T2 or NAFLD? ...or, a funny thing happened on the way to the surgery

[Tiggy63#]

Well done enjoyed reading all the issues you raised in your post

 

[Chris24Main]

Wow - if you've just gotten through 38 pages of my rambling prose, I would have to say the same..!!

 

[Chris24Main]

Given that one of my key goals in this thread (and that this thread is supposed to be at heart a "warts and all" record of my attempt to uncover answers) is to get to the bottom of what insulin resistance is.. there is one aspect of it that I want to just poke at.

It's something that does come up time and again, but cards on the table, this particular thought arose from an interview by Jordan Peterson and Ben Bikman. It was the first time I'd seen Peterson interview anyone, he's not usually my cup of tea, but I wanted to see how that conversation developed, and anyway; it's good to take in views that don't directly align with ones you already have, at least some of the time. Anyway, I only mention to give full transparency; this has no bearing on the detail of that conversation.

We - because of course we do.. tend to hold in our minds, a scope of what insulin is and what it does.
For Type ones, it's the thing we inject to stay alive, and you match it to the carbs you eat.
For Type twos, it may also be part of the medication milieu, or something you know that at some point you may end up taking, or not long ago, it was the primary med. So - clearly it plays a role in reducing blood glucose.

So - that builds up an idea that insulin is something that meekly gets into the blood stream and reduces blood glucose.

And - it does do that, but we should also - all the time - be aware that insulin (that humble hormone from the pancreas) is the master regulator of energy throughout the body - there isn't a single cell in the whole body that exists without a receptor for insulin - so insulin affects every single cell, and has more than one hundred different functions.

For example, in ovarian cells, insulin is responsible for converting testosterone into oestradiol (more commonly referred to as estrogen, but really the most common of the estrogens in women). Even more precisely, it inhibits that transformation, so if insulin is high, less estrogen is being generated than there should be. That effect is amplified, the higher the level of insulin.

So - to get to the point - there are two sides to insulin resistance. Some cells become "blind" to insulin, but insulin is also high at the same time, and other cells do not get blinded - so they go into an accelerated state - whatever their particular function is.

This is why it's so tricky to get a grip on what insulin resistance is, and why it's so impactful on so many health conditions - it isn't that we become less able to use insulin to bring down blood glucose -

- well, it is, but even that is only a tiny part of the total disruption of the fat and glucose (energy) regulation that insulin sits on top of, but at the same time, other cells and organs; it's like someone has their foot stuck down on the gas pedal.

Another example (and I apologise for both examples being totally female centric, maybe as an encore I can go into erectile dysfunction) - breast tissue. The connection between insulin and pregnancy is pretty clear, so one of the things that happens with breast tissue, is that it should (from an evolutionary demand perspective) draw in more sugar to build into milk. Obvious, right? - so when insulin is high, that leads directly to breast tissue cells developing many more glucose transport ports - the cells literally become more greedy for glucose; and that leads to them simply having too much sugar energy in the cells themselves - an excess of energy that can overwhelm the mitochondria, and which may explain the strong association with breast cancer. Note that I say may, but reading through Thomas Seyfreid, he goes much further, and the statistical association is very strong.
https://aacrjournals.org/cebp/article/11/11/1361/166673/Fasting-Glucose-Is-a-Risk-Factor-For-Breast (just picking one at random for the sake of holding myself to the rule on providing a reference anything which is outside my own experience)

The key thing is that we limit our thinking to what insulin is doing or not doing to bring down our blood glucose - that isn't it's job - if we live in a way that keeps insulin high, it takes a wrecking ball to a whole bunch of other things throughout our body.

 

[Chris24Main]

So - I learned about Cholecystokinin today - anyone interested?

Not a name that rolls of the keyboard - but it comes up a lot in the kind of stuff I listen to, so I thought I should dig into it.
Pronounced "colo - site-oh - kine - een" so it actually rolls off the tongue quite nicely, but not so easy to spell.

Anyway - it's a stomach hormone, primarily for regulating stomach acid, but of course does more than that, and when you zoom out a bit, I think it gives a little more insight into how we are specialised...

