The Physics Police

The Physics Police

Monday, October 28, 2013

Protecting the Gray Wolf

I care about saving endangered species. A lot. Protecting biodiversity is imperative to human survival. That's why one of my favorite laws is the Endangered Species Act. This law aims to "halt and reverse the trend toward species extinction, whatever the cost." I dare say signing this bad-ass law was the best thing Richard Nixon ever did.

Here's how it works. When a species is listed as endangered, a recovery plan is created. This plan describes objective, measurable criteria to tell how well a species is recovering. The end goal is that species are successfully recovered and delisted.

When a species gets delisted, it's time to break out the champagne. Delisting is a declaration that we've successfully saved a species from the brink of extinction! This is not to make light of the serious business of continuing to protect all species, especially those recently delisted. Rather, it's an opportunity to show the Fish and Wildlife Service some well-deserved appreciation.

Recovery of the Gray Wolf is a wonderful yet complex example of such success. There are three distinct populations of wolves in the United States.

I will refer to the yellow areas as Great Lakes and Rocky Mountains, and to the blue area as Southwest.

The Great Lakes population was first listed as endangered in 1967, followed by the Rocky Mountain population in 1973, and finally the Southwest population in 1976.

In 1978, the whole species was listed as endangered, since each of its subspecies populations were also listed as endangered. Makes sense, right? If all the subspecies of Gray Wolves are endangered, then the whole species of Gray Wolves is endangered, too.

Well, technically, this is not how the Endangered Species Act is supposed to work. The Gray Wolf, as a whole species, is not endangered, given its abundance across the whole arctic range! So, it shouldn't be listed as endangered, just because the subspecies which happen to lie in the United States are, themselves, threatened.

By 2012, both yellow populations had recovered by the measures described in their respective recovery plans. Accordingly, they were delisted. Champagne time! But, since the majority of subspecies of Gray Wolf are now delisted, it makes even less sense to keep the species, as a whole, on the list. Taxonomical specificity is important to prevent exemptions, which nobody wants.

So, in June of 2013, the Fish and Wildlife Service proposed a rule to delist the species, on the whole, while maintaining the endangered status of the Southwest population. Sounds reasonable, right?

Well, not according to Richard Steiner, who is adamant that wolves should remain on the endangered species list. He acknowledges the restoration of those yellow populations. But he tells his readers "this success is about to be undone" by the proposed rule.

This demonstrates a lack of understanding of how the Endangered Species Act is supposed to work. Remember that, to the end of species recovery, delisting is the goal. A baseball player's running of the bases is not undone when he reaches home plate and goes back to the dugout.

Steiner talks about the "horror of wolves ... being caught in traps and snares" as though such illegal activity would be condoned by the proposed rule. It most certainly would not. In the yellow regions, states are already in full control.
Across the subspecies' range any legal take is regulated by provincial or state law to maintain sustainable wolf populations...
Steiner says that "people tend to fear and hate that which they don't understand", which is true. That's why he confuses his readers with emotionally compelling non-arguments rather than explain the real reasons for delisting. If you don't know why the Gray Wolf species is being delisted, it sounds scary!

Leda Huta thinks that the proposed rule means the Fish and Wildlife Services are abandoning Gray Wolves. They aren't. Under the proposed rule, they would continue to protect the Southwest endangered population. The proposed rule does not change the status of the yellow populations.

Delisting does not "turn the clock back", as Huta claims. It marks our progress forward.

Hunta also mentions how inhumane trapping can be. I dislike trapping for this reason. There are better methods for population management. But this isn't an argument against delisting. It's an argument for humane management! It's also an issue for states to decide on their own.

Megan Gannon posted on LiveScience that Gray Wolves may lose endangered status. In this headline, the verb is the problem. Wolves lose nothing by our taxonomical classification. Federal protections for the three distinct populations are not being changed.

However, some people believe wolves should be reintroduced to Colorado, Utah, and California. This would expand their territory, and be super awesome. I want this to happen. Sadly, delisting the Gray Wolf on the species level might make this more difficult. Does that tempt me to dislike the proposed rule? Sure, it's tempting.

That's where integrity comes in. The original classification on the species level was a mistake. This taxonomical mistake needs to be corrected. My love for wolves doesn't trick me into taxonomical dishonesty. Furthermore, it's clearly not worth it to abuse the Endangered Species Act to support one's political viewpoint. For the law to remain respected and effective, it must not be abused.

