Scientists narrow down the mechanism whereby cancer cells metabolise sugar
sciencealert.com
sciencealert.com
Is it reasonable to talk about the health impact of sugar at all? For example, the article says:
> This link between sugar and cancer has sweeping consequences.
Does that refer to sugar I eat? Or sugar my body makes from carbohydrates I eat? And are glucose and fructose equally linked to cancer? What about all the other sugars?
I also recommend the rest of the channel.
Hmm.. So they could have used any opisthokont's cells for a model, but they chose a fungus, a type of organism that travels readily in the environment as micrometer-sized spores and on even forms yeast, a zoomorphism which just so happens to match the growth and feeding patterns of cancer.. makes sense.
Conversely, the above has resulted in a big number of yeast trained molecular biologists, who end up applying yeast work wherever they can (see: law of the instrument). Sometimes it works, sometimes it doesn't.
Cancer: A Metabolic Disease With Metabolic Solutions. https://www.youtube.com/watch?v=SEE-oU8_NSU
Ketosis has shown to be good for quicker recovery from chemotherapy.
But that only holds if growing out of control has no impact on normal function. If, say, cancer cells reproduced faster than their own mitochondria, then those cancer cells would function differently from normal cells in a particular sense: they could metabolize sugars into pyruvate but not all the way to CO2 + H2O. And that in turn could have other consequences.
This statement glosses over how important the molecular processes of cellular metabolism and mitosis are, how they are linked, and why cancer cells are aberrant. I don't think one can call a cancer cell a normal cell that is growing out of control.
This is pretty much the characteristic ability that cancerous cells have.
I can be more specific if you'd like.
I'm getting javascript framework diet fad of the week fatigue
humans are fully capable of doing the statistics to get proper answers on these questions without ML. we just cannot trust the data enough,because to get a reliable data set we would have to imprison a few tens of thousands of people for 60 years and control every aspect of their exercise and diet, and that sort of thing usually gets you arrested.
I don't think this is a problem with our learning, but a problem with our unrelenting desire to compress complex subjects and findings into easily digestible morsels that people can understand without too much thought.
Deep learning isn't going to help with that.
I lost my uncle last year to small-cell lung cancer (age 40). Doctors gave him 12 months after the diagnosis, turns out he barely had 3 months (mostly due to a very bad response to chemotherapy). In his last months he turned to one of these alternative medicine gurus who told him that the tumor (quote) „would eat itself“ if he stops eating sugars.
Sorry if this is too personal of a question.
- him being a heavy smoker (SCLC almost exclusively in smokers)
- running a car repair shop and inhaling fine dust frequently
Despite these factors he was very unlucky developing cancer at such an early age.
Survival rates for SCLC: http://www.cancercenter.com/lung-cancer/statistics/tab/lung-...
The best one can do is try to minimize risk factors to either avoid cancerous growth or at least to slow it down to the extent that it does not affect life expectancy.
THe actual paper is about the https://en.wikipedia.org/wiki/Warburg_effect Warburg effect (the observation that cancerous cells rely heavily on glycolysis). People have wondered about causation, and this group has offered some mechanistic answers that help get us closer to knowing if glycolysis spikes _because_ you have cancer, or you get cancer because you lean on glycolysis.
This mechanism is the glycolysis (something used in fermentation), which is much less effective than the other mechanism which uses oxygen (used indeed in respiration) to produce ATP.
From the article abstract, they hint that the cell cycle is quicker with glycolyse than with respiration.
Fructose-1,6-bisphosphate couples glycolytic flux to activation of Ras (2017)
https://www.nature.com/articles/s41467-017-01019-z
Background: https://en.wikipedia.org/wiki/Warburg_effect
However I agree in that sugar and carbs are a big factor, and one can go a long way avoiding them.
the issue would be to reduce fat consumption as much as humanly possible, while taking regular blood sugar measurement, only diabetics do this and it's already late by then.
I cannot find a single study showing insuline resistance due to high fat consumption when consuming <5% of calories in carbs and <25% in protein.
Our ancestors only found carbs accompanied by lots of fiber. Fiber causes satiety. Carbs cause insulin secretion, which indirectly converts carbs to fat and puts the body in fat storage mode. Storing fat was an advantage to our ancestors because they couldn't ever store fat all year round. But nowadays 30% of calories in carbs is considered "normal" or even "low", but it's actually absurdly high considering the rest of the diet (low fiber, way too much fructose) and our activity.