Category Archives: Human Genetics

The world's rarest and most debilitating diseases can potentially be cured thanks to genomics and gene editing breakthroughs.

And this next-generation wave of technologies and medicines presents a hugely exciting opportunity for investors.

Innovation is hot right now, and the cost of sequencing a human genome has fallen drastically, making it a feasible solution to many modern health problems.

To date, scientists have sequenced around 0.2% of the human genome. Incredibly, this has led them to discover cures for approximately 5% of an estimated 5,000 rare diseases, according to industry estimates.

Therefore, further sequencing is sure to reveal new opportunities for cures and advancements. This is an inspiring growth story to be a part of.

Between 1980 and 2000, biotech enjoyed a revolution. This was prompted by the discovery of recombinant DNA technology along with Genentech's 1980 IPO. Genentech became a subsidiary of Roche (SWX: RO) in 2009.

From the turn of the Millennium, the rise of genetics, company consolidations, and less innovation led to a downturn.

Now leading ETF provider, ARK Invest sees a revival in fortunes for the biotech industry, particularly in the genomics space.

Understanding how the human body is constructed on a molecular basis has come on leaps and bounds in recent years. And with it, a reduction in the cost of genome sequencing. Lower prices mean widespread adoption, furthering data collection and analysis.

All this could lead to miracle cures for cancer and many other debilitating illnesses.

The time will come when an individual's genetic background will be included in their computer health records. Indeed, this has already begun.

A genetic family tree will show genetic mutations in close or distant relatives and predict potential offspring irregularities. Artificial Intelligence (AI) technologies can then diagnose, notify health practitioners and implement a tailored health plan.

AI technologies include deep neural networks and machine learning and are far superior to current medical computer systems.

AI can analyze vast quantities of data from many sources. Plus, it can detect patterns and disease characteristics that humans might miss.

Unlocking the secrets of DNA is paramount to curing diseases and chronic illnesses.

Thanks to breakthroughs in genomics, the approval of new genomic drugs could transform the modern healthcare system to ensure longer, healthier lives and fewer surgeries. This would result in a more robust economy, a happier society, and less economic burden from health.

Some genomics stocks to consider investing in include:

One of ARK Invest's favorite genomics stocks is Switzerland-based CRISPR Therapeutics. Its proprietary platform, CRISPR/Cas9-based therapeutics, allows for precise and directed changes to genomic DNA.

One of its founders is Emmanuelle Charpentier, who, along with Jennifer Doudna, recently won the Nobel Prize for her breakthrough research on CRISPR technology.

CRISPR stock has endured a volatile year. The CRSP share price is down over 45% year-to-date, although it has risen 320% in the past five years.

Illumina is a life sciences company making the tools and systems required for large-scale genetic variation and function analysis. It recently re-acquired subsidiary Grail in an $8bn acquisition.

Illumina founded Grail, an early cancer detection specialist, in 2016, then spun it off shortly after but retained a 12% stake.

The fact it was willing to pay such a large sum to re-acquire shows it must see value in Grail and have confidence in its future. Indeed, early detection of cancer is desperately needed. Therefore the potential target market is enormous.

Unfortunately, the Grail acquisition has been fraught with regulatory tension, which has triggered a share price decline in Illumina.

Illumina is a $59bn company with a solid reputation. Its machines and platform are used for COVID-19 variant tracking across 70 countries. And the very first COVID-19 viral sequence was detected on an Illumina machine.

It already screens for early-stage diabetes and high cholesterol, so adding cancer detection is sure to add the opportunity for growth to the company.

In March, the New York Times reported, "According to the Federal Trade Commission, Illumina controls roughly 90 percent of the market for sequencing machines in the US".

Meanwhile, Illumina claims to compile 80% of the world's genomic information.

Editas is on a mission to repair broken genes. Using CRISPR, it is developing a pipeline of medicines for serious diseases. These include In Vivo Medicines for ocular and neurological disorders and Ex Vivo Cell Medicines for Sickle Cell Disease and Thalassemia. It is also developing Cellular Therapy Medicines.

It will soon be reporting its results in a trial for inherited blindness. It aims to create a cure (EDIT-101) for LCA10, a leading cause of blindness in children with no treatment. If the trial results are positive, the share price is likely to respond well.

Editas, like CRISPR Therapeutics and Intellia, uses Cas9, but it also works with the Cas12a nuclease. It believes this gives it scope to expand the capabilities of CRISPR gene editing greatly.

Co-founded by Jennifer Doudna, Mammoth Biosciences is still a privately funded company. It develops diagnostics and is branching into gene editing medicines.

The biotech start-up is escalating its foray into developing CRISPR cures for disease. It recently raised $150m in a Series D funding round to help it expand. This reportedly values it at over $1bn.

Mammoth Biosciences CTO, Janice Chen said:

"Traditionally, Mammoth has been positioned as a diagnostics company, but really, our vision is much broader than that. We're thinking about CRISPR as a search engine at large."

Mammoth will focus on researching gene editing with CRISPR as a way to modify patients' cells directly inside the body. It aims to target tougher-to-reach disease points.

In early 2021 Mammoth developed a diagnostic test for COVID-19 based on CRISPR.

There is speculation Mammoth may go public via IPO, but so far, nothing has been confirmed.

ARK Invest offers its Genomic Revolution ETF, which contains between 30 and 50 companies operating in genomics. Their focus includes:

DNA Sequencing

Gene Editing

Gene Therapy

Agricultural Biology

Targeted Therapeutics

Molecular Diagnostics

Bioinformatics

Living Drugs

Investing in healthcare and biotech stocks is notoriously risky. They are hugely speculative and, therefore, volatile. The upside potential is massive when trial results come good, but share prices regularly plunge when results disappoint.

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Investing in Genomics - Value The Markets

THOUSAND OAKS, Calif., Nov. 29, 2021 /PRNewswire/ -- Amgen (NASDAQ:AMGN) today announced that it has been named to the Dow Jones Sustainability World Index for the eighth consecutive year, reflecting the company's enduring commitment to environmental, social, and governance (ESG) issues.Amgen also was named to the DJSI North America Index for the ninth straight year.

The DJSI Indices are among the best indicators of a company's ESG performance due to the breadth of companies evaluated nearly 11,000 this year and the rigorous nature of the annual assessment process. The DJSI World Index recognizes the top 10% of companies in the S&P Global Broad Market Index for performance on ESG issues, which S&P Global considers critical to generating long-term stakeholder value.

"Our mission is to serve patients and our ESG framework guides how we go about successfully accomplishing that mission," said Judy Brown, senior vice president, Corporate Affairs. "As we look to the future, we will continue to do our part to build a better, healthier world by addressing the challenges facing society that matter most to our business and to our stakeholders."

Amgen's four ESG pillars Healthy People, Healthy Society, Healthy Environment and a Healthy Amgen include commitments to:

"We congratulate Amgen for being included in the Dow Jones Sustainability Index for DJSI World and DJSI North America," said Manjit Jus, Global Head of ESG Research, S&P Global. "A DJSI distinction is a reflection of being a sustainability leader in your industry. The record number of companies participating in the 2021 S&P Global Corporate Sustainability Assessment is testament to the growing movement for ESG disclosure and transparency."

In May 2021, Amgen published a comprehensive Environmental, Social, and Governance Report, which is available here.

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

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

Amgen is one of the 30 companies that comprise the Dow Jones Industrial Average and is also part of the Nasdaq-100 index. In 2021, Amgen was named one of the 25 World's Best Workplaces by Fortune and Great Place to Work and one of the 100 most sustainable companies in the world by Barron's.

For more information, visit http://www.amgen.comand follow us on http://www.twitter.com/amgen.

CONTACT: Amgen, Thousand Oaks Trish Rowland, 805-447-5631 (Media) Megan Fox, 805-447-1423 (Media) Arvind Sood, 805-447-1060 (Investors)

SOURCE Amgen

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Amgen Named To Dow Jones Sustainability World Index For Eighth Consecutive Year - PRNewswire

Sekar Kathiresan was driving home when his cell phone rang. The voice on the other end belonged to his father. It was the evening of Sept. 12, 2012, his father's 65th birthday. But that wasn't why he was calling.

"Senthil collapsed at home," Kathiresan's father said. "He's in the hospital."

Senthil, Kathiresan's older brother, was a seemingly healthy 42-year-old, training for a race. But that night he returned from a run dizzy and sweating profusely. He called 911, then had a seizure as paramedics arrived.

Senthil had had a heart attack; his brain starved of oxygen for minutes. He died a little over a week later.

His death devastated Kathiresan, an immigrant from India who spent his early childhood overseas with his brother, waiting for the day they'd join their parents in the U.S. "We relied on each other," Kathiresan said. Both had thrived in the U.S. They were married the same year and each had young children.

This story might be familiar to the millions of people and families affected by heart disease, the world's leading cause of death. But it's more than that for Kathiresan, who, when Senthil died, was a cardiologist and emerging as one of the field's leading geneticists.

"It really shook Sek. It shook all of us," said David Altshuler, the former Broad Institute of MIT and Harvard geneticist, a Vertex Pharmaceuticals executive and mentor to Kathiresan. "It was a tragic irony."

Kathiresan channeled his despair into motivation. He rose to the top of his profession, making discoveries that changed the way people think about heart disease. He launched a startup with an exceptionally ambitious aim to prevent heart attacks, for life, with a single treatment. Nearly a decade after his brother's death, the startup, called Verve Therapeutics, could soon test that treatment in people.

"I tried to turn that negative energy into Verve," Kathiresan said, "to make sure what happened to Senthil doesn't happen to others."

The road ahead is daunting still. Kathiresan is an academic-turned-CEO on a personal mission, not a seasoned biotech executive. His company is attempting a scientific moonshot, relying on cutting-edge, but unproven, gene editing technology to develop a one-time medicine for one of the most prevalent diseases. In doing so, he will have to prove the world needs what is essentially a longer-lasting version of cholesterol-lowering drugs that are already available.

"It's a pretty high bar to say gene editing has an important role to play here," said Richard Lifton, the president of Rockefeller University and a geneticist known for research into heart disease.