I suppose from O-level biology, I'd always thought of our digestive system as a stomach for digesting food, and then a long pipe coming off it that takes out the trash. It's much better to think of the stomach as "food triage", or as a kind of holding bay for the start of digestion proper.

There is a whole thing about needing much longer intestines (or more stomachs) to fully digest some plant foods, but I'm not going there so much as - it's much more instructive to look at the portal vein;

I mean, look at that beauty!!

Or maybe not, but at least consider what's at the end of it - the portal vein takes up ... everything, from the stomach, the intestine, the pancreas, the kidneys - the entirety of the digestive system - and it isn't about makeing sure that these have adequate blood supply - it's about "porting" all of that blood output straight into the liver - so everything that goes on in processing food; your liver is the primary player.

We also (being diabetic) have some clue about foods that easily break down into sugar - we know that this goes straight to the liver (via the pancreas, where it's done all the insulin-stimulatin).

So - I'd heard the term cholecystokinin in the realms of satiety - along side the GLP-1 response, but the GLP-1 hormone is released in the lower intestine in response to fat - so what is cholecystokinin all about?

Well - it turns out that it's kind of a "nothing to see here, move along now" kind of hormone, for the stomach, if there is nothing for it to do..

Let me back up. There are quite a few emotional responses to food, most obviously you literally salivate, thinking about something nice to eat; well that's going on in multiple places - we just tend to notice it more when we dribble.

So, you're all primed for food, and you start to drop it into your stomach, which has also been busy preparing stomach acid to start to break down foods. But not all foods - mainly the foods that it can port directly to the liver. There is no point expending energy on moving stuff all around the intestine if it can go straight to the liver - that's where everything is going to end up anyway...

So, as we know, this applies to sugars, starches and shorter chain fatty acids. Everything else gets a dose of Pancreas digestive juices as it's dumped into the top of the intestines and away we go.

But - this is where cholecystokinin comes in - in response to fat and protein, it's stimulated, and dials back stomach acid and sends satiety signals to the brain, and sets up the intestines.

In other words, in a low-carb high-fat meal, it will tell the stomach to stand down - this is all going to need a full job through the rest of the system, and you can stop putting in more food now, we got this.

I'd noticed this effect sometimes in the morning - having a bullet-proof coffee. I can be quite hungry, and drinking that blended butter and coconut oil, I can feel ... nothing ... in the sense of food being in my "system" - yet, at the same time, I can feel that hunger dialing down to zero, almost in real time. It's pretty amazing, a single mug of coffee, and I'm not "full" - but I'm totally satisfied for hours. I think I now understand this to be the cholecystokinin effect.

 

[Chris24Main]

OK then - here is an attempt to dig into the split cause side of insulin resistance.
From listening to Ben Bikman a few times on this topic, it's finally sunk in that it's important - from the perspective of what you really need to understand if you want to be successful in the long term in reversing insulin resistance. (with the obvious caveat that all of this is only my regurgitation of the work of others, and represents only my opinion, and could be totally wrong, and certainly should not be taken as advice to do anything).

I've talked recently about needing to think of the effects of insulin resistance as being two things at once - both that the level of circulating insulin is too high, and at the same time, some tissues in the body (most obviously adipose tissue) become "deaf" to the effect of insulin, leading to this weird dual state, where some parts of the body speed up their insulin-driven processes, and some slow down - but it's all insulin resistance.

Well - that's on the "effect" side of the equation, but you also need to consider that on the "cause" side - there are two equally different things going on. Ben Bikman calls these "fast insulin resistance" and "slow insulin resistance".

It's not complicated to follow the mechanisms, but I think it's more intuitive to compare to something we should understand without going into cell biology. Decision and Habit. Anyone can make a decision and that will lead to a single outcome, but it takes making a decision over and over to form a habit. Eventually, once that habit has formed, you no longer need to consciously decide to do that initial thing - you just do it out of habit. Of course, you can form a habit just by doing the same thing over and over, there doesn't need to be a conscious decision at the start of it - but there does if you intend to turn the habit around. This is why the concept is so important (in my humble opinion) when it comes to attempting to reverse insulin resistance.

