The Year of the Fat

During the first few months of this year, we’ve seen at least three strong signs suggesting that health authorities have misled the public for several decades about dietary fats. This finding is of particular interest because later this year the 2015 Dietary Guidelines for Americans will be published.

Ever since the beginning of the 1960s, “eat less fat, in particular, less saturated fat and cholesterol” has been repeatedly emphasized by medical professionals and other experts.

The Year of the Fat

Food manufacturers have played along by emphasizing low-fat food varieties of all possible kinds, whether it’s dairy products or something else. Butter consumption has decreased, and cooking oils have become very popular, all according to public health advice with the aim to eliminate cholesterol and saturated fat from our dishes.

What started all this was observational data showing an association between blood cholesterol and the risk of cardiovascular disease. Many health experts assumed that by reducing cholesterol and saturated fat in our diet the epidemic of heart disease might be stopped because these interventions would lower blood cholesterol. However, this was an untested hypothesis.

Nobody knew what would happen after the first US dietary recommendations were launched in 1980 because the implications of such an advice had never been tested in a scientific study.

Today, these guidelines may be regarded as a research protocol for the biggest dietary intervention trial so far performed. The trial was designed without a control group; everybody had the same advice. There was no informed consent and the trial wasn’t performed according to defined ethical principles for medical research involving human subjects (1).

However, to be fair, the death rated from coronary heart disease has dropped dramatically in most western countries for the past 30 years. Of course, this achievement is due both to modification of risk factors and improved treatment. Data from the US and many other countries suggest that lowering of cholesterol in the population may have contributed to this benefit (2).

On the other hand, since the introduction of the dietary guidelines, rates of obesity and diabetes have risen dramatically.

In fact, questions have repeatedly been asked about the Dietary Guidelines for Americans. It has been pointed out that the guidelines were implemented despite lack of supportive evidence and in the face of contradictory evidence (3).

Recently, the Dietary Guidelines Advisory Committee published its Scientific Report (4) preparing for the upcoming 2015 edition of the Dietary Guidelines for Americans. The U.S. Department of Health and Human Services (HHS) and the U.S. Department of Agriculture (USDA) jointly publish the Dietary Guidelines every five years.

The Scientific Report reflects important changes regarding dietary fats compared with previous guidelines. At the same time, two recent scientific publications suggest that our basic assumptions on dietary fats may have been wrong from the beginning.

Dietary Cholesterol

Recommendations to reduce dietary cholesterol were initiated by the American Heart Association (AHA) in the 1960s and have been a mainstay of the USDA and other public health guidelines for many years. All this time, excess dietary cholesterol has been regarded as a public health concern.

According to the Recent Scientific Report from the Dietary Guidelines Advisory Committee (4), ”Cholesterol is not considered a nutrient of concern for overconsumption.” It is assumed that this change of direction will make it to the final guidelines that will be published later this year.

Although blood levels of cholesterol are still considered an important risk factor for cardiovascular disease, the abrupt change of direction reflects scientific data suggesting that cholesterol consumed in food appears to play a minor role in determining the blood levels of this substance.

So apparently, the guidelines have been wrong for decades. There is no reason anymore to believe that eating eggs or other food rich in cholesterol will cause heart disease.

It will be interesting to see how the AHA will approach this recent change of heart.

The Year of the Fat

Saturated Fat and Heart Disease

From the beginning, dietary guidelines have underscored the importance of limiting the amount of saturated fat in our diet. This advice was based on observational data showing an association between the intake of saturated fats and death rate from heart disease.

It is well known that although observational studies may show an association between two variables, they can very rarely prove a causative relationship. Although dietary guideline committees have always been aware of this fact, they have been determined to stick with their initial approach regarding saturated fat, most likely because of their immense respect for blood levels of LDL cholesterol (5).

For decades, LDL cholesterol has been regarded as an important target when it comes to reducing the risk of heart disease. It’s often assumed the almost every measure able to lower LDL cholesterol will be beneficial.

There is some evidence linking the consumption of some types of saturated fat with raised LDL cholesterol. Accordingly, these fats will increase risk. But, using surrogate markers like LDL cholesterol to determine risk may be misleading (6).

Only randomized clinical trials can prove that the intake of saturated fats will increase the risk of heart disease. Interestingly, results from such trials were available the time of the publication of the first dietary guidelines

Last month, British investigators published a systematic review and meta-analysis of results from randomized clinical trials that were available when the first US and UK dietary guidelines were published in the late 1970s and early 1980s (7).

The authors found six dietary trials, including a total of 2.467 male participants. The intervention differed somewhat between studies but all aimed at reducing total fat and/or saturated fat consumption in the intervention group.

There were no differences in all-cause mortality and non-significant differences in mortality from heart disease, resulting from the dietary interventions. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups.

So despite lowering cholesterol, interventions aimed at reducing saturated fat intake did not lower mortality nor decrease death rate from heart disease.

The authors arrived at three pretty sobering conclusions:

Government dietary fat recommendations were untested in any trial prior to being introduced

Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from randomized clinical trials

The present review concludes that dietary advice not merely needs review; it should not have been introduced

Macronutrient Consumption Data

In 1977 the U.S. Senate Selection Committee on Nutrition and Human Needs issued Dietary Goals for the United States, which recommends that fat consumption be reduced to 30% of energy intake, and that carbohydrate consumption be increased to account for 55-60% of energy intake (8).

The focus on the relative contribution of different macronutrients was maintained by the first Dietary Guidelines for Americans that were launched by the USDA in 1980 and have remained largely unchanged since then.

There were two reasons experts believed reducing fats and increasing carbohydrates would be beneficial. Firstly, this would lower blood cholesterol and thereby the risk of heart disease. Secondly, because one gram of fat contains more calories than one gram of carbohydrates, the intervention would reduce the risk of obesity.

A recently published U.S. paper addresses the long-term dietary consumption of the U.S. population from 1965-2011 based on NHANES (National Health and Nutrition Examination Survey) data focusing on Americans aged 18-64 (9).

The main goal of the study was to address whether Americans have been following dietary guidelines with regards to the macronutrient composition of the diet.

Untitled
Cohen et al, Statistical review of U.S. macronutrient consumption data, 1965–2011 Americans have been following dietary guidelines, coincident with the rise in obesity doi:10.1016/j.nut.2015.02.007

In 1965, fat consumption comprised 44.7% of calories of adult Americans’ diets, compared with 39% for carbohydrate. By 1999, fat consumption reached a through of 32.4% while carbohydrate consumption hit its peak at 52.1%. Protein consumption remained relatively constant throughout the period.

In 1971, saturated fat comprised 13.5% of total calories. By 2011, Americans were eating 10.7% of their calories as saturated fat (a 20.5% reduction since 1971).

Per capita cholesterol consumption decreased down below 300 mg/day, from over 400 mg/day in 1971.

The study also confirms a clear shift towards more obesity during the study period.

The authors underscore that there is a strong correlation between the increase in carbohydrate share of total intake and obesity.

They also address the question whether the increased prevalence of obesity can be explained by an increase in overall calorie intake by conducting their tests over two subsamples of participants who consumed similar calories over time. They conclude “the increase in calorie consumption since 1971 is not likely to offer any significant explanation for the increase in BMI (body mass index) over the last four decades.”