"But the flip side of that," he added, is a drug "that could last, potentially, a lifetime."

Kathiresan was only four years old when his world upended.

Kathiresan's father, an aspiring engineer, had received a full scholarship at the University of Pittsburgh, thousands of miles away from the tiny southern India village of Viramathi he, his wife and three children called home. He dreamed of coming to the U.S. and pursuing a higher education, but couldn't afford to bring the whole family, Kathiresan said. So, in 1975, he left for the U.S. with his wife, baby daughter Davi and about $40. Sek and Senthil stayed in India.

Kathiresan remembers a sense of loss, a "yearning." He didn't see his parents or hear their voices for five years. There were no phones in the house the brothers shared with their grandparents, nor at the boarding school they attended. They communicated through letters sent across the ocean. "I'm not sure I would have had the courage to leave my kids behind," he said, reflecting on his father's decision.

But the plan worked. Kathiresan's father earned a Ph.D. and saved enough money to bring his sons to the U.S.

Kathiresan vividly remembers the flight from Mumbai to New York. The brothers, who had never seen a plane before, were awestruck. They flew by themselves, with an attendant as their guardian. Picked up at the airport by their father, their first meal in the U.S. was at McDonald's, where Kathiresan had french fries for the first time. He devoured them and asked for more.

"We can't afford another one," his father told him.

The Kathiresan family in 1975. Sek is second from left. Courtesy of Sekar Kathiresan

Senthil and Sek Kathiresan, aged 10 and 9, in India in 1980, just before leaving for the U.S. Courtesy of Sekar Kathiresan

The Kathiresan family soon moved into a house outside of Pittsburgh. The brothers, who spent half their childhood in a town with no running water, would live the other half in a middle-class and predominantly White U.S. suburb, an upbringing each wrestled with.

Growing up, Kathiresan was one of the few people of color in his school. Though he made fast friends, he wasn't comfortable, caught between his two worlds: weekly prayers at a nearby Hindu temple and weekend football games at school. His mother pushed him and Senthil to remember their heritage, anxious they would become "too American."

While Kathiresan dated and met his wife in college, Senthil had an arranged marriage. "We respected each other's approach," he said. "Some immigrants want to jump right in and be all in," and others "want to keep as much of their home culture as possible."

Kathiresan majored in history and even flirted with a career in finance before finding medicine, which he said "offered a sense of purpose and a mission."

His choice of profession was also personal, even before Senthil's death. Kathiresan's uncle, a physician, had died of a heart attack. So had his grandmother. His father had a heart attack at 54. Each time Kathiresan was more certain he'd become a cardiologist.

He embraced the grueling hours and sleepless nights that came with residency training at Massachusetts General Hospital, undeterred even when accidentally stuck by a needle that had been in the neck of an HIV patient. "I saw my whole life flash in front of me," he recalled, yet, after initially panicking, he took antiviral drugs and went back to the hospital.

"It comes with the territory," he said. "You're teaching, you're trying to help, but there's risk, you know?"

Kathiresan wasn't satisfied being a doctor, though. He wanted to understand why the people closest to him were getting sick and learn how to do something about it.

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David Altshuler recalls sitting in his office at MGH one morning in 2000 when he heard a knock on the door.

Altshuler was already well on his way to being recognized as one of the world's top geneticists. His academic lab would soon co-lead three large genetic research studies the 1,000 Genome Project, the SNP Consortium and the International HapMap Project and he would become one of the founding members of the Broad Institute.

Kathiresan, then a young cardiology fellow, sought him out and burst into his office.

"I want to figure out what causes people to have premature heart attacks," Kathiresan exclaimed, according to Altshuler.

Dressed in scrubs, Kathiresan looked exhausted, having gone to Altshuler's office straight from an overnight shift at the hospital. Altshuler can still recall the big, dark circles under Kathiresan's eyes.

Many people can talk a good game. But Sek is the real deal. He reminds us of why we do what we do.

David Altshuler, chief scientific officer of Vertex Pharmaceuticals

"How are you going to do that?" he asked.

Kathiresan laid out a plan to discover what puts people at risk for heart attacks. Then he'd figure out which risk factors were actually important, before finding a way to intervene before health problems began.

"I need to learn genetics," Kathiresan told Altshuler. "That's why I'm here."

Altshuler was impressed. "He was personally compelling," he said, "and obviously incredibly motivated." When Kathiresan finished his doctoral training three years later, he went to work for Altshuler at the newly founded Broad Institute.

Kathiresan (front row, third from left) during his time as chief resident in internal medicine at Massachusetts General Hospital. Source: Sekar Kathiresan

The experience was a crash course in genetics. Altshuler pushed Kathiresan to answer scientific questions that mattered, not just the ones he could solve. He taught Kathiresan how to manage and develop talent, skills he'd call on in the future. "He had an immeasurable influence on me," Kathiresan said.

Over the next decade, the two wrote grants together and teamed up on studies aimed at identifying genetic markers for heart attacks. They became good friends and confidants. Along the way, Kathiresan emerged as "the leading person in the world studying the genetics of coronary artery disease, certainly of his generation," Altshuler said.

"Many people can talk a good game," Altshuler said. "But Sek is the real deal. He reminds us of why we do what we do."

A research lab is like a small company. There's money to raise, a budget to manage. A team to put together, mold and motivate. Careers to foster and a vision to rally a team around. Kathiresan got that chance in 2008, when he started a lab at MGH and the Broad to search for genetic clues into the underpinnings of heart disease.

As a first-time lab leader, Kathiresan had to convince people to believe in him. One of the first was Kiran Musunuru, a young heart doctor doing a fellowship at Johns Hopkins University.

At the time, Musunuru was disillusioned with cardiology. There were plenty of ways to treat heart disease, he said, but not enough tools to prevent it. Musunuru thought genetic research was the key and desperately wanted to be a part of the building "wave" of studies. That led him to Kathiresan's lab at MGH.

Kathiresan didn't have experience. His lab was brand new and his future there wasn't secure. But Musunuru felt a kinship with him. "In the same way that I was, he was all in," he said. "You've got to take some risks, right?"

Kiran Musunuru, professor of cardiovascular medicine and genetics at UPenn Source: American Heart Association

What followed was a prolific partnership. Musunuru became Kathiresan's mentee, one of his first post-doctorate students, and eventually, the head of his own lab at the University of Pennsylvania and a Verve co-founder. They were willing to put in "insane amounts of time" to finish work and publish papers as quickly as possible, according to Musunuru. Conditioned by working long hospital shifts, they'd each wake up before dawn, texting and calling one another.

The two partnered on a number of important research papers, looking into, among other things, the genetic basis of cholesterol and a protective gene known as ANGPTL3 that would become a top therapeutic target of drugmakers including, years later, Verve.

In the meantime, Kathiresan's lab turned into a training ground for dozens of other young scientists. By the time he stepped away, Kathiresan taught more than 60, many of whom are now faculty members. And he had discredited a long-held belief about heart disease.

For many years, Ethan Weiss, a cardiologist at the University of California, San Francisco, told his patients to exercise so their levels of "good cholesterol" would increase. He wasn't alone. Doctors were taught in medical school that high levels of high-density lipoprotein, or HDL, were associated with fewer heart attacks. Conventional wisdom was "you wanted to do everything you could to get your HDL up," Weiss said.

But researchers didn't know much about HDL and its relationship to fats in the blood called triglycerides, which were also linked to heart disease. High HDL, for example, was associated with low triglycerides and vice versa. "The question has been, which of these is the dominant one? Which one carries risks?" said Lifton, of Rockefeller. "It's been very hard to disentangle."

Researchers and drugmakers were nonetheless convinced HDL was the key, and that medicines that raised it would prevent heart attacks. Years of research led to drugs, known as CETP inhibitors, that could boost HDL. Several were thrust into large clinical trials early last decade, poised to become the next big thing in heart medicine.

"But correlation," Kathiresan said, "does not mean causation."

He basically changed a paradigm that we had clung to forever.

Ethan Weiss, cardiologist at the University of California, San Francisco

In 2012, Kathiresan's lab at MGH made a startling discovery: Good cholesterol isn't so good after all. By studying the genes of more than 100,000 people, they separated the effects of triglyceride levels from HDL. They found people with more HDL weren't safer from heart attacks.

HDL appeared to be a mirage, its link to heart disease perhaps conflated with other factors. Drugs that raise it likely wouldn't protect people from heart attacks, the team wrote in a paper published in The Lancet in May 2012.

The news stunned cardiologists. "He basically changed a paradigm that we had clung to forever," said Weiss, who now tells patients to ignore HDL levels because "it doesn't seem to matter."

The findings rippled across the pharmaceutical industry. One by one, CETP inhibitors from Roche, Amgen, Merck & Co. and Eli Lilly failed in clinical trials or were dropped by their developers. The class was largely shelved, along with a long-running hypothesis.

"It was a beautiful demonstration of using large-scale genomics to address a clinically vexing and important problem," Lifton said.

Just a few months after the paper's publication, Kathiresan's brother died of a premature heart attack.

Kathiresan took time off work and reexamined his own health. He went for heart tests, committed to being more active and dropped weight hed put on in college but hadn't lost.

"You mourn," Kathiresan said, and then "focus on the things you have control over."

So Kathiresan kept going. He and his labmates found more genes associated with either risk of early heart attacks or protection against them, confirming research by others in the process. They used a trove of genetic data from the U.K. to develop a diagnostic test that can identify higher risks of coronary artery disease, diabetes and other conditions in seemingly healthy people. "He decided, 'I will redouble myself to this effort,'" Altshuler said. "That took courage."

David Altshuler, Vertex's chief scientific officer Source: Vertex Pharmaceuticals

By 2018, they'd amassed a body of work so impactful that Kathiresan received the same Curt Stern award an honor given to pioneering human geneticists by the American Society of Human Genetics that Altshuler previously won.

In his acceptance speech, Kathiresan recalled the journey that took him from a small town in India to an awards stage in San Diego.

