Did you know we’re in the midst of a vitamin D deficiency epidemic? By the standards of the Endocrine Society, 80% of Americans have inadequate vitamin D levels. You better go buy some pills! You better buy Michael Holick’s books! He’s the guy who is obsessed with warning everyone about their dangerously low vitamin D, and he’s not kooky at all.

The Boston University endocrinologist, who perhaps more than anyone else is responsible for creating a billion-dollar vitamin D sales and testing juggernaut, elevates his own levels of the stuff with supplements and fortified milk. When he bikes outdoors, he won’t put sunscreen on his limbs. He has written book-length odes to vitamin D, and has warned in multiple scholarly articles about a “vitamin D deficiency pandemic” that explains disease and suboptimal health across the world.

His fixation is so intense that it extends to the dinosaurs. What if the real problem with that asteroid 65 million years ago wasn’t a lack of food, but the weak bones that follow a lack of sunlight? “I sometimes wonder,” Holick has written, “did the dinosaurs die of rickets and osteomalacia?”

I’ve seen this phenomenon in educated people before: they latch onto one explanation for something, and suddenly they apply it to everything, regardless of the evidence or lack thereof, and insist that it is the One True Theory, and all must bow before it. For other examples, see the Aquatic Ape Absurdity and Brian Ford’s Bullshit. It’s the lure of the Umbrella Hypothesis, braced by a little factlet of truth.

So yes, you can be deficient in vitamin D, and it can lead to real diseases. It’s just that here in developed countries with actual policies that lead to reasonable monitoring and addition of supplements to key foods (milk has been supplemented with vitamin D for over a hundred years to prevent rickets), we’re fine. You don’t need to go to extremes to correct an imaginary deficiency.

Except that inventing imaginary problems and selling the cure is extremely profitable.

Since 2011, Holick’s advocacy has been embraced by the wellness-industrial complex. Gwyneth Paltrow’s website, Goop, cites his writing. Dr. Mehmet Oz has described vitamin D as “the No. 1 thing you need more of,” telling his audience that it can help them avoid heart disease, depression, weight gain, memory loss and cancer. And Oprah Winfrey’s website tells readers that “knowing your vitamin D levels might save your life.” Mainstream doctors have pushed the hormone, including Dr. Walter Willett, a widely respected professor at Harvard Medical School.

He’s been getting paid a thousand dollars every month for his vitamin D promotion! He’s received hundreds of thousands of dollars from pharmaceutical companies! The tanning bed industry donated $150,000 to his research!

I’ve been missing out on the gravy train, and I’ve got to start hawking my own supplement. I thought of one. You know, I bet you’ve eaten hardly any spiders lately. It’s true, isn’t it — they aren’t part of our usual cuisine, and no one spices their food with ground-up spider bits, except for those wierdos in Cambodia, so I can argue without being gainsaid that almost all of us have a spider deficiency. I can even make up statistics, like that 99.7% of Americans haven’t eaten any spider at all lately, and trust that no one will say I’m wrong.

Now I just need a common disease that I can blame entirely on arachnoinsufficiency, and before you know it, Gwyneth Paltrow will be knocking on my door.

A creationist told me I had to explain the origin of life to him. So I did.

There’s this article in the popular press titled “Scientists calculate the speed of death in cells, and it’s surprisingly slow”, and the title is backwards. It’s summarizing an article in Science magazine which measured the speed of a wave of apoptotic signaling in dying cells that concludes the exact opposite: cells die fast.

Apoptosis is an evolutionarily conserved form of programmed cell death critical for development and tissue homeostasis in animals. The apoptotic control network includes several positive feedback loops that may allow apoptosis to spread through the cytoplasm in self-regenerating trigger waves. We tested this possibility in cell-free Xenopus laevis egg extracts and observed apoptotic trigger waves with speeds of ~30 micrometers per minute. Fractionation and inhibitor studies implicated multiple feedback loops in generating the waves. Apoptotic oocytes and eggs exhibited surface waves with speeds of ~30 micrometers per minute, which were tightly correlated with caspase activation. Thus, apoptosis spreads through trigger waves in both extracts and intact cells. Our findings show how apoptosis can spread over large distances within a cell and emphasize the general importance of trigger waves in cell signaling.

To put that in context, 30 µm/min is more than 40,000 µm/day, or 40mm/day. Back in the day when I’d stick proteins in one end of a cell and wait for them to get to the other end, we’d estimate that the rate of transport was a couple of millimeters per day — so if you were working with an axon that was a couple of centimeters long, you might have to wait a week or two for a complete traverse. I’m impressed with 30 µm/min.