The main findings of the study were

  • Americans have been adhering to federal dietary guidelines for the past 40 years
  • Fat consumption by U.S. adults has decreased from 45% to 34% between 1965 and 2011
  • Carbohydrate consumption has increased from 39% to 51% over this same period
  • There is a high correlation between the change in diet and the rise of obesity
  • The percentage of overweight adults has increased from 42% to 66% since 1971

The Bottom Line

Recently we have seen important evidence suggesting that the fear of dietary fats, in particular, the fear of saturated fats and cholesterol is not based on reliable scientific data.

This evidence adds further to the belief that we have been misinformed for decades by public authorities about dietary fat intake.

Although authors of dietary guidelines seem to have admitted that there is no reason to avoid dietary cholesterol, I’m still afraid they haven’t got it right. For example, the advice to avoid saturated fats was never based on evidence from randomized clinical trials.

It is hard to accept that public health recommendations are not based on solid scientific evidence.

A  part of the problem is that the guideline process is too complicated, and recommendations are often hard to change.

The dietary fat history is a tragic example of how easy it is to mess things up for years when you get it wrong from the beginning.

Guideline writers should acknowledge the lack of evidence for most recommendations and write shorter guidelines. They should stick to hard evidence. Who needs hundreds of pages of expert consensus? The public deserves to be guided by real science.

Finally, despite the forthcoming 2015 Dietary Guidelines for Americans, this could be the year of the fat.

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davebrown9
davebrown9
5 years ago

Good commentary. Indeed, the Dietary Guidelines Advisory Committee would do well to stick to hard science. There is no hard science linking saturated fat intakes to heart disease. There is hard science indicating that intakes of linoleic acid exceeding 2 percent of calories causes problems. For example, “Linoleic acid (LA) is the most abundant polyunsaturated fatty acid in human diets, a major component of human tissues, and the direct precursor to the bioactive oxidized LA metabolites (OXLAMs), 9- and 13 hydroxy-octadecadienoic acid (9- and 13-HODE) and 9- and 13-oxo-octadecadienoic acid (9- and 13-oxoODE). These four OXLAMs have been mechanistically linked… Read more »

Nina Teicholz
5 years ago

Dear Dr. Sigurdsson,
I’d greatly appreciate a reference to my work in your post. These ideas are nearly all derived from my work, including my recent op-eds in the New York Times and the Wall Street Journal, as well as my book, The Big Fat Surprise.
Thank you very much!
Nina Teicholz

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Nina Teicholz

Dear Nina As you know I’ve read your book and respect your writing and research. I’ve previously mentioned your book on my blog in the context of dietary fats and will be happy to do so again. It so happens that I’ve been writing blog articles about dietary fats for some years now, starting long before your book was published. I don’t think you’ve referred to any of my writings. The three issues/studies I bring up in this particular blog article are based on my own studies and opinion. The fact that some of my writing may coincide with your… Read more »

Charles Grashow
Charles Grashow
5 years ago
Reply to  Nina Teicholz

And how many of the ideas in your book were derived from GCBC by Gary Taubes?

Are we supposed to bow down to the all knowing Nina Teicholz??

Research is research – live with it!

Robert
Robert
5 years ago
Reply to  Nina Teicholz

Mrs. Teicholz, quite a few of us readers, just like Dr. Sigurdsson, are trained medical doctors with primary knowledge and sometimes primary research in the matter, and as much I’m sure your book (which I haven’t and will not read) is a wonderful compilation by a non-technical bright popularizer, please rest assured that most of us build our medical knowledge from trusted peer reviewed articles and not the last greatest book or personal hypothesis we’ve read about. So maybe there’s some sense lost in translation (I am not an English mothertongue speaker) but to me your statement sounds like a… Read more »

Chris
Chris
5 years ago
Reply to  Robert

This is great. Thanks for stepping down from your pedestal to share your opinion. I found Ms. Teicholz’s work far more informative than anything here, which is amazing considering she doesn’t have your privileged education.

Bob Johnston
5 years ago
Reply to  Robert

I was gonna let this one slide but what the heck… Robert – you’re kidding yourself if you think that “peer review” means diddly squat when it comes to the correctness of a study. The abuses of peer review are shameless in many fields, nutrition and climatology spring to mind as supreme examples. Having actually read The Big Fat Surprise I feel like I can make an educated comment about it – it’s a terrific expose of just how poor nutritional guidelines are that delves not into just the science and history but also the personalities, which is quite important.… Read more »

George
George
4 years ago
Reply to  Robert

Perhaps the point is that Big Fat Surprise had a major influence on the attitudes to fat in mainstream media that are an important part of the subject being discussed, not that Axel has necessarily used any of Ms Teicholz’s intellectual property in this post.

Amy
Amy
5 years ago

Hi re the cholesteroland dietary fat esp saturated fat what do you suggest if someone has high lpa and should reduce unsaturated fat and carbs but increase saturated fat ..BUT has the apoe 3/4 gene which calls for very very low fat from all sources..little to no saturated at all little to no animal protein and high carb and low to NO cholesterol as apoe4 s over absorb cholesterol and fat from the food we eat ..im a rock stuck in a hard place

Charles Grashow
Charles Grashow
5 years ago

“In 1965, fat consumption comprised 44.7% of calories of adult Americans’ diets, compared with 39% for carbohydrate. By 1999, fat consumption reached a through of 32.4% while carbohydrate consumption hit its peak at 52.1%. Protein consumption remained relatively constant throughout the period.

In 1971, saturated fat comprised 13.5% of total calories. By 2011, Americans were eating 10.7% of their calories as saturated fat (a 20.5% reduction since 1971).”

If total calories increased then the percentage increase/decrease would be affected by that and people are just playing around with numbers to prove a point.

Mie
Mie
5 years ago

Indeed. Carbsane appropriately demolishes this nonsense – which Axel sadly seems to have swallowed just like that.

davebrown9
davebrown9
5 years ago
Reply to  Mie

What puzzles me is that nobody on either side of the saturated fat divide pays attention to linoleic acid research.

“Linoleic acid (LA) is the most abundant polyunsaturated fatty acid in human diets, a major component of human tissues, and the direct precursor to the bioactive oxidized LA metabolites (OXLAMs), 9- and 13 hydroxy-octadecadienoic acid (9- and 13-HODE) and 9- and 13-oxo-octadecadienoic acid (9- and 13-oxoODE). These four OXLAMs have been mechanistically linked to pathological conditions ranging from cardiovascular disease to chronic pain.”
https://www.ncbi.nlm.nih.gov/pubmed/22959954

Mie
Mie
5 years ago
Reply to  Mie

What bothers ME about that comment Dave is that it’s a strawman. Plain and simple.

You’ve been told before that normal consumption of n-6 fatty acids is by no means detrimental. You’ve paid no heed to this.

George
George
4 years ago
Reply to  Mie

“You’ve been told before that normal consumption of n-6 fatty acids is by no means detrimental.”
That depends what you want to die of
https://www.ncbi.nlm.nih.gov/pubmed/16573374

Joe
Joe
5 years ago

I had gone over to the low carb crowd years ago, getting 70% of my cals from saturated fat, about 20 from protein and 5 or less from carbs. My total C went from 185 to 404, LDL from 105 to 305. All other numbers good. So, within the low carb crowd there are some that say whoa, that is too high and others who say, under 500 or 600 its still not a problem.

