Cochrane: No Health Benefits By Reducing Saturated Fat

Via That Paleo Guy:

There are no clear health benefits of replacing saturated fats with starchy foods (reducing the total amount of fat we eat).

Oh my.

Clearly the people at Cochrane just don't know how to look for the "proper" evidence. After all, haven't we be told for decades that Saturated Fat is THE bogey man? What's next? That they tell us that statins don't work?

More Animal Fat & Less Seed Oils = Longevity!

Stan the Heretic has the details:

1. New study on the topics of mono-unsaturated and saturated versus polyunsaturated fats:

"Lipidomics of Familial Longevity.", by Gonzalez-Covarrubias V, et al.
Aging Cell. 2013 Mar 2. doi: 10.1111/acel.12064. [Epub ahead of print]

Quote:

In addition, the longevity-associated lipid profile was characterized by a higher ratio of monounsaturated (MUFA) over polyunsaturated (PUFA) lipid species suggesting that female offspring have a plasma lipidome less prone to oxidative stress. Ether PC and SM species were identified as novel longevity markers in females, independent of total triglycerides levels. Several longevity-associated lipids correlated with a lower risk of hypertension and diabetes in the Leiden Longevity Study cohort.

2. Longevity marker = MUFA/PUFA ratio in cellullar membranes:

"Fatty acid profile of erythrocyte membranes as possible biomarker of longevity.", Puca AA, et al., Rejuvenation Res. 2008 Feb;11(1):63-72.

Quote:

Erythrocyte membranes from nonagenarian offspring had significantly higher content of C16:1 n-7, trans C18:1 n-9,[mono-unsaturated] and total trans-fatty acids, and reduced content of C18:2 n-6 and C20:4 n-6 [polyunsaturated fats].

(comments in brackets added by me)
 

It Is The PUFA Overconsumption, Not The n-6/n-3 Ratio, Stupid!

Science – do an experiment, find out things:

Metabolic markers in Ossabaw pigs fed high fat diets enriched in regular or low α-linolenic acid soy oil

Ramesh B Potu, Hang Lu, Olayiwola Adeola and Kolapo M Ajuwon*

Abstract

Background
Soy oil is a major vegetable oil consumed in the US. A recently developed soybean variety produces oil with a lower concentration of α-linolenic acid, hence a higher (n-6)/(n-3) ratio, than regular soy oil. The study was conducted to determine the metabolic impact of the low α-linolenic acid containing soy oil.
Methods

Ossabaw pigs were fed diets supplemented with either 13% regular soybean oil (SBO), or 13% of the low α-linolenic soybean oil (LLO) or a control diet (CON) without extra oil supplementation, for 8 weeks.

Results
Serum and adipose tissue α-linolenic acid concentration was higher in pigs fed the SBO diet than those on the CON and LLO diets. In the serum, the concentration of saturated fatty acids (SFA) was lower in the LLO group than in CON and SBO groups polyunsaturated fatty acid (PUFA) concentration was higher in the LLO group compared to CON and SBO groups. Glucose, insulin, triglycerides and LDL-cholesterol were higher in pigs fed the SBO diet than those fed the CON and LLO diets. HDL-cholesterol was lower in pigs on the SBO diet than those on the CON and LLO diets. Pigs fed SBO and LLO diets had lower CRP concentration than those on the CON diet. Adipose tissue expression of Interleukin 6 (IL-6) was higher in the SBO and LLO diets than the CON. Expression of ECM genes, COLVIA and fibronectin, was significantly reduced in the SBO diet relative to the CON and LLO diets whereas expression of inflammation-related genes, cluster of differentiation 68 (CD68) and monocyte chemoattractant protein 1 (MCP-1), was not different across treatments.

Conclusions
Results suggest that lowering the content of α-linolenic acid in the context of a high fat diet could lead to mitigation of development of hyperinsulinemia and dyslipidemia without significant effects on adipose tissue inflammation.

For those of you who don't know right of the back of their heads, α-linolenic acid is an Omega-3 fatty acid (n-3). So a lower consumption of it makes the n-6/n-3 ratio higher – with a higher n-6/n-3 ratio usually considered (erroneously) to be the main problems with seed oils. Yet a lower consumption of only this fatty acid decreases the absolute amount of PUFAs consumed – and that seems to be beneficial (if you are an mammal).

Let me put this in other words: Lower PUFA consumption (even Omega-3!), means better health. 

