As a biologist, I always think in evolutionary terms. All mammals share a single ancestor who had developed a warm-blooded metabolism. Many mammals hibernate: bears, ground squirrels, skunks, bats, anteaters, etc. To hibernate, you have to throttle back your warm-blooded metabolism to a torpid one allowing your metabolic rate and body temperature to drop. Since at least 171 species of mammals all along the mammalian tree of life are known to enter into torpor1, it seems likely that the ancestral creature that we all evolved from could enter torpor.
All three branches of the mammalian family – monotremes (egg-layers like platypuses and anteaters), marsupials and those with placentas – contain animals who enter torpor. So if our common ancestor didn’t have the ability to enter torpor, it would have had to have evolved independently in each branch of mammal. Further consider that birds are ALSO warm blooded and that at least 43 species of bird can also enter into torpor. I would argue that the most likely explanation is that there was an original species that had a warm-blooded metabolism AND the ability to enter torpor to save energy and that birds and mammals both evolved from this ancestor.
When I wrote the SCD1 Theory of Obesity I pointed out that polyunsaturated fat (PUFA), had the effect of down-regulating SCD1 up to a point, but if too much PUFA – especially linoleic acid (LA) – was consumed the situation flipped and body fat accumulated PUFA and monounsaturated fat (MUFA) in parallel. At the time I believed that this was pathological dys-regulation. Now I believe that the consumption of linoleic acid is an evolutionarily conserved switch that all mammals share that turns our metabolism from a warm-blooded one to a torpid one.
Looked at in this way, the linoleic acid is the switch, but the definition of torpor is an upregulated SCD1/PPAR gamma/ELOVL axis.
Sufficient LA is Required to Induce Deep Torpor and a Full Hibernation Period
This paper2 shows us how much linoleic acid is necessary to upregulate SCD1 and become torpid in Golden-mantled Ground Squirrels, a hibernating species. The LA composition of the diets are my calculations from the author’s description which are reasonably clear but also vague in places. For instance, “The base of the diets was finely ground barley seeds, with small amounts of high-nitrogen casein and Purina Rat Chow added to produce the desired protein content.” The low-LA diet used 5% of supplemental coconut oil, the medium LA diet used 5% supplemental corn oil and the high LA diet used 12% supplemental sunflower oil. I’m using the desaturase index (DI) – the ratio of oleic acid (the endproduct of SCD1) to stearic acid (the raw material of SCD1) – as an indicator of SCD1 activity. The absolute numbers weren’t given – only a graph – so the calculated DI is approximate but unambiguous. Ground Squirrels seem to have higher DIs than humans for some reason.
After being fed the three diets, hibernation was induced by lowering the atmospheric temperature. The first two months the temperature was 3.5. After two months the temperature was lowered to -2.5 C to see how low the squirrels could drop their body temperature. Here are the results:
| Dietary LA | Lo-LA ~1.5 % | Med-LA ~ 3% | Hi-LA ~ 8% |
| Number Of Animals Entering Hibernation | 0/4 | 3/4 | 4/4 |
| Number Who Stayed in Hibernation | 0/4 | 0/4 | 4/4 |
| LA Content of Body Fat % | 10 | 18 | 30 |
| Oleic Content BF % | 58 | 56 | 45 |
| Stearic Content BF % | 2.2 | 2.1 | 0.6 |
| Desaturase Index Before Hibernation | 26:1 | 27:1 | 75:1 |
| Number of Fasted Hours Before Hibernation | 112 | 216 | |
| Weight Before Hibernation | 267g | 273g | 283g |
| Body Fat % Before Hibernation | 45.3 | 47.3 | 48.7 |
| Mean Body Temp Hib Month 1 | 4.5 C | 4.0 C | |
| Mean Body Temp Hib Month 2 | 4.6 C | 4.3 C |
What happened to the animals on the Low LA diet when the atmospheric temperature was lowered? “After 9 d of fasting at Ta = 3.5 C, none of the four animals in the minimum linoleic acid group had entered hibernation. The mean (+SE) body masses of this group decreased to 153g … were thus removed from the
study at this point, since they appeared to have depleted their fat stores”.
