[Content warning: fat, anorexia, dieting]
[Epistemic status: crazy speculation from someone who isn’t an expert in the field. Please don’t take too seriously.]
Some anorexics I talk to describe their condition as falling into two phases.
In Phase 1, they’re a model or a ballerina or something where they’re under a lot of pressure to become thin. So they go on a diet, they have trouble just like everyone else, but they stick to it and gradually get thinner. People praise them for their thinness. They win the Ballerina Of The Year award. They’re pretty happy with how things are going, and their dieting is ego syntonic – ie they agree with it and can explain the reasons they think it’s a good decision.
In Phase 2, somebody tells them, wait, this is unhealthy. Maybe they end up in the hospital. Maybe some friends stage an intervention. They admit that they have anorexia and decide to get better and gain weight. And then they can’t. The exact way that this presents varies among people. A few say they never feel hungry – as if they’re always so stuffed they couldn’t eat another bite. More often they still feel hungry, but they feel a sense of horror at their fatness, even if they rationally understand they’re really thin. This makes it very hard to regain weight.
This reminds me of the model of obesity I talked about the other day. People start overeating for social reasons (specifically, because our society is full of tasty food). Then they find they can’t stop – their body has adjusted to its higher weight as a new set point and will defend it vigorously, producing hunger pangs and food obsessions if they try to diet.
The brain system producing these effects is called the “lipostat”, and it seems to work through a control loop. Fat cells produce a hormone called leptin. The hypothalamus measures the amount of leptin, compares to its preferred set point, and based on the result generates strong urges to eat/exercise/fidget either more or less. This in turn makes the person gain or lose weight, increasing or decreasing the amount of fat and the concentration of leptin, and completing the loop.
In (at least some cases of) obesity, constant overeating makes the hypothalamus leptin-resistant – that is, it systematically underestimates the blood level of leptin. Suppose a healthy person weighs 150 lbs, his body is on board with that, and his lipostat is set to defend a 150 lb set point. Then for some reason he becomes leptin-resistant, so that the brain is only half as good at detecting leptin as it should be. Now he will have to be 300 lbs before his brain “believes” he is the right weight and stops encouraging him to eat more. If he goes down to a “mere” 250 lbs, his brain will panic, believe he’s starving, and demand he eat more.
One point that The Hungry Brain stressed again and again is the cognitive complexity of the hunger response. For example, from Ancel Keys’ Starvation Experiment:
Over the course of their weight loss, Keys’s subjects developed a remarkable obsession with food. In addition to their inescapable, gnawing hunger, their conversations, thoughts, fantasies, and dreams revolved around food and eating – part of a phenomenon Keys called “semistarvation neurosis”. They became fascinated by recipes and cookbooks, and some even began collecting cooking utensils. Like leptin-deficient adolescents, their lives revolved around food. Also like leptin-deficient adolescents, they had very low leptin levels due to their semi-starved state.
And from studies of leptin-deficient children:
Farooqi explains that the primary reason leptin-deficient children develop obesity is that they have “an incredible drive to eat”…leptin-deficient children are nearly always hungry, and they almost always want to eat, even shortly after meals. Their appetite is so exaggerated that it’s almost impossible to put them on a diet: if their food is restricted, they find some way to eat, including retrieving stale morsels from the trash can and gnawing on fish sticks directly from the freezer. This is the desperation of starvation […] Unlike normal teenagers, those with leptin deficiency don’t have much interest in films, dating, or other teenage pursuits. They want to talk about food, about recipes. “Everything they do, think about, talk about, has to do with food” says [Dr.] Farooqi. This shows that the [leptin system] does much more than simply regulate appetite – it’s so deeply rooted in the brain that it has the ability to hijack a broad swath of brain functions, including emotions and cognition.
Once again, it’s not really clear how people’s metabolic set point drifts up, but it seems to maybe have something to do with overeating junk food.
So suppose there was an exactly opposite process. People who severely undereat find that their metabolic set point drifts down, with their hypothalamus becoming hypersensitive to leptin. Again, consider a person who would ideally weight 150 lbs. If they become twice as sensitive to leptin, their body won’t be happy unless they weigh 75 pounds. If they gain weight to be 100 pounds instead, they’ll be getting “too much” leptin, their brain will feel like they’re too fat, and their bodies will vigorously “defend against” weight gain to try to return to the distorted set point. This sounds a lot like anorexia nervosa.
Some more evidence: people with anorexia fidget like crazy. This is the conventional wisdom among generations of psychiatrists, and has been confirmed in studies – see for example Measurement Of Fidgeting In Patients With Anorexia Nervosa Using A Novel Shoe-Based Monitor, which found anorexics fidget almost twice as much as healthy controls. This seems really damning to me. Consciously deciding to fidget is hard. If you don’t believe me, try to fidget as much as possible for the next two hours (the length of the study linked above) and see how well it goes. Most people just can’t do it. On the other hand, fidgeting (renamed to the more dignified “non-exercise activity thermogenesis”) is the classic strategy that the lipostat uses to maintain unconscious control over weight:
The research of James Levine, an endocrinologist who works with the Mayo Clinic and Arizona State University, explains this puzzling phenomenon. In a carefully controlled overfeeding study, his team showed that the primary reason some people readily burn off excess calories is that they ramp up a form of calorie-burning called “non-exercise activity thermogenesis” (NEAT). NEAT is basically a fancy term for fidgeting. When certain people overeat, their brains boost calorie expenditure by making them fidget, change posture frequently, and make other small movements throughout the day. It’s an involuntary process, and Levine’s data show that it can incinerate nearly 700 calories per day.
A purely social paradigm of anorexia can’t explain the fidgeting; a biological paradigm outright predicts it.
I’m not an expert on anorexia, so for all I know lots of people have thought of this and I’m late to the party. But a quick Google search only reveals a few small leads. Heidebrand et al have studied leptin in anorexia nervosa, but only because they think it might affect symptoms. They find circulating levels are low – which makes sense given anorexics’ low BMI, and which neither confirms nor disconfirms a leptin hypersensitivity hypothesis. They also find that leptin increases more quickly when anorexics gain weight than when healthy people gain weight, which is suggestive but doesn’t prove that much.
I also found a paper, the appropriately-named Treasure (2005) which described anorexia nervosa apparently due to brain lesions. For example:
Of the seven anorexia cases associated with primary tumours in the area of brain stem and the fourth ventricle (Table 1: cases 24–30),12,25–30 two (24 and 25) presented as typical restrictive anorexia nervosa with fear of fatness; surgical removal of the tumours led to remission and sustained weight gain in both cases.
Thirteen cases of eating disorders associated with lesions in the cerebral hemispheres were identified (Table 1: 31–43).31–38 The damage was predominantly localised in the frontal and temporal lobes (six frontal, four temporal, three frontotemporal) of the right hemisphere (nine right, three left, one bilateral)…seven cases presented as “typical” anorexia nervosa with weight and shape preoccupations.
Most of these cases weren’t typical anorexia, and almost all of them involved other obviously-neurological symptoms that ordinary anorexics lack. And most of the relevant tumors were not the hypothalamus (although a similar paper by Chipkevitch finds a disproportionately high number of hypothalamic lesions). But it does prove that excessive concern about becoming fat isn’t just caused by ballet coaches and the patriarchy. It can also be induced by purely neurological mechanisms.
(and a complicating factor – most brain tumors increase intracranial pressure, which seems to increase the ability of leptin to enter the cerebrospinal fluid in ways that might cause obesity or something. There’s actually some suggestive literature that “leptin resistance” might just be serum leptin not making it into the cerebrospinal fluid, and a bunch of studies show that anorexics have proportionally much higher – and obese people proportionally much lower – CSF:serum leptin ratios. But these studies don’t explore causality and it might just be that if you’re too fat your leptin transporters get overloaded.)
I probably shouldn’t focus on leptin so much. Everybody agrees that leptin is only one part of the biology of weight gain, that other hormones are probably more important in weight loss, and that using leptin to represent the entire biological regulation of obesity is kind of a streetlight effect.
But I feel like something like this might be true. There must be some reason why the symptoms of anorexia resemble lipostat action so closely. There must be some reason why anorexics fidget so much. And there must be some reason why brain tumors can mimic some of the most striking symptoms of anorexia, like obsessive fear of becoming fat. All of these make sense only in the context of metabolic set point theory, and I hope more people start trying to link these two ideas up.
One oddity is that anorexia and obesity have strong (and opposite) class correlations.
Perhaps fast food increases your set point and biologically farmed romaine lettuce lowers it 🙂
It’s an oddity that’s explained by the suggestion that the initial trigger is likely to be a culturally/socially based intentional weight restriction, though.
Ditto the fact that anorexia is largely a culture-bound syndrome of the West.
But anorexia nervosa is not a culture bound illness. It occurs in “third world” countries, as well as developed countries. Much like OCD, and other mental illnesses, like schizophrenia, environment can shape how the illness is expressed and may be a PART of triggering it.
There are lots of potential explanations, but the fact that we socially reward anorexia more than obesity would be the first. Though perhaps if anorexics fidget they’d exhibit other tendencies which were considered pro-social or pro-economic as well. That’d be interesting.
Also, stress can induce eating as a response, and less healthy foods could lead to insulin resistance. I wouldn’t be completely surprised if sleep disturbances related to poverty factored in here.
I briefly had a dorm roommate who was anorexic, but his origin story was the opposite of Phase 1. He’d been a high school football player, and he had to gain a lot of weight for the position he played. He said it messed up his body image for good, and the problem started his senior year of high school.
I know nothing about your friend, so I could very well be wrong, but humans are good at telling themselves stories as explanations/origins. Religions/creation myths are one obvious example. Maybe some lady has a sick son and he gets a “miracle” transplant/recovery and the cause is obviously that she prayed in some specific way the day before.
I’ve seen people say they’re not good at maths… and proceed to explain that it’s because their 6th grade math teacher was mean or some really random story like that.
Even closer to home: I have had mild to moderate allergies to cat hair earlier in life and it is now much milder to almost nonexistent. I haven’t had shots, I’ve actually moved from a cat-owning household to a non-cat owning household in that span of time and haven’t started praying to the dog god. Any explanation I can think of doesn’t fit in with the change, so I of course don’t explain it using those explanations.
