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AaronJeep t1_j48nig1 wrote

Apparently a 12oz coke has 39 grams of sugar. I have one cup of highly overpriced coffee in the morning. I do like my three teaspoons of sugar in it. That comes out to about 13 grams of sugar.

So the question is, is that the same bad habit (gram for gram) as someone drinking cokes and energy drinks? Obviously, if someone drinks three or four cokes a day they are getting about 150 grams of sugar to my 13 (all other things ignored), but is all sugar bad, period. Or is there a reasonable amount you can have and not feel like you are poisoning yourself?


Cleistheknees t1_j493eoa wrote

> but is all sugar bad, period

The molecule is the same, but the “badness” is based on where it goes, and metabolism is contextual and prioritized. A lot of absolutist sucrose defenders put these studies on blast by saying things like “what about fruit!!!”, noting that the epidemiological data on “fruit” isn’t nearly as bad as on SSBs. Obviously, though, they’re either consciously or mistakenly forgetting that the concentration of sucrose in SSBs is much higher than almost all fruits, and lacks a single gram of fiber, which nearly all fruits have. There is the added problem that “fruit” is a very nonspecific term. An apple and fig have substantially different sugar concentrations and fiber ratios.

The most important factor is time. The longer you can stretch out your liver’s exposure to a given sugar bolus, the better. This is exactly what fiber does: slows motility. The liver (and most peripheral tissues) can metabolize glucose without insulin, but when you’re at rest it’s only at a basal rate, which is the homeostatic demand for hepatic glucose output. The closer you can get your sugar intake to match that “background level” of insulin-independent glucose metabolism, the less negative effect (ie insulin requirement) it would have. Endothelial tissue gets it’s glucose via GLUT1 transporters, which are insulin independent. It’s why the vasculature takes the brunt of chronic hyperglycemia: it isn’t able to prevent all that glucose from diffusing in and wreaking havoc on its internal machinery via glycation.

Low-intensity exercise (ie Zone 2) also opens up an insulin-independent glucose pathway, but into skeletal muscle. That’s why taking a brisk walk after meals is consistently so effective at improving glycemia in diabetics.

So, the “good or bad” gist would be that any sugar which exceeds the ability of the liver to metabolize, which they gets exported as VLDL or contributes to chronic insulin spikes, is bad. I guess the problem isn’t the molecule from a certain point of view, it’s just that it has nowhere to go without a pattern of insulin secretion that is desensitizing in the long-term. Any sugar which is metabolized normally (especially into skeletal muscle) and without chronic insulin spikes is fine. Obviously this is just based on energy and ignores the other 99% of nutritional quality.


KetosisMD t1_j49fysl wrote

Love your post. Knowledge is power.

Thoughts on this ?

> get glucose intake to match glucose-independent uptake

If blood glucose was stable and it went up 18mg/dl (1 mmol) wouldn’t that indicate the intake was too high ?


Cleistheknees t1_j49r5gs wrote

What Eades is saying doesn’t really make sense. If a type 1 diabetic (ie, complete lack of endogenous insulin) consumes 15g of glucose or 150g, the change in serum glucose will be wildly different, and commensurate with the amount ingested. If what he’s saying was correct, that insulin-independent glucose disposal can account for even large boluses in the form of a meal, then the change in serum glucose in a T1D would the same regardless of intake, as that change would be from hepatic output, not from the meal, which in the absence of insulin will be the same whether you’re eating a bowl of pasta or arugula with salmon. As someone who’s last endogenous secretion of insulin was about 26 years ago, I can pretty confidently tell you that is not the reality. I can eat a turkey sandwich before a 20mi bike ride no problem, but a 16oz soda with 70g of sucrose is going to put me past 500mg/dL even with the same exercise.

It is true that the effect of insulin on serum glucose in the advanced T2D patient specifically seems mostly based on suppressing hepatic output, and not entirely on opening GLUT4 channels in skeletal muscle as was thought before, but that doesn’t mean it’s black and white. GLUT4 exists, and is activated via IRS1, and GLUT1 is virtually unexpressed in skeletal muscle after the first year of life (Gaster et al, 2000). That is beyond contestation at this point. If Eades has a good argument as to why this exquisitely architected system of insulin-dependent glucose uptake into muscles that are perfectly prepped for its immediate oxidation would all exist for no reason, I would love to hear it. In fact, we have a version of what Eades is describing, in the form of AMPk activated GLUT4 translocation, skipping IRS1 and the need for insulin, but that’s in situations where the myocyte senses energy deficiency, not at rest. You probably know as well as I do how inefficient exercise is for disposing calories, so unless Eades expects us all to take 6 hour zone 2 jogs after every meal, at some point insulin-mediated glucose disposal has to be accepted.

Plus, we and our predecessors in Homo have been consuming starches for hundreds of thousands of years, there is evidence of strong selection on regions like AMY1 that extends long before our genus, etc. It’s clearly just as native to us at this point as any other nutrient. What’s not native is—like I said before—the context. The liver obviously can’t handle 3 100g boluses of refined glucose per day, for 30 years, especially in a sedentary person. That doesn’t mean glucose, or insulin, is a thing to be suppressed at all costs, just like the mechanistic connection between fatty acids and cardiovascular disease doesn’t mean fatty acids should be suppressed at all costs. IMO, an insulin sensitive person who exercises 4-6 times per week can eat whatever combination of whole foods they like and have basically zero fear of MetS or accelerated atherosclerosis. Remember that JAMA paper in Jan 2021 that computed the WHI biomarkers HR for CVD? LDL was like 1.6, lipoprotein insulin resistance was higher, near to obesity, and T2D was like 10.5. To my mind, insulin resistance is the smoking gun, whether it’s the initial causative agent or not, it seems pretty clear that if you’re weight stable and insulin sensitive, you’re safe.

Plus, I feel like he of all people shouldn’t be relying entirely on rodent data. Isn’t that usually his thing? That metabolic observations from rats shouldn’t be extrapolated to humans?

> If blood glucose was stable and it went up 18mg/dl (1 mmol) wouldn’t that indicate the intake was too high ?

I mean, maybe in an absolute sense it means intake was greater than the ability of basal glucose disposal to completely account for, but “too high” seems like it suggests pathology, and I don’t see that small of a disturbance to serum glucose being anywhere near such a threshold. Any healthy person’s glucose will rise more than that simply by waking up, or lifting weights for a bit.

Plus, insulin shuttling glucose into muscle and adipose tissue isn’t bad. It’s a normal physiological process. Provided both of those tissue categories remain sensitive to insulin and the person is at stable weight, I don’t see how you could sneak your way into MetS.