DNA Science

As a New RNA Biomarker Test for Alzheimer’s Nears, I Can’t Help but Wonder if my Grandmother Was Better Off Not Knowing

Ricki Lewis, PhD — Thu, 02 Jul 2026 13:14:03 +0000

My grandmother had what must have been Alzheimer’s disease, but no one ever called it that.

When I visited her in the 1970s from college, all I’d noted was that her mind was in the past. She still appeared to remember me and my husband-to-be Larry, but she would repeat the same stories from her deep, deep past every time we saw her – about my then sixty-something uncle Bernie who’d lost his coat when he was 6 years old. As a budding biologist, I was transfixed by the brain’s ability to conjure great detail in a very distant memory. I didn’t think of her as being sick, as having a disease.

Grandma Sarah was extremely fortunate to have spent her final months in what may have been one of the first dementia facilities at what was then Long Island Jewish Medical Center, now Northwell Health. My two uncles – her sons – were prominent physicians there, and they made sure that their mother had the most expert care available at the time.

Although Alzheimer’s disease was officially named in 1910, I’m glad my mother and uncles never uttered that term, at least to me, to describe my grandmother. My uncles had to have known.

My mother only rarely used the word dementia to describe her mother. And to me, my grandmother wasn’t sick. She was just Grandma Sarah, living in the past, happy to have her many visitors. A spinal tap, brain scan, blood marker test, or a disease name weren’t needed to see that she was losing some of who she was, transitioning, painlessly, to who she had been, to a happier time, when two of her four children were very young. I like to believe that she was at peace, her brain somehow, protectively, returning, again and again, to a cherished memory.

For more the past 15 years, diagnosing Alzheimer’s disease has included assaying levels of two telltale proteins, amyloid beta and tau. Now, RNA is being tracked too. Researchers at the Icahn Genomics Institute at Mount Sinai have identified patterns of RNA-containing nanoparticles in the blood that may serve as a new type of biomarker for impending Alzheimer’s disease. The report appears in the June 22 Nature Communications.

My Recent Experience with Alzheimer’s Testing

A few months ago, I began revising the most complicated chapters of my human genetics textbook, the ones that update CRISPR and other biotechnologies. New editions have evolved into simpler revisions as paper books have become extinct. I’m a long-time author – the term content creator is demeaning.

I’ve been writing and revising this book since I scribbled the table of contents on a napkin at a publishing meeting circa 1990, so swapping in new examples, cases, and stories should be a no-brainer. Yet this time around, I found myself repeating revisions I’d already written. Most alarming was my addition of the recent case of a young woman from a prominent family whose chromosome 3 had spontaneously inverted, placing a sleeping oncogene next to a gene that revs up cell division. The result was a deadly leukemia.

I wrote the leukemia story on a Wednesday, scribbling in red marker in an actual paper textbook in the upper left corner of a page.

On Thursday morning, I picked up where I’d left off. And in the lower right corner, in green marker, I scribbled in the details of the case. Then I sat back and noticed the other add-in-edit in the upper left corner of the page. I’d written the same story, with disturbingly few differences – but enough to reveal that I’d completely forgotten that I’d already written up the case.

After this happened a few more times, I made an appointment with a neurologist.

I “aced” all the cognitive tests, just like our brilliant president, exhibiting a heretofore unrecognized special flair for rapidly counting backwards from a random number by 7s. The PA was astonished, but couldn’t stump me with math. And I lucked out – the “name as many animals as you can in one minute” challenge was easy for a biologist. I easily babbled out a rapid-fire roster of insects and rare mammals. I shudder to think how I would have fared if asked to name car parts or members of a football team.

Then, the PA took my blood to look for levels of the telltale Alzheimer’s biomarker proteins. I requested the new early Alzheimer’s test that probes the ratio of standard biomarkers amyloid beta and tau, but apparently Medicare wasn’t quite up to date – I had to settle for the older amyloid 42/40 ratio. But that was okay. I was right in the middle range of normal. (DNA Science covered new Alzheimer’s tests here.)

Disclosure: For a few years I participated in the Alzheimer’s Disease Neuroimaging Initiative, and was even a spokesperson, describing how the study had identified two brain tumors in a friend, saving her life. Participation entailed taking cognitive tests every 6 months, then, eventually, brain scans, like my friend had had. You have to listen to a short story and then repeat it. My story, the day ADNI fired me, was about a little girl finding a fossil – something that had actually happened to me, so you’d think I’d remember it. Well, my husband decided that would be a good time to clean out the cat box just a few feet away from me, shattering whatever concentration I had with the repetitive motion of scraping feline feces from the bottoms of the boxes. I had a meltdown, screaming about cat shit, all thoughts of little girls and fossils leaving my brain. So I failed. An email soon informed me that the study was over — which apparently it isn’t.

A Tale of Two Proteins

Quick review: In Alzheimer’s disease, two types of protein accumulate in brain neurons. Amyloid beta forms plaques outside neurons, while tau forms tangles mostly inside the cells, particularly in the emanating axons.

Some brain regions become more blocked in proteinaceous gunk than others – the amygdala (seat of emotion) and hippocampus (the memory center) are especially vulnerable. Changes also unfold among the several types of glial cells that are part of the brain.

FDA approved two drugs that can slow the progression of Alzheimer’s disease by targeting amyloid beta: Leqembi (lecanemab) in 2023 and Kisunla (donanemab) in 2024. Both are infusions. Symptoms may progress once treatment stops, and long-term effects aren’t yet known.

A year later, new blood tests came along. One assay measures the ratio of specific variants of tau and amyloid, and the most recent test assesses the level of pTau181. The number denotes a phosphate (a phosphorus atom bound to three oxygen atoms) attached to the 181th amino acid in the sequence of Tau protein.

For now, pTau181 testing is used to rule out eventual Alzheimer’s in patients with mild cognitive impairment (MCI) or mild dementia. It isn’t yet clear what elevated pTau181 means in an individual with normal cognition. Investigations that look backwards from people with Alzheimer’s indicate that elevated tau is a highly predictive biomarker. So people with Alzheimer’s once had elevated pTau181, but not everyone with greater-than-average levels of the biomarker goes on to develop Alzheimer’s. Time will tell.

RNA Reflects Gene Expression as a Disease Unfolds

RNA biomarkers in blood are joining amyloid and tau proteins in revealing early Alzheimer’s changes. Unlike the slow buildup of these diagnostic proteins, RNA is a more fleeting molecule, its levels reflecting the undulations of a particular gene’s expression as a pathological process progresses. The collective set of mRNAs in a cell at any given time is termed its transcriptome; transcription means RNA synthesis.

(Another quick review: DNA encodes RNA, which encodes proteins, such as tau and amyloid. So mRNA levels and identities, aka gene expression, mirror what’s going on in a body.)

