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Testosterone Replacement Therapy Market Projections From 2020-2026 With Research Data on Consumption Analysis, Investment Cost, Profits Data and…

Posted: January 8, 2020 at 8:46 pm

The global Testosterone Replacement Therapy market is broadly and deeply studied in the report with key focus on the competitive landscape, regional growth, market segmentation, and market dynamics. We have used latest primary and secondary research techniques for compiling this comprehensive research study. The report offers Porters Five Forces analysis, PESTLE analysis, competitive analysis, manufacturing cost analysis, revenue and production analysis, and various other types of analysis to provide a complete view of the global Testosterone Replacement Therapy market. Each segment of the global Testosterone Replacement Therapy market is carefully analyzed on the basis of market share, CAGR, and other vital factors. The global Testosterone Replacement Therapy market is also statistically presented with the help of Y-o-Y growth, CAGR, revenue, production, and other important calculations.

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We can customize the report as per your requirements. Our analysts are experts in market research and analysis and have a healthy experience in report customization after having served tons of clients to date. The main objective behind preparing the research study is to inform you about future market challenges and opportunities. The report is one of the best resources you could use to secure a strong position in the global Testosterone Replacement Therapy market.

Market Segmentation:

Following are the segments covered by the report are:GelsInjectionsPatchesOtherBy Application:HospitalsClinicsOthersKey Players:The Key manufacturers that are operating in the global Testosterone Replacement Therapy market are:AbbVieEndo InternationalEli lillyPfizerActavis (Allergan)BayerNovartisTevaMylanUpsher-SmithFerring PharmaceuticalsKyowa KirinAcerus Pharmaceuticals

Regional GrowthThe report offers in-depth analysis of key regional and country-level Testosterone Replacement Therapy markets, taking into account their market size, CAGR, market potential, future developments, and other significant parameters. The Middle East and Africa (GCC Countries and Egypt) North America (the United States, Mexico, and Canada) South America (Brazil etc.) Europe (Turkey, Germany, Russia UK, Italy, France, etc.) Asia-Pacific (Vietnam, China, Malaysia, Japan, Philippines, Korea, Thailand, India, Indonesia, and Australia)

Key Questions Answered What will be the size and CAGR of the global Testosterone Replacement Therapy market in 2025? Which product will gain the highest demand in the global Testosterone Replacement Therapy market? Which application could show the best growth in the global Testosterone Replacement Therapy market? What will be the nature of the competitive landscape in future? Which players will lead the global Testosterone Replacement Therapy market in the coming years? Which region will gain the largest share of the global Testosterone Replacement Therapy market?

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Table of Contents

Report Overview: It includes six chapters, viz. research scope, major manufacturers covered, market segments by type, Testosterone Replacement Therapy market segments by application, study objectives, and years considered.

Global Growth Trends: There are three chapters included in this section, i.e. industry trends, the growth rate of key producers, and production analysis.

Testosterone Replacement Therapy Market Share by Manufacturer: Here, production, revenue, and price analysis by the manufacturer are included along with other chapters such as expansion plans and merger and acquisition, products offered by key manufacturers, and areas served and headquarters distribution.

Market Size by Type: It includes analysis of price, production value market share, and production market share by type.

Market Size by Application: This section includes Testosterone Replacement Therapy market consumption analysis by application.

Profiles of Manufacturers: Here, leading players of the global market are studied based on sales area, key products, gross margin, revenue, price, and production.

Testosterone Replacement Therapy Market Value Chain and Sales Channel Analysis: It includes customer, distributor, Testosterone Replacement Therapy market value chain, and sales channel analysis.

Market Forecast Production Side: In this part of the report, the authors have focused on production and production value forecast, key producers forecast, and production and production value forecast by type.

About Us:QYResearch always pursuits high product quality with the belief that quality is the soul of business. Through years of effort and supports from huge number of customer supports, QYResearch consulting group has accumulated creative design methods on many high-quality markets investigation and research team with rich experience. Today, QYResearch has become the brand of quality assurance in consulting industry.

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Scientists Figured Out the Indian Cobra’s Genomeat Last – WIRED

Posted: January 8, 2020 at 8:45 pm

In 1891, a French physician named Albert Calmette opened a research outpost in what was then Saigon (now Ho Chi Minh City, Vietnam) to develop new vaccines for rabies and smallpox. Then the Indian cobras showed up.

The invaders sank their fangs into several of Calmettes new neighbors, injecting molecules that rotted muscles, ruptured blood vessels, and paralyzed the nerves that told their hearts to beat and lungs to breathe. Their grisly deaths prompted him to drop infectious disease and focus on snake venom. When he returned to France, he injected Indian cobra venom into rabbits in small doses and discovered that the animals produced a serum with a protective effect: the first antivenom. Calmette began producing his anti-cobra cocktail of antibodies in donkeys and horses and in 1895, for the first time, successfully treated a human snakebite victim.

Calmettes method still dominates antivenom production todaya practically medieval process of snake milking and horse blood harvesting that is laborious, expensive, and error-prone. What scientists have needed in order to modernize this operation is the source code for a snakes noxious protein soup, the actual genes and nearby DNA that turn them on or off.

After two years of work, an international team of scientists has now published, in Nature Genetics, an atlas of all 38 of the Indian cobras chromosomes, the most complete snake genome ever assembled. It contains information no one has ever been able to piece together before: the genetic recipe for the snakes deadly venom cocktail. Theyre hoping it will serve as a roadmap to bring antivenom production into the 21st century.

It seems like something we should have figured out 20 years ago, but until now those areas of the snake genome have been total black boxes, says Todd Castoe, an evolutionary geneticist at the University of Texas at Arlington who was not involved in the work. Initially, scientists believe, the genes that generate venoms carried out totally different functions, usually some innocuous cellular housekeeping task. But along the way they duplicated, a common DNA-copying error. And then the extra copies acquired mutations. That happened over and over, and the proteins they produced became deadly in different ways. The result of all this evolution is that the stretches of DNA that code for venom toxins are full of repetitive sequences, making them exceedingly difficult to properly assemble. Imagine trying to solve a jigsaw puzzle where the same fluffy clouds are scattered six, eight, a dozen times in the same corner of the sky. How do you know which piece goes where?

To finally fit together these elusive sections of the genome, Somasekar Seshagiri, a geneticist and president of the SciGenom Research Foundation in Bangalore, and his collaborators used a combination of older sequencing methods with new ones that read out very long stretches of DNA. They also employed a technique that detects the 3D shape of DNA to further refine their guesses about how exactly to stitch together the structurally finicky venom regions. With the full genome in hand, the researchers then analyzed which sections of it are turned on in the venom gland but not in other tissues. That allowed them to identify the code that spells death or disablement for anyone who encounters the cobras bite.

Antivenoms will no longer just be like some magic potion we pull out of a horse.

Somasekar Seshagiri

Indian cobra venom isnt just one poison; it consists of more than a dozen toxins and other substances that together launch a coordinated attack on the snakes prey (or a hapless human victim). In the Nature Genetics paper, Seshagiris team identified 19 genes key to producing this lethal brew. For the first time, it establishes the links between a snakes toxins and the genes that encode them.

The achievement not only shows scientists how to use the same methods to sequence other venomous snake species, it also unlocks the door to modernizing antivenom production. The value of genomics is that it will allow us to produce medicines that are more concretely defined, says Seshagiri. Antivenoms will no longer just be like some magic potion we pull out of a horse.

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Mouse Lemurs Just Might Be the Next Big Thing in Genetics – Nature World News

Posted: January 8, 2020 at 8:45 pm

Jan 08, 2020 11:04 AM EST

There are 500 animals studied so far in the mouse lemur project, a collaboration that aims to parse the genetics of this diminutive, prosimian primate. It is the brainchild of Stanford biochemist Mark Krasnow.

Because all 24 species of mouse lemurs look similar, the most reliable way for scientists to tell them apart is through genetic testing. (Scientists have recently identified three new species of mouse lemurs in Madagascar.)

They are quite possibly the answer to medical researchers' dreams.

This world's smallest primate may soon replace fruit flies, worms, and even mice as the primary lab animal for scientific research.

According to Stanford University School of Medicine researchers, they have the potential to serve as an ideal model for a wide range of primate biology, behavior, and medicine, including cardiovascular disease and Alzheimer's disease.

Mice, fruit flies, and worms as genetic models have routinely failed to mimic many aspects of primate biology, including many human diseases, said Mark Krasnow, MD, Ph.D., professor of biochemistry.

Krasnow and his colleagues turned to the mouse lemur and began conducting detailed physiologic and genetic studies on them.

It was reported that they already have identified more than 20 individual lemurs with unique genetic traits, including obesity, high cholesterol, high blood sugar, cardiac arrhythmias, progressive eye disease and motor and personality disorders.

The researchers hope it will soon become a genetic model organism that will help us better understand many aspects of primate biology, behavior, and health, including lemur and human diseases.

According to the June issue of GENETICS, Ezran et al.'s genetic research on these primates began as a project for three high school laboratory interns to find an appropriate model organism for primate genetics.

Mouse lemurs are more human than mice, as genetic research on mice has led to countless important discoveries, but their physiology and behavior differ in many ways from that of humans and other primates. They potentially rival the common laboratory mouse Mus musculus, at least for certain questions.

Mice, fruit flies, and worms were the prototypical lab specimen because they were inexpensive to maintain, easy to study, and reproduced quickly enough to offer researchers a constant stream of samples. According to Krasnow, MD, Ph.D., a professor of biochemistry at Stanford University, the genetic makeup of the 3 animals hasn't been a close enough match to humans to work well for the studies today's researchers need to conduct.

Krasnow's project is studying a large population of grey and brown mouse lemurs - Microcebus murinus and Microcebus rufus, respectively - in the wild to work out how their genes link to differences in biology, health, and behavior.

Other than being closely related to humans, they still have many of the advantages of mice in terms of small size, rapid reproduction, and relatively large litters.

These researchers hope that continued study of these abundant primates could lead to a better understanding, and possibly better treatments, of these and other conditions in lemurs and humans.

