Essential fatty acids (6), deposition of LA in depot fat

I was having a conversation with a friend about this old article: Seed Oils and Body Fatness: A Problematic Revisit

These are my thoughts:

So he (Guyenet) has like 7 papers for his nice linear graph. All of them use different populations. Some of them are women only, some are men only, some are both. But he lumps them together and plots them over time. Ok, the problem with this is that, first men’s requirements for LA are more than women by quite a bit so you can’t just lump this all together and plot this over time that is a big FAIL.

The second thing is that deposited LA in fat stores tells you nothing about utilization or consumption habits. This has been demonstrated as early as 1936. In fat free diets when you add small amounts of LA something like 1-2% there is a marked increase in deposited LA, as in, almost all of it gets deposited in fat depot tissue because it shuts down de novo lipogenesis. This seems to be a direct function of LA by decreasing expression of SREBP-1c, which is major regulator of DNL, which is interesting because if you aren’t eating LA and eating a fat free diet in some people this causes RAPID weight gain, fat that is laid down is more oleate instead of palmitate which probably makes it increasingly hard over time to go without food.

But when you add medium chain and long chain fatty acids to the diet and you feed LA, LA is dramatically reduced in adipose tissue as LA utilization (metabolically as opposed to bio-synthetically) is a function of the chain length of the fatty acid. For example, in rats fed fat free diets, diets with MCTs, and diets with LCTs, fat depot LA levels are respectively 21%, 11%, and 6%.

So, EVEN if there is more LA in adipose tissue, it doesn’t tell you anything about actual CONSUMPTION, all it tells you loosely is the composition of fats and carbohydrates in a person’s diet, it does not tell you about CONSUMPTION habits AT ALL because you can take someone on a low fat diet who eats low amounts of LA and it all will be deposited into depot fat, but you can take a person who is on a moderate or higher fat diet eating the same amount of LA as the person on the low fat diet and they will have LESS LA in their depot fat.

That’s literally the only conclusion you can draw, so you can not copy and paste historical soybean oil availability charts and paste them on top of depot fat composition on mixed groups of people over time and then say boom we are eating more LA because of soybean oil and look there is also more in our fat, doesn’t work that way.


P.S. Next post will be why you don’t want your mitochondria to be depleted of LA. It’s not good.

Essential fatty acids (5), notes

  • IV glucose w/o fat induces EFA deficiency w/ accompanying symptomatology
  • Hydrogenated coconut oil and tallow are used to induce EFA deficiency in lab animals
  • PUFA induced NAFLD seems to be dependent on what mouse model is being used, for example, diabetic prone mice already have deranged EFA metabolism, as a result EFA would be implicated much like cholesterol is implicated in various disease states but interventions fail, flawed logic, do you biology? LOL.
  • Symptoms of EFA deficiency take weeks not years to appear (even when nutrition is adequate)
  • Reversal of EFA deficiencies with sources of LA and ALA largely resolve acute symptomatology within weeks not years, the idea it takes years to deplete PUFA stores is unrealistic
  • Common symptoms of chronic EFA deficiency are hair loss, increased shedding, and skin abnormalities, hair and skin is one of the most metabolically active tissues, the idea that EFAs slow metabolism is an unrealistic mechanism; same for improvements in skin quality
  • LA and ALA seem to spare the B vitamins and vice versa
  • Symptoms of EFA deficiency are reminiscent of hypothyroidism (thinning of hair, thinning of outer eyebrows)
  • EFAs are required for proper epithelial differentiation and proliferation, this not only has implications for hair and skin but ALL epithelial cells including the GI tract along with gut permeability
  • EFA deficient animals manifest with slowed wound healing, this is a problem as the longer a wound takes to heal the more susceptible one is to infection and scarring
  • The immune system requires LA and ALA to function properly, immune cells hoard EFAs and use the peroxides generated from EFAs to disable viruses and bacteria
  • EFAs are required for the proper metabolism of saturated fatty acids (the mechanism is not clear yet)
  • EFAs are required for myofibrillar and sarcoplasmic hypertrophy
  • EFAs are required for some hormone production, especially some of the stress hormones, a failure in the production of stress hormones would inhibit the stress response, thus adaptation, leading to maladaptive and degenerative state
  • EFA deficiencies manifest psychologically with the following traits: depression, aggression, hostility, changes in attention, motivation, changes in reactivity to stimuli and reward, general personality disorders such as obsessive compulsive behavior, apathy, and eating disorders
  • EFAs required for proper sex organ function and development in both males and females
  • EFA metabolism is complex, supplemental EFAs can resolve EFA symptomatology in most cases, however, perturbations of desaturase and elongase activity such as those seen different disease phenotypes can prove difficult to treat though because the underlying machinery is deranged
  • EFA derangement is seen in the following conditions, alloxan and streptozotocin treated diabetic rats, diabetes, vitamin E and selenium deficiencies, cystic fibrosis, copper deficiency, Kwashiorkor, adult respiratory distress syndrome, chronic and acute carbon tetrachloride poisoning, multiple sclerosis, most chronic and acute neurological diseases, LEC rat models of fulminant hepatitis, hepatic cancer, Wilson’s disease, sudden cardiac death, beta-Thalassaemia major, abnormal umbilical cord blood cells
  • Mead acid is increased during EFA deficiency, the largest reservoir of mead acid is the cartilage, after stores of oleic acid are exhausted soft tissues particularly in the joints are robbed of mead acid stores, it is plausible this can lead to joint degeneration, stiffening of joints, loss of flexibility, calcification of joints
  • LA and ALA are the only known essential fatty acids (in humans, mice have different available desaturase and elongase enzymes, as do other species along with varying capacities), other fatty acids sometimes associated with EFAs such as DHA, EPA, AA, are what are known as ‘conditional essential fatty acids’
  • Contrary to the antioxidant hypothesis, Vitamin E may not be involved with stabilizing polyunsaturated fat i.e. reducing its proneness towards oxidation, rather Vitamin E is involved with the function of desaturation ezymes, which of course is a more plausible mechanism
  • LA probably is an important part of the mammalian antioxidant system
  • There are sex differences in EFA metabolism that are proportional to muscle mass

