Nu Skin teams with Dr. Cox to find a cure for Alzheimer's Part I - Dr. Cox walking

Dr. Cox is set to find a cure for Alzheimer's, Part I

Moxie Beauty Care Admin

Doctor Paul Cox, creator of our epoch® beauty line, has set his goals pretty high. His research is very interesting and thought of sharing it with you. This article was published in the FORTUNE Magazine, enjoy the read of part I of a series!

In a small lab in Jackson Hole, Wyo., 65-year-old Paul Cox believes he’s closing in on a treatment that might prevent Alzheimer’s disease. And ALS. And a host of other neurodegenerative diseases, for that matter. Cox, we should point out, isn’t a neurologist. He isn’t a physician of any kind. He doesn’t work at a big drug company or an academic medical center or a government laboratory. His ideas come from so far outside the mainstream of neurological research that you might think he’s crazy or deluded or worse. But then, some very credible people think he might be on to something big—which might make the improbable, quixotic story you are about to read one of the most important as well.

Our unusual tale begins with ethnobotany: the study of the way indigenous people use plants in their customs and diet. You see, Cox is an ethnobotanist, and a darn good one by all accounts. “You’d enjoy walking through a jungle with me,” he once told me. He’s a cheerful gray slouch of a man, quick-witted and sincere, given to club ties and blockish suits when he’s not rocking a fleece. But neurology? When it comes to the study of neurons—the critical cells of the central nervous system that degenerate and die in diseases such as Alzheimer’s and ALS—Cox describes himself as something of a piker. “One colleague says I know about as much neurology as a neurologist’s spouse,” he added with a grin.

Nonetheless, neurons are precisely what you’ll find Cox and a covey of researchers studying at his nonprofit Brain Chemistry Labs. If you happen to be visiting Jackson this winter, you’ll recognize the lab by the cartoonish wood carving of a bespectacled bear (holding a beaker, naturally) just above the front portico. You might even spot a wealthy local patron wearing one of the lab’s “Serine Dipity” sweatshirts. That’s a wordplay on L‑serine, an amino acid that serves critical functions in the central nervous system, among other things. That’s the second strange part of this story: How extraordinarily unlikely and yet wonderful would it be if Cox and his colleagues were right—and the best prevention for some of these terrifying diseases turns out to be a naturally occurring protein building block rather than a high-priced drug?

You can buy a kilo of powdered L-serine for $53 on Amazon. A Serine Dipity sweatshirt, on the other hand, will cost you a $150,000 donation to Cox’s lab. Which leads us to the third twist in this marvelously odd tale. The sweatshirt buyers (and Cox’s wealthy backers) seem to believe just as fervently in the man’s innovative research model as they do in his purported cure. Indeed, it’s fair to say that whether or not Cox’s theory pans out, the style of medical investigation he’s pioneering is gaining fans—even in some traditional and elite academic quarters. So if Cox and his colleagues do push the science forward on Alzheimer’s, ALS, or any other neurological disease even a little, it may have an added benefit of offering the culture of medical research a fresh model to emulate.

And that—in a nutshell—is what the Paul Cox story is all about.

Cox’s interest in neuro­degeneration began when he set out to solve a puzzle that had bedeviled researchers for decades: Why did an extraordinary number of the Chamorro people of Guam develop an odd hybrid of ALS and Alzheimer’s symptoms? Cox’s answer: They had been poisoning themselves every time they indulged in their greatest culinary delight, a bat boiled in milk—eyeballs, wings, and all. That was 16 years ago. Since then, Cox has been trying to see if that insight could eventually lead to some kind of treatment against brain diseases.

Cycad Tree with a head of developing seeds attached to small leaf-like structures - Moxie Nu Skin

Working on a tiny budget, Cox has built a consortium of 50 scientists from a wide range of disciplines, who share their unpublished research with one another and push Cox’s theories in directions he never would have anticipated. Within this loose-knit group, the spirit of inquiry seems to thrive, uninhibited by strictures that rein in scientists in academic research centers and pharmaceutical labs. “He’s a visionary,” said Deborah Mash, who runs the Brain Endowment Bank at the University of Miami’s Miller School of Medicine and who has worked with Cox on several experiments. “I was a skeptic. But he’s a fiercely intelligent man. The way he’s pushed this forward is unbelievable.” Cox’s “virtual pharma,” as he calls it, has fostered a more innovative, organic, and patient-focused form of scientific research than what’s often found at the world’s leading drug companies, its members say.

