Science on Cocoa Butter

(PJ) #1

All the other cocoa butter threads are a/ old and b/ not in the science section, so I’m starting a new one here.

This is a white paper that was studying mice, different kinds of fat, and the effects of that on (a) body weight, (b) gut biome diversity/quantity, and © a variety of intestinal issues including metaplasia.

Oils: Control, Beef, Lard, Coconut, Linseed, Corn, Olive, Soybean, Cocoa[butter]

I found the bits about cocoa butter to be very interesting. It was by far, of the list, the best results in every area. To the degree I was looking at the funding etc. to see if it was related hahaha. Doesn’t seem like it.

Brief excerpts:

We compared eight kinds of HFDs adjusted to 60% kcal from fat. In spite of the fact that food intake was similar among all HFDs, body weight gains were different. Increased body mass can be caused by the digestibility and absorption of fat. Cocoa butter has been known to be a low-energy fat. In general, lipid digestibility is less than 95%. In contrast, cocoa butter digestibility is 60–70%, as the binding of calcium to form poorly digested fatty acid-calcium complexes results in low absorption…

and

Cocoa butter is composed of similar fatty acids as lard and beef tallow, however, the mice fed Cocoa diet kept lean with a healthy gastric mucosa. Moreover, dietary cocoa ameliorates the inflammatory mediators, IL-6 and MCP-1, in diet-induced obese mice [19] and inhibits colorectal cancer induced by AOM/DSS…

and

In addition, it has been reported the Cocoa diet suppressed permeability of intestine by sustained occludin and ZO-1, tight junction molecules used for the maintenance of intestinal epithelial barrier [45]. Through these mechanisms, it can support mucosal integrity and suppress dysregulation of stemness.

and

All HFDs tended to increase microbial number and higher occupancy of Lactobacillus in the stomach. These effects were most pronounced in the Olive and Cocoa groups, in which these diets failed onset of intestinal metaplasia. Furthermore, in Cocoa-fed mice, the microbial community in both the stomach and large intestine tended to increase in diversity more than the other diet groups.

(Bob M) #2

But wait…doesn’t cacao butter have EVIL palmitic acid in it? :wink:

#3

Does better actually mean healthy?

(Bob M) #4

Hard to know what to do with this. The cacao butter group ate more than most other diets, but weighed the least:

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How did that happen?

And lard weighed the most but ate the least…

(PJ) #5

So here is where I found it and this guy has a theory about why I would LOVE to see but I canceled my Twitter account long ago and don’t want to make a new one and most the thread is hidden behind a link. And threadreader says its too old. So if anybody has Tw it would be great if you could copy his posts or open them all up and make a PDF or in some way other convey why he thinks this is.

Something to do with how cocoa butter vs. beef attaches its fats in the triglyceride…

https://twitter.com/matthewjdalby/status/1310966867566178307

#6

Theobromine addiction and its effects on fat metabolism.

https://www.google.com/search?q=theobromine%20ppar

(PJ) #7

That’s what I need a new reason to eat chocolate :rofl:

(Bob M) #8

Explains cacao perhaps, but not lard.

#9

Not saying this necessarily is the case, as I haven’t looked into it, but a few possibilities based on that chart:

The group that ate Cocoa butter had a higher metabolism (as a result?), and so used more energy despite eating more / The group eating more Lard had a lower metabolism (as a result?) so used less energy despite eating less.

Similar to the above, but simply eating more resulted in greater metabolism/usage of energy (type of fat may related, but could be the amounts have a causal link between each other on their own, even if it goes against conventional expectations).

While we’d assume they all had the same starting weight and lean mass/fat ratio, we don’t know that from the chart alone, so could be the different groups happened to differ a bit making things look a bit skewed. The one is showing gain in body weight, after all, so if one started larger, they could still eat more and gain less than ones that started smaller.

Since this appears to measure the food intake as a whole, rather than absorption of nutrients or what have you, it could be the Cocoa Butter had a lot more that simply was passed through the digestive system, thus having less impact on anything retained. As an analogy, a huge portion of it could be like fiber to the mice, so they just get rid of it. Lard could be more percentage usable to their bodies, so they may retain it more rather than passing it.

