Dietary Monounsaturated Fat, The SCD1 Theory of Obesity, Part 3


This is the third part of my SCD1 Theory of Obesity series.  Here are part 1 and part 2.  There is a brief synopsis of the theory below if you don’t want to start from the beginning.

Since I published the ROS theory of obesity, one of the most common questions I’ve gotten is, “What about monounsaturated fat(MUFA)?”  My answer is it depends on whether it is dietary MUFA or derived in fat or liver cells from production of SCD1.    We’ve already seen that when saturated fat is produced through de novo lipogenesis (when the body makes saturated fat from starch), some SCD1 is produced to unsaturate it, leading to a balance of saturates and unsaturates.  

If you ate something very high in monounsaturated fat, the expectation should be that the body saturates it to get it to the same place of balance.  Except that we lack an enzyme that can turn MUFA into saturated fat.  Instead what happens is that a signalling molecule called  oleoylethanolimide (OEA) is produced by our small intestine from ingested oleic acid, the most common dietary MUFA famously found in olive oil.  OEA sets in motion a chain of events which saturates our dietary fat!  It does this by cranking up saturated fat production in the liver and increasing the movement of fat throughout the organism.  

The Caveman Pantry

For at least 400,000 years humans have been using bone marrow as a storage form of calories, leaving it in the whole bone for as many as nine weeks before cracking apart the bone and eating it.​1​  It appears to be the original pantry item.  Another pantry item: at least 170,000 years ago modern humans were roasting high starch, low fiber, potato like tubers in a cave in Africa​2​, well proceeding the fully modern human diaspora from Africa​3​.  Tubers store well in caves, especially when buried in sand or ash.

Thank you to Libbie Summers. This is a great post.

I find it likely that on rainy days in Africa 170,000 years ago, humans were roasting marrow bones and potatoes in their caves and eating them together.  Many bone fragments have been found in the same cave where the roasted tubers were found.​4​  It may come as a surprise to some that bone marrow fat is one of the richest sources of monounsaturated fat (MUFA) on the planet, even rivaling olive oil at times!​5​  This is only surprising because of the culturally common but completely inaccurate assumption that all fat from animal sources is highly saturated.  The cave dwellers were in my opinion the predecessors to modern Mediterranean people eating pasta with olive oil.

Deer Bone Marrow66%23654
Olive Oil73141171

If you’ve already read The SCD1 Theory of Obesity Part 1 and Part 2, you’ll already see the problem here.  Stored monounsaturated fat seems to be sufficient to cause fat accumulation in mammals.  Furthermore, if a cave dweller were to simply store enough of the MUFA rich bone marrow fat as bodyfat, they might lose the ability to do leptin induced thermogensis in the fat cells and wind up with a post-obese metabolism.

Summary of the SCD1 Theory of Obesity

Fat cells release a hormone called leptin.  The more fat mass you have, the more circulating leptin.  If you have sufficiently saturated fat – both from diet and stored body fat – you respond to leptin by upregulating genes involved in thermogenesis, the process of burning off calories as heat.  If your fat becomes too unsaturated, you lose the ability to do leptin induced thermogenesis.  Your body temperature drops and you become prone to obesity.

SCD1 is an enzyme that converts saturated fat (SFA) to monounsaturated fat (MUFA).  Obese humans make a lot of SCD1 and have highly unsaturated bodyfat. Overexpressing SCD1 is sufficient to cause heart muscle cells to store fat.  Mice lacking SCD1 are largely protected from leptin-deficiency induced obesity.  

Leptin is supposed to work by increasing fat burning in the fat cells (fat cells both produce leptin and have leptin receptors) which produces Reactive Oxygen Species (ROS) in the mitochondria which is a signal to both decrease SCD1 and turn on thermogenesis. If stored fat becomes too unsaturated, insufficient ROS are generated in response to leptin leading to a nasty cycle of ever increasing SCD1 and decreasing fat saturation levels, leading to lowered body temperature and obesity.

