Thank God It's FriGAINZZZ

See correction and acknowledgement at post's end. By the way, the end is probably a good place to start -- this guy doing the What I've Learned videos puts this pretty succinctly.

Today's GAINZZZ thread is about re-GAINZZZing your insulin sensitivity.

I get a lot of people who seem to be sort of normal-weight pushing back against this whole low-carb/fasting thing.

Let me explain it more than I have previously.

Many of these people think that they're not prone to weight gain because they don't "eat too much" and "get some exercise."

In fact, it's the opposite. They don't eat too much and they get some exercise because they're not prone to weight gain.

It sounds strange, but fatness itself causes fatness. And giving advice to those prone to weight gain based upon what "works" for a person without that problem is like a non-diabetic instructing a diabetic that "a few donuts here and there won't kill you."

Well, for a diabetic, they just might. Different metabolisms respond differently to different stimuli.

Okay, so here's what insulin resistance is.

By the way -- that term might sound strange. Insulin resistance is the bad thing, and insulin sensitivity is actually the good thing -- though it would be easy to assume the "resistance" is the good thing and the sensitivity the bad one.



Let's look at how insulin is supposed to work -- and how it does work, in a normal, not-disturbed metabolism.

1. You eat protein or especially carbs.

2. These get broken down and enter the blood as glucose. (Protein would take longer to enter as glucose, but it can and does happen, to a lesser extent).

3. Your body cannot take too much glucose in the bloodstream at once -- I think it can only tolerate 10 grams of dissolved glucose in the blood at any one time, or something. But a big carb heavy meal might dump 70 or more grams of glucose into the blood in the hour or two after a meal. Having too much glucose in your blood is called hyperglycemia, a potentially very serious condition frequently experienced by diabetics.

4. Your body senses that there's too much glucose and your pancreas begins pumping out insulin.

5. The cells of your muscle and liver and your fat cell storage sites -- having a normal level of sensitivity to insulin, and let me repeat, assuming a normal level of sensitivity to insulin -- bond at the cells' receptor sites. The insulin molecules, bonded at the receptors, now tell the various cells to start taking in glucose, to get it out of the blood stream. A certain amount of glucose can be stored (in the form of glycogen) in the muscle, and some in the liver. Some can be used immediately by muscle if you're exercising at the time. The rest goes to fat cells, to be packaged away for long-term storage as fatty triglycerides.

6. Once your blood glucose levels are in an acceptable range, the body detects this too, and tells the pancreas to stop pumping out insulin. Again: assuming a normal sensitivity to insulin.

7. Over a period of minutes to hours, the insulin begins unbonding from cell receptors and gets recycled or excreted. This is important, because it means 1, no further glucose will be swept out of the blood (which can cause lethargy, or even low blood sugar (hypoglycemia)), and 2, it means you can begin burning fat again.

See, the thing I don't talk about much is that most normal weight or athletic people are routinely in the state of "ketosis" -- fat burning. Ketosis is not some weird body function that weird dieters trick their body into. It's the state that most healthy people are supposed to be in, at least periodically, between meals.

If you don't have any glucose coming into your body, and you need some, the body is supposed to send out hormone-sensitive lipase (and other fat-burning hormones) to your fat cells and tells them: We need energy, start breaking that fat down into smaller molecules which can be metabolized for energy.

Here's the thing:

The various fat burning hormones are opposed by, and blocked by, insulin. Hormones tend to work in pairs, one "on" and the other "off," and "insulin" is the "on" switch for gaining fat (sending glucose to fat cells) and the "off" switch for hormones which tell fat cells to release their stored energy to be made into ketones.

So when you have a lot of insulin in your body, you can't burn fat. (Or, at least, you can burn very little.)

So let me finish up this long step: In a person with normal sensitivity to insulin, their insulin levels aren't all that high, and insulin starts getting swept away to be disposed of when it's no longer needed, and now cell receptor sites are free to accept the fat burning hormones which tells fat cells "start burning fat."

