Category Archives: Transhuman News

A new method that cleverly uses CRISPR to simultaneously make thousands of point mutations in human genes is helping researchers at Columbia University Vagelos College of Physicians and Surgeons understand how subtle changes to genes contribute to cancer and other diseases.

The new research is featured in "CRISPR base editor screens identify variant function at scale,"a perspective published in Molecular Cell, and in "Finding function with base editing screens," in Nature Reviews Genetics.

The method, created by a team led byAlberto Ciccia, PhD, associate professor of genetics and development in the Herbert Irving Comprehensive Cancer Center, was designed to study genes involved in DNA repairbutcould be applied to the study of any type of gene.

The findings,published in the Feb. 18 issue of Cell, could lead to precision medicines tailored to a patients exact genetic abnormality.

Researchers trying to understand how a gene impacts disease have generally been limited to making changes that disable an entire gene and its respective protein. Although this can reveal the genes dominant function, it doesnt tell us about all the other functions it may have, Ciccia says.

With a new type of gene editingcalled CRISPR-dependent cytosine base editinga single cytosine (C) in a gene can be replaced by a single thymine (T).

With base editors, we can make subtle changes in any part of the gene, much like what happens in nature, Ciccia says.

Making the technique even more powerful, the Ciccia laboratory has devised a way to make cytosine base edits across an entire gene and in dozens of genes at the same timea high-throughput approach that will greatly accelerate the discovery and analysis of clinically important mutations.

Using the new screening method, Ciccia and his team made thousands of mutations in 86 different DNA repair genes and exposed cells with the mutations to DNA-damaging agents to determine if the point mutations altered the function of these genes.

DNA repair genessense and correct errors in DNA, but mutations within the repair genes can hinder this natural proofreading mechanism. Genetic alterations of DNA repair genes have been implicated in breast and other cancers, along with other human genetic disorders.

The screen successfully identified more than 100 new, likely pathogenic mutations in DNA repair genes, including several in the breast cancer genes, BRCA1 and BRCA2.The full results of the screen are available on the Ciccia laboratorys website.

We anticipate this resource will expedite studies of DNA repair genes in human disease, Ciccia says, and that base-editing screening technologies will help researchers determine the causes of many different human diseases and accelerate the path to precision medicine.

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New CRISPR Method Allows Scientists to Understand Impact of Subtle Mutations - Columbia University Irving Medical Center

THOUSAND OAKS, Calif., Feb. 24, 2021 /PRNewswire/ -- Amgen (NASDAQ:AMGN) will present at the Cowen 41st AnnualVirtual Healthcare Conference at 12:50 p.m. ET on Thursday, March 4, 2021. Murdo Gordon, executive vice president of Global Commercial Operations and Peter H. Griffith, executive vice president and chief financial officer at Amgen will present at the conference. Live audio of the presentation can be accessed from the Events Calendar on Amgen's website, http://www.amgen.com, under Investors. A replay of the webcast will also be available on Amgen's website for at least 90 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 OaksMegan Fox, 805-447-1423 (media)Trish Rowland, 805-447-5631(media)Arvind Sood, 805-447-1060 (investors)

SOURCE Amgen

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Amgen To Present At The Cowen 41st Annual Healthcare Conference - PRNewswire - PRNewswire

For more than a decade, archaeologists thought they were looking at a bear. Known to experts as PP-00128, the fragment of bone found in a southeastern Alaskan cave seemed to be from some large mammal that lived in the area thousands of years ago. But ancient DNA evidence has given this unassuming shard of bone a new identity. The sliver did not belong to a bear, but at 10,150 years old, the most ancient dog yet found in the Americas.

The surprising realization was published today in a study in the Proceedings of the Royal Society B. While looking for Ice Age bear bones to examine, University of Buffalo geneticist Charlotte Lindqvist set about analyzing PP-00128. Perhaps the DNA would reveal what sort of bear the bone came from and how it was related to other ursids. But when Lindqvist and colleagues analyzed the DNA extracted from the bone, they found something very different. This bear was a dog.

Ten or twenty years ago, we would have looked through a pile of bone fragments and not seen this, says Durham University archaeologist Angela Perri, who was not involved in the new study. This is a nice example of what can be done with some of these advanced methods, she adds, noting that mass screening of archaeological material can turn up new clues that might otherwise be missed. Advances in how ancient DNA is extracted, corrected for any modern contaminants and sequenced have allowed researchers to quickly assess the genetics of organisms much faster than ever before, building a growing database that can be used to detect broader patterns. The more ancient DNA thats recovered, analyzed and placed in the database, the bigger the sample researchers have to work from when trying to understand how organismsbe it dogs or humans relate to each other.