But, in an alternative world where I somehow moved to a cat-owning household but everything else remained the same, it would be very hard to not think that was the obvious explanation for my reduced reactions.
There are other examples more emotionally-involved/similar to your friend’s story, but I don’t feel like sharing them. At any rate, my point is that what one person says the cause is, isn’t necessarily the actual cause, regardless of their sincerity.
I’ve had the same cat allergy when younger that seems to be mostly gone now development. Is it common for that kind of allergy to become milder with age? I know allergies generally are immune over-reactions, does it have something to do with the general weakening of the immune system with age?
For some reason, cat allergies seem to be unusually prone to the placebo effect. This drug showed a 60% improvement in cat allergy sufferers, but still failed it’s trial because it did not better than a placebo. Not sure exactly how that applies but always thought it was interesting. http://www.circassia.com/media/press-releases/circassia-announces-top-line-results-from-cat-allergy-phase-iii-study/
When I was quite young, I had a couple of allergies that later went away, but that might not be the same thing you guys are talking about, since it sounds like your allergies faded when you were much older. For example, I was lactose intolerant from around 2 years old until I was 5 or so. I was one of those “constant ear infections” kids, though, so it’s possible someone just mistook symptoms of an infection of some sort as an allergy. (I’ve had that happen separately too: my father became convinced that I was allergic to skittles when I was 9, because I started getting rashes around my mouth. These were from licking my lips excessively in cold weather.)
The change in my response to cats was much later; they bothered me significantly into my early 30s at least, but haven’t really been much of a problem for the past several years (I’m in my 40s now).
I think I am not understanding the point you are trying to make. You say you had mild allergic reactions to cat hair when younger, these have more or less gone now, and you moved from a cat-owning household to a non-cat owning household in the meantime.
I am going to assume you mean “In the normal course of events, the natural human instinct to explain things by stories would have me going ‘the reason my cat hair allergy is gone is because I moved to a non-cat owning household’, but if I had moved to a cat-owning household and the allergy still disappeared, plainly that shows the story wasn’t true and the real reason was something else”.
Which, okay yeah, but why should that mean that the friend’s explanation of “I didn’t start having a messed-up body image until I had to put on a lot of weight, against my natural inclination and appetite so I had to force myself to eat to what I considered excess” isn’t the reason? Your “it’s only a story like humans tell themselves about miracles” explanation only works if he was ‘really’ anorexic all along and would have started a crash diet even if he had not had to put on extra weight that he wanted to get rid of, but we don’t know that since we don’t have access to the alternate world where everything else was the same except he never was picked for the football team and had to put on weight but still went on the crash dieting.
Let’s assume the football player and the ballerina are both ‘really’ anorexic; that the trigger in the ballerina’s case was “I was told I needed to lose weight” and the trigger in the football player’s case was “I was told I needed to gain weight”, and that gaining weight is different to losing weight does not mean that they are ‘telling stories’ to explain why their anorexia was triggered, just that both of them had their body image problems triggered for reasons that are different on the surface, but the underlying similarity is that both of them were forced by outside pressures into an unnatural relationship with monitoring their eating and their body for the sake of their sports (classing dance as a sport for convenience sake).
It’s the opposite actually, as I have informal reasons to believe that being exposed to a stimulus on a daily basis reduces reactions to it (acclimatization). This underlying “story”/assumption would be hard to reject in the cat allergy case if it had turned out that I had made the no-cat to cat move instead of the other way around.
I didn’t say that. In fact, I started the comment with:
and ended with:
I’m expressing skepticism about the idea of inferring cause from reported cause. Maybe the friend is right, but maybe they aren’t. The point there is that the comment I was replying to was integrating new information (from Scott’s article) based on the friend’s story. I’m suggesting that in case those two don’t match up, it might very well be that Scott’s information is incorrect, but it is valuable to also consider that the story might not be the incorrect information in such a case, too.
Any complete explanation for anorexia must include the remarkable effect that the microbiome has on appetite and behavior.
You can take gut bacteria from obese mice, transplant it into skinny mice, and they’ll gain weight. The same things works in reverse too.
If I were a psychiatrist, I’d be registering a clinical trial to test the effects of FMT from obese people into anorexics and vice-versa. Think they’d give me two Nobel Prizes if I cured both conditions?
Sure, but diet can obviously affect the microbiome.
Isn’t that one explanation for why most diets (vegetarian/low carb/etc) work? By drastically altering the composition of our food, we are drastically altering the makeup of our gut bacteria.
The generic explanation for why diets work is that change works. One guy I knew claimed to have lost 20+ lbs on the beer and ice cream diet, of course the diet had an explanation (cold food requires the body to burn more calories to maintain its temperature), but the common theme in diets that work is “eliminate X because Y”, all the heavy lifting seems to be done by the elimination factor.
I know a man who lost weight because he added ice cream to what he was eating. He stopped the excess ice cream because he found it was driving his cholesterol too high.
People are weird. Biology is weird. My friends are weird. I know someone who got 18 hours of deep sleep from taking modafinil.
Is there any evidence that exposure to coldness is an effective weight loss strategy? Fat from dairy seems to be less lipogenic than fat from other sources. It’s an open question why. People have tried to point to the calcium content of dairy, but I’m suspicious. If that were true, people would have been taking calcium pills a long time ago (even if they did cause arterial calcification. People have endured far worse for weight loss.)
Here are a few relevant articles, which relate to cold exposure activating brown fat to increase metabolism:
(no free full text or abstract)
“The new work shows that cold exposure, like dietary change, provokes alterations in the gut microbiota of mice. Moreover, when cold-adapted flora are transferred to a germ-free animal, the recipient mouse loses fat mass and has improved insulin sensitivity, which is brought about by a process that involves enhanced browning”
(no free full text)
“Although it remains to be proven, a sustained activation of AT (adaptive thermogenesis) is probably insufficient to cause clinically significant weight loss, and the ensuing compensatory mechanisms will likely nullify the modest increase in EE. Nonetheless, a modest but prolonged activation in the AT response modulates carbohydrate metabolism 76 ; 79, to a degree that could affect clinically significant endpoints, similar to the response elicited by moderate physical activity . In this regard, the expansion of AT response capacity represents a prime target for therapeutic interventions.”
(Short review article from Nature)
(free full text article from American Diabetes Association)
From a brief look at those articles (and I’m not a good judge of this kind of literature), it seems like cold exposure can induce weight loss, but not a lot of evidence about it has been compiled yet, so people are skeptical about how great it is as a long-term weight loss/maintenance strategy.
i recall G Cochran writing that the person he knew who had done the math on a cold diet didn’t realize that food calories were really kilocalories. Changes the numbers a bit.
Are there relationships between being fidgety, smoking, and anorexia?
My experience with large numbers of anorexics was when I was living in an apartment building that had quietly rented out one floor to a residential anorexia clinic. It took me awhile to figure out who were all these skinny, blonde, rich-looking, disdainful teenage girls who came outside to smoke with their minder.
Presumably, some of the anorexics didn’t smoke, but I didn’t see them.
Any anorexic worth their salt knows smoking helps suppress the appetite.
Which is sort of true. Nicotine is a stimulant, and it’s well documented that quitting smoking will cause some weight gain. Smoking’s effectiveness for weight loss is probably all anecdotal as I doubt anyone is going to run that study, maybe there’s some old ones from the 50s.
Still the use of smoking for weight loss is pretty common knowledge amoung models, teenage girls and other people who care about staying super thin.
Nicotine is super interesting to me, as there’s a huge amount of anecdotal evidence about its effectiveness as a “bio-hack”, but since it has “smoking cooties” researchers won’t touch it– even though nicotine (given as a mist, gum, or patch) is quite likely to be less dangerous than many of the drugs currently used.
It’s a stimulant, of course; you’d expect that to increase the fidgeting and consequent calorie burning. But I’ve heard many people tell me that it also helps them with intrusive thoughts– whether that’s sex, food, aggression, whatever. Most of the people who have told me this were not diagnosed with any illness, I should add. (I myself have never taken nicotine, so this is all second-hand for me.)
Last year Scott wrote a post about smoking as a coping mechanism for schizophrenia that you might find interesting.
I have been diagnosed with ADHD as an adult (although the diagnosis really doesn’t fit) and have tried a variety of stimulant drugs, including amphetamine, ritalin, modafinil, nicotine, and caffeine, at various doses and in various combinations. Personally, I find nicotine to be qualitatively superior to the rest, no contest.
Nicotine radically and uniquely improves my ability to generate mental representations of purposeful action alternatives. It wouldn’t be much of an exaggeration to say that nicotine introduced me to the subjective experience of having “free will”. It blew my mind. It was like I could suddenly use the Force to see into the future. Maybe this is actually just what regular people have going on all the time, since outside evaluations of my behavior shifted from the usual “inexplicably chaotic and self-defeating” to “surprisingly well-organized and sustainable-looking”.
Unfortunately, this effect wears off abruptly after about a week, takes many weeks of abstinence to reset, and I can’t find a suitable alternative. Regular stimulants can give me “energy”, or keep me fixated on a particular task (regardless of whether performing that task makes any sense) but only nicotine provides any actual *agency*.
Plenty of people with anorexia nervosa do not smoke (me). and not all of them are rich, blonde teenagers. (me) I didn’t get why when went to treatment how some of them actually started up smoking; or restarted. The few I talked to, it was to take the edge off of the anxiety. Most people don’t realize that in some sense, eating disorders are very much anxiety disorders, and add to that the cognitive distortions, that can be in part *just* from starvation alone. If you read the Minnesota Semi-Starvation Experiment, it is noted how the men start acting like those with eating disorders.
This suggests an experiment – induce leptin resistance in anorexics.
I would not like to try to get that past an ethics board.
Also, if anorexia has a related but different hormonal cause, this combination could have any number of effects.
Isn’t the stereotype that boys are more fidgety than girls? But girls are more likely to be anorexic.
