A Polar Affair
Lloyd Spencer Davis
Pegasus Books, $29.95

On March 29, 1912, British explorer
Robert Falcon Scott wrote the final diary entry of his ill-fated quest to reach
the South Pole. That same day, more than 350 kilometers away, naval surgeon and
zoologist George Murray Levick was hunkered down within a snowbank at Cape
Adare, observing Adélie penguins.

Levick had accompanied Scott to
Antarctica, but was not one of the five expedition members on the final trek to
the pole. The return journey claimed the lives of all five. Levick survived the
expedition, however, and in 1914, published a manuscript summarizing his
observations — the first scientific descriptions of Antarctic penguins.

But he left something out.

During his months observing Adélie
penguins, which included an entire breeding cycle, Levick witnessed the birds
engaging in same-sex mating rituals. He also saw the birds engage in a variety
of other sexual behaviors that in humans we might call promiscuity, infidelity,
even prostitution. Levick recorded these scandalous details in a second
manuscript, “The sexual habits of the Adélie penguin,” in 1915. But the
manuscript was stamped “Not for Publication” and remained unpublished for
nearly a century.

In 2012, the manuscript resurfaced in a
scientific journal. Penguin biologist and author Lloyd Spencer Davis, who had
thought he was the first to record same-sex behavior in Antarctic penguins in
1996, was dismayed and intrigued. So Davis embarked on a personal quest to
understand how and why Levick’s observations had been buried in the first place
— seemingly by his own wishes.

The result of that quest is Davis’ book
A Polar Affair, an entertaining, chatty and sometimes salacious romp
through polar exploration history, penguin biology and Victorian mores.

Each of the book’s five sections opens
with a brief essay — Homosexuality, Divorce, Infidelity, Rape, Prostitution — that
highlights how tempting it can be, whether in Victorian or modern times, to
view penguin sexual behaviors through an anthropomorphic lens.

But the driving force of A Polar
Affair isn’t really to understand these sexual behaviors, Davis writes.
Instead, what he really wants to understand is “why Murray Levick would
discover the dirty side of penguins and then try to cover it up.”

Davis delves into Levick’s personal
history, hunting down his field notes and retracing his long, frostbitten
months studying Cape Adare’s penguin colony.

Davis’ investigations are interspersed
with a sweeping history of polar exploration that is by turns fascinating and
frustrating. He also includes stories from his own penguin studies. The
narrative meanders through the exploits of a wide-ranging cast of explorers who
have since lent their names to bits of Antarctica’s geography, from James Clark
Ross to Fabian Gottlieb von Bellingshausen.

Early expeditions led to key
innovations to manage challenges such as the bitter cold and ever-present
nutrient deprivation. And many of those innovations, we learn, came to bear in
the 1911–1912 race to the South Pole between Robert Falcon Scott and Norwegian
Roald Amundsen. (Amundsen got there first, beating Scott by about one month.)
This rich and often intimate history can be riveting stuff. But much of it is
also well-trodden ground, and at times, I found myself flipping ahead, wanting
to get back to Levick and his penguins.

Other digressions, though, particularly
Davis’ discussions of whether there are evolutionary benefits to penguins’ same-sex
mating or nonmonogamous behaviors, are fascinating. Is same-sex mating a case
of mistaken identity, in that male and female penguins are monomorphic, looking
much alike? Is promiscuity among penguins related to the female’s inclination
to build a stronger nest, one that is shored up by stones earned through
offering sex?

These are questions with which Davis and other penguin biologists still wrestle. And A Polar Affair doesn’t come to a tidy answer for why Levick suppressed his most startling findings. But the book’s unique approach to polar exploration history makes for an engaging read. And by the end, Davis does come to terms with his need to understand his predecessor and with his own dismay at being scooped a century ago. The journey in discovery, he suggests, was satisfying. “It doesn’t really matter who was the first to see a bit of male-on-male action in penguins,” he writes, “any more than it probably matters who was first to stand on an arbitrary piece of ice and drive a flagpole into it.”

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Trends in inequality, Science News, December 6, 1969 —

The share of the total national income going to the poorest 20 percent of the [United States] has increased very little in the past 20 years … only from 5.1 to 5.4 percent … between 1947 and 1967. The proportion of the low-earning group that is nonwhite has remained at about 21 percent, which is more than twice the proportion of nonwhite families in the country as a whole. And census figures reveal that a greater proportion of the bottom fifth … reside in the South.

Update

There’s still a wide gap between the haves and the have-nots in the United States. In 2018, the lowest-earning fifth of the population earned only about 3 percent of the nation’s total income, while the highest-earning fifth raked in about 52 percent. 

