That's a good counterargument

Reiterating my claim to focus on how your claim relates to it:

"I fear that we have a risk budget, so when STD risk is reduced via a cure or prophylaxis, humans increase the amount of sex they have until the STD rate stabilizes again."

You mention:

" I don’t think there’s some other STD killing tens of thousands per year to fill that gap."

They of course look contradictory at first glance, but is it possible that both claims are consistent?

My claim was about individual decision-making. Not that the effort made by researchers in developing cures, treatment or prophylaxis that reduces death rates is going to be counteracted.

For a couple of reasons the gap will not be filled:

1- 40k was a peak that triggered a reaction, we know that it crossed a threshold of tolerance for STD, and we know that that the upper bound for that threshold is 40k, but it is possible that such a threshold was lower, and that there is latency in the technologic and behavioural reaction that causes the rates to plateau and drop. If for example that threshold was 10k deaths per year, then my theory would argue that the std rate would approach the 10k threshold before triggering a reaction.

2- My claim was about individual decision-making, and I used the term STD risk, which we might naïvely mathematically model as p * QALE, where p is probability and QALE is (Quality Adjusted) Life Expectancy.

Quality of Life is part of the STD risk, and the STD risk might even be purely aesthetic without affecting health at all, for that reason, I wouldn't only measure death rates, but infection rates. So this comes down to what metric you multiply by p, I used QALE, you used LE, I would go as far as using u (utility), this would weigh low lethality and low damage STDs like mouth herpes a bit more, since they have rare complications, but are very visible, chronic, and carry 'stigma' that reduces dating/mate perceived value.

There's other differences between risk rate and lethality, especially as it relates to p and uncertainty over the future, the risk not only accounts for current incidence but for projected rates, in the middle of an epidemic one doesn't know where it will peak, and data often lags behind, 1 to 2 months of incubation period for AIDS plus procedural data gathering and publishing delays and aggregation periods. So the risk can be much higher than the incident rate suggests due to psychological uncertainty! I wasn't alive during the aids epidemic, but I read this was very documented, people were overtly cautious (for good cause).

I also assume it can work in the inverse, if there have been 20 years without an epidemic, people will get, uuhhh, 'cocky'.

3- Some stats, I'm not good at this, and there's no obvious conclusion.

https://www.cdc.gov/sti-statistics/annual/index.html

"In the United States, a total of 30,115 new cases of HPV-associated cancer were reported in 1999 and 43,371 in 2015 "

https://wonder.cdc.gov/controller/datarequest/D127;jsessioni...

Chlamydia rising a lot

https://wonder.cdc.gov/controller/datarequest/D127;jsessioni...

Diseases with similar epidemiology as AIDS dropping with ADS in the 90s, and then seeing a slow rise again.

It's worth noting that these charts don't track HPV or Herpes. I think in general medicine has a bias towards lethal diseases, which seems to explain why they were cut. (I don't think HPV was known at the time (1984-2014) to be known to have such a high lethality, and most was just attributed to cancer)

4- My theory would pose that there std risk oscillates between a high and a low threshold, even if we ignore the threshold/trigger issue and the QALE vs LE issue, then still we wouldn't expect the "gap to be filled", rather we would expect the std risk (and possibly the std rates or std lethality by proxy), to slowly rise until that risk rate, so it's not inconsistent.

Does that make sense?