He then showed an ambulance report from the 911 call a 42-year-old made before he suffered a heart attack. He shared the man's electrocardiogram, his cholesterol and triglyceride levels and troubling family history. He explained how he died. He went through all the work he and his team had done to understand why the same thing happens to millions of other people.

The patient was his brother, he explained. New drugs were needed to avert the same tragedy in others, he said, and that was something he was working on. A high-profile competition he had recently lost gave him an opportunity.

Kathiresan, accepting the Curt Stern award from the American Society of Human Genetics on Oct. 18, 2018. Source: American Society of Human Genetics, via YouTube

In January 2016, the American Heart Association, the British drugmaker AstraZeneca and Google's life sciences arm Verily came up with an idea for a competition. Called "One Brave Idea," they promised a $75 million award and partnership opportunities to a researcher with the best idea to cure heart disease.

"What we're seeing is this growing epidemic of cardiovascular disease worldwide," said AHA CEO Nancy Brown, in a video describing the competition, "and we know that we need a new answer."

The AHA received 349 applications from research teams in 22 different countries. Kathiresan submitted one of them. Musunuru, then at UPenn, wrote another.

Unknown to one another, both pitched the same idea: a single shot of a gene editing drug that could drive down "bad cholesterol," or LDL, as low as possible for as long as possible.

Kathiresan cowrote an application with Anthony Philippakis, another Altshuler trainee who worked with the venture firm GV; and Feng Zhang, also of the Broad and one of the leaders of CRISPR gene editing research. Musunuru's team included UPenn gene therapy pioneer James Wilson.

The proposals were "eerily similar," Musunuru said. "Almost interchangeable."

Neither even made it to the competition's final round. The award went to a group of researchers led by Calum MacRae, chief of cardiovascular medicine at Brigham and Women's Hospital, who won for a genomics project meant to detail the biological changes that occur when heart disease begins.

The loss still bothers both of them. "I was bitterly disappointed," Kathiresan said. Musunuru calls it a "big, lost opportunity for the AHA."

Musunuru turned his attention back to research. Kathiresan decided to change careers.

Academia and the drug industry are closely linked. Academic researchers, after all, often make the discoveries that companies turn into medicines.

But that doesn't make it easy to leave the research bench for an industry job. The switch involves learning an entirely new language. Kathiresan, for example, had never heard the term "CMC," which is industry parlance for the process and regulation of drug manufacturing.

Jumping from academia to biotech can also mean giving up a secure position for a role in a company that, history would suggest, is likely to fail. Scientific glory isn't the only goal for a biotech, either: it has to eventually make money.

Kathiresan said he didn't have the "antipathy to the for-profit model that some people have." Previously, he had been focused on research, turning down industry job offers along the way. But his perspective changed after Altshuler left the Broad Institute in 2015 for a job as Vertex's top scientist. That "opened my eyes to the fact that there's a much larger world out there, and ways to have impact," he said.

So after losing the One Brave Idea competition, Kathiresan turned to Philippakis. It was a role reversal, of sorts: Kathiresan had advised Philippakis throughout medical school and after. "I really consider him a mentor in my life," Philippakis said.

Now it was Kathiresan who needed help. Philippakis cowrote the AHA application, he said, to help figure out how to build a company around the one-shot project. And Philippakis, who was well-versed in the biotech business because of his role with GV, could teach Kathiresan how to make that happen.

For almost two years, they gathered a small group every Friday to go through all the steps and potential roadblocks ahead. They tried to convince themselves "that this was actually doable," Philippakis said. They discussed how and where they'd get the intellectual property. The type of gene editing medicines they'd make. The business plan. How to raise the money and which firms to contact. Who the founders would be.

They came up with the name Endcadia Therapeutics a nod to ending coronary artery disease and prepared a pitch for GV.

Krishna Yeshwant is a venture capitalist who has worked with GV since its inception more than a decade ago. Over that time he's invested in dozens of healthcare startups. He's been asked to back plenty more.

Yeshwant has heard plenty of stories like the one Kathiresan told. Different versions of how "this family member of mine, this boyfriend or girlfriend, came down with this condition and I've devoted my life to it," he said. An emotional pitch only goes so far, though. And venture capitalists don't often invest in heart drugs because of how expensive they are to develop and test. In recent years, they've taken a back seat to promising new cancer and rare disease medicines.

But Yeshwant, who had joined Kathiresan and Philippakis for many of those Friday morning meetings, thought they were on to something. The treatment they envisioned, if successful, could change "how society works," he said, and Kathiresan was devoted to seeing it through. The plan they'd laid out was realistic as well: First they would prove the drug could work in a rare, inherited heart disease, a faster and less expensive clinical development path. Then they would go bigger and broader.

"It's aspirational," Yeshwant said, "but there was a nice on-road to it."

Krishna Yeshwant, managing partner at GV Source: GV

The others agreed. The startup became the first drugmaker GV better known for forming digital health companies ever incubated. The firm led a $59 million financing that closed in August 2018 and was announced the following year.

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Heart attacks struck Sek Kathiresan's family. He's devoted his life to stopping them. - BioPharma Dive

It was one of those rare, almost magical, summer evenings. Warm enough to sit outside in a T-shirt, listening to birdsong; warm enough to stay out late, savouring a meal; warm enough not to notice night settling in, the visitor that slipped into the party unannounced.

It was 11 June 2021. Jenny McCann sat in the garden of her home in north London with her twin brother, John Eyers, their parents, Lyn and Derek, and Jennys husband and children. It was her sons 10th birthday party. John and their parents had come down from Southport in Merseyside for the weekend to celebrate. Jenny made Lebanese lamb and parathas. The adults were buzzed on wine, the kids on birthday cake. Life felt really good, says Jenny.

She cant remember how the argument about the Covid vaccine started. John started saying really crazy things that didnt make sense, she says. About how people were only getting the vaccine for free McDonalds, and there was formaldehyde in it. The rest of the family remonstrated with him, pulling out their phones to factcheck what he was saying. But John was unmoving. He kept saying: I wont be a guinea pig.

Eventually, he made a joke and changed the subject that was his way of defusing tension. He would make a joke about everything, says Jenny, who is 43 and works as an operations manager.

Argument aside, it was a great get-together. John was on really good, funny form, says Jenny. They went for dinner at a Turkish restaurant and played darts in the garden. John scored a bullseye with his eyes closed and bragged about it all weekend. There was only one other difficult moment, when the family went to a local health club. John refused to wear a mask. The twins had a fight in reception.

I said: John, put your face mask on, Jenny remembers. He said: You arent my mother dont tell me what to do. John eventually acquiesced, then made another easy joke. They went swimming and played tennis and forgot about it.

A perfect weekend, then. Twins enjoying each others company after the enforced separation of the pandemic. Neither had any idea it would be their last time together.

John and Jenny were born in Southport in 1978. As children, they were diametrically opposed. Jenny was a bookish goody two-shoes; John was mischievous, good at sport and uninterested in school.

Despite their differences, they shared a formidable bond. When we were very young, we were shadows of each other, says Jenny. Into adulthood, she always knew when her brother was lying like the time he told their mother he hurt his shoulder tripping over a witch on Halloween. (He had been knocked off his bike by a lorry.) He didnt want Mum to worry, she says.

Jenny left home at 18 to go to university, leaving her brother behind. He worked in their parents carpet business for a while, but didnt enjoy it, then joined the erotic dance troupe the Chippendales, performing all over Europe. He had piercings in places you dont want to know about your brother having piercings in, Jenny shudders.

Around this time, he had a child, Macey, who is now 19. The relationship with her mother didnt work out, but John was a committed and loving father. His stripping days over, he returned to Southport and began working as a product specialist in the flooring industry. He worked to keep the lights on, but sport was his big thing. John had always been a gifted athlete.

He would do something and get obsessed with it, Jenny says. In his teens, he was a champion pole-vaulter and hockey player. In adulthood, he went through phases. He got into triathlons for a while, then bodybuilding competitions, then mountain climbing. He was a fixture at his local gym, which is where he met his best friend, Jonathan Cohen, 37, a chartered surveyor. Hed spot me in the gym with a set of weights and it was a natural progression from there, says Jonathan. Suddenly, we were going out every weekend together.

Johns dedication to fitness was something to behold. He really pushed his body to the limit, says Jonathan. John would be in the gym most mornings at 6am. On a holiday to Marbella in May 2016, John kept getting stopped by other men on the beach they wanted to know his training regimen. Jonathan cropped John out of their holiday photos. I wasnt having a photo stood next to him with his six-pack, he laughs. No! Not having that.

John was gregarious and fun-loving. He was a social butterfly, Jenny says. He liked being out, working a room, being charismatic and laughing and joking. He was a big piss-taker hed insult you, but in a funny way, so you ended up laughing. From his first girlfriend, at 10, John was a serial monogamist, prone to the odd grand gesture; he once proposed to a girlfriend at a festive grotto while dressed as Santa. He was an old romantic, says Jenny. He really wanted the happily-ever-after. (That relationship didnt work out and John never married.)

From January onwards, John struggled with his mental health. Covid restrictions weighed heavily on him. He hated not being able to go to the gym, hated not being able to go climbing, hated not seeing his friends. He lived alone, having broken up with a girlfriend at Christmas, and was lonely. He confided in his sister. I was really worried about him, Jenny says. He was in a bad place. I had to call him every day to make sure he was OK. Their grandmother died in March. When Jenny saw him at the funeral, she was horrified. Hed lost so much weight, she says.

Jonathan thinks this is, in part, what drove his friends Covid scepticism. He was frustrated at the way he couldnt go and do normal things, he says. He didnt want another lockdown, or to be in a situation where he wasnt able to go and see people. John felt that Covid was real, but that it had been dramatically overstated by the authorities. Nobody he knew in Southport had contracted Covid. If he got the virus, he would be fine. It got to the point where he refused to wear a mask at all, says Jenny.

Many of the people in his life tried to argue with him. I would tell him: Why wont you get the jab? Youll need it if you want to go away on holiday, says Jonathan. He kept saying that he wanted to wait. It wasnt that he would never get it. But it was more the misinformation, really. For whatever reason, he would not listen to whatever message was coming out of the government. Id say to him: John, why are you listening to that rubbish?

