Hi @Sean_Raymond - very curious and interesting that after reading about the low carb approach to type two diabetes, you take on the idea that it works so well because - it allows us to eat less. (That old tired - and wrong - idea about weight loss by simply eating less.)
As someone that practices basically every method out there to keep body-fat - particularly around my waist - to a healthier/protective state (apparently which is less than half one's height) (https://pubmed.ncbi.nlm.nih.gov/20819243/) the idea that I would spend the rest of my life being hungry all the time in order to do this is beyond comprehension. I am not alone - I am pretty sure that this is the reason that 'simply eating less' (ie calorie deficit) to be a healthy weight (ie have healthy fat cells) has not worked for soooo many.
Hunger is a normal physical response to not eating enough in order to get the nutrients and energy in order to keep you alive, let alone think clearly, and do things and lift things and move. Hunger is a good thing, not a bad thing and is natural and healthy. It is how we eat enough, after all.
Many with type two understand that their systems have been mucked up, and how their hunger and satiation hormones are not working well is part of the dysruption of the blood glucose regulation system. I agree with Gary Taubes, and Phinney and Volek (https://www.amazon.com/Art-Science-Low-Carbohydrate-Living/dp/0983490708), and et al ,that excessive carbohydrates, especially in the form of sugar, as yummy as they are, are the culprit for this, and that mammals like us have not evolved to eat carbs in the amounts that has become mandated from above and as normal, as we are seeing in our societies in the last 40 or so years. Also, the new fats that were introduced to our diets in order to lower the amount of saturated fats in our diets that became the dietary demon around the same time, uncoincidentally.
The amazingly complex diagrams about blood glucose regulation, called the Randle cycle, I have seen and refer to jokingly from time to time, absolutely involve dietary fat. But in those diagrams the raised glucose levels which bring about the raised insulin levels which tip the system way into chaos, seem obviously to be the point where chaos begins. (https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/randle-cycle)
This is not a personal individual dietary/regulatory phenomenon - this is us being an omniverous mammal. I don't think this is particularly controversial! The degree to which folks can take high carbs with high fat - and I would say - these new fats which we cannot digest properly or well - before their bodies break down is what is individual and different - not that it can break down big time. That is part of us being human and having human bodies which have evolved on certain dietary parameters. This is why type two diabetes is spiralling out of control into being a - dare I say it? - a global big health problem. (And especially in the wake of our big enemy - a very nasty virus - currently being a global health problem.)
Anyway - to go low carb, and when one has type two - to go as low sugar and carb as one can (and oh yes, that level can differ enormously between individuals, due, imho, to how sick your fat cells are) is not about not having enough nutrition and energy, ie to not have enough food and going hungry. It is about lowering the very foods (for me - anything with sugar added, and made from milk, and wheat, and I would add - with the new wheat strain,as with the new potatoes, maize and rice - https://croplife.org/news/the-evolutionary-story-of-four-vital-crops/ ) that have caused the hugely raised blood glucose levels which caused the insulin cascade and inflammed and sickened my ever expanding fat cells into the state they are in today. (https://www.frontiersin.org/articles/10.3389/fcvm.2020.00022/full).
As part of the low-fat eating folk since the late 1970s when it was governmentally mandated in the countries I have lived in, it was not the saturated fat and cholesterol-high food (eggs! for instance, and fatty cuts of meat) I unfortunately was not eating (I believed these governments - one of my greatest regrets), but the sugar and carb-heavy food I substituted, that got me here in this forum discussing this with you all today.
There can be limitations to the eating less approach and it hasn't been effective for many. I have worked with people that it has been very effective in also and used low Carb diets which were not tolerable. However I recognise a low carbohydrate diet is a great alternative option as many do find it just works better for them in achieving whatever particular goal they have. There are ways of manipulating a specifically calorie reduced diet to provide bulk, mitigate effects on satiety etc but it is a challenging area. Hunger is indeed a major barrier with the eat less/consume less calorie idea.
