BPA-free plastics leach endocrine disruptors, sometimes even moreso than plastics WITH BPA. Thoughts?


I am in love with Soylent 2.0, but this study makes me hesitant to drink it, or at least very much of it. I did read official confirmation that the plastic used in Soylent 2.0 bottles is BPA-free, but this study shows that many kinds of plastic that are BPA-free can have even more endocrine disrupting chemicals leaching out into food and water than those with BPA present.

There are two purposes I am interested in discussing in this thread:

  1. What are your thoughts on this? Is it a valid concern? What is the worst that can happen from drinking too much of these endocrine disruptors?

  2. This study’s conclusion says that they have found that there are very easy and inexpensive methods to making plastic bottles which do not have ANY endocrine disrupting chemicals. Would anyone from Soylent comment on the possiblity of the company reaching out to the manufacturers of plastic bottles to find options that are completely free of endocrine disruptors? I haven’t seen the shape of the Soylent 2.0 bottles anywhere else, so I assume they are custom made for Soylent. Would it be a possibilty for Soylent to ask their bottle manufacturer to use whatever method the researchers in this article suggest to prevent endocrine disruptors being present in the bottles?

Disclaimer: I am not trying to stir up any FUD on Soylent. I am very open to opposing views, as long as they are backed up with scientific evidence.

I think a lot of people in the Soylent community pay very careful attention to many dietary issues, so I would assume this would be a rather important issue for the community to discuss.


I trust the company to take studies like this into effect and respond appropriately. I’m not going to worry about it.

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My takeaways:

  1. There are unrecognized problematic chemicals which can cause EA
  2. BPA, being a recognized problematic chemical, is still best left out
  3. Plastics thought to be EA-free can become EA through common stresses like microwaving, UV exposure, and heating
  4. There are unrecognized nonproblematic chemicals which don’t become EA when stressed, which we should switch to using

This doesn’t impact Soylent much because the bottles are single-use, not cooked or heated, and spend all their time in a cupboard or refrigerator. Assuming the bottles were EA-free to start, which is fair given they’re BPA-free, without stresses they shouldn’t become EA.

I thought we knew all this anyway, doesn’t everyone know not to leave your water bottle in the sun or in a hot car?

edit: might as well make the bottles with a better plastic. All things being equal I’d rather use a material with at least one less known defect.


Someone posted this in another thread (forgot who, but thanks).


That’s who is bottling 2.0. Maybe ask them about it? Would be curious to see their response.

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First, I’d like to state that I’m against leachable ergogenically-active compounds in our plastics, or anywhere from where they can get into people - whether through food or other contact.

I’d like to see more and continued testing for what gets out from plastics, and which ones constitute a hazard, and what levels are necessary for a hazard to exist.

Those having been said - I think the BPA scare was overblown, and it was overblown in large part because popular bloggers and self-informed “health fanatics” made a big deal out of it. It is likely that BPA is not as bad as it was made out to be, it is likely that BPA is not the most worrisome chemical in our plastics. But the scaremongering led to a focus on BPA, and when BPA was removed from foodstuffs, people falsely felt “safe.”

As a side note, your real risk of BPA exposure never came from bottles; you are exposed to a lot more of it - and still are - from handling thermoprinted receipts from the grocery stores where you buy your BPA-free bottled goods.

I’d like to see MORE good, solid research into the problems and our materials. Research like the 2011 study that was cited here; research like the studies that have followed it.

I’d like to see LESS people picking up one study and challenging a company to address it and make their product “safer.” That just leads to the kind of knee-jerk reactions that led people to think we’ve ameliorated a huge problem by banning BPA, when it was actually a minor issue, and the time and effort spent on it distracted from the real work that needs to be done - which is to understand all the ergogenically active compounds, and what levels of them should really matter to us.


Very well said, MN, and it applies to so many “fearful things” these days.

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It is likely that BPA is not as bad as it was made out to be, it is likely that BPA is not the most worrisome chemical in our plastics. But the scaremongering led to a focus on BPA, and when BPA was removed from foodstuffs, people falsely felt “safe.”

Can I see your source on this?

As a side note, your real risk of BPA exposure never came from bottles; you are exposed to a lot more of it - and still are - from handling thermoprinted receipts from the grocery stores where you buy your BPA-free bottled goods.