Upshot: In a person with a non-dysfunctional metabolism, all this hormonal signalling works pretty well. If they have too much glucose in their blood, the pancreas sends out some insulin -- not a ton, just enough to do the job! -- and some glucose gets swept out. Then the insulin goes away, and fat-burning hormones are now free to tell fat-storage sites to burn fat when it's needed.

Result: You don't feel tired or lethargic after meals. You don't feel hungry soon after meals, because your blood has enough glucose in it to keep going. And you don't gain much fat, because your insulin-sensitive hormone is frequently able to tell your fat storage sites to give up fat as needed, and they're not cockblocked from doing so by insulin.

Okay. Now let's look at a person with a disturbed or dysfunctional or "dysregulated" metatolism:





1. You eat some protein or -- bad news! -- carbs.

2. These are broken down and enter your blood as glucose.

3. Just as with a person without a dysregulated metabolism, your body senses there's too much glucose in your blood, and

4, signals your pancreas to start pumping out insulin.

5. Here's the problem. The cells of the body can learn to tolerate insulin, if they've seen too much of it. Just as an alcoholic develops a tolerance to alcohol, or a smoker finds he needs three cigarettes to give him the lift that one used to do, so too can cell receptors grow to tolerate insulin, and develop a resistance to insulin -- a resistance which can only be overcome with an even bigger dose of insulin.

In other words, the normal dose of insulin which is supposed to bond to cells and tell them "start taking glucose out of the blood" fails to do so. The insulin level is just too low to get the cells to do what they're supposed to.

So the pancreas pumps out more insulin. It still doesn't trigger the cells to take in glucose.

6. In a normally-insulin-sensitive person, at this point the pancreas would detect that glucose levels are now in an acceptable range, and will stop pumping out insulin.

But in an insulin-resistant person, the normal dose of insulin hasn't worked.

So the pancreas pumps out more. It still doesn't activate the cells to take in insulin.

After pumping out a level of insulin which can be 300-400% higher (or even higher) than that which a normal-weight person produces, the cells finally get the message and start letting glucose into the liver and muscles.

The amount of insulin that gets flooded into the blood in an insulin-resistant person -- also known as a "fat person" -- can be pretty dramatic, compared to that in the blood of a normal-weight person throughout the day; you can see where the meals are eaten. It's pretty obvious.

This chart has colors. You may not believe in Science, but you believe in colors, don't you?

Few things to note from that chart:

* A fat person's fasted insulin -- that is, his default blood insulin even in the fasted (pre-meal) state -- is already higher, permanently, 24-hours-round-the-clock, than the normal weight person.

* His insulin rises far, far higher than the normal weight person's, even above his normal fasted insulin, which is, again, already elevated.

* His insulin remains at high levels longer than the normal weight person's.

Now, finally, yes, the insulin works here, and glucose gets swept out of the blood into the cells, and the pancreas turns off the insulin pumps.

7. But since there's now such a high level of insulin in the blood, too much glucose gets swept out, and the fat person now experiences the very weird condition of being tired and being hungry, though having just eaten. (See Provisional Retraction below -- a physician weighs in to say this bit about the obese having lower blood glucose due to higher insulin levels isn't true.)

Why? Because his damn blood has no sugar in it and that's a universal signal to the hunger centers to tell him to eat again.

And he's not going to be doing any damn exercise in his low-blood sugar state.

And notice the really bad consequence here of high insulin levels combined with high duration of high insulin levels: His fat burning hormones, which would normally tell the fat cells to give up their stored energy between meals, are blocked from telling fat cells to do so due to the swamp of insulin in his blood.

His insulin starts high in a fasted state, gets very high after a meal, stays pretty damn high even between meals -- all the time blocking the fat-burning magic of insulin's opposite-function fat-burning hormones from doing what the body is supposed to do between meals, that is, go into a slightly ketogenic state where fat is being burned to produce the other sort of molecule that can be burned for energy, ketones.

