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And that would be the kind of thing I would look for - take a food we've seen as generally harmless, find someone who is off the charts on a satiety index with it, and see if it can possibly get them obese. Until that's demonstrated, the whole satiety thing seems more like a 2nd or 3rd order effect than a core reason for obesity.

Palatability, not satiety (satiety is how filling it is).

The better test would be to have people rate the relative palatability of different foods. Build them a diet around those foods, and see how well the palatability tracks with weight change.

But even then there's the difficulty carrying out the study, changing palatability preferences (and what that means), maybe the fat prone people find everything tastier, etc. It sounds like a study with a lot of moving parts that's hard to do properly.

I leave it to Lustig to talk further on that, especially regarding the difference between fructose taken in juice form versus whole fruit (he seems to imply there is a difference in digestive process that mitigates the deleterious effects in that case).

Or that's the only way he can get rid of most of the non-industrial populations. After all how many non-industrial cultures drink a bunch of juice sweetened with refined sugar? Oops, found one (the Kuna)

I just thought of something - we could test this stuff on someone with no taste buds. By the satiety hypothesis, such a person would be unable to overeat, because nothing is tasty. The insulin hypothesis supposes that given insulin resistance, even if the tongue doesn't recognize that something is tasty, the muscles will know if they are being starved or not, and drive hunger.

Palatability not satiety.

I couldn't find anything on that but there seems to be an inverse correlation between taste bud sensitivity and weight. I'm not really sure what to make of it. Sweet and sour lower but bitterness, saltiness, and unami were depressed the most, I don't even know if that would balance out into increasing total palatability (less bitter) or decreasing (less salt). Could be a result of overstimulus, a defensive measure to reduce palatability, or causal somehow.

This nature article seems to imply we become less sensitive to flavours after eating a lot, though I'm not certain how that would related to palatability or satiety.

So you're asserting that there is in fact, some universal addictive properties that berries simply don't have? You deny the possibility of someone being addicted to berries because they find them so tasty?

Maybe if there is in fact certain things that cannot possibly be addictive (in this case, taking the Hazda diet, apparently by the tastiness hypothesis, nothing they eat can possibly be addictive since they don't get overweight), we can identify the biological mechanism of addiction.

Surely, my experience has shown sugar to be a particularly addictive substance, and it may be that simple...but I'd be interested in other proposed biomechanisms.

For some people maybe they are addictive enough to cause obesity, but for non-industrial cultures this doesn't seem to be a problem and even for industrial I don't think unprocessed berries are a signficant cause of obesity.

Well, you can separate the two - Lustig claims that a certain amount of fructose is what develops the carbohydrate allergy (aka, insulin resistance). Whether or not "non-industrial cultures can eat any macronutrient balance they want" begs the question as to the insulin response from those foods. Perhaps it's better to say "non-industrial cultures can eat low glycemic in any macronutrient balance they want".

Except we answered that question and they can eat rice and root crops that are high GI.

The only plausible mechanism you have left is fructose causing a 'carbohydrate allergy' in industrial populations, but even this is contradicted by non-industrial populations eating a lot of fruit and berries.

You only took a partial quote. The full quote is "The more easily digestible and refined the carbohydrates", and as shown by the lack of sugar consumption in Japan, they don't have more refined carbohydrates.

So again, no disagreement with Taubes except perhaps in the semantics of "easily digestible and refined" versus "easily digestible or refined".

Outside of increasing the GI what else does refining do other than making food more palatable? By adding refinement on top of GI you're conflating it with patabability for no reason, if you want to test his insulin hypothesis then look at less palatable foods that cause a high insulin response like plain rice.

Refuted elsewhere - the error bars on both porridge and fish for the 40 out of 41 subjects who didn't actually test all the foods were so large as to easily encompass fish being lower than porridge.

Ahh yes, that single pairing of carb vs protein shows porridge might have a slightly higher insulin response, devastatingly refuted.

But, they don't. They're innocent victims of insulin resistance and elevated insulin levels. You're trying to implicate protein and fat when they're just along for the ride. (Well, fat is certainly along for the ride - protein does have some insulin response, but that pales in comparison with that of carbohydrates - caveat that I know you still disagree on the 41 person fish study).

Exactly what do you think happens to the fat we eat?

Insulin resistance means that insulin, that stores excess blood sugar, leaves no blood sugar for muscles to use and inhibits the fat cells from release alternate energy (ketone bodies) for the muscles to use.

If your muscles are starving, why wouldn't you feel hungry?

Shouldn't type - 1 diabetes patients, before treatment get fat not thin then?

What about someone who *does* think berries are tasty, and potato chips aren't? After all, people can have different addictions. Can someone addicted to berries in the Hazda tribe get fat because of their subjective tastiness?

Someone who doesn't like chips probably won't get fat off them. But for berries factors like fibre, flavour, and moisture content might mean berries can reach that same level of addictivness.

And none of the data you've shown has contradicted that. You might have an example of certain carbs with a low glycemic index being *less* damaging, and therefore possibly negligible in effect, but you've caricatured Taubes into "all carbs must show a high insulin response and cause weight gain", instead of accepting that there is a spectrum of badness.

