Category Archives: Molecular Genetics

Ever since the earliest reports of a pneumonia-like illness spreading within Hubei province in China, the resemblance to the SARS outbreak of 2002-2003 has been uncanny: probable origins in the wild-animal markets of China; an illness that in some people resembles the common cold or a flu, but in others leads to pneumonia-like symptoms that can cause respiratory failure; community transmission that often occurs undetected; super-spreader events; and reported vertical transmission in high-rises or other living spaces where the waste systems are improperly engineered or drain catch-basins are dry, allowing aerosolized particles to pass from one floor of a building to another (see The SARS Scare for an in-depth description of the epidemiology and virology of the SARS outbreaks of 2002-2003 and 2003-2004).

At first, this latest outbreak was referred to as a novel coronavirus, then in the media as COVID-19 (formally, the name for the disease in an infected person who has become sick, a distinction analogous to that between a person who is HIV positive and one who has developed AIDS). Now that the virus has been characterized and its relationship to SARS firmly established, its designation is SARS-CoV-2severe acute respiratory syndrome coronavirus 2.

Will public-health measures be sufficient to contain its spread? How infectious is it? What is the incubation period? Is this a pandemic? What role does the immune-system response play in the progression of the disease? Which populations are most at risk? Can scientists develop a vaccine, and how quickly? These are some of the questions that scientists worldwide are asking, and that a collaboration among Harvard University and Chinese researchers will address as part of a $115-million research initiative funded by China Evergrande Group, which has previously supported Universitygreen-buildings research at the Graduate School of Design, research onimmunologic diseases, and work inmathematics. (See below for the University press release describing the initiative.)

Harvard Magazinespoke with some of the researchers involved in fighting the first SARS outbreak, and those who will be collaborating with Chinese colleagues, in what is already a worldwide effort to control SARS-CoV-2.

Michael Farzan 82, Ph.D. 97, who in 2002 was an assistant professor of microbiology and molecular genetics at Harvard Medical School (HMS) studying the mechanism that viruses use to enter cells, was the first person to identify the receptor that SARS used to bind and infect human cells. SARS-CoV-2 is a close cousin to SARS, and uses the same human receptor, ACE2, reports Farzan, who is now co-chair of the department of immunology and microbiology at Scripps Research. The ACE2 receptor is expressed almost exclusively in the lungs, gastrointestinal tract, and the kidneys, which explains why the disease is so effectively transmitted via both the respiratory and fecal-oral routes.

But there are subtle differences in the new virus behind the current outbreak, he explained in an interview. The viruss receptor binding domainthe part that attaches to the human receptorhas undergone a lot of what we call positive selection, meaning there has been a good deal of evolutionary pressure on that region from natural antibodies, probably in bats or some other animal host that is a reservoir for this disease. So while the virus retains its ability to bind ACE2, Farzan explains, it no longer binds the same antibodies. That is unfortunate, because as the first SARS epidemic wound down, HMS professor of medicine Wayne Marasco had identified a single antibodyfrom what was then a 27-billion antibody librarythat blocked the virus from entering human cells. (Marasco is actively testing new antibodies, hoping to find one that will have the same effect on SARS-CoV-2.) Still, we are not starting from square one, says Farzan.

In animal studies,Remdesivir [a new and experimental antiviral drug] has seemed to work against SARS-like viruses, he says. Its effectiveness will probably hinge on getting it early enough, in the same way that the antiviral drug Tamifluis most effective against the seasonal flu when given to patients early in the course of infection.

And there is a reasonable hope that a vaccine canbe developed, Farzan adds, because the part of the virus that binds the human receptor is exposed and accessible, making it vulnerable to the immune systems antibodies. In addition, the viral genome is relatively stable. That means SARS CoV-2 wont evolve much over the course of an epidemic, so a vaccine that is relatively protective at the beginning of an epidemic will remain effective until its end.

Another reason for optimismdespite the long road to deploying any vaccine in humansis that the science that allows researchers to understand the viruss structure, life cycle, and vulnerabilities is progressing far more rapidly today than during the first SARS outbreak 17 years ago. So, too, is the understanding of the human immune response to the virus, and of the most effective public-health strategies based on the epidemiology of the disease.

When epidemiologists assess the severity of an epidemic, they want to know how effectively the disease can propagate in a population. The first measure they attempt to calculate is the reproductive number (R0)the number of people that an infected individual will in turn infect in an unexposed population, in the absence of interventions. When the reproductive number is greater than 1 (meaning each infected person in turn infects more than one other person), more and more people become infected, and an epidemic begins. Public-health interventions are therefore designed to lower the rate of transmission below 1, which eventually causes the epidemic to wind down. The second number epidemiologists focus on is the serial intervalhow long it takes one infected person at a particular stage of the disease to infect another person to the point of the same stage of the disease. The serial interval thus suggests how rapidly the disease can spread, which in turn determines whether public-health officials can identify and quarantine all known contacts of an infected individual to prevent their retransmitting the disease to others.

Marc Lipsitch, a professor of epidemiology at the Harvard Chan School of Public Health (HSPH), and director of the schoolsCenter for Communicable Disease Dynamics, helped lead one of the two teams that first calculated the reproductive number of SARS in the 2002-2003 outbreak. SARS had an R0 of 3, he recalls: each case led to three others. In that outbreak, about 10 percent of those who became sick died. The good news is that SARS CoV-2 appears to have a much lower R0 than SARS, ranging from the high ones to low twos, and only 1 percent to 2 percent of those who become sick have died. On the other hand, the serial intervalstill being worked outappears to be shorter, meaning the new virus has the potential to spread faster.

In the current epidemic, Lipsitch notes a further concern: the fact that the incubation-period distribution and the serial-interval distribution are almost identical. Thats a mathematical way of saying that people can start transmitting the virus even when they are pre-symptomatic, or just beginning to exhibit symptoms. That makes tracing and quarantining contacts of infected individualsa classic, frontline public-health measurenearly impossible.

Tracing, quarantining, and other public-health interventions, such as distancing measures (closing workplaces or asking employees to work from home, for example) proved sufficient to defeat SARS in the early 2000s. But with SARS-CoV-2, public-health measures alone may prove inadequate. Controlling this version of SARS may require antivirals, stopgap antibody therapies, and ultimately, vaccines, deployedtogetherwith robust public-health containment strategies.

Unfortunately, SARS-CoV-2 is almost certainly already a pandemic, Lipsitch continues: demonstrating sustained transmission in multiple locations that will eventually reach most, if not all places on the globe. The disease appears to be transmitting pretty effectively, probably in Korea, probably in Japan, and probably in Iran. He has estimated that 40 to 70 percent of the adult global population will eventually become infected.

That said, Infected is different from sick, he is careful to point out. Only some of those people who become infected will become sick. As noted above, only about 1 percent to 2 percent of those who have becomesickthus far have died, he says. But the number of people who areinfectedmay be far greater than the number of those who are sick. In a way, he says, thats really good news. Because if every person who had the disease was also sick, then that would imply gigantic numbers of deaths from the disease.

I'm very gratified, Lipsitch continues, to see that both China and Harvard recognize the complementarity between public health and epidemiology on the one hand, and countermeasure-development on the other hand. We can help target the use of scarce countermeasures [such as antivirals or experimental vaccines] better if we understand the epidemiology; and we will understand the epidemiology better if we have good diagnostics, which is one of the things being developed in this proposal. These approaches are truly complementary.

In the short term, Lipsitchwho has sought to expand the modeling activities of the Center for Communicable Disease Dynamics to better understand the current outbreaks epidemiologysays, It would be great toexpand collaborations with Chinese experts. Longer term, I see a really good opportunity for developing new methods for analyzing data better, as we have in previous epidemics. After the first SARS outbreak, for example, epidemiologists developed software for calculating the reproductive number of novel diseases; that software now runs on the desktop computers of epidemiologists around the world. And in 2009, during an outbreak of swine flu in Mexico, Lipsitch and others developed a method for using the incidence of the disease among awell-documented cohort of travelerswho had left Mexico, to estimate the extent of the disease among amuch larger and less well surveyedpopulation of Mexican residents.

What they found then was that the estimated number of cases in Mexican residents likely exceeded the number of confirmed cases by two to three orders of magnitude. The same method is being used to assess the extent of SARS-CoV-2 in China right nowso far without any hiccups. In the Mexican case, Lipsitchreports, the estimates suggested that severe cases of the disease were uncommon, since thetotal numberof cases was likely much larger than the number ofconfirmedcases. So I think we have learned from each epidemic how to do more things. And in between them, you solidify that less visible, less high-profile research that builds the foundation for doing better the next time. His group, for example, has been developing ways to make vaccine trials faster and better once a vaccine candidate exists.

A vaccine is the best long-term hope for controlling a disease like SARS-CoV-2. Higgins professor of microbiology and molecular genetics David Knipe, who like Lipsitch will participate in the newly announced collaboration, works on vaccine delivery from a molecular perspective. Knipe has developed methods to use the herpes simplex virus (HSV) as a vaccine vector and has even made HSV recombinants that express the SARS spike proteinthe part of the virus that binds the human ACE2 receptor. He now seeks to make HSV recombinants that express the new coronavirus spike protein as a potential vaccine vector.

But Knipe also studies the initial host-cell response to virus infection, which is sometimes called the innate immune response. And he has used HSV vectors that expressed the first SARS spike protein to study how it activates innate immune signaling. That is important because inSARS 1, initial symptoms lasted about a week, but it was the second phasecharacterized by a massive immune-system response that began to damage lung tissuethat led to low levels of oxygen saturation in the blood, and even death.The inflammation in the lungs is basically a cytokine storm, an overwhelming and destructive immune response thats the result of innate signaling, Knipe explains. So were going to look at that with the new coronavirus spike protein, as well. This could help to determine the actual mechanism of inflammation, and then we can screen for inhibitors of that that might be able to alleviate the disease symptoms.

