I have several friends with Parkinson’s and Alzheimer’s.
Bacterial blood infection, computer illustration.
My grandfather died of Alzheimer’s 35 years ago, and I was there when his wife took her own life rather than face another winter with someone who didn’t know who she was.
These science stories may inevitably turn out to be down the rabbit hole, but I present them so folks know what is being discussed, BS or not.
Salmonella is a bacteria that causes an intestinal tract infection from contaminated food or water. It was recently discovered that salmonella in the gut is linked to neurological diseases like Parkinson’s and Alzheimer’s.
A collaboration between Vaccine and Infectious Disease Organization-International Vaccine Centre (VIDO-InterVac) at the University of Saskatchewan (USask) and Temple University (Philadelphia, U.S.) analyzed the effect of Salmonella biofilm protein on animals. They observed that bacteria can cause arthritis and autoimmune responses.
Salmonella biofilms typically form in the environment such as surfaces where raw meat is prepared. Biofilms are bacteria that densely stuck together in response to harmful conditions like disinfectants and antibiotics.
Dr. Aaron White, an expert on salmonella biofilms and curli amyloids, alongside his team found Salmonella biofilms forming on the intestines of infected mice models. The biofilm protein ‘curli’ appeared as the scientists replicated the food-borne illness associated with the bacteria.
Within four to six weeks, curli formed in the colon and cecum, or the beginning of the large intestine, of the mice. The scientists also ruled out that curli was produced solely by Salmonella and not by other bacterial species.
This is not food safety but could be. A colleague never knew this story, so I found it and shared it with him.
And know all of youse who don’t like it, start your own blog.
Oh, and hit delete.
That’s me and grandma, 1963.
Wrote this for the Globe and Mail in 1994
How We Die
Reflections on Life’s Final Chapter
Sherwin B. Nuland
Alfred A. Knopf
A Gentle Death
Marilynne Seguin, R.N.
Key Porter Books
Review by Douglas Powell
My grandmother ended her own life. After five years of painstaking care for her husband, who was slowly deteriorating from the cerebral ravages of Alzheimer’s disease, she decided that a sixth was not worth facing.
Her death was quick and without warning. One moment we were saying goodbye before a routine trip to the store, the next I was transferring her from car to wheelchair at the hospital emergency ward. Within 30 minutes she was officially deceased, the result of a major pharmaceutical overdose.
Looking back, I’ve often wondered what I would say to her, given the chance. Don’t do it, life is really okay. You are not alone. Things will get better.
But in reality, life is often harsh, she was often alone, and the prospects of yet another winter, trekking to the hospital each day to watch the person she had spent the vast majority of her life with become even more unfamiliar, meant that things certainly were not about to get better; at least not in any foreseeable future.
Western society is finally being forced to grapple with some of the difficult consequences that arise when medical technology conflicts with individual rights and freedoms. In Canada, Nancy B., a 25 year-old quadriplegic, and Sue Rodriquez, who suffered from the degenerative wasting of Lou Gehrig’s disease, have challenged existing laws and brought the question of when to say enough is enough to the arena of public debate. The discussion is welcome and the only antidote to the private anguish of such decisions, as is forcefully brought home in two new books.
Humans have created powerful myths and rituals to accompany death, writes Sherwin Nuland in How We Die, but perhaps none more bizarre than the modern hospital, “where it can be hidden, cleansed of its organic blight, and finally packaged for modern burial. We can now deny the power not only of death but of nature itself. We hide our faces from its face, but still we spread our fingers just a bit, because there is something in us that cannot resist a peek.”
Dr. Nuland, a physician who has authored several books about the medical profession and continues to teach surgery and the history of medicine at Yale University, says this book was written to demythologize the process of dying, to present it in its biological and clinical realities. The changes at a cellular and organ-level that accompany heart attacks, stroke and cancer are presented in detail that may be intimidating to the uninitiated. Then again, any person who is faced with life-threatening disease can quite rapidly assimilate the medical jargon — they have to. Physicians capable of talking in clear, simple language are rare.
Nuland is blunt. Despite the gripping television constructs, few of the 350,000 Americans who suffer cardiac arrest each year actually survive. Nuland observes that after the vain attempts at resuscitation, the critical response team eventually stops and the mood is transformed from heroic rescue to dejected gloom of failure. But it’s the patient and their families that Nuland, like any good — and increasingly rare — general practitioner focuses on. “The patient dies alone among strangers: well-meaning, empathetic, determinedly committed to sustaining his life — but strangers nonetheless. There is no dignity here.”