The Body Seeks Balance

We know humans can create ONLY saturated fat from starch through a process called de novo lipogenesis.  Humans cannot exist on pure saturated fat so they upregulate SCD1 a bit in response to starch consumption.  Conversely, if humans eat highly unsaturated sources of fat – such as bone marrow – they reduce SCD1.  Either way the human body is trying to achieve the correct balance of monounsaturated and saturated fats that will allow for an appropriate response to leptin.

But what happens when the amount of dietary MUFA is enough to overwhelm the system?  Reducing SCD1 can’t INCREASE saturation level of dietary fat, it can only prevent a further decrease.


Thanks to Tucker Goodrich for initially turning me onto a molecule called oleoylethanolamide (OEA).  OEA is produced in our small intestine from oleic acid – the 18 carbon MUFA which is the primary component of both bone marrow and olive oil.  We know that it’s important in energy regulation because it has been evolutionarily conserved for a very long time.  The mammalian response to OEA presumably evolved in a common ancestor before mammals split off of the tree of life.  That was over 178 million years ago.​6​  Remember that small mammals and dinosaurs co-existed!  Due to the deeply conserved evolutionary nature of OEA signalling, OEA both combats obesity in rats​7​ and reduces non-alcoholic fatty liver disease (NAFLD) symptoms in humans.​8​

The Flinstones: an observational documentary of a time and place where neolithic humans and dinosaurs co-existed.

As a signalling molecule, OEA has several mechanisms of action:

  1. It suppresses appetite​9​ 
  2. It upregulates PPAR alpha, a master fat metabolism up-regulator​9​
  3. It downregulates SCD1​7​

This is very clever.  

The first thing is to minimize the amount of incoming MUFA.  That’s straight forward enough.  OEA decreases appetite through a mechanism that requires PPAR alpha.  Consuming MUFA leads to a cessation in consuming MUFA.

PPAR alpha is a transcription factor that turns on all facets of fat metabolism: fat oxidation rates in the mitochondria, fat transport by increasing lipolysis in fat cells and export from the liver and fat production in the liver​10​. It also increases SCD1​11​ leading to an appropriately saturated/unsaturated fat blend coming out of the liver.  At least that is what happens when PPAR alpha is stimulated by a “normal” activator, such as the fibrate drugs​11​, which have been known to improve blood lipids (according to the traditional model)  since the 1960’s.​12​

But in the specific case of OEA stimulation, PPAR alpha has all of those same effects except that the liver is now cranking out saturated fat in the absence of SCD1.  Of course the bone marrow consumer is getting other specific inhibitors of SCD1 from the bone marrow – palmitoleic acid and CLA, among others – but the olive oil consumer has to rely on OEA alone.

OEA sets in motion a series of events which saturates incoming dietary MUFA by limiting the amount consumed, increasing fat oxidation rates to burn the MUFA off and increasing saturated fat production and export from the liver.

A Dynamic System

Let’s think a little more about what’s happening if you are the cave dweller who has just eaten bone marrow and potatoes.  

Your insulin level will rise in response to the starch.  Your fat cells will be relatively insulin sensitive, so insulin will reduce lipolysis but this will be somewhat countered by OEAs effect on PPAR alpha, which increases lipolysis. 

MUFA from the marrow will be absorbed and released from your small intestine in floating “boats” (as Dave Feldman calls them) called chylomicrons, which are ultimately transported in the bloodstream.  These chylomicrons will “dock” at tissues that express something called LPL (lipoprotein lipase) – predominantly your fat cells – where they unload their cargo.  Much of the fat will be transported into your fat cells but much will also be “spilled” in the bloodstream, becoming free fatty acids.​13​  Since your fat metabolism is turned up due to PPAR alpha, much of the MUFA that enters the fat cells will be metabolized immediately.  

