Ricki Lewis

Choosing a medical treatment based on patient traits historically used to define races is fundamentally flawed, because race in the context of humans is a social construct, while medicine is based on biology. Race-based prescribing robs some individuals of drugs that could help them, while prescribing them to people who likely will not respond, or even be harmed. Fortunately, the practice of basing treatment decisions on the superficial traits used to define human races is on the decline.

Blood thinners and blood pressure medications have for decades dominated discussions of race-based prescribing. A more recent example of the dangers of using superficial features as guidelines for providing appropriate care is flawed interpretation of a standard measure of kidney function, used to prioritize patients for kidney transplants. Due to a fudge factor of sorts, until very recently Blacks have been given lower priority on the lists for organs.

Perhaps the starkest example I've encountered of race obscuring delivery of adequate health care comes from California-based pediatrician Richard Garcia, who wrote in The Chronicle of Higher Education in 2003 "The Misuse of Race in Medical Diagnosis":

"My childhood friend Lela wasn't diagnosed with cystic fibrosis until she was 8 years old. Over the years, her doctors had described her as a '2-year-old black female with fever and cough' and 'a 4-year-old black girl with another pneumonia. Lela is back.' Had she been a white child, or had no visible 'race' at all, she would probably have gotten the correct diagnosis and treatment much earlier. Only when she was 8 did a radiologist, who had never seen her face to face, notice her chest X-ray and ask, 'Who's the kid with CF?'"

To continue reading, go to DNA Science, where this post first appeared.

The pandemic ignited public interest in science, introducing the phrase "doing my research." But the persistence of the idea that science aims to "prove" anything reveals a fundamental misunderstanding of what scientists actually do.

What Science Is, and Isn't

Scientists test hypotheses based on observations of the natural world, then deduce possible explanations, using experiments and further observations. We analyze data, draw tentative conclusions, then ask more questions. The scientific method is, as I've called it in my textbooks, a cycle of inquiry. Variations on the theme are spawned from creative thinking.

So when ideas and advice about responses to COVID changed, it wasn't because science or scientists had been "wrong." It's that what we thought we knew changed as we learned more. Advice to not use, or use, masks is a good example. We needed to know the size of the droplets and their speed of transit and proximity to an inhaling nose, to predict parameters for infection transmission and hypothesize how we could best respond.

Science isn't a static proof of anything. And it is dynamic.

The public could gain a good understanding of what science is, and is not, by observing the scientific method on display at science fairs.

I've judged science fairs, at all levels, for a long time, through pre-Internet posters done with magic markers and oaktag (whatever that was), to the zoom renditions of the past three years, to a fantastic in-person experience last weekend. Participants display the results of sometimes years-long projects, in posters and powerpoint presentations and demonstrations, that adhere to and elaborate on the steps of the scientific method. Sophistication of projects has paralleled the growth of information science, including wide availability of data ripe for comparison, interpretation, and further hypothesizing.

To continue reading, go to DNA Science, where this post first appeared.

In early 2020, COVID appeared to be mostly respiratory, with blame for the shattering of delicate lung tissues initially placed on the violent "cytokine storms" unleashed from overactive immune responses. At first, autopsy series focused on the inflammation and antibodies, not finding evidence of the virus itself. But that view has changed.

As the fourth year of the pandemic dawns, a study published in Nature from Daniel Chertow, MD, MPH, head of the Emerging Pathogens Section at the NIH Clinical Center and colleagues, finds the virus in many body parts – particularly, the brain. The discovery may explain cases of long COVID.

Indirect Attack on the Brain

At first, researchers thought the role of the virus on the brain was indirect.

In July 2022, Avindra Nath, MD, clinical director of the National Institute of Neurological Disorders and Stroke and colleagues reported in the journal Brain changes in the brains of nine people who died quickly from COVID. Autopsies revealed antibodies glommed onto viral antigens on the tile-like endothelial cells that form the blood-brain barrier. As capillaries disintegrated, the risk of stroke skyrocketed amid catastrophic destruction.

The COVID-infected brain is a mess.

