9.6 to 12.3 billion people on Earth by year 2100? — 80 percent probability, says a study based on United Nations population data through 2012

© 2014 Peter Free

Citation — to study

Patrick Gerland, Adrian E. Raftery, Hana Ševčíková, Nan Li, Danan Gu, Thomas Spoorenberg, Leontine Alkema, Bailey K. Fosdick, Jennifer Chunn, Nevena Lalic, Guiomar Bay, Thomas Buettner, Gerhard K. Heilig, and John Wilmoth, World population stabilization unlikely this century, Science [Express], DOI: 10.1126/science.1257469 (18 September 2014)

Citation — to press release

Hannah Hickey, World population to keep growing this century, hit 11 billion by 2100, University of Washington (18 September 2014)

Method and findings

From the abstract:

The United Nations recently released population projections based on data until 2012 and a Bayesian probabilistic methodology. Analysis of these data reveals that, contrary to previous literature, world population is unlikely to stop growing this century.

There is an 80% probability that world population, now 7.2 billion, will increase to between 9.6 and 12.3 billion in 2100.

This uncertainty is much smaller than the range from the traditional UN high and low variants.

© 2014 Patrick Gerland, Adrian E. Raftery, Hana Ševčíková, Nan Li, Danan Gu, Thomas Spoorenberg, Leontine Alkema, Bailey K. Fosdick, Jennifer Chunn, Nevena Lalic, Guiomar Bay, Thomas Buettner, Gerhard K. Heilig, and John Wilmoth, World population stabilization unlikely this century, Science [Express], DOI: 10.1126/science.1257469 (18 September 2014) (paragraph split)

Caveat

Obviously, if one cannot foresee massively acting constraints on human population growth — on a planet that may (or may not) be close to its carrying capacity — one cannot accurately assess all the variables that will probablistically be controlling that growth.

The moral? — Maybe and maybe not, followed by policy planners’ shrugs

The nice thing about comparatively loose probabilities like this one is that their ballpark is big enough not to get egg on one’s face, if one acts on (or against) them:

(a) There is a noticeably big difference between 9.6 billion and 12.3 billion, as compared to our current world population of 7.2 billion people.

(b) If you factor in an “only” 80 percent change of hitting that rather expansive range, then you have some rather large “error bar” doors to walk out.

This scientifically unavoidable ambiguity simply means that I doubt that this growth projection is going to affect policy planning very much. Which, of course, is not at all a criticism of the study.

Americans may still be getting fatter — a study of 32,816 men and women — in the National Health and Nutrition Examination Survey (NHANES) (1999-2012)

© 2014 Peter Free

Citation — to study

Earl S. Ford, Leah M. Maynard, and Chaoyang Li, Trends in Mean Waist Circumference and Abdominal Obesity Among US Adults, 1999-2012, JAMA 312(11): 1151-1153, DOI:10.1001/jama.2014.8362 (17 September 2014)

Citation — to press release

For the Media, Waistlines of U.S. Adults Continue to Increase, JAMA (16 September 2014)

Ballooning waist girth — method and findings

From the Journal of the American Medical Association press relations arm — here reformatted with portions underlined:

Earl S. Ford . . . and colleagues used data from seven 2-year cycles of the National Health and Nutrition Examination Survey (NHANES) [see here]

starting with 1999-2000 and concluding with 2011-2012

to determine trends in average waist circumference and prevalence of abdominal obesity among adults in the United States.

Data from 32,816 men and nonpregnant women ages 20 years or older were analyzed.

The overall age-adjusted average waist circumference increased progressively and significantly, from 37.6 inches in 1999-2000 to 38.8 inches in 2011-2012.

Significant increases [in average waist circumference] occurred in

men (0.8 inch),

women (1.5 inch),

non-Hispanic whites (1.2 inch),

non­Hispanic blacks (1.6 inch),

and

Mexican Americans (1.8 inch).

The overall age-adjusted prevalence of abdominal obesity increased significantly from 46.4 percent in 1999-2000 to 54.2 percent in 2011-2012.

Abdominal obesity was defined as a waist circumference greater than 40.2 inches (102 cm) in men and greater than 34.6 inches (88 cm) in women.

Significant increases [in abdominal obesity] were present in

men (37.1 percent to 43.5 percent),

women (55.4 percent to 64.7 percent),

non-Hispanic whites (45.8 percent to 53.8 percent),

non-Hispanic blacks (52.4 percent to 60.9 percent),

and

Mexican Americans (48.1 percent to 57.4 percent).

