Searching for long-term success in weight management? Forget dieting, eat regularly
 

I almost put this one in the war zone, I'm highly suspicious of it. What if I told you that people who tread water are more likely to drown than people who don't? I think that's probably true, because people who tread water are more likely to be in water that's deep, less likely to be wearing a life jacket, etc. People who don't struggle to maintain their weight may very well be those people who don't need to struggle to maintain their weight.

Here's a news bulletin:


Now if they only knew how to tell people what constitutes "regular eating habits" that actually lead to good health.

My other observation of articles like this is the use of the term "study" as if it carries some degree of credibility. However, studies can be poorly constructed and when they include answering questionnaires, are notoriously inaccurate. It truly doesn't matter how many participants were involved, as the inaccuracies simply magnify the distortions with more participants. Yet, if it's a "study," then we must pay attention.

oooooookaaaay! If that were true, I would be completely sc#w#d! I spent those crucial years between 15 and 25 with an ED and lots of weight issues.

okeee, wait, lemesee here. I have this straight?

my best protection against getting fat would have been . . . not to get fat? If I had done that all along (but especially as a young adult), I wouldn't have gotten myself in this predicament in the first place? It was that easy?

You have to ask yourself. Is this the best they can come up with?

Insulin-induced lipohypertrophy

Occurs over time, irreversible by diet alone. Mechanistic culprit - insulin, specifically chronic hyperinsulinemia. Primary culprit - dietary carbohydrates. In diabetes type 1, it occurs as a result of injecting insulin in the same spot for years, and it occurs only in that spot, resulting in local fat mass. In everybody else, it occurs systemically, but most especially around the waistline and where there is normally already more fat than elsewhere on the body.

None of this can be explained merely by "eating irregularly", nor can it be fixed by "eating regularly".

However, if we consider the Minnesota semi-starvation experiment and the subsequent follow-up that shows subjects regained weight and then some extra fat on top of that, we can reasonably conclude that deprivation eventually leads to overcompensation, and if this overcompensation is done mostly in the form of eating dietary carbohydrates, it will result in chronic hyperinsulinemia and insulin-induced lipohypertrophy. On the other hand, we can already reasonably conclude that none of that is required for chronic hyperinsulinemia - we can just eat lots of carbs now at every meal - we can just "eat regularly".

There's that Minnesota starvation study again. Google "fat overshoot" and you see that study and the name Duloo. There was fat overshoot with the refeeding. Was there obesity? Did the men remain fat?
Quote;
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although binge-eating continued to be a problem for a few. Participants did not, after the end of the study, eat and eat until they were obese: in general, they regained their original weight plus about 10% in the rehabilitation phase, and their weight then gradually declined towards the pre-experiment levels during the the follow-up period.
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Dulloo has suggested recovery of lean mass for the fat overshoot--fat mass recovered first, and the appetite didn't return to prestarvation levels until recovery of lean mass.
Binges are a slightly different issue, although obviously relevant. Rodent models of binge disorder often do not involve excess body fat.



https://www.psychologytoday.com/us/...ness-starvation

I definitely agree with Teaser on this. Comparing naturally metabolically healthy individuals to those who aren't and tend to gain weight (and therefore diet, skip meals etc. trying to not gain) is comparing apples to oranges.


The physical adaptations that come from pregnancy (promote survival in case of pregnancy/birth during a famine) definitely gave me weight gain issues. Too much sugar and carbohydrate in general during the height of the low-fat era, too. And if we're talking about the same women who gave birth to two or more little ones, "poor contentment with life" just might translate to exhaustion from lack of sleep and keeping up with all the constant needs of small loved but helpless human beings. Mothers of young children tend to rate lower on those types of psychological scores, but maternal contentment goes up as as children grow more independent at self care and things like mom's sleep and more personal time return. Interesting that smoking increased likelihood of men's weight gain. Possibly a marker for poor personal health habits in general, as I've heard women used to smoke to keep their weight down.

Recovery of lean mass as the cause for fat overshoot? No.

Fuel partitioning. If more energy goes to fat tissue, less goes to lean tissue. However, fat tissue and lean tissue are made up of completely different stuff. So, it's not a question of fuel partitioning after a meal, but the content of the meal that determines beforehand where that energy will go once eaten. In other words, protein cannot convert to fat, nor can fat convert to protein, nor can carbs convert to protein, but carbs can convert to fat, and some amino acids can convert to glucose.

Suggesting lean tissue recovery as cause for fat overshoot is the same as suggesting protein converts to fat and fat converts to protein.