Your liver, also jolted into action by the PPAR alpha, will be very busy: taking in these Free Fatty Acids that were spilled, using the blood glucose provided by the potatoes as raw material to build saturated fat by de novo lipogenesis, then re-esterifying it all together into triglycerides that it will pack into VLDL and release into the bloodstream.  The VLDL, much like the chylomicrons, dock at tissues expressing LPL to unload their cargo.  Some of this will also be spilled, making its way back to the liver to get up-satuaretd again before being packed into VLDL and returned to the blood.  

All of this happens quite quickly.  After a large meal, your intestine can continue to release dietary fat for several hours.  The half-life of a chylomicron is typically under an hour.  The half-life of VLDL is 30-60 minutes.​14​  So dietary MUFA can get up-saturated through several cycles after a large fatty meal.

Two hours post meal, the effect of insulin begins to wane and from there on out lipolysis from fat cells rapidly increases.  Again, this behavior is spurred on by the up-regulated PPAR alpha due to OEA being released by the small intestine.  The effect of PPAR up-regulation is to increase fat flux through the whole system.  The recently stored MUFA rapidly re-enter the pool of circulating free fatty acids and head to the liver to get up-saturated.


The difference between dietary monounsaturated fat (MUFA) and MUFA created in fat cells by SCD1 is that dietary MUFA leads to the production of OEA.  OEA blunts appetite, upregulates PPAR alpha and downregulates SCD1.  This leads to increased fat oxidation, increased fat flux through the system and steadily increasing saturation levels of circulating fat in the hours after a meal.  Ultimately, in cultures that are metabolically healthy, this seems to lead to fat saturation levels reaching an acceptable level before being stored.

Would I recommend olive oil if you’re trying to lose weight?  I wouldn’t.

I’ll leave you with a thought question and I don’t know the answer.  If I figure out the answer it’ll make a fun post.  Feel free to comment. The question is this:  If a healthy person eats JUST bone marrow, is there a tissue where PPAR alpha activation combined with SCD1 suppression leads to MUFA being broken down into acetyl-CoA which is then rebuilt into saturated fat before being exported or stored?

  1. 1.
    Blasco R, Rosell J, Arilla M, et al. Bone marrow storage and delayed consumption at Middle Pleistocene Qesem Cave, Israel (420 to 200 ka). Sci Adv. 2019;5(10):eaav9822. doi:10.1126/sciadv.aav9822
  2. 2.
    Wadley L, Backwell L, d’Errico F, Sievers C. Cooked starchy rhizomes in Africa 170 thousand years ago. Science. Published online January 2, 2020:87-91. doi:10.1126/science.aaz5926
  3. 3.
    deMenocal P, Stringer C. Human migration: Climate and the peopling of the world. Nature. 2016;538(7623):49-50. doi:10.1038/nature19471
  4. 4.
    Klein RG. The Mammalian Fauna from the Middle and Later Stone Age (Later Pleistocene) Levels of Border Cave, Natal Province, South Africa. The South African Archaeological Bulletin. Published online June 1977:14. doi:10.2307/3887843
  5. 5.
    Cordain L, Watkins B, Florant G, Kelher M, Rogers L, Li Y. Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Eur J Clin Nutr. 2002;56(3):181-191. doi:10.1038/sj.ejcn.1601307
  6. 6.
    Pickrell J. How the earliest mammals thrived alongside dinosaurs. Nature. Published online October 23, 2019:468-472. doi:10.1038/d41586-019-03170-7
  7. 7.
    Suarez J, Rivera P, Arrabal S, et al. Oleoylethanolamide enhances  -adrenergic-mediated thermogenesis and white-to-brown adipocyte phenotype in epididymal white adipose tissue in rat. Disease Models & Mechanisms. Published online October 23, 2013:129-141. doi:10.1242/dmm.013110
  8. 8.
    Tutunchi H. The effects of oleoylethanolamide, an endogenous PPAR-α agonist, on risk factors for NAFLD: A systematic review. Obesity Reviews. Published online July 7, 2019.
  9. 9.
    Caillon A, Duszka K, Wahli W, Rohner-Jeanrenaud F, Altirriba J. The OEA effect on food intake is independent from the presence of PPARα in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARα in mice. Metabolism. Published online October 2018:13-17. doi:10.1016/j.metabol.2018.06.005
  10. 10.
    Rakhshandehroo M, Knoch B, Müller M, Kersten S. Peroxisome Proliferator-Activated Receptor Alpha Target Genes. PPAR Research. Published online 2010:1-20. doi:10.1155/2010/612089
  11. 11.
    Jo E, Li S, Liang Q, et al. Chronic activation of PPARα with fenofibrate reduces autophagic proteins in the liver of mice independent of FGF21. Guillou H, ed. PLoS ONE. Published online April 19, 2017:e0173676. doi:10.1371/journal.pone.0173676
  12. 12.
    Acheson J, Hutchinson EC. A controlled trial of atromid in cerebral vascular disease a preliminary report. Journal of Atherosclerosis Research. Published online September 1963:711-715. doi:10.1016/s0368-1319(63)80056-3
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    Lambert J, Parks E. Postprandial metabolism of meal triglyceride in humans. Biochim Biophys Acta. 2012;1821(5):721-726. doi:10.1016/j.bbalip.2012.01.006
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    Feldman D. Remnant Cholesterol – What Every Low Carber Should Know. Cholesterol Code. Published January 19, 2019.