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Joe

Hi Joe

It’s well known that eating much saturated fats raises total, LDL and HDL cholesterol. What this means in terms of risk is still a matter of debate.

We also have to keep in mind that not recommending a limitation of saturated fat intake is not the same thing as encouraging high intakes.

Jennifer Elliott
5 years ago

I’d like to understand more about the saturated fat and total cholesterol connection. Could you comment on my thinking that for a rise in TC to be attributable to saturated fat, the fatty acids would need to be extracted and fed separately. Otherwise, aren’t we observing what happens when foods are eaten and then attributing the effect to different components? Ancel Keys made up his equation by doing this, which led to the belief that sat fat raises chol, PUS reduces it and MUS is neutral. He deemed butter to be sat fat and the short term rise in TC… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago

Hi Jennifer

This is a complex issue. Stephan Guyenet covers some of the literature nicely here.

Mie
Mie
5 years ago

Guyenet’s post has several problems in it. 1) If you want to know accurately about the role of nutrient X on lipid levels, you need to conduct a metabolic ward study. Period. Observational studies among free-living individuals are BY DEFAULT incapable of examining this – they of course have their uses (more of which below) – as it is simply impossible to get free-living individuals to comply & report accurately. Guyenet’s comment on the “poor quality” of such studies suggests that he hasn’t actually read the original papers or e.g. Mensink et al (2003) meta-analysis of such studies – otherwise… Read more »

Mie
Mie
5 years ago

As for Jennifer’s question: based on her article, it seems that there simply isn’t (nor will there be) evidence that would satisfy her request. E.g. this “Could you comment on my thinking that for a rise in TC to be attributable to saturated fat, the fatty acids would need to be extracted and fed separately. Otherwise, aren’t we observing what happens when foods are eaten and then attributing the effect to different components?” shows remarkable ignorance on the question of e.g. individual safas and carrier foods (which I commented upon, the fermented cheese part). Findings in met.ward studies clearly indicate… Read more »

George
George
4 years ago
Reply to  Mie

Findings from very low carb studies show that increased SFA can’t raise LDL if there’s little CHO in the diet in most subjects, in fact LDL usually drops a tiny bit.
Which begs the question, what are feeding studies really looking at?
And then, of course LDL is not a discrete entity, the way glucose is, say, or insulin. The putative atherogenicity of the LDL particle is modified by CHO.

Charles Grashow
Charles Grashow
5 years ago
Reply to  Joe

@Joe

Have you had your LDL-P checked?

Kevin O'Connell
Kevin O'Connell
5 years ago

I would not bet against something along the lines of ‘Our recommendations remain just as correct as the day we coined them*, but because there may have been some increase in overall calorific consumption, we must do MORE of the same. We therefore now recommend a reduction in total fat intake to below 25% of total energy intake (SFA 5% or less) and that CHO be increased to a minimum of 60%.’ There might even be a mention in favour of PCSK9 cholesterol-lowering drugs.

*Note the cunning wording, allowing a get-out-of-jail-free play if ever required. (Cynical? Moi?)

Jennifer Elliott
5 years ago

And I meant to say thank you for another great article!

Jennifer Elliott
5 years ago

Hi Axel

Thank you for the link. I think Stephan may be saying the same thing; that Ancel Keys metabolic ward studies from the 60s are the basis of the sat fat/ chol connection. I’ll ask him though.
I’ve looked at those studies in some detail and the flaws are incredible. The Aust Heart Foundation admitted in a position paper that their dietary recommendations are based on Key’s work.
My paper was published last year and if you have time to have a look, I would really appreciate your opinion
https://dx.doi.org/10.4236/fns.2014.519201
Thank you, Jen

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago

That’s interesting Jennifer.
Thanks for the link.

Mie
Mie
5 years ago

Repeating the low carb/cholesterol denialist mispresentation about Keys (which Seth, BTW, has addressed here),

https://thescienceofnutrition.wordpress.com/2014/04/21/fat-in-the-diet-and-mortality-from-heart-disease-a-plagiaristic-note/

misrepresenting the case of FH by cherrypicking one man’s opinion etc. etc. – and, in general, amusement that results from referring to select number of ancient papers as somehow being evidence showing that lipid hypothesis as we know it in 2014 would be fundamentally wrong.

What did you hope to accomplish with this, Jennifer?

George
George
4 years ago
Reply to  Mie

To make people think, Mie.
People are still allowed to think, aren’t they?

tannngl
5 years ago

Dr. Sigurdsson,

Thank you for keeping me up to date on the latest in regards to dietary fat and its causal relationship to disease-or, rather, non-relationship to disease.

I’m surprised the news media hasn’t picked this up in the states. I haven’t seen a single report on this on any of the news networks.

Could it have that little value?

So happy to have found your blog.

davebrown9
davebrown9
5 years ago

@ Jennifer Elliott, Around 1980 I read a book by Hal Huggins, DDS entitled “Why Raise Ugly Kids?” He recommended consuming 2 eggs and a quarter pound of butter to bring total cholesterol up if it was low and lower cholesterol if it was high. Charting cholesterol changes in patients who followed his advice, there was a convergence around 220 mg/dL. That value falls close to the lowest point of the cholesterol/ all cause mortality curve. https://healthcorrelator.blogspot.com/2009/12/total-cholesterol-and-cardiovascular.html When asked how doing the same thing could produce different results, he noted that his advice always contained the recommendation to reduce sugar… Read more »

Max_Headroom
Max_Headroom
5 years ago

The year of the Fat…indeed! For me it’s a historic year since all my basic knowledge is shattered in pieces and now I wonder how I should raise my family! Since I’m having heterozygous hypercholesterolemia type IIa and ApoE 3/4 allele I was teached all my life (and still am) that a carb-rich, low-fat diet should be my goal. Now I’m testing for the 2nd time LCHF (lowCarb – high fat – the opposite!) and never had such fantastic LDL- and HDL-levels. Even under statins (atorvastatin 40 mg) and ezetimibe LDL hardly made it unter 100 and now it has… Read more »

Max_Headroom
Max_Headroom
5 years ago
Reply to  Max_Headroom

It’s weird that there’s no updated advice for guys like me. Heterozygous FH is said to be quite common – 1:500 and we’re leaving the field to all those drug companies selling statins and that’s it? Despite the fact that 80% of the tretated patients keep failing in reaching their recommended LDL?

I’ll need to figure it out by myself, I guess….

Max

Mie
Mie
5 years ago
Reply to  Max_Headroom

Updated dietary advice based on …? FH cannot be managed by diet alone. Of course, when you lose weight your lipid levels improve, but that cannot go on forever. Surely you knew that?

Max_Headroom
Max_Headroom
5 years ago
Reply to  Max_Headroom

I won’t doubt that I’ll need statins all my life long – that’s o.k.,
But guys like me are still told we should keep a carb-rich diet (60%) and reduce fat esspec. saturated fats.

But since I’ve tried LCHF my blood fats are better than ever and this effect can not be explained by weight loss alone (I’ve hardly lost any remarkable weight in 4 weeks). I wonder how much focus I should pay on this in educating my kid…sparing on the bread or on the butter, that’s the point!

