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.

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.

Cannibidiol for pain: a partial retraction

Earlier I described CBD as having absolutely no effect on cognition.  This turns out to be wrong.  I’ve subsequently found that CBD does impair cognition somewhat relative to optimal, it just does so less than pain.  And at least for me, it doesn’t wear off quickly: if I take it at night I’m in less pain the next day, but I also have trouble focusing for long periods and doing truly complex work.  It feels like I can’t get far enough away from problems to see the whole of a thing.  If my choices are “in pain and dumb” or “not in pain and dumb”, I choose door 2, but this does make me more forgiving of NSAIDs.

In other news, they finally took my bone spur out and wow, I’m in a lot less pain.

Why Jezebel is Wrong that Cats Don’t Care About You.

Jezebel has a post titled “Why House Cats Generally Don’t Care (About You)“, in which they assert that cats don’t care about humans because they’re so close to wild cats.  Where do I start with this?

  1. The claim that domestic cats are closely related to wild cats is not backed up by numbers.  Jezebel claims ” house cats may not be that genetically different from wild cats”, citing sister site io9, which in turn cites a summary (warning: PDF) of the base article for its claim that the feline genome is “highly conserved.”  (Jezebel eventually links to the full article, but only the abstract is accessible)
    1. I’m not sure it’s actually wrong to describe an entire genome as highly conserved, but the term is usually applied to specific genes or even gene sequences, not entire genomes.
    2. You know what is a good system for measuring how different two things are?  Numbers.  For example: humans and common chimpanzees share 97% of their DNA.  Eyeballing it, it would not surprise me at all if domestic cats were more related to their ancestral wildcat than humans to chimpanzees.  I don’t see any numbers in either blog post or any of the article summaries I have access to.
  2. Despite numbers being excellent at measuring things, genetic similarity does not correlate very strongly with behavioral similarity.  For a fascinating example of see the fox domestication experiment, in researchers attempted to breed fur-farm foxes for tolerance of humans.  They succeeded in less than 40 years.  

     

     

    1. Domesticated foxes vary from undomesticated fur-farm foxes by only 40 genes.  They tragically don’t give a total gene count, but farm + domesticated foxes different from wild foxes by 2,700  genes, so 40 is almost 0%.  Nonetheless, undomesticated adult farm foxes will either bite your face off or cower from you, and domesticated ones want tummy rubs.

      .  We’ve had thousands of years with cats, we could make them want tummy rubs if we wanted.

  3. Which we have done.  Jezebel seems to be ignoring variation between breeds and individuals.  Certain breeds, like burmese, scottish fold, and Maine coon, really love and orient towards humans.  They don’t have dogs ability to read human facial expressions, but they do seek out their owners for attention, even when no food is on offer.  My cat loves tummy rubs and will fetch his favorite toy, although he has yet to realize people other than me can throw them.
  4. Meanwhile chow chows, one of the earliest dog breeds, possibly originally intended as food, are described as “cat like” because they’re so independent, and need extensive socialization to even tolerate strangers.
  5. Jezebel also comments on cats’ hunting behavior.  What they say is true, but it’s equally true of dogs: domestic and wild, feline or canine, animals have hunting behavior built in but need to be taught to eat what they kill.

And thus concludes your daily dose of Someone Is Wrong on the Internet

Different things for the same name

I’ve picked up enough scientific/medical Latin and Greek that I can often guess what a new term refers to without looking it up. Of course 50% of that comes from knowing “itis” means “inflammation”, but I’ve picked up other terms too.

The problem is that even English -> Science translations are ambiguous. In psychology, “displacement” means redirecting an emotion from the cause to a new target (e.g. you’re mad at your boss so you punch a wall). In the closely related field of animal behavior, displacement means taking the energy of a negative emotion it can’t act on and investing it in something positive (e.g. your cat licking itself after it hears thunder).  Over in physics, it means physically moving something out of the way, which is probably the closest to the conversational definition.

Latin -> Science -> English is even worse. Take parabiosis. It literally translates to “living next to”, which could mean the perfectly reasonable “two species living in very close association with each other, without noticeable benefit or cost to either”. Or it could mean “sewing the circulatory systems of two different animals together so they can share blood forever.” This is useful when you want to test if blood borne chemicals are relevant to a system but have no idea which chemical might be relevant, e.g. testing how aging affects recovery from trauma. AKA Elizabeth Bathory was on the right track.

If you read that and are wondering if you can maintain eternal youth by sewing yourself to a college student, the answer is probably no. The mice must be heavily immunocompromised to avoid mutual destruction via the immune system (although I wonder if this could be combated with cloning.  Hypothetically.). But having discovered that pigeon-rats are a very real possibility, I am excited/afraid to discover what other Simpson’s Halloween episodes we can make real.

On a more serious vocabulary note note, I’ve been using Iodine’s in-browser medical translator, and I’m shocked at how helpful it is.  You wouldn’t think Highlight-rclick-google search is that taxing, but compared to seeing the definition instantaneously and in context, it feels like an enormous waste of working memory.    My only complaints are that it doesn’t autotranslate words in links, which are often exactly the words I want to know the meaning of, and that it’s strictly medical rather than biological, so it skips a lot of basic science words.

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.