SerialStateLineXer t1_je9670e wrote

In this study it specifically refers to children under the age of 5, but stats for overall homicide rates are very similar.

Justifiable homicide is relatively rare, but likely has the same pattern.


SerialStateLineXer t1_je83s9x wrote

People who take antidepressants are more depressed than people who do not. If we just look at the correlation, we might assume that antidepressants cause depression, but the opposite is true.

In this case, there's still a correlation, but the sign is the opposite of the true causal effect of taking antidepressants.

Alternatively, consider a car being driven over a hilly road at a constant speed. When the car is going uphill, it's burning more gas. There's no correlation between speed and gas consumption, but gas consumption increases speed.


SerialStateLineXer t1_jcjnfj7 wrote

To be clear, you can't reverse aging just by heating up or overfeeding an old person. The point is that aging and death on human time scales are not an inevitable consequence of the laws of thermodynamics. Entropic changes can be reversed using an external source of energy (e.g. you can use energy to set up bowling pins after knocking them down). With the right technology, it is absolutely possible to repair aging-associated damage and restore an old person to a youthful state. It's a very difficult engineering problem, but there's no theoretical reason it can't be done.


SerialStateLineXer t1_jc66n69 wrote

Would a negative-pressure ventilator like an iron lung solve some of these problems, and if so, is there active research into developing more lightweight alternatives? What about diaphragmatic stimulation?


SerialStateLineXer t1_jc65u3d wrote

OP asked about accident-induced coma, while this study specifically excludes trauma-induced comas, concentrating on comas arising from medical conditions like diabetes, heart attack, or stroke.

I looked around a bit, and while I wasn't able to find any relevant papers quite as explicit as this is one, from what I found it doesn't look like the odds of recovery from trauma-induced comas are much better, and they may be worse.


SerialStateLineXer t1_jb5l8n8 wrote

Are you under the impression that heritability of height is defined as the correlation between children's heights and the average of their parents' heights? Obviously you can determine that by calculating said correlation, but that's not what heritability means.

Heritability refers specifically to share of variation in a trait attributable to genetic variation. I suppose it's possible that there's some field other than genetics in which the term is used to refer to the degree to which children are similar to their parents, but the original question specifically referred to the definition used in genetics, and you definitely can't calculate that by comparing children to their parents. If you could, twin studies would never have been invented. That's the exact problem they were invented to solve.


SerialStateLineXer t1_jb0xois wrote

>So to estimate heritability, you regress your height against the average of your parents' heights.

No, you can't estimate heritability that way, because this can't distinguish between genetic and environmental transmission of traits.

Traditionally, heritability is estimated with twin studies, using Falconer's formula. You compare the correlation between pairs of monozygotic twins to the correlation between pairs of same-sex dizygotic twins. You can exploit the fact that MZ twins are twice as genetically similar as DZ twins but MZ and DZ twins are raised in equally similar environments to determine heritability.

So if the MZ correlation is 0.7 and the DZ correlation is 0.4, this implies that 60% (2 * (0.7 - 0.4)) of the variation in the trait can be attributed to genetics, 30% (1.0 - 0.7) to non-shared environment (environmental factors that differ between twins) and the remaining 10% to shared environment (environmental factors that are the same for both twins).

There are some additional adjustments you can do for things like gene-environment correlation, but that's the simplified version.


SerialStateLineXer t1_jb0vxw2 wrote

>It means 100% of the phenotypic variation depends on genes, which is quite different.

More precisely, it usually refers to share of the variation within the specific population being studied. For example, when measuring the heritability of height in a wealthy country, you will get a very high heritability estimate, perhaps 0.8-0.9. When measuring the heritability of height in a global population, you'll get a lower heritability estimate, because a significant fraction of your sample will have had their growth somewhat limited by environmental factors like undernutrition or disease. Conversely, if you're studying a population of clones, the heritability will be zero, because there's no genetic variation and all variation must be due to environment.

None of these estimates is more correct than the other, because heritability can only be defined for specific populations with specific distributions of genetic and environmental factors. There is no "ideal heritability."


SerialStateLineXer t1_jazyfer wrote

>“Vaccinations can have serious side effects that cause more harm than some of the diseases that they are supposed to prevent.”

That's technically true. The COVID-19 vaccines could very rarely cause GBS, anaphylaxis, and dangerous blood clots, all of which are more dangerous than COVID-19 for the typical person.