RELATED ARTICLE: DNA Analysis Helps Researchers Identify New Mouse Lemur Species

2018 NatureWorldNews.com All rights reserved. Do not reproduce without permission.

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Amgen To Present At The Goldman Sachs 12th Annual Healthcare CEOs Unscripted Conference – PRNewswire

Posted: January 8, 2020 at 8:45 pm

THOUSAND OAKS, Calif., Jan. 7, 2020 /PRNewswire/ -- Amgen (NASDAQ:AMGN) will present via video conference at theGoldman Sachs 12th Annual Healthcare CEOs Unscripted Conference at1p.m.PT on Thursday, Jan. 9, 2020. Robert A. Bradway, chairman and chief executive officeratAmgen, and Peter H. Griffith, executive vice president and chief financial officerat Amgen, will present.Live audio of the presentation can be accessed from the Events Calendar on Amgen's website,www.amgen.com, under Investors.A replay of the webcast will also be available on Amgen's website forat least90 days following the event.

About AmgenAmgen is committed to unlocking the potential of biology for patients suffering from serious illnesses by discovering, developing, manufacturing and delivering innovative human therapeutics. This approach begins by using tools like advanced human genetics to unravel the complexities of disease and understand the fundamentals of human biology.

Amgen focuses on areas of high unmet medical need and leverages its expertise to strive for solutions that improve health outcomes and dramatically improve people's lives. A biotechnology pioneer since 1980, Amgen has grown to beone ofthe world'sleadingindependent biotechnology companies, has reached millions of patients around the world and is developing a pipeline of medicines with breakaway potential.

For more information, visitwww.amgen.comand follow us onwww.twitter.com/amgen.

CONTACT: Amgen, Thousand OaksJessica Akopyan, 805-447-0974 (media)Trish Hawkins, 805-447-5631(media)Arvind Sood, 805-447-1060 (investors)

SOURCE Amgen

http://www.amgen.com

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Largest-ever study on genetics of anxiety points to new treatments – Inverse

Posted: January 8, 2020 at 8:45 pm

The future of anxiety treatments could go the way of oncology and cardiology, as scientists inch closer to treating the condition using precision medicine drug treatments that are specifically tailored to ones genetic and biochemical profile. Anxiety is notoriously hard to treat using standard therapies, but a precision medicine approach promises to actually work.

But to know what genes to target using precision medicine, you have to know where to look. In the largest genetics study of its kind to date, scientists reveal regions in the human genome that appear directly related to anxiety risk five are found in the genomes of Americans of European descent, and one in black Americans.

The findings were published this week in the American Journal of Psychiatry.

The researchers used data from nearly 200,000 participants in the United States Million Veteran Program one of the worlds largest genetic biobanks. Daniel Levey, a postdoctoral associate at Yale School of Medicine and co-lead author of the study, described the dataset as one of the greatest resources in the world for conducting this kind of research.

Levey tells Inverse that the study identifies the locations in the genome where genetic variation is common in most people. In turn, people who have variation in these locations have increased risk for anxiety symptoms.

But theres a chance that people at a higher genetic risk for anxiety will not develop the disorder, Levey says.

Genetics are an important piece of the puzzle for understanding human health, but they are not fate, Levey says. The variants we identified are responsible for an increase in overall risk, but that genetic risk interacts with other environmental and lifestyle factors.

The team analyzed the genomes of 199,611 participants and looked at whether they had a self-reported diagnosis of anxiety or panic disorder.

In Americans of European descent, the researchers identified five locations on the human genome related to anxiety. The study is notable because it is may be the first to produce significant findings on the genetics of anxiety among people of African ancestry (about 18 percent of the participants were black). The identified region is at the TRPV6 gene the genetic variant only occurs in people of African ancestry.

A risk region of particular interest is one near the gene SATB1, Levey says. This gene interacts with the hypothalamic-pituitary-adrenal axis, which is the biological pathway associated with the stress response. The result may point to a novel understanding of how genetics influence the stress response and anxiety, he says.

The findings jibe with the theory that the traits of some psychiatric conditions overlap because they share genetic roots. The researchers found high genetic overlap between anxiety symptoms and depression, post-traumatic stress disorder, and neuroticism.

Historically, the genetics of anxiety disorders has lagged behind other related conditions, including depression. In 2018, scientists discovered that there are at least 82 genes linked to depression in part explaining why 50 percent of cases are caused by genetics.

The authors of the 2018 study hoped that identifying genes could lead to new treatments. Levey shares the same hope: Other researchers can take what this study has accomplished, and expand upon the findings to develop novel therapies. Theres also a need for larger studies that can identifying more of the genetic architecture underlying anxiety disorders, he says.

In the future, perhaps awareness of increased risk for anxiety disorders may lead people to seek out treatment and empower them to seek training in coping strategies to be more resilient, Levey says.

Partial abstract:

Background: Anxiety disorders are common and often disabling. They are also frequently comorbid with other mental disorders such as major depressive disorder with which they may share commonalities in their underlying genetic architecture.

Methods: We used one of the largest homogeneously phenotyped cohorts available, the Million Veteran Program, to perform a genome-wide association study (GWAS) a continuous trait for anxiety (GAD-2, N=199,611) as the primary analysis and self-report of physician diagnosis of anxiety disorder (SR-ANX, N=224,330) as a secondary analysis).

Conclusions: We present the largest GWAS of anxiety traits to date. We identified novel genome-wide significant associations near genes involved with global regulation of gene expression (SATB1) and the estrogen receptor (ESR1). Additionally, we identified a locus (MAD1L1) which may have implications for genetic vulnerability across several psychiatric disorders. This work provides new insights into genetic risk mechanisms underpinning anxiety and related psychiatric disorders.

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Autism heritability: It probably does not mean what you think it means – Spectrum

Posted: January 8, 2020 at 8:45 pm

Brian Lee

Associate professor, Drexel University

The question of autisms heritability is compelling for researchers and laypeople alike, but many people in both groups misunderstand its definition.

Heritability is defined as the proportion of variation in a condition that is attributable to variation in genetics. Heritability estimates can influence how much time and money researchers like me think should be allocated to studying genetic factors versus environmental ones. For families with a history of autism, heritability estimates get right to the heart of the nature-versus-nurture debate, by offering clues about which factors led to an individuals diagnosis.

These numbers have substantial implications; they probably should not. Autism arises from a complex interplay of genetic and environmental factors, and most heritability studies oversimplify these relationships.

Several studies on autism heritability published in the past few years have drawn considerable attention. Those published from 2011 to 2014 estimated heritability to be in the 35 to 50 percent range, but studies published since 2017 have put the number at 64 to 85 percent.

What do these estimates actually mean?

Heritability is often misinterpreted as the proportion of a condition that is caused by genes. However, that interpretation is not quite correct. Or rather, so many asterisks must be attached in order for it to be correct, that it could not be, by any stretch of the imagination, considered to be correct.

Heritability estimates may tell us to what extent a persons genetics predispose them to a condition. But they tell us nothing about how different environments cause those genetics to play out.

First, let me explain why most estimates of heritability are incorrect. Studies that estimate autisms heritability use a statistical model to try to attribute the condition to either genetics or environment. Mounting evidence suggests this model is too simplistic to explain how autism arises.

The model generally looks something like this: Observed characteristics, or phenotype (P) = genotype (G) + environment (E). The G and E components can each be broken down further to get at specific types of genetic or environmental contributions, but the core point of the model is to separate G and E.

A statistical model is merely a caricature of the real world, though; the extent to which it is useful depends on how well the model reflects reality. The P = G + E model assumes that genetic and environmental influences are independent of each other and that genes do not interact with the environment or with other genes to influence phenotype.

We know in fact that networks of genes interact to influence a persons odds of having autism and that genetic factors raise the odds of having autism caused by environmental exposures such as infection, air pollution or nutrition.

In short, if reality is more complex than the model, that model may produce inaccurate heritability estimates. There are many more technical reasons why published heritability estimates are likely to be inaccurate1.

There is also a much simpler reason why heritability estimates should not be taken at face value: High heritability does not equal genetic causation, and it does not exclude the possibility of environmental influence.

Here are two thought experiments that demonstrate why.

Borrowing an example from the great evolutionary biologist Richard Lewontin, imagine planting a set of identical seeds in a uniform environment that ensures all the seeds receive equal amounts of light and nutrients. Any variation in the heights of the plants that grow from those seeds is solely attributable to genetic variation among the plants. The heritability in this scenario is 100 percent.

Now imagine taking another set of the same seeds and planting them in uniformly suboptimal growing conditions, with limited light and nutrients. The plants growth would be stunted, and again the heritability would be 100 percent.

The point is: Even where heritability is estimated to be 100 percent, the environment can influence phenotype. Of course, this is not limited to plants. For example, the heritability of human height is estimated to be approximately 80 percent, but height is still strongly regulated by a persons nutritional environment.

Next, consider this example from David S. Moore and David Shenk2. Imagine a bucket of water into which person A pours 40 liters of water and person B pours 60 liters of water. Clearly, 40 percent of the water is attributable to person A, 60 percent to person B. Now imagine the same bucket, but this time person A turns on the faucet and person B holds the hose. How much of the water in the bucket is due to person A and how much is due to person B?

In short, when causes interact to create an outcome, it becomes nonsensical to try to apportion credit (or blame) to one cause independent of the other.

The bucket example is not just a thought experiment; it represents conditions that have both genetic and environmental components.

Consider the condition phenylketonuria, which occurs in people who have genetic variants that affect how their bodies metabolize the amino acid phenylalanine. The condition does not occur in the absence of the genetic variants, but it also does not occur if phenylalanine is removed from the diet. So how much of it can be attributed to genes versus the environment?

The consequences of miscasting heritability as the contribution of genetics to any given individuals diagnosis are potentially dire. As well as misinforming the public, it could throw funding for research on the etiology of autism entirely into genetic research rather than into how genes and environment interact.

This should cause genetic and environmental researchers alike great concern.

