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

[Chris24Main]

Could it possibly be that there is a corner of the internet where friendly discussion can take place?

I hope so - If I come across as thinking that I know anything, I don't feel it. All of this is fiendishly complicated, and I find that trying to explain a thing is the best way to learn how little you know about it.

And lots of topics all of a sudden..

On whether the link between saturated fat and heart disease has ever been proven; I'll choose my words carefully. The most obvious point is that in 2006, the biggest study of it's kind - the Women's Health Initiative, set out to do exactly that (partly because of this ongoing argument) - and concluded quite the reverse. "The diet had no significant effects on incidence of CHD"

More broadly - it's a difficult thing to prove. In most of science, you forward a hypothesis, then try to dis-prove it - if you repeatedly cannot, then it's likely to be true, but if you disprove it once, it's false. It really is true to say that no study has proven a causal link.. there are many that appear to do so... but you can (and I have, and there are many sources that will go through a history of all studies done) see that there is a history of trying to 'show' the right data to make the case, not try to disprove.

The most glaring example is the famous seven country study, that shows quite a striking connection between levels of heart disease and consumption of saturated fat. Really conclusive, to the point that you can only agree with the 'this is a known thing' perspective. Except, inconveniently, if you know that at the time, data for 23 countries existed, and if you plot them all, the full picture proves absolutely nothing.

So - especially when you understand that even the initial trial results that underpin all of this, published by Ancel Keys, were careful to state that this was an association, not a proof, and further that when you realise that people involved in those studies went back after the event and showed that sugar consumption was a better statistical fit to the data.... it really is factually correct to say that the link between saturated fat and heart disease is still an unproven working hypothesis.

@HairySmurf - I congratulate you on hitting your weight goal - bravo. I am also prescribed Statins, and this is very much a bone of contention with my GP, because I stopped taking them. I kind of feel like Pfizer are quite happy for us to all take moderate to high levels of statins and then eat what we like, but I'm not sure it's a very good plan.

The main problem with Statins is that they require the saturated fat hypothesis to be true, and if it isn't, then there are well studied risks.. most obviously about an equal risk of developing Diabetes (statistically compared to the benefit in terms of reduced risk of CHD). And a 1 in 20 risk of muscle problems, and a long list of additional risks. I would point you at Dr Malcolm Kendrick on that one...

I dropped in to his blog to see if there was any link to the 'Rice Diet' - which I agree on the face looks interesting (at least within the confines of what you could get away with in 1937) - and his comment was simply, "Let us see if anyone else can replicate this work." - which says it better than I can.

I don't think I have a problem with the study that shows an increase in LDL receptors with increased fat consumption of any kind; that would be totally normal. The problem is the assumption that it's a bad thing... Every cell needs Cholesterol to function, and LDL receptors are what trigger LDL particles to engage with the cells, and drop off their load of Cholesterol - they are only transport vessels for that purpose. But they are constructed in the Liver. The lower intestine will create Chylomicrons from dietary fat. Plus, the Cholesterol present in them is different from then crystalline Cholesterol present in blood clots that become Plaque.

 

[Chris24Main]

I guess I have a different starting point - it almost feels like whatever I do will be better than what I've done before.

The long-term implications of my choices is something that enters my mind on a fairly regular basis. Like yourself, I often tend to end up with a conclusion that no one really knows, and then hoping that if I'm doing something really harmful to my self my body will let me know sooner rather than later and that I just need to listen out.

@Chris24Main - sorry to hijack your thread here. Really enjoyed reading about your journey and your passion for data and process - it almost sounded like I could have written this about me and my journey.

Not at all, I'm only another traveller...

 

[Outlier]

We do well always to bear in mind that today's "scientific fact" becomes tomorrow's "we used to think". And to remember that saying about "You can't serve God and Mammon". This Board is so good with bringing in different "facts" and giving them perspective.

 

[Antje77]

On whether the link between saturated fat and heart disease has ever been proven

Most of your thread goes way above my head, mainly because the subjects aren't of great interest to me, my personal money is on keeping my BG in a normal range and ignore all else, including risks from smoking and too much alcohol.

lower carbs, lower fats, lose weight, all good. I hit my weight loss target yesterday, and a problem I now face and a place where fact and fiction are mixed together, is around cholesterol and it's risks. The practical outcome of getting that wrong might be a stroke or a heart attack

It only takes some 6 months to a year to your next lipids test as a diabetic, and you might be pleasantly surprised.
I know I was, and I do not watch the types of fats I eat at all, bacon, mayonnaise, pork scratchings, butter all feature heavily in my diet.