Seems kind of like a false dichotomy to me. We can have a risk from both sources. Also, from what I understand, while there is a serious BPA risk from receipts, it is mainly only absorbed if you use moisturizing lotion before touching the receipt.

Again, I am not scaremongering. I am open to sources from any side.

Where does it say that these plastics only leach endocrine disruptors through microwaving, UV exposure, and heating? Just legitimately wondering about the source.

Thanks for the info. I tried using their contact form but it doesn’t even work. It amazes me how any business nowadays can not notice that their whole business’ contact form doesn’t.

It doesn’t say “only” and neither did I, but those are the ones mentioned in the study you linked.

There are chemicals which are/were used in plastic compounds that leak endocrine disruptors without being stressed, and there are some that don’t unless stressed, and according to the researchers in this paper there are some chemicals that don’t even when stressed.

E-Mail: info@jasperproducts.com

Haven’t tried the email addy or the form, but I disable scripts and cookies on most websites. No idea if any of it works or not.

We want plastiglass (plastic on the outside and glass on the inside) bottles :smile:

Or if its too expensive, how about metal bottles? With these two ,no need to recycle, RL can take them back clean them and re-use them (this will be cheaper in the longer run for RL than buying new plastic bottles everytime). From home use customers atleast. If not now by next couple of years.

I made no dichotomy at all - I’m not saying these are opposed to each other or wholly different. They are two sources which can both lead to BPA exposure. But it turns out that receipts may pose more real risk, in two ways - the BPA can get more directly to through the bloodstream, while the oral route has to go through more digestive and metabolic processes, and receipts provide a way for BPA to get into us is massively higher amounts.

There is always some absorption through the skin. The use of hand sanitizers causes the rate of absorption to skyrocket, but that’s not the same as saying there’s no absorption without the sanitizers.

The effect comes form dermal penetration enhancers which are used in sanitizers, moisturizers, and topical lotions of all kinds; these enhancers include things like propylene glycol, eugenol, some alcohols and esters, basil oil, Vitamin E - in fact, most lipids, applied topically, enhance penetration. Even “naturally oilier skin” can transfers these BPA molecules more easily. These penetration enhancers lead to easier absorption not just of BPA, but of other ergogenically-active compounds in the environment, as well.

[quote=“andrewb, post:7, topic:23602”]

On the BPA fears from the oral route (from plastic bottles, can linings, and food containers), you can look at a number of studies pursued by the FDA:


Research studies pursued by FDA’s National Center for Toxicological Research have:

Found evidence in rodent studies that the level of the active form of BPA passed from expectant mothers to their unborn offspring, following oral exposure, was so low it could not be measured. The study orally dosed pregnant rodents with 100-1000 times more BPA than people are exposed to through food, and could not detect the active form of BPA in the fetus 8 hours after the mother’s exposure.

Demonstrated that oral BPA administration results in rapid metabolism of BPA to an inactive form. This results in much lower internal exposure of BPA (i.e., the active form) than what occurs from other routes of exposure such as injection.

Found that primates (including humans) of all ages effectively metabolize and excrete BPA much more rapidly and efficiently than rodents.

Developed physiologically based pharmacokinetic models that can be used to predict the level of internal exposure to the active and inactive forms of BPA. Based on the effects of metabolism, internal exposures to the active form of BPA following oral administration are predicted to be below 1% or less of the total BPA level administered.

Recently completed a rodent subchronic study [7] intended to provide information that would help in designing a long-term study that is now underway (see below). The subchronic study was designed to characterize potential effects of BPA in a wide range of endpoints, including prostate and mammary glands, metabolic changes, and cardiovascular endpoints. The study included an in utero phase, direct dosing to pups to mimic bottle feeding in neonates, and employed a dose range covering the low doses where effects have been previously reported in some animal studies, as well as higher doses where estrogenic effects have been measured in guideline oral studies. The results of this study showed no effects of BPA at any dose in the low-dose range.