The idea, he says, is to stop theinflammatoryresponse now killing people in the respiratory phase of the disease by targeting the specific molecular interaction between the virus and the host cell. This, he explains, aligns with one of the principal initial goals of the collaboration, which is to support research both in China and at Harvard to address the acute medical needs of infected individuals during the current crisis.

In the last days of 2019 and the first days after the New Year, we started hearing about a pneumonia-like illness in China, says Dan Barouch, an HMS professor of medicine and of immunology known for his anti-HIV work, whose lab has developed a platform for rapid vaccine development. (During the Zika virus outbreak of 2016, for example, his group was the first to report, within a month, a vaccine protective in animal models.) When the genome of the virus was released on Friday, January 10, we started reviewing the sequence that same evening, working through the weekend. By Monday morning, we were ready to grow it.

His concern about this latest outbreak was that the rate of spread seemed to be very rapid. In addition, the outbreak had the clinical features of an epidemic. We reasoned that this might make it difficult to control solely by public-health measures, he says, particularly because the virus can be transmitted by asymptomatic individuals. Thus, if the epidemic is still spreading toward the end of this year or early 2021, by which point a vaccine might be available, Barouch explains, such a remedy could prove essential. Historically, when viral epidemics don't self-attenuate, the best method of control is a vaccine.

Although Barouchs lab is working on DNA and RNA vaccines, a new technology that has the potential to cut vaccine development times in half, large-scale manufacturing using so-called nucleotide vaccines is unproven. That's why I think there needs to be multiple parallel vaccine efforts, he emphasizes. Ultimately, we don't know which one will be the fastest and most protective. At the moment, he reports, there are at least a half dozen scientifically distinct vaccine platforms that are being developed and he believes that vaccine development for this pathogen will probably go faster than for any other vaccine target in human history.

Ever since I graduated from medical school, he points out, there have been new emerging or re-emerging infectious disease outbreaks of global significance with a surprising and disturbing sense of regularity. There is Ebola. There was Zika. There were SARS, MERS; the list keeps growing. With climate change, increasing globalization, increasing travel, and population shifts, the expectation is that epidemics will not go away, and might even become more frequent.

In this global context, Barouch emphasizes the importance of a collaborative response that involves governments, physicians, scientists in academiaandin industry, and public-health officials. It has to be a coordinated approach, he says. No one group can do everything. But I do think that the world has a greater sense of readiness this time to develop knowledge, drugs, and therapeutics very rapidly. The scientific knowledge that will be gained from the vaccine efforts [will] be hugely valuable in the biomedical research field, against future outbreaks, and in the development of a vaccine to terminate this epidemic.

University provost Alan Garber, a physician himself, adds that Global crises of such magnitude demand scientific and humanitarian collaborations across borders. Harvard and other institutions in the Boston area conduct research on diagnostics, virology, vaccine and therapeutics development, immunology, epidemiology, and many other areas.With its tremendous range of expertise and experience, our community can be an important resource for any effort to address a major global infectious disease outbreak. Our scientists and clinicians feel an obligation to be part of a promising collaboration to overcome the worldwide humanitarian crisis posed by this novel virus.

The official Harvard press release follows:

Harvard University Scientists to Collaborate with Chinese Researcherson Development of Novel Coronavirus Therapies, Improved Diagnostics

At a glance:

Since its identification in December, the novel coronavirus has quickly evolved into a global threat, taking a toll on human health, overwhelming vulnerable health care systems and destabilizing economies worldwide.

To address these challenges, Harvard University scientists will join forces with colleagues from China on a quest to develop therapies that would prevent new infections and design treatments that would alleviate existing ones.

The U.S. efforts will be spearheaded by scientists at Harvard Medical School, led by DeanGeorge Q. Daley, working alongside colleagues from the Harvard T.H. Chan School of Public Health. Harvard Medical School will serve as the hub that brings together the expertise of basic scientists, translational investigators and clinical researchers working throughout the medical school and its affiliated hospitals and institutes, along with other regional institutions and biotech companies.

The Chinese efforts will be led by Guangzhou Institute of Respiratory Health and Zhong Nanshan, a renowned pulmonologist and epidemiologist. Zhong is also head of the Chinese 2019n-CoV Expert Taskforce and a member of the Chinese Academy of Engineering.

Through a five-year collaborative research initiative, Harvard University and Guangzhou Institute for Respiratory Health will share $115 million in research funding provided by China Evergrande Group, aFortuneGlobal 500 company in China.

We are confident that the collaboration of Harvard and Guangzhou Institute of Respiratory Health will contribute valuable discoveries to this worldwide effort, said Harvard University President Lawrence Bacow. We are grateful for Evergrandes leadership and generosity in facilitating this collaboration and for all the scientists and clinicians rising to the call of action in combating this emerging threat to global well-being.

Evergrande is honored to have the opportunity to contribute to the fight against this global public health threat, said Hui Ka Yan, chair of the China Evergrande Group. We thank all the scientists who responded so swiftly and enthusiastically from the Harvard community and are deeply moved by Harvard and Dr. Zhongs teams dedication and commitment to this humanitarian cause. We have the utmost confidence in this global collaborative team to reach impactful discoveries against the outbreak soon.

While formal details of the collaboration are being finalized, the overarching goal of the effort is to elucidate the basic biology of the virus and its behavior and to inform disease detection and therapeutic design. The main areas of investigation will include:

With the extraordinary scale and depth of relevant clinical and scientific capabilities in our community, Harvard Medical School is uniquely positioned to convene experts in virology, infectious disease, structural biology, pathology, vaccine development, epidemiology and public health to confront this rapidly evolving crisis, Daley said. Harnessing our science to tackle global health challenges is at the very heart of our mission as an institution dedicated to improving human health and well-being worldwide.

We are extremely encouraged by the generous gesture from Evergrande to coordinate and supportthe collaboration and by the overwhelmingly positive response from our Harvard colleagues, said Zhong, who in 2003 identified another novel pathogen, the severe acute respiratory syndrome (SARS) coronavirus and described the clinical course of the infection.

We look forward to leveraging each of our respective strengths to address the immediate and longer-term challenges and a fruitful collaboration to advance the global well-being of all people, Zhong added.

Harvard University ProvostAlan M. Garbersaid outbreaks of novel infections can move quickly, with a deadly effect.

This means the response needs to be global, rapid and driven by the best science. We believe that the partnershipwhich includes Harvard and its affiliated institutions, other regional and U.S.-based organizations and Chinese researchers and clinicians at the front linesoffers the hope that we will soon be able to contain the threat of this novel virus, Garber said. The lessons we learn from this outbreak should enable us to respond to infectious disease emergencies more quickly and effectively in the future.

Excerpt from:
Harvard and the Guangzhou Institute of Respiratory Health Team to Fight SARS-CoV - Harvard Magazine

University Showcase 2/21 8a: Alzheimers and dementia represent a growing crisis around the world and New Mexico faces many challenges in addressing these illnesses.

On this episode we highlight a conference organized by the Alzheimer's Foundation of America coming to the University of New Mexico on February 25.

It is open to the public and no tickets are required, but participants can register here.

We also talk with Dr. Gary Rosenberg, founder of the UNM Memory & Aging Center.

The center opened in 2016 and focuses on advancing research on dementia and helping expand care around the state.

And we check in one with Nicole Maphis, Ph.D candidate in UNMs Biomedical Sciences Graduate Program, who is working on a vaccine for Alzheimers with Kiran Bhaskar, an associate professor in UNMs Department of Molecular Genetics & Microbiology, and Bryce Chackerian, Professor and Vice Chair, Molecular Genetics and Microbiology. Find the previous interview we did with these researchers here.

Guests:

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Tackling Alzheimer's and dementia in New Mexico - KUNM

NEW YORK, Feb. 20, 2020 /PRNewswire/ -- Kallyope Inc., a leading biotechnology company focused on identifying and pursuing therapeutic opportunities involving the gut-brain axis, today announced that Peter Hecht, Ph.D., CEO of Cyclerion Therapeutics, has been appointed to the company's Board of Directors.

Prior to joining Cyclerion in 2019, Peter was co-founder and CEO of Ironwood Pharmaceuticals from 1998 to 2019. Under his leadership, Ironwood grew into a fully integrated research, development and commercial organization with more than 700 employees. During his tenure the company discovered, developed and commercialized LINZESS (linaclotide) globally for irritable bowel syndrome with constipation and chronic constipation. In 2019, Peter led the tax-free separation of Ironwood's non-gastrointestinal (GI) assets and R&D team into Cyclerion, enabling Ironwood to be a profitable GI therapeutics-focused leader. After completion of the spin-off, Hecht joined Cyclerion as its first CEO. He holds a Ph.D. in molecular biology from the University of California at Berkeley and was a post-doctoral research fellow at the Whitehead Institute.

"It is an exciting time to join Kallyope," said Hecht. "Their unique platform of integrated technologies has led to a new understanding of gut-brain circuits that has, in turn, resulted in the discovery of novel approaches to diseases of high unmet need in multiple therapeutic areas. I look forward to working with the team as the company begins to advance its portfolio of programs towards the clinic."

"We are delighted to welcome Peter to our Board of Directors at this pivotal time," said Nancy Thornberry, CEO of Kallyope. "As we progress our lead programs and expand our pipeline and novel platform, Peter's experience in building innovation-driven biotech startups into mature biopharmaceutical companies will be invaluable for us."