But here's what happened to my lipids during the 7+ years of changing my diet from officially 'moderately healthy' to LCHF: https://www.diabetes.co.uk/forum/th...tion-book-recommendations.201616/post-2674018
I'm only N=1, but the theory of sat fats increasing HDL doesn't seem applicable to me.

 

[HairySmurf]

On whether the link between saturated fat and heart disease has ever been proven; I'll choose my words carefully. The most obvious point is that in 2006, the biggest study of it's kind - the Women's Health Initiative, set out to do exactly that (partly because of this ongoing argument) - and concluded quite the reverse. "The diet had no significant effects on incidence of CHD"

News to me, so I looked it up. That would be this Women's Health Initiative? - Link

If so, under 'Dietary Intake and CVD risk' on the page labelled #265 I see that the intervention aimed to limit total fat intake to 20% of calories in the diet. 'Reductions in both saturated and unsaturated fatty acids in the intervention group were equivalent'. Also - 'low density lipoprotein cholesterol was modestly lower in the intervention group'. So, not a study that set out to investigate saturated fat specifically, but one which showed a small change in LDL nonetheless, due to a small change in saturated fat perhaps? If that's the most obvious point, then I'm missing it. Counterpoint - this article, and the list of references at the end (some actual saturated fat studies): Link

I highly recommend watching the learned lipidologist to learn what an LDL receptor in the liver does. Marvel at how every cell in the human body can and does manufacture it's own cholesterol. Be shocked at the revelation that the body does not get it's cholesterol from the blood - very very little 'dropping off' of a load of cholesterol occurs for any useful purpose, except back at the liver, where the cholesterol is recycled or dumped into the intestine via bile acids. HDL is a disposal system for waste , excess cholesterol coming back from cells that don't need it and LDLs are a remnant of the structure of the delivery mechanism for fat in the body, VLDL particles ('triglycerides'). And no, ordinary cholesterol crystalizes, which is why waste cholesterol needs to be mopped up by HDL particles and rushed back to the liver for reuse or dumping, otherwise excess cholesterol crystalizes in cells and kills them.

Apologies for entering your thread - it was rude and obnoxious of me. It just makes me very angry that the 'best minds' of the low carb world are also often a source of what I see as dangerous medical misinformation.

 

[Chris24Main]

Thanks - I don't find it rude or obnoxious at all, @HairySmurf - honestly, the more we mere mortals question our own understanding, the better. I don't have any hold over 'the correct' way to think about anything. I will go through the lipidologist info, and I welcome your input, whether or not I agree.

I also did watch the video on the rice diet that you suggested, or at least up to the point that it talked about some of the subjects suing the guy for beating them physically. I actually think it was closer to a starvation regime than anything. The overwhelming medical view on diabetes before injectable insulin was developed, was that very severe dietary restriction was so obviously the only solution, that a study was not even worth the effort. I suppose the other thing I thought, but have no actual insight to was that this rice diet was aimed at reversing hypertension; there was no mention of diabetes, or what the effect of this diet was in those terms. But fundamentally, I'm not going to put much into a single study done so long ago that required the doctor to beat his patients...

Womens Health Initiative, yes - that's the study. The obvious point is the one that I highlighted - this is a massive study, and still ongoing, but to expand the point - (being whether saturated fat intake really has a bearing on expectation of heart disease ... that being the critical point since most diabetics die of heart disease, so in my mind you cannot separate one from the other) - I'll paste the full paragraph that I clipped:

levels of high-density lipoprotein cholesterol, triglycerides, glucose, and insulin did not significantly differ in the intervention vs comparison groups. The numbers who developed CHD, stroke, and CVD (annualized incidence rates) were 1000 (0.63%), 434 (0.28%), and 1357 (0.86%) in the intervention and 1549 (0.65%), 642 (0.27%), and 2088 (0.88%) in the comparison group. The diet had no significant effects on incidence of CHD (hazard ratio

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, 0.97; 95% confidence interval [CI], 0.90-1.06), stroke.

