Amazing "Croissant Diet" Experiment Results (Stearic Acid/Saturated Fat)

[GorillaHead]

The results of this experiment are amazing...

I recently found a blog article by a guy who decided to go on a croissant diet with a high amount of stearic acid to see if he could prove that eating this way would cause him to lose weight/body fat.

The hypothesis of his experiment was based on a study that showed that mice who ate a high amount of Stearic Acid and low amount of unsaturated fat diet had a reduction of visceral fat by 70% and an increase in lean mass.

This is the article:
Introducing The Croissant Diet - Fire In A Bottle

The before and after pictures are pretty stunning. The question is.. what is actually causing the fat loss. Is it just the saturated fat vs unsaturated fat ratio? Or is it the Stearic Acid? Or is there more going on?

What are your thoughts?

My thoughts is hes after shot is by far one of the worst things i have ever seen as an example as document to show lost weight.

 

[Inaut]

I read the title of this thread and was so excited to start eating croissants! I'm glad my impulses are more tamed these days :)

 

[S-VV]

Do you think eating st. acid long term (providing it worked well initially for fat loss) would have some downsides?
Thanks

That’s the question. Well, either the body urinates the glucose, like a Type I diabetics do, or it up-regulates insulin independent glucose transporters, like GLUT1, or it up-regulates metabolic rate. Or none, and diabetic gangrene sets in.

 

[Vinny]

That’s the question. Well, either the body urinates the glucose, like a Type I diabetics do, or it up-regulates insulin independent glucose transporters, like GLUT1, or it up-regulates metabolic rate. Or none, and diabetic gangrene sets in.

So, basically, you wouldn,t mess with it long term, correct?

 

[S-VV]

So, basically, you wouldn,t mess with it long term, correct?

Personally, I would, and am planning to. But daily fasted BS readings are a must. This is unexplored territory.

 

[Vinny]

D

Personally, I would, and am planning to. But daily fasted BS readings are a must. This is unexplored territory.

Thanks for all, and for suggesting to watch the BS levels too.

 

[ecstatichamster]

I'm pretty sure the mechanism is mitochondrial fusion which occurs best with stearic acid. I am not sure why this leads to fat loss, increased metabolic rate, etc. but I think it does.

 

[yerrag]

I'm pretty sure the mechanism is mitochondrial fusion which occurs best with stearic acid. I am not sure why this leads to fat loss, increased metabolic rate, etc. but I think it does.

Should I read further on the ROS Theory of Obesity to brush up on that concept, that of Mitochondrial Fusion? It's a totally new buzzword to me.

 

[ecstatichamster]

Should I read further on the ROS Theory of Obesity to brush up on that concept, that of Mitochondrial Fusion? It's a totally new buzzword to me.

i don’t think one has much to do with the other. I am researching how mitochondrial fusion leads to fat loss and higher energy expenditure. Stearic acid is best at stimulating mitofusin-2 and leading to mitochondrial fusion.

One theory is that genetically‑engineered mice lacking mitofusin‑2 have a lower metabolic rate, lower uncoupling protein, and increased weight gain. Glucose and insulin tolerance tests have led the researchers to hypothesize that mitochondrial fusion is geared towards carbohydrate metabolism for energy production, while mitochondrial dissociation / fission is involved in fatty acid synthesis from carbohydrates.

 

[Julian]

Just saw someone post this on the Saturated Fat Reddit:

BTW, Mr Turnbuckle at Longecity says stearic acid must be cooked to be bioavailable. He also mentions that glycerol monosterate can be substituted. This looks to be both a food additive and body building supplement so it can be found on Amazon and elsewhere.

Manipulating mitochondrial dynamics - Page 46 - Aging Theories - LONGECITY - Page 46

Checked out what the guy said on the forum. Glycerol monosterate could be interesting too...

 

[Julian]

From what I can gather from the Saturaed Fat Reddit, this seems to be the only place known so far that sells pure Stearic Acid:

Stearic acid S4751

The other stuff out there is probably just 50% Stearic Acid and 50% Palmitic Acid. Which you don't want to consume I think.

 

[Julian]

From what I can gather from the Saturaed Fat Reddit, this seems to be the only place known so far that sells pure Stearic Acid:

Stearic acid S4751

The other stuff out there is probably just 50% Stearic Acid and 50% Palmitic Acid. Which you don't want to consume I think.

Hmm that website seems wayyy to expensive... haha

 

[tankasnowgod]

From what I can gather from the Saturaed Fat Reddit, this seems to be the only place known so far that sells pure Stearic Acid:

Stearic acid S4751

The other stuff out there is probably just 50% Stearic Acid and 50% Palmitic Acid. Which you don't want to consume I think.

Where did you get this idea from, that somehow they are selling 50% Palmitic Acid without disclosing it?