© 2014 For the Media, Waistlines of U.S. Adults Continue to Increase, JAMA (16 September 2014) (reformatted and reordered, underlines added)

The moral? — Public health concern about overweightness appears not to have much impacted the public, at least that portion captured by NHANES

Not a surprise, given the persistence of human behaviors.

Progress with discovering the cause of variability in schizophrenia? — 8 distinct gene clusters — an apparently brilliantly done study

© 2014 Peter Free

Citation — to study

Javier Arnedo, Dragan M. Svrakic, Coral del Val, Rocío Romero-Zaliz, Helena Hernández-Cuervo, Ayman H. Fanous, Michele T. Pato, Carlos N. Pato, Gabriel A. de Erausquin, C. Robert Cloninger, and Igor Zwir, Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies, American Journal of Psychiatry, DOI:10.1176/appi.ajp.2014.14040435 (in advance publication, 14 September 2014)

Citation — to press release

Jim Dryden, Schizophrenia not a single disease but multiple genetically distinct disorders, Washington University in St Louis (15 September 2014)

If accurate, this is a brilliant study

The key — to understanding that schizophrenia is not one disease, but several, and linked to a handful of interacting gene clusters — lay in the research team’s realization that they had to group symptom types, so as to properly correlate them with the displaying patients’ genetics:

[Dragan] Svrakic said it was only when the research team was able to organize the genetic variations and the patients’ symptoms into groups that they could see that particular clusters of DNA variations acted together to cause specific types of symptoms.

[T]hey divided patients according to the type and severity of their symptoms, such as different types of hallucinations or delusions, and other symptoms, such as lack of initiative, problems organizing thoughts or a lack of connection between emotions and thoughts.

The results indicated that those symptom profiles describe eight qualitatively distinct disorders based on underlying genetic conditions.

© 2014 Jim Dryden, Schizophrenia not a single disease but multiple genetically distinct disorders, Washington University in St Louis (15 September 2014)

In other words, if we aren’t looking in the right place with the correct perspective, we are not going to see much.

Hypotheses and methods of data examination really matter.

More on the method

The abstract implicitly explains the team’s scientific reasoning:

In a large genome-wide association study of cases with schizophrenia and controls, the authors first identified sets of interacting single-nucleotide polymorphisms (SNPs) that cluster within particular individuals (SNP sets) regardless of clinical status.

Second, they examined the risk of schizophrenia for each SNP set and tested replicability in two independent samples.

Third, they identified genotypic networks composed of SNP sets sharing SNPs or subjects.

Fourth, they identified sets of distinct clinical features that cluster in particular cases (phenotypic sets or clinical syndromes) without regard for their genetic background.

Fifth, they tested whether SNP sets were associated with distinct phenotypic sets in a replicable manner across the three studies.

© 2014 Javier Arnedo, Dragan M. Svrakic, Coral del Val, Rocío Romero-Zaliz, Helena Hernández-Cuervo, Ayman H. Fanous, Michele T. Pato, Carlos N. Pato, Gabriel A. de Erausquin, C. Robert Cloninger, and Igor Zwir, Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies, American Journal of Psychiatry, DOI:10.1176/appi.ajp.2014.14040435 (in advance publication, 14 September 2014) (paragraph split)

Detailed findings

From the abstract:

The authors identified 42 SNP sets associated with a 70% or greater risk of schizophrenia, and confirmed 34 (81%) or more with similar high risk of schizophrenia in two independent samples.

Seventeen networks of SNP sets did not share any SNP or subject.

These disjoint genotypic networks were associated with distinct gene products and clinical syndromes (i.e., the schizophrenias) varying in symptoms and severity.

Associations between genotypic networks and clinical syndromes were complex, showing multifinality and equifinality. The interactive networks explained the risk of schizophrenia more than the average effects of all SNPs (24%).

Schizophrenia is a group of heritable disorders caused by a moderate number of separate genotypic networks associated with several distinct clinical syndromes.

© 2014 Javier Arnedo, Dragan M. Svrakic, Coral del Val, Rocío Romero-Zaliz, Helena Hernández-Cuervo, Ayman H. Fanous, Michele T. Pato, Carlos N. Pato, Gabriel A. de Erausquin, C. Robert Cloninger, and Igor Zwir, Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies, American Journal of Psychiatry, DOI:10.1176/appi.ajp.2014.14040435 (in advance publication, 14 September 2014) (paragraphs split)

In Jim Dryden’s plainer lay language

From his excellent press release:

In all, the researchers analyzed nearly 700,000 sites within the genome where a single unit of DNA is changed, often referred to as a single nucleotide polymorphism (SNP).