About Kallyope Inc.

Kallyope, headquartered at the Alexandria Centerfor Life Science in New York City, is a biotechnology company dedicated to unlocking the therapeutic potential of the gut-brain axis. The company's cross-disciplinary team integrates advanced technologies in sequencing, bioinformatics, neural imaging, cellular and molecular biology, and human genetics to provide an understanding of gut-brain biology that leads to transformational therapeutics to improve human health. The company's founders are Charles Zuker, Ph.D., Lasker Award winner Tom Maniatis, Ph.D., and Nobel laureate Richard Axel, M.D. For more information visitwww.kallyope.com.

Contact

Danielle Cantey(202) 337-0808dcantey@gpg.com

Morgan Warners(202) 337-0808mwarners@gpg.com

View original content to download multimedia:http://www.prnewswire.com/news-releases/kallyope-inc-appoints-peter-hecht-to-board-of-directors-301008114.html

SOURCE Kallyope Inc.

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Kallyope Inc. Appoints Peter Hecht to Board of Directors - BioSpace

A map , built to tell the spread of the infection from new coronavirus in Italy . As the case count grows and the first two victims are registered, one 78 enne Paduan and a 75 enne lodigiana, Wired has decided to launch this tool to map the progress of the disease now arrived in Italy (NB: the map is not updated in real time, it takes time to verify the data).

As the virologist Giovanni Maga , director of the Cnr Institute of Molecular Genetics, comments in a press release, we are facing to an outbreak of virus Sars-Cov-2 infection. The numbers do not yet allow to speak of an epidemic. Of course, he adds, the picture could obviously change in the coming days, but our health system is in a state of maximum alert and capable of managing effectively also the possible appearance of other small outbreaks such as the current one .

To avoid excessive alarmism , continues Maga, is good to remember first that 19 cases [alla mattina del 22 febbraio, ndr] out of a population of 60 millions of inhabitants, however, make the risk of infection very low. Only in the areas currently affected by traffic is the risk higher and citizens must follow the indications of the health authorities. Outside of these, the situation remains as in the past weeks .

Here is what the information collected so far in the world tell : The infection, from epidemiological data available today on tens of thousands of cases, causes mild / moderate symptoms (a kind of flu) in the 80 90% of cases. In 10-15% pneumonia can develop, the course of which is however benign in the absolute majority. It is estimated that only 4% of patients require ICU admission. The risk of serious complications increases with age, and people over 65 years and / or with pre-existing or immunosuppressed diseases are obviously more at risk, as they would be for the flu .

Don't panic , in short. And precisely in an attempt to make an informative contribution to map the outbreaks of Covid 19 in Italy, Wired has created a dataset that everyone can update. Anyone with information to provide, can do so by filling out this form. Once verified by the editorial staff, the information will be entered and published.

The dataset feeds the map that opens this piece, but obviously anyone can use it to build their own. The goal, in fact, is to help provide information as accurate as possible about the spread of coronavirus in Italy.

You may also be interested in

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New coronavirus, a map to tell the story of the infection - NJ MMA News

Famous celebrities, coverage makers and consultants from the nation's agriculture sector are collaborating within the Outlook Agriculture Conclave to be held in New Delhi on Monday and professional periods to be held underneath it. In addition to the farmers within the Conclave, awards shall be given in varied classes to different organizations and establishments lively in agriculture. The winners who made particular contributions have been chosen by a jury of consultants in agriculture. The awards shall be offered by Union Agriculture Minister Narendra Singh Tomar on the concluding ceremony of the Conclave. Meghalaya Deputy Chief Minister Prestone Tiansoong, Agriculture Minister of Haryana, Jai Prakash Dalal will inaugurate the Conclave.

->Madhya Pradesh Agriculture Minister Sachin Yadav, Telangana Agriculture Minister S. Niranjan Reddy will deal with. The consultants and jury members becoming a member of the Conclave are as follows.

Haryana Agriculture Minister Jai Prakash Dalal

Haryana Agriculture Minister Jai Prakash Dalal would be the particular visitor. Brokers are very lively in fixing the present issues of farmers and enhancing their financial situation. He made nice efforts to implement the suggestions of the Swaminathan Commission.

Madhya Pradesh Agriculture Minister Sachin Yadav

Madhya Pradesh Agriculture Minister Sachin Yadav is working for the betterment of farmers. He is working to supply reduction to the farmers dealing with many issues within the state and to take ahead on the financial progress.

Meghalaya Deputy Chief Minister Prestone Tiansong

Meghalaya Deputy Chief Minister Meghalaya Prestone Tiansoong would be the particular visitor. 80 % of the inhabitants in Meghalaya depends on the agricultural sector. Due to this, agriculture sector is essential within the financial improvement of the state. The position of chief Tiansoong as deputy chief minister is essential.

Harish Chavan

Harish Chavan Mahindra & Mahindra Ltd. Okay. Swaraj is the Chief Executive Officer of the Division. He has 28 years of expertise in varied fields together with manufacturing, administration, technique planning, abroad business in India and overseas. Prior to taking cost of the Swaraj division, he held varied different vital positions within the Mahindra Group.

Vasudha Mishra

Vasudha Mishra, a 1987 batch IAS officer of Telangana cadre, is Special Secretary within the Ministry of Agriculture and Farmers Welfare. Prior to this she was Additional Secretary within the Department of Administrative Reforms and Public Grievances. She additionally held the place of Managing Director of National Cooperative Development Corporation. Prior to that, she has additionally dealt with a number of departments in Andhra Pradesh.

Dr. Trilochan Mohapatra

Dr. Trilochan Mohapatra is the Director General of the Indian Council of Agricultural Research (ICAR). Dr. Mahapatra, identified for his particular contribution within the area of molecular genetics and genomics, was awarded the National Biosciences Award by the federal government, one of many highest awards of Indian scientists for his contribution within the area of biosciences.

Vijay Sardana

Vijay Sardana, convener of the Food Security and Sustainable Agriculture Foundation, is the Vice President and Head of Food Security and Agribusiness, Policy and Program at UPL Group. They are related in several roles in lots of organizations of the nation. Sardana has additionally been concerned within the actions of the World Economic Forum, World Business Council for Sustainable Development, Initiative for Global Development and International Food Policy Research Institute.

Rajeev Rallan

Rajeev Rallan is the top of gross sales and advertising and marketing of Mahindra & Mahindra's Swaraj division. Rallan has been instrumental in popularizing Swaraj tractors and connecting farmers. He has taken initiative to attach farmers by taking initiative like cellular app to beat the issues of the day.

Sanjay gakhar

BTech Gakhar is the Vice President of MCX in Agriculture Engineering. He focuses on fields resembling commodity futures, provide chains and buying and selling. Prior to becoming a member of MCX in August 2005, he labored in establishments resembling Nafed and Britannia.

Sanjay Chhabra

Mr. Sanjay Chhabra is the President and Business Head of Shriram Farm Solutions of DCM Shriram. He has 27 years of in depth expertise within the area of Agri Input and Rural Market. Chhabra was instrumental within the improvement of greenery by DCS Shriram, the primary rural retail initiative within the nation.

Dan elf

Counselor Dan Elf of the International Development Cooperation, Science and Agriculture on the Israeli Embassy has held managerial positions within the agricultural sector. Dan Elph, who focuses on agriculture, has intensive expertise in gardening and crops administration. He obtained an MBA diploma after learning agriculture in Hebrew University from Hebrew University.

Anoop Vikal

Anoop Vikal is the Chief Financial Officer of Naira Energy. When he joined Naira Energy, the corporate was going via a transition. He performed a key position in management, threat administration and planning. He additionally oversees authorized and CSR actions within the firm. He has held senior positions at Snapdeal and Bharti Airtel.

Vineet Durani

Vineet Durani is the director of Microsoft and is accountable for buyer and partnership engagements. He has 24 years of expertise within the area of business administration. Durani has efficiently held a number of different tasks at Microsoft. Prior to Microsoft, he additionally served at Samsung and Modi Enterprises.

Sanjay agarwal

Sanjay Aggarwal, Secretary, Union Ministry of Agriculture and Farmers Welfare is a 1984 batch UP cadre IAS. He earned BTech and MTech levels from IIT Kanpur. Sanjay Agarwal, who held a number of posts within the Government of Uttar Pradesh, was additionally the Principal Secretary of the Department of Electricity. He additionally grew to become the Additional Chief Secretary of the state. Being on the post of Secretary within the Ministry of Agriculture, he has an vital position in figuring out the insurance policies of this sector. The most important accountability of doubling the revenue of farmers and implementing vital schemes of Modi authorities like Kisan Samman Nidhi is his personal ministry.

Dr. T. Haque

Dr. T. Haque has been the Chairman of the Commission for Agricultural Costs and Prices CACP and the top of Land Policy Cell of NITI Aayog. Eminent agricultural economist Dr. Haque is an professional within the area of agricultural improvement and insurance policies. He has been a senior marketing consultant in a number of organizations together with International Labor Organization, Food and Agriculture Organization and World Bank. Apart from the central authorities, he additionally served on a number of professional committees of the governments of Punjab and Andhra Pradesh. Dr. Haque has written a couple of dozen books and greater than 100 analysis papers. The most important emphasis of his books and articles was on matters like rural improvement, total coverage formulation for growing international locations, land reforms, agrarian reforms.

Sandeep Nayak

Sandeep Nayak, Managing Director of National Cooperative Development Corporation-NCDC has a variety of expertise within the cooperative sector. He has seen intently the position of cooperative sector in agriculture and upliftment of farmers. National Cooperative Development Corporation is doing important work on this space. Shri Nayak, an IAS from Jammu and Kashmir batch, has held a number of different posts apart from principal secretary of the agriculture division in Jammu and Kashmir. An International Cooperative Trade Fair was organized underneath his supervision.

