Most importantly, though, that study doesn't indicate whether the effects, if they end up being reproducible, are caused by BPA alone, or the combination of BPA+sugar. It's well known in other scenarios that toxins, when combined with inflammatory foods like sugar, are far worse than they are in the absence of inflammatory foods.
I'm fairly convinced that BPA is slightly bad, I just think alternative plastics may turn out to have other compounds that are also bad, given horrible diets, and the best solution may be to fix the diet, rather than try to eliminate all toxins related to modern plastics (and the same argument may apply to pesticides). Other toxins from modern living will undoubtedly pop up, and if they all cause different and problematic diseases in combination with bad diets, but not so much in combination with good diets, how much energy do we really need to put into studying and eliminating toxins in a giant game of whack-a-mole?
This really does make sense. When that pathway is suppressed, the adipogenic program is activated, which turns on the SREBP-1 pathway and stores lipid droplets. Without this pathway activated, fructose is processed and exported out of the liver, preventing harm to the liver.
I would argue that we should really test every new manmade chemical against a library of our proteins before we synthesize anything new and introduce millions of tons of it to the world. Not doing so can have disasterous consequences.
Samuel Epstein, before he died, documented a great many examples of horror stories we just barely averted. https://www.youtube.com/watch?v=rQoc6WP3QJo
Aside from that though, there are many other mouse studies.
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2605....
As well as studies showing that BPA in human urine is associated with insulin resistance and obesity
People reach obesity from overeating, no matter what their choice of calorie-dense foods, but it's typically sugar or fats, and sugar is the cheapest/most available.
Being obese is clearly a causative factor towards T2B [1]. How are these obvious truths 'running on a treadmill'?
High fat consumption raises inflammatory profiles through mechanisms that are poorly understood. Carbohydrates seem to cause similar inflammation, but this is largely do to advanced gylcation end-products created from fructose, specifically.
Overeating is not interesting. The reason people do overeat is very interesting, and if you hit the literature you find that this is largely driven by damage to the hypothalamus by environmental exposure.
What if it's not. What if people just overeat because life is boring, and food tastes good, and we all have differing levels of willpower & education on nutrition?
> if you hit the literature you find that this is largely driven by damage to the hypothalamus by environmental exposure.
Sounds like nonsense, can you elaborate?
Then we need to explain why this suddenly became a problem in the 1970s. Life is more boring now? We all lost our willpower? People understood nutrition better before that? Something has changed, either in humanity or the environment. My bet is the environment.
Since theres no blood brain barrier here, these neurons get damaged easily due to things in the blood. When that happens, they don't see leptin anymore, and obesity develops. Fructose and high fat diets have both been shown to cause inflammation here. (hypothalamic gliosis)
heres a random selection of many papers http://diabetes.diabetesjournals.org/content/65/3/551.figure...
We also know that certain viruses show up in obese people (adenovirus36). As the field develops, I would not be surprised if labs demonstrate both viral infection of the hypothalamic ARC and damage by endocrine disruptors there.
Yes, let's ignore 50+ years of established science that is parsimonious with everything we know about the molecular biology of insulin resistance, and dump it in favor of a fringe theory, based on a single paper about a mouse study, where there's not even a plausible explanatory mechanism.
Folks, stop downvoting simply because someone provides a link. The parent is spouting pseudo-scientific nonsense.
https://www.ucsusa.org/our-work/center-science-and-democracy...
There are literally not. The review you've linked to cites a handful of papers involving minor effects observed in mouse studies.
Moreover, the paper you originally cited proves nothing even approximating a mechanism. I'm not suggesting anything about the safety of BPA, but it's utter nonsense to claim that it is a more plausible explanation for the diabetes epidemic than sugar consumption.
A few mouse studies do not change 50+ years of established science on the relationship between sugar and diabetes.
Elevated blood glucose, as in Type 2 Diabetes, has LONG been known to be primarily driven by excessive production of glucose by the liver due to liver insulin resistance. In fact, the way that the drug metformin improves diabetes is by shutting that pathway down.
http://diabetes.diabetesjournals.org/content/50/8/1807.short
Thats not dietary, thats the hormone insulin being ignored by the liver. This is further complicated by the fact that peripheral tissues, like muscle, are themselves insulin resistant.
The TCF7L2 pathway has been shown to be down-regulated in all of these tissues in diabetics.
Observing that it is downregulated in diabetics provides no evidence for or against any theories concerning BPA.
And out of a compound library of 20k chemicals, BPA had the top effect on it.
Seems significant to me
Also worth noting that BPA has been shown to specifically effect the occupancy of TCF7L2 at transcription factor binding sites in Chip-Seq experiments.
http://press.endocrine.org/doi/abs/10.1210/endo-meetings.201...
Lastly, before calling someone else's claims psuedoscientific, you may want to do some homework and check your previous biases. We could certainly use someone with your skills to help model BPAs interaction with the Androgen receptor. Might just save millions of lives....
https://www.ncbi.nlm.nih.gov/pubmed/?term=bisphenol+a
Forgive me, but I don't have time for this.
It’s pretty interesting to think about how easy it is to muddy the waters like this. Something starts off as a direct medical concern, but then sprals into a secondary contamination problem. Both are bad. Plastics are bad for a variety of reasons, and sugars definitely contribute to obesity.
But, horomonal factors really cannot be shrugged at. There’s some serious distortion affecting people for the past 20 or more years, and it’s nothing normal. Is it birth control pills being dumped down the drain, and recirculating into the drinking water? Is it ibuprofen messing with people who have over dosed on their analgesic NSAIDs?
One thing’s for sure modern civilization has inteoduced many complications, all simultaneously, and that is likely the biggest mistake of all.
Also, I’m not sure you’ve used the word “parsimonious” correctly? Are you trying to say they’ve been “very careful” or “strict”? I think it’d be more appropriate to replace it with “well aligned” or “concomitant” if a vocabulary word should be preferred.
Diabetes in Asia and the Pacific: Implications for the Global Epidemic, https://doi.org/10.2337/dc15-1536 ( http://care.diabetesjournals.org/content/39/3/472 )
Someone needs to do a dietary and sociological study of Vietnam, because it looks like they've been least affected by the diabetes epidemic, up until the early 2010s at least.
Check out this study, where they fed mice water, water+fructose, or water+fructose+BPA. At the end of the experiment, only the BPA containing solutions had elevated liver fat
https://www.sciencedirect.com/science/article/pii/S0300483X1...