Some companies claim remote work hurts wellbeing. Research shows the opposite.
Leaders at Google and other companies are trying to get workers to return to the office, saying remote and hybrid work disrupt work-life boundaries and well-being. These arguments conflict with research on remote work and wellness.
Many leaders at top companies are trying to get workers to return to the office. They say remote and hybrid work are bad for their employees’ mental well-being and lead to a sense of social isolation, meaninglessness, and lack of work-life boundaries, so we should just all go back to office-centric work.
One example is Google, where the company’s leadership is defending its requirement of mostly in-office work for all staff as necessary to protect social capital, meaning people’s connections to and trust in one another. That’s despite a survey of over 1,000 Google employees showing that two-thirds feel unhappy about being forced to work in the office three days per week. In internal meetings and public letters, many have threatened to leave, and some are already quitting to go to other companies with more flexible options.
Last month, GM rolled out a policy similar to Google’s, but had to backtrack because of intense employee opposition. The same is happening in some places outside of the U.S. For instance, three-fifths of all Chinese employers are refusing to offer permanent remote work options, according to a survey this year from The Paper.
For their claims that remote work hurts well-being, some of these office-centric traditionalists cite a number of prominent articles. For example, Arthur Brooks claimed in an essay that “aggravation from commuting is no match for the misery of loneliness, which can lead to depression, substance abuse, sedentary behavior, and relationship damage, among other ills.” An article in Forbes reported that over two-thirds of employees who work from home at least part of the time had trouble getting away from work at the end of the day. And Fast Company has a piece about how remote work can “exacerbate existing mental health issues” like depression and anxiety.
For his part, author Malcolm Gladwell has also championed a swift return to the office, saying there is a “core psychological truth, which is we want you to have a feeling of belonging and to feel necessary…I know it’s a hassle to come into the office, but if you’re just sitting in your pajamas in your bedroom, is that the work life you want to live?”
These arguments may sound logical to some, but they fly in the face of research and my own experience as a behavioral scientist and as a consultant to Fortune 500 companies. In these roles, I have seen the pitfalls of in-person work, which can be just as problematic, if not more so. Remote work is not without its own challenges, but I have helped 21 companies implement a series of simple steps to address them.
Research finds that remote work is actually better for you
The trouble with the articles described above - and claims by traditionalist business leaders and gurus - stems from a sneaky misdirection. They decry the negative impact of remote and hybrid work for wellbeing. Yet they gloss over the damage to wellbeing caused by the alternative, namely office-centric work.
It’s like comparing remote and hybrid work to a state of leisure. Sure, people would feel less isolated if they could hang out and have a beer with their friends instead of working. They could take care of their existing mental health issues if they could visit a therapist. But that’s not in the cards. What’s in the cards is office-centric work. That means the frustration of a long commute to the office, sitting at your desk in an often-uncomfortable and oppressive open office for at least 8 hours, having a sad desk lunch and unhealthy snacks, sometimes at an insanely expensive cost and, for making it through this series of insults, you’re rewarded with more frustration while commuting back home.
In a 2022 survey, the vast majority of respondents felt that working remotely improved their work-life balance. Much of that improvement stemmed from saving time due to not needing to commute and having a more flexible schedule.
So what happens when we compare apples to apples? That’s when we need to hear from the horse’s mouth: namely, surveys of employees themselves, who experienced both in-office work before the pandemic, and hybrid and remote work after COVID struck.
Consider a 2022 survey by Cisco of 28,000 full-time employees around the globe. Nearly 80 percent of respondents say that remote and hybrid work improved their overall well-being: that applies to 83 percent of Millennials, 82 percent of Gen Z, 76 percent of Gen Z, and 66 percent of Baby Boomers. The vast majority of respondents felt that working remotely improved their work-life balance.
Much of that improvement stemmed from saving time due to not needing to commute and having a more flexible schedule: 90 percent saved 4 to 8 hours or more per week. What did they do with that extra time? The top choice for almost half was spending more time with family, friends and pets, which certainly helped address the problem of isolation from the workplace. Indeed, three-quarters of them report that working from home improved their family relationships, and 51 percent strengthened their friendships. Twenty percent used the freed up hours for self-care.
Of the small number who report their work-life balance has not improved or even worsened, the number one reason is the difficulty of disconnecting from work, but 82 percent report that working from anywhere has made them happier. Over half say that remote work decreased their stress levels.
Other surveys back up Cisco’s findings. For example, a 2022 Future Forum survey compared knowledge workers who worked full-time in the office, in a hybrid modality, and fully remote. It found that full-time in-office workers felt the least satisfied with work-life balance, hybrid workers were in the middle, and fully remote workers felt most satisfied. The same distribution applied to questions about stress and anxiety. A mental health website called Tracking Happiness found in a 2022 survey of over 12,000 workers that fully remote employees report a happiness level about 20 percent greater than office-centric ones. Another survey by CNBC in June found that fully remote workers are more often very satisfied with their jobs than workers who are fully in-person.
