Tag Archives: Death

WHAT REALLY KILLED ROBIN WILLIAMS

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On August 11, 2014, entertainment genius Robin Williams took his own life inside his Paradise Cay, California home near San Francisco. The coroner initially ruled that Williams, age 63, died by suicide—asphyxia by hanging antecedent to, or caused by, clinical depression. However, when the final autopsy results were in, an entirely different picture played out. Robin Williams was in the advanced stage of a somewhat common, but almost always undiagnosed, brain disease called Lewy Body Dementia or LBD.

As Williams’ window, Susan Schneider Williams who now represents the Lewy Body Dementia Association, stated, “The disease was a terrorist in my husband’s head. Any way you look at it, the presence of Lewy bodies in his brain took his life. Depression was only a symptom. Unfortunately, we as a culture don’t have the vocabulary to discuss brain disease in the way we do about depression. Depression is only a side effect of LBD—it’s rooted in neurology. His brain was literally falling apart, and not one thing could be done about it.”

Lewy Body is a strange term. We’ll examine where that name came from, what exactly LBD is, what causes it, and how this always-fatal disease can be managed in its three progressive stages: early, mid, and late. But first, let’s have a brief look at this remarkable man’s achievements. Perhaps “remarkable” isn’t a powerful enough word for Robin Williams.

Robin McLaurin Williams was born on July 21, 1951, into an average American family. But from an early age, there was nothing average about him. He showed a God-given gift for improvision comedy and acting. By the early 1970s, Williams was in high demand as a San Francisco-based stand-up comedian, and he went on to be one of the funniest funnies of all time.

Few can forget many of Robin Williams’ outstanding character roles. He got his television start in Mork & Mindy and went on to film. Popeye. Hook. Good Will Hunting. Dead Poets Society. Good Morning Vietnam. The World According to Garp. World’s Greatest Dad. Night at the Museum. The Birdcage. Moscow on the Hudson. Jumanji. And, of course, Mrs. Doubtfire.

Williams also did voice-overs in Aladdin, Robots, and Happy Feet. He won numerous awards—six Golden Globes, five Grammys, two Primetime Emmys, two Screen Actors Guilds, and an Oscar for Best Supporting Actor. As well, Williams won the Cecille B. DeMille award in 2005.

Robin Williams had his struggles through life, though. He was addicted to cocaine and alcohol which set him into fitful mood swings. He was in and out of rehab for years. However, by 2010 he was stable and substance free, except for therapeutic prescriptions issues to combat what was thought to be clinical depression.

It was not. Robin Williams had an undiagnosed brain disorder. A disease that was only discovered after his death and was verified by brain sectioning at his autopsy. What was suspected to be Alzheimer’s or Parkinson’s in the last year of his life turned out to be Lewy’s Body Dementia—a condition under the general dementia umbrella and an extremely deadly disease.

You’re likely wondering what this weird name is and what it entails. Rather than me paraphrasing the information, let’s go to the best source available. No, not Wikipedia or ChatGPT.  It’s the website of the Lewy Body Dementia Association, and here’s what it says:

Lewy body dementia (LBD) is the 2nd most common type of progressive dementia after Alzheimer’s disease. The name comes from a discovery by Dr. Friedrich Lewy in the early 1900s of abnormal bodies or deposits of alpha-synuclein proteins in areas of the brain that can only be verified through an autopsy. These bodies alter the production of dopamine and acetylcholine that are vital neural transmitters.

LBD is not a rare disease. It affects more than a million people in the United States alone. Because LBD symptoms may closely resemble other, more commonly known disorders like Alzheimer’s and Parkinson’s disease, it is widely under-diagnosed.

LBD is an umbrella term for two related diagnoses:

  • A person with dementia with Lewy bodies will develop dementia and other LBD symptoms, one of which may be changes in movement, like a tremor (parkinsonism).
  • With the other form of LBD, people will present first with changes in movement, leading to a Parkinson’s disease diagnosis; over time many will develop dementia years later. This is diagnosed as Parkinson’s disease dementia.

As time passes, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. The earliest symptoms of dementia with Lewy bodies and Parkinson’s disease dementia are different, but both are due to the same underlying biological changes in the brain.

