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
I'm not talking about technical difficulties, the Python dev experience is top notch and I have no complaints in that area. What I mean is that it's hard to form a mental model of what's going on because it's as though you were using two different languages: the "fast" API calls and the "slow" munging of the results.
The frustrating part is that the language doesn't seem to "compose" any longer, it doesn't feel uniform: you can't really do things the simple way without paying a hefty peformance penalty.
With that said, the #1 reason why any code in any language is slow is "you're using the wrong algorithm", either explicitly or implicitly (wrong data structure, wrong SQL query, wrong caching policy, etc.), and in that sense Python definitely helps you because it makes it easier (or at least less tedious) to use the correct algorithm.
I think that complaint applies to the (vast, essential) ecosystem, not to the language and standard library. AFAIK, there aren't serious performance potholes to hit in the language and standard library any more. You're not paying a huge performance penalty for writing things the simple way, but things are uniformly pretty slow.
It's when you pull in fast libraries that composition breaks down e.g. the many-fold difference between numpy's sum method and summing a numpy array with a python for-loop and an accumulator.
I agree, the standard library doesn't have those problems. As you said though, the ecosystem is kind of the point of using Python in the first place.
Again, I'm not really a fan of Python as a general purpose language for large projects, but it really, really excels at being a kind of "universal glue", and it's why I use it again and again.
In that role, "uniformly slow" is better than "performance rollercoaster".
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.
> 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 :)
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.
> No point in focusing on hormones so much. I somehow don't see people fretting over their ACTH or progesterone.
I respectfully disagree. When I go to USA or Mexico in particular, the frequency of obesity is astonishing. Perhaps with more understanding of the mechanisms around the phenomenon, there would be more success in dealing with the problem. As I mentioned earlier, around 25% of the entire human population has NAFLD, which is also an astonishing figure.
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.
> insulin IS NOT needed for glucose absorption
I'm not aware of anyone claiming insulin is needed for glucose absorption. The brain, liver, and red blood cells, for example, cannot function properly if they are sensitive to blood insulin levels; this may be because the RBC and brain rely on a steady supply of glucose, and the liver must be able to take up or release glucose on its own schedule.
On the other hand, muscle and adipose tissue DO have insulin-sensitive GLUT4 transporters. The GLUT family of transporters are passive, so glucose flows down its concentration gradient, unlike the sodium-linked transporters of the gut and kidney, which actively transport glucose against a gradient.
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. In a person without diabetes, insulin is released from the vesicles when the body detects the amino acids leucine and arginine, or the sugars glucose and mannose. So typically, insulin will also be present, and having its usual effect on the GLUT4 transporters.
This is all covered, to some degree, in the appendices to Fung's book on obesity, by the way.
> Adipose tissue is [...] 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.
It doesn't seem fair to even compare Fung's work with the claims of Myolean, because Fung is a trained scientist and knows how to read, interpret, and communicate scientific information in the traditional manner that others can understand. Even if Fung's arguments were wrong, at a superficial level he would be more persuasive because he knows how to use the language and standards of science.
However, examining the discussion in some details will reveal that Fung is correct in all the major points covering this topic, as best as is known at present. (Of course there are major unknowns when it comes to human metabolism, but there is also a lot that is known).
From the link you provided, it seems quite apparent that Myolean does not understand what a non-linear feedback system is (e.g. human metabolism), and doesn't understand the role of motivation and willpower (for compliance) involved in maintaining a calorie-deficient or calorie-neutral diet.
At no point does Fung say the laws of thermodynamics don't apply, but rather that they aren't very relevant when you incorporate the variability of basal metabolism, and motivation/willpower, into the model. One of Fung's major points is that in reality, when people try to follow restrictive diets, doing it in a way that leaves you constantly hungry, with low willpower, and continuously high insulin production leads to failure of achieving desired results.
Lastly, it would be easier to take Myoleanfitness more seriously if I didn't get the feeling they are trying to sexually manipulate me with a hit of dopamine and testosterone with their ads such as [2] and [3].
The point is, the substance of the Myoleanfitness argument is not even wrong, its just irrelevant. But the form in this case matches the content. Distracting and irrelevant.
> 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.
> As we go on you reference Fung (and defend him) a fair bit
I defend Jason Fung because he's one of the few in this area of science and medicine who has gone to the trouble of writing books that ordinary people can understand, and yet still have some scientific rigor. I could cite innumerable scientific papers that very few have the training to read, or the one author who took the time to write something anyone literate can at least follow along with.