Income disparities between racial groups have also endured, according to U.S. Census Bureau data. In 2018, the average income was about $87,200 for Asian American households, $70,600 for white households, $51,500 for Hispanic households and $41,400 for black households. Poverty rates follow a similar trend: about 10.1 percent of Asian, 8 percent of white, 17.6 percent of Hispanic and 20.8 percent of black households fell below the poverty line, in which a household’s income isn’t enough to meet the family’s basic needs. 

America’s poorer populations are still concentrated in the South. In 2018, residents of the Northeast, West and Midwest earned an average $70,100, $69,500 and $64,100, respectively. Those in the South earned a substantially lower $57,300. Southern communities also suffer higher poverty rates — about 13.6 percent in 2018, compared with 10.3, 11.2 and 10.4 percent in the Northeast, West and Midwest, respectively. And those regional contrasts could become more severe with climate change (SN: 6/29/17). 

Being
single-celled doesn’t necessarily doom a creature to a simple life. A fresh
look at a long-dismissed, century-old experiment suggests that so-called primitive
organisms can behave in surprisingly complex
ways.

Stentor roeseli, a tiny trumpet-shaped protist, can dodge,
duck or flee in response to an irritating stimulus,
changing its behavior when one strategy fails, researchers report online
December 5 in Current Biology. The study suggests that single
cells, rather than being preprogrammed to react in a certain way, are capable
of “changing their minds” based on experience.

“This fascinating
experiment reminds us that primitive organisms can do complicated things,” says
Sindy Tang, a cellular engineer at Stanford University who wasn’t involved in
the study.

S. roeseli rose to prominence in 1906, when the American zoologist Herbert
Spencer Jennings described
some of the most complex behaviors ever reported for a
single-celled organism. The millimeter-long freshwater protist spends much of
its life fastened to drifting algae, using hairlike cilia on its body to sweep
food into its mouth.

Jennings messed with S.
roeseli, disturbing them with a pipette-delivered stream of a chemical
irritant. Instead of simple reflexive behaviors, he documented a complex
hierarchy of avoidance tactics. First, the protist would bend to dodge the
onslaught. If that failed, it would repel the irritant by using its cilia to “spit”
water out of its mouth. When Jennings persisted, it would contract its whole
body to shrink away. Its final act was to escape by detaching from its
substrate and floating away. 

At the time,
biologists considered single cells to be capable only of rudimentary behaviors,
such as moving toward or away from some stimulus. Consequently, Jennings’ work
garnered much attention. But attempts to replicate it failed, and eventually
his observations were dismissed.

But when Jeremy Gunawardena, a systems biologist at Harvard Medical School in Boston, learned of Jennings’ work from a colleague’s lecture, “I was surprised and immediately fascinated,” he says. It suggested that single cells can have a sort of autonomy that we don’t consider nowadays.” Gunawardena tracked down some of the major replication studies and noticed a major flaw: They all used a different species of Stentor with a more mobile lifestyle than S. roeseli.

With the right species in hand, Gunawardena and his colleagues set out to replicate the century-old experiment. Instead of chemicals, they shot pulses of tiny plastic beads at S. roeseli each time the cells appeared to be in a resting state and recorded their behaviors.

Over 57 experiments,
the researchers observed each of the behaviors first described by Jennings, but
noted substantially more variability than in the original experiment. Some of
the cells repeated the same steps or skipped some altogether. 

Initially the
researchers were puzzled. But when they analyzed the behaviors of all S.
roeseli used in the experiments, a hierarchy emerged. More often than not,
an irritated S. roeseli cell will first bend away or try to spit out the
beads. Then, it will either contract or detach, but the researchers never saw a
cell detach without contracting first.

These results suggest
that S. roeseli can, in a sense, change its mind about how to respond to
an irritant, the researcher say. “We showed that a single cell is capable of
fairly sophisticated decision-making,” Gunawardena says. 

The team was
especially surprised to find that, after contracting once, there’s a 50-50
chance that S. roeseli will either contract again or detach. That’s a
decision-making process that seems akin to flipping a coin. Such
unpredictability could give S. roeseli an advantage in keeping predators
on their toes, Gunawardena says.

Kirsty Wan, a
biophysicist at the University of Exeter in England, welcomes revisiting
Jennings’ work. It’s “a great start toward understanding how these particular
cells make decisions,” she says. Using software to denote certain behavioral
states, instead of relying on a researcher’s subjective assessment, could
strengthen future studies, she says.