To continue reading go to DNA Science, where this post first appeared.

I stopped eating beef 5 years ago, following a trip to Costa Rica just days after being diagnosed with breast cancer. Our daughter had been urging us to give up red meat for more than a decade, but a lecture and slide show on the effect of cattle ranching on Costa Rica's spectacular biodiversity, right after my diagnosis, finally did the trick. So compelling were the environmental and human health reasons to no longer eat beef that I barely dwelled on the obvious animal cruelty aspect.

Back home, I wrote about another anti-beef argument here at DNA Science: a sugar (a type of sialic acid) on our cell surfaces that is slightly different than versions on muscle cells of cattle and pigs. The cells of these animals make an enzyme that dismantles their form of sialic acid, but our cells don't. As a result, the human immune system reacts to cow and pig muscle cells bearing sialic acid with its inflammatory response. Over time, thanks to hamburgers and steaks and ribs, risks of cardiovascular disease, arthritis, and cancer rise.

A few days ago, my husband and I returned from a second trip to Costa Rica. This time, we saw firsthand the stark difference between cattle grazing land and the plants-upon-plants-upon-plants that make up natural ecosystems.

To continue reading, go to DNA Science, where this post first appeared.

When a headline in the Washington Post dubbed COVID "A Plague of the Elderly," I cringed, envisioning Logan's Run, the sci-fi classic in which people past a certain age voluntarily die. The film came out in 1976, the year I graduated college.

That would make me, well, elderly.

Yes, older folks are over-represented among those who get very sick or die from COVID, with "nearly 9 out of 10 deaths now in people 65 or older," WaPo reminds us. That is striking for an age group that makes up only 16 percent of the population. But while media reports trumpet the damning statistics, few delve into the biology behind the elevated risk: it could be that our shorter chromosomes hamper the immune response.

The WaPo article, like others, states the obvious:

"The vulnerability of older people to viruses is neither surprising nor new. The more we age, the more we accumulate scars from previous illness and chronic conditions that put us at higher risk of severe illness."

Yes, a 75-year-old with COPD is less likely to survive COVID pneumonia than a 75-year-old with healthy lungs. And developing COPD is more likely after decades of exposure to irritants. But number of years by itself may be a surrogate for some other factor.

Might the culprit be telomeres, the tips of chromosomes? They shrink as time passes, like candles burning down.

To continue reading, go to DNA Science, where this post first appeared.

Three years ago, health officials in China announced the first cases of infection with a "novel coronavirus."

Dr. Zhang Jixian reported the first case on December 26, 2019 in a senior couple living in the residential community near her hospital in Wuhan. An expert in SARS, she recognized the triad of fever, cough, and an unusual pneumonia.

The earliest events remain a bit murky.

"On December 30th, China reported an outbreak of respiratory disease in Wuhan City, a major transportation hub about 700 miles south of Beijing with a population of more than 11 million people," declared Nancy Messonnier, director of CDC's National Center for Immunization and Respiratory Diseases, on January 17, 2020.

But I heard about it on NPR shortly after New Years.

My first COVID post was January 23: "I'm astonished at the speed with which geneticists and epidemiologists are zeroing in on the Wuhan coronavirus," referring to the first viral genome sequence announced January 15. Sequencing viral genomes would evolve into a powerful tool of, well, viral evolution, with the US caught behind.

It's been a hellish roller coaster ride, with terrible tragedy juxtaposed against some of the most astonishingly brilliant science I've ever encountered. I switched from covering rare genetic disease to following the erupting pandemic, reporting news, interpreting technical reports, and delving into the history of epidemiology.

To continue reading, go to DNA Science, where this post first appeared.

Do our genes predispose us to follow a religion? I searched Google Scholar for reports on the inheritance of religiosity.

I sought something scientific – does being religious favor the survival-to-reproduce that fuels natural selection of an adaptive inherited trait?

I skipped regular Google and mainstream media, seeking data and not opinions, and included "inheritance" and "religiosity" in my search. To me inheritance means genes that encode proteins that affect the phenotype (trait or illness). But inheritance also means passing something from parents to offspring – such as money, property, possessions, or ideals.