So - in my words, but this is referred to in several books that try (much better than I can) to lay out the reasons why the saturated fat hypothesis is both wrong and at the same time held to be true... the biggest, gold standard study that there has ever been in history set out to prove the link between saturated fat intake and risk of heart disease, and found no significant effect. Nothing so comprehensive, before or since, has ever been undertaken.

I totally, totally agree on the general idea that this subject is complicated... and honestly, I've only read maybe a dozen books in a four month period, so I'm definitely no expert on anything... but there is more detail behind what I typically post, I'm generally trying to simplify things, though I recognise that leaves me open to calls of dumbing down.

In some of what you are saying in your paragraph about Cholesterol, you are actually agreeing with me. Couple of points, I'm not sure what you mean by 'ordinary Colesterol' - there is only Cholesterol, and the majority of it is produced in the liver. I think we agree on that. Crystals of Cholesterol are interesting because they only appear in red blood cells - Cholesterol is really quite important, you make testosterone and oestrogen from it, for example.. But, yes, Chylomicrons and VLDL particles are transports for triglycerides and Cholesterol - I think we are agreeing on that, though I think you are saying that there is no Cholesterol in the blood. That is true on it's face, because Cholesterol is insoluble, but these transport particles travel through the blood, so that's what I mean - and as they drop off the triglycerides, they become smaller and eventually become LDL particles, with only Cholesterol.

When you are getting into HDL, and 'waste' recycling, I'm not sure if you realise you are describing part of the thrombogenic hypothesis - the very opposite of the saturated fat hypothesis.. essentially, this goes 'everything you have been told about fat and heart disease is wrong, there is a natural process of clotting to react to damage to the arterial lining called the endothelium, and if you overwhelm that by causing damage too often, by smoking, or having high blood glucose, or having blood cells shaped like sickles, you will end up with unstable plaques on top of other plaques, which will block the arteries, or break off and cause a stroke.'

In among that (fiendishly complicated) hypothesis, the generation of the initial blood clot in the arteries, is super interesting, and I could go on all day just about that, but suffice to say that a big part of the clot, is red blood cells (as it is on the skin when you get a clot) and that's why the presence of crystalline Cholesterol is interesting, because the Cholesterol inside LDL (or Chylomicron or VLDL) cannot crystallise - in other words, the Cholesterol that is observed in Plaques - which gave rise to the saturated fat hypothesis in the first place - simply cannot have come from LDL particles, whether or not you subscribe to the thrombogenic or saturated fat hypothesis.

And - then much of the rest of the discussion about Cholesterol and lipids and LDL and statins just falls away - the central thing that underpins "what we know to be true, that saturated fat causes heart disease" - firstly medical science has failed to prove that for about 70 years, and secondly, the Cholesterol that they saw, has nothing to do with the diet at all - it can only be from blood cells used in the clotting mechanism.

Incidentally, HDL particles are part of the clear up. Once the damage under a clot has been repaired (assuming a healthy and not overwhelmed repair system) - the liver wants it's valuable Cholesterol back - so HDLs bring them back. I don't see waste at all.

But - please expand. Lots of this makes me angry too, but not at you @HairySmurf - I'd just like to investigate what you see as dangerous misinformation, and see if there is any common ground... there should be much more that we agree on....

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[Chris24Main]

So I've dipped into the Artherosclerosis.org article that you refer to and can immediately tell that it's another "so - we know this to be true, let's gather some evidence to show it to be so" I mean, this isn't just my opinion, the initial paragraphs lay it out, and even get in some defense about how it's not on to disagree.

Fundamentally - it talks about the progressive nature of atherosclerosis - the build-up of plaque - the literal furring up of the arteries, due to the 'quality' of the dietary fat you consume.

Indigenous Inuit communities were studied alongside the initial work done on saturated fat - these people exist on whale blubber. They do not get heart disease. That by itself should be enough to disprove the saturated fat hypothesis - it simply cannot be true if these people do not get heart disease (and it's the most obvious example of many). However, the guy involved (forget his name) was pilloried, de-funded and essentially squeezed out of work.

and - if you do not accept the central premise, all the rest of it falls away -

But - keep it simple - this article - it's all about the 'quality' of fat eaten. In most diets, the majority of 'fat' that is stored in your body, came from Carbohydrates that you ate, that your liver turned into saturated fat (fatty acid chains in the form of Triglycerides that were packaged in very large density lipoproteins, all in the Liver; the liver only creates saturated fat).