No, I've talked extensively about carbs with a high GI and insulin response like rice.

Not at all. I'm asserting the following - obesity is a sign of a carbohydrate allergy. Regardless of its genesis (say, fructose ala Lustig, or some other hormonal defect), the treatment is carbohydrate restriction. You cannot fix someone's insulin resistance (once they are insulin resistant), by feeding them starchy foods.

So by eating fructose we've developed some sort of insulin allergy that isn't present in non-industrial (ie ancestral) cultures. And that's why non-industrial cultures can eat any macronutrient balance they want and not get fat?

Did you come to this conclusion before or after the evidence the insulin hypothesis didn't work in non-industrial cultures?

Granted, let's assume for the moment that you have no alternate mechanism, and that Guynet's assertions are just hand waving. Let's be clear about the important questions still open about the insulin hypothesis:
1) what causes insulin resistance (see Lustig for one option)
2) what other mechanism could account for MHO (if say, further investigation shows that indeed, these large waisted people are able to accumulate fat in the absence of insulin). Perhaps this might end up being some sort of thyroid issue, who knows.

MHO==MOH==Morbidly Obese Humans?

Insulin resistance is more complicated than you think.

1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.

Mostly just in the sense that fat is very energy dense and make foods more palatable leading us to overeat. It may be linked to heart disease in industrial societies but not non-industrial.

2. The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis—the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.

Except easily digestible carbs like rice are fine in Japan, and countless non-industrial nations the only real common factor in obesity is industrial societies (though some like Japan avoid this).

That and protein also causes a similar effect on insulin (ie fish).

3. Sugars—sucrose and high-fructose corn syrup specifically—are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.

I agree, but for different reasons

4. Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization.

Maybe they're factors but my BS meter is go

You'd have to dig further into the 41 subjects that were a part of that survey. Further, it'd be nice if more than a single subject actually consumed all of the foods listed (http://ajcn.nutrition.org/content/66/5/1264.full.pdf). Even worse that only 15 subjects did more than two food categories.

Always look closely at the data before believing it.

That's what they have statistics for. Having the same subject consume both lets you run a paired T-test which lets you push the variance lower (I don't know if they did that with the 15) but having the 41 subjects consume foods from different categories is fine. If they did it your way you'd be complaining because they either tested fewer foods or did it with fewer volunteers. The only issue is like all studies of their kind it's done on a bunch of western university students.

And it's not the only study that decouples insulin and GI.

You've decided the only possible way to get fat is via insulin resistance (well at least for the 70% who have both conditions), so if palatability contributes to obesity you're assuming it must work in this bizarre fashion.

That's correct. We haven't shown any mechanism for fat accumulation outside of insulin resistance and elevated insulin levels, although some MHO data suggests it might be possible for say, 30% of the population.

We haven't shown any mechanism for fat accumulation outside of insulin. But that doesn't mean you can't get fat without insulin resistance or chronically elevated insulin. You haven't even accounted for glucagon!

How about this, define palatability. How can you tell one food is more or less palatable than another? Does this vary between individuals? Does it vary over time within individuals? What's your specific definition?

Some people have done some serious research into hyperpalatable foods. There are some characteristics of palatability, crunchiness, low bitterness, sugar, fat, salt. But the fact you don't want to accept a fuzzy definition doesn't mean its not a real thing. Are you seriously going to claim that we can't look at tastiness because I can't prove why icecream tastes better than a block of vegetable shortening?

That doesn't mean people haven't tried but you're not going to get a simple story.

You'd have to dig further into the 41 subjects that were a part of that survey. Further, it'd be nice if more than a single subject actually consumed all of the foods listed (http://ajcn.nutrition.org/content/66/5/1264.full.pdf). Even worse that only 15 subjects did more than two food categories.

Always look closely at the data before believing it.

That's what they have statistics for. Having the same subject consume both lets you run a paired T-test which lets you push the variance lower (I don't know if they did that with the 15) but having the 41 subjects consume foods from different categories is fine. If they did it your way you'd be complaining because they either tested fewer foods or did it with fewer volunteers. The only issue is like all studies of their kind it's done on a bunch of western university students.

And it's not the only study that decouples insulin and GI.

You've decided the only possible way to get fat is via insulin resistance (well at least for the 70% who have both conditions), so if palatability contributes to obesity you're assuming it must work in this bizarre fashion.

That's correct. We haven't shown any mechanism for fat accumulation outside of insulin resistance and elevated insulin levels, although some MHO data suggests it might be possible for say, 30% of the population.

We haven't shown any mechanism for fat accumulation outside of insulin. But that doesn't mean you can't get fat without insulin resistance or chronically elevated insulin. You haven't even accounted for glucagon!

How about this, define palatability. How can you tell one food is more or less palatable than another? Does this vary between individuals? Does it vary over time within individuals? What's your specific definition?