Regardless, the original post was likely using consumer level USP/Food Grade Steric Acid. He made no mention of ordering it directly from Sigma Aldrich.

 

[Terma]

His idea is too incomplete to hold up as described, in the research. SCD1 has different effects depending on the tissues and state, and the duration. The popular alternative is ceramide (The Role of Ceramides in Insulin Resistance). Ceramides don't always explain insulin resistance but its overload is a reliable sign of pathology.

You get mitochondrial fission (Mitochondrial fission mediates ceramide-induced metabolic disruption in skeletal muscle. - PubMed - NCBI) and various problems while compounds like adiponectin (probably improved if combined with AMPK: Adiponectin serenades ceramidase to improve metabolism) help lower ceramides accumulation by degradation (to sphingosine). The ceramides are made de novo (this is where palmitic acid gets blamed) and through sphingolipid/sphingomyelin breakdown, which can come from various inflammatory or oxidative insults commonly mentioned. The latter means eventually you need to rebuild sphingolipids, requiring phospholipids to upgrade the ceramides, energy, and well-coordinated cells because their formation is complex. Mitochondria and ceramides have reciprocal/counterbalanced relationships to an extent greater than I'm aware (Novel function of ceramide for regulation of mitochondrial ATP release in astrocytes). Inevitably the work of the mitochondria must fuel some of the work done to handle ceramides.

Oleic acid is beneficial insofar as it can divert from inappropriate palmitic acid overload in ceramide synthesis (which requires and probably wastes serine) into triglycerides instead (just as it is better to store polyunsaturated acids as triglycerides than as phospholipids, but I'm not sure how oleic affects that). But eventually that overloads and it stops doing good. Meanwhile stearic acid diverts away from triglycerides and ceramides and seems to prefer either oxidation or incorporation into DAG for cell signaling or phospholipids, depending on the tissue and the study you read, and probably the state of the cell, and where SDC1 ablation improves oxidation so the other fatty acids get dealt with (https://www.physiology.org/doi/full/10.1152/ajpendo.00439.2004). In fact stearic acid could improve insulin resistance at one level/tissue or another, and SCD1 knockouts can have opposing effects depending on study/tissue. Commonality is that both stearic acid and ceramides can induce apoptosis but seemingly under different conditions.

Lower SCD1 means both more stearic acid and less oleic acid. Meanwhile, in his experiment, more stearic acid will inevitably lead to less oleic absorption. Meaning in all the experiments, the effects of more stearic acid will inevitably get conflated with the effects of less oleic acid. If it worked, it could be a double whammy. Of course that also depends because possibly only low amounts of stearic acid make it across the gut barrier as Kartflullel posted. In that case it could be more about excretion of oleic acid and the absence of the effects it would've had than the effects of stearic acid.

I think stearic acid has value. I was interested in it for its potential lean-tissue-preserving properties, and very specifically as a sleep-time activities promoter. It would be an interesting mechanism to be able to eat glucose most of the day and then before you go to bed, "switch on" fat burning in the night with something of a surge (the idea of the nighttime spike in growth hormone) while minimizing the stress of the signal (would you rather growth hormone or norepinephrine?). I already started using L-serine 2-4g before bed (with low-dose melatonin for the intestines and the usual magnuseum and other things) and maybe some stearic acid would make a gay addition (other things). In fact, I would consider the experience of the user with worsening glucose a good sign because states of pseudo insulin resistance are normal at nighttime and so in the worst case I trigger something relatively physiological for the time of day, although I guess if it persists strongly into daytime readings that's something else. Although nothing replaces some good ketones. If stearic acid increased beta-oxidation, in the right cell types (liver, astrocytes) then it could increase ketogenesis from fatty acids I guess including itself. You can also just drink them. [Carnitine deficiency would be bad]

I'm not sure in other tissues but in the brain stearic acid predominantly incorporates into phosphatidylethanolamine and phosphatidylserine, which are important to mitochondria but also are the most unsaturated, so it serves to counterbalance the unsaturated fats although I'm not sure if it would actually encourage their incorporation. In particular it has a special role in phosphatidylserine because it associates with DHA there (Phosphatidylserine in the Brain: Metabolism and Function) as the other side of the coin (based on best guess I would agree with Travis that a small amount of o-3 is necessary in the brain - specifically because phosphatidylserine-C18:0-C22:6 seems like a valuable compound - although highly vulnerable - which is why it's preferable to make as endogenously to its point of use as possible, rather than overloading on sardines). When you combine this with the idea that ceramide is blamed for insults to astrocytes it seems very desirable, if you could get it across the BBB or improve stearic endogenous synthesis in the brain, such as find a natural SCD1 inhibitor endogenous or otherwise that affects the brain likely combined with not eating carbs or protein too late, or only non-insulinogenic non-carb overload type things - probably you'd rather want to promote ketogenesis by the liver and astrocytes, after which the ketones compete with glutamate to help us sleep (Sci-Hub | Ketone body metabolism and sleep homeostasis in mice. Neuropharmacology, 79, 399–404 | 10.1016/j.neuropharm.2013.12.009). Basically you'd want a strong carbohydrate daytime/ketogenic nighttime cycle for optimal effects, ofc depends on the duration of the effects on the SCD1 mRNA/protein levels, I'm not sure - you might have a winner. Throw PPARalpha activators in there to make your allopregnanolone endogenously in the astrocytes along with more ketones (Regulation of Ketone Body Metabolism and the Role of PPARα), that gives a lot of clues, and there's a point to keeping insulin down or modify the fructose/glucose ratio. Meanwhile in this environment you can handle DHA and phosphatidylserine in a calmer environment not stimulated by glutamate but rather by GABA and fueled by more ketones (relatively clean-burning, while the astrocytes do the fatty acid oxidation), and maybe that translates to a relative lower level of peroxidation in the CNS, and better sleep and brain development, or health and reorganization.