Max

davebrown9
davebrown9
5 years ago
Reply to  Max_Headroom

Max, What is the target LDL you are trying to achieve? It may be too low in view of this. https://www.eurekalert.org/pub_releases/2011-05/tau-cn050511.php

Max_Headroom
Max_Headroom
5 years ago
Reply to  Max_Headroom

The target LDL – that’s a good point. Our “official” recommendations are: LDL-Cholesterol < 160 mg/dl (4,14 mmol/l) That's no problem at all – since November 2013 I'm well below 100 and since I'm doing LCHF (lowCarb-highFat) I circle around 60 (with the help of 40 mg Atorvastatin and Ezetimibe). Without Ezetimibe and a less potential statin (Simvastatin) I had 156-172 LDL cholesterol. Before that, I used Cholestyramine only which caused a high variation of the LDL values (maybe a more dietary influence?) – between 100 and more than 400 but most of the time well above the recommended values.… Read more »

davebrown9
davebrown9
5 years ago
Reply to  Max_Headroom

Max, I’ve studied the supposed connection between saturated fat and inflammation. The only connection is between serum saturated fats caused by high carbohydrate intake or saturated fats injected directly into the bloodstream or brain. Dietary saturated fat alone doesn’t promote inflammation. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0113605

Mie
Mie
5 years ago
Reply to  davebrown9

Not only is the Volek study problematic in terms of its methodology

https://carbsanity.blogspot.fi/2014/11/de-novo-lipogenesis-to-palmitoleic-acid.html

https://carbsanity.blogspot.fi/2014/12/that-new-volek-phinney-study-part-iii.html

https://nutrevolve.blogspot.fi/2014/11/carbs-sfas-and-circulating-fatty-acids.html

but palmitoleic acid isn’t “consistently associated” with adverse health outcomes. See e.g. Chowdhury et al (2014).

As far as inflammation is concerned, safa is about the same as average carbs. Pufa (n-3 in particular) is somewhat anti-inflammatory.

George
George
4 years ago
Reply to  Mie

Chowdhury?
That the paper that’s too badly flawed and full of errors – until a low-fatter finds something in it to use?

davebrown9
davebrown9
5 years ago
Reply to  davebrown9

Mie said, “but palmitoleic acid isn’t ‘consistently associated’ with adverse health outcomes. See e.g. Chowdhury et al (2014).

As far as inflammation is concerned, safa is about the same as average carbs.”

Need clarification. Palmitoleic acid is not a saturated fatty acid. What’s your point.

While I’m commenting, these two papers suggest that swapping linoleic acid for saturated fat is beneficial.

https://ajcn.nutrition.org/content/95/5/1003.full

https://diabetes.diabetesjournals.org/content/63/7/2222.full.pdf

By way of contrast:
https://medicalresearch.com/weight-research/genetically-modified-soybean-oil-plenish-only-slightly-healthier/12425/

Mie
Mie
5 years ago
Reply to  davebrown9

“Need clarification. Palmitoleic acid is not a saturated fatty acid. What’s your point.”

Indeed it isn’t. But Volek et al. suggest that higher amount of palmitoleic acid associated with the high carb phase is the result of DNL – because of higher carb intake.

And yes, the two studies do indeed suggest the benefits of safa –> n-6 exchange.

davebrown9
davebrown9
5 years ago
Reply to  davebrown9

@Mie

“So, to clarify your position, we are to accept this?
Swapping saturated fat and carbohydrates for linoleic acid – the main polyunsaturated fat found in vegetable oil, nuts, and seeds – lowers risk of coronary heart disease…”
https://www.hsph.harvard.edu/nutritionsource/2014/11/05/dietary-linoleic-acid-and-risk-of-coronary-heart-disease/

And ignore this because?
medicalresearch.com/weight-research/genetically-modified-soybean-oil-plenish-only-slightly-healthier/12425/

Mie
Mie
5 years ago
Reply to  davebrown9

“And ignore this because?”

Because – and this applies to the gorilla study below too – animal studies on dietary fatty acids, carbs etc. etc. have little relevance in humans. To give just one example, consider carbs & DNL: paleonistas/low carbers love citing rat studies because DNL is of totally different magnitude in rats whereas in humans it’s virtually insignificant (therefore, eating carbs per se doesn’t make one fat). If soybean oil is bad for human consumption, it needs to be confirmed in studies conducted on humans.

davebrown9
davebrown9
5 years ago
Reply to  davebrown9

@Mie And how are gorillas like rats? “If soybean oil is bad for human consumption, it needs to be confirmed in studies conducted on humans.” Pregnancy https://press.endocrine.org/doi/full/10.1210/jc.2012-2482 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3206402/ https://www.ncbi.nlm.nih.gov/pubmed/25172360 Heart health Careful evaluation of recent evidence, however, suggests that allowing a health claim for vegetable oils rich in omega-6 linoleic acid but relatively poor in omega-3 α-linolenic acid may not be warranted https://www.cmaj.ca/content/186/6/434.extract Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death. https://www.ncbi.nlm.nih.gov/pubmed/21118617 “…a number of important questions remain… Read more »

Mie
Mie
5 years ago
Reply to  davebrown9

“And how are gorillas like rats?” Because they’re both animals? Then the others: 1) Cognitive skills: bear in mind the study designs (cross-sectional), notice the large n-3/n-6 ratios and the large amount of LA in general. Not to mention the dietary choices for linoleic acid, which usually tend NOT to be those recommended by e.g. the guidelines. A lot of variables. N-3 fatty acids may indeed beneficial for cognition, yes – or rather their deficiency may be detrimental (as there’s little data to suggest the benefits of supplementation/higher dietary intake among people who already have a balanced, healthy diet). Or… Read more »

davebrown9
davebrown9
5 years ago
Reply to  davebrown9

@ Mie “the etiology of obesity or DM2 cannot be reduced to a single factor …” I never implied that. I said, “Something is causing the rapid world-wide deterioration in the public health and it is not excessive saturated fat in conjunction with inadequate linoleic acid intake.” The public health message is, “Swapping saturated fat and carbohydrates for linoleic acid – the main polyunsaturated fat found in vegetable oil, nuts, and seeds – lowers risk of coronary heart disease…” https://www.hsph.harvard.edu/nutritionsource/2014/11/05/dietary-linoleic-acid-and-risk-of-coronary-heart-disease/ Do you agree with that or not? Humour me. Present the short version of your argument in response to this… Read more »

davebrown9
davebrown9
5 years ago
Reply to  davebrown9

@ Dr. Sigurdsson, Several times Mie has raised objections to my practice of including snippets of the articles I discuss and/or reference when I post comments. I do that by way of illustration so that readers don’t have to wade through entire articles trying to figure out what I was getting at. Also, opinions and data can be located and viewed in context. I like being able to do that when I read scientific papers. Do you or any other readers of this blog object to what I do? And if so, can you offer suggestions? Should I report on… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  davebrown9

I get your point Dave. I don’t object. It’s a difficult road. I’m not in favour of much copy/pasting but if it’s clearly done in order to make a point I will accept it. Secondly, I prefer comments not to be too long, mostly because I believe very few people read lengthy comments. Then of course, it’s always better if you use your own words instead of someone else’s. But, I guess everybody has their style and I there’s no reason to let Mie dictate how you should do it.