When we look at the diets of our ancestors, evidence typically favours diets that were higher in animal products than something like the 'eatwell' plate although tribes that come closest to hunter gatherers in the modern world do eat large amount sof plant foods (unprocessed).
Gary Taubes believes Insulin stimulates hunger driving over consumption of foods however the body of evidence indicates that insulin promotes satiety as a part of its role in energy homeostasis. Some may dismiss what research finds and prefer to be guided by their lived results, which I understand, but Gary is no different to me in offering a hypothesis and research to back it up. But I haven't seen research that definitively backs up the notion insulin makes you hungry (frank hypos which insulin has a role in can stimulate hunger).
The ease of access and availability to highly palatable high energy foods continues to increase and it makes sense that as a species which evolved seeking out high calorie foods to survive in an environment where food wasn't guaranteed we will be really attracted to them. Adding this to more sedentary behaviours is for me most likely the main factors driving the obesity epidemic rather than it being because of a particular macronutrient or hormone. We have not undergone a major genetic shift in just 50 years and I do not believe most people are inherently inflicted with greediness so maybe it is the unconscious aspects of the brain forged in a time of feast and famine that is what drives what are now unhealthy behaviours.
The topic of saturated fat as a cause of heart disease is a rabbit hole. I do not hold a firm opinion that it is as bad as some say or benign as others. Evidence exists linking it to heart disease and other evidence suggest there is not. People then argue over the strength of the studies on either side. My view is that whilst people do respond differently to fat, generally saturated fat does raise LDL cholesterol (if a person is losing weight on a high fat diet this potential rise may be offset by the cholesterol lowering effects of the weight loss). I've looked at many low CHO v High CHO studies and LDL does tend to go up more than down.
If we accept that saturated fat raises LDL cholesterol (as I do -many do not), it then follows that the next question should be, is this a risk for health? Again, we find studies that contradict each other over this. I cannot conclusively say either way. But even If we were to say it does a low CHO/high fat/sat fat diets also may cause an increase in HDL and decrease in TAG - so just because LDL went up have we increased our overall cardiovascular risk? Then we must consider that increasing LDL itself may not be as important as the number and size of LDL particles rather than the amount of cholesterol being carried. Large LDL particles may confer less atherogenic risk. When we look at MUFA/PUFA, in theory they do not raise LDL and so it is said that they are less likely to cause a furrying of the arteries. But, saturated fat in the arteries is unlikely to be oxidised because it is a saturated fat. This means the inflammation which sparks creation of plaque in arteries may not occur whilst MUFA/PUFA can be oxidised. So whilst unsaturated fats may be less likely to cause deposition of cholesterol in artery walls might be more readily oxidised if they do. Simply put - unsaturated fats may be more pro-inflammatory.
Again, this all needs to be considered in the context of energy balance, weight, other factors etc. So, I do not fear saturated fat however I am not sure MUFA/PUFA are the disaster some say. Saying that, I do try to avoid processed vegetable oils and get MUFA/PUFA from nuts, olive oil for example. So it may be not so much the type of fat per se but a shift towards consuming more unnatural oils in replace of natural SFA which may have had some unhealthy effects. So I can find some agreement with you on unsaturated fats but maybe not in quite the way. Sorry if I went on there.
The Randall cycle is interesting, it actually is closest to the topic I first raised about how dietary fat may exert an acute insulin resistant effect and consuming carbohydrate at the same time may mean the carbohydrate is less efficiently metabolised. This is in keeping with the Randall cycle principle but may not wholly be explained by it (this cycle looks at competition between fatty acids and glucose for fuel useage not acute insulin resistant effects of fat). If we look to our ancestors it is likely animal and plant foods were not generally consumed together (animal caught and eaten, berries forged and eaten). I think you do raise an interesting point here.
Unfortunately as we progress advice changes and advice once taught as healthy is shown not to be.