Edit: But maybe the stearic gets in the way, and has to be compensated in some ways: Fatty acid chain length and saturation influences PPARα transcriptional activation and repression in HepG2 cells. - PubMed - NCBI

 

[Vinny]

Where did you get this idea from, that somehow they are selling 50% Palmitic Acid without disclosing it?

Wondering the same. It,s getting very complicated and expensive if true. Otherwise, I,ll just order some st acid for soap/candels from ebay for pennies, and I,m good to go...

 

[Jeemmy]

Sorry guys noob here, why 16:0 is considered a bad SFA? I mean if medium length is good and 18:0 is good what's wrong with 16:0?

 

[Broken man]

Super interesting!
How would you guys rate cacao butter ? Too much mufa?
Also hydrogenated coconut oil has like 7 percent stearic acid and by far the best ratio of sfa to pufa.

You need high amount od stearic acid I think .....

 

[Broken man]

Cocoa butter is higher in stearic acid than enhanced butter at 33% according to the same guy.
The Croissant Diet Specification - Fire In A Bottle

But the ratio Is what Is important.

 

[Broken man]

Sorry guys noob here, why 16:0 is considered a bad SFA? I mean if medium length is good and 18:0 is good what's wrong with 16:0?

Palmitic acid Is good but the advantage of stearic acid Is that Its displacing linoleic acid from Its position. That Is what Travis said.

 

[Broken man]

I tried to read this. The ROS Theory of Obesity as explained here The ROS Theory of Obesity - Fire In A Bottle goes against what I believe to be our understanding of saturated fats vs PUFAs, if we are to believe in Ray Peat's ideas on the subject.

According to the author, as he explains the ROS Theory of Obesity, saturated fats generate ROS and PUFAs don't. I just had to stop reading this.

I think that dietary stearic acid would be able to help with combating obesity, but not for the reasons being discussed in this thread. I think that dietary stearic acid is helpful with obesity for a different reason: that it transports endotoxins out of our system, and in so doing restores our ability to metabolize sugar well. In addition, saturated fats have an antibiotic effect, and it would be able to kill bacteria as well. This reduces the need of our innate immune system, to phagocytize bacteria, which requires the production of ROS to kill bacteria. The ROS spillover to adjacent tissues is an oxidative stress, and it requires the use of endogenous anti-oxidants such as glutathione, uric acid, and albumin, to neutralize the stress.

Because the use of stearic acid leads to lower production of ROS and lower usage of endogenous anti-oxidants, this would conserve anti-oxidants for use in quelling the natural production of ROS during mitochondrial respiration. This would allow a higher rate of mitochondrial respiration, and the increased metabolic rate leads to higher energy usage, and the burning of calories would be facilitated. This would lead to weight reduction.

Not only that, lowering the state of inflammation from reduced endotoxin levels allows the whole body tissues to be absorb and metabolize sugar freely. This leads to the salutary effect of good sugar regulation throughout the body, avoiding the peaks and valleys of blood sugar, and keeps the stress response to a minimum. It would lead to less fat production by the liver which results from high blood sugar condition being relieved by the liver through de novo lipogenesis, as signalled by an insulin response. It would lead to eliminating hunger, the result of insulin causing blood sugar to become too low, and cause another meal to be eaten, in the process increasing caloric intake. Speaking of hunger, this would not happen as well as good blood sugar regulation prevents fatty tissue buildup in the liver, and this allows more room in the liver to store glycogen. Glycogen comes into use when it's converted to glucose by the liver when blood sugar gets low - in between meals and during a day fast.

I don't buy the ROS theory of obesity. The theory is anti-peat but the idea of using stearic acid isn't though.

I thought that Its because increased mitochondrial function leading to higher fatty acid uptake like with pregnenolone And insulin, study was posted earlier.....