When you’re looking at outlier cases like Anoerexia that hits only a small proportion of the population, looking at averages isn’t that informative. This is also probably a case of Simpson’s Paradox, where the trend within sexes is for fidgeting to be associated with low weight, while the difference between genders tells the opposite story. (And, entirely anecdotally, I think the fidgeting boy stereotype applies most to elementary and middle school aged boys, while fidgeting starts to mellow out by the time high school comes along, which is also when anoerexia starts ticking up.)
But there is still the important question of how to explain the gender differential. I don’t think anyone is positing a purely biological model, where all difference comes from random genetic variance, but it’s still not something that is a natural consequence of random variation in leptin or the microbiome. On the surface at least, it seems cultural attitudes would have to make up some significant part of the explanation.
I remember watching a lecture of Jordan B Peterson’s in which he discusses how the Big 5 personality trait of Conscientious divides into Industriousness and Orderliness. He suggested orderliness was strongly associated with feelings of disgust and he speculated that it served a variety of purposes such as protection against certain classes of foods and the establishment of a disgust towards those significantly lower then you in social status (protection of social status).
It seems possible to me that perhaps we are born with a provisional model of things we should be disgusted towards (Certain animals – dead bodies – excrement) but that such a model is updated to reflect the things people find sacred/disgusting in a given culture. Now – let’s assume that orderliness is a moderately heritable human trait and that it – likes all traits – falls over a distribution. Let’s posit that women have an increased tendency towards orderliness (This doesn’t seem implausible to me but it would need to be investigated) and cultural influences make it more likely that women sacralize body weight more often then men. Let’s posit that there is a subset of women (and even smaller subset of men) that score very high in this trait.
Now – let’s posit you have a group of would-be ballerinas. Thinness is favourable in ballerinas so there exists pressure for ballerinas to become thin. Only those that successfully sacralize body weight are able to lose enough weight for them to be successful ballerinas. We can then take Scott’s model from here. They push themselves low enough such that their lipostat stops working correctly and this breakdown results in a biology that prevents weight gain. In careers such as modelling/ballerinas/(some third type of thing that requires you to be really thin) you tend to find anorexia nervosa not because these careers make you develop anorexia nervosa but because you typically need to be able to develop something-like-anorexia nervosa to succeed.
Such an explanation may also be applicable to monks and/or other devoutly religious people in the past who did extraordinary things. These people are sufficiently able to sacralize certain things and the ability to do so was a prerequisite for membership in such a group. Food – in particular – seems quite easy to sacralize as (as discussed above) disgust seems to have utility in protecting people from harmful foods. Perhaps a person with anorexia develops a feeling of disgust towards all foods while sacralizing a thin body as pure.
Whoa, whoa, whoa. I want to hear more about this!
Disgust toward people of lower social status? Is that a recognized and documented phenomenon?
How about disgust toward specific body features associated with low status?
It seems plausible that, say, a dedicated anti-Semite might develop sincere disgust at large noses. But has this kind of thing ever been demonstrated?
Disgust and similar disgust-like reactions towards certain professions (and habits) is relatively well recognized, I think. Certainly (incoming confident statement backed up by zero facts) there are a bunch of unrelated cultures with an “untouchable” class that performs some set of disfavored professions. And in our own culture, people often seem to have a disgust-type reaction to, say, (stereotypical) drug addicts. I don’t think the disgust reaction fits the typical expression of racial/ethnic bias, though, except maybe when people are deliberately trying to spread the bias (eg “slimy jews”, caricatures of jews and Asians). It seems like more of a within-culture thing.
there are a bunch of unrelated cultures with an “untouchable” class that performs some set of disfavored professions. And in our own culture, people often seem to have a disgust-type reaction to, say, (stereotypical) drug addicts.
I’d say that varies by tribe. Reds tend to feel that disgust toward stereotypical criminals/drug addicts. Blues feel it toward stereotypical rednecks/white trash.
The lecture in which this is discussed is: here. Point of interest seems to start around 39:32 in which he talks about the breakdown of the big-five personality theory into sub-factors. Around 44:38 he talks about the orderliness of Hitler and Germans in general. This is roughly where he gets to this topic. Disclaimer: It can be sort of rambly at times – and it’s also pretty speculative. I’ve tried to summarize the lecture below.
He starts down the path towards disgust and social status by discussing how Hitler seemed very orderly. For example, when Hitler first came into power he spent a fair amount of time vaccinating the population and eliminating vermin in factories (I don’t have a citation for this – but he mentions it). Reviewing Hitler’s dinner conversations suggests that Hitler didn’t hate the Jewish population in Germany but rather saw them as contaminants. An interesting point here is a paper (Here) discussing the correlation between disease outbreaks and the rise of a totalitarian regime and finding it to be quite strong. Perhaps in the face of a disease outbreak orderly people are particularly good at stabilizing the situation and are awarded prestige as a consequence of their success. This increased prestige permits totalitarian personalities to ascend in status leading to the rise of totalitarian governments.
If people feel disgust towards the outgroup why should they feel disgust towards the outgroup? The link between disgust sensitivity and social status begins to be developed at 57:07. Typically, you associate with people pretty close to you in social status. If you we’re to mate/associate with someone significantly lower then you in social status you would likely get a reaction from your peer group. Disgust towards associating with those of lower status is a form of contamination – as associating with them affects how others perceive your own social status. Theoretically, this would underpin disgust towards the outgroup as associating with the outgroup (and people of much lower status would be one such outgroup) would also lower your status. However, we do not have much evidence for this yet.
So – let’s see if there’s much evidence. There’s a paper discussing disgust sensitivity and attitude towards immigration here: link and here: link. People who experience more disgust tend to have harsher views towards immigration. This may support the above idea. Also, in general, conservatives tend to exhibit higher disgust sensitivity (they also are more orderly) which perhaps could explain why they are typically more hostile towards immigrants. This evidence is pretty limited and we’d certainly need more before this amounts to more then speculation.
So – it seems plausible (like you said) that disgust could be shown towards features (such as large noses) of the outgroup but we don’t really know – yet. People might be too effective at self-censorship but I wonder if items associated with different social status could be used in a clever way as proxies to investigate this phenomenon. Do people dislike things like Mcdonalds and Walmart for the reasons they present or are the reasons merely rationalizations for their disgust? Perhaps Mcdonalds is associated with people of lower status and people avoid it as it is a contaminant of social status. Seems possible – but I don’t really know.
Let’s not get into the red/blue division. My guess is that it’s not all that relevant here.
Disgust toward drug addicts is surely a subset of general disgust toward those who are unhealthy/dying/dead. And disgust toward people who are physically dirty (or live in dirty places, like slum tenements) may tend to uphold class lines, but again, germ phobias and other health issues would explain that already.
What about sincere, visceral disgust toward things that are pure class markers, not symptoms of poor health?
Disgust toward drug addicts is surely a subset of general disgust toward those who are unhealthy/dying/dead.
I assumed the disgust in question was more of a moral disgust (maybe contempt would be a better word) than a purely physical “ew, that’s icky” kind of thing. The two can certainly overlap. But if someone has cancer and is covered with oozing tumors, people might get grossed out, but they’re probably not going to be morally outraged. If anything, they’ll feel sympathy or pity.
With drug addicts, on the other hand, there seems to be a perception that they’re weak-willed/selfish/harming society with their bad choices, etc.
With regard to the red/blue thing, I don’t want to derail too much but it does seem relevant that different people have a different perception of “who is the lower class we should feel disgusted toward?”
What about sincere, visceral disgust toward things that are pure class markers, not symptoms of poor health?
I personally find myself creeped out by those really long press-on nails, which some people see as a “ghetto” thing, so maybe that qualifies? And if someone has them I find that does lower my opinion of them a bit, in the sense of perceiving them as tacky (though I try to work against that perception).
I don’t know how much of that is a class thing, though, and how much is just that I’m weirded out by really long nails in general. I worry that they’ll break and make that awful cracking sound.
I personally find myself creeped out by those really long press-on nails, which some people see as a “ghetto” thing, so maybe that qualifies? And if someone has them I find that does lower my opinion of them a bit, in the sense of perceiving them as tacky (though I try to work against that perception).
You mentioning nails makes me think of fashion and music. I remember sitting on a friend’s couch while him and his girlfriend discussed whether or not a given song was socially appropriate to put on a playlist – the topic was rather arcane to me but they seemed to be giving this quite serious consideration. They had concerns over whether the song was old enough to be hip again or whether it was still in that awkward period between recent and old.
Now knowing what songs are currently in (or not) and their fear of being judged for not knowing sure seems like they we’re afraid of being judged and they sure seemed disgusted by the prospect of playing such music. Couldn’t this and things like fashion be pure class markers? I’m not sure – but it sure begs for an explanation.
“Disgust toward people of lower social status? Is that a recognized and documented phenomenon?”
Also, a lot of other cultures have a small scale caste system where a few jobs are stigmatized. For example, in the Middle East, being a blacksmith was often a job for reserved for sub-Saharan blacks.
I have this vague theory that a culture that was pro-blacksmith tended to technologically advance faster than a culture that was anti-blacksmith, like much of the Middle East, where there was Indian-style caste prejudice against blacksmiths.
In contrast, American culture, for example, was pro-blacksmith. Here’s the opening of Longfellow’s popular 1842 poem “The Village Blacksmith:”
Under a spreading chestnut-tree
The village smithy stands;
The smith, a mighty man is he,
With large and sinewy hands;
And the muscles of his brawny arms
Are strong as iron bands.
His hair is crisp, and black, and long,
His face is like the tan;
His brow is wet with honest sweat,
He earns whate’er he can,
And looks the whole world in the face,
For he owes not any man.
So presumably someone should try the leptin injections again, but as spinal fluid injections?
It seems to me that there are three phenomena of interest. One is the minority of anorexics who don’t feel hunger. They are candidates for the hypothesis of anorexia adjusting their low-level leptin mechanism, rather than simply ignoring hunger. The second is the creation of the disgust reaction. This seems like the stereotype of anorexia, that the high-level social feedback produces the lower-level, but still fairly high-level “psychological” feelings of disgust to balance feelings of hunger from the low-level physiological systems that it cannot directly manipulate.
Finally is the fidgeting. In principle, this is pretty similar to the lack of hunger, but it has two advantages for study: that is more common and directly observable.