LBD is a multi-system disease and usually requires a comprehensive treatment approach with a collaborative team of physicians and other health care professionals like occupational, physical, or speech therapists. Early diagnosis and treatment may extend your quality of life and independence. Many people with LBD enjoy significant lifestyle improvement with a comprehensive treatment approach, and some may even experience little change from year to year.

For a more in-depth explanation of Lewy Body Dementia disease, here’s a trip to the medical research department at Johns Hopkins University:

Lewy Body Disease (LBD) is a complex and often misunderstood neurodegenerative disorder that affects millions of individuals worldwide. Characterized by the accumulation of abnormal protein deposits called Lewy bodies in the brain, LBD poses significant challenges to both patients and caregivers. In this article, we delve into the neurological aspects of LBD, exploring its development, detection, effects on the human body, and its associated symptoms.

Development of Lewy Body Disease

Lewy Body Disease primarily affects older adults, typically manifesting after the age of 50. While the exact cause of LBD remains unknown, researchers believe that a combination of genetic, environmental, and lifestyle factors may contribute to its development. Genetic mutations, particularly in genes associated with the production and clearance of alpha-synuclein protein, have been implicated in some cases of familial LBD. However, most cases of LBD occur sporadically without a clear genetic link.

Neurological Pathology

At the core of LBD pathology is the abnormal accumulation of alpha-synuclein protein, forming Lewy bodies within neurons. These protein aggregates disrupt normal cellular function and communication within the brain, leading to widespread neurodegeneration. Areas of the brain particularly affected by Lewy bodies include the substantia nigra, which plays a crucial role in movement control, and the cerebral cortex, responsible for cognitive functions.

Detection and Diagnosis

Diagnosing LBD can be challenging due to its overlapping symptoms with other neurodegenerative disorders such as Parkinson’s disease and Alzheimer’s disease. A comprehensive medical history, neurological examination, and a battery of neuropsychological tests are often employed to assess cognitive function, motor abilities, and psychiatric symptoms.

Brain imaging techniques, such as MRI and PET scans, may reveal characteristic patterns of brain atrophy and dysfunction associated with LBD. Additionally, a definitive diagnosis of LBD can only be made post-mortem through the examination of brain tissue for the presence of Lewy bodies.

Effects on the Human Body

Lewy Body Disease has profound effects on both motor and non-motor functions, significantly impacting quality of life. Motor symptoms include bradykinesia (slowed movements), rigidity, tremors, and gait disturbances resembling those seen in Parkinson’s disease. Non-motor symptoms encompass cognitive impairment, hallucinations, fluctuations in attention and alertness, sleep disturbances, autonomic dysfunction (such as orthostatic hypotension and urinary incontinence), and psychiatric manifestations like depression and anxiety.

Treatment and Management

While there is no cure for Lewy Body Disease, various treatment strategies aim to alleviate symptoms and improve patients’ quality of life. Medications targeting dopamine levels in the brain, such as levodopa, may help alleviate motor symptoms. Cholinesterase inhibitors, commonly used in Alzheimer’s disease, may improve cognitive function and psychiatric symptoms in some LBD patients. Multidisciplinary approaches involving physical therapy, occupational therapy, speech therapy, and psychological support are essential for managing the diverse array of symptoms associated with LBD.

Takeaway

Lewy Body Disease presents a complex clinical picture characterized by the interplay of motor, cognitive, and psychiatric symptoms. Understanding its neurological underpinnings is crucial for early detection, accurate diagnosis, and effective management of the disease. Ongoing research efforts aimed at unraveling the molecular mechanisms underlying LBD pathogenesis hold promise for the development of targeted therapies that can ultimately improve outcomes for individuals living with this challenging condition.

I’ll jump back to the Lewy Body Dementia Association for the diagnostic symptoms of the disease.

