mdomans · HackerTrans

In general optimising Python is: * understanding that pure Python is not a language to write CPU-heavy computational code in it and was never intended as such * understanding that Python lets you write 3-4 solutions to a problem easy and 1 will be slow, two will be OK and one will be optimal - often that involves using generators, collections, sets and is a bit nuaced * I'd say that optimising Python, compared to something like C or C++ is far easier - I can set up a decent testing and profiling environment for most of my problems easy with pip and ipython which is borderline simple compared to valgrind

mdomans

5 lat temudiscuss

Oh boy, the IJF is going to have an epic hissy fit

mdomans

6 lat temudiscuss

Mostly because both JavaVM and ErlangVM are solid but Java VM is much more popular.

If you're looking for a technology to run a service focused on privacy and security one of the things to consider is the amount of use and thus testing something gets. In case of Java that's testing in enterprise setting.

mdomans

6 lat temudiscuss

Best regard to you too :)

mdomans

6 lat temudiscuss

> I'm not saying that every person must study these metabolic pathways in detail, but rather that the quick and simple rules and choices people make in daily life should take advantage of what is known, hopefully for a better outcome than what is currently observed.

I agree. I'm simply pointing out the fact that with the picture as complex as we know it is I have a knee jerk reaction to people going from "how to have normal BF%" to "ok, let's talk about insulin". It's the same thing with people talking about brain, attention span and productivity. 10 seconds into the discussions it's "dopamine, dopamine ... DOPAMINE"

> So in the case of adipose tissue, it does require glucose in order to store fat. The glycerol backbone for intracellular triglyceride synthesis is provided by glucose.

Yes. And? Glucose to some extent is always present in the blood. Drop the glucose low enough and brain will die. One could say that adipose tissue will always figure out how to store fat.

As we go on you reference Fung (and defend him) a fair bit. I'd like to take this opportunity to state the obvious. Jason Fung is a trained and certified nephrologist, book author, popular doctor and so on. He does not hold (to my knowledge) a PhD nor has he published any peer-reviewed studies.

Thus calling him a quack on my part was bad (I was pulling your leg a bit) but he cannot be considered a scientist either. He's an expert in his field but his books can't be considered textbooks on human endocrinolongy. He's allowed to have his own opinion but asking anybody to agree or disagree with his views without in-depth study of them is asking too much and he haven't (to my knowledge) presented them in the form of some kind of scientific paper it's not worth arguing whether he's right or not.

That being said - the link you provided on FFA is about cholesterol. I fail to see how that's relevant to discussion about FFA impact on insulin resistance?

Alas, to make my point. Obesity is certainly a multifaceted problem. Thermodynamics certainly matter, human psyche, inflammation, hormones - essentially all of that has its place. Looking from a systems point of view there's no reason (and probably there isn't one) to look for single causative agent though some certainly play a grater role.

In my experience both time-restricted feeding, caloric restriction and macro restriction work and have their place depending on the individual. Generally as a rule IF and low-carb are certainly good ideas, I'm not a fan of keto for everything.

mdomans

6 lat temudiscuss

> I didn't understand that the main point was "debunking the idea that insulin is what makes us fat", since I don't know anyone who believes that. Chronic poor nutrition can make you fat, sure, and rising basal insulin levels tend to occur as a result of that, but saying "insulin is what makes us fat" sounds a lot like "yellow fingertips cause lung cancer". Nobody I know believes that is true. I have to keep up on these things for my work, in drug development.

Insane amount of people believes and promotes that. As in INSANE. Just check any sports/diet related magazine :)

mdomans

6 lat temudiscuss

Insulin is mostly (in humans, not rats) a hormone signalling energy availability. That's why many humans secret insulin when we smell or taste food, way before it hits GI tract.

> Maintaining the insulin/glucagon cycle is important in maintenance of a healthy metabolism.

No point in focusing on hormones so much. I somehow don't see people fretting over their ACTH or progesterone.

> Insulin mediates glucose transport and promotes absorption of blood glucose into the liver, fat and muscle cells.

If you look at data from humans - insulin IS NOT needed for glucose absorption. Studies on diabetic people clearly show that glucose gradient into the cell is higher, not lower, despite them being incredibly insulin resistant. 1st role of insulin in humans that's critical is shutting down liver glucogenesis and gluconeogenesis.

The problem with insulin/glucose narration is omitting the role of FFA. Intracellular FFA levels drive down the glucose absorption gradient. If the glucose absorption gradient is low and we still have glucose - that will stimulate more insulin release to drive that glucose level to normal.

Problem is that as more insulin is present cells eventually start being resistant to insulin requiring more insulin for the same job. Which makes for a problem because if insulin is there to shut down liver glucogenesis and cells are now more resistant to insulin - bad news, we need more insulin to get blood glucose to same levels with a meal that used to be no problem.

Adipose tissue is simply the number #1 a-hole here because it's usually the least resistant to insulin and the least resistant to nutrient storage since it's its primary role. It will just pack more in.

P.S. Isn't Fung a quack? E.g. https://www.myoleanfitness.com/evidence-caloric-restriction/

mdomans

6 lat temudiscuss

No. I can elaborate but generally it's the glucose that stimulates the insulin release (the pancreas has glucose receptors).

Weight gain IS NOT driven by insulin or glucose. You can put someone on euglycemic clamp literally pumping him with insulin and glucose and he won't get fat from that. He will hover start storing fat IF we give him too much glucose for his needs.

Frankly, if you were a very mad you could theoretically put yourself on insulin/protein infusion to lose fat.

Idea being that insulin will drop your blood glucose (via insulin-dependant glucose transporter translocation) forcing liver to balance that out. When liver runs out of stored glucose it will start breaking down fat.

The downside of that is that eventually muscles won't store more glucose (you'd somehow need to get rid of that) and the risk of dying is pretty high.

mdomans

7 lat temudiscuss

You can't force or even ask someone to be a role model because than that's not being a role model. Much like telling someone to volunteer makes them "not a volunteer".

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