The Land Sub Experiment

Gary Taubes penned a column in Nature last month arguing for a rigorous test of the energy balance hypothesis versus what he calls the hormonal hypothesis for the cause of obesity.  Taubes writes

Before the Second World War, European investigators believed that obesity was a hormonal or regulatory disorder. Gustav von Bergmann, a German authority on internal medicine, proposed this hypothesis in the early 1900s.

The theory evaporated with the war. After the lingua franca of science switched from German to English, the German-language literature on obesity was rarely cited. (Imagine the world today if physicists had chosen to ignore the thinking that emerged from Germany and Austria before the war.)

Instead, physicians embraced the ideas of the University of Michigan physician Louis Newburgh, who argued that obese individuals had a “perverted appetite” that failed to match the calories that they consumed with their bodies’ metabolic needs. “All obese persons are alike in one fundamental respect,” Newburgh insisted, “they literally overeat.” This paradigm of energy balance/overeating/gluttony/sloth became the conventional, unquestioned explanation for why we get fat. It is, as Bernard would say, the fixed idea.

This history would be no more than an interesting footnote in obesity science if there were not compelling reason to believe that the overeating hypothesis has failed. In the United States, and elsewhere, obesity and diabetes rates have climbed to crisis levels in the time that Newburgh’s energy-balance idea has held sway, despite the ubiquity of the advice based on it: if we want to lose fat, we have to eat less and/or move more. Yet rather than blame the advice, we have taken to blaming individuals for not following it ‘properly’.

The alternative hypothesis — that obesity is a hormonal, regulatory defect — leads to a different prescription. In this paradigm, it is not excess calories that cause obesity, but the quantity and quality of carbohydrates consumed. The carbohydrate content of the diet must be rectified to restore health.

As I have argued before (see here and here), these two hypotheses are not conflicting.  The question of whether or not carbs make you fat is not an either-or issue but a quantitative one.  I also agree that we don’t yet know the answer and a definitive carefully controlled experiment is required.  I call this the “Land Sub Experiment” because what we need to do is to completely sequester individuals from the outside world for up to a year or more so that we can precisely measure everything they eat and how much energy they expend.  We can then compare a group that consumes mostly carbs to one that doesn’t.  The NIH will actually be involved in the NuSi study that Taubes describes and Kevin Hall is directly involved in the planning.  I anxiously await the outcome.  On a side note, a recent meta-analysis (see here) reports that being overweight actually lowers your mortality rate.


12 thoughts on “The Land Sub Experiment

  1. I’ve been intermiitently following your comments about diet for a while. However, I’m sure that I’m misrepresenting what I think that you are driving at.

    Would you be willing to clarify your position on several issues?
    If I know for certain what your position is, then I may be able to throw out some alternative (scientifically and clinically based) observations that may point you in new directions. Or maybe I don’t have jack to offer; I don’t know.

    1) The principle cause of obesity in America is ?

    2) My mathematical models suggest that the best way to treat obesity is through ?

    3) Possible weakness in the assumptions in my models are include?

    4) Can you list all of your factors accounted for in your obesity model, and also list any factors that you may have omitted, and why?

    5) The likelyhood of getting a given patient to follow the advice for weightloss implied by my model is?

    I’m thinking that your answers will be something like:
    1) excess calorie consumption
    2) reduce caloric intake
    3) My models of obesity are based upon rock-solid fundamentals.
    4) I have accounted for all important factors in modeling obesity, and have overlooked nothing.
    5) 2% because it’s hard to get anyone to eat less.



  2. @Tom

    1) I believe excessive food production is the cause for the rise in body weight in the US. It seems that about 1/3 of the population is extremely likely to increase food consumption when more food is available, 1/3 is moderately susceptible and 1/3 is immune to excesses in food. We have no idea what sets the categories.

    2) Reduction of intake or increase in activity can reduce weight. However, this is a tautological statement. The model does not suggest any way to achieve these ends. I personally do not have any solution for the obesity epidemic.

    3) The model is very simple and is based on known physiological and clinical data. However, there is a large uncertainty in the parameter values for individuals, in particular the relationship between energy expenditure and body weight. Thus the model can accurately predict an average over a population with good confidence and less confidence for individuals. So I would say our assessment of the US population is solid while specific predictions for particular individuals would be tenuous.