They looked at SNPs in 4,200 people with schizophrenia and 3,800 healthy controls, learning how individual genetic variations interacted with each other to produce the illness.

In some patients with hallucinations or delusions, for example, the researchers matched distinct genetic features to patients’ symptoms, demonstrating that specific genetic variations interacted to create a 95 percent certainty of schizophrenia.

In another group, they found that disorganized speech and behavior were specifically associated with a set of DNA variations that carried a 100 percent risk of schizophrenia.

In all, the researchers identified 42 clusters of genetic variations that dramatically increased the risk of schizophrenia.

“In the past, scientists had been looking for associations between individual genes and schizophrenia,” explained Dragan Svrakic . . . .

“When one study would identify an association, no one else could replicate it. What was missing was the idea that these genes don’t act independently. They work in concert to disrupt the brain’s structure and function, and that results in the illness.”

The investigators . . . replicated their findings in two additional DNA databases of people with schizophrenia, an indicator that identifying the gene variations that are working together is a valid avenue to explore for improving diagnosis and treatment.

© 2014 Jim Dryden, Schizophrenia not a single disease but multiple genetically distinct disorders, Washington University in St Louis (15 September 2014) (extracts)

 Caveat(s)

In a study of this kind of quantitatively near-overwhelming complexity, findings will obviously require corroboration.

It is conceivable that a wish to find links between (a) behavior and (b) interacting complexes of single nucleotide polymorphisms led to (c) seeing patterns where there were none or only partially some. Intricacies like those described in team’s methods lay fertile ground for inadvertently making errors, either in basic technique or as to data interpretation afterward.

But that is not my main point.

Instead, essentially turning my own caveat on its head, I am in admiration of the apparent sophistication and sheer diligence with which this team approached a very difficult conceptual and empirical problem.

The moral? — A brilliant attempt at making sense of a previously very confusing mental illness

A salute is in order.

Ixodes scapularis (deer/blacklegged ticks) — carrying Borrelia burgdorferi bacteria (Lyme disease) — are apparently moving westward in the United States — now discovered in North Dakota — And an illustration of the worth of professional societies in communicating medicine and science

© 2014 Peter Free

Citation — to study

Nathan M. Russart, Michael W. Dougherty, and Jefferson A. Vaughan, Survey of Ticks (Acari: Ixodidae) and Tick-Borne Pathogens in North Dakota, Journal of Medical Entomology 51(5):1087-1090, DOI: 10.1603/ME14053 (September 2014)

Citation — to press release

Entomological Society of America, Ticks that vector Lyme disease move west into North Dakota, ScienceDaily (11 September 2014)

In the terse, but reasonably complete wording of the abstract

Left to your own devices, would you have paid much attention to this blurb?

Ticks were sampled at nine locations throughout North Dakota during early summer of 2010, using flagging techniques and small mammals trapping.

In total, 1,762 ticks were collected from eight of the nine locations.

The dominant species were Dermacentor variabilis . . . (82%), found throughout the state, and Ixodes scapularis . . . (17%), found in northeastern counties.

A few nymphal and adult Iscapularis tested positive for Borrelia burgdorferi (3%) and Anaplasma phagocytophilum (8%).

This is the first report of Iscapularis and associated pathogens occurring in North Dakota and provides evidence for continued westward expansion of this important vector tick species in the United States.

© 2014 Nathan M. Russart, Michael W. Dougherty, and Jefferson A. Vaughan, Survey of Ticks (Acari: Ixodidae) and Tick-Borne Pathogens in North Dakota, Journal of Medical Entomology 51(5):1087-1090, DOI: 10.1603/ME14053 (September 2014) (paragraph split)

Maybe not. Unless you were a medical or public health professional interested in infectious diseases.

Enter a professional society with a sense of responsibility regarding the communication of science

From an excellent press release by the Entomological Society of America:

According to the U.S. Centers for Disease Control, there are more than 300,000 cases of Lyme disease in the U.S. each year. Last year, most Lyme disease cases reported to the CDC were concentrated heavily in the Northeast and upper Midwest, with 96 percent of cases in 13 states. In fact, the disease gets its name from the northeastern town of Lyme, Connecticut, where it was first discovered.

However, a new article published in the Journal of Medical Entomology reports that the ticks that vector Lyme disease — Ixodes scapularis, also known as blacklegged ticks or deer ticks — are moving westward, and for the first time have been found to be established in North Dakota.

[D]eer ticks that were infected with the bacterium that causes Lyme disease (Borrelia burgdorferi) were found as well.

