is this an example of high sensitivity and low specificity? Since you can determine a positive for sure (the 80X example) but can’t determine if the negative is truly a negative or false negative (the latter example)

Is it just coincidence that you referenced the dosage range of Vyvanse? 😂

I can't speak to science, only my own experience with nutrition, vitamin deficiency, and health conditions (the ones negativity affecting me the most being hypothyroidism and ADHD).

My hypothyroidism definitely affects my ADHD negativity when not properly managed. (Makes sense because out of whack hormones would create out of whack brain chemicals).

Vitamin D deficiency gave me chronic brain fog and negatively affected my ADHD until found and supplemented.

Processed foods (especially food dyes) negatively affect my ADHD....too much creates massive brain fog and kills my ability to function...

My take on it is that vitamin deficiencies would affect anybody negatively whether neurodivergent or not. I think that maybe ADHD or autistic people may be more sensitive to nutrition factors but you would really need to ask a dietician (or multiple) and see if they've noticed a correlation.

Is there typically difficulty in getting the specific prescription information from this suspect/victim instead of having to work with all these assumptions?

Hmmm well in practice fruit trees are propagated from cuttings and thus are clones and are not grown from seeds. Propagation ensures the consistency. Keep in mind that fruit trees are highly altered and manipulated from their wild ancestral form. Many tree varietals found in nurseries cannot be grown from seeds at all. But that’s about as much as I know. Hope this helps and I look forward to more detailed answers. Great question!

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There was a recent study that found mothers' low levels of vitamin D during pregnancy to increase the risk of adhd. https://www.sciencedirect.com/science/article/abs/pii/S0890856719322324?via%3Dihub

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I did my PhD on this, but for living patients ;)

As you say, there are many factors at play, most importantly distribution volume and drug elimination rate. For all of these factors, you can estimate the typical value and the between-individual variability in the population. We call this a population pharmacokinetic model.

With just a single concentration, you assume this person is a "typical individual". You can back-calculate (based on time of death and time of taking the drug) what the dosage typically could have been. You need the administration time though, the time of death, and you better hope the drug concentration remained stable between time of death and time of autopsy. In clinical studies, blood samples are often stored in solid co2 (-80C), and for good reason.

Using the known variability in the population, you can also give a confidence range for your initial dose prediction. You can make predictions more precise by adding information. Bodyweight influences likely drug distribution volume. A second drug (with known dosage and administration time) could help you too.

Usually, this technique is done for drugs that need to be in a precise concentration range. Give a dose, measure concentration, estimate blood volume and calculate the optimal dose for that patient. We call this Model Informed Precision Dosing: MIPD. You can apply the same in autopsies, but I doubt it is routinely applied. Cool question!

For many drugs if you knew the route of administration (orally for example) and the time, you could get a pretty good feeling of the dose.

The pharmacokinetics of drugs give you a curve or a line of some kind and it is possible to back calculate.

There are certain caveats. For some things , the original drug is labile and the metabolite in stable, so you would just measure that. But this is a technical thing, like measuring an oxidized version rather than not. Some things are in bound and free forms and it is technically difficult to get both. Some things have endogenous versions that make it hard to tell what you ate vs what you had (erythropoietin , testosterone) because they are indistinguishable. Some things have such a long or short half life that it becomes complicated. Some things that are stored in fat are tricky to figure out doses of. And all sorts of other little quirks. But , a qualified yes is really the answer.

As most of the answers have said, it depends. When monitoring a patient on certain medications, we will test what is called "peak and trough." Peak is when the medication should be at its highest concentration in the bloodstream, which is typically an hour after dose, although this can vary a little with some drugs. Trough is when the concentration should be at its lowest, which is typically just before the next dose. I believe drug half-life has been mentioned previously, so i wont rehash that. Drug interactions, disease, and things like grapefruit can interfere with drug metabolism rates. Most drugs dosing is calculated using amount of drug/weight of patient/time. Blood volume is assumed. Again, not all drugs are the same, and not all humans react the same, but you could roughly guesstimate the initial dose, which was your actual question. This information isn't terribly useful in most clinical settings. I am a clinical laboratory scientist, so this is a bit of what I do.

This is a very exact science called pharmacokinetics. But we need some pretty exact info, like time of the last dose and rough dosing history before that. For most marketed drugs we’ll have a population pharmacokinetic model that we could use to give a prediction interval around a likely concentration for a given dose, or to estimate the most likely dose given an observed concentration.

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Yep, skin sheds over time so the ones that added melanin to protect from future sun exposure are lost, and the new ones that formed when you weren't in the sun as much aren't expecting to need that extra melanin. (Melanin is what makes skin brown and reduces the risk of sunburn)

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What’s the age of the person?

100mg is a bit high. Even for someone with tolerance. I personally have never seen a prescription for Norco 10-325 to be taken 10 pills at a time.

But two major concerns present itself:

1. Respiratory depression induced by opioids
2. Liver damage caused by the acetaminophen in the Norco; assuming you are from the US where just getting hydrocodone by itself is not really a thing, minus special cases.

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Adding on to some of the good comments here, many drugs have physical properties that cause them to distribute in body tissues beyond the blood. For instance, when we give patients oral antibiotics for infections of a specific organ (prostatitis, for example), we need to choose an antibiotic that has good penetration to the prostate. Or good bone penetration for osteomyelitis. If a drug is extremely lipophilic and is given to an obese person, the volume of distribution can be effectively limitless and difficult to ascertain, because it distributes beyond the blood and into the fat tissue. The log P value of a drug will give us a clue to how widely the drug distributes, but we would need multiple samples to truly understand the kinetics how the drug is eliminated in a specific patient.

There are also special circumstances that complicate this “2-compartment pharmacokinetics” process. When we give a cancer patient high dose methotrexate infusions, the drug will distribute into any excess body fluid in the patient, like edema. The body will then clear the blood of the drug, but the methotrexate-laden body fluid will effectively re-bolus the patient with the drug and raise their blood levels again, long after we’ve stopped the infusion.