So non-torpid ground squirrels depleted their fat stores and lost 43% of their body weight when subjected to 9 days of fasting at around 40 degrees F. Torpid ground squirrels went into hibernation within 5 days to preserve their body fat! They did this by lowering their body temperature and metabolic rate.
Humans Also Respond to Dietary Linoleic Acid levels of 8% By Up-regulating SCD1
Being a member of a hibernating species doesn’t necessarily mean that you can get into torpor. You also need linoleic acid. I think that being a member of a non-hibernating species doesn’t guarantee that you CAN’T get into torpor. Let’s look again at what happened to the stored body fat of Americans between 1962 and 1991 compared to a tribe of Nigerians in 1962 living on mostly starch and a tribe of Nigerians living on the relatively oily grains of sorghum and millet.
| Nigeria ’62 Starch | Nigeria ’62 Oily Grain | USA ’62 | USA ’91 | |
| Dietary LA | 2-3% | 5.5% | 6-8% | 10-12% |
| Body Fat % | ||||
| Linoleic Acid | 7.9 | 8.7 | 7.9 | 17.2 |
| Oleic Acid | 46.2 | 42.3 | 52.3 | 41.5 |
| Stearic Acid | 5.9 | 9.6 | 6.7 | 2.9 |
| Desaturase Index | 7.8 | 4.4 | 6.6 | 14.3 |
| Torpid? | N | N | N | Y |
The majority of Americans became torpid between 1962 and 1991 as dietary linoleic acid levels rose due primarily to increasing consumption of soybean oil.
In Nigeria, when dietary linoleic acid increased to 5.5% of calories, SCD1 activity and therefore the DI were lowered. This is what happens in a non-torpid metabolism. In America, a threshold was crossed before 1991. Linoleic acid levels and SCD1 activity increased in parallel. That is the definition of a torpid metabolism.
Sterculia Oil Inhibits SCD1
Epilogue
You may be wondering about what happened to the ground squirrels on the medium LA diet, the semi-torpid squirrels who incororated some LA but who didn’t upregulate SCD1. The ones who didn’t complete the hibernation period.
“To determine the minimum body temperatures defended by the two groups during torpor, the Ta of the environmental chamber was lowered by 1-2 C/d for five consecutive days during the third month (November 1990) of hibernation. Body temperatures were recorded after the animals had been allowed to habituate to the new T for 24 h (fig. 2). When the T was decreased to below -2.5″C during the fifth day of the experiment, two of the animals from the medium linoleic acid group died during torpor, and the third animal awoke from hibernation.”
For hibernating animals there are real consequences for failing to enter torpor. For non-hibernating animals, there are real consequences for succeeding.
- 1.Ruf T, Geiser F. Daily torpor and hibernation in birds and mammals. Biol Rev. Published online August 15, 2014:891-926. doi:10.1111/brv.12137
- 2.Frank CL. The Influence of Dietary Fatty Acids on Hibernation by Golden-Mantled Ground Squirrels (Spermophilus lateralis). Physiological Zoology. Published online September 1992:906-920. doi:10.1086/physzool.65.5.30158549
This is just a random question about animals, but do hibernating animals increase linoleic acid intake by preferentially seeking it out when it gets colder, or does linoleic acid become a larger portion of the food supply (because plants change what they produce?) when it gets colder? I’m just curious how this signal was setup in the first place. I’m guessing it’s more that just a signal since there are physical benefits to having less saturated fat when it’s cold out (it’s easier to keep it from solidifying).
It does seem that animals seek out specific high PUFA foods before hibernating but of course there also are more high PUFA foods available in the fall – acorns, seeds, etc.