42 thoughts on “Dietary Monounsaturated Fat, The SCD1 Theory of Obesity, Part 3”

  1. Reading this makes me wonder if meditation-induced body heating would also be a useful tool in the fat management tool chest, and if it’s even a real thing.
    It seems to exist, and this video is a pretty convincing example:
    Although in the latter part of the video it’s hard to determine if the extra body temperature is due to muscle work or thermogenesis.
    Here’s an article looking at the practice,takes%20the%20shape%20of%20a but it doesn’t really seem to answe that question.

    1. I should add that inspired by this, I was able to make my cold fingers warm just by sitting, staring somewhat intensely and somewhat angry at my screen, imagining being a Super Saiyan, and since that didn’t seem to do much, tensing my leg, arm and torso muscles for a minute. The finger heat came 5-10 minutes after the tensing.
      Not quite convinced but pretty cool

    2. definitly real, If you are experienced, you can keep the warmth the whole day. I feel like I can save money on heating.

      it is nevertheless a somewhat advanced technique. Shortcuts to get there:
      – Loving kindness meditation and radiation of love (start with a wish for a benefactor, someone who has done you good. Thankfulness, or just the wish: might you be happy; you can mix in visualisation of loved ones; smile during meditation; try to feel it in body)

      – another technique is imagining a fire (for me, it i easier to start with the earth element and then water, then fire)

      – all of the techniques demand strong concentration, in “the mind illuminated” you find the most detailed description how to get there as a lay person.

      – kasina meditation can speed up concentration skill development

    1. I actually just got some! Going to try it for appetite suppression for intermittent fasting.


  2. Carlos R Dick Izas

    Hello Bard, I love the work you’ve done so far. I wonder about this balance you mention. I understand that if you eat monounsaturated fat then your liver saturates it, and if your body needs monounsaturated fat; fat-cells produce it through SCD1. Does that mean that if you hypothetically eat a meticulously balanced diet of these two fats, then your liver and fat-cells wouldn’t try to create more?
    Also, wouldn’t consuming stearic acid increase SCD1 thus making you more prone to store all that fat?

    1. I think the system is quite good at adjusting to changes in the proportion of dietary fat that is MUFA versus SFA as long as PUFA levels are low. A billion years of evolution will get things pretty fine tuned.

      And yes there is a danger that stearic cid will cause up-regulation of SCD1. We have to hope this is outweighed by dietary stearic acid producing enough ROS to outweigh that effect. The ROS effect seems to trump the direct up-regulation by saturated fat. This is why I like to “macro-dose” with saturated fat. The idea is if I consume a LOT of very highly saturated fat at one time I will be able to overwhelm the effect of my stored fat.