Here are the direct references for those statements:

a) Churchwell MI, Camacho L, Vanlandingham MM, Twaddle NC, Sepehr E, Delclos KB, Fisher JW, Doerge DR. Comparison of life-stage-dependent internal dosimetry for bisphenol a, ethinyl estradiol, a reference estrogen, and endogenous estradiol to test an estrogenic mode of action in Sprague Dawley rats. Toxicol Sci. 2014 May;139(1):4-20. doi: 10.1093/toxsci/kfu021. Epub 2014 Feb 4.

b) Delclos KB, Camacho L, Lewis SM, Vanlandingham MM, Latendresse JR, Olson GR, Davis KJ, Patton RE, Gamboa da Costa G, Woodling KA, Bryant MS, Chidambaram M, Trbojevich R, Juliar BE, Felton RP, Thorn BT. Toxicity evaluation of bisphenol a administered by gavage to sprague dawley rats from gestation day 6 through postnatal day 90. Toxicol Sci. 2014 May;139(1):174-97. doi: 10.1093/toxsci/kfu022. Epub 2014 Feb 4.

c) Doerge DR, Twaddle NC, Vanlandingham M, Fisher JW. Pharmacokinetics of bisphenol A in neonatal and adult Sprague-Dawley rats. Toxicol Appl Pharmacol. 2010 Sep 1;247(2):158-65.

d) Doerge DR, Twaddle NC, Vanlandingham M, Brown RP, Fisher JW. Distribution of bisphenol A into tissues of adult, neonatal, and fetal Sprague-Dawley rats. Toxicol Appl Pharmacol. 2011 Sep 15;255(3):261-70.

e) Doerge DR, Twaddle NC, Vanlandingham M, Fisher JW. Pharmacokinetics of bisphenol A in neonatal and adult CD-1 mice: inter-species comparisons with Sprague-Dawley rats and rhesus monkeys. Toxicol Lett. 2011 Dec 15;207(3):298-305.

f) Doerge DR, Twaddle NC, Vanlandingham M, Fisher JW. Pharmacokinetics of bisphenol A in serum and adipose tissue following intravenous administration to adult female CD-1 mice. Toxicol Lett. 2012 Jun 1;211(2):114-9.

g) Doerge DR, Twaddle NC, Woodling KA, Fisher JW. Pharmacokinetics of bisphenol A in neonatal and adult rhesus monkeys. Toxicol Appl Pharmacol. 2010 Oct 1;248(1):1-11.

h) Fisher JW, Twaddle NC, Vanlandingham M, Doerge DR. Pharmacokinetic modeling: prediction and evaluation of route dependent dosimetry of bisphenol A in monkeys with extrapolation to humans. Toxicol Appl Pharmacol. 2011 Nov 15;257(1):122-36.

i) Doerge DR, Vanlandingham M, Twaddle NC, Delclos KB. Lactational transfer of bisphenol A in Sprague-Dawley rats. Toxicol Lett. 2010 Dec 15;199(3):372-6.

j) Ferguson SA, Law CD Jr, Abshire JS. Developmental treatment with bisphenol A or ethinyl estradiol causes few alterations on early preweaning measures. Toxicol Sci. 2011 Nov;124(1):149-60.

k) He Z, Paule MG, Ferguson SA. Low oral doses of bisphenol A increase volume of the sexually dimorphic nucleus of the preoptic area in male, but not female, rats at postnatal day 21. Neurotoxicol Teratol. 2012 May-Jun;34(3):331-7.

l) Patterson TA, Twaddle NC, Roegge CS, Callicott RJ, Fisher JW, Doerge DR. Concurrent determination of bisphenol A pharmacokinetics in maternal and fetal rhesus monkeys. Toxicol Appl Pharmacol. 2013 Feb 15;267(1):41-8.

m) Twaddle NC, Churchwell MI, Vanlandingham M, Doerge DR. Quantification of deuterated bisphenol A in serum, tissues, and excreta from adult Sprague-Dawley rats using liquid chromatography with tandem mass spectrometry. Rapid Commun Mass Spectrom. 2010 Oct 30;24(20):3011-20.

n) Yang X, Doerge DR, Fisher JW. Prediction and evaluation of route dependent dosimetry of BPA in rats at different life stages using a physiologically based pharmacokinetic model. Toxicol Appl Pharmacol. 2013 Jul 1;270(1):45-59.


Thanks for the outstanding reply! Very edifying. Just a couple questions though:

  1. Regarding the rodent subchronic study, wouldn’t that finding be relatively meaningless since the concerns of BPA causing cancer in humans would be from a long term consumption or exposure to BPA? Rodents have much shorter life spans than humans.