It’s worth pointing out that mammals evolved before flowering plants, so it’s not that the first mammal was seeking out acorns! It’s unclear what was happening back then. But yes! Hibernators, in addition to lowering their metabolic rate also need to keep their fats liquid so they have multiple reasons to unsaturate.
Thanks, that’s really interesting!
So linoleic acid is like a signal from mammals feed that it’s time to hibernate? It looks like it’s only available in a natural diet on a seasonal cycle and by pumping our modern diet full of it we’re basically telling ourselves to add fat and hibernate right?
Exactly! The deeper problem is that once we’ve made the metabolic switch to SCD1/PPAR gamma we get “stuck” in torpor. The question is how we get out of it.
Brad
I think you’ve already covered that brilliantly. We consume more saturated fats(higher SA the better) and lower PUFA/LA to 0 if possible. Coupled with steady state cardio(an inference from me…we walked alot as hunter gatherers) for oxidation of stored body fat.
A normal body have multiple switches with controlsystems wired into it,
those system can be damaged, when the body can’t repair itself anymore,
after Dr. Stasha Gominak from RightSleep Switches are repaired and maintained in Deep Sleep. To get into it, you need the right amount of Vitamin D and a sack full of the B Vitamins, if you didn’t get them from your bugs.
So the question is, can sleep repair the metabolic switch too?
It’s an interesting suggestion. Neither of my parents are great sleepers, nor am I. There is certainly evidence that lack of sleep is associated with diabetes/obesity.
Just discovered Dr. Gominak last month and have added a multi-B vitamin every other day. Definitely an improved, deeper sleep. Problem is cancer cells like abundant vitamin B’s so taking daily is probably not wise (per Paul and Shou-Ching Jaminet, Ph.D.). Am hoping that a three-month trial of alternate multi-B intake will be sufficient to reestablish my own gut into producing adequate amounts of the B’s, as needed.
Hibernating animals, come out of torpor because ambient temperature increases and fat stores reach a minimum amount of pufa
Fascinating stuff – you are mining a really interesting seam at the moment Brad. I am logging into your site every day just to see if there is anything new!
It will be really interesting to see what will I guess be a key outcome of this work eventually, namely whether simply sustaining a suitably low LA level over time is enough to reduce SCD1 and get us back out of torpor (sooner or later). Or whether assistance is needed via increased stearic acid consumption, sterculia oil etc – either just to make it happen at all, or to speed it up to some reasonable timescale.
Wild thought just occurred to me. What happens to Americans who stay outside in the cold too often during winter?
I wonder if all this LA in our fat stores and/or diet…. if cold weather accelerates the metabolic problem even further.
Haha! I know some people who spend their winters in something very much like torpor! Barely getting out of bed.
Teenagers?
My experience is that is upregulates body temperature. The result is I can feel quite comfortable wearing shorts and a tanktop even in temperatures as low as 35 f and people standing near me will sometimes comment it is like being near a furnace. To be fair I am hot blooded in general, but cold temperatures further enhances this.
If I overate PUFA (especially oxidized) enough I do wonder if this would change.
Yeah, I’ve read about multiple sources supporting that idea. Cold exposure in and of itself is known to brown fat and improve metabolism and feelings of alertness. Would be unsurprised if excess LA in the body blunted this response but did not eliminate it.
Second question-
Is there any evidence that, folks who go through weight loss / weight regain cycles, especially if the weight regain includes lots of LA, does the body fat’s store of LA as a % of total fat steadily increase?
I.e.- when you burn body fat- do the “better fuels” preferentially burn first, i.e. saturated & MUFA, leaving some PUFAs hanging around (burning slower) and upon weight regain with SFA/MUFA/PUFA it happens in the context of higher quantities of unburned PUFA left behind, causing the net PUFA % of fat stores to increase over years/decades of weight loss/regain cycles
A bear, by contrast, burns off most of its fat stores over a long hibernation period. So when it refeeds in the spring, there’s much less PUFA in the fat stores to start; but most Americans don’t lose most of their fat stores when they diet, they lose 10% or maybe a bit more and end up regaining…
Actually, unsaturated fats seem to be (slightly) preferentially oxidized. A bear still has body fat stores in the spring, but they are higher in saturates and lower than unsaturates than they were in the fall. So the bear can seemingly escape torpor with a 6 month fast. Tricky for humans, though!