If a fat person's insulin is always making his blood low in sugar, thus making him both tired and hungry, and his always-high insulin levels are always blocking his body from burning fat for non-glucose energy, how in the hell is a fat person ever supposed to lose weight?

A normal weight person does store fat away from time to time -- but his insulin is at fairly low levels, and falls to a low fasted state quickly, thus permitting him to frequently dip into his fat stores as needed. He may gain a pound or two here or there -- but he also has no particular problem losing that pound or two.

But for a fat person, the process of tapping into those fat stores is completely taken off-line by the ever-present ocean of insulin that is always in his blood. (And note that a fat person's fasted insulin levels can be even higher than a normal-weight person's post-meal levels!)

In a normal weight person, fat is put away into a closet. It is stored, but it can be accessed when needed.

In a fat person, fat is put into the closet, but that closet is then locked shut by chains and padlocks called "excess resting-state, always-present insulin," which forbids the body from opening that door and getting to that fat.

In a normal weight person, whose insulin is not dysregulated, his insulin fades and allows insulin-sensitive hormone to burn fat whenever he needs it. It's a two way street -- fat goes in, sure, but it comes out, too.

But in a fat person, that fat is now on a one-way journey only -- it can only be put into the closet, and never (or almost never) taken out again.

The high insulin levels he has now make it such that while fat is always being put into his fat cells, it is nearly impossible to ever access them to burn off for energy. Note this bitter vicious cycle aspect: the fatter you are, automatically, the higher insulin levels you'll produce; your fatness is the mechanism by which you will produce more fatness, and block you from burning fat.

Fat people have insulin resistance. Period. This is the Syndrome X, a complex of high blood pressure, obesity, diabetes, etc., scientists noted a long time ago, which is now called "metabolic syndrome."

To reduce weight, they have to eat foods that produce less of an insulin response, and maybe seriously deplete their blood of insulin -- by not eating at all for long periods of time -- to prod their cells into becoming sensitive to insulin again, so that they react to lower doses of the hormone.

This chart compares post-meal insulin levels in an overweight person versus a normal weight person, when either of those two have a High Carb (HC) or High Fat (HF) meal.

The top line is overweight eating carbs; the second is normal weight eating carbs; the third is overweight eating fat; the last is normal weight eating fat.





Note a couple of points: Insulin spikes in the obese and normal weight fairly high after high carb meals, though (of course) higher in the obese; and after high fat meals, while overweight people still react with higher insulin, notice the difference there is barely visible. The obese and normal-weight react kinda the same to high-fat meals.

The point of Dr. Fung's program is actually to cure diabetes 2 sufferers, but the plan can help increase insulin sensitivity for normally overweight or obese people or people who are sadly, let's say it plainly, pre- diabetic, or maybe pre-pre-diabetic.

Warning: Dr. Fung carefully monitors his diabetes 2 patients. Do not try to cure yourself of diabetes 2 with this plan except under strict medical supervision. Playing around with sugar and insulin while suffering from diabetes can kill you.

The idea is to kill the tolerance to insulin by greatly reducing the insulin present in the blood. The idea -- which I hope works, though I'm only on month seven of trying it, and it might take 1-2 years -- is to re-sensitize cells to insulin by always keeping to foods that cause a lower insulin response, and then having longer periods (fasted states) where there's no food at all coming in that could jack up insulin levels.

And just as someone who has grown tolerant to alcohol might, if he quits booze for a year, suddenly find that two drinks is enough to make him tipsy, the idea is that starving the cells of insulin might help them regain a normal-weight person's sensitivity to insulin, too.

I don't know if this works, obviously. I'm not a doctor. But Dr. Fung says his program is a success.

Anyway, I was going to talk about other issues but I seem to have used up all my allotted time on this one thing.

