Is Stephen Hawking Full of Sh*t?

He knows more about cosmology, general relativity, and quantum gravity than anyone on Earth. And yet the famed physicist recently offered an incredibly reductionist theory on obesity. We ran with it. Here’s our extended “correction” of the record.


Here’s a mea culpa for a Wednesday morning.

Every once in a while — my editors would probably say I underestimate — I allow sanctimony to get the better of reason.

Even in this space, which is dedicated to science, technology, and innovation, sometimes fervor overcomes data.

That’s what happens when we abandon rationality and do stuff like make specious appeals to authority, for example.

I plead guilty to the charge of committing that logical fallacy in highlighting Stephen Hawking’s latest pronouncement on great threats to humanity.

The bottom line is this: Obesity may not be about eating too much and moving too little.

It doesn’t take a Ph.D. in theoretical physics to understand this particular problem. It might, however, require one in endocrinology.

That’s what I learned after reading an excerpt from Sylvia Tara’s new book The Secret Life of Fat: The Science Behind the Body’s Least Understood Organ and What It Means for You.

Tara — who received her Ph.D. in biochemistry from my alma mater, the University of California, San Diego, and also earned an MBA from the Wharton School at the University of Pennsylvania — details compelling research that suggests a virus first found in chickens causes fat to accumulate in humans.

Wired published the excerpt, “The Mysterious Virus That Could Cause Obesity,” on December 27, 2016, the day Tara’s book was published.

It doesn’t take a Ph.D. in theoretical physics to understand this particular problem. It might, however, require one in endocrinology.

“Patient Zero” in this story is a former Illinois farm boy who was once skinny and industrious. One morning, while doing his morning chores, he was clawed by “a particularly large and perturbed rooster.” He was never the same.

“Some days later,” Tara writes, “Randy noticed a change in his appetite. He was constantly hungry. He felt drawn to food and thought about it all the time. He started eating in between meals and overeating when he finally sat down to dinner.”

Over the next year or so, Randy, who was 11 at the time of the rooster incident, gained about 10 pounds. Despite earnest efforts and the support of his family, by the time he reached his teens, he was 30–40 pounds overweight.

The bottom line is this: Obesity may not be about eating too much and moving too little.

Eventually, in his late 30s, he crossed the 300-pound threshold.

Later, when he submitted a urine sample and then a blood sample as part of an application for a commercial driver’s license, Randy learned his glucose levels were extraordinarily high.

He was an extreme diabetic.

And then his doctor referred him to University of Wisconsin-Madison endocrinologist Dr. Richard Atkinson, who along with postdoctoral fellow Nikhil Dhurandhar had already established some fascinating connections between obesity and a chicken virus.

Dhurandhar needed to know whether what seemed possible — “that sneezing on somebody can transmit obesity” — could be validated with human data.

Dhurandhar’s Ph.D. work in India provided some of the most remarkable data, as he conducted a series of experiments designed to understand the pathology of a virus spreading through the Indian poultry industry.

Here’s Tara’s description of the series of events:

Dhurandhar pushed ahead and arranged an experiment using 20 healthy chickens. He infected half of them with SMAM-1 and left the other half uninfected. During the experiment, both groups of chickens consumed the same amount of food. By the end of the experiment, only the chickens infected with the SMAM-1 virus had become fat. However, even though the infected chickens were fatter, they had lower cholesterol and triglyceride levels in their blood than the uninfected birds. “It was quite paradoxical,” Dhurandhar remembers, “because if you have a fatter chicken, you would expect them to have greater cholesterol and circulating triglycerides, but instead those levels went in the wrong direction.”

To confirm the results, he set up a repeat experiment, this time using 100 chickens. Again, only the chickens with the SMAM-1 virus in their blood became fat. Dhurandhar was intrigued. A virus, it seemed, was causing obesity. Dhurandhar thought of a way to test this. He arranged three groups of chickens in separate cages: one group that was not infected, a second group that was infected with the virus, and a third group that caged infected and uninfected chickens together. Within three weeks, the uninfected chickens that shared a cage with infected ones had caught the virus and gained a significant amount of body fat compared to the isolated uninfected birds.

Fat, it seemed, could indeed be contagious.

That’s pretty crazy stuff.

Dhurandhar needed to know whether what seemed possible — “that sneezing on somebody can transmit obesity” — could be validated with human data.