I don't need to condone Steiner's emotional non-arguments, or his slight-of-hand tricks of misinformation in order to be a good environmentalist.

My love for wolves goes back to childhood, when my pretend Native American name was Black Eagle Wolf. This love doesn't make Leda Huta's dishonest claims any more true.

So I show appreciation for the hard work done by the Fish and Wildlife Service.

I'm glad the Gray Wolf is being delisted and will continue to roam these United States.

Friday, October 18, 2013

Rats, Oreos, and Drugs

The science media circus has pitched its tent around a Connecticut College News article claiming:
Connecticut College students and a professor of psychology have found “America’s favorite cookie” is just as addictive as cocaine – at least for lab rats.
This is, of course, a false conclusion. The research by Joseph Schroeder and his students actually shows that "conditioned place preference" can be accomplished by administering addictive drugs or a food reward.

No direct comparison was made between the drugs and food.

In the presentation abstract, the researchers draw a subtly different conclusion than the article:
These findings suggest that high fat/sugar foods and drugs of abuse trigger brain addictive processes to the same degree and lend support to the hypothesis that maladaptive eating behaviors contributing to obesity can be compared to drug addiction.  
Maladaptive eating behaviors can be compared to drug addiction. This is fairly obvious, for anyone who has ever seen someone eat a whole pint of ice cream. Or eaten one, themselves.

Nobody would question the fact that food is a profound motivator. Motivation and reward are involved in addiction. But the claim that one substance is "just as addictive as" another requires evidence. This research provides no such evidence. They didn't even look for it.

Here's how the study was conducted:
On one side of a maze, they would give hungry rats Oreos and on the other, they would give them a control – in this case, rice cakes... Then, they would give the rats the option of spending time on either side of the maze and measure how long they would spend on the side where they were typically fed Oreos.

They compared the results of the Oreo and rice cake test with results from rats that were given an injection of cocaine or morphine, known addictive substances, on one side of the maze and a shot of saline on the other. Professor Schroeder is licensed by the U.S. Drug Enforcement Administration to purchase and use controlled substances for research.

The research showed the rats conditioned with Oreos spent as much time on the “drug” side of the maze as the rats conditioned with cocaine or morphine.
This is called "conditioned place preference" and is a staple of High School science projects. The conditioning worked equally well for both drugs and Oreos, so they are both equally addictive, right?


All that has been demonstrated is that drugs and Oreos both work equally well for conditioned place preference. You can't extrapolate from this to addiction!

Rats are smart. They quickly identify areas on a maze with reward. It could be cheese. It could be a shot of morphine. It could be a chocolate chip cookie. Or an oatmeal cookie. Or an Oreo cookie.

If the rats ran the maze equally well for cheese as Oreos, would we, by the transitive property of addiction, conclude that cheese is "just as addictive" as cocaine? I think not.

If you wanted to actually compare Oreos to drugs, you would have to administer Oreo plus the saline control on one side of the maze, and drugs plus the control cracker on the other side. The researchers didn't perform this test.

Why not? Because they weren't studying the relative addictive properties of drugs and food in the first place. They were studying the nucleus accumbens!
Stimulation of the nucleus accumbens by addictive substances, including high fat/sugar foods triggers expression of immediate early genes, the measurement of which can be used as an indicator of cellular activation. 
Their experimental design was setup to demonstrate this hypothesis.

But "Nucleus accumbens C-Fos expression is correlated with conditioned place preference" isn't a headline that pops. So they added misleading language into their conclusion, and hooked up with Amy Martin, the Manager of Media Relations at Connecticut College.

Together, they produced this garbage news article, which was quickly picked up by the media.

Now, we have crazy headlines like Will Oreos Be Outlawed Next? and Lab rats find Oreos more pleasurable than drugs. This isn't just annoying and wrong. It's dangerous. The constant stream of bad science from the media harms people's brains. Bad science teaches people bad thinking patterns. The end results are bad decisions that harm individuals and the society as a whole. This is not just about one brand of cookies. It's not okay to lie to people and call it science.

Injecting Oreos with drugs because, why not?

Oh, and where was this study published, you ask?

Nowhere. It's not peer-reviewed. It's unpublished.

It's not even science.

It's careerism and dishonesty.

Okay, now I want Oreos.

UPDATE: I called Deborah MacDonnell, the Director of Public Relations at Connecticut College, and voiced my concerns about the article. She told me that "Connecticut College stands behind [Joseph Schroeder's] research." So much for their reputation.

