Are the BPA-Free Plastics Like Tritan Safe?

Do BPA-free plastics such as Tritan, have human hormone-disrupting effects? And what about BPS and BPF?

Recent human studies indicate that exposure to the plastics chemical BPA may be associated with infertility, miscarriage, premature delivery, reduced male sexual function, polycystic ovaries, altered thyroid and immune function, diabetes, heart disease, and more. Yet, “[a]s recently as March 2012, FDA stated that low levels of BPA in food are considered safe.” However, just months later, to its credit, the agency banned the use of BPA plastics in baby bottles and sippy cups. Regulators standing up to industry? Maybe I shouldn’t be so cynical! But, wait. The ban was at the behest of the plastics industry. It had already stopped using BPA in baby bottles so it was their idea to ban it.

The industry had switched from BPA to similar compounds like BPF and BPS. So, our diets now contain everything from BPA to BPZ, and the majority of us have these new chemicals in our bodies as well. Are they any safer?

As I discuss in my video Are the BPA-Free Alternatives Safe?, based on the similarities of their chemical structures, they are all predicted to affect testosterone production and estrogen receptor activity, as you can see at 1:40 in my video. However, they were only recently put to the test.

As you can see at 1:50 in my video, we’ve known BPA significantly suppresses testosterone production, and, from “the first report describing BPS and BPF adverse effects on physiologic function in humans,” we know those compounds do, too. Well, kind of. The experiments were performed on the testicles of aborted human fetuses. But, the bottom line is that BPS and BPF seem to have “antiandrogenic anti-male hormone effects that are similar to those of BPA.” So when you’re assured you shouldn’t worry because your sales slip is BPA-free, the thermal paper may just contain BPS instead. What’s more, BPS receipts may contain up to 40 percent more BPS than they would have contained BPA. So BPA-free could be even worse. In fact, all BPA-replacement products tested to date released “chemicals having reliably detectable EA,” estrogenic activity.

This includes Tritan, which is specifically marketed as being estrogen-activity-free. As you can see at 3:06 in my video, however, researchers dripped an extract of Tritan on human breast cancer cells in a petri dish, and it accelerated their growth. This estrogenic effect was successfully abolished by an estrogen blocker, reinforcing it was an estrogen effect. Now, the accelerated growth of the cancer cells from the Tritan extract occurred after the plastic was exposed to the stressed state of simulated sunlight. Only one out of three Tritan products showed estrogen activity in an unstressed state, for instance when they weren’t exposed to microwaving, heat, or UV rays. “Because there would be no value in trading one health hazard for another, we should urgently focus on the human health risk assessment of BPA substitutes.”

In the meanwhile, there are steps we can take to limit our exposure. We can reduce our use of polycarbonate plastics, which are usually labeled with recycle codes three or seven, and we can opt for fresh and frozen foods over canned goods, especially when it comes to tuna and condensed soups. Canned fruit consumption doesn’t seem to matter, but weekly canned vegetable consumption has been associated with increased BPA exposure. If you do use plastics, don’t microwave them, put them in the dishwasher, leave them in the sun or a hot car, or use once they’re scratched. But using glass, ceramic, or stainless steel containers is probably best.


For more on BPA, check out my videos:

Unfortunately, BPA isn’t the only plastics chemical that may have adverse health effects. See:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

One Way to Treat Asthma and Autoimmune Diseases with Diet

Cutting two teaspoons of salt’s worth of sodium from one’s daily diet can significantly improve lung function in asthmatics

In the 1960s and 1970s, a mystery was emerging. Why were childhood asthma rates between 2 to 5 percent in the developed world but as low as 0.007 percent in the developing world? For example, in the developing world, instead of 1 in 20 kids affected, or even 1 in 50 kids, it could be more like 1 in 10,000 kids—extremely rare. And, when kids moved from a low-risk area to a high-risk area, their risk went up. What was going on? Were they exposed to something new? Did they leave some protective factor behind?

As I discuss in my video How to Treat Asthma with a Low-Salt Diet, all the way back in 1938, scientists showed they could stop asthma attacks by lowering children’s sodium levels. That was done with a diuretic drug, but subsequent dietary experiments showed that diets high in salt seemed to increase asthmatic symptoms, while “lowering the salt decreased the asthmatic symptoms…” This body of evidence was apparently forgotten…until it was picked up again in the 1980s as a possible explanation for why Western countries had higher asthma rates.

Maybe it was the salt.

