Should Your Employer Have Access to Your Fitbit Data?
The modern world today has become more dependent on technology than ever. We want to achieve maximal tasks with minimal human effort. And increasingly, we want our technology to go wherever we go.
Wearable devices operate by collecting massive amounts of personal information on unsuspecting users.
At work, we are leveraging the immense computing power of tablet computers. To supplement social interaction, we have turned to smartphones and social media. Lately, another novel and exciting technology is on the rise: wearable devices that track our personal data, like the FitBit and the Apple Watch. The interest and demand for these devices is soaring. CCS Insight, an organization that studies developments in digital markets, has reported that the market for wearables will be worth $25 billion by next year. By 2020, it is estimated that a staggering 411 million smart wearable devices will be sold.
Although wearables include smartwatches, fitness bands, and VR/AR headsets, devices that monitor and track health data are gaining most of the traction. Apple has announced the release of Apple Health Records, a new feature for their iOS operating system that will allow users to view and store medical records on their smart devices. Hospitals such as NYU Langone have started to use this feature on Apple Watch to send push notifications to ER doctors for vital lab results, so that they can review and respond immediately. Previously, Google partnered with Novartis to develop smart contact lens that can monitor blood glucose levels in diabetic patients, although the idea has been in limbo.
As these examples illustrate, these wearable devices present unique opportunities to address some of the most intractable problems in modern healthcare. At the same time, these devices operate by collecting massive personal information on unsuspecting users and pose unique ethical challenges regarding informed consent, user privacy, and health data security. If there is a lesson from the recent Facebook debacle, it is that big data applications, even those using anonymized data, are not immune from malicious third-party data-miners.
On consent: do users of wearable devices really know what they are getting into? There is very little evidence to support the claim that consent obtained on signing up can be considered 'informed.' A few months ago, researchers from Australia published an interesting study that surveyed users of wearable devices that monitor and track health data. The survey reported that users were "highly concerned" regarding issues of privacy and considered informed consent "very important" when asked about data sharing with third parties (for advertising or data analysis).
However, users were not aware of how privacy and informed consent were related. In essence, while they seemed to understand the abstract importance of privacy, they were unaware that clicking on the "I agree" dialog box entailed giving up control of their personal health information. This is not surprising, given that most user agreements for online applications or wearable devices are often in lengthy legalese.
Companies could theoretically use their employees' data to motivate desired behavior, throwing a modern wrench into the concept of work/life balance.
Privacy of health data is another unexamined ethical question. Although wearable devices have traditionally been used for promotion of healthy lifestyles (through fitness tracking) and ease of use (such as the call and message features on Apple Watch), increasing interest is coming from corporations. Tractica, a market research firm that studies trends in wearable devices, reports that corporate consumers will account for 17 percent of the market share in wearable devices by 2020 (current market share stands at 1 percent). This is because wearable devices, loaded with several sensors, provide unique insights to track workers' physical activity, stress levels, sleep, and health information. Companies could theoretically use this information to motivate desired behavior, throwing a modern wrench into the concept of work/life balance.
Since paying for employees' healthcare tends to be one of the largest expenses for employers, using wearable devices is seen as something that can boost the bottom line, while enhancing productivity. Even if one considers it reasonable to devise policies that promote productivity, we have yet to determine ethical frameworks that can prevent discrimination against those who may not be able-bodied, and to determine how much control employers ought to exert over the lifestyle of employees.
To be clear, wearable smart devices can address unique challenges in healthcare and elsewhere, but the focus needs to shift toward the user's needs. Data collection practices should also reflect this shift.
Privacy needs to be incorporated bydesign and not as an afterthought. If we were to read privacy policies properly, it could take some 180 to 300 hours per year per person. This needs to change. Privacy and consent policies ought to be in clear, simple language. If using your device means ultimately sharing your data with doctors, food manufacturers, insurers, companies, dating apps, or whoever might want access to it, then you should know that loud and clear.
The recent implementation of European Union's General Data Protection Regulation (GDPR) is also a move in the right direction. These protections include firm guidelines for consent, and an ability to withdraw consent; a right to access data, and to know what is being done with user's collected data; inherent privacy protections; notifications of security breach; and, strict penalties for companies that do not comply. For wearable devices in healthcare, collaborations with frontline providers would also reveal which areas can benefit from integrating wearable technology for maximum clinical benefit.
