Fire in a Bottle - The ROS Theory of Obesity and The Proton Theory


(PJ) #61

Thanks Mary. I’m actually familiar with that stuff. I water-fasted off and on much of last year – two weeks in April was the longest. I’ve gone through Fung’s books and videos (back then).

For medical (not psyche) reasons I had too-little appetite for many years, + years of chronic loss of nutrients (medical), so unless I’m pointedly fasting, I want to be eating enough to be getting a fairly dense-nutrient intake, I will be in body-rebuild ‘recovery’ for years still.

Also getting a lot of protein dramatically changes (improves) my psychology, never mind my ability to function well, so I target 30-35% protein if I can. This is hard if I’m not hungry lol. I normally put all my caloric intake from around 2pm-7pm, but I think I’m just going to start doing the coffee by 9am, despite it blows my IF. :smiley:

Now that I’ve read all this ROS stuff, I want to work on shifting the % of SFA in my body, oy! I am certain it is probably very high in PUFA. I don’t find much when I search on topics like: what makes the body select some fat cells over others when it’s going to use some fat for energy? I suspect nobody’s done the research or maybe it’s just too technologically advanced to be done at this moment.

(Utility Muffin Research Kitchen) #62

Good question, hope someone answers this :slight_smile: I know that there is some work done on what reduces visceral fat vs. subcutaneous fat (

But PUFAs isn’t the only concern: Fat cells store toxins too. Hence my quest to get rid of them, but slow enough limit the amount of toxins released into the bloodstream.

(Bob M) #63

This is in mice, but it’s very interesting:

Also, I heard an interview with Cate Shanahan, who said that when fat cells burn PUFAs, interesting things happen, like feeling bad or getting hot. She was mainly discussing fasting and bad effects that can occur there, but if we’re eating SFA and it’s causing fat to be burnt, could that have any short-term detrimental effects? (I haven’t felt any, but I’ve also been doing this 6 years.)

This is Dr. Cate:

(Michael - When reality fails to meet expectations, the problem is not reality.) #64

Thanks, Bob. I think this would be very interesting to many folks around here :thinking:


Our main finding was that dietary stearic acid leads to dramatically reduced visceral adipose tissue (VAT). Our data also indicated that total body fat was reduced by 25% compared to the low fat diet group when standardized to total body weight. Specifically, when VAT was normalized to total body weight, the stearic acid group had 67%±4% (SEM) less VAT as compared to the other diet groups. A conservative estimate of the normal percentage of VAT compared to total mouse fat is 60% [21] and a 67% reduction in VAT would reduce total body fat by 40% which is more than enough to account for the 25% loss of total body fat measured by DXA (which was also standardized to total body weight). Thus our data strongly point to VAT as being the primary fat depot being affected by dietary stearic acid. However we did not measure possible changes in other fat depots and cannot rule out the possibility that fat was lost or gained from other depots. Also we don't know the long term effects of dramatically reducing VAT. Nevertheless it is clear that excess VAT is not healthy and a diet that reduces VAT in a setting of excess VAT may be beneficial.

You don’t say. Qualifies for the understatement of the day award.

(Bob M) #65

In my tests so far of eating higher saturated fat (mainly cocoa butter and shea butter), it does seem as if my belly fat is going down and I’m getting leaner with more muscle. Brad Marshall (of The Croissant Diet) said he found the same thing:

That mouse study has some interesting theories and results. They think stearic acid causes apoptosis of “new” fat cells, for instance. They found the mice with stearic acid diet had lower blood sugar. That perplexes me, as I thought the mice on high PUFA would have a lower blood sugar, as if their fat cells (on high PUFA) are insulin sensitive, they should be sucking up blood sugar. Conversely, if SFA causes fat cells to be insulin resistant, they shouldn’t take in blood sugar, and therefore there should be higher blood sugar. But maybe there’s more involved than I realize for blood sugar. Leptin (a hunger hormone) also went down on the stearic acid diet.

