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Saturated fats and type 2

kokhongw said:
Just for completeness, this is their views on Ketones...
https://www.masteringdiabetes.org/what-are-ketones/



Good for all to learn to separate the wheat from the chaff...
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Their list of adverse symptoms 'caused' by low carb diets reads just like my heart med, and my PPI med, and several form part of the watch list for my diabetes meds too. Living and breathing can also cause most of these problems, I note that many of the referenced studies were indeed carried out and ascribed to the Seventh Day Adventists. I note ADVENT 2 is one of them.
 
Guzzler said:
Per Seventh Dayers, the Bible contradicts itself right left and centre, it is the ultimate cherry picking source.
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Having spoken with Mormons recently regarding LC diets and Diabetes, I note that although not the same as the Adventists, these folk do indeed like to follow a clean living lifestyle. They favour vegetarianism, but do not mandate it for their followers.

What interests me is that if they have many followers doing whole plant diets, then there should be evidence of them living till old age gracefully, How come then in this country we only see young mormons? Or is that just me being selective in my observations? (tongue firmly in cheek)
 
I've learnt something new. Learnt where the source of saturated fats cause insulin resistance and diabetes, to reverse it by plant based diet, which people have spouted nonsense. Now I know now why I can contradict this. No idea why people belI've this nonsense. It's amazing how who do not have access to fresh foods only saturated fats do not develop diabetes. develop T2 and heart disease through processed foods
 
bulkbiker said:
And of course none of them will ever stand a chance of developing Type 2....
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Maybe the Higher Authority steps in to punish their sins by bringing down a plague or two? It is a condition that unfortunaltely seems to disregard religious beliefs and strikes mercilessly and they do not seem to be immune in any special way. Anyway the leaders I spoke to took the LCHF message with them when they left mine humble abode.
 

Fats around the liver/pancreas do inhibit insulin production. But it is debatable whether it kills pancreas....

Unfortunate that Dr Roy Taylor studies shy away from measuring ketones or consider absolute water fasting as comparison to a 3 month long 800 calorie diet. I wonder why the fixation with 800 calories...

It was already observed in 1966 that in extended 14 day fast, "the glucose tolerance test approached normal".
https://pmj.bmj.com/content/postgradmedj/44/507/58.full.pdf




And fasting up to 200+ days are not unheard of...
https://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S0140673666929254/first-page-pdf

 

They are simply propagating their religious conviction. Nothing more. Nothing less. They will not change their mind irregardless of the evidence before them.

So flatline glucose and meat based ketogenic diets are dangerous.
 
The first study is a submission for a postgraduate Doctorate, so is not necessarily a bone fide rigorous study but merely a thesis submission. Thus it may be safer to downgrade the importance of the findings. The fasting occurred, but was then followed by a prolonged restricted calorie diet for some time, so in fact does much what the Newcastle Diet study did, but preceded it with a fast to get the bgl down quickly. It is not clear when the OGTT was performed, or how often. It is also not clear what type of diabetes the 3 patients suffered from, or what their HbA1c did before or after the fast, No attempt made to measure insulin or c-peptide levels so no clues there either. There were only 3 diabetic subjects so n=3 in 46. Presume they were on insulin before the trial, but when did they stop needing insulin? seems to imply they were T2D if they were able to stop but this is not stated anywhere.

This is. I think, a poor quality observational study, and its conclusions are not IMO reliable,

Edit to add: I see that the subjects are noted as experiencing euphoria, i.e. light headedness, which I believe shows a potentially dangerous malnutrition condition if prolonged. It is probably the entry into ketosis, but if they were insulin dependant, then this needed to be monitored carefully - the report does not give this impression.
 
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Oldvatr said:
This is. I think, a poor quality observational study, and its conclusions are not IMO reliable,
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It may well be...except that fifty years on...Dr Jason Fung has much success with his fasting protocol.
http://casereports.bmj.com/content/2018/bcr-2017-221854.full

Fifty years later...if big food and pharma continue with their high successful marketing and evidence suppression/misdirection...we may still look back and discard these case studies as poor quality observational studies rather than extracting nuggets of truth and value from these experiences.
 