As opposed to dropping your blood glucose level once. You can probably see where this is going...

Anyway - that said, let's look at the things that cause fast insulin resistance:
1. High insulin
2. High inflammatory particles
3. High stress hormones
Now - how do we know this, and what can that tell us?
Cells, in a culture, in the lab can be stimulated with various chemicals, and the effects can be measured. So - a petri dish can be bathed in cytokines (the inflammatory particles which cells create as a kind of alarm signal for the body to send out the emergency services) and the cells can be observed to become resistant to the effect of insulin.

There are a couple of things to mention here. First - this is a lab, not a real body, but that does mean that lots of different stimuli can be tested, so that this can be discussed as real, direct evidence - it isn't necessary to talk about epidemiological studies and the difference between association and causation - inflammatory particles in high concentration will cause insulin resistance directly (with no other cause, and quickly) in fat storage cells.

The second thing to consider is - this isn't a body - but is it likely in a body? One stimulus that you may have heard of is that saturated fat will directly cause insulin resistance - and that is true - in that same petri dish, bathing the same cells in high concentration of saturated fat will cause the same cells to become insulin resistant. So - why is saturated fat not on that list above? The answer is that it just cannot happen in a real body - the entire digestive system is arranged to allow us to transport fat in a way that works given what can and cannot dissolve in blood (mainly water) - fat cannot dissolve in blood, therefore we have all these complicated transport particles called lipoproteins to do the job. A fat storage cell just cannot find itself surrounded by fat. But it can be surrounded by inflammatory particles, insulin or stress hormones.

On a side note, the mechanism also passes the smell test - if an organ, or body is stressed, or inflamed, it shouldn't want to continue growing normally (a process which consumes energy) - it should want to first relieve that stress or inflammation, so prioritises that energy - insulin being the master regulator of energy, it makes sense that the cells should quickly become "deaf" to insulin.

So - these three things can cause insulin resistance very quickly - but - and this is the important bit - that will reverse itself just as quickly if you take away the stimulus. That also makes sense - when the stress is gone, and balance restored, the body should go back to normal.

The confusing thing is the high insulin (why would insulin cause resistance to insulin?) - but only on first glance - it's also just a question of balance - if insulin is very high; it's the master regulator of energy and growth - so you will grow, but you can't just keep growing out of control, so there has to be a self-regulating aspect - that also just makes sense, the more you grow, the more you resist growing - that reaches balance, quickly insulin drops, and everything goes back to normal.

All of this so far is really just explaining what should happen - there is a response - and cells react quickly - and then things go back to normal. So; what's the problem?

Well, it's mainly about the first cause - insulin itself. If it's high too often, that leads to what is referred to as "slow insulin resistance" - where fat cells are being expected to keep swelling beyond what they want (this is called hypertrophy). They are able, biologically speaking, to grow to hundreds of times their original size, but if that needs to keep happening, then major structural changes need to occur around the cell (new blood vessels to keep the cell supplied, for example).

This is more like now, think about the difference between fixing a pothole in the road, and building a bypass. One may involve diverting traffic for an afternoon, the other can cause grief all around the area for months.

I'll leave it there - at that level of dumb analogy - but you should be able to see the interconnection between the fast and slow mechanisms, and also that not all of this relates to food - it's just more unusual for repeated high inflammation or stress to occur, day after day (though it does happen, and my own mother succumbed exactly to that, it's what Malignant Cushing's syndrome is). But what can lead to repeatedly high circulating insulin? Well, that one is simple, just follow the dietary guidelines that most of us grew up with - Three meals a day with snacks in between, and the majority of that from carbs.

Now - what happens to you will be unique to you, for all the reasons discussed in this thread and elsewhere, and there is still very strong belief in the "calories in - calories out" narrative leading to obesity and obesity leading to T2DM. I'm not so much interested in "which approach is the right one" - more than I am in - well, fast and slow insulin resistance makes sense to me, and makes sense of a person gradually putting on weight at a freakishly steady rate (try to calculate how difficult it would be to deliberately eat exactly the right amount of unneeded calories every day in order to put on the couple of pounds a year that so many people do like clockwork).