Mie
Mie
5 years ago
Reply to  davebrown9

Dave, “Do you agree with that or not?” The benefits of exchanging safa –> pufa? Yes, I do agree there are benefits. “And I don’t care to wade through all the previous comments you made in search of the relevant information.” That’s too bad. Perhaps you OUGHT to, however, instead of copy/pasting lengthy portions of various studies the methodology, focus etc. etc. of which is ALL OVER the place. If you see no point in trying, why should I repeat myself to you? Your choice. Reply to my criticism or don’t. Whether we’ll continue on the topic is up to… Read more »

George
George
4 years ago
Reply to  Mie

Dave posts links to studies and you question the methodology, Then you post links to blogs.
I presume these are peer-reviewed blogs.

Erik Arnesen
5 years ago

Quote: “For example, the advice to avoid saturated fats was never based on evidence from randomized clinical trials.” First of all, there never were any advice to *avoid* saturated fats, as you know (since I presume you actually read the recommendations). Second, regarding evidence from RCT’s. There are no RCT’s showing that trans fats directly increase risk for cardiovascular disease either. Would you say it’s unfair to recommend avoiding trans fats anyway? Similarly with added sugar etc. Since no RCTs have been done with hard endpoints, would you say that recommending a low sugar intake will be the next ”… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Erik Arnesen

Erik There was advice to “avoid too much” fat, saturated fat and cholesterol. When you’re informing patients like I do it practically means “avoid” because “too much” is obviously a matter of definition. I accept your criticism regarding RCT’s. I know we often have to rely on observational data (smoking, trans-fats, added sugars etc). But that doesn’t mean we can ignore results from RCT’s when they’re available. I know I’m a bit harsh calling the guidelines a research protocol. But, sometimes you have to stretch a bit beyond to be heard. Maybe it’s emotional. As a cardiologist I have been… Read more »

Mie
Mie
5 years ago

Axel, if you instruct your patients with certain simple choices for food and/or ACTUAL diets, they more or less automatically get it right. And as it has been commented multiple times here: if the RCT’s have failed to even test modification X properly, you CANNOT reason that the modification X doesn’t work per se. You can, of course, reason that recommending modification X has little value in clinical practice as it is, but that’s a different thing. If you were to follow the SAME short-sighted reasoning with dietary advice in general, you’d have to STOP recommending any kind of dietary… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

Mie

Why would/should I recommend I dietary intervention that hasn’t been shown to work (like the one in the paper you cited)?

Mie
Mie
5 years ago

“But, sometimes you have to stretch a bit beyond to be heard.”

I’m afraid that in this case you’re not just “stretching”. You’re misrepresenting. Sadly, Erik’s points on the double standard don’t seem to be that far-fetched.

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

Mie (and Erik) Mie wrote: “I’m afraid that in this case you’re not just “stretching”. You’re misrepresenting. Sadly, Erik’s points on the double standard don’t seem to be that far-fetched.” Calling it double standard is fine with me if you prefer to make things personal. I guess I’m happy if my writing raises some eyebrows and makes people think.” My purpose was to highlight the huge responsibility associated with providing lifestyle/dietary guidelines to millions of people. I’m sure we agree that such an advice should be based on very strong scientific data. If it’s based on a hypothesis, or an… Read more »

Mie
Mie
5 years ago

Axel:

“Why would/should I recommend I dietary intervention that hasn’t been shown to work (like the one in the paper you cited)?”

That was for ALL dietary interventions.

If you were to rely on RCT data alone, you couldn’t really recommend anything but Med. diet (best results), could you?

Evelyn aka Carbsane
5 years ago

What RCT evidence is being ignored?

You linked to the Nutrition article that shows that Americans have NOT altered diets in response to recommendations.

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago

The meta-analysis paper (Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis) suggests that results of available RCT’s were not taken into account when the first US and UK guidelines were launched.

The authors of the Nutrition article concluded that Americans HAVE altered diets isn response to recommendations. I assume you don’t agree 🙂

Mie
Mie
5 years ago

Axel, I suggest you read what Charles wrote above:

“If total calories increased then the percentage increase/decrease would be affected by that and people are just playing around with numbers to prove a point.”

Americans are now consuming more calories. The actual amount of e.g. fat hasn’t thus changed virtually at all.

Furthermore, when it comes to e.g. fat sources, intake of fruits and veggies etc. etc. Americans seem to be pretty far from guidelines.

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

Mie I agree with that. I do realize that calories play a role. This is a peer reviewed paper and all I did was summarize the findings and the authors’ main conclusions. These conclusions weren’t mine although I found them interesting (and bold I guess). I don’t believe the obesity epidemic is only due to shift in relative contribution of macronutrients in the diet but it may have played some part as the authors suggest. Maybe recommending fats out and carbs in wasn’t that clever after all (which shouldn’t come as a surprise as it wasn’t supported by strong scientific… Read more »

Mie
Mie
5 years ago

Axel, I’m afraid that this “I just copypasted it” argument doesn’t really cut it. First of all, you of all people should know that CRITICAL examination of any study is essential (I’m referring to the error you spotted in that one study of which you blogged about). Furthermore, why would you mention these in the context of making an argument about the alleged failure of guidelines UNLESS you yourself believed the conclusions needed to be taken at face value? Defend your position if you can. If you can’t, change it. That’s how it should be. Both Charles and Erik, not… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

Mie I don’t have to “defend my position” I’m on the attack. All my arguments can be found in the above blog article. I know you, Charles and Erik “have pointed at flaws in my reasoning”. But I still have a few supporters. My colleague, Steve Nissen at the Cleveland Clinic obviously shares my opinion. He’s renowned for his scientific thinking, and well I guess he’s quite “mainstream” as well. He, just like you and I, knows that CRITICAL examination of any study is essential. His words reflect the view of many other cardiologists today (as well as my own).… Read more »

Mie
Mie
5 years ago

Axel, are you seriously resorting to argument from authority now? If Nissen has anything convincing to say on the matter, let him author a review or a new meta-analysis etc. to indicate e.g. that advice to avoid fat led to people eating more crappy carbs as part of SAD (Standard American Diet) – despite the fact that the QUALITY of the carbs was always a part of the recommendations! Opinions in popular press are irrelevant compared to peer reviewed work, regardless of who we’re talking about

Please. At least try, will you?

Erik Arnesen (@erik_arnesen)
Reply to  Erik Arnesen

Regarding Harcombe’s metaanalysis, one important question is: Were these RCT’s fair tests of the recommendations or the lipid-hypothesis? Except the Sydney trial (which is difficult to extrapolate), none of the RCT’s tested a diet with maximally 30 % energy from fat and 10 % energy from saturated fat. If the authors read the papers the cite, they should not have ignored this advice in ‘Which clinical studies provide the best evidence?’ https://www.bmj.com/content/321/7256/255: “Limited randomised controlled trials need other forms of evidence to be appraised and considered. … the weight given to each bit of evidence should be determined by a… Read more »

Erik Arnesen
5 years ago

“The focus on the relative contribution of different macronutrients was maintained by the first Dietary Guidelines for Americans that were launched by the USDA in 1980 and have remained largely unchanged since then.”