The combination of hunger and fidgeting in the same person demonstrates that there is more than one control mechanism, with different set points.
You suggest that the social feedback has created the lack of hunger or the fidgeting, but it might be that it is instead a filtering mechanism. Maybe people with a normal fidget control mechanism can’t lose enough weight to be diagnosed with anorexia. Or maybe when they diet they become lethargic and thus poor ballerinas.
Perhaps the disgust reaction is class/caste related? Perhaps anorexia’s positive class correlation has something to do with higher class people tending to feel disgust more strongly?
Really? Systematically across the entire class structure, or just among a few anomalous subrgoups? Has this been specifically studied?
Class? Seriously? Poor people get eating disorders as well. They can get anorexia nervosa as well. This “disgust” you talk about has nothing to do with class or caste. It has to do with how the brain processes things, in an errant way, misidentifying food as a threat (think phobias/ anxiety disorders when fear is there when it “shouldn’t” be.)
On eating disorder wards fidgeting is something they try to suppress in the people closest to death. It’s entirely common for people with anorexia to both be skeletons who’s kidneys are failing due to extreme starvation who still want to pace and will constantly jiggle their legs and arms if given the chance.
I’m not exactly sure how this is related, but since it regards under-eating and leptin from an angle you might not have considered, I thought i would share.
There’s a condition called hypothalamic amenorrhea, which is basically when the menstrual cycle stops due to some combination of over-exercise, under-eating, and/or stress. Lots of anorexic women develop HA, but so do lots of women who exercise a ton but eat fairly normally, or exercise moderately and under-eat moderately. You can even develop HA when you are overweight from a BMI standpoint. The usual treatment is to stop exercising and gain weight.
Women with HA also tend to have low leptin levels, and one study found that administering leptin resulted in the return of ovulation, even though they didn’t gain any weight during the study.
You’d also need to explain the modern increase in anorexia. I’ve read one book claiming that anorexia isn’t all that modern (title escapes me), but (from memory) it includes fraudelent fasting girls from the middle ages where the miracle was that they didn’t loose weight and the fraud was that food was being smuggled to them, and one Victorian young woman who didn’t eat because of opposition to her family, so I’m dubious about the premise.
As for fidgeting not being something most people can increase voluntarily, well, most people can’t starve themselves voluntarily, let alone doing extreme exercise while starving, so I don’t know about anorexics and fidgeting.
One question would be whether anorexia was much of a problem during the Lily Langtry era when being well-insulated was a sign of higher social class (e.g., roughly up through the time of President Taft).
Wikipedia says the term goes back about 140+ years, but that it started to be a bigger deal in general society with a book in 1978 and Karen Carpenter’s death in 1983.
In my experience, the most typical explanation for the modern rise in anorexia is that exposure to unrealistic and hyperattractive images of people plus an increasing focus on appearance increase the pressure that people feel to become thin. This and similar popular explanations fit fine with what Scott describes, since they can be the cause that leads to the first phase that he describes.
Well, okay, but isn’t it common knowledge that the median skinny clothes model is well below the level of curviness that the median man finds attractive? If both these things are true, that’s another mystery.
My vague subjective impression is that anorexia tends to plague girls who are more driven by status competition versus other girls than by boy craziness.
This is also my impression. Speaking as a former teen girl who didn’t enjoy that time period.
There is a related rabbithole which might be explored, related to the incidence of anorexia in traditional age stratified schooling, vs that in societies where older people took a better hand in helping teens manage sexuality/marriage, instead of just assuming that they would work it out.
(I say rabbithole because there is a tremendous number of issues here regarding individual liberty and neglect and parental overcontrol and teenage stupidity, and returning to the bad old days is not an option but can’t we do better than what we’ve got?)
From someone I know who works in eating disorders sometimes parental overcontrol can be a massive massive factor.
They’re not supposed to blame the parents but sometimes when mom is hyper-controlling and has decided that her daughter is going to be a supermodel-doctor and makes repeated attempts to smuggle diet pills to her daughter who’s already hospitalized and near death and comments on her daughter with a BMI of 12 “getting tubby”….. sometimes they want to physically beat the parents with a stick. A heavy stick.
Sometimes the parents are a huge huge part of the problem/cause and hyper-controlling parents is part of one of the major “types” in eating disorders.
What’s the mystery? Fashion models (and women’s fashion in general) are not designed to appeal to men.
Huh. I’ve read about both of those in Ethan Watters’ Crazy Like Us: The Globalization of the American Psyche, which has the opposite claim – that anorexia is modern. iirc the chapter on anorexia says it wasn’t widespread/existent in China (people did starve themselves, but not for the reasons associated with anorexia) until Western psychiatry introduced it into the cultural psyche.
In absolute terms anorexia is still quite rare.
Go back not very far at all and in the poorer population it wouldn’t be obvious since it would get hidden by normal starvation and in the richer population it would probably just get lumped in with “wasting disorders” or some such. Lots of people wasted away through various causes . If a small fraction of them were actually suffering from anorexia it would be really hard to distinguish them.
Now that food is so easy to acquire that they stopped tracking deaths due to “lack of food” simple starvation no longer hides anorexia in the crowd and we’ve defeated so many of the various diseases that anorexia is part of the tiny pool of what’s left.
I suspect the book your referring to is historian Joan Brumberg’s Fasting Girls: The Emergence of Anorexia Nervosa as A Modern Disease. (Disclosure: I’m friends with the author.) I think her argument is subtler than you suggest, and actually fits with the above.
First, she distinguishes between several different types of anorexia (which just means loss of appetite, and can include appetite loss from other factors); the religious fasting is known (not her original term) as anorexia mirabilis; the modern disease is formally called anorexia nervosa. She doesn’t equate the two. And while cases of anorexia mirabilis did include some fraud, i.e. they didn’t live on literally nothing as some claimed, they definitely ate quite, quite little – in line with modern cases of anorexia nervosa.
Brumberg posits a two-stage model (with some similarities to Scott’s two stages). First is what she calls the “recruitment” stage (where it’s cultural, not individuals doing the recruiting; it’s not deliberate), in which people are induced to extreme fasting. This is cultural and social, and differs radically by society: in medieval times, attempts at piety recruited women to fast; in modern times, attempts to look thin. The rise of anorexia nervosa in modern times is explained by a rise in the changing culture, and hence increased “recruitment”. (She certainly discusses the dramatic spike in anorexia nervosa in the 1970s/80s.)
The second stage is when, so to speak, the physical takes over. Brumberg doesn’t go into depth about the biology (not her field), and the book was first published in the 1980s, so lipostat is not mentioned (IMS). But basically we’re talking Scott’s stage 2. And here, since humans are humans, anorexia mirabilis and anorexia nervosa work similarly, even if the first stage was quite different. I don’t recall her discussing brain tumors, but presumably that’s a case of yet a third type of anorexia, mirroring the second stage of the various socially/culturally induced anorexias.
Yes, that was the book. Thank you for the details.
Here’s a 1985 article on Brumberg’s book “Fasting Girls:”
Sure, you should ask anorexics if they fidget intentionally. Here is unsystematic poll in which most of the respondents say that they fidget unintentionally. Since it is a pro-ana site, I think that they’re probably telling the truth.
I got interested to see what I could find. I found the same paper you did, but also this one on anorexia following upon disease:
Interestingly, the paper claims that leptin resistance is increasingly in doubt and being replaced by the idea of “central leptin insufficiency”.
I mention this because your last two posts seem to be predicated on the leptin resistance idea. The central leptin insufficiency idea seems to be that if the leptin were delivered to the appropriate sites in the hypothalamus where it isn’t reaching due to being interfered with elsewhere, it would be effective.
So if the lipostat set point is messed with and this theory is correct, somehow the lipostat is presumably stopping leptin from reaching the sites where it is needed, I guess.
Now, in the case of anorexia cachexia syndrome, the paper I found states that other factors (inflammatory cytokines, among others) are messing with the hypothalamus’s normal response to low leptin levels. So in at least that particular kind of anorexia (different from anorexia nervosa) they have a different explanation.
However, it’s hard to see how the more normal AN relates to a reverse of central leptin insufficiency due to increased set point in an obese person. If the mechanism by which the lipostat sets the set point too high for leptin to stop him or her from eating is to prevent the leptin from reaching specific sites in the brain, what would the reverse be? I guess somehow ensuring an excess amount reaches those sites? Or maybe some other factor that mimics leptin? It seems slightly asymmetric, but I guess it’s possible.
The implication I got from Scott’s last post was that leptin doesn’t explain the body’s defense against increasing weight/fat, or at least doesn’t explain it as well. If there’s some unknown factor that normally defends against weight gain, we can assume that AN includes an increase in this factor, as well as / in addition to a decrease in the anti-weight-loss factor.
I didn’t read it that way. I thought his point was that it is in insufficient explanation, as something seems to alter the response, and he was interested in what that something was.
Why does the set point drop in the anorexic case, but not for most people who try dieting? And are there some overweight people for whom the set point drops but not to the anorexic extreme?
My guess: for the set point to drop, the dieting has to be excessive and prolonged; the sort of thing that would be caused by wanting to be the best ballerina, best figure skater, or because of patriarchal pressure to be thin or whatever. But then, even after their original reason for wanting to be extremely thin goes away, their set point has been lowered and they’re screwed. Simply dieting to get a nice swimsuit body isn’t enough motivation for this to happen, even if the diet is intense.
In anecdatal support of this, I have seen instances of extreme weight loss regimes that end up sticking without conscious effort after the initial loss, but we’re talking positively unhealthy regimes here, like halving your weight in 3 months from 140 to 70 kg or similar.
Edit: the end result is perfectly healthy, but the method of getting there carries significant risk.
A couple of comment …
It sounds from your discussion as though what normally prevents weight loss is something that makes you feel hungry or want food when you shouldn’t. That isn’t consistent with my experience. If I cut my food intake well down I lose weight. I don’t feel very hungry, don’t have to use lots of will power.
The limitation on that is that I enjoy eating, but that was as much true when I was at my old set point as at the level I have been holding for the past few years, fifteen pounds or so lower.
