Agreed. And I'd make the assertion that for the vast majority of 400 pound fat people chowing down large pizzas, they're doing so because their muscles are starving, and their appetite is triggered on high, thanks to the partitioning of energy due to insulin into their fat cells.
Further, if we have, say, a model of appetite where one can increase it by reducing caloric intake, and increasing caloric output (as say, when you're told to "bring your appetite", and you skip a meal, or go exercise more to work up your hunger), it seems that focusing on calories in/calories out is going to be self defeating.
Now, imagining that it's all about taste, calorie density, texture, and "filling" begs the question - what are the biochemical processes at work there?
I guess for me it's hard to assert that those particular bits are nearly as important as insulin resistance, and insulin response, especially since we have such a wide variety of response to the same diet.
The insulin hypothesis deals rather neatly with the appetite response observations, since the partitioning of fuel into fat cells starves muscles, driving more eating, which we can then call "overeating" (because it drove fat accumulation - a skinny person, by definition, can never overeat).
It might cause obesity but the fact you can create obesity by simulating a specific disorder doesn't mean that disorder causes obesity.
I can see perhaps asserting there might be some alternate causes of obesity (in some small percent of people), but I'm not sure if you've identified a confounding factor yet.
If Taubes is right there should be a strong correlation between % of calories from carbohydrates, particularly simple ones like rice, and obesity
You're missing a variable - insulin resistance. If you go by Lustig, if someone eats nothing but starch, but never touches fruit, they never develop insulin resistance.
They overeat as a result of non-insulin factors. The excess food causes excess blood sugar, this causes an insulin spike and eventual resistance.
How can excess fat intake (in the absence of significant carbohydrate intake) raise blood sugar levels? Isn't the problem that they "overeat" carbohydrates?
Scientists follow the evidence, not government guidelines,
Your optimism is refreshing:) Try get a government grant on research that doesn't toe the line of the government position on something.
they spend a lot of time talking about why people eat more calories, how many they burn being active, how many they burn while inactive, metabolic factors, etc....
So, they blame character flaws (gluttony and sloth), and then make observations of "calories in/calories out", without actually asking "what is the metabolic *cause*". Lustig has done some great stuff on that.
If you want to go all in on the insulin theory and start drenching everything in butter all I can do is wish you good luck and hand you the number of a contractor who can widen your front door.
I have, and I've lost weight. In nutritional ketosis, eating 3000+ calories a day, with a sedentary lifestyle, I simply don't gain any weight. You may of course, consider this simply a single anecdote, not data, but you'd have a very difficult time making the case that the insulin hypothesis isn't true in my individual case.
Take the Japan example, he was asked about it directly, and he unambiguously dodged the question.
What's there to dodge? The question of "look, rice" is like asking "have you stopped beating your wife?" Holding up a country as an example of "look, insulin is wrong" is like the whole race and intelligence crap - you can't start doing your comparison unless you *control* for environment, and in the case of "lots of rice countries", that means controlling for insulin resistance, which might very well vary between populations.
It's funny, it seems as if you're unwilling to entertain the idea that as per the Taiwan study you cited, the vast majority of cases of obesity *support* Taubes' hypothesis. Would you be more forgiving of Taubes if he said simply "in the vast majority of cases", rather than giving you the notion that he believed 100% of the cases followed?
Lipohypertrophy simply confirms insulin as the mechanism for fat storage which everyone agrees on.
Okay, with you there.
What you'd need to show is insulin injections can cause obesity (not just lipohypertrophy) in healthy patients.
That's only with the caveat of a healthy patient with insulin resistance, but it begs the question - if we all agree insulin is a mechanism for fat storage, why *wouldn't* insulin injections cause obesity?
But the real measure is to see what their % of calories from carbohydrates is (which I couldn't find)
Not sure what you're driving at here - you think obese native Hawaiians must not be eating much rice? Or that it's not a high enough percentage of their diet?
I agree the other 70% have insulin issues, but I challenge that their obesity is caused by those insulin issues instead of insulin issues caused by obesity.
So you think fat accumulation happens *first*, and *then* insulin rises? Given the agreement on insulin as the mechanism for fat storage, exactly how does that jibe together?