No, the 1980’s U.S. guidelines did not say anything about the proportion of fat. They said “Avoid too much”. However, in the Scandinavian countries, the first official advice to limt fat to 35% (to lower the energy density) came already in 1968.

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Erik Arnesen

Erik

Thanks for the clarification.

The U.S. Senate Selection Committee on Nutrition and Human Needs launched the macronutrient composition goals in their 1977 report; Dietary Goals for the United States.

And you’re right. It say’s “avoid too much” fat, saturated fat and cholesterol in the 1980 guidelines.

michael goroncy
michael goroncy
5 years ago

Teicholz’s Book is less than useless, riddled with mis-information and plagiarism.
Instead of giving it to an op-shop (where someone else could be misinformed) I binned it.

But all is not lost…..I learnt not to pay attention to ‘book reviews’

The ilk of this woman and her shameless self promotion is evident in her comment and insult to Axel.

Bob Johnston
5 years ago

Axel – excellent article. Thanks for your good work.

Sissa Wallin
5 years ago

Great article. Amazing how easy it is for society to get lost in all the science and to forget that if we just eat real, quality, preferably ethic and organic produce from all food groups and home cooked from scratch, we will not have to think about macro or micro nutrients, but can just have a really good time over food with our families and friends…

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Sissa Wallin

Thanks Sissa

You make an interesting point. The macronutrient discussion is probably outdated. I agree it’s time to talk about food.

The Dietary Guidelines Advisory Committee says it nicely in its recent Scientific Report: “Additional strong evidence shows that it is not necessary to eliminate food groups or conform to a single dietary pattern to achieve healthy dietary patterns. Rather, individuals can combine foods in a variety of flexible ways to achieve healthy dietary patterns, and these strategies should be tailored to meet the individual’s health needs, dietary preferences and cultural traditions.”

Mie
Mie
5 years ago

Indeed. Focus should be on diets as a whole. Not to mention on HOW to improve people’s compliance.

This – inevitably, in my opinion – requires state-level interventions on e.g. taxation and health care services. If it were just a matter of educating people, we’d have much less CVD, diabetes, obesity etc. etc.

davebrown9
davebrown9
5 years ago

Dr. Sigurdsson,

It’s interesting that linoleic acid (LA) is excluded from debate regarding the causes of obesity and heart disease. Why is there so little interest in LA research? It exists, it’s accessible, and it’s compelling. Have you read “The Modern Nutritional Diseases: and how to prevent them by Fred and Alice Ottoboni? In my opinion, it’s the definitive popular nutrition book on inflammation. https://www.amazon.com/The-Modern-Nutritional-Diseases-Prevent/dp/0915241056

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  davebrown9

Thanks Dave.
I agree.
LA is probably something we should be discussing more.
I’ve read a lot you have written about it.
I must admit I haven’t dug into the literature really. I guess I should.

davebrown9
davebrown9
5 years ago

I suggest you start with the Modern Nutritional Diseases. You can familiarize yourself with the Ottoboni’s work at this site: https://ketopia.com/author/ottoboni/

Erik Arnesen
5 years ago

Will you consider studies like these too? – Long-chain conversion of [13C]linoleic acid and α-linolenic acid in response to marked changes in their dietary intake in men – Increasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic review – Comparison of dietary conjugated linoleic acid with safflower oil on body composition in obese postmenopausal women with type 2 diabetes mellitus. – Effects of n−6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial – Effect of dietary linoleic acid on markers of inflammation… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Erik Arnesen

… or maybe you should write a guest article on the subject on Doc’s Opinion Erik and I’ll stick with Cardiology.

davebrown9
davebrown9
5 years ago

@Erik Arnesen,

I have collected all the studies you posted except this one – Long-chain conversion of [13C]linoleic acid and α-linolenic acid in response to marked changes in their dietary intake in men. Thanks. However, there are a number of aspects of LA research not addressed in the above papers. One example: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC41359/ Figure 3. “… the fractional PUFA content is the primary determinant of oxidation and PUFA compose 20% of total fatty acids in LDL.”

davebrown9
davebrown9
5 years ago

Mie says, “You’ve been told before that normal consumption of n-6 fatty acids is by no means detrimental. You’ve paid no heed to this.” What is meant by normal consumption of n-6 fatty acids? Vague statement. Were the gorillas in the Cleveland Zoo that developed heart disease on a diet that included 6.5% fat calories supplied by soybean oil not consuming enough n-6 to keep their arteries clear? https://www.marionzoological.com/leaf-eater/nutrition/ Or were they getting too much sugar? Or were they not getting enough fiber? Or was it the reverse; too much n-6, not enough sugar, and too much fiber? Whatever the… Read more »

Mie
Mie
5 years ago
Reply to  davebrown9

1) Gorillas? WTF?

2) N-6 benefits: see e.g. the new Farvid et al (2014) on cohort data.

Or read the Ramsden et al (2010) which you mentioned: it showed that a) mixed n-3 & n-6 exchange was beneficial & the finding statistically significant whereas b) diets VERY rich in n-6 (consumption of 12-16% of tot.E as n-6) was worse but NOT in statistically significant way. Doesn’t lend any support to your pufa phobia.

3) And where’s the evidence of harm “with linoleic acid intakes exceeding 1 to 2% of calories”? Hmm?

davebrown9
davebrown9
5 years ago

Update: Responding to my request, Dr. Ayoob kindly sent me a link to the “recent” meta-analysis he referred to: https://circ.ahajournals.org/content/130/18/1568.abstract

From the abstract: “When the highest category was compared with the lowest category, dietary LA was associated with a 15% lower risk of CHD events and a 21% lower risk of CHD deaths.” Contrast this with the Lyon Diet Heart Study in which linoleic acid intake was substantially lowered with a resultant 70% drop in CVD morbidity and mortality. https://circ.ahajournals.org/content/99/6/733.full

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  davebrown9

Dave.
Can you give any explanation for the discrepancy between these studies. The Circulation meta-analysis suggests that replacing saturated fat with LA ma be beneficial in terms of CHD risk. I know it’s cohort studies, but it’s a large database. What do you think?

davebrown9
davebrown9
5 years ago

I am still studying this out. I’m about to request a Full Text of the Harvard meta-analysis Dr. Ayoob referred to in his commentary. https://circ.ahajournals.org/content/early/2014/08/26/CIRCULATIONAHA.114.010236.abstract Here’s a thought. We know that heart disease mortality increased dramatically in the 1930s, 40s, and 50s and declined considerably beginning in the early 60s, coincident with a steep rise in lenoleic acid intake. (See Figure 6 in this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076650/) The micronutrient and fatty profile of the food supply have undergone many changes through the years but the most striking change has been the increase in linoleic acid consumption. It’s possible that increased linoleic… Read more »

Mie
Mie
5 years ago

“But if it does so by shifting the cause of death to a variety of other fatal conditions related to the various effects noted in linoleic acid research literature, then that needs to come out in the analysis.”

There’s no data to indicate that moderate intake of LA is harmful in the case of cancer: neither in RCTs (the old ones where the intake was, to put it mildly, sky-high) or in cohort studies.