Saurabh Kumar

Mr. Saurabh Kumar is the Chief Executive Officer of ICICI Foundation. He contributed considerably to the event of ICICI Digital Village. This expanded the market in rural areas and benefited the villages.

Dr. DN Nobleman

Dr. DN Thakur Sahkar is the nationwide vp of Bharti. Prior to this, Dr. Thakur served within the Ministry of Agriculture and Cooperation for a few years and gained intensive expertise within the area of cooperatives. He has additionally been the deputy MD of the National Cooperative Development Corporation (NCDC).

Vm Lion

Shri VM Singh is a outstanding farmer chief. Former MLA Mr. Singh can also be the National Convener of the All India Kisan Sangharsh Coordination Committee. They have been elevating the difficulty of entitlement of farmers from varied boards.

Dr. Ron Malka

Dr. Ron Malka is the Israeli Ambassador to India. After serving in economics and business administration, he served within the Israeli military. He then held senior positions within the Financial Advisory Unit of the IDF Intelligence Corporation and Chief of Staff. Having a eager understanding of financial and monetary issues, Dr. Malka can also be related to financial and monetary organizations in Israel and has instructing expertise.

R .s. Sodhi

RS Sodhi, managing director of Gujarat Cooperative Milk Marketing Federation Limited (Amul), has a big presence within the jury. Sodhi has performed an vital position in giving new route to the White Revolution. Such a mannequin of Amul developed in Gujarat that the milk farming business obtained a brand new route by adopting it everywhere in the nation. Sodhi focuses on market analysis, meals processing, FMCG and business improvement.

Dr . A.okay. Lion

Dr. A.Okay. Singh is the deputy director normal of the Indian Council of Agricultural Research-ICAR and is in control of the agricultural extension sector. Their presence within the jury is vital as a result of theyve been related to agricultural analysis for a very long time. Due to the vital position of agricultural analysis in doubling the revenue of farmers, their expertise and contribution is essential.

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Well-known agricultural sector consultants and coverage makers are sharing their expertise within the Outlook Agriculture Conclave - Sahiwal Tv

Social media typically represents what a person wants to show about themselves.

But sometimes, its also what they dont want to be seen as.

Kaplan Test Prep administered a survey that was made public Jan. 13, reporting that roughly 36% of college admissions officers look at the social media accounts of university applicants. This is a marked increase from the reported 25% last year and an indication of the rising relevance of social media in society.

Online posts are public information and easily searchable, making them fair game for college admissions officers.

When hopeful students apply to colleges, many dont realize that admissions officers would consider anything beyond whats included in their applications. However, its in universities best interests to look at their candidates as holistically as possible.

After all, they arent accepting an application theyre accepting the person behind it.

UCLA and universities nationwide not only have the ability to check applicants social media profiles, but they also owe it to themselves to select candidates using all the information they have at their disposal. Universities are completely justified in using public, online information regarding candidates as a part of the admissions process.

And that includes social media.

Perhaps the most obvious reason for colleges to judge applicants through social media is simply because its available to them. Combined with the fact that social media can provide meaningful insight into an applicants personality, it seems like a no-brainer that colleges should look at an applicants profiles.

Mitchell Chang, UCLA education and Asian American studies professor, said in an emailed statement that looking at social media may help admissions committees make more informed decisions regarding specific applicants.

If an applicant expresses him/herself in ways that raise serious concerns, such harmful expressions should not be overlooked, Chang wrote. If applied carefully, social media will have an insignificant impact overall, but when it does make a difference, it could be immeasurable.}

This alludes to the crux of the issue: Social media provides a way for colleges to judge applicants in a relatively unfiltered manner. In other words, it offers a unique perspective on an applicant that an admissions officers may not get from an application.

And more importantly, social media can alert colleges as to whether applicants have posted something derogatory or demeaning in some way. It can reflect integrity and maturity, or a lack thereof and that can be vital in difficult admissions decisions.

A school wouldnt want someone who has bad moral character to represent them, said Maya Andari, a third-year microbiology, immunology, and molecular genetics student. With that being known, youre expected to be conscious about what you post.

But social media doesnt just act as a check on poor character.

It can positively supplement students application in certain cases. An applicants social media presence may focus around an activity or passion that reflects personality or good character. It gives the admissions officer another perspective of the candidate, with the possibility of exposing more positive qualifications and experiences.

Madeline Buecheler, a second-year economics and world arts and cultures student, said that social media has helped her with landing an internship.

Social media helped me demonstrate my passion for fashion, and its a big thing to have a social media handle in my field, Buecheler said. Its a great way of having different people see your image.

And this method of personal screening isnt new or exclusive by any stretch. Employers often check the social media presence of potential hires and one of the primary goals of college is preparing students for future careers.

Employers wont hesitate to hire or fire people based on social media presence, which students will come to learn once they enter their careers postgraduation. Cognizance regarding social media presence is a must for jobs, and college admissions following suit is good preparation for common hiring practices.

Many would argue that colleges looking at social media illustrates a blatant violation of privacy. People typically associate these platforms with personal use, and nobody expects it to bleed over into their professional life. But what most fail to understand is that public profiles on social media represent information made available of ones own volition.

As such, its not a violation of privacy its an indication of how you represent yourself on the most public sphere there is: the internet.

Another common misconception is that colleges may judge applicants for personal beliefs or ideologies not included in their applications but emblazoned on their social media. But that would only play a role if those beliefs were actively meant to hurt or demean others and colleges are justified in being wary of that.

So if, hypothetically, an applicant posts derogatory remarks toward other groups or other people, college admissions officers should have the right to use that information when coming to a decision about a candidate.

At the end of the day, colleges can and should use all the information they have available to make their decisions on applicants.

Students are more than just their applications, and universities need to understand who theyre choosing to represent them.

And if that means checking Instagram, so be it.

Read the original post:
Social media may prove to be a valuable tool for college admissions officers - Daily Bruin

The Scottish scientist in the frontline of the battle against the deadly coronavirus is warning the need for a vaccine is even more critical with more than 31,000 confirmed cases and around 630 deaths.

Dr Kate Broderick, is working round the clock with her team of researchers at the pharmaceutical company Inovio in San Diego to develop a jab in just six months.

The 42-year-old, who is originally from Dunfermline, and has been living in California for 20 years, says the aim is to make a vaccine faster than theyve made any other in our history.

Broderick has helped create successful vaccines for ebola, zika, lassa fever and Mers (Middle East Respiratory Syndrome) moving from Glasgow to develop her work in molecular genetics.

She first read about the coronavirus outbreak on Hogmanay and saw that the World Health Organisation had reported a couple of cases.

From there the Chinese authorities published the DNA sequence online which was the trigger for Broderick and her team to start working on a new vaccine.

She said: Seeing it online was like 100 per cent confirmation that this was a new virus but even before that from the disease symptoms it wasnt fitting into any particular box.

So, we already suspected that this was something new.

We downloaded the sequences and the first stage of our development is done on a computer which is why our technology at Novio allows us to go so far.

We ran the sequences through a computer algorithm and three hours later we actually had a full design for the vaccine and the next day we were able to put that into manufacturing.

She added: Its definitely 100 per cent a race against the clock were working here 24/7 and thats not an exaggeration to get this thing out.

What were trying to do here is make a vaccine faster than weve ever made any other vaccine in our history.

Our fastest in the past was seven months from sequence to patient and that was for the Zika outbreak where kids were being born with these terrible neurological deficits and we really sprang into action there.

We got the viral sequence and we got it tested in humans within seven months and we were so proud of that and here for the novel coronavirus were trying to do it significantly faster than that.

We need international support and I think were seeing that in the scientific community.

Theres a lot of organisations working together but its absolutely a race against time.

The UK government announced earlier this week that it has pledged 20 million to develop new vaccines to combat the worlds deadliest diseases, amid concerns over the novel coronavirus, 2019-nCoV.

Dr Broderick welcomed the funding which will go to the Coalition for Epidemic Preparedness Innovations (CEPI), originally formed in response to the Ebola epidemic in West Africa.

She added: Thats what we need now funding to support this work.

We have to follow all the established protocols and work with the authorities thats absolutely critical.

So, all we would do first is a phase one clinical trial which we plan to do early summer.

Thats testing it on completely healthy people just to get a read-out of the fact the vaccine is safe and its doing what we hope its going to do.

We hope to roll that out in the US in the early summer and well also be working with our colleagues in China to do similar kinds of trials there with an eye to discussing with the Chinese authorities to get the vaccine out to people who need it as soon as its available.

Dr Broderick has retained her Scottish accent having gone to St Columbas High School in Dunfermline before studying genetics at the University of Glasgow, where she also completed her PhD.

Her father was a physicist, her mother a therapist, one of her sisters is a nurse and the other is a social worker.

She met her husband, Steve, in California, and 20 years on is still there. She has two children, Rory, aged eight, and four-year-old Isla.

She said: Every single day almost someone will ask me if Im here on vacation and Ill say no Ive been here for 20 years.

I come back to Scotland at least once a year and my whole family are still in Scotland and I feel very, very Scottish.

Im proud of my adopted home in California but I very much consider myself Scottish.

The rest is here:
Coronavirus: Meet the Scottish doctor working to create life-saving vaccine - Scotland on Sunday

Congratulations, you recently won a Science Foundation Ireland award for outstanding contribution to Stem communication. Tell us about Cell Explorers.