In our pursuit of advancement, we must not erode fundamental rights to privacy and security, and not infringe on the rights of the vulnerable and marginalized.
If current trends are any indication, wearable devices will play a central role in our future lives. In fact, the next generation of wearables will be implanted under our skin. This future is already visible when looking at the worrying rise in biohacking – or grinding, or cybernetic enhancement – where people attempt to enhance the physical capabilities of their bodies with do-it-yourself cybernetic devices (using hacker ethics to justify the practice).
Already, a company in Wisconsin called Three Square Market has become the first U.S. employer to provide rice-grained-sized radio-frequency identification (RFID) chips implanted under the skin between the thumb and forefinger of their employees. The company stated that these RFID chips (also available as wearable rings or bracelets) can be used to login to computers, open doors, or use the copy machines.
Humans have always used technology to push the boundaries of what we can do. But in our pursuit of advancement, we must not erode fundamental rights to privacy and security, and not infringe on the rights of the vulnerable and marginalized. The rise of powerful wearables will also necessitate a global discussion on moral questions such as: what are the boundaries for artificially enhancing the human body, and is hacking our bodies ethically acceptable? We should think long and hard before we answer.
A new competition by the XPRIZE Foundation is offering $101 million to researchers who discover therapies that give a boost to people aged 65-80 so their bodies perform more like when they were middle-aged.
For today’s podcast episode, I talked with Dr. Peter Diamandis, XPRIZE’s founder and executive chairman. Under Peter’s leadership, XPRIZE has launched 27 previous competitions with over $300 million in prize purses. The latest contest aims to enhance healthspan, or the period of life when older people can play with their grandkids without any restriction, disability or disease. Such breakthroughs could help prevent chronic diseases that are closely linked to aging. These illnesses are costly to manage and threaten to overwhelm the healthcare system, as the number of Americans over age 65 is rising fast.
In this competition, called XPRIZE Healthspan, multiple awards are available, depending on what’s achieved, with support from the nonprofit Hevolution Foundation and Chip Wilson, the founder of Lululemon and nonprofit SOLVE FSHD. The biggest prize, $81 million, is for improvements in cognition, muscle and immunity by 20 years. An improvement of 15 years will net $71 million, and 10 years will net $61 million.
In our conversation for this episode, Peter talks about his plans for XPRIZE Healthspan and why exponential technologies make the current era - even with all of its challenges - the most exciting time in human history. We discuss the best mental outlook that supports a person in becoming truly innovative, as well as the downsides of too much risk aversion. We talk about how to overcome the negativity bias in ourselves and in mainstream media, how Peter has shifted his own mindset to become more positive over the years, how to inspire a culture of innovation, Peter’s personal recommendations for lifestyle strategies to live longer and healthier, the innovations we can expect in various fields by 2030, the future of education and the importance of democratizing tech and innovation.
In addition to Peter’s pioneering leadership of XPRIZE, he is also the Executive Founder of Singularity University. In 2014, he was named by Fortune as one of the “World’s 50 Greatest Leaders.” As an entrepreneur, he’s started over 25 companies in the areas of health-tech, space, venture capital and education. He’s Co-founder and Vice-Chairman of two public companies, Celularity and Vaxxinity, plus being Co-founder & Chairman of Fountain Life, a fully-integrated platform delivering predictive, preventative, personalized and data-driven health. He also serves as Co-founder of BOLD Capital Partners, a venture fund with a half-billion dollars under management being invested in exponential technologies and longevity companies. Peter is a New York Times Bestselling author of four books, noted during our conversation and in the show notes of this episode. He has degrees in molecular genetics and aerospace engineering from MIT and holds an M.D. from Harvard Medical School.
- Peter Diamandis bio
- New XPRIZE Healthspan
- Peter Diamandis books
- Longevity Insider newsletter – AI identifies the news
- Peter Diamandis Longevity Handbook
- Hevolution funding for longevity
XPRIZE Founder Peter Diamandis speaks with Mehmoud Khan, CEO of Hevolution Foundation, at the launch of XPRIZE Healthspan.