In 2007, researchers identified RNA molecules outside cells, transported in body fluids in tiny membranous bubbles called extracellular vesicles (EVs). The surface is identical to that of a cell membrane – a lipid bilayer with embedded proteins and sugars. EVs can harbor bits of DNA too. Another mode of transport, an extracellular particle (EP), does not have the outer membrane – it’s more like a simple bubble.

DNA, RNA, and proteins can also travel in the bloodstream unfettered, dubbed “cell-free.” These bits of bloodstream matter, once discarded as debris, may be emissaries of gene activity and provide clues to physiology – and pathology.

The surfaces of vesicles and particles are festooned with “molecular signatures” that indicate the cell type of origin, a little like a person wearing a tee shirt from a college or town. And surface features can function as biomarkers.

EVs reflect activities at their sources. Circulating EVs from the brain offer a soup of biomarkers that reveal not only how cells are communicating, but how efficiently brain tissue is clearing out damaged cells – such as telltale plaques and tangles. More specifically, EVs in a blood sample can reveal the high levels of pTau181 that may foretell Alzheimer’s disease.

The New Findings

The Mount Sinai researchers compared RNA and protein signatures from EVs in brains and blood of 26 deceased individuals, 10 of whom had died of Alzheimer’s disease.

Their main question: could the circulating RNAs act similarly to a “liquid biopsy” used to detect tumor DNA in a blood sample? Indeed, they could. And the team discovered a variety of small blood nanoparticles, dubbed “SECmeres,” which carry the telltale molecular signs of Alzheimer’s-related brain signals more clearly than do standard extracellular vesicles. Detecting these nanoparticles, enriched with brain-specific markers, may offer a minimally invasive way to diagnose the beginnings of Alzheimer’s.

“SECmeres may hold promise as a real-time, non-invasive diagnostic tool for the living human brain. Our study demonstrates that blood EVPs (extra-vesicular particles) carry brain-specific RNA information that could be used for liquid biopsy approaches, pending validation in larger blinded clinical trials. EVP-derived RNAs may reveal disease-related changes earlier in the disease process, before proteins or pathology become detectable,” said investigator Navneet Dogra.

The several new ways to detect early or even future Alzheimer’s disease are astonishing. Will that knowledge enable intervention? I can’t help but wonder whether my grandmother was better off not knowing.

NOTE: I’ve just learned that my blog DNA Science, which I’ve written since 2012, is being discontinued, along with other PLoS blogs. I’m sad. But I will continue to post my thoughts on genetics occasionally at my website, www.rickilewis.com. I’m open to finding a new blog host!

The post As a New RNA Biomarker Test for Alzheimer’s Nears, I Can’t Help but Wonder if my Grandmother Was Better Off Not Knowing appeared first on DNA Science.

Genomic Analysis Sets Back Timeline of Plague to Hunter-Gatherer Children in Siberia

Ricki Lewis, PhD — Thu, 18 Jun 2026 19:00:09 +0000

Bubonic plague conjures images of wheelbarrows heaped with bodies in the streets of medieval Europe from 1347 to 1352. It’s estimated that 25 to 30 million people died. Fleas and perhaps other insects carried on scurrying brown rats transmitted the infecting bacteria, Yersinia pestis. Mongol traders and fighters had unwittingly brought the scourge from central Asia to the Crimea, traveling through Italy to the rest of Europe aboard ships from the Black Sea.

The infectious disease takes the name Black Death from the black sores, called buboes, that form beneath the skin over swollen lymph nodes. Excruciating joint pain and fever also happen. Bubonic plague kills, often within three days, in up to 75% of cases.

The high mortality rate of the plague rippled through medieval European society for decades, taking two centuries to restore population numbers. Many human settlements were completely abandoned.

The circumstances of the Black Death in Europe led to the idea that human crowding facilitated spread of the infection – it likely did, but the disease did not originate in fourteenth century Europe. A new study, published in Nature, identifies and interprets changes in the pathogen’s genome that point to an earlier presence than the rat-infested, crowded cities of medieval Europe. Genetic evidence, archeological tools, and radiocarbon dating complemented to paint a portrait of an ancient infectious disease that was especially lethal to the young.

Clues in a Cemetery

Ruairidh Macleod, Eske Willerslev, and colleagues at the University of Copenhagen analyzed ancient DNA collected from 42 hunter-gatherer individuals whose remains lay in four cemeteries around Lake Baikal in southeast Siberia. In 18 of the bodies, Y. pestis was the predominant pathogen, reflecting outbreaks from 5520–5265 cal BP and 5315–4235. “Cal BP” is a measurement from geology and archeology that stands for “calibrated years Before Present.” It approximates the calendar age of biological specimens more accurately than does radiocarbon dating, which can fluctuate with climate change.

Comparison of the DNA sequences from exhumed individuals enabled reconstruction of their familial relationships, and the investigators deduced family structures and likely transmission patterns of the infectious disease. But it turns out that bodies discovered together were not genetically related, as might be expected among sick people, but instead may have been left by dying young friends.

The most severe infections were in 8-to-11-year-olds.

“The unusually high number of children and the short timespan was a real puzzle that we’ve been trying to solve since the 1990s. Finding out that plague was the cause is extraordinary, but it makes so much sense,” explained archaeologist Andrzej Weber of the University of Alberta, and principal investigator of the Baikal Archaeology Project.

A Superantigen and Exoneration of Rats

Genome sequencing also revealed a likely mechanism behind the extraordinary lethality of this older plague – genes that encode proteins that function as “superantigens.” These protein toxins rev up the host’s immune response to a devastating level of inflammation. The genome of the more familiar medieval strain of the pathogen doesn’t harbor coding for a superantigen.

“Whether the earliest forms of plague were mild or virulent has been a matter of debate, but our findings demonstrate that these ancient strains were already highly lethal,” said Eske Willerslev. That seems especially so for children, even without flea-borne transmission.

Rats may not have been implicated in these earlier episodes of bubonic plague. Archaeological evidence from marmots near the cemetery site suggests that these large, burrowing mammals may have been part of the transmission train. Marmots carry plague today too, as do prairie dogs, ground squirrels, chipmunks, and wood rats in North America; gerbils, and susliks in Asia; and a variety of rats, mice, and gerbils in Africa and South America. (I’ve had a few of these as pets or rescued them from my cats.)

The new findings “challenge the notion that higher population densities and lifestyle changes during the Neolithic agricultural transition were prerequisites for plague epidemics,” the researchers write.

Together, the findings suggest that the earliest known plague outbreaks may already have been as deadly as later historical forms of the disease, especially for children, even without flea-borne transmission. Perhaps in a broader sense, the findings highlight the incredible adaptability of pathogens to different times and places.

The post Genomic Analysis Sets Back Timeline of Plague to Hunter-Gatherer Children in Siberia appeared first on DNA Science.

