Some bacterial infections don't necessarily require an adaptive immunity response. Our innate immunity cells have receptors that recognize common pathogens. We even have a system that is just an elegant sequence of proteins being modified to create a pore in bacteria. This is just kicked off by sugars on the outside of the bacteria cell wall (although one such pathway is initiated by antibodies). In fact, certain organs are "immune privileged" and (mostly) do not allow T cells and B cells to infiltrate. But in all cases the invaders are destroyed by the immune system and the debris will find its way (whether or not it goes to the spleen first) to the liver or kidneys and get excreted like any other waste.

However, if someone is lactose intolerant they might not be able to absorb as much of those nutrients due to inflammation.

Animals are no longer used for epinephrine production. If we still did this, it would be pretty harmful to the animals and the environment. I imagine we would not use the same animals used for food. They would be raised in labs. If there was a use for other organs, we might keep those but most of the animal would be incinerated. BUT! that's not happening anymore. The precursors are just mixed together and probably there's some heating and maybe some refluxing and some form of purification. No animals necessary. That's way too expensive and wasteful.

Just to add on here- You're probably not going to get IRB approval for raising kids on any vitamin deficit. You could do this with pregnant rats and then perform behavior tests on them during development. Or you might be able to enroll pregnant women in a study where vitamin levels/diets are tracked but not altered in anyway. Then follow up with the children at different time points.

To answer the original question- I'd probably say that the main issue is that it's hard to get a study funded without having reliable data to back up your hypothesis. I skimmed a few papers and there's not a lot of rational behind the idea that vitamin deficiencies play a role in ADHD pathogenesis. No one is presenting a good reason for thinking vitamin deficiencies are important in ADHD. On top of that it looks like there isn't any compelling data that can be cited.

Another issue you'd run into is that ADHD has such strong genetic links, and none of the genes implicated in ADHD are related to vitamin metabolism. They're all related to neurotransmitter/neuromodulatory molecule signaling and handling and neuronal proliferation. So, it doesn't make a lot of sense to argue a vitamin deficiency involvement when all the observations point elsewhere.

So, sometimes when you read that it's hard to get to the bottom of an issue, with no clear explanation of why, it might just mean it's not a great hypothesis.

Interesting point because humans are not particularly sexually dimorphic when compared to other animals, and even other primates. Sexual selection is often overlooked in evolution, but females play a large role in what traits are conserved and which are lost. For humans, parental involvement was favored over size/strength of males. This is why we pair-bond and are mostly monogamous with fewer offspring.

The short answer to all your questions is, yes. Adipocytes (fat cells) store energy in large lipid droplets that are encased in their own single-layer phospholipid membrane. People tend to describe lypolysis (the breakdown of of fat) as though it doesn't happen until your body has completely exhausted all blood sugar and stored carbohydrates. That's probably (I'm saying probably because I didn't look this part up, but I'm pretty confident) not true, it's more like you are using all forms of energy all the time, but you may increase or decrease the retrieval of different energy stores depending on your metabolic needs.

Lipids tend to be stored as triglycerides (larger, more complex lipids) and then are broken down into free fatty acids (smaller, simpler lipids) and transported out of adipocytes in a few different ways. Some are carried by proteins, some are carried by small vesicles. It probably depends on the pathway that is being used/what process has led to lypolysis.

Different signals that induce lipolysis are going to come from fasting, growth, stress, and disfunction of things like the thyroid. All the pathways lead to some amount of stored lipids leaving adipocytes in one way or another. For different people these processes may be more or less efficient. There are a lot of steps in signaling lypolysis and if any of them are impaired, it will be harder to release stored lipids.

I imagine that you have a balance of storing and releasing lipids that is constantly happening. If you expend more energy than you consume, the balance will shift towards fat loss. When this happens, your fat cells essentially shrink as their droplets become depleted. Since you are (again, educated assumption) constantly breaking down and replacing lipids, the effects of the shift won't be noticeable immediately after initiation. But if you keep the balance of fat loss and production on the loss end, you will eventually lose enough lipid mass that you see a difference.

So, even though the signaling that leads to "burning fat" may be somewhat different during exercise or fasting, the end result for your fat cells is more or less the same. Following exercise, depending on how efficiently you can signal for lypolysis, you may have a minute net loss of lipids in your fat cells. But they have to be further broken down and the byproducts have to leave your body at a higher rate than you generate new lipids for you to notice a loss of body fat.

I hope this helps!

Similarly, for identifying genetic variations linked to diseases and how other genes may be related or interact with those genes.

Look up cold habituation or sensory adaptation. I think it either that the cells that have thermoreceptors become harder to activate due to changes in thermoreceptor expression, or the connection between these peripheral cells and the cells in your brain that interpret the signals a "ow, cold" becomes less efficient. Or both!

I'm going to take a guess and say you are wondering how new cells obtain RNA polymerases. If you're thinking about the problem of making RNA polymerase without RNA polymerase, don't worry. When cells split, they kind of divide stuff up between them like marital assets during a divorce. So, each new cell already has RNA polymerases available to make new polymerases. Similarly, after meiosis, gametes will have RNA polymerases from the parent cell.

https://www.nature.com/articles/s41580-019-0208-1

If that's not what you are wondering, then RNA polymerase is made just like any other protein complex. It starts by transcribing the DNA (done by an RNA polymerase) to mRNA. This is occurring in the nucleus. The mRNA then goes to a ribosome witch will attach complimentary tRNA to produce a peptide. The peptides of each RNA polymerase domain will then fold (probably with the help of some chaperone protein) and then somehow be joined together.

If you really want to twist your noodle, look up the RNA world hypothesis. The theory is that before there were proteins, RNA did all the work that proteins do. So, replication of nucleic acids was carried out by self-replicating RNA. So then the question is, where did individual ribonucleotides come from?

Two things need to happen for insulin receptors (or really any receptors) to work. 1) The receptors need to be expressed. This is the actual production (transcription/translation)of the protein. There are a lot of steps between transcription and getting the insulin receptors to the cell membrane. Any of them could be disrupted and then there's always post translational modifications such as glycosylation that can muck things up. 2) Binding of the insulin receptor has result in an intracellular signal cascade, leading to glucose receptors being transported to the cell membrane. I think what is meant by cytosolic signal impedence is that something gets interrupted between insulin receptor binding to glucose receptor translocation. Or even cell signaling to initiate insulin receptor expression.

It's hard to accurately describe the process of insulin resistance as being linear or having a single inciting event. It's more of a breakdown of the entire, circular(ish) system. But I suppose I think of insulin resistance "starting" in the cells that have the most insulin receptors like fat cells.