Weight in an Elevator

According to their website, Science World is a Canadian nonprofit that engages people in science and inspires future science and technology leadership. They are famous for something called ambient marketing, where they put up entertaining and often funny posters and other types of media in an urban setting. Clearly, their goal is to get people's attention on science. I like it.

However, some of their media boast dubious scientific claims. I also found one that was simply incorrect. This scale was placed inside an elevator:

You weigh less on the way down.

The purpose of this seems to be drawing attention to the Elevator Problem. This physics thought experiment considers the effect of Newton's second law on the forces felt in an elevator. When you are accelerating upward, you feel heavier. When you are accelerating downward, you feel lighter.

This particular ad confuses velocity for acceleration.

Consider a trip from the 2nd floor to the 3rd floor. When the doors close, you are rest, using the building as a reference frame. You are also at rest, hopefully, before the doors open again. On this trip, the elevator had to accelerate upwards to begin moving, then decelerate, to stop.

This happens when you drive a car, too. Going from stop light on 2nd street to the stop light at 3rd street, you hit the gas to accelerate, drive one block, then hit the break to stop. When you hit the gas, if you drive anything like I do, you can feel your head pushed back into the headrest. When you hit the breaks, your head is pushed forward a bit.

Saying that "you weigh less on the way down" is like saying your head is pressed against the headrest going towards downtown. That's silly, because the same is true going the other way. It's not which direction you're moving, it's which direction you're accelerating!

On the way down, you weight less, then more.

On the way up, you weigh more, then less.

Since this bothered me enough to blog about it, clearly their marketing campaign is a success.

Thursday, October 3, 2013

Glyphosate and Aflatoxin

Misrepresentation of science really pisses me off. I'm tired of talking about GMOs. These days, though, the topic is just too ripe with science abuse for me to ignore. Sayer Ji of Green Med Info is one of the worst offenders.

In a recent blog post titled Study Links Roundup 'Weedkiller' To Overgrowth of Deadly Fungal Toxins, he references a study published by an Argentinian team in the Journal of Environmental Science and Health which concludes:
... that these Aspergillus flavus and A. parasiticus strains are able to grow effectively and produce aflatoxins in high nutrient status media over a range of glyphosate concentrations under different water activity conditions.
It's not surprising that fungus can grow in high nutrient media, with or without the presence of an herbicide. You see, glyphosate isn't simply a poison. It's a chemical that interferes with the production of aromatic amino acids in plants, and only in plants. It is not a fungicide, so it doesn't kill fungus!

The interesting thing about this study is that the growth of these fungi was actually increased by glyphosate. This stimulation of soil biology is a feature of glyphosate, not a bug. The proliferating fungi attack dying weeds, completing the nitrogen cycle.

It's also important to notice that while growth was stimulated, aflatoxin production was not:
Aflatoxin B1 production did not show noticeable differences among different pesticide concentrations assayed at all aW in both strains.
So, why did glyphosate stimulate these fungi to grow, anyway? It's possible that growth stimulation may have been nutritional, not enzymatic. Before administering the glyphosate, fungi were starved overnight to halt their growth. This is standard practice in microbiology to establish an adjacent control colony which experienced identical conditions.

If the growth-limiting nutrients in this study were phosphorus or carbon, then digestion alone could explain the stimulated growth. Yes, fungi can eat glyphosate!

That raises the question, what were the concentrations of glyphosate used in this study?
The glyphosate increased significantly the growth of all Aspergillus section Flavi strains in different percentages with respect to control depending on pesticide concentration. At 5.0 and 10 mM this fact was more evident; however significant differences between both concentrations were not observed in most strains.
That unusual unit mM stands for millimolar. So, is this dose environmentally relevant?
(10 mM) * (169.07 g/mol) = 1,691 mg/L = 1,691 ppm
That's a thousand times larger than the tolerance on corn forage, 13 ppm!

So, we certainly can't conclude anything about human exposure, in food, from this in vitro study.