Some people have done some serious research into hyperpalatable foods. There are some characteristics of palatability, crunchiness, low bitterness, sugar, fat, salt. But the fact you don't want to accept a fuzzy definition doesn't mean its not a real thing. Are you seriously going to claim that we can't look at tastiness because I can't prove why icecream tastes better than a block of vegetable shortening?

That doesn't mean people haven't tried but you're not going to get a simple story.

Even if you assume an epigenetic factor is at work in western populations you still need to explain why it was activated in western populations and not ancestral populations eating lots of sugar, fructose, and carbs.

I thought you agreed that there is no ancestral population eating lots of sugar (i.e., like comparing sugar comparison between Japan and the US).

Name a single ancestral population eating lots of sugar, fructose and carbs.

Ok

No, I'm saying "the study you cited contradicts the other study you cited". Which one is wrong, do you think? Do you think that insulin doesn't cause fat accumulation as shown by study A, or do you believe that insulin does cause fat accumulation by study B?

I'm not sure what this study B you're talking about is. Outside of lipohypertrophy (something different) or insulin used to treat a specific disorder (very specific circumstances and I don't think I posted it anyways) I can't remember posting anything like that.

A metabolic ward is by definition a highly a-typical environment and putting someone in a metabolic ward introduces a pile of confounders that don't show up in the normal population.

So you're asserting that somehow the psychological effect of being in a metabolic ward causes biochemistry to behave differently?

Look, in order to get down to the biomechanisms here, you need to be able to observe things in frightening detail - are you positing some sort of heisenberg uncertainty principle for diet, in that it changes when observed?

You can examine what happens when you eat specific foods in detail and that very valuable. But obesity is caused by our entire lifestyle and can't replicate their lifestyles in a metabolic ward.

Your evidence that two generations of nutritional scientists are complete bunk and someone publishing thousands of papers without actually doing any useful work is largely based on a book by a journalist.

A journalist who has painstakingly cited every finding he's shown. He's just the messenger, the real data is there, and that needs to be contended with.

WTF do you think I've been doing?!? I've shown real data he's misrepresented. I've shown counter examples he's ignored. I've shown how everyone else knows about this 'real data' but also knows the other data that leads to different conclusions!

All Taubes has done is cherrypicked and misrepresented some data and ended up with some fame and a pile of money.

You can eat pretty much whatever balance of macronutrients you want, but if you're not in a developed economy you're probably not obese.

Maybe your idea of a "developed economy" differs than mine. Obesity is a form of malnutrition, and there are plenty of third world countries where obesity is rampant. Now granted, that's not an "ancestral diet", but I think it's difficult to find, much less define "ancestral diets". Do you have a specific example that would help illustrate what you mean?

In 3rd world countries the fat people are generally just the city dwellers. I guess 'developed economy' was a bad way to put it, populations who's lifestyle hasn't changed significantly in the past 500-1000 years. Subsistence hunters or populations using traditional farming techniques.

r. You think there's something with fructose in particular that causes insulin resistance with the same insulin levels?

Lustig posits (and I think it's fairly reasonable as at least one method) that fructose causes insulin resistance, and that before that point, insulin levels are perfectly well handled (allowing for the high starch/no insulin resistance == not much obesity populations). I think it's also possible that chronically elevated insulin levels in the absence of significant fructose could also be doing something to drive insulin resistance, but that's not as clearly outlined in biomechanical process as Lustig has with his fructose theory. It may be, as with insulin resistance, fructose effect occurs on a spectrum.

So it looks like fructose can be a factor in insulin resistance and it plays a role in abdominal fat. But I'm still not convinced that insulin resistance itself is a cause, and not a symptom of obesity.

So none of those Chinese people are adapted to fat? Is that genetic or environmental?

I'm claiming that any population you identify with a high carb diet and low obesity rates does not have significant allergies to carbohydrates. What triggers an allergy to carbohydrates may be a combination of genetic or environmental factors.

I'd approach the claim of genetic factors with extreme skepticism. Unless the entire western world under went a mutation in the last 100 years and everyone who moves to a western society undergoes the same mutation.

There's a genetic component to obesity obviously, but the smoking gun lies in modern diet and lifestyles.

Are you claiming that mice don't experience lipophypertrophy

I thought that was your claim - insulin given to mice, according to your cite, did not cause fat accumulation.

Lipohypertrophy is a specific form of localized weight gain. The cite said that injecting insulin did not cause total fat gain. Claiming insulin works significantly differently in mice is a VERY bold claim, evolutionary biologists would likely be astonished if a shared basic metabolic hormone had different effects between our species (and that nutritionists were so impossibly daft as to never notice it).

Show me an insulin sensitive person who isn't overweight, and loses 140 pounds on low carb, and then we'll be able to find out if there are any other reasons why low carb works :)

Sure (just a joke in poor taste, I have no idea what her actual diet was).

Well, I think the gold standard is the whole metabolic ward stuff. Peter Attia shares some of his experiences there: http://www.youtube.com/watch?v=NqwvcrA7oe8&feature=player_embedded

Our brain is actively maintaining the level of fatness. If your brain feels it has too much fat and your muscles need energy is will try to take calories from the fat instead of food.