Also, I’m curious as to how many calories can be burned up by fidgeting. It seems like a pretty low intensity form of exercise.
I experience the same thing, but only up to within a range of 15 pounds or so. If I try to go lower, I start feeling incredibly hungry, all the time. And the point where that happens is still well above what is called “normal” weight for a person of my age and height. This (anecdotally of course) supports the idea that the body thinks you need a certain particular weight and won’t let you go below it.
From Scott’s last post.
One place where the analogy breaks down is that anorexic people have delusions that they are too fat and need to lose weight, but obese people don’t have delusions that they are too thin and need to gain weight.
Supposedly, male bodybuilders are sometimes prey to mirror image delusions that they are pathetically skinny. But in America, at least, few fat people worry they aren’t fat enough.
Perhaps in a culture that prizes obesity, such as Mauritania, this happens?
I don’t have documentation for this, but it seems anecdotally true that many fat people apparently have no idea either that they’re overweight, or just how overweight they really are. Of course, most fat people probably know they’re fat on an intellectual level, but perhaps it’s similar to the anorexics Scott describes. They know on an intellectual level that they’re too skinny, but it’s the fact that they feel fat that’s much more important. Lots of fat people don’t feel fat, or at least not as fat as they truly are, no matter what the scale or their pants might tell them.
Or even if they do feel fat, they don’t necessarily feel that their eating is unusual, when in fact they are consuming much more than average.
Last September, I ate some raw meat at a restaurant and–I don’t know if it was food poisoning or if my stomach was upset because it wasn’t used to raw meat–but I was acutely sick for a few weeks. But then I stopped puking everything up, and it still took a lot less food to make me full than it used to. I was eating the amount that felt natural to me, but when I was with others I’d suddenly become conscious of the fact that it was taking me an hour to finish the small side I ordered at a restaurant, and then I noticed most of my clothes were loose. I had recently moved, so the new people in my life weren’t really familiar with my previous habits, but when I saw my family over Christmas they noted that I’d lost weight. People keep telling me I’m fidgety, but I thought I had always been fidgety.
I’m still eating the amount of food that feels natural to me–and I love food–but it still takes less of it to make me full, sometimes concerningly so. But despite that, I feel like I’m stuffing myself when I eat past feeling full. I’m not worried about being fat, I’m concerned with the weight I’ve lost and I think I’d be fine with my body if I gained it back, but eating when I’m full is physically uncomfortable and the desire to avoid acute discomfort usually wins.
A few days before your last post on this subject, I found that I’m able to eat ice cream and gelato even when I feel full, and they don’t seem to make me full as quickly despite being high in fat and calories. After your last post, I was wondering if temporarily losing weight due to food poisoning had lowered my lipostat in the long term and that, if so, eating more junk food would set it back to normal. After this post, I’m worried I might end up with an eating disorder and I’m wondering what I can do before it’s too late.
I don’t normally favor calorie counting, but if you estimate your average daily caloric intake and think it’s too low, you could try a daily dose of ice cream to make up the difference.
You should go to the doctor. You may have tapeworms. (no joke)
Hmm. Calorie restriction reduces fidgeting.
Stimulant ADHD medications commonly cause reduced hunger.
So it seems reasonable that some portion of the efficacy of these drugs is caused by the calorie restriction. Maybe just a small fraction of the effect, and maybe it only works on the physical hyperactivity part, but it should be measurable.
Why don’t I see any studies measuring the effect of calorie restriction on childhood ADHD symptoms?
Continuing on from the previous post, about the difference between “the scientific consensus” and “the establishment” when it comes to the ‘conventional wisdom’ on things like diet and exercise, I saw this in the news today:
The scientific consensus, as represented by the British Medical Journal: hey guys, turns out saturated fats may not be the demons responsible for clogged arteries and coronary heart disease! What actually helps are fats like olive oil, eating properly, taking 30 minutes of exercise like walking a day, and reducing stress!
The establishment, as represented by the Irish Heart Foundation and many aggrieved others: this is dangerous, simplistic nonsense which is going to confuse ordinary people and make them stuff their faces with junk food so they keel over and die!
It’s a complicated matter 🙂
What does research say about the difference between those who become anorexic vs. bulemic? Does binging and purging affect leptin differently than starving?
Try to _stop_ fidgeting consciously. I would bet that people who try that fidget more than their baseline, and more than people trying to fidget more. Anyone want to put a study together and apply for a grant? I don’t need to be a coauthor, just put me in a footnote or something.
It’s interesting that both anorexia and extreme obesity are gender correlated, and much more common among women. From the NIH, men are somewhat more likely to be overweight, men and women are equally likely to be obese, but women are twice as likely to be extremely obese.
So on the one hand, the theory that social pressure to be thin affects women more strongly would explain increased anorexia, but makes the extreme obesity statistics counterintuitive. What’s going on?
At least for the upper end of the scale, women have a bit more body fat generally. Is it possible that this increased baseline means (whether directly or though a more complicated hormonal mechanism) that a woman will gain more weight on a fattening diet than a man on an identical diet? There’s a stereotype of fat eunuchs in literature; does this have any basis in fact? If so, it would point in favor of the hormonal picture. I note that I don’t have any stereotype of fat trans women in my mind, though, which points in the opposite direction.
There’s also the cliche that men loose weight more easily from dieting/exercise than women do.
Is there any evidence the cliche is true? If it is, it would potentially dovetail well with the set point theory. Perhaps women have stronger set points – more difficult to move, but therefore also more likely to cause a serious disorder if something temporarily moves them hard over to the “thin” or “fat” side?
I don’t know whether the cliche is true– now that I think about it, I haven’t heard it lately, but it was common wisdom maybe twenty years ago.
A thing I’ve only heard once is that the first diet is the easiest– if that’s true, then it’s plausible that dieting used to be a lot more common among women.
I think there is some, but I’m not sure how strong it is. I recall reading about a small study where the scientists locked a bunch of people in the lab, calculated how many calories these people needed to maintain weight, and then had the people diet and fast. Exact measurements were taken as to how many calories everyone was burning. Turned out some people in the study had “thrifty” metabolisms: they started burning many fewer calories in response to fasting. The women in the study were much more likely to belong to that group.
Men exercise more hours than women on average, which obviously can explain why exercise is perceived as working better for men. If you do more, it’s not strange to get better results.
I’ve also seen it claimed that women tend to exercise with less intensity, although I don’t know if this is true. There is research that suggests that it is harder for women to exercise with high intensity.
I wonder if this doesn’t fully explain it: women are, on average, smaller and have less muscle mass than men. In other words, they burn fewer calories per day, on average.
But restaurants, dinner parties, etc. don’t serve women smaller portions (would rightly be considered cheap/sexist). In other words, in a world which encourages portion size invariability (of course, women can order or take less food, or not finish/take home their food, but we are culturally encouraged to clean our plate and it’s tempting to eat what’s in front of you if it’s tasty, even if you’re already full), our idea about appropriate portion size is probably informed by that which is an appropriate size for a (large, active) man, since people would be annoyed at a restaurant/dinner party that sent a large, active man home hungry.
If this were accurate, I guess one would also expect smaller men to be more obese than taller.
The average American woman is 5’3″. “Extremely obese” is a BMI of at least 40, which for a 5’3″ woman is 230 lbs. That’s really big.
Your explanation might work for overweight/obese, but in that 25-39 range, women aren’t over represented. I think to get into that “extremely obese” level (we’re talking only 8% of women here) it probably takes more than big burgers at Applebee’s.
Anyway I was mostly curious if there’s potentially an explanation that gives you both more anorexia and more extreme obesity for women.
About the control system:
As I understood it, the theory is that it works like this: Fat produces leptin, brain detect leptin levels, compares to set point, then orders us to eat or fidget. Leptin detector is imperfect, and can sometimes read wildly off causing error. I didn’t see how the brain goes about determining what the set point should be.
It seems unlikely that the leptin detector can only exist in a state of functioning perfectly and being wildly off, much more likely is that it’s accuracy varies, and is probably never really perfect.
If I was designing this control system, I would be tempted to eliminate a step. Rather than setting/changing the setpoint, I would have a constant setpoint and only adjust the sensitivity of the leptin detector. It’s considerably less intuitive, but it’s a step simpler. So the brain under this system would always want to be 100lbs, but based on whatever conditions alter things, would change what it perceives itself to be at any given point.
Of course how I would design a system isn’t really important, so my overall point is “are we sure that’s not what is happening?”
How you would design the system is important insofar as it points us to likelier solutions. Evolution certainly favors the parsimonious. Great suggestion.
While evolution favors small changes step by step, it doesn’t usually end up with a parsimonious solution, as we learned when we tried to copy it for nanotechnology.
AFAIK this is incorrect:
If I remember correctly, the number of fat cells never goes down. If at all, only slightly. In people who lose (enormous) volumes of weight, the number stays the same, only the size decreases. Which probably makes gaining weight back easier and makes our lives miserable.
And being obese at some period of life may increase your mortality risk for the rest of your life. At least this study suggests so:
Anyone have an overview of the process of anorexics regaining weight? My impression in that there’s a lot of variety in how easy it is physically to regain weight.
As for the social environment, it isn’t just overt competition for prizes. I’ve seen alot of accounts from people who were being complimented on their weight loss and asked for diet tips when they were sick from malnoursihment.
I’ve heard of one case of what I call poverty anorexia– feeling unentitled to food because there wasn’t much around.
More information on the cultural side: http://www.slate.com/articles/double_x/doublex/2014/03/eating_disorders_and_women_of_color_anorexia_and_bulimia_are_not_just_white.html
This is anecdotal, but I (formerly anorexic around the age of 14/15) had an experience whereby after being convinced by a therapist to start eating normally, I gained a tremendous amount of weight (going from ~110lb to 145lb in the space of maybe 6 months), and for at least three or four years thereafter, had every indication of a metabolic rate severely below what would have been normal for a girl my age. My interpretation of it at the time was “I managed to re-engineer my metabolism to a new starvation-normal of many fewer calories, and it was hard to engineer back out of that”, but I’m not sure how widespread/validated by evidence that interpretation is.