Academic peer-reviewed research provides further support. Consider a 2022 study published in the International Journal of Environmental Research and Public Health of bank workers who worked on the same tasks of advising customers either remotely or in-person. It found that fully remote workers experienced higher meaningfulness, self-actualization, happiness, and commitment than in-person workers. Another study, published by the National Bureau of Economic Research, reported that hybrid workers, compared to office-centric ones, experienced higher satisfaction with work and had 35 percent more job retention.
What about the supposed burnout crisis associated with remote work? Indeed, burnout is a concern. A survey by Deloitte finds that 77 percent of workers experienced burnout at their current job. Gallup came up with a slightly lower number of 67 percent in its survey. But guess what? Both of those surveys are from 2018, long before the era of widespread remote work.
By contrast, in a Gallup survey in late 2021, 58 percent of respondents reported less burnout. An April 2021 McKinsey survey found burnout in 54 percent of Americans and 49 percent globally. A September 2021 survey by The Hartford reported 61 percent burnout. Arguably, the increase in full or part-time remote opportunities during the pandemic helped to address feelings of burnout, rather than increasing them. Indeed, that finding aligns with the earlier surveys and peer-reviewed research suggesting remote and hybrid work improves wellbeing.
Remote work isn’t perfect – here’s how to fix its shortcomings
Still, burnout is a real problem for hybrid and remote workers, as it is for in-office workers. Employers need to offer mental health benefits with online options to help employees address these challenges, regardless of where they’re working.
Moreover, while they’re better overall for wellbeing, remote and hybrid work arrangements do have specific disadvantages around work-life separation. To address work-life issues, I advise my clients who I helped make the transition to hybrid and remote work to establish norms and policies that focus on clear expectations and setting boundaries.
For working at home and collaborating with others, there’s sometimes an unhealthy expectation that once you start your workday in your home office chair, and that you’ll work continuously while sitting there.
Some people expect their Slack or Microsoft Teams messages to be answered within an hour, while others check Slack once a day. Some believe email requires a response within three hours, and others feel three days is fine. As a result of such uncertainty and lack of clarity about what’s appropriate, too many people feel uncomfortable disconnecting and not replying to messages or doing work tasks after hours. That might stem from a fear of not meeting their boss’s expectations or not wanting to let their colleagues down.
To solve this problem, companies need to establish and incentivize clear expectations and boundaries. They should develop policies and norms around response times for different channels of communication. They also need to clarify work-life boundaries – for example, the frequency and types of unusual circumstances that will require employees to work outside of regular hours.
Moreover, for working at home and collaborating with others, there’s sometimes an unhealthy expectation that once you start your workday in your home office chair, and that you’ll work continuously while sitting there (except for your lunch break). That’s not how things work in the office, which has physical and mental breaks built in throughout the day. You took 5-10 minutes to walk from one meeting to another, or you went to get your copies from the printer and chatted with a coworker on the way.
Those and similar physical and mental breaks, research shows, decrease burnout, improve productivity, and reduce mistakes. That’s why companies should strongly encourage employees to take at least a 10-minute break every hour during remote work. At least half of those breaks should involve physical activity, such as stretching or walking around, to counteract the dangerous effects of prolonged sitting. Other breaks should be restorative mental activities, such as meditation, brief naps, walking outdoors, or whatever else feels restorative to you.
To facilitate such breaks, my client organizations such as the University of Southern California’s Information Sciences Institute shortened hour-long meetings to 50 minutes and half-hour meetings to 25 minutes, to give everyone – both in-person and remote workers – a mental and physical break and transition time.
Very few people will be reluctant to have shorter meetings. After that works out, move to other aspects of setting boundaries and expectations. Doing so will require helping team members get on the same page and reduce conflicts and tensions. By setting clear expectations, you’ll address the biggest challenge for wellbeing for remote and hybrid work: establishing clear work-life boundaries.
Researchers at Stanford have found that the virus that causes Covid-19 can infect fat cells, which could help explain why obesity is linked to worse outcomes for those who catch Covid-19.
Obesity is a risk factor for worse outcomes for a variety of medical conditions ranging from cancer to Covid-19. Most experts attribute it simply to underlying low-grade inflammation and added weight that make breathing more difficult.
Now researchers have found a more direct reason: SARS-CoV-2, the virus that causes Covid-19, can infect adipocytes, more commonly known as fat cells, and macrophages, immune cells that are part of the broader matrix of cells that support fat tissue. Stanford University researchers Catherine Blish and Tracey McLaughlin are senior authors of the study.