There’s probably not enough information on this to say for sure from just one study, and, as always, we have to keep in mind mice are not humans so some things will work differently for them.

(Bob M) #10

After gaining 20+ pounds while trying the croissant diet, I have a hard time with these studies. I can go to Hyperlipid and see the theory, but when I apply that to myself, I find it’s way more complex than just eating a lot of saturated fat and - BAM - you won’t be hungry and lose weight.

Part of that is definitely because we aren’t mice. Let’s face it, a mouse would never really eat any of this crap anyway.

I do like @djindy’s theory about what passes through the mice.

They do include more data in a supplement:

image

I’d have to spend at least an hour or more to attempt to make sense of this.

(PJ) #11

Well if someone can get that Twitter thread we could see that guy’s theory which may be interesting, about why.

As for lard since most of it nowdays is so much PUFA I kinda don’t trust any science done with it as representing a super high SFA fat.

#12

11.7% Polyunsaturated fat isn’t particularly high for fats. Certainly not as high as Corn Oil and Soybean Oil that are also tested in the set and show up more in the middle for both charts.

#13

Running in parallel to this topic is this podcast. An intriguing listen. Peter discusses the rodent models, which he finds ‘convincing’.

And if you can bear Dr. Saladino, there’s this:

(Michael - When reality fails to meet expectations, the problem is not reality.) #14

Unless I’m misunderstanding something, the study linked in the OP basically says we’re all doomed to cancer of one sort or another from eating fat. I find that claim farfetched. Before I get too excited about this, I’d like to see someone who understands human fat metabolism well review and comment. I suppose that’s too much to hope for - so I’ll just carry on.

Maybe @amber would find this interesting enough to read and comment.

(Bob M) #15

I’ve listened to part of the one with Peter, and it’s great. He theorizes that if you’re eating a low PUFA (i.e., linoleic acid, not O3s) diet, you probably don’t need to have fish oil or fish. He says ALA should be converted by the liver to what’s necessary.

I think this might be correct, though when I got my levels tested, my O3 levels were quite low. But this is on the scale provided by the company, and it’s tough to know whether this is relevant for people who are low carb.

WARNING: Peter does say that very high carb, low fat can work. And that starches aren’t necessarily evil. I’m only 35 minutes into this, though.

As for Saladino, I personally can’t take him. Hi beliefs sometimes are just so far out there, I can’t do it.

(Bacon is a many-splendoured thing) #16

The key is, apparently, extremely low fat intake. And note that Peter says that it’s not necessarily a healthy diet, even though it does reverse insulin resistance. He is basically talking about the Kempner rice diet, here, which was documented to reverse people’s diabetes.

P.S.—Thinking about the starch business, it would explain the “but [these people] ate [some kind of starch] and they lived for ever”—they may have eaten a lot of rice, but their traditional fat intake was very low in PUFA. Switching to the same oils as we use today caused them to develop the same problems as we have today.

(Bob M) #17

I agree, Paul.

When I was on Pritikin (very low fat, very high carb), that was probably what Peter was referring to.

I mainly have an issue with treating PUFAs (not O3) as the sine qua non of obesity. For instance, I ate what I believe was a low PUFA diet (good beer, pizza from pizza places - not boxed, ice cream) yet got fat.

Also, I’ve been trying to remove PUFAs from my diet for years, though I do eat some chicken and some pork at times. But I’ve switched to beef mainly. Some fish, just to test the O3 theory.

One would think therefore that I could eat croissants with butter and get a satiety effect. But I don’t. I can eat as many of those as I want, or at least I did the one time I tried this.

The same with potatoes fried in tallow made from suet. As many as I want.

I could get satiety if I ate a TON of saturated fat using Ghee and stearic acid, packed into some type of starch (potato, sweet potato, even spaghetti squash). But if I ate less than that, I got no satiety effect I could tell.