On the previous thread, I wrote something that as stated amounted to a tautology and was called out on it. Since we’re still more or less on the same topic, I’ll explain what I actually meant in somewhat more words here:
– we know that insulin, the hormone that governs how the body handles sugar is triggered by sugar intake.
– we know that anabolic hormone, the one that governs how the body handles proteins is triggered by protein intake.
– therefore it is not unreasonable to suspect that leptin, the hormone that governs how the body handles lipids is triggered by lipid intake.
If this is the case, this is a good explanation for why high fat diets work as well as why it seems to be slimming to eat olive oil in the morning. Also, it makes Guyenet’s lipostat theory fully compatible with a low-carb diet, albeit with a different mechanism.
And lo and behold: most studies regarding the relationship between high-fat diet and concentration of leptin were found that there is a positive association between intake of higher fats and leptin level.
“most studies” seems to be few and far between, but still at least not contradictory. As usual, this comes with the caveat that things are more complicated and which types of lipids you ingest seems to make a significant difference.
>A purely social paradigm of anorexia can’t explain the fidgeting; a biological paradigm outright predicts it.
At the risk of saying something trivial, it has to be both, right?
Social paradigms essentially create internal pressures, or feedback loops, that result in our semi-consciously reprogramming our brain. Anorexia might get triggered by a social paradigm, but (similar to what you wrote about with the women who can’t stop feeling like she’s suffocating), but then the biological feedback loop kicks in.
I think as we discover and learn more about learning algorithms, their preliminary use as an analogy-based scientific paradigm to humans is shockingly strong. There is some learning state of our brains that we don’t have explicit control over, but we can use our prefrontal cortex to influence the inputs into this hidden part of our brain, to change its state.
I recently broke my leg. Before this I worked out 5-10 hours a week. As my leg recovers I’ve lost the motivation to go to the gym. This state of my brain has reverted to a natural energy-saving steady state, which evolution tells it should be the baseline. I can only keep it in a state of constant physical activity with constant reinforcement: I work out-> I feel good -> I look good.
I, prefrontally, am well aware this hidden state has changed. Still, it is challenging to discipline myself to reteach it to do what I want it to do.
I’m sorry to hear about your leg, I hope it heals quickly.
Thanks! At least I did it Skiing in Alaska, so it wasn’t boring. After a couple months I’m starting to walk again, hopefully in time for my wedding.
If this was a humble brag, it’s a very well done one 😉 congrats on your upcoming nuptials!
Haha thanks 🙂 I wanted to put a positive spin on the downer vibe of injuring myself. Having a rod hammered into my shattered bone and the recovery ranks low on my ranking of life events.
On the plus side, after the fact, “having a rod hammered into my shattered bone” sounds really bad ass.
Tangential, mostly related to the previous post. Given the parallels between hyperstimulation of junk food and internet, can there be a parallel “switch to single-type bland food” — “switch to single-type long-form distractions”? I.e., treat procrastination by sticking to procrastinating with one series of verbose articles or one web serial at a time instead of a variety of lolcats and outrage fodder and clickbait?
Anecdotally, this does exactly the opposite. If I browse Reddit when I should be working, I’ll chew through the front page of links, then realize how far I’ve gotten and go back to work. If I discover a new web novel, I could lose half a day bingeing on the archives. Each link on Reddit is distinct, each chapter of a long work leads into the next one.
The way I manage procrastination is by raising the effort required to get to whatever I’m procrastinating with – install Siteblock and block Reddit, turn off my phone so I don’t have constant access to procrastination material in my pocket. Procrastination feels like following the path of least resistance – a minor issue in work stops my flow, and while I can resolve it easily, it still puts enough of a barrier in my way to make me not want to. And conversely, creating minor issues in my procrastination makes it easier to start working again.
How might the leptin set-point relate or correlate to insulin and/or blood sugar? Could something similar to what you describe in anorexics be going on in an insulin-dependent diabetic who consistently lets his blood sugar fall way to low.
I ask because my father was an insulin-dependent diabetic for 50 years, until he was 78. He seemed to intuit early on that high blood sugar was the cause of many of the long-term debilities of diabetics. So he had rigorous control, or at least that’s the way it would be described by his endocrinologists. But his ‘control’ was actually a dangerous lack of control at the low end of the blood sugar range. Reading this has me asking whether his control was partly a low set-point for blood sugar, or a high set point for leptin, which may work out to something similar. I’m intrigued by the idea of a cognitive element to the situation.
My dad would frequently have severe hypoglycemic episodes. He lost a job in his field in part because of ‘insulin reactions’. Then tried to become a teacher, somehow not realizing that losing consciousness when you’re the primary person watching a group of children might limit job prospects, and he was underemployed for the last decade of his working life. He crashed at least 3 cars. He had insulin reactions at family holiday gatherings and at my wedding. This was very difficult for my mom. He spent a lot of evenings going to political meetings and volunteering. Other wives might have worried that a husband frequently out of the house was having an affair. My mom was worried that he’d crash the car and kill himself or someone else. We’re not certain about his death – he fell, and it might have been a stroke, or it might have been hypoglycemia leading to him falling and hitting his head on concrete.
At any rate, I sometimes remarked that I felt his approach to his insulin was similar to that of an anorexic to food – that even when he knew he was sliding, when he demonstrably couldn’t focus, maybe reading a passage over and over, unable to take it in, when a couple bites of an apple or a slice of bread would have brought him back, he would often insist he was fine. Sometimes sluggishly raising his drooping head to say he was fine.
My aunt, a counselor, (I think that’s the professional term – ie, not a psychologist, but someone with a certificate who works with people on their emotional and psychological difficulties) felt that his resistance to eating was very different, that it was a more standard resistance to being nagged. I don’t know, but wonder whether she might have argued that it ultimately became pathological because of the long feedback loop of being nagged by my mother to eat more. (Not unlike the way dance coaches and their pressure are blamed for their anorexic charges.) Reading what you’ve written about the deep cognitive relationships has me wondering. Very interesting.
An interesting question is how the neurological and psychological/behavioral implications of set-point theory might extend if you substitute other key hormones, say, testosterone or estrogen, for leptin.
Please don’t reach reflexively for the mighty ban hammer. I fully realize anything relating to sex must be handled in an exceedingly careful, civil, and professional manner so as to avoid any potential for unwarranted inflammation of deeply-felt sentiments. However, I’m genuinely trying to make a serious point here, and so I’d respectfully request that everyone please be dignified and refrain from baselessly accusing me of trolling or derailing the conversation or something along those lines. It’s unfortunate that these days I have to interrupt my own comment to make the equivalent of a disclaimer, but here we are.
I stipulate that, epistemically, this is some very low-confidence speculation, but it doesn’t seem wildly implausible to me that set-point theory might have something to do with the autogynephile species of transgendered individuals. The observational pattern is that many of these rare individuals were once extremely masculine characters such as star athletes, military veterans, and so forth, or otherwise excelling in stereotypically male-dominated fields, and sometimes having multiple female mates and many children. Examples could include Jenner, McCloskey, Rothblatt, Pritzker, Ware, and perhaps the Wachowskis.
Again, this is mere speculation. But if hormonal-neurological set-point theory can be extended in this way, it doesn’t seem crazy to say that these individuals were born male and their brains were perhaps accustomed from an early age to what would be an extraordinarily high level of testosterone for a normal male. But, like all males, those high levels of testosterone began to diminish with age. A normal male can certainly feel the effects of a gradual and mild decline in himself, and the process of adjustment is probably easy and nearly imperceptible. But for these individuals it must have ‘felt’ to their brains as if their testosterone levels had really and suddenly fallen off a cliff. And perhaps this drop so far from baseline could generates an interpreted signal which could have been a contributing factor in the brain’s own analysis of what gendered behaviors and impulses it should be manifesting.
(Nitpick: “Autogynephile” doesn’t seem important for this hypothesis. If “not neurologically intersex” is important for the hypothesis, note that those aren’t the same thing; maybe there are an intersex and a non-intersex, psychologically-motivated group of trans women, but autogynephilia isn’t really the fundamental feature of the latter group [in fact I think this is probably true, but that’s not important here]. I don’t mention this because autogynephilia is bad to bring up, but because (a) there’s no need to add [politically touchy] burdensome detail to an interesting hypothesis (b) I often see, and don’t want to see more of, the equivocation that if being MTF trans isn’t an intersex condition then it must be autogynephilia / the entire Blanchard-Bailey model must be correct.)
I have no idea what it means to be neurologically intersex or not neurologically intersex, and it seems like trans lesbians also have a good case for neurological intersexuality. For instance, one could make the argument “straight trans women generally transition for psychological reasons, because they fit in better as straight women than as flamboyant gay men; trans lesbians have a localized intersex condition which causes gender dysphoria”, and it seems equally consistent with the data. (I don’t believe that argument; I think there are two separate causes of gender dysphoria.)
That’s a pretty good analogy, but here’s one issue: my impression is that anorexics tend to come from the skinnier classes of society, so anorexia seems like taking what your culture tells you to do too far.
In contrast, male to female transgenders don’t seem to come all that often from the ranks of society that particularly subscribe to pro-transgender ideology, so transgenderism seems more random and harder to explain.
As far as I can tell, male to female transgenders were almost never average or a little below average in masculinity as men. You virtually never hear of some gentle NPR announcer-type deciding to transition. You might expect that NPR-type institutions that favor transgenderism ideologically would have lots of middle-aged men deciding they were always women on the inside. But it doesn’t seem to work like that. Instead it tends to be the rightwing edge of high IQ professions: e.g., the Harvard football player turned libertarian economist.
Instead, it’s usually somebody who was either very effeminate as a boy or somebody who was above average in masculinity.
For example, in business school in 1981, I spent about 20 hours working on a small team with a man who is now sometimes listed as the highest paid woman CEO in America. Even by the standards of MBA students, this fellow was one of the two most arrogant students I knew at B-school, along with an Israeli fighter pilot.
And the B-school was likely one of the least liberal parts of UCLA.
