It's very plausible that sugar (I.E. sucrose) damages POMC cells that regulates appetite and energy expenditure during childhood, then the person grows up to be intolerant of carbs making them suffer from metabolic disorder. That's why fat Westerners (like myself) do well on low carb high fat diets, whereas low sugar societies (like the Japanese) stay skinny despite having lots of carbs later in life.
There's quite a bit of evidence for that, but we need some large scale studies to be made to confirm it with more confidence.
>> The absence of causality in the CI-CO = dW has been well established for centuries > >It's pure PHYSICS that if you need a certain number of calories, and if you do not consume enough, you will lose weight.
That's what I said... CI-CO = dW But CI-CO => dW is obviously wrong because it doesn't work. and CI-CO = dW is obviously wrong because a change in weight can't force you to do anything.
>That might be because the whole calorie counting thing is pure BS.
This.
The absence of causality in the CI-CO = dW has been well established for centuries. It was lost briefly in a period between the 1970s and mid 2000s, but I think we're back on track mostly, provided that you don't listen to doctors.
>No. bitcoins are accepted almost nowhere, they thus don't have the liquidity of money
I'm working on bringing my wife's yarn store up to speed accepting bitcoins. Why not? It's a hell of a lot easier than putting together code for PCI-DSS compliant credit card transactions, or paypal.
Was that your homework assignment for a rhetoric class or do you actually go around talking like that while people quietly wish you would go somewhere else?
There's a guy who does an excellent job of reviewing serious health and nutrition research and explaining it. He's covered many of the statin studies. His web site is most useful here because I can point to explanations that point to real studies, rather than pointing to real studies and writing a bucket load of explanations.
The serum LDL does go up and down in inverse relationship to the LDLR LDL receptors. However the liver is generally pumping out the same amount of LDL. The serum LDL is low because it gets pulled into cells more quickly and LDLR activty on cell surfaces increase. So the same amount of LDL reaches cells.
People with PCSK9 mutations that increase LDLR benefit from lower heart disease because there is less LDL oxidation, because there is a lower density of LDL and each LDL blob spends less time getting from liver to cell. The LDL oxidation is known to be the starting point for plaque formation.
So, yes, low serum LDL as part of a natural bodily response is great. But LDL is part of a repair mechanism. If you lower LDL using drugs, then there is less LDL around to transfer the repair materials.
>beneficial not just in lowering LDLs, but also rates of myocardial infarctions(heart attacks), coronary heart disease, and overall mortality. While raising the rates of other diseases like cancer to a greater extent and in significant populations (like women) offering no benefit at all.
>"Fructose and sucrose appear to promote obesity more strongly than equivalent amounts of starch or glucose;". Different result.
Yes. I'm saying there isn't a significant difference between the metabolic processing of sucrose and HFCS. Glucose and starchy precursors of glucose are obviously differently processed by the body because they lack the fructose and the metabolic processing of fructose is very different.
Fructose != sucrose != glucose. But sucrose is very close to HFCS. Sufficiently close that difference in health outcomes are not apparent.
Slashdot Mirror
It's very plausible that sugar (I.E. sucrose) damages POMC cells that regulates appetite and energy expenditure during childhood, then the person grows up to be intolerant of carbs making them suffer from metabolic disorder. That's why fat Westerners (like myself) do well on low carb high fat diets, whereas low sugar societies (like the Japanese) stay skinny despite having lots of carbs later in life.
There's quite a bit of evidence for that, but we need some large scale studies to be made to confirm it with more confidence.
>> The absence of causality in the CI-CO = dW has been well established for centuries
>
>It's pure PHYSICS that if you need a certain number of calories, and if you do not consume enough, you will lose weight.
That's what I said... CI-CO = dW
But CI-CO => dW is obviously wrong because it doesn't work.
and CI-CO = dW is obviously wrong because a change in weight can't force you to do anything.
Please keep up.
No it isn't.
FFS. We seem to have this discussion weekly on Slashdot.
A little review of the literature: http://www.ketotic.org/2013/09/the-ketogenic-diet-reverses-indicators.html
>3 eggs + bacon is like 400-500 calories? That's a large glass of orange juice.
Well technically, orange juice is a bunch of fuctose and some fiber (if it's unfiltered) to help your gut bacteria make you fat.
3 eggs + bacon is food.
>found the soylent concoction particularly tasty
Or found it particularly not tasty and upped the FIAF instead: http://high-fat-nutrition.blogspot.com/2007/12/fiaf-whos-fat-is-it-anyway.html
>That might be because the whole calorie counting thing is pure BS.
This.
The absence of causality in the CI-CO = dW has been well established for centuries. It was lost briefly in a period between the 1970s and mid 2000s, but I think we're back on track mostly, provided that you don't listen to doctors.
>I thought the exact property of bitcoin is having its trail un-followable.
Er. No.
>No. bitcoins are accepted almost nowhere, they thus don't have the liquidity of money
I'm working on bringing my wife's yarn store up to speed accepting bitcoins. Why not? It's a hell of a lot easier than putting together code for PCI-DSS compliant credit card transactions, or paypal.