The Curious Coloration of Eggplants

Ricki Lewis, PhD — Thu, 04 Jun 2026 20:35:42 +0000

I love eggplant. Although common supermarket varieties are dark purple, or a pricier stripy lavender, the fruits may also be white or green. Standard chlorophyll provides the green, and anthocyanin pigments add purple, red, and even essence of blue.

A new study from researchers at South China Agricultural University, the Hunan Vegetable Research Institute, and the University of Kentucky identifies the odd genetics behind the curious colors of eggplants. Their report appears in Horticulture Research.

Three Types of Genetic Information
The new study reveals a form of genetic information beyond the sequences of the bases A, C, T, and G: patterns of short repeats. This alternate DNA language forms a subtext encoded in a repetition pattern. It lies behind more than sixty human conditions, including Huntington’s disease, a form of ALS, fragile X syndrome, frontotemporal dementia, and several types of ataxia.

Yet a third form of genetic information is gene expression – that is, which genes are turned on or off under specific circumstances. Gene expression arises from the patterns of binding of three types of small molecules to a gene’s DNA sequence: acetyls, methyls, and phosphates.

To Sun or Not to Sun
Most eggplants are photosensitive – they require sunlight to survive through the chemical reactions of photosynthesis. But the rare nonphotosensitive eggplants maintain their purpleness even in shade or short daylight hours.

In contrast, most eggplants are photosensitive. Typically, exposure to sunlight turns on production of the anthocyanin pigment that imparts the characteristic dark purple, nearly black color. In these plants, prolonged shady conditions result in a pale or splotchy fruit – an important consideration for growers and gardeners.

In contrast, nonphotosensitive eggplants seemingly ignore the lack of sunlight, producing purple fruits even in the shade. The ability comes from a “stutter“ of short repeats in the sequence of a gene called SMMYB113. The variation affects the beginning part of the gene that encodes the promoter, which is an “on” switch. The stutter, a stretch of 725 DNA base pairs repeated four times, enables the plant to crank out dark anthocyanin pigments even if the sun isn’t shining. The researchers call it “reshap(ing) visible traits by rewiring gene expression.”

“Our findings offer new insights into the molecular mechanisms controlling fruit color in eggplant and lay the groundwork for the development of molecular markers to facilitate breeding for nonphotosensitive and other fruit color variants,” the researchers write.

Perhaps the color-controlling DNA repeat can be bred into other crop species, enabling a fine-tuned control over the colors of specific plants and widening growing conditions.

The post The Curious Coloration of Eggplants appeared first on DNA Science.

The Genetics of Heirloom Tomatoes

Ricki Lewis, PhD — Thu, 28 May 2026 12:24:44 +0000

Come summertime, I enjoy the marvelous diversity, and exquisite if fleeting taste and texture, of heirloom tomatoes. They are nothing at all like the uniformly hard, shiny orange round and ovoid things that stand in for tomatoes mid-winter, more like a Spaulding pinky ball than a juicy fruit.

Heirloom tomatoes come in a variety of hues, from pale yellow to dark purple to everything in between. The skins are thin, the flesh sweet, and softening rapid. The fruits range from small and round to huge and multi-lobed. Their delectability is fleeting – they’re best eaten within two days of picking, or right off the vine. If nurtured and spaced correctly, the plants become towers of deliciousness.

I do not have a particularly green thumb, but I try, and every summer grow the components of salads for months. Here’s a useful video for nurturing heirloom tomatoes.

This season, I’m attempting to grow my own, with heirloom seeds sprouting in tiny dissolvable pots in a closet repurposed with a red glowing growing lamp. They are Cherokee purples. Other colorful names are Hungarian heart, pineapple, rosella, apricot zebra, tulip, beefsteak, globe, oxheart, plum, cherry, lucky tiger, and Brad’s Atomic Grape, “a visually striking, elongated cherry tomato developed by Brad Gates of Wild Boar Farms in California,” a sweet fruit with stripy purply coloring and a hard texture. I love them.

Breeding True
Heirloom tomatoes originated in South America as the Aztecs selected and cultivated them for their palate-pleasing traits. Spanish explorers brought the fruits to Europe in the 16th century, and by the 1800s, many varieties were being grown, the seeds typically saved and passed down in human families. They are, technically, ancient cultivars.

By definition, heirloom seeds must have been handed down for at least 50 years. They lack the gene variants bred into cultured plants that provide the expected orange color and thick skins of the bounceable supermarket versions, and are homozygous for the recessive traits that endow the fruits with their spectacular colors and offbeat shapes. In people, the homozygous recessive state lies behind many single-gene conditions, including cystic fibrosis, sickle cell and Tay-Sachs diseases, and many “inborn errors of metabolism.”

Insects and breezes spread the seeds of heirlooms. Because the two copies of the genes that provide the fruit traits are homozygous – that is, two copies of the same variant, rather than hybrids – the pleasing qualities are consistent from generation to generation. A more familiar term for homozygote is “breeding true.”

Tackling the Biochemistry
A team from the Council for Agricultural Research and Economics Research Centre for Vegetable and Ornamental Crops in Pontecagnano, Italy analyzed the biochemistry of 60 accessions of heirlooms (technically Solanum lycopersicum). In agriculture, an accession is seeds, clones, or other tissue sampled from a specific site, one time, and cultured at a gene bank, for use by researchers. An accession may be a cultivar, landrace, or wild relative.

The researchers identified and tracked ascorbic acid, the colorful carotenoid pigments (such as lycopene and β-carotene), and other compounds to specifically define the characteristics of the many variations on the heirloom theme. They tracked thousands of genetic markers called SNPs, which vary at single bases in the DNA sequence, deducing how a plum hue differs from cherry and yellow, and fruits with globe shapes differ genetically from tiny orbs and the enormous flattened, purply kinds.

The researchers identified two genes that control fruit weight and a single gene that controls a precursor molecule to the carotenoid pigments. Identifying the basis of these traits and how they vary could suggest even more variations on the heirloom tomato theme.

CODA

Next week: how the eggplant got its purple color. Against the profoundly anti-science stance of the current US administration, I’m going to stick to writing about vegetables for awhile.

The post The Genetics of Heirloom Tomatoes appeared first on DNA Science.

The Last Carolina Girl, a Novel, Echoes the Famous Case of Carrie Buck and the Eugenics Movement

Ricki Lewis, PhD — Thu, 14 May 2026 18:54:29 +0000

In early spring, when I pull out the puniest of garden plants and toss them aside to make room for the more robust, my thoughts turn to eugenics.

I recently discovered a compelling work of historical fiction, Meagan Church’s 2023 The Last Carolina Girl, which captures the horror of the movement in the first half of the twentieth century in the US to force eugenic measures on women.

Church is a master of describing the abuses against women that were once ignored and accepted. She wrote 2025’s The Mad Wife, which looks at a tranquilized housewife in the 1950s, and 2024’sThe Girls We Sent Away, about the fate of an unwed pregnant teen in the 1960s.

