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Friday, 3 May 2013

"The Truth was Still Putting on its Shoes", my first article to be published IRL

I haven't had my Diet Wars writing published before, unless you count my many letters to the editors of The Herald, Listener, and Otago Daily Times, letters which, I'm pleased to say, do often get published.
This is the first hard copy of an article that wasn't just a response to some piece of stupidity in the press.

It was commissioned for inclusion in the first edition of the free Café  Reader. This will hopefully be available in every café in New Zealand. Apart from my polemic, it also contains writing from the finest local talent. I opened it at random (after checking my piece for typos, phew!) and Simon Sweetman's party piece is the funniest thing I've read in ages. Put together by Phantom Billstickers, thanks to Jim and Kelly Wilson and no doubt other committed team members that I haven't had dealings with.

And there we have it. I will reprint the whole article in a few weeks for overseas readers.

Meanwhile, some exciting science news; expert scienticians have finally invented a high-fat diet that DOESN'T produce fatty liver in Wistar rats, even with prodigious overfeeding!

Long term highly saturated fat diet does not induce NASH in Wistar rats


Understanding of nonalcoholic steatohepatitis (NASH) is hampered by the lack of a suitable model. Our aim was to investigate whether long term high saturated-fat feeding would induce NASH in rats.


21 day-old rats fed high fat diets for 14 weeks, with either coconut oil or butter, and were compared with rats feeding a standard diet or a methionine choline-deficient (MCD) diet, a non physiological model of NASH.


MCDD fed rats rapidly lost weight and showed NASH features. Rats fed coconut (86% of saturated fatty acid) or butter (51% of saturated fatty acid) had an increased caloric intake (+143% and +30%). At the end of the study period, total lipid ingestion in term of percentage of energy intake was higher in both coconut (45%) and butter (42%) groups than in the standard (7%) diet group. No change in body mass was observed as compared with standard rats at the end of the experiment. However, high fat fed rats were fattier with enlarged white and brown adipose tissue (BAT) depots, but they showed no liver steatosis and no difference in triglyceride content in hepatocytes, as compared with standard rats. Absence of hepatic lipid accumulation with high fat diets was not related to a higher lipid oxidation by isolated hepatocytes (unchanged ketogenesis and oxygen consumption) or hepatic mitochondrial respiration but was rather associated with a rise in BAT uncoupling protein UCP1 (+25–28% vs standard).


Long term high saturated fat feeding led to increased "peripheral" fat storage and BAT thermogenesis but did not induce hepatic steatosis and NASH.

The full text paper is here


john said...

It is sort of strange that even the coconut rats were fatter, but it does happen sometimes. Their metabolic rate per mass was high though, considering their calorie intake was incredibly high!

George Henderson said...

They were fatter peripherally without changing mass. I am sure there is more to this than muscle wasting, which isn't mentioned in the paper.

Ilya said...

In view of recent studies housing temp is important with rodents. When kept under 30C rodents are cold-acclimated and display an evolutionary established preference for lipolysis (Walsberg et al.) and respectively active BAT. Energy expenditure obviously was not matched with nutritional intake so in this case BAT of HF fed rats was compensating for both-cold acclimation and excess food intake thru increased thermogenesis hence increased UCP-1 in HD rats. The rest was stored as WAT. Now about the main point of the study, the idea that dietary fats cause NAFL or obesity in humans is long time dead. Cause for NAFL and AFL too is increased hyperglycemia insulin-induced SREBP-1c transcriptional and translational factor in cold acclimated human subjects result of *endogenous* LC acyl-FA, the ones formed from glucose and especially sucrose and fructose via DNL. There is a study from Alcoholic Reports confirming that alcohol is not *necessary* and respectively not a cause for so-called AFL. The reason for increased DNL in humans is the same as in rats, simply the thermoneutrality point is above 33C. Everything below evolutionaty requires lipolysis as predominant metabolic path of Randle cycle. HF LC diets drive DNL to fit that pattern with a detrimental impact on mitochondria causing oxidative stress- from increased NADPH+ ROS (H2O2) and increased NOS (from inhibited AMPK). Final result is mitochondria dysfunction, the one, and founding, cause of modern morbidity.

George Henderson said...

Thanks Ilya. I consider increased ambient heat in dwellings, workplace, hospitals, cars etc a cause of modern morbidity. I believe that Colorado has the lowest obesity rate in the USA. Mitochondrial dysfunction especially at ETC Complex 1 is common to a wide range of disorders.
You can cause steatosis in humans with excess linoleic acid, probably easier if fructose is also included. Human cases of NASH will have extremely high n-6/n-3 ratios; up to 144:1.

George Henderson said...

The idea that alcohol is not required or sufficient in itself to produce AFL is covered very ably in these two papers:
fats and AFL:
microbiota and AFL:

Bill said...

Interesting interesting. I tend to think some exogenous fats, like George mentioned linoleate also play an important/"causative" role in liver dysfunction.

I wouldn't expect MCTs to deteriorate mitochondrial function at any ambient temperature, but even more so in the cold when BAT is already activated. Is this where you guys were going: MCT-induced BAT activity drives DNL to fuel thermogenesis (as opposed to MCTs themselves being burned)?

George Henderson said...

What does it mean that the coconut rats had to eat more of EVERYTHING, not just fat, to keep the same shape as the butter rats?

George Henderson said...

Does anyone think it's relevant that coconut is only a staple food in hot places? I wonder if there is a pattern towards eating more thermogenic foods around nightfall in those places? In fact, is this the original evolutionary reason for the big evening meal in general?

George Henderson said...

Bill, I think DNL fats are ligands for PPAR-alpha, which is the fasting-state "fat burning" transcription factor. This seems paradoxical, but it might well be how coconut oil works.