Fiber: the Mr. Rogers of nutrition

I have consciously decided to let the arguments for high protein diets pass me by, despite how convincing some of the research and underlying mechanistic claims sound.  Humans have been cycling through high -protien, -fat, and -carb diets since we developed enough of a surplus to choose, and I’m pretty sure if any of them were that superior to the others it wouldn’t have been supplanted.  I would say “everything in moderation”, but that is just a zen way of saying “Eat the correct amount.  Idiot.” which I don’t think is very helpful.

HAES brings up a more constructive suggestion: eat fiber.  Fiber* is usually left out of the macronutrient triumvirate, but so is water, and water is extremely useful.  Off the top of my head: Fiber has the advantage of being natural**, because our ancestral foods had much more fiber than our current ones, yet its lack of calories is well suited to our current, couch-based, lifestyle.  It evens out digestion of other nutrients, reducing the destructive sugar/insulin boom and bust cycle.  It simultaneously treats diarrhea and constipation (if you drink enough water, which you should anyway).  Have you ever wished you could eat a good thing and have it cancel out a bad thing?

mitch-hedberg-onion-ring

Well, that might actually be true if the good thing is fiber, and the bad thing is not cocaine.

Here is where I meant to track down all the good things HAES says about fiber, but when I read it more carefully.  I realized most of what it was praising was fruit, with the implication that fiber was the reason fruit is beneficial.  The one actual fiber claim is that high-glyemic diets increase the risk of type 2 diabetes unless the diet is also high in fiber (five sources, all of which say nice things about fiber, one of which is actually about type 2 diabetes.  The paper did conclude that fiber fights type 2 diabetes, but it was a post-hoc survey, which is a weak methodology).  However, those other four sources also say pretty good things about fiber, just not the one the book claims they did.  I think we are all on board with “fruit and whole grains” > “potato chips and soda”, although I’m severely disappointed that this of all books is backing that up with data on weight loss, rather than actual health outcomes.

But Dr. Wikipedia has many very specific nice things to say about fiber, and it cites much more relevant sources.  Fiber increases micronutrient absorption (a little).  Fiber increases nutrient absorption (more).  Fiber fights inflammation.  Basically, it does everything good and nothing bad.  So while HAES didn’t lay out its case properly, fiber is definitely good, and I look forward to finding out who takes this too far and what the negative effects are.

*Definition of fiber varies a little from institution to institution, so for clarity: I am defining fiber as carbohydrates that are not broken down for energy in the human body.  It’s worth noting that there are two contributors to whether an organism can digest food: its own enzymes, and the bacteria in its digestive track.  Termites can’t naturally digest wood, but they house a bacteria that can.

**It’s easy to oversell “naturalness”, but when you have a mission critical system made of complex legacy code no one understands, sticking close to its original environment is a good default strategy.

Bariatric Surgery

I had a pretty poor opinion of weight loss surgery already, but Health At Every Size all but says any doctor recommending it should lose their license for malpractice.  That claim seems worth investigating.  Luckily, she cites her sources.

First, I feel it’s important to note that bariatric is medical Greek for “obesity related medicine.”  I’m already not thrilled with that because I think excess fat is a symptom of health problems, but rarely a health problem in and of itself.  “Bariatric surgery” is often sold as something that is fixing a problem, the way an appendectomy fixes appendicitis, but it is at best undoing the damage of something else that is making you fat.

That said, let’s start with the immediate death rate.  HAES quotes a study as reporting a 4.6% death rate within the year: what it doesn’t say is that that study was done on Medicare recipients, meaning they were older than 65 or disabled.    Moreover, the 4.6% number is based on death from any cause, not what would be expected above and beyond what is normal for patients’ age and health.  Controlling for age, sex, and likelihood they would have died anyway* the researchers found that surgery increased your risk of death in the 90 days after surgery by somewhere between 90% and 200% (=3 times as likely to die), depending on which demographic you were in.  Inexperienced surgeons make this worse (which they do not back out of their model).  This is not just the stress of surgery: that’s twice the death rate following coronary revascularization or hip replacement, neither of which are minor.

HAES cites another study, published in JAMA as reporting a 6.4% four-year death rate.  This study has a number of problems.  Its only control was matched for age- and sex- but not health status.  A lot of the deaths stem from heart disease, which could plausibly be caused by being fat or having been fat, which is not a case against weight loss surgery.  Worse, that was the death rate only among people considered “at risk” enough to justify four years of follow ups.  The article doesn’t explain what qualified someone as “at risk”, but rarely does that risk mean “at risk of living too long”.  HAES cites a blogger who cites the study as demonstrating a 250%-360% increase in mortality over four years, relative to age- and BMI- matched controls, but I don’t see that anywhere in the original paper.