The search for rare genetic variants that may cause autism has yielded many important findings, but the search for common variants, whose influence combines to raise autisms odds, has been less fruitful. There are likely to be many of these variants, each exerting only weak effects, which makes them undetectable except in massive study samples. It is also highly likely that many common variants do not exert an effect unless they are present along with another genetic or environmental factor.

Animal models that explore genetic factors in the absence of relevant environmental interactions could be doomed never to recapitulate those genetic factors effects in people.

In short, many heritability estimates of autism in the literature are likely to be inaccurate and, more importantly, prone to misinterpretation. Rather than asking: Are genes or the environment responsible for autism? we should be asking: How are genes and the environment responsible for autism?

Brian Lee is associate professor of epidemiology and biostatistics at Drexel University in Philadelphia, Pennsylvania.

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Nature Reviews Genetics Pseudogene Function Is Prematurely Dismissed – Discovery Institute

Posted: January 8, 2020 at 8:45 pm

A new paper in Nature Reviews Genetics, Overcoming challenges and dogmas to understand the functions of pseudogenes, is simply incredible. It documents not only that pseudogenes have been found to have widespread function but also that under current dogma in biology, and given the technical limitations, we are failing to recognize their functions. As Seth W. Cheetham and his co-authors put it, biology suffers from demotivation into exploring pseudogene function by the a priori assumption that they are functionless where The dominant limitation in advancing the investigation of pseudogenes now lies in the trappings of the prevailing mindset that pseudogenic regions are intrinsically non-functional.

The abstract lays out exactly what they think:

Pseudogenes are defined as regions of the genome that contain defective copies of genes. They exist across almost all forms of life, and in mammalian genomes are annotated in similar numbers to recognized protein-coding genes. Although often presumed to lack function, growing numbers of pseudogenes are being found to play important biological roles. In consideration of their evolutionary origins and inherent limitations in genome annotation practices, we posit that pseudogenes have been classified on a scientifically unsubstantiated basis. We reflect that a broad misunderstanding of pseudogenes, perpetuated in part by the pejorative inference of the pseudogene label, has led to their frequent dismissal from functional assessment and exclusion from genomic analyses. With the advent of technologies that simplify the study of pseudogenes, we propose that an objective reassessment of these genomic elements will reveal valuable insights into genome function and evolution.

They immediately caution that there are many instances where DNA that was dismissed as pseudogene junk was later found to be functional: with a growing number of instances of pseudogene-annotated regions later found to exhibit biological function, there is an emerging risk that these regions of the genome are prematurely dismissed as pseudogenic and therefore regarded as void of function.

In 2003, Francisco Ayala and Evgeniy Balakirev wrote in Annual Review of Genetics that pseudogenes that have been suitably investigated often exhibit functional roles. This new Nature Reviews Genetics paper offers a very similar statement: Where pseudogenes have been studied directly they are often found to have quantifiable biological roles. Its a long narrative that recounts how many scientists mistakenly dismissed stretches of DNA as pseudogenes. They document dozens of instances where pseudogenes in humans and other organisms have been found to have function.

Some of these functions are protein-based, meaning the pseudogene actually generates a functional protein. But other functions can be RNA-based or DNA-based. For example, most evolutionists would presume that a pseudogene that does not produce a protein cant be functional. But the paper observes that pseudogenes that cannot be translated into a protein may still have a function through their RNA transcript:

Many pseudogenes contain a frequency of mutations that render them unlikely to be (or incapable of being) translated into proteins. However, such mutations do not necessarily preclude pseudogenes from performing a biological function.

The paper notes that even if the RNA transcript of a pseudogene cant be translated into protein, a myriad of RNA-based regulatory mechanisms have been described for pseudogenes, including processing into small interfering RNAs (siRNAs) that may regulate their parent genes, acting as a decoy for transcription factors and, most prominently, as molecular sponges for microRNAs.

Many evolutionists would forcefully assume that if a pseudogene cant even produce an RNA transcript then it cant be functional. But it turns out that pseudogenes that dont produce any RNA transcript (i.e., arent transcribed) can still have important functions:

Another mechanism through which pseudogenes can function is by influencing chromatin or genomic architecture. HBBP1, a pseudogene residing within the haemoglobin locus, enables the dynamic chromatin changes that regulate expression of fetal and adult globin genes during development. Notably, although inhibiting HBBP1 transcription has no effect, deletion of the genomic locus reactivates fetal globin expression. HBBP1 DNA contacts, but not transcription, are required for suppressing the expression of fetal globin genes in adult erythroid cells.

A variety of other non-transcriptional functions are documented in the paper, including stabilizing chromosomes, mediating transcript-splicing, and regulating recombination. Thus, in many cases copy numbers of pseudogenes seem to have functional importance, where deviations from the normal genetic state causes disease. They predict: It is expected that further links between human pseudogene polymorphisms and complex diseases will be identified in the coming years

The implication is that one reason we presume pseudogenes are functionless is because we havent been looking for their functions. And why didnt we look for their functions? Because we presumed they were functionless! So theres a circular aspect to the reasoning here. It has created the science-stopping junk-DNA paradigm, which has prevented us from understanding what pseudogenes really do.

The typical response from evolutionists would be that all of these examples of functional pseudogenes are just isolated rare cases, and that the bulk of pseudogenes are clearly junk. The authors of the paper who give no indication of sympathy for intelligent design, but definitely oppose dismissing pseudogenes as junk are aware of this objection. They say the following in direct rebuttal to it:

The examples of pseudogene function elaborated on here should not imply that pseudogene functionality is likely to be confined to isolated instances. At least 15% of pseudogenes are transcriptionally active across three phyla, many of which are proximal to conserved regulatory regions. It is estimated that at least 63 new human-specific protein-coding genes were formed by retrotransposition since the divergence from other primates. Numerous retrogenes continue to be recognized as functional protein-coding genes rather than pseudogenes across species. High-throughput mass spectrometry and ribosomal profiling approaches have identified hundreds of pseudogenes that are translated into peptides. Although the functions of these peptides remain to be experimentally determined, such examples illustrate the challenge in substantiating a genepseudogene dichotomy.

They continue: As the abundance of such [non-coding-DNA] acquired functions does not appear to be an especially rare or isolated phenomenon, it would seem remiss to take the default perspective that processed pseudogenes are functionless. Instead, it is probable that pseudogene-containing regions of the genome harbour important biological functions that are yet to be revealed.

They point out that current algorithmic and computational methods employed for differentiating pseudogenes and protein-coding genes may overestimate the proportion of the genome that is composed of pseudogenes. Why? Because the properties that are used to define many pseudogenes are also often found in normal protein-coding genes. For example:

Because of this, they argue that computational differentiation of pseudogenes from genes on a purely rule-based system is unlikely to be feasible as it will inherently conflict with many protein-coding genes. They therefore propose markedly softening claims that a stretch of DNA is a pseudogene: it may be useful to consider the annotation of pseudogenes in genomes as a prediction or a hypothesis rather than a classification.

As the authors show, the presumption that a pseudogene is functionless needs to be abandoned. But then, why are we still presuming they are functionless? There are three main reasons: (1) evolutionary thinking has presumed that pseudogenes are functionless junk, (2) terminological dogma reinforces a mindset that pseudogenic regions are intrinsically non-functional, and (3) technological limitations prevent us from discovering their function. The paper acknowledges that problem (3) stems from problem (2), but it fails to explicitly recognize that both problems (2) and (3) ultimately stem from problem (1). In fact it doesnt even identify problem (1) as a problem. Yet the whole situation traces back to bad evolutionary predictions. Lets look at these causes briefly, in reverse order:

The proximal cause that prevents us from understanding pseudogene functions are technological limitations. Because of the junk DNA paradigm, a lot of our biochemical techniques and technologies are set up only to identify standard protein-coding genes. They ignore and dismiss DNA that doesnt fit that mold. Only by updating our technology to detect functional DNA elements that dont necessarily fit the standard definition of a gene can be we begin to understand what pseudogenes really do. The paper explains that technical limitations, informed by our biases and assumptions, demotivate the study of pseudogene functions:

In addition to the demotivation into exploring pseudogene function by the apriori assumption that they are functionless, their systematic study has also been hindered by a lack of robust methodologies capable of distinguishing the biological activities of pseudogenes from the functions of the genes from which they are derived.

They compare the situation to that of long non-coding RNAs (lncRNAs), which were similarly dismissed initially as emanating from junk DNA or as transcriptional noise, largely by virtue of their definition as non-protein-coding. But as technology developed, lncRNAs are now widely recognized as functional and we regularly screen for their functions:

Following a combination of technology developments, genome-wide studies and detailed biochemical studies, lncRNAs are now routinely included in genome-wide analyses, and their functional potential as cellular regulators is widely recognized.

However, at present, the authors note, due in part to the experimental challenge of investigating their function and expression, pseudogenes are typically excluded from genome-wide functional screens and expression analyses. In other words, one of the main reasons we arent finding function for pseudogenes is because we arent looking for it. This needs to change, and they argue that it can.

For example, according to the paper, processed pseudogenes were presumed to have been rendered transcriptionally silent by the loss of cis-regulatory elements. But we now know that thousands of retrotransposed gene copies are transcribed and are often spliced into known protein-coding transcripts and up to 10,000 mouse pseudogenes have evidence of transcription. By trying to study these transcripts we can understand what they may be doing.

One complication is that pseudogene transcription shows cell-type specificity and dynamic expression meaning they may only be transcribed in particular places at particular times. This is all the more reason not to assume that lack of evidence for the function of a pseudogene is evidence that the pseudogene has no function! It very likely may be functional in a cell-type or a situation that we just havent properly investigated yet. As they put it, The use of assays ill-suited to analysis of pseudogenes has arguably stymied elucidation of their biological roles. But they are hopeful: CRISPR-based approaches, carefully applied, have the potential to revolutionize our ability to dissect the functions of pseudogenes. They conclude that its time to stop excluding pseudogenes from biochemical analyses and start using techniques that can identify their functions:

The use of a liberal definition of pseudogenes is attractive as it simplifies genomic analyses. This approach, often unknowingly to the researcher, leads to the consolidation of the pseudogene classification that is, their exclusion by convenience in functional studies. Many regions now considered to be dead genes potentially encode cis-regulatory elements, non-coding RNAs and proteins with impacts in human biology and health. Accordingly, determining the functions of putative pseudogenes warrants active pursuit by their inclusion in functional screens and analyses of genomic, transcriptomic and proteomic data. With innovations in long-read sequencing and CRISPR-based methodologies now readily accessible, the technological limitations that formerly motivated the exclusion from functional investigation are largely resolved.