Most of us think of fat as the spare tire that can accumulate around the middle as we age, but fat also is present closer to most internal organs. McLaughlin's research has focused on epicardial fat, “which sits right on top of the heart with no physical barrier at all,” she says. So if that fat got infected and inflamed, it might directly affect the heart.” That could help explain cardiovascular problems associated with Covid-19 infections.
Looking at tissue taken from autopsy, there was evidence of SARS-CoV-2 virus inside the fat cells as well as surrounding inflammation. In fat cells and immune cells harvested from health humans, infection in the laboratory drove "an inflammatory response, particularly in the macrophages…They secreted proteins that are typically seen in a cytokine storm” where the immune response runs amok with potential life-threatening consequences. This suggests to McLaughlin “that there could be a regional and even a systemic inflammatory response following infection in fat.”
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
The macrophages studied by McLaughlin and Blish were spewing out inflammatory proteins, While the the virus within them was replicating, the new viral particles were not able to replicate within those cells. It was a different story in the fat cells. “When [the virus] gets into the fat cells, it not only replicates, it's a productive infection, which means the resulting viral particles can infect another cell,” including microphages, McLaughlin explains. It seems to be a symbiotic tango of the virus between the two cell types that keeps the cycle going.
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
Macrophages are mobile; they engulf and carry invading pathogens to lymphoid tissue in the lymph nodes, tonsils and elsewhere in the body to alert T cells of the immune system to the pathogen. Perhaps some of them also carry the virus through the bloodstream to more distant tissue.
ACE2 receptors are the means by which SARS-CoV-2 latches on to and enters most cells. They are not thought to be common on fat cells, so initially most researchers thought it unlikely they would become infected.
However, while some cell receptors always sit on the surface of the cell, other receptors are expressed on the surface only under certain conditions. Philipp Scherer, a professor of internal medicine and director of the Touchstone Diabetes Center at the University of Texas Southwestern Medical Center, suggests that, in people who have obesity, “There might be higher levels of dysfunctional [fat cells] that facilitate entry of the virus,” either through transiently expressed ACE2 or other receptors. Inflammatory proteins generated by macrophages might contribute to this process.
Another hypothesis is that viral RNA might be smuggled into fat cells as cargo in small bits of material called extracellular vesicles, or EVs, that can travel between cells. Other researchers have shown that when EVs express ACE2 receptors, they can act as decoys for SARS-CoV-2, where the virus binds to them rather than a cell. These scientists are working to create drugs that mimic this decoy effect as an approach to therapy.
Do fat cells play a role in Long Covid? “Fat cells are a great place to hide. You have all the energy you need and fat cells turn over very slowly; they have a half-life of ten years,” says Scherer. Observational studies suggest that acute Covid-19 can trigger the onset of diabetes especially in people who are overweight, and that patients taking medicines to regulate their diabetes “were actually quite protective” against acute Covid-19. Scherer has funding to study the risks and benefits of those drugs in animal models of Long Covid.
McLaughlin says there are two areas of potential concern with fat tissue and Long Covid. One is that this tissue might serve as a “big reservoir where the virus continues to replicate and is sent out” to other parts of the body. The second is that inflammation due to infected fat cells and macrophages can result in fibrosis or scar tissue forming around organs, inhibiting their function. Once scar tissue forms, the tissue damage becomes more difficult to repair.
Current Covid-19 treatments work by stopping the virus from entering cells through the ACE2 receptor, so they likely would have no effect on virus that uses a different mechanism. That means another approach will have to be developed to complement the treatments we already have. So the best advice McLaughlin can offer today is to keep current on vaccinations and boosters and lose weight to reduce the risk associated with obesity.
Air pollution can lead to lung cancer. The connection suggests new ways to stop cancer in its tracks.
Researchers at Francis Crick Institute found that air pollution can "wake up" existing mutations, triggering them to turn into lung cancer. The scientists used their new understanding about this connection to prevent cancer in mice.
Forget taking a deep breath. Around the world, 99 percent of people breathe air polluted to unsafe levels, according to data from the World Health Organization. Activities such as burning fossil fuels release greenhouse gases that contribute to air pollution, which could lead to heart disease, stroke, asthma, emphysema, and some types of cancer.
“The burden of disease attributable to air pollution is now estimated to be on a par with other major global health risks such as unhealthy diet and tobacco smoking, and air pollution is now recognized as the single biggest environmental threat to human health,” wrote the authors of a 2021 WHO report.
The majority of lung cancer is attributed to smoking. But as pollution levels have increased, and anti-smoking campaigns have discouraged smoking, the proportion of lung cancers diagnosed in non-smokers has grown. The CDC estimates that 10 to 20 percent of lung cancers in the U.S. currently occur in non-smokers.