Nevertheless, Ji concludes that glyphosate is:
... seriously undermining the quality of our global food supply, and may help to explain recent observations that GM corn heavy markets, such as the U.S., have a significant aflatoxin problem.
This is a strong accusation, not at all justified from this one study. Let's take a look at another, older study published in 2007 by the USDA. Like the Argentinian study, this one looked at fungi aflatoxin production in a Petri Dish. They didn't find any.
No aflatoxin production was detected on water agar regardless of strain or glyphosate treatment.
They also tested glyphosate on soil fungi. It didn't effect them, and they explained why.
In soil, no effect of glyphosate was observed on the recovery of A. flavus cfu from soil regardless of rate, formulation or time after treatment. Glyphosate is readily bound by soil colloids and less material would be bioavailable to interfere with growth.
Finally, they looked for significant contamination in real-life corn fields. They didn't find any.
Although mycotoxin contamination was minimal in the 4 years of this study, there was no evidence that rotation of corn with cotton had any affect on reducing inoculum potential in soil and there was no consistent effect of glyphosate on propagule density of A. flavus. 
Clearly, the use of glyphosate on corn crops doesn't put humans at risk from aflatoxin poisoning.

Then, what does cause dangerously high aflatoxin production? According to Cornell:
Water stress, high-temperature stress, and insect damage of the host plant are major determining factors in mold infestation and toxin production. Similarly, specific crop growth stages, poor fertility, high crop densities, and weed competition have been associated with increased mold growth and toxin production
Weed competition! Hey, you know what's good at fighting weeds? Herbicides.

Herbicides kill plants, not fungus.

Or people!

Tuesday, October 1, 2013

Titanium Dioxide

The motto of the shock blog Green Med Info is "education equals empowerment". Its founder, Sayer Ji (one of the worst human beings alive), has a degree in Philosophy with a specialty in existential phenomenology. Naturally, this makes him an expert in the study of molecular biology. Did I say expert? I meant dangerous know-nothing.

In a recent post, he asks the villainous and leading question Why Is The Food Industry Poisoning Us With Trillions of Nanoparticles?

The short answer is, of course, they're doing no such thing!

The nanoparticles in question are titanium dioxide, a white pigment used as a food additive. These particles are manufactured using chemical processes from rocks called ilmenite and rutile.

Nanotechnology is not involved in their manufacture. However, the resulting molecules are small. Normal people call that a "powder" but I guess you can call them "nanoparticles" because many are 100 nanometers in size.

Of course, lots of things we eat are less than 100 nanometers in size. When you caramelize sugars with heat, for example, carbon nanoparticles are produced. Is the food industry poisoning us with grilled onions and caramel candy? Other nanoparticles commonly found in nature include water ice in clouds, smoke from a fire, volcanic ash, ocean spray, fine sand and dust, and even viruses.

Clearly, particle size alone is no way to evaluate food safety.

Let's take a look at the science.

The recent study cited in this post is titled Effects of titanium dioxide nanoparticles in human gastric epithelial cells in vitro, and was published by a Portuguese team in the journal Biomedicine & Pharmacotherapy.
Our results demonstrate for the first time that nanoparticles induce tumor-like phenotypes in human gastric epithelial cells.
As the title suggests, it examined the effect of titanium dioxide nanoparticles on cell lines taken from human stomach lining, which are a specialized type of skin cells. The "tumor-like phenotypes" observed were DNA damage, oxidative stress, and increased cell proliferation. Sounds scary, right?
 Well, don't worry. These results are completely irrelevant to dietary sources! There are two major differences between the form of titanium dioxide that makes white pigment used in foods, and the stuff exposed to in this study.

First, the nanoparticles used in this study are engineered, industrial grade particles smaller than 25 nanometers, and have regular geometric shapes. The food additive particles are largely around 100 nanometers, and have irregular shapes. The biological action of these two, very different products are not comparable.

Second, the concentrations of nanoparticles in the study are ludicrously high. DNA damage and oxidative stress were seen only at a 15% solution. That's a really high concentration, environmentally unrealistic when compared with the 0.1% concentration in many whitened food products. Some products have much less, like Nestle Original Coffee Creamer, for example, which only has 0.004% titanium dioxide.

Cell proliferation, on the other hand, became significant around 6%.

Still, we know that oxidative stress, DNA damage, increased cell proliferation are involved in the formation of cancer, right? So, does this study show that high concentrations of engineered titanium dioxide nanoparticles are a carcinogen?

No. Here's the problem with that interpretation. The study used AGS cells, which are line of human stomach cancer cells. Yes, cancer cells. (Remind you of Séralini?)

To attribute the "tumor-like phenotype" of these cancer cells to the act of drowning them in white pigment is just ridiculous!

They were cancer before you painted them white!

