What we call type 2 diabetes is complicated. Strictly speaking, it means non-insulin dependent diabetes, but more commonly it is thought of as a form of diabetes that is not due to the immune system destroying the insulin producing cells of the pancreas.
There are major flaws in those descriptions. First, type II diabetes can progress to destruction of the beta cells of the pancreas, first by overworking them, and actually in the late stages by the immune system destroying beta cells which have been overworked and over-secreting insulin. Type 2 might also be mediated by allergens or enteroviruses that get through a permeable gut. Gut permeability can be reversed fast with IF. Type II and type I often run in the same families, and Type 2 is far more genetically linked than type 1 (If one twin has type two the other will have it like 85% of the time versus around 30% for twins and type I).
Type II also has several probably unrelated forms.
There can be insulin resistance caused by buildup of fat/fatty liver that makes the liver not respond to insulin, so that it tries to release glucose into the blood stream. This is generally caused by obesity but linked to fructose and alcohol intake.
There can be type II where the cell receptors for insulin are flawed, or there are not enough of them, and so even if insulin is release, cells don’t respond.
There can be type II where the pancreas is naturally deficient in its ability to produce insulin, but there is not destruction of beta cells, however, it should be noted that pancreatic cells are among the first to die in the presence of high blood sugar and rapid blood sugar changes, so high blood sugar alone will destroy the pancreas.
Technically, when the pancreatic beta cells are mostly gone, diabetes should be referred to as type I or insulin dependent diabetes whether it was caused by a juvenile autoimmune reaction or by chronic hyperglycemia. It appears now that even after beta cells are killed, they can regenerate, or that a few resilient cells can stay alive and produce more if the metabolic and immunological conditions improve.
It has been pretty clearly established in the last 10 years that over the course of a week, the amount of insulin you secrete, or need to inject does not depend largelyon the macro-nutrient breakdown, but rather the total calories. Lower carb, higher fat diets require more insulin per gram of carbs because the body makes less enzymes to burn up carbs for fuel. (In fact, insulin is MORE important in signalling cells to make glucose burning enzymes over a 2 day to 2 week period than it is at moing glucose into muscle cells). Protein requires almost as much insulin as carbs per gram over the course of 24 hours. (The metabolic fate of ALL protein is either glucose or ketones, and most amino acids end up as glucose-see glucogenic and ketogenic amino acids).
Type II diabetics need to inject less insulin with lower carb, higher fat diets because the rise in glucose is slower, and their pancreas can still make enough over 4 hours or so. By the way, Al Dente Pasta raises blood sugar very slowly, not fast as I expected. Same for really crusty wheat based starches and starches mixed with fat.
At a certain point, a type II diabetic does not make enough insulin to even keep their liver from raising their blood sugar to hyperglycemic state even in a fasted state. About 30% of a normal persons daily insulin release is simply to keep the liver from releasing glucose and blood sugar will tend to rise about 25-40 points an hour without insulin even if someone doesn’t eat, if they have no insulin. Ketones will accumulate and terminal DKA can be reached in 12-18 hours. Ketones cause insulin resistance so that even more insulin is needed to manage blood sugar in the presence of ketones.
So its important to describe the state of the type II diabetic. There is insulin resistance. There is insulin resistance where the individual’s pancreas can not manage post meal glucose without additional insulin. There is insulin resistance where the individual’s pancreas cannot manage meals OR even their liver output (basal insulin), and there is insulin resistance/pancreatic insufficiency where runaway ketoacidosis will occur without injected insulin. The degree to which this is causes by fatty buildup, by genetic cell receptor flaws, or by pancreatic destruction has to be assessed to determine the effects of diet.
I suspect that the form that results in a latent onset pancreatic destruction might respond fast to IF. Others simply require not overeating, others require agents to make cells more sensitive.