Then there’s the story of Dr. Nuland as young intern and his first crisis when a patient went into massive cardiac. Using all his training, Nuland opened the man’s chest and began to massage his heart, as was the routine practice at the time, but to no avail. The man died. Yet suddenly he “threw back his head once more and, staring upward at the ceiling with the glassy unseeing gaze of open dead eyes, roared out to the distant heavens a dreadful rasping whoop that sounded like the hounds of hell were barking. Only later did I realize that what I heard was McCarty’s version of the death rattle, a sound made by spasm in the muscles of the voice box, caused by the increased acidity in the blood of a newly dead man. It was his way, it seemed, of telling me to desist — my efforts to bring him back to life could only be in vain.” Or, as Nuland constantly reminds the reader, “we rarely go gentle into that good night.”
Marilynne Seguin’s A Gentle Death is an attempt to help ease that journey for patients and their families. Sequin, a registered nurse for over 30 years as well as a founding member and executive director of the Toronto-based Dying With Dignity tells how she, like Nuland, was trained to prolong life at all costs. Experience has taught her to question prevailing attitudes of the medical establishment and she stresses that patients must become informed and responsible for the medical decisions that affects their lives.
In presenting the many examples of people approaching death who Sequin has cared for, a common theme emerges. Rather than a passive silence, many approaching death wish to be at home, surrounded by the noise of children — the noise of life — rather than the sobering silence of loneliness.
Both books try to dispel the hero myth, the one where the nurse or physician is never to allow the patient to lose hope. Yet hope and wishing for miracles get in the way of true discussion; it robs people of their death. Nuland confronts this reality head on when he describes how, when his brother Harvey was diagnosed with bowel cancer in 1989, he made “a series of mistakes. … I became convinced that telling my brother the absolute truth would ‘take away his only hope.’ I did exactly what I have warned others against.” Harvey was enrolled in an experimental therapy that showed initial promise but in the end increased and prolonged his anguish. Eventually, Harvey returned home to die.
These two books, and others, are a continuation of an expanding public interest in death. Certainly part of that interest can be attributed to the demographics of baby boomers. The group that first discovered drugs, free love, parenthood, the mid-life crisis and menopause has now discovered death. And along with those who want to face biological realities there will be those who desire to live beyond their biological means. Nuland writes we are currently in the vitamin era, following previous attempts to prolong life through the pseudoscience of monkey glands, mother’s milk, and, as King David tried, sleeping between two virgins. Coming soon will be expanded attempts to prolong life through the mass availability of human growth hormone, derived by genetic engineering, and gene therapy. Only “accurate knowledge of how a disease kills,” writes Nuland, “serves to free us from unnecessary terrors of what we might be fated to endure when we die. We may thus be better prepared to recognize the stations at which it is appropriate to ask for relief, or perhaps to begin contemplating whether to end the journey altogether.”
Which leads to the hotly debated topic of physician-assisted suicide and the right of rational individuals to decide how and when to end their lives. At this point the two books differ strongly. Nuland approves of Living Wills and other advanced care directives, instructing physicians what treatments to withhold in the face of terminal illness, but he strongly disapproves of physician-assisted suicide. Seguin, however, sees no distinction. Much of her book is devoted to a frank discussion of the practical advantages and limitations of such approaches.
Nuland, however, fails to come clean on the topic, when he mentions in passing that, “Like so many of my colleagues, I have more than once broken the law to ease a patient’s going, because my promise, spoken or implied, could not be kept unless I did so.” Seguin states quite clearly that many physicians have engaged in such activity, so why not create clear, legally-binding rules, as has been done in the Netherlands.
One Dutch physician who supports the new law says society needs a counterweight for the enormous technology of modern medicine. But more importantly he says, it gives the patient a chance to take leave openly of his children, his grandchildren, and others.
That openness seems crucial to further public discussion of death and dying. I still wonder what I would say to someone who is about to leave this earth on their own accord. Both books provide unique and moving insight into such conversations. Perhaps I now know what I might have said to my grandmother.
Douglas Powell is a graduate student at the University of Guelph.
I wonder about prion diseases because I watched my grandfather degenerate from Alzheimers, and carried my suicidal grandmother into the Barrie, Ontario (that’s in Canada) hospital when I was 20 (that’s her, right, when I was a kid)
It sucked, and has scared me for 35 years.
But after years of therapy, I may be learning to deal with it.
My first book in 1997 was called Mad Cows and Mothers Milk for a reason.
A very personal reason.
A new study has shed light on the mechanisms underlying the progression of prion diseases and identified a potential target for treatment.
Prion diseases are a group of fatal neurological disorders that includes Creutzfeldt-Jakob disease and bovine spongiform encephalopathy (“mad cow disease”). They are caused by the spread of “prions”, which are altered forms of normal cellular proteins. These abnormal molecules then interact with normal proteins to promote misfolding. While we understand that this process of converting normal to abnormal protein is what causes the symptoms of prion disease (including rapidly progressive dementia, seizures and personality changes), the exact mechanism of damage to the neuronal connections in the brain and spinal cord has been poorly understood.