In my opinion, the cell proliferation is easily explained by the oxidative stress. This is a well known phenomena, and makes sense for tissues that need to quickly regrow after being damaged. The stomach lining exactly fits that bill. Except, in this example, since titanium is so easily chelated, cell death is minimal. This results in a weird situation for these cells, indeed.

Consider, though, how contrived is this experiment. Results relied on nanoparticles of just the right size (25 nanometers) and shape (Degussa showed dose-response, Sigma did not). Statistically significant results were seen only at extremely high concentrations (6% solution).

Sounds like a lot of fine-tuning, doesn't it? Wait, there's more!

The team's first attempt failed to find increased cell proliferation:
First, we used RPMI supplemented with FBS for the suspension of TiO2 nanoparticles. This treatment caused no alteration on cell proliferation. These results are explained by the effect of the protein adsorption ability of metal oxide nanoparticles on the cytotoxicity.
FBS stands for fetal bovine serum. Basically, this is the food they used to wake up the starved cells, so they would keep growing. When they performed the experiment the first time around, the presence of proteins in the FBS prevented the nanoparticles from causing cell damage.

These proteins seem to be sticky to the nanoparticles used. They act like sponges, having a tenancy to round up nanoparticles. Like a sort of molecular lint roller, this seems to have been enough to prevent any significant damage to the cells.

Consider that, inside your gut, there are a lot of proteins and other potentially sticky things, like bacteria. After all, it's pretty messy in there! This same protective effect would likely keep your cells from absorbing too much titanium, even if you chugged a tall glass of white paint.

Consider, also, that your gut epithelium is a type of tissue called a mucous membrane. It secretes a mucus made up of, among other things, mucin proteins. These presumably act as an effective barrier protecting the stomach lining from damage due to ingested nanoparticles.

After all, evolution has adapted the gut to handle nanoparticles from ingested dust, dust, soot, and dissolved metal oxides in water.

Nanotechnology is new, and its development and use should be performed cautiously, especially when human exposure is possible.

Let's not get distracted by fear mongers like Sayer Ji, frantically grasping at straws in order to push their anti-science, anti-medicine agenda.

Titanium dioxide is far better than the zinc- and lead-based pigments it replaces.

In reasonable quantities, it's safe to ingest, just like iron oxide, or any other trace mineral.

Before I end this post, I want to share one more funny story involving titanium nanoparticles.

Rightfully published in the "rumors" section of MSN News is an article by Sally Deneen titled Toxic nanoparticles are entering the food supply. The article includes this tangled paragraph:
Titanium dioxide, a common additive in kid-tempting candies, marshmallows, icing and more, says this study, was found in recent studies to inflame rats' lungs when non-food-grade nano-sized titanium dioxide is inhaled, Kavanagh said. Whether eating it causes problems is being investigated in animal studies, he said, all of which tend to use high doses.
As the article disclaims, this study, too, uses engineered titanium dioxide particles, less than 25 nanometers in size, administered in high doses. At least, for the sake of relevance, it's performed on mammals, not cancer cells.

Of course the article does get everything else wrong. The results were negative for rats. It was the lungs of mice, not rats, where an effect was identified. Also, inflammation was not directly measured, but inferred from the ratio of neutrophils to other types of white blood cells.

In this study, too, we see the same shady pattern, where they didn't get desired results, so they tuned the experiment to fit their preconceived conclusion:
The first round of in vivo studies involved three independent labs, all of which used SD rats that were exposed to either TiO2-P25 or TiO2-A in DM. None of the treatment groups reported statistically significant changes in lung inflammatory parameters relative to DM controls; therefore, the scope of the consortium studies was expanded to include another rat strain (F344) and another species (mouse, C57BL6).
Rats didn't work? Let's try more, different rats. Oh, and mice too. Because, why not, right?

Three different doses were administered to the poor mice, 10, 20, or 40 micrograms. This was mixed with 100% ethanol and sprayed into their lungs. Sorry, mice. A statistically significant raise in neutrophils was only seen at the highest dose.

For fun, let's scale up this dose proportionately from a 25 gram mouse to a 75 kg human.

How much Nestle Original Coffee Creamer would I have to inhale, to inflame my lungs?

((40 µg / 25 g) * (75 kg)) / ((0.04 µg/mg) * (1,000 kg/m³)) = 3 Liters

That's a lot of coffee creamer to snort!

Don't try this at home.