I'd agree that what the ADA (and the AHA - but that's a different discusion)is doing is essentially malpractice on a large scale.
I'd also agree that T2DM is reversable for *most* people. I have doubts about people who have had it so long they're suffering 'beta cell exhaustion', essentially becoming T1DM, but those are just doubts - and I have seen no research on that. Maybe those cells can recover(?)
That said the hows of reversability are interesting. In myocytes (skeletal muscle cells) where insulin resistance starts in humans (and is the beginning of the rising insulin levels that can eventually - but don't have to - create IR in hepatocytes (liver cells)). That IR comes from diglygerides* essentially jamming the molecular chain reaction that starts with insulin at the cell wall and ends with glucose transporters poking through the cell wall. Exercise (and to a lesser degree chromium picolinate) can also prompt those transporters to poke through the cell wall but seem to use an alternate pathway. So it makes sense that neither exercise nor chromium are sorting the issue long term - but that increasing fat flux and reducing the load within myocytes can. I've seen at least one study in which 1200 kCal/day restriction reversed IR in myocytes (no need to drop to 800 - although that might be a matter of exercising-some vs sedentary).
That said, T2DM has associated higher risks of a number of chronic diseases (e.g. AD, CVD) and cancer - and it's not clear that it's high glucose or high insulin (or both) that's the issue. To the extent that 80ish percent of us have some degree of IR (but glucose completely under control, just rising amounts of insulin to maintain those 'normal' levels) those higher levels of insulin might also be raising the risk of those diseases it's IMO worth paying attention to IR. One issue is that it's not easy to test insulin. I haven't seen a cheap test, something done easily at home, like a glucose strip - or even the ones for lactate.
Not credentialled in this area, just have had an interest since my dad was diagnosed with T2DM in the late 80s - and I have a skill set that includes reading studies. Wish I knew then what I know now.

*a diglyceride is a triglyceride with one fatty acid replaced with a hydroxyl - so you have a glycerol holding two hydrophobic molecules together with one hydrophillic molecule. It's not a shock that some isoforms (picture two FAs in the lipid bilayer with a hydroxyl hanging out, potentially grabbing another molecule) can cause issues. Gerald Shulman did pioneering MR cellular work in this; I'd point anyone interested in the interview he did with Peter Attia as a starting point - or look through PubMed for 'G. Shulman'. [question for any readers: would a footnote like this work better for you as a reply to my reply - or is it OK like this?]