How does the brain actively maintain the level of fatness? Are you saying that even in the presence of insulin resistance, that your brain can override your fat and muscle tissue and make them partition fuel despite the influence of insulin?

Insulin resistance will screw with the regulation but that doesn't mean it started the obesity or is the main driver.

I don't know exactly how the brain understands its weight level, but the set point certainly does exist and I can't see how insulin responding to blood sugar alone could be responsible for this.

If a Japanese or Vietnamese person can be thin with a bunch of calories from white rice why can't I?

If a two pack a day smoker can live until 94 years old without lung cancer, why can't everyone?

In the case of people living in Japan or Vietnam, more things than just their caloric intake of white rice vary - other portions of diet, other environmental factors, all can create a situation that isn't applicable to other locations.

Show me a country where 2-pack a day smokers have a drastically lower lung cancer rate and we'll talk.

Here's the big problem with the Taubes idea.

We weren't always fat. Virtually no ancestral cultures have high levels of obesity, but tons have high levels of carb intake. Some even eat a ton of fruit and honey.
You can also swap out a bunch of fat for sugar and not gain weight with modern people.

And if carbs are responsible for obesity then why did we eat more calories from carbs 100 years ago than we do today? And why isn't there a correlation between that macronutrient graph and obesity rates over the same period

If your interpretation of the biochemistry tells you that insulin is driving obesity then your interpretation is wrong because the evidence is pretty overwhelming that carbs are not the culprit.

Our brain is actively maintaining the level of fatness. If your brain feels it has too much fat and your muscles need energy is will try to take calories from the fat instead of food.

How does the brain actively maintain the level of fatness? Are you saying that even in the presence of insulin resistance, that your brain can override your fat and muscle tissue and make them partition fuel despite the influence of insulin?

Insulin resistance will screw with the regulation but that doesn't mean it started the obesity or is the main driver.

I don't know exactly how the brain understands its weight level, but the set point certainly does exist and I can't see how insulin responding to blood sugar alone could be responsible for this.

If a Japanese or Vietnamese person can be thin with a bunch of calories from white rice why can't I?

If a two pack a day smoker can live until 94 years old without lung cancer, why can't everyone?

In the case of people living in Japan or Vietnam, more things than just their caloric intake of white rice vary - other portions of diet, other environmental factors, all can create a situation that isn't applicable to other locations.

Show me a country where 2-pack a day smokers have a drastically lower lung cancer rate and we'll talk.

Here's the big problem with the Taubes idea.

We weren't always fat. Virtually no ancestral cultures have high levels of obesity, but tons have high levels of carb intake. Some even eat a ton of fruit and honey.
You can also swap out a bunch of fat for sugar and not gain weight with modern people.

And if carbs are responsible for obesity then why did we eat more calories from carbs 100 years ago than we do today? And why isn't there a correlation between that macronutrient graph and obesity rates over the same period

If your interpretation of the biochemistry tells you that insulin is driving obesity then your interpretation is wrong because the evidence is pretty overwhelming that carbs are not the culprit.

Our brain is actively maintaining the level of fatness. If your brain feels it has too much fat and your muscles need energy is will try to take calories from the fat instead of food.

How does the brain actively maintain the level of fatness? Are you saying that even in the presence of insulin resistance, that your brain can override your fat and muscle tissue and make them partition fuel despite the influence of insulin?

Insulin resistance will screw with the regulation but that doesn't mean it started the obesity or is the main driver.

I don't know exactly how the brain understands its weight level, but the set point certainly does exist and I can't see how insulin responding to blood sugar alone could be responsible for this.

If a Japanese or Vietnamese person can be thin with a bunch of calories from white rice why can't I?

If a two pack a day smoker can live until 94 years old without lung cancer, why can't everyone?

In the case of people living in Japan or Vietnam, more things than just their caloric intake of white rice vary - other portions of diet, other environmental factors, all can create a situation that isn't applicable to other locations.

Show me a country where 2-pack a day smokers have a drastically lower lung cancer rate and we'll talk.

Here's the big problem with the Taubes idea.

We weren't always fat. Virtually no ancestral cultures have high levels of obesity, but tons have high levels of carb intake. Some even eat a ton of fruit and honey.
You can also swap out a bunch of fat for sugar and not gain weight with modern people.

And if carbs are responsible for obesity then why did we eat more calories from carbs 100 years ago than we do today? And why isn't there a correlation between that macronutrient graph and obesity rates over the same period

If your interpretation of the biochemistry tells you that insulin is driving obesity then your interpretation is wrong because the evidence is pretty overwhelming that carbs are not the culprit.

High school chemistry classes should be teaching that paper burns at 451 C not 451 F. Units people!

Considering the insulin index of white rice compared to fruit [wikipedia.org] I find this claim pretty dubious.

Lustig makes the point that fructose consumption starts insulin resistance, and *then* the insulin index really matters. Check out his youtube lecture "sugar: the bitter truth" - he goes into serious depth there.

But that doesn't mean insulin is driving the hunger.