Meanwhile, the American Society for Metabolic and Bariatric Surgery aka “the people doing the surgeries” is happy to report a mere 0.2%-0.5% mortality rate after the first month of gastric bypass surgery.

That’s everything the book cites on mortality, which I found unsatisfying, so I turned to Dr. Google.  This Swedish study actually bothered to match controls (although surgery was not assigned at random, introducing the possibility that the surgical patients varied on a factor they didn’t think of) and found a 30% reduction in death over 10 years.

But I hate it when people act like death is the only bad thing that could ever happen to you.  What about people who don’t die, but do suffer for the surgery?  HAES cites six studies showing long term nutritional deficiency.  Of the five I was able to find online, all showed serious deficencies and none had a control.  Interestingly they all found a vitamin D deficiency, when vitamin D is primarily produced by your skin in response to sunlight, unless you live in Seattle, in which case you mostly get it through supplements.  Either way, food is not a major source of it, and if bariatric surgery effects vitamin D levels (which these studies have not demonstrated) I am extremely curious as to why.  Given the current controversy as to the efficacy of vitamins even in people with normal stomachs, it’s not clear how much this issue could be fixed with supplementation.

Every study I’ve read agrees that people lose substantial weight after surgery and then gain some of it back, I’m not even bothering looking for citations for this.

CONCLUSION: bariatric surgery has severe risks.  These may be partially compensated for by a skilled surgeon and good nutritional technique.  For extremely obese patients the benefits may outweigh the risks.  We don’t know where the cut off is for “fat enough to benefit.”  The strongest piece of evidence against bariatric surgery is that no one has done the fairly obvious studies that would conclusively demonstrate their effectiveness.

Some of the benefits probably stem from societal approval rather than genuine health issues, and the long term fix for that is for society to stop shaming people for their weight.  Another part of the benefit may be a forcing function, i.e. if patients ate like they’d had the surgery they’d lose weight whether or not they actually had it.  For an individual living in the society they live in and who has already tried dietary changes, this is sad but irrelevant to the decision.

I’m really uncomfortable with this conclusion.  It doesn’t fit my prior model, and I prefer the tribal affiliation of strong weight loss surgery opponents to strong weight loss surgery advocates.  I consider the evidence I’m basing this on somewhat iffy,  but in all honesty if it had come out the way I expected I would be fine with it.  I’m also pretty disappointed in HAES for so blatantly misrepresenting the evidence.

*Risk of death was calculated using the  Charlson Comorbidity Index.   I have no idea if that is a good model, but it appears to be standard.  This doesn’t prevent the researchers from being wrong but it does mean they’re probably not being deliberately manipulative.

Poverty, Medicine, and Research

John: http://gap.hks.harvard.edu/women%E2%80%99s-empowerment-action-evidence-randomized-control-trial-africa
[Women’s Empowerment in Action: Evidence from a Randomized Control Trial in Africa]
Me: That’s awesome. Wait, why are they jumping between percentage points and absolute percentages? And they don’t give the absolute numbers at all.*
John: http://www.ucl.ac.uk/~uctpimr/research/ELA.pdf
Me: Sweet. Wait, so they plopped some afterschool clubs down and then measured outcomes for girls that attended them? That’s a hell of a confound.**
Paper: Nope, this is an RCT, and we compared both attendees and non-attendees (will overestimate impact due to confounds, but miss any spillover affects on non-attendees) and treatment communities with control communities (will underestimate impact because only 20% of girls attended the club, will catch spillover effects).
Me: But mobility is high, what if girls leave the area?
Paper: we track them. Plus attendees, members of treatment communities, and members of control communities had similar attrition rates.
Me: I’m still distraught you’re only giving rates of change, not absolute numbers.
Paper: Jesus Christ, not everyone loves numbers as much as you. The numbers are in the appendix.
Me: This looks like you made it worse.
Paper: Maybe it would help if you read the part that explains how to read the numbers.
Me: Your sexual health knowledge test includes questions like “A woman cannot catch HIV while on her period. T/F”. That’s the opposite of true.
Paper: You see why we’re concerned.
Me: HA! You said you calculated based on living in a treatment area, not participation, but table 2 is contingent on participation.
Paper: Table 2 describes duration and intensity of club attendance.
Me: Fine. Your study was perfect and its results are amazing. But you said Africa and the study takes place entirely in Uganda and treating Africa as a uniform mass is racist.  Why don’t you just talk about your tiger prevention efficacy?