John was a fan of the pearlescent-toothed Tony Robbins, whose brand of adrenalised motivational speaking has earned him an estimated fortune of $500m (375m), plus a private island in Fiji and celebrity fans including Serena Williams and Hugh Jackman. Robbins, while steering clear of outright anti-vaccine statements, has made comments throughout the pandemic that play down the severity of Covid, or imply that lockdown restrictions are overblown. (Confusingly, he has also touted a Covid vaccine that is being developed by Covaxx, a company that has received funding from a venture capital firm in which Robbins is a partner. He has made no secret of that financial interest.)

In September 2020, Robbins posted a link to an article by the Kremlin-funded news site RT that said lockdowns achieved almost precisely nothing with regard to Covid. No deaths were prevented. In September 2021, he appeared at a conference in Florida where he mocked Australias Covid restrictions, cast doubt on the efficacy of vaccines and told a cheering audience not to let fear be the thing that controls you.

John mentioned to me once that one of his beliefs was that we shouldnt live in a climate of fear around Covid, says Jenny. If you were young and fit and well, youd be fine.

In this assumption, John wasnt entirely wrong. He was extremely unlikely to die from Covid, as a physically fit 42-year-old with no underlying conditions. The Covid mortality rate for a 40-year-old with no underlying health conditions is about one in every 1,490 people infected.

But his calculus when it came to understanding the risk-to-benefit ratio of Covid vaccination was off. If infected, someone who is unvaccinated is 32 times more likely to die of Covid than someone who has been vaccinated. While vaccination carries a risk of side-effects, this risk is far smaller than the risk of being unvaccinated during a pandemic. Out of 46.3 million fully vaccinated people in the UK, 77 have died of blood clots thought to be related to a Covid vaccine.

There is a huge asymmetry with risk, says Dr Tom Stafford, a psychology lecturer at the University of Sheffield. If you can get away with things that are low probability, you dont know how dangerous they are until its too late. Stafford uses the example of driving without a seatbelt: most of the time, you will be absolutely fine. But the one time you are in an accident, things might get very bad very quickly.

Its the same with the vaccine, says Stafford. Its a low-probability event that you will get the virus and need hospitalisation. But if you do, then the vaccine shows its benefit.

Stafford says that decisions about vaccination, particularly for Covid, are some of the hardest that people have to make. Risk calculus can be particularly hard in certain circumstances, he says. Risks where we dont always see the outcome, so we have to trust people. And new risks. Coronavirus is both of those things.

But why would someone such as John be inclined to take his information about the pandemic from social media influencers rather than scientific experts?

In 2009, Stafford co-authored a paper that surveyed people who lived on brownfield sites that might have been contaminated with pollutants. The survey asked the residents whom they trusted to tell them about the risks associated with living on the land. While most of the people trusted scientists to tell them the truth, they were almost as likely to take their information from family and friends, despite their total lack of expertise. It wasnt that they didnt trust the expertise of the scientists, Stafford says. They knew that scientists knew about pollution. They just thought that the scientists didnt have their interests at heart, whereas they knew that family and friends did.

The internet replicates this fundamental human impulse to trust family and friends almost as much as we trust experts at scale. We feel a connection to the people who are telling us things in a way that we dont feel a connection to the Centers for Disease Control or the Joint Council on Vaccination and Immunisation, Stafford says.

In the age of social media, we dont even need to have met the people we trust as much as established experts. Thats why social media is so dangerous, says Stafford. Because people share that emotional connection with influencers they might never have met. But its an asymmetrical intimacy. I may think I know that vlogger and they are talking to me. But really theyre talking to millions of people and the advertisers generating them their revenue.

The falsehoods that John repeated to his family and friends in the months leading up to his death are common tropes in online anti-vaccine spaces and easy to find: the vaccine has dangerous levels of formaldehyde in it; the vaccine is experimental; people are only getting the vaccine for free McDonalds.

The best thing that people can do is realise that social media platforms are fundamentally unsafe environments to gain facts about a pandemic that might kill you, says Imran Ahmed, the CEO of the Center for Countering Digital Hate. Social media contains vast amounts of misinformation that mingles seamlessly with good information. The misinformation might kill you.

John was a heavy user of social media. He was what Id call a Facebook ranter, says Jenny. Occasionally, she would challenge him on the content of his posts about Covid. When he was at her house, Jenny told him off for spending too much time on his phone. He wouldnt put his phone down, she says.

Ahmed is scathing about the social media companies that profit from misinformation. They dont want you to find the truth, he says. They want you to keep scrolling. If you find the truth, you dont need to scroll any more. They want you to keep scrolling and arguing and looking for more bullshit.

John tested positive for Covid on 29 June. By 3 July, he was seriously unwell. Amy, the woman who had recently become his girlfriend, had to force him to call 111 for help. Later that day, he was taken to Southport & Ormskirk hospital by ambulance.

Jonathan texted his friend as soon as he heard the news. He said that he couldnt type, but that he was in hospital with pneumonia, he remembers. He wouldnt admit at that point that it was Covid.

John had a raging temperature and difficulty breathing. Doctors put him on a Cpap machine, to assist his breathing, and swathed him in cooling blankets. On 4 July, John was up all night vomiting blood. He sent Jonathan a voice note the next morning.

It is the worst voice note I have ever heard in my life, says Jonathan. I burst out crying halfway through it. The voice note is a minute and a half long. In that time, John speaks about 12 words. I will never send it to anyone, but if anyone questioned whether Covid is real, I would play it to them, says Jonathan. It is the worst thing in the world. I can hear the fear in him. He is literally gasping for air. This is someone I knew who could run 10k or climb a mountain without struggling.

On 6 July, Jenny was in the supermarket when a feeling of great panic settled upon her. I just had this feeling that something wasnt right with John, she says. She left without doing her shopping. That afternoon, she got the phone call. John was in the ICU. She immediately got a train to Southport, sobbing the whole way.

By 11 July, John needed to go on a ventilator. Jenny spoke to him on the phone before he was sedated. She told him she loved him. He couldnt respond, but he texted her: Dont let them give up on me. It was the last message she received from her twin.

On the morning of 27 July, Johns family got the call they had been dreading. He was dying; they should come in right away. They raced to the hospital, but John had stabilised by the time they arrived. Staff told them to go home and said they would call back if there was any change.

About an hour later, the hospital called back. The family piled into the car and started driving to the hospital at top speed. Nurses kept calling, telling them to hurry. They raced to the ICU, where staff were waiting with PPE. Jenny could hear the alarms going off in her brothers room. I couldnt stop shaking, she says. It felt like a monster was about to come out of my mouth and I couldnt control it.

When they had finally tugged on the PPE, they ran into his room. It was full of ICU staff, all in tears. John had just died. Jennys stepdad collapsed to the floor. Her mum was wailing. The matron grabbed my mum and was holding her, says Jenny. Everyone was crying. The consultant was crying. All the staff were crying. Because he was so young. And they couldnt save him.

How do you explain how a supremely fit 42-year-old man died of a disease typically thought to afflict older people or those with underlying conditions?

Genetics makes the most sense, says Dr Guillaume Butler-Laporte, a genetic epidemiologist at McGill University. ButlerLaporte is part of a global research programme to analyse the genomes of more than 100,000 people with Covid, in an effort to understand why some people are more severely affected than others.

When he began his research in March 2020, Butler-Laporte did not expect to find much, he says. We thought Covid would affect everyone, but be worse for old people and not as bad for young people. But as we included more patients, we saw a clear story develop. It was surprising.

Butler-Laporte and his colleagues found that people with variants in up to a dozen locations on the human genome were at higher risk of developing severe Covid, should they be unfortunate enough to be infected with the virus. People with variants on the chromosome 3 region alone were up to twice as likely to develop severe Covid as someone without that genetic mutation. Chromosome 3 mutations are carried in about 10% of people of European ancestry, meaning that such people have a 10% chance of being twice as susceptible to severe Covid infection.

There is no question there is a genetic underpinning to this, says Butler-Laporte. As to whether genetics is more important than other factors, like age, I wouldnt want to comment. But it is clear that there are other determinants of severe disease and genetics is one of them. He is almost certain that John fits the profile of someone with a genetic variation that made him more vulnerable to severe Covid. Its impossible to know specifically what genes he carried, but its very likely he carried this genetic predisposition, says Butler-Laporte.

Unbeknown to John, his body was primed to react with maximum violence to the Covid virus. When he was unfortunate enough to breathe in infected air carrying infinitesimally small virus particles, his body gradually failed.

Had he been vaccinated, the best case would have been that he developed sterilising immunity, meaning that, when the virus landed in his nostrils, it got picked up by antibodies and never set up an infection, says Dr Tom Lawton, an intensive care doctor. If hed had a lower level of immunity from the vaccine, he would have had non-sterilising immunity, meaning that the virus did start to infect cells, but his body fought it and was able to clear out the virus before it ramped up rapidly. But John was not vaccinated.

The Covid virus infected his cells, replicating in his body. He eventually managed to expunge the virus but then his immune system went into overdrive. The virus seems to set something up in the body and the damage comes from there, says Lawton. It wouldnt have happened had the virus not been there.

First, his lungs were affected. There will have been blood clots forming, as well as a thickening of the membrane that separates the air and the blood in his lungs, says Lawton. As a result, the blood couldnt carry sufficient oxygen to Johns organs.

Doctors treated him with steroids, to damp down his immune response. But these immune suppressants made John vulnerable to bacterial and fungal infections. He developed infections in his lungs. His liver and kidneys began to malfunction, causing waste products to build up in his blood.

Doctors put John on dialysis to clear out the toxins, but by this point many of his organs were failing and he had unsurvivably low oxygen levels. He expended an inconceivably huge metabolic effort to stay alive. Although it looks like someone is just lying there asleep, the amount of work theyre doing is really impressive, says Lawton. He compares it to walking a marathon for every day the patient is hospitalised.