Motor Symptoms

  • Bradykinesia (slowed movements)
  • Rigidity (stiffness)
  • Tremors (usually less prominent than in Parkinson’s disease)
  • Gait disturbances (shuffling gait, balance problems)

Cognitive Symptoms

  • Fluctuating attention and alertness
  • Memory loss
  • Executive dysfunction (problems with planning, organizing, and problem-solving)
  • Visuospatial difficulties (problems with spatial awareness and perception)

Psychiatric Symptoms

  • Hallucinations (visual hallucinations are particularly common)
  • Delusions (often related to the hallucinations)
  • Depression
  • Anxiety
  • Apathy
  • Irritability or aggression
  • Sleep disturbances (REM sleep behavior disorder, vivid dreams, acting out dreams)

Autonomic Dysfunction

  • Orthostatic hypotension (drop in blood pressure upon standing)
  • Urinary incontinence or urgency
  • Constipation
  • Erectile dysfunction (in men)

Other Symptoms

  • REM sleep behavior disorder (acting out dreams physically)
  • Sensitivity to neuroleptic medications (may worsen symptoms)
  • Changes in sense of smell
  • Difficulty swallowing (dysphagia)

Note that not all individuals with LBD will experience all of these symptoms, and the severity and combination of symptoms can vary widely from person to person. Additionally, symptoms may fluctuate over time, with periods of relative stability interspersed with episodes of worsening symptoms. Early recognition and management of these symptoms are crucial for improving the quality of life for individuals living with LBD.

Detecting and verifying Lewy Body Disease (LBD) involves a comprehensive approach that combines clinical evaluation, neurological assessments, and diagnostic tests. Here’s a breakdown of the steps involved in the detection and verification process.

Clinical Evaluation

  • A thorough medical history is obtained from the patient and their caregivers, focusing on the onset and progression of symptoms.
  • A neurological examination is conducted to assess motor function, cognitive abilities, and psychiatric symptoms. This may include assessing gait, muscle tone, reflexes, coordination, memory, attention, and mood.
  • Careful observation of symptom patterns, including fluctuations in cognition and alertness, visual hallucinations, and motor symptoms resembling Parkinson’s disease.

Diagnostic Criteria

  • LBD is diagnosed based on established clinical criteria, such as the consensus criteria proposed by the DLB Consortium or the McKeith criteria.
  • These criteria outline the characteristic features and diagnostic markers of LBD, including cognitive fluctuations, visual hallucinations, Parkinsonism, and rapid eye movement (REM) sleep behavior disorder.
  • Criteria may also specify supportive features, such as neuroimaging findings and autonomic dysfunction, which further support the diagnosis of LBD.

Neuropsychological Assessment

  • Neuropsychological tests are administered to evaluate cognitive function, including memory, attention, executive function, and visuospatial abilities.
  • These tests help quantify cognitive impairment and track changes over time.

Neuroimaging Studies

  • Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans may be performed to assess brain structure and function.
  • MRI may reveal patterns of cortical atrophy and changes in brain volume associated with LBD.
  • PET imaging with radiotracers targeting dopamine transporters or amyloid plaques can provide additional evidence supporting the diagnosis and differentiate LBD from other neurodegenerative disorders like Alzheimer’s disease.

Cerebrospinal Fluid Analysis

  • Lumbar puncture may be performed to analyze cerebrospinal fluid (CSF) biomarkers associated with LBD, such as levels of alpha-synuclein protein and markers of neuroinflammation.
  • While not routinely performed, CSF analysis can provide supplementary information to support the diagnosis of LBD in some cases.

Genetic Testing

  • Genetic testing may be considered in cases of familial LBD or when there is a strong family history of neurodegenerative diseases.
  • However, genetic testing is not typically performed as part of routine diagnostic evaluation for sporadic LBD.

Multidisciplinary Evaluation

  • A multidisciplinary team approach involving neurologists, neuropsychologists, geriatricians, psychiatrists, and other healthcare professionals is often utilized to ensure a comprehensive assessment and accurate diagnosis of LBD.
  • Verification of LBD relies on the integration of clinical findings, diagnostic tests, and adherence to established diagnostic criteria.
  • Given the complexity and variability of LBD presentation, accurate diagnosis and ongoing monitoring are essential for effective management and supportive care.

Treatment Options

  • LBD is a multi-system disease and typically requires a comprehensive treatment approach, meaning a team of physicians from different specialties, who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms.  ​
  • A comprehensive treatment plan may involve medications, physical, occupational, speech or other types of therapy, and counseling.

Medications

  • There are many treatments that can help with the symptoms; all medications prescribed for LBD are approved by the Food and Drug Administration to treat symptoms in other diseases, like Alzheimer’s disease and Parkinson’s disease.
  • These medications can offer symptomatic benefits for cognitive, movement, sleep, mood and behavioral changes in LBD.
  • There are not yet any medications that slow or stop the progression of LBD.