Until we develop and apply these technologies to put pseudogenes to the proper test, the assumption that they are functionless junk is completely unwarranted. And its not hard to predict what the outcome will be. As Ayala and Balakirev noted, pseudogenes that have been suitably investigated often exhibit functional roles. Or as this new paper observes, Where pseudogenes have been studied directly they are often found to have quantifiable biological roles.

Technology only reflects what people want to do, and there are reasons why biologists have created hardly any technology to investigate pseudogenes: biologists presume (wrongly) that pseudogenes are nonfunctional junk. The paper argues that the terminology associated with the junk DNA paradigm discourages investigation into their function. Thus, we have terms like pseudogene which by their very nature imply that the DNA isnt a gene but something like a wannabe gene that doesnt do anything. As the authors note, the definition of a pseudogene as defective means the non-functionality of pseudogenes remains the dominant and default perception. Citing Thomas Kuhn and his concept of a dominant paradigm that is intolerant of criticisms, they lash the junk-pseudogene paradigm in strong terms:

[T]he term pseudogene itself asserts a paradigm of non-functionality through its taxonomic construction. Pseudogenes are defined as defective and not genes. This point is highlighted because impartial language in science is known to inherently restrict the neutral investigation between conflicting paradigms. In the case of pseudogenes, the term itself is constructed to support the dominant paradigm and therefore limit, consciously or unconsciously, scientific objectivity in their investigation.

Its hard to imagine a greater indictment of the idea that pseudogenes are generally functionless. They continue to explain how use of the term pseudogene hinders scientific research:

Although the pseudogene concept arose to describe an individual molecular phenomenon, the term was rapidly adopted to annotate tens of thousands of genomic regions that met only loosely defined criteria and was effectively axiomatized without being subject to any rigorous scientific debate. This lack of consensus-seeking process has left genome biology with a legacy concept that obscures objective investigation of genome function.

They recommend using different language where [t]he automated classification of gene-like sequences as pseudogenes should be avoided. Instead, we propose that descriptive terms that do not make functional inferences should be used in reference to genomic elements that arose from gene duplication and retrotransposition and terminology should not impose any unsubstantiated assumption on end users.

So what is now stopping us from elucidating the functions of pseudogenes? The only obstacle is a mental block not a technical or evidential one:

The dominant limitation in advancing the investigation of pseudogenes now lies in the trappings of the prevailing mindset that pseudogenic regions are intrinsically non-functional.

The paper predicts that as soon as we lose this mindset, there will remain no technical limitations blocking us from progress in understanding the functions of pseudogenes: With renewed scientific objectivity, we anticipate that a wealth of discoveries to understand genome function, its role in disease and the development of new treatments is within reach.

Thats good news, but we must ask a question the paper fails to ask: Why did this terminology develop in the first place?

Evolutionary thinking is the cause that ultimately created, nurtured, and sustained the junk DNA paradigm. Yet the paper adopts a wholly evolutionary approach, and for this reason never identifies evolutionary thinking as the root problem. The closest the authors get is when they recount how the very first paper to identify a pseudogene (published in 1977) dismissed its potential function as a relic of evolution:

In the absence of evidence that the 5S pseudogenes were transcribed, Jacq etal. concluded that the most probable explanation for the existence of the pseudogenes is that they are a relic ofevolution and are functionless1. Since the coining of the term pseudogene, its definition has broadened and is now widely accepted to define any genomic sequence that is similar to another gene and is defective.

This 1977 paper by Jacq et al. was published in the journal Cell and found a pseudogene in an African frog. That paper concluded:

We are thus forced to the conclusion that the most probable explanation for the existence of the pseudogene is that it is a relic of evolution. During the evolution of the 55 DNA of Xenopus laevis, a gene duplication occurred producing the pseudogene. Presumably the pseudogene initially functioned as a 55 gene, but then, by mutation, diverged sufficiently from the gene in its sequence so that it was no longer transcribed into an RNA product.

And there you have it: The pseudogene is seen as a mere a relic produced by mutation until it diverged so much that it was no longer transcribed into an RNA product. This is the classic view of a pseudogene.

Ironically, the 1977 paper went on to speculate that perhaps there is evidence for function for the pseudogene, but the authors privilege the relic view as the right answer until a function can be proven:

This evolutionary explanation for the presence of the pseudogene, however, is incomplete by itself in that it ignores the conservation in sequence of the pseudogene, and indeed of the entire G + C-rich spacer of 55 DNA. In an attempt to explain this, it has been suggested that the pseudogene may be a transcribed spacer corresponding to a primary transcript of 55 RNA, which is a transient precursor and has not so far been detected. If this is so, then most of the G + C-rich region of 55 DNA would be the structural gene for 5S RNA. This function, if true, would provide the necessary selective pressure to conserve the sequence of the linker and pseudogene region so that the correct processing of the postulated 300-long precursor was maintained. In the absence of any experimental evidence for such a long precursor, however, this suggestion must be regarded as speculative; it is more probable that the pseudogene is a relic of evolution.

The recent Nature Reviews Genetics paper hopes to remedy this problem by reviewing much of the overwhelming evidence for pseudogene function and emphasizing how the the non-functionality of pseudogenes remains the dominant and default perception. This will limit, consciously or unconsciously, scientific objectivity in their investigation. The authors are to be commended. However, experience teaches that unless you address the root cause of a problem, it rarely goes away. The tendency to view pseudogenes as a relic of evolution probably wont change as long as you presume that the entire genome is the product of blind evolution. The paper fully endorses the latter view, providing all kinds of narrative gloss that describes pseudogenes (whether functional or not) as retrocopies that arose from gene duplication and transposition. They emphasize:

In the fundamental reductionist approach often assumed in genetics and molecular biology, the perspective is often lost that life as we observe it today is not only the product of billions of years of evolutionary processes but also still subject to these same processes.

They are welcome to take the reductionist approach often assumed in genetics and molecular biology. But until those fundamental evolutionary views of the genome are on the table for questioning, they wont make much progress in shaking the science-stopping assumptions of the junk-DNA paradigm.

Photo: Xenopus laevis, by Brian Gratwicke [CC BY 2.0], via Wikimedia Commons.

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Is ‘No Kill’ Changing the Genetics of Pit Bulls? – City Watch

Posted: January 8, 2020 at 8:45 pm

But a newphenomenon is also developing as a common occurrence -- multiple Pit Bulls attacking as a pack.

Colleen Lynn, founder ofDogsBite.org,which tracks and investigates fatal dog maulings, reports that,of all fatalities,65% involved two or more dogs, a reversal from early CDC (Centers for Disease Control) study years when 70% of fatalities involved a single dog.

Could the number of dogs involved in attacks listed below signal that these expanding policies -- which allow unlimited adoption, ownership, or keeping of Pit Bulls per household be influencing and changing the genetics of Pit Bulls -- and not in a good way?

The following is a single Pit Bull attack that occurred recently.I am providing it to show what was required to stop this dog in an enclosed location with animal-handling experts present.Imagine the terror and damage if there had been more Pit Bulls involved:

Attacking Pit Bull Shot in Animal Shelter to Save Life of Supervisor

Here is a terrifying example of the relentless nature of a Pit Bull attack. It was recorded on the kennel video in the Oakland County animal shelter and reported this week by theDetroit Free Press. The severely injured supervisor was a 25-year veteran of animal care and control.

The four-year-old Pit Bull involved, Roscoe, and had been surrendered after he attacked an adult and two children in the family that had reportedly loved and raised him since a puppy.

"When three Oakland County dog shelter workers couldnt dislodge a ragingpit bull mauling the kennel supervisor, a policeofficer shot thedog in the head, saving the supervisor. . . Yet, the 80-pound dog after being shot at point-blank range, between the eyes, seemingly rose from the dead, the Oakland County spokesman said.

The officer returned to the hallway of the six kennels housing dangerous dogs and found that the pit bull had regained consciousness and "now posed a fresh threat."

The officer saw it was now a wounded animal and the possible threat played through his mind, so he immediately ended its suffering with a second shot that was fatal," the spokesperson said.

The report states that,even after the incident was conveyed to the family, the mother refused to give permission to euthanize the dog, blaming the serious attack on herself and her two children to the fact she had been "talking too loud."

Roscoe had also previously bitten a shelter worker who took him out for a walk.

RECENT ATTACKS BY MULTIPLE PIT BULLS

Three Pit Bulls Kill Womanin Houston, TX on December 21, 2019.DogsBite.orgreports one woman is dead and another severely injured after a vicious dog attack in north Houston, according to police. . .KTRK reports thatall three dogs are pit bulls.

Woman Attacked by 6 Pit Bulls While Walking Dog. . .

Apr 26, 2019 -Awomanis recovering after police say she wasattackedbysix pit bullswhile walking her daughter's dog Wednesday night in Taunton, Massachusetts.. . .The officer then witnessedsix pit bullsfollowing andattacking51-year-old Rochelle Silva.

4 Pit Bulls Attack Woman Walking Dog. . .

Jun 24, 2019 -Awomanwas recovering after she wasattackedbyfour pit bullswhile walking her roommate's dog in Calgary, Canada, on Friday night.

Woman critically injured in Maryland pit bull attack

Nov 14, 2019 -Awomanwas critically injured in anattackby twopit bulls. . .Helicopters were used to searchforthe dog. . .