Cell Explorers is an outreach programme, where volunteers who are scientists go to primary schools and festivals and do hands-on experiments with children. The volunteers come from universities and institutes of technology around Ireland, and the idea is for them to build their communication skills and share their passion for science with young people.

We tend to work with schoolchildren who are between age 10 and 12. Research shows this is the age around which they form opinions about science including whether they like it or not, and if it is for them so an important aspect of the programme is to provide a positive hands-on experience of engaging with science, with facilitators who might act as science role models and dont look like the stereotypical scientist.

How did you get the idea?

I was a researcher at NUI Galway, working on how cells can detect damage in DNA, and activate ways to repair the DNA. Part of my job was to teach undergraduate students, and I did some training to become a better lecturer.

I saw how you can encourage people to learn by co-creating with them, and I got the idea to work with undergraduates to design molecular biology workshops for school students, where they could do experiments themselves and learn more about it.

And that was the start of Cell Explorers?

Yes. I got some funding from NUIG to start a staff-student collaborative project. I asked biotechnology students would they like to join the project and work with my sons school. Ten of them volunteered and designed four workshops, including Fantastic DNA, which we are still running now.

Everyone really enjoyed it and from this Cell Explorers was started. We got successive funding from the RDS, the Wellcome Trust and Science Foundation Ireland for going into more schools and taking part in science festivals. In eight years we built a network of 13 Cell Explorers teams across 15 institutions around Ireland.

How do you assess its impact?

I have taken a scientific approach with the evaluation of Cell Explorers, gathering the evidence about it from the very beginning. This is to the point that it has become my research and I dont do molecular genetics in the lab any more. Between 2012 and the end of 2019 we reached about 40,000 people.

Throughout that time we have been reflective, documenting and improving our practice and sharing our findings with others. In addition to our evaluation, one PhD student and one postdoctoral researcher are looking at the potential impact of our programme on how children perceive science and scientists.

What keeps you going with it?

I find it very rewarding to see the responses of the children in the classroom, of the teacher and of our young volunteer scientists. I cant put numbers on this part, it is a feeling that you are making a connection and it is worth it. It is why I do this.

How do you take a break?

At home, I like to spend time with my family. I am French and I love to cook, especially with my children. We love cats my husband is counting the number that are turning up in our garden! We are also a family of readers, we enjoy reading books and discussing them.

And what was the last book you read?

In English? That would be Normal People by Sally Rooney. I also recently read and enjoyed Notes to Self by Emilie Pine. Over Christmas, I read a lot of books in French, including books that my children read too, and we had fun talking about them.

See more here:
Exploring a hands-on approach to engaging with science - The Irish Times

"We know villages were destroyed and people were being taken," says Vicky Oelze. "We want to put numbers on it. I'm interested in individual histories." (Photo by Fred Deakin)

This geological map of equatorial Africa shows strontium isotope sampling locations Oelze's team will use to create the first-ever strontium isotope map of the region, a tool researchers will use to help trace the origins of Africans who were abducted during the transatlantic slave trade. (Map courtesy of Vicky Oelze)

Vicky Oelze, an assistant professor of anthropology, should introduce herself as a detective. Who else would attempt to fill in the gaps of the transatlantic slave trade by gathering clues from cemeteries in South Carolina and the shores of West Africa?

Four hundred years after the forced displacement of millions of Africans began, Oelze wants to use isotope biogeochemistry to trace back and identify the origins of individuals who were abducted and perished in the Americas.

Skeletal remains of slaves hold the clues that Oelze will use to identify where in Africa individuals were born and raisedinformation that has been lost to history.

"The narrative we have now is based on log books written by people who were deporting hundreds of Africans on ships," said Oelze. "They documented only the numbershow many left and how many arrived in the respective harbors. There was no recordkeeping of where people were actually from."

Archaeologists have had great success in parts of the developed Western world using strontium isotopes to identify the geological origin of prehistoric people, matching data to detailed strontium isotope maps researchers have developed. This type of map does not exist for tropical Africa, a gap Oelze will fill with over 400 environmental samples from 40 field sites that cover most major geological formations in tropical Africa. The principle is simple: Vegetation takes up a specific isotopic makeup of the trace element strontium from bedrock, and, in tiny quantities, that isotopic "signature" becomes locked in the teeth of people and animals that consume it. Oelze will use samples of African flora and fauna to build a strontium isotope map to match the signatures in skeletal remains of slaves to specific regions in Africa.

With support from the Helen and Will Webster Foundation, Oelze is hiring a postdoctoral researcher for two years to work in partnership with collaborators at the Max Planck Institute for Evolutionary Anthropology in Germany. In a second step, the team will start examining human remains from the Americas for their strontium isotope values. Strontium isotope analysis is particularly valuable when deterioration of skeletal material has ruled out genetic analyses as an option, and it is a much more precise way to assess human mobility on an individual, rather than population, level, said Oelze. The team will also analyze human remains from urban centers of the West African slave trade in collaboration with UCSC archaeologist Cameron Monroe.

"We know villages were destroyed and people were being taken," said Oelze. "We want to put numbers on it. I'm interested in individual histories."

The remains of millions of slaves are buried in designated slave cemeteries and near slave trade centers in the Caribbean and the Americas, as well as in informal burial plots that have been lost to history, noted Oelze. "It is imperative to include descendant communities in the process, she said. Many have a genuine interest in their ancestors. It's important to them, which is why so many are turning to 23andMe."

However, genetics from Africa are postcolonial and therefore flawed, said Oelze. As people were displaced by the pressures of slave raids, they effectively erased their geographic origins; strontium isotope analysis holds the promise of retracing movements from the past, she said.

Oelze's results will also aid wildlife conservation. "Trafficking of endangered animals is of growing concern to conservation, and this map of strontium isotopes in tropical Africa will help identify hotspots of illegal poaching activity," said Oelze, who plans to share her data internationally in open-access publications. She is also eager to use the findings to spark interest in STEM fields among students from Historically Black Colleges and from high schools with diverse student populations.

A hub of excellence

UC Santa Cruz has the potential to lead the field in tracing the histories, geographies, and molecular archaeology of the slave trade, according to Katharyne Mitchell, dean of the Division of Social Sciences. In Anthropology, Lars Fehren-Schmitz brings expertise in the analysis of ancient DNA, and Monroe has conducted extensive research in Bnin and Togo on the transformation of West African communities during the slave trade, as well as related archaeological research in the Caribbean. In History, Professor Greg O'Malley has done pathbreaking work on the transatlantic slave trade.

"This cohort of brilliant scholars is doing transformational work," said Mitchell. "Vicky is a powerhouse, and I'm delighted the Webster family wanted to support her research. I see great things emerging from this."

Oelze, who joined the faculty in 2016 from the Max Planck Institute for Evolutionary Anthropology, will organize a symposium on campus on the molecular forensics of the transatlantic slave trade, drawing historians, archaeologists, isotope geochemists, and geneticists to campus.

See the rest here:
Using isotopes to reconstruct life histories within the transatlantic slave trade - UC Santa Cruz

The spurious chemical imbalance theory of depression is arguably the most destructive thing that psychiatry has ever done. Worldwide, millions of individuals are taking antidepressants, often with a cocktail of other drugs, because they have been told the blatant falsehood that they need the pills to combat a brain illnessa real illness just like diabetes.

Many of these individuals were told the additional lie that they needed to take the pills for life and are now addicted to the products.

At the present time, some psychiatrists and psychiatric facilities are backing away from the hoax. Most of these recantations take the form: We didnt mean it literally. The chemical imbalance thing was just a metaphor.

But what needs to be stressed is that the impetus for these diluted recantations came, not from psychiatry, but rather from the anti-psychiatry movement. It was the thousands of protesting voices that finally persuaded psychiatry that some backing off was needed, particularly as no proof of the theory had ever been uncovered.

The response from psychiatry, however, has not been commensurate with the damage done. What we need to see are full page ads in all major newspapers and cyber news outlets acknowledging that the chemical imbalance theory was a hoax; that it induced millions of people worldwide to take these drugs; and that it was developed and propagated to increase psychiatrys prestige and earnings. But thats not what we are seeing.

Instead, the general response from psychiatry continues to be one of denial, minimization, and excuse-making. The very eminent and learned Ronald Pies, MD, is the master of denial in this area, but minimizers and self-excusers abound. We are told that patients needed a simple formula for understanding their problems. They didnt. They needed the truth. We are told that patients needed a biological explanation to reduce stigma and alleviate their feelings of guilt. They didnt. They needed valid explanations. Besides, biological explanations actually increase stigma (here, here, here, and here).

The essential point is that as the drugs began to come on stream in the 50s, 60s and 70s, psychiatry needed illnessesreal illnesses with clear-cut biological etiologiesto cash in on the pharma-generated bonanza. Real illnesses were not to hand, so they invented their various chemical imbalance theories and promoted them as fact with all the vigor and energy that they could muster. Since then, psychiatrists have produced a truly overwhelming volume of research all aimed at proving the theory correct, but with no success. The simplistic shortage-of-serotonin-in-the-brain nonsense remains stubbornly unproven. As mentioned above, psychiatrists have backed off the more blatant expressions of this theory, but, remarkably, the treatments remain the same: Take these pills every day and come back in three months for more.

All of which is very interesting. But of even more interest is the recent development of a new approach to validatingor rather attempting to validatepsychiatric illness.