africa

The paper graciously conceded my last point, but it knew my heart wasn’t in it. There is no end to the number of follow up studies one can suggest, but this is as good as a single study can be, and I accepted their conclusions. Founding afterschool clubs for girls in Uganda, with a mix of social activities and vocational, and health education, has pretty amazing results. $17.90 US (I know the exact number because the paper specifies it, which I love) spent on a girl translates to an additional $1.70 in monthly spending, almost a 50% increase (they tracked spending rather than earnings because self-employment earnings tend to be feast or famine. Employment also went up significantly), and a decrease in rape and child bearing. That means the program pays for itself in less than a year, and they get some additional benefits on the side. And to the researchers’ credit, the abstract trumpeted the less impressive community-wide numbers, when they could just as easily have used the confounded but shiny attendee numbers.

I mention this for two reasons. One: someone found a way to improve the bodily autonomy and earnings of African young women, basically for free. That’s neat. Two, I read this paper the morning after spending hours on a HAES post (which you may or may not ever read because wordpress ate it, thank you very much. WordPress ate this one halfway through too, so what you read is a cliff’s notes version of my original Socratic dialogue). The HAES post was enormously frustrating, because of the two claims I investigated, I found one (that cyclic dieting, rather than current weight, increases blood pressure) to be pretty misprepresentative of the data, and the other (high blood pressure hurts thin people more than fat people) pretty well supported…for a medical claim. By which I meant the evidence came from either retrospective studies (too many confounds to contemplate) or rats specifically bred to have the physical fitness of an aging Tony Soprano. That is genuinely good for medical research, and that fact is really frightening given how much is riding on getting the correct answer.

So when I read this paper, and see the study is well designed, they explain their modeling in a way an educated non-expert can understand, and they refuted every one of my criticisms, I felt a kind of relief. I’m not quite ready to say “trust the experts”, but at least I didn’t spend two hours tracking down reasons to not trust them

*If something goes from 10% to 20%, that’s an increase of 100% but only 10 percentage points. Switching between the two and failing to give the absolute percentages is a common trick for making data look more impressive than it is.

**Confounding variable, i.e. something that varies between your control and treatment group that is not the thing you are studying, and affects outcomes. The most popular confounding variable is time, e.g.

Pirate_Global_Warming_Graph
But here I’m worried about motivation: girls who show up to a club to learn entrepreneurial and life skills are probably more likely to start businesses and delay marriage than those that don’t attend,

Leptin: Catching Chemicals

Leptn is often considered the anti-ghrelin.    It is produced by fat cells to say “I exist and am full, you do not need to feed me.”  Animals with their leptin gene knocked out grow enormously fat.  This is a perfectly lovely story that can be conclusively proven by a picture of a fat rat.

Figure2diabetes
Bring me Solo and the wookie

If you do not find this story compelling, please consider that I also have a photo of a fat mouse.

Well, if it isn't Lone Star. And his sidekick, Puke
Well, if it isn’t Lone Star. And his sidekick, Puke

Are you convinced yet?  Look, I know last week I said all hormones are almost fractally complicated and anyone who says they completely understand one is lying, but that entry forever to write (thanks for publishing that a week early, wordpress), and this entry has pictures of obese rodents.  Surely you believe the rodents?

Original source: http://commons.wikimedia.org/wiki/File:Big_Fat_Red_Cat.jpg
If no, would a cat be sufficient?

*sigh* I’ve created a monster.

Like ghrelin, leptin is important to fetal lung development because, and I quote, “I don’t know stop asking me.”  Leptin is also produced by the ovaries, skeletal muscle, stomach (some cells produce both ghrelin and leptin), mammary epithelial cells, bone marrow, pituitary, liver, and of course adipose tissue.

Leptin stimulates ovulation and sperm production, which makes some evolutionary sense: getting pregnant when you don’t have the resources to carry it to term in a healthy way is extremely costly (men have to be nearly dying before they stop producing sperm entirely, but levels can drop incompletely before then).  This doesn’t explain why the ovaries (but not testicles) produce leptin, since they don’t have any independent information about fat stores.  This may be an example of an override (in which the ovaries decide they want a baby even though the rest of the body doesn’t believe it has enough fat), but the fact that I can come up with a clever anthropomorphization does not make an explanation legitimate.  You can sort of see why leptin facilitates the onset of puberty, since puberty takes a lot of energy.