All of the agonising about quality of fat (meaning - plant-based polyunsaturated is good) is nonsense. There is no point worrying about dietary fat - we need a broad range of fats, with the exception of plant or seed oils. I eat far more fat today than I've ever done in my life. I've always enjoyed food, but I'm having a bit of a revelation with the possibilities of cooking with fats - the 'French Paradox' is another big red BS flag pointing at the unlikeliness of the Saturated fat hypothesis being correct. I've never in my life found it so easy to manage my weight - and specifically my visceral fat.

And also - if you eat less Cholesterol - your liver will simply make more...

Finally - those same indigenous Inuit communities now all suffer from high rates of diabetes and heart disease - what happened ? they switched their diets to highly processed carb-laden food. Like the rest of us.

 

[Chris24Main]

I've had a skim through Anil Gupta's book. Very comprehensive (and hugely expensive, it's really a medical resource rather than a book for the masses).
Nothing I could see that I would object to.

One point that I keep meaning to make on the topic of insulin resistance and it's inherent complexity. There is a growing body of work that talks about this in the sense of "you're not getting it if you only think of insulin"..

Most control functions in the body have a balance to them, testosterone/ oestrogen, Adrenaline/ Cortisol, Omega-3/ Omega-6 .. and so on, and so it is with insulin and Glucagon.

Not going further than that, but there are some who talk about insulin not being the primary reaction to sugar, but the side effect of Glucagon, and this gives the whole question yet another angle.

Indeed - I caught something a while ago about there being a hope that the rDNA vaccine methods developed for Covid, could offer new drugs that could effect Glucagon, as a totally different way of addressing Diabetes as a process, rather than the symptom.. it's not quite making sense as I write, so don't take that as that I think this makes sense, it really is very confusing..

 

[Chris24Main]

@HairySmurf - could you please link to what you refer to here:
"I highly recommend watching the learned lipidologist to learn what an LDL receptor in the liver does"

I'd like to do that, but I'm not sure who you are referring to.

 

[Peanut234]

Oh, I had forgotten about Glucagon. So many jigsaw pieces...!

 

[HairySmurf]

So - in my words, but this is referred to in several books that try (much better than I can) to lay out the reasons why the saturated fat hypothesis is both wrong and at the same time held to be true... the biggest, gold standard study that there has ever been in history set out to prove the link between saturated fat intake and risk of heart disease, and found no significant effect. Nothing so comprehensive, before or since, has ever been undertaken.

The Rice Diet - the story is wild it has to be said. Nobody in their right mind would try an all carb diet these days - it will never be reproduced as an intervention. The guy had to beat people to get them to stick to the diet! The reason I give that as an example is because it was a prescribed, extreme high-carb intervention that resulted in weight loss and an improvement in diabetes. It goes against the idea that carbs lock-up fat in a Type 2 preventing weight loss due to high insulin levels, making fasting and a low-carb diet a necessity. I myself spent the first 3 months after diagnosis on a low fat, moderate carb weight-loss diet and lost 1Kg per week just fine. There was toast. Fruit. There were bagels. Pasta was eaten. I didn't feast on carbs, but I didn't restrict them very much either - I went straight at calorie counting and sticking as closely as possible to a familiar diet that I knew I could stick to to get weight loss happening at 1Kg per week as fast as I knew how - low carb experiments came much later. I've read an account on another forum of a person who went into remission using Slimming World - not exactly low-carb. That's not to say intermittent fasting and low-carb don't work for weight loss, I'm sure they're great, just that the logic that says it's the best way or the only way to lose weight as a Type 2 is flawed. Someone could try to disprove it properly and conclusively I suppose, but who would bother?