More importantly - for me at least, it points the way; and provides the motivation for sticking to an eating regime that aims to lower insulin, because if you do that you can start to unpick the Gordian knot of insulin resistance.

More than that - you can see why it isn't just about what you eat - you have to look at that whole list, and figure out what you can do to reduce inflammation more generally and stress hormones too. (though I can't help but point out that the same dietary guidelines will affect both - that feeling of being "hangry" is very much about stress hormones caused by the brain craving carbs, and there is nothing more pro-inflammatory than industrially processed seed oils).

 

[jjraak]

noticed this effect sometimes in the morning - having a bullet-proof coffee. I can be quite hungry, and drinking that blended butter and coconut oil, I can feel ... nothing ... in the sense of food being in my "system" - yet, at the same time, I can feel that hunger dialing down to zero, almost in real time. It's pretty amazing, a single mug of coffee, and I'm not "full" - but I'm totally satisfied for hours. I think I now understand this to be the cholecystokinin effect.

Interesting point @Chris24Main .

I dislike coffee but did try the bulletproof one .. disgusting to my tastes.

However I did find rather by accident a few Brazil nuts before work kept me satiated until lunch time.

I used to be rather amazed at intrepid explorers who entered the Amazon for instance & met tribesmen who could run for days hunting animals for food, who could sustain themselves on the journey with little more than a handful of berries & nuts...how on earth is that possible I used to think.

Now I know how.

Maybe it's time I revisited that bulletproof coffee.....mmhh


Interesting thread, thank you for posting

 

[Chris24Main]

So, maybe a lesson in humility overnight. I was only spouting on a couple of days ago that acid reflux was entirely caused by digestion of carbs in the stomach causing excessive stomach acid, so by cutting out carbs, you just can't get acid reflux, or even indigestion, and having suffered from some level of indigestion all my life, I've just had no discernible symptoms in the last year. Case closed.

Except that I had some indigestion over the weekend, and acid reflux last night. I had my "standard" meal of a couple of good quality burgers, air fried with a couple of slices of halloumi cheese, and a side of rocket, with a couple of teaspoons of clotted cream and 85% chocolate to finish, all before 8pm. So, according to the grand theory of everything, I should not have been up at 2am with acid reflux; yet there I was, feeling more humbled in the face of my own hubris than anything.

I'm pretty sure I have been fighting off an infection of some sort through the weekend (some other symptoms, and otherwise unexplainable high blood glucose on Saturday morning) and I have woken up this morning with very robust ketone levels, which may indicate that whatever it was, I'm beating it (figuring out infections when you don't get the same symptoms you expect is still confusing me, as smug as I'm sure that sounds - I'm still of the opinion that if you have a given inflammation response capability, then giving it less to do means that you have more available to deal with infection, so you shouldn't be aware of as much.)

So - the point of this post is simply to say - as much as I like to think that I have everything tied down and figured out - I was just as lost and confused by my body's response last night. Totally perplexed - my thought was that you shouldn't hold yourself to too high a standard - things have been going well for me, but you shouldn't become accustomed to it. Expect some dips, otherwise they can be discouraging when they inevitably happen.

For what it's worth - I was complaining a little at dinner time last night, and had made some tacos for the family, and had said that I couldn't stomach the taco mince myself - the truth was that the thought of it was making me feel nauseous. Not in an emotional way (I'm aware of how triggering that language can be) - in an "upset stomach" kind of way. So, I reverted to something I knew to be "safe". Maybe a better way of thinking might have been that my body was telling me that for whatever reason, I needed to allow my stomach to fully empty, and that the night time acid was simply a reaction to food in my stomach when my stomach just wanted to be left alone - after all the intermittent fasting I've done, I know without doubt that I can skip an evening meal with no consequence.

So - that's what I'm going to do today; just roll into a fast and see how that feels.

There is a lot of Noravirus going around, and there are all sorts of infections that can leave you with an upset stomach - if a viable strategy is simply to give your stomach a break and let it rest for a day; that might be an incredibly useful tool to have in the first aid toolbox - and totally free.