What you can’t see is why, despite everything we know about pregnancy and eating, the placenta produces leptin. Excess amounts appear to cause hyperemesis gravidarum (extreme morning sickness aka Kate Middleton’s one weakness).

katemiddleton

High amounts of leptin appear to be good for your brain.  Just so story: brains are extraordinarily expensive, so if you don’t have sufficient savings your body turns on the dimmer switch.  They also have a long term protective effect against Alzheimers.  On the other hand, high levels of leptin alter the immune system in a way that encourages artery hardening.  I am way more afraid of living with Alzheimers than I am of dying of a heart attack, so I will count this as one point for fat.

Leptin’s overall effect on the immune system is complicated.  Leptin is an inflammatory agent, possibly to prevent damage from overreating as your body suddenly tries to shove extra calories that won’t fit in the white adipose tissue under the bed and in the coat closet (the organs).  Which may explain why ghrelin is an anti-inflammatory.  Leptin and ghrelin chose opposite powers and color schemes, like an early 90s superhero cartoon.

Or an early 90s cartoon
The safe represents the hypothalamus

Fatness in humans does not appear to be a problem of inadequate leptin production, and more leptin does not make people thinner.  Instead, it appears that the brains of obese individuals are less sensitive to leptin.  No one knows exactly why, but “crash dieting” is high on the list of suspects.  Two people with identical body compositions but different genes or life history may produce very different amounts of leptin, which means they may require very different behavior to stay the same weight, in ways we do not understand at all.  Which I could have told you before we went on this magical photographic tour of my childhood.  But now we know for sure, plus I learned that fetal lung development is creepily intertwined with food in a way no other organ is.  Let us go forth and use this new knowledge

The Rescue Rangers also want me to play video games.
The Rescue Rangers also want me to play video games.

Now I’m learning about hypothalamusing

Lots of people, including HAES subscribers, believe human beings have a set point or range where their weight will always be.  It takes great effort to get your weight above or below your set point, although repeated attempts can probably raise it.  If there is a set point, one likely candidate for its controller is the hypothalamus.  It comes up enough that it seems worth my time to find out what the hypothalamus is.

The hypothalamus is part of the brain.*  It translates the electrical impulses in your brain into signals to endocrine glands to produce and release hormones, which signal the rest of your organs to do their thing.  In this way, the brain is like general.  It dictates orders to its secretary, the hypothalamus.  The secretary than copies all the orders and sends them to the relevant lieutenant generals (glands), who respond by releasing the appropriate hormones.  For example, it coordinates the ebb and flow of melatonin (produced by the pineal gland) and cortisol (produced primarily by the adrenal glands), so that you can wake up in the morning and fall asleep at night.  It also translates from hormones to the brain, turning “I’m hungry” into cooking, or “I’m horny” into hitting on someone.

What does this have to do with food and weight?  If I had a definitive answer to that I would be rich (and better nourished).  Damaging specific parts of the hypothalamus while keeping environment constant causes weight change in rats that previously maintained a stable weight.  Damaging other parts causes the rat’s weight to be more affected by an environment (i.e. before damage they previously maintained a particular weight regardless of what food was offered.  After damage they lost weight when food was unpalatable and gained weight when it was more palatable).  And we’ve tracked several hormones that communicate status between the hypothalamus, adipose tissue, and digestive organs, in ways too complicated to fit into this overview post.

In summary, the hypothalamus is the connection point between the brain and your hormones, and no one really knows what either one is saying.

*One thing that always bugs me when I hear the phrase “part of the brain” is  “how sharp is the distinction between this part and other parts?  Can there be cells where it’s a matter of judgement which section they fall into?  Can you just look at an arbitrary brain and say “there, that’s the hypothalamus”?”  I eventually found this video, which very explicitly detailed how each part of the brain is separated, except for the hypothalamus, which he just sort of gestured around.  As we’ll read later, scientists are able to precisely destroy sub sections of of the hypothalamus so I guess its boundaries are pretty sharp.

Ghrelin: The Hunger and Lung Development Games

Writing about hormones is hard because anything I say will be incomplete by necessity.  I can only do so much research,  and will undoubtedly miss something.  More worryingly, there’s a lot nobody knows about our endocrine system, and all available overviews tend to overstate our level of certainty.  I will be ecstatic if in 10 years this entry turns out to be 60% true.  But we go to war with the facts we have, so:

Ghrelin is best known as… well if you’re me it’s “proof calories in/calories out is bullshit“, but it’s more commonly known as “the hunger hormone”.  The simple story is that cells in your stomach produce ghrelin in response to perceived space in the stomach (which may be one way gastic bypass surgery leads to decrease in food consumption: your stomach reports fullness almost immediately).  Your hypothalamus detects this and informs the brain, which interprets it as hunger, which should lead you to get food.

