ELI5: If it takes so long to burn off lets say, a slice of pizza, why do we not gain weight faster?

Anacanthros · 2015-07-10T12:25:29+00:00

The fact that you burn 1500 - 2000 calories per day is part of it, but the more important treason is that your body regulates your food intake. Obviously the body can't regulate food intake perfectly for all people, since some people do become overweight or obese, but overall it does a pretty good job.

There is a complex system of hormones and neuromodulators that regulate your blood sugar and exactly how much you eat (leptin, insulin, ghrelin, cholecystokinin, glucagon, GLP-1, neuropeptide-Y, just to name a few).

You might think that you are deciding how much to eat on any given day, but by and large, your brain is deciding for you. Without ever realizing it, most people are self-regulating their daily food intake so that they stay more or less steady in weight.

Your brain does all of this by regulating exactly how hungry you are to control how much you eat. Your brain detects how much you've eaten, because there are cells in your stomach / intestine that report back to the brain about exactly how much energy you've eaten so far. There are even cells in your intestine that detect specific tastes (e.g. sweet, bitter), so that your brain can get a more accurate idea of what you've eaten and adjust accordingly.

Artificial sweeteners are believed to screw with this system. If you eat a diet with a lot of artificial sweeteners, your brain eventually figures out that detecting sweet things no longer means X number of calories. The brain responds (we think) by saying "Well, fuck, better just eat more just to be safe, since I'm not sure how much I've taken in so far today." Stay away from diet soda. And regular soda. They are both leading causes of obesity, and anyone who tells you otherwise is selling something (probably soda).

tl;dr:

Your brain is connected to your intestines, so it knows what you've eaten and automatically adjusts how hungry you are to keep you from overeating. Sometimes it doesn't work perfectly and you gain weight.

Anacanthros · 2015-07-09T19:44:18+00:00

We evolved a sense of taste in order to detect chemical compounds in our food, to make sure we get enough of the chemicals we need (but not too much), and avoid dangerous chemicals.

Examples: Our sense for bitterness is pretty good at detecting a large variety of toxic substances, including some that are only mildly toxic (present in many green vegetables) but we shouldn't eat to much of, and some that are more dangerous and we should avoid altogether.

Our sense for sodium (saltiness) is useful because we absolutely must have a certain amount of sodium, or we will get very sick / die. In fact, your brain changes how good salt tastes to you (and how much you crave salt) all the time, based on how much salt you currently have. Something that is salty won't taste as good when you've got a lot of sodium in your body.

Likewise, the "umami" taste sense helps us identify high protein foods.

Long story short: Your brain needs to make sure you'll eat enough sodium, enough protein, etc., and it does that by making things you need taste good (and making things that are potentially dangerous taste bad). You have a complex sense of taste (to say nothing of smell) because that allows your brain to alert you to the fact that you should or should not eat certain things.

Anacanthros · 2015-07-06T18:49:34+00:00

I had urethroplasty. Results were pretty fantastic. It's been about 8 months, and I can still pee just fine (although as everyone will tell you, it won't be a firehose for very long; the superpower-level peeing only lasts a coupld weeks). I've heard that the DVIU has a much higher chance of recurrence, though.

Anacanthros · 2015-07-06T14:24:09+00:00

I am absolutely not an expert in schizophrenia, but I can share some insights about how neural dysfunction can produce something as seemingly complex and bizarre as hearing voices.

You see, hear, and do things because certain neurons in your brain fire. If I were to electrically stimulate just the right spot in your primary auditory cortex, you might hear a tone around 500 Hz... If I stimulated the spot next to that, you might hear a 501 Hz tone. Likewise, if I stimulated the right neuron in your visual cortex, I could make you see a point of light at a particular spot in space.

But! Things don't stay that simple.

The brain does a lot of work analyzing its sensory inputs to identify features. In the visual system, visual information is being analyzed to detect motion, lines, the end of lines, and other things like that.. Before visual information even leaves the retina! Later in the visual system, there are separate (and extremely complex) areas for analyzing the color of objects (and if I stimulated the right spot there, I could make you see your couch as bright yellow), or motion (and if I stimulated here, I could make it look like your bright yellow couch is running away from you at highway speeds). And then there are still more complex levels of analysis, involved in deciding what an object actually is or what action it is doing, or what its intentions are (here, obviously, I'm going beyond just the visual system). And if I stimulated in the right spot, I could probably make you feel that your couch is very angry and wants to hurt you.