 

[Chris24Main]

Maybe it's time I revisited that bulletproof coffee.....mmhh

I have to admit that it took me several weeks before I actually tried something that seemed to be so antithetic to what coffee is to me - chuck a lump of butter in it and how can you call that coffee? I shudder at the idea of adding milk to a good coffee; but I do (or at least used to) enjoy a cappuccino, and my thought now is that properly frothed milk is really about using the steam to mechanically alter the structure of the protein strands in the milk, so how is that different to mechanically blending in milk that's just been churned a bit first.

I'd also say that having been raving about it for weeks now, I've had to dial back the butter a bit, and I'm experimenting with coffee with coconut oil alone - it tastes more of coffee, less rich, and just about as filling.. more experimentation needed.

 

[Chris24Main]

May be a strange thing to post here, but @AloeSvea - if you're happy to post here, I'd be really interested in your take as our resident Swede. No worries if not, I'm actually just trying not to derail another thread, but there is one thing that touches on my post about fast and slow insulin resistance that maybe you can shed some unique light on.

Sweden is unique (I think) in classifying T2DM according to the level of insulin resistance, and I sometimes wonder if this is just another way of making them seem different to the Danes (and I say that with respect and affection for both countries, each which I have personal connections to). Denmark has typically leaned more into the "fat is bad" narrative, and is also (co-incidentally?) the home of Novo-Novartis.

Anyway - this isn't a dig at pharma companies, I was just curious how, in Sweden, you might find your diagnosis of severe insulin resistant diabetes explained to you ...

It would seem to me, that thinking through the way that slow and fast insulin resistance works (in theory) would give a clue - the more it's about the acute state of the liver, the quicker it can be reversed; the more it's about long-term structural change to your adipose tissue, the longer it might take to reverse (though acting first on the liver would have to be step one).

There is a confounding point too, which has more to do with the amount of seed/ vegetable oils you have eaten over the long term. Anything we eat will be used as the starting point for building our body - that is totally non-controversial. If you eat a high proportion of poly-unsaturated fats (as we are all told to) - then these will be incorporated into our cell linings at that proportion.

This is relevant if you look at the historic proportion of the human diet that polyunsaturated fats represent.
It's difficult to be totally objective in this, but there is good evidence that the historic level of polyunsaturated fats in the human body has been less than 1% for most of the time humans have existed (don't forget that in all real food, fat is a mixture of types, and that we do need some unsaturated fat for our inflammatory system to function). Now, the recommended daily intake is that around 5-10% of calories should be polyunsaturated (and depending on how much ultra processed or even restaurant food you eat it could be much higher and still considered healthy) - so this inevitably means that the proportion of the structure of our cells which are made from unstable, unsaturated fats is higher than has ever been throughout human history. That is just fact - again, it's difficult to be objective and make any conclusion from that, but it simply has to be fact.

and - there has simply never (whatever you think of in relation to what "healthy fat" actually means) ever been any evidence that changing the proportion of fat in this way is a good thing for the human animal. And it's a significant change we're talking about.

So - the half-life of an adipose cell is around 2 years, which means that it takes a long time to re-build your cells with "more appropriate" fats.

Which - (and if this is correct, I can only say it makes sense to me, but what do I know) - if severe insulin resistance is a combination of long-term impairment of insulin sensitivity in the adipose tissue, complicated by inherent inflammation because of the structure of that adipose tissue... the solution is still to cut carbs, and replace with healthy fats (meaning saturated and mono-unsaturated, and with a mix of short-chain and medium-chain fatty acids) - focus on sleep and stress - but also keep out poly-unsaturated fats, doing whatever exercise you can with ketosis...

Because - one of the ways you can reverse the longer-term issue, is to become fat-adapted, allow your body to burn fat for fuel, and then mobilise those PUFAs and burn them. They won't burn as well (that gets even deeper into mitochondrial function and energy pathways, so I'll skip it) but they will burn.

That should significantly reduce the amount of time it takes to bring the ratios back to what they have been historically, and will lower the level of inflammation at the "whole body" level -

Win-win; no?

 

[Chris24Main]

I've just discovered something entirely new, and amazingly positive.