  3. Another awesome article.
    Thinking about a comment someone made under your last post questioning whether higher MUFA ground beef should be avoided and replaced with leaner sources of beef and added butter… What’s your recommendation?
    Is this mechanism you described in this article sufficient in practise to deal with conventional high MUFA beef fat or should lean beef + suet or lean beef + butter be preferentially consumed?
    I mean for someone who struggles a bit with not becoming fat.

    1. The truth is it’s not that clear to me. I think for everyone it will be different. I’m curious to hear others experience with this going forward.


  4. Pingback: Most TCD ice cream… – Easy TCD 🥐for Fat Loss

  5. I have been adding SA to ghee and adding that to my eggs every morning and my lean ground beef for dinner for about a month now. I’d say it’s been about a Tablespoon per dish. Plus, I’ve cut out nuts and oils. And I drink butter coffee in the morning. Result, I went from 117 to 124 as of this morning. I’m 5’2 and this is definitely not the direction I want the scale to go. Question, am I adding too little fat, am I “post-obese”, never been overweight but definitely was eating a lot of PUFAs, has it not been enough time, do I need more carbs? I am so confused! I ‘m really frustrated since in theory I really like this way of eating but in practice it just doesn’t seem to be working out. Any help would be greatly appreciated since I don’t know what else to try.

    1. Hi Liza!

      It’s always frustrating when the best laid plans don’t work out. If I were you’ I’d get my desaturase index tested. Then you’d know where you stood. I know that it costs some $.

      Couple questions:
      1) Did you change your level of carb intake? One thing that will happen if you do that is that your glycogen stores can fill back up. This effect alone can add 6 lbs or more.
      2) Are you using a tape measure? I find the tape measure to be a much less anxiety inducing way to track changes since they don’t bounce up and down like scales do.

      And of course it’s possible that you’ve added some extra fat to your diet, but your stored PUFA and MUFA are trumping any desired effects and so the extra fat winds up just being extra calories until you deal with stored PUFA.


  6. Thx Brad. Incredible how you even come up with those ideas 😀
    Something i am wondering though when reading your stuff, is what differs in a ketogenic/low carb context…?
    Why do those folks loose weight and stay incredibly lean while often consuming huge amounts of linoleic acid? (I personally know 3 people who shove in sunflower oil based pesto, bacon, BBQ sauces and stuff like that all day and it works for them… Additionally I have heard many low carb doctors say their patients have success independent of PUFA intake).
    Also on Peters blog something like that was mentioned once in the comments .. how a keto context lets you deal better with PUFA but I can’t remember the reasoning.
    So what’s your opinion on that issue? Why does a keto diet still work even with high PUFA – at least to a certain extent but for many completely?
    What’s the mechanism?

    1. Hey Alex!

      Great question! Obviously this is a complex subject. Many people remain lean eating the standard american diet. But like… why? IDK.

      But to answer your question, there are multiple factors here and a major player is insulin. Fat stimulates insulin less than the other macros and PUFA stimulates insulin the least of all of the fats. PUFA also down-regulates SCD1. So the body will adjust by making less MUFA and overall insulin levels will be very low.

      Am I surprised that this approach works for some people? I’m not. Is this the approach I’d want to use? It’s not.


  7. Kristin Ellermann

    Macadamia Nuts are so much lower in linoleic acid that I had switched to them from almonds. I don’t find true satiation if I don’t eat an ounce. But, they are very high in Oleic acid. All the things I have read suggest that olive oil helps fat burning because of the oleic acid, so I thought that was okay. Reading your article, now I am worried. Do foods with high oleic acid actually cause fat storage? Are macadamia nuts not a healthy choice? I just don’t seem to feel full without a few Pili or Macadama nuts.

    1. I doubt a few Macadamia nuts will tip the balance of an overall balanced diet, but perhaps it’s something to consider if you find out you have a high desaturase index. Someone just pointed out that macadamia not oil is also fairly high in palmitoleic acid, which is interesting. It’s probably not a bad choice if your desaturase index is under control.