    4) The model accounts for energy expenditure as a function of body composition, energy density of body tissue, how the body partitions excess energy into various body compartments, the efficiency of processing food, and changes in body energy when body weight changes. We have attempted to account for all available data.

    5) The model can predict how much one should eat to lose a given amount of weight on average. I have no idea what the likelihood of anyone following the prediction and wouldn’t even want to hazard a guess.


  3. Carson, thanks for your answers. I have 2 parts to throw out there which you may or may not find useful. I do see that our jobs force us to focus on obesity from 2 different directions. You are more likely interesting in modeling parameters for populations and don’t care about individual situations. I am stuck trying to find solutions for the obesity of the person sitting in front of me, but am not responsible for the population at large.
    That being said, I have found that the most efficient way to coach for weight loss is in a specific group of patients; namely those with truncal obesity, middle age, family history of diabetes, and slowly rising blood sugars. Yapping away about constructing a diet with 20% fats, 30% proteins, more exercise, reduced portion size, etc, etc, has never once worked for me. Their eyes glaze over, their diet doesn’t change, and their wieght never goes down. I have had better luck with the following approach. I list common high-carb foods and invariably hear the comment “well, what am I suppose to eat?”, as they, in general, eat a carb-rich diet. I then tell them to simply restrict total carbs (from the high-carb-food-list) to 50g per meal. They can eat whatever else they want. Veggies, meat, cheese, etc, etc. I don’t tell them to exercise more, and I don’t tell them to limit portions. Just limit total carbs to 150g per day.
    At a 3 month recheck, I typically find that 1/2 don’t do this at all, and their weight is the same or higher. 1/3 do it to varying degrees, and achieve some degree of weight loss. The last group take it to heart, and low and behold, find that they drop 10-30 lbs and are excited about it. They all tell the same story that it took about a week of dietary changes for them to stop craving the carbs, and then they didn’t miss them. Once they stopped craving carbs, they stopped eating as much because they reported that they weren’t so hungry. (Notice that I did not counsel them on restricting portion size or increasing activity.) The weight tends to stay off until more carbs start trickling into their diet 1-2 years later.
    For many undoubtedly complex reasons, in people predisposed to type II diabetes, having them only focus on avoiding high carb foods causes a number of patients to drop their caloric intake of their own volition, and result in clinically measureable weight loss. Their cholesterol usually improves too.
    These instructions don’t work at all if the patient doesn’t have a family history of diabetes and slowly elevating blood sugar.
    Why? People with type II diabetes tend to initially overproduce insulin, before their insulin production gradually falls later in the disease. Yet, I acknowledge that the the role of insulin and the causes of insulin resistance in the setting of weight loss are very controversial. But, from my personal experience, I’ve found that advice to work in a segment of the population. I strongly suspect that the diabetes susceptibility genes and focus on low fat (which turns into high-carb) account for part of your 2/3 of the population who are susceptible to excess food availability.
    As I look at what I think is your picture on Google images, you do not seem to have the body type of metabolic syndrome. You likely don’t have any response to low carb diets, and can’t personally figure out what anyone sees in those diets. But, there is a way to simulate that feeling. Just stay up for 24 hours, and for breakfast (at hour 24), have a large breakfast of pancakes, lots of orange juice, toast, donuts, and hashbrowns. Then go about your day, but keep some nice high-carb foods around your office. You will be tired, grouchy, and about 11am, you will have a pretty intense craving of whatever high-carb foods you can get your hands on. Those cravings for carbs are what many with prediabetes feel on a daily basis.
    Sleep deprivation releases many stress hormones, and creates temporary insulin resistance. The end result is that carbs taste really good in that situation, and after feasting on high carb foods, you will soon be hungry for more carbs several hours later. Try it for yourself to see what I mean.
    For that matter, fasting for 24 hours seems to reduce insulin resistance in most people. The first meal after a fast is very filling, and one tends not to eat as much.
    OK, this is a bit lengthy, but the point is that for a substantial part of the general population, their personal biochemistry seems to push them to the carbs>increased hunger>overeating paradigm, and likely plays some role in the 2/3 of the population who are susceptible to excess food availability.
    The second part I alluded to is in a different direction all together.


  4. noi nation of islam who i disagree with extremley did just take all that garbage out of the hood or maybe put it up in bethesda and nih half a mice day got em hear


  5. My second observation will shed further light into why your estimate of 2/3 of people are variably unresponsive to satiety cues. Simply put, many eat to affect their brain chemistry, and not to satisfy their metabolic energy requirements. It’s been known for > 40 years that eating carbs will raise brain serotonin levels.

