To my readers

As you may or may not have noticed, I have been pre-occupied of late caring for a family member.  This has taken a bit of a toll on me both mentally and at times physically.  This past weekend marked the beginning of the end of this chapter, as this person has made it to the in-patient rehab phase of their journey towards recovery.

I've tried to welcome every newbie who comments here, but, as traffic has picked up, this has been difficult to keep track of.  And I embarrassingly mixed up two different people with the same screen name, for which I hope my apology has been accepted.

I wanted to take the time this morning to thank each and every one of you for reading and offering your input here.  If I don't always get to acknowledge or answer your comments, it's not because I don't want to, it's because I do have more than this blog in my life, much as I like to "goof off" about the internet!   Couple that with one of my failings - getting easily distracted and drawn into discussions on "pet subjects" - and ... well...

Regular contributors via comments probably noticed some changes in that area.  Up until sometime in February of this year, I didn't moderate comments.  Amazingly in all that time I had to delete exactly one comment for abusive content regarding me, and a few where someone insisted on trying to use my blog to launch all caps attacks on others irrelevant to the discussion at hand.  Then Kurt G. Harris MD decided to grace us with his presence here.  His purpose seemed to be to save all you from yourselves lest I confuse you with my inability to read, think and interpret research to his liking.  I didn't realize this at first, as the general high esteem with which many seemed to hold Kurt, led me to believe he was interested in honest debate on some of the topics I present and discuss here.  I now realize this wasn't the case and I vastly overestimated his nature as being one of well meaning.  Kurt, if that's not you, re-think your approach is all I can suggest.

When Kurt posted the comment I'll include at the end of this post, I deleted it because prior comments were scattered about threads, and my family member situation was critical at the time.  I just didn't have time to deal with the bullshit.  What time I had, and this blog provides me with much relief in the form of distraction and interaction, I preferred to channel to positive ventures.  So ... on went the comment moderation.

In the ensuing weeks it became clear that after the initial brew ha ha, it wasn't necessary.  So off it goes, for now, but I'm hopeful forever.   At this point so much time has gone by that it's silly to even publish this one, but I made a promise that I would and therefore I'm doing so now.

If anyone is interested, HERE are the exchanges leading up to this summarized in one place:

This exchange ultimately elicited this comment:



I've since published the remaining comments by Kurt as far as I'm aware.  Made good.  Moving on.

I don't see how Stephan, Kurt and Peter agree on some over-arching opposite to my way of looking at things.  Stephan seems perfectly willing and able to conduct himself in a calm professional manner here and I only suggest that, since this is a focus of mine, I might have more knowledge on the topic.  I, for one, am proud of the readership I've drawn who seem more than capable of reading and judging for themselves the merit of what I write here.  Kurt seems unable to go a comment or two here or elsewhere without making statements such as that I'm confused, can't read, don't understand what I'm reading, don't think or don't think deeply enough.  Whatever.

His commentary on his blog leads me to say I've misjudged Peter as well, and I'll just leave it at that and twaddle on.

Kurt, it is a juvenile argument to make that because I use a whimsical avatar, you do not "personally attack" me.  If anyone is still entertaining notions that I'm not a singular person who demonstrates through her writing the truthfulness of how I've presented myself, I can't change that.  Please, then, do realize that the Asylum door swings both ways, and be careful not to let it hit you on the way out.  Otherwise, at least respect that there is a real person under the bunny ears and treat me accordingly, as I would have the courtesy to do so on your blogs and such.   I chose CarbSane, as stated, so that when I read and comment around the web, at least people know the persona with whom they're conversing.  So many don't even bother to do that on various blogs that allow anonymous postings.  Clearly some of these people are prolific on various sites but can't take the time to sign up for a free Blogger or OpenID or whatnot.  And yet I'M not to be taken seriously?  Again, whatever.

Thanks again to all who contribute so positively to this little corner of the web!  It is meaningful to me in many ways I cannot express.  God bless.

Edit 9/12/11:  I'm C&P'ing the rest of Kurts comments from that time in to this post so anyone who wonders over the full nature of our exchange has seen all of it.  I'm not going to waste time with formatting.  I'm also going to include some later comments where he demonstrates he's capable of making a post without insulting me or my readers.

Stephan said:"Looking at that last graph, I...
from My Carb Sane-Asylum by Kurt G. Harris MD
\Stephan said:

"Looking at that last graph, I don't find it alarming at all. Fasting FFA levels were similar in the HF and HC groups "

"Glucose and FFA are reciprocally regulated energy sources; the transition is orchestrated by insulin.

I don't think VLC is a great idea for most people in general, but these data do not strike me as alarming."

Exactly. If you are alarmed it means you don't understand it well enough.

@SanjeevCS was the one who brought up qualificat...
from My Carb Sane-Asylum by Kurt G. Harris MD


CS was the one who brought up qualifications, no? Her claim was that I haven't read as much as she has, making her more "qualified" to know whether her claims are true. Apart from the obvious flaw that she has no way of knowing how much I have read about anything, I pointed out that it was not just a case of one person who read a lot disagreeing with only me. Rather, she disagrees with SEVERAL people with a wealth of diverse clinical and research experience, experience which does enable us to evaluate claims like hers.

Not that our combined experience and knowledge trump reading, but they certainly are valid to consider for others who might wonder if we are qualified to judge CS's claims.

I could hardly have claimed CS lacks qualification in any case, as she insists on anonymity. She could claim to be Walter Willett and how could I prove she isn't : )

"Regarding qualifications and background, I&#...from My Carb Sane-Asylum by Kurt G. Harris MD

"Regarding qualifications and background, I'll only state that mine are similar to yours"

Your anonymous bio states you have an MS. Do you have a PhD like Stephan does? Aren't you minimizing the value of a PhD just a little bit?

I am not questioning your credentials. You were th...
from My Carb Sane-Asylum by Kurt G. Harris MD
I am not questioning your credentials. You were the one who stated that your credentials were equivalent to Stephan's. I thought perhaps you really did have a PhD, and had just not told us for anonymity purposes. I know quite a few people who very nearly completed PhDs as well. Having a PhD is certainly not the same qualification as "almost having one". I think to imply that is to diminish the value of the credential. that's all.

If you really find my deleted comment that offensive, just keep it deleted.I am indifferent to whether you respond to it.

You are certainly creating the impression, intentionally or not, that it is a much bigger deal than it is. How much preparation do you need to respond to a few paragraphs of sarcastic commentary pointing out that you disagree with three of us and not just one about the dangers of NEFA on VLC?

@CS"I also think you owe King an apology fo...
from My Carb Sane-Asylum by Kurt G. Harris MD


"I also think you owe King an apology for your rude response to him. Remember where you are."

Who is KIng? rude response? I literally have no idea what you mean...

If King is you, Sanjeev, then I apologize for thinking that you were addressing me, but not for rudeness, just making a dumb mistake, as my comment would have been appropriate had you been addressing me. I simply had not seen Stephan's comment yet.

Assuming he is "King....."

You seem to see rudeness everywhere but in your own behavior. I don't devote entire posts to ridiculing Gary Taubes and spelling his name with a dollar sign, do I? You do a fair amount of mockery of others here. I think the pot is definitely calling the kettle black.

Now that I have read Stephan's quote, I would add that you should pay attention when someone like Stephan is saying that your claims can be easily debunked with textbook physiology, because they can. His post is as close to an admonishment as you will ever get from him.

You have deleted my sarcastic comment that you claim attacks you "personally" even though I've no idea who you are. The comment was short, and by your standards of personal attack and slander, pretty mild, you must admit. I

The other readers deserve to know what I said, which was essentially that you are disagreeing with an MD, a clinical veterinarian who is quite knowledgeable about physiology, and Stephan, who is as he points out very highly qualified to comment. The wealth of our experience is as relevant to consider as is the number of papers or abstracts you have read. That was my point.

You had make it sound like it is just you and me, and it is not.

You had asked if it was possible that I was wrong and you were right. My sarcastic response was that I and Peter and Stephan would all have to be wrong. I'll let you and the other readers translate that into an odds ratio.

Hello CSYou said:"Here's my plain and...
from My Carb Sane-Asylum by Kurt G. Harris MD

Hello CS
You said:

"Here's my plain and simple explanation. People gain weight when intake > expenditure and vice versa. You're right, it's not a hypothesis, it's a fact. "

Christian is pointing out, and I agree, that that this is neither an explanation nor a hypothesis. It is a tautology that tells us nothing. Like saying morphine has opiate properties. Or that adding heat is accompanied by a higher temperature. In each case there is no explanation at all, as the one is simply contained in the definition of the other.

I've read Peter's post and can find nothing wrong with his explanation, nor can I find him endorsing the cartoon "carbohydrate/insulin hypothesis" that you keep using as your straw man, as if anyone believes insulin operates in a total vacuum to create fat without any constraints- regardless of whether your mouth is sewn shut or if you are force fed.

He quite explicitly says that liver insulin resistance determines your tolerance for carbohydrate. This would apply to the Kitavans or any other non NAD damaged cultures, as well as to me personally. I never was fat. I could eat anything I want if I only cared about weight. My own clinical experience with patients also supports this, as well as the experience of many other clinicians. The formerly obese and diabetics I know all do best on real food relatively low carb diets. If they are still fat on LC, they are either really broken or have emotional eating issues - basal ganglia overriding the hypothalamus I suppose. Probably very common, actually.

I am sure it would suck to be so broken you might have to go LC and ALSO count and measure for the rest of your life, but maybe that's you? If it is you, that's unfortunate but does that mean the rest of us that don't weigh and measure and can eat anything we want must be lying? Or that carbs and their metabolic effects have NOTHING to do with weight loss for the more mildly broken who want to lose weight? You are promoting a false dichotomy here: CICO vs Insulin explains everything. Both are nonsense.

CS, you really could do some useful thinking here if you were to lose your "I hate Gary Taubes" filter. It seems to be distorting your view of just about everything you read... That and your NEFA phobia.

"IMO, most obese have long since - for whatev...
from My Carb Sane-Asylum by Kurt G. Harris MD

"IMO, most obese have long since - for whatever reason - kissed "natural" homeostasis goodbye."

But that is precisely the point. If that is so, why? Because they failed to weigh and measure? Why are the obese different and what does the tautology of CI=CO tell us about this difference? Is tells us zero about it.

@HarryLosing weight IS a negative energy balance...
from My Carb Sane-Asylum by Kurt G. Harris MD


Losing weight IS a negative energy balance. I would find a new doctor if I was the patient in your scenario. Especially if I were doing hours of cardio a week and was hungry all the time like all the fat people I see working out at my gym on stairmasters.

Customer: Did you find out why my tire is flat?

Useless Mechanic: It is leaking air.

Helpful mechanic: It has a nail in the carcass causing a leak.


You said:

"let's see you try ALL possible solutions, including all that require creation of new mass/energy from nothing. "

Sanjeev, there is no one on this board, certainly not me, who believes that mass or energy is created from nothing. I stipulate CS's and your tautology, that there must be an energy deficit. The question is how to achieve it.

I.Normal weight people eating a healthy whole foods diet don't need to do anything - their weight is spontaneously regulated with zero conscious thought the same way their breathing and thier thirst are regulated, They don't accidentaly die of cerebral edema from polydypsia, nor do they die of dehydration because they forget to drink enough. If the brain and gut and liver are as unbroken as the kidneys, no conscious thought need be given to the weight or energy content of food, ever.

II. Some metabolically damaged people can heal their damage with time and abstinence from what caused the damage. Then they can be like the people in I, and need never weigh, or measure their food or their exercise output, ever. These people exist. I am one of them.

III. Some metabolically damaged people may be so metabolically deranged that they must always eat a particular diet, say low carbohydrate diet, in order to maintain weight. Otherwise, they gain.

IV. Some people may be further damaged, and have to eat LC and consciously eat to less than satiety - probably because of persistent leptin resistance. Such people, in their frustration, may then speculate that categories I-III don't exist. It is not fair, but these people may be stuck with being food conscious forever, like alcoholics who can't avoid the drink without daily AA meetings. It's not their fault. But the existence of such people doesn't prove that CICO is the only thing we can say about fat loss, anymore than the existence of people with diabetes insipidus would imply that all people have to worry about how much water they drink al the time.

V. The regulation of fat stores involves the whole organism. It follows there may be at least as many ways that a person can gain or lose fat as there are parts to the regulatory whole. Like insanity, brain damage, inflammation, conscious over-riding of the satiety signals, etc. - think Bobby Sands or Dick Gregory.

It is totally obvious to me that all these categories exist, and they are all interesting. They are not at all mutually exclusive.

Why perseverate on CICO? It is true but it tells us nothing. It is not interesting.

@ AllI agree about the poor title but I do happe...
from My Carb Sane-Asylum by Kurt G. Harris MD

@ All

I agree about the poor title but I do happen to believe that gluttony exists and some people are fat because of it. (perhaps unlike GT, I hesitate to add)

The brain is a powerful organ and normal homeostasis can be overriden. Even when there is no organic pathology. Think of Hollywood actors like DeNiro in raging bull or Christian Bale - twice now - gaining or losing substantial weight for movie parts.

I also have no doubt that some who are "broken" need conscious control to avoid obesity or to avoid death (Anorexia Nervosa) - maybe forever. I don't think this is most people, though. And if you are an emotional eater you can VLC all day long and gain like heck. I've seen it.

Much of the problem with dietary discussions and the nutrition literature is that obesity is a SIGN, not a disease. It can be a sign of excess intake due to metabolic derangement - a la metsyn, or a sign of conscious overeating like DeNiro in the latter half of the movie. We know that obesity can occur early and protect us from type II DM, or it can occur late and be a sign of its presence.

Just like blood pressure, it can indicate lots of different states, physiologic or not. With BP, we can predict someone who has it is likely to have metabolic syndrome, but they may have a pheocromocytoma instead.

With obesity, it's the same. Marlon Brando showed up obese on the set of apocalypse now and it was a surprise. DeNiro overate on purpose for his part in raging bull. Which one was more likely to have liver IR? Or to spontaneously return to normal weight?

Physiologic starvation causes fat wasting to keep us alive. Anorexia Nervosa results in death in the presence of abundance. Cancer causes cachexia - wasting. Who thinks simply being thin means you have to have AN or cancer?

So I continue to say there are many different reasons one displays the sign of obesity.

It's not all carbs. It's also not only failure to weigh and measure and "move".

Because obesity per se is not a disease. It is just a physical sign that in our culture happens to correlate quite often with metabolic syndrome.

@CSI don't disagree that it's possible t...from My Carb Sane-Asylum by Kurt G. Harris MD


I don't disagree that it's possible that you may be in a state now where you have to monitor the amount you eat or even that you must tolerate hunger.

I do disagree that this is the normal state of nature.

And my central thesis is indeed that the western diet has particular agents - the NAD - that can upset the normal fat homeostasis we are all born with

If I were to consciously overeat and be totally sendentary, my weight might climb to 170. When I go VLC with fasting workouts and two meals a day, I drop to 150. (Currently I am 158 due to more weight training) This, I am sure you would admit, is a very narrow range. My fat setpoint allows a narrrower range with dietary variety than is typically found in folks who have trouble with fat gain.

In an earlier post, you mentioned that you had margarine growing up. I have eaten butter, eggs and red meat, and whole milk since day one and have never eaten margarine, ever.

What makes you so sure the difference between us has nothing to do with omega 6 or trans fats, or even fructose exposure? Have you read Stephan's posts on how metsyn and obesity track omega 6 consumption or Peter's posts on n-6 and n-3 and fatty liver?

The Kitavans and the plains indians at any age didn't need to count, weigh or measure, or "work out" and neither do I. Although I had a fair amount of sugar growing up, it was a very animal fat heavy diet relatively light on wheat and excess LA compared to the SAD.

I think there are explanations for these observations, and dietary history of exposure to particular factors outside of our evolutionary experience may account for them.

And contra the assertions of Nigel or others who claim that we must be sure to "keep moving", both my weight and fat mass vary inversely with total physical exercise. When i ran 25 miles per week on the SAD, I weighed 170. When I was VLC and dropped to one workout per 10 days a la McGuff my intake sponateously dropped and I weighed 149 lbs. Now I run and lift 3 times per week and I weigh 158. And remember, I never count or measure. The point is just as Taubes says, exercise makes me eat more, and I add both muscle and fat with more exercise.

I am not saying that applies to everyone, but I am saying lack of exercise is absolutely not the "cause" of diseases of civilization. Fat people I see at the "Y" burn more calories weekly than many HG tribes, who basically hang around when they don't have to do work, just like I do most of the time...

@MirrorballThese are the same type of observatio...from My Carb Sane-Asylum by Kurt G. Harris MD


These are the same type of observational studies that show meat consumption increases mortality. They are confounded by other healthy behaviors. Although PaNu and PHD are in practice nearly the same, I don't agree with all of Jaminet's claims. I also don't think "infection" is the TOE (theory of everything) he makes it out to be. So bottom line is I stand by my assertion - distinguishing exercise from normal activity of course. lying in bed is not good but running marathons is not good either. Exercise may help mitigate the damage of the SAD, but is a tweak if you eat properly and are metabolically healthy.


I've seen no evidence that consumption of 12% of calories as n-6, or 150 lbs a year of sugar or any amount of wheat improves life expectancy. Have you? Uness you mean these "foods" are preferable to starvation.

Life expectancy aside, these are the agents that differ most between current and ancestral diets - the diets where even old people are free of hypertension, obesity, diabetes.

If you want to wait for a randomized trial, fine, but I go on the assumption that avoiding things that are not food has little downside when there are other things to eat that are better, even if the DOCs turn out to be caused by "infections" or whatever...

And that is all I advocate, and all I do.


In another post here I referred to a heirarchy of metabolic damage. If you are in a category that LC and avoiding the NAD ala PaNU or PHD does not work for, then more conscious effort may be required, I agree. I don't agree with using that as an argument to say that LC does not work long term or that CICO and ELMM is the only real way to lose weight and keep it off. For you activity may suppress appetite, for me it makes me ravenous and I have to be careful not to eat the whole house post workout!

I've had and seen to much success for me to believe either of those.

As far as women and LC, no doubt women that were morbidly obese have more difficulty in general - women always have higher obesity rates in almost all cultures, that's the way it is. It should not surprise us if morbibly obese females have the most trouble losing weight with the double whammy of sex and likely metabolic damage that may be permanent (that's what morbid obesity indicates, IMO).

My wife has eaten VLC/LC for 4 years -5' 6"" aged 52 - initial weight 138lbs, dropped to 119 over few months and steady at that weight ever since with no weighing or measuring, ever and no regular exercise (although very physically active - walking and gardening etc.) Had she been heavier for many years, maybe it would not work, but ask any woman who feels like she doesn't look good as a size 8 that being able to drop to size 3/4 is not "success" - see what they say. And every health parameter we've measured is better as well.. And no more cold sores or yeast infections or UTIs. ever. But then, it's not just LC, its PaNu.

Paleo 2.0

@CS"I've never said the diabesity epide...
from My Carb Sane-Asylum by Kurt G. Harris MD


"I've never said the diabesity epidemic was due to some failure to weigh and measure. But it cannot be explained by some sort of mass metabolic derangement due to a particular macronutrient or even subclasses thereof."

Forgive me for thinking that was your explanation.

If the first sentence - basically saying that humans normally need to monitor and have knowledge of the energy content of food before they consume it - is not your hypothesis, and you also disagree with me and Stephan and Peter and GT and many others that there indeed might have been some mass metabolic derangement due to particular agents that are outside of our evolutionary experience, then what is your explanation?

And Sanjeev and others:

The failure of real foods paleo or PaNu or any particular approach to reverse obesity or indeed any disease at all does not mean that adopting such a strategy will not PREVENT these diseases. It may just be too late.

For example, Type I DM is autoimmune and likely related to wheat consumption. But no one thinks that once you've been shooting up insulin for 20 years you are going to be cured of Type I by going off wheat. But wheat avoidance in a population would help decrease the incidence.

This kind of thinking indeed informs my approach. If someone eats low carb junk all his waking hours because of something related more to his brain than his liver, that doesn't prove anything fundamental about LC or VLC eating, anymore than knowing someone who died of pneumonia despite antibiotics would prove the inefficacy of antibiotics.

Just because something is the best we have doesn't mean it will always work. Even the most efficacious medical regimens are never 100%. Why should diet be any different?

So if Sanjeev could not avoid weight gain on paleo, that doesn't prove that if we took 100 people and applied it to them it would not on average make them, or even Sanjeev, healthier - just that one person may not have responded the way we wanted in terms of fat loss.

I admit that much of what I advocate is based on informed guessing and reasoning, and that fat loss is a minor concern for me. But on average the people I see minimizing the NAD see big health benefits and there is essentially no downside to their limitation.

They don't all necessarily find love and happiness and their stocks don't all go up. But most don't want to go back. A few of them don't lose much weight, especially if they were morbidly obese or if they are emotional eaters (think brain, not liver). But if Sanjeev was one of my patients and he got fatter just by limiting wheat fructose and LA, he would definitely be the first.

Your insistence that the point of how he lost weig...from My Carb Sane-Asylum by Kurt G. Harris MD

Your insistence that the point of how he lost weight is that he "ate less" continues to boggle the mind.

NO ONE disagrees that he ate less.

The only interesting question to someone who thinks, and is not just playing the nihilist, could posssibly be WHY did he lose the weight while consciously overeating?

I think the best explanation is monotony.

Your explanation was that he counted and measured in order to undereat, which has now been falsified, by exactly 180 degrees.

And this is your response -"How, why, schmow, schwhy"?

Your explanation, as usual wrong, was that he consciously underate.

It is only because you have absolutely nothing novel to say about fat loss that you don't even find it disturbing that you are totally wrong about whether he consciously overate or underate.

You suffer no "cerebral stress" because you are not thinking.

Endlessly repeating that there must be a caloric deficit as if that means something, which no one commenting on your blog has contested, and insisting all the while that it does not matter and you do not care why anything happens.

- this behavior is not stressful, because it is speech that requires....

no thought.

We get that you are really, really angry at Gary Taubes and anything that even looks like it might be one of his ideas.

Is there anything else you'd like to discuss?

"Thing is the O6:O3 ratios of grass vs. grain...
from My Carb Sane-Asylum by Kurt G. Harris MD

"Thing is the O6:O3 ratios of grass vs. grain beef is of negligible difference and amount"


The difference is quite significant, and in the context of a veggie-oil-free diet, the n-3 in grass fed meat (including muscle cuts) and dairy is plenty enough to have a healthy 6:3 ratio.

The difference is due to n-3, not n-6 content. N-3 is part of the chloroplasts found in grass. You don't get it from grain, which is seeds.

And Loren Cordain is your most credible source? His stuff is mostly nonsense.

Try googling "William Lands" and discover that there is more to healthy diet than calories, scales and 20th century macronutrients.

The standard american diet is 12 to 15% total PUFA. Mine is less than 4% with a 2:1 ratio. It's not hard to do at all.

Kurt G. Harris MD,"Is there anything else y...from My Carb Sane-Asylum by Robert

Kurt G. Harris MD,

"Is there anything else you'd like to discuss?"

This is the internet. If you're not interested in discussing what you think is the same thing over and over here, then LEAVE. You're not required to read this blog or comment on this blog.

@JamesI freely grant that CICO is true and I con...from My Carb Sane-Asylum by Kurt G. Harris MD


I freely grant that CICO is true and I concede that some people think that they can eat any amount of total calories and lose fat by magic. I don't personally know anyone like that, but you may.

Some people who eat ad lib LC lose substantial fat with no counting or measuring. I have seen and treated many such people with better success than with any other approach. None of them think it is magic. They all notice spontaneously lower hunger.

Some people have even better results specifically restricting excess fructose and PUFA - including reversing fatty liver and diabetes and many other non-weight related metabolic derangements. They don't need to count or weigh or measure either. Many such people go back to higher carbs as starch and do not re-gain the weight.

Some people have no luck with either of these maneuvers. They may need to give it more time, or try something else, perhaps even weighing or measuring! Or having their thyroid function checked, or seeing a clinical psychologist or psychiatrist about why they are self-medicating with a gallon of Bryer's every evening.

But to say over and over again that CI=CO is to terminate the conversation a bit early, isn't it?

How can we explain WHY these methods work when they do (and they do, even if not for everyone) if we keep perseverating on a fact that we all agree on?

A fact that is true, but by itself explains nothing, and is therapeutically useful only in the specific case of someone who thinks they can overeat and lose weight, but is not?

Why initially treat with the expensive drug before we know if the cheap and easy one works?

Dietary maneuvers are all likely to be variants of ways to induce a caloric deficit.

One can lesion the brain, do a vertical banded gastroplasty, remove the pancreas surgically - all of these will make you lose weight.

More reasonably, one can decrease carbs or increase protein.

More reasonably yet, one can restrict excess fructose and wheat specifically.

FInally, if nothing else works, you can count and measure and weigh to ensure a deficit, and if you can tolerate the hunger, that might finally work for you.

But why is that last, desperate step the only thing worth discussing?

Do you view the human organism as simply a neutral caloric sink without complex hormonal appetite regulation and no organ sensitivity to toxins?

We are stipulating that there must be a caloric deficit, somehow. In a murder trial, one might stipulate that the victim is dead, but then argue it was self defense, or someone else besides the defendant who did it, etc.

Continually invoking an inarguable, stipulated condition this way is like the prosecutor blurting out "but the victim is dead" every five minutes or so during the trial.

The judge might well interrupt and say "Yes, that's been stipulated by the defense, and they are denying that the defendant killed them! Move on, counselor".

Make your case. That is, tell us why some people don't need to count or weigh and they can lose weight. We've stipulated a caloric deficit. Now let's move on to how that happens.

@James"However, obviously the vast majority...from My Carb Sane-Asylum by Kurt G. Harris MD
"However, obviously the vast majority of people wanting to lose weight don't understand CICO, or have been misled by individuals like Taubes."
Is that your experience? I find that hard to believe. I've met some people who lost weight successfully with Atkins who believe that, but the vast majority of people? I doubt it.
Where I live everyone believes the precise opposite, that math is the only way to lose weight, and a calorie is a calorie. They all eat dry salads and low fat garbage and spend hours on stairmasters and treadmills at the Y.
They are all fat because the only thing they have ever been taught is that calories count - so they count them and starve, or stay fat.


Mirrorball said…
Appeal to authority, Kurt? Really? What a disappointment. :( And I thought only T. Colin Campbell believed he is automatically right about everything because of all the hundreds of research papers he has published.
Nigel Kinbrum said…
"Please, then, do realize that the Asylum door swings both ways, and be careful not to let it hit you on the way out."
I don't know why (as I'm in a really bad mood after the events of earlier today) but that made me laugh.

Looking after sick family members takes its toll. {{{{{CarbSane}}}}}
Anonymous said…
I always learn something reading this blog. Keep up the good work, even in the midst of crises, if you can. You're always worth reading, carbsane!
Unknown said…

Wow, I've finally got my name in a thread title!

" ....just found his attitude towards diet induced tachychardia or risks of heart attacks to be somewhat flippant."

Yes, I offered an actual physiologic explanation, based on my clinical experience (gasp!) for your tachycardia and tried to reassure you it had no bearing on NEFA.

How inconsiderate of me.

Thanks for finally publishing all those - I stand by everything I said.

As far as "asylum doors", I post here to suit my own purposes, as you allow me to post here to serve yours. Your blog thrives on argument and controversy - was built on it in fact.

If you'd prefer I don't ever post here, just say so and I'll disappear for good. You're not doing anything for me, and I'm not ever going to change your mind on a single thing, that seems obvious by now.

I'm only addressing your readers and trying to help them out. Quite obviously, I can do so through my own blog just as well.

This is just more fun, although I'll missed being attacked by all your bulldogs if I go for good....


You read the whole thread and all you see is an appeal to authority? Huh??
Mirrorball said…

I know you've got some good arguments and important things to say. You didn't need to appeal to authority or resort to ad hominem attacks to make your point.
Thomas said…
I'm a litle disapointed to hear that from Kurt, although I know he can get riled up a bit. I still respect his opinions, however, as well as yours. The blogasphere can be a nasty place-it's easier to be rude to people when you are not talking face to face. Keep up the good work, carbsane, and don't let it get under your skin.
kds said…
Ugh, it feels like so much of this blog has just degenerated into random personal noise and any discussion which could actually yield some fruitful consensus is being lost piecemeal. I agree with Mirrorball in that ad hominems aren't really productive, whether they be $s or making fun of bunny ears or whatever the hell else. It's just more noise.