My central beef with Taubes is nutritionists already know a huge amount of the story of what causes obesity.
That's categorically untrue. Nutritionists have ignored the basic biochemistry for years, and been driven by misguided government guidelines put out by the USDA (see the 1978 McGovern commission). Like the example of a full dining hall, it is *trivially* true that it is full because more people entered than left, but it that statement gives you *no* information as to *why* people enter and *why* people leave. The typical nutritionist story about obesity is "more calories were stored in fat cells than were removed" - which is simply an observation, not a statement of cause.
I'd like to be thinner, but I also ate some cookies when I wasn't really hungry last night. The carbs in the cookies weren't the problem, the problem was that they were cookies.
The cookies are only a problem if they cause fat accumulation. We know that's driven by insulin. If the cookie was made out of say, 100% butter, 0% carbohydrate, the cookie wouldn't have the same effect on your fat accumulation.
Taubes is part of a long line of fad diets
I believe you truly misunderstand him. Taubes is a science history reporter, not a diet guru. He's done a great job of exposing the fallacies of the fat-hypothesis, and a great job of showing the strong support of the insulin hypothesis, but the diet conclusions from that aren't really the point, other than to show us that our current dietary guidelines have been based on mistaken premises.
other causes are at work and the insulin is just along for the ride.
So in essence, you posit a confounding variable, that drives insulin, unrelated to carbohydrate intake? I mean, if we drive deeper, leptin/insulin track (http://www.ncbi.nlm.nih.gov/pubmed/10567012) to carbohydrate consumption...are you suggesting it's possible for someone to be "metabolically healthy" with good insulin levels, but out of control leptin levels? Or are you suggesting some other driver of insulin besides blood sugar levels, and some other driver of blood sugar levels besides dietary carbohydrate?
Say we posit that "other causes are at work" with insulin *not* along for the ride in some % of cases (30% stipulated, for example)...does that still mean you're asserting that those *same* "other causes" also drive the other 70% of insulin resistant folks?
It could be that all you're interested in doing here is pointing out the holes in the insulin hypothesis without replacing it with an alternative, which I'm *perfectly* fine with (that's how good science is done, after all)...but do you believe that the insulin hypothesis is simply untenable in any conditions, or needs to be modified for certain, non-majority scenarios?
The NASA example was obviously just for rhetorical purposes. But I've included numerous links to scientific papers, and the Guyenet links I included all used multiple citations.
Yes, we've addressed the issues with rat models, and conflicting papers:)
And my apologies - I wasn't clear that I was critiquing your rhetorical appeal to unnamed authorities. I do appreciate the *actual* references and papers you've cited!
Good luck getting approval to inject insulin into healthy people to see if it makes them fat.
That's been done before, they even have a word for it:
Cultures that eat a ton of white rice? They stay thin.
Um, try Hawaii and obesity levels amongst native Hawaiians, who have a *ton* of white rice in their diet.
Inject insulin into rats? Thin
Again, animal model versus human reality. If the rat model was an accurate depiction, anorexics who were treated with insulin would lose weight:)
Fat people without insulin issues? Significant portion.
As per my other reply, let's say we stipulate to 30% of fat people without insulin issues...are you agreeing that the other 70%, the vast majority, *do* have insulin issues?
So you're arguing that the 30% may have still been insulin resistant because they didn't test insulin resistance directly, just blood glucose levels and blood pressure.
Not only that, but they only tested waist size.
As for a writeup of a fat person without insulin resistance or elevated insulin levels, why would someone do that clinical writeup if it's a completely ordinary phenomena?
Always check your premises in science:)
That all being said, let's say we stipulate to 30% of the obese population being driven by say, some odd thyroid problem rather than chronically elevated insulin levels - do you accept that 70% of the obese population has their fat accumulation driven by insulin?
Perhaps I'm driving too hard a bargain, and can convince you that for the overwhelming majority of obese people insulin is a problem, rather than for 100%.
Creationist journals are cargo-cult science, nutrition is real science doing real experiments.
A nutritionist who ignores the biochemical role of insulin in fat accumulation, and insists it's all "calories in/calories out" is a creationist then.
Appealing to a scientific authority about a scientific question they study is hardly an "unnamed authorities fallacy".
