4 ms·

Even if sperm count doesn't impact overall male fertility, the fact that sperm count is declining potentially indicates some type of endocrine disruption. Also,

by sumy23 4y ago

Even if sperm count doesn't impact overall male fertility, the fact that sperm count is declining potentially indicates some type of endocrine disruption. Also, your comment kind of glosses over the fact that though-to-be cause hormonal interference were found at levels 17 times what is considered safe in the median sample from the study.

mike_hearn 4y ago
The point of the scientists quoted above is that those aren't safe assumptions. 1. Sperm count might not be falling at all. 2. If it is, that might be some sort of natural variation, or an effect rather than a cause (maybe sperm counts fall if you aren't regularly impregnating women, which is to some extent a social choice). 3. Even if there is a natural cause, it might not be chemicals. 4. Even if it is, that might not actually be a problem worth worrying about. "17 times what is considered safe" Considered safe by who? Epidemiologists?
- sumy23 4y ago
  > Considered safe by who? Epidemiologists? Did you read the paper? The authors specifically chose chemicals that have been shown to reduce male sperm counts. The hazard levels they chose were based on the observed effects on sperm production from those studies. We know these chemicals reduce sperm count and they are being found in high quantities in urine, so it doesn't seem likely that the measured decrease in sperm is due to measurement error or some other cause.
  - mike_hearn 4y ago
    "The authors specifically chose chemicals that have been shown to reduce male sperm counts" No, they chose chemicals that predictive modelling claims would reduce male sperm counts. This is epidemiology remember, they hardly care about real experiments. From their cited paper Kortenkamp2020: "combinations of chemicals with different mechanisms of action are predicted that should result in cumulative effects. These predictions are then mapped against evidence from experimental mixture studies with relevant combinations" If we check the Table 2 RfD data to explore the citations, e.g. for the very first entry in the table, we find: "Due to variations in the no-observed adverse effect levels (NOAELs) in high confidence studies, possible reference doses ranged from 0.0001 to 0.0099 μg/kg/d. In choosing 0.003 μg/kg/d we struck a balance between caution suggested by studies at the lower end of the doses and the weight of evidence from studies with higher NOAEL. BPA exposures currently experienced by European populations and beyond are in excess of 0.003 μg/kg/d ... The precise mechanisms by which BPA affects semen quality are not resolved" So their figure for safe BPA exposure level is made up. The evidence gave them an enormously varied range of possibilities, and they picked one of the lowest values allowable given that evidence because they wanted to incorporate "caution", and - totally coincidentally - because that level would let them say that most Europeans are being exposed to dangerous levels (according to their made up estimate). They also have no idea how this is meant to work biologically, which raises the risk of a correlation=causation fallacy, and their direct evidence comes from studies on baby rats. They exclude experiments on adult rats because, well, who the hell knows, they don't explain that, and they then go to include epidemiological studies on adult men so it's not like there's anything meaningful behind that choice. One might ask whether this evidence tells us much about humans given the frequency with which cancer has been successfully cured in rats. So what about the evidence from people? "In adult men, the best timing of exposure measurements would be around 90 days before taking a semen sample, because spermatogenesis takes approximately 75 days, with an additional 12 days of maturation as the sperm travels through the epididymis. However, none of the eligible studies adopted such a timing. Instead, most studies collected urine samples for BPA measurements at the same time, or near the time of semen analysis" So their studies aren't measuring sperm counts at the right time and they know this, but use the data anyway. Where do they find these men? "These studies are case-control, cohort or cross-sectional with participants drawn from the general population, occupational cohorts, or couples from infertility clinics" Infertility clinics! With epidemiology papers it's always like this. We learned that from COVID. You don't actually need to read the work of these sorts of 'scientists' to know they're going to be filled with wild suppositions, unverified assumptions, garbage quality data and nonsensical methodologies. It's just a totally corrupt field. Life is too short to double check everything coming out of public health research; at some point we have to learn to stop listening.

by sumy23 4y ago

mike_hearn 4y ago

The point of the scientists quoted above is that those aren't safe assumptions. 1. Sperm count might not be falling at all. 2. If it is, that might be some sort of natural variation, or an effect rather than a cause (maybe sperm counts fall if you aren't regularly impregnating women, which is to some extent a social choice). 3. Even if there is a natural cause, it might not be chemicals. 4. Even if it is, that might not actually be a problem worth worrying about. "17 times what is considered safe" Considered safe by who? Epidemiologists?

sumy23 4y ago
> Considered safe by who? Epidemiologists? Did you read the paper? The authors specifically chose chemicals that have been shown to reduce male sperm counts. The hazard levels they chose were based on the observed effects on sperm production from those studies. We know these chemicals reduce sperm count and they are being found in high quantities in urine, so it doesn't seem likely that the measured decrease in sperm is due to measurement error or some other cause.
- mike_hearn 4y ago
  "The authors specifically chose chemicals that have been shown to reduce male sperm counts" No, they chose chemicals that predictive modelling claims would reduce male sperm counts. This is epidemiology remember, they hardly care about real experiments. From their cited paper Kortenkamp2020: "combinations of chemicals with different mechanisms of action are predicted that should result in cumulative effects. These predictions are then mapped against evidence from experimental mixture studies with relevant combinations" If we check the Table 2 RfD data to explore the citations, e.g. for the very first entry in the table, we find: "Due to variations in the no-observed adverse effect levels (NOAELs) in high confidence studies, possible reference doses ranged from 0.0001 to 0.0099 μg/kg/d. In choosing 0.003 μg/kg/d we struck a balance between caution suggested by studies at the lower end of the doses and the weight of evidence from studies with higher NOAEL. BPA exposures currently experienced by European populations and beyond are in excess of 0.003 μg/kg/d ... The precise mechanisms by which BPA affects semen quality are not resolved" So their figure for safe BPA exposure level is made up. The evidence gave them an enormously varied range of possibilities, and they picked one of the lowest values allowable given that evidence because they wanted to incorporate "caution", and - totally coincidentally - because that level would let them say that most Europeans are being exposed to dangerous levels (according to their made up estimate). They also have no idea how this is meant to work biologically, which raises the risk of a correlation=causation fallacy, and their direct evidence comes from studies on baby rats. They exclude experiments on adult rats because, well, who the hell knows, they don't explain that, and they then go to include epidemiological studies on adult men so it's not like there's anything meaningful behind that choice. One might ask whether this evidence tells us much about humans given the frequency with which cancer has been successfully cured in rats. So what about the evidence from people? "In adult men, the best timing of exposure measurements would be around 90 days before taking a semen sample, because spermatogenesis takes approximately 75 days, with an additional 12 days of maturation as the sperm travels through the epididymis. However, none of the eligible studies adopted such a timing. Instead, most studies collected urine samples for BPA measurements at the same time, or near the time of semen analysis" So their studies aren't measuring sperm counts at the right time and they know this, but use the data anyway. Where do they find these men? "These studies are case-control, cohort or cross-sectional with participants drawn from the general population, occupational cohorts, or couples from infertility clinics" Infertility clinics! With epidemiology papers it's always like this. We learned that from COVID. You don't actually need to read the work of these sorts of 'scientists' to know they're going to be filled with wild suppositions, unverified assumptions, garbage quality data and nonsensical methodologies. It's just a totally corrupt field. Life is too short to double check everything coming out of public health research; at some point we have to learn to stop listening.