@CS- maybe I'm off base but it seems as if you've been antagonized (or you think you've been antagonized) into committing to the NEFA hypothesis in much the same way Taubes has committed himself to carb-bashing. Regardless of whatever personal insults you think Kurt has dished your way, he still has a point in that in the real world (and not in the world of clamps and Intralipid infusions) there is simply no controlled evidence showing that reduced-calorie VLC diets have done anything but improve TII DM clinical endpoints. Do IR/metsyn folks who habitually stuff their faces with hypercaloric carb PLUS fat feedings have elevated NEFA? Absolutely. Do VLC dieters and starving people have elevated NEFA? Sure. Is there much of a similarity in their outcomes as it pertains to lipotoxicity? That's for you to demonstrate.

I know I posted this before, but I want to reiterate that relying on absolute NEFA levels can be misleading, and I still think you're jumping to conclusions by extrapolating from raw data in some of the studies you've posted.

Per Joslin:

"Plasma concentrations of FFAs reflect the balance between their release and uptake, but this relationship is not linear over the physiologic range. At low flux rates, a disproportionate decrease in plasma concentrations of FFAs occurs, whereas at very high flux rates, plasma levels of FFAs may increase to a greater degree than would be predicted if the relationship between flux and concentrations were linear. Basal FFA flux typically exceeds the fatty acid oxidation rate (measured by indirect calorimetry) by 50% to 100%; the excess FFAs are thought to be reesterified into triglycerides in the liver and muscle. FFA clearance increases dramatically with exercise, such that at the onset of exercise plasma concentrations of FFAs may decrease even while rates of FFA release are increasing. Thus, although FFA concentrations are a reasonable indicator of FFA release, it is not possible to use concentration values to make quantitative estimates of release rates, and in some circumstances FFA concentrations can be misleading with respect to changes in lipolysis."
@CarbSane, whether Kurt/KGH realizes this or not, he's effectively conveyed to us that he thinks it's worth his time to visit here, read what you have to say, and respond with his own comments.

"This is just more fun," - KGH

Fair enough. Although now any excuses about not having the time to write posts or respond to readers' questions, quite honestly reads a little more like insincere bullshit. But hey, it's a privately-owned blog, and KGH owes no reader a thing, and readers are certainly free to NOT visit, comment (or donate). I generally like and respect Dr. KGH, but if he's sitting around reading these comments, then he probably isn't working writing on writing articles worth reading.
Anonymous said…
'If you'd prefer I don't ever post here, just say so and I'll disappear for good. You're not doing anything for me, and I'm not ever going to change your mind on a single thing, that seems obvious by now.'

I think I got a note passed to me in study hall when I was in high school that sounded just like this.

Thanks for the trip down memory lane!
Anonymous said…
I'm glad your family member has rounded a corner, Carb Sane!
Flavia said…
Good to hear you will have more time now, CarbSane. Taking care of sick family members can be quite a toll.

Argument by authority, also known as ipse dixit (AKA he said it)is a fallacious type of logic. It does not prove the point.

When resorting to ad hominems, I believe the argument is lost. The lowest form of argumentation is appeals to authority, anecdotal evidence, and ad hominems.

BTW when someone or CS has time, can they quickly explain what the FFA theory would be? How does one get extra FFA in the system anyway? From being fat? Does that mean that being fat causes us to be fat?
MM said…

I'm glad to hear your family member is improving. I hope this gives you a much needed break.

Re Joslin: do you think this quote is referring to people on a typical mixed diet, and that it doesn't apply to people on a VLC diet where FFAs are high all the time? (
CarbSane said…
@euler: Welcome to the Asylum and Thank You!

@Mary & Flavia, thanks for the thoughts. :)

@Kurt, bottom line, "because I say so" doesn't cut it and your behavior undermines whatever message you feel compelled to deliver to readers here. Carry on!

@KDS: I'm not sure what hypothesis I'm "falling for" really. I do believe that Frayn, Boden and McGarry - to name just three - are more qualified to review and interpret the science than I or anyone else here. There is a murky area as to whether it's levels themselves or flux rates, but given the facilitated diffusion means by which FFA's are delivered (one way street it seems in all but fat and liver cells) there is reason to be concerned, IMO, by any prolonged elevated FFA level.

The way I see it boils down to this. Diabetes and MetS are characterized by elevated circulating levels of TWO substrates: glucose and NEFA. We accept glucotoxicity. Low carbers seem to reject lipotoxicity mostly because the "goal" of low carbing is to increase NEFA.

Still waiting for anyone to address the results for diabetics in Shai. They sure are inconvenient.
Frank said…

I personnally enjoy the fact that you are posting here, as you are offering another perspective, which is always very important to keep thing in balance. I'm sure, tho, you could do this with less ad hominems and hostility toward CS. Simply pointing out where she is wrong and why you believe so, by bringing valide references other than "I think so" or "i'm an MD, I must therefore be right" would certainly make this debate much more interesting and enjoyable for everyone.
CarbSane said…
Thanks Frank. I could do without all the snipes about how I don't know how to read or think too, but at this point those diminish Kurt more than they impact me.
Mario Iwakura said…

I think that the results for diabetics in Shai are very easy to explain. From Shai description of the low carb diet:

"the participants were counseled to choose vegetarian sources of fat and protein and to avoid trans fat"

Israel has one of the highest consumption of linoleic acid of the entire world:

Linoleic acid is not a very good fat source for a diabetic:

So, if you ask a jewish to increase his fat from a vegetarian source, for me it seems reasonable to assume that he would increase linoleic acid, or not?
CarbSane said…
Somewhat plausible but not likely, IMO, because the LC group actually reduced fat intake slightly from baseline (a few grams) throughout the study. One has to estimate LA intake indirectly, but they only reduced sat fat intake by a fraction of a gram (an increase by % of diet from 9 to 12%) so perhaps they didn't heed the advice on the veggie sources after all.