(Michael - When reality fails to meet expectations, the problem is not reality.) #66

I haven’t read all the nitty gritty yet, but unless I’m mistaken (very possible) I think they say that stearic acid specifically has that effect on glucose and insulin, not all SFAs. Might have something to do with increase in glucagon.

(Bob M) #67

It could be glucagon. I think stearic acid is the “safe” saturated fat, as it supposedly increases HDL without an increase in LDL, or some crap like that. Meanwhile, palmitic acid is the “evil” saturated fat, which supposedly increases LDL while decreasing or not changing HDL, or other crap like that. (Yes, I believe these tests were likely garbage and even if true, are meaningless.)

However, he actually used a “stearic acid” which is actually a mixture of stearic and palmitic, about 50/50 supposedly. And the calculations they’ve been doing here:

Indicate that palmitic acid is just below stearic acid in the ability to make a fat cell insulin resistant.

Anyway, I wish I would have taken measurements before I started taking higher saturated fat. But I really had no idea the effect would be as strong as it is for me. My response truly shocked me. I’ve believed in this theory a long time, but I didn’t think just eating a lot more saturated fat (relatively speaking) would have this effect. Never dreamed it could.

Edit: Meant to say that because palmitic acid is considered “evil incarnate”, you don’t see a lot of studies done with it.

(PJ) #68

I see what you mean. But… maybe I misunderstand. I didn’t think the body was stuffing glucose into fat cells. I thought it was making glucose into triglycerides and stuffing those into fat cells. So if the fat cell is resistant, that would not leave glucose in the blood, it would leave fat (tg) in the blood… right? No? Hence we are not hungry because we have circulating energy. But we don’t have an insulin fit because it’s not going “omg look at all that glucose in the blood still.”

Just watched this last night about LDL and energy, very interesting.

(PJ) #69

This is an email I sent to my friend that I want to cc here because it seems associated with my daily cocoa butter bolus this week.

The last several days, whatever I eat (which is not really incorporating the extra-SFA theory yet, I’m eating what I have), I have a protein drink when I wake up (part of a meditation), then several hours later I eat all my daily food fairly at once or within about an hour, and with that meal (which is my last) or right after it, I have the cocoa butter coffee. Once, I had two meals separated by hours and had the second half of my coffee with the second meal, first half with the first meal.

So far it has worked fine and I’m very satiated. Even the next morning I’m not hungry.

Today I skipped the morning protein, and had my CB coffee then instead. Then I had my food as one meal to include a protein drink, around 4:30-5pm. I didn’t even think about it… so what.

Around 7:40 I basically passed out. I was sitting with my computer and just… gone into ‘abrupt severe sleep.’

I recognize that blood sugar crash. Before I lost so much weight, I was much more inclined to do that if I ate pasta or something for example. And after I first lost a bunch of weight super fast, I was getting reactive-hypo even to high protein and fat meals (like eggs and sausage) – not uncommon in people who’ve lost a lot of weight suddenly, and eggs especially can trigger it. Anyway I should not be getting BG drop severely like that for either reason.

I would not even be awake now (despite waking up 3x but being so deep in my brain state I could not bring myself out) at like 10:45pm except apparently every emergency siren in my city was called to something and had to go down main straight past my house (I’m on a frontage road about 500yd from main/route66). And even then it wasn’t until the last of them went past that I was finally able to drag myself up to alertness. And I was not sleep deprived mind you.

That is super bizarre and scary. I mean… I did not eat anything too weird and I did not eat anything unusual and this does not normally happen to me now, that hasn’t happened in years!

The one thing that IS diff is that

a/ I ate most things pretty close together like a 1MAD diet, so there’s more body-impact from doing that, and

b/ I did the CB coffee hours before all that – instead of with it or after.

I guess if you had a hard blood sugar response to something, would SFA modify the body response, by telling the cells they could skip accepting fat, so the glucose gets converted to triglycerides and then wanders around staying in the blood. But without the SFA, the insulin stuffs all energy into the fat cells, perhaps if the triggered insulin response was much too high, does it so overly-well that suddenly you have far too little energy in the blood and now you’re hypo. Like an exaggerated version of the basic model we talked about at first.