Researchers from Boston University School of Medicine (BUSM) used a method they previously described for culturing nerve cells from the hippocampal region of the brain, and then exposing them to prions, to illustrate the damage to nerve cell connections usually seen in these diseases. They then added a number of different chemical compounds with known inhibitory effects on cellular responses to stressful stimuli, with the objective of identifying which pathways may be involved.
They found that inhibition of p38 MAPKα (an enzyme that typically responds to stress, such as ultraviolet radiation and heat shock) prevented injury to nerve connections and promoted recovery from the initial damage. Hippocampal nerve cells that had a mutation preventing normal function of p38 MAPKα were also protected, seeming to confirm the role the enzyme plays in this disease process.
David. A. Harris, MD, PhD, professor and chair of the Department of Biochemistry at Boston University School of Medicine and corresponding author of the study, sees these findings as a major breakthrough in trying to understand and treat these diseases. “Our results provide new insights into the pathogenesis of prion diseases, they uncover new drug targets for treating these diseases, and they allow us to compare prion diseases to other, more common neurodegenerative disorders like Alzheimer’s disease.”
My grandfather died of Alzheimer’s in the 1980s, when I was a 20-something.
It wasn’t pretty, so stark that my grandmother took her own life rather than spend winter days going to a hospital where the man she had been with for all those years increasingly didn’t recognize her.
Glen Campbell’s death yesterday from Alzheimer’s, and Gene Wilder’s before that, rekindled lots of conflicting emotions.
In 1995, I was a cocky PhD student and about to be a father for the fourth time, when I was summoned to a meeting with, Ken Murray.
I rode my bike to a local golf club, met the former long-time president of Schneiders Meats, and established a lifelong friendship.
When Ken told me about a project he had established at the University of Waterloo in 1993, the Murray Alzheimer Research and Education Program (MAREP), after his wife’s demise from the disease, I said, I can’t understand the hell of being the primary caregiver for so long, but I know of the side-effects.
Ken had heard I might know something of science-and-society stuff, and he actually funded my faculty position at the University of Guelph for the first two years.
Sure, other weasels at Guelph tried to appropriate the money, but Ken would have none of it.
For over 20 years now, I’ve tried to promote Ken’s vision, of making the best technology available to enhance the safety of the food supply.
I’ve got lots of demons, and what I’ve learned is that it’s best to be public about them. It removes the stigma. It makes one recognize they are not alone. It’s humbling (and that is good).
In addition to being an unbelievably gifted songwriter, session player, and hit maker, Glen Campbell was – directly or not – an outstanding advocate of awareness about Alzheimer’s.
Michael Pollack writes in The New York Times obituary that Glen Campbell, the sweet-voiced, guitar-picking son of a sharecropper who became a recording, television and movie star in the 1960s and ’70s, waged a publicized battle with alcohol and drugs and gave his last performances while in the early stages of Alzheimer’s disease, died on Tuesday in Nashville. He was 81.
Tim Plumley, his publicist, said the cause was Alzheimer’s.
Mr. Campbell revealed that he had the disease in June 2011, saying it had been diagnosed six months earlier. He also announced that he was going ahead with a farewell tour later that year in support of his new album, “Ghost on the Canvas.” He and his wife, Kimberly Campbell, told People magazine that they wanted his fans to be aware of his condition if he appeared disoriented onstage.
What was envisioned as a five-week tour turned into 151 shows over 15 months. Mr. Campbell’s last performance was in Napa, Calif., on Nov. 30, 2012, and by the spring of 2014 he had moved into a long-term care and treatment center near Nashville.
Mr. Campbell released his final studio album, “Adiós,” in June. The album, which included guest appearances by Willie Nelson, Vince Gill and three of Mr. Campbell’s children, was recorded after his farewell tour.
That tour and the way he and his family dealt with the sometimes painful progress of his disease were chronicled in a 2014 documentary, “Glen Campbell: I’ll Be Me,” directed by the actor James Keach. Former President Bill Clinton, a fellow Arkansas native, appears in the film and praises Mr. Campbell for having the courage to become a public face of Alzheimer’s.
At the height of his career, Mr. Campbell was one of the biggest names in show business, his appeal based not just on his music but also on his easygoing manner and his apple-cheeked, all-American good looks. From 1969 to 1972 he had his own weekly television show, “The Glen Campbell Goodtime Hour.” He sold an estimated 45 million records and had numerous hits on both the pop and country charts. He was inducted into the Country Music Hall of Fame in 2005.
Decades after Mr. Campbell recorded his biggest hits — including “Wichita Lineman,” “By the Time I Get to Phoenix” and “Galveston” (all written by Jimmy Webb, his frequent collaborator for nearly 40 years) and “Southern Nights” (1977), written by Allen Toussaint, which went to No. 1 on pop as well as country charts — a resurgence of interest in older country stars brought him back onto radio stations.