If you are not an mammal, or if your livelihood depends on selling PUFA supplements in the form of fish oil or seed oil (I'm looking at you USDA, ADA and AHA), then go ahead and advertise an increased PUFA consumption. I just hope that in everybody's interest that you die of natural causes before people start to pick up pitchforks.

More Evidence That Seed Oil Might Be Bad For Your Health

Low serum eicosapentaenoic acid / arachidonic acid ratio in male subjects with visceral obesity

Kana Inoue, Ken Kishida, Ayumu Hirata, Tohru Funahashi and Iichiro Shimomura

Nutrition & Metabolism 2013, 10:25 doi:10.1186/1743-7075-10-25
Published: 12 March 2013

Abstract (provisional)

Background
Visceral fat accumulation is caused by over-nutrition and physical inactivity. Excess accumulation of visceral fat associates with atherosclerosis. Polyunsaturated fatty acids have an important role in human nutrition, but imbalance of dietary long-chain polyunsaturated fatty acids, especially low eicosapentaenoic acid (EPA) / arachidonic acid (AA) ratio, is associated with increased risk of cardiovascular disease. The present study investigated the correlation between EPA, docosahexaenoic acid (DHA), AA parameters and clinical features in male subjects.

Findings:
The study subjects were 134 Japanese with diabetes, hypertension and/or dyslipidemia who underwent measurement of visceral fat area (eVFA) by the bioelectrical impedance method and serum levels of EPA, DHA and AA. EPA/AA ratio correlated positively with age, and negatively with waist circumference and eVFA. Stepwise regression analysis demonstrated that age and eVFA correlated significantly and independently with serum EPA/AA ratio. Serum EPA/AA ratio, but not serum DHA/AA and (EPA+DHA)/AA ratios, was significantly lower in subjects with eVFA >=100 cm2, compared to those with eVFA <100 cm2 (p=0.049). Subjects with eVFA >=100 cm2 were significantly more likely to have the metabolic syndrome and history of cardiovascular diseases, compared to those with eVFA <100 cm2 (p<0.001, p=0.028, respectively).

Conclusions
Imbalance of dietary long-chain polyunsaturated fatty acids (low serum EPA/AA ratio) correlated with visceral fat accumulation in male subjects.

Or in other words:
Evidence that obese people consume disproportionate more seed oil than non-obese people.

The obese of the world have been eating seed oils like crazy the good patients they are, as ordered by the good doctors at the ADA and AHA.

What does that tell us about the advise of the ADA and AHA to consume more seed oil to avoid obesity? (Hint: It's a two letter word that starts with an capital B and ends with an capital S)

To rehash for all of you haven't internalized human essential fatty acid metabolism (shame on you):

Linoleic acid (LA) gets metabolized into arachidonic acid (AA).

Alpha-linolenic acid (ALA) gets metabolized into eicosapentaenoic acid (EPA).

Seed oil has an high content in poly-unsaturated fatty acids "PUFAs" (seed oil has an high content of ALA, and even higher content of LA), and seed oil has a low ALA/LA ratio.

Consumption of seed oil (with its low ALA/LA ratio) will lead to a low EPA/AA ratio (like no other food) and it will increase the AA level like no other food.

And this low EPA/AA ratio (that plausibly could only be caused by seed oil) correlates with obesity.

You have been warned.

BTW: AA in turn gets metabolized into "series 2 prostaglandins" which are considered to be "more inflammatory" (red box above).

Furthermore PUFAs do negatively influence the carbohydrate metabolism and muck up the way insulin works (which will drive fat into fat cells).

And again:

No other food contains as much PUFAs as seed oil.

No other food allows you to raise your AA level like seed oil.

No other foods allows you to lower your EPA/AA ratio like seed oil.

So in my maybe not so humble opinion:
No other food besides seed oil is necessary to explain obesity.

Or put bluntly:
Obesity? Caused by increased seed oil consumption.

And look! Seed oil consumption has increased! Consumption of butter and lard have gone way down! We are doing what the ADA and AHA are telling us! Thank god!


And look! Obesity is up! Wonderful to see the marvellous advise of the ADA and AHA bearing such beautiful fruits!

 And look at this! Diabetes is going up like crazy! It brings water to my eyes to see the success of the ADA and AHA!

And look here! Heart disease is at an all time high! If that doesn't tell you that the ADA and AHA are doing a top job, I don't know what will.

So avoid seed oils, if you do not want to become obese and run the risk of getting other "diseases of civilization".