So I’m curious: what are these “other fatal conditions” that you speak of?

davebrown9
davebrown9
5 years ago

@ Mie, Linoleic acid (LA) is the most abundant polyunsaturated fatty acid in human diets, a major component of human tissues, and the direct precursor to the bioactive oxidized LA metabolites (OXLAMs), 9- and 13 hydroxy-octadecadienoic acid (9- and 13-HODE) and 9- and 13-oxo- octadecadienoic acid (9- and 13-oxoODE). These four OXLAMs have been mechanistically linked to pathological conditions ranging from cardiovascular disease to chronic pain…lowering dietary LA can reduce the synthesis and/or accumulation of oxidized LA derivatives that have been implicated in a variety of pathological conditions.” https://www.ncbi.nlm.nih.gov/pubmed/22959954 Regarding chronic pain: “A dietary intervention increasing n-3 and reducing n-6… Read more »

davebrown9
davebrown9
5 years ago

@ Charles
Thanks for the link.

Mie
Mie
5 years ago

Dave, next time please just send the link/include the reference AND your own comments instead of needless, lengthy copy-paste. First one https://www.ncbi.nlm.nih.gov/pubmed/22959954 was about chronic headaches. Unfortunately, the study didn’t measure actual feelings of pain (unlike the other study) nor have a control group which would’ve resumed the regular diet with more n-6. Second one https://www.ncbi.nlm.nih.gov/pubmed/23886520 Unlike the first one, this study seemed to suggest particular benefit in increasing the n-3 intake (still, no control group with a regular diet, though). Ok. Now please elaborate how big a problem chronic headpain is in terms of e.g. mortality or hospitalizations and… Read more »

davebrown9
davebrown9
5 years ago

@Mie, Aw Shucks! I like animal research. To me, ignoring what linoleic acid does to animals is like a crime scene investigator ignoring all evidence besides blood spatter and finger prints. I especially like this 1973 research because for the first time, researchers demonstrated they could boost the linoleic content of meat and milk by protecting linoleic acid from microbial hydrogenation in the rumen with a protective casein-formaldehyde safflower oil coating. They also demonstrated that they could prevent the linoleic acid from killing the calves if it was protected with vitamin E. Too bad humans are never warned to boost… Read more »

Frank
5 years ago

I don’t understand the sudden change regarding dietary cholesterol and TC level. As there been any new evidences that i’m not aware of? Because: Dietary cholesterol and coronary heart disease. ”Confusion about dietary cholesterol has arisen because amounts above a certain quantity (the ceiling) do not elevate plasma cholesterol and low-density lipoprotein cholesterol. The therapeutic threshold for dietary cholesterol is below 100 mg/d.” Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis ”Dietary cholesterol raises the ratio of total to HDL cholesterol and, therefore, adversely affects the cholesterol profile. The advice… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Frank

Frank. Here‘s a recent meta-analysis.

We have to look at clinical endpoints.
I don’t think there has been a study showing a significant association between intake of cholesterol rich food (like eggs) and the incidence or mortality from coronary heart disease.

Frank
5 years ago

Well, here’s one study Egg Consumption and Risk of Heart Failure in the Physicians’ Health Study and here’s another Incident Heart Failure Is Associated with Lower Whole-Grain Intake and Greater High-Fat Dairy and Egg Intake in the Atherosclerosis Risk in Communities (ARIC) Study also, the same years that the meta that you linked to was published, another one was, which came to a different conclusion. Egg consumption and risk of cardiovascular diseases and diabetes: a meta-analysis. ”Our study suggests that there is a dose-response positive association between egg consumption and the risk of CVD and diabetes.” Another one found no… Read more »

Mie
Mie
5 years ago
Reply to  Frank

Frank, just like you quoted: “Serum cholesterol concentration is clearly increased by added dietary cholesterol but the magnitude of predicted change is modulated by baseline dietary cholesterol” The effect is not only considerably smaller when compared to safa or trans fat, but you also need to consider the sources (carrier foods). E.g. shellfish and eggs: rich in cholesterol, but also nutritious. Of course, if you have high LDL, you may want to choose foods that have a clearly beneficial effect. The overall picture is, nonetheless, still what counts. In addition, it seems (based on the very reviews/meta-analyses you referred to)… Read more »

Frank
5 years ago
Reply to  Mie

My understanding of this quote is that studying the effect of eggs consumption in a population with an already cholesterol-rich diet, with a high serum TC level is not likely to really show the arms associated with eggs consumption. The effect could only be seen in people with low tc level and eating a plant-based diet. So it’s no surprise that it appears that eggs are harmless in the general population given that most american eat already too much cholesterol and have high serum cholesterol. I also agree that we should consider the food as a whole. I’m not sure… Read more »

Mie
Mie
5 years ago
Reply to  Mie

“My understanding of this quote is that studying the effect of eggs consumption in a population with an already cholesterol-rich diet, with a high serum TC level is not likely to really show the arms associated with eggs consumption.” But perhaps the consumption of eggs in met.ward studies conducted among vegetarians isn’t likely that show that either? We know that the human body can adjust cholesterol synthesis according to dietary intake of cholesterol. Now, doesn’t this mean that if the dietary intake of cholesterol is markedly higher for a period of time, the body will then ADAPT – resulting to… Read more »

Frank
5 years ago
Reply to  Mie

Replying here Mie as I can’t under your last reply. ”But perhaps the consumption of eggs in met.ward studies conducted among vegetarians isn’t likely that show that either?” Strong designed studies (such as cross-over) have shown many times that dietary cholesterol do raise serum TC if baseline serum TC/dietary cholesterol are low enough. This is an harm to me, since I think the lipid hypothesis is well supported. Any food that increase TC level is not beneficial to me in this regard. No met ward studies could be long enough to study clinical endpoint such as CVD or mortality so… Read more »

Mie
Mie
5 years ago
Reply to  Mie

“Strong designed studies (such as cross-over) have shown many times that dietary cholesterol do raise serum TC if baseline serum TC/dietary cholesterol are low enough.” I’m not arguing against that, so why repeat it? “It might adapt – or not, see this (1) – but it adapts when it’s too late.” ??? As these met. ward studies clearly show, if there’s baseline intake of any kind then the effect of added dietary cholesterol is clearly reduced – because the body indeed synthesizes LESS cholesterol if it gets more from the diet (this is not an opinion, you know). Now, this… Read more »

Frank
5 years ago
Reply to  Mie

I’m keeping this going althought from reading your comments I know we agree on much more than we seem to disagree on, and I would probably not quite call this disagreement but just a matter of drawing a line somewhere in regard to our own standard. ”I’m not arguing against that, so why repeat it?” I just repeated it because you said, in the other reply that ”Because it’s not a shortcoming in general population?”. My point is simply that any food that increase cholesterol, and that carries cholesterol, has and is a shortcoming to me when I consider what… Read more »

Erik Arnesen
5 years ago
Reply to  Mie

Since you’re talking about eggs and cholesterol, I just found this paper that looks intriguing: “The influence of consuming an egg or an egg-yolk buttermilk drink for 12 wk on serum lipids, inflammation, and liver function markers in human volunteers.”