Turns out it certainly could.

After he came under Dr. Atkinson’s wing here in the States, Dhurandhar’s testing focus shifted to the human adenovirus Ad-36.

As Tara notes: “It turned out that Ad-36 had similar qualities to SMAM-1 in chickens. Atkinson thought Ad-36 might very well be a mutated form of SMAM-1. When Dhurandhar infected chickens with Ad-36, their fat increased and their cholesterol and triglycerides decreased, just as had happened with SMAM-1.”

Dhurandhar and Atkinson then shifted from chickens to humans.

They “found that 30% of subjects who were obese tested positive for Ad-36, but only 11% of nonobese individuals did — a 3-to-1 ratio. In addition, nonobese individuals who tested positive for Ad-36 were significantly heavier than those who had never been exposed to the virus.”

Here’s Atkinson explaining the relationship between a virus and obesity:

There are three ways that we think Ad-36 makes people fatter:

(1) It increases the uptake of glucose from the blood and converts it to fat; (2) it increases the creation of fat molecules through fatty acid synthase, an enzyme that creates fat; and (3) it enables the creation of more fat cells to hold all the fat by committing stem cells, which can turn into either bone or fat, into fat. So the fat cells that exist are getting bigger, and the body is creating more of them.

Randy’s relationship with Atkinson is the point of my comeuppance. The doctor was not judgmental. He was solution-oriented, constructive.

“Fat shaming” — writing stuff with headlines like “Want to Save the World? Get off Your Ass!” — is anti-science.

My wife is Philadelphia born and bred; she and I met as first-year students at Villanova University School of Law. We’re Flyers fans.

So intellectual honesty requires that I cop to worshiping at the altar of Stephen Hawking, a tremendous astrophysicist, sure, but certainly no endocrinologist.

Our daughter — who got her start in the Philly suburbs but is now most definitely a northern Virginian — is a fervent Washington Capitals fan.

She had a babysitting gig one night during her winter break from classes at James Madison University. As it happened, the Caps were playing the New Jersey Devils that night and fell behind 1-0.

I texted her teasingly: “Dude, what’s the score of the Caps game.”

We settled the fact that I did indeed know the score.

The next day, I followed up with: “I can’t believe you didn’t call me out for not using a question mark when I asked if you knew the score of the Caps game last night.”

“Are you calling yourself out?” she replied.

“It would be intellectually dishonest if I did not… So the answer to your question is yes.”

So intellectual honesty requires that I cop to worshiping at the altar of Stephen Hawking, a tremendous astrophysicist, sure, but certainly no endocrinologist.

As Atkinson notes for Tara: “People are really stuck on eating and exercise as the only contributors to fatness. But there is more to it.”

But it’s Dhurandhar who really sums it all up: “Science is not about belief, it is about fact.”


NBNBC

Mayfield Robotics was founded in 2015 with significant financial support from global technology outfit Bosch’s Startup Platform.

Yesterday, Mayfield introduced Kuri, “a loyal little home robot with a cheerful personality.”

Here’s IEEE Spectrum’s Evan Ackerman’s description:

Kuri has some fairly sophisticated technology inside of it. Besides what you’d expect (a camera, microphone array, speakers, and touch sensors), Kuri also has some sort of “laser-based sensor array” that it uses for obstacle detection, localization, and navigation. If Kuri can map your house by itself and then remember where things are, that would be slick, and we’re looking forward to seeing how much autonomy is there. We’re also unsure how much of what Kuri does relies on the cloud, but we do know that it’ll run for a couple hours straight, and then autonomously recharge itself on a floor dock.

Besides mobility, what makes Kuri unique is the fact that it has no display (besides a color-changing light on its chest), and that it doesn’t even try to talk to you, as Pepper and Jibo do. There’s speech recognition, but Kuri won’t talk back, instead relying on a variety of beepy noises and its expressive head and eyes to communicate. Essentially, it’s R2-D2-ing, which is a verb now, meaning to have effective nonspeech interactions.

Smart Investing,

David Dittman
Editorial Director, Wall Street Daily

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He knows more about cosmology, general relativity, and quantum gravity than anyone on Earth. And yet the famed physicist recently offered an incredibly reductionist theory on obesity. We ran with it. Here’s our extended “correction” of the record. Here’s a mea culpa for a Wednesday morning. Every once in a while — my editors would...

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