If on the other hand you do want to become obese, then follow the advise of the ADA and AHA and make sure you consume lots and lots of seed oil.

One more thing, while we are at it: If you think you are a bird or a mouse – and who am I to judge – then I guess eating nothing but seeds (and the occasional bottle of cold-pressed olive oil) is a viable and healthy diet for you and other members of your species – but please don't counsel humans on their nutrition.

"No Change In AHA Recommendations On Saturated Or Poly-unsaturated Fat"

Tuck at the blog Yelling Stop: "No Change In AHA Recommendations On Saturated Or Poly-unsaturated Fat"

AHA stays the course with their Omega-6 Seed Oil Insanity.

On Nutrition: Seed Oils, Omega-6 and First Principles

An attempt to a (sometimes polemic) precursor post on seed oils ("vegetable oils"), Omega-6 fatty acids ("n-6 fats") and Eicosanoids – with special attention to linoleic acid (18:2), which is one of the main fatty acids in seed oils.

This post will be followed by a longer post on seed oils in the hopeful near future.

I shall try to show from "first principles" alone the likely negative health implications resulting from the generally recommended increased consumption of n-6 fats – with organizations like ADA and AHA being two of worst offenders.

All points in this post should be (bloody) obvious and indisputable for anybody slightly versed in the fields of chemistry, biology, evolution and medicine.

0. Linoleic acid is essential

As the human body can not produce linoleic acid, yet various functions in the body depend on it as precursors to other molecules, linoleic acid needs to be consumed.

(I think much of the confusion over the "healthyness" of seed oils stems from this fact. Water is by the same measure essential, yet the consumption of supranatural amounts of water can kill you, and given enough persistence will in fact kill you.)

1. An increased consumption of linoleic acid increases levels of said fats in the stomach, in the blood, and finally in the tissues.

Otherwise the recommendations of the ADA and AHA would be completely nonsensical.

2. The body has no mechanism to regulate the tissue levels of linoleic acid

It is always hard to prove a negative. I am however not aware of any mechanisms by which the body would regulate the levels of specific fatty acids.

Furthermore I think it should be obvious that no such mechanism was necessary in evolutionary past, as we see in the next point:

3. No other naturally occurring food besides seed oils enables to consume such large amounts of linoleic acid

Every other naturally food in this world contains comparatively low levels of linoleic acids.

Even if someone consumes seeds (and nothing but seeds) it is difficult to reach these amounts of linoleic acid that one can consume with seed oils (and should consume, according to the ADA and AHA).

Once more: Only with seed oils is it possible to massively increase the consumption linoleic acid – no other food in the world can do that.

(Furthermore seed oils makes it possible to consume massively more n-6 than n-3 fatty acids, unlike most other foods. Usually food contains – with pork and fish being two prominent exceptions – roughly equal amounts of n-3 and n-6 fatty acids. That will be important for the eicosanoid point further down the list.)

The proof for this point (the linoleic acid content of various foods) is left as exercise to the reader – the data is available. (E.g. I can recommend the very excellent German Bundeslebensmittelschlüssel BLS, which can be searched in German for free on this commercial website. The BLS data is even available in English.)

4. Consumption of seed oils in large amounts is only possible for about a century

Before the industrial production of seeds oils, it was simply not possible to consume linoleic acid in large amounts. I think this should be self evident.

5. The recommendations of the ADA and AHA should be considered as consumption of supranatural levels of linoleic acid

As far as I know no identified deficit is addressed by the the recommendation to consume supranatural levels of linoleic acid. As far as I know no mechanism is stated by which the need would arise to consume supranatural levels of linoleic acid. Supposedly n-6 fatty acids are more healthy than saturated fat, but no mechanism has been shown so far despite decades of research.

The practice of the ADA and AHA to recommend the consumption of supranatural levels of linoleic acid reminds me of those who recommend various supplements  based on cherry-picked, slim and vague data – with arguably the volume of cherry-picked slim and vague data from the ADA and AHA being quite large.

6. There was not enough evolutionary time to adapt to the massively increased consumption of linoleic acids

Should be obvious for anybody with a little bit of experience with evolution that there was not enough evolutionary pressure and not enough time to adapt to a diet high in seed oils – if you dispute this fact, I'm afraid there is nothing I can do for you.

7. Supranatural amounts of linoleic acid in the tissue will lead to supranatural levels of series 2 prostaglandins in the tissue

So let me present my strongest evidence:

"It's the eicosanoid metabolism, stupid!"