I see – that is actually encouraging! Seems then outside of any other hormones I’m not aware of (and there are probably thousands of them), the key here is to dig deep into fat loss, and use anti-PPARgamma therapies to close the filler plug before you start gaining weight again on a more “relaxed” dietary regimen.
This is the hope: if we get out of the cycle of torpor and lose the stored MUFA and PUFA we can essentially reset our metabolism and start behaving like a person with a normal metabolic rate.
I wonder if animals who hibernate have less cancer?
Reading through this that was actually my thought…theoretically couldn’t humans perform some extended fasts to try and reverse this? Seems like if we’re preparing a body for hibernation the best thing to do would be to not fight the biology. I agree though, compliance would be an issue.
Does that mean dietary unsaturated is stored as body fat more readily than dietary saturated, however the unsaturated portion of body fat is used for energy (and not kept in storage) slightly more readily than the saturated portion? This seems somewhat contradictory. Or perhaps the slight preference to use unsaturated fat stores applies to the specific situation of hibernating bears but not people on the Standard American Diet?
I don’t know that unsaturated fat is stored more readily. This article has a good review of how different fat lengths and saturation levels are oxidized. For instance, DeLaney reported that 9h after a mixed meal, 13% of stearic acid had been oxidized, 18% of oleic, 20% of linoleic and 27% of linolenic (Omega 3). Sometimes people see this as evidence that PUFA leads to higher metabolic rates, but I don’t think so, I just it just gets burned first. If you didn’t eat it something else would get burned first.
Little of topic question:
Do you know those “competitive eaters”.
Like Kate Ovens or furious Pete and such.
What u can say bout them:
– incredible lean and shredded
– often eat 2kg of mayo, or bacon, chicken wings, or Donuts (high PUFA, high sugar, high insuliogenic foods) at one sitting.
(If u don’t know what I mean just YouTube these names)
How do they remain lean? How can u be shredded as f*** while eating just the worst possible foods in astronomical quantities?
I don’t wanna know their weekly PUFA intake.
So what’s your opinion?
Wild guess- The ills of PUFAs become less prevalent if you burn them off in a short period of time, and if they’re actually exercising hard enough to create ATP deficit, AMPK->PPARa is naturally occurring here… Not sure if that’s the case but data point:
“Last year I did four or five and I’ve only done two during lockdown. Weirdly, I think I’m the fittest I’ve been for about four years.”
https://www.gq-magazine.co.uk/lifestyle/article/kate-ovens-competitive-eater
I know eating a lot tends to surge my thermogenesis – now this is more a question for Brad – Would eating a lot of PUFAs and sugars in the context of a large acute calorie load, with thermogenesis (by what mechanism?), protect one from long-term torpor? Is the real problem with the American diet the slow, daily, ordinary doses of PUFAs we get?
Oh boy! Haha, THAT opens a can of worms. SO you’re suggesting that PUFA and sugar together might be fine as long as we only eat them in huge feast meals so that our metabolic rate increases and we burn them off? I mean, I like the idea… I suspect not.
Brad
I know most don’t eat like that all the time. I remember watching a documentary on Kobayashi and he was pretty serious about his nutrition except when competing/preparing to compete. He also was an avid exerciser as well.
To complicate matters, bears do not go into hibernation until spring. They make come out of hibernation several times during the winter, then return to it.
I’m not following. I feel certain that bears go into hibernation in the fall.
I think he means the bears are not in continuous hibernation from fall until spring. Instead, they intermittently come out of hibernation and then go back into hibernation before fully coming out of hibernation in the spring.
