I've been reading Roy Taylor's book laying out the Newcastle view of diabetes.
Very conflicted about all of this. On the one hand Prof Roy Taylor has achieved much, and there must be thousands of people living normal lives now who owe that to his insights, tenacity and ability to popularise his methods so that people actually follow them rather than view them as some kind of fringe, dangerous oddity.
On the other, his book, his central thesis, his treatment method, all exist in lock-step with the abiding narrative that people generally eat more food than they need, and that this leads to fat "clogging up" things - in his case, the liver and pancreas. If you suddenly drop your weight by 15kg, you will reverse your Type 2 diabetes. This will first strip the fatty deposits in your liver and "wake up" the beta cells in your pancreas (which have been going dormant under the "attack" of fat).
'Consider the source' - as Dr Eric Westman might say, and you look back at the career of Roy Taylor - and he talks about having various insights into the state of the pancreas in healthy and diabetic people, and the genuinely revolutionary development of the magnetic resonance imaging equipment, and department that he brought together out of determination and virtually nothing else, which gave him the ability to measure the level of fat and gylcogen in the pancreas and muscles - in a way that nobody else could. You could say then, that it isn't much of a surprise that his major thesis is that T2DM is primarily a question of excess fat in the liver and pancreas, and that a big sign of developing the condition is the lack of ability to store additional glycogen in muscle cells.
Almost his first word is insulin, then he goes on to virtually ignore the wider implications and effects of insulin. He talks about there being a small number of critical hormones, and that insulin's major job being the regulation of glucose uptake. He mentions ketones as an emergency replacement of glucose for the brain in the event of starvation, but repeatedly talks about the brain needing glucose, and that there are only two fuels, glucose and fat.
In other words, there is no recognition of the role insulin plays in fat mobilisation. You can read his book and come away with the idea that "food" results in an insulin response, and that you burn fat and glucose for fuel. Anyone wanting a better understanding should look into the Randal cycle, but essentially glucose and fat "burning" are in competition with each other, and one has to win out - and when insulin is high, the winner is alway glucose, because all your cells are under instruction to store any available fat, and to lock it away in storage.
The "method" is to suddenly reduce weight by 15kg by using prepared meal-replacement shakes. These were developed entirely as a lab tool to induce sudden weight loss. He recognises that there needs to be more research into how to transition into a more sustainable "diet" to keep the weight down, but totally ignores the effect of hunger, or any of the hormones that affect hunger, or even that the sympathetic nervous system can over-ride what the liver thinks it should do. You should read some Gary Taubes to get a better understanding of how absurd it is to simply say that people should eat less food.
Fundamentally, he describes T2DM as a state of fat toxicity, where I think it's better described as a hormone imbalance.
But - all of that doesn't mean that I think he's wrong. How could I with the results he has demonstrated?
I have to come back to a medical phrase that just opens all of this up:
In the presence of elevated insulin, and sufficient energy, adipose tissue will hypertrophy
It's an enormously loaded phrase, and it means a lot of things at the same time:
1. Insulin is the master switch between energy storage and energy release.
2. If BOTH high insulin and sufficent energy - then fat storage cells will pull in available fat and swell up to accommodate. Hypertrophy means to swell up, not to create new, small fat cells.
3. If insulin is low (like if there is no carbs or too much protein in the food) then the body will carry on burning fat.
4. If insulin is high (like if there is some carbs or lots of protein) then the body is stuck storing energy, and only burning glucose.
5. The definition of "elevated" is entirely dependent on you - your current normal level will depend on your insulin sensitivity, your genetics, and genetic expression, your level of stress, and infection and inflammation.
6. The definition of "sufficent" is also entirely dependent on you. But - your abIlity to dial down your metabolism by up to 40% means that you need to eat very little before your body decides that there is not sufficient energy. Essentially - 50% less than normal, whatever normal is, but you can pretty much guarantee that the body will react by making you feel like you should eat something - we're pretty well adapted not to just starve without a fight.
So - this is where you end up with both views of weight loss -
- If you eat in a way that reduces insulin, you will burn energy, and ketones come in to play as a kind of relief valve, but the amount you eat (within reason) is not so important, and you don't need to be hungry.
- If you eat in a way that reduces calories, you have to significantly reduce calories before anything changes (assuming you are following the standard high carb diet) - but you can lose weight, at least in the short term, if you can get over the hunger (or the "pathological hunger" that Dr Catherine Stranahan talks about - stress-driving hunger triggered in the central part of the brain )
both are true, and either can be successful, the biggest differential of course being individual motivation and beliefs.
The insulin approach of course smacks head-first into the "fat is bad" mantra, because if you reduce carbs, and limit protein; of course the consequence will be that more of your intake will be fat, and some of that will inevitably be saturated fat. (forgive me if I just brush that aside for a minute).
But - where does all of this leave us -? Clearly the Newcastle approach can work, but also the low-carb, insulin reducing approach also works; what gives?
So - in my humble opinion, I have some issues with the "twin-cycle" hypothesis - but without going too far into the long grass with this, I can explain a lot of the observations and conclusions from direct effects of insulin and insulin resistance, but the short version is simply that there is a fine line between cause and effect, the end result - as the title of this very thread attests - is that you end up with fat in the liver.
There are very different mechanisms in play as to how it could be occurring, but in the end, does it matter? The end result is the same.
Very quickly, you come to the question on how to treat the excess fat in the liver and pancreas, and you come back to the key statement, for my money, even if you buy the entire thesis, you are still better trying to reduce the visceral fat with lowering insulin through low-carb and intermittent fasting; but that's another thread entirely.
There is far, far more to agree on than there is to argue about.
One thing that was really interesting - in fact made reading the whole book worth the effort by itself; is around the question of what exactly is it that is degrading the pancreas? I have more to say on that.
, I have recently been watching Youtube videos (have not got the book yet) of Stacy Sims including this one: 