In JAMA Psychiatry, October 2019, Kenneth Kendler, MD, published an essay titled From Many to One to Many-the Search for Causes of Psychiatric Illness. Dr. Kendlers essential thesis is as follows. Prior to about 1850, causes of illness were anecdotally recorded from individual cases, resulting in long and diverse lists for all disorders. In the second half of the nineteenth century, single causes were found for many infectious diseases. Causal thinking shifted from multicausal approaches to monocausal theories of etiology. Dr. Kendler writes, Indeed proving monocausal etiology became a way to establish the legitimacy of a disorder. In the mid 20th century, general medicine shifted to a chronic disease model in which paradigmatic disorders, such as cancer and cardiovascular disease, were shown to be highly multicausal. Psychiatry, however, continued to pursue monocausal theories in their attempt to legitimize their activity. Despite ample evidence to the contrary, monocausal thinking continues to influence our field, for example, in the popular but improbable view that we can, with a few key advances, move easily from descriptive to etiologically based diagnoses.

Dr. Kendler works for Virginia Commonwealth University. He is a Distinguished Professor of Psychiatry, Professor of Human Genetics, and Director of the Virginia Institute of Psychiatric and Behavioral Genetics. He served on the DSM-III-R Work Group, on the DSM-IV Task Force, and on the DSM-5 Work Group for mood disorders.

Dr. Kendlers essay highlights two main themes: firstly, that psychiatry is not blameworthy in the promotion of spurious and monocausal etiologies; and secondly, that even though the quest has failed dismally, this is not a problem because a multicausal approach is better anyway.

Here are some pertinent quotes from Dr. Kendlers paper, interspersed with my thoughts and observations.

The second epidemiologic phase, termed infectious disease, had as its paradigm the germ theory, lasted roughly from 1850 to 1950, and was dominated by monocausal etiologic theories in which the relationship between putative etiologic agents and specific diseases was one to one (although most investigators recognized such modifying factors as host resistance). The third epidemiological phase, termed chronic disease, had a dominant black box paradigm. It incorporated a multifactorial disease model for what was termed chronic noncommunicable diseases (eg, diabetes, heart disease, certain forms of cancer, and hypertension), diseases often associated with particular lifestyles that could not be explained by a single salient causal factor. In this paradigm, the goal of epidemiology was to determine the magnitude and causal nature of the associations between a wide range of putative risk factors and these chronic noncommunicable diseases. This phase began around 1950 and has lasted until current times. (p 1087)

The essential point that Dr. Kendler is making here is that there is a fundamental distinction between these two phases. But is this really so? Let us compare scarlet fever, a classic monocausal infectious disease, with diabetes, which is the first example Dr. Kendler gives of a multicausal chronic disease.

Scarlet fever is caused by a streptococcal infection of the throat, while diabetes is widely considered to arise from many causes, or risk factors, as they are sometimes called. These include inheritance, lifestyle factors, and diet. However, the essential cause of diabetes is an inability of the pancreas to produce enough insulin to adequately process and utilize the sugar in the blood stream. This in turn stems from a damaged or compromised pancreas, ingestion of more sugar than the pancreas can cope with, or other causes. When considered in this light, diabetes is a monocausal illness, even though there are multiple pathways to the final cause.

Applying the same logic in reverse, one can make a case that scarlet fever is multicausal. Firstly, the individuals throat has to be exposed to the streptococcal infection. Secondly, the germ has to survive the initial immune system response. Thirdly, as hand-washing is one of the major protections against contracting this illness, anything that militates against frequent hand-washing could be considered a cause, e.g., living in crowded unsanitary conditions.

In addition, the time period leading up to the contraction of an illness can be analyzed and re-analyzed almost indefinitely. Any incident or event in that time frame has the potential to be considered a contributing cause. Let us say, for instance, that a child contracted scarlet fever at a birthday party given by one of his friends. We could legitimately say that the invitation caused the illness; or that the childs acceptance of the invitation was the cause. Or let us become even more imaginative and say that the child in question was rather shy and didnt want to go to the party, but was prevailed upon by his parents to do so, in the belief that it would do him good. So the illness was caused inadvertently by the parents! And so on.

Back to Dr. Kendlers essay.

During the second half of the 20th century, the approach to disease causation of major parts of psychiatry was out of step with the rest of medicine and medical epidemiology. Instead of multicausal models, the rising and soon to be dominant field of biological psychiatry pursued monocausal models for their major disorders. (p 1088)

The reader will have no difficulty seeing where this is going. Psychiatrists were chasing single causes, for their so-called illnesses, when they should have been looking for many causes. So the great failure of psychiatry to deliver the promised causes wasnt a failure at all. They were simply looking for the wrong kind of explanation. Butand this is the point that Dr. Kendler glosses overit wasnt a benign error. Psychiatry needed clear-cut biological explanations in order to take advantage of the drugs and to establish themselves as bona fide doctors. In this regard they routinely prioritized their own guild interests over the welfare of their clients.

In the early to mid-1960s, through histofluorescence stains, the cell bodies and neuronal pathways of the 3 monoamine neurotransmitters were identified: dopamine, norepinephrine, and serotonin. This further spurred the development of 3 long-lived monocausal neurochemical theories for psychiatric illness. All were proposed in the mid-to-late 1960s: the catecholamine hypothesis of affective disorders, the dopamine hypothesis of schizophrenia, and the serotonin hypothesis of depression. Although based on a range of evidence, the primary support for these theories was reasoning backward from therapeutic mechanisms to etiology. That is, for Parkinson disease the logic was sound: clarification of cause leading to a proposed treatment. By contrast, psychiatry followed the more problematic approach of extrapolating backward from a proposed mechanism of treatment to the cause of the disease. Although the original articles proposing these theories were couched in qualifications, as a psychiatry resident in the late 1970s, I was taught these theories as monocausal explanations. Schizophrenia was caused by excess dopamine transmission. Decades later, I would commonly see patients who would say some version of my psychiatrist said I have a chemical imbalance in my brain and then proceed to summarize one or more of these theories. It is now widely accepted that these theories, claiming a dominant causal pathway to illness, are false although debate continues regarding the dopamine hypothesis. (p 1088) [Emphases added]

Theres a lot in this quote. Firstly, note the phrase Although based on a range of evidence. In fact the evidence supporting these chemical imbalance theories was flawed, i.e. it was not evidence at all. Secondly, note the sentence By contrast, psychiatry followed the more problematic approach of extrapolating backward from a proposed mechanism of treatment to the cause of the disease. [Emphasis added] This was not a more problematic approach; it was a bogus approach; a hoax. And if the psychiatrists who promoted these theories couldnt see the deception, then they had no business presenting themselves as a helping profession. It becameand perhaps still isroutine for mental health workers who drew attention in case conferences to critical psychosocial realities to be told by the psychiatrists that first we have to treat the depression, which invariably meant drugs or electric shocks.

Although the original articles proposing these theories were couched in qualifications, as a psychiatry resident in the late 1970s, I was taught these theories as monocausal explanations. (p 1088)

Dr. Kendler did his psychiatry residence at Yale University, during which, he tells us, he was taught the various chemical imbalance theories, presumably as valid, factual explanations. This seems straightforward enough, and presents no surprises. But there is some ambiguity. If I were to say that my father taught me how to ride a bike, I am actually making two statements. Firstly, I am asserting that my father expended some time and effort in this process, and secondly, that his efforts were successful. In his essay, however, Dr. Kendler leaves this issue vague. Did he believe the hoax, and did he in turn foist it on his customers? It is obvious that Dr. Kendler is a very bright person and, given the fact that the original articles proposing these theories were couched in qualifications, it is reasonable to believe that he did see through the whole sordid deception. So what did he say to the trusting victims who parroted back the bogus theories to him? Did he tell them the truth? Or did he play along?

It is not my intention to pressure Dr. Kendler on this matter. Economics can make cowards of us all. But if he genuinely wants to promote honesty and integrity in this area, it would be helpful if he were to write an expos of sorts concerning the pressures he experienced in these matters during his psychiatric residency at Yale. Such an endeavor would be unlikely to endear him to his colleagues, but would shed light on a facet of psychiatry that has for too long been kept hidden, and might even encourage other psychiatrists to follow suit.

Psychiatry has had a long-term love affair with monocausal theories of illness dating at least from the late 19th century, heavily influenced by our success at the identification and effective eradication of GPI [general paresis of the insane]. In the latter half of the 20th century, with both neurochemical and molecular genetic theories of illness, our enthusiasm for monocausal theories outran our common sense. Emerging from decades of psychoanalytic dominance, we were deeply committed to reestablishing our medical legitimacy. What better way to show that we treated real diseases than to show that they were monocausal? (p 1089)

There is a distinct exculpatory tone to this passage. Instead of acknowledging that psychiatrists were systematically deceiving their customers for their own benefit, Dr. Kendler tells us that it was just a long-term love affair, in which their enthusiasm for monocausal theories outran [their] common sense.

Indeed, as mentioned earlier, this exculpatory stance is one of the dominant themes of the essay. Here are some additional quotes:

Our long yearning for monocausal theories of etiology drives, at least in part, our heartfelt calls for the abandonment of our descriptive nosologic systems in favor of an etiologic model. (p 1089)

There have not been heartfelt calls or long yearning from psychiatry on this matter. Rather, they simply declared the matter resolved, and promoted the chemical imbalance theories as fact. I have written extensively on this subject here.

This search has 2 prominent phases, both fueled by new scientific developments. The first was neurochemical. The stage was set in 1957 by Montagus discovery of dopamine in brain tissue quickly followed, in 1960, by the dramatic finds from Ehringer and Hornykiewicz of the decreased content of dopamine in the postmortem brains of patients with Parkinson disease. Here was a major neurologic disorder fitting apparently into a monocausal neurochemical theory. What could be more exciting for the then young and ambitious field of biological psychiatry? (p 1088) [Emphasis added]

So the systematic, self-serving, and widespread deception perpetrated by psychiatry stemmed from their excitement! How eminently understandable.