Sure it is. You refer to some large group (say NASA), and make a baseless assertion without specific attribution. Name the individual, cite the work, or you're simply hand waving.
BOOM!!/me does a rude dance
Wow, if only everything that happens to rats happened to humans:)
Also interesting that you cite a paper "Identification and characterization of metabolically benign obesity in humans", while also citing the other paper that concludes, "Results of the present study indicate that obesity in the absence of the metabolic abnormalities is not such a rare condition in Taiwan. Furthermore, obesity and weight gain are associated with an increased risk for incidences of hypertension, T2DM and the metabolic syndrome in the metabolically healthy, middle-aged population. As such, weight management should continue to be a target for reducing cardiometabolic diseases in all obese indi- viduals."
Trying to have your cake and eat it too?:)
Stephan Guyenet seems to have decided to rewrite the Kreb's cycle...seems like wishful thinking in search of evidence:)
"No data of serum insulin or hs- C-reactive protein (CRP) for further exclusion of metab- olically abnormality in our study was a limitation of re- search; therefore we adopted a metabolic syndrome crite- rion to exclude subjects with insulin resistant characters. It is rare to be insulin-resistant while subject’s blood glu- cose levels were less than 5.6 mmol/L, triglyceride 1.7 mmol/L, HDL-C 1.0 mmol/L in men, 1.3 mmol/L in women and blood pressure 130/85 mmHg."
but at 102 cm you're carrying a lot of fat no matter what height you are.
Again, an assertion, not an observation. The study doesn't purport to show what you think it does. What you're looking for is a clinical writeup of a single individual with a fat accumulation problem that doesn't have insulin resistance, or elevated insulin levels. This study clearly has limitations, including the critical statement "To date, there is no uniform definition for MHO."
You're editorializing - they didn't say they had normal insulin sensitivity, they said "Subjects included were 1,547 men and women (age range, 18-59 years), who were free of components of the metabolic syndrome except waist criteria."
While EGIR has a definition for insulin resistance, none of the other definitions require it for a definition of metabolic syndrome. WHO lists it, but doesn't *require* it.
The study itself claims this caveat:
"It is rare to be insulin-resistant while subject’s blood glu- cose levels were less than 5.6 mmol/L, triglyceride http://apjcn.nhri.org.tw/server/APJCN/21/2/227.pdf
The other question is "does waist criteria represent obesity"? I knew plenty of people who would've failed on the BMI scale, but did not have a fat accumulation problem. So while it's fairly provocative, I think the study fails to demonstrate what you editorialized in your link text.
No though I've heard/read a number of extended interviews.
I highly suggest giving it a read, especially the footnotes. You may not walk away agreeing with him, but you'll be better informed.
That's not true, there's a lot of obese people with no insulin issues.
Just one example, please. Any example. A single obese person that has neither insulin resistance, nor elevated insulin levels.
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.
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. 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:)
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.
To believe Taubes you need to believe the entire field of nutrition science has been spectacularly incompetent for the past half century
That's not surprising at all. Have you read his book, "Good Calories, Bad Calories"? Thanks to zealots like Ancel Keys, the direction of government sanctioned research went in a singular direction with blinders, masking and disparaging any divergent opinions.
Look, no matter what your particular axe to grind with Taubes, the fact of the matter is that for every obese person, you've got a combination of insulin resistance and high insulin levels, period. It simply doesn't happen by any other biochemical mechanism.
Actually, no, insulin resistance/sensitivity counts for a lot. Sort of a "square/rectangle" thing - not everyone with elevated insulin levels is going to get obese, but anyone who is obese is so because of elevated insulin levels.
Lustig posits that insulin sensitivity is driven by fructose consumption and its effect on the liver, which seems plausible, but I'm sure a great deal of it has to do with genetics as well. There are bean pole skinny guys out there with high cholesterol and diabetes who don't have any fat accumulation problem, but still get all the other "benefits" of high insulin.
Actually, you'd be surprised. When I hit fast food joints, they're more than happy to hold the bun, the fries, and the sugary drink. At the store, I buy pork rinds instead of chips. At restaurants, I ask them to replace whatever starch with something like broccoli dripping in cheese or butter. I've never had a situation where I haven't been able to avoid carbohydrates.