5 Pit Bulls Attack Woman On Bike, 'Tore Her Apart', Husband. . .

Apr 2, 2019 -A Florida woman underwent surgery Monday after suffering serious injuries following anattackbyfive pit bullson March 28.

Five Pit Bulls Maul Philadelphia Toddler to Death

Aug 2, 2018 -A 2-year-old boy was mauled to death byfive pit bullsat his aunt's house in the Port Richmond area of Philadelphia, local police have said. Officers responding to the incident at around5:35 p.m. Wednesday fired at the dogs to stop theattack, killing one and injuring two others, reported WPVI.

For shocking and informative quick-stats and graphs, see:Deadly Dog Attacks.

Read also:CA Hits Record High in Fatal Dog Attacks in 2019 -- Are Animal ControlPolicies Protecting Us?

HISTORY:PIT BULLSUSED FOR FIGHTING - NOT NANNY DOGS

Human aggression by Pit Bulls was not acceptable in past generations, including by dog fighters.The early 1900's photos which are now purported to be "Nanny Dogs" were actually ads used to show that the breeding stock by a dog man was NOT human aggressive and would not attack a human at a dog fight/match -- it did not mean they were house pets.

Dog fighting was legal in the U.S. at that time and advertising Pits bred for that purpose was rampant. They were bred to attack another dog without provocation andkill quickly and efficiently. They werenotintended to be released into society.(Google 'Pit Bulls for Sale' ads in the early 1900's inDog Fanciermagazine.)

PIT BULLS THAT ATTACK HUMANS NOT KEPT BY DOG FIGHTERS

Following an ad for pups from the line of "Old Family Red Noses and "Red Devils" with photos of "Wilder Red Inferno" and "Mean Girl, " here areexcerptsfrom an op-ed that appears in theAmerican Pit Bull Terrier Gazette(FALL 1997).

SIMPLY RETROSPECT OR RESPECT?(by Charlie Stephens,President, Lone Star APBT Club.)

"LET'S LOOK AT THE 1920'S AND1930'S. Things were very different then.We went to church on Sunday with no thought of burglary or theft, and the dog we had didn't dare bite a human being.If a dog, any dog, was aggressive toward humans it was killed.No, not gassed or injected, it was shot! It was a simple time and that type of dog simply was not tolerated.And this was especially true for the American Pit Bull Terrier. Dogmen of the 1920's and '30's would not allow it!

Today, however, it is different.People are scared, real scared, and they believe they need protection.So, they go out and buy a dog.

(He mentions five incidents of APBT attacks.)

In closing, I make a plea to all dog owners of America. Please take responsibility for your dog. . . If you must own a dog that is human aggressive, then keep it away from humans.And, keep it away from windows too.

PIT BULLS/FIGHTING DOGS CHANGED BY ADAPTATION

AJanuary 18, 2019 article, "The so-called modern bloodlines,"byNeylor Zaurisio, discusses and documents his personal study ofhow, since the 1800's, modern living necessitated adaptations that changed the name of the breed and also affected its size.

"In the late 1800's,with the industrial revolution, thousands of families migrated from rural areas to large industrial centers in search of employment.

Some of these families had as a form of extra income and tradition sold and bet on fighting dogs, Pit Bull dogs. When they saw the opportunity of a better future in the big cities they started to move and took their dogs with them, changing drastically from a habitat where they developed completely, to small spaces in apartments and other cheap options where they were confined most of the time, [loss of] exercise and losing their habit, combined with the selection for smaller dogs, caused a visible reduction in muscular and bone structure.

PIT BULLS HAVE ALSO ADAPTED BY SELECTIVE BREEDING

Pit Bull genetics have been changed several times.In theUnited Kingdom, bull-and-terriers were used inblood sports, such as,bull baitingandbear baitinguntil this was officially eliminated in 1835 when Britain introducedanimal welfare laws.

Sincedog fightingis cheap to organize and far easier to conceal from the law, blood-sport enthusiasts begin to develop dogs that could be pittedagainst each other.

DOG FIGHTERS OPPOSE BSL AND "MANDATORY SPAY/NEUTER"

Dog fighting was used as both a blood sport (usually involving gambling) and a way to continue to test the gameness and maintain fighting blood lines. Maintaining these bloodlines is the reason dog fighters do NOT want "Breed Specific Legislation" (BSL) nor mandatory spay/neuter laws.

If this centuries-old lineage is destroyed, it cannot be replicated.The characteristic of "gameness" means the animals will attack and kill without provocation--includingits own breed.It also means it will continue to fight until it is dead or physically incapable of movement.

PIT BULLS HISTORICALLY KEPT IN ISOLATION

Pit Bulls have traditionally been kept as the only dog in a household, chained or caged in isolation because of their propensity to attack/kill. (Dog fighters keep them caged or "tied out" on chains in their yards.A yard can be any size property, and many keep dozens of dogs -- each far enough from the others to be unable to engage physically. They did not indulge in "play groups."

MULTI-DOG HOUSEHOLDS, NO BSL AND NO PET LIMITS

The "No Kill" movement as prescribed by Best Friends Animal Society has imposed rigid rules for animal shelters and animal owners regardingeuthanizing a dangerous dog, and many veterinarians are afraid to take this risk because of the criticism that can be generated on the Internet.

Prior to this, rules and laws of animal ownership were created and enforced for public and animal health and safety, animals were limited to the number that did not create excessive noise and exhibit behavior issues that decreased or threatened the safety and quality of life of a community.

Best Friends policies links:

Save Them All - Best Friends Animal Society- Best Friends Animal Societyis leading the way.

Best Friends Position Statements on Issues -BestFriendsis opposed tomandatory spayandneuterlaws.

Dog Breed Labels | Best Friends Animal Society-Apr 6, 2018-Labelingshelterdogs as a particularbreedis problematic.Shelterstaff are wrong a majority of the time when identifying a dogs prominent breed. . .

Pet Limit Laws in Los Angeles | The Best Friends Blog

Dec 14, 2010 -Los Angeles is looking to raise itsanimal limit laws. Five reasons whypet limitsare a bad idea in the first place.

Pit Bulls, Dog Breed Discrimination & BSL | Best Friends.

One ofBest Friends' primary goals is to end pit bull breed discrimination,breed-specific legislation(BSL) and the killing of pit bulls in shelters.

Read also:Best Friends Animal Society in Dog Fight over Shock Collars(Nov 25, 2019)

MULTIPLEPIT BULLSMAY BE THE NEXT GATHERING STORM

In 1990, Donald H. Clifford, DVM, and two other noted staff members at the medical College of Ohio, published THE PIT BULL DILEMMA - The Gathering Storm," annotating 1.000 abstracts from books, journals, magazines, newspapers and reports of dog fighting and Pit Bull Attacks.

This was a warning that a new threat was being unleashed on society.(CA enacted a No Breed Specific Legislation prohibition in 1989.)

After Pit Bulls began to be kept as pets, owners generally kept only one orperhaps with a dog of the opposite gender (but even this may not stop them from inevitably fighting or killing each other.)

However, the basic behavior seems to be changing--perhaps as an adaptation to multiple-Pit households--so that numerous Pit Bulls can live together without killing each other but attack as a pack.Is this an anomaly, or is there a change occurring in the genetic structure of the dogs?

IS THE MULTIPLE-PIT BULL ENVIRONMENT CHANGING THE GENETICS OF PIT BULLS?

In the study, "Both Environment and Genetic Makeup Influence Behavior," the following conclusion was reached:

How do genes and the environment come together to shape animal behavior? Both play important roles. Genes capture the evolutionary responses of prior populations to selection on behavior. Environmental flexibility gives animals the opportunity to adjust to changes during their own lifetime.

I am not a geneticist, but I think it is worth questioning whether creating a living environment for Pit Bulls as pets in large or unlimited numbers in the same household is also creating changes in genetics which allows them to act in unison during attacks, but not turn on each other?

And, if so, judging from the recent increase in multiple Pit Bulls attacking as a pack, what issues does this pose for the future of society and community safety?

(Phyllis M. Daugherty is a former City of Los Angeles employee and a contributor to CityWatch.) Edited for CityWatch by Linda Abrams.

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A World Without Pain – The New Yorker

Posted: January 8, 2020 at 8:45 pm

We like to think that what doesnt kill us makes us stronger, or more resilient, or... something. Deeper. Wiser. Enlarged. There is glory in our sufferings, the Bible promises. Suffering produces perseverance; perseverance, character; and character, hope. In this equation, no pain is too great to be good. The darker the night, the brighter the stars, Dostoyevsky wrote. The deeper the grief, the closer is God! We atheists get in on the action by insisting that the agony of loss elucidates the worth of love. The hours spent staring into the dark, looping around our own personal grand prix of anxieties, are not a waste of time but a fundamental expression of our humanity. And so on. To be a person is to suffer.

But what if our worst feelings are just vestigial garbage? Hypervigilance and pricking fear were useful when survival depended on evading lions; they are not particularly productive when the predators are Alzheimers and cancer. Other excruciating feelings, like consuming sadness and aching regret, may never have had a function in the evolutionary sense. But religion, art, literature, and Oprah have convinced us that they are valuablethe bitter kick that enhances lifes intermittent sweetness. Pain is what makes joy, gratitude, mercy, hilarity, and empathy so precious. Unless it isnt.

I know the word pain, and I know people are in pain, because you can see it, Joanne Cameron, a seventy-two-year-old retired teacher, told me, in the cluttered kitchen of her century-old stone cottage in the Scottish Highlands. Cameron has never experienced the extremes of rage, dread, grief, anxiety, or fear. She handed a cup of tea to Jim, her husband of twenty-five years, with whom shes never had a fight. I see stress, she continued, and Ive seen pain, what it does, but Im talking about an abstract thing.

Because of a combination of genetic quirks, Camerons negative emotional range is limited to the kinds of bearable suffering one sees in a Nora Ephron movie. If someone tells Cameron a sad story, she crieseasily! Oh, Im such a softie. When she reads about the latest transgression by Boris Johnson or Donald Trump, she feels righteous indignation. But then you just go to a protest march, dont you? And thats all you can do. When something bad happens, Camerons brain immediately searches for a way to ameliorate the situation, but it does not dwell on unhappiness. She inadvertently follows the creed of the Stoics (and of every twelve-step recovery program): Accept the things you cannot change.