Dogs have been with humans for a very long time. Around 23,000 years ago, in whats now Siberia, humans and gray wolves were hemmed in by the encroaching glaciers of the last Ice Age. No one knows for sure exactly how the two species started their relationship, with the leading hypothesis being that the friendlier wolves got used to people who gave them scraps or let them raid garbage piles, but that was the crucible in which the first domesticated dogs were born.

From there, the history of people and dogs was intertwined. Genetic evidence of both humans and dogs, published earlier this year by Perri and colleagues, suggest that they left Eurasia together as people and their pooches crossed the Bering Land Bridge to the ancient Americas together. Now, hot on the heels of that discovery, Lindqvist and colleagues have identified PP-00128 as a genetic cousin of those first Siberian dogs.

In this particular case, the happenstance discovery helps bring some resolution to a disjunction in the archaeological record. The archaeological evidence for humans and dogs in the New World is sparse and there is a gap in time between archaeological evidence and genetic estimates when it comes to both the entrance of humans and dogs to the Americas south of the ice sheets, Lindqvist says. The genetics seemed to suggest earlier arrivals for both dogs and people, but the archaeological evidence was often much younger than what the genetics suggested. But by looking at both where PP-00128 existed in time, as well as its genetic connections to both Eurasian and American dogs, a new perspective is starting to come together.

The bone comes from a critical time. Its age is a shade older than other early dog bones found in current-day Illinois, indicating that dogs domesticated in Eurasia spread with people through the Americas. The dogs from the Midwest form a genetic group together with others from places like Alabama and Missouri, part of the dispersal of people through the continent. What makes PP-00128 distinct is that its from an earlier group of dogs with ties to Siberia, and its location is especially important. The bone fragment was uncovered in a cave that is close to another archaeological site containing human remains of similar age along the Alaskan coast.

Archaeologists and anthropologists have long debated when and how people traveled from Eurasia across the Bering Land Bridge to the Americas. For decades, the prevailing thought was that migrating groups took advantage of receding ice sheets to take a central corridor between the continents, going through the middle of whats now Alaska before venturing further south. But the discovery of a domesticated dog along Alaskas Blake Channel points to a growing body of evidence that people traveled between the continents by moving along the coast, perhaps using early watercraft to move across the wetter stretches. Ice retreated from the coast before the interior, with estimates suggesting that people could have traveled through the area as early as 17,000 years ago and certainly by 15,000 years ago. I think that their paper most importantly makes a strong case for coastal migration into the Americas, Perri says, with the peopling of the continent starting with the coasts and later expanding more inland as the ice continued to withdraw.

Additional finds and analysis will test the ideaPerri notes that even earlier dogs are likely to be found along the route between Siberia and Alaska. But the close association between people and dogs so far back in time underscores an important point. The movement and locations of ancient dogs are proxies to the movement of people, and vice versa, because our histories are closely linked, Lindqvist says. Not far from where the 10,150-year-old dog bone was found, archaeologists have found 10,300-year-old human remains in a cave called Shuk Ka on nearby Prince of Wales Island, underscoring that people and dogs were here together. As Perri notes, Where people go, dogs go.

The emerging picture doesnt rest on any single discovery, but many different threads. The location, time and genetics of PP-00128 lined up with new hypotheses about when and where both dogs and people arrived in the Americas. Encroaching ice may have brought people and the ancestors of dogs together in Siberia, but when the ice thawed they could begin to travel together. Sometimes in science it is very exciting when multiple different pieces of evidence come together, Lindqvist says.

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Ancient DNA Reveals the Oldest Domesticated Dog in the Americas - Smithsonian Magazine

Most of us living on planet Earth have to make it through some amount of cold weather for at least part of the year, and new research has identified a specific genetic mutation that makes a fifth of us more resilient to cold conditions.

The genetic mutation in question stops the production of the protein -actinin-3, which is important for skeletal muscle fibre: The protein is only found in fast-twitch (or white) fibres and not in slow-twitch (or red) fibres.

Based on the new study's results, people without -actinin-3 have a higher proportion of slow-twitch fibres, and one of the consequences is that the body tends to conserve energy by building up muscle tone through contractions rather than shivering.

"This suggests that people lacking -actinin-3 are better at keeping warm and, energy-wise, at enduring a tougher climate, but there hasn't been any direct experimental evidence for this before," says physiologist Hkan Westerblad, from the Karolinska Institutet in Sweden.