    Consider that the most common targeted pathway for antidepressants is through the brain serotonergic pathway. Well, you can get a similar effect through eating lots of carbs. And, it’s more fun to eat fun foods than take a pill. I mean, the law of conservation of energy ties weight gain to energy consumption minus energy usage. You clearly have the equations governing those connections pretty well established. However, to really investigate how this goes astray, you should consider looking in a direction orthogonal to energy balance to account for other causative effects.

    Chasing a certain transient state of brain chemistry leads to overeating behavior that is not constrained by satiety cues. Unfortunately, that I suspect that makes the mathematics of energy regulation very messy when they are intertwined with the vagrancies of abnormal human psychology.

    Consider bariatric surgery. Surgeons love it because it’s a major operation that they can charge for. Yet, the fraction of patients who return to pre-surgical weight was 1/3 at 5 years and 2/3 at 10 years. If the cause of obesity was unintentional overeating, then surgery should fix the problem. Yet, all surgery does is cause about a 100 lb weight loss in the first 6 months, until the patients figure out how to eat around it (i.e. high carb drinks like soda/shakes/etc). Then, weight loss stops and begins to reverse. Surgeons throw up their hands and tell these patients to take it up with their primary care provider.

    These people are not overeating because they accidentally missed satiety cues, they are overeating to force desired changes in their brain chemistry in order to ‘feel’ better. I could tell you story after story, but will just share one. One lady was proud of her bariatric surgery and her 100 lb weight loss. Twelve months after the surgery, she was with friends, and asked them to stop at Dairy Queen to celebrate. Everyone else exchanged nervous glances, and tried to suggest other activities, but she was insistant. Sure enough, she ordered some big ice cream dish. About half way through, her eyes began to bug out because she was having stomach pains from trying to eat so much. Yet, she doubled down, and eventually ate the whole thing. She then excused herself and began pacing around the parking lot outside, muttering “not again”. Soon enough, she had her husband take her to the ER because she grossly overate what her now-surgically altered intestines could handle, and had severe abdominal pains. Unfortuantely, she probably averaged 1 trip to the ER a week. She regained all of her weight, but now she permanently altered her body through surgery. Remember, she had to mentally tough it out to physically consume this quantity of food, despite real pain.
    This is an example of the 2/3 of individuals in your example who don’t respond to normal satiety cues.


  6. @Tom
    I actually have argued previously that low carb diets may work by curbing appetite, i.e. a purely neurological effect. Interestingly, Gary Taubes has always been negative about this idea, which I have never understood why.


  7. This is a bit delayed, but let me clarify a different way to approach obesity.

    A common treatment for depression is Selective Serotonin Uptake Inhibitors (i.e. SSRI’s like Prozac). Increasing serotonin in the brain seems to help some with depression. Of course, a detailed understanding of all causes of depression is not currently known.

    Now, from the link given above
    eating carbs increases serotonin in the brain. There are detailed reasons for this, but consider that the GI tract produces 95% of the serotonin in the body.

    And, serotonin receptors in the liver regulate insulin sensitivity.

    Not surprisingly, certain SSRI’s can improve insulin sensitivity in the liver.

    Finally, low serotonin levels are seen with diabetes

    And, depression is more common in those with diabetes

    Soooo…. in an abreviated way, it would suggest that diabetes could be thought of as a low-serotonin activity state predisposing to depression. As evidenced by the first link above, a “natural” way to increase brain serotonin levels (and “feel better”) is by eating lots of carbs….leading to weight gain…leading to insulin resistance…leading to diabetes.

    Thus, folks are eating for reasons completely unrelated to satiety as they are utilizing food to influence their brain chemistry in ways other than hunger regulation….which is why bariatric surgery doesn’t work long term because it’s not fixing the serotonin problem…

    This is just a rough sketch, but hopefully, it provides enough research to show how factors other than energy balance contribute to the obesity problem.

    Two more recent stories:
    Sweet sodas raise your risk of depression

    And, in last week’s JAMA
    Fructose and glucose activate different parts of the brain (giving different ways to affect brain chemistry and activity through food selection)

    However, I suggest that the solutions to many (but not all) types of obesity will be found by considering these neural pathways and mechanisms.


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