(Now my brain is wondering. If under severe, growing nearly diabetic conditions, the insulin resistance in fat cells from being over-stuff causes the insulin to keep working to find a place to stuff it somewhere, and so it does it in skeletal muscle and organs, which is bad… Why is it not doing that in our new SFA model, but instead it’s all wandering the blood, and the insulin is like oh well, whatever, and laying off?)

(Now I’m also wondering, does giving the fat cells the regular ability to control their own fat intake, so over some time they get used to being INsensitive with that control; does that somehow potentially make them MORE insulin-sensitive when they suddenly don’t have that control anymore?)

Tomorrow I am going to eat exactly what I did today, except instead of having the CB coffee in the morning, I am going to drink it starting just after I eat. I want to see if there is a difference, which there seems to be, but I need to put it against the same foods at the same time of day for a better test.

I cannot think of a single example right now, unfortunately, but the back of my brain is telling me that I have run into things before in life where, when you finally ‘give proper control’ or improvement to something, that if you suddenly remove that control or improvement, often the result is much more extreme/worse than it had been to begin with.

To analogy it in human psyche terms, like when things get much better in some area in your life, and you suddenly realize how good it can be and how bad it was, and then later when the bad situation returns, it seems much worse, and you are way less tolerant of it.

So now I’m wondering if having consistently had this bolus of SFA present just after I’ve eaten, has somehow made me more insulin sensitive when I do not have that.

(Utility Muffin Research Kitchen) #70

I see no change in satiety with about 50g cocoa butter a day. Actually I seem to have put on 2 pounds in the last month and tend to be more hungry, after losing 20 pounds in the 5 months before that. But it may be due to muscle buildup as my diet is also higher in protein. In any case I have abandoned my cocoa butter coffee in the morning for now and went back to strict OMAD, and will have some cocoa butter variety as dessert.

However, today I measured my morning fasting blood glucose for the first time in weeks and was very surprised to get a 90 (compared to my usual ~105). I actually measured a second time, 87. Huh? The 105 was consistent with the dawn effect for insulin resistant people (my morning BG went up 10 points when I went keto). Got to monitor this during the next days.

I don’t think SFAs should cause higher blood glucose. Excess glucose is converted to triglycerides, this process should not be affected by SFAs at all.

Haven’t read the paper yet. Will give it a go later today.

(Bob M) #71

The problem is that the scale is basically useless, at least for me. I had three DEXA scans done, over the course of a year. I lost about 6 pounds of fat and gained about 4 pounds of muscle in a YEAR, so a scale difference of 2 pounds. That’s beneath the level of “noise” my scale generates.

I postulate that in addition to potentially affecting belly fat, SFA might also cause an increase in basal metabolic rate and cause a preference for muscle over fat. I do not know the mechanisms. But at night now, I go through periods of being overly hot, taking off some or all of our covers (and we keep the temperature in the low 60s), then getting slightly colder, and having to add back in some or all of the covers. I also seem to look better, with less belly fat.

I am going to start taking waist and other measurements, as soon as I can find my tape measure. (I used to take waist measurements, too, but they seemed to have too much error in them to be of use. But maybe this time will be better.) I’d love to do DEXA scans, but they cost $150 each where I am and are typically over an hour’s drive away. (I can find tons of DEXA scans near me for bone health, but very few for fat/muscle analyses.)

Will report back over time.

(Bob M) #72

Also, just thinking out loud, does the starch + SFA have anything to do with it? That is, perhaps the combination of the two is better than each alone? I don’t know, but I may also try to test this. I’m still not a fan of starch, as it causes a blood sugar rise for me. I am going to try to get a CGM (have to go through a freaking doctor for a prescription where i am), and see what happens.

(Windmill Tilter) #73

Random unexplained hypo is definitely not good. Loss of consciousness is worse than not good; it’s actually dangerous. Might be worth talking to a Doctor.

Hard to believe the timing of your coffee had a material impact. At the very least, maybe switch to 2MAD for a couple days to see if that evens things out. Time to start monitoring blood sugar after meal times to see what the F is happening!