Cost-benefit analysis heavily favored getting vaccinated, of course, but that's a very badly designed survey question.


SerialStateLineXer t1_jadlscb wrote

Cells produce molecules which circulate in the blood, so you don't have to wait for circulating cancer cells. The tricky part is finding molecular signatures that identify cancer with high sensitivity and specificity.

For example, elevated prostate-specific antigen is a sign of something wonky going on in the prostate, which may be cancer, but also may not.

Edit: See responses. This comment isn't relevant to this particular device, which actually looks for cancer cells in the blood.


SerialStateLineXer t1_ja6vkwg wrote

What the other commenter said. Environment has made recent generations fatter than older generations, and makes people in rich countries fatter than people in poor countries, but in wealthy countries, within the current generation, genetics explains most of the variance in obesity, while upbringing explains very little.

This paper is based on a sample in Macao, and I don't know of any twin studies that were conducted in Macao specifically, so it's possible that they've found a causal factor that's peculiar to Macao or other wealthy East Asian countries. But we should be skeptical of this as a general causal explanation for obesity, given that it's contradicted by twin studies.

Edit: Note that the heritability of obesity doesn't mean that different people with the same lifestyle end up with wildly different BMIs because of genetics. Behavioral traits are also strongly heritable, and it's likely that much of the genetic contribution to obesity is mediated by genetic influences on lifestyle choices, rather than by genetic influences on metabolism.


SerialStateLineXer t1_ja2xnqq wrote

It's important to note here that twin studies have found obesity to be very strongly heritable with minimal contribution from shared environment.

Since this study used mediation analysis, which can't be used to demonstrate causality, we should be skeptical of causal claims made by the authors.


SerialStateLineXer t1_j9e5pgq wrote

>I don't think young toddlers know what a calorie is, or how many they need - or the difference between a good calorie and a bad calorie.

Perhaps also worth noting that obesity is a relatively new problem in Thailand. While the obesity rate is rapidly increasing, it was below 5% only 20 years ago. It's not a problem they've been dealing with for multiple generations the way we have in the West, and the grandparents of today's children grew up in a time when hunger was a much bigger problem than obesity.


SerialStateLineXer t1_j9e4owm wrote

I can think of at least three possible explanations:

  1. Executive function is heritable, and parents with poor executive function are more likely to overfeed their children.

  2. Children with poor executive function behave in a manner that prompts parents to overfeed them.

  3. Overeating and obesity impair executive function, even in young children.


SerialStateLineXer t1_j99apep wrote

As I understand it, the claim here is not that subcutaneous fat is protective, but that visceral fat is extra harmful, and that, holding total fat constant, a tendency to store fat subcutaneously is protective because the alternative is storing it viscerally.


SerialStateLineXer t1_j8i3gwk wrote

You got the title wrong. The numbers you cite in the title are relative mortality risk, not the reduction in risk of mortality. So people age 60-79 were 27% as likely to die (i.e. 73% less likely), not 27% less likely (73% as likely), as implied by your title.


SerialStateLineXer t1_j8c8hox wrote

It's worth keeping in mind that most common neurodegenerative diseases are syndromes: clusters of diseases defined by symptoms and certain aspects of the disease process rather than by root cause. Even Huntington disease is actually a class of genetic mutation rather than one specific mutation: a sequence of three nucleotides is repeated many times, but the number of repetitions varies and affects the severity and age of onset. There are dozens of different mutations known to cause ALS, and severity, age of onset, and specific symptoms vary accordingly.


SerialStateLineXer t1_j7v1k9e wrote


SerialStateLineXer t1_j7e4iax wrote

> The Bristol team, led by Professor Paolo Madeddu, has found that a single administration of the mutant anti-aging gene halted the decay of heart function in middle-age mice. Even more remarkably, when given to elderly mice, whose hearts exhibit the same alterations observed in elderly patients, the gene rewound the heart’s biological clock age by the human equivalent of more than ten years.

That's where "rewind" comes from. It restored cardiac function in elderly mice when administered late in life.


SerialStateLineXer t1_j6cnwjw wrote

>You're probably not going to get IRB approval for raising kids on any vitamin deficit.

You can't do that, but can't you select a group of children and give some of them supplements? If some of the kids in the control group don't get enough of certain nutrients...well, that was going to happen anyway.