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Nudges: four reasons to doubt popular technique to shape people’s behaviour

Can you really nudge people into washing their hands more? The evidence is far from perfect.

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Can food labelling really help us make 'better' choices? AntGor/Shutterstock

Throughout the pandemic, many governments have had to rely on people doing the right thing to reduce the spread of the coronavirus – ranging from social distancing to handwashing. Many enlisted the help of psychologists for advice on how to “nudge” the public to do what was deemed appropriate.

Nudges have been around since the 1940s and originally were referred to as behavioural engineering. They are a set of techniques developed by psychologists to promote “better” behaviour through “soft” interventions rather than “hard” ones (mandates, bans, fines). In other words, people aren’t punished if they fail to follow them. The nudges are based on psychological and behavioural economic research into human behaviour and cognition.

The nudges can involve subtle as well as obvious methods. Authorities may set a “better” choice, such as donating your organs, as a default – so people have to opt out of a register rather than opt in. Or they could make a healthy option more attractive through food labelling.

But, despite the soft approach, many people aren’t keen on being nudged. During the pandemic, for example, scientists examined people’s attitudes to nudging in social and news media in the UK, and discovered that half of the sentiments expressed in social media posts were negative.

1. Nudges can be limited and fragile

Informational nudges were common during the pandemic. In response to such campaigns, people said they would wash their hands more – with a 7% increase in India and a 2% boost in Colombia. In Brazil, such nudges increased people’s willingness to wear a mask by 3%.

image of people sitting on a bench, socially distancing.
Nudges were used to encourage social distancing. Kzenon/Shutterstock

So much is made of the power of nudging because because large field studies, involving millions of people and conducted by government-funded behavioural change organisations, and have reported that they work. Even though the effects are small, when scaled to a population, one to two percentage point increases in positive effects on behaviour may translate into thousands or even millions of changed minds (depending on the country). But this is similar to the level of effects that are achieved in psychological experiments using a placebo. The effect sizes are also similar to statistical noise (random irregularity in data) in scientific studies.

There is also work showing that when compared to hard interventions (for example, economic incentives) nudges deliver a lower overall benefit over time. Long-term studies into environmental nudges also show that nudge effects are feeble, don’t last and only work on those already motivated to be pro-environmental. Also, there are several moderating factors that help to explain the fleeting effects of nudging, such as socioeconomic factors, personal motivation to change behaviour, and the context in which a nudge is introduced.

To be worthwhile, then, the costs of implementing nudges need to be outweighed by the benefits in behavioural change achieved. Moreover, in evaluting the costs and benefits, the effects of nudging need to be demonstrated to sustain over time, and as yet the jury is out on this.

2. Nudges can be unethical

Nudges may also present ethical concerns. For instance, nudging is now combined with genetics, dubbed “nudgeomics”, meaning DNA is used to tailor nudges that can improve people’s health. This is so new that there’s little evidence to assess effectiveness. But using someone’s DNA to try to manipulate their behaviour may have implications for insurance purposes, for example.

Nudging may also be aided by artificial intelligence – so-called smart nudging. Intelligent software algorithms can be used to influence people’s behaviour by targeting emotional, social and cognitive processes. We experience this in video games, news recommendation aggregation engines, fitness trackers and tailored advertising – which all try to influence us based on what they know about our behaviour.

We have yet to tackle the basic concerns with the ethics of nudging in its current form, let alone its expansion into areas with their own ethical issues such as genetics and AI.

3. Nudges can backfire

Nudges can fail – and even backfire. An environmental nudge removing bottled water to try to reduce plastic waste, for example, directly increased sugary drink consumption – resulting in a similar number of discarded bottles as before.

The failure rate of nudging is still unknown, partly because of publication bias, which is not uncommon in psychology – typically only studies of successful nudges are submitted to scientific journals for publication.

Image of a urinal with a housefly painted onto the ceramic.
Can a housefly painted onto a urinal get men to aim better? wikipedia, CC BY-SA

So a lot of cherry picking may be going on. One way to address this is through pre-registering studies before they are run, though this isn’t standard convention yet, and has its own problems.

4. Nudges lack theoretical backing

There are no comprehensive theories of nudging per se. Instead, there are general frameworks that loosely connect work from psychology and behavioural economics to speculative arguments for using public policy interventions. Having a theory is key to predicting and interpreting the psychological and contextual causal factors that account for the successes and failures of nudges.

The public should be more involved in discussions around the use of nudging so that everyone comes to a better understanding of the practical advantages balanced against honest communication of the scientific and ethical issues.

A resolute belief in something despite contrary evidence is nothing more than an act of faith those using behavioural change in public and private policy domains would do well to avoid. Ultimately, claims about the power of nudging need to be balanced against the obvious limitations that still need to be overcome.

Magda Osman receives funding from ESRC, EPSRC, ARC, Wellcome Trust

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VIRI: Enrollment Complete in FORTRESS Trial; Results Expected in September 2022…

By David Bautz, PhD
NASDAQ:VIRI
READ THE FULL VIRI RESEARCH REPORT
Business Update
FORTRESS Trial Fully Enrolled; Topline Results in September 2022
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By David Bautz, PhD

NASDAQ:VIRI

READ THE FULL VIRI RESEARCH REPORT

Business Update

FORTRESS Trial Fully Enrolled; Topline Results in September 2022

On April 28, 2022, Virios Therapeutics, Inc. (NASDAQ: VIRI) announced that it has completed enrollment of 425 fibromyalgia patients into the Phase 2b FORTRESS (Fibromyalgia Outcome Research Trial Evaluating Synergistic Suppression of Herpes Simplex Virus-1) trial, a randomized, double blind, placebo controlled study of IMC-1. The primary endpoint of the trial is reduction in pain and secondary endpoints include change in fatigue, sleep disturbance, global health status, and patient functionality (NCT04748705). An outline of the trial is shown below.

In parallel with the FORTRESS trial, Virios is continuing the chronic toxicology studies of IMC-1 in two animal species. The results of these studies are required by regulators before Virios will be allowed to dose patients for one year or more, which is the plan for the Phase 3 program. The results of the chronic toxicology studies should be known around the time of the completion of the FORTRESS trial, thus the company should be able to move into a final Phase 3 program following completion of the current study, pending positive results.

Testing Combination Antiviral Therapy for the Treatment of Long COVID

In February 2022, Virios announced a collaboration with the Bateman Horne Center (BHC) to test combination antiviral therapy for the treatment of Long COVID. Following an infection with SARS-CoV-2, the virus that causes COVID-19, approximately 30% of patients will experience symptoms that last for weeks or months, which is referred to as Long COVID. The range of symptoms varies from patient to patient, however the most commonly reported (from a recent meta analysis) were fatigue (58%), headache (44%), attention disorder (27%), hair loss (25%), and dyspnea (24%) (Lopez-Leon et al., 2021).

The main theories for what might be causing ...

Full story available on Benzinga.com

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Type-I interferon stops immune system ‘going rogue’ during viral infections

Hamilton, ON (May 17, 2022) – McMaster University researchers have found not only how some viral infections cause severe tissue damage, but also how…

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Hamilton, ON (May 17, 2022) – McMaster University researchers have found not only how some viral infections cause severe tissue damage, but also how to reduce that damage.

Credit: Georgia Kirkos/McMaster University

Hamilton, ON (May 17, 2022) – McMaster University researchers have found not only how some viral infections cause severe tissue damage, but also how to reduce that damage.

 

They have discovered how Type I interferon (IFN) stops the immune system ‘going rogue’ and attacking the body’s own tissues when fighting viral infections, including COVID-19.

 

Their paper was published in the journal PLOS Pathogens today.

  

Senior author Ali Ashkar said IFN is a well-known anti-viral signalling molecule released by the body’s cells that can trigger a powerful immune response against harmful viruses.

 

“What we have found is that it is also critical to stop white blood cells from releasing protease enzymes, which can damage organ tissue. It has this unique dual function to kick start an immune response against a viral infection on the one hand, as well as restrain that same response to prevent significant bystander tissue damage on the other,” he said.

 

The research team investigated IFN’s ability to regulate a potentially dangerous immune response by testing it on both flu and the HSV-2 virus, a highly prevalent sexually transmitted pathogen, using mice. Data from COVID-19 patients in Germany, including post-mortem lung samples, was also used in the study.

 

“For many viral infections, it is not actually the virus that causes most of the tissue damage, it is our heightened immune activation towards the virus,” said Ashkar, a professor of medicine at McMaster.

  

First co-author of the study and PhD student Emily Feng said: “Our body’s immune response is trying to fight off the virus infection, but there’s a risk of damaging innocent healthy tissue in the process. IFNs regulates the immune response to only target tissues that are infected.

 

“By discovering the mechanisms the immune system uses that can inadvertently cause tissue damage, we can intervene during infection to prevent this damage and not necessarily have to wait until vaccines are developed to develop life-saving treatments,” she added.

 

“This applies not just to COVID-19, but also other highly infectious viruses such as flu and Ebola, which can cause tremendous and often life-threatening damage to the body’s organs,” said first study co-author Amanda Lee, a family medicine resident. 

 

Ashkar said the release of harmful proteases is the result of a ‘cytokine storm’, which is life-threatening inflammation sometimes triggered by viral infections. It has been a common cause of death in patients with COVID-19, but treatment has been developed to prevent and suppress the cytokine storm.