Some quick context - I'm trying to lean into the "fat isn't as bad as we've been taught" line of thought since day one, because it instinctively made sense to me, and because almost everything I started to learn reinforced it, but one of the underlying themes since has been "but, it's more complicated than you think" - fat does play a role in T2DM; just not the way you might think. Fat does play a role in heart disease, just not the way you might think. Much of this thread has been about trying to sort the chaff from the wheat (to use an oddly inappropriate metaphor - we know it's all chaff!!)

Anyway - you may have noticed that despite the above paragraph, I tend to use more specific language around "fat" - getting into not just saturation, what "Omega-3" actually means, short-chain fatty acids, how medium chain saturated fatty acids can be absorbed straight into the liver... that kind of thing... Well, it turns out that there is something really quite important about even versus odd lengths of saturated fatty acids (mainly, I think, because the body chops these down and thus the smallest end product must be different).

Anyway - there is a marvellous story involving trying to look after Dolphins, which gets to observing that a very specific type of fat (C15, meaning an odd chain of 15 carbon atoms in a fatty acid chain) looks really interesting relating to the health of a group of extremely well documented Dolphins, to looking at the ramifications for humans... to testing that end molecule against a bunch of diseases in the lab...

When I say that C15 activates AMPK and inhibits MTOR - all the nerds in the back will be fist-pumping as much as I did...

for the rest of you normal people... this is genuinely something to look into - this is maybe the biggest discovery of an essential nutrient, and why it has become lacking in our diet, and what the effect has been ... certainly, in decades.
I don't like posting links but google "discover C15" and you'll be there - the whole story is fascinating, but be warned that there is a pharmaceutical angle; and you will see C15 supplements soon enough.

The really good news (for those of us on a certain kind of diet) - is that as well as some fish (clearly, given the Dolphin connection) is that this amazing anti-inflammatory, anti-aging, glucose moderating, mitochondria-enhancing disease-protective and demonstrably safe molecule is highly available in full fat dairy, including cream and cheese.

The fact that it is both so demonstrably good for humans (study after study, it's really gotten quite the record) and is a saturated fat - may start to really swing the pendulum back to a sensible view on what fats are healthy.

 

[Chris24Main]

Really really quick one today - I'm reading a book by Dr Georgia Ede - a real gentle soul; a practicing psychiatrist, who came to question the role of diet on the world of mental health after some of her own experience led her to experiment. "Change your diet, change your mind"

It's just striking when you see the same things over and over, from different specialists ... she lays out the three big drivers of the progression of almost all mental health issues as;

1. Insulin resistance
2. Inflammation
3. Oxidative stress

Now, where have we seen that list before...?

So - I think we're on the right path in trying to figure out what these mean and how to combat them.

The really good news is - if all of this is correct, or even just a little bit correct, then reducing these three things by any means will have huge long-term effects on all sorts of aspects of physical and mental wellbeing - not simply getting blood glucose under control.

If that sounds a bit Pollyanna - it's worth repeating that the keto diet in its original form was invented as a (quite successful) treatment for epilepsy in children in the 1920s.

 

[Melgar]

That’s interesting @Chris24Main . I have recently seen research on ADHD and its association with inflammatory disorders, such as arthritis - Inflammation causing structural changes in the brain. There is an upcoming webinar by James Kustow on Thursday on the subject , entitled The Surprising Association Between ADHD and Inflammatory Disorders.
And here is a link to more research on this.

Inflammation, Anxiety, and Stress in Attention-Deficit/Hyperactivity Disorder - PMC

Attention-deficit/hyperactivity disorder (ADHD) is a prevalent and serious neurodevelopmental disorder characterized by symptoms of inattention and/or hyperactivity/impulsivity. Chronic and childhood stress is involved in ADHD development, and ADHD ...

pmc.ncbi.nlm.nih.gov

 

[Chris24Main]

Huge connection.
In the whole space - there is probably more progress going on in the treatment of mental disorders. Partly that's because it's where the keto diet comes from, but there is some speculation that it's been done in a way that doesn't threaten the drug companies...

... and I really don't mean to disparage drug companies ...

The thinking is that (you know, from the likes of bolshy upstarts like me) - you get a cry of "you don't need any of these drugs - just make these simple changes in your lifestyle and everything will be fine!!"

