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I realize this title look like troll-bait, but please hear me out. Given the revived "DHA-Accelerated Aging Hypothesis Validated" thread, I noticed a surprising omission from the discussion. With all the focus on excess O-3 fats (which are clearly a problem), very little attention has been paid to to the fact that the group of mice fed a high-lard diet lived the longest!


MR does touch on it here :


(It may, however, be worth noting that high SaFA intake may have an indirect effect that is beneficial on this narrow question of tissue membrane PL unsaturatioin index if you're also consuming a lot of PUFA, because high SaFA intake increases the activity of delta-9 desaturase, which converts some of the SaFA to MUFA (especially, stearic (18:0) [thanks Brian!] to oleic (18:1)). So a high-SaFA diet can (inefficiently) increase the availability of oleic to compete with PUFA at the sn-2 position, even tho' it has no effect on the am't of SaFA in the tissue membranes. You can see this for animals fed lard in several previous studies linked in my appendix below. But consuming more MUFA directly while limiting PUFA is a more efficient way of doing this).
And, finally: remember, while I advocate for this "DHA-accelerated aging hypothesis," it remains an untested one in an experimental sense -- and even I think that its effects will be felt on the margin of things, and only in people on CR. By contrast, the epidemiology and clinical trials are pretty clear that SaFA will kill you dead of a heart attack or occlusive stroke, irrespective of whether you're aging a little slower because of an altered cell membrane composition.



A lot of the biochemistry is above my head right now, but I understand this to say that eating SaFA is basically a bad way to get your MUFAs. But here is my question:


Is the fatty-acid profile of lard improving lifespan by another mechanism(s), perhaps helped along being consumed with a good dose of SaFA?


According to Self Nutrition Data, 100g of lard has around 40g of SaFAs and 45g of MUFAs. Similarly, there are considerable SaFA's in human adipose: "compared with adipose fat composition, 27.1 ± 4.2% saturated, 49.6 ± 5.7% monounsaturated, and 23.4 ± 3.9% diunsaturated" according to http://www.jlr.org/content/49/9/2055.full. It seems counterintuitive that our bodies would store SaFA as fuel if if were simply going to kill us dead. And I say this with much much respect to Michael, who I have followed closely. Not in a creepy way :)


Thank you for considering this question!

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Good questions. I'm no expert on the various fatty acids, and hopefully Michael will chime in to answer you. I'm just responding to point to an interesting article from yesterday by one of Michael's favorites, Dr Greger :-), discussing the evidence that one mechanism by which saturated fat does harm is through impairing insulin sensitivity - more so than other types of fat.
One other observation. You wrote:
It seems counterintuitive that our bodies would store SaFA as fuel if if were simply going to kill us dead.


The key is that it kills us dead slowly. Cardiovascular disease takes decades to develop. Overt symptoms and death don't typically strike until our 5th decade on earth, long after our ancestors typically died of other causes. So our bodies (and evolution) don't care that saturated fat will eventually kill us from heart disease. In the short run SFA is a highly efficient way to store energy, which is much more important for short-term survival and reproduction in our ancestral environment.


Plus in our ancestral environment, dietary sources of saturated fat were hard to come by.  They were rare and took a lot of energy expenditure to procure - burning off a lot of fat in the process.


Plus even the animals sources of SFA that were available had a lot less saturated fat than the animals people eat today. So it is no wonder that our bodies don't 'recognize' that too much saturated fat is unhealthy - since they were very rarely exposed to excessive amounts during the long period in which such recognition could have evolved.


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(First, for anyone who has no idea what David is talking about, please see my major post on the DHA-Accelerated Aging Hypothesis).