Many years ago some of our ancestors experimented with eating animal products, and demonstrated that one could live quite happily and healthily on a carnivorous diet. They documented it (on cave walls) and these were set in stone. Many millenia later we are being told that eating animals is WRONGGGGG and so unhealthy, and many believe this to be true, The exponents of this new thinking have impressive credentials, and carry institutional weight too from the universities anf governments, So we need to look at all the evidence from both sides of the divide to decipher the good evidence from the bad.

So when someone uses the term MD or Dr to imply authority, it is helpful to know if this is a genuine medical certificate, or an agricultural or vetinarian qualification. In the case we have here, I was pointing out that the authors were postgraduate students, and that this report may not be properly peer reviewed or tested.

I too follow Jason Fung, and believe his principles to be valid, but this does not stop me from querying and questioning the evidence I see presented before me as 'proof' for a theory or hypothesis. It is even more important in these days of Fake News and evidence massaging. Anyone can postulate a new theory and publish it in the media and indeed many times here we see things presented as fact to the Forum, only to discover that it is merely someone's opinion or blog. As a scientist I care not if it is in the headlines or number one in the viral charts, I care that someone takes it and tests it then someone else analyses and repeats the tests to show it is a valid repeatable result, Then it becomes more than urban myth and magic.

So Ancel Keys put forward his thoughts on the role of fat in diet, no one seems to have questioned it or tested at the time, but recently it has been reviewed again, and found to not carry the weight it should when being used as the yardstick for public health, We here are apparently paying the price for that blind acceptance as 'fact'. There are now RCT studies and trials being conducted around the world to provide the evidence so even though I currently believe the opposite to Keys, I may be proven wrong in time too.
 
By low carbing and high fat diet, forces the body to burn fat as fuel. The body starts using the internal fats, the fat around the organs and the liver. This increases insulin sensitivity. People having a high carb diet, if its not burnt off it turns to fat, once all the fat cells have been used then it lays fat around the organs and liver. It's not saturated fats per Se which causes diabetes, neither is the calorie intake. It's what actual foods and activity, It's the highly processed foods which are high in both carbohydrates and fats or non processed food but eating both carbs and fats together. I think its high carbohydrate diet which is the problem.
 
"He doesn't say anything about saturated fat being causal for Type 2 diabetes." No, That was why I specifically took the trouble to point that out - if you read what I said!!! "This was not about the type of fat that people were eating but the fat they were wearing. It was also about overfeeding rather than saturated fat specifically."
It was fat you wear, caused by "overfeeding", the word he uses, that he was talking about as causing the fat on the pancreas that kills the beta cells. He was talking about fat generally, not any particular type of fat. My point was that beta cells can be killed by fat in a living human, not just in a petri dish as you claimed. Taylor says that fat on the pancreas kills and damages beta cells and therefore (in combination with the genetic contribution of course) is the cause of T2. And that if you lose the fat on the pancreas and the liver that feeds it you can reverse your T2 for as long as you keep that fat off.
As to what Prof Taylor says you might be less confused if you tried reading some of his articles :
http://www.ncl.ac.uk/press/articles/archive/2017/09/type2diabetesisreversible/
http://care.diabetesjournals.org/content/36/4/1047

https://www.sciencedaily.com/releases/2016/03/160322080542.htm:

https://www.sciencedaily.com/releases/2015/12/151201141231.htm
 
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"He doesn't say anything about saturated fat being causal for Type 2 diabetes."

Well I have to say I lost an awful lot of fat by eating far less carbs but carried on eating meat and upped fats though I did also restrict calories as well does the prof say what is the origin of this excess fat and don't lose sight of the fact that this thread is about saturated fats not any old fats as stated in the opening post " saturated fats are the direct cause of type 2 diabetes"
 
Tannith said:
Taylor says that fat on the pancreas kills and damages beta cells and therefore (in combination with the genetic contribution of course) is the cause of T2.
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No he doesn't... he says that it impairs the function of the pancreas and liver.. he cannot possibly know that it "kills off the beta cells" as its not currently possible to test or see that except in the case of Type 1's where they just cease to function completely. The quote I gave was from your hero himself.
 