  8. Great stuff as always. Question: You’ve mentioned on occasion that you are a big fan of red wine. How does alcohol metabolism fit in with SCD1 and ROS? And how does it scale from say drinking a small glass to a bottle or two?

    1. Unfortunately, alcohol is the least studied macromolecule, so I can’t always find the answer. But I AM planning to do a series on it…


  9. Great thread here again.
    I was following pretty nicely up until OEA and PPAR… and got lost. Sorry, now I can’t understand. I guess I need more background.

    1. Here’s the summary: when you eat monunsaturated fat, the body has to saturate it. It does that by cranking the handle faster…

      Fat cells start releasing, up-taking and burning fat. The liver starts up-taking, releasing and producing saturated fat.

      In this way the octane of the incoming blend is increased so that it can be stored.

      OEA and PPAR alpha mediate this, but you don’t really have to remember that part.


  10. Hi Brad, something i dont quite understand.. please help:
    why is it fat tissue which is preferentially targeted by insulin resistance created by sat FA? There are cells of way faster metabolism that burn through way more fat (eg the heart) and thus should become IR sooner..  in fact i would say almost all lean tissue burn more fat than adipocytes do.. 
    The theory goes, that adipocytes become IR first so you dont lose kcal into adipocytes thus more are remaining for the lean tissue to feast on it… right?..
    But wouldnt you expect the opposite to be true? The cells burning the most fat, aka the lean tissue becoming IR first thus reducing their uptake of energy leaving more for the adipocytes..?Whats my mistake in logic here? Im confused haha

    1. Hi Luke!

      Tissues targeted by dietary fat are the ones that most strongly express a protein called lipoprotein lipase (LPL). That’s the protein that actually “unloads” the fat from chylomicrons and VLDL. Adipose tissues have the highest LPL activity.

      I think the fat tissue itself is a primary regulator of body fatness levels. That’s why they are the most sensitive to changes in saturation levels mediated by LPL.


  11. As far as I understand: Saturated fat while going through the krebs cycle, produce reactive oxygen species of byproducts that your fat cell use to determine if it is full or not. If the fat cell is full of energy then it will stop more energy storage by becoming insulin resistant. So, is not a pathological IR but just cells working properly. There is no consideration from the cell if other cells need more fuel or not but simply each cell doing its job. Excess energy will circulate through your blood and if the excess continues then your body can increase metabolism or even store it if the energy becomes too high.

    1. Yeah. I think that’s about right. Fat storage is pretty dynamic, with fat cells taking it in and releasing it all the time and the liver doing the same.


  12. Would macadamia nuts be a good source of monounsaturated fats then? Especially since it is high in palmitoleic acid.

    1. Macadamia nut oil is the best high MUFA/Low MUFA source that I know of. An good call on the palmitoleic, I didn’t realize that but you’re right! 15-24% palmitoleic.

      1. Brad, do you mean “high MUFA/low PUFA”? Or something else? I was under the impression that macadamia nuts are (relative to other nuts) higher sat fat, ok MUFA, lower PUFA. Other nuts are way higher in PUFAs.

        I just wish there was a way to determine what fats we’re really getting. For instance, I buy 2 chickens every two weeks from the local farm. What’s the PUFA content relative to chickens from a massive supplier? I have no idea.

        Obviously, moving to eating only meat from ruminants (primarily beef in the US), with maybe some fish thrown in, might be the best diet, if one is low carb and looking to decrease PUFAs. But after 7 years low carb, I like some variety, and my wife finds cooking chicken easier than cooking beef. So, I have to eat some chicken, some pork. The question I have is, how much is okay and how much too much? I don’t know the answer to that.

        1. Macadamia not oil is majority MUFA by far. It may have less Saturated Fat than other plant oils, but it’s mainly MUFA.