As you can see at 1:34 in my video, researchers graphed out childhood death from asthma versus family salt purchases, and it seemed more salt meant more death. Just because a family buys more salt doesn’t necessarily mean the kids are eating more, though. The way to find out how much salt someone is eating is to collect their urine over a 24-hour period and measure the amount of sodium, since how much salt we eat is pretty much how much salt we excrete. The way to test for asthma, called a bronchial challenge test, is to look for an exaggerated response to an inhaled chemical. And, indeed, there was a strong correlation between how their lungs reacted and how much sodium they were taking in. However, there are all sorts of food additives, like preservatives, that can trigger these so-called hypersensitivity reactions, so maybe high sodium intake was just a marker for high processed food intake. Maybe it wasn’t the salt at all.

Or maybe it was other components of the diet. For example, the reason sodium may be a risk factor for another inflammatory disease, rheumatoid arthritis, may be that sodium intake is just a marker for increased fish and other meat intake or decreased fruit and vegetable intake. We needed a study where researchers would take asthmatics, change the amount of salt in their diets, and see what happened—and that’s just what came next.

As you can see at 3:16 in my video, researchers doubled the salt intake of ten asthmatics, and lung sensitivity worsened in nine out of ten. There was no control group, though. Is it possible the subjects would have gotten worse anyway?

In a randomized, double-blind, placebo-controlled trial, researchers put everyone on a low-salt diet, but then gave half of the subjects sustained-release sodium pills to bring their salt intake back up to a more normal level and the other half a placebo. After five weeks, the groups switched regimes for another five weeks. That’s how you can randomize people to a true low-sodium diet without them even realizing it. Genius! So what happened? Asthmatics on the salt got worse. Their lung function got worse, their asthma symptoms got worse, and they had to take more puffs on their inhalers. This study compared asthmatics consuming about three teaspoons’ worth of salt a day to those consuming less than one, so they were effectively able to drop their sodium intake by two teaspoons’ worth of salt, as you can see at 4:04 in my video. If you do a more “pragmatic” trial and only effectively reduce people’s salt intake by a half a teaspoon a day, it doesn’t work.

Even if you are able to cut down your sodium intake enough to get a therapeutic effect, though, it should be considered an adjunct treatment. Do not stop your asthma medications without your doctor’s approval.

Millions suffer from asthma attacks triggered by exercise. Within five minutes of starting to exercise, people can get short of breath and start coughing and wheezing such that lung function significantly drops, as you can see at 0:19 in my video Sodium and Autoimmune Disease: Rubbing Salt in the Wound?. On a high-salt diet, however, the attack is even worse, whereas on a low-salt diet, there’s hardly a significant drop in function at all. To figure out why, researchers had the subjects cough up sputum from their lungs and found that those on the high-salt diet had triple the inflammatory cells and up to double the concentration of inflammatory mediators, as you can see at 0:43 in my video. But why? What does salt intake have to do with inflammation? We didn’t know…until now.

“The ‘Western diet,’ high in saturated fatty acids and salt, has long been postulated as one potential…cause for the increasing incidence of autoimmune diseases in developed countries…” The rapidly increasing incidence of autoimmune diseases may be due to an overactivation of immune cells called T helper 17 (Th17) cells. “The development of…multiple sclerosis, psoriasis, type I diabetes, Sjögren’s syndrome, asthma, and rheumatoid arthritis are all shown to involve Th17-driven inflammation,” and one trigger for the activation of those Th17 cells may be elevated levels of salt in our bloodstream. “The sodium content of processed foods and ‘fast foods’…can be more than 100 times higher in comparison to similar homemade meals.”

And, sodium chloride—salt—appears to drive autoimmune disease by the induction of these disease-causing Th17 cells. It turns out there is a salt-sensing enzyme responsible for triggering the formation of these Th17 cells, as you can see at 2:07 in my video.

Organ damage caused by high-salt diets may also activate another type of inflammatory immune cell. A high-salt diet can overwork the kidneys, starving them of oxygen and triggering inflammation, as you can see at 2:17 in my video. The more salt researchers gave people, the more activation of inflammatory monocyte cells, associated with high-salt intake induced kidney oxygen deficiency. But that study only lasted two weeks. What happens over the long term?

One of the difficulties in doing sodium experiments is that it’s hard to get free-living folks to maintain a specific salt intake. You can do so-called metabolic ward studies, where people are essentially locked in a hospital ward for a few days and their food intake is controlled, but you can’t do that long term—unless you can lock people in a space capsule. Mars520 was a 520-day space flight simulation to see how people might do on the way to Mars and back. As you can see at 3:17 in my video, the researchers found that those on a high-salt diet “displayed a markedly higher number of monocytes,” which are a type of immune cell you often see increased in settings of chronic inflammation and autoimmune disorders. This may “reveal one of the consequences of excess salt consumption in our everyday lives,” since that so-called high-salt intake may actually just be the average-salt intake. Furthermore, there was an increase in the levels of pro-inflammatory mediators and a decrease in the level of anti-inflammatory mediators, suggesting that a “high-salt diet had a potential to bring about an excessive immune response,” which may damage the immune balance, “resulting in either difficulties on getting rid of inflammation or even an increased risk of autoimmune disease.”