If we accept the premise that fat accumulates through lipoprotein lipase activation by insulin, which then esterifies fatty acids to triglycerides, driven by glucose metabolism resulting in production of glycerol, we could hypothesize that somehow dietary protein has the ability to convert to glucose (at least some amino acids) then stimulate insulin then convert this glucose to fat, but when protein is ingested, insulin is secreted, this insulin then dictates only one path for protein (for amino acids, more appropriately) to go - lean tissue. Insulin inhibits gluconeogenesis, inhibits proteolysis, stimulates protein synthesis. Insulin also stimulate LPL in fat tissue, which allows the hypothesis that dietary protein can lead to excess fat accumulation, but there's no new glucose, there's no new glycerol, there can't be fat accumulation.

This means that in order for excess fat accumulation and lean tissue recovery to occur simultaneously, there must be both dietary protein and dietary carbs. This then refutes any suggestion of causality from lean tissue recovery to fat overshoot. Instead, it's parallel effects by two distinct dietary agents.

Finally, excess fat accumulation doesn't occur during a meal, but in-between meals. During a meal, it's merely called storage. And in order for excess fat accumulation to occur in-between meals, insulin must remain higher than otherwise, this means dietary carbs. Neither can dietary fat nor dietary protein produce this. On the contrary, dietary fat has the unique ability to cause insulin to drop in-between meals, while dietary protein has a similar ability because it does not cause blood glucose to rise, but less so because it still stimulates insulin during a meal.

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Apples and oranges? Let's see.

Are lean people more or less prone to growing fatter than fat people? Would a meal that makes a lean person fat, make a fat person fatter too? Would it make him fatter more or less easily? Are the mechanisms that make a lean person fat, the same mechanisms that make a fat person fatter?

This forum is dedicated to a low-carb diet, and to discussion about how a low-carb diet makes us leaner (support, science, media, recipes, journals, success stories, etc). We're fat. Does this same low-carb diet make lean people leaner too?

I prefer to see it as different points on the same spectrum.

I think it likely is an artifact at least in part, of the sort of food taken in. But also likely, given the diet refed, that the subjects did keep "overeating" after fat mass was recovered, due to signals from the still-depleted lean mass.

One thing mentioned is a decrease in the thermal response to food--read carbohydrate. Until lean mass is recovered, the biggest sink for glucose in the body is basically missing.

Let's do a thought experiment based on the Minnesota semi-starvation experiment. We put half the subjects on a low-carb diet after the experiment so they recover. Now there's two questions. Which tissue recovers quicker, lean or fat? Does any tissue grow in excess, i.e. excess fat accumulation or excess lean tissue growth? I tend to think that fat tissue recovers quickest of all tissues (in either direction), and no tissue grows in excess (due to diet alone) in the relative absence of carbs.

Now we compare this thought experiment to what actually happened. Since there was excess fat accumulation, we can reasonably conclude that there was lots of carbs. Hyperglycemia inhibits growth hormone, and growth hormone is the most potent growth factor for lean tissue. From this, we can then conclude that lean tissue recovery was slower than it could have been, had the subjects been put on a low-carb diet, which would have prevented inhibition of GH by hyperglycemia. For fat tissue, we got the carbs, we got the insulin, combined with inhibition of GH, we got effective fuel partitioning favoring excess fat accumulation and slower lean tissue recovery.

If we accept the premise of lean tissue being the biggest glucose sink, we still can't ignore the effect of low-carb on us today, we still can't ignore the effect of hyperglycemia on GH and then on lean tissue, we still can't ignore carbs->insulin->excess fat accumulation. I'd have to say that the potency of the missing biggest glucose sink is rather weak by comparison. Maybe it contributes to glucose being shuttled mostly toward fat tissue (where we get glycerol, esterification, etc) as lean tissue recovers, but I prefer to think that insulin can do that all on its own without ever knowing what happens with lean tissue, precisely because when we start with a healthy young man in his 20's and feed him a high-carb diet for 20 years, that's exactly what happens. We get excess fat accumulation and systemic insulin-induced lipohypertrophy.

For the Minnesota subjects, insulin-induced lipohypertrophy is probably not a concern, but for young people who choose between eating irregularly and eating regularly, we advise them to eat 300 grams of carbs per day, which is likely to be in the ball park of the diet eaten by the Minnesota subjects after the experiment. Fat tissue will grow, and I bet it won't matter whether they eat regularly or not.

I'm not sure who said we had to (or whether you're suggesting that I said that).

I don't contest



But don't see this as an argument vs. a role of recovery of lean mass in this.