The second wave of monocausal theories in psychiatry was genetic. Despite much evidence from family studies that major psychiatric disorders did not segregate in pedigrees as expected for a mendelian condition, the first successful linkage study of Huntington disease in 1983elicited intense excitement in psychiatric genetics and launched a large number of linkage studies, especially of schizophrenia and bipolar illness. (p 1088) [Emphasis added]

Even more excitement!

Yet the ghost of GPIof monocausal psychiatric disorderslurks in our memory. To this day, it influences our nosologic thinking. It makes us too willing to adopt a monocausal perspective in our clinical work and in our explanations of psychiatric disorders to patients. Monocausal thinking continues to support hard reductionist approaches that seek the cause of our major disorders and is one of several factors inhibiting collaborative psychiatric research work across scientific levels. (pp 1089-1090)

So it is the ghost of GPI lurking in psychiatrists collective memories that inhibits them from acknowledging the non-medical nature of depression, painful memories, paranoid thinking, distractibility, etc

Despite the wide acceptance of the chronic noncommunicable disease model in modern medicine, there remains in our culture a sense that disorders with many causes have reduced legitimacy. Therefore, both clinicians and their patients would feel more secure if a large indisputable cause were found for their disorders. This, however, is a social and not a scientific problem. (p 1089-1090) [Emphasis added]

So a monocausal breakthrough would make clinicians and their patients feel more secure. So, telling a bereaved woman that her sadness is the expected and reasonable response to the death of her spouse will make her feel less secure than telling her the gross falsehood that there is something wrong with her brain. Or telling a battered wife that her sadness is the understandable response to the violence would make her feel less secure than telling her it stems from a brain disease. This is exculpation taken to a new level. We lie to our customers because it makes them feel more secure.

Dr. Kendler closes his essay on an upbeat, exhortative note.

The stigma of psychiatric illness and the low status of the psychiatric profession need to be addressed at both social and political levels and will not likely be solved through the discovery of major single causes for our illnesses. The legitimacy of the discipline of psychiatry does not rest on our ability to find single major causes of our disorders. (p 1090)

How does one address the stigma associated with psychiatric disorders and the low status of the psychiatric profession at social and political levels? PR campaigns? Lobbying politicians to pass psychiatry-friendly laws? These things are happening already, but the routine prescribing of pills and electric shocks continues to be psychiatrys only stock in trade, and the self-centered promotion of biological psychiatry continues to dominate the field.

Rather than grieving for the loss of our visions of another GPI around the corner, we can positively embrace the etiologic complexity of our disorders. (p 1090)

Actually they are not psychiatrists disorders. Rather, they are the disorders that psychiatrists self-servingly foist on their hapless clients.

If the common, morbid dysfunctions of the human cardiovascular, immune,hormonal, musculoskeletal, and gastrointestinal systems, which cause most of the morbidity in our country, are highly multifactorial, could we realistically expect anything else from the parallel dysfunctions of our mind/brain system? (p 1090)

In other words, psychiatric illnesses have as much ontological reality as diabetes, heart disease, cancers, hypertension, etc. Dr. Kendler encourages his colleagues not to grieve the abandonment of the quest, but rather to positively embrace the etiological complexity of psychiatric illnesses.

But what does etiologic complexity actually mean in this context, and why is it so important to Dr. Kendler?

Dr. Kendler uses various terms to describe etiologic complexity. For instance, he describes the illnesses in question as multifactorial, chronic noncommunicable, often associated with particular life styles, multicausal, etc.

Dr. Kendler has been working on this general theme for quite some time. In 2012 he published an article in Molecular Psychiatry calledLevels of explanation in psychiatric and substance use disorders: implications for the development of an etiologically based nosology (2012: 17, 11-21). Here are two quotes from the abstract:

The soft medical model for psychiatric illness, which was operationalized in DSM-III, defines psychiatric disorders as syndromes with shared symptoms, signs, course of illness and response to treatment. Many in our field want to move to a hard medical model based on etiological mechanisms. (p 11)

a move toward an etiologically based diagnostic system cannot assume that one level of explanation will stand out as the obvious candidate on which to base the nosology. This leaves two options. Either a hard medical model will be implemented that will require a consensus about a preferred level of explanation which must reflect value judgments as well as science. To take this approach, we need to agree on what we most want from our explanations. Alternatively, we will need to move away from the traditional hard medical model that requires that we ground our diagnoses in single biological essences, and focus instead on fuzzy, cross-level mechanisms, which may more realistically capture the true nature of psychiatric disorders. (p 11)

Theres a lot here. Firstly, there is what many readers might consider a contradiction in the first sentence: The soft medical model for psychiatric illness, which was operationalized in DSM-III, defines psychiatric disorders as syndromes [Emphases added] But syndromes are not illnesses. Heres how DSM-III defines a syndrome:

A grouping of symptoms that occur together and that constitute a recognizable condition. The term syndrome is less specific than disorder or disease. The term disease generally implies a specific etiology or pathophysiological process. In DSM-III most of the disorders are, in fact, syndromes. (p 368)

And elsewhere in the text (p 6), the term mental disorders is defined as a clinically significant behavioral or psychological syndrome. However, even before DSM-III was published (in 1980), it was widely accepted and promoted by psychiatrists that many psychiatric disorders, including depression, were genuine bona fide illnesses. (In my entire career I have encountered only one psychiatrist who acknowledged that psychiatric disorders were syndromes, not real illnesses.) This massive deception has been discussed at great length in various venues and need not be labored here. But what is noteworthy is Dr. Kendlers next sentence: Many in our field want to move to a hard medical model based on etiological mechanisms. But in fact almost all psychiatrists have already made this move and have been promoting the chemical imbalance hoax for decades. Many psychiatrists who are now retired practiced nothing but bio-bio-bio psychiatry for their entire careers.

Obviously Dr. Kendler is aware of this. So, what point is he making?

a move toward an etiologically based diagnostic system cannot assume that one level of explanation will stand out as the obvious candidate on which to base the nosology. (p 11)

In other words: if psychiatrists continue down their present road trying to use science to prove their various disease theories, they are just as likely to discover that major depression, schizophrenia, PTSD, etc., stem from psychosocial and economic causes rather than from their cherished brain diseases. In effect Dr. Kendler is saying: abandon the search or we run the risk of losing everything. (We) cannot assume that one level of explanation will stand out as the obvious candidate on which to base the nosology. In other words, we cannot assume that biological explanations will emerge as the dominant perspective. Dr. Kendler warns his colleagues, we need to agree on what we most want from our explanations. What does he mean by this? Read on.

Here are some quotes from the body of the 2012 article:

Let me sketch what we might find for MD [major depression]. Single gene effects for MD are even smaller and less well established than for AD [alcohol dependence]. Aggregate genetic effects are also somewhat weaker and are modified by a range of environmental exposures. Structural and functional magnetic resonance imaging studies have suggested a range of central nervous system abnormalities that correlate with MD but the specificity and strength of these associations, as well as their causal status, remain uncertain. A number of physiological abnormalities including endocrine and immune function have been reported in cases of MD but again, sensitivity and specificity have typically remained modest. Several aspects of personality are strongly correlated with risk for MDespecially neuroticism. This association is almost certainly causal but is nonspecific as high levels of neuroticism predispose to many internalizing disorders. Some cognitive processes may be more specific and here their causal role has been clearly demonstrated by many randomized controlled trials of cognitive behavior therapy. A range of early environmental risk factors have been well established for MD (for example, poor parenting and sexual abuse) and are generalizable across cultures but are quite nonspecific. Stressful life events can be quite strongly associated with risk for MD. Much, but not all, of this association is likely causal and some classes of events are moderately specific for MD. However, stressful life events are likely to be quite distal influences on risk pathways to MD and many such events predispose to other psychiatric disorders. Economic factors can impact on risk for MD via levels of unemployment and cultural factors can shape the expression and help-seeking behavior of those with depressive syndromes. (p 16)

Nature does not appear to have provided us one critical level of explanation for psychiatric illness that stands out from the background. For CF [cystic fibrosis], explanatory power is highly concentrated in the level of DNA base-pair variation. For psychiatric disorders, explanatory power is dispersed and diffuse. (p 16)

So, genuine scientific investigation might show that depression, say, is as likely to stem from sad events in peoples lives as from any kind of brain disease.

The current status of our science, and, most probably, the nature of psychiatric disorders themselves, does not yield up unambiguous choices for the best level at which to define psychiatric illness etiologically. (p 16) [Emphasis added]

Or might even show that depression is much more likely to stem from sad events.

But, despite these obvious concessions to a bio-psycho-social-cultural-economic perspective, Dr. Kendler is careful not to jettison the baby with the bathwater. He still seeks to preserve the notion that psychiatric disorders are real illnesses.

a rejection of the hard medical model for psychiatric disorders should not be misunderstood as setting up a deep divide between etiologic models for psychiatric and medical disorders. (p 16)

If, as our review of the data suggest, there is no a priori way to pick a single level of explanation on which to base an etiological nosology, we could try to argue it out on pragmatic grounds. What do we most want as a field from our explanations? (p 17)

What indeed? To date, psychiatrys primary motivations have been enhanced prestige, expansion of scope, and increased earning power, all of which were well-served by the chemical imbalance hoax.

What Dr. Kendler is telling his colleagues here is that the hoax is exposed; that science will not give them what they seek; and that by continuing to promote a purely biological perspective they are running the risk of losing what they want most: the reality of psychiatric illness. In other words, the science is not going our way, so we need to ask ourselves what do we most want, and then promote concepts that will help us achieve this. Dr. Kendlers wording is carefully chosen, but it seems to be that he is encouraging his colleagues to dispense with the formalities and neutrality of science and promote concepts that will retain psychiatrys hegemony in the field: what we want most.