Quote from abstract: “The increase in serum TC and LDL-C concentration was no longer significant in women consuming the same egg yolk incorporated in a buttermilk drink (0.33 mmol/L [P = 0.66] and 0.31 mmol/L [P = 0.55], respectively).”

https://www.ncbi.nlm.nih.gov/pubmed/23911216

davebrown9
davebrown9
5 years ago
Reply to  Frank

@ Frank, It may not be wise to rely on the opinions of Plant positive no matter how many studies he cites. For example, he says, “… the most basic assumption seems to be that it is an asset of saturated fats that they are resistant to oxidation. Don’t believe it. Actually, it is this resistance to oxidation along with its stiffer structure that makes saturated fat such a difficult thing for your body to deal with. If saturated fatty acids aren’t easily oxidized, that means they are not easily used for energy and other purposes. They tend to linger… Read more »

Frank
5 years ago
Reply to  davebrown9

I’m kind of perplex why you think that this quote from plant positive, and what you said next, discredit him.

I also don’t understand why you say that I should not listen to his opinion even if he cites studies. He just so happens to be citing studies that anyone with an internet connection can access for themselves and review, and they all clearly show that dietary cholesterol increases serum cholesterol.

Charles Grashow
Charles Grashow
5 years ago
Reply to  davebrown9

@Frank

Even Ancel Keys said that dietary cholesterol had no effect on serum cholesterol.

davebrown9
davebrown9
5 years ago
Reply to  davebrown9

Frank, I didn’t say you shouldn’t listen to plant positive’s opinion. I merely cautioned you to be careful about relying on his opinion. In truth, only the facts are reliable. When a person misrepresents the facts, his opinions should be regarded with suspicion.

This is the quote I referred to.
Also, plant positive did a review about did and found 19 studies which clearly show that dietary cholesterol increases TC level, as long as the TC level is low to beggin with, which is exactly what is being shown in all those reviews that i’ve put here.
https://www.docsopinion.com/2015/03/02/the-year-of-the-fat/#comment-19554

Charles Grashow
Charles Grashow
5 years ago
Reply to  davebrown9

@Frank https://circ.ahajournals.org/content/5/1/115.full.pdf Human Atherosclerosis and the Diet By ANCEL KEYS, PH.D. In summary, then, we may remark that direct evidence on the effect of the diet on human atherosclerosis is very little and is likely to remain unsatisfactory for a long time. But such evidence as there is, plus valid inferences from indirect evidence, suggests that a substantial measure of control of the development of atherosclerosis in man may be achieved by control of the intake of calories and of all kinds of fats, with no special attention to the cholesterol intake. This means: (1) avoidance of obesity, with restriction… Read more »

Charles Grashow
Charles Grashow
5 years ago

https://ajcn.nutrition.org/content/32/5/1051.full.pdf
Effect of dietary egg on human serum cholesterol and triglycerides

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1245349/pdf/bmjcred00006-0011.pdf
Effect ofdietary cholesterol on plasma cholesterol concentration in subjects following reduced fat, high fibre diet

Frank
5 years ago

It seems Keys was mistaken on this issue. We have now plenty of evidence clearly showing that dietary cholesterol do raise serum cholesterol. See the multiples meta I’ve posted above.

Charles Grashow
Charles Grashow
5 years ago
Reply to  Frank

” My point was only that it seems that cholesterol level stabilize once they are high. These studies clearly show that if you have low TC and dietary cholesterol intake, increasing dietary cholesterol intake will increase your TC level over 150mg/dl and then it might stop increasing, but that’s too high already in regard to athero plaques progression.” I’m going in for new blood work in a couple of months and we shall see but my last blood work had TC 120, LDL-C 56, HDL-C 54 I eat meat and eggs among other things so is juts the stain I… Read more »

Frank
5 years ago
Reply to  Frank

Hi Charles Do you take statins or was that sarcastic? If you do that certainly must be influencinbg what’s going on. There is clearly also genetical factors at play, maybe you have geneticaly low TC level and are not affected much by the food you eat. Who knows. Good for you in any case. Those are very good numbers. Again, I think my prudent approach makes sens : Avoid food that have clear downside, especially if they don’t have anything interesting to offer. Eggs have been shown to increase TC level, LDL, Apo-b, inflammatory markers such as c-reactive p and… Read more »

Charles Grashow
Charles Grashow
5 years ago
Reply to  Frank

@Frank

Last hsCRP was 0.9, fasting glucose was 83

Charles Grashow
Charles Grashow
5 years ago

https://blogs.plos.org/dnascience/2015/03/05/man-ate-25-eggs-day/ The Man Who Ate 25 Eggs a Day Fred Kern Jr., MD, a gastroenterologist at the University of Colorado School of Medicine, heard about the man and saw an opportunity to study individual differences in how diet affects serum cholesterol level. And so the 88-year-old egg eater joined such famous patients as French-Canadian explorer Alexis St. Martin and Henrietta Lacks. First, Dr. Kern tested the man’s lipid levels, which were normal: 200 milligrams per deciliter total cholesterol and 142 for LDL. Then he compared the extent to which the man’s body compensated for the cholesterol overload in the 25… Read more »

Charles Grashow
Charles Grashow
5 years ago

https://healthcorrelator.blogspot.com/2012/10/the-man-who-ate-25-eggs-per-day-what.html
The man who ate 25 eggs per day: What does this case really tell us?

Michael Suede
5 years ago

This is what the study said verbatim: https://www.nutritionjrnl.com/article/S0899-9007%2815%2900077-5/abstract “Since 1971, the shift in macronutrient share from fat to carbohydrate is primarily due to an increase in absolute consumption of carbohydrate as opposed to a change in total fat consumption. General adherence to recommendations to reduce fat consumption has coincided with a substantial increase in obesity.” So people are fatter now because they eat more, not because they decreased fat consumption. This article is misleading in this regard. Along with obesity comes a host of other related metabolic illnesses. I’m curious why the billion Asians subsisting primarily on rice and vegetables… Read more »

David_Brown
David_Brown
5 years ago
Reply to  Michael Suede

Michael, Americans ended up swapping saturated fats for linoleic acid which has decidedly obesiogenic effects. Here’s what happened. “The incidence of obesity in the U.S. has increased from 15% to 35% in the last 40 years and is expected to rise to 42% by 2030. Paralleling this increase in obesity are a number of dietary changes, most pronounced of which is a >1000 fold increase in consumption of soybean oil from 0.01 to11.6 kg/yr/capita from 1909-1999: soybean oil consists of 50-60% linoleic acid (LA), so the energy intake from LA has increased from 2% to >7%/day. LA is an essential… Read more »

Michael Suede
5 years ago
Reply to  David_Brown

I don’t think it has to do with fatty acids, it has to do with the protein. High fat dairy is typically fermented, and the fermentation breaks down the proteins, which is why there is an associated reduction in type 2 diabetes. We see the same thing in the Masai tribe with their high consumption of fermented dairy and low consumption of meat.

Animal protein is the killer.

David_Brown
David_Brown
5 years ago
Reply to  Michael Suede

“I’m curious why the billion Asians subsisting primarily on rice and
vegetables didn’t get fat until they started adopting the rich western
diet.”

You changed the subject. You were wondering about the factors causing obesity, not cancer. Here’s more commentary that speaks to the obesity issue. https://www.doyoueven.com/2015/03/the-fat-that-makes-you-fat/

Michael Suede
5 years ago
Reply to  David_Brown

That’s an interesting article on LA. I’m not sure if it can explain the Chinese cancer and obesity explosion though. Perhaps a combination of LA and casein are at work.

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