HUH!? This caused a double take! Thoughts?

https://www.youtube.com/watch?v=MiUyjMjuLl0

Thanks for posting the video. This is the first time I've seen news of this study--or any study--from NuSi. I'm no scientist, but I think it's premature to say that this study "falsifies" the insulin hypothesis. I will follow the further discussion. I do like Dr. Yoni Freedhof (the interviewer on this video) and will look for his comments as well.

I'm taking my personal comments over to my journal.

Thank you for starting a new thread on this study.
Discussion started on this thread at post 24, but really should be separate: http://forum.lowcarber.org/showthre...83&page=2&pp=15

Dr. Fung's response: https://intensivedietarymanagement....diet-explained/

http://forum.lowcarber.org/showthread.php?t=473283

The study's come up on the thread above.

Recapping some of my points from the other thread;

This study didn't compare a standard american diet to a ketogenic diet. What it did was first put people on a standard american diet, on the calories it took to put them in calorie balance in a metabolic chamber. Then after a month of this as a baseline, they were put on the ketogenic diet.


Most of the study wasn't in the metabolic chamber it was in a metabolic ward, and according to Hall, subjects burned about 500 calories more a day when in the metabolic ward than when in the metabolic chamber--making what was supposed to be weight maintenance, at least during the baseline standard American diet into weight loss during both the baseline and the ketogenic diet phases. This shows that environment, for whatever reason, had a strong effect on metabolic rate--and you can't rule out that there might be some interaction between environment and diet that would obscure metabolic advantage. Metabolic advantage might occur in free-living subjects on a particular diet, but not under the conditions of the study.

The fact that the baseline, which was supposed by design to keep people at their original bodyweight, resulted in weight loss is a big problem--it means that once people went on the ketogenic diet, they'd already been on a weight-loss diet for a month. This might be long enough for some of the "low hanging fruit" of fat loss to have been already picked, setting up the ketogenic diet phase for a reduce rate of fat loss. But it also might have not been long enough for the people in the study to have experienced very much of the decrease in metabolism that can come after a more extensive weight loss. David Ludwig's study where weight reduced people ate low carb or low fat found less of a decrease in metabolism in people eating low carb--here, the metabolic advantage shown wasn't an increased metabolism in people at their top bodyweights, but less of a decrease in metabolism in people who had lost a fair amount of bodyweight. People going into a study like this are probably screened, to make sure they haven't been recently on a diet, since that would be a major confounder. The people out in the real world, who claim to experience a metabolic advantage on low carb--have not been screened, it's possible that metabolic advantage shows up more in people who have struggled with calorie restriction, had some success but were walking around with a reduced metabolism as a consequence.

There is spontaneous reduction of overall food intake when we go low-carb. In that experiment, they clamped food intake, therefore this spontaneous reduction was not allowed to occur. Hall stated as such in the first minute. I guess that's his next experiment.

My paradigm can explain partly the slowing of fat loss in the first couple weeks. Ketones signal the liver to open up insulin receptors, once the liver receives insulin, insulin shuts down ketogenesis. The more ketones, the stronger this effect. The second part is insulin-degrading enzyme, which degrades insulin once it's done its job in the liver. However, doing this at this point early in fat loss, where there's basically a flooding of FFA's from fat tissue, will subsequently flood the bloodstream with both ketones and FFAs even further. There must be some mechanism that regulates insulin-degrading enzyme precisely to prevent this from happening. So, while insulin drops as a result of low-carb, and while this causes a flood of FFAs and ketones, either FFAs or ketones must somehow signal the liver to not produce so much insulin-degrading enzyme.

It's likely that FFAs signal the liver to shut down insulin receptors (which then allows the liver to convert FFAs to ketones), and in turn ketones signal the liver to open up insulin receptors (which then regulates ketones production).

So, while it appears that there isn't an advantage specifically for fat loss from fat tissue, the experiment (and my paradigm) illustrates how finely adapted the liver is to rapidly fluctuating fat flow. Furthermore, the quick weight loss in the first couple weeks cannot simply be explained as a loss of protein, no matter what Hall says about it. The protein loss is likely due significantly to a degradation of corrupted protein through the CMA process induced by ketones (chaperone-mediated autophagy). This is seen, for example, as a drop in HbA1c.

Growth hormone is inhibited by glucose, therefore inhibited by a high-carb diet. Low-carb, therefore, restores proper GH production and secretion. This in turn should prevent abnormal loss of actual lean tissue, which supports the idea that most of the protein lost during this time comes from CMA. Furthermore, low-carb is high-fat, and fat is necessary for production of steroid hormones, namely testosterone, which suggests that going low-carb will also restore T production and secretion, further supporting the idea that in spite of nitrogen loss, little of it is due to losing useful lean tissue. On the other hand, when we lose weight, the muscles that grew to compensate for increased weight are no longer needed, and so they would respond by shrinking accordingly, however this is unlikely to occur in the first couple weeks.

Finally, for those of you who really like gut bugs, they've been thriving on a high-carb diet, then you suddenly starve them. They gonna die. Well, they got protein too, and this too should be accounted for when measuring nitrogen loss. There's billions of them buggers after all.

Yes. Calorie restriction, even if spontaneous food intake would have had a person eating a similar amount of food, could cause some sort of a stress response and have an effect on metabolism. It's always possible that under free-living conditions, some people would eat more, but otherwise become spontaneously more active or twitchy or experience some sort of increase in metabolism that made up for an increase in calories.