The Last Carolina Girl is set in 1935 North Carolina. When 14-year-old Leah Payne is orphaned, kind neighbors, who cannot afford to raise her, send her to a family willing to take her in – but, as Leah soon discovers, not as a foster child, but as an abused “helpmate.” The tale is loosely based on the author’s great aunt.

Comparisons to Delia Owens’ Where the Crawdads Sing, published in 2018 and a film four years later, led me toThe Last Carolina Girl, also about a nature-loving, adventurous North Carolina girl. But it is much more.

The eugenics theme at the core of the plot emerges subtly in the middle of the tale, then hits with staggering force when Leah is tricked into being sterilized. The reason – her blackout “spells” – seizures likely stemming from fever in early childhood, not an errant gene that could be passed on.

When the narrative turns to eugenics, Leah’s story begins to echo the tale of Carrie Buck.

A Famous Case
In 1927, 17-year-old Carrie Buck was tried as a criminal in her hometown of Charlottesville because her mother lived in an asylum for the “feebleminded” and Carrie had given birth out-of-wedlock, despite having been raped by her foster parents’ nephew. She was blamed for the forced pregnancy, deemed “promiscuous.”

Carrie was declared feebleminded too, although she was a B student in school. Sir Oliver Wendell Holmes Jr., in Buck v Belle (1927), famously ruled “three generations of imbeciles are enough” in approving her forced sterilization.

Carrie Buck joined her mother Emma at the Virginia State Colony for Epileptics and Feeble-Minded in Madison Heights, near Lynchburg, and became the first person sterilized to prevent having another “socially inadequate offspring.” A crude pedigree drawn at the time depicted Carrie Buck and her “inherited trait” of feeblemindedness.

According to the DNA Learning Center, Carrie Buck’s trial was an intentional test case for the state’s 1924 sterilization law, and her lawyer was in on it. After Carrie was released, she went on to a life of apparent mental normalcy, as did her supposedly feebleminded daughter Vivian, whose teachers reported her intelligence as above-average.

The Supreme Court’s decision in Buck v Bell led to an estimated 65,000 to 70,000 forced sterilizations.

A Horrific Tale Unfolds Slowly
The Last Carolina Girl’s plotline revolves around the fact that the mean woman who takes Leah in as a helpmate is actually her aunt, who harbors a long-simmering revenge agenda.

The eugenics theme emerges halfway through the narrative, when protagonist Leah and her friend Jesse are at a country fair, Leah sneaking away for a bit from her evil guardian. Leah and Jesse are riveted by a man addressing the crowd with posters depicting black and white rats, illustrating “genetic Inheritance.”

“Dr. Foster addressed the crowd:

When you take a pure white and a pure white, what are the results? Pure white, of course. No tainted abnormalities. But mix in a black with a pure white, and you’re not guaranteed what you’ll get. Any impure abnormality can result.

How many generations of abnormalities is too many?” the doc continued, echoing Oliver Wendell Holmes.

He went on, “Especially when we have the ability to do something about it? To stop it. To sterilize the offender—the feebleminded, the promiscuous—so future generations don’t have to suffer. Sterilization is a simple procedure that will ensure that those people won’t have future generations who will drain our society.” The mesmerized crowd nodded in agreement.

The Examination
Later on, Leah’s mistress, Mrs. Griffin, forces her to see the doctor from the fair. He conducts a terrifying pelvic exam, and then seeks to demonstrate the three strikes against her: seizures, promiscuity, and subnormal intelligence.

Paramount are the seizures.

“He asked me about my flashes, though he called them my absences. I wondered how he knew. Of course Mrs. Griffin had to’ve told him. I knew she’d spotted a couple in my months with them, but apparently she’d seen more than I’d realized,” Leah thinks.

The doctor steps back, addressing Mrs. Griffin. “From my examination of her, there’s clearly something wrong. Not having seen one of her episodes for myself, I have to take your word for them, but I’m inclined to say she’s suffering from absence seizures.”

Next came demonstration of promiscuity. “Just the other day at the fair, I caught her behind a tent with a boy who isn’t from around here. I can’t even imagine what would’ve happened had I not found them then,” Mrs. Griffin told the doctor.

Finally, when Leah appeared puzzled at being handed a book meant for a young child, the doc assumed she couldn’t read. “It’s clear that she is not as mentally astute as others her age,” he concluded. “Thankfully we do have a procedure to help with this sort of situation.”

After the procedure, Leah eventually realizes what has happened:

“I was one of those rats hanging on the poster board. I was one of the tainted ones, the burden needing fixing.”

The repercussions of the assumption that Leah was not mentally fit echo throughout what would be a very long life.

In The Last Carolina Girl, Meagan Church has vividly knitted a compelling story around a time tainted with profound prejudice and cruelty, superimposed on the subjugation of women.

The post The Last Carolina Girl, a Novel, Echoes the Famous Case of Carrie Buck and the Eugenics Movement appeared first on DNA Science.

Memories of Craig Venter

Ricki Lewis, PhD — Thu, 30 Apr 2026 21:12:03 +0000

I was saddened to hear of Craig Venter’s passing at the age of 79, today, April 30, 2026. Often portrayed as the bad guy, sometimes to Francis Collin’s good guy, my handful of interactions with the man were positive and memorable. He was a genius, inventing technologies through a string of institutes and businesses that earned him the label of a “serial entrepreneur.”

A True Genius

Dr. Venter is best known to the public as the “other” researcher “racing” to complete the first, in retrospect quite spotty, human genome sequence. The official announcement came on June 26, 2000, in the White House Rose garden (now desecrated with stone and yellow umbrellas), Venter and Francis Collins outwardly convivial after a sometimes bitter, headline-inspiring race.

But I needed to know who’d gotten to the finish line first – Venter’s Celera Genomics or the National Human Genome Research Institute in March, because I was working on the new edition of my human genetics textbook and wanted to include that information. My deadline was looming.

I’d recently met Venter to interview him for an article in The Scientist, so I e-mailed him. No, he answered immediately, he wouldn’t update me directly, but if I emailed him a multiple choice question, something to the effect of who got there first, Celera, NHGRI, both or neither, he’d answer, but I couldn’t publish that info. He answered that indeed, it was he. I was able to get the shared announcement in June into my textbook before another semester rolled around.

Dr. Venter invited me back to interview for a remote job, helping to assemble a compendium of intriguing human genes, chromosome-by-chromosome. When I walked down the long hallway to his expansive office, I felt like Dorothy approaching the great Wizard of Oz. But my nervousness vanished instantly, as we fell into conversation and excitement about all the gene discoveries, quickly finishing each other’s sentences. And I helped, briefly, with the project.

Next I saw him at an international genetics conference in Sweden, 3 weeks after 9/11, a scary time to fly. He was in tears as he opened the meeting.