Eventually, John exhausted his physiological reserve. His body was oxygen-deprived and wrung out. His heart stopped beating and he died.

Before he died, John told the doctor treating him how much he regretted not getting the vaccine. The doctor said that he was beating himself up so much before they put him on the ventilator, Jenny says. He was saying: Why didnt I get vaccinated? Why didnt I do it? Why didnt I listen?

It is for this reason that his family has agreed to share his story. He probably wouldnt be dead if hed had the vaccine, says Jenny. Its really quite simple. He made a bad decision. We all make bad decisions all the time. And he paid the ultimate price for it. Which is so unfair.

Jenny says she just wants people to be vaccinated and, if they have doubts, to get medical advice not advice from the internet. And to realise that Covid is brutal. Its just brutal.

She is struggling to adapt to life without her brother. I dont know that it will ever feel real, she says. How can my healthy, outgoing, silly brother be dead? It doesnt make sense in my brain. How can I be a twin without a twin?

At Johns funeral, on 16 August, Jonathan delivered a eulogy. He spoke about that holiday in Marbella in 2016. They spent a day drinking champagne at a beach club, laughing, messing around. As the sun set, a rainbow formed over the sea.

This is how Jonathan likes to remember John. They are sunburned, drunk, a little unsteady on their feet. Suffused with love for each other. The night is drawing in and Jonathan turns to his best friend and says: shall we carry on? And John says: of course.

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The life and tragic death of John Eyers a fitness fanatic who refused the vaccine - The Guardian

The neuroscientist Alon Chen, director of the Weizmann Institute of Science in Israel.Santi Burgos

Like every Israeli, Alon Chen had to do three years of military service, and was posted with the paratroopers to the middle of the war in Lebanon. I lost a friend. When you go and you treat the person that is injured and is dying, and you cannot help him, it leaves its mark, he recalls. From then on, he knew he wanted to dedicate the rest of his life to understanding what happens to a brain that suffers a traumatic experience.

The son of Moroccan Jews who emigrated to Israel in the 1950s, Chen is the first generation in his family to go to university. He received his PhD in neurobiology and spent time in the United States specializing in the effect of stress on the brain at the molecular level. He currently leads the Weizmann Institute of Science in Israel, one of the most prestigious research organizations in the world, as well as a center studying stress-related mental illnesses run jointly by the Weizmann and the Max Planck Institute in Germany.

Speaking ahead of a recent lecture at the Ramn Areces Foundation in Madrid, Chen asserted that society today exacerbates depression, anxiety, bulimia and other diseases that we do not understand properly. These conditions are treated with the same drugs as 50 years ago, which do not work on one of every three patients, he added, amounting to a modern mental health crisis.

Question. You study the effect of stress on our brains at almost a molecular level. You cannot get into peoples brains, so how do you approach your field of study?

Answer. The best model for humans is other humans, but unfortunately, we cannot take out [live] human brains. We can image the brain, we can do blood tests and learn a lot, and we can use post-mortem brains. Stress eventually causes and affects many, many pathologies, like depression and anxiety. We do have access from different brain banks, for people who committed suicide, for example, because of depression or some other reason. So we do have human brain samples, but first, we use animal models.

Q. Isnt animal and human stress very different?

A. We think the same genes, the same proteins, the same brain circuit, the regulatory response to stress exists all the way from fish to humans.

Q. And what does that response look like?

A. Its a survival response. You know, if Im sitting with you here now and a lion enters the room, both of us perceive the lion as a challenge, as a stress, as a threat. The brain will activate what we call the central stress response. Its a response which will activate the entire body, but also your brain, which will cause a cascade of events. You will have your heart rate increasing and your blood pressure, glucose level, your respiration. It doesnt have to be a lion by the way. You can just now get a very, very upsetting phone call. Any psychological stress.

Q. And why does all that happen?

A. Your brain will prepare your body to escape, and that is the reason its increasing the glucose level because you need energy to escape, of course. But your cortisol level, your stress hormone will go high, and cortisol has many effects on the brain. Also within your brain there are a lot of changes. Your cognition will change. You will remember this event very well. You are going to have changes in your area of the brain which affect your attention, focus, your appetite. You dont need to think about your lunch now and you dont need to think about sex. Almost every major brain region will change its activity because of this lion. And collectively, all these systems will go out of balance, out of homeostasis. Its a normal and healthy response because you want to survive this. However, if we activated all the systems and we survived the challenge or the lion just left, the system has to switch off. Part of the stress response is not only to activate. The response is to switch off, and the people who cannot control this may develop stress-related disorders.

Q. What are these disorders?

A. Not only psychiatric disorders, not only depression. We all know about depression and anxiety and post-trauma, and eating disorders, but also metabolic-related [disorders], you know, Type 2 diabetes and obesity. But the question is why? Why is someone who is exposed to chronic stress or the traumatic stress of a bomb blast, a rape, an accident, why do they develop trauma and not less importantly, why are other people resilient? In the last 50 or 100 years, scientists were mainly busy asking why someone is sick. However, the majority of the population are resilient. So what we try to do now is ask why?

Q. Do you know how they manage to stay resilient?

A. The mechanism of resilience is not the opposite of the mechanism of being susceptible or vulnerable, so if you have a gene that makes you more susceptible and this goes up, it doesnt mean that if it goes down youre more resilient. Resilient [people] also have a different mechanism, or a separate one, that if you can study them, we can mimic them, we can copy them and help people.

Q. Is the predisposition to become ill from stress genetic?

A. We know that these diseases and disorders have a genetic component. We see it in the family tree. This is what we call genetic predisposition. Most of us carry a genetic predisposition to something, for depression, Alzheimers, cancer. If I just look at mental health, you can see that schizophrenia has a much stronger genetic contribution, 70% or 80%. Depression is probably less: 40% or 50% genetics. So how come you develop a disease or not if its 50%? Its the environment. The environment is everything you drink, you eat, you smoke, you breathe in. Stress is the most significant factor that affects it, which will eventually interact with your genetic predisposition and will determine whether you develop a disease.

Q. Could you provide an example?

A. If you have an identical twin from the same fertilized egg, meaning both of you inherit the same genetic predisposition, but you were separated at birth and you grow up in Madrid in nice neighborhoods and your brother grows up in a war zone, in a very stressful environment, the chance he will develop depression or post-trauma is significantly higher. You have the same genes, so genetics are important, but the environment is no less important. Your environment can come out at a different time of your life, so you can be exposed now as an adult to stress, as a teenager, as a young kid, as a baby and even as an embryo, meaning that your mother was the one who was exposed to stress and she transmitted some signals to you while you developed, and made you more or less susceptible to develop disease later in life.

Q. What happens when you suffer stress very early in life?

A. You can have a totally normal life. Normal childhood, teenager, high school, not a problem. And then suddenly you have a trigger. And this trigger could be anything. A trauma could be rape. Trauma could be, you know, you lost someone you love. It could be just an accident. Something you experience could be war. It can activate this embryonic signature and suddenly the disease is floating.

Q. Can you identify those genetic markers yet?

A. Its what we call epigenetics. Epigenetics are chemical modifications on top of your DNA. And the environmental signature is in this domain, in this epigenetic mark. Today we can measure epigenetic markers, and we can sequence not only the DNA, we can also sequence your epigenome, not only your genes.

Q. Can you identify which people are most at risk for stress-related diseases?

A. We are not there yet. In other fields like cancer, for example, women that carry mutations to a gene called BRCA1, well we know the chances those women will develop breast cancer are significant. So this is a genetic predisposition to develop breast cancer, or depression, or anxiety, or schizophrenia. But this is exactly where research is being done now. Maybe in the future before we send soldiers [to war] they will screen their genome or even epigenome and tell them no, look, they are prone to develop trauma.

Q. You often say that todays drugs for depression or anxiety are the same as they were 50 years ago?

A. The majority of the available drug treatment today is based on a very similar mechanism discovered more than 50 years ago, which is fine if they are working. The problem is the efficiency of SSRIs or selective serotonin reuptake inhibitors like Prozac and others: you still have 30% to 35% of patients not responding to anything. And when I give you the treatment, you need between five to eight weeks usually until the drug even starts to be effective. Some of them have major side effects, from migraine to sexual dysfunction, so people prefer not to get treatment. So we definitely need new solutions, and that will only come from understanding the brain.

Q. How close are we to being able to mimic these genetic mechanisms of stress resistance?

A. There has been major progress in the last decade. We still have a very long way to go because a disease that is composed of genetic predisposition is very complex, not from a single gene. Its not a mutation that causes blindness or deafness, its many, many genes and interaction between those genes, and then the environment. Your depression and my depression could be totally different depressions. You may have the same symptoms, but the underlying mechanism for depression could be totally different. So we may end up having 100 different types of depression. So we first need to start with better diagnostics.

Q. How has the pandemic affected societys stress levels and mental health?

A. We all talk about the physiological, clinical symptoms and how people are suffering from [Covid-19] infection and thats very, very important. But when this pandemic ends, we wont see those people anymore. But you know what will happen? Were going to continue seeing people who develop trauma and depression and anxiety because of the pandemic. You go now to a psychiatric hospital, and they are loaded with people. They cannot cope with the pressure. The number of depressed kids, young adults suffering from trauma because of lost jobs, lost businesses. The impact of the pandemic on mental health is already huge, but people dont talk about it enough and its going to stay with us for years after this pandemic.

Q. What does work against stress, besides medication?

A. Probably the most scientifically proven approach is exercise. Exercise is the best way to cope with depression and anxiety. You dont need to run a marathon or be an Ironman, just any type of combination of aerobic and anaerobic activities. The majority of the population that suffers from depression can still do those things. They can go and do something that they feel is making them feel better. I have a very stressful work life but I like the sea, and I do sea kayaking. Three times a week I wake up at 5am and go to the sea. I do 10 kilometers, or I like to work in my garden. The pandemic taught us how critical this is, and we are very social organisms. We like to be with people, we like to kiss, we like to hug, we like to be with partners and therefore not having this is affecting you. Meditation is another scientifically proven practice. It doesnt work for everybody, but it works for many.

