

No tinfoil hats here, and nothing "a priori" about it. Just going by the empirical evidence.

Of course a fair summary is easy: very low CHO diets if not of the eco-atkins type are quite damn toxic

How so?

Edit: my mistake Atkins did not die of a heart attack

Anyway, I had a nutritionist in my health class last week who said it's not healthy to be on either side of the extreme (low fat or low carb) that you should have a balanced diet. He mentioned something about people putting a strain on their hearts when they're at both ends of the extreme.

Anyway, I know there are some tribal people which some of you use as examples for the low carb diets, but don't those tribal people also eat fruits and yet people here seem to treat fruits as if they were the plague.

Edited by Dmitri, 31 October 2010 - 08:17 PM.

[JLL]

It annoys me to no end when people take it as an absolute truth that "balance" is somehow magically always better than any extreme.

Is a "balance" between war and peace better than absolute peace? Is a "balance" between feeling good and feeling suicidal better than feeling good all the time? Is a "balance" between health and disease better than extreme health?

Shit no. There is no reason why an extreme diet could not be better than a "balanced" diet. We may not know what the optimal extreme diet is, but that doesn't prove the argument that we should strive for balance. Do we really need to include bread in our diets, just because it makes a diet "balanced"? Why don't we include gravel and cyanide just for the sake of balance?

I hate nutritionists.

[Dmitri]

It annoys me to no end when people take it as an absolute truth that "balance" is somehow magically always better than any extreme.

Is a "balance" between war and peace better than absolute peace? Is a "balance" between feeling good and feeling suicidal better than feeling good all the time? Is a "balance" between health and disease better than extreme health?

Shit no. There is no reason why an extreme diet could not be better than a "balanced" diet. We may not know what the optimal extreme diet is, but that doesn't prove the argument that we should strive for balance. Do we really need to include bread in our diets, just because it makes a diet "balanced"? Why don't we include gravel and cyanide just for the sake of balance?

I hate nutritionists.

I believe you're taking this to a whole other level and I don't see how you can compare some of those things you mentioned to a diet. Either way we were discussing the more extreme low carb diets the types that almost exclude carbs altogether (which some people here seem to do as they're even afraid of eating a fruit).

[xEva]

The verdict against salt is clear cut. (although, it may have paradoxical effects on lipid metabolism)

What paradoxical effects? I'm interested in the subject of salt. Googling was not helpful. Thanks.

[kismet]

I have been asked to elaborate on a few questions, if anyone still remembers, and I will get to answering some of them. I decided to deal with arguments that seem novel to me and to try to ignore those that probably have been discussed at length already. First, a few general remarks. Second, Lp(a) and fatty acid intake. Third, a quick glance at oxidative stress and fatty acid intake (later on).

Low-carbohydrate diets: Science is inaccurately represented
Of course a fair summary is easy: very low CHO diets if not of the eco-atkins type are quite damn toxic.

Toxic in what way?

Atkins very low carb as done in the literature and by its followers usually ranges between "the SAD taken to the extreme and stripped off carbs" and a very low carb diet without much emphasis on vegetarian food sources. If you accept either premise (or both) that a. fruits and vegetables are healthy, b. nuts, EVOO, legumes, etc are healthy it definitionally follows that your regular atkins diet (violating both a & b) has to be unhealthy.
Then I simply use "toxic" and "pretty unhealthy" exchangably.

"The conclusion of the DGAC Report suggests that the replacement of SFA with monounsaturated fatty acids or PUFA creates unequivocally positive cardiovascular risk factor outcomes; this is not the case. Studies cited by the DGAC Report demonstrate increases in atherogenic lipoprotein levels or triacylglycerols, decreases in high-density lipoprotein cholesterol, and varied metabolic responses to lowered dietary SFA in subpopulations"
The evidence in favour of MUFA and surrogates is strong and the evidence in favour of mixed MUFA/PUFA sources is incredibly strong e.g. nuts and EVOO.

In favour of MUFA or in favour of olive oil polyphenols?

In favour of both, of course. As I said the data on MUFA and surrogates is strong, as shown by the non-EVOO literature, e.g. KANWU. There is good evidence for MUFA, very strong evidence for MUFA-rich plant sources (nuts and EVOO). The point is that you cannot get the latter w/o the MUFA (and often quite some PUFA).

So your average SAFA source is usually a. less studied and/or b. proven to be less beneficial than your typical plant-based MUFA-source. If you do not want to promote MUFA for its inherent (putative) benefits, you basically have to recommend it indirectly in the form of nuts and EVOO. In fact, the latter seems more prudent anyway.

