OK now you have freaked me out as I can see neither in your post…
I agree. Yet this will be an enormous uphill battle to get everybody else to change how they do it. IF/EF is massively established.
Yeah, Paul - so does that mean a regular pattern or not? I fear it does, but personally prefer no fixed periodicity here, as with Iced saying “done randomly throughout my week with no fixed pattern.”
Totally agree here too, Robert. The whole language thing, i.e. “break (the) fast” is arrayed against us, though.
For most of us here, the context is a lot different than it was for Thag the Caveman. Breaking the fast - eating again - was a really great thing for him. Now, we’re mostly looking for the good things that happen in the absence of eating.
I don’t take it as meaning a regular pattern and only a regular pattern, but I do take it as including a regular pattern as well as random offs and ons.
But if you don’t want to call 16:8 intermittent fasting, then don’t, but please be gentle with those of us who do.
I hear you, brother. It’s one of those things where I’m conscious of being biased from the get-go, and that the language is broader than my nutty little niche.
The intermittent thing is more interesting than I’d ever considered. We know that by definition it’s not going to be continuous, but the “regular or not” meaning is influenced by context, in my opinion. Perhaps there are other qualifiers that would tip the balance.
A river or lake that ‘regularly’ dries up will be both intermittently wet and dry, according to the definition.
Yet if we have intermittent garbage-pickup service, doesn’t that imply that something is wrong with the system, i.e. that some pickups get missed? Or would it need to be said like, “We only had intermittent garbage pickup…”?
Well I look on intermittent fasting as the variable element in my regime. Sometimes I have lunch at 1 pm sometimes at 4 pm and sometimes not at all. Always have dinner usually at 7 ish so my TRE would be variable too but usually a 17/7 regime or 23/1 or something else. I think TRE would be a stricter time fixed regime and IF more flexible?
Those for IF seem to be flexible and those for TRE seem to be strict
Imagine my shock ~
I totally get that… after about a month of reading and re-reading the definition a dozen or so times and reading numerous articles. My hang up is the average person wants to ask the question “Why am I fat?” and the answer is insulin resistance… but isn’t the real problem chronically elevated insulin levels and that’s what causes the resistance on a cellular level? So why not call the problem something that better describes the cause, rather the effect.
I dunno, maybe it’s just me.
BTW, I got the quote notification five days after your post…
There are variety of reasons, I think, Carl. In the beginning, most of us get fat because we eat more than we burn, and our insulin and cells work just fine - they make glucose go into fat cells when we’re in a fully-fed, high-energy state. Increased insulin really fires up the glucose transporter proteins.
Over time, higher insulin levels mean less sensitivity to it, and less energy getting to the cells that need it, thus more hunger and less satiation, even with enough glucose already being present - the body being stuck in ‘fat storage’ mode due to high insulin. Obviously a bad cycle to be in - wanting to eat more and getting less satisfaction from it.
Over more time, after substantial weight gain, we’re adding more fat cells (that aren’t going to go away later) and some of the existing cells are getting really full of fat.
Past a point, the outer layer of the fat cell (which contains the normal components we think about in cells) is going to start getting tight, the cell is full-up on fat and really doesn’t “want” to take in any more. I think this is when the cells effectively give insulin the finger by shutting down the receptors. True physiological insulin resistance - the fat cells are too full to take in any more.
First, I can’t relate to this. I’ve been insulin sensitive for most of my life…able to eat ice cream and cookies in lieu of real food at meals and not gain an ounce. It wasn’t until I was in my 40s that I started gaining weight.
Second, I thought the fat storage process was insulin’s job as it tries lower BG levels to maintain homeostasis. Even if our insulin and cell receptors are behaving properly, constantly high BG levels means insulin is constantly at work and shoving energy into fat cells.
LOL, well said.
I’d have to agree, If it’s the same thing every day it’s not intermittent, that would defy the definition of the word. I always hate when people say their doing an “extended” fast and it’s a 24/48hr one. To me you gotta hit at LEAST 4-5 days to say that. Sadly nothing official about the terms.
I made it until my late 20s. Some people go ‘forever.’ There is a genetic component to how well we maintain insulin sensitivity, and the amounts of high-glycemic index foods (rather than just their presence in one’s diet) matters a lot too. Pizza is one thing. Two large pizzas at one sitting (me) is another. Ice cream, yeah. A half gallon or 3 quarts of ice cream in an evening; another matter.
For sure. Constantly high BG levels mean something is already screwed up, though. To an extent, insulin is then trying to work, and trying and trying…
I think you are implying that its hyperinsulinaemia rather than IR which causes the problems I think its Ben Bikman who says the same thing.
Hurray someone agrees with me.
Coincidentally, I just watched my first Benjamin Bikman video yesterday (The relevance of dietary protein). I’m definitely going to have to look up more of his work.
This does make sense - especially early on. There need not be insulin resistance.
Hyperinsulinaemia doesn’t usually develop ‘in a vacuum’ though. Just eating too much, too often, too high a percentage of carbs - kicks it off, and then it can be a vicious cycle - high insulin diverting more energy into storage, leaving the person hungrier, likely eating more, stimulating even more insulin. If by “problems” we mean weight gain/obesity, it’s not just high insulin that is doing it.