The study I referred to massive as it is (48835 participants) is not ongoing (though the wider Women's Health Initiative is) and did not intervene in saturated fat levels specifically - just examined a modest reduction in total fat. The change in saturated fat levels eaten in the intervention group was small (2.9% of energy intake) as was the change in LDL (0.09 mmol/L) and so CHD risk differences were indeed found to be non-significant. To study saturated fat you must test significantly different levels and measure results from those different levels - very hard to do in a massive study. A practical study like that requires controlled conditions, which often means small, and small often means accurate. You can't ethically ask tens of thousands of people to feast on red meat for six years (as an example), and it's extremely hard to get that many people to cut out red meat entirely.

To choose that study specifically, ignore the ones which actually focus on saturated fat, refer to it as 'massive, biggest of it's kind', and fail to mention that it doesn't even examine saturated fat as an objective is emblematic of bending over backwards to cherry-pick an impressive sounding bit of science to back up a dodgy claim. Several books do this you say? Do these books actually list all the available evidence to the contrary and offer detailed explanations on why all that evidence is invalid? Or do these books mostly list the science that agrees with the exciting selling point of the book with maybe an odd reference to an easily-attacked study from the 1970s? What about the 80s? The 90s? All the work that went on to try and test and explain the 70s stuff? All the work which an actual expert must read and understand to become an actual expert.

'The biggest, gold standard study that there has ever been in history set out to prove the link between saturated fat intake and risk of heart disease' which was actually a study on the effects of a moderately low-fat diet versus whatever is going on in the wild. It's stated objective was "To test the hypothesis that a dietary intervention, intended to be low in fat and high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk." In short - did the (primarily) cancer prevention diet we tested work for heart disease. The answer was no. The cancer prevention diet did not even attempt to control saturated fat specifically. Is the study actually described that way in these books you refer to? Surely the lie couldn't be that blatant.

 

[HairySmurf]

Indigenous Inuit communities were studied alongside the initial work done on saturated fat - these people exist on whale blubber. They do not get heart disease. That by itself should be enough to disprove the saturated fat hypothesis - it simply cannot be true if these people do not get heart disease (and it's the most obvious example of many). However, the guy involved (forget his name) was pilloried, de-funded and essentially squeezed out of work.

Finally - those same indigenous Inuit communities now all suffer from high rates of diabetes and heart disease - what happened ? they switched their diets to highly processed carb-laden food. Like the rest of us.

The Inuit have been eating mostly fat for a very long time - so much so that they have evolved to suit the diet - Link I'm going to guess that has something to do with it.

Incidentally, some people are basically immune to the effects of negative effects of high cholesterol. Nobody knows how exactly - presumably genetics.

The learned lipidologist videos are the Thomas Dayspring series - link here which includes links to the three YouTube videos - Link

 

[Chris24Main]

Great, thanks- I'll check that out and report back.

I could list my sources if you like - I'm trying to be as rounded as possible, considering sleep, stress, metabolism, inflammation, brain function and development, reasoning, as well as everything I can learn related to diabetes and Heart health (and of course wider implications for diabetics). It seems like you are suggesting I'm presenting or supporting a lie in some way; I'm not really sure and I don't want to put words in your mouth. But, if you think I have some kind of angle here other than attempting to make sense of the same things you are, please let me know directly. I'm not, (at least, I don't believe I am, but I'm as susceptible to bias as anyone).

The problem I have with your response above - there is this vague reason that this population have not conformed - is that there are simply too many of them through decades of literature (and again, I can list them if you want) - when it's much, much easier to go back to basics - right at the start, there wasn't an overwhelming consensus that saturated fat was the villain. Sugar was the suspect just as much, but Fat won the argument.

Sugar and carb intake (and the rise in the intake of seed oils) make sense of all the data I've seen.. whereas you have to tie yourself in knots to hold to the saturated fat hypothesis.
Actually, that's not complete - the best total explanation I've come across (and again, you really have to come back to heart disease rather than diabetes) is this - there are only 2 direct causes of heart disease that require nothing else - Sickle cell anaemia, and Lupus.
Absent that, you have a combination of Smoking, High blood sugar, Elevated stress hormones, and high blood pressure.

Anything else is an association.
Which means you can gather data, and make an argument, and people have been doing just that for decades. But for every positive piece of data, there is a compelling negative. So then it becomes a question of narrative and the power of a good story, which is where it got interesting for me.