Another way to look at it is that if your typical cell is about 10µm across, once the apoptotic enzymes in one spot are activated, the whole cell is self-destructing in 20 seconds. The pop sci article uses a different example: “That means, for instance, that a nerve cell, whose body can reach a size of 100 micrometers, could take as long as 3 minutes and 20 seconds to die.” That’s still fast. That’s faster than diffusion. The authors ruled out diffusion as the mechanism, and suggest that it’s a wave of activation.

The unusual size of the Xenopus egg raises the question of how an all-or-none, global process such as apoptosis spreads through the cell. One possibility is that apoptosis spreads through the egg by random walk diffusion, ultimately taking over all of the cytoplasm. A second possibility is suggested by the existence of multiple positive and double-negative feedback loops in the regulatory network that controls apoptosis. These loops may allow apoptosis to propagate through self-regenerating trigger waves. Trigger waves are propagating fronts of chemical activity that maintain a constant speed and amplitude over large distances. They can arise when bistable biochemical reactions are subject to diffusion or, more generally, when bistability or something akin to bistability (e.g., excitability or relaxation oscillation) is combined with a spatial coupling mechanism (e.g., diffusion or cell-cell communication). Familiar examples include action potentials; calcium waves; and the spread of a fire through a field, a favorable allele through a population, or a meme through the internet. Trigger waves are an important general mechanism for long-range biological communication, and apoptotic trigger waves may allow death signals to spread rapidly and without diminishing in amplitude, even through a cell as large as a frog egg.

That makes sense. The apoptotic enzymes are distributed throughout the cell in an inactive state at all times; you don’t have to physically move the proteins around, you just have to switch one on, which then switches on its neighbor, which switches on its neighbor, and so on.

I’ve seen many cells die, as I’m watching them in the microscope. It’s always impressively swift and thorough: one minute, round, plump healthy cell; next minute, membranes are blebbing out all over the place, the cytoplasm goes all granular and curdled, and at the speed of light I’m cussing over yet another failed experiment.

I’m not sure why the editor or whoever slapped that confusing title on the article. There may have been some confusion about scale: a 2 meter tall human doesn’t die by the propagation of a signal from a single point on a cell, spreading at a rate of 40mm/day (if it worked that way, you’d stub your toe, a cell would die, and you’d have to wait a month and a half for the death signal to reach your brain). That would be slow. Multicellular organisms die by systemic failure of a network, not the progressive collapse, cell by cell, of all of its components.

I was asked to summarize my Ph.D. thesis research…I usually think of this kind of question as more relevant for someone currently or recently working on their thesis, but hey, OK, I can take a trip down memory lane.

Man, memory lane keeps getting longer and longer. This was 3 or 4 decades ago.

I’d love to know what this dark matter stuff is, and you know that physicists want to know even more.

So, why does dark matter, matter, anyway? Well, this stuff makes up a huge chunk of the Universe, and we want to know what the Universe is made of. If it turns out to be an elementary particle that isn’t part of the Standard Model of particle physics, then that means the Standard Model is wrong, and we’ve got some cool new physics! If, on the other hand, it somehow turns out to be that our understanding of gravity is fundamentally flawed, we still get new physics. And new physics is always exciting! Either way, it’s about learning about our Universe. Think about it: right now, the stuff we know and are familiar with accounts for just 5% of the Universe’s contents. Imagine what ticking off another 25% of the Universe would mean. Don’t know? Neither do I, but that’s what’s so exciting about it! My bet is that it’s a new particle, and the Standard Model is wrong. Maybe it’ll be SIDM, maybe WIMPs, or Kaluza-Klein dark matter. Maybe it’ll be several types of dark matter, with new forces in the dark sector; I mean, why shouldn’t it be, when the visible sector is a particle zoo? Whatever it turns out to be, unraveling this mystery will be a ground-smashing achievement in the world of physics.

That comes from a pretty good summary of many of the current models for dark matter (well, I thought it was an informative summary, but I’m a biologist, so what do I know?). Some day I’m going to need a physicist to sit down with me over a beer and explain this stuff in little words.

After that blustering buffoon badgering bison, it would be nice to see a thoughtful man behaving competently. How about this? Mark Levy was one of 21 pilots flying WWII aircraft in a British airshow, when the engine on his P-51 conked out, and he had to sputter to a landing in a cornfield. And best of all, there’s full cockpit video of the whole thing! You get to watch these magnificent old planes flying in formation, and then crisis as the engine begins to fail (and you know the pilot is going to be fine).

It’s less than two minutes between engine failure and grinding to a stop in a cornfield, but the video goes on for over a half hour as the pilot discusses what he was thinking and what he did and what his concerns and priorities were. I don’t know about you, but I love this stuff: glamorous machines and thoughtful people behind them.

I’m also even more impressed with the WWII pilots. Imagine managing this beast while other airplanes are shooting at you, over ground with big anti-aircraft guns intentionally trying to knock you out of the sky.