Saturday, September 18, 2010

Fathead Supersize Me and Sweden (2)

An addendum to the mouse trans fat fibrosis paper: It's junk. Utter junk. Even the title is wrong. There are NO trans fats in the experiment, NONE what so ever!

The mice were fed on the Surwit Diet. Here's the pdf from Research Diets.

I thought medium chain trans fats were a bit of a strange animal....


So the mice are being fed on fully hydrogenated coconut oil, which has minimal PUFA to begin with and gets hydrogenated to fully saturated, mostly medium chain triglycerides. Plus non hydrogenated soya oil, which is mostly omega 6 PUFA and a little omega 3 PUFA.

The ONLY source of carbohydrate in the diet was sucrose and maltodextrin, which made up 25% of calories. To which they added sucrose in the drinking water, plus added fructose in the drinking water.

THERE ARE NO TRANS FATS IN THIS DIET.

Fructose, beyond human comprehension, with adequate soya oil, is enough to fibrose a mouse's liver. Not even Bill Clinton could eat this much fructose a day for life.

Who scrutineered this paper? Who wrote the title? How much money was wasted? What is happening in the world?

Arghhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhh!

Ouch. Ouch. Ouch.

Ouch.

I'm trying to stop banging my head on the table but (Ouch)......

Peter

21 comments:

john said...

Hi Peter,

You just can't win...

Off topic question: why/how does t3 induce hepatic lipogenic enzymes* yet regress fatty liver**?

*http://jn.nutrition.org/cgi/reprint/120/6/625.pdf

**http://www.ncbi.nlm.nih.gov/pubmed/18434432

Peter said...

Hi John,

Probably have to look very carefully at the methods there. The choline/methionine deficient rat has nothing to do with NAFLD or NASH in humans and the first study is quite specific about what it is saying and needs reading very carefully....

Peter

john said...

Thanks...it's a learning process...

Emily Deans, M.D. said...

I know, I'm on call too.

Rohit Kohli lead author's email address is right there on pubmed. Maybe we could ask him directly what the hell he was thinking.

john said...

...And on that note, how about some more quick help: Nick Lane (in PSS) says that in hot climates, uncoupling is down regulated (which is intuitive) and therefore contributes to excess free radicals, "especially with a high fat diet." Now this is counter-intuitive, considering your "metabolism nuts and bolts" posts: am I missing something?

By the way, it's in the epilogue.

Peter said...

Hi John,

I have to say that I felt the applied physiology to human global distributions were the most arguable points in an otherwise excellent book. However all of my books are now in cardboard boxes and will go in to storage on Friday, so I don't think I'll be checking anything too much over the next 3 months!

BTW, I've still not ploughed through the implications of the T3 paper in detail but one thing that occured to me is that is nothing wrong with lipogenesis per se, after all fat is good. It's what you do with the fat which matters. Leaving it in your liver is dumb. Exporting it and using it for calories is good. T3 undoubtedly affects metabolic rate and PUFA undoubtedly inhibit fat export. And PUFA might affect the thyroid receptor in the supraphysiological concentrations the AHA advise to drum up business. There would be many aspects to consider.

Hi Emily, I think I'm a bit rude to get replies from serious researchers, if anyone ever googles Dobromylskyj! If I had the time it would be better to write a letter to the editor of the journal, but it's a bit like Axen and Axen with the move coming up on Friday....

Peter

Peter said...

Hi Emily,

I just roughed out an email

Peter

Peter said...

Hi Emily,

I got a very prompt reply, the oil was MCTs with the longer remaining PUFA extracted, if I understand correctly.

I'm not going to argue any points as the chap was kind enough to reply promptly.

But it does show us that, when everything they eat and drink is seriously contaminated with fructose and sucrose, even MCTs cannot prevent the fibrosis of a mouse's liver. There's about 4% PUFA in the diet, the rest is saturated MCTs as the lipid.

J A Deep, looks like there is a level of fructose which is intolerable on a quite low PUFA background, w/o trans fats. Let's not go there!

Peter

Emily Deans, M.D. said...

It was very nice of him to reply! Guess I will return my vat of HFCS to the chemist's. And that gallon of vodka.

William A. Ryan said...

Peter,

You wrote: "But it does show us that, when everything they eat and drink is seriously contaminated with fructose and sucrose, even MCTs cannot prevent the fibrosis of a mouse's liver."

I know you have some lingering concern about MCTs, due to their extremely rapid processing by the liver. Couldn't this study be interpreted as evidence of the harmfulness of MCTs? Are there studies with this level of fructose doing equivalent damage without the other known agents of hepatic damage?