But nothing in the human body does just one thing.  For one, ghrelin is produced in other areas of the body.  Pancreas, intestines (sure, they have information about current digestion status), placenta (okay, the fetus needs a way to direct you to eat more), gonads, adrenal cortex, pituitary gland (well those are pretty general hormone production factories), kidneys (for…water…consumption?), and lungs (the hell)?

Ghrelin encourages storage of calories as fat, which could mean that eating more (to suppress ghrelin production)  would help you avoid fat gain or even allow fat loss.  But (one form of) ghrelin also triggers production of human growth hormone (in fact, that’s where the name comes from: Growth Hormone RELease INducing factor), which encourages burning fat and building muscle.  The important lesson here is that if someone every tells you “Do X lose weight because hormone Y does Z”, you should laugh at them, even if Y and Z are correct, because Y does 4 million other things, some of which are the opposite of Z.  Ghrelin’s presence in the lungs might be a mechanism to trigger HGH to trigger fetal lung development.  Or maybe not.  We don’t know.

Still in the realm of possibility, high ghrelin levels delay puberty and discourages ovulation.   This is a reasonable second job for the hunger hormone to have because transforming a zygote into a baby is an epic amount of work and you want to be well fed.   I seriously wonder about the effects on ghrelin on libido: given that humans have sex for both reproduction and social bonding,** I could see the effect going either way.

Ghrelin appears to have some mood effects.  When I first read this I assumed high ghrelin -> stress and depression, which would be a convenient way of explaining why I was so jumpy before my hypochlorhydria was treated.  Turns out, nope, ghrelin is an anti-depressant* , which may be one mechanism reinforcing anorexia.  But ghrelin also makes pleasant activities (eating, but also drugs, and it’s at least in the same brain neighborhood as sex) more rewarding.  It also has a bunch of effects on learning and memory and stress-based learning, mostly apparently positive.  This is the opposite of what I would have predicted, given how I and people I know act when hungry.

I'm sorry for what I said when I was hungry

Lastly, ghrelin inhibits inflammation. To the point it may be useful as a treatment for autoimmune diseases like rheumatoid arthritis and multiple sclerosis.   This concerns and confuses me, possibly even more than growth hormone effects. Hunger and long term calorie deficits are associated with increased susceptibility to disease (as your body prioritizes short term goals over long term health), so maybe this is a happy accident?  But no, ghrelin promotes development of at least one kind of white blood cell.  The anti-inflammatory effect may explain why people often don’t want to eat while injured- your body lowers ghrelin levels to allow healing to occur, and the loss of appetite is a side effect.  But that’s highly speculative, the truth is we just don’t know.

For all that, ghrelin is one of the simplest hormones I’ve studied.  It has one obvious primary job, and several of its lessen effects seem at least related to that job.  We know where it is produced and a good chunk of how it achieves its (known) effects.  More fundamental hormones like progesterone, testosterone, or oxytocin are infinitely more complicated.  So this post is a little bit about the science of hunger, and a lot about how the human body is complicated and people with simple answers are liars.

*Should you be laughing at me right now?  Maybe.  The study in question shows actual behavior change, not a potential mechanism of behavior change (that’s this paper), but it is just one study.  Perhaps compromise on chuckling.

**What about pleasure, you ask?  Irrelevant from an evolutionary standpoint.  We feel pleasure because there is some actual useful purpose served.

Damnit

1.5 years ago I did a food sensitivity test, and it came back “yes”.  I gave up wheat, eggs, and milk.  After 4 weeks my chronic heartburn was gone and I generally felt better.  Not better enough to stick with it indefinitely- at the beginning of 2014 I fell off the wagon due to a combination of stress and changes in my access to food.  The problem with sensitivities is that it’s a very delayed feedback mechanism.  One bite of foods I am sensitive too doesn’t bother me at all, in the moment or later.  Conversely, giving up all those (delicious) foods doesn’t immediately make me feel better.

After many false starts, I re-gave up all the sensitivity inducing foods in August, and was pretty irked when my heartburn continued for weeks.  But like last year, I suddenly noticed that only do I not have heart burn, but I haven’t for weeks.  I forgot that it was a thing I had.  And sometime in the last three weeks my skin became flawless.

No, one subject-aware case study does not prove a thing.  But when you consider how much the subject wanted the opposite result because that was where the ice cream was, it becomes deserving of further study.