Lindeberg's studies with Paleo are often lauded but they too demonstrate the utility of much higher carb consumption than most low carbers would "tolerate".
Mario Iwakura said…
ok, but If you take in account the advice to the Mediterranean group to eat more olive oil and thus displacing some LA, then this could easily explain the diferences.
CarbSane said…
Well, I'm certainly not pushing LA on anyone, but OK, cutting LA improves diabetes, cutting carbs does not. ;)

Again, the records are indirect but at 2 years Meds cut total fat 10.5g of which 4.6 were sat fat. Their MUFA/SFA ratio changed +0.11. The Low carbers cut total fat 1.7g of which 0.56g were sat fat. Their MUFA/SFA ratio went down -0.01. I'm not sure how those relatively minor differences (10.5g fat is <5% of total calories in a 2000 cal diet) would have such an impact. A 30+ point reduction in fasting bg is impressive.
CarbSane said…
Oops missed my virtual hug. I know of your situation with your Mum Nigel and greatly appreciate this!

@BTE - quite insightful there!
CarbSane said…
BTW blue tooth: Your comment went to spam - might be the username?
CarbSane said…
@KDS: I made a considered decision early on to drop the $ and such from my posts about Taubes. But I'll not apologize or go back and delete the 2 (or maybe 3) prior posts that contained this. And yet this is what folks, including Jimmy Moore when he interviewed me months later - and aired that interview even more months later b/c of how his scheduling works - wish to fixate on.

I'm not going to be bullied into not mentioning Taubes' name when it's appropriate. It's funny, really, how some of this stuff just falls in my lap when I look at topics that interest me. For example, it was the recently posted FFA & beta cell function study bearing McGarry's name that I stumbled upon first. The name rang a bell, and lookie what turns up - more Taubes misrepresenting the science. When I find it, I'm going to blog on it!
Mario Iwakura said…
Ok, around 15g of diference in LA (from 30ml of sunflower oil versus 30ml of olive oil) in TWO single isocaloric 1100 cal meals produced an increase of around 18 mg/dl in glucose levels.

The Med group was instructed to eat 30 to 45g of olive oil. If they follow this recommendation they were replacing a considerable amount of LA (for two years instead of two meals!).
Sue said…
This comment has been removed by a blog administrator.
kds said…
This comment has been removed by the author.
kds said…
@CS- I’m not sure why you put “falling for” in quotes- I hope anyone reading your post understands that I never used that phrase and those are your words. I think it’s understandable that one can reach the conclusions you have even after a large amount of meticulous reading, but the synthesis of your reading just seems premature without controlled, longer-term in vivo studies. It’s pretty well established that glucotoxicity and lipotoxicity are phenomena that can be observed in persons who are already IR or frankly diabetic. What I believe you’ve prematurely committed to is the notion that A. snapshot-in-time NEFA levels are good indicators of flux, B. elevated NEFA levels/flux are always representative of pathology, C. reduced-calorie LC/HF cohort NEFA is analogous to metsyn cohort NEFA levels, and D. this presumed analogous pathology is severe enough to lead to permanent beta cell, muscle, and hepatocyte dysfunction. Even if first three steps were individually confirmed, linear causation among them would still need to be established. It’s not sufficient imo to note that artificially infusing FFA causes clamped beta cells to be sluggish, LC folks have elevated NEFA, ergo elevated NEFA can cause LC’ers to become permanently insulin resistant.

As for Shai, I think the study would be causing me more concern if the results actually appeared consistent. In particular, I’m troubled by the fact that the MDTN group had a fasting BG drop of 32.8 mg/dl, but yet “Among the participants with diabetes, the proportion of glycated hemoglobin at 24 months decreased by 0.4±1.3% in the low-fat group, 0.5±1.1% in the Mediterranean-diet group, and 0.9±0.8% in the low-carbohydrate group. The changes were significant (P<0.05) only in the low-carbohydrate group (P=0.45 for the comparison among groups).” IMO, the significance of the result demonstrating that MDTN significantly lowers fasting BG is tremendously weakened by the lack of statistical significance in the A1C comparison. If MDTN is really that effective, a 2 year study should’ve had sufficient power to clearly and unconditionally demonstrate a comparatively superior improvement in the best marker of long-term glycemic control. Do you not agree?