Venter’s Inventions

Craig Venter notoriously saw what others didn’t.

His invention of “shotgun sequencing” quickly overshadowed the slower “clone-by-clone” technique of the government effort. His approach blasted several copies of a genome into smithereens and rebuilt the overall sequences by overlapping the pieces. Meanwhile, the NHGRI approach proceeded by inching across whole chromosomes. (“Clone” refers to a piece of DNA.)

Another famous Venter invention is expressed sequence tags, aka ESTs.

When everyone was yammering on about “racing” to decipher “the” human genome sequence, never mind that we all have millions of distinctions, Venter was focusing on the 200-to-500 DNA base ESTs. These bits of DNA were created (“reverse transcribed”) from mRNA molecules, and dubbed cDNAs (c stands for complementary). The collection of transient mRNAs in a particular cell under particular conditions, represented as the more stable cDNAs, provides a glimpse of gene expression in that tissue and time.

The invention of ESTs perhaps presaged the mRNA vaccines that today target viral diseases and cancer. But at the time, James Watson dismissed ESTs as “bits of junk” that would actually slow the sequencing effort, and objected to Venter’s patent.

Sequencing Genomes

His interests extended well beyond human health. He pioneered metagenomics, the strategy of sampling all of the DNA in an environment and deducing the resident organisms. He described deep sea life forms from their shed genetic material, constituting the marine microbiome.

And who else but Craig Venter would attempt to invent life, from basic chemicals up? His Synthetic Genomics effort became Viridos, which filed for bankruptcy last year.

He introduced the first “hypothetical minimal genome” in 2010, whittling it down from the natural genome of tiny microbe Mycoplasma genitalium. Its half-a-million or so DNA bases encode a mere 473 genes. Venter named it JCVI-syn3.0, JCVI for the J. Craig Venter Institute. Beat that, Donald!

Venter monetized personal genome sequencing, at first charging $25,000 and pitching the data as a life extension tool. To that end, in 2014 he founded Human Longevity Inc. “to advance precision, pre‑symptomatic medicine.” At the time, the idea to combine genome sequencing with all manner of tests and scans to predict an individual’s lifespan was indeed novel. The effort amasses genome sequences and tons of clinical data, from people of all backgrounds, ages, experiences, and health status.

After some legal tussles and changes in leadership, including a dismissed lawsuit against Venter, the company still exists, in San Diego and South San Francisco. And of course now the idea of combining genome sequencing with scans and many other testing modalities is everywhere, for those who can afford it of course.

Most recently, Venter founded Diploid Genomics (DGI) in January 2026. The company’s strategy is to combine complete sequencing of each chromosome (including the repeats and other parts that do not encode protein) in a diploid cell, to assess the contributions of both parents, with clinical data and imaging, to derive “an AI-driven unified patient profile, transforming how early stage disease is predicted, detected, and treated.”

CODA

It is sadly ironic that Venter’s final focus, as far as I know, was extending the human life span, through Human Longevity Inc.

But even the most sophisticated, data-drenched predictive models can’t foretell all – getting hit by a truck, struck by lightning, attacked by an ICE agent, or sent to war.

Ironically, all those data can’t predict the somatic mutations that happen in our non-sex cells all the time, as natural errors of the imperfect process of DNA replication. Nature makes mistakes. And that’s how one errant cell, with an activated oncogene or dampened tumor suppressor gene, divides to produce another, and they divide, and on and on until a tumor grows.

We can’t predict who will die from what, and when. I’ve had cancer twice, and I’m so sorry that the unforgettable Craig Venter died at age 79 from a cancer treatment. But I’m so glad that I met him, even just briefly.

Said Anders Dale, president of JCVI, “Craig believed that science moves forward when people are willing to think differently, move decisively, and build what doesn’t yet exist. His leadership and vision reshaped genomics and helped ignite synthetic biology. We will honor his legacy by continuing the mission he built—advancing genomic science, championing the public investments that make discovery possible, and partnering broadly to turn knowledge into impact.”

(photo credit Brett Shipe, JCVI.org)

The post Memories of Craig Venter appeared first on DNA Science.

A Goldilocks Genetic Strategy to Combat Tomato Yellow Leaf Curl Disease

Ricki Lewis, PhD — Thu, 23 Apr 2026 12:36:25 +0000

My favorite part of the arrival of spring is getting back to the garden – especially tomatoes. But I’ve learned not to plant too soon, especially in my neck of the woods where snow can come as late as May.

Starting seedlings indoors is fine, but you can’t cheat by buying a plant already festooned with fruits, which I unfortunately smugly did last year. One-by-one, the beautiful tomatoes turned red and quickly rotted from the bottom up into brown mush.

So I was intrigued by a study just published from professor Sota Koeda and graduate student Moeno Shimoide at the Graduate School of Agriculture at Kindai University in Japan, in the journal Euphytica. They tackled begomoviruses, a large group of pathogens known to decimate crops of beans, squash, cassava, cotton and tomatoes, causing tomato leaf curl disease. Whiteflies transmit it in the southern US as far north as North Carolina, and in the Caribbean, Mexico, Southeast Asia, Japan, and the Mediterranean.

Infected plants are stunted and festooned with upward curling, yellowing young small leaflets, and halted flowering.

But nature may have provided a tool to save domesticated tomatoes from yellow leaf curl disease. Certain wild relatives of tomatoes carry resistance genes, which are introduced into cultivars to protect them. A more-is-better approach is to breed in variants of six specific resistance genes, called Ty-1 through Ty-6, into tomato cultivars. But that can harm crop plants too, a phenomenon known as linkage drag.

The new work finds that the magic number of protective genes is two – either Ty-1 or Ty-3, plus Ty-6.

“To control aggressive begomoviruses distributed in Southeast Asia, which are one of the most virulent species globally, relying on a single resistance gene common in Europe and Japan is insufficient. Thus, determining which combinations of resistance genes are necessary and sufficient for effective control is important for breeding tomatoes with enhanced viral resistance,” said Koeda.

First, they tested a trio of resistance genes that differed the most in DNA sequence from each other. They used common Japanese varieties with tomato yellow leaf curl virus resistance, as well as fancier ones from World Vegetable Center specifically bred to be highly resistant to the disease. And it turned out that plants that carried the Ty-1 and Ty-6 genes, or Ty-3 and Ty-6, fared best. Four didn’t improve resistance to the virus.

“Our study suggests that the introduction of fewer resistance genes than expected can substantially enhance resistance. It offers a promising approach for improving tomato varieties while balancing resistance, productivity, and fruit quality. Overall, our findings may provide valuable guidance for enhancing begomovirus resistance in other crops and represent a discovery that could contribute to the long-term stable production of food,” said Koeda.