I don't know the value. I know the price. I go to coinbase.com to find the price.
Was that your homework assignment for a rhetoric class or do you actually go around talking like that while people quietly wish you would go somewhere else?
The value of bitcoins was obviously spiking in the past few days. So no. A drop was entirely expected irrespective of any silkroadyness.
There's a guy who does an excellent job of reviewing serious health and nutrition research and explaining it. He's covered many of the statin studies. His web site is most useful here because I can point to explanations that point to real studies, rather than pointing to real studies and writing a bucket load of explanations.
Here we go...
Lower LDL post heart attack predicts an higher chance of being dead in the next 3 years:
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20and%20heart%20attack%20survival
Statins give cancer to men who respond well to statins
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20and%20the%20J-LIT%20study
If you're in the lowest cholesterol group as a result of taking statins, you have a 600% increase in the risk of a cardiovascular death
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20and%20the%20J-LIT%20update
10 year all cause mortality in low dose statins is lowest at 250 mg/dl. Higher at lower and higher levels. Dramatically so for cardiac events.
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20and%20Son%20of%20J-LIT
A little bit on statins fixing the wrong properties of LDL and HDL. I.E. total volume rather than size and number.
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20and%20Son%20of%20J-LIT
A 50% increase in being dead on Crestor, courtesy of the JUPITER study, buried in the data so as not to cause embarassment.
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20heart%20attacks%20and%20JUPITER
A more complete review of the JUPITER study with fewer difficult words.
http://junkfoodscience.blogspot.com/2008/11/when-news-sounds-too-good-statins-new.html
Lets hope you don't have Familial hypercholesterolemia and take this drug.. 1000% increased chance of stroke or heart attack. Yay for statins!
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20pacitimbe%20and%20ACAT
Oh dear. Statins increase the oxidation of LDL. No wonder they kill so many people.
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%3A%20statins%20and%20oxLDL
The traditional piss taking of Ancel Keys massaging of saturated fat data to get the wrong result, extended to statins.
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%20presentation%3A%20Between%20countries
Lowering of LDL does not correlate with atheroma volume decrease. Whoops. Where did my hypothesis go?
http://high-fat-nutrition.blogspot.com/search/label/Cholesterol%3A%20ASTEROID%20destroys%20lipid%20hypothesis
Killing more unsuspecting patients with torcetrapib in the RADIANCE1 and RADIANCE2 studies.
http://high
The serum LDL does go up and down in inverse relationship to the LDLR LDL receptors. However the liver is generally pumping out the same amount of LDL. The serum LDL is low because it gets pulled into cells more quickly and LDLR activty on cell surfaces increase. So the same amount of LDL reaches cells.
People with PCSK9 mutations that increase LDLR benefit from lower heart disease because there is less LDL oxidation, because there is a lower density of LDL and each LDL blob spends less time getting from liver to cell. The LDL oxidation is known to be the starting point for plaque formation.
So, yes, low serum LDL as part of a natural bodily response is great. But LDL is part of a repair mechanism. If you lower LDL using drugs, then there is less LDL around to transfer the repair materials.
>beneficial not just in lowering LDLs, but also rates of myocardial infarctions(heart attacks), coronary heart disease, and overall mortality.
While raising the rates of other diseases like cancer to a greater extent and in significant populations (like women) offering no benefit at all.
So if you limit your view to heart disease and related diseases statins sometimes appear to work.
http://www.ncbi.nlm.nih.gov/pubmed/22677075
But if you measure all cause mortality, they're a disaster.
If you do a quite big study and report it honestly, you might find the statins don't help much with anything
http://high-fat-nutrition.blogspot.com/2008/11/cholesterol-heart-attacks-and-jupiter.html
But sometimes you have to stop the study before the evidence becomes too clear.
http://en.wikipedia.org/wiki/JUPITER_trial
Yes. But today is the deadline for SP800-90 comment submissions. So not today. I haven't got my comments submitted yet.
Or tinted layers with a volumizing mousse cut in an attractive bob.
You are not alone.
I first hit this when fetching subversion. I think it gave me an Ask Jeeves toolbar pox instead.
"plans to launch their HEAT2X lift vehicle loaded with the TRS-80 capsule"
Wow. That is old school.
>"Fructose and sucrose appear to promote obesity more strongly than equivalent amounts of starch or glucose;". Different result.
Yes. I'm saying there isn't a significant difference between the metabolic processing of sucrose and HFCS. Glucose and starchy precursors of glucose are obviously differently processed by the body because they lack the fructose and the metabolic processing of fructose is very different.
Fructose != sucrose != glucose.
But sucrose is very close to HFCS. Sufficiently close that difference in health outcomes are not apparent.
Yes. You can use lard. Beware of some cheaper brands that sneakily hydrogenate. Check the label.
Or better still, render your own.
They should fully hydrogenate themselves.
Vegetables are overrated. I avoid them except as decoration for meat.
I had to look up PHVO. Now I know.
Unfermented Soy is bad all on its own. Partially Hydrogenate it FTW!
>Ketosis for the win.
Indeed. Peeing on sticks for pleasure and profit.
Monoculture in food production leading to a fragile food supply maybe.