Q. And how can you help those other people?

A. You always have to remember that we have that fraction of people who are very, very sick, and you know, you can take 10-year-old kids, even six sometimes and the only thing they want is to die. Right? Why does a six-year-old go into the playground slide and want to jump head down because she wants to die? This is something in the chemistry, the electricity in the brain that is not working, its a brain disease. We need to stop thinking about mental health. There is a soul, but this is your brain. I can put electrodes in your brain and I can make you more anxious or less anxious. Its electricity and chemistry, and we need to understand this. And we need to educate the public that mental health is a disease like any other disease, its like cancer or Alzheimers. So we need to educate the public about this.

Q. Israel has been in conflict with its neighbors for most of its history. How has this affected citizens mental health?

A. In Israel, every few years we have tough periods with conflict and missiles and sirens. In a way, there is some resilience in the population. And I think this is one of the reasons Israel was very good at handling this pandemic. We were extremely organized. The system is organized for emergencies.

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Alon Chen: Were going to continue seeing people who develop trauma and depression and anxiety because of the - EL PAS in English

Although verdicts vary, and some progresswas clearly made, the climate changeconsensusemerging among scientists post-Glasgow is thatthe world continueson a path toexceedthe threshold of 1.5 degrees Celsius identified in Paris in 2015 to avoid the worst impacts of climate change.But there is a course, so far too much neglected, that could magnify the tangibleprogress against carbon emissionseveryone wants:embracingbiotechnologyinnovation.

Strangely, Glasgow was marked by thealmost complete absenceof any discussion ofagriculture, which is widely charged withcontributing 20 to 30 percentof the greenhouse gas emissions driving global climate change. This is an unfortunate omission as advances in genetics over just the past decade have given uspowerfultoolsto tailor precisely the metabolisms of plants and animals. Living organisms are major sources and sinks for atmospheric carbon, so researchers are developing ways toapply genetic toolsto reduce emissions andincreasecarbon capture and sequestration.

Biotechnology cannot solve the whole climate problem on its own, but unlike nuclear fusion, which has been 30 years off for the last 50 years, bioengineered innovations havealready transformedagriculture, and gene-edited improvements are rapidly expanding those successes. The first research programs have alreadytweaked photosynthesisto deliver productivity increases of 20 to 40 percent in greenhouse tests that are now being scaled up and broadened. Doubling agricultural productivity by 2050 is well within reach.

The methane that cows and other ruminant animals produce is a significant contributor to global warming, but while U.S. herds have doubled their productivity in the past half-century, they have done so witholder technologies. Dairy farmers are now poised to apply the new technologies toacceleratefurther changes and achievecarbon neutralityin a generation or less.

Another huge opportunity is food waste, which accounts for roughly half of agricultural emissions. Gene editing isreducing wasteby extending the shelf life of fruits and vegetables while also enhancing nutritional value and quality.

Meanwhile, bioengineering and gene editing are increasingbiofuel crop yieldsby producing larger harvests and improving microbial digestion of cellulose. This is a welcome boon for the emissions-heavy transportation sector.

Myriad human activitiescontributeto non-biogenic greenhouse gas emissionsfrom lighting, warming, and cooling buildings to producing cement and steelso simply cutting agricultural emissions obviously will not be enough. But bioengineering and gene editing are also being applied in other ways that can help offset some of the difference, such as enhancing the ability of grasses, trees, crops, and algae to capture and sequester carbon at the required scale.

John Kerry, President Bidens Special Envoy for climate,recently said, The measure of success at Glasgow is we will have the largest, most significant increase in ambition [on cutting emissions] by more countries than everyone ever imagined possible. A much larger group of people are stepping up. He went on to note, There is a massive amount of money and energy going to bringing these [clean technologies] up to scale. That is necessary, but not sufficient. Governments also must take steps to unchain and liberate the innovative potential of these new technologies.

COP26 missed a chance to make a giant step forward bygalvanizing governmentsto take specific steps to capitalize on biotechnology innovation. Thefirst priorityshould beeliminatingunscientific regulatory burdens and barriers thathinderthe development of safe gene-edited products forno reasonother than unfounded fearmongering. Governments also shouldincrease their investmentsin and coordination of research and development (R&D) priorities such as advancing CRISPR tools, enhancing photosynthesis, and improving methods to measure and increase soil carbon. Finally, they should expand incentives that will spur rapid adoption of novel gene-edited technologies in the marketplace.

As the financial think tank Carbon Trackerhas noted, Mitigating climate change is no longer an expensive collective action problem; it is a technology revolution with enormous wealth-generating andredistributive potential. The solutions are within our grasp. It istimeto make the policy changes needed to capitalize on them.

Val Giddings is a senior fellow at the Information Technology and Innovation Foundation (ITIF). Giddings received his Ph.D. in genetics and evolutionary biology from the University of Hawaii in 1980. Val can be found on Twitter@prometheusgreen

This article was originally posted at theInformation Technology & Innovation Foundationand is reposted here with permission. Follow ITIF on Twitter@ITIFdc

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Viewpoint: By failing to endorse carbon-cutting biotechnology innovations, Glasgow climate summit missed 'low hanging fruit' - Genetic Literacy...

Natural selection, the evolutionary process that guides which traits become more common in a population, has been acting on us for the past 3,000 years, right up to the modern day, new research suggests.

And it seems to be acting in surprising ways on complex traits encoded by multiple genes, such as those tied to intelligence, mental illness and even cancer.

In natural selection, genes that confer some sort of survival or reproductive advantage get passed down and persist in a population, while those that lead to lower survival or fewer offspring become less common. There's no question that natural selection shaped the evolution of humans in our more distant past. But the impact of natural selection in the recent past is a much more controversial question.

The new research suggests that natural selection is indeed an important factor in modern times, though the methods used in the study have led to missteps before, said John Novembre, a computational biologist at the University of Chicago who was not involved in the new research. This means the findings should not be taken as the final word in modern-day natural selection.

Related: How would Earth be different if modern humans never existed?

The new study focuses on traits that emerge from a combination of multiple gene variants, such as intelligence and skin pigmentation. The complex genetics of these traits makes unraveling the action of individual genes difficult. To find these subtle effects, researchers conduct genome-wide association studies (GWAS), in which they scan for genetic markers across the entire genome to find short genetic sequences that are more common in certain traits than in others.

These results can be challenging to interpret even comparing people at a single point in time. Newer studies up the ante by looking not only for genes associated with complex traits, but also for signs of natural selection on these traits. In essence, genes that become more common over time are under positive selection: They're beneficial in some way and are thus likely to be passed down. Genes that become less common with time are under negative selection. They're somehow harmful to survival or reproduction, and thus are less likely to be passed down.

"There is quite a lot of controversy about whether GWAS is ready for this type of application," Novembre told Live Science.

In their study, published Nov. 15 in the journal Nature Human Behaviour, the researchers found a total of 755 traits showing signs of selection in the last 2,000 to 3,000 years.

For the modern samples, the researchers used data from people of European ancestry in the U.K. BioBank, a repository of genetic and health data from 500,000 participants. To look deeper into history, the researchers also used three datasets of ancient human DNA from the pre-Neolithic, Neolithic and after the advent of agriculture in the Near East, comprising a total of 512 individuals. The researchers looked in three timeframes: The modern era, the past 2,000 to 3,000 years, and up to about 100,000 years ago. The oldest data is the most unreliable, said study leader Guan Nin Ling, a professor in the school of biomedical engineering at Shanghai Jiao Tong University.

While the researchers had detailed health and lifestyle information from the U.K. BioBank, they had only partial genetics to go on for the older samples, and no direct information about things like how many children a person had or what they ate. Thus, they used the genes themselves to infer traits. If a gene known to be involved in height increased in frequency over time, the researchers took that as a signal that height might have been under positive natural selection.

The traits that seemed to be under selection ranged from skin traits such as "ease of tanning" to various body measurements. Somewhat surprisingly, genes associated with some seemingly undesirable traits increased in prevalence over time, including genes associated with conditions like skin cancer, inflammatory bowel disease and anorexia nervosa. This suggests that some of these disorders arise as side effects of genes that are beneficial for other reasons, the researchers suggested.

"If one variant elevates the risk of one disease but decreases the risk of another, natural selection would have little power to eliminate this variant," Lin told Live Science.

Ling and his colleagues were most interested in the question of why disorders with complex genetics, such as schizophrenia or attention deficit hyperactivity disorder (ADHD), persist despite natural selection.

But GWAS can be a tricky tool for trying to unravel natural selection, Novembre told Live Science. One of the biggest problems is something called "stratification." Differences between two populations can appear genetic, when they are actually environmental. Because GWAS can't show that a gene causes a trait, only that they're associated, the results can get weird, fast. To use a classic example from a 1994 paper, chopstick skills are clearly not a gift of DNA: They're a matter of practice from a young age. But a GWAS study in a diverse population like San Francisco might very easily turn up evidence of genes associated with chopstick skills simply by revealing genes that are more common in East Asian populations than in European populations.

This mistake has actually happened. In the last decade, a number of papers came out claiming that height-conferring gene variants are more prevalent in Northern Europe than in Southern Europe and that natural selection was pushing Northern Europeans to become taller, on average, according to research published in 2012 in the journal Nature Genetics.

But it turned out the impact of these genetic variants was overestimated, Novembre said. When looking at those same genetic variants in less diverse populations (a strategy for reducing the stratification problem), the evidence for natural selection vanished. The study had been picking up on so-far-unknown environmental differences between northern and southern Europeans and mistaking them for something purely genetic. Researchers had to completely rethink the results and are still uncertain about whether natural selection has anything to do with height differences across Europe, according to a 2019 paper in the journal eLife.

The use of data from people of only European ancestry helps limit the stratification problem, Novembre said. But there are still opportunities for the stratification problem to arise, he warned.

Among the hundreds of traits the researchers found might be under natural selection, a few stood out. When focusing on modern-day data, the researchers found that higher IQ was associated with having more sexual partners but fewer children. Meanwhile, ADHD and schizophrenia were both associated with having more sexual partners. These two conditions are examples of traits that might be a challenge in daily life, yet improve mating success, Lin told Live Science.