Cognitive Symptoms

  • Medications called cholinesterase inhibitors are considered the standard treatment for cognitive symptoms in LBD.
  • These medications were developed to treat Alzheimer’s disease. However, some researchers believe that people with LBD may be even more responsive to these types of medications than those with Alzheimer’s.
  • These drugs sometimes help control behavior problems and hallucinations as well.
  • Another medication that may be helpful is memantine (Namenda).

Movement Symptoms

  • Movement symptoms may be treated with a Parkinson’s medication called carbidopa/levodopa (Sinemet), but if the symptoms are mild, it may be best to not treat them in order to avoid potential medication side effects.

Visual Hallucinations

  • If the hallucinations are not disruptive, they may not need to be treated. However, if they are frightening or create challenging behavioral changes, a physician may recommend treatment.
  • Cholinesterase inhibitors are sometimes effective in treating hallucinations and other psychiatric symptoms of LBD. In addition, newer ‘atypical’ antipsychotic medications may be tried.
  • Most LBD experts prefer quetiapine or clozapine when treatment is necessary for safety or quality of life concerns.
  • Caution is required to find the lowest effective dose in this situation.
  • A newer medication, pimavanserin, was approved to treat psychosis in Parkinson’s disease; results from another clinical trial of this medication in people with dementia and psychosis are pending.
  • While older ‘traditional’ antipsychotic medications such as thorazine and haloperidol are commonly prescribed for Alzheimer’s patients with disruptive behavior, these medications may cause severe side effects in those with LBD.
  • For this reason, older traditional antipsychotic medications like haloperidol should be avoided.

WARNING: Up to 50% of LBD patients treated with any antipsychotic medication may have a severe reaction, such as worsening confusion, heavy sedation, and increased or possibly irreversible parkinsonism. If severe fever or muscle rigidity occurs, contact your doctor immediately; you may have a potentially life-threatening condition that is treated by stopping the medication.

REM Sleep Behavior Disorder (RBD)

  • RBD can be quite responsive to treatment, so your physician may recommend a medication like melatonin and/or clonazepam.

Medication Side Effects

  • Speak with your doctor about possible side effects.
  • The following drugs may cause sedation, motor impairment, or confusion:
  • Benzodiazepines, tranquilizers like diazepam and lorazepam
  • Anticholinergics (antispasmodics), such as oxybutynin and glycopyrrolate
  • Older antidepressants
  • Certain over-the-counter medications, including diphenhydramine and dimenhydrinate.
  • Some medications, like anticholinergics, amantadine, and dopamine agonists, which help relieve parkinsonian symptoms, might increase confusion, delusions, or hallucinations.

Surgery and Anesthesia

  • Be sure to meet with your anesthesiologist in advance of any surgery to discuss medication sensitivities and risks unique to LBD.
  • People with LBD often respond to certain anesthetics and surgery with acute states of confusion or delirium and may have a sudden significant drop in functional abilities, which may or may not be permanent.
  • Possible alternatives to general anesthesia include a spinal or regional block. These methods are less likely to result in postoperative confusion.
  • If you are told to stop taking all medications prior to surgery, consult with your doctor to develop a plan for careful withdrawal.

Other Types of Treatments

  • Lifestyle interventions include eating a healthy diet, exercising, and remaining socially active.
  • Physical therapy includes cardiovascular, strengthening and flexibility exercises, as well as gait training.
  • Speech therapy may improve low voice volume, poor enunciation, muscular strength, and swallowing difficulties.
  • Occupational therapy helps maintain skills and promotes functional ability and independence.
  • Music and aromatherapy may reduce anxiety and improve mood.
  • Individual and family psychotherapy may be useful for learning strategies to manage emotional and behavioral symptoms and to help make plans that address individual and family concerns about the future.
  • Support groups may be helpful for caregivers and persons with LBD to identify practical solutions to day-to-day frustrations and to obtain emotional support from others.

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This might be a lot of cut & pasted material—some maybe repetitive—however I think it’s important to be aware of Lewy Body Dementia.

So far, LBD is incurable but somewhat manageable if detected early-on. Our population is aging. Today’s demographics represent an ever-increasing older population, and the numbers are that many of our folks and friends around us