HAES pre-check

I’ve been meaning to do a “science of fat and health and food” series for a while now, but have never quite gotten it together. There’s too much stuff I remember reading in some blog years ago but can no longer find.  The library has finally delivered Health at Every Size to me (just in time for Thanksgiving), and I’m hoping to use that as both a serious source and a jumping off point for other research I want to do.  In the spirit of inquiry, here are my basic beliefs, as cobbled together from an undergrad biology degree, personal experience, things people said on the internet, and scientific studies I read the abstracts of.  When possible I’ve included a citation but mostly this is just stuff from my brain.

  1. Some diets are lead to a better functioning body than others.
    1. The healthiest diets supply all necessary trace nutrients, including ones we haven’t identified as necessary yet.
    2. Protein, fat (of multiple kinds) and carbohydrates are all necessary for proper functioning.  Right now a lot of people are pretty sure that you should minimize carbs and especially sugars, but 20 years ago they were equally sure fat was evil, so I’m unconvinced even though their numbers look very shiny.
  2. Exercise is super good for you right up until the point it is super damaging.
  3. Despite our astonishing lack of genetic diversity, humans have a pretty wide range of how they react to identical food and exercise inputs.  Additionally, the same person can react differently to things over time.
    1. For example, people’s beliefs about the deliciousness of the milkshake they are about to receive affects ghrelin production, which definitely affects satiety and probably affects nutrient and calorie absorption.
    2. Medication can do the same.  Cortisol makes you gain weight. Several psychiatric medications lead to severe weight gain.  Hormonal birth control definitely used to make you gain weight. Many scientists claim the newer drugs haven’t been shown to do so, but my feeling is that “baby chemicals lead to weight gain” is the default assumption and the burden on them is to prove it doesn’t.
    3. Past deprivation, including in utero, can decrease basal metabolic level, or make it more likely to decrease in the face of further calorie deficits.
  4. At the same time, people are remarkably resilient to environmental changes.  A given person can eat a wide range of calories and stay at the same weight.  No one understands why.
  5. So while calories in/calories out is literally true, in the sense that everyone is taking in and using calories, it’s not useful, because so many things affect intake and output.
  6. It is possible to have an excellent diet and exercise routine and still be fat.
  7. But any given person will probably be fatter the worse their diet and exercise.
  8. When you tease these out, fat is mostly a symptom of things that lead to bad health, not a cause of bad health.  Extreme amounts of fat are hard on the joints and heart.  But all evidence says (good diet, good exercise, 40% body fat) > (bad diet, no exercise, 20% body fat)
  9. Nonetheless, the general and medical public alike seem extremely fixated on fat, and this is hurting fat people.
  10. Shame around fat seems to contribute to both fat and the negative health outcomes associated with being fat.  Shaming fat people for the health is right up there with rescuing prostitutes by arresting them.
  11. To the extent fat itself affects health, the ideal body fat % from a health perspective is much higher than the ideal body fat % from an American aesthetic perspective.
  12. Lab animals are fatter than they were a generation ago despite provably identical conditions.  This has got to mean something about our food, and it’s probably not good.
  13. It is possible to be both fat and undernourished.  Most poor Americans are.
  14. Your body needs calories to run.  Faced with a calorie deficit, your body may choose to cut programs (like the immune system, or thinking) rather than dip into savings (stored fat).  This means that maintaining even an “unhealthy” weight may be the healthiest choice a person can make.