"We can now show that the loss of this protein gives a greater resilience to cold and we've also found a possible mechanism for this."

The researchers recruited 42 men to sit in 14-degree Celsius (57.2-degree Fahrenheit) water while their temperatures and muscles were measured. The chilly immersion lasted 20 minutes at a time with 10-minute breaks, for up to two hours in total.

The proportion of participants who could keep their body temperature above 35.5 degrees Celsius (95.9 degrees Fahrenheit) was higher in those with the -actinin-3 mutation versus those without 69 percent of volunteers versus 30 percent.

In other words, the genetic mutation appeared to help these participants to conserve energy more efficiently and build up a greater resilience to the cold.

The team also conducted follow-up experiments in mice with the same mutation in order to check whether having this mutation could have something to do with increasing brown fat stores a well-known heat-generating tissue in mammals but that didn't turn out to be the case.

People lacking -actinin-3 might be better braced for a cold water swim or a bout of wintry weather, but it could also leave them more vulnerable to obesity and type-2 diabetes if they're inactive, the researchers say. It might also increase the risk of falling as they get older, as fast-twitch fibres handle speedy muscle movements.

"The mutation probably gave an evolutionary advantage during the migration to a colder climate, but in today's modern society this energy-saving ability might instead increase the risk of [these] diseases, which is something we now want to turn our attention to," says Westerblad.

As previous research has shown, -actinin-3 deficiency has increased across the population as humans have moved from warmer to colder climes, although questions remain about whether this mutation is present at birth and affects infant mortality.

It's also interesting to note that athletes who excel at sports involving explosiveness and strength (such as sprinting) are more likely to not have this lack of -actinin-3, while for endurance sports the stats are reversed.

As for future research, the team is keen to look at how this might all work at the molecular level, as well as how it could affect muscle disease. For now, it's an important new discovery about this genetic mutation and the allele or gene form associated with it.

"These findings provide a mechanism for the increase in [these gene variants'] frequency as modern humans migrated from Africa to the colder climates of central and northern Europe over 50,000 years ago," conclude the researchers in their published paper.

The research has been published in the American Journal of Human Genetics.

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Don't Suffer in The Cold? Turns Out There's a Genetic Mutation For That - ScienceAlert

20 years ago, humans first discovered the richness and complexity of their genetic heritage. A long-term venture that has monopolized hundreds of researchers for 15 years, but it has changed biology and medicine.

February 15, 2001, first snatch Genome Humans have revealed Famous newspaper Nature. This publication will forever change the history of biology and medicine. For the first time, humanity has its marrow, its ADN And his Genoa. Although incomplete, this is the first Sequencing The human genome requires the work of hundreds of researchers from around the world, all working together in the same consortium: Human Genome Project.

Twentieth anniversary of the publication of the article in Nature It is an opportunity to return to this incredible scientific adventure that began in the late 1970s. Before daring to attack 23 pairs, several researchers tested their sequencing technique to test simple organisms. Chromosomes Of the human genome.

It all started in the mid-1980s, when all three scientists had the same awareness. For the discovery of the 1975 Nobel Laureate Renato Dalbeco without consulting each other Oncogenes, Robert Sinsheimer and Charles Delisi of the University of California, Santa Cruz, argue to fill an important gap: the human genome continues to grow deeper and deeper. At that point, sequencing Genetic It is still in its infancy. Scientists rubbed his shoulder with his genome phage X174 and its 5.375 Nucleotides In 1977, to the 1978 SV40 with 5,224 nucleotides. In the early 1980s, scientists achieved further growth by aligning elongated genomes, including phase 2 of 1982 and its 48,502 nucleotides. On the human side, theADN Mitochondrial, Its 16,569 nucleotides pass through the sequencing mill for the first time. The latter 16 genes are identified.

These first works are the fertile ground for a more ambitious project to be formed in 1985. To create a comprehensive genetic map of the human genome. The Human Genome Project Born in 1988, with him Human Genome Organization (Hugo), responsible for coordinating the efforts of scientists around the world. The project takes 15 years to learn about the human genome, as well as others Model creatures Important in biology and medicine. thats all National Institute of Health, Its first director Francis Crick, Co-discovery of the dual helix structure of the project-leading DNA.

Scientists in 1995 Human Genome Project Together in Bermuda make a decision to change everything. When the sequencing is complete, it should be available to everyone. Each decrypted sequence must be shared in an Internet database, thus forming an invisible treasure that is the genetic heritage of mankind. Thus, three years before the deadline, the first raw sequences appear in the review Nature What do they say about the abyss that was the human genome at the time?