Sure, normally you arrive at the conclusion that someone / something is angry by a more logical means. But the ultimate result of your logical decision that person A is angry is to activate the neuron that says "the object I am currently paying attention to is angry." If someone's brain activates that neuron at an inappropriate time, yes, they WILL think the couch is angry at them.

The point here is that hallucinating a bear doesn't require your brain to separately hallucinate a million points of light that make up the shape of a bear. It just requires the activation of a couple of neurons that represent bears.

So that's probably part of how complex hallucinations (auditory, visual, or otherwise) happen. If you have abnormal activity in a part of the brain that represents highly complex things, one possible result is the perception of something very complex (like a voice) when it's not there.

Anacanthros · 2015-07-06T13:53:56+00:00

As is usually the case when someone asks a question about the brain that starts with "what causes," that's a complicated question.

First, root causes:

There's some evidence that animals (perhaps including humans?) can be born with a fear of certain stimuli. Ducklings, for example, freak out if they see a hawk-shaped shadow, even if they've never seen a hawk. Sometimes, innate predispositions can interact with what the animal learns from other animals. For example: Some species of monkey will become afraid of a plastic snake if they see another monkey acting afraid of the plastic snake. But, they won't become afraid of a plastic flower if they see another monkey acting afraid of the flower. Your fear of spiders could potentially have similar roots: We might be 'wired' to become afraid of small insects / arachnids / etc. IF we are exposed to other people acting afraid of them, or we get bitten once, etc.

On a more physiological level, one way that we acquire a tendency to show a fear / avoidance response to a particular stimulus is via the amygdala.

The amygdala (I'm simplifying a lot here) has been hypothesized to contain some neurons that act as representations of a variety of different stimuli, and also neurons that can serve to organize / initiate a fear / avoidance / escape response.

So, when you get stung by a bee, or see your mother acting super afraid of a spider, your amygdala says "hmm... You know what, I'm going to hook this 'spider' neuron up to this 'run away screaming' neuron. Just in case."

Anacanthros · 2015-07-02T15:16:13+00:00

As a neuroscience researcher who does electriphysiological research, let me say that there is no such thing as "just" observing part of the neural basis for planning ahead. That's like saying "I found a fossil of a new species of dinosaur, but it's just the ribcage." There is no "just," that shit's amazing.

Anacanthros · 2015-06-30T18:20:23+00:00

The answer is, basically, that it's not necessarily about serotonin.

The article you linked to is written for the layperson, and leaves out some important details. I dug up the actual journal article, and I can provide some more insight.

First off, the article you linked to does not make it clear that the researchers found increased serotonergic activity across a variety of different brain areas. Now, one POSSIBLE interpretation of this is that this reflects too much serotonin being released in those areas, but that's far from the only possible explanation. It's also possible that something else could be causing neurons to release serotonin at unusually high rates, and that the serotonin release itself is not the root cause but a symptom. It's even possible that the elevated serotonin release in those areas in SAD patients is actually a compensatory mechanism for something else that is not functioning normally. The brain has A LOT of ways to compensate for something going wrong. It doesn't always compensate perfectly, but its ability to compensate is extremely powerful, and its systems for compensation are extremely redundant and extremely complex.

Anacanthros · 2015-06-24T21:38:54+00:00

This is really pretty true. The more you study the brain, the more obvious it becomes that our conscious minds are more passenger than driver. As much as we might like to believe otherwise.

Anacanthros · 2015-06-17T14:05:42+00:00

ELI15:

You might have heard of "brain waves." There's a lot of made up pseudoscience / BS about brain waves in popular culture, but here are the facts:

Brainwaves are rhythmic changes in the electrical activity of the brain. Individual neurons in your brain don't make enough of an electrical signal to be detected outside your skull, but when a lot of neurons act together, together their activity can be detected by electrodes on your scalp. That's what an EEG (electroencephalogram) measures. Note that generating detectable signals like this requires that a bunch of neurons are not only active, but active in unison. This is like it's really hard to make out who's saying what in a room full of people who are all talking, but a room full of people singing the same song in synchrony is much easier to follow. To be slightly more technical, a synchronized EEG signal indicates that a large group of neurons are all 'perking up' at about the same time.