Researchers sampled ticks at nine locations throughout North Dakota by trapping small mammals and then removing the attached ticks.

When they found I. scapularis, they screened them for Borrelia burgdorferi and for two other types of bacteria that can lead to two other tick-borne diseases called Anaplasmosis and Babesiosis.

I. scapularisticks were collected in six of the nine counties surveyed, and two of the counties seemed to have established populations because all life stages — eggs, larvae, nymphs, and adults — were present.

“This represents an expansion of the predicted range for this tick species and is of concern because of the ability of this tick species to transmit various disease-causing agents,” the authors wrote.

I. scapularis and associated pathogens have become established in northeastern North Dakota.”

© 2014 Entomological Society of America, Ticks that vector Lyme disease move west into North Dakota, ScienceDaily (11 September 2014)

The moral? — Medically important study, well communicated to lay readers

The spread of Lyme disease’s stomping grounds is obviously important to medical professionals. The abstract indicates as much.

Building on the abstract’s foundation, the Entomological Society of America demonstrated how more comprehensively presenting such findings is important in communicating with people unfamiliar with the subject matter.

Well done on everyone’s part.

People already prone to aggression respond neurally differently to violent movies — as compared to more placidly wired folks — a study of 54 men

© 2014 Peter Free

Citation — to study

Nelly Alia-Klein, Gene-Jack Wang, Rebecca N. Preston-Campbell, Scott J. Moeller, Muhammad A. Parvaz, Wei Zhu, Millard C. Jayne, Chris Wong, Dardo Tomasi, Rita Z. Goldstein, Joanna S. Fowler, and Nora D. Volkow, Reactions to Media Violence: It’s in the Brain of the Beholder, PLoS ONE, 9 (9): e107260, DOI: 10.1371/journal.pone.0107260 (10 September 2014)

Citation — to press release

Mount Sinai Medical Center, Impact of violent media on the brain: Depends on each individual’s brain circuitry, study finds, ScienceDaily (10 September 2014)

The research team’s common sense hypothesis . . .

Aggressive people will respond differently to violent movies than non-aggressive people.

And so it turned out — method and results

Mount Sinai Medical Center did an excellent job of communicating what it had done and found.

I include a lengthy quotation from the Center’s press release as an example of outstanding science writing for a lay audience:

“Our aim was to investigate what is going on in the brains of people when they watch violent movies,” said lead investigator Nelly Alia-Klein . . . .

“We hypothesized that if people have aggressive traits to begin with, they will process violent media in a very different way as compared to non-aggressive people, a theory supported by these findings.”

After answering a questionnaire, a group of 54 men were split by the research team into two groups — one with individuals possessing aggressive traits, including a history of physical assault, and a second group without these tendencies.

The participants’ brains were then scanned as they watched a succession of violent scenes (shootings and street fights) on day one, emotional, but non-violent scenes (people interacting during a natural disaster) on day two, and nothing on day three.

The scans measured the subjects’ brain metabolic activity, a marker of brain function. Participants also had their blood pressure taken every 5 minutes, and were asked how they were feeling at 15 minute intervals.

Investigators discovered that during mind wandering, when no movies were presented, the participants with aggressive traits had unusually high brain activity in a network of regions that are known to be active when not doing anything in particular.

This suggests that participants with aggressive traits have a different brain function map than non-aggressive participants, researchers said.

Interestingly, while watching scenes from violent movies, the aggressive group had less brain activity than the non-aggressive group in the orbitofrontal cortex, a brain region associated by past studies with emotion-related decision making and self-control.

The aggressive subjects described feeling more inspired and determined and less upset or nervous than non-aggressive participants when watching violent (day 1) versus just emotional (day 2) media. In line with these responses, while watching the violent media, aggressive participants’ blood pressure went down progressively with time while the non-aggressive participants experienced a rise in blood pressure.

“How an individual responds to their environment depends on the brain of the beholder,” said Dr. Alia-Klein.

© 2014 Mount Sinai Medical Center, Impact of violent media on the brain: Depends on each individual’s brain circuitry, study finds, ScienceDaily (10 September 2014) (paragraphs split, underlines added)

Caveat

Obviously, this is too small a study to put great stock in.

And one could quarrel, I imagine, with its interpretations of the functional meanings of different brain regions and their levels of metabolic activity. And so on — to nitpick heaven.

Yet, its primary finding is congruent with common sense and many people’s experience with aggressive and violent people. My own included.

The moral? — Aggressive people’s brains may be wired to like or accept violence

Which would presumably make behavior modification that much more difficult for them.