Essential fatty acids (4), what about B6?

P.S. I can ABSOLUTELY tell you without a doubt B6 won’t fix that. LOL.

Bold claim? Nope. Demonstrated in 1938.

These results show that rats may develop acrodynia-like dermatitis if the diet is free from fat even when moderately large amounts of B6 are given. The possibility that the disease observed by Burr and Burr might be due to a low intake of vitamin B6 is ruled out by the finding that even with 10 times the minimum curative dose, unsaturated fatty acid is necessary for normal health and growth. The fatty acid factor is, therefore, an essential constituent of the diet for rats.

Essential fatty acids (1), to be continued…

Everybody loves a little click bait. And this is click bait. As part of my ongoing “Unifying biology” series I had planned to do a post on essential fatty acids. It was one of the first things I planned on covering. Initially, as you can see below I have a good start. But then I got side tracked by other things I wanted to cover and because the more I read about EFA’s and the history of their research and their relationship with B vitamins the more I realized this particular topic was not going to be easy to neatly fold and place in the drawer. The truth is while I have been silent on the necessity of the classical essential fatty acids, I have been quite adamant of my position on polyunsaturated fats. Essential fatty acids have always been a sort of moot point for me, my assumption was always that if you are eating animal products you are going to get some depending on your favorite animal. That is true. But it turns out there is a story to be told. Stay tuned for the next post in my “Unifying biology” series.

L. reuteri (2) effects of linoleic acid

This past week I’ve been spending quite a bit of time thinking about L. reuteri. One of the interesting things I’ve mentioned in the past and why I think that this particular strain is interesting out of all the other different species is because L. reuteri was a dominant species in the human gut in the middle twentieth century according to literature and samplings done during that time period. Present day this seems to not be the case. In fact, it seems to be quite rare.

One of the interesting things about L. reuteri is that the antimicrobial compound it produces, reuterin, is produced in the presence of glycerol. Glycerol as you know forms the backbone of triglycerides i.e. fat. In the lab, reuterin can be synthesized simply by culturing L. reuteri with glycerol. L. reuteri is unique in that it will thrive in 16:0 and 18:0 i.e palmitic and stearic acid growth medium.

It’s growth however, can be inhibited by excess consumption of polyunsaturated fat and in particular 18:2 or linoleic acid. While some strains have been shown to mutate in the presence of LA and evolve defense mechanisms to protect itself from LA, they don’t thrive as much as they do when LA is low. In other words LA is bactericidal/bacteriostatic. A bactericidal compound literally kills bacteria whereas a bacteriostatic compound simple inhibits growth. The effect that LA has on bacteria has been known since the early 20th century.If we take a look at these figures for sources of LA in the diet we can see that LA has dramatically increased mostly from increased soybean oil and poultry consumption.

If we take a look at these figures for sources of LA in the diet we can see that LA has dramatically increased mostly from increased soybean oil and poultry consumption.

That is a very interesting coincidence along with the falls in palmitic and stearic acid.

When bile is released it breaks down triglycerides into it’s basic components, free glycerol and 3 free fatty acids. The free glycerol would have provided substrates for L. reuteri to produce reuterin and the free fatty acids would have provided the approperiate energy substrates for L. reuteri to continue to thrive and remain dominant.

However, with declining saturated fat and meat intake and the increase in 18:2 since the middle part of the 20th century, this would have proved unhospitable to L. reuteri thus destroying any benefit to a symbiotic relationship. No more free lunch.While most bacterial strains can thrive with a variety of different energy substrates, they proliferate and dominate when they are provided with the right energy substrates that allow them to effectively compete. When you remove those things and simultaneously introduce a hostile environment they vacate.