And - more to try to address your challenge on fasting... I don't think anywhere I have said that calorie reduction isn't a possible treatment for T2DM - in fact before insulin, it was the only treatment. I think the rice diet was closer to a starvation diet, certainly it was a reduced calorie diet, regardless, I did that myself for 3 years - of course I accept that you can lose weight by reducing calories - and you have, and I did. But, the statistical reality is that most don't, or at least put it all back on. The fundamental thing I have a problem with is that in 77 the dietary guidelines (due to the increase in heart disease) were to increase Carbs and reduce saturated fat. Largely that happened, yet the rates of heart disease are still very high (the risk was mainly smoking which has reduced) and the rates of T2DM have skyrocketed.

For me, fasting works great, but it's never going to be for everyone, and I'm not pushing it. Also for me, as evidenced in the title of the thread, I started off thinking that I probably should have been diagnosed with non-alcoholic fatty liver in the first place; so my plan was to target the liver - and I think we agree that the liver amongst other things has a store of glycogen. Thus - I was convinced that rather than keep taking Metformin, I should regularly fast for what I reckoned was longer than the time it would take to use up that Glycogen, and have the liver turn some of the fat to glucose.

I can also say that this has produced staggering results (for me) in terms of my belly, that 3 years of very dedicated calorie restriction did not. But, your milage may vary, and my results do not invalidate yours - after all, we are all unique.

 

[Chris24Main]

Dr Thomas Dayspring is an excellent communicator, and clearly understands lipid transport (probably better than anyone I've heard or seen) and I instantly learned a couple of things, finally understand my Apo-A from Apo-B - and now understand the comment about all cells being able to synthesise Cholesterol. But nothing at all that I disagree with or that gave me pause for thought..

He is a lipidologist, and thus nothing that he was talking about is related to the absorption of carbs directly in the stomach and how the liver turns them into lipids - or the other issues surrounding carbs and sugars. That's not to say anything he said was wrong, but that it's not in conflict with focusing on reducing carbs as a treatment to a disease that's all about too much sugar.

Secondly, when it comes to Atherosclerosis in particular, I follow what he was saying, and get a lot of it, but this is by no means the consensus - Drs Malcolm Kendrick, Robert Cywes, Tim Noakes, Philip Ovadia.. and many others talk about this being a symptom view, and that the better way to think about it is that the sclerosis (formation of plaque) is not a process by itself (otherwise, you're back to the Inuit, and have they somehow evolved into super fat-resistant humans and back again) but as a response to damage to the Endothelium, caused by smoke particles, the glycation from excess glucose, stress hormones causing inflammation, and all of it under excess blood pressure (as opposed to veins where there is otherwise mysteriously no sclerosis with identical conditions).

Dayspring does cover this, but if it was just pressure, why is there never any plaque on any vein, and if the structure was different, why can you transplant veins into arteries (and why do they then start to develop plaque)

Malcolm Kendrick talks about this being the thrombogenic hypothesis, and it's not a new idea, in fact there was a company who produced a report in 1992 - "Pathologic triggers – new insights into cardiovascular risks". I can pass on the details, and I actually dug out a copy of the report, in support of a new drug that was aimed at platelets, ie helping to dial down the formation of clots - because repeated clotting led to Plaque formation. However, instead, the company decided it's future was much better served by not publishing that and instead pushing the new drug it had just acquired - Atorvastatin.

And it was right - Pfizer has made a ton of money with it.

But - as far as all the detail on lipid transport - totally agree with all of that... except where he gets a bit fuzzy about the starting point of atherosclerosis

I think I would have to ask - so we've developed this super amazing capability as a species to manufacture and transport these incredible collection of molecules back and forward through the body - but you're saying that they just go wrong and clog up half the blood vessels in our bodies? and nobody can explain why?

And one of the key points of contention (I suppose) is that Dayspring and others talk about stopping the Apo-B from getting through the endothelium to the arterial wall .. so all the measurement is aimed at making sure you reduce your Apo-B count (I know it's not, but let's call that 'bad Colestesterol' cause that ties with what people are told)... but other equally experienced doctors will say - look, it's simply impossible for that particle to blast through an endothelial cell - firstly it's like a ping pong ball compared to a blimp. Secondly, it can only enter the cell through the action of the LDL receptor, and thirdly, it's absorbed in the cell as part of the process.