Of course - I'm not and never would say that, but it's pretty obvious that that is how it sounds a lot of the time, and you get drowned out by the combination of the conservative "you can't say that, it's dangerous - even if you say you feel healthier than you ever have" and the threatened "you can't say that, it threatens our profit margins, we're lawyering up, or sending conflicting information to the press, or sponsoring this research that proves that you are dead wrong, or paying this rather attractive person to be on our side"

or so on. Again, I'm not a conspiracist, I've just read the histories of this happening.. for much much longer than you would think.

Anyway - in the mental health space - it's much more "try the drugs first, and if they don`t work, and none of them work very well, then try this"

plus - it's really a whole other level of ketosis - where the kind of thing I'm doing is baby ketosis - ketosis as a treatment for mental pathology is more about flooding the brain with ketones on the assumption that they are just not getting sufficient energy from glucose any more for various reasons. Do that at the same time as take away the thing causing the inflammation, and you can have remarkable success stories - and there are lots of success stories.

 

[Chris24Main]

In other news - I had a bit of a revelation this morning making my bacon and eggs - about plant sterols.

Anyone been encouraged to take, like, yoghurt with plant sterols to lower cholesterol? - I have, and did - it sounded like a great idea, the "plant sterol" bit sounded sciency enough, and it did seem that it could lower your cholesterol (proven, even!), so I think I bought a bunch of Benecol, and quite liked it.

The revelation side of things - was that the penny dropped as to why it might not be such a good idea - file this under "things that cause insulin resistance that have nothing to do with carbs"

So - this is all a bit techy (fair warning) - but it's biology, not opinion. What actually happens in any given person is unique, so I'm not saying A therefore B for you... but the principle is sound.

ok?

Right then; you eat, or drink yoghurt with plant sterols in it. Plant sterols are the same kind of thing as cholesterol, in fact they are all sterols - and as an example form the basis for steroids (one of the many things that cholesterol is made into).

Your liver sees these - and says (with apologies for the kind of lazy personification I usually complain about) "right, here are some sterols, let's use them and make a little less ourselves, let's cut this shift short for a change" - generally speaking, you need much more in the way of cholesterol than anyone can eat - like 6 eggs worth a day.

This is primarily why plant sterols reduce "cholesterol" so efficiently - they out-compete them in effect. (ref Dr Malcolm Kendrick who has studied this for years, and I think in "The Clot Thickens" but I'm not 100% - this is all from memory)

Now you have your circulating sterols - but a portion of them are plant sterols - quite similar, but not the same as the cholesterol you can only get from animal products, or make yourself.

One of the things (again, totally non-controversial) that cholesterol is used for is making up cell linings. Not exclusively, but just enough to get the right amount of flexibility - think of it as part of the mix of concrete to make sure it's not too brittle. This happens all over the body, including in the humble pancreas.

Now, we come back to that "it's pretty similar but not identical to cholesterol" problem-

You have areas on the cell lining of the beta cells in the pancreas (yes, those cells) that act as a kind of solid platform for insulin receptors - called, imaginatively enough - "insulin receptor cell islands" - (Ref Dr Paul Mason in a lecture given on this topic to "low carb down under")

and you can probably guess by now what I'm about to say - insulin receptors built on islands where there are too many plant sterols, simply don't function. It's like they are switched off (in fact, they are switched off - all of this of course only shown in lab cultures, but it was verifiable).

So - the cell becomes a little bit more blind to insulin because the receptor cannot be triggered - or in other words - insulin resistant.

It's an interesting thing to try to weigh up then, plant sterols are very definitely recommended to reduce cholesterol - and they will, and you may feel that's a good thing, I'm only talking biology here...
But you should be at least informed about the effect they can have directly on insulin resistance in the pancreas, and how much (as a T2 diabetic) you should want to encourage the very best for your pancreas.

