Given that it's this odd period between Christmas and New Year, and we have an unusual amount of time, I wanted to get to the bottom of something that's been troubling me for a while - the Newcastle diet.
More specifically, why it is that the research underpinning this (and there is some resultant debate, even on this thread) still seems to point to something fundamental about fat intake and how it relates to the progression of T2DM. Is there a way of fitting this square peg in the round hole that is insulin resistance - more specifically, you can read some of the background on the Newcastle web page, and come away having never read the phrase "insulin resistance" - so why is this, and is there any common ground - the mechanism seems to be totally different...
So - firstly, let me say that I'm in no way "doubting" the clinical results that have been achieved by following the Newcastle meal replacement program. I don't personally think it's as effective as cutting carbs and intermittent fasting, but there is bound to be some confirmation bias on my part - I've never done the Newcastle thing, but I did have really great success following my own plan around fasting and lowering insulin through cutting carbs. No one plan is perfect for everyone, and if you understand the key principle of energy management - revolving around elevated insulin and sufficient energy - then reducing energy significantly should have similar effects - which is essentially what the treatment plan is. I'd love to see some comparison research between the two routes, but that doesn't exist. My personal opinion is that switching to a low carb eating regime, then reducing the frequency of fasting will be easier to maintain permanently than a 12-week crash diet followed by ... something ... (the "what to do following the 12 weeks is a little vague, but I assume that there is some support, though the phrase "you can go back to eating the things you like" does worry me).
Anyway - there are pros and cons, and there are some people that will gravitate to a 12-week plan, and have some success - fine. The more people helped the better.
But - what about the underlying mechanisms... why the focus on fat and the relative absence of focus on insulin resistance...?
So - there are bound to be many reasons for this, and I'm not party to all the facts - so some of this is clearly my opinion, but the more I learn, the more overlap I see - and it's kind of about the title of this thread - Fatty Liver.
From the background info: taken directly from the website (and understanding that this research was all done around 2008 ish..
"We now know that type 2 diabetes is caused by excess fat inside liver and pancreas"
Well - that's describing non-alcoholic fatty liver - so the theory is that NAFLD is a direct cause of T2DM -
Most of the newer research that focuses on Insulin resistance is just a little later - 2010 and onward, with the significant realisation that type 2 is characterised by Too much insulin - not too little- hyperinsulinemia leading to insulin resistance, leading to greater need of insulin - and so on. Could it be that the focus of the research just shifted to insulin, and that the Newcastle research which was so revolutionary in 2008 just seems behind now?
Additionally, the research in Newcastle seems to me to be really focusing on the point in the curve below (taken from their own published paper) where the fasting glucose jumps up - we would call that the point of beta-cell failure, where the pancreas can no longer keep up with the demand for increased insulin, so the insulin level drops, and blood glucose shoots up, leading to the classically diagnosable HbA1c reading we all know.
Again - no real controversy there, but if all the research you were doing was prior to the work on insulin resistance, you would be focused on - what is causing the problem in the pancreas?
Fair enough.
Also - from published paper in the introduction section:
"What is the basic nature of Type 2 diabetes? What causes it? It is associated with obesity, and both insulin resistance and a β cell defect are involved."
So - there is no attempt to discount the effect of insulin resistance here either - it looks like there should be significant overlap.
There then follows quite a complicated passage that goes into specific types of fat and talks about how they end up in the area around the liver and pancreas, and sets this out as "the twin cycle hypothesis":
Once again copy and pasting (I tend to avoid doing this, but I need to in this case - all from the Banting Memorial Lecture 2012.
"The twin cycle hypothesis postulates that chronic calorie excess leads to accumulation of liver fat with eventual spill over into the pancreas. These self-reinforcing cycles between liver and pancreas eventually cause metabolic inhibition of insulin secretion after meals and onset of hyperglycaemia."
So - if you are looking at the world through the lens of "calories are bad" and "failure of the pancreas" is the cause of T2DM - this sounds like it makes sense.
However - we also know that it isn't just about calories, and that the types of food we eat matter in the way that the body has to deal with them, and the hormonal response. Fat doesn't just "spill over" - indeed if fat could somehow "spill" - we would just die - we have incredibly complicated mechanisms for handling and transporting fat around the body - waving your hands and talking about "spilling over" - just doesn't cut it.
So - back to basics - fat digested in the intestine is packaged up into Chylomicrons and transported to the liver - I'll use a diagram to aviod explaining the entire thing.
The short version is that you can see two distinct routes - fat via Chylomicrons from the Gut, and then the Liver packaging up triglycerides (the actual "fat" bit) into VLDL which becomes LDL.
At the same time, excess carbs are ported straight into the liver via the hepatic artery, where the liver attempts to convert and store as glycogen or converts to fat, also packaging the resulting triglycerides into VLDL.
At the same time, any fructose or alcohol must be dealt with first by being metabolised by the liver into fat, and stored in the liver.
So - you may get the idea from all of this that I'm arguing against the Newcastle twin cycle hypothesis - but not really - I'm just saying that it's an over-simplification based on the prevailing narrative that fat is bad. When they talk about "a chronic calorie excess" - it's just the same as saying that we eat in a way that presents the liver with too much to do, and triggering the release of too much insulin, which causes all of the fat it deals with to have to be stored.
In a different eating regime, the person will simply find that they cannot keep eating (imagine now a plate of fatty meat, can you imagine carrying on eating beyond the point that you feel full?) - and any "calorie excess" will be turned into ketones which will be peed and breathed out - none of that happens in a high-insulin state, where everything must be converted to fat and stored.
That concept of fat "spilling over" into the pancreas, is more accurately a state of hypertrophy in the surrounding adipose tissue - or fat storage cells swelling up to accommodate the fat that the insulin is driving into them - directly causing insulin resistance, which directly drives everything else.
Of course, that is also an over-simplification, there are many, many direct causes of insulin resistance, the result of which is the viscous cycle of increased demand for insulin, and increased insulin resistance - but simply, it's a better explanation than the "excess calories causing fat to spill over" - that may have seemed viable in 2008.
All of which to say - there really isn't anything directly controversial in the Newcastle research, except that it has somewhat been superseded with better research that better explains how fat builds up in the liver - because of insulin, not simply because of excess calories.
With that - you may be more prone to think about treatment focused on reducing insulin, not reducing calories. However - reducing calories (substantially) will also work, and may be a better route for some.