Reduced lean mass-->reduced glucose sink, and hormonal consequences of this, and increased appetite due to a drive for recovery of lean mass, and, and, and-->insulin-->excess fat accumulation doesn't really sidestep a role for insulin.



A problem for me here is that I only have the thought experiment to work from. I don't think it's clear that carbs are the problem in this particular instance, while obviously I think they are a problem in certain contexts, or what would I be doing here? As far as quicker recovery of lean mass goes, I think what there's the most evidence for here is increased, better quality protein compared to the diet they were refed (the same poor quality diet of the restriction period, but in unlimited quantities) paired with some sort of resistance training.

As far as whether a low carb diet can support excess fat growth--it can. It's far less likely to in certain contexts. Whether this is true post starvation--we may never know, unless maybe somebody looks into it as an anorexia nervosa recovery diet. My suspicion here actually generally runs in the same direction as your "tend to think," just with a little less confidence. :lol:

Oops. I edited too much.

I asked Teaser about recovery from starvation, and Dr. Lutz's Life Without Bread.

I apologize for "messing up" this post.

On the topic of recovery from starvation.

Here is an excerpt from:


Human pattern of food intake and fuel-partitioningduring weight recovery after starvation: a theory of autoregulation of body composition

BY A. G.DULLOO

http://doc.rero.ch/record/303329/fi...65197000803.pdf




A CONCEPTUAL MODEL OF AUTOREGULATION OF BODY COMPOSITION DURING WEIGHT RECOVERY

The control systems operating through energy partitioning, thermogenesis, and hunger-appetite have been incorporated in a conceptual model of autoregulation of body weight and body composition depicted in Fig. 8, and are outlined below.

1. Energy partitioning between lean and fat tissue compartments is a characteristic of the individual based on the observation that for a particular adult individual, the proportion of the total body energy mobilized as protein during weight loss (i.e. the P ratio) is strongly correlated with the proportion of body energy deposited as protein during weight recovery, and that variability in P ratio between individuals is very strongly determined by the initial (pre-starvation) percentage body fat. This leads to the concept that the initial percentage body fat provides a ‘lean-fat compartmental memory’ which defines the P ratio of the individual and dictates not only his (her) pattern of lean and fat tissue mobilization during energy deficit, but also the way that energy deposited during refeeding is repartitioned into lean and fat tissue compartments.

2. Thermogenesis is suppressed during weight recovery, and by a magnitude which is proportional to the degree of fat depletion, but unrelated to the degree of FFM depletion. This leads to the concept that there exists a memory of the largest fat stores reached in a given individual, i.e. a ‘fat-stores memory’ which governs the suppression of thermo- genesis as a function of the replenishment of the fat stores. The functional importance of the economy in thermogenesis during weight recovery is, therefore, to accelerate specifi- cally the replenishment of the fat stores, thereby contributing to the disproportionate rate of fat relative to lean tissue recovery. This control of ‘fat-specific’thermogenesis functions as a specific accelerator of body fat during weight recovery, and is distinct from the control of
‘non-specific’ thermogenesis which functions as an attenuator of energy imbalance.

3. Hunger-appetite drive leads to hyperphagia during weight recovery, and the magnitude of this hyperphagic response is determined at least in part by the extent to which body fat and FFM are depleted, with the degree of fat depletion being the stronger determinant. The hyperphagic response, therefore, seems to be dictated not only by a memory of the initial fat stores but also by a memory of the initial FFM (hence, lean tissue) compartment.

The functional importance of this increase in the hunger-appetite sensation,with consequential hyperphagia, is to accelerate the restoration of both lean and fat compartments, as defined by the energy-partitioning characteristic of the individual.

Not really. Dr. Ludwig's study showing lack of reduction in metabolic rate with a ketogenic diet following weight loss vs. a higher carb diet is suggestive, but I guess maybe waiting to see how his bigger study looking at this turns out makes sense. There are rat studies showing different results in refeed depending on whether the animals were calorie restricted or just plain starved, and also where letting the animals choose their own macronutrient ratio had effects on their recovery.

I read Life Without Bread a while ago, it is interesting. Hard to know whether there were some undiagnosed celiacs, or people just eating too little protein, or something. Even borderline diabetes, somebody could produce enough insulin to support a healthy body-weight on a low carb diet, but be deficient if they eat high carbs.

Most of what I've seen looking at recovery of lean mass doesn't care about fat overshoot, they're just looking at protein vs. energy, fat vs. carbohydrate energy effects on nitrogen balance.