If insulin is driving energy into fat cells, and making it unavailable to muscles, and that unavailability is what triggers some sort of hunger response (as we see when say, someone is starving), isn't it simply obvious that in that case insulin is driving the hunger?

I mean, if instead of putting energy into your mouth, and putting it directly into fat storage, you simply didn't put that energy into the body, wouldn't a body get *hungrier*? Isn't that a reasonable assumption?

Even when gaining weight there's only a small difference in the average calories we ingest and the average we burn. Our brain is actively maintaining the level of fatness. If your brain feels it has too much fat and your muscles need energy is will try to take calories from the fat instead of food.

How does Taubes think the body regulates fatness? Does he think maintaining blood glucose at X level is the only mechanism?

If you really wanted to compare this to race vs intelligence then note you're the one positing that populations react differently to the same diets.

I'm positing that populations with different internal biochemical *environments* react differently to the same diets, whereas the race and intelligence folk posit that populations differ, *regardless* of environment.

How are their internal biochemical environments different? If a Japanese or Vietnamese person can be thin with a bunch of calories from white rice why can't I?

it's also consistent with mainstream nutrition

Would you critique mainstream nutrition with the same tactic, that there are some % of cases that don't follow their hypothesis?

Well there's 30% of obesity in Taiwan that doesn't follow Taubes hypothesis on why they're fat, and entire regions of the world (including examples he used) that defy his theory. If mainstream nutrition had this problem I think they'd be in trouble too.

I'd really suggest reading the series on Why Do We Eat? A Neurobiological Perspective. I think you'll be surprised by how complex the picture is and how thorough the literature is.

How are they having a debate and presenting evidence about a possible small regulatory role while completely missing the massive regulatory role that Taubes claims?

They're in denial. They have a trope, and even though the data doesn't match it, they refuse to give it up. Very typical of cargo-cult science.

Creationist journals are cargo-cult science, nutrition is real science doing real experiments.

Saying researchers put on blinders and never looked there would be like saying NASA put on blinders and never looked at the sun as the thing holding the solar system together.

Appeal to unnamed authorities fallacy.

Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".

That being said, NASA has put on blinders when it comes to the sun as the thing driving the earth's climate when it comes to the whole catastrophic anthropogenic global warming trope :)

See my 10 foot pole?

It's not even coming close :P

Look, you want to show a single clinical case of an obese person with no insulin resistance, or insulin issues, please, feel free - hopefully whatever happened in that one in a million case is identified and understood. But when it comes to the basic biochemistry of fat accumulation, it is simply incorrect to believe that insulin plays anything but a predominant role.

"Experimentally preventing the increase in circulating insulin that occurs on fattening diets does not alter the course of fat gain in rodents or dogs

Experimentally elevating circulating insulin by creating liver insulin resistance does not lead to fat gain in rodents

Experimentally increasing circulating insulin by infusing it directly into the blood does not cause fat gain in rodents, but instead makes them leaner

Roughly a quarter of obese humans have normal circulating insulin and normal insulin sensitivity ("metabolically healthy" obese)"

BOOM!! /me does a rude dance

How are they having a debate and presenting evidence about a possible small regulatory role while completely missing the massive regulatory role that Taubes claims?

They're in denial. They have a trope, and even though the data doesn't match it, they refuse to give it up. Very typical of cargo-cult science.

Creationist journals are cargo-cult science, nutrition is real science doing real experiments.

Saying researchers put on blinders and never looked there would be like saying NASA put on blinders and never looked at the sun as the thing holding the solar system together.

Appeal to unnamed authorities fallacy.

Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".

That being said, NASA has put on blinders when it comes to the sun as the thing driving the earth's climate when it comes to the whole catastrophic anthropogenic global warming trope :)

See my 10 foot pole?

It's not even coming close :P

Look, you want to show a single clinical case of an obese person with no insulin resistance, or insulin issues, please, feel free - hopefully whatever happened in that one in a million case is identified and understood. But when it comes to the basic biochemistry of fat accumulation, it is simply incorrect to believe that insulin plays anything but a predominant role.

"Experimentally preventing the increase in circulating insulin that occurs on fattening diets does not alter the course of fat gain in rodents or dogs

Experimentally elevating circulating insulin by creating liver insulin resistance does not lead to fat gain in rodents

Experimentally increasing circulating insulin by infusing it directly into the blood does not cause fat gain in rodents, but instead makes them leaner

Roughly a quarter of obese humans have normal circulating insulin and normal insulin sensitivity ("metabolically healthy" obese)"

BOOM!! /me does a rude dance

How are they having a debate and presenting evidence about a possible small regulatory role while completely missing the massive regulatory role that Taubes claims?

They're in denial. They have a trope, and even though the data doesn't match it, they refuse to give it up. Very typical of cargo-cult science.

Creationist journals are cargo-cult science, nutrition is real science doing real experiments.

Saying researchers put on blinders and never looked there would be like saying NASA put on blinders and never looked at the sun as the thing holding the solar system together.

Appeal to unnamed authorities fallacy.

Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".

That being said, NASA has put on blinders when it comes to the sun as the thing driving the earth's climate when it comes to the whole catastrophic anthropogenic global warming trope :)

See my 10 foot pole?

It's not even coming close :P

Look, you want to show a single clinical case of an obese person with no insulin resistance, or insulin issues, please, feel free - hopefully whatever happened in that one in a million case is identified and understood. But when it comes to the basic biochemistry of fat accumulation, it is simply incorrect to believe that insulin plays anything but a predominant role.

"Experimentally preventing the increase in circulating insulin that occurs on fattening diets does not alter the course of fat gain in rodents or dogs

Experimentally elevating circulating insulin by creating liver insulin resistance does not lead to fat gain in rodents

Experimentally increasing circulating insulin by infusing it directly into the blood does not cause fat gain in rodents, but instead makes them leaner

Roughly a quarter of obese humans have normal circulating insulin and normal insulin sensitivity ("metabolically healthy" obese)"

BOOM!! /me does a rude dance

How are they having a debate and presenting evidence about a possible small regulatory role while completely missing the massive regulatory role that Taubes claims?

They're in denial. They have a trope, and even though the data doesn't match it, they refuse to give it up. Very typical of cargo-cult science.

Creationist journals are cargo-cult science, nutrition is real science doing real experiments.

Saying researchers put on blinders and never looked there would be like saying NASA put on blinders and never looked at the sun as the thing holding the solar system together.

Appeal to unnamed authorities fallacy.

Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".

That being said, NASA has put on blinders when it comes to the sun as the thing driving the earth's climate when it comes to the whole catastrophic anthropogenic global warming trope :)

See my 10 foot pole?

It's not even coming close :P

Look, you want to show a single clinical case of an obese person with no insulin resistance, or insulin issues, please, feel free - hopefully whatever happened in that one in a million case is identified and understood. But when it comes to the basic biochemistry of fat accumulation, it is simply incorrect to believe that insulin plays anything but a predominant role.

"Experimentally preventing the increase in circulating insulin that occurs on fattening diets does not alter the course of fat gain in rodents or dogs

Experimentally elevating circulating insulin by creating liver insulin resistance does not lead to fat gain in rodents

Experimentally increasing circulating insulin by infusing it directly into the blood does not cause fat gain in rodents, but instead makes them leaner

Roughly a quarter of obese humans have normal circulating insulin and normal insulin sensitivity ("metabolically healthy" obese)"

BOOM!! /me does a rude dance

Although Taubes did the seminal work "Good Calories, Bad Calories", which references the undisputed biochemistry I've cited, he isn't the guy who actually did the work - he just reported on it. Calling him a "crank" is to misunderstand how we actually got to understand the Kreb's cycle and the role of insulin in fat accumulation.

Now, Stephan Guyenet has an axe to grind against Taubes, and that's fine, but nothing he's written or cited contraindicates the role of insulin in fat accumulation. There's some question as to what triggers initial insulin resistance (since there are a group of people out there who have no fat accumulation problems despite high carbohydrate intake, although other problems invisible to the naked eye do occur), but there's absolutely no question that the mechanism for fat accumulation in the obese is insulin.

There's a big difference between insulin being required for fat storage and insulin regulating fat storage.

My big beef with Taubes is he basically assumes researchers made a mistake in the 50s, and then... well I'm not sure what.

Have they been doing public advocacy the past 60 years and never bothered to do anymore research?

Are they all such spectacularly bad researchers that no one ever noticed insulin was regulating obesity?

Did they have incredible tunnelvision and haven't looked at how insulin reacts with fat at all?

To believe Taubes you need to believe the entire field of nutrition science has been spectacularly incompetent for the past half century, somehow never considering that the hormone that enables fat accumulation also regulates it. Yet some science reporter somehow stumbled on the truth and is giving you a completely unbiased account of it.

Just look at how he responds when asked about the Japanese and their rice consumption. He starts talking about Japanese eating brown rice until 50 years ago and being healthy then. Ok, so what about the Japanese eating white rice now and still being healthy!! He also says that maybe the real problem is sugar. So the goalposts have moved, high carb isn't bad, it has to be high refined carbs, and maybe it isn't even high refined carbs, it has to be actual sugar! So I'm glad that Taubes apparently endorses a primarily brown rice diet as the key to being thin.

Of course, he didn't need to move the goalposts when talking about the Massa, since most people don't really know what the Massa eat it's safe to simply misrepresent their diet.

Although Taubes did the seminal work "Good Calories, Bad Calories", which references the undisputed biochemistry I've cited, he isn't the guy who actually did the work - he just reported on it. Calling him a "crank" is to misunderstand how we actually got to understand the Kreb's cycle and the role of insulin in fat accumulation.

Now, Stephan Guyenet has an axe to grind against Taubes, and that's fine, but nothing he's written or cited contraindicates the role of insulin in fat accumulation. There's some question as to what triggers initial insulin resistance (since there are a group of people out there who have no fat accumulation problems despite high carbohydrate intake, although other problems invisible to the naked eye do occur), but there's absolutely no question that the mechanism for fat accumulation in the obese is insulin.

