I called it ‘curable’ but the right words seems to be ‘remissionable’ or ‘reversible.’ For me the core insight is the 15 Kg. weight loss necessary for remission to take effect. I went from 90 Kg. to 70 Kg and then back up to 75 Kg. I don’t know if the extra 5 Kg. affected my diabetes but I did feel less well and I tired sooner. Having lost three out of the five the knees no longer hurt and I can again take longer walks.
The best part, no need for drugs, just lose weight!
Long-Term Remission of Type 2 Diabetes Is Durable | Roy Taylor, MD & M. Scott Moore, DO
You got it bass-ackwards. The core insight is to avoid anything like a 15kg weight gain in the first place. Respond to the first 5-10 lb gain with intent because, once that becomes acceptable and excusable, 50-100lbs (and beyond) happens as if by magic
This isn’t as facetious as it might appear, as increasing adiposity inevitably brings a departure from healthy homeostasis long before those biomarkers that are routinely
ignored raise a warning flag…and a really long time before a diagnosis of even “pre” diabetes. That’s why central adiposity (belly fat) and other manifestations of excess fat have a place on the metabolic syndrome/metabolic dysfunction rap sheet.
The reason why “curable” isn’t routinely used when discussing therapeutic lifestyle interventions is because, once a tipping point is reached for most folk, all the healthy eating in the world doesn’t restore the body to the metabolical flexibility of the pre craptaculous eating/lifestyle days.
It’s a complex topic, for sure, but this piece of marketing by Peter Attia (together with the hyperlinks and list of his various podcasts on the subject) ought to be enough to explain a bit of it
Additionally, it’d be a mistake to infer that all examples of non insulin dependent diabetes are the result of craptaculous lifestyle choices. In the same way that an unfavorable genetic profile can be an underlying cause of ASCVD … independent of diet … such is the case for “diabetes”. A bit of Goggling on such disorders as LADA and MODY will be a bit of an eye opener here.
Manifestly, just a few genetic polymorphisms that’re approaching the genotype of these diseases are going to make a dramatic difference to the ability of diet and exercise alone to reverse what, on first blush, looks like bog standard “diabesity” caused by consistent poor dietary choices and sedentary behavior once that “tipping point” on the departure from healthy homeostasis is reached
Old Lags from the H&N board might remember this research from discussions we had there when Roy Taylor’s very early studies were published over a decade ago now. I even remember the poster who first introduced it …swiing (with 2 "i"s)
It captured my imagination at the time as it struck me as one of those examples of someone noticing something and thinking “Now, that’s peculiar”(in this instance, the sudden, dramatic improvement in the biomarkers of T2D after bariatric surgery and before appreciable weight loss has occured) and following up with “I wonder if…” (in this instance, could the effects of bariatric surgery be reproduced non surgically by putting willing volunteers on an 800 Cal a day diet)
I think the department at Newcastle has gotten a lot of mileage out of the results on those first few patients with books and what have you. Here’s the details of the Newcastle diet fleshed out…
It should also be noted that the Newcastle diet wasn’t based on Real Food or what’s generally considered healthy eating habits. Most of the daily Calorie intake (800 Cals, remember) came from those shakes and pre packaged soups that MLMs like Optavia and Medifast are based on. That was one of the criticisms of the diet at the time … and advocates of eating Real Food would still make, I guess. Except when they don’t.
—I called it ‘curable’ but the right words seems to be ‘remissionable’ or ‘reversible.’
Think of it more like being a recovering addict. You are never cured, you take the appropriate steps one day at a time. Once you have developed DM2, you will pretty much always have the propensity to do it again, even if you’ve taken all the appropriate steps.
—For me the core insight is the 15 Kg. weight loss necessary for remission to take effect. I went from 90 Kg. to 70 Kg and then back up to 75 Kg. I don’t know if the extra 5 Kg. affected my diabetes but I did feel less well and I tired sooner. Having lost three out of the five the knees no longer hurt and I can again take longer walks.
Weight without context gives little insight. Are you tall? Active? Muscle mass? etc, etc. I see 70kg and think that is a small person. I see 90 kg and think that is my weight when training for a long race.
I will say this, joints only “see” weight. Doesn’t matter if it is extra fat or extra muscle they are carrying around. So if losing 5kg makes your knees feel better, probably should keep those 5kg off. I’m the same way but it is going from 95kg to 93kg.
Dr. Roy Taylor brought up the 15 Kg. number which he said was supported by their findings. I have no way of verifying the assertion. At 72.5 Kg. my current wight, the BMI is 22.9 which seems to be in the healthy range. Aiming at 22.1 at 70Kg.
The reasoning behind the 15 Kg. number instead of a ratio to body mass is that all that is needed is to reduce the fat in the liver and pancreas, fat elsewhere seems to have little effect on insulin resistance because it is the liver and the pancreas that control the digestion of sugar and fat and the secretion of insulin. Like I said above, I have no way of verifying the assertion but it sounds reasonable.
EDIT: While I was losing weight I had bouts of low blood pressure. My doctor told me to eat some salt which worked just fine. Dr. Roy Taylor also talked about the low salt condition which I experienced.
Here it is. The study that put Prof Taylor’s department on the diabetes map…
I see I was wrong. It was a diet of 600 Cals a day and not 800. Additionally, it was followed as directed for only 8 weeks (except when it wasn’t and patients left the study) and, as mentioned in the study discussion, patients were all in the obese category, had super high fasting glucose, A1c and really abnormal OGTT. This puts the “magic” number of 15 kg (or 15% of bodyweight) into a bit more perspective…as this was the average weight loss over a brief period of a major energy restriction. In other words, a “crash” diet of Optifast meal replacement shakes and a few lettuce leaves.
As I mentioned upstream, the popular press (and, yes, commentators on the H&N biard) were uniformly negative in their comments. The usual stuff…“crash diet”, no Real Food, unsustainable etc.etc . All true…but irrelevant to the stated purposes of that pilot study. That is: is it possible to achieve the superficial responses of bariatric surgery but without the bariatric surgery and to identify a putative mechanism for those results. It seemed to do that pretty well at the time…and since.
Of course, it’s most definitely not a cure for diabetes and, as plenty of research since has demonstrated, only effects a reversal when folk continue to eat down to the diminished capacity of their liver and pancreas to cope and their insulin resistant muscles to dispose of circulating glucose.
Don’t dump the Novo Nordisk stock just yet.
Edit: conversion table for folk like me who’ve lost the ability to think in mm/L
This final comment is important enough to warrant its own post as it’s something that Prof Taylor’s research didn’t address fully.
Peripheral insulin resistance is something of a “Canary in the Coalmine” of metabolic dysfunction and has effects long before the Darwin Award of even “pre diabetes”. Skeletal muscle is the body’s largest disposal unit for circulating glucose …depending, of course on muscle mass and degree of insulin resistance.
Even if a brief crash diet restored a diseased pancreas and liver to rude good health and normal function, without a place to go, that circulating blood glucose and the extra insulin produced in an attempt to utilise it are free to continue to causing damage. Hence the designation of “skinny fat” i.e. metabolically obese, normal weight. Body composition does matter.
Edit: should anyone be wondering about their own insulin sensitivity, ask for insulin to be measured at your next annual physical. It’s better than assuming/hoping…