Surely someone had done a genome-wide association study for "religiosity." A "GWAS" is a survey of single-DNA-base positions (SNPs) in a genome where individuals vary, having any of the four DNA bases. These studies have been around for two decades, seeking evidence for genetic underpinnings of such traits as antisocial behavior, loneliness, and even political ideologies.

Today researchers use an abbreviated "polygenic risk score" to describe so-called complex traits – those influenced by several genes as well as environmental factors. In contrast to an either-or diagnosis like cystic fibrosis, a PRS tallies variants of many genes that contribute to a trait or illness.

The investigations that Google Scholar returned came more from the social sciences, using language with which I am admittedly unfamiliar. Here's a brief chronology of five studies that probed whether religiosity is in our genes.

To continue reading, go to DNA Science, where this post was first published. 

The reconstruction of a once-living landscape in northern Greenland from 2 million years ago, deduced from bits of DNA bound to minerals, reveals an Ice Age ecosystem in the throes of climate change that may suggest ways to mitigate rising global temperatures today. The collection, analysis, and interpretation of environmental DNA from this distant time and place provides a "genetic roadmap" for how organisms can adapt to a warming climate. The work is the cover story in Nature this week. Six of the 40-member multinational team discussed the findings at a news conference.

eDNA

Environmental DNA – eDNA – is used to describe habitats both ancient and contemporary. Until now, the oldest eDNA was from a mammoth that lived in Siberia one million years ago.

To continue reading, go to DNA Science, where this post first appeared. Image credit Beth Zaiken.

The latest phrase borrowed from biology in COVID conversations is convergent evolution. It refers to pairs of unrelated species that look similar because their ancestors evolved under similar environmental conditions. Natural selection favored adaptive (helpful) inherited traits, and millennia later, two unrelated species of mammals or birds look remarkably alike.

Convergent evolution happens to viruses, too. It is unspooling right now as SARS-CoV-2 genome evolution coalesces into variations on the Omicron theme.

The natural history of SARS-CoV-2 began with the wild type, another term from classical genetics. It means "most common," not "normal" as the media often misuses it.

As the virus changed, we grouped sets of new mutations, which substitute one RNA base of the genome at a time, into "variants." We named them, which biologists tend to do.

Alpha, recognized in November 2020, begat beta, gamma, and delta, all of which stayed with us for a bit. The next few versions were fleeting. The International Committee on Taxonomy of Viruses and WHO skipped Nu (because it sounds like "new") and Xi (a common surname), landing on Omicron. And natural selection has favored its collection of mutations. No new Greek letters necessary.

When Species Look Alike

Biologists term traits that are alike in two species that arise from recent shared ancestors homologous, while similar structures or behaviors that arise from similar environmental exposures are analogous. Convergent evolution reflects responses to similar environments (analogy), rather than descent from recent shared ancestors (homology).

Striking examples of convergent evolution are pairs of placental mammals and Australian marsupials. These include anteaters, moles, wolves, ocelots and native cats, flying squirrels and flying phalangers, and groundhogs and wombats.

To continue reading, go to DNA Science, where this post first appeared.

Planning for the next pandemic begins with acknowledging what we did wrong for COVID-19. As the situation has calmed, experts are weighing in on what we did, and didn't do, as the months unfolded. I've distilled and organized their comments from the medical literature and webinars. Several of the opinions are from Preventing the Next Pandemic: New Tools for Global Surveillance, which the Harvard T. H. Chan School of Public Health held for journalists October 17, 2022.

Next time, we should:

1. Recognize the field of ethics as practical, not just an academic discipline.
Determining the 'right' course of action in many circumstances proved more vexing and controversial than solving the technical challenges, such as developing vaccines and treatments, wrote Ezekiel Emanuel, Vice Provost for Global Initiatives at the University of Pennsylvania and colleagues, in The New England Journal of Medicine ("What COVID Has Taught the World About Ethics").

To continue reading, go to DNA Science, where this post first appeared.