Cameron, who has white hair and was wearing denim overalls over a purple striped shirt, has a bouncy, elfin energy. She described the closest shed ever come to experiencing real terror: an incident when her son, Jeremy, a musician, was beaten up so badly at a gig that he had to be hospitalized. He was defending someone, Cameron said. The lead singer was gaywere talking a good few years ago, when they werent quite as toleratedand they started calling the gay chappie names, and then suddenly the whole lot of them came on top of Jeremy.

They punched him, and kicked him, stamped his head, Jim, a tall, genial man, with a white beard and a thick brogue, added gravely.

When Cameron got the call, she remembers, initially, I thought, Oh, God, I hope he doesnt dieI felt that. Then we got in the car. I wasnt fretting, I was just thinking, Weve got to get to him, he needs me. They drove a hundred and thirty miles on the single-track roads that wind east from their home in Foyers, near the snaky banks of Loch Ness, to Peterhead. We got to the hospital about four or five in the morning. He looked like an elephant man, my handsome boy did, Cameron said, laughing. He looked like nothing on earth!

In addition to Jeremy, who is forty-two, Cameron has a daughter, Amy, who is thirty. Her experience of motherhood has entailed none of the rumbling terror that most parents feel over their childrens safety. Some time ago, someone said to me, When the baby comes, the first thing you do is count the fingers and toes. I thought, I never looked at anything! Cameron said. I never dreamed of there being anything wrong.

In sharp contrast to her near-inability to feel awful, Cameron has an expansive capacity for positive emotions. She is exceedingly loving and affectionate with her husband. When I first came to the door, she greeted me with an embrace, crying, Ooh, Im very huggy! Her seventeen years as a special-education teacher required great reserves of compassion. I had a Down-syndrome girlwho was actually quite high-functioningand she would come in every morning and shed walk up to me and spit in my face, and say, I hate you, Jo Cameron! I hate you! And Id stand there and say, I dont like being spat on, but I dont hate you! Cameron told me, smiling. Oh, Ive had some very difficult students. Ive been bitten; Ive been spat on; Ive been kicked! Over the years, the Camerons have provided short-term foster care for four children. One of them stole all their vacation money from the cookie jar. She did take things for the sake of taking them, Cameron said pleasantly. It took us years to catch up! When eight hundred pounds is gone from your vacation kitty, it takes a long time to recoup.

Even seemingly sorrowful things, like the loss of her mother a year ago, can fill Cameron with appreciation and pleasure. My mothers death was the least saddest thing ever, Cameron declared. She used to say, Ive had the most wonderful life. And she died after she had an iced lolly and went to sleep. When the doctor arrived, Cameron recalled, she said, Dont take this the wrong way, but thats the most beautiful corpse Ive ever seen. Then we sat in the kitchen and had a fantastic wake: we toasted Mum with Tia Maria till the early morning.

Cameron plans to leave her own corpse to science when she dies. Theyll whisk the body away, and stick us in a drawer somewhere and chop us up, wont they? she said. I dont mind. She will also spend a good deal of her remaining time alive being studied by scientists, who hope that her genetics will provide a path to new treatments for anxiety and trauma, as well as for pain management and healing. In addition to her unusual emotional composition, Cameron is entirely insensitive to physical pain. As a child, she fell and hurt her arm while roller-skating, but had no idea shed broken it until her mother noticed that it was hanging strangely. Giving birth was no worse. When I was having Jeremy, it was the height of everyone doing natural childbirths, she said. My friends would come up to me and say, Dont listenits murder. If youre in pain, take everything they give you. I went in thinking, As soon as it gets painful, Ill ask for the drugs. But it was over before I knew it.

Remarkably, Cameron didnt realize that she was any different from other people until she was sixty-five. Lots of people have high pain thresholds, she said. I didnt think people were silly for crying. I could tell people were upset or hurt and stuff. I went through life and I just thought, I havent hurt myself as much as they have.

Devjit Srivastava was an officer in the Indian Navy for a decadean experience that taught him to stay cool under pressure. Composure is also important in his current job, which is unpredictable and high-stakes: Srivastava is the consultant anesthetist at what he calls a frontier hospitalRaigmore, in Inverness, which serves the whole of the vast and remote Scottish Highlands. His first day on call, he was pulled into a helicopter to help with a field amputation on a farmer who had got caught in a thresher.

When Srivastava met Jo Cameron, six years ago, she told him that she wouldnt need painkillers for the surgery she was about to undergo. He assumed that he was just dealing with a kindred imperturbable spirit. The Scottish are known to be stoic people, Srivastava said, drinking coffee in the bustling hospital cafeteria. I thought, Shes just trying to tell me she can tolerate pain very well. And, actually, its a busy list, and we have to crack on.

Cameron was having a trapeziectomy, an operation to remove a small bone at the base of the thumb joint. Though her hands never hurt, theyd become so deformed by arthritis that she couldnt hold a pen properly. Shed had a similar experience with her hip, which had recently been replaced; it didnt hurt, but her family noticed that she wasnt walking normally. She saw her local doctor about it several times, but the first question was always How much pain are you in? And the answer was always None. (The third time I was there I think they figured, Well just take an X-ray to shut this woman up, Cameron told me. Then the X-ray came in and it was really bad. Everything was all distorted and mangled and crumbling. He said, Wow. This has got to be done.)

Srivastava told Cameron that, Scottish stoicism notwithstanding, he intended to use an anesthetic block during the operation. After she left the hospital, he reviewed her chart: She had only one paracetamola Tylenolimmediately after the operation in the recovery area. And that was only because the nurses give everybody a paracetamol after surgery. I checked the full records of hip replacement the previous year: after hip surgery it was the same thingnothing taken for pain. Thats when I called her in.

He remained slightly skeptical until Cameron let him perform a maneuver that anesthesiologists use on patients who are having difficulty regaining consciousness after sedation: they press hard on the inner edges of the eye sockets, and the pain shocks people awake. Cameron, of course, felt only pressure.

Srivastava was surprised that no doctor or nurse had been curious about her pain insensitivity before. (Cameron told me that she didnt think it was particularly notable: Theyve got so many people demanding their attention, screamingtheyre the ones you focus on.) Srivastava recognized that her case was extraordinaryThis doesnt fall into every anesthetists life, he saidand also that understanding it would require him to supplement his own expertise. He developed a research protocol, and enlisted highly regarded scientists from around the world to try to figure out what caused her condition.

Cameron is beguiled by the idea that she can help alleviate others sufferingshe remembers the terrible migraines that tormented her mother. Her father, however, was pain-free. I never saw him take an aspirin, Cameron said. Im convinced he was the same as me, because I never heard my father complaining about any pain, ever. He died suddenly, of a brain hemorrhageI think other people would have had a warning. She continued, He was the kindest man youll ever meet. Every morning hed wake us with a cup of tea and a carrot from the garden and tell us a poem. Then hed accompany Cameron to school, hand in hand and skipping all the way.

The scientists who took on Jo Camerons case were working in a young field. Geneticists have been studying congenital insensitivity to pain only since the nineteen-nineties. In that time, several hundred cases have been reported; presumably there are others, but no one knows how many. The condition is almost always caused by neuropathy, an interruption in the transmission of painful sensation along nerve fibres. People with severe congenital neuropathy tend to die young, because they injure themselves so frequently and severely. (Without pain, children are in constant danger. They swallow something burning hot, the esophagus ruptures, bacteria spill into the internal organs, and terminal sepsis sets in. They break their necks roughhousing. To protect some patients, doctors have removed all their teeth to prevent them from chewing off their tongues and bleeding to death.) There are also people whose neurons stop working, as the result of a disease: syphilis, lupus, diabetes, rheumatoid arthritis.

In recent years, advances in genetic science have made it possible to link particular variants of pain insensitivity to mutations in specific genes. Six members of the Marsili family in Italy, for instance, share a mutation in the gene ZFHX2; consequently, they rarely sweat, experience pain only fleetingly, and are completely insensitive to heat. We live a very normal life, perhaps better than the rest of the population, Letizia Marsili, the matriarch of the family, said in 2017. (She once broke her shoulder while skiing in the Italian alps; she continued skiing without any pain for the rest of the afternoon, and got around to seeing a doctor only days later, when it was convenient.) There are downsides, though, to whats been named Marsili syndrome. Letizias mother suffered multiple fractures in her youth without noticing them; her bones were never set properly, and they healed awry.

In 2006, Geoff Woods, a geneticist at Cambridge, published his findings on members of several families in a remote region of northern Pakistan, who share a mutation in the gene SCN9A, which renders them both pain-free and unable to process smell. (Since then, people with the same mutation have been identified all over the world, but the Pakistani patients were an ideal group to study: they were all the products of cousin-to-cousin marriages, making their gene pool unusually easy to map.) The lack of a sense of smell is really helpful, because it provides us with a simple question we can ask new patients, James Cox, a former researcher of Woodss who is now a prominent geneticist at University College London, said. Cox has been studying Camerons DNA for five years, and has co-authored a paper with Srivastava about her case, which was published last March, in the British Journal of Anaesthesia. Jo is quite unique, he said.

Cameron does not have neuropathy: she can feel all the sensations the rest of us do, except pain. The most striking difference between her and everyone else is the way she processes endocannabinoidschemicals that exist naturally in every human brain. Endocannabinoids mitigate our stress response, and they bind to the same receptors as the THC in the kind of cannabis you smoke. Normally, they are broken down by an enzyme called fatty acid amide hydrolase, or FAAH. But Cameron has a mutation on her FAAH gene that makes the enzyme less effectiveso her endocannabinoids build up. She has extraordinarily high levels of one in particular: anandamide, whose name is derived from the Sanskrit word for bliss.

