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Are the negative effects of antibiotics on male fertility permanent?


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18 minutes ago, Alfred001 said:

I have been posting for two pages now about all the literature I've read on this subject. I know the subject and that various things affect sperm parameters is not a revelation to me, as I think I've made clear in the thread. What is a revelation is that amoxicillin after a single day of administration caused abnormalities in 90% of sperm. That is a figure you don't see even in animal studies where they're fed long courses of extreme doses, if you know the subject. (Setting aside that spermatogenic arrest can be induced, I'm talking strictly about the rate of abnormalities.)

So, with that in mind, I'm curious to see a study showing reversability of amoxicillin's effect on sperm parameters and/or histology of reproductive organs, because the magnitude of the effect makes me wonder.

How am I picking and choosing elements from different studies and what conclusions am I making, I haven't arrived at any conclusion?

The difference very well may be attributable to physiological differences. The only study of the impact of rifabutin on male fertility showed no effect in mice and baboons and a pretty significant effect in rats. It's possible amox has a more dramatic impact on the human reproductive system than that of the mouse. This is, of course, speculation, because we have (AFAIK) too little evidence.

The bottom line is, the only human evidence we have for amox, suggests a pretty dramatic impact on sperm parameters, way out of line with effects commonly observed in animal studies of antibiotics.

Yet clearly it has little long term effect in practice, since amoxicillin is widely prescribed (in the US, as much as 24% of all antibiotic prescriptions:https://www.definitivehc.com/resources/healthcare-insights/most-prescribed-antibiotics) and we do not see any mass outbreak of sterility in the population.

Edited by exchemist
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59 minutes ago, Alfred001 said:

How am I picking and choosing elements from different studies and what conclusions am I making, I haven't arrived at any conclusion?

The effect size in  the one human was big but it was mostly a  method paper for optimizing protein extraction and had no replicates. In the animal studies, effect size is more moderate. As we do not know what particular issues were with this person, the conclusion would be that more data is needed, especially for humans.

 

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11 hours ago, CharonY said:

 

Having difficulty posting!

Many of your posts on this thread have been very informative, balanced and representative of science.

Context is needed to interprete data.

I also agree with INow that anxiety may be leading the way in reading and interpreting the data.

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2 hours ago, exchemist said:

Yet clearly it has little long term effect in practice, since amoxicillin is widely prescribed (in the US, as much as 24% of all antibiotic prescriptions:https://www.definitivehc.com/resources/healthcare-insights/most-prescribed-antibiotics) and we do not see any mass outbreak of sterility in the population.

We went over that argument on the 2nd page, it doesn't refute the hypothesis.

1 hour ago, CharonY said:

The effect size in  the one human was big but it was mostly a  method paper for optimizing protein extraction and had no replicates. In the animal studies, effect size is more moderate. As we do not know what particular issues were with this person, the conclusion would be that more data is needed, especially for humans.

As I say, the difference in effect size could be explained by the difference in physiology. We see such different effects between species.

But, obviously, conclusions cannot be reached based on n=1, but it's the only data we have for amox in humans (that I know of) and it's worriesome.

35 minutes ago, Luc Turpin said:

I also agree with INow that anxiety may be leading the way in reading and interpreting the data.

So there's a non-anxious way of reading the data that would say there's no reason for concern here and we don't need human data?

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2 minutes ago, Alfred001 said:

We went over that argument on the 2nd page, it doesn't refute the hypothesis.

 

I may have misunderstood then. What exactly is the hypothesis that has not been refuted? 

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1 minute ago, exchemist said:

I may have misunderstood then. What exactly is the hypothesis that has not been refuted? 

That some antibiotics may permanently impair fertility in some % of people.

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9 minutes ago, Alfred001 said:

That some antibiotics may permanently impair fertility in some % of people.

OK, well in that case what I posted shows it cannot be a widespread effect, at least. But I suppose it does not rule it out as an effect in certain individuals.

 

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8 minutes ago, exchemist said:

OK, well in that case what I posted shows it cannot be a widespread effect, at least. But I suppose it does not rule it out as an effect in certain individuals.

 

Basically the point I made as well. Antibiotics use in children is rampant, a third to half of kids 4 and under are prescribed each year in the US, and in some countries the average is 5 per year

“Children in low- and middle-income countries (LMICs) are receiving an average of 25 antibiotic prescriptions during their first five years of life”

https://news.harvard.edu/gazette/story/2019/12/high-rate-of-antibiotic-use-in-low-income-countries-alarming/

https://meps.ahrq.gov/data_files/publications/st35/stat35.shtml

You’d expect to see a bigger effect in countries where more antibiotics are used. Do we see such an effect?

 

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43 minutes ago, Alfred001 said:

So there's a non-anxious way of reading the data that would say there's no reason for concern here and we don't need human data?

Analysing data without being too anxious about it, generally leads to a different understanding of the situation. I know this, because when I am anxious, I almost always get it wrong.

My take on it is that there is some, but not major concern.

We need human data; we need also other kinds of data points and analyse all of this within context.

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