The generally agreed-upon eicosanoid metabolism

To summarize:

• Eicosanoids are signalling molecules derived from n-3 and n-6 fatty acids, involved in processes like inflammation.
• The left column is the n-3 cascade, the one on the right the n-6 cascade 
• n-3 fatty acids are converted among others into PG3s (series 3 prostaglandins, a type of eicosanoids, the box to the right of EPA)
• n-6 fatty acids converted among others into PG1s and PG2s (series 1 and series 2 prostaglandins, the boxes to the left of DGLA and AA)
• Both the n-3 and n-6 fatty metabolism shares the same enzymes (e.g. delta6-desaturase, elongase, delta5-sesaturase, and so on) to produce their various eicosanoids.
• While it is considered that n-3 fatty acids have a greater "affinity" to these enzymes, if you massively increase the amount of linoleic acid (on the top of the right column) – through say the ADA and AHA recommended consumption of seed oils – this will massively increase the amount of PG1 (turquoise box) and PG2 (red box, uh-huh, red isn't good, is it?)
• PG3s (produced from n-3 fatty acids) are generally considered "less inflammatory" 
• PG2s (produced from n-6 fatty acids) are generally considered "more inflammatory" (again, the red box) – seed oil, a bona fide candidate for a disease mechanism involved in heart disease. *

So, in one sentence:
If you eat seed oils, you increase the levels of the pro-inflammatory series 2 prostaglandins above what would be considered "natural" – no other food can do that.

If you think this is good, then you might be an idiot.

People at the ADA and AHA think that the consumption of supranatural levels of seed oil is good.

People at the ADA and AHA might be idiots.

Further studies are warranted.

--

* Be advised that this is not the only mechanism by which seed oils and the overconsumption of linoleic acid will cause disease – see here for a mechanism by which seed oils and the overconsumption of PUFAs could cause obesity and T2DM.

On Nutrition: Trans Fatty Acids

I'm starting a series "On Nutrition" to gather some basic health information regarding foodstuff – be warned, it will be based on evolutionary principles, the Paleo Diet and hopefully quite heretic.

First of all I want to collect what foodstuff can be involved in disease, and should therefore be avoided on a precautionary basis.

What is it and where can I find it?
Trans Fatty Acids are a type of fatty acids (of simply known as "fat"). The technical name typically used is "partially hydrogenated vegetable oil"*.

Typically Trans Fatty Acids are found in Margarine (or "Vegetable Shortening") produced from seed oils ("vegetable oils").

Unlike most seed oils, which are an oil at room temperature, Trans Fatty Acids are an solid fat, and can be used like butter.

Furthermore, partially hydrogenated vegetable oil is used as an ingredient in some industrially produced foods (AKA "crap in a box").

Novel food? Industrial!
Trans Fatty Acids can be found in small quantities in naturally occurring foods. These levels are however low.

Only the industrial production made it possible to produce large amounts of seed oil and the hydrogenation of seed oils. Only since about 100 years is it possible to consume large amounts of Trans Fatty Acids. It was sold as an cheap replacement for Lard and Butter, and was being branded as "healthy" already back then.

It is chemically different enough from e.g. animal fats that it can cause disease, and it has in evolutionary terms only recently been introduced into human nutrition – so it is unlikely that we are evolutionary adopted to eating Trans Fatty Acids in any substantial amounts we can encounter with products like margarine.

Pathogenic pathways?
As the Trans Fatty Acids are close relatives of Omega-6 Polyunsaturated Fatty Acids (n-6 PUFAs), they have the potential to interfere with n-6 metabolism in the human body. Especially the potential to be metabolize into substances that are close relatives of Series-2 Prostaglandines, but might have functional differences, has the potential to cause disease – especially considering the role of prostaglandines in inflammation.

Furthermore some of the health problems caused by the overconsumption of n-6 PUFAs might apply to Trans Fatty Acids as well, as they are related and chemically similar.

Self-Test?
If you regularly consume margarine, you might want to try to substitute it for at least a couple of weeks with Ghee ("Clarified Butter") or Coconut Oil ("Palm Oil") to see if it has influence on your health.

I never consumed large amounts of margarine, so I don't have any personal experience.

Verdict: AVOID
The role of Trans Fatty Acids in disease are more and more being realized. Personally I think the evidence is already clear enough, and I would not wait until the evidence gets more clear to stop ASAP the consumption of Trans Fatty Acids.

The low levels of Trans Fatty Acids in naturally occurring foods should be OK though – the dose makes the poison in this case.