Like Bobbie Gentry, with whom he recorded two Top 40 duets, and his friend Roger Miller, Mr. Campbell was a hybrid stylist, a crossover artist at home in both country and pop music.
He could be a cut-up in recording sessions. “With his humor and energetic talents, he kept many a record date in stitches as well as fun to do,” the electric bassist Carol Kaye, who often played alongside Mr. Campbell, said in an interview in 2011. “Even on some of the most boring, he’d stand up and sing some off-color country song — we’d almost have a baby trying not to bust a gut laughing.”
After playing on many Beach Boys sessions, Mr. Campbell became a touring member of the band in late 1964, when its leader, Brian Wilson, decided to leave the road to concentrate on writing and recording. He remained a Beach Boy into the first few months of 1965.
Mr. Campbell had his most famous movie role in 1969, in the original version of “True Grit.” He had the non-singing part of a Texas Ranger who joins forces with John Wayne and Kim Darby to hunt down the killer of Ms. Darby’s father. (Matt Damon had the role in a 2010 remake.) The next year, Mr. Campbell and the New York Jets quarterback Joe Namath played ex-Marines in “Norwood,” based on a novel by Charles Portis, the author of “True Grit.”
Mr. Campbell made his Las Vegas debut in 1970 and, a year later, performed at the White House for President Richard M. Nixon and for Queen Elizabeth II in London.
But his life in those years had a dark side. “Frankly, it is very hard to remember things from the 1970s,” he wrote in his autobiography. Though his recording and touring career was booming, he began drinking heavily and later started using cocaine. He would annoy his friends by quoting from the Bible while high. “The public had no idea how I was living,” he recalled.
In 1980, after his third divorce, he said: “Perhaps I’ve found the secret for an unhappy private life. Every three years I go and marry a girl who doesn’t love me, and then she proceeds to take all my money.” That year, he had a short, tempestuous and very public affair with the singer Tanya Tucker, who was about half his age.
He credited his fourth wife, the former Kimberly Woollen, with keeping him alive and straightening him out — although he would continue to have occasional relapses for many years. He was arrested in November 2003 in Phoenix and charged with extreme drunken driving and leaving the scene of an accident. He pleaded guilty and served 10 nights in jail in 2004.
I cried with many emotions when I first watched his documentary, I’ll Be Me.
And I’ll watch it again today with humility, respect and gratitude, to people like Glen and Ken.
I’ve got lots of demons, and what I’ve learned is that it’s best to be public about them. It removes the stigma. It makes one recognize they are not alone. It’s humbling (and that is good).
Gene Wilder was born Jerome Silberman in Milwaukee on June 11, 1933. His father, William, a manufacturer and salesman of novelty items, was an immigrant from Russia. His mother, the former Jeanne Baer, suffered from a rheumatic heart and a temperament that sometimes led her to punish him angrily and then smother him with
“I don’t like show business, I realized,” he said in 2008. “I like show, but I don’t like the business.”
He was by then enjoying a new career as a novelist. His “My French Whore,” published in 2007, was the story of a naïve young American who impersonates a German spy in World War I (“just fluff, but sweet fluff,” the novelist Carolyn See wrote in her review in The Washington Post). It was followed by two more novels, “The Woman Who Wouldn’t” and “Something to Remember You By,” and a story collection, “What Is This Thing Called Love?”
Gina Kolata of The New York Times reports on new research by a team of investigators at Harvard which suggests Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection.
It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease.
The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s.
So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains.
“It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence.
The work began when Robert D. Moir, of Harvard Medical School and Massachusetts General Hospital, had an idea about the function of amyloid proteins, normal brain proteins whose role had long been a mystery.
The proteins were traditionally thought to be garbage that accumulates in the brain with age. But Dr. Moir noticed that they looked a lot like proteins of the innate immune system, a primitive system that is the body’s first line of defense against infections.
Elsewhere in the body, such proteins trap microbes — viruses, fungi, yeast and bacteria. Then white blood cells come by and clear up the mess. Perhaps amyloid was part of this system, Dr. Moir thought.
He began collaborating with Rudolph E. Tanzi, also at Harvard Medical School and Massachusetts General Hospital, in a study funded by the National Institutes of Health and the Cure Alzheimer’s Fund. The idea was to see if amyloid trapped microbes in living animals and if mice without amyloid proteins were quickly ravaged by infections that amyloid could have stopped.
The answers, they reported, were yes and yes.
In one study, the group injected Salmonella bacteria into the brains of young mice that did not have plaques.
“Overnight, the bacteria seeded plaques,” Dr. Tanzi said. “The hippocampus was full of plaques, and each plaque had a single bacterium at its center.”
In contrast, mice that did not make beta amyloid succumbed more quickly to the bacterial infection, and did not make plaques.