Monday, July 29, 2013

Could grain-fed beef liver be particularly nutritious?


There is a pervasive belief today that grain-fed beef is unhealthy, a belief that I addressed before in this blog () and that I think is exaggerated. This general belief seems to also apply to a related meat, one that is widely acknowledged as a major micronutrient “powerhouse”, namely grain-fed beef liver.

Regarding grain-fed beef liver, the idea is that cattle that are grain-fed tend to develop a mild form of fatty liver disease. This I am inclined to agree with.

However, I am not convinced that this is such a bad thing for those who eat grain-fed beef liver.

In most animals, including Homo sapiens, fatty liver disease seems to be associated with extra load being put on the liver. Possible reasons for this are accelerated growth, abnormally high levels of body fat, and ingestion of toxins beyond a certain hormetic threshold (e.g., alcohol).

In these cases, what would one expect to see as a body response? The extra load is associated with high oxidative stress and rate of metabolic work. In response, the body should shuttle more antioxidants and metabolism catalysts to the organ being overloaded. Fat-soluble vitamins can act as antioxidants and catalysts in various metabolic processes, among other important functions. They require fat to be stored, and can then be released over time, which is a major advantage over water-soluble vitamins; fat-soluble vitamins are longer-acting.

So you would expect an overloaded liver to have more fat in it, and also a greater concentration of fat-soluble vitamins. This would include vitamin A, which would give the liver an unnatural color, toward the orange-yellow range of the spectrum.

Grain-fed beef liver, like the muscle meat of grain-fed cattle, tends to have more fat than that of grass-fed animals. One function of this extra fat could be to store fat-soluble vitamins. This extra fat appears to have a higher omega-6 fat content as well. Still, beef liver is a fairly lean meat; with about 5 g of fat per 100 g of weight, and only 20 mg or so of omega-6 fat. Clearly consumption of beef liver in moderation is unlikely to lead to a significant increase in omega-6 fat content in one’s diet (). By consumption in moderation I mean approximately once a week.

The photo below, from Wikipedia, is of a dish prepared with foie gras. That is essentially the liver of a duck or goose that has been fattened through force-feeding, until the animal develops fatty liver disease. This “diseased” liver is particularly rich in fat-soluble vitamins; e.g., it is the best known source of the all-important vitamin K2.



Could the same happen, although to a lesser extent, with grain-fed beef liver? I don’t think it is unreasonable to speculate that it could.

21 comments:

Bill said...

Interesting article, Ned. What's your take on liver from conventional vs. "organic" (eg, antibiotic-free, etc.) cattle?

js290 said...

A story on foie gras.

Anonymous said...

What about conventionally-fed (whatever that is) chicken and pork liver? I ask, because that's what seems to be in virtually every type of pate or liverwurst available where I live, be it commercial or 'artisan' pate or wurst. I never see beef/lamb liver on the ingredient list. Of course, I should make my own...
Cheers, Michael

Ned Kock said...

Below is exchange with Sean Baker on Facebook, regarding this post, which may be of interest here.

Sean Baker:

I know the bulk of the article is about beef liver, but re: foie gras. ducks will actually gorge themselves. no force-feeding required. either way, I would think the Ω-6 in foie gras may be more problematic than grain-fed beef liver. beef liver is pretty lean, but foie gras seems to be VERY fatty. I haven't seen nutrition info on it, but it sure as hell renders a lot of fat when you sear it in a pan, a pan that requires no fat to keep it from sticking, and needless to say, i'm not talking about a nonstick pan. you can sear it dry in a stainless steel pan, and it won't stick.

Ned Kock:

Indeed, foie gras is very fatty. Most of the fat is monounsaturated and saturated (44 g per 100 g of weight), with a comparatively small amount of n-6. About 0.5 g of n-6 per 100 g of weight. Most of what melts into the pan is "olive oil", so to speak.

Ned Kock said...

Hi Bill. Generally speaking, I think that both the advantages and degree to which products are really organic are exaggerated.

Ned Kock said...

Hi Anon. Liver is nutritious, one way or the other. Foie gras seems to be particularly rich in K2, but the measures of this vitamin for organ meats in general are often unreliable. Chris has a good article on this. I think the link is the one below, but it was not working at the time of this writing:

www.westonaprice.org/fat-soluble-activators/x-factor-is-vitamin-k2

VEGF antibody said...

Thank you for the article.

Nate said...

yellowing shows incomplete conversion of beta carotene to retinol

water buffalo butter is white in appearance showing an almost complete conversion

still would eat as it is so dense nutritionally

raphi said...

Hi Ned,

Interesting post and great timing for me as I am back home in France now perusing the isles for duck fat and foie gras while wondering how common an item they should be for myself (considering that I'm aiming for a 1:2 - 1:4 omega-6 to omega-3 ratio).


I read Chris Masterjohn's "How Essential are the Essential Fatty Acids?" report and would like your opinion on some of the aspects relating to your article.


Firstly

"all of the same enzymes and cofactors are used to convert linoleate to arachidonate, ALA to EPA, and EPA to DHA. Linoleate from vegetable oil, ALA from flax oil, and EPA from fish oil will not only compete with each other for these enzymes but an excess of any of them will decrease the production of those enzymes, aggravating the effect of the competition" - p.17

Wouldn't this suggest that our priority should be to limit omega-6 FAs rather than 'overload' ourselves with omega-3 FAs due to the available enzymes and cofactors for their conversions? It'd seem like an up-hill battle otherwise...


