I truly think conventional medicine does not understand Type 2 Diabetes, and that is why its solutions are so unsuccessful.
Type 2 diabetes is not primarily a problem of high blood sugar but of impaired mitochondrial energy utilization.
Glucose and fatty acids are both broken down into acetyl-CoA, which feeds into the TCA cycle. The cycle generates electron carriers, NADH and FADH2, which deliver electrons and protons to the ETC. When functioning well, electrons flow down the ETC to oxygen, protons are pumped across the inner mitochondrial membrane, and ATP is produced efficiently through oxidative phosphorylation. This coupling between substrate oxidation and energy demand keeps the system in balance.
This is basic mitochondrial biology we all learn in med school (but is never integrated into working with people).
In metabolic disease, however, the mitochondria are flooded with fuel. Chronic excess of glucose, free fatty acids, and triglycerides means the cell receives far more input than it can oxidize. But the issue is also often combined with impaired oxidation itself for which the bottleneck can be found in many different places. This is what doesn't get enough attention.
Both fats and sugars converge on the same mitochondrial machinery, and when the influx of electrons from NADH and FADH2 exceeds the ETC’s capacity to pass them to oxygen, the chain becomes over-reduced (flooded with electrons essentially).
You get hyperpolarization of the mitochondrial membrane. Electrons begin to leak from complexes I and III, generating oxidative stress.
When produced excessively high levels of ROS will damage mitochondrial proteins, lipids, and membranes, impairing oxidative capacity further - vicious cycle as with most chronic diseases.
The oxidative stress will blunt insulin signalling itself. Meanwhile, build up of diacylglycerol and ceramides due to fuel overload reinforce insulin resistance. This creates a self-perpetuating loop of mitochondrial stress and signalling dysfunction.
The cell, in essence, becomes insulin resistant as a defence mechanism. When mitochondria are already overloaded, the cell reduces glucose uptake to prevent further electron pressure and oxidative damage. Systemically, this appears as hyperglycaemia and hyperinsulinemia, but the problem began within the mitochondria, not the bloodstream. It is an issue of energy oversupply and disposal, not merely sugar toxicity.
At its core, type 2 diabetes is a mitochondrial problem, a breakdown in the handling of electrons, not simply a surplus of glucose. The blood abnormalities are the visible signs of this deeper bioenergetic congestion - but they are not the disease itself. So you should not optimise these markers as you can “fix” those while making the issue worse.
