An introduction to rates and potency

[Stats]

It has become increasingly apparent in the forums I've read of late that there is a profound and widespread misunderstanding about drug comparisons in terms of strength or potency, perceived or otherwise, in relation to weight and in some cases, the hue or aroma emitted from a substance.

It bothers me to see this widespread misunderstanding so I make this post as a contribution to accurate knowledge on why ODs happen and what determines the perceived strength of ingesting or delivering a substance into ones system.

The effects of a substance can be broken down directly to the rate of absorption, with one possible definition being the rate of excretion by the body of amphetamines in different alkaline environments.

To continue with that example, we know baking soda and tums, or any alkalizing hcl agent in the general case, produces stronger effects with longer duration as compared to the same experience without the poteniating compound. Ever wondered why?

It's the same weight, and thus the amount of active substance ingested is the same in both cases. What you have manipulated is the rate of delivery (excretion) of the substance into (out of) the bloodstream. This results in sometimes weaker or stronger effects depending on the individuals body and state at the time.

This is also why it is futile and erroneous to compare klonopin and xanax. Yes, klonopin is weaker in perceived effects. Yes this is true for 1mg=1mg of each. Why? Because klonopin is absorbed over a longer period of time, distributing its 1mg over a much longer time frame than xanax.

Know your rates!


Will be making more short posts on this topic regarding ODs and tolerance.

 

[falsifiedhypothesi]

I'm sorry but I believe your theory is wrong, or at least incomplete. It's not just rate of absorption that effects potency it's also the binding affinity of certain drugs in the brain, bioavailability, the liver enzyme's effects on the substance, and other variations in individual body chemistry.

Im not sure what your next post will bring but I just want anyone reading this to understand that the processing and subsequent effects of drugs in the body is not a simple thing.

 

[Jekyl Anhydride]

^ This

..and there's two sides to the pH coin, going in and coming out.

It's pee pH that can slow excretion of unmetabolized amps (or speed it up). Amphs excretion is strongly affected by urinary pH, and faster the more acidic it is.

It's not easy to change your pee pH, but mega doses of vitamin C would do it. That much has data out there, but I bet phosphoric acid, as found in the dark-colored sodas, has an effect (how much diet coke? no idea).

Other things can acidify your pee, but you'd risk hurting yourself more than an amph overdose.

And then, aim for citric acid salts and blood pressure meds (thiuridizide class) to keep your pee pH more neurtral for retention.

Don't eat a box of baking soda, even if it could work. You'd be pretty funny foaming from your mouth and nose and choking to death but then you'd die.

EDIT: missed you tubbs, but there's two things: absorption of oral amphs by your GI tract is dependent on pH, and that's separate from excretion of unmetabolized amphs (pee pH).

So acidic foods mean less absorption. Acidic pee means faster excretion.

All the texts out there blame it on the amine, but that makes no sense. Or at least, it's gotta be way more complicated than that. You [wikipedia] want me to believe you can't absorb a water soluble molecule out of your intestines? The makers of Vyvanse believe that.

 

[HoldBack]

I?m sorry, but this is so incomplete that it?s incorrect. To say that the only difference between Xanax and kpin is the rate at which it?s absorbed.

So do oxy and morphine differ ONLY by the rate at which they are absorbed?

There are so many factors that impact the perceived and real effects of a drug that cause people to have different experiences that saying the rate is as significant as potency is misinformation.

 

[Stats]

I am sorry you don't agree. What I have stated is indeed all accurate with the caveat of falsifiedhypothesis's comment. It is not meant to serve as a one page summary of every detail of drug pharmacology--for I would have posted that outside of basic drug discussion.

It is a simplified version meant to guide conversations on conversion ratios because it is indeed true, at a minimum, that any present state of the body can be summed up or at least deduced by the makeup of the blood in that given moment. So instead of saying yeah I'm used to doing X amount of morphine and so I can do X amount of heroine--they are the same substance and I even know the dealer got the same potency! This could be a fatal miscalculation as the conversion is really:

cX = bX * a for some x > 0 grams of substance

where c is the rate of absorption of heroine and b is the rate of absorption of morphine. unless c = b, and most of the time it will not, then you need to consider a as the "1-to-1" ratio factor in order to ingest similar dosages and achieve desired effects. Meaning, if c > b (I honestly don't know if morphine < heroine) then you really want to take c/a * X or a fraction c/a of the normal amount of morphine you'd take to achieve the same effects over the same amount of time you are used to while using heroine.

I.e., you need to dilute the substance which is stronger by 1/a or strengthen that which is weaker by a multiple of a, BUT YOU MUST ACCOUNT FOR ABSOROPTION. We overdose because at the beginning or origin time of OD, the present state of the blood is one in which enough toxins have accumulated to reach a threshold necessary for an adverse event to occur inside the body. If the rate of the substance is not reduced or at best, stopped, the OD will continue until the person expires.

Key to chemistry are rates, and as such, all of the things you all have pointed out again redirect back to rates.

Define Y to be the payload of the dose D in weight of drug X. Consider further we have two rates of absorption r1 > r2 with r1 being the baseline (lab setting) absorption rate of the substance and r2 really just being a transformation of r1 by taking r1 over a divisor such as r1 * 1/2. r2 represents the absorption rate conditioned on an individual's unique body and levels of hormones, neurotransmitters, etc.

Then r1 and r2 are obviously related to the effects of any drug through the following:

Y = D*(r1[x] + C) where r1[x] is the rate of absorption for drug X and C is a baseline shift in absorption unique to each persons anatomical makeup at the time of ingestion. This has intra-individual variation. Then r1[x] + C can represent the baseline C=0 or another individual's shifted c from the base line. Subbing r2[x] = (r1[x] + C) + C2 and now we have the same thing again.

Y = D*r2[x] + C2
where rate r2[x] and so forth. The point is that once the individual threshold for OD to begin is met, the rate becomes the sole causal influence on survival outcome. I.e., the paramedics job is too stop or slow the rate of drug being absorbed or else the person will die.