You’d be off base in questioning any of that, at least as the central premise that “X person didn’t have Y effects because they ate too much Z macro.”
Keto, when strictly followed, provides a great reduction to bolus needs (in personal experience, 80-90% reduction, depending on protein intake), and a lesser, but still significant, reduction to basal needs (30% in my case); however, both types of insulin are absolutely still needed to prevent high blood sugars in an environment with no insulin, which is a significant risk of DKA (and death). Protein metabolizes into excess sugar in the blood stream as well, so unless you’re eating a pure fat diet, you will still need insulin. In addition to that, there are hormones (cortisol for sure), and other non-macro nutrients and alkaloids (a common report is caffeine, but this very much depends on individual biochemistry) that can cause rises in blood sugar, which require insulin to compensate for.
A type 1 diabetic without honeymoon insulin production will still die after a period of even the strictest of ketogenic diets. It was the treatment prior to the introduction of insulin, and was effective at extending the lives of diabetics; they would typically be able to live up to 3 or 4 years post-diagnosis before eventually dying.
For the record, my body enters keto at or around 45g/day, as measured by the presence and amounts of ketones; anyone who says “you need exactly N grams per day or it isn’t keto” is extrapolating from generalized experience at best.
The problem with keto isn’t that it isn’t effective for some things, it’s that people go a long way to oversimplify both the science behind it and the impacts it can have on other conditions by over applying that lens of simplification. It’s a good diet for some, but it isn’t a free lunch (pun not intended) - and it’s far from something that can eliminate the needs of insulin in type 1 populations, as this article alludes to.
Coronary heart disease. CVD (cardiovascular disease) may be more appropriate as it’s less specific but still covers the linkage between the two conditions.
It’s not without tradeoffs. There’s a substantial overlap between T1 and CHD, and the impacts of keto on CHD in non-normal populations (hyper-responders, metabolic patients) are even more poorly understood than they are in the general population.
Lowering carbs is one thing; LCHF is an entirely different beast (and I say this both as a T1 and a T1 who tried LCHF for nearly a year).
It’s an option for some, but billing it as “remission” is going to make people think it’s a cure-all, when it’s far from that, and isn’t exactly “new” for the treatment of T1 - it’s both part of the general instruction set (“reduce carbs”) and even prior to insulin therapy, was the only treatment for T1, and it had a pretty poor success rate.
Curious if they have any clearer definition of what they mean by “recently diagnosed.”
Based on the article, it looks like all patients were in their honeymoon period, which certainly makes for a substantial difference from what most would think of as remission - the difference between “clinical remission” and “clinical remission in very controlled circumstances while patients were still capable of producing some insulin.”
It’s pretty well known that LCHF reduces overall insulin requirements, and it’s not surprising that in new patients who are still capable of some production that LCHF would be enough to effectively lengthen the honeymoon period, but in any case I’d argue that the word remission is a pretty poor choice of words for describing the effect seen.
Keto, when strictly followed, provides a great reduction to bolus needs (in personal experience, 80-90% reduction, depending on protein intake), and a lesser, but still significant, reduction to basal needs (30% in my case); however, both types of insulin are absolutely still needed to prevent high blood sugars in an environment with no insulin, which is a significant risk of DKA (and death). Protein metabolizes into excess sugar in the blood stream as well, so unless you’re eating a pure fat diet, you will still need insulin. In addition to that, there are hormones (cortisol for sure), and other non-macro nutrients and alkaloids (a common report is caffeine, but this very much depends on individual biochemistry) that can cause rises in blood sugar, which require insulin to compensate for.
A type 1 diabetic without honeymoon insulin production will still die after a period of even the strictest of ketogenic diets. It was the treatment prior to the introduction of insulin, and was effective at extending the lives of diabetics; they would typically be able to live up to 3 or 4 years post-diagnosis before eventually dying.
For the record, my body enters keto at or around 45g/day, as measured by the presence and amounts of ketones; anyone who says “you need exactly N grams per day or it isn’t keto” is extrapolating from generalized experience at best.
The problem with keto isn’t that it isn’t effective for some things, it’s that people go a long way to oversimplify both the science behind it and the impacts it can have on other conditions by over applying that lens of simplification. It’s a good diet for some, but it isn’t a free lunch (pun not intended) - and it’s far from something that can eliminate the needs of insulin in type 1 populations, as this article alludes to.