Secondly

"On a diet low in sugar and rich in essential minerals, the requirement for EFA during periods of growth is likely to be well under 0.5 percent of calories if supplied by animal fats and well under 0.1 percent of calories if supplied completely by liver." - p.23

Would your recommendation differ from Chris Masterjohns?

Ned Kock said...

Hi raphi. I would normally tend to agree with Chris, who is a genius, but I am increasingly suspicious of the applicability of ratios and the like regarding n-6 and n-3, as long as they come from natural sources. It seems that the really problematic sources are unnatural, or industrial, foods rich in n-6. Have you seen the post below, about the man who ate 25 eggs a day?

http://bit.ly/QPV5g6

raphi said...

Yes I'd already read that a while ago, but didn't seem to grasp just how significant a point it raised in terms of the un/healthfulness of some foods being affected by ingested cofactors, timing etc..

How do we normally figure out how much activity/concentration of a particular compound starts crowding out receptor sites, leaving other compounds with sub-optimal receptor site accessibility?

Would looking at the intracellular polyunsaturated FA profile help us make the determination of an 'unbalanced' ratio or should we figure out a way of answering my previous question first? (i.e., knowing how much is too much before trying to observe apparent 'crowding out' in vivo)

Ned Kock said...

Hi raphi. Biochemistry-based arguments can be very misleading. Yet, biochemistry can be extremely useful in the elucidation of diet and lifestyle effects that are suggested by well-designed studies of humans.

If you start with a biochemistry-based argument though, and ignore actual studies of humans, you can easily convince someone that glycogen-depleting exercise (e.g., weight training) is unhealthy, because many health markers change for the worse after that type of exercise. But it is the damage caused by glycogen-depleting exercise that leads to health improvements, via short- and long-term compensatory adaptations.

The same applies to n-3 and n-6 amounts, their ratios etc. After looking at a number of studies, it seems that if n-3 and n-6 come largely from natural sources, it will be difficult to find pathological cases. Another example is the consumption of the mongongo nut by the traditional San bushmen, for whom it is a dietary staple.

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

Keeping in mind that:

(1) epidemiological evidence strongly suggest that omega-6 & 3 FA ratios are important variables for overall mortality and especially CV health,

and

(2) a substantial amount of in vivo and in vitro experimental evidence suggest that omega-6 & 3 FA ratios count, but who's 'effect' is also limited by the absolute concentrations of each

The argument seems to come from both lines of evidence leaning on each other.

Yet the high omega-6 consumption of the !Kung apparently contradicts both point 1 & 2...but
neither the '!Kung' argument or 1 & 2 are strong enough to refute the another.

So, one plausible explanation that seems worth investigating is: could our 'modern' consumption of polyunsaturated FA (whether from extracts or whole products) in their (often) denatured from (high heat, few anti-oxidants) 'confound' the results we observe in the !Kung which (seems reasonable to assume) consume these polyunsaturated FA in their 'optimal' state?

Ned Kock said...

There is a lot of evidence contradicting the idea that n-6 consumption per se causes health problems. I think that what you listed is a reasonable alternative hypothesis. The more I study health issues, the more it becomes clear that life is not simple.

Having said that, it seems that one can take relatively simple actions that will very likely minimize health problems. Among the most important are: doing moderate glycogen-depleting exercise, being physically active, avoiding highly industrialized foods, and minimizing one’s waist-to-weight ratio.

If one feels good in the short and long term while doing these things, it is a good sign.

Christel said...

Cool!

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comprar Cialis said...

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Jack C said...

Ned, I think you and Chris Masterjohn are both brilliant guys but I thoroughly disagree with your contention that excessive intake of n-6 linoleic acid has only minor adverse consequences. I think that a vast amount of research on the endocannabinoid system has proven that excessive intake of n-6 LA, which is a precursor to n-AA that is the backbone of n-6 endocannabinoids, results in the dysregulation of many physiological functions including memory, learning metabolism and appetite. Endocannabinoids derived from n-6 AA activate the same receptors that are activated by marijuana.

Excess intake of n-6 LA, like smoking too much pot, makes people fatter and dumber.

Jack C said...

Ned, the primary cause of non-alcoholic fatty liver disease (NAFLD) is excessive intake of linoleic acid and the consequent depletion of n-3 fatty acids from the liver.

From PMID 21853118

"n-3 PUFA depletion in liver phospholipids leads to activation of SREBP-1c and lipogenesis, which contributes to hepatic steatosis. (NAFLD)"

PMC 3154437 Free PMC Article

The increase in n-6 LA intake results increases in endocannabinoids which "predisposes mice to ectopic lipid storage (belly fat) and hepatic insulin resistance by promoting centrally mediated (via the brain) hypothyroidism. The reduction in energy expenditure caused by hypothyroidism results in increased "feed efficiency" (weight gain per calories of food intake). Calories not used for energy are diverted to synthesis of fats from carbohydrates which causes the weight gain.

Saturated fat does not cause non-alcoholic fatty liver.


Mohammad Mahmudul Hasan said...
This comment has been removed by the author.