Yes… This is likely true, most animals cycle through states of torpor. Deep torpor is full hibernation, there are also arousal periods.
I wonder if glucose is also a factor, like bears eating a lot of berries to put on the pounds before hibernation.
Brad,
Your thoughts on using the suggested supplements (Berberine, Sterculia Oil, AMPK, CLA) during longer term fasting (3 – 7 days)? Or should one pause those supplements when not eating?
I’m not sure. I’m also a bit of a throw caution to the wind type… Maybe while fasting you should double them! See what happens!
Brad
I have a theory. A bunch of us, including myself, gained weight on the croissant diet. While I did get some satiety if I ate enough saturated fat, I still gained over 20 pounds. The really confusing part was that I tried eating regular croissants (without the stearic acid) and could eat them, even with extra butter, without bounds. There was no limit.
I did the same with fries fried in tallow I made myself from suet. I ate them all and was still hungry. Again, no off switch.
My wife was the same way. In fact, she forbade me from making any more croissants or fries.
What’s similar between my wife and I? We both have a large percentage of “Polish” heritage.
My family on my mother’s side is mainly Polish. All of them, save a few (as in one or two), are obese. And I remember their dinners being high starch plus high butter. Pierogies fried in butter, anyone? Cabbage + butter + rice? That should be perfect croissant-like food: starch (flour, potato; rice) + butter (and lots of it). Yet they were all obese.
You start looking into this:
https://blog.23andme.com/23andme-research/genes-and-geography/
http://www.khazaria.com/genetics/poles.html
And you realize the French are different genetically from the Polish. (And I’m using “Polish” generically, since my great grandmother was from Czechoslovakia.)
So, my theory is that starch + butter might not work for certain people, because of their genetics.
Unfortunately, I cannot find anything studying this. Nothing at all.
But it doesn’t make sense to me that there are some who can eat croissants and get full, whereas I can eat as many as I want, with gobs of extra butter, and not get full. At all.
Yet if I combine high saturated fat and low carb/keto, I find some amount of satiety. (It’s just a bit hard to eat high saturated fat without starch.)
So, that’s my theory. I’ve yet to question others who gained weight from the croissant diet to see what their genealogy is, to verify. But it would be an interesting endeavor.
Brad I was wondering a few of things, reading ALL your articles (as soon as I get a couple more supps and your SA flakes I’m starting a cycle experiment of TCD. Thanks for the horrific tasting oil, I’m excited about it :-))
1 – would any herb/food historically known for appetite suppressant be a good place to look for substances that reduce SCD1? Quick search example https://draxe.com/wp-content/uploads/2017/01/canva-photo-editor-2019-10-06T121229.128.png
2 – When you say CoQ10 “bottleneck” — that the quantity of ROS is overwhelming the CoQ10 that can deal with it, is that a correct understanding? — is it quantity or something else that is rate-limiting? We make and store vastly less CoQ10 as we age, so it seems my ‘bottleneck means limited quantity’ must be wrong. But how does it bottleneck? (I take CoQ10 for my heart. Prior to heart surgery I learned from experience it is gigantically helpful. So I don’t want to stop taking it, but I don’t want to screw up my TCD experiment, either.)
3 – Recipes to get stearic and starch mated edibly might be helped by using the sweet-tasting amino acids in some fashion (glycine, alanine, threonine, proline, serine, glutamine) — I don’t know if some of those taste horrific, glycine is not bad in smoothies, tempers the bitter of cocoa a bit — but I’m having a hard time finding the possible effect on SCD1 or PPARalpha any of those beyond Glycine have. I hope you run across this kind of info at some point and I get it by virtual osmosis, like all the rest of this awesome content. 🙂
I am supersized, have lost a LOT of weight, but keto, IF, even fasting, is no longer doing anything. I can lose weight in total fast, but it returns so fast even on keto calorie controlled I’ve been assuming it’s merely water. Same with keto vs. eating even a small but not ketogenic number of carbs. Something is going on! And I think that Peter and you have stumbled on what it might be. Very exciting even to have a doorway for hope and experiment. I’m taking the Omega3 complete test prior to this and will do it a couple months later to see the result. Otherwise I can only do scale, measure, temp, resting pulse. This leads me to a question:
Is there a place people can send their test results etc. to kind of centrally share this info, for others looking on?