I live in the northeast so my plants won’t encounter this type of virus, but I can appreciate the difficulty of launching each spring’s tomato crop – a sudden rainstorm early in the season can wipe out hours of work instantly. But there’s nothing better than harvesting an armful of tomatoes, especially heirlooms, from a garden into the fall.

The post A Goldilocks Genetic Strategy to Combat Tomato Yellow Leaf Curl Disease appeared first on DNA Science.

“Upgrade” Chillingly Conjures a Genetically-Enhanced World

Ricki Lewis, PhD — Thu, 16 Apr 2026 14:14:52 +0000

It was inevitable that sci-fi would take on genetic enhancement, but I somehow missed Blake Crouch’s brilliant 2022 dystopian novel Upgrade. He’s one of my favorite authors, the brains behind Wayward Pines and five other novels, as well as 2024’s Dark Matter on Apple TV+.

Because I’m working on the zillionth edition of my human genetics textbook, I’m ultra-sensitive to accuracy, and Upgrade doesn’t disappoint. The tale’s compelling view of what could be is far more detailed, and entertaining, than the gloom of GATTACA.

A Gene Drive with Unforeseen Consequences
I admit I’ve never thought much about genetic enhancement; my books and articles have always been about preventing or combating disease. But the invention of CRISPR gene editing in 2012, its ease and versatility, quickly changed what was possible.

In Upgrade, protagonist Logan Ramsay is an agent for the Gene Protection Agency. His notorious mother, geneticist Miriam, was responsible for a gene drive (which eliminates a specific genotype) that unintentionally killed millions. Gene editing is now banned, parents who edit their sick kids’ DNA imprisoned, but novel DNA tweaks still happen in “dark gene labs.” Billboards announce “GENE EDITING IS A FEDERAL CRIME.”

Mom Miriam also ran a company called “The Story of You,” which held millions of peoples’ genome sequences in its databases. It’s mentioned briefly, overshadowed by her major contribution of Scythe, “the most powerful genome-modifying system ever created” that spawned “the largest accidental mass killing in human history.”

Scythe was used to engineer locusts to deliver viruses genetically modified to protect indica rice plants growing in Zhaoqing, China, from a bacterial leaf blight. But Scythe veered off-target, as gene editors can do, knocking out genes for seed production. Oops! “Within a year, the vector locusts began propagating exponentially.”

When the modified viruses spread to other crops, the resulting “Great Starvation” radiated out along the food webs that interconnect all life on Earth. The cascade of environmental changes eventually plunged coastal cities under water as an island of glomming microplastics emerged in the Indian Ocean.

“My mother had tried to edit a few rice paddies and ending up killing two hundred million people,” explains protagonist Logan. He’d worked in her lab, helped the gene editing take root in China, and ended up in prison for the crime of germline modification.

Skewing Mendelian Ratios
Gene drives were envisioned to knock out populations of insects that carry pathogens, like the mosquitoes behind malaria. The technology erases the contribution of one parent of a sexually-reproducing organism, altering Mendel’s first law of gene segregation.

Crouch explains it well:

“Say the mother has brown eyes, the father blue. With a gene drive, you can overwrite the mother’s genes for eye color in the embryo, thus guaranteeing that their child will have blue eyes. But the real kicker is that the child will pass on the targeting system to their children in turn. All of their children will now have blue eyes too, and so on. Within a few generations, the gene drive will pervade the entire population – and the natural, unedited copy of the gene will be wiped out completely. All Homo sapiens will have blue eyes.”

(He doesn’t explain that the edit would need to affect the embryo’s primordial germ cells, which give rise to sperm or eggs, to be passed on. That’s important.)

Logan leaves prison, after many years. And his mother Miriam has disappeared. Or has she?

Before we find out what’s happened to Miriam, a description of this strange, genetically modified world unfurls.

Zootopia
Scythe leaves CRISPR in the dust, enabling creation and propagation of populations of creatures with selected genetic changes. These include the expected designer pets, ultra-strong cannabis, spider-silk clothing, and GMO foods, plus the more inventive “exotic synthetic creatures” nurtured in lab-grown, free-standing uteri. The syn beasts include

• giant hornets that make taipan snake multi-venoms
• “an eel with a head at each end”
• Pompeii worms adapted to deep-sea hot thermal vents
• tiny pink gorillas as toys
• “sex dolls wrapped in synthetic human muscle and skin”
• “four biology undergrads at Brown who had simply wanted to see if they could make a dire wolf”- prophetic years before Colossal Biosciences made this very claim, providing the inspiration for my post De-extincted Dire Wolf Pups Have a Few Genetic Tweaks – That’s It).

Miriam is able to take her technology to humans, thanks to her 23andMe-like company and its millions of stored human genome sequences.

Evading the Gene Protection Act
All genetic tinkering has gone underground since evocation of the Gene Protection Act, which outlawed genetic research and made geneticists and molecular biologists instant criminals. Editing one’s own genes also became verboten.

Miriam Ramsay’s plan went far beyond engineered insects and skewed eye color. Her goal: building a better human.

But “better” is a highly subjective term, and genetic manipulations tend to have unforeseen consequences.

To start, she arranges for son Logan to have his genome enhanced in a dark lab, without his knowledge, just as hers has been enhanced. That takes the form of a sudden shower of tiny, glowing ice shards, each delivering into his unsuspecting cells a slew of genes carried aboard viruses. As the story unfolds, these genes unspool his enhancement.

A Menu of Genes
Blake Crouch traipses through an impressive laundry list of genes to tweak (with assistance from real-life geneticist Michael Wiles):
• SKI, PGC-1alpha, and IGF-1 pack muscle cells with mitochondria.
• Altered LRP5 builds denser bones.
• A slew of genes enhance brain function: GRIN2B regulates early learning and memory, GluK4 synaptic plasticity, and NLGN3 molds synapses.
• PDE4B, encoding an enzyme involved in inflammation and cell division, is implicated in COPD, asthma, cancer, and schizophrenia.
• TERT, which controls telomere length, affects rate of aging.

Oddly, protagonist Logan is flummoxed by one of the best-known genes, FOXP2, which gave our species speech.

The roster includes some targeted genes that don’t seem obviously to provide enhancement – the mutation behind the inborn error of metabolism PKU, a cystic fibrosis gene variant, an interleukin variant here, hemoglobin variant there, a tumor suppressor and oncogene thrown in.

A clever interlude complete with sequences of A, T, C, and G – the DNA bases – reveals how genetic code, read backwards and forwards, from one strand or the other, can be tweaked to hide information. This becomes important later on, when characters meet up.

Alas, the accurate gene descriptions lapse into classic anti-science word choices. Logan’s genome, for example, has the “primary goal of survival of the species.” That’s not at all how mutation and natural selection affect evolution.

So what can the genetically enhanced Logan do? The changes unfold slowly.