I Swallowed A Bug

Here are the arguments in favor of bug eating:
  1. Relative to traditional meats (chicken, cow, pig, sheep), bugs require many fewer resources. (This and all future comparisons will be done on a per unit edible protein basis, rather than per unit animal weight)
  2. Bugs have more trace nutrients and less fat.
  3. We care less about bug suffering than chordate suffering.  Possibly we don’t care at all.
Here are the arguments against bug eating:
  1. Bugs are gross.
Here is where 28 years of being unable to digest food becomes a super power.  Most food and essentially all protein sources strike me as gross.  So bugs aren’t that much worse than any other source, and I have a lot of practice overcoming disgust in order to eat.
My friend Brian held a bug eating night.  He explains the rationale and practicalities pretty well, so I’ll restrict myself to talking about my personal experience, which can be summed up as “a million times better than I thought it would be.”
For background: I’m trying to train myself to eat meat.  This quarter I’ve taken to cutting off slivers of salmon (for the omega-3s) and more recently duck (which is a wonderful combination of delicious when dead and malicious towards conspecifics while alive, which makes it feel a little more moral) and sauteing them until they’re charred through.  When I say slivers, I mean slivers.  I’ve been working on duck for a week and I eat at most two fingernail-clipping sized bits, prepared and eaten separately.  For salmon I might do as much as 1/2 the volume of my pinky. I have small hands.
I pre-committed to eating at least one cricket, but that was all.  The other bug was supposed to be waxworms, and waxworms are squishy.  I don’t do squishy even when it’s not bugs.  And I was going to be extremely proud of myself for just that one cricket.  Eating a new anything is a big deal for me, and it takes time to adjust.
When the moment came I ate several (along with some HCl pills), and walked away, supremely satisfied in myself for trying a new thing and not freaking out about it.  And then I started getting that itch to eat more, that means the thing in front of me has some trace nutrient I’m short on.    So I did.  And I asked for some to take home.
I got off easy on the waxworms because they were burnt so badly they ended up not serving them.  But there were mealworms.  Mealworms were served as taco fillings, but as it turns out I’d rather eat a bug than a taco (the variation in textures freaks me out).  Mealworms were wetter and more fibrous, so you had to chew them more (although don’t skimp on chewing crickets, catching a leg in your throat feels gross).  The had their own taste, which I didn’t care for at first but could probably grow to be okay with.  I think I like it better than chicken (aka bad tofu) and beef, but not as much as duck or pork, and by pork I mean bacon.
At the end of the night I had a slight stomach ache.  I’d brought HCl but no digestive enzymes, and my stomach was clearly struggling to keep up.  But I get that with all new foods and any significant amount of protein, so I don’t hold it against the bugs.
Some of ease of eating was undoubtedly the environment.  Brian, John, and their blogless roommates have a pre-existing tradition of communal meals that I love, and that makes eating easier.  it was also supremely gratifying to have other people share my attitude that the food in front of us was gross but we were going to eat it anyway.  Constantly being the only one that thinks that gets really lonely.  I flinched a little bit when I went to eat the cricket leftovers this morning.  But then I ate them, and it was fine.  Definitely better than duck, and duck is delicious.
Honestly, the biggest down side is that for all that bugs take many fewer resources than chordate meat, they are currently much more expensive.  One pound of edible cricket is ~$13/pound, which is as much as the grass fed free range humanely cuddled duck I get at the fancy grocery store.  I could probably grow them at home at essentially no cost, since they can live on food waste I would otherwise toss, but I’m not yet committed enough to deal with the noise.  But even at this price I plan on eating more bugs.

Pain, part 2: Options for Treating Pain

Anesthetic (e.g. Novocain):  This is a very good option for when you need to block an extraordinary amount of pain in a very specific area for a short period of time (e.g. dental work).  However, as someone who received nerve damage from surgery that exactly mimics the effects of local anesthetic, I can tell you that it is not a long term solution.  Feeling nothing is actually very weird, and makes it easy to injure yourself.

Non-steroidal anti-inflammatories (e.g. ibuprofen):  These are great for occasional use, and have their place for long term pain caused by inflammation (e.g. arthritis).  But they carry some heavy risks for long term use.  One, inflammation is often a helpful reaction.  Topical NSAIDs helped my cat’s pain but retarded the growth of blood vessels in the eye which ultimately made the problem worse*.  Suppressing a fever can prolong illnesses.

NSAIDS are also hard on the stomach, which is bad for everyone, but especially bad for someone like me, who has long running stomach problems that interfere with my ability to absorb nutrition.  I completely wrecked my stomach with naproxen the week before surgery.

COX-2 inhibitors are a subclass of NSAIDs that target pain pathways more specifically, while sparing the gastic pathways that cause so many problems.  The problem is they also increase the risk of coronary events, to the point many were taken off the market and others restricted to single use post-surgery.  They’re so out of favor for pain relief that the three different medical professionals I begged for dental pain relief didn’t think to suggest them, even though I have many gastric risk factors and essentially no coronary risk factors.

Even before realizing COX-2 inhibitors might be perfect for me, I was very angry that they had been taken off the market.  The coronary risk was limited to a small subset of patients, of even of those, some might very well choose to live a shorter life in less pain, because pain is depressing.

Non-NSAID analgesics (e.g. tylenol and asprin): You know how new drugs like to advertise themselves as “safer than asprin?”  That’s because asprin is actually pretty dangerous.  Not super dangerous, but dangerous enough it might well be denied FDA approval today.  Asprin is also a blood thinner, which is great for coronary patients but terrible for dental patients because it can melt the blood clot protecting the surgical site, leading to dry socket.  Some descriptions down play dry socket, but it is in fact both extremely painful (because it exposes a nerve to open air), and dangerous (because it leaves the wound open to infection).   Tylenol is the world’s worst way to commit suicide, because there are several days between the point of no return and actual death, and they are extremely painful.