My own gains: two pounds down -- 168 -- bodyfat down quite a bit over a few weeks, two inches lost on my waist (which hadn't shed any inches for a while).

The one meal a day thing seems to be what I needed. Maybe my body had adapted to the 16/8 thing to the point where it just didn't consider it a metabolic stress enough to burn fat. So maybe it needed a shake-up.

It's not easy, but I'd also say it isn't particularly hard. Not after seven months on a 16-20 hour fast regime. Doesn't take much more to get it to 23/24 hours.

Right now though I'm hungry enough to eat a rotten pig's ass so I'm going to do that.

In the meantime: Tell me about your GAINZZZ.

Oh, and sure, let the people without dysregulated metabolisms tell me how they solved all the weight problems that they've never actually had, and why people who have this metabolic disorder should just do what people without metabolic disorders do to keep weight off (that is, nothing at all, letting your properly-functioning insulin metabolism keep you at ideal weight, all working smoothly in the background, while you do nothing in particular except say "eat less, move more, rinse, lather, repeat").

Note/Correction: I got most of this, at least this week (I've read the basics a lot before), from these very good videos I've previously recommended by What I've Learned, especially this one, and this one I recommended last week.

The hormone that tells fat cells to release triglycerides for processing into ketones (energy bodies) is "hormone-sensitive lipase," not "insulin-sensitive hormone," as I called it.

Actually, there are several hormones that tell fat cells to burn fat for fuel, such as epinephrine, cortisol,* testosterone, human growth hormone, grehlin, and glucagon, but almost all of them are antagonistic to insulin, or opposed by insulin. Broadly, one could describe them as "insulin sensitive hormones," but none are named that.

Sorry for the garbling. I've changed my botched language to specify "hormone-sensitive lipase" or "lipase and other fat-burning hormones" or "fat burning hormones" generally to get rid of the just-plain-wrong "insulin-sensitive hormone" term I mistakenly used.

* Cortisol is a hormone with a few effects. It's the "stress hormone," but it's also the alertness hormone. If you wake up pretty quickly in the morning, that's your body giving you a jolt of cortisol to stress it up (out of its hibernating state) and get you moving.

Apparently it has some fat-burning function. However, it also gets branded as a fat-hoarding hormone, in people with too much stress, or who don't get enough sleep and therefore have a lot of cortisol in their bodies all day long.

I don't know much about anything, and I certainly don't know at what point cortisol goes from being a useful wake-up hormone into a stress-monster fat-hoarding-because-winter-is-coming hormone.

Cortisol, like most of the other fat-burning hormones, is opposed by insulin. Cortisol promotes alertness, awakeness, stress, and fat-burning (in some situations, at least); insulin promotes lethargy, sleepiness (you get sleepy after a big Thanksgiving meal, right?) and fat-storage.

Provisional Retraction. Another GAINZZZ Correction. I don't know on this one either way, but a physician pops in to say that, while he agrees with most of the GAINZZZ post, he disagrees with my assertion that the high insulin response of an obese person sweeps too much glucose out of the blood and leads to feeling both tired and hungry. He says the obese have simultaneously a high fasted insulin level and a high fasted blood glucose level.



I don't know if he's right. I thought the feeling of being tired -- the famous "spike your blood sugar, then crash with lower blood sugar" -- was related to insulin level, and I thought I read people connecting that to higher insulin levels in the blood. Or maybe I just speculated myself that the two things were directly connected.



Maybe both points are true: High quickly-bioavailable carbs do cause the spike-and-crash effect, but they cause this in all people, and it's not true that people with high insulin levels have it worse. Maybe they just have it like anyone else.

He says he's a doctor, and I gotta admit my understanding here is based on a few pop-science books I only remember in broad outline, so let me provisionally retract this.



If the poster making this point, or any other doctor, would be so kind as to illuminate me on this point, I'd appreciate it.