The first rough map of the human genome actually contains the genetic heritage of several unknown donors. Each donor gave their consent before taking five to ten DNA samples.

To form this genetic map, we first had to cut the DNA into a thousand pieces. Bacterial synthetic chromosomes (BACs) contained fragments of DNA with a base of 100 to 200 kPa formed a large library. Its like separating and storing each sheet of a book. To reconstruct the book, the BACs were arranged individually, as we read each page of the book, before putting the whole story together before putting them back together. The resulting genetic map includes 4.26 gigabases or 4.26.109 The letters A, T, C or G that follow each other, we have never understood such a long genome!

Although this is only a draft of the human genome, it has identified important points in our genetic heritage:

It required two years of work Human genome tweaking, Final sequences Finally published Nature In October 2004. Since then, knowledge about our genes, their effects on diseases, and how they work has been growing. Currently, this is the mapping done Genome Reference Consortium Based on the performance of in 2019 Human Genome Project, Is considered Reference.

Today, artificial intelligence is pushing human genetics backwards as computers can create from scratch. Human genomes that do not match the genetic makeup of any living human being.

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20 years ago, humans first adjusted their genome - SwordsToday.ie

Although Dr Kendler is internationally renowned and highly respected for his work in psychiatric genetics, he has been further catapulted into fame over the past 2 decades through his widely read commentaries on the philosophical foundations of psychiatry. I recently had the pleasure of reading the book Toward a Philosophical Approach to Psychiatry: The Writings of Kenneth Kendler. The book is a selection of 21 of his most important philosophical and historical papers published throughout his career, addressing topics such as the classification and nature of mental disorders, mind-body relationship, causality and explanation in psychiatry, and historical studies in psychiatric nosology. My admiration of Kendler is no secret at this point.

AFTAB: I really like your description of how psychiatric nosology sits in a historically contingent developmental arc. How is this history relevant to ongoing nosological debates in psychiatry, and how has ignorance of this history impeded our efforts at making progress?

KENDLER: With respect to psychiatric nosology, there is quite a bit of truth to 2 worn maxims: (1) If you dont know where you have been it is hard to see where you are going, and (2) if you dont know your history, youre are at high risk to repeat your prior mistakes. So, I think history can provide a context and a background for what nosology can do and where it has taken wrong roads in the past.

AFTAB: I read that you collaborated with a translator to obtain English translations of Kraepelins previously untranslated works. Will these translations be published or see the day of light in some manner?

KENDLER: They are all sitting on my hard drive, and that of the translator Ms Astrid Klee, but there is a lot more there than just Kraepelin. A very small percentage of the relevant German psychiatric literature of the late 19th and early 20th centuries have been translated. I have thought about trying to set up a website to make these widely available. That will take time, energy, and a bit of resources. If any of these readers want to help, be in touch.

AFTAB: You have argued for a scientific pluralism where there are multiple explanatory perspectives available to us to understand psychiatric disorders, and one perspective cannot be reduced to another perspective. You describe your pluralism as empirical and hard-nosed, by which you mean that risk factors must earn their place at the table. It is a little unfortunate that many discussions of pluralism in psychiatry tend to get stuck in debating the merits and demerits of the biopsychosocial model. For the most part, you have managed to stay away from those controversies and have successfully charted a course for pluralism independent of any baggage that the biopsychosocial model brings. Is it time for our field to abandon the biopsychosocial model?

KENDLER: Its core idea was on target, but its implementation was so non-specific as to blunt any rigor it might have once had and its ultimate utility. I would not mourn its passing, but it did some important historical work.

AFTAB: DSM-5 defines mental disorder as a syndrome that, among other things, reflects a dysfunction in the psychological, biological, or developmental processes underlying mental functioning. What is the intended meaning of the term dysfunction? Did the members of the DSM committee have any clarity or consensus regarding what it means?

KENDLER: The hope that we could have a crisp set of inclusion and exclusion criteria for what constitutes a psychiatric dysfunction is a wonderful idea but (in my view, not for lack of trying) impossible. There are too many social and conceptual nuances. So, although there is a general idea of what dysfunction means, operationalizing in the way that would give substantial sharp precision to the definition has not proved possible.

AFTAB: Could you articulate what that general idea of dysfunction is? I am also interested in whether dysfunction necessarily implies that the locus of the problem is primarily inside the individual and not in interpersonal relations and social context? And, if there is such an implication, does this relegate interpersonal and social causal risk factors to a more secondary status?