Now, that being said, it is true that carbohydrates are in fact, addictive, and weaning oneself off of the sugar rush/crash cycle is as difficult as stopping the use of other drugs like tobacco, alcohol, methamphetamine, or even cocaine. It *can* be sustainable, but it's not something that happens without effort.
The only "calorie in/calorie out" that counts is the calories that are partitioned into fat accumulation, versus those that are partitioned into energy use. This is driven not by the gross amount of calories, but by the insulin response from those calories (and the insulin sensitivity/resistance of the subject).
The second law of thermodynamics applies, but not at the macro level of "mouth/body", but rather the micro level of the fat cell.
Scientifically, the only proven mechanic is the regulation of insulin levels.
Yes, I've permanently changed they way I live - I *always* avoid eating carbohydrates, and will do so for the rest of my life.
I lost 50 pounds in 6 months after understanding the biochemistry behind fat accumulation and the reasons behind it, and have kept that off for 6 years.
As for selling books/videos, I've got no dog in that fight - and frankly, recommending carbohydrate restriction is so simple and effective, it doesn't *require* any sort of expensive book or video to understand and implement.
Having someone who is insulin sensitive semi-starve themselves while eating only potatoes can certainly cause weight loss. Applying an isocaloric potato diet, increasing the % of carbohydrates, to someone who is insulin resistant is going to cause obesity.
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.
I've been in ketosis for going on six years now, and never had any sort of kidney issue. In fact, my wife's kidneys, which had some signs of malfunction ever since her 20s, got *better*.
Nutritional ketosis might not be for everyone, but I've yet to see any credible information showing that it is harmful in any way whatsoever.
For me, after two years of low-calorie/low-fat diet and 5 miles a day of running, and a 10 pound weight *gain*, keeping carbs under 20g a day lost me 50 pounds in 6 months, and kept it off for the past 6 years.
The sad thing is that people still keep pushing the calories in/calories out dogma, which takes well intentioned people down the completely wrong path.
Look up the Kreb's cycle - insulin levels simply are not driven at all by fat calories, and only marginally by protein calories. Carbohydrates drive insulin levels, and insulin levels drive fat accumulation.
You can refuse to believe the basic, biochemical facts, and attempt to apply a tinker toy physics model of "e-in/e-out", but it simply doesn't apply.
Fat accumulation isn't driven by caloric intake levels, it's driven by insulin.
If you consume calories which drive insulin up, you'll accumulate more fat. Consume calories which don't drive insulin up, and you won't accumulate more fat.
The concept is pretty simple: to lose weight, don't consume calories that cause fat accumulation. We call these "carbohydrates".
Slashdot Mirror
What does that mean, biochemically?
Agreed. And I'd make the assertion that for the vast majority of 400 pound fat people chowing down large pizzas, they're doing so because their muscles are starving, and their appetite is triggered on high, thanks to the partitioning of energy due to insulin into their fat cells.
Further, if we have, say, a model of appetite where one can increase it by reducing caloric intake, and increasing caloric output (as say, when you're told to "bring your appetite", and you skip a meal, or go exercise more to work up your hunger), it seems that focusing on calories in/calories out is going to be self defeating.
Now, imagining that it's all about taste, calorie density, texture, and "filling" begs the question - what are the biochemical processes at work there?
I guess for me it's hard to assert that those particular bits are nearly as important as insulin resistance, and insulin response, especially since we have such a wide variety of response to the same diet.
The insulin hypothesis deals rather neatly with the appetite response observations, since the partitioning of fuel into fat cells starves muscles, driving more eating, which we can then call "overeating" (because it drove fat accumulation - a skinny person, by definition, can never overeat).
I can see perhaps asserting there might be some alternate causes of obesity (in some small percent of people), but I'm not sure if you've identified a confounding factor yet.
You're missing a variable - insulin resistance. If you go by Lustig, if someone eats nothing but starch, but never touches fruit, they never develop insulin resistance.
How can excess fat intake (in the absence of significant carbohydrate intake) raise blood sugar levels? Isn't the problem that they "overeat" carbohydrates?
Your optimism is refreshing :) Try get a government grant on research that doesn't toe the line of the government position on something.