Dietary fiber and whole grains: Conclusions do not reflect the quantity and/or quality of science
Justified criticism but ultimately futile: strong evidence suggests that foods rich in fibre are healthy whether because or in spite of fibre is only secondary.

Wrong, because you're essentially talking about vegetables and fruits, while the fiber theory is used to promote whole-grain wheat products. And where is the evidence whole grain wheat is healthy?

Where is the evidence that whole grains are unhealthy that you speak of? The evidence both for and against moderate hole-grain intake (esp. non-wheat, low GI varieties) is mixed. Thus if recommendations to increase fibre-intake promote both whole-grain, vegetable and fruit intake, they would be largely beneficial. But I concur that a stronger focus on foods or food categories over nutrients may be called for in this and many other cases.

continued in the next post...

Edited by kismet, 13 November 2010 - 07:59 PM.

[kismet]

Keep in mind, lipoprotein metabolism is not my area of expertise, caveat emptor, as they say.

I will not address the "cholesterol con" claim that TC is irrelevant. It is bogus and not really pertinent to the discussion because TC/HDL is indeed a better predictor as you said yourself. Of course, neither LDL/HDL nor TC/HDL would be any better a marker than HDL alone if TC were irrelevant. I do not know what your stance is since you seem to concede that TC/HDL is important to some degree.

Anyway, for my answer, I will rephrase your question: Does PUFA & MUFA improve the TC/HDL ratio and would this outweigh the putative effects on Lp(a) and oxLDL?

Lipoprotein(A) and its relation to CVD as well as fatty acid intake
First, it remains to be seen if Lp(a) is a causal risk factor. Correlation does not mandate causation: in epidemiology detrimental changes will be very difficult to discern from positively adaptive ones. Based on the biological role of Lp(a) a protective role, at least under specific circumstances, has been suggested:
"In a similar manner, we hypothesize that under certain settings, Lp[a] acts as an acute-phase reactant and its levels are increased in plasma within the context of the genetically determined set point. In turn, we postulate that the physiological role of Lp[a] may be to preferentially bind and transport OxPLs that are derived from apoptosis and cell death, as occurs during inflammation and oxidative stress, or when OxPLs are mobilized from tissues during iatrogenic plaque rupture during PCI or during lesion regression in response to therapeutic interventions. Lp[a] may possibly even detoxify OxPL." [1]

If we entertain the notion that, yes, LP(a) is a true risk factor, then it is still a rather modest one [2]:
“In a common set of participants, the adjusted RR for CHD per 1-SD higher Lp(a) concentration was considerably weaker than the corresponding RR with non-HDL cholesterol (1.14 vs 1.66, respectively)”
Keep in mind that TC/HDL is even more powerful than non-HDL cholesterol!
“Lipoprotein(a) concentration is, however, a relatively modest coronary risk factor, being only about one-quarter as strong overall as non–HDL cholesterol, although Lp(a) may become proportionally more important to CHD at very high concentrations owing to its potentially curvilinear risk relationship.”

I don't know where the idea that Lp(a) is an exceptionally strong risk factor originated. Perhaps people did not notice that risk estimates successively diminished in more recent meta-analyses; that the effects may be only pronounced at extremely high Lp(a) levels or under other specific circumstances. (see [2] among others)

To play the numbers game if we wish to back up the above notion (read [2] to follow the back of the envelope calculations):
-10% SAFA, +20% LP(A); this likely overestimates the increase when replacing SAFA with fat a little but may work for CHO (see e.g. KANWU) [3, 4]. Note that not all studies find SAFA to lower Lp(a), though, many or most do.
+20%/+350% (1 SD) = 0.057 factor
Let’s use the highest estimate for mortality: Coronary death RR 1.14 (1.07-1.22) per one standard deviation of Lp(a)
New RR: 1.013; even if we generously round a modest ~2%

Different fatty acids and the TC/HDL ratio
Yes, what about different fatty acids and TC/HDL? Based on the Mensink et al. meta-analysis [5] (but calculated by Mozaffarian et al. [6]):
“In short-term feeding trials, each 5%E of PUFA replacing SFA lowers low-density lipoprotein cholesterol (LDL-C) by 10 mg/dl, without an appreciable reduction in HDL-C, producing a lowering of the TC:HDL-C ratio by 0.16 [Mensink et al.]... In observational studies of adults aged 40–59 y, each 1 unit lower TC:HDL-C is associated with 44% lower risk of CHD [Prospective Studies Collaboration, my ref. 8] Based on these two sets of data, a 5%E increase in PUFA replacing SFA would be predicted, based on TC:HDL-C effects alone, to reduce occurrence of CHD by 9%” [6]