When looking back over more than 100,000 years of human history, the researchers found that traits having to do with skin tone and body measurements were the most common to show selection pressure. These included things like facial measurements, height and torso length. For example, genes associated with face shape and size were apparently under natural selection over the past 100,000 years, the researchers found, which might have to do with changes to the jaw and skull associated with diet and brain growth.

Looking back as far as 3,000 years ago, the researchers found that inflammatory bowel disease seemed to be favored by natural selection. This could be an example of a trait that is helpful in one context and harmful in another, Lin said.

"We hypothesize that in ancient times with poor hygiene conditions, a highly activated immune system in the intestine would protect us from infection," he wrote in an email to Live Science. "However, a highly activated immune system in modern society only causes our intestine to attack itself."

But it can be very hard to show why a particular trait relates to evolutionary success. To use height as an example, being tall might benefit reproduction by making someone more appealing to potential sexual partners. Or maybe height is just a side effect of an efficient metabolism, which improves survival rates, and that increased likelihood of surviving to reproductive age could lead to the genes getting passed down to the next generation. If genes tend to vary together and many do natural selection could be acting on a totally different trait than the one that seems most intuitive. For example, Novembre said, the variants that made skin tanning easier, which showed up as highly selected in the new research, are likely related to a lot of other traits, like rates of skin cancer, freckling and hair color. It's hard to know what path, exactly, leads to someone reaching reproductive age, attracting a fertile mate, and having lots of babies, and which genes are just lucky hangers-ons in that process.

Making matters more complicated, there are times when the genetics of a trait may be completely swamped by the environment. Something like this could theoretically happen with human intelligence. IQ is partially hereditary, so if it's true that higher-IQ people do have fewer children, that would arguably push the collective IQ of the population downward over time. But if the environment became more conducive to brain development better nutrition, reductions in lead or other pollutants the population might well become brighter.

"Just because the apparent genetic basis for something is changing doesn't mean the population has even been evolving in that direction," Novembre said.

One approach to nailing down natural selection would combine large-scale GWAS with studies on the genomes of single families, Novembre said. Family members, especially siblings, usually grow up in fairly similar environments, so it's easier to tell when genes are affecting any given trait. These family studies could be used to ground-truth claims from large GWAS samples, teasing out which genes still show impacts when you remove as much of the environment as possible from the equation.

Lin and his colleagues plan to conduct family studies to learn more about the genetics of complex conditions like schizophrenia. They're also working to quantify genetic variants that can give rise to both beneficial and harmful effects simultaneously, he said. The findings of the new study are a starting point, Lin said, and a reminder that natural selection is still a force in human biology.

"It is simply not true that humans have stopped evolving by natural selection, even given our capacity to change the environment towards facilitating and reducing physical tasks, minimizing the energetic costs to get better food, and better health care system," Lin said.

Originally published on Live Science

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Natural selection has been acting on hundreds of human genes in the last 3,000 years - Livescience.com

Growth of Animal Genetics Market is attributed to rise in production of porcine and increase in pork consumption across the globe. The same segment is likely to register highest CAGR in the global animal genetics market during the forecast period.

PUNE, India, Nov. 25, 2021 /PRNewswire/ -- According to The Insight Partners study on "Animal Genetics Market to 2027 Global Analysis and Forecast by Animal Genetic Material, Genetic Material and Service" the animal genetics market was valued at US$ 4,778.67 million in 2019 and is projected to reach US$ 7,705.23 million by 2027; it is expected to grow at a CAGR of 6.3% during 20192027. The growth of the market is attributed to the growing preference for animal derived proteins supplements and food products and rising adoption of progressive genetic practices such as artificial insemination (AI) and embryo transfer. However, limited number of skilled professionals in veterinary research and stringent government regulations for animal genetics is expected to hinder the market growth.

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The North American region holds the largest market share of this market and is expected to grow in forecasted years. The growth in North America is characterized by the presence of new market players, various product launches and increasing government initiatives.

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Likewise, Mexico is likely to offer attractive business opportunities for livestock genetics. Over the last decades, Mexico's beef, pork, and dairy productions have undergone valuable developments. Mexican generators in the expanding livestock intensive systems are frequently using modern genetic improvement technologies such as artificial insemination and embryo transfers.

In North America, the US is the largest market for animal genetics market. Livestock groups provide consumers with different products and services, including meat, milk, eggs, fiber, and draught power. The genetic variation within livestock communities produces the raw material for evolving through natural selection in answer to changing conditions and human-managed genetic improvement plans. As per the Food and Agriculture Organization (FAO), animal genetics is one of the livestock development support. It is a wide field, ranging from characterization to conservation to genetic development. According to the National Institute of Food and Agriculture (NIFA), there have been dramatic improvements in animal production yields and efficiencies. Therefore, the ever-increasing demand for dietary protein in the United States has been observed. These demands are achieved by one the best Animal breeding is one strategy by which these improvements may be performed. NIFA, with the help of scientists from universities and research organizations and food animal industries, provides national leadership and funding opportunities to conduct basic, applied, and integrated research to increase knowledge of animal genetics and genomics.

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The COVID-19 outbreak has disturbed various trades and businesses across the world. The incidence of corona virus or COVID 19 has not yet been registered the animals. Also, there is no evidence that companion animals are the prime source of the spreading epidemic in humans. However, various studies have been conducted to check the spread of disease from animals to humans. In many cases, zoonotic diseases were found in humans due to interaction with animals. Therefore, government bodies are taking more precautions and safety measures to prevent the spread of corona virus in the animals. The measures are widely carried out for companion animals as they frequently come in contact with their owners. Also, it is essential to report the cases to a veterinary authority. For instance, in the region, to report the cases of detection of COVID-19 is done to OIE through WAHIS, in accordance with the OIE Terrestrial Animal Health Code as an emerging disease.

The OIE is actively working by providing assistance to research for their on-going research and other implications of COVID-19 for animal health and veterinary public health. The assistance is also providing risk assessment, risk management, and risk communication. Also, the OIE has put in place an Incident Coordination System to coordinate these activities. In addition, OIE is also working with the Wildlife Working Group and other partners to develop a long-term work program. The aims are to provide better understandings, dynamics, and risks around wildlife trade and consumption. Also, it aims to develop strategies to reduce the risk of future spillover events.

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Additionally, various product and service launches have been initiated, which is helping the US market to grow. For instance, The Veterinary Genetics Laboratory (VGL) at the UC Davis School of Veterinary Medicine has launched an updated and advanced website along with several new tests for veterinary community. As the VGL is one of the foremost genetic testing laboratories in the world, the new site and tests will bring yet another level of global impact to the top-ranked veterinary school. Thus, the consistent support for combating addiction in the country undertaken by various organizations likely to augment the growth of animal genetics market during the forecast years.

The Asia Pacific region is expected to be the fastest-growing region among all other regions. The growth of the market in the region is majorly due to countries like China, India and Japan, which drives the major consumption of animal derived products. Moreover, growing preference for animal derived proteins supplements and food products, and rising adoption of progressive genetic practices such as artificial insemination (AI) and embryo transfer are also likely to contribute to market growth. On the other hand, significant investment by government in various breeding programs is supporting the growth of market. For instance, the central and local governments have invested more than RMB 5 billion to build breeding or multiplier farms and conservation farms for breed improvement programs and the building of centers for testing the quality of breeding stock, semen, and embryos.

Based on product, the animal genetics market is segmented poultry, porcine, bovine, canine, and others. The porcine segment accounted for more than 35.84% of the market share in 2019. In terms of genetic material, the animal genetics market is segmented into semen, and embryo. The embryo segment held the largest share of the market in 2019. In terms of service, the animal genetics market is segmented into DNA typing, genetic trait tests, genetic disease tests, and others.The DNA typing segment held the largest share of the market in 2019.

Rising Adoption of Progressive Genetic Practices Such as Artificial Insemination (AI) and Embryo Transfer in Animal Genetics Market:

Growing focus on developing superior animal breeds using genetic engineering to obtain high reproduction rates for large-scale production of modified breeds is expected to drive animal genetics market during the forecast period. Animal genetics emphasizes the inheritance and genetic variations in wild and domestic animals. This science is used at a commercial level for services such as testing genetic disorders, screening genetic traits, and typing DNA. For identifying genetic hybridizations, animal genetics uses various genetic practices, such as artificial insemination, embryo transfer, and cytological studies. Moreover, artificial insemination (AI) can reduce various risks involved in animal breeding and disease transmission. It is found that female offspring cattle born through artificial insemination yield more milk than normal offspring. Additionally, the use of antibiotic-containing semen extensors is effective in preventing bacterial infectious diseases. Therefore, the entire AI process is considered hygienic than natural mating.

The market players are focusing on partnerships, collaboration, and acquisitions to develop genetically modified breeds and maintain their market share. For instance, in August 2020, Cogent and AB Europe collaborated to launch a novel sexed semen service for sheep producers in the UK. In May 2018, Recombinetics entered into partnership agreement with SEMEX for the implementation of a precision breeding program, which is expected to improve animal health and well-being through hornless dairy cattle genetics. According to the Brazilian Association of Artificial Insemination, the number of commercialized doses of semen increased from 7 million in 2003 to ~14 million in 2017. Thus, rising adoption of genetic practices will support the market growth in coming years.

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Market: Segmental Overview

In terms of product, porcine segment is anticipated to register the highest CAGR during the forecast period. Growing production of porcine and increase in pork consumption is likely to favor the growth of the market. Pork is the most consumed meat across the globe. In the US, pork production generates $23.4 billion output per year. Additionally, 26% that is around 2.2 million metric tons of pork and its products are exported to other countries. Despite of the challenges such as tariffs, labor and disease risks, the pork industry in US is still growing with around 66,000 sows in 2019. Also, developments by the major pork producers in the country is likely to grow the pork production industry. For instance, in 2017, 123-year-old Clemens Food Group partnered with 12 independent hog farmers to establish a new packing plant in Michigan. Thus, growing pork production industry is likely to favor market growth. In terms of genetic material, the animal genetics market is segmented into semen, and embryo. The embryo segment held the largest share of the market in 2019. In terms of service, the animal genetics market is segmented into DNA typing, genetic trait tests, genetic disease tests, and others.The DNA typing segment held the largest share of the market in 2019.