It seems counterintuitive that our bodies would store SaFA as fuel [MR emphasis] if if were simply going to kill us dead. And I say this with much much respect to Michael, who I have followed closely. Not in a creepy way :)

I was  initially skeptical about the narrow empirical basis your empirical premise, because the study you link is only a single time-slice of "Twenty healthy adults (twelve females and eight males) age 22–52 years (average 34 years; without diabetes or known vascular disease)", otherwise uncharacterized: we know nothing about their diets, or anything else, but there's a good chance that they're just impoverished medical students at the University of Texas Southwestern Medical Center in Dallas, who I'd venture to say probably get their share of saturated fat ;) . However, their results are pretty consistent with a paper reviewing dietary and other influences on fatty acid composition of adipose tissue TG and other tissue FA (1) with data in 4258 and 3096 healthy men and women from 19 studies shows 43.5% 18:1 and 7.2% 16:1, with 21.5% 16:0 and 6% total 14:0 + 18:0.  That's also consistent with the "Positional distributions of fatty acids (mol %) in triacyl-sn-glycerols of animal depot fats" in this American Oil Chemists’ Society article on triacylglycerols, which shows that there's a fair amount of 16:0 in the typical human's adipose tissue TG sn-1 position, but little in sn-2 or -3, whereas there's a very large amount of 18:1). But of course, humans consume very little n-3 as a percentage of total fat (and it wold be dangerous for us to dramatically increase it, as the typical American intakes of n-6 in the late 20th century were excessive), so it's not surprising that it has to be comprised of something. In any case, you can see that it's MUFA and not SaFA that predominate.
Now, as to the line of reasoning in your question: first, you're making a variation on the signature error of the more doctrinaire Paleo diet people. You have to remember that evolution has not optimized to keep you free of cardiovascular disease within a modern human's life expectancy, but a Paleo person's: i.e., the principal selective pressure is to optimize to survive childbirth, followed by early-childhood and lifelong infection, trauma, starvation, and warfare. It is not making any significant effort to make sure that your arteries are kept clean for 80+ years, or that you're well-suited to sustain energy balance and remain healthy in a world of unlimited and continuous access and exposure to Calorie-dense, highly-palatable food.
It's also, similarly, not optimizing to slow your aging down any more than it is already slowed down relative to our evolutionary ancestors (which is a tautology, of course). The 'default' of having a lot of HUFA in your tissue phospholipids, and only being remodeled to the slower-aging short-chain PUFA as part of a response to something as radical as periods of famine, is not because evolution wants to kill you earlier; nor, for that matter, are faster-aging animals' higher tissue HUFA evidence of evolution trying to kill them any faster than us. It's because natural selection has other priorities, which are met with faster activity of cell membrane proteins, easier synthesis of  eicosanoids, etc.
Second major point: you've unconsciously revealed part of the key here, which I've highlighted in red. Fat that is sequestered in adipose tissue TG is exactly that: storage fat, not metabolically-active fat or fat in metabolically-active tissue membrane. Remember, as I've reviewed, the fat in tissue cell membrane phospholipids, which is used for metabolic purposes (as raw material for eicosanoid synthesis, to govern the activity of cell-surface proteins and transporters, etc) is genetically determined to be one saturated and one unsaturated fatty acyl group, with the diet and metabolism determining which saturated and unsaturated fatty acids take up the respective sn- positions. So you have to put any excess SaFA somewhere. Having it disproportionately stored up in a (mostly, and directly) metabolically-inert place, but available to simply and safely burn off as energy in times of need, is the best thing for it!
And also, remember that adipose is where you store excess energy in general, and not just from fat: you have a limited capacity to build muscle or other proteins from dietary protein, and to store excess carb as glycogen, and the rest gets converted into fat by de novo lipogenesis. And what kind of fat does DNL make? Saturated and monounsaturated fatty acids, of course! In fact, no vertebrate animal can synthesize its own PUFA. So that's where all that extra Snackwell is going.
There are also a lot of other reasons why different spp favor different FA for adipose composition. In humans, for instance, much of our fat tissue is not just storage, but includes structural fat, too — notably breast and the ass, as well as visceral fat when not in excess.  And different spp have other idiosyncratic reasons why particular FA wind up in their adipose tissue that have nothing to do with their long-term health:

Ruminant animals, such as the cow and sheep, have relatively saturated fats because the dietary unsaturated fatty acids are subjected to biohydrogenation in the rumen, a process that also generates trans fatty acids as by-products. These animals also tend to have relatively higher concentrations of odd- and branched-chain fatty acids from the rumen microflora. Non-ruminant herbivores, such as the horse, can have appreciable amounts of linolenic acid from grass in their adipose tissue, while that of marine mammals is characterized by high concentrations of long-chain mono- and polyenoic fatty acids because of their diet of fish. ... The fatty acid compositions of triacylglycerols of fish oils reflect their diet and usually comprise high concentrations of long-chain monoenoic and polyunsaturated fatty acids, especially those of the omega-3 biosynthetic family. ...

Marked differences have been observed in the distributions of fatty acids among the three positions of the glycerol moiety in most species examined. There are also appreciable interspecies differences. A few representative results are listed in Table 2. [AOCS op cit]


1: Hodson L, Skeaff CM, Fielding BA. Fatty acid composition of adipose tissue and blood in humans and its use as a biomarker of dietary intake. Prog Lipid Res. 2008 Sep;47(5):348-80. doi: 10.1016/j.plipres.2008.03.003. Epub 2008 Apr 4. Review. PubMed PMID: 18435934.

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Omega-3 fatty acids partially revert the metabolic gene expression profile induced by long-term calorie restriction.

López-Domínguez JA, Cánovas Á, Medrano JF, Islas-Trejo A, Kim K, Taylor SL, Villalba JM, López-Lluch G, Navas P, Ramsey JJ.

Exp Gerontol. 2016 Feb 10. pii: S0531-5565(16)30031-6. doi: 10.1016/j.exger.2016.02.002. [Epub ahead of print]

PMID: 26875793




Calorie restriction (CR) consistently extends longevity and delays age-related diseases across several animal models. We have previously shown that different dietary fat sources can modulate life span and mitochondrial ultrastructure, function and membrane fatty acid composition in mice maintained on a 40% CR. In particular, animals consuming lard as the main fat source (CR-Lard) lived longer than CR mice consuming diets with soybean oil (CR-Soy) or fish oil (CR-Fish) as the predominant lipid source. In the present work, a transcriptomic analysis in the liver and skeletal muscle was performed in order to elucidate possible mechanisms underlying the changes in energy metabolism and longevity induced by dietary fat in CR mice. After 8months of CR, transcription downstream of several mediators of inflammation was inhibited in liver. In contrast, proinflammatory signaling was increased in the CR-Fish versus other CR groups. Dietary fish oil induced a gene expression pattern consistent with increased transcriptional regulation by several cytokines (TNF, GM-CSF, TGF-β) and sex hormones when compared to the other CR groups. The CR-Fish also had lower expression of genes involved in fatty acid biosynthesis and increased expression of mitochondrial and peroxisomal fatty acid β-oxidation genes than the other CR diet groups. Our data suggest that a diet high in n-3 PUFA, partially reverts CR-related changes in gene expression of key processes, such as inflammation and steroid hormone signaling, and this may mitigate life span extension with CR in mice consuming diets high in fish oil.




Calorie restriction; Dietary fat; Gene expression; Omega-3 fatty acids

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Thank you all for the well-informed responses. I completely with Michael and Dean that we are not necessarily designed to live long but to live long enough to reproduce and pass on a few survival tips to our offspring. Yes, the Paleo-folk often appeal to this fallacy of doing what is natural instead of doing what will improve vigorous longevity. However, that doesn't mean that their conclusions are necessarily wrong - it just means they are using the wrong line of reasoning.



There is something about this lard study that sets off my spider sense. Like I said, I am not in the same league, either in terms of biochemistry or CR, as most of you. I will need to digest your responses and references for a while, and hopefully come to some conclusions later.

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