I do arrive at different, though, pretty similar results both using their data (for 40-59yo) and estimates better applicable to the population at large:
TC/HDL change when 1%E PUFA is substituted for CHO or SAFA*
-0.032 (-0.042, -0.022)

for 10E% and a 33% risk reduction** per -1.33 units TC/HDL (see [8]) we get:
-7.9% (-10.4%, -5.4%) IHD mortality

If you prefer to have all your results from one solid RCT look again at KANWU [3]. I arrive at a qualitatively similar result for MUFA when I calculate their change in TC/HDL and use that instead of Mensinks' meta-analysis (data not shown).
Note, that these calculations are consistent w/ RCTs (Mozaffarian et al. [6]) and the epidemiology (Jakobsen et al. [7]***) and further drive home the point: TC/HDL may be the key risk factor here and PUFA really is superior to SAFA in the population at large.

Again I am comparing "worst-case" scenarios for unsaturated fatty acids (lowest conceivable risk reduction via TC/HDL lowering) with a "best-case" scenario for SAFA (largest imaginable risk reduction via Lp(a)), but, based on my data, the CIs still do not come close to overlapping.
Conclusion, positive effects on Lp(a) from SAFA do not come close to outweighing benefits to the TC/HDL ratio that unsaturated FAs show under normal circumstances.

Usually one way to counter the evidence is to dismiss Mensink et al. for analysing short-term data (e.g. Stephan from wholehealthsource.blogspot.com). However, this also massively weakens one's argument against PUFA. If adaptation to high SAFA intakes takes place, the same might be true for PUFA in regards to ALL its postulated side-effects (LP(a) and ox. stress, see below). This line of reasoning is interesting and I haven't reviewed it in any detail, but the data reviewed by Mozaffarain et al. [6] clearly refutes key aspects of this hypothesis: long term PUFA RCTs do lead to reduced TC.

*since substitution of CHO with SAFA is neutral I used the pre-calculated table for CHO given by Mensink not the actual equations; MUFA lowers the TC/HDL ratio a little less than PUFA (not significant)
**I suppose here it would be better also to use the confidence intervals given by [8] for best accuracy but I cannot find them for the whole set in the given pdf, though, the lowest available risk estimate is -26% (70-89yo group). This is so pessimistic as to be ridiculous and would give a lower bound of -4.3% for PUFA.
***for the sake of completeness: this is the study showing MUFA to be neutral or very slightly detrimental vs SAFA; why this may be artifactual is discussed by the authors and has been addressed on this forum and elsewhere -- but this is not contrary to my point, which is simply that both PUFA and MUFA edge out SAFA when all lines of evidence are considered. Though, some studies point towards a risk from MUFA, currently, this remains the weaker proposition IMHO.

[1] A novel function of lipoprotein [a] as a preferential carrier of oxidized phospholipids in human plasma. Bergmark C, Dewan A, Orsoni A, Merki E, Miller ER, Shin MJ, Binder CJ, Hörkkö S, Krauss RM, Chapman MJ, Witztum JL, Tsimikas S.
J Lipid Res. 2008 Oct;49(10):2230-9. Epub 2008 Jul 1. http://www.jlr.org/c...49/10/2230.full
[2] JAMA. 2009 Jul 22;302(4):412-23.
Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. Emerging Risk Factors Collaboration
http://jama.ama-assn.../full/302/4/412
[3] Atherosclerosis. 2003 Mar;167(1):149-58.
Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects.
Rivellese et al.
[4] Am J Clin Nutr. 2007 Dec;86(6):1611-20.
Comparison of monounsaturated fat with carbohydrates as a replacement for saturated fat in subjects with a high metabolic risk profile: studies in the fasting and postprandial states. Berglund et al.
http://www.ajcn.org/.../full/86/6/1611
[5] Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003; 77: 1146–1155.
http://www.ajcn.org/.../full/77/5/1146
[6] Mozaffarian D, Micha R, Wallace S (2010) Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLoS Med 7(3): e1000252. doi:10.1371/journal.pmed.1000252
http://clinicaltrial...al.pmed.1000252
[7] Am J Clin Nutr. 2009 May;89(5):1425-32. Epub 2009 Feb 11.
Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Jakobsen et al.
http://www.ajcn.org/.../full/89/5/1425
[8] Lancet. 2007 Dec 1;370(9602):1829-39.
Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths.
Prospective Studies Collaboration et al.

Edited by kismet, 13 November 2010 - 11:41 PM.

[Sillewater]

wow, missed this gem, luckily kismet you linked to it from another post. Let the calculations begin.

[Sillewater]

If anyone is interested there is a great book:

http://www.pjbarnes.co.uk/op/nut.htm

It was published over 10 years ago but it was still a great read and in my opinion accurate.