Those companies have failed miserably in their own efforts to attack Alzheimer’s. The FDA has approved just five treatments for Alzheimer’s, and they provide only limited, temporary relief. The agency hasn’t signed off on any new ones since 2003, despite more than 500 clinical trials of Alzheimer’s drugs. In 2018 alone, trials of once-high-profile drugs made by AstraZeneca, Eli Lilly, Johnson & Johnson, Merck, Takeda, and others collapsed or faded away in a statistical whimper. Some big companies, including Pfizer, have completely abandoned the field. (For more on this epic washout, see “Can Biogen Beat the Memory Thief?”).

What do these serial failures have in common? The great majority of the drugs were built on a single idea, the “amyloid hypothesis,” which posits that clumps of protein fragments called beta-amyloid—which are found in the brain of every Alzheimer’s patient—are the primary cause of the disease. (Another hallmark is the presence of neurofibrillary tangles of a protein called tau.) The amyloid theory is based on decades of perfectly good science, and the idea that if you eliminate those plaques you might also slow or reverse the disease still holds sway. But it’s not the only science—and targeting these plaques directly may not ultimately be the best (or only) way to fend off or treat Alzheimer’s.

For decades, though, Big Pharma hasn’t been very interested in less conventional theories. Seeking an enormous payout of perhaps $10 billion a year in sales, they have thrown thousands of scientists and billions of dollars at this one idea, again and again, with no luck.

“You know that definition of insanity?” Cox asked, the first time we met. “Doing the same thing over and over again despite getting the same results? Each trial is a billion bucks; each targets the same thing. None have worked. It seems to me that if you’d put in a billion bucks and failed, you’d say, ‘Let’s try something else.’ ”

If there is any good news about Alzheimer’s, it might be this: After three decades of cureless consensus, the scientific community may finally be ready to seriously consider alternative approaches. One sign of change has been the entreaties in top-tier journals ranging from The New England Journal of Medicine to Brain to Frontiers in Neuroscience to rethink the orthodoxy. (As a New England Journal editorialist put it: “We may very well be nearing the end of the amyloid-hypothesis rope, at which point one or two more failures will cause us to loosen our grip and let go.”) Another sign, perhaps, is the willingness of scores of scientists to sign on to the exploration of a bizarre moonshot of a theory born in the rain forests of Guam.

The epiphany came while Cox was reading a book, The Call of Service, by Robert Coles. “Coles writes that when your experience, interest, and talents are orthogonal to a societal need, you are hearing a call,” Cox explained to me in Jackson in 2016. We had repaired to the foyer of a bed and breakfast near his lab. Cox was tired after seven hours of meetings with his board of directors, and he sank into a wingback chair, yellow legal pages full of scribbled notes threatening to escape from the binder on his lap.

His mother had died of cancer in 1985, and Coles’s call to arms offered a way forward apart from grieving. So he grabbed some paper and began jotting down his experiences, interests, and talents. “I’m fluent in a couple of Polynesian languages, I’m a marine forest biologist, I’ve studied with the world’s greatest ethnobotanist, and I really want to defeat disease,” he recalled. “If I become an oncologist, maybe I can help dozens of people. If I could discover a new drug, I could help millions of people. What are the chances of that? Oh, about next to zero. But why not give it a shot?”

Two months after his mother’s death, he, his wife, Barbara, and their three kids set off for Falealupo, a tiny village on Savai’i, a Samoan island where they would live, off and on, for several years. The funding came from a 1985 Presidential Young Investigator Award, presented by President Reagan.

Cox didn’t discover a cure for cancer in Samoa. He did, however, find a substance in tree bark that local healers ground into a salve, which Cox suspected might have activity against HIV. (He later licensed the compound to the AIDS Research Alliance of America, but it was never developed into a drug.) He also brokered a deal that helped save 30,000 acres of Samoan rain forest—home to many native species, including Pteropus samoensis, a flying fox, or genus of bat, whose wingspan can stretch nearly three feet wide. Cox and a tribal chief named Fuiono Senio were awarded the Goldman Environmental Prize for the rain forest agreement.

Bats studied by Dr. Cox in Guam - Nu Skin by Moxie

Cox’s interest in bats led him to Guam, and to the mysterious ailment the Chamorro people called lytico-bodig. In the years after World War II, the Chamorro were up to 100 times as likely as people elsewhere in the world to develop symptoms often associated with neuro­degenerative diseases like ALS, Alzheimer’s, and Parkinson’s: slurred speech, facial paralysis, loss of motor skills, immobility and dementia. Believing that this cluster might hold essential clues to neurodegeneration, scientists advanced several theories. Some targeted a toxin found in the seeds of local cycad trees. Called BMAA, it killed nerve cells in lab tests and induced symptoms of lytico-bodig when fed to monkeys. The Chamorro cleaned the seeds thoroughly before grinding them into a flour for their version of tortillas. But later research suggested that humans would have to ingest, literally, a ton of cycad flour each month for the toxin to have any effect, and the purported BMAA link fell out of favor.