About a third of the population has a mutation in the FAAH gene, which provides increased levels of anandamide. That phenotypelow levels of anxiety, forgetfulness, a happy-go-lucky demeanorisnt representative of how everyone responds to cannabis, but you see a lot of the prototypical changes in them that occur when people consume cannabis, said Matthew Hill, a biologist at the University of Calgarys Hotchkiss Brain Institute, who was a co-author of the Cameron paper. The FAAH gene, like every gene, comes in a pair. People who have the mutation in one allele of the gene seem a little high; people who have it in both even more so. Jo Cameron is fully baked.

When I met Jo for the first time, I was just struck by her, Cox, an affable forty-year-old with a scruffy beard, told me, one afternoon in his lab at U.C.L. She was very chatty. Did you notice that? (Its hard to miss.) I said to her, Are you worried about whats going to happen today? Because she was meeting our clinicians to have a skin biopsy and do quantitative sensory testingpain-threshold tests. She said, No. In fact, Im never worried about anything. Cox told me that it was difficult to get through everything in the time theyd allotted, because Cameron was so friendly and loquacious with the scientists, even as they burned her, stuck her with pins, and pinched her with tweezers until she bled. This imperviousness to pain is what makes her distinct from everyone else with a FAAH mutation. They, like even the most committed stoners, can still get hurt.

Cameron had the same FAAH mutation that many other people havebut there had to be something else at play. The scientists started their inquiry by isolating DNA from her blood, and then analyzing the protein-coding subset of her genomethe part thats traditionally considered to be significant. We didnt really find anything, Cox said. So we decided, O.K., why dont we look across the whole genome for bits that are deleted or duplicated? And, at the time, this new chip was just available, which enabled us to scan the whole genome and look for deletionssnippets missing from her genetic code. It was a lucky strike: we found that there was this deletion. But it was distinct from FAAH. It was away from FAAH, just downstream.

The scientists noticed that the right edge of the deletion overlapped a gene that was annotated as a pseudogene, Cox said, and frowned. Which is a term I dont like. A pseudogene is whats been thought of as genetic detritusa copy of a gene thats just sitting there, not doing anything productive. One biochemist I spoke to likened a pseudogene to a rusted-out car you stumble on in the forestonly, in Camerons case, they put a key in the ignition and the car turned on. To call it a pseudogene is misleading, because this is a gene that is expressedit makes a product, a sequence in the DNA, Cox said, with excitement. Its a real fascinating class of genes which have been severely overlooked in genetics until very recently. Cox and his colleagues named this particular pseudogeneIts nicer to call it a gene, he insistedFAAH OUT. It was a wordplay, really, he said sheepishly. The challenge now is to understand what its doing. Jo is the first person in the world that we know of with this.

Camerons case is important in genetics, partly because it may supply evidence that pseudogenes are more significant than they were previously thought to be. Moreover, if scientists can replicate her neurochemistry they might be able to develop treatments that alleviate the opioid epidemic. They could potentially treat otherwise intractable anxiety and depression. Perhaps we could all be a little more like Jo Cameron: joyful, compassionate, unperturbed by all the nasty, roiling feelings that turn us, from time to time, into goblins.

I asked Matthew Hilla renowned expert on cannabinoids and stressif there was any downside to Camerons biology, and he laughed out loud. Yes! From an evolutionary perspective, it would be tremendously destructive for a species to have that, he said. Without fear, you drown in waves that you shouldnt be swimming in; you take late-night strolls in cities that you dont know; you go to work at a construction site and neglect to put on a hard hat. Her phenotype is only beneficial in an environment where there is no danger, Hill asserted. If you cant be concerned about a situation where youd be at risk of something adverse happening to you, you are more likely to put yourself in one. Anxiety is a highly adaptive process: thats why every mammalian species exhibits some form of it.

Unlike other pain-insensitive people, Cameron has made it into her seventies without getting badly hurt. Sometimes she realizes that shes burning her hand on the stove because she smells singeing; sometimes she cuts herself in the garden and sees that shes bleeding. But none of that has been severe, and Cameron did raise two children safely into adulthood.

The human brain is very capable of learning, This is whats appropriate to do in this situation, Hill said. Camerons relative cautiousness may have developed imitatively. And there may not have been that much threat presented to hershes lived in a rural community in Scotland, he concluded. Maybe she hasnt had to deal with that much that would physically or emotionally harm her.

Scotland is notorious for one of the vilest climates under heaven, Robert Louis Stevenson, who was born in Edinburgh, wrote. The weather is raw and boisterous in winter, shifty and ungenial in summer, and a downright meteorological purgatory in the spring. But the week in autumn when I visited was blissfully sunny. Farmland rolled under a gleaming blue sky for miles around the Camerons property, green and gold and dotted with sheep. Behind their cottage, they grow vegetables in little plastic greenhouses, and their chickens peck about in a modest orchard of pears, apples, and plums. We look after the hens very well, Cameron said. (She is a vegan; her husband is a vegetarian who sometimes indulges in an egg.)

The Camerons do everything together, Jo said. They make wine, and take weekly trips to Edinburgh to visit Amy; theyre in a local theatre troupe, for which Jo is the stage manager. (She doesnt act, because she cant remember the lines. As we were walking through the garden, a pizza was burning in the oven: Cameron had forgotten that she was making one for lunch.) I love Jim to bits, Cameron said. Hes smashingIm so lucky. Having had a marriage before where... She trailed off, thinking about her previous husband. I mean, I loved him. But you never knew what you were coming home to.

Camerons first husband, Phil, died after a prolonged battle with mental illness. Hed either be full of fun and laughter, or hed be so depressed hed be curled up in the corner in the fetal position, she said. He was like this She mimed a seesaw going violently up and down. Bipolar.

They met when they were both university students near Birmingham, England, where Cameron grew up. He was lovely, she said. But he always had a dark side. He would get down, and I would be the one that would bring him up again. You know, thered be a game going: Oh, its not that bad, come on.

Phil had his first major episode as the family was on its way to a vacation in Sardinia, when Jeremy was little. He just cracked, Cameron said. On the plane, all the way there, he was kicking me, pinching me. (Its impossible to say how hard; it didnt hurt.) We got to the hotel, and I said, Can someone please come and help me? My husband is having a breakdown. She recalled the difficulty of finding a flight home on short notice, of thinking of an excuse to give Jeremy. He always had it under control, she said. But suddenly he couldnt control it. Phil tried a variety of medications and saw several psychiatrists over the years. I always went to every session, Cameron said. The last time he went to see somebody, the doctor said to me, This is terminal, you know. At some point, he will... And six months later, sure enough, he did.

I asked Cameron what she felt when the psychiatrist said that. (And I imagined how I would feel: desperate, heartsick, powerless, distraught.) I looked at the state he was in, and I thought, Maybe its good, she said. Cameron was back at work the day after the funeral. It sounds cold. But you say to people, Im not being cold! Look, horrible things happen. Im not in airy-fairy land. Horrible things are going to happen. You have to cope with it. You have to say to yourself, I cant help that person. You help them as much as you can, but when you cant help them anymore, then you have to help everyone else.

Amy was a year old at the time, and Jeremy was thirteen. We all went to the beach every weekend after Phil died, Cameron recalled. I said to Jeremy, What well do every Sunday is well put Amy in the back of the car, and you get a mapbecause he loved mapsand I wont know where were going, just direct me. Hed go, Turn left, now turn right, go along here. And wed turn up in all sorts of places, and wed have Sunday lunch. We had a great time doing that. Whenever I pressed Cameron for details about a seemingly devastating occurrence, she wasnt evasive; she was mystifyingalways ending up on a lovely memory, via a route so unforeseeable it was as if it, too, were determined by a child with a map.

Cameron began dating Jim, who was teaching science at the time, and had known her late husband from their village chapter of Roundtable, a kind of Scottish Rotary Club. Five years later, they married, and Jim adopted Amy. (Jeremy was already a young adult.) Cameron said of her daughter, Shes geometrically opposite me. She worries about everything. From an early age, Amy demonstrated talent as an artist, and her work has been exhibited across Europe. Her portfolio includes sculpture, earthworks, and intricate, realistic drawings, often interspersed with text. In one piece, above the image of a sleeping baby, float the words feeling/the sacrifice/cut through/and sectioned/kept alive by/these unfortunate animals of emotionsfear, disgust, anger, etc. Odder still people feel nothing.

Amy finds her mothers equanimity confounding. Shell say, Why cant you be a normal mom? Cameron told me. When Cameron asked, Whats a normal mom? Amy replied, Well, its not you. They shout! Cameron shook her head at the memory. I sometimes think to myself, Im being horrible. If someone is really in a rage and really upset, and youre saying, Its all right!, then they get angrier. I can be very annoyingespecially when youre a teen-ager and you dont want your problems solved. You just want someone to shout at.

Paul Bloom, a professor of psychology at Yale and the author of the book Against Empathy, maintains that relating to suffering has little to do with the capacity to be helpful and kind. He has published research suggesting that compassion, not empathy, drives altruistic behavior. (Most research on the subject blurs together empathy and compassion, but Bloom argues that this is a failure of experimental design: The standard measures suck.) Empathy can actually get in the wayif you are in terrible pain and I feel so much empathy for you that, being with you, I feel it, too, I may decide to stay home, he told me. The Buddhists knew this. Theres all this teaching that says, Dont get sentimental. Joyously and lovingly help others, but dont get in their heads. Cameron, he told me, was a perfect illustration of his point: Shes my dream girl. She doesnt feel the pain of others, so she doesnt feel empathy per se. But she cares for others.

For nearly a decade, pharmaceutical firms have tried, without success, to create medications that act on FAAH. In 2016, the Portuguese company Bial Pharmaceuticals abandoned one such drug after a Phase 1 clinical trial in which six participants were hospitalized, and one died. (Scientists believe that there may have been a dosing accident, or that the drug had off target effectsit ended up binding to a receptor other than FAAH.) Pfizer gave up its own attempts at a FAAH inhibitor in 2012, because the drug didnt work. Recently, though, it started research again, and Vernalis funded a study at Brigham and Womens Hospital, in Boston, which is undergoing peer review. The prospect of a breakthrough is too promising to relinquish.