Inflamed (or oxidised) LDL particles due to the instability of Phytosterols (back to seed oils ) causing damage to the endothelial cell itself, and causing it to curl up and expose part of the arterial wall that triggers an immune response and the clot formation cascade - thrombogenesis.. now that is surprisingly similar, but explainable, and works alongside the other things that can cause damage to those cells - smoke, glucose etc.. but if you are sold on the 'its only the lipids themselves' hypothesis, you still have to explain how you can get atherosclerosis with only the wrong shaped blood cells, and nothing wrong with your lipids.

And again - one of the uses that Cholesterol is put to, is in the cell boundary of red blood cells - and as crystals. (part of the physical structure of these unique cells) - while inside the Apo-B particle, the Cholesterol cannot be crystalline - it would kill the particle. But - the Plaques are full of red blood cells, and crystalline Cholesterol. So - even if everything he said was true (recognising he is a lipidologist now and not a cardiovascular surgeon, some of who's books I've read being among this group) there is still no link between the Cholesterol in the Plaque and in the LDL..

 

[Chris24Main]

See - the problem with the 'it must be evolution, stupid' argument - bearing in mind that at the very start of the 'Inuit metabolism revisited' report, there is this warning - "leading researchers and clinicians to warn that our understanding of the long term effects of very low carbohydrate intake is not sufficient to justify broader claims regarding optimal health effects" ... so that gives you some clue to what the report really wants to prove.

.. is that the guy who did the original study was so impressed that he took on the same diet, and lived totally happily on it for the rest of his life, even when he returned to the US - Did he experience an instant evolution?

And for how long do you suppose the rest of the human race throughout history managed to survive without a steady source of Carbohydrates...?

 

[Chris24Main]

I realise nobody asked, but here's a screenshot of the top of my book library - I haven't managed the Elon Musk biography yet, but everything else has been totally worth the time.

But - it should be clear from that that I'm not here selling anything...

Oh - and I should say - I'm a big audiobook listener, all of these are books that I read (why it's all non-fiction)

 

[TheSecretCarbAddict]

I love a good book recommendation or two... I need to pace myself, though, as I already have quite a few books waiting in my reading queues (diabetes, studies, work). I tend to do books in two passes, listen to audio book if I can (Audible/Spotify) at 1.5x speed while walking dog, and then, if I feel inspired, read it with my note taking appliances.

 

[Chris24Main]

Another audio booker... fantastic.. I'm not necessarily saying anyone else should read any of this, more that this is genuinely wide ranging thing for me..

Ironically (maybe) - if I had to recommend one of these above - it would be "Why we sleep" - that was a real life changer... has no bearing directly on Diabetes; but it's just extraordinary..

Love for you to expand on the 'note taking appliances' angle, by the way, - I'm a huge (like 10% of my iPad is full with) OneNote guy, and my second obsession at the moment is trying to decide which of the new iPads to upgrade to...

 

[TheSecretCarbAddict]

I like my fineliners and bullet journals when I'm analogue. When on my devices, I moved from OneNote to Obsidian, which manages all info as non-proprietary markdown files + allows me to geek out with automating my personal knowledge management (I'm a big fan of Second Brain and related methodologies).

I'm still trying to reconcile analogue with digital, have looked at remarkable 2, but haven't been sold on it 100%

 

[Chris24Main]

Interesting (at least for us, @TheSecretCarbAddict - I'll keep this short for anyone else...) I like the look of Obsidian, and Notion, and I actually use Scrivener for planning and writing long-form, but I got heavily into Evernote back in the day, and had to bail to OneNote... so I'm wary about straying off the path, and I'm heavily leaning on OneNote professionally, I help run a small company, and with OneNote, for example, we have 15 years of weekly meeting minutes in one file, all searchable, and I use multiple devices, and access my notes in Windows, Android and IOS, so I need bomb proof syncing and the same experience everywhere, and equally good for digital handwriting, typing and screen clipping - and OneNote is really the only option that ticks all those boxes. - I guess I've been paperless since about 2009 in various ways, but an iPad, a PaperLike screen and an Adonit Star (iPad pencil in the shape of a proper fountain pen) is the best solution to it all that I've come to.
I do find myself looking at the remarkable as well (and the Boox) - but remarkable (not being able to run OneNote) is probably not going to work for me.