Gunawardena hopes this study will push biologists to think about cells differently. Rather than being genetically programmed to respond uniformly to some stimulus, he says individual cells might instead be programmed with “machinery that allows the cell to have some autonomy about what it does depending on the context.”

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Call it a comeback — maybe. After being shelved earlier this year for lackluster preliminary results, a drug designed to slow Alzheimer’s progression is showing new signs of life. A more in-depth look at the data from two clinical trials suggests that patients on the biggest doses of the drug, called aducanumab, may indeed benefit, the company reported December 5. 

People who took the highest
amounts of the drug declined about 30 percent less, as measured by a commonly
used Alzheimer’s scale, than people who took a placebo, Samantha Haeberlein of the
biotechnology company Biogen reported at the Clinical Trials on Alzheimer’s
Disease meeting in San Diego. With these encouraging results in hand, Biogen,
based in Cambridge, Mass., plans to seek drug approval from the U.S. Food and
Drug Administration in early 2020.

The results are
“exhilarating, not just to the scientific community but our patients as well,”
Sharon Cohen, a behavioral neurologist at the Toronto Memory Program, said during
a panel discussion at the meeting. Cohen participated in the clinical trials
and has received funding from Biogen.

The presentation marks “an
important moment for the Alzheimer’s field,” says Rebecca Edelmayer, director of
scientific engagement for the Alzheimer’s Association in Chicago. Alzheimer’s
disease slowly kills cells in the brain, gradually erasing people’s abilities to
remember, navigate and think clearly. Current Alzheimer’s medicines can hold
off symptoms temporarily, but don’t fight the underlying brain destruction. A
treatment that could actually slow or even stop the damage would have a “huge
impact for patients and their caregivers,” she says.

If confirmed, the results
also bolster the idea that the build-up of amyloid, a sticky protein that
accumulates in the brains of people with Alzheimer’s, is a key early step
of the disease, as opposed to a red herring, as some have argued (SN: 2/25/11).

Aducanumab is an antibody
designed to target both small clusters and larger clumps of amyloid, called
fibrils, for removal. But the drug has had a roller coaster history. Early on, the
drug was shown to clear amyloid
from the brain (SN: 8/31/16). Researchers
launched two phase III trials, designed
to prove a drug’s worth by pitting it against standard treatments or a placebo,that enrolled people around age 70 who showed early signs of
Alzheimer’s. Preliminary data from those two trials showed that the drug was
unlikely to hit its goals of slowing symptoms along with the underlying brain
signs of the disease more than a placebo treatment.

Those lackluster findings
led Biogen to stop the trials in March before they were finished.

But then in October, after rolling
in three more months of data that became available after the initial analyses, Biogen
decided that the drug showed promise after all, particularly among people who
received the highest dose, which was 10 milligrams of the drug per kilogram of
body weight. The company had decided midway through the trial to increase the
doses of some people who had previously been assigned to lower doses for fear
of side effects.

Updated results included a
total of 3,285 people who had early signs of cognitive slipping. Surveys
measured participants’ abilities on six aspects of life, including memory,
orientation, personal care and problem solving. Analyses on a subset of 288
people in one trial who received the highest dose showed that, while they still lost some mental
abilities over the year and a half of the study, they declined 30 percent less than those who received the placebo. A
similar subset of 282 people in the other trial declined 27 percent less than
those who took a placebo. Brain scans showed that, compared with people on the
placebo, the brains of people taking aducanumab had less amyloid — and less tau, another protein associated with
Alzheimer’s. Both the tau and amyloid results indicate that the drug was in
fact slowing the disease.

The treatment did cause some
side effects. Around 40 percent of the people who received the highest dose of
aducanumab showed signs of brain swelling or bleeding, brain scans revealed.
Most didn’t exhibit any symptoms of those problems, though.

The extent of improvement
seen in these results, particularly on measurements of day-to-day abilities, is
“a big deal,” Cohen says. “Those of us who know this disease well know what it
means to lose yourself slice by slice. Anything you can hang onto, and do well,
is a triumph.”

Two major changes to the trials
— the change in dosing midway through and the trials’ early ends — complicate
the analyses. Those complexities, and the whiplash they have caused, has left
some researchers wary of the newest results.

Neurologist Samuel Gandy, of the Icahn School of Medicine at Mount Sinai in New York City, is withholding judgement until more data is available. Biogen ought to share its data with other scientists for independent analyses, as it did with a different Alzheimer’s drug called solenezumab, he says. “This complete open sharing is now the gold standard, and is especially important for aducanumab, where there now exists such controversy,” he says.

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