Towards the end of the article Dr. Kendler provides us with more descriptors of the psychiatric diagnostic system that he envisions for the future. These include disorders (of) complex, mutually reinforcing networks of causal mechanisms, disordered multi-level mechanisms, and higher-order disturbances in multi-level mechanisms. [Emphases added]

Note the words disorders, disordered, and disturbances. Dr. Kendler, as in the 2019 paper, affords no recognition to the fact that the thoughts, feelings, and actions in question are not actually illnesses, and in many (perhaps most) cases are clearly adaptive.

Four years later (2016) Dr. Kendler published The Nature of Psychiatric Disorders (World Psychiatry, 2016: 15: 5-12). Heres a quote from the abstract:

Therefore, we should argue more confidently for the reality of broader constructs of psychiatric illness rather than our current diagnostic categories, which remain tentative. Finally, instead of thinking that our disorders are true because they correspond to clear entities in the world, we should consider a coherence theory of truth by which disorders become more true when they fit better into what else we know about the world. In our ongoing project to study and justify the nature of psychiatric disorders, we ought to be broadly pragmatic but not lose sight of an underlying commitment, despite the associated difficulties, to the reality of psychiatric illness. (p 5)

Note the phrase we ought to not lose sight of an underlying commitment, despite the associated difficulties, to the reality of psychiatric illness. To which I can only ask: why not? The common and accepted meaning of the word illness is something going significantly awry with the structure or function of an organ. If what psychiatrists call major depression doesnt actually conform to this description, why should psychiatry maintain an underlying commitment to the reality of psychiatric illness? Also, note the phrase In our ongoing project to study and justify the nature of psychiatric disorders [Emphasis added]. Isnt this arguably the very opposite of valid science? Didnt most of the great errors of science stem from efforts to justify the status quo often for the benefit of various powerful conflicting interests?

Despite Dr. Kendlers writings on these matters, his polycausal model is not attracting a large following. Here are quotes from the websites of some psychiatric facilities:

Harvard Medical School: What causes depression?

Certain areas of the brain help regulate mood. Researchers believe that more important than levels of specific brain chemicals nerve cell connections, nerve cell growth, and the functioning of nerve circuits have a major impact on depression. Still, their understanding of the neurological underpinnings of mood is incomplete. [Note how the simplistic chemical imbalance theory is being nudged aside, and being replaced by the more generic notion of nerve functioning.]

This quote is followed by five pages of closely-written type under the following headings: (Brain) regions that affect mood; Areas of the brain affected by depression (with picture); Nerve cell communication; How the (neurological) system works; When the (neurological) system falters; Kinds of neurotransmitters; How neurons communicate (with picture); Genes effect on mood and depression; Temperament shapes behavior; Stressful life events; How stress affects the body; Early losses and trauma; Seasonal affective disorder; Medical problems; and Depression medications.

The material is heavily slanted towards a biological perspective. Even the headings that sound psychosocial are slanted. The section on stressful life events contains:

Disturbances in hormonal systems, therefore, may well affect neurotransmitters, and vice versa.

The section on early losses and trauma contains:

Many researchers believe that early trauma causes subtle changes in brain function that account for symptoms of depression and anxiety. The key brain regions involved in the stress response may be altered at the chemical or cellular level.

Mayo Clinics article Depression (major depressive disorder) under the section Causes:

Its not known exactly what causes depression. As with many mental disorders, a variety of factors may be involved, such as:

Biological differences.People with depression appear to have physical changes in their brains. The significance of these changes is still uncertain, but may eventually help pinpoint causes.

Brain chemistry.Neurotransmitters are naturally occurring brain chemicals that likely play a role in depression. Recent research indicates that changes in the function and effect of these neurotransmitters and how they interact with neurocircuits involved in maintaining mood stability may play a significant role in depression and its treatment.

Hormones.Changes in the bodys balance of hormones may be involved in causing or triggering depression. Hormone changes can result with pregnancy and during the weeks or months after delivery (postpartum) and from thyroid problems, menopause or a number of other conditions.

Inherited traits.Depression is more common in people whose blood relatives also have this condition. Researchers are trying to find genes that may be involved in causing depression.

University of Rochester Medical Center, Major Depression, under the heading What causes depression?

Researchers are studying the causes of depression. Several factors seem to play a role. It may be caused by chemical changes in the brain. It also tends to run in families. Depression can be triggered by life events or certain illnesses. It can also develop without a clear trigger.

And so on. Its clear that most pro-psychiatry writers have received the message to downplay the simplistic too-little-serotonin-in-the-brain theory. Many, however, are still relying on this notion but couching it in different terms or adding some token psychosocial material, usually referred to as triggers.

In psychiatry there is no actual illness behind the symptoms. Major depressive disorder and psychiatrys other functional disorders are nothing more than loose collections of vaguely and arbitrarily defined thoughts, feelings, and behaviors. Psychiatrys clear objective in the past fifty years has been to pathologize every significant difficulty of thinking, feeling, and/or behaving, and to sell these bogus illnesses to the general public, the media, insurance companies, and government officials. The only essential difference between psychiatrists and street-corner drug-pushers is that the latter dont pretend that they are treating or curing illnesses.

Dr. Kendler has written an interesting and thought-provoking essay, but, in my view, has missed the central point: that depression, regardless of severity, duration, or impact, is not an illness. In fact, the opposite is the case. Depression is an adaptive mechanism that encourages us to make changes in our lives, habits, or circumstances. Just as pain provides an incentive to remove our hand from a hot stove, so depression encourages us to leave home, change jobs, develop some assertion skills, find a partner, etc. It is a mechanism that we share with virtually all other animal species, though the precise nature, complexity, and impact of the depression varies enormously.

As a species we can experience a wide range of emotions. We have this ability because we have machinery in our brains, and other organs, that enables this to happen. It is widely believed in psychiatric circles that if neurobiologists could uncover the precise mechanisms involved in experiencing depression, this would prove that depression is an illness. But, in fact, uncovering such mechanisms would no more pathologize depression than the neurobiology of walking or seeing or writing poetry would pathologize these activities. All human activity has a neurobiological underpinning, without which the activity cannot occur. We cannot see without eyes and optic nerves, etc.; we cannot feel without feeling machinery though we dont know exactly what this machinery is or how it works.

It certainly needs to be acknowledged that a persons feeling apparatus can malfunction, but such malfunctions are almost certainly rare, and cannot be routinely inferred from the presence of depression, regardless of severity. I have personally worked with hundreds of depressed individuals in my career, but have never encountered anyone whose level of depression was incommensurate with his/her story. Psychiatrists have essentially numbed themselves to this reality, firstly because of their spurious atheoretical approach (if youve got the symptomsregardless of why youve got themthen you have the illness); and secondly because their primary, or perhaps only, agenda is to clinch the diagnosis. It is particularly interesting in this regard that before the arrival of the pills, psychiatrists, most of whom practiced some kind of psychotherapy, had no difficulty recognizing the reality: that if people are given the opportunity to talk, they can tell you very clearly why they are depressed.

For several decades psychiatry has been lying to its customers that depression is a pathological state caused by a shortage of serotonin, and can, apparently miraculously, be diagnosed without ever examining the brain but simply by scoring yes on five of the nine items on the facile checklist. Some of the more prestigious facilities and colleges are stepping back from the serotonin hypothesis, largely as a result of being outed by the anti-psychiatry movement. But the diagnostic criteria are still the same, and the treatment hasnt changed. Its still eat these pills every day and come back in three months. And if that doesnt work, well try electric shocks.

Sometimes people feel trapped in their circumstances and are unable to muster the resources or skills to effect the necessary changes. An abused wife, for instance, might lack the economic or emotional means to leave her abusive husband. A man stuck in a job that he hates might not be able to see a way out. In cases like these, the depression can appear permanent and unrelenting. What people in these kinds of circumstances need is genuine help to identify the nature of the issues, generate positive targets, and begin the process of change. An abused wife needs a safe home for herself and her children, an effective safety network, and ongoing emotional and practical support. She does not need a diagnosis of major depressive disorder and a bottle of serotonin reuptake inhibitors.

Drugging a perfectly effective depression mechanism out of existence in order to reduce the immediate sense of discomfort and misery is a bit like sticking duct tape over the check engine light on ones dashboard. It may reduce ones negative feelings on the matter, but will produce no lasting benefits. Physicians who participate in these pharma-sponsored activities are not practicing medicine in any true sense of the term. Rather, they are drug pushers, pure and simple.

Dr. Kendler is proposing that psychiatry abandon the search for monocausal explanations of psychiatric illness and embrace the multicausal perspective. His reasoning is that this is a better perspective and is more in tune with present-day approaches to chronic non-communicable illnesses.

But he has perhaps revealed his true motivation in the 2016 paper:

In our ongoing project to study and justify the nature of psychiatric disorders, we ought to be broadly pragmatic but not lose sight of an underlying commitment, despite the associated difficulties, to the reality of psychiatric illness. (p 5)

In this very clear statement, Dr. Kendler is acknowledging an ongoing and underlying commitment to justify psychiatric disorders and to affirm their reality. But isnt this the very antithesis of science? Isnt it a fundamental requirement of science that we leave our beliefsno matter how deeply cherishedat the door, and go where the science takes us? How much credence should we afford a scholar who acknowledges, apparently without compunction, that in his work and writings his agenda includes an underlying commitment to the reality of psychiatric illness?

Go here to see the original:
The Chemical Imbalance Theory of Depression: Where Is It Going? - James Moore