KENDLER: The general idea of dysfunction is commonsensicalthat the relevant psychobiological system is not doing what it is supposed to do. Examples might include providing your higher centers with an approximately veridical sense of the world around you, keeping levels of anxiety roughly appropriate to the real dangers being confronted, producing mood states approximately congruent to the environmental situation, etc. The DSMs have traditionally seen disorders as existing within individuals and, for example, avoided providing diagnoses for dysfunctional marriages or families. So, in that sense, the underlying disturbance is seen to exist within individuals. I do not see that definition having much of anything to do with the causes. Environmental experiences like severe childhood sexual abuse can clearly cause dysfunctional mood-modulation systems as well as a high genetic vulnerability.

AFTAB: To what extent is the dappled distribution of causal risk factors of psychiatric disorders a result of the heterogeneity of constructs? For example, a discussion of the distribution of causal risk factors of chronic fever disorder is not likely to be very meaningful. Furthermore, it is true for major depressive disorderas a category that no single causal risk factor has dominant explanatory power, but it may be the case for specific individuals with depression that there are causal risk factors of large explanatory power. What are your thoughts?

KENDLER: I dont buy it. Most psychiatric disorders are, I think, multifactorial all the way down. I also think that for a few affected individuals they do suffer from disorders largely as a result of one major cause. I sometimes call your model the mental handicap model. Imagine you were a physician in the mid-19th century caring for what would then have been called idiots or imbeciles. If you could apply modern diagnostic methods to that group, a fair proportion would have a range of specific causes: Down syndrome, fragile X, a host of autosomal recessive disorders impacting on all kinds of brain-relevant genes that, when mutated, produce widespread central nervous system dysfunction, a range of small deletions, and a whole bunch would be nonspecific multifactorial. That is, a lot of your cases (but far from all) would have largely monocausal conditions. This has been long postulated for psychiatric illness. It has, in my judgment, been largely a pipe dream. I think that lesson applies more broadly.

AFTAB: Your philosophical writings are published and featured prominently in leading American psychiatric journals, which do not usually publish articles related to philosophy of psychiatry. I have wondered if one of the reasons mainstream journals are so receptive to your philosophical workaside from the undisputed academic quality and rigoris that your conclusions do not threaten or destabilize the status quo in a way that conclusions of some of the other philosophical commentators do. It was interesting to me that one of your more controversial articleson the dopamine hypothesis of schizophreniawas also the one that had a difficult time getting accepted. Why are leading American psychiatry journals publishing so few philosophical articles and so afraid of controversy?

KENDLER: I have made a deliberate attempt over the past 15-plus years to try to crack open the leading psychiatric journals for articles with a primary philosophical and/or historical content.

I agree with you that my ability to do that has been, in part, a result of the fact that I have achieved some standing in empirical areas of psychiatric research. To be vernacular, I have accumulated some street cred. I also think the papers were written in a way the audience could understand and that spoke to their concerns. I did not consciously edit the papers to make them less controversial. I still think that nonscholarly issues impacted on the problems we had with the dopamine hypothesis paperthat was perhaps a special case. I do not want to blow up psychiatry. I believe quite deeply in our clinical and research mission, but we surely can think more clearly about a number of issues in our clinical work, nosology and research.

AFTAB: Some critics hold the view that if a classification can be misused, it will be misused. To what extent should the concern for misuse constrain classification decisions? Do the creators of DSM have a responsibility to make academic as well as public educational efforts to reduce the ways in which the diagnostic manual is misunderstood and misused?

KENDLER: Our primary responsibility on DSM is to our patients and the research community that we assist. But possible misuse does, appropriately, arise in nosologic debates. For example, it played a key role in the opposition to the late-luteal-phase dysphoric debate in DSM-IVthat the diagnoses would be used in ways prejudicial to women. So, it would be unrealistic for DSM to ignore completely the possible misuse of the document. But, if the chips are down, I think serving our patients and research is the more important mission. It is impossible to control all the possible misuses of DSM and, if you took that concern too far, it would be paralyzing.

AFTAB: You have argued persuasively that the conditions we call psychiatric disorders are not merely constructed by individuals and cultures, and that these conditions have some basis in the objective reality, but what do you say about the construct of mental disorder itself? To what extent are concepts of health and disease, and characterizations of disorder grounded in objective reality?