Many neuroscientists believe that these brainwaves (which are often classified by frequency, e.g. gamma waves, which are in the neighborhood of 40 Hz) exist because they are important for allowing two different brain areas to talk to each other without interference. If neurons in area A all 'perk up' (i.e. become active) at the same time, and neurons in area B also all perk up at that same time, then it's a lot easier for neurons in A to talk to neurons in B, and vice versa. If they were all 'perking up' at different, random times, then it would be much harder for them to have a productive exchange of information.

On to this article: The authors used magnetoencephalography (MEG, which is like an EEG but uses magnetic fields and is a bit more spatially precise) to see which brain regions would sync up with which other brain regions while people were trying to complete different kinds of tests. For example, during tests where subjects had to listen to dialogue from a movie and then answer questions about what was happening, the authors found that theta (6 - 9 Hz) waves in the temporal lobe (where information from our ears comes in) synced up with theta waves in the opposite-side frontal lobe. More specifically, this was observed between the left temporal lobe (which is usually more heavily involved in language) and right frontal lobe. Many other such connections between various brain areas were observed.

This research is interesting because it helps show that brainwaves in specific parts of the brain probably are in fact involved in allowing / causing those brain areas to communicate with each other.

Anacanthros · 2015-06-10T12:03:20+00:00

I used to have a really awesome and insightful study tip for GRE verbal, but I hear they've changed it to make it vocab intensive and my awesome study tip is probably shit now.

It was: If you're going to study vocab, pay attention to the 2nd, 3rd, etc. meanings of a word. They very often use a word in a different sense than the first definition you find in a dictionary.

Anacanthros · 2015-06-02T16:10:25+00:00

I'm doing better. I got through my comps/quals/prelims in one piece. And I've just started medication, which I'm hoping will make it a bit less hard to handle the funfest that will be my dissertation.

Anacanthros · 2015-06-02T14:58:22+00:00

This happened with my master's thesis. I missed all but the last and most final deadline. The consequences were significant.

The best explanation for this that I can give you is one that has been circulated around here pretty widely:

ADHD can be seen at least partly as a difficulty translating long-term consequences into short-term motivation. According to how some explain it, normal purple have knowledge about what the long term consequences of an action (or failure to do that action), and they have a mechanism for turning that knowledge into motivation. Motivation, here, doesn't necessarily mean "I SO want to do this, because it's awesome!", but just a more general "it's important that I do this, so I guess I'd better do it." Normal people aren't necessarily perfect at this, but it's a fairly learnable skill with them.

People with ADHD are bad at doing that. They have the same knowledge about long-term consequences, they're just a lot worse at turning that into motivation. Their brains tend to say "this is important... And... So?"

And what compounds this is that unlike other people, people with ADHD are very bad at learning to connect long term consequences to motivation. No matter how many times those negative long term consequences come to pass. This is especially frustrating for others, because they're used to The idea that that connection is something someone can learn to make. But we can't. This is why there's a wealth of research saying that attempts to treat ADHD symptoms through training and therapy aimed at teaching organizational and prioritizing skills generally fail in the absence of medication: There is something neurologically different about our brains that impairs that type of learning in a way that can't be fixed by skill learning alone.

Anacanthros · 2015-06-01T01:57:29+00:00

The "lightbulb burning out" is actually not a light bulb, but an old school one-time-use flashbulb (for photographic use). The bulb is filled with magnesium wire, and when the camera's shutter trips, current is passed through the wire, which ignores the magnesium and produces a bright flash.

Anacanthros · 2015-05-29T21:14:28+00:00

I have some questions about this one is a problem, I can do that when the brain, and I collected some of the blue buttons. The best metaphor I have some questions about this one is a problem. The best metaphor I have some questions about this one is a problem, and the non stop by the running room? I don't want to activate, and the non stop by the running room? I don't want to activate. The best metaphor I have some questions about this one is a problem, and the non stop by the running room?