Given the long evolutionary history we have seemed to have had with L. reuteri and the increasing amounts of carbohydrate and LA in the human diet and the decreasing prevalence of L. reuteri, I’d venture to say that this particular species is well suited to thrive in a diet low in carbohydrate and rich in fat. In other words it doesn’t need carbohydrate to thrive. I’ve often thought of the gut biomass as only being relevant in the context of diets that contain elevated amounts of ruffage. Clearly this is not always the case as L. reuteri likes glycerol, amino acids, and saturated fat, and doesn’t like LA, so as far as I’m concerned me and L. reuteri can be friends.

Given that L. reuteri thrives at physiological temperatures, culturing at 37C probably is fine.

December 4, 2017 updates

Wrapping things up around here at home, we’ll be picking up the our Airstream travel trailer sometime at the beginning of January. We are looking forward to the new adventure. I also am looking forward to doing more with the blog and writing more. In the interim I’ve added Discord support, you should be able to join the server using the widget on the right sidebar.

If for some reason you can not connect to Discord, leave a comment, or send me an email and I’ll send you an invite.

As always, best wishes, Ed.

The Apocalypse: Conquest

It’s kind of funny how I have changed as I’ve gotten older. I just turned 34 last month and despite oscillations over the years the trend since I’ve been born is linear improvement. I feel better than I felt last year and so on. The funny part is that I eat just about everything these days and the only thing that has stayed universally consistent over the years is my general avoidance of polyunsaturated fat and more recently my willingness to embrace childhood favorites on a regular basis including things like Doritos, commercial pizza and cheeseburgers. A paradox I know—but that’s about it.

There are a couple of things that you might find interesting as well.

I come from the band camp that sings the tune that a high metabolism is not the same thing as an efficient metabolism. Now efficiency i.e. “achieving maximum productivity with minimum wasted effort or expense” is what gives a person the ability to eat less than another despite matched efforts. And depending on what is going on this could mean a person is producing more ATP per log of wood thrown onto the fire or a person is using ATP more—how do I say this proper—more soundly. Or both.

Bottom line if you can’t go without food for a day there is something wrong. You might want to upgrade from a bonfire to a wood burning stove. Or from two sticks to a match. Or from wet sticks to dry sticks. Ha.

For myself, I eat the bulk of my calories after work. Sometimes I’ll bring something “small” to work like Creepy Uncle Ed’s 6-yolk hot chocolate (have lost interesting coffee for some time) or I’ll pick one up at the coffee shop (sadly no yolks in that), and sometimes a few 1 gram salt tablets during the day mostly preemptive preparation for my evening weightlifting.

I eat all of the macronutrients in any combination that I am hungry for. The only rule I follow is to avoid polyunsaturated fat. Now avoid doesn’t mean always. When I’m in Rome (traveling), I do as the Romans do, and indulge in a bit of pro-oxidative behavior. For example, recently I was up in Chicago and ate the local cuisine. If I happen to be hungry for some childhood favorites such as Doritos which seem to be magical in instances I do so.

I even eat wheat things, like pancakes, using un-crapified wheat flour. Basically unbleached, unbrominated, unenriched flour. Enriched flours acutely bother me. So I’ve been baking a little more as of late even have made my own sandwich bread which I use for cheese burgers. You could live off cheeseburgers and milkshakes by the way and only lack in potassium so take your pick, banana split or fries (air fried or cooked in coconut oil or peanut oil—Five Guys Cajun fries anyone?)

One of the most interesting accidental discoveries I made this year was after I purchased a pressure cooker. Starch gelatinization on digestibility is pretty incredible, rice and potatoes no longer bother me.

I smoke off and on though less then I used to and I drink off and on as well sometimes excessively other times nothing. I sleep when I’m tired although increased tobacco use and moderate alcohol consumption seems to improve my sleeping patterns to acceptable societal norms whereas without those things I tend to have irregular sleeping patterns like when I was growing up.

On workdays, Monday through Friday I tend to eat less calories on average then on the weekend.

Not much in the way of supplements, maybe a quarter tablet of Aspirin on occasion, salt tablets pretty regularly (I sweat a lot, as in puddles on the lifting platform when I work out), and infrequently magnesium, I just took some the other day last time I took it was in December. I’ve never taken any single supplement on a regular basis without having some sort of eventual negative effect. Sometimes I take 12.5 mcg of Cynomel.

Aspirin, Benadryl, Cynomel, and magnesium all reduce my maximal strength. A small amount of Benadryl (1/4 to 1/2 a tablet) is enough to knock my maximum efforts down 10-15kg for 24-36 hours. 12.5 mcg of Cynomel will increase my strength for 6 hours but subsequently reduce it for the next 24 hours. A steady dose of ¼ a tablet of Aspirin will eventually cause difficulty in breathing—eosinophilia. A steady dose of 500mg of magnesium per day also reduces my strength although not as predictably as the other supplements. Whey protein, I essentially have completely negative effects with. It essentially interferes with my vision temporarily which is interesting, not willing to fuck around with that since I have better than perfect vision yet.

Essentially, I eat things I want and justify those crappy foods I grew up with as beneficial pro-oxidants. Isn’t that fucked up?