Animal Genetics Market: Competition Landscape and Key Developments

Neogen Corporation, Genus, Groupe Grimaud, Topigs Norsvin, Zoetis Services Llc, Hendrix Genetics Bv, Envigo, Vetgen, Animal Genetics Inc, Alta Genetics Inc. and among others are among the key companies operating in the animal genetics market. These players are focusing on the expansion and diversification of their market presence and the acquisition of a new customer base, thereby tapping prevailing business opportunities.

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In September 2020, Genus Plc and Tropic Bioscience entered into collaboration. Tropic Biosciences the pioneering agricultural-biotechnology company entered into collaboration with Genus in order to explore the application of Tropic's Gene Editing induced Gene Silencing (GEiGS) technology in porcine and bovine genetics.

In July 2020, Topigs Norsvin entered into strategic partnership with Acuity swine genetics company. This partnership will provide the opportunity for joint collaboration and expansion of technical expertise, commercial product testing and supply chain infrastructure in animal genetics market across the North America region.

In April 2020, Zoetis Animal Genetics and Angus Australia have entered into a strategic partnership that will aid Australian Angus breed stock and commercial breeders an additional benefit from genomic, or DNA-based technology. Zoetis have made a considerable investment in the expansion of the Angus genomic reference population through the provision of genotyping services and sponsorship.

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Animal Genetics Market Worth ($7,705.23 Mn by 2027) by (6.3% CAGR) with Impact of Coronavirus Outbreak and Global Analysis & Forecast by The...

Cannabis exerts its effects on the body by binding to cannabinoid receptors. These cannabinoid receptors also bind to endogenous cannabinoids that the body makes, called endocannabinoids.

Endocannabinoids are involved in the modulation of numerous biological processes, including metabolism, pain, inflammation, and transmission of information in the brain. The release of endocannabinoids, along with opioids, is also responsible for the feeling of euphoria that people generally experience after an intense workout.

A new study has shown that daily physical exercise is effective in lowering the levels of inflammation-related markers. Moreover, the study suggests that the endocannabinoid system may interact with gut microorganisms to produce such a reduction in inflammatory markers.

Researchers at the University of Nottingham led the research, which appears in the journal Gut Microbes.

Endocannabinoids bind to cannabinoid receptors present in the brain, peripheral nervous system, and immune system. The enteric nervous system, which controls the gut, also expresses cannabinoid receptors.

The dysregulation of the endocannabinoid system is associated with obesity and metabolic disorders.

Microorganisms present in the gut, which people collectively refer to as the gut microbiota, also have a significant influence on metabolism. Changes in the composition of these microorganisms, including reduced diversity of gut microorganisms, are associated with obesity and other metabolic disorders.

Studies suggest that the endocannabinoid system interacts with the gut microbiota to influence metabolism and energy homeostasis.

For instance, gut microbiota composition can influence endocannabinoid and cannabinoid receptor levels in the intestine. Specifically, changes in gut microbiome composition in obesity occur alongside lower endocannabinoid levels.

Obesity and other metabolic disorders are also associated with chronic, low grade inflammation. Both endocannabinoids and gut microbiota are involved in the modulation of inflammation, including in the aforementioned conditions.

Certain gut bacteria species can break down dietary fiber to produce short-chain fatty acids. These short-chain fatty acids have a link with lower inflammation and may exert protective effects against obesity.

Similarly, the endocannabinoid system can limit inflammation, and changes in the endocannabinoid system are observed in irritable bowel syndrome (IBS) and obesity.

Scientists do not fully understand whether the short-chain fatty acids that gut microorganisms produce can interact with the endocannabinoid system to produce anti-inflammatory effects.

The present study reports that the endocannabinoid system may mediate, in part, the anti-inflammatory effects of short-chain fatty acids that the gut microbiota produces, and vice versa.

Exercise is associated with an increase in endocannabinoid levels and long-term anti-inflammatory effects. The researchers used a 6-week exercise intervention to investigate further the association between endocannabinoids, inflammation, and short-chain fatty acids produced by gut microorganisms.

The researchers found that physical exercise was associated with lower inflammation, which higher short-chain fatty acid and endocannabinoid levels accompanied.

The studys first author, Dr. Amrita Vijay, a research associate at the University of Nottingham, told Medical News Today:

The findings from the current study highlight that simple lifestyle interventions such as exercise can modulate endocannabinoids, and this is a timely discovery, especially in the time when there is increasing interest around the use of cannabidiol and other related supplements in reducing levels of inflammation.

The present study involved two cohorts. The first cohort consisted of 78 adults who were aged over 45 years, living with knee arthritis, and residing in a community setting.

The researchers examined the relationship between the endocannabinoid system, gut microbiota, and inflammation in this cohort at baseline. They then confirmed these results in a second cohort consisting of 35 individuals over 18 years of age.

The researchers also assessed the effects of a 6-week exercise intervention tailored to people with osteoarthritis on the relationship between the endocannabinoid system, inflammation, and gut microbiota in the first cohort. To do this, they divided the participants into a treatment group, consisting of 38 participants, and a control group, involving 40 individuals.

The researchers used blood samples from the participants to evaluate the serum levels of endocannabinoids, short-chain fatty acids, and inflammatory markers. The inflammatory markers included cytokines, a class of immune proteins that have either pro-inflammatory or anti-inflammatory effects.

The team used stool samples and conducted DNA sequencing to assess the abundance of various gut microbiota species.

Before the onset of the exercise intervention in the first cohort, the researchers found that endocannabinoid levels had a positive correlation with gut microbial diversity, short-chain fatty acids levels, and levels of gut microbiota species that produce these short-chain fatty acids.

In contrast, higher endocannabinoid levels were associated with lower levels of Collinsella, a gut bacteria genus that is linked with increased inflammation.

Consistent with these results, endocannabinoid levels were positively correlated with anti-inflammatory cytokines levels but had a negative relationship with pro-inflammatory cytokine levels. These results from the first cohort were similar to those that the team obtained from the second cohort.

The researchers then estimated the contribution of endocannabinoids to mediating the anti-inflammatory effects of short-chain fatty acids. They used a statistical method called mediation analysis, which can help estimate the extent to which a third factor plays a role in mediating the relationship between two variables.

They found that endocannabinoids mediated roughly one-third of the effects of short-chain fatty acids on inflammatory markers. This suggests that other biological factors or pathways, in addition to the endocannabinoid system, may play a role in mediating the anti-inflammatory effects of short-chain fatty acids that the gut microbiome produces.

Likewise, the researchers investigated the extent to which short-chain fatty acids mediated the effects of endocannabinoids on inflammation. They estimated that short-chain fatty acids mediated about half of these effects.

However, the authors caution that such estimates, which they obtained using mediation analysis, do not imply causality.

Next, the researchers examined how the 6-week exercise intervention affected the association between endocannabinoids levels on one hand and short-chain fatty acid levels, gut microbiome composition, and inflammatory markers on the other.

They found that endocannabinoid and short-chain fatty acid levels increased in the exercise group but did not show any changes in the control group. At the same time, there was a decline in the level of pro-inflammatory cytokines in the participants in the exercise group.

Changes in the levels of the endocannabinoid anandamide correlated with the short-chain fatty acid butyrate after 6 weeks across the two groups. Moreover, the researcher found a positive correlation between the changes in endocannabinoid levels and the increase in the abundance of short-chain fatty acid-producing bacteria.

On the other hand, changes in endocannabinoid levels were negatively correlated with the changes in the abundance of bacteria and cytokines associated with pro-inflammatory effects.

Lastly, the endocannabinoid levels were positively associated with the expression levels of the genes for the short-chain fatty acid receptor FFAR2 and the cannabinoid receptor CNR2.

The short-chain fatty acid receptor is associated with a lower risk of obesity, whereas CNR2 is associated with anti-inflammatory effects.

These results suggest that the anti-inflammatory effects resulting from physical exercise could potentially involve an interaction between endocannabinoids and short-chain fatty acids.

Highlighting the studys salience, Dr. Vijay said, The findings are novel, as we may have found a key link between how substances produced by gut microbes interact with the substances produced by our own bodies, which tell us how physical exercise reduces inflammation.

The authors note that their findings are observational and do not establish causation. Furthermore, Dr. Vijay added, The exercise intervention we carried out was performed in individuals with painful knee osteoarthritis and may not be directly relevant to other groups.

It would be interesting to test if different forms of exercise have different effects on our bodies in relation to the levels of these substances being produced and thereby influencing inflammation. It is also important to consider the effect of diet on these relationships.

Dr. Vijay

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Exercise may lower inflammation by increasing endocannabinoids - Medical News Today

THOUSAND OAKS, Calif., Nov. 24, 2021 /PRNewswire/ -- Amgen (NASDAQ:AMGN) will present at the 2021 Evercore ISI Healthcare Conference at 5:10 p.m. ET on Tuesday, Nov. 30, 2021. Rob Lenz, M.D., Ph.D., senior vice president of Global Development at Amgen will present at the conference. Live audio of the conference call will be broadcast over the internet simultaneously and will be available to members of the news media, investors and the general public.

The webcast, as with other selected presentations regarding developments in Amgen's business given at certain investor and medical conferences, can be accessed on Amgen's website, http://www.amgen.com, under Investors. Information regarding presentation times, webcast availability and webcast links are noted on Amgen's Investor Relations Events Calendar. The webcast will be archived and available for replay for at least 90 days after the event.

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

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

For more information, visit http://www.amgen.com and follow us on http://www.twitter.com/amgen.

CONTACT: Amgen, Thousand Oaks Megan Fox, 805-447-1423 (media)Trish Rowland, 805-447-5631 (media)Arvind Sood, 805-447-1060 (investors)

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