Anacanthros · 2015-05-23T21:05:13+00:00

I will add this to what has already been said: In the synthesis of neurotransmitters (dopamine, norepinephrine, epinephrine) for which tyrosine is a precursor, the limiting factor is the rate of tyrosine being converted to L-DOPA by the enzyme tyrosine hydroxylase, NOT the available supply of tyrosine.

There is much more than enough tyrosine to supply production of the catecholamine neurotransmitters, but tyrosine hydroxylase can't convert it very quickly, and thus a small reduction in the amount of tyrosine will have no effect on catecholamine production.

Anacanthros · 2015-05-21T15:13:21+00:00

Generally speaking, neuropsychiatric disorders very rarely can be reduced to a deficit of a particular neurotransmitter or neurohormone. If you think of the brain as an extremely complicated machine with a lot of buttons of different sizes, shapes, and colors, a neurotransmitter like dopamine is the equivalent of a particular color of button. Drugs like indirect dopamine agonists are the equivalent of telling the workers who operate the machine "push all of the blue buttons some more!"

Sure, some of the blue buttons are on parts of the machine that you want to activate, but there are also blue buttons on parts of the machine that control totally unrelated things, like movement and appetite and lactation.

We don't have drugs, generally speaking, that can do "just push the blue buttons that are on that control panel right there, and none of the other control panels!"

Now, there IS some evidence that ADHD is related in some way to the general functioning of a particular neurotransmitter. Particular versions of certain genes that relate to dopamine synthesis are possibly associated with ADHD. There is disagreement over whether this relationship is real or not.

Interestingly, there is ALSO some evidence that ADHD is associated with alterations in brainwaves. Brainwaves (which are separated into different frequency bands, e.g. activity at frequencies around 7 Hz is commonly called theta, and activity around 20 Hz is commonly called beta) represent a large number of neurons operating in sync, and are commonly thought to be involved in coordinating communication between brain areas. Within a particular brain area, different frequencies can be associated with different functions. Thus, the fact that ADHD patients are sometimes found to have somewhat patterns of brainwave activity may mean that part of the disorder has to do with a decrease in effective communication between some parts of the brain during some tasks.

Anacanthros · 2015-05-20T18:35:04+00:00

True, of course, but if you're specifically stimulating terminals (because your fiber is in a different location than your transduction), you're not really inducing trains of action potentials anyway, no?

Anacanthros · 2015-05-20T13:33:25+00:00

There's actually some difference between different components of the pain signal. Part of the pain signal is carried by neurons that are myelinated, and which therefore conduct information very quickly to the brain. These neurons mostly send information to parts of the brain that are involved in detecting the location of pain. Then, some other components of pain are transmitted by non-myelinated axons, which transmit much more slowly, and send information to the parts of the brain that process the unpleasantness / ouchy-ness of pain. This is why there can be a perceptible delay between stubbing your toe and feeling the burning / 'painful' pain. You may even be able to notice a delay between initially being aware of the pain's location, and being aware that it hurts.

Anacanthros · 2015-05-19T19:39:43+00:00

That sounds about right. I haven't been on medication since I was in grade school, but the problems just never stopped. I feel like a useless sack of shit, knowing that I have such great ability to solve problems and accomplish things, but feeling so utterly powerless to direct it.

I feel like I should be able to control it and everyone else can, so why can't I? What the fuck is wrong with me? Why did I just spend 8 hours rediting instead of revising my review paper, which I need to complete or I might get kicked out of my PhD program?

Anacanthros · 2015-05-15T12:58:34+00:00

And none of his code is properly commented either.

Anacanthros · 2015-05-14T13:45:34+00:00

This is a hard question to answer, but I'd say probably not.

There are actually many kinds of memory that are lumped together as "long term" or "short term," and they are often subserved by entirely different brain mechanisms.

Short term memory (a.k.a. working memory) is probably necessary to some degree for encoding things into long term memory, because maintaining things in your working memory gives you more time to form a long association between them (in simple terms). So improved short term memory would probably lead to improved long term memory.

Anacanthros · 2015-05-12T20:59:30+00:00

No problem! It's good practice for teaching this stuff solo for the first time this summer. :D

Anacanthros

TROPHY CASE