There’s a lot of trouble trying to come to a better understanding of these things by noticing observable patterns. First, there is high causal density – a definite nature, nurture issue, with interactions and feedbacks too – and so there are a lot of important influences to tease apart. Second, we are dealing with a rare condition and small n, with the n that we have seeming to heterogeneous enough to make the task even harder. Third, lots of folks are very private about these things, and so we are limited only to very prominent examples, which is bound to skew our perceptions. And fourth, there is good reason to be skeptical of a lot of the information we get from self-reporting and surveys – not just on this matter but almost any culturally sensitive topic – because there is bound to be a lot of socially-conscious self-deception and memory auto-retconning so that the details fit in with the narrative one is supposed to support. Eye-witnesses often come to sincerely believe even wildly erroneous elements of their testimony, and act with genuine shock when you can prove to them that their memories are totally inconsistent with better evidence, e.g. video.
All that being said, one signal of a pattern that seems so striking and consistent that it seems to force itself to emerge from the noise is the set of these smart, highly accomplished men pursuing stereotypically male-dominated professions and, despite their later statements to the contrary, having early lives that give every sign of being ultra-masculine characters completely untroubled and even relishing their macho sexual personae, having lots of exclusively female sexual partners, showing off to females, having multiple children, and so forth.
And then they get old, their testosterone falls, probably by a lot compared to their youthful baseline, and something apparently quite dramatic happens, to the point where even their close friends (many of a class without much naivete on matters of sexuality), report being quite surprised at the revelation. These instances are self-reported as as typical ‘coming out of the closet’ experiences, but again, we are justified in taking any first-person stories about these matters with a grain of salt.
So, focusing in on this very narrow slice of the population, the question is whether neurological-hormonal set-point theory is consistent with the sudden shift in presentation and self-perception of gendered impulses and behaviors. My hunch – and again it’s only a guess – is that it is consistent.
One additional complicating or perception-skewing factor might be that smart, prestigious, ultra-masculine, high-achievers could tend to be much more comfortable bucking social conventions, making prominent displays of themselves, and accustomed to asserting dominance and being obeyed or submitted to. Think of a military command, or movie director, or star athlete (especially team captain), or authoritative professor. These people get quite used to having all their whims catered-to, and being able to easily make other people accept and parrot their ideas. Losing this suddenly, as when a top politician leaves office, or a top officer retires, is apparently psychologically excruciating.
That socially-dominant and ‘insistent’ (or ‘domineering’ / ‘bullying’) aspect of their long-ingrained personality seems to be much less sensitive to sex hormones, even to estrogen supplements, and to survive their transition.
Steve, is your sample mostly from the news? If so, you could be biased towards the most dramatic stories.
I know three MtF transgendered people. One was started out masculine but not dramatically so (occupation was and continued to be truck driver, but a gentle person and not ambitious), one was a cross-dresser (big beard with very feminine clothes, computer programmer, I think, no taste for physical danger that I know of), and one transitioned early enough that I didn’t know them as male but I think more weird in general than anything else– didn’t show an obvious taste for risk or status.
Okay, but where are the prominent individuals from not strongly masculine backgrounds? It’s hard to notice the dogs that aren’t barking, but when you stop and think about it, the disconnect between who believes in transgender theory and in who practices it is notable.
In contrast, with anorexia, most anorexics come from social milieus favorable to weight loss and take socially approved behavior too far. With late onset M to F transgenderism, however, the best known examples come from social milieus less favorable to transgenderism than the ones that don’t supply many prominent individuals.
This doesn’t mean that Handle’s set-point reaction analogy to anorexia is wrong.
Maybe we could polish up the analogy like this: Perhaps anorexic girls tend to develop a self-image of themselves as being as slender and low body-fat as they were at, say, 14, and find repulsive their natural womanly putting on of weight in later years? Similarly, perhaps late onset M to F trans people develop a self-image of themselves as being as masculine as they were at 22 or whenever and thus find their subsequent natural decline in masculinity over the decades to be alarming and profoundly unsettling, setting off a mental retconning of their pasts.
The latter is still more complicated than the former, but we may be approaching a model that makes both more understandable.
Trans lesbians are a lot less late-onset than they used to be. I am personally aware of dozens of trans lesbians (and gay trans men) who transitioned in college, some as early as high school, which is basically something you wouldn’t see at all in the eighties. I think that this points to a social explanation for trans lesbians being late-onset: heterosexual trans women are more likely to have a community with lots of other trans women, who provide possibility models for transition; with the rise of the Internet and trans politics, this difference no longer exists.
Also, anecdotally, trans lesbians tend to start feeling dysphoria in childhood or adolescence. (Even Anne Lawrence writes about how erotic crossdressing usually begins by puberty.)
I wouldn’t consider erotic crossdressing a symptom of dysphoria.
If I understand correctly, the theory is that MtF transexuals with male-oriented sexual preferences (“heterosexual transwomen”) have gender dysphoria, while MtF transexuals with female-oriented sexual preferences (“translesbians”) have autogynephilia.
The former usually tries to transition early, maybe because dysphoria is highly mentally taxing, the latter may not transition at all, partially transition (e.g. crossdress) or transition late (when it is more convenient), because autogynephilia is merely a fetish which doesn’t disrupt their psyche too much.
The mainstream Blanchardian belief is that both trans lesbians and heterosexual trans women have gender dysphoria. The etiology for heterosexual trans women goes “femininity in childhood –> difficulty adjusting –> gender dysphoria”, while the etiology for autogynephiles goes “autogynephilia –> gender dysphoria.” But no Blanchardian who’s had any experience with trans people at all denies the importance attached to transitioning and pain of not transitioning, for both types.
What is a Blanchardian? Google isn’t helping.
Blanchard is the guy who invented the theory you’re talking about.
Steve, I did miss that you were talking about late onset transexuals. The third person I mentioned transitioned fairly early.
The first two would count as late, I think, and I’ve thought of a fourth, also not hypermasculine and late.
I agree that anorexia is over-compliance with social norms, while becoming transgender is going in opposition.
” Perhaps anorexic girls tend to develop a self-image of themselves as being as slender and low body-fat as they were at, say, 14, and find repulsive their natural womanly putting on of weight in later years?”
Not so much from what I’ve read– or at least it hits much earlier. At least anorexic accounts include wanting to fight puberty off.
Late onset anorexia
“Major life events are usually the cause of these disorders. “The person can lose their job, suffer a bereavement, have a child or see their relationship break down. As a result, their mood deteriorates and they develop a depressive illness. They lose their appetite and then lose weight,” said Dahabra. “They then notice that they feel better when they don’t eat, that they look ‘better’ and might even get compliments, and this then distracts them from what really bothers them and gives them a new focus.””
It’s possible that being MtF transexual is so much more aggravation for someone famous that only the most aggressve/assertative people will go that route. If this theory is correct, then we’ll see people with more average male termperaments choosing to transition if that gets considered to be more normal.
Just another bit of anecdata; the two mtfs I know personally both come from the category that you say one almost never hears of.
Are we sure this is true? I just tried it and didn’t find it difficult. (It’s definitely possible I’m just different, but I’d be interested in seeing where the claim came from.)
In fact, I’m having trouble stopping now, as I’ve had fidget fidget fidget fidget in the back of my head for the last two hours.
I did the same, with the same result.
(I am somewhat fidgety in general, so I tried maintaining multiple fidgets — tapping fingers, jiggling leg, etc — and had no trouble keeping 3-6 separate fidgets going on at any given time for two hours.)
Relevant personal anecdata: I had a healthy relationship to food and a healthy, stable body weight until about a year ago when, over the course of a few months, I lost a *lot* of weight when I had to get intensive chemotherapy to treat cancer. That was followed by another few months in which it would have been nearly impossible to try to regain weight because of various health issues related to the recovery from chemo.
By now, though, my digestive system has long since returned to normal, and yet I’ve been struggling to regain the weight I lost. It has surprised me quite a bit since I had read about metabolic set points in the past and assumed that, after sufficient recovery along other dimensions, my set point would kick back in and I would have an increased appetite for a while until re-approaching my set point. Instead, my appetite has been stubbornly uncooperative: I feel full after consuming a frustratingly small number of calories at each meal and have had to resort to more creative methods (e.g. marijuana to stimulate appetite) to slowly regain weight.
So when I read the line in your post about many Phase II anorexics also struggling with lack of appetite and feeling full, my eyes lit up, because I hadn’t been aware of another group that systematically experiences the same combination of low body weight and low hunger! And as I continued reading, my eyes lit up again, because a couple months ago I had started to independently posit essentially the same theory for myself as you propose for these anorexics: That the metabolic set point may shift after a sustained period of being forced away from its previous position.
And so that immediately led me to the further thought that there are probably a bunch of groups that could enable someone to test the weight-loss (as opposed to gain) version of this shifting-set-point hypothesis, independent of the anorexic population*: just study the experience of any group without eating disorders that is forced, for some external reason, to have a lower body weight for some extended period of time.
* which, you’ve convinced me, should also be further investigated but will nevertheless remain fraught, because people tend to have strong pre-existing theories and feelings about the causes of eating disorders
As an aside, I’d be interested to know if low cortisol might mediate these slow-recovery effects.
I gather people who have trouble making enough cortisol — whether due to Addison’s or some less dramatic problem with the adrenal glands — can experience loss of appetite (and nausea). And likewise, increases in cortisol can increase appetite.
I wonder if a big physical stressor (like chronic fasting with anorexia nervosa or multiple rounds of chemotherapy treatment) can lower cortisol production which then may suppress appetite for some months until the adrenal glands recover.
Well, I am anorexic. I’ve always been thin (female, height 157 cm, past weight around 45-47 kg), then I married, gave birth to a boy, and my weight became 42 kg. I couldn’t keep in touch with my previous circle of friends, ate horrible bland food for almost two years of breast-feeding and eventually just gave up on all of it. + I did think that gaining weight, the way women often do, will make me “one of them”, who cannot & would not want to return to their professional life and former interests, so I decided I would not at least gain weight. Now I weigh 40 kg, feel neither good nor bad, and shrug off my endocrinologist who says that 1) I cannot, with this weight, have regular menses (I do), & 2) that women of my weight are unable to beget children (I did explain that I was heavier). I would like to return to my 47 kg, though, to get people off my back and maybe have a stronger immune system (?, I don’t get ill more frequent than before or compared to my more well-rounded colleagues).
