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Nutrition Facts - Glyphosate Series Part 3 dropped
I'm somewhat surprised (pleasantly) by the quantitative emphasis and sharing of the Zoller and Connolly publications. Few understand there importance and how these represent important data poorly handled by the ECHA/EFSA assessments that rely heavily on rodent bioavailability. I would also note some surprise in the citations. Pointing out conflicts of interest has its place (both sides), but too often it seems to substitute for evaluating the actual evidence. Seriously ➡️ assess the data. Play the ball, not the players.
Zoller O, Rhyn P, Zarn JA, Dudler V. Urine glyphosate level as a quantitative biomarker of oral exposure. Int J Hyg Environ Health. 2020 Jul;228:113526. doi: 10.1016/j.ijheh.2020.113526. Epub 2020 Apr 16. PMID: 32305862. doi.org/10.1016/j.ijheh…
Zoller (2020) can be supported by Faniband (2021)
Faniband MH, Norén E, Littorin M, Lindh CH. Human experimental exposure to glyphosate and biomonitoring of young Swedish adults. Int J Hyg Environ Health. 2021 Jan;231:113657. doi: 10.1016/j.ijheh.2020.113657. Epub 2020 Oct 30. PMID: 33130428. doi.org/10.1016/j.ijheh…
What isn't discussed here and matters
how current reference values and regulatory limits are based on clinical signs and observations rather than mechanistic biomarkers (or cancer risk, see OEHHA NSRL discussions, statement of reasons);
whether the 'threshold of toxicological concern' framework is even applicable here, given PK-based exclusion criteria;
the bone-retention signal that "no bioaccumulation" talking points gloss over, compounded by the absence of validated PBPK models; and
how in vitro in vivo techniques and data feed into toxicological and regulatory risk assessments, and how these are routinely extrapolated across gaps that can span several orders of magnitude and
how discussions real-world exposure concentrations and the microbiome narrative, ignores basic biochemistry and microbiology.
rarely considers the feedback regulation of the shikimate pathway,
that a substantial fraction of human gut microbes do not possess a complete shikimate pathway, or
that estimated human gut concentrations following typical exposures are likely to be only a tiny fraction of experimentally determined minimum inhibitory concentrations (MICs).
Details that matter when evaluating biological plausibility (and toxicological sciences).
Do the Math:
Start from known dietary exposure, use 1–3% oral bioavailability (or go ahead and use 30%), and you can get a reasonable estimate of absolute peak blood levels (Cmax). Then realize that these real-world dietary exposures are a small fraction of the MRL such that actual Cmax values likely fall in the ng/mL–pg/mL range. These steps are almost always missing from both scientific and lay treatments and publications. Mechanistic findings and observations at millimolar-to-molar in vitro concentrations tell you almost nothing about physiological plausibility until someone does that arithmetic. I’m not disparaging in vitro data like many others, or make statements like ‘only in mice’, but do ask at what concentrations observations are made and what is expected, ordinarily, or actually achievable at the target sites. - There is so much more, but I’ll stop for today.
<I did run a ‘fact check’ and ‘critique’ on my note, also pleasantly surprised, will post follow-up & did see the Forbes opinion on glyphosate - pretty poor>