--

* "Fully hydrogenated vegetable oils" are by the way simple (and healthy) saturated fats.

Vegetable Oils, PUFAs, Omega-6? Don't eat it.

If you need any more evidence that seed oil (aka "vegetable oil") is bad for your health, here it is:

Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis
…
Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction.

However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established.

In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease.

An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit.

These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats. 

To sum it up: The advise of the past decades for a "heart healthy" not only has no health benefits, it actually creates the problem it perpetuates to fight.

Don't eat vegetable oils, because vegetable oils cause disease.

Eat saturated fat, because saturated fat does not cause disease.

I know this will make most doctors unhappy, but hey: go fuck yourselves. Handing out murderous advise for decades? If people find out, there'll be a shortage of pitch-forks, I hope – one can dream, right?

(via)

[Update] Stan the Heretic an his take on the matter:

…
This high multiple factor seems to be confirm by the data from Table 5 indicating that for every 5% PUFA increase (in absolute energy%) the All cause mortality, the Cardiovascular disease mortality and the Coronary heart disease mortality increased by 31%, 35% and 26% respectively (relative risk factor).

This implies a proportionality factor of about 5-7. That is, for every 1% added Poly-Unsaturated Fatty Acids ( PUFA) in absolute calories % of the total, cardiovascular mortality INCREASED by 5 to 7%. This is big news!
…

[Update] Chris Kresser on the same topic.

Getting insulin sensitive when you don't want it

Peter over at Hyperlipid has a go at why consumption of seed oil (with a high linoleic acid content, aka omega 6 PUFA) is a stupid idea – excellently written, as always.

Protons: Physiological insulin resistance:

… Under full starvation a rat lives off of its fat. If linoleic acid is what is being released from the adipocytes under fasting conditions it provides significantly less FADH2 relative to NADH in to the electron transport chain of all fat burning cells than the mix of fatty acids from the adipocytes of lard fed rats. ie there is less physiological insulin resistance. This failure means you fail to keep glucose levels normal during starvation. Let's rub that in: Failure to develop physiological insulin resistance during starvation results in hypoglycaemia and hunger.

Exactly the same will happen in any soy oil fed USA citizen. The end result will still be the failure to develop the essential physiological insulin resistance which is needed to keep blood glucose normal during fasting.

When the average soy oil fattened American is asleep they HAVE to, finally, stop snacking on carbohydrate crap, which is the only way they can maintain a decent blood glucose level. At this time blood glucose falls, simply because their muscles stay insulin sensitive and glucose falls in to them. The brain will not accept hypoglycaemia. Some time, in the middle of the night, there has to be a Refrigerator Raid.

And, OMG, they eat calories! And calories count! Did I ever mention gluttony? Or, perhaps, is the Refrigerator Raid simple physiology?

The 22h daily fasted rats have a locked refrigerator. However hungry they feel due to hypoglycaemia, they are not getting any extra food. But why is there extra weight loss under starvation? Insulin was tricky to measure from a rat in the 1970s, but I know that the safflower loaded then starved rats had the lowest insulin as they are both insulin sensitive and hypoglycaemic. Low insulin = more lipolysis = more ketones and more weight loss. Logical.

Now let's go a step further. Blood glucose is low. It's low because the F:N ratio of linoleic acid is low and that's what is being released from adipocytes. This is metabolism. Individual cell by individual cell, it's a metabolic phenomenon. Picked up by the brain as hypoglycaemia. …

Protons: Physiological insulin resistance addendum:

… The whole point of a ketogenic diet (epilepsy excepted) is to induce starvation-appropriate physiological insulin resistance. What is the point of setting up a ketogenic diet which does not have the ability to convert from running on glucose to running on fat? …

That Paleo Guy On Omega-6 Fatty Acids

Are diets high in omega-6 polyunsaturated fatty acids unhealthy?

Yes, so don’t eat ‘em. Thanks for reading.

Whaddya mean you want more of an explanation? They just are, okay!?

Look, there are plenty of health professionals who tell you to eat or avoid certain things with little in the way of an explanation, so why can’t I?

Tough crowd.

For the vast majority of you, I am preaching to the converted when it comes to warning of the perils of consuming large amounts of vegetable and seed oils, and the many processed foods that contain them, due to their relatively high omega-6 polyunsaturated fatty acid content (herein abbreviated as n6 PUFA). Specifically, we are talking about the n6 PUFA – linoleic acid (LA). Others might require a bit more convincing. Here goes…