That’s my two cents anyway…

(Bob M) #74

That’s not the theory. The theory is that your fat cells become insulin resistant by eating SFA. If your glucose does not go into your fat cells, where does it go?

Of course, this theory only explains fat cells. It does not explain the entire body’s response to extra SFA. There is much, much more that happens when we eat, including a bazillion different hormones.

In accordance with my previous comment, maybe you NEED the starch for some reason? Maybe SFA + keto isn’t the best? More to test…

(Bob M) #75

By the way, I’m not trying to belittle anyone with this statement. I assume there are some people who can see say a 2 pound scale increase and know something is wrong/different. That’s not me. I can get 5+ pound movements on the scale. See this, from back when I actually used my scale:

(Justin Jordan) #76

I can easily bounce fifteen pounds in a day. Which, actually I did just yesterday.

I do still find the scale useful, though, but it’s a big picture kind of thing.

(Utility Muffin Research Kitchen) #77

From what I’ve understood, glucose can’t physically go into fat cells for storage. In fact glucose is toxic for many processes, that’s why excess glucose is stored as glycogen which is not toxic. The only way for glucose into fat cells is via the liver and conversion to triglycerides.

Insulin however will cause fat cells to store triglycerides from your blood, absence of insulin will make them release the fatty acids. However, fat we eat is also stored in our fat cells. I’m not sure how exactly insulin resistance in fat cells will help with satiation. However, leptin is driven by insulin, and leptin is produced in adipose cells (I think). Maybe the reverse electron flow simply drives leptin production?

Bugger, I’ll really have to go to hyperlipid and try to understand the protons theory. Or at least watch Mike Eades talk again. I know that we get satiated a lot quicker if we eat saturated fat with carbs vs. polyunsaturated fat, which Mike Eades attributes to the different ratio of FADH2 to NADH. But if we eat carbs, shouldn’t the mitochondria burn glucose? Why would they burn fat at all?

All I know right now is that I don’t have a clue what’s going on :slight_smile:

(Central Florida Bob ) #78

FWIW, I tend to mentally draw error bars on anything from the scale. At my weight, my Renpho scale says it should be +/- 0.8 lbs. It turns out even that’s not enough to cover day to day variation.

Weight is such a crude measure. I increase that speculation to things like DEXA scans. It says we’re some percent body fat, say 25%. OK, what does that mean? That’s based on a weight which comes from a nice precision balance. What’s its tolerance? There’s a tolerance for the % body fat measurement on top of the scale’s. Do we end up 25 +/- 1 or 2 or what percentage?

I’m used to measurements being reliable to fractions of 1%. It just doesn’t seem to happen with our bodies.

(PJ) #79

No kidding! But in the two years I’ve been back on keto (and the two years before, after heart surgery) I’ve not even had mild BG issues let alone severe. And I tracked my BG and BK religiously off an on last year.

I’m still losing water weight from Dec-off (I’m not on Keto in Decembers). Gotta get to 1/21 where I officially call it done before I start measuring. It confounds everything.

I was mysteriously carb-hungry from the time I woke up, and I should have been very full until today, which to me indicated that I really did get all that stuffed into fat cells leaving me energy low. I ended up eating 3 eggs with some cheese at 3am, and since I’m not working at the moment, not waking up until noon. But I feel fine for now. I will avoid eating that major amount of protein+fast-protein all at once again.

(Utility Muffin Research Kitchen) #80

The croissant diet relies heavily on stearic acid, which is kinda hard to get. The only easy source seems to be cocoa butter, which has a strong smell and taste of, well, cocoa. Which is fine when making chocolate, but not so much if you want to do something else.

According to the protons theory, palmitate should be almost as good as stearic acid (0.486 to 0.484). Palm oil contains over 40% palmitate and is cheaper than cocoa butter, and cocoa butter contains only 30% to 35% stearic acid.

Shouldn’t we use palm oil for these experiments? Mind you, I’ve never used palm oil before. Don’t even know how it tastes and smells. But since it’s used in many commercial products (or was, until we demonized saturated fat) it should be fine, shouldn’t it?