Opioids, besides being addictive, dont always work: some kinds of chronic pain dont respond to drugs that target the opioid system, or to other analgesics, such as ibuprofen and corticosteroids, which operate on the prostaglandin system. Cameron may provide the key to a new class of drugs that operate on the endocannabinoid system. Srivastava told me that the paper he worked on with his colleagues was just the beginning. You realize that this is sort of nature revealing its secret to you, he said, and you only worked on part of that secret, but if you worked on the full secret, so to say, it could be astounding.

For half a century, scientists have accumulated evidence that pain is not simply the result of a one-way flow of sensory information from an injury to the brain. Before the brain gets involved, gates in the spinal cord modulate the way we feel painwhether it is fast-travelling information, as in a stab wound, or the dull, slow-moving kind that characterizes chronic pain. These spinal gates can be opened or closed by a variety of factors. A distracting physical sensation can temporarily close them; when you bump your head and instinctively rub that spot, you are overriding the nerves that register pain with the nerves that register rubbing. Your emotional state, too, can have an effect. Its evolutionarily advantageous for pain gates to be wide open when youre stressed: if you were anxiously evading a predator, your body would want to let you know if you were stepping on something sharp that might hinder your ability to escape. Conversely, if you are very relaxed, your gates are less apt to be open. One of the things Srivastava and his colleagues want to explore is the extent to which Camerons pain insensitivity is the result of her peaceful state of mindand vice versa.

The second phase of Srivastavas research will include Camerons son, Jeremy, who has the FAAH mutation on one but not both alleles of the gene, and who has a high tolerance for pain. (Unlike many FAAH people, Jeremy, who declined to be interviewed, is painfully shy.) But this goes much beyond genetics, Srivastava continued. We are deconstructing pain mechanisms in Jo. Because she has sensation but no pain, she presents unique possibilities for research. We know this nerve carries that, this is how it is done, bit by bit we have progressedbut here is a golden opportunity to do it all at once, and confirm, rebut, or come up with new findings, Srivastava said. He has been contacted by doctors and scientists in Sweden, France, England, and the United States, who want to collaborate. Srivastava, who is fifty, is an impassive man, but he looked a little fretful as he talked about the research. I feel slightly overwhelmed, he admitted,like I dont have enough time in this life to properly do it.

One complicating question is how much of Camerons Cameronness is really a consequence of her FAAH mutation and FAAH OUT deletion. She has plenty of other genes, after all, and her upbringing and her early environment also played a role in making her who she is. Since the paper was published, Matthew Hill has heard from half a dozen people with pain insensitivity, and he told me that many of them seemed nuts. If you had this phenotype and werent a generally pleasant person like Jomaybe youre, like, a douche-y frat boythe way that you would process this might be entirely different. Our whole perception of this phenotype is explicitly based on the fact that it was Jo who presented it.

Srivastava is intent on solving the scientific riddles that Cameron poses. But, in a wistful moment, he suggested that the work also raised profound social questions. Spending time with her, you realize that if we only had more people like Jowho are genuinely nice, pleasant, do not give in to anger... well, he said, you know.

Misery may not be all its cracked up to be. Paul Bloom, who is writing a book about suffering, told me, Theres a big movement in psychology to say, What doesnt kill you makes you stronger. People talk about post-traumatic growth. I think a lot of it is bullshit. Look at the data: bad things are bad. You arent healthier after you have cancer or fall down a flight of steps. And its only in the movies that getting hit by a bolt of lightning turns you into a superhero; in life, it turns you into a fritter.

The entire time I spent behind the wheel in Scotland I was suffering what psychologists call an aversive experiencethat is, I was afraid for my life. The Scots drive on the left side of the road, which is already a challenge, but in the Highlands near Loch Ness there is only one lane. When another car comes barrelling at you, youre supposed to pull over on the (nonexistent) shoulder, but this can be hard to remember when you come around a sharp curvewhich happens roughly every two secondsand find yourself in the glare of rapidly oncoming headlights. I was pretty sure that one of these encounters would send me over a cliff, plummeting toward the dark water like Toonces the Driving Cat.

I relaxed slightly when I was back in Inverness, where my only foes were the baffling roundabouts, with their unique Scottish etiquette. I had just navigated such a rotary and was on a seemingly easy stretch of highway when I felt an explosion underneath me, then heard the hideous sound of metal scraping asphalt. Id hit the curb with such force that Id popped my front left tire.

I felt my blood pumping and my skin prickling, and I whipped my head around to see how many people Id killed. In the process, I scratched my forehead on the sharp corner of the seat-belt mechanism, and it hurt. There was nowhere to pull over, so I rumbled loudly onward, afraid that something worse was about to happenmind racing, pain gates open, tire rim scraping the street. I felt panic about getting to the airport, followed by irate self-recrimination (why am I such a bad driver?), then by irate spousal recrimination (why didnt he get his stinking passport renewed in time, so he could come with me on this trip and drive?). I was a wounded, furious, frantic goblin.

Then I thought about Jo Cameron, and what she would do in this situation. She would keep going until there was a place to pull over, and she wouldnt worry about how far that might be or what might happen before then, because thered be nothing she could do about it. Shed park, call the rental-car place, and take it from therecalmly, kindly, without losing her mind or her sense of humor.

Gradually, my heartbeat slowed, and I saw in the rearview mirror that the scratch on my forehead hadnt even broken the skin. I remembered something that Matthew Hill had said about how a stress response is biologically designed to reallocate energy for survivalthe goblin feelings are just a weird side effect. Cortisols main job is to boost your blood sugar, and adrenalines main job is to jack up your blood pressure, so you have fuel and a delivery method to sustain your muscles and brain in dealing with an aversive threat, hed explained. But we have so rapidly out-evolved the requirements of those processes they are almost like an evolutionary throwback. When we check a Facebook page and find out our partner has cheated on us, our brain still mounts that same biological response, even though it has zero value to us anymore. Even Hillwho told me how disastrous it would be for human beings to float through life without anxietyconceded, Maybe Jo is the next evolutionary step.

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A World Without Pain - The New Yorker

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How the 1920s Can Inform the 2020s in Health Care – InsideSources

Posted: January 8, 2020 at 8:45 pm

Dr. John H. Bell was the superintendent at the Virginia State Colony for Epileptics and Feebleminded

The 2020s have arrived. Science and technology are poised to revolutionize health care, spawning moral questions we cant yet imagine. Such questions will tempt governments to mandate or prohibit new technologies. Unintended consequences will follow.

2020 marks a good time for medical professionals, ethicists and policymakers to examine events that transpired in the previous 20s the 1920s a similar period of foment. In 1920, nobody quite knew the nature of the coming medical revolution. Before the decade was out, hope turned to hubris, and public policy veered in abominable directions.

In the 1920s, scientific and political consensus led to appalling abuses of human rights, including the forcible sterilization of tens of thousands of Americans.

In teaching medical professionals, Ive always devoted a week or two to the 1920s, never telling the students exactly why we were covering this period or exactly what they were supposed to learn from it. They were left to draw their own lessons on what that period means for our own time. Ill do the same here.

First, a bit of context. From around the 1830s on, Western medicine sank into therapeutic nihilism the idea that then-existing medical interventions did more harm than good, so doctors should limit their activities to observing and comforting patients not trying to heal them. In the late 1800s, the field of statistics emerged, and researchers zealously applied new mathematical tools to the study of physical and mental illness. Knowledge grew rapidly, but confidence in that knowledge grew even faster. Therapeutic medicine was back. The 1920s produced insulin and penicillin, but it also generated an awful consensus around eugenics the highly politicized junk-science predecessor to genetics.

Eugenics was purportedly the science of good breeding. Armed with statistical tools and modern medical techniques, eugenicists believed they could and should breed a superior race of humans by encouraging fit people to mate and discouraging unfit people from procreating. In 1927, the Supreme Court signed onto this agenda.

In Buck v. Bell, the Commonwealth of Virginia argued that a young woman, Carrie Buck, her mother, and Carries infant daughter exemplified hereditary feeblemindedness. The case was built on sham science and sleazy legal shenanigans, but the Supreme Court bought the states arguments. Virginia and other states were now free to forcibly sterilize people like Buck to prevent the birth of future generations of unfit people.

Bucks mother was a suspected prostitute. Buck was judged immoral for giving birth out of wedlock (after being raped). A local nurse testified that Bucks infant daughter was somewhat peculiar somehow. These paltry facts were taken as scientific proof of genetic illness and doomed Bucks life. In the decision, Oliver Wendell Holmes penned some of the most appalling words that ever emerged from the Supreme Court:

It is better for all the world if, instead of waiting to execute degenerate offspring for crime or to let them starve for their imbecility, society can prevent those who are manifestly unfit from continuing their kind. The principle that sustains compulsory vaccination is broad enough to cover cutting the Fallopian tubes. Three generations of imbeciles are enough.

Buck v. Bell led to the forcible sterilization of more than 70,000 Americans 8,300 in my own state of Virginia. The story of Buck v. Bell and eugenics is told painfully and movingly in an eerie 49-minute 1993 documentary called The Lynchburg Story and in Edwin Blacks book War Against the Weak: Eugenics and Americas Campaign to Create a Master Race. I consider them must-watch and must-read for this topic.

People in the 1920s were thrilled by the power that statistical, pharmacological, diagnostical, and surgical innovations brought to medicine. But popular enthusiasm for these techniques led to a grotesque overestimation of the wisdom of experts and the desirability of state micromanagement of human beings.

Today, were equally thrilled by the prospects of genomic medicine, CRISPR, Big Data, and sharing intimate data through wearable devices and genetic testing companies. I myself am enthusiastic about these innovations. But the history of eugenics tempers my enthusiasm, making me wary of efforts to manipulate individual lives, based on this explosion of information. Theres reason to fear both the mandates and the prohibitions that governments will summon forth. Tread lightly.

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How the 1920s Can Inform the 2020s in Health Care - InsideSources

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