KENDLER: As an aggregate concept, I think psychiatric illness (or mental illness) is a real thing out in the world. Going from that to specific disorders, be it schizophrenia or narcissistic personality disorder, that is harder, and the role of social construction or historical accident becomes greater. A metaphor (not my own) is to imagine rewinding the tape of history, say, to 20 centuries BCE and re-running it 100 times until society and medicine developed enough to establish something like what we call psychiatry. I would bet that some construct like insanity/schizophrenia would be there almost all the time. I would not say that for a number of more specific disorders in our manual.

AFTAB: You have stated that psychiatric disorders are multicausal, similar to how coronary artery disease, hypertension, and type 2 diabetes are multicausal in medicine. Multifactorial disorders can still have final common pathways onto which those risk factors converge, and those final common pathways provide a lot of explanatory power.

For example, multiple causal risk factors for diabetes converge onto insulin production or insulin resistance. Do you imagine that various causal risk factors for psychiatric disorders also converge onto final common pathways? If it turns out that psychiatric disorders are more like homeostatic property clusters, then it may very well be the case that there may be no final common pathway. In that situation would it still be fair to say that psychiatric disorders are multicausal in the same way as diabetes mellitus is?

KENDLER: Great question and topical. I have been involved with a research team trying to determine the biological coherence of the signals emerging from genome-wide association studies. This is a question rather closely related to the one you pose. I guess my main answer is I hope so. As you note, that is the case for lots of other complex disorders. To be a bit more precise, I think it is realistic that our big syndromes (eg, schizophrenia, alcohol use disorder, depression, anxiety disorders) reflect broad syndromes with some meaningful subtypes within them for which different therapies might have different success. It is awfully optimistic to think that all of them go through one tight final common pathway at which an intervention, properly designed, could be nearly curative for all cases. But similarly, the idea that there are hundreds of kinds of each disorder, each with its own needed therapy, is both very pessimistic and likely unrealistic.

AFTAB: You may not remember during the 2016 American Psychiatric Association Annual Meeting, I approached you nervously after a session to express my admiration of your philosophical work. I was a second-year resident at that time. You gave me advice that was something along the lines of It is very important that you read a lot and that you read very widely. That often comes to my mind because every day I discover that there is so much more to learn. I am impressed by how you have managed to apply ideas from other areas of philosophy of science to psychiatry. Given that you have limited time, how do you prioritize and decide what you will read?

KENDLER: There is never enough time to read everything of interest; I often think of the metaphor of trying to drink a waterfall. I am rather disciplined in what I read. I am good at skimming, and if the first 20 pages dont look good, then I bail. The older I have gotten, the less patient I am with philosophical books written for other professional philosophers, filled with philosophy-speak. If they are not interested in communicating with me, I have to be very, very interested in what they are saying to soldier on.

I read 5 or 6 books at once. I am now reading about the history of genetics and cannot get enough of it. I read very little fiction. But I do keep up other lines of reading, usually late at night, that help keep me rounded, or listen to Audible when I bike or commute. Recently, I have been reading more history of psychiatry than philosophy. I have lots of bookshelves at my home and work office, but I am running out of space.

AFTAB: This may be an unfair question: If posterity could remember you predominantly for either your research work in psychiatric genetics or your philosophical work in psychiatry, what would you prefer it to be?

KENDLER: I have to laughyes unfairSophies choice that I cannot answer. I hope I am remembered, if at all, as someone who has tried to weave together empirical and conceptual work. It has been a wonderful career, and the older I get, the harder it is to pull these 2 parts of what I do apart. My identity is with the whole of it.

Conversations in Critical Psychiatry is an interview series that explores critical and philosophical perspectives in psychiatry and engages with prominent commentators within and outside the profession who have made meaningful criticisms of the status quo. The opinions expressed in the interviews are those of the participants and do not necessarily reflect the opinions of Psychiatric TimesTM.

Interviews published in this series can be accessed at http://www.psychiatrictimes.com/series/critical-conversations-in-psychiatry.

Dr Aftab is a psychiatrist in Cleveland, Ohio, and clinical assistant professor of psychiatry at Case Western Reserve University. He has been actively involved in initiatives to educate psychiatrists and trainees on the intersection of philosophy and psychiatry. He is also a member of the Psychiatric TimesTM Advisory Board.

An earlier version of this article, Weaving Conceptual and Empirical Work in Psychiatry: Kenneth S. Kendler, MD, was published online ahead of print on May 26, 2020. -Ed

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A Psychiatrist Weaving Conceptual and Empirical Work - Psychiatric Times