Wednesday, February 14, 2018

Collateral damage from saturophobia. People really do get hurt.

I've spent the last few posts talking about the parlous state of research in to NAFLD and the techniques for justifying saturophobia. This current post is one I wrote a few months ago but never got round to putting up. It's still fairly current, so here it is.

The president of the AHA had a heart attack at an AHA scientific conference recently. This is almost, but not quite, funny. After all, no-one got hurt (much), a little money changed hands and the president is still alive and as healthy as any other cardiologist, still able to go on promoting the ideas which led to his brief trip to the cath lab.

Not everyone is so lucky. I recently finished reading the (very depressing) biography of Tina Mokotoff, written by her husband and documenting her descent in to alcoholism and her subsequent death from alcoholic liver disease at the age of 45.

Mrs Mokotoff had an unremitting need for alcohol. It was the primary drug which allowed her to cope with the emotional scars from her childhood abuse injuries. Her husband, a interventional cardiologist, watched with palpable frustration at the failure of the gastroenterologists to manage her cirrhosis and the failure of repeated rehabs to control her need for alcohol.

WARNING: Epidemiology and rodent studies ahead.

There is significant variation in mortality between populations from alcohol related liver disease (ALD) per unit alcohol consumption. It's interesting to speculate as to why this might be and it was a recurrent thought throughout the persistently depressing account of Tina Mokotoff's journey to death. Let's start with epidemiology:

Correlations between deviations from expected cirrhosis mortality and serum uric acid and dietary protein intake

Mortality from cirrhosis in a population can range from 80% less than predicted (ie two cirrhosis deaths per 100,000 when the alcohol intake predicts 10 per 100,000) through to over 80% more deaths than predicted (ie over 18 per 100,000). That's a nine fold difference between lowest and highest risk, at the same alcohol intake. Something is real here.

In this epidemiological study, animal protein intake is associated with a markedly reduced cirrhosis death rate. The animal protein may be protective per se but I tend towards thinking of it as being a marker for saturated fat intake. But then I would.

To support this biased mindset we know that, in rodent models at least, saturated fat is either completely protective against alcoholic liver disease or shows a dose response in its protective effect up to near complete protection at 30% of calories from saturated fat, even when the other 15% of calories in the 45% calories-from-fat-diet are still PUFA. We also know that even mice fed a low carbohydrate diet derive no protection from ALD when the carbohydrate is replaced by PUFA from corn oil. I doubt anyone would argue that PUFA are good for your liver. Hepatologists have known for decades that lipid peroxides are the drivers of cirrhosis and these only come from damaged PUFA.

Through the 1990s, during his wife's descent in to cirrhosis, Dr Mokotoff worked tirelessly in the cath lab placing stents and "curing" people of occlusive coronary artery disease. His life must have been very simple. Here is a blocked artery. Here is a bit of pipework to open it. Let's put this in there and the patient is fixed. Just occasionally he might even have done some good (though far from as often as he might have thought he had done). During this period the cardiological community was deeply under the influence of the "obvious" benefits from a low fat, low saturated fat and low cholesterol diet.

Unless you are going to indulge in some weird Ornisheque low fat diet, eating a saturated fat depleted diet will will undoubtedly involve a significant intake of PUFA. This should never, under any circumstances, be combined with alcohol. Would the Morokoffs have avoided saturated fat? Dr Mokotoff was an interventional cardiologist. Just guess.

Having a cardiologist, the president of the AHA, inflict a minor injury on himself, without getting really hurt, is ironic. Reading an account of a real human being being driven to a very unpleasant death through cirrhosis is not funny. Inflicting a population wide epidemic of assorted PUFA induced diseases is, absolutely, not funny either.

Thank you, AHA.



Unknown said...

According to this paper:
we do not even need Ethanol to destroy the Liver.

PUFA can do the job alone!

Dophamn said...

*Tries not to laugh about the AHA president and about it not quite being funny*

raphi said...

"I doubt anyone would argue that PUFA are good for your liver."

Oooohhh do i have a surprise for you, if you ever make it to Twitter...

Unknown said...

Peter: I just found this one in my database. I'm not sure if you have commented on it already:

Peter said...

JW, I've had that one on my hard drive for some time. The Protons concept makes it more comprehensible but I think the generic response will be that swilling PUFA will deplete liver fat, visceral fat and (probably, from other the group's other study) make you ripped. Not so good for the long term health of the sheeple [ref raphi's comment].

Not sure if there will be time to post on this one. We'll see. It's along the same old lines.


Unknown said...

Here's a nice analysis of the AJCN-Paper by Chris Masterjohn:

The real interesting part begins at "What We Do and Don’t Know About Veggie Oils and Fatty Liver".

Peter said...


Chris M has no Protons concept to provide any sort of logical explanation. We have no shared terminology. I have convinced myself that I have a valid concept here, with explanatory power. That's hard to let go of.

Chris does have lots of facts.


Puddleg said...

PUFA are also not a food for gram +ve microbiota, and in the absence of SFA and presence of alcohol and PUFA gram -ve microbes will thrive. Their LPS will tigger hepatis via TLR4 in a fatty liver (which has become acutely sensitive to LPS).
This is the tipping point at which alcoholic steatosis, viral steatosis, NAFLD become alcoholic or viral hepatitis, NASH and so on, leading to cirrhosis.
Think about it - what do you make yogurt from? The two highest SFA foods in the diet - milk (and you can culture cream and butter), or, if unfortunate, coconut milk or cream.
Not so far as I know nut milk and I've never seen cultured peanut butter though no doubt the KGB tried.
Good bacteria like good fats. Kirpich et al, the heirs of Nanji and French, have worked this out from - drum roll - a 1930's citation.

Peter said...

George, that citation is bang on topic but comes from 2016. Did you mean to copy paste a 1930s link? I love those old papers. Often so innocent and so focused on answering a genuine question with limited but effective tools....


Puddleg said...

I had to dig a bit, but here it is - 1945 so I wasn't off much

Kodicek, E. The effect of unsaturated fatty acids on Lactobacillus helveticus and other Gram-positive micro-organisms. Biochem J. 1945;39:78–85.

full text at

It's a basic question - what fatty acids can sour milk microbes metabolise? If more people had thought to ask it they wouldn't have made fools of themselves wittering on about "fatty" diets and the microbiome.
From the look of it gram +ve microbes might lack saturase enzymes in their beta-oxidation pathways.

Oleic, linoleic and linolenic acids, and also their
sodium salts, inhibited growth and acid production
(Table 1). This effect, which was contrary to that of
stearic and palnitic acids, depended upon: the concentration
of bacteria, the amount and nature of
the acid added, the time of incubation, and the
presence of other lipids in the medium. The methyl
esters of oleic, linoleic and linolenic acids were
without effect.

Reference in here; this, not the one I linked to, is the team that dug it up.

Peter said...

Thanks George, some nice stuff there. The histo pics in are lovely, especially the 4-hydroxy nonenal, only present in the livers of PUFA fed alcoholic rats.........


karl said...

@Jürgen Wildhardt

The papers in question are correlative diet surveys - in other words junk science. There are papers that show that the diet surveys don't work - people don't remember, lie, and it is impossible to do a proper multivariate study.

When people eat more PUFA they almost always are eating other bits as well - in order to make this point one would have to do the other part of science - a controlled study.

Correlation does not show causation.