  2. Even if the amount of the active form of BPA which was measured interally is 1% or less, I’m not sure what that really proves. I think it is important to execrise a certain level of criticism with most things, so with this finidng I wonder what it actually proves. Is it a constant 1% even with greatly varying levels of ingested BPA? Even if it is less than 1%, does that mean that it is not unhealthy? I am sure there are other chemicals which you could drink 1% of a certain amount which would have very bad effects on you. And who is to say that that 1% isn’t building up? If it is not building up, then wouldn’t that mean that there is really nothing to worry about since we would just excrete or urinate all the BPA out at some point anyway? If it does, wouldn’t that have major implications for our health?

  3. Wouldn’t “humans of all ages effectively metabolizing BPA much more rapidly and efficiently than rodents” mean that studying the health effects of BPA in rodents isn’t a very good method? Why not use pigs or something else?

  4. Don’t we absorb all kinds of things very easily from our mouths before ingesting them? For example, there are drugs which you don’t have to swallow, but instead just hold under your tongue and it will be absorbed directly into your bloodstream.

Just out of curiousity, I take it you are a researcher of some sort?


Wouldn’t it be a simple matter of testing V 2.0 samples for “said” chemicals to see if plastic leeching is even an issue?

Personally I’d prefer glass because it is totally inert as I’m no fan of Endocrine Disruptors, GMOs, weed killers (ex. glyphosate) or any other “additive” in our food. The only things that should be in our food is our food.

Personally, I do prefer weed killers in my Soylent. I find it gives that little ‘kick’ that I need to get up in the morning. Also adds a nice variety to the flavor. Plus… I accidentally swallowed some lemon seeds a while back and I need to make sure that I don’t have a tree growing inside of me, that would hurt!

Rodents are a well-analyzed area in science. Yes, rodents have shorter life spans, which is exactly why they are used. Research often takes several life-generation of the subject creature to produce a result. If you work with an organism with a longer lifespan, you may not get results within human lifetimes.

Also, rodents go through substantially the same processes in their short lives. They are not just shorter lives, they are faster lives, so they do as much biological “living” in that short period as we do. They may suffer “old age” in their second year, but they do so with extraordinarily similar effects to our own, including the production of cancers at the typical developmental ages.

Most importantly, BPA is not even of note as a direct carcinogen, as your statement implies. It is of note as an endocrine disruptor, and the effects of endocrine disruption can be tested in these non-human mammals, which have the same chemicals in play in their endocrine systems. For example, there was some question of BPA increasing breast cancer risk - but that was based on perinatal exposure, not based on exposure when the breast cancer develops at maturity. Exposure to an endocrine disruptor during the perinatal period (around the time of birth) changes the course of development, especially for sex-linked features, potential pre-disposing the organism to later problems, like cancers. That’s part of why the use of BPA in baby bottles was phased out so early, because that’s where the perinatal exposure was coming from, so that was the focus of the concern.

You don’t need long-term cancer studies to see whether something is an endocrine disruptor in the perinatal period.

It just means we use scaling methods to calculate comparable doses to create the same effects in humans. Again, well-studied.

Why not pigs? Compare a 25 gram mouse, housed in a shoebox, to a 68,000 gram pig (and that’s not a big pig.) Which requires more food? Water? Care? You need several thousand times the input per pig… and if the substance you’re studying is expensive, well, you still needs thousands of times as much of that, too. Study 500 mice; you can fit them in a walk-in closet. 500 pigs? You need a warehouse or a farm. Again, thousands of times the cost. And how long do you run the study, if the subject need to reach maturity or old age?

If we didn’t work with rodents, we would be able to investigate only a tiny, tiny fraction as much as we do… and the results wouldn’t be available for decades longer.

Some things, yes. Others, no. And we absorb some through the external skin, too.
That’s why we have to actually swallow Soylent to get most of the nutrition, swirling it under the tongue or applying directly to the skin does not work! But now we’re just asking general questions about “things,” and not talking about the subject in question.

Not by trade, but I spent a too many years collecting degrees and have developed some research skills which I still use.


What about this?

I would love to see Soylent partner with them and produce a bottle out of it. Obviously the capsules are small and might be weird for a lot of people, but the creative minds and scientific prowess already part of Soylent could probably advance the idea enough to make something in bottle form.