Logan’s Run
The first improvements are barely noticeable. Beating his daughter in chess (like Larry suddenly beating me in Scrabble). Remembering details of journal articles and books he read decades ago. Ultra speed-reading; “You’re turning a page, like, every thirty seconds,” says his wife one night.

Logan suddenly recalls events from years past in excruciating detail.

He reads tiny, subtle facial cues that convey instantly how people will act – that’s invaluable, especially when gambling, for example. Senses sharpen, as pain tolerance soars. He’s stronger, and takes multitasking to a new level. Perhaps most importantly, Logan’s focus, concentration, and ability to ignore unimportant stimuli – collectively called sensory gating -skyrocket.

“I hadn’t been capable of this intensity of concentration and focus in, well, ever: Something was different. As I closed my eyes, a quiet voice whispered from the further corner of my mind. Not something. It’s you that’s different,” Logan muses.

In short, Miriam was attempting to use her Scythe superior gene editing to alter how humans think, and her son was a guinea pig. She told him before committing her crime against humanity, “It’s one thing to build a new life-form, cure illness, or even attempt the work we’re doing now with our locusts. But to change how members of a fully sentient species THINK is surely the ultimate expression of the power of gene editing.”

(I’m glad that our president doesn’t know how to read and most certainly doesn’t know anything about genetics, or any science.)

A rather convoluted plot complete with the requisite chase scenes, perhaps a requirement for an eventual film adaptation, finally reveals that Miriam and her two offspring, Logan and his sister Kara, have had their genomes enhanced. But the classic unpredictability of gene expression and interaction turns Kara to the dark side.

Collateral Damage
If a technology seems too good to be true, it generally is.

I guessed the Achille’s heel of Miriam’s technology when the narrative settles on Glasgow, Montana, a small town where everyone has been enhanced. Some of the guinea pigs suddenly break out in “maniacal laughter,” for no apparent reason, and soon perish. If you’re familiar with protein folding (hint), it is an ingenious and plausible plot point. The explanation rhymes with “scion,” but I won’t give it away.

The second half of the book takes place a year later. Miriam had been planning to upgrade all of humanity, to make up for her killing millions, but she died before she could do so. Meanwhile, Logan struggles with the challenges of the genomically enhanced, struggling with too many stimuli.

How will he stop his evil sister from disseminating the genome enhancement?

Can he preemptively save the millions who will be collateral damage, spiraling into the deadly laughter?

I won’t give away the ending, but it does wrap up all the dangling plot tendrils.

CODA
Alas, much as I loved Upgrade, near the end it devolves into a prolonged chase, presumably to ease translation to the big screen and satisfy adolescent viewers with Y chromosomes.

The action becomes a traipse through what was once lower Manhattan, the skyscraper pinnacles poking up from what was submerged, with remnants of human culture dotting the apocalyptic landscape. I skimmed about 50 pages of it.

I awoke when the last two pages suddenly evoke a pair of sci-fi classics.

“Music effervesced from the crowd” of survivors brought me instantly back to the brilliant Station Eleven’s band of scorched-earth traveling troubadours. And Logan catching “a glimpse of the Statue of Liberty” of course conjured the final scene of Planet of the Apes, as a stunned Taylor gazes at the ruined crown of the great statue and instantly sees the past and the future.

End-of-the-world scenarios, split humanity, genome tinkering, good versus evil – they’ve all been done many times. Upgrade is a thought-provoking take on a classic theme.

The post “Upgrade” Chillingly Conjures a Genetically-Enhanced World appeared first on DNA Science.

Is Measles Returning in a More Vicious Form?

Ricki Lewis, PhD — Thu, 02 Apr 2026 18:06:06 +0000

Eman, our informally adopted son who is a physician in Monrovia, Liberia, is recovering from the measles. He contracted it from a teen patient.

“It started with a slight fever and chills, and became a burning fever. Then I had cough and red, watery eyes. I treated myself for malaria and went for a checkup. The doctor saw the rashes on my face and hands, and said it didn’t look like a typical measles rash. Initially I was treated as an outpatient and told to isolate. Then in two days, I got shortness of breath at home, and had to get admitted. I experienced respiratory distress and had to get supplemental oxygen. It reminded me of having COVID.”

He had measles vaccine as a child, and thought he had some cross-protection from having had chickenpox.

“I’ve been looking up papers on why a previously vaccinated person or an adult would get measles. A lot of them are pointing to incomplete dosages, improper handling of the vaccines, waning immunity, or being immunocompromised. There are many other previously vaccinated adults with measles for the first time. This should be happening in mostly immunocompromised people, and I’m not. The measles outbreak has been terrible.”

Perhaps the scariest thing about infectious diseases is that they change. That’s what nucleic acids – DNA and RNA – do.

Measles in Many Nations
Liberia has faced measles outbreaks before, a particularly serious and widespread one in 2022. And the disease is creeping back in many places.

Health officials in Australia fear loss of the nation’s measles-free status, with recent cases attributed to people returning from visiting southeast Asia, where they became infected.

The disease is on the rise in Indonesia, Thailand, and Vietnam, and is endemic in India, Bangladesh, Myanmar, Nepal, Angola, Yemen, and Mexico. Cases have recently been reported from Bolivia, Canada, Guatemala, and Mexico.

“Measles elimination in the Americas was a historic achievement, but recent events demonstrate that this progress is fragile and can be reversed without consistently high vaccination coverage. Coordinated action now can save lives, prevent further outbreaks, and ensure the health security of the region,” said Jarbas Barbosa, director of the Pan American Health Organization, in a report issued February 3.

And of course, measles is returning to the US.

The CDC reported 2,285 confirmed measles cases in 2025, and as of March 26, 2026, 1,575 cases, from 31 states. The new year has seen 16 new outbreaks.

The Natural Cycle of Mutation and Selection
Two interpretations of Eman’s experience – contracting measles despite having been vaccinated – are possible.

An anti-vaxxer might say “Measles vaccine doesn’t work.”

A biologist like me would say “Pathogen genomes mutate.”

A viral genome changes, as all genomes do, as the genetic material replicates and occasionally, errors happen. That’s mutation, a natural process arising from the underlying chemical reactions. If new viral variants arise that can evade vaccine protection, they may come to persist. Then cases of the infectious disease start popping up. That’s selection.

The cycle of mutation and selection is about as basic as biology gets.

But measles is especially dangerous, for it can shut down immunity to past, non-measles infections, too. This recent DNA Science post explains the details.

The Fear Factor
Perhaps I appreciate vaccines because I remember having the diseases that some of them now protect against.

Getting the handful of “childhood diseases” was just part of being a kid in the 1960s. I had measles for a month, German measles (aka rubella), mumps, and chickenpox. I recounted how my younger sister and I straddled the time of the invention of the measles vaccine here – I had the disease, she had the shots. Now that measles is back, I’m likely still protected – she may need an MMR booster.

Why are infectious diseases once almost completely gone returning?