From infections with no symptoms to why men are more likely to be hospitalized in the ICU and die of COVID-19, new research shows that your genes play a significant role
Early in the pandemic, genetic research focused on the virus because it was readily available. Plus, the virus contains only 30,000 bases in a dozen functional genes, so it's relatively easy and affordable to sequence. Additionally, the rapid mutation of the virus and its ability to escape antibody control fueled waves of different variants and provided a reason to follow viral genetics.
In comparison, there are many more genes of the human immune system and cellular functions that affect viral replication, with about 3.2 billion base pairs. Human studies require samples from large numbers of people, the analysis of each sample is vastly more complex, and sophisticated computer analysis often is required to make sense of the raw data. All of this takes time and large amounts of money, but important findings are beginning to emerge.
About half the people exposed to SARS-CoV-2, the virus that causes the COVID-19 disease, never develop symptoms of this disease, or their symptoms are so mild they often go unnoticed. One piece of understanding the phenomena came when researchers showed that exposure to OC43, a common coronavirus that results in symptoms of a cold, generates immune system T cells that also help protect against SARS-CoV-2.
Jill Hollenbach, an immunologist at the University of California at San Francisco, sought to identify the gene behind that immune protection. Most COVID-19 genetic studies are done with the most seriously ill patients because they are hospitalized and thus available. “But 99 percent of people who get it will never see the inside of a hospital for COVID-19,” she says. “They are home, they are not interacting with the health care system.”
Early in the pandemic, when most labs were shut down, she tapped into the National Bone Marrow Donor Program database. It contains detailed information on donor human leukocyte antigens (HLAs), key genes in the immune system that must match up between donor and recipient for successful transplants of marrow or organs. Each HLA can contain alleles, slight molecular differences in the DNA of the HLA, which can affect its function. Potential HLA combinations can number in the tens of thousands across the world, says Hollenbach, but each person has a smaller number of those possible variants.
She teamed up with the COVID-19 Citizen Science Study a smartphone-based study to track COVID-19 symptoms and outcomes, to ask persons in the bone marrow donor registry about COVID-19. The study enlisted more than 30,000 volunteers. Those volunteers already had their HLAs annotated by the registry, and 1,428 tested positive for the virus.
Analyzing five key HLAs, she found an allele in the gene HLA-B*15:01 that was significantly overrepresented in people who didn’t have any symptoms. The effect was even stronger if a person had inherited the allele from both parents; these persons were “more than eight times more likely to remain asymptomatic than persons who did not carry the genetic variant,” she says. Altogether this HLA was present in about 10 percent of the general European population but double that percentage in the asymptomatic group. Hollenbach and her colleagues were able confirm this in other different groups of patients.
What made the allele so potent against SARS-CoV-2? Part of the answer came from x-ray crystallography. A key element was the molecular shape of parts of the cold virus OC43 and SARS-CoV-2. They were virtually identical, and the allele could bind very tightly to them, present their molecular antigens to T cells, and generate an extremely potent T cell response to the viruses. And “for whatever reasons that generated a lot of memory T cells that are going to stick around for a long time,” says Hollenbach. “This T cell response is very early in infection and ramps up very quickly, even before the antibody response.”
Understanding the genetics of the immune response to SARS-CoV-2 is important because it provides clues into the conditions of T cells and antigens that support a response without any symptoms, she says. “It gives us an opportunity to think about whether this might be a vaccine design strategy.”
A researcher at the Leibniz Institute of Virology in Hamburg Germany, Guelsah Gabriel, was drawn to a question at the other end of the COVID-19 spectrum: why men more likely to be hospitalized and die from the infection. It wasn't that men were any more likely to be exposed to the virus but more likely, how their immune system reacted to it
Several studies had noted that testosterone levels were significantly lower in men hospitalized with COVID-19. And, in general, the lower the testosterone, the worse the prognosis. A year after recovery, about 30 percent of men still had lower than normal levels of testosterone, a condition known as hypogonadism. Most of the men also had elevated levels of estradiol, a female hormone (https://pubmed.ncbi.nlm.nih.gov/34402750/).