There's a big difference between insulin being required for fat storage and insulin regulating fat storage.

My big beef with Taubes is he basically assumes researchers made a mistake in the 50s, and then... well I'm not sure what.

Have they been doing public advocacy the past 60 years and never bothered to do anymore research?

Are they all such spectacularly bad researchers that no one ever noticed insulin was regulating obesity?

Did they have incredible tunnelvision and haven't looked at how insulin reacts with fat at all?

To believe Taubes you need to believe the entire field of nutrition science has been spectacularly incompetent for the past half century, somehow never considering that the hormone that enables fat accumulation also regulates it. Yet some science reporter somehow stumbled on the truth and is giving you a completely unbiased account of it.

Just look at how he responds when asked about the Japanese and their rice consumption. He starts talking about Japanese eating brown rice until 50 years ago and being healthy then. Ok, so what about the Japanese eating white rice now and still being healthy!! He also says that maybe the real problem is sugar. So the goalposts have moved, high carb isn't bad, it has to be high refined carbs, and maybe it isn't even high refined carbs, it has to be actual sugar! So I'm glad that Taubes apparently endorses a primarily brown rice diet as the key to being thin.

Of course, he didn't need to move the goalposts when talking about the Massa, since most people don't really know what the Massa eat it's safe to simply misrepresent their diet.

Fat accumulation is driven by the hormone insulin. Undisputed biochemistry.

Insulin levels are driven by blood sugar levels. Undisputed biochemistry.

Blood sugar levels are driven by carbohydrate intake. Undisputed biochemistry.

I'm sorry to inform you but Gary Taubes is a crank.

Stop eating carbohydrates. It's simple.

Low carb diets work, but not for the reason you think they do.

Fat accumulation is driven by the hormone insulin. Undisputed biochemistry.

Insulin levels are driven by blood sugar levels. Undisputed biochemistry.

Blood sugar levels are driven by carbohydrate intake. Undisputed biochemistry.

I'm sorry to inform you but Gary Taubes is a crank.

Stop eating carbohydrates. It's simple.

Low carb diets work, but not for the reason you think they do.

One thing people might want to check out is a blog by an actual obesity researcher

Simply put there's a lot of factors of which the author summarized a few with an 8 part series on what motivates people to eat. One of the main hypothesis he pushes is the particularly depressing palatability hypothesis that says the tastier food is the more of it we'll eat.

He also takes down the nonsense of Gary Taubes.

One thing people might want to check out is a blog by an actual obesity researcher

Simply put there's a lot of factors of which the author summarized a few with an 8 part series on what motivates people to eat. One of the main hypothesis he pushes is the particularly depressing palatability hypothesis that says the tastier food is the more of it we'll eat.

He also takes down the nonsense of Gary Taubes.

One thing people might want to check out is a blog by an actual obesity researcher

Simply put there's a lot of factors of which the author summarized a few with an 8 part series on what motivates people to eat. One of the main hypothesis he pushes is the particularly depressing palatability hypothesis that says the tastier food is the more of it we'll eat.

He also takes down the nonsense of Gary Taubes.

The ghastly-little-soldering has been dissuading me; but apparently the move toward eDisplayPort (rather than LVDS) in recent iPads means that you can successfully connect their screens to ordinary DisplayPort sources, given a suitable physical adapter and a power supply for the backlight.

I don't know if the same is true of the Surface Pro or not. If it's an LVDS panel, the conversion hardware isn't wildly expensive (but the ebay cheapy boards aren't nearly small enough to fit neatly); if it's eDP, some moderately heroic soldering and a custom flexPCB might actually make it happen...

Here's some worthwhile reading on why Lisp has trouble staying put—possibly a little flamebait-y: Lisp is not an acceptable Lisp, The Lisp Curse, and Revenge of the Nerds. The core arguments seem to be (a) it's really easy to invent things in Lisp so no one can agree on how to do it, and (b) the lack of a coherent standard platform means there is no easy target for university courses or job descriptions.

the casual thief might get caught by this, for a while. .. when I started writing this, I was thinking "SIM cards aren't RFID, are they?" I was wrong. So maybe they're just reading RFID tags?

What's the cost of an RFID-blocking smartphone wallet these days? Passport wallets that advertise RFID blocking are about $20 us or so...

by MS, who took ownership of the 32-bit follow-on OS.

Of course, this was before they turned this OS/2 2.0 project into an entire fiasco that I have very bad words against MS about.

All the examples you give predate the "nearly four decades" timespan that I wrote about in my post. With those you just have--inadvertently-- confirmed my point.

Academics made great contributions to programming languages until the "programming languages=type theory" and "usability improvements=syntactic sugar" mindsets crept in. I am far from the first person to observe this btw, e.g.:

http://matt-welsh.blogspot.ca/2013/04/the-other-side-of-academic-freedom.html?showComment=1366600358822#c5765593833050647322

Don't get me wrong, I'm all in favor of research. I'm just pointing out that the PL community has chosen a narrow focus of their discipline to the detriment of progress in real life PLs.