And on Twitter, I found a bunch of others would also gained 15, 20, 25 pounds on the croissant diet.

Until someone can say why there is a group of us who gain weight (I was under 200 and not “obese” before the diet and over 220 at the doctor’s office afterwards) on the diet while others lose weight, I’m not convinced that simply avoiding PUFAs and eating saturated fat is what will magically keep everyone thin.

I still will prioritize saturated fat at times, but I’m back to eating lower fat, higher protein again. And I’ve lost a lot of the weight I gained, though I still can’t get into many/most of my 34 waist pants. I’m getting closer, though.

As always, it’s incredibly confusing, as a high P:F (I don’t eat many carbs, so I’m not using “E”) is by definition a low PUFA diet, in that I eat little fat most times. Does the lack of PUFAs contribute to the effects I’m getting? It’s impossible to tell.

I personally think that I’m relatively insulin sensitive, so I have access to my body fat. I’m also lifting several times a week, further providing an insulin/glucose sink. And I’ve gained quite a bit of strength while in the pandemic, again providing more of an insulin/glucose sink. Couple that with the thermic effect of having to burn and use protein, and I think that’s why this is working.

But I have no real idea, and no way to test this.

And, I’m also back to fasting when I can. I’ll do two days of OMAD this week, attempting to eat as few calories as I can. This has to play a role, too.

So, while Peter’s (and Brad’s) theories are interesting, I can’t tell how much they apply to actual humans like me. Or at least when I tested them, I gained weight instead of lost.

(L. Amber O'Hearn) #18

I think Matthew Dalby’s thread referenced above is worth reading. He makes the case that it’s absorption, and that this has to do with the triglyceride position, so it is specific to cocoa butter as opposed to, say, stearic in tallow or lard, and further, that humans absorb it better than mice, so the effect shouldn’t generalize well to humans. I haven’t taken a look at the study itself, but Matthew’s reasoning looks pretty good.

It would also be worth looking to see if Peter Dobromylskyj has addressed this counterargument.

One last thing: I don’t know that Dobromylskyj is fully on board with the croissant diet application of the idea. That’s Brad Marshall’s extension and it makes some sense given the theory, but it’s not identical to it. I suspect that once you have metabolic syndrome, the way you process carbs may be out of whack. That is, it would be consistent if a croissant diet doesn’t cause obesity, but doesn’t cure it either.

(Bob M) #19

One more note. Peter was never fat. According to him, he had 2kg of fat around his waist, which he lost immediately by going on Atkins. In this way, he’s similar to Ted Naiman, who weighs the same now (with muscles) as he did when he was a vegetarian.

I often think that we look through our lenses. The lenses for these two might be different than for those of us who aren’t like them.

When I went in the military, I lost weight and was quite thin after basic training. I then went into classes and gained a bunch of weight. How? Eating ice cream.

Under Peter’s theory, that shouldn’t make me fat, as it’s high in saturated fat, and we don’t care about sugar. But it did. (And still does, as I can EASILY overeat with ice cream. Three pieces of ice cream “cake”? No problem.)

So, what works for some people might not work for others.

(Bob M) #20

I think Brad was trying a multi-pronged attack. High saturated fat, low PUFA. But at the same time make it taste good, as one theory is that things that taste good make us fat (best exemplified by Stephan Guyenet? Or the guy – can’t remember his name – who always tests “processed food” and keto for less than two weeks).

And I’ve found that if you want to take in a very high amount of saturated fat, you pretty much have to do what Brad recommends. I’ve tried something similar with cacao butter and suet, and even high fat dairy, but it’s really difficult to eat those to any large degree.

Edit: Kevin Hall

Edit: And I don’t think it’s saturated fat causing me to not be able to eat cacao butter/suet/full fat dairy, it’s just these are hard to eat, particularly the first two. And, unlike many, if I eat chunks of cheese, I really am OK with a few, then I’m done. I don’t want more. My Pritikin influence may show up there, as I didn’t eat any cheese at all – other than on pizza – for decades.