Every cell has a sex, expressing receptors for male and female hormones on their surface. Hormones docking with these receptors affect the cells' internal function and the signals they send to other cells. The number and role of these receptors varies from tissue to tissue.
Gabriel began her search by examining whole exome sequences, the protein-coding part of the genome, for key enzymes involved in the metabolism of sex hormones. The research team quickly zeroed in on CYP19A1, an enzyme that converts testosterone to estradiol. The gene that produces this enzyme has a number of different alleles, the molecular variants that affect the enzyme's rate of metabolizing the sex hormones. One genetic variant, CYP19A1 (Thr201Met), is typically found in 6.2 percent of all people, both men and women, but remarkably, they found it in 68.7 percent of men who were hospitalized with COVID-19.
Lungs are the tissue most affected in COVID-19 disease. Gabriel wondered if the virus might be affecting expression of their target gene in the lung so that it produces more of the enzyme that converts testosterone to estradiol. Studying cells in a petri dish, they saw no change in gene expression when they infected cells of lung tissue with influenza and the original SARS-CoV viruses that caused the SARS outbreak in 2002. But exposure to SARS-CoV-2, the virus responsible for COVID-19, increased gene expression up to 40-fold, Gabriel says.
Did the same thing happen in humans? Autopsy examination of patients in three different cites found that “CYP19A1 was abundantly expressed in the lungs of COVID-19 males but not those who died of other respiratory infections,” says Gabriel. This increased enzyme production led likely to higher levels of estradiol in the lungs of men, which “is highly inflammatory, damages the tissue, and can result in fibrosis or scarring that inhibits lung function and repair long after the virus itself has disappeared.” Somehow the virus had acquired the capacity to upregulate expression of CYP19A1.
Only two COVID-19 positive females showed increased expression of this gene. The menopause status of these women, or whether they were on hormone replacement therapy was not known. That could be important because female hormones have a protective effect for cardiovascular disease, which women often lose after going through menopause, especially if they don’t start hormone replacement therapy. That sex-specific protection might also extend to COVID-19 and merits further study.
The team was able to confirm their findings in golden hamsters, the animal model of choice for studying COVID-19. Testosterone levels in male animals dropped 5-fold three days after infection and began to recover as viral levels declined. CYP19A1 transcription increased up to 15-fold in the lungs of the male but not the females. The study authors wrote, “Virus replication in the male lungs was negatively associated with testosterone levels.”
The medical community studying COVID-19 has slowly come to recognize the importance of adipose tissue, or fat cells. They are known to express abundant levels of CYP19A1 and play a significant role as metabolic tissue in COVID-19. Gabriel adds, “One of the key findings of our study is that upon SARS-CoV-2 infection, the lung suddenly turns into a metabolic organ by highly expressing” CYP19A1.
She also found evidence that SARS-CoV-2 can infect the gonads of hamsters, thereby likely depressing circulating levels of sex hormones. The researchers did not have autopsy samples to confirm this in humans, but others have shown that the virus can replicate in those tissues.
A possible treatment
Back in the lab, substituting low and high doses of testosterone in SARS-COV-2 infected male hamsters had opposite effects depending on testosterone dosage used. Gabriel says that hormone levels can vary so much, depending on health status and age and even may change throughout the day, that “it probably is much better to inhibit the enzyme” produced by CYP19A1 than try to balance the hormones.
Results were better with letrozole, a drug approved to treat hypogonadism in males, which reduces estradiol levels. The drug also showed benefit in male hamsters in terms of less severe disease and faster recovery. She says more details need to be worked out in using letrozole to treat COVID-19, but they are talking with hospitals about clinical trials of the drug.
Gabriel has proposed a four hit explanation of how COVID-19 can be so deadly for men: the metabolic quartet. First is the genetic risk factor of CYP19A1 (Thr201Met), then comes SARS-CoV-2 infection that induces even greater expression of this gene and the deleterious increase of estradiol in the lung. Age-related hypogonadism and the heightened inflammation of obesity, known to affect CYP19A1 activity, are contributing factors in this deadly perfect storm of events.
Studying host genetics, says Gabriel, can reveal new mechanisms that yield promising avenues for further study. It’s also uniting different fields of science into a new, collaborative approach they’re calling “infection endocrinology,” she says.