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.

Nestle Nutrition Workshop: Dairy might be bad for you – Oops

Nestle Nutr Workshop Ser Pediatr Program. 2011;67:131-45. doi: 10.1159/000325580. Epub 2011 Feb 16.

Evidence for acne-promoting effects of milk and other insulinotropic dairy products.

Melnik BC.

Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Osnabrück, Germany.

Abstract:
Acne vulgaris, the most common skin disease of western civilization, has evolved to an epidemic affecting more than 85% of adolescents.

Acne can be regarded as an indicator disease of exaggerated insulinotropic western nutrition.

Especially milk and whey protein-based products contribute to elevations of postprandial insulin and basal insulin-like growth factor-I (IGF-I) plasma levels.

It is the evolutional principle of mammalian milk to promote growth and support anabolic conditions for the neonate during the nursing period.

Whey proteins are most potent inducers of glucose-dependent insulinotropic polypeptide secreted by enteroendocrine K cells which in concert with hydrolyzed whey protein-derived essential amino acids stimulate insulin secretion of pancreatic β-cells.

Increased insulin/IGF-I signaling activates the phosphoinositide-3 kinase/Akt pathway, thereby reducing the nuclear content of the transcription factor FoxO1, the key nutrigenomic regulator of acne target genes.

Nuclear FoxO1 deficiency has been linked to all major factors of acne pathogenesis, i.e. androgen receptor transactivation, comedogenesis, increased sebaceous lipogenesis, and follicular inflammation.

The elimination of the whey protein-based insulinotropic mechanisms of milk will be the most important future challenge for nutrition research.

Both, restriction of milk consumption or generation of less insulinotropic milk will have an enormous impact on the prevention of epidemic western diseases like obesity, diabetes mellitus, cancer, neurodegenerative diseases and acne.

o.O

Speculation on Type 2 Diabetes

I just wanted to post here one more piece of speculation, that it is seed oils that cause or primarily contribute to Type 2 Diabetes (and possibly Obesity) – so in two or three decades I can say: "Told you."

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? …

Raw milk, acne and blood sugar – An update

As I wrote before, my acne is caused by milk. While I sometimes get very very very small furuncles (which i haven't been able to track down to a cause yet), I just need to east a bit of dairy to get several nasty furuncles and sometimes even nasty pimples. No doubt, milk caused my acne, which I can say with certainty after being dairy-free for quite some time now.

Now I wanted to see if raw dairy (from non-pasteurized milk) makes a difference, as I read something to that effect. I got some really nice raw-milk "Bergkäse" cheese, and ate a nice piece of it.

And what can I say about raw-milk dairy, after a sample size of 1?

The good: 
No acne. None whatsoever. And the Bergkäse was really nice.

The bad and ugly:
I ate the cheese at 10 in the morning and about half an hour later I got a rather low blood sugar: All the symptoms like "that jittery feeling", and the confirmation by several measurements of blood sugar (blood glucose) during the day. Eating some glucose, and then some more didn't help much. And then some potatoes, and then some more. I was jittery to some degree all day. And had (slighter) problems with blood sugar for some days.

Hmmm.

I need to try this experiment again, in some weeks, to see if this is not some random fluke.

At least for now, and for me, it seems that (pasteurized) milk is able to provoke an immune reaction (in the form of acne) in my body – this could provide an plausible mechanism for some autoimmune conditions.

And it seems possible (for now) that milk fucks up the insulin/blood sugar regulation of my body – something I need to confirm† or rule out‡. Next time

Update: Just one short update, a second try with raw-milk cheese, and I did not get any noticeable bad health results. Let's see.

--

† Confirmation that milk fucks up insulin/glucose regulation would be really really cool, as it would provide an mechanism for some of the diseases we see – say: obesity, "metabolic syndrome", T1DM and T2DM (type 1/2 diabetes mellitus)

‡ Ruling out negative health effects (for me) of raw milk would be really really cool, as I could eat cheese again, in the form of raw milk cheese.

Insulin and Obesity?

A nail in someone's coffin?

Apparently these rats are a nail in the coffin of the insulin hypothesis of obesity.

Peter at Hyperlipid destroys the "insulin and obesity" theory – what fun.

iPOP (integrative personal omics profile) – tracking proteins, metabolites, metabolism, microRNAs, cytokines, antibodies, and gene transcripts in one person

Michael Snyder tracks his health status with iPOP and finds a virus causing his Type 2 Diabetes (T2DM)?

Snyder had a cold at the first blood draw, which allowed the researchers to track how a rhinovirus infection alters the human body in perhaps more detail than ever before. The initial sequencing of his genome had also showed that he had an increased risk for type 2 diabetes, but he initially paid that little heed because he did not know anyone in his family who had had the disease and he himself was not overweight. Still he and his team decided to closely monitor biomarkers associated with the diabetes, including insulin and glucose pathways. The scientist later became infected with respiratory syncytial virus, and his group saw that a sharp rise in glucose levels followed almost immediately. "We weren't expecting that," Snyder says. "I went to get a very fancy glucose metabolism test at Stanford and the woman looked at me and said, 'There's no way you have diabetes.' I said, 'I know that's true, but my genome says something funny here.' "

So much for "These people eat too much."

Topol writes in an e-mail, "this type of 'pan-ar-omic' study of individuals is now not only feasible but in select individuals with medical conditions, particularly useful clinically."

We'll have to wait until this will be used more often in research, and then it will take some considerable time, but it will reach clinical use some time, maybe in the next decade.

Read it all.

[Update] Here's another blog post about this.

I think there is something wrong here

There is definitely something wrong here – and it looks like the CDC is not able to handle it. Bonus points for recording it, though.