Likewise, the high insulin/insulin resistance thing seems very self-reinforcing to me, in essence two sides of the same coin - persistently high insulin causes insulin resistance, causing even higher insulin secretion…
Certainly there are other things that can influence obesity like genetics, cortisol and leptin reistance to name a few, but aren’t those things just triggers for spiking insulin directly or spiking BG which leads to spiking insulin? I mean how else is possible to add fat without the fat storage hormone being involved? I’m not disputing, I am truly curious.
It’s definitely a vicious cycle.
I’m really not disputing, much, either, believe it or not… I think the differences may just be in approaching things in slightly different ways.
It’s certainly involved - look at Type 1 diabetics before they knew to add insulin - most simply could not gain weight or even avoid emaciation, no matter what…
But insulin is rarely just going to start going high “by itself.” Most of the time, I do see it as going hand-in-hand with developing insulin resistance. Especially as pertains to longer-duration high insulin levels, rather than to ‘spikes’ that occur in response to diet, high insulin results from the pancreas secreting more of it, since the body’s cells aren’t responding well to earlier insulin releases. The body is freaking out over high blood sugar levels and continues trying to lower them.
Going back to the “Why am I fat?” question - high insulin need not be involved. If one eats more than they burn, it’s gonna happen, even with perfect insulin sensitivity and normal insulin levels. The body’s cells are nourished, the liver and muscles have their fill of glycogen, so into fat-storage mode we go.
Despite the over-generalized title of the video, there is a ton of good information in this deal from Chris Masterjohn. Why Insulin Doesn’t Make Us Fat – it’s really not so simple as that, but he does a good job covering the bases and I like the explanation: Although insulin promotes storage of fat in adipose tissue, this occurs in the context of multiple layers of regulation where energy balance is the final determinant of how much fat we store.
Excellent point. Superficially, this makes us look fat but if glycogen is basically carbon, water and oxygen stored in the muscles and liver, it isn’t actual fat but certainly contributes to gaining weight. I’m still struggling to take this in context with my 20s and 30s when I would eat insane amounts of calories and literally not gain a pound. For sure it can be argued that the energy has to go somewhere and for me I am pretty sure the excess was flushed down the commode. I had been told by more than one person that my needing to take two or three craps per day was highly unusual.
Alas it is late here but I will definitely take a look at the video Doug. Thanks for it and your thoughts.
It is actual fat, though - the body has its fill of glycogen and goes into fat-storage mode - we get triglycerides from food and our liver also makes it - the liver sends triglycerides to fat cells for storage (our stored fat is triglycerides).
It was the same for me, Carl. Even when I was gaining weight, it was 5 lbs per year, when I had many weeks where I should have gained that much, just looking at caloric intake. Increased metabolism is one factor - I tended to run ‘hot’ and I picture the body being as free with energy as it can be, rather than trying to conserve. This probably does not go very far, however, as far as offsetting such a huge caloric surplus.
Waste - stuff not being absorbed - I agree that this must be a large thing.
Around 50 hours for the total time from eating to elimination? Time to go through just the large intestine and colon averaging 40 hours, with men at 33 hours and women at 47?
That seems very high, to me. I’m used to it being “the next day” fairly uniformly, and faster sometimes. I’ll go days without eating any really hot, peppery stuff, and then do it. Often it’s 14 to 16 hours later and I know, without question, that it’s made it all the way through.
I do think that for almost all of us, trouble begins with just plain “eating too much.” A positive energy balance is what kicks off the vicious cycles.
Eat more than we burn (positive energy balance) --> Over a long time --> Increases liver fat --> Increases liver insulin resistance (but not muscle IR, different thing there) --> Slowly increases insulin secretion in the pancreas as the body seeks to normalize liver function --> Higher insulin increases fat formation in the liver and we have one vicious cycle at work.
2nd cycle = Over time, liver fat increases until it starts to enter the bloodstream as VLDL and triglycerides --> The fat goes all over the body, with different parts varying in their uptake and accumulation --> The pancreas readily takes up some of this fat --> This reduces the beta cells’ ability to produce insulin --> Higher blood sugar --> Further increased demand for insulin from the pancreas and another vicious cycle in place.
Pretty grim stuff, but it’s not hard to break the cycles.
1.) Eat less. Especially, eat less carbohydrates - the liver makes triglycerides from them more readily than from protein or ingested fat.
2.) Eat less often. “Normal liver function” includes storing glucose as glycogen after we eat, to be used later on. Between meals and when sleeping, the liver reverses course, goes into glycogenolysis and makes glucose for the body’s needs. Spend enough time in the “unfed” state and liver fat accumulation and a vicious cycle is prevented.
3.) Eat a ketogenic diet. The liver storing glucose or manufacturing it is regulated by insulin and glucagon. That video you mentioned - Dr. Benjamin Bikman - ‘Insulin vs. Glucagon: The relevance of dietary protein’ - is the single most eye-opening one I’ve ever seen. The difference between eating a S.A.D. diet and a ketogenic one is not just substantial, in some respects, it is astounding.
Well, yes, because hyperinsulinaemia causes insulin resistance.
What? It’s the insulin level that determines whether the fat tissue stores or releases fat. This is why people have gotten fat on a calorically inadequate, but high-carbohydrate intake. The blocking effect of insulin on leptin in the hypothalamus keeps hunger up, thus stimulating further intake, and eventually tipping the energy balance. Energy balance isn’t the cause, it’s the effect. This is endocrinology 101.
But of course, I got fat because I ate too much and didn’t exercise enough. My fault!