I do not fully agree with Taylor that his study proves that abdominal fat around the liver and pancreas kills beta cells. I think all he has demonstrated is that reducing adipose fat leads to a reduction of Insulin Resistance, which is a symptom of T2D (not necessarily beta cell extinction). Endocrinologists have for years shown that the number of beta cells in the body is determined at birth, and is one of the few cells in the body that is not created as required (such as adipose fat cells that can be created from stem cells, and once created cannot be removed or reprogrammed. All we can do is empty them, but they never go away while we live. If beta cells could be created then T1D would have a better chance of finding a cure, but diet alone would not suffice.

Taylor managed with difficulty to observe and measure liver and pancreas mass, and determine that it was the fat that shrank following the diet. He did NOT measure beta cell mass, and as far as I can see, that measurement can only be done post mortem.

The effects of IR can be measured in vivo but that is not a confidence check on beta cell mass either, merely that they start working again. The fact that T2D can be reversed/ put into remission by diet is great news, but if beta cell death was being reversed, then that would indeed be counter current understanding of the endocrine system. Like any cell in the body the beta cell needs certain nutrients, and oxygen to survive, so maybe prolonged high levels of fat are choking the beta cells irreversibly, and this leads to insulin dependance T2D which is the progressive condition we recognise as end stage.

But fat stored in the adipose tissue is No Longer SAFA or satfat, since they do not travel well as lipids. No, SAFA's get broken down by metabolism before they enter the bloodstream. So the argument that Satfat causes T2D is not in itself true, but satfats do break down to give more lipids to transport and store. If we do not burn off the adipose fat, then that will lead to trouble in all sorts of ways. In essence, Low Calorie diets and exercise try to prevent fat buildup, and keto + exercise works to reduce the fat once stored. What Taylor demonstrates is that there is crossover possible between them. I suspect Fasting is also able to join in too.
 
In simplistic terms that I like, lipids in the plasma stream comprise of cholesterol bubbles containing various fatty acids. Now the fatty acids are stripped out of our dietary intake of oils and fats, and comprise Saturated Fatty Acid (SFA), Poly Unsaturated Fatty Acid(PUFA) and monounsaturated Fatty Acids (MUFA) Please be careful here, we are talking fragments of acid chains that have been stripped out of the diet, and NOT (repeat NOT) talking about dietary SAFA, PUFA, and MUFA as eaten. For example Coconut oil is a medium chain fat (MCT) that breaks down to give all variants of fatty acids. So our metabolism mixes and matches as it thinks we need in our bodies, and in normal people that seems to work well, but in some people it goes wrong. This is the added risk that diabetes carries, as does being obese.

Now here comes the entertainment
https://www.karger.com/Article/PDF/366324

This report,as I read it (and yes I did read it) shows that there are some fatty acids that lead to inflammation markers being increased, but many do not. Again, my warning here about SFA etc not being the same thing as eaten fats.

Now each of us is different, and my take on it is that variations in our metabolisms leads to fats being broken up in different ways, so some produce more inflammation than others even when eating the same food.

The real evil ones according to Greger et al is animal fats, which he classes as SAT FAT, but is actually a right royal mashup of all sorts of fatty acids, so not actually fully saturated. Olive Oil is almost pure saturated fat. So it is more likely that we are able to metabolise olive oil into the healthier chain acids, but the animal fat mixture breaks down into more of the harmful ones, Not sure on this and its above my pay grade, but thats MY theory,
 
"Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis "Prof Taylor. I have already given you the reference for this but obviously you didn't bother reading it before making rash and inaccurate statements about it.
 
Tannith said:
β-Cell loss appears to increase as duration of diabetes increases
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Appears being the operative word.. he's guessing.. the piece is full of likely and maybe.. he hasn't proved anything which is what you were implying or in fact reported that was what Prof Taylor said. As I said he says nothing of the sort. You really should not make unsubstantiated claims.
Anyway what's your latest HbA1c? Are you still doing well after your ND?
 

Following link at 66, they speak of amylin deposits. Little is known about these plaques but research into Alzheimer's Disease suggest that it may be the bodys way (at first) of protecting against apoptosis but that it gets out of hand.
 
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