So, they blame character flaws (gluttony and sloth), and then make observations of "calories in/calories out", without actually asking "what is the metabolic *cause*". Lustig has done some great stuff on that.
I have, and I've lost weight. In nutritional ketosis, eating 3000+ calories a day, with a sedentary lifestyle, I simply don't gain any weight. You may of course, consider this simply a single anecdote, not data, but you'd have a very difficult time making the case that the insulin hypothesis isn't true in my individual case.
What's there to dodge? The question of "look, rice" is like asking "have you stopped beating your wife?" Holding up a country as an example of "look, insulin is wrong" is like the whole race and intelligence crap - you can't start doing your comparison unless you *control* for environment, and in the case of "lots of rice countries", that means controlling for insulin resistance, which might very well vary between populations.
It's funny, it seems as if you're unwilling to entertain the idea that as per the Taiwan study you cited, the vast majority of cases of obesity *support* Taubes' hypothesis. Would you be more forgiving of Taubes if he said simply "in the vast majority of cases", rather than giving you the notion that he believed 100% of the cases followed?
Okay, with you there.
That's only with the caveat of a healthy patient with insulin resistance, but it begs the question - if we all agree insulin is a mechanism for fat storage, why *wouldn't* insulin injections cause obesity?
Not sure what you're driving at here - you think obese native Hawaiians must not be eating much rice? Or that it's not a high enough percentage of their diet?
So you think fat accumulation happens *first*, and *then* insulin rises? Given the agreement on insulin as the mechanism for fat storage, exactly how does that jibe together?
That's categorically untrue. Nutritionists have ignored the basic biochemistry for years, and been driven by misguided government guidelines put out by the USDA (see the 1978 McGovern commission). Like the example of a full dining hall, it is *trivially* true that it is full because more people entered than left, but it that statement gives you *no* information as to *why* people enter and *why* people leave. The typical nutritionist story about obesity is "more calories were stored in fat cells than were removed" - which is simply an observation, not a statement of cause.
The cookies are only a problem if they cause fat accumulation. We know that's driven by insulin. If the cookie was made out of say, 100% butter, 0% carbohydrate, the cookie wouldn't have the same effect on your fat accumulation.
I believe you truly misunderstand him. Taubes is a science history reporter, not a diet guru. He's done a great job of exposing the fallacies of the fat-hypothesis, and a great job of showing the strong support of the insulin hypothesis, but the diet conclusions from that aren't really the point, other than to show us that our current dietary guidelines have been based on mistaken premises.
So in essence, you posit a confounding variable, that drives insulin, unrelated to carbohydrate intake? I mean, if we drive deeper, leptin/insulin track (http://www.ncbi.nlm.nih.gov/pubmed/10567012) to carbohydrate consumption...are you suggesting it's possible for someone to be "metabolically healthy" with good insulin levels, but out of control leptin levels? Or are you suggesting some other driver of insulin besides blood sugar levels, and some other driver of blood sugar levels besides dietary carbohydrate?
Say we posit that "other causes are at work" with insulin *not* along for the ride in some % of cases (30% stipulated, for example)...does that still mean you're asserting that those *same* "other causes" also drive the other 70% of insulin resistant folks?
It could be that all you're interested in doing here is pointing out the holes in the insulin hypothesis without replacing it with an alternative, which I'm *perfectly* fine with (that's how good science is done, after all)...but do you believe that the insulin hypothesis is simply untenable in any conditions, or needs to be modified for certain, non-majority scenarios?
Yes, we've addressed the issues with rat models, and conflicting papers :)
And my apologies - I wasn't clear that I was critiquing your rhetorical appeal to unnamed authorities. I do appreciate the *actual* references and papers you've cited!
That's been done before, they even have a word for it:
http://en.wikipedia.org/wiki/Lipohypertrophy
http://garytaubes.com/2012/02/on-the-greatly-exaggerated-demise-of-the-insulin-hypothesis/
Heck, they even use it as a therapy for anorexia:
http://www.psychologytoday.com/blog/evolutionary-psychiatry/201206/evolution-and-anorexia-nervosa
Um, try Hawaii and obesity levels amongst native Hawaiians, who have a *ton* of white rice in their diet.