Because people are actually encouraging it, their fear overwhelming any knowledge of biology. And they may listen to non-experts with impressive titles and in positions of power (See A Pop Quiz in Biology for RFK J).

Individuals choosing not to vaccinate their children are enabling nature to take its course, providing a breeding ground for the measles virus to spread and change, shattering herd immunity. And as a result, resistance mutations, which arise naturally, are more likely to persist, perhaps to flourish. Will the virus mutate enough for even natural immune protection to become insufficient?

Ignorance and selfishness are a potentially deadly combination.

The post Is Measles Returning in a More Vicious Form? appeared first on DNA Science.

New Study Suggests Why the Mediterranean Diet is so Healthy – and a Recipe

Ricki Lewis, PhD — Thu, 26 Mar 2026 13:40:50 +0000

A Mediterranean diet emphasizes fruits, vegetables, whole grains, legumes, seeds, nuts, and especially olive oil, with a few heart-healthy cheese choices – mozzarella, ricotta, and especially feta – and some lean poultry and fish. It has long been associated with lower risk of diabetes, heart disease, and cognitive decline, but how it does so has been mostly a mystery. I’ve followed this way of eating for years – this post ends with an easy recipe for a vegetarian Moroccan stew.

A new report in Frontiers in Nutrition suggests the source of the benefits of the Mediterranean diet at the molecular level: two tiny proteins made in the mitochondria, the tiny, footprint-shaped organelles that house the biochemical reactions that extract energy from nutrient molecules.

Mighty Mitochondria

In middle school biology classes, the mitochondrion is dubbed “the powerhouse of the cell” for good reason. Festooned along the intricate infoldings of the organelle, the energy “currency,” the molecule ATP (adenosine triphosphate), runs the cell using the energy captured in its chemical bonds.

A cell may have a few hundred to tens of thousands of mitochondria, depending on activity level. A rather sedentary liver cell has about 1,700 mitochondria, but a highly active skeletal muscle cell may have 10,000 or more.

Mitochondria don’t just sit there. They move about within a cell and can transport DNA from one cell to another, a recent discovery. They coalesce and break apart, like bubbles in a bathtub, assuming different volumes.

Most intriguing is that mitochondria have their own genome, consisting of 37 genes. They reproduce, release heat, and send and receive molecular signals.

These eclectic organelles have a bad reputation when they cause mitochondrial diseases, which typically cause great fatigue and other symptoms. But they also hold a special place in the history of biology as the basis of the endosymbiont theory. This is the idea that mitochondria were once free-living microorganisms that were captured by larger single-celled microorganisms, contributing to the evolution of our own more complex, eukaryotic cells.

More practically speaking, the hardier and smaller mitochondrial DNA is more likely to survive the harsh conditions of disaster than DNA from a cell’s nucleus, and so they serve as a forensic tool. (See Maui Fires: How Mitochondrial DNA Will Identify Human Remains.)

Two Tiny Proteins
In the new study, Roberto Vicinanza, a gerontologist at USC and colleagues identified two tiny proteins from mitochondria, called humanin and SHMOOSE (an acronym far more exciting than what it stands for), that may be intimately involved in how age-related diseases arise – and how some people manage to avoid them.

The microproteins are so small, under 100 amino acids long, that their genes were too tiny to have been picked up in human genome sequencing efforts. The new study found that adherents to a Mediterranean diet have higher levels of the microproteins, both of which have been linked to protection against neurodegenerative and cardiovascular disease.

“These microproteins may act as molecular messengers that translate what we eat into how our cells function and age. It’s a new biological pathway that helps explain why the Mediterranean diet is so powerful,” Vicinanza said.

That might be a bit of an overstatement.

A Preliminary Investigation
The study looked at markers of oxidative stress, a key driver of aging and chronic disease, in only 49 patients, average age 78, recruited from an observational study of atrial fibrillation. The participants took the “9-item Med-Diet questionnaire,” which provides a score, from 0 (low) to 18 (high), based on how frequently people reported having eaten foods from nine categories: fruit, vegetables, meat, cereals, dairy, alcohol, olive oil, legumes, and fish.

Twenty patients reported following a Mediterranean diet. The folks who ate more olive oil, fish and legumes had higher levels of SHMOOSE and humanin in their blood, while those who didn’t had higher markers of oxidative stress. Specific correlations suggested that olive oil is the healthiest component of the diet, legumes came in second, and refined bread the worst, according to the oxidative stress markers.

“These findings suggest that specific components of the Mediterranean diet may directly influence mitochondrial biology. Humanin and SHMOOSE could serve as biomarkers for adherence to the Mediterranean diet and have clinical significance,” said senior author Pinchas Cohen. He discovered humanin in 2003, which has been linked to improved insulin sensitivity, cardiovascular protection, preservation of cognitive function, and longevity. SHMOOSE was more recently discovered and is linked to brain health. A variant of the gene is associated with increased Alzheimer’s disease risk and the normal variant may protect brain neurons from amyloid-induced damage.

“These peptides are emerging as key regulators of aging biology,” Cohen said. “They connect mitochondrial function to diseases like Alzheimer’s and heart disease and now, potentially, to nutrition.” And so the Mediterranean diet may work two ways: lowering oxidative stress while boosting levels of mitochondrial microproteins that further dampen damage.

Vicinanza put the work into perspective. “We’re connecting centuries-old dietary traditions with cutting-edge molecular biology. It supports the idea that healthy eating patterns with little to no ultra-processed foods reflect how humans have eaten over long periods and may create conditions to which mitochondria—ancient cellular organelles—are likely adapted.”

The researchers envision the two tiny proteins as biomarkers that could help people tailor their diets to optimize brain health and longevity. “Our goal is to move from observing associations to understanding causality,” Vicinanza said. “If we can harness these pathways, we may be able to design nutritional strategies that promote healthy aging at the molecular level.” But don’t we already know this?

A Culinary Coda
I love the idea of finding biological reasons for an observation, like a diet linked to improved heart or brain health. But an observational study of a few dozen people, who report what they’ve eaten, isn’t very powerful.

Instead, it’s easier to just eat foods that include those of a Mediterranean diet. Here’s one of my faves.

Moroccan Chickpea + Eggplant Stew

Ingredients (2 big servings)

Half a large eggplant or a small one, cut into strips
Half an onion, chopped (or more)
3 cloves garlic, shredded
1 can chickpeas
1 can tomatoes
dried fruit (handful): prunes, apricots, dates, cranberries, yellow raisins
dried Mediterranean (Moroccan) spice mix

Sautee eggplant strips, onion, and garlic with salt + pepper. Add most or all of the tomatoes, chickpeas, and dried fruit. Add 1 teaspoon dried spices

Cook for awhile and eat, or put in crockpot for a few hours.

Enjoy!

The post New Study Suggests Why the Mediterranean Diet is so Healthy – and a Recipe appeared first on DNA Science.