And now my husband’s dieting, and I don’t have time to cook separately some food, maybe spicy or something, that would inspire any interest in me (beyond the thought: “gotta eat”).
Edit to add: I simply don’t feel like I should eat more. I have to think about it, plan it, whatever.
So… meh. There’s cultural anorexia, and then there’s less cultural.
Weren’t you worried that you’d undereat while pregnant and mess up your child?
Not here to judge or change anyone’s mind. Someone close to me is also anorexic and this is something I worry about for her.
But I didn’t undereat when I was pregnant, I think. I gained 10 kg during pregnancy, and was told it was normal.
A brief google search says underweight women should gain between 28 and 40 lbs during pregnancy.
You claim to have gained 22 lbs. Even with an extended range, this is still on the low end. Additionally, as someone who doesn’t know you personally, my guess is that there is a reasonable chance you are underreporting the weight gain. Although you have more self-information than I do, so please don’t take my guess personally.
Regardless, this is actually a red herring. Even if you gain the expected amount of weight, you’re still pregnant and underweight. How do you know that all 22lbs went to the pregnancy? What if 5-10 lbs went into your own tissue?
You can ask this same question of a person at any body weight, but it is much more likely for a “starved” person to misallocate weight than a normal-weight person.
There are also epigentic concerns. I am very far from an expert but I’m sure I’ve read research somewhere that obese parents may contribute to their childrens’ obesity via their obesity “priming” the fetus for a food-scarce environment.
It also feels like there should be a pretty strong precautionary principle when raising children. There’s no benefit to being very underweight while pregnant, and at least a small chance of significant harm.
I’m not sure I understand what you mean by a red herring. When a woman gives birth, there is the weight of the baby and the weight of the mother. My own was low, the baby’s was ok, so I wasn’t worried on his behalf. On my own, I knew I had to eat, eat, and eat, and I ate what I could (and yes, it felt mostly awful, but there still wasn’t much I could do about it; it’s just life). There was simply nothing else to it.
As to priming him for obesity, I guess it’s possible, but not probable. Everybody on my side is thin, everybody on his father’s side is portly, & beyond that, I know nothing for certain. He is too thin for his age, but he’s also on a diet for having inherited my gallbladder.
What precautionary principle do you mean?
Incidentally, at some point after breast-feeding I took my tea without sugar for a month or two, in a misguided attempt to not bother the person who brought it. Lost a kilogram. Started taking it again and gained it back. So sugar is, for me, a strong source of calories.
Your weight is far more stable than mine if you can meaningfully detect a difference of a kilogram. Mine bounces around more than that constantly:
Also, it just doesn’t make sense to me that a 48-calorie tablespoon of sugar could add up to anything significant. I think you were worried about it and looked for evidence it was making a difference.
I am something of a tea addict, when I am within reach of a kettle, so it was several cups a day. Maybe it was the change in taste, though. But yes, my weight is rather stable.
Where do hunger pangs come in, under this approach? Sometimes, even in the absence of appetite, hunger pain can be a difficult sensation to ignore even for a person who is very set on dieting. What happens when a person’s leptin levels and their hunger sensation are mismatched, how does that person ultimately behave?
One consequence of SA’s crazy speculation from someone who isn’t an expert in the field is that it suggests that junk food and eating at food courts may be particularly effective at helping anorexics overcome unwillingness to eat.
One thought occurred to me: I wonder if it makes more sense to hypothesize a similar but reverse mechanism of action with *ghrelin* as the factor in AN, compared to *leptin* and obesity?
If obesity comes about due to a breakdown in the lipostat leading to central leptin insufficiency (leptin somehow getting intercepted in the hypothalamus), perhaps AN works through a parallel interference with ghrelin?
Also, while I’m tossing in stray thoughts, I might as well contribute another:
I wonder if anyone has looked at the possible contribution of food and drink *temperature* to hyperpalatibility (this kind of goes more to the point of the previous post, but it might work here in reverse)?
It has sometimes struck me with the ubiquity of microwave ovens and the like how seldom people are stuck with eating cold food or drink. You can even walk your partially-drunk mug of coffee back over the microwave for a rezap multiple times so you need never consume any of it cold.
My back of the envelope estimate tells me this probably would contribute at most about 5 or 10 calorie equivalents a day to one’s food intake compared to a person who didn’t find it equally easy and convenient to heat up food and therefore ate more cold foods and drinks, but on the other hand, if it’s a difference the system is not well-calibrated to account for, those could be an extra 5 or 10 calories that are flying under the lipostat’s radar.
I’ll throw in one more wild idea: I heard about the set point notion years ago, long before I had ever heard about leptin or ghrelin, and I recall hearing that raising the set point happens after spending a certain amount of time at or above a given weight, like three months or six months, but lowering the set point back down took three or four times as long. This was folklore, basically, but I’ve heard it repeated over the years.
I have no idea if it’s true, (well, I suspect it’s not true, in any exact sense, as it’s way too simple) but I had long since absorbed a background assumption that there’s a big asymmetry in toying with the mechanisms that make you less satiated (easy) vs. less hungry (hard). This is part of what makes me suggest maybe it involves the two different hormones.
Posted about this to Scott on twitter, although obviously longer form here.
Contrave, which is welbutrin+naltrexone is an effective weight loss drug.
I’ve been on it for a few months, sort of (I was on the welbutrin before, added the naltrexone). It (the naltrexone; welbutrin on its own had no effect on eating) has, for me, destroyed the enjoyment of most foods and much of my appetite.
One of the effects is that it makes things not taste as good past a certain amount, which I know is the way humans are supposed to work, but is not the way I worked before the drug. The other is that certain flavors (salt, fat, sweet) can be easily overpowering to the point of being distasteful. It’s been a fascinating way to finally lose some weight.
Anyway, I was wondering if Scott had run into this (ok, he’s a psychiatrist, he knows people on welbutrin and people on naltrexone, but heroin and alcohol addicts don’t tend to be that fat)
I’ve occasionally lost the ability to enjoy cheese– it will just taste like fat and salt. This is rare and brief, but I have no idea what’s going on with it– no correlation with anything obvious and no theories about the mechanism.
What still seems strange to me (though I understand it’s not fully understood):
It would seem like something like being on “The Biggest Loser,” where they force you to focus intensely on this goal of weight loss and strongly associate “weight lost=good” in your mind, and where you do, in fact, drop a lot of weight in a short time, would be just as good as having a mean ballet coach for lowering your set point, if, indeed, something like that can lower your set point. But these contestants notoriously cannot keep the weight off.
Also, it seems like periods of deprivation resulting in a reduced set point is the opposite of what evolution would lead one to expect: one would expect a body which goes through periods of serious deprivation would interpret that as “clearly we weren’t fat enough–raise the set point!” And, in fact, some claim that repeated crash dieting can slow your metabolism and make later diets even harder (though I don’t know if that’s actually true). What then, is the deciding factor between: excessive weight loss–>lowered set point and difficulty maintaining a healthy weight vs. excessive weight loss–>decreased metabolism, food obsessions, etc. to get you back to the set point?
Is it just that, in people predisposed to develop anorexia due to genetic or childhood trauma factors, the addition of a period of chronic undereating will result in a depressed set point, but in others, the set point will just keep defending a certain weight? Or?
I wonder if this is where psychological factors play an important role?
In the literature, anorexia nervosa seems often to be associated with perfectionism. And in instances where it may be a behavioral response to trauma, I gather it’s often about control.
Though obesity may in some instances have its own control dynamic but in the direction of keeping weight on rather than off. The research that led to the ACE studies (adverse childhood experiences) came about because of Felitti and Anda’s work at an obesity clinic for Kaiser. They discovered IIRC that the people who put the weight right back on had more significant trauma histories. This has been written about elsewhere too I think, that for some people, obesity is another kind of behavioral response to trauma that also involves control.
I don’t know that we understand yet how genetic, physiological, social, and psychological factors combine to drive anorexia or obesity. It may be that we all have some of these factors at play but that they cancel each other out to some degree, whereas with people at either extreme perhaps they’ve got multiple reinforcing variables working in the same direction.
Had a thought, which seems overly simplistic, but, which, upon further reflection, rings true to me:
What if it’s about the difference between wanting to gain something you don’t currently have (a positive self-image dependent on being thin) and being afraid of losing something you do currently have (a positive self-image dependent on being thin).
The anorexics in the story Scott mentions (and I have known at least one person who told a similar story: she was always very thin as a little girl and people always complemented her on this; it made her feel special and she was afraid of losing that thing that made her special ever since). Big generalization, but I think people tend to fear losing what they already have more strongly than they crave something they don’t have–especially if they’ve never had it.
If we generalize to say that people who are chronically overweight are likely to have a negative-ish self image dependent on being overweight, then actually improvements in self image relative to baseline are somewhat low-hanging fruit. Conversely, if we generalize that anorexics of the “everyone complemented me on how thin I was when I was a kid” variety have a positive-ish self image, but one that is dependent on a continued self-perception as “thin,” then those people might, paradoxically, be in a more precarious position in terms of maintenance of some baseline level of self-regard, especially if we assume there is some “hedonic treadmill” aspect to self esteem, as seems likely to me (that it, regardless of what you look like, you’re going to tend to revert somewhat to a baseline of thinking you look “ok” unless you’re looking better or worse than usual).
I don’t know how typical my past experiences with disordered eating are, but:
* I was very hungry almost all of the time. Very small amounts of food could provide a feeling of satiety, but the duration was much shorter than an actually filling meal would provide for a typical person.
* I experienced the starvation study food obsession: I dreamed about food very frequently and spent a lot of time researching recipes and talking about food online.
* I could (and can) gain or maintain weight on fewer calories than most calculators would predict, which probably has to do with loss of muscle mass. I still have a lot less muscle than typical for my weight and height (confirmed via DXA scan).
* I’m sure I fidgeted a lot due to overconsumption of caffeine. Coffee and caffeine pills got me through the day.
The flip side of this is weight loss after bariatric surgery. Apparently the surgeons know ahead of time what weight you will stabilize at.