I know. It was hardly the worst thing about the MS OS/2 2.0 fiasco though (for which I have a very bad opinion against MS).

Personally, if you can't tell from my comments, my personal favorite is the MS OS/2 2.0 fiasco.

Here's the lowdown on how BZGF works, as one example. In this case, there are many short distinct of DNA being stored together, each with offset and quality information, many of which may be identical. The compression is localized to smaller blocks (I'm not sure if they're 4096-byte disk sectors or something else.) You're right that there's probably some performance lost due to the misalignment, but 6 and 8 line up every 24 bits, so at worst that means patterns of four codons or three bytes—and a step of four amino acids is ideal for alpha helix motifs, so it's not all a loss.

And, yes, regarding individual genomes: I'm pretty sure that'd be all anyone stored if they didn't have to hold onto the FASTQ files for auditability.

The missing link: Google Voice for Calgary only in Canada

http://21stdigitalhome.blogspot.ca/2013/06/vcp200-voice-recognition-ic.html

I wrote a blog article about MS's bad decision here:
http://yuhongbao.blogspot.ca/2012/12/about-ms-os2-20-fiasco-px00307-and-dr.html

Though the best solution would have been not making this mistake back in 1990 in the first place.

Also see the original MS OS/2 2.0 SDK announcement from 1989:
http://www.os2museum.com/wp/wp-content/uploads/2012/03/1989-12-29-m3974.html
And my blog post on is at here (notice the mention of DR-DOS and PX00307, which is another exhibit that don't seem to be well known:
http://yuhongbao.blogspot.ca/2012/12/about-ms-os2-20-fiasco-px00307-and-dr.html

My personal favorite is the MS OS/2 2.0 fiasco:
http://yuhongbao.blogspot.ca/2012/12/about-ms-os2-20-fiasco-px00307-and-dr.html

I've been using ifttt and gmail since just after they announced retiring Google reader. It works pretty good so far: http://prlj13-whatimupto.blogspot.ca/2013/06/rss-replacing-google-reader-with-ifttt.html

They do it well.

Not to mention that MS was not exactly good during the Gates era either. My personal favorite is the MS OS/2 2.0 fiasco, but of course that is not the only one.

Ah, DR-DOS. I mentioned in my blog post about the OS/2 2.0 fiasco that Caldera took advantage of the fact that Win9x ran on top of DOS to continue its lawsuit against MS, and that OS/2 was designed as a full OS from the beginning.

Bad news. The card companies cannot disable this on their end and the limits are set by the merchants rather than the bank. I've tried to get them to disable it to no effect (which I think is BS -- if you can accept it, you can choose to *not* accept it). In any event, there is a site that shows you how to cut the NFC antenna in your card.

AFAIK this helped DR's lawsuit against MS. In contrast, as mentioned in my blog post, OS/2 never depended on DOS at all.

The MS OS/2 2.0 fiasco is my favorite MS fiasco: http://yuhongbao.blogspot.ca/2012/12/about-ms-os2-20-fiasco-px00307-and-dr.html

Don't have time to read the article, but I was curious if the government collude in that. Thats the problem we have here.

No, but there is a visa program that's being abused by employers similar to the H1B's in the US. Blazing Cat Fur did a story on it a few days ago(for those that don't know BCF, he is one of the newstrenders here in Canada, he usually breaks a story 2-3 days before hand and the media picks up on it), and the majority of the input workers are going into fastfood especially in places like Alberta. Interestingly enough the last time something similar happened the federal government(conservatives) intervened and changed the law regarding this.

Ah, the MS OS/2 2.0 fiasco:
http://yuhongbao.blogspot.ca/2012/12/about-ms-os2-20-fiasco-px00307-and-dr.html

How about their parents? They had them, they raised them or failed to raise them. They are responsible.

Not a chance, governments worldwide have spent the last 25 years or so doing their best to make people believe that they're not responsible for raising them. Hell even up here in Canada we have schoolboard trustees who believe they're actually the parents or co-parents. So, if that's the case, I say we blame those instead.

There are many logical, reasoned arguments one can make against the existence of God.

But there are emotional ones, too, and ones that don't involve such arguments as "God doesn't exist, and atheists hate Him.", like some apologists pithily quote (I'm looking at you, Dinesh D'Souza).

For me, it's summed up in this (possibly NSFW) one picture. Kevin Carter, the photographer of this picture, has claimed that the child proceeded to get up and make their way to a UN famine relief centre, but the truth is no one knows for sure.

It's very, very hard to hear apologists argue about faith with that image in my mind, I find.

I have a blog article about the MS OS/2 2.0 fiasco: http://yuhongbao.blogspot.ca/2012/12/about-ms-os2-20-fiasco-px00307-and-dr.html

Personally my favorite topic is the MS OS/2 2.0 fiasco that is about the 386, which is much much worse: http://yuhongbao.blogspot.ca/2012/12/about-ms-os2-20-fiasco-px00307-and-dr.html