Opioids (e.g. heroin): I’m told these are super fun for some people, but I have had many different kinds over the years (as one dentist after another fucked up trying to fix my mouth), and I hate them.  The milder ones (everything short of percoset) do nothing for me, and the stronger ones (percoset) are so supremely unpleasant I would rather be in pain.  The only exceptions were when I was literally dying of norovirus, and whatever opioid they gave me was apparently integral to me not dying, and when I got dry socket.  And even with dry socket, I only took them to sleep, because they were just so awful. I refused to even get a prescription this time, because they just don’t work for me.

But even for people who find opioids tolerable, they have serious risks.  They depress respiratory function, cause constipation, and reduce mental function.  They’re insanely addictive on a chemical level- which doesn’t mean everyone who takes them once is hooked forever, but does mean that most people who take them will go through an unpleasant withdrawal period, no matter how “legitimate” their reason for use.  People develop tolerance to the pain relief faster than to the negative side effects, and quitting them may leave them in more pain than they were when they started.  For all these reasons, opioids are pretty much exclusively used for acute pain management and terminal patients.  Doctors who stray outside this risk serious sanctions from the DEA and FDA.  Even if I found opioids tolerable, there is absolutely no way I could have safely used them for the months of surgery + recovery I am going through.

And because I’m working my cat into everything: he doesn’t like opioids either.  Even after having four teeth pulled he fought me on taking his medicine, and then he just stood around in a stupor and drooled.

Tricyclic antidepressants: This is a cutting edge use of a very old drug.  I was prescribed topical doxepin by the doctor who did the research proving it was useful for oral pain- and even then, he was researching a different kind of oral pain.  It had some ugly side effects: I fell asleep immediately upon taking it, and couldn’t stand being touched (anywhere) the next day.  It left some numbness that lasted indefinitely- when I ate spicy food I could feel in my throat where the liquid had trickled down.  On the plus side- it left some numbness that lasted indefinitely.  That was a huge improvement over the shooting pain I’d had before.  I eventually stopped because the permanent effects had boosted me to the point it didn’t hurt that much, and the side effects were getting worse, but it was overall a great experience.  If I hadn’t found something better it’s what I’d ask my doctors for now.

Capsacin (aka spicy food): This really only works for dental pain.  When you eat capsacin it activates all your pain receptors at once.  Which hurts a lot, but then you’re good for a couple of hours.

Cannibidiol (i.e. marijuana): This one isn’t as well researched as the others because it’s illegal at the federal level (although, I must stress, legal in my state for both medical and recreational use).  But everything we know about it is awesome.  People tend to use THC and marijuana interchangeably, but that’s not true at all.  Any given strain can very in the amount of THC and CBD, and some strains may not have any THC at all, or the treatment may not activate it.  THC causes a lot of the symptoms traditionally associated with marijuana use, like munchies everything being funny.  CBD causes nerves to stop hurting for no reason, and may do a bunch of other awesome things like reduce inflammation, encourage bone growth, decrease anxiety, fight cancer, and (I can only assume) whiten your teeth while you sleep.  There is essentially no way to kill yourself with it** and there’s no physical dependency.  I used this off and on after all three surgeries, and my use naturally trailed off after each one.  It either doesn’t have any effect on me mentally, or the effect was less than the pain it was stopping.

THC may work synergisticly with CBD.  In my case it makes me sleepy, which is a terrible trait for a recreational drug but an amazing one for convalescent therapy.

A note for dental use in particular:  you are not even allowed to use a straw, so you definitely cannot smoke anything.  The nice people at the medical dispensaries have precisely dosed pills, and if you are lucky, CBD tinctures.  These are meant to be taken sublingually, but if your pain is in your mouth you can apply them to the area and everything stops hurting really really rapidly.  It gave me an amazing sense of control over my pain and enabled me to take more risks, in terms of eating and talking to people, which really sped up my recovery.

I don’t want to get too much on the “yay marijuana” bandwagon, because it’s entirely possible that as its usage becomes more widespread we’ll find out it has some rare but nasty side effects too.  But I do think it’s a travesty it is treated as worse than ibuprofen or alcohol, when it is clearly better.

*I think his infection was also resistant to the first antibiotics they gave him.

**Weirdly, this may be true for humans but not pets.  When I investigated using CBD to treat pain from my cat’s corneal ulcer, I discovered that we are pretty sure there is no amount so high it can kill your pet in one sitting, but chronic use may lead to something resembling serotonin syndrome (aka the reason you have to be so careful when taking MAOI inhibitors).