 

[Outlier]

**** right @Chris24Main! Nursie, who is much nicer to me now than she was when I was first diagnosed, has suggested plant sterols, as she knows I am refusing statins. She says as all my other readings are A-OK, my cholesterol readings must be "familial". This is very big of her as I know she is under considerable pressure to get me on statins. She is also surprisingly supportive of my investigations into modern research on cholesterol. BUT as a woman, an old woman at that, I suspect "lowering" my blood cholesterol even with something like plant sterols, will actually do me no good at all. I am torn between conducting a short-term experiment on myself using plant sterols from an excellent source just to placate the box-ticking, and staying as I am. I'd love to see what difference they would make, but fear damage could be done, and if it ain't broke.......

So many thanks for describing what actually happens in the body when plant sterols are taken - it's made my mind up to leave well alone.

 

[IanBish]

I remember the GP suggesting I try plant sterols. My cholesterol came down a bit, but I remember saying that the reduction was artificial. I didn't know why, but your explanation makes sense.

 

[Chris24Main]

Maybe because we all might need a little positivity just now...

I was out on the river first thing this morning, it's a short stretch of river, and I go up and down on my paddleboard, so turning at the western-most end of the river, to come back downstream, I get the reveal of the sun in my face, and the promise of paddling with the current.

Anyway, this morning, the sun is very bright, but it's still minus 1 degrees, so there is a fine layer of mist over the surface, about a foot deep, and illuminated by the sunlight. As I turn, there is a duck, arcing down and in to land on the water.

In a slow, graceful curve, it drops through this mist, which parts and leaves a perfect duck-sized wake, but through the air - it's difficult to capture with words, but it was so beautiful, it brought tears to my eyes.

I had to just stop and take it all in.

 

[Melgar]

Sounds lovely @Chris24Main. I love to see the mist. We have it form in cloud like formations just above the forests, we call it dragons breath. I do miss the mist that firms over the water. I had a lakeside property in Quebec. The mist would form, Loons would call out in that haunting sound they make to each other when the mating pairs drift apart in the night, then start calling back to each other.

 

[Melgar]

@Chris24Main Would I be right in thinking that plant Sterols interfere with beta cell insulin receptors, which are by their very nature extremely sensitive to minute rises in blood sugar. If I recall correctly they are positioned close to capillaries so they can detect slight variances in blood sugars in the blood. Am I also right in thinking that as these Sterols attach themselves to insulin receptors, effectively dulling their glucose sensitivity, making the beta cell mass as a whole insensitive to fluctuations in blood sugars, and impeding the proper function of the pancreas in keeping blood sugars in homeostasis, a form if insulin resistance ?

 

[Chris24Main]

Not quite - it's a lot more direct than that.
If I can use the term sterols (not accurate, but I'm invoking that plant and animal sterols are processed the same in the liver, so .. sterols) - these are waxy - this is their purpose in a cellular structure perspective - they are waxy where fatty acids are gooey, so you need the right mix to make firm but flexible cell membranes.

So- sterols are packaged up in the liver and transported around the body in lipoprotiens - they have to be delivered to cells, because lumps of wax cannot dissolve in blood - this is why lipoproteins contain triglycerides and cholesterol.

After most of the triglycerides are delivered, the lipoprotein is small, contains mainly cholesterol - and is called an LDL.
If a given cell needs some cholesterol (all cells do, and most can produce their own) - it hangs up an LDL receptor
That allows a passing LDL to come in, deliver its cholesterol, and the LDL is consumed in the process.

All of which to say that there is a really complicated delivery mechanism (this is the simple version) - in fact the level of LDL particles the liver makes is related to the number of LDL receptors expressed - ie, the numbed of LDL particles is related directly to the need for cholesterol (I'll just let that one sink in for a second)..

So - the cell has it's cholesterol molecule and does something with it. In this scenario, the cholesterol molecule is like a tub of putty, and cell is the size of the entire town. There are a bunch of things it can be used for, including the cell lining.

On the cell lining - think the town boundary... there are firmer patches made of much more cholesterol, so that they are firm enough to build something specific on - now think foundations for a border post. That border post is the insulin receptor.

Except the border post never opens, because the building is judged unsafe, because the wrong material was used in the foundation.

So - yes plant sterols interfere with insulin receptors, but not in the sense that they interact - it's that insulin receptors built on platforms made with plant sterols do not function properly.