There are hundreds if not thousands of researchers and practitioners in this area, so it is convenient to point to someone that anybody literate can read and rely on. His books (several of them overlap greatly) cite hundreds of papers, so that work mostly a compilation of other's work (as it should be).
> He does not hold (to my knowledge) a PhD nor has he published any peer-reviewed studies.
I'm not sure what a PhD has to do with anything, most of my scientific work was published before I got mine, or even started it, as is common in industry and applied sciences.
> 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?
I'm sorry you don't see the connection regarding FFA, perhaps you can re-read what he wrote and click through to the underlying reference to get a better idea (the title is "Fat Oxidation, Body Composition and Insulin Sensitivity in Diabetic and Normoglycaemic Obese Adults 5 Years After Weight Loss"). I couldn't find the text of Fung's book online, but the other paper he references in this connection is "The role of fatty acids in insulin resistance" (2015) which I did find online, here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587882/ .
> 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.
I agree in general. I think IF is fine, I'm favor of balanced diets not very low or high in anything in general, and I believe without regular blood work and expert supervision, keto is downright dangerous for most. Thermodynamics are present, true, but this is in practice perhaps not the most helpful perspective, since things like willpower, hunger, and sustainably maintaining a healthy diet matter more; the thermodynamic perspective fails to model the feedback control system that regulates the human behavior component. Nonetheless, I agree with the overall thrust of your comment.
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.
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".
tl;dr somebody who has little idea about economy or history tries to write about economy and politics, fails miserably
longer read:
It's hard to consider Foucault serious basis for in-depth political analysis. I'm not a total fan of Chomsky, but he was 100% right about Foucault - it's gibberish without any scientific basis.
Neoliberalism never was intended a COMPLETE fix to prevent fascism. Much the same way markets were never meant to be a source of justice. Idea that there's some inherent justice that can be achieved through free market is a straw man.
The interpretation author has of the invisible hand suggests he never really read Adam Smith, just heard of it.
Then follows an interesting conclusion - "we are using the market to justify government action" - which is entirely false. We can try to analyse markets to verify effects of certain government action (and it's incredibly hard, often laden with error stemming from too small amount of factors considered) and politicians sometimes use such arguments - but that's false equivalency.
What follows is critique of Donald Trump and Republicans ending in authors conclusion that economics is hard. It is, that's why even someone like Varoufakis initially wanted to leave it to economists.
Finally we have this ad absurdum rhetoric of "what ifs". Well, what if my aunt had mustache - should I call her "uncle"?
"Neoliberalism’s very frugality and subsequent demands for efficiency dovetail all too well with the rational efficiency of fascist genocide. " Wow. I think the author never really read about neoliberalism's notion of the state not interfering in the markets or what happens under nationalism to enterprise and commerce (hint: heavy state intervention). Actually, anybody sane would say that it's the exact opposite. One has to be mentally ill to kill people who would work for you for free. And you had to be an idiot to say there was any rational efficiency in genocide. Genocide is the most irrational and inefficient thing you can do, since you're effectively killing people who would be willing to work as slaves (most people prefer slavery, at least initially, to death). To do that, as Nazis did during WW2 is a proof on how ideology elevated to the level of religion can lead to worst possible outcome.
Apart from that - author would benefit from reading on something like discretionary versus rule-based economic policies and generally, spending more time reading about macroeconomy before writing about that.
This is pure honesty and wanting to help. People who feel better on cycle usually a) in fact do need TRT and b) should consider professional counsel in regard to their psychological help. Testosterone is very potent antidepressant - if you only feel good on T it means you only feel good on antidepressants. This information with the context you mentioned (trenbolone which has net negative effect on serotonin metabolism in the brain) suggests you should visit a doc and talk about SSRIs. Seriously.
They usually have underlying psychological condition which they fail to address. Note that all the "regain" studies were done in cohorts that had either severe problems or lacked proper professional assistance (which these days you can get online for 100USD).
The fact that you can loose weight is simple physics. The fact that these people often have endocrine issues is near tautology because adipose tissue HAS endocrine activity and thus ones changes hormonal profile if in excess. Usual set of changes include: insulin resistance, lower testosterone, low thyroid hormones, leptin resistance, higher SHBG and usually higher estrogen.
Doesn't mean dieting won't work but if someone is long-term overweight he needs more work than just a difference in bodyweight.
