2015 Interview w Joseph Kraft, father of insulin array

[hill dweller]

Just watched this interview with 95 year old Dr. Joseph Kraft. It's a very interesting history of diabetes research and treatment. Long but you can speed up to 2x. https://www.youtube.com/watch?v=w0nV-_ddXoc

"Those with cardiovascular disease not identified with diabetes . . . are simply undiagnosed" -- Joseph Kraft

[circular]

Thanks for the link! I've been listing to podcasts with people influenced by him but not yet listened to him

[circular]

Have had a listen. I would like to see his position discusses more here.

Dr. Kraft says fasting BG, fasting insulin, PPBG, A1c, etc *do not* tell if one has insulin issues. It sounds like according to his view they are largely irrelevant? Is that your takeaway too?

For others, he devised an insulin sensitivity test that involves a five-hour glucose tolerance test that also measures insulin response over that time. He identified four patterns, and only one suggests insulin sensitivity. The others show abnormal insulin in the presence of normal fasting BG and A1c.

This page is a good introduction that will take less time than listening to the podcast:'Early Detection of Insulin Resistance for Improved Patient Outcomes'

...we could say that of the original 3650 patients who were administered the OGTT, only 15% (not 53%) were truly normal.

http://www.townsendletter.com/Jan2015/early0115.html

[apod]

Very interesting, but a bit long. Is Kraft looking at elevated levels of insulin itself being a driver of heart disease, or is that simply a marker of insulin resistance which is associated with other downstream contributors to heart disease (elevated trigs, lower HDL, higher LDL-p, higher sdLDL, higher inflammation, higher A1C / oxidized cholesterol, higher blood pressure, lower physical fitness, lower muscle mass, lower activity levels, other poor dietary/lifestyle factors & genetic predispositions?)

If hyperinsulinemia is a driver of heart disease, I'm curious how dairy protein (highly insulinogenic, but associated with improved insulin sensitivity), safe starches (highly insulinogenic) and combining fats + carbohydrates (which elevates insulin more than eating carbohydrates without them) might be viewed -- does kraft tend to look at a higher carb / lower protein / low fat traditional diet rich in legumes and whole grains (rich in lectins, but associated with improved insulin sensitivity and lower levels of serum insulin) as being useful here for improving the glucose tolerance and insulin secretion for a 100g load, or is he into the newer lower-carbohydrate / moderate-protein / higher fat atkins-style diets which might introduce some level of physiological insulin resistance and produce higher levels of serum cholesterol & glucose?

I've read that increased amounts of coffee increase fasting insulin levels and decrease insulin sensitivity, yet coffee consumption seems to have a dose-dependent ability to lower heart disease risk. In this study, a diet containing 538 grams of carbohydrates per day (close to 300 grams of simple sugars per day) was shown to help decrease fasting insulin levels, increase insulin sensitivity, and improve blood lipids: https://www.researchgate.net/publicatio ... Old_Adults Perhaps there's some nuance here to dialing in the diet besides looking at fasting insulin / post-prandial insulin secretion?

[circular]

In the podcast the fat emperor asks him if he supports a low carb diet to address the dysfunctional insulin patterns. He replied that he refers these patients to a dietician and wasn't sure what she did, but I think that it involved balancing blood sugars ... May have said protein at every meal? I got the feeling a moderate approach and that it got the desired results, but precious little said on it so I don't really know.

[apod]

In the podcast the fat emperor asks him if he supports a low carb diet to address the dysfunctional insulin patterns. He replied that he refers these patients to a dietician and wasn't sure what she did, but I think that it involved balancing blood sugars ... May have said protein at every meal? I got the feeling a moderate approach and that it got the desired results, but precious little said on it so I don't really know.

It seems like protein at every meal would be insulinogenic and keep IGF1 / insulin up? (Particularly useful for building muscle / lean mass / gaining weight.) I was thinking the message was that blood glucose was a poor measure, as normal people with healthy glucose levels yet higher post-prandial / fasting insulin might be considered prediabetic and susceptible to heart disease from his perspective.

[hill dweller]

I'm not seeing a 5-hour Glucose Tolerance Insulin Resistant test offered anywhere online other than here:
http://meridianvalleylab.com/Kraft-Prediabetes-Profile

They have a finger prick (bloodspot) test that you can do yourself and mail back. The fee is $40 handling (nonrefundable) plus $159 analysis for a total of $199. They request that you do this with someone else present (family, friend) to guard against fainting.

Any one go with Meridian Valley Lab? Or another, to do the "Kraft" assay?

[circular]

I haven't looked at Kraft's papers, but one thing I wonder is whether he ran this test more than once in his study participants. (Was it even a formal, peer reviewed study?) Is it possible that one's pattern can actually fluctuate and you'd need to do, say, one a week for five weeks and see if the results are consistent before concluding anything?

[hill dweller]

Kraft did 14,384 assays from 1972 to 1998, at St Joseph's Hospital in Chicago. He was dept chair and replaced the standard GTT with his GTIR assay, at least in these 14,384 patients.

His book is The Diabetes Epidemic & You (2008). The writing style is bit dated and definitely preachy, but it's for laymen.

Yes, insulin resistance levels change throughout life, largely based on diet.

[circular]

I've noticed that a parent and I are both homozygous on a SNP that reduces the first phase insulin response.

46% of European non-diabetic offspring of type-2 diabetes patients are rs13266634(C;C) homozygotes; they are diabetes-prone [3x risk of diabetes] and characterised by a 19% decrease in first-phase insulin release following an intravenous glucose load. [Emphasis added; SNPedia]

The distribution bar at Promethease indicates that 56.6% of people with Northern and Western European ancestry have this result, so it's very common. I wonder how this would affect analysis of his results, if at all. I imagine that being in Chicago his patients were very diverse, and it's certainly a large n=14,384. It would seem to be a good dataset to look more closely at SLC30A8 C,C vis insulin response.