          As to how much PUFA is too much, surely it depends on how metabolically healthy you are. I’m going to be publishing some articles about native American diets. Often the main source of fat was bear grease, which tends to be around 10% PUFA with fairly high MUFA. This seemed to work OK.

          Once you metabolically deranged can you still consume that much MUFA/PUFA? Time will tell.


  13. What about Elovls? My biochem-fu is low so dunno if it makes sense but this paper links PPAR with elovl3
    or this one which states that mice with elovl6 removed have more C16:0 then C18:0

    but as i said my biochem is poor so i don’t know if Elovls are just trees in the forest here. On the other hand if we could trigger SFA’s elongation then we could have more stearic without eating it with spoon ;]

    1. Typically, the PPAR’s upregulate a suite of genes involved in fat metabolism including synthases, elongases and desaturases. SCD1 is “special” in that it behaves somewhat independently of the others, who tend to act more in concert. That’s one of the reasons it appears to be significant.


      1. This sort of makes me curious if fibrates and sterculic acid could sort of complement each other(as I’ve read fibrates induce SCD1 but otherwise seem to have benefits on lipolysis)

  14. I wonder if the ROS & SCD1 theory might explain why some people first gain fat when they enter the carnivore diet, but after some variable amount of time they start loosing and become very lean? If the person happens to be quite unsaturated to begin with, it takes time before the mixture becomes saturated enough for enough ROS production. If there is caloric surplus, the process of saturation would mostly mean storing saturated fat but not so much burning of the unsaturated, leading to overall fat gain before the person gets saturated enough. What do you think?

    1. Yeah, this may go a ways towards explaining t, especially if the person moving to carnivore is doing all beef carnivore.

  15. Long time Hyperlipid reader here, and I’ve been following TCD since you first came out with it. Having just read the three articles in this series in one sitting, I’m a little confused.

    1. In parts 1 and 2 we get the distinct impression that dietary MUFA = bad. Also that the metabolism can only unsaturate fats (from sat to MUFA), it can’t saturate them. But now in part 3 we learn about OEA and how cranking the system faster can actually up-saturate fats as they are moved around in the body. Did your thinking evolve, or am I missing something? I don’t use olive oil anymore, but I do eat a few avocados a week. No nuts.

    2. Of course your focus, as well as that of almost every low-carb blog out there, is weight loss. Never having been obese (just +20 lbs, long gone now), but having the pleasure of a mystery neuropathy that is thought to be autoimmune, started me on the low-carb path 10 years ago. A little breast cancer blip 14 months ago had me eliminate dietary PUFA as much as possible while concentrating on stearic acid; PUFA and MUFA are tumorigenic. I had thought my metabolism was never that broken, but now the information about low body temperature — 97.5° — might indicate otherwise. Anyway, there’s also always a little head scratching when trying to interpret these things to decide what’s good for someone who is metabolically normal. Any thoughts?

    3. I’m pretty sure in the introductory TCD post you said you only included the starch in order to prove that any weight loss was not due to a ketogenic affect, in addition to being handy for absorbing all that butter. But now it’s starting to sound like a little bit of starch might not be such a bad thing. Because of the autoimmune thing I still avoid grains, but now I occasionally indulge in potato chips, only coconut oil or avocado oil ones. What’s your thought on coconut oil, which is medium-chain?

    1. Sorry it’s taken me so long to respond to this…

      My thinking has evolved a bit on dietary MUFA. If you’re metabolically healthy, the body has ways of dealing with it. That’s not to say that it’s ideal for weight loss, but of course that’s not your concern. Having said that, things like olive oil and Avocado oil also carry a not insignificant amount of PUFA – 10-20% – in addition to there being concerns about the oils being adulterated.

      I don’t think a little starch will hurt you as long as you have good glycemic control/etc.

      Coconut oil I think is a fine fat. Very stable. It lacks Stearic Acid, so it may not have the same metabolic punch as some other fats but it certainly won’t lead you down the path of lipid peroxidation/destructive oxidative stress.


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