I have no idea what the answer is myself. I like my coconut oil and trust your intuition...

Will

blogblog said...

Hi John,

a highly experinced physician once told me taht Inuits could eat a high fat diet because they lived in a cold climate. I simply replied that all humans haver a core temprature of 37C so his argument was total nonsense.

john said...

blogblog,

I'm not quite sure what you're saying. It is easier to maintain body temperature in Africa than in Greenland.

My point was that with decreased uncoupling (seemingly a negative), a high fat diet shouldn't be an additional negative, considering http://high-fat-nutrition.blogspot.com/2008/04/metabolism-nuts-and-bolts.html

Anyway, I just thought it was odd that Lane said it (he does mention a "Western diet" right after--maybe within the paragraph, "Western" = "high fat").

john said...

Peter,

"...nothing wrong with lipogenesis per se..."

Lipogenesis includes "subsequent triglyceride synthesis," but do the enzymes (FAS, g-6-p d, malic) imply trig synthesis, or can it end at free fatty acids?

Insulin and t3 administration both increase FAS activity, but it is pretty counterintuitive for the end results to be the same.

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

John said:
"I'm not quite sure what you're saying. It is easier to maintain body temperature in Africa than in Greenland."

This isn't really correct:

- The East African Highlands where humans evolved rarely get above 25C. The nights are cold - only a few degrees above freezing. If you're naked you will certainly notice the cold.

- Stefansson describes the traditional Inuit fur clothing as being very warm and lightweight in any weather conditions.In addition the Iuits housing was kept so warm and humid that they sweated profusely.

john said...
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Owen said...

John,

The Clarke and Hembree PDF you linked to is somewhat disturbing. This is the first data I've seen implicating long-chain saturated fat (tallow) as a T3 inhibitor along with o-6 PUFA.

I looked around and found this as well:

http://www.ncbi.nlm.nih.gov/pubmed/3900181

I suppose you can look at it from two different perspectives... the T3 either dropped in both groups because they were isocaloric and too low-carb, or the T3 dropped in both (to different degrees) as a direct correlation with the amount of PUFA they were being fed.

I've been deferring to Broda Barnes as an expert on thyroid treatment and his two dietary suggestions were to not eat PUFA and to not go below 50g of carbs a day. Interestingly, his other "radical" idea relating to hypothyroidism is that excessive GAG production in tissue leads to various disease states involving the heart and skin:

http://tinyurl.com/29hlobd

Could this apply to liver pathology as well?

Also, if dietary fat does compete with T3, but you are supplementing with a T3 containing thyroid extract (I take a generic version of Armour, but Cytomel would be another option) it may be a wash once you balance your dose out with the amount of fat you are consuming. Consuming twice as much fat as carbs might require an extra grain or two of thyroid to maintain the same blood level compared to eating an equal ratio of fat and carbs, but does it matter?

MCTs are interesting as well. Coconut oil seems to have good reputation as being pro-metabolic. My understanding was that this results from it being preferably metabolized over PUFA, thus temporarily blocking PUFA's anti-metabolic effects.

john said...

Owen,

Here is something in regards to 50g carbs per day, http://www.ncbi.nlm.nih.gov/pubmed/1249190

...But, the diets are very low calorie--here is one where thyroxine is measured, and it actually goes up with a ketogenic diet (although I don't think it's too high in sat fat), http://www.nature.com/oby/journal/v12/n11s/full/oby2004276a.html

...Here, the same occurs, but t3 is also measured and there was a nonsignificant change, http://www.ncbi.nlm.nih.gov/pubmed/12077732?dopt=Abstract&holding=f1000,f1000m,isrctn

Does this mean, as you said, fat competes with t3, or is the conversion rate simply lowered a bit? It would seem the increase in t4 balances things out though.

john said...

Owen, sorry, the second link is a review and actually references the third--I didn't check the reference from link 2 when I first commented. With the full text we would be able to see t3 uptake changes, but I can't find it.

Jordan said...

Why is it that I keep seeing 'saturated fat' in the title and trans fat in the full text?

http://www.ncbi.nlm.nih.gov/pubmed/18560126

Peter said...

Hi Jordan,

In this case the fats really were saturated, no trans fats if the hydrogenation eliminates all double bonds. It's the partially hydrogenated oils that provide the industrial tans fats.

The paper is still a total waste of money. If MCTs were that bad all of the Tokelau would have forgotten where they left their car keys...

Peter