This from Dr. Fung. Help me out here. When Dr. F refers to "calories out" he is mainly talking about maintaining basal metabolism, right? How do other forms of "calories out" figure in this theory? Does that mean we all have to be out busting our butts on the track or treadmill just to stay even?

As it happens (N=1), I've always had the most success at weight loss when I've been, well, busting my butt in the gym, or otherwise. I've always maintained a regular schedule of resistance training, but often (oh, baby, it's cold outside!) neglected the cardio part. Weight loss? Slow going at this point. Maybe now that spring has arrived, I'll kick up the pace a little and see if combining weekly fasting with more calorie-burning through exercise might get me past that plateau.

I have no idea what's happening with my basal metabolism. It's not something I can conveniently keep up with, unless you have a suggestion for actually measuring it at home--or what tests might be provided in a clinical setting.

I believe Dr Fung is saying that we need to eat in a way that doesn't slow our metabolism and thereby decrease calories out. If I am remembering correctly this means to not eat a low fat high carb diet but to instead eat a lchf perhaps ketogenic diet. It doesn't necessarily mean busting your butt. Each one of us, of course, has to still do the n=1 experiment to find out what exactly that means for us individually. At least I think this is What Dr Fung is saying but neither my memory nor my ability to comprehend the science is as good as I would like it.

Jean

With the busting your butt=faster weight loss, I have to wonder, which causes which, or does the causation go both ways? When I've restricted calories, often it's resulted in a decreased tendency to move.

I've just about always intended to be active. But especially in the early days of low carb, when I still had lots of body fat to lose, eating this way seemed to translate my intention to be active into actual activity, ready access to fat stores might drive the exercise.

Well, continuing to speak as N=1, I've always found that exercise was driven by my psychological capacity to flog myself into doing it! When I was confined to an office day after day, I took a lot of walks during the day to "think." Also, for several years, I used a fitness ball as a desk chair--a risky behavior frowned upon by the OSHA gendarmerie. I used to ice skate regularly during my lunch hour. None of these activities had much to do, I think, with boosting the effectiveness of my weight loss, although I'm sure they had everything to do with not becoming a blimp over time. I hated it when "experts" said that fidgeting could result in weight loss. Just try increasing your fidget-rate on a conscious level.

Ability to bully yourself into exercise might also come down to metabolic state.

Fidgeting--yeah, probably easier to do a forced march than to pointlessly make yourself fidget all day.

I am so glad to hear of NuSI doing something!

And no matter what their outcomes, I feel glad to think that the people doing this research are planning it well and performing it with integrity.

And what we learn NO MATTER WHAT is something learned, the way science is supposed to be. Then the protocol can be adjusted for "knowing better now than we knew then" and another inquiry can be made.

There are no head games or end games or just get my bloody paper in a press release so I get massive free as-if-its-news-publicity games.

I love that. I really do.

P

Kevin Hall was biased going in, but that was the deal, people always have at least a suspicion of what the results will be--and I do think that if the study had gone another way, he would have been just as happy with the new finding as he is with what he probably sees as a reconfirmation of something he already knew. Maybe happier, proving a metabolic advantage would probably be pretty good for a person's career. I hope that if that had been the result, I'd still be blabbing on about how the findings might be particular to things in the study design in addition to the carbohydrate content.

My problem here is with the idea that this might be looked at as "case closed."

Sometimes rodent studies get people to rolling their eyes when they're applied to humans. One thing rodent studies do show, though--is that findings in a very carefully controlled experiment are sort of specific to the conditions of the experiment. Changing just one thing shows the results of changing that one thing in a controlled environment--not necessarily in all controlled environments. One example is fructose. Take two groups of rats, add fructose to the chow of one group, feed the other only chow. Bad stuff might happen to the fructose group. But give them extra glycine, or choline, or something, and the fructose group might have done just fine.

At the same time, adding glycine or choline for the plain chow group might have had no appreciable effect--meaning that if the researchers had happened to choose a diet higher in glycine or choline for the control diet, adding fructose might not have done any harm.

What time you turn on the lights, temperature the cage is kept at, whether there's a running wheel, meal timing, food texture (hard food can hurt the roof of an animal's mouth, decreasing food intake)--in the Hall study, were people fed just discrete meals, or did they just have to make sure they ate all of the food they were prescribed, with a few small floating snacks that they could eat when they wanted, as long as they ate them before bed)? All sorts of things might make a difference. There's the story, and it might be apocryphal, that the benefits of intermittent fasting were discovered when lazy grad students started feeding lab rats twice as much food on Monday, Wednesday, and Friday--true or not, it's plausible, especially if going in they had no idea that changing the feeding pattern would have an effect.

I think if you took every metabolic ward study ever done in humans, and replicated these studies as much as possible in rats or mice, and knew nothing of the zillion other studies done on these animals--you'd know only a fraction of what's already known about these animals.

Something else, this might be silly, it might not. A common claim we make here in low carb land is that eating the SAD causes hypoglycemic swings, this is something a ketogenic diet can protect from, between the decrease in insulin/glucose excursions and the directly protective effect of ketones.

David Jenkins did a study where he fed people 50 grams of glucose all at once, or slowly over a 3.5 hour period. Fed slowly, insulin went up way less, and free fatty acids went down and stayed down, which is probably why people were more insulin sensitive.

Gulped down all at once, glucose and insulin spike, fatty acids plummet--but then free fatty acids go well above baseline, as part of the counter-regulatory response. Another way to fight hypoglycemia is to just eat more, and to eat more often. Not really an option in a metabolic ward.