Thanks for all your documentation and being a center for a crowd-sourcing N=1. Super appreciate your efforts… could change the world, seriously.
Hi! Thanks for the nice note. I’m sorry, my answers may be disappointing, so much yet to be learned, but here goes.
1) Maybe? A couple of things on that list definitely DO… Green tea, citrus polyphenols, IDK about the others but I DID recently read a paper that capsaicin (the hot compound in chilis) could help weight loss, which only increases my Sriracha addiction…
2) This gets into the kind of nano-physics that is REALLY hard to study and I don’t know if anyone really could say with any kind of certainty.
3) There are some interactions between amino acids and SCD1, PPAR gamma, etc… I haven’t gotten there yet, but it’s on the list.
4) I’d LIKE to have a central repository for the data… ala ownyourlabs.com and the Citizen Science Foundation. I asked Dave Feldman about it but he’s too overwhelmed to take on any new projects….
One other thing. I’ve become interested in micro RNAs as regulatory elements. As a for instance:
https://www.sciencedirect.com/science/article/abs/pii/S095528631831235X
miRNA 122 is downregulated by hesperidin, a citrus polyphenol.
Brad
Now here is an interesting breed of pig, that I just became aware of through a local (SC) butcher – Ossabaw Island Pigs.
Brad given your love of all-thing pigs, what is your take on these animals?
From https://texastinypigs.com/ossabaw-island-pigs
“The Ossabaw pig breed is unusual and important for three reasons. Its history as an isolated island population has meant that the Ossabaw is the closest genetic representative of historic stocks brought over by the Spanish. Second, the presence of pigs on Ossabaw Island provides scientists with an exceptional opportunity to study a long-term natural population. Third, the Ossabaw breed is biologically unique, having been shaped by natural selection in a challenging environment known for heat, humidity, and seasonal scarcity of food. Ossabaw hogs may be as small as 100 pounds, but they are able to store astounding amounts of body fat in order to survive during the seasons when there is little to eat. This biochemical adaptation is similar to non-insulin dependent diabetes in humans, making the pigs a natural animal model for this disease. The pigs are also highly tolerant of dietary salt. Ossabaw Island hogs on the mainland, once removed from the selective pressures of their island home, have lost some of their unique survival adaptations. Their ability to fatten is both an advantage and a disadvantage, and breeders must watch their feed intake to prevent obesity.”
And from a farmer in Virginia https://www.autumnolivefarms.com/the-ossabaw-island-hog
“Ossabaws are indeed unique with meat and fat loaded with fatty acids, omega 3’s, unsaturated fat and oleic acid which is predominant in olives. The Ossabaw fat is so unsaturated that it nearly turns to liquid and melts at mere room temperature.
What that means to the buyers is that beyond the amazing health data the foraging Ossabaw meat, cured or fresh, is spectacular and firmly established in the debate regarding the finest pork to be had on this planet. We finish ours on the amazing Shenandoah Valley forages of acorns, hickory nuts, and walnuts. Add in the fruits of Autumn Olive and Wild Cherry which are predominate here and you should expect to have an amazing and uncompromising product. “
Ossabaw island pigs are indeed a unique and interesting American breed with their list of positive attributes.
I have my own biases, though. I have been and continue to be interested in saving the American Mulefoot, a homestead breed that is also descended from old Spanish stock but is larger and probably not QUITE as fatty, but still QUITE fatty.
Pig breeds are actually a good thought exercise. The fatty breeds, like Ossabaw and Mangalitsa, are very high in monounsaturated fats. They have a high desaturase inex and therefore they are able to hold onto their fat stores for lean times.
Think about it.