 

Ashkar said that steroids like dexamethasone are already used to rein in an extreme immune response to viral infections. The authors used doxycycline in their study, an antibiotic used for bacterial infections and as an anti-inflammatory agent, inhibits the function of proteases causing the bystander tissue damage.

 

Lee added: “This has the potential in the future to be used to alleviate virus-induced life-threatening inflammation and warrants further research.” 

 

The study was funded by the Canadian Institutes of Health Research.

 

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Editors:

Pictures of Ali Ashkar and Emily Feng may be found at https://bit.ly/3wmSw0D

  

 

 


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mRNA vaccines like Pfizer and Moderna fare better against COVID-19 variants of concern

A comparison of four COVID-19 vaccinations shows that messenger RNA (mRNA) vaccines — Pfizer-BioNTech and Moderna — perform better against the World…

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A comparison of four COVID-19 vaccinations shows that messenger RNA (mRNA) vaccines — Pfizer-BioNTech and Moderna — perform better against the World Health Organization’s variants of concern (VOCs) than viral vector vaccines — AstraZeneca and J&J/Janssen. Although they all effectively prevent severe disease by VOCs, the research, publishing May 17th in the open access journal PLOS Medicine, suggests that people receiving a viral vector vaccine are more vulnerable to infection by new variants.

Credit: Carlos Reusser Monsalvez, Flickr (CC0, https://creativecommons.org/publicdomain/zero/1.0/)

A comparison of four COVID-19 vaccinations shows that messenger RNA (mRNA) vaccines — Pfizer-BioNTech and Moderna — perform better against the World Health Organization’s variants of concern (VOCs) than viral vector vaccines — AstraZeneca and J&J/Janssen. Although they all effectively prevent severe disease by VOCs, the research, publishing May 17th in the open access journal PLOS Medicine, suggests that people receiving a viral vector vaccine are more vulnerable to infection by new variants.

By March 2022, COVID-19 had caused over 450 million confirmed infections and six million reported deaths. The first vaccines approved in the US and Europe that protect against serious infection are Pfizer-BioNTech and Moderna, which deliver genetic code, known as mRNA, to the bodies’ cells, whereas Oxford/AstraZeneca and J&J/Janssen are viral vector vaccines that use a modified version of a different virus — a vector — to deliver instructions to our cells. Three vaccines are delivered as two separate injections a few weeks apart, and J&J/Janssen as a single dose.

Marit J. van Gils at the University of Amsterdam, Netherlands, and colleagues, took blood samples from 165 healthcare workers, three and four weeks after first and second vaccination respectively, and for J&J/Janssen at four to five and eight weeks after vaccination. Samples were collected before, and four weeks after a Pfizer-BioNTech booster.

Four weeks after the initial two doses, antibody responses to the original SARS-CoV-2 viral strain were highest in recipients of Moderna, followed closely by Pfizer-BioNTech, and were substantially lower in those who received viral vector vaccines. Tested against the VOCs – Alpha, Beta, Gamma, Delta and Omicron – neutralizing antibodies were higher in the mRNA vaccine recipients compared to those who had viral vector vaccines. The ability to neutralize VOCs was reduced in all vaccine groups, with the greatest reduction against Omicron. The Pfizer-BioNTech booster increased antibody responses in all groups with substantial improvement against VOCs, including Omicron.

The researchers caution that their AstraZeneca group was significantly older, because of safety concerns for the vaccine in younger age groups. As immune responses tend to weaken with age, this could affect the results. This group was also smaller because the Dutch government halted use for a period.

van Gils concludes, “Four COVID-19 vaccines induce substantially different antibody responses.”

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In your coverage, please use this URL to provide access to the freely available paper in PLOS Medicine:

http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1003991

Citation: van Gils MJ, Lavell A, van der Straten K, Appelman B, Bontjer I, Poniman M, et al. (2022) Antibody responses against SARS-CoV-2 variants induced by four different SARS-CoV-2 vaccines in health care workers in the Netherlands: A prospective cohort study. PLoS Med 19(5): e1003991. https://doi.org/10.1371/journal.pmed.1003991

 

Author Countries: The Netherlands, United States

 

Funding: This work was supported by the Netherlands Organization for Scientific Research (NWO) ZonMw (Vici grant no. 91818627 to R.W.S., S3 study, grant agreement no. 10430022010023 to M.K.B.; RECoVERED, grant agreement no. 10150062010002 to M.D.d.J.), by the Bill & Melinda Gates Foundation (grant no. INV002022 and INV008818 to R.W.S. and INV-024617 to M.J.v.G.), by Amsterdam UMC through the AMC Fellowship (to M.J.v.G.) and the Corona Research Fund (to M.K.B.), and by the European Union’s Horizon 2020 program (RECoVER, grant no. 101003589 to M.D.d.J). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.


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