What if you already have an autoimmune disease? In the study titled “Sodium intake is associated with increased disease activity in multiple sclerosis,” researchers followed MS patients for a few years and found that those patients eating more salt had three to four times the exacerbation rate, were three times more likely to develop new MS lesions in their brains, and, on average, had 8 more lesions in their brain—14 lesions compared to 6 in the low-salt group. The next step is to try treating patients with salt reduction to see if they get better. But, since reducing our salt intake is a healthy thing to do anyway, I don’t see why we have to wait.


What else can we do for asthma? See:

Have you heard that salt reduction was controversial? That’s what the processed food industry wants you to think. Check out the science in:

What are some of the most powerful dietary interventions we have for autoimmune disease? See, for example:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

How to Foster a Healthy Gut Flora

What’s more important: probiotics or prebiotics? And where can we best get them?

“Virtually every day we are all confronted with the activity of our intestine, and it is no surprise that at least some of us have developed a fascination for our intestinal condition and its relation to health and disease.”

“Over the last years the intestinal microbiota [our gut flora] has been identified as a fascinating ‘new organ’” with all sorts of functions. Well, if the bacteria in our gut make up an entire, separate organ inside our body, what about doing an organ transplant? I discuss this in my video How to Become a Fecal Transplant Super Donor.

What would happen if you transferred intestinal bacteria from lean donors into obese subjects? Researchers figured that rebalancing the obesity-causing bacteria with an infusion of gut bacteria from a lean donor might help. They had wanted the study to be placebo-controlled, which, for drugs is easy, because the control subjects can just be given a sugar pill. But, when you’re inserting a tube down people’s throats and transplanting feces, what do you use as the placebo—or poocebo, if you will? Both the donors and the subjects brought in fresh stools, and the subjects were randomized to either get a donor’s stool or their own collected feces. So, the placebo was simply getting their own stool back.

What happened? As you can see at 1:32 in my video, the insulin sensitivity of the skinny donors was up around 50, which is a good thing. High insulin sensitivity means a low level of insulin resistance, which is the cause of both type 2 diabetes and prediabetes. The obese subjects started out around 20 and, after an infusion of their own feces, stayed around 20. The group of obese donors getting the skinny fecal infusion similarly started out low but then shot up near to where the slim folks were.

It’s interesting that not all lean donors’ stools conveyed the same effect on insulin sensitivity. Some donors, the so-called super-fecal donors, had very significant effects, whereas others had little or no effect, as you can see at 2:02 in my video. It turns out this super-donor effect is most probably conveyed by the amounts of short-chain fatty acid-producing intestinal bacteria in their feces. These are the food bacteria that thrive off of the fiber we eat. The short-chain fatty acids produced by fiber-eating bacteria may contribute to the release of gut hormones that may be the cause of this beneficial, improved insulin sensitivity.

“The use of fecal transplantation has recently attracted considerable attention because of its success in treatments as well as its capacity to provide cause–effect relations,” that is, cause-and-effect evidence that the bacteria we have in our gut can affect our metabolism. Within a few months, however, the bacterial composition returned back to baseline, so the effects on the obese subjects were temporary.

We can get similar benefits by just feeding what few good gut bacteria we may already have. If you have a house full of rabbits and feed them pork rinds, all the bunnies will die. Yes, you can repopulate your house by infusing new bunnies, but if you keep feeding them pork rinds, they’ll eventually die off as well. Instead, even if you start off with just a few rabbits but if you feed them what they’re meant to eat, they’ll grow and multiply, and your house will soon be full of fiber-eating bunnies. Fecal transplants and probiotics are only temporary fixes if we keep putting the wrong fuel into our guts. But, by eating prebiotics, such as fiber, which means “increasing whole plant food consumption,” we may select for—and foster the growth of—our own good bacteria.

However, such effects may abate once the high-fiber intake ceases. Therefore, our dietary habits should include a continuous consumption of large quantities of high-fiber foods to improve our health. Otherwise, we may be starving our microbial selves.


The microbiome is one of the most exciting research areas in medicine these days. For more information, see, for example:

For more on health sources of prebiotics, check out:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations: