Now today’s gift via his generosity of spirit is very interesting. He’s done a pretty detailed analysis of a study that was published in Feb (and in Googling the title did the rounds of the usual SBPR sources at the time…with the usual level of uncritical stenographic reproduction of the press release) Sure enough, full analysis of the primary document shows a bit more nuance etc.
Now, the interesting thing about this alternative presentation of the facts is that it’s from Peter Attia who , at one time was a huge advocate of Gary Taubes’s Carbohydrate-Insulin Model of obesity. To the extent…as he mentions here…that he hooked up with him and his NuSi “charity” designed to fund “better” research" i.e. studies that would somehow prove this model. Inconveniently, the studies didn’t prove that at all. Still, it’s an interesting addition to fundamental understanding…
T2D my BIL an endocrinologist would not blame on carbs.
The difference according to him between fat, carbs and proteins in the liver, think glucose, is much much less than the fad books tell us. There is no carb cutting angle that is so glorious. But if you cut calories you lose weight until you add more other the carbs you cut.
Well, in a general sense, he’s not that wrong (except fat isn’t an equal source of glucose…by a long way) For sure, given a high quality diet, metabolic health and an energy intake that’s not obesogenic, individual micronutrients don’t play that big a role in weight management (the focus of the article)
However, in T2D…and even before that for a good many folk…the above scenario doesn’t hold, does it? Once there’s a big enough departure from healthy homeostasis and you start to develop a degree of insulin resistance, carb intake does seem to count. I’ve gotten interested in the use of continuous read glucose monitors in the “non diabetic” individual (I put that in quotes, BTW, because you don’t know until you know) Physicians whose practice is clogged with folk with metabolic syndrome and beyond tend to pour scorn on the use but I suspect that in a few years time, that departure from healthy homeostasis will be detected much earlier and the impact of carbohydrates in further progression will be recognised.
There was a lot of information to be had on this topic on the old Diabetic Fools board…along with insight into future technology/investment opportunities and general future proofing for those who are keen on health and well-being
Oh I was pointing out politely you are totally unqualified to have much of an opinion. You do not understand the research topics because you are untrained. On the practical side you are making a mess of things from what I am reading.
Stop obsessing over your health. The stress makes your problems worse. Certainly wont help you.
And treat people the way you want to be treated without donning other specialists’ roles in life.
38, it is off the rails because passing ones self off as an expert when one does not know the topic is problematic.
This below is well accepted by actual endocrinologists. While junk sugars are not smart to the calorie count endocrinologists believe sweet foods do damage mostly by raising brain signaling creating more hunger. Other carbs complex are not sweet and do not induce more hunger. All that “science” about complex v simple carbs is mostly a waste. Still fiber takes lipids out of the blood stream to a degree.
The only solution is to eat healthily and eat less. The science wont do anything else for anyone. Worriers need not apply.
Can too much fat raise blood sugar?
High-fat overfeeding increases fasting glucose levels due to increased hepatic glucose production. The increased insulin secretion may compensate for hepatic insulin resistance possibly mediated by elevated GIP secretion.
My BIL a top endocrinologist at Beth Israel would say the difference in metabolism between fat, protein and carbs is so slight it is a non issue. Yes there is a ton of nonsense literature for decades now to the opposite.
I guess your father’s advice that studies are junk doesn’t apply if you can cherry pick something that you think supports your opinion?
Did you read your study and compare it with what my reply to your comment was…you reproduced it above so, if you didn’t other posters will be able to.
So these study subjects …who per the protocol weren’t overweight/obese and appeared to be metabolically healthy (no T2D) and looking at the results, you could be duped into thinking that the HFHC diet did produce a higher fasting glucose than the control diet. It says it does right there in the results. However, this HFHC diet was well above the energy content of the standard weight maintenance diet of the study subjects …by a long way!!
Now, if you look closely, the macronutrient profile of the 2 diets is given in % and not gram amounts. The extra energy content of the high fat diet was 50% extra to the control diet so, yes, there’s much more fat being eaten but look at the carbs…32% in the HFHC vs 50% in the maintenance but that 32% was of a greater energy content. A rough calculation puts it about the same in absolute amounts. Once you throw in the protein (another potential source of glucose) that greater amount of glucose in the study diet doesn’t look quite so significant.
This is probably the sort of study that your father could rightly encourage you to disregard if it were attempting to claim equivalent glucose production from fat (it’snot)…“weighted” as it is towards inevitably producing a higher fasting glucose. Had the study authors then gone on to compare isocaloric diets with the same micronutrient profile (and they may well have done) I suspect that fasting glucose would tell a different story.
Can’t help you much there…it’s an area I know enough about to realise I don’t know enough to let myself wander around the Google field of cow pats. So no Dunning-Kruger award for me, I guess.
I do recall that the IF proponents tend to bang on about it a lot…and I think it’s relatively easy to demonstrate whatever demonstrates the phenom via biomarkers etc. in rodent research. I seem to remember listening to a podcast during my early days of subscribing to the Attia site and that focused more on the evidence for human applications. One of the reasons the particular researcher gave for distinguishing between the different protocols under the IF umbrella (i.e. Time Restricted Feeding vs true fasting) was that trying to reproduce what was noted in rodent research with the same time frames (12 hour fast 16 hour fast etc) didn’t work to a significant degree. Primarily because rodent metabolism is hugely different and you don’t get a long enough period with zero digestive activity going on with, say, an 8 hour feeding window in a 24 hour block. That makes sense when you think about it…if you finish a nutritionally sound dinner at, say 5 pm, you have a good few hours with it still roiling around your innards before it’s all done with, right.
I’d have to double check but I want to say a 3 day fast was what was necessary and I didn’t hear anything that convinced me to go that route.