The mechanism between air pollution and the development of lung cancer has been unclear, but researchers at London’s Francis Crick Institute recently made an important breakthrough in understanding the connection. Lead investigator Charles Swanton presented this research last month at a conference in Paris.
Pollution awakens mutations
The Crick Institute scientists were able to identify a new link between common air pollutants and non-small cell lung cancer (NSCLC). They focused on pollutants called particulate matter, or PM, that are 2.5 microns wide, narrower than human cells.
Most cancer diagnosed in non-smoking people is NSCLC, but this type of cancer hasn’t received the same research attention as more common lung cancers found in smokers, according to Clare Weeden, a cancer researcher at the Crick Institute and a co-author of the study.
“This is a really underserved and under-researched population that we really need to tackle, as well as lung cancers that occur in smokers,” she says. “Lung cancer is the number one cancer killer worldwide.”
In the past, some researchers believed air pollution caused mutations that led to cancer. Others believed these mutations could remain dormant without any detriment to health until pollutants or other stressors triggered them to become cancerous. Reviving the latter hypothesis that carcinogens may activate pre-existing mutations, instead of directly causing them, the Crick researchers analyzed samples from 463,679 people in the UK and parts of Asia, noting mutations and comparing changes in gene expression in mice and human cells.
“The mutation can exist in a nascent clone without causing cancer,” says Emilia Lim, a bioinformatics expert and a co-first author of the Crick study. “It is the carcinogen that promotes a conducive environment for this one little clone to grow and expand into cancer. Through our work, we were able to revive excitement for this hypothesis and bring it to light.”
The study explains a confusing pattern of lung cancer developing, particularly in women, despite a lack of environmental risk factors like smoking, secondhand smoke, or radon exposure. The culprit in these cases may have been too much PM 2.5 exposure.
Other researchers had previously identified a link between mutations in certain genes that control epidermal growth factor receptors, or EGFR mutations, and the development of NSCLC. In a 2019 study of 250 people with this type of cancer, about 32 percent had the mutation. Women are more likely to have EGFR mutations than men.
Not everyone who has the EGFR mutation will develop lung cancer. Respirologist Stephen Lam studies lung cancer at the BC Cancer Research Centre in Vancouver, Canada, but was not involved in the Crick Institute research. He says the study explains a confusing pattern of lung cancer developing, particularly in women, despite a lack of environmental risk factors like smoking, secondhand smoke, or radon exposure. The culprit in these cases may have been too much PM 2.5 exposure.
More exposure leads to inflammation and lesions
The Crick researchers found that an excess of PM 2.5 in the air sparked an inflammatory process in cells within the lung. This inflammation set the stage for NSCLC to develop in people and mice with existing EGFR mutations.
The researchers also exposed mice without EGFR mutations to PM 2.5 pollution—an experiment that couldn’t be ethically conducted in humans—to link pollution exposure to NSCLC. The mice experiments also showed that NSCLC is dose-dependent; higher levels of exposure were associated with higher number of cancerous lesions forming.
Ultimately, the study “fundamentally changed how we view lung cancer in people who have never smoked,” said Swanton in a Crick Institute press release. “Cells with cancer-causing mutations accumulate naturally as we age, but they are normally inactive. We’ve demonstrated that air pollution wakes these cells up in the lungs, encouraging them to grow and potentially form tumors.”
Preventing cancer before it begins
Targeted therapies already exist for people with EGFR mutations who’ve developed NSCLC, but they have many side effects, according to Weeden. Researchers hope that making more definitive links between pollutants and cancer could help prevent people with EGFR or other mutations from developing lung cancer in the first place.
Along those lines, as an additional component of their study presented last month, the Crick researchers were able to prevent cancer in mice that had the EGFR mutations by blocking inflammation. They used an antibody to inhibit a protein called interleukin 1 beta, which plays a key role in inflammation. Scientists could eventually use such antibodies or other therapies to make a drug treatment that people can take to stop cancer in its tracks, even if they live in highly polluted areas.
Such potential could reach beyond lung cancer; in the past, Crick and other researchers have also found associations between exposure to air pollution and mesothelioma, as well as cancers of the small intestine, lip, mouth, and throat. These links could be meaningful to a growing number of people as climate change intensifies, and with increases in air pollution from fossil fuel combustion and natural disasters like forest fires.
Plus, air pollution is just one external condition that can flip the switch of these inflammatory pathways. Identifying a link between pollution and cancer “has wide ramifications for many other environmental factors that may [play] similar roles,” Weedon says. She hopes that the Crick study and future research in this area will offer some hope for non-smokers frustrated by cancer diagnoses.