Again, animal model versus human reality. If the rat model was an accurate depiction, anorexics who were treated with insulin would lose weight :)
As per my other reply, let's say we stipulate to 30% of fat people without insulin issues...are you agreeing that the other 70%, the vast majority, *do* have insulin issues?
Maybe we already have 70% agreement :)
Not only that, but they only tested waist size.
Always check your premises in science :)
That all being said, let's say we stipulate to 30% of the obese population being driven by say, some odd thyroid problem rather than chronically elevated insulin levels - do you accept that 70% of the obese population has their fat accumulation driven by insulin?
Perhaps I'm driving too hard a bargain, and can convince you that for the overwhelming majority of obese people insulin is a problem, rather than for 100%.
A nutritionist who ignores the biochemical role of insulin in fat accumulation, and insists it's all "calories in/calories out" is a creationist then.
Sure it is. You refer to some large group (say NASA), and make a baseless assertion without specific attribution. Name the individual, cite the work, or you're simply hand waving.
Wow, if only everything that happens to rats happened to humans :)
Also interesting that you cite a paper "Identification and characterization of metabolically benign obesity in humans", while also citing the other paper that concludes, "Results of the present study indicate that obesity in the absence of the metabolic abnormalities is not such a rare condition in Taiwan. Furthermore, obesity and weight gain are associated with an increased risk for incidences of hypertension, T2DM and the metabolic syndrome in the metabolically healthy, middle-aged population. As such, weight management should continue to be a target for reducing cardiometabolic diseases in all obese indi- viduals."
Trying to have your cake and eat it too? :)
Stephan Guyenet seems to have decided to rewrite the Kreb's cycle...seems like wishful thinking in search of evidence :)
Read the study directly, it'll be more informative for you than the abstract:
http://apjcn.nhri.org.tw/server/APJCN/21/2/227.pdf
"No data of serum insulin or hs- C-reactive protein (CRP) for further exclusion of metab- olically abnormality in our study was a limitation of re- search; therefore we adopted a metabolic syndrome crite- rion to exclude subjects with insulin resistant characters. It is rare to be insulin-resistant while subject’s blood glu- cose levels were less than 5.6 mmol/L, triglyceride 1.7 mmol/L, HDL-C 1.0 mmol/L in men, 1.3 mmol/L in women and blood pressure 130/85 mmHg."
Again, an assertion, not an observation. The study doesn't purport to show what you think it does. What you're looking for is a clinical writeup of a single individual with a fat accumulation problem that doesn't have insulin resistance, or elevated insulin levels. This study clearly has limitations, including the critical statement "To date, there is no uniform definition for MHO."
http://circ.ahajournals.org/content/112/17/e285/T1.expansion.html
Note the elevated waist requirement doesn't even factor in height:
Elevated waist circumference*
102 cm (40 inches) in men
88 cm (35 inches) in women
Hard to consider that an accurate proxy for a fat accumulation problem of obesity.
You're editorializing - they didn't say they had normal insulin sensitivity, they said "Subjects included were 1,547 men and women (age range, 18-59 years), who were free of components of the metabolic syndrome except waist criteria."
See: http://en.wikipedia.org/wiki/Metabolic_syndrome#Definitions_and_diagnosis
While EGIR has a definition for insulin resistance, none of the other definitions require it for a definition of metabolic syndrome. WHO lists it, but doesn't *require* it.
The study itself claims this caveat:
"It is rare to be insulin-resistant while subject’s blood glu- cose levels were less than 5.6 mmol/L, triglyceride http://apjcn.nhri.org.tw/server/APJCN/21/2/227.pdf
The other question is "does waist criteria represent obesity"? I knew plenty of people who would've failed on the BMI scale, but did not have a fat accumulation problem. So while it's fairly provocative, I think the study fails to demonstrate what you editorialized in your link text.
I highly suggest giving it a read, especially the footnotes. You may not walk away agreeing with him, but you'll be better informed.
Just one example, please. Any example. A single obese person that has neither insulin resistance, nor elevated insulin levels.
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.
Appeal to 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 :)
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.
That's not surprising at all. Have you read his book, "Good Calories, Bad Calories"? Thanks to zealots like Ancel Keys, the direction of government sanctioned research went in a singular direction with blinders, masking and disparaging any divergent opinions.
Look, no matter what your particular axe to grind with Taubes, the fact of the matter is that for every obese person, you've got a combination of insulin resistance and high insulin levels, period. It simply doesn't happen by any other biochemical mechanism.
Actually, no, insulin resistance/sensitivity counts for a lot. Sort of a "square/rectangle" thing - not everyone with elevated insulin levels is going to get obese, but anyone who is obese is so because of elevated insulin levels.
Lustig posits that insulin sensitivity is driven by fructose consumption and its effect on the liver, which seems plausible, but I'm sure a great deal of it has to do with genetics as well. There are bean pole skinny guys out there with high cholesterol and diabetes who don't have any fat accumulation problem, but still get all the other "benefits" of high insulin.
Actually, you'd be surprised. When I hit fast food joints, they're more than happy to hold the bun, the fries, and the sugary drink. At the store, I buy pork rinds instead of chips. At restaurants, I ask them to replace whatever starch with something like broccoli dripping in cheese or butter. I've never had a situation where I haven't been able to avoid carbohydrates.
Now, that being said, it is true that carbohydrates are in fact, addictive, and weaning oneself off of the sugar rush/crash cycle is as difficult as stopping the use of other drugs like tobacco, alcohol, methamphetamine, or even cocaine. It *can* be sustainable, but it's not something that happens without effort.
The only "calorie in/calorie out" that counts is the calories that are partitioned into fat accumulation, versus those that are partitioned into energy use. This is driven not by the gross amount of calories, but by the insulin response from those calories (and the insulin sensitivity/resistance of the subject).
The second law of thermodynamics applies, but not at the macro level of "mouth/body", but rather the micro level of the fat cell.
Scientifically, the only proven mechanic is the regulation of insulin levels.
Yes, I've permanently changed they way I live - I *always* avoid eating carbohydrates, and will do so for the rest of my life.
I lost 50 pounds in 6 months after understanding the biochemistry behind fat accumulation and the reasons behind it, and have kept that off for 6 years.
As for selling books/videos, I've got no dog in that fight - and frankly, recommending carbohydrate restriction is so simple and effective, it doesn't *require* any sort of expensive book or video to understand and implement.
Consistently?
Having someone who is insulin sensitive semi-starve themselves while eating only potatoes can certainly cause weight loss. Applying an isocaloric potato diet, increasing the % of carbohydrates, to someone who is insulin resistant is going to cause obesity.
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.
I've been in ketosis for going on six years now, and never had any sort of kidney issue. In fact, my wife's kidneys, which had some signs of malfunction ever since her 20s, got *better*.
Nutritional ketosis might not be for everyone, but I've yet to see any credible information showing that it is harmful in any way whatsoever.
For me, after two years of low-calorie/low-fat diet and 5 miles a day of running, and a 10 pound weight *gain*, keeping carbs under 20g a day lost me 50 pounds in 6 months, and kept it off for the past 6 years.
The sad thing is that people still keep pushing the calories in/calories out dogma, which takes well intentioned people down the completely wrong path.
Look up the Kreb's cycle - insulin levels simply are not driven at all by fat calories, and only marginally by protein calories. Carbohydrates drive insulin levels, and insulin levels drive fat accumulation.
You can refuse to believe the basic, biochemical facts, and attempt to apply a tinker toy physics model of "e-in/e-out", but it simply doesn't apply.
Fat accumulation isn't driven by caloric intake levels, it's driven by insulin.
If you consume calories which drive insulin up, you'll accumulate more fat. Consume calories which don't drive insulin up, and you won't accumulate more fat.
The concept is pretty simple: to lose weight, don't consume calories that cause fat accumulation. We call these "carbohydrates".
C'mon, mod parent up. It's *completely* on topic.
Imagine for a moment you were invited to a gourmet dinner, and your host said "bring your appetite". What might you do?
Maybe skip a meal? (eat less)
Maybe work up an appetite with a brisk walk? (exercise more)
Now, what makes you think advice that makes people *hungry* is going to help them lose weight?
Fat accumulation is driven by insulin, which is driven by blood sugar, which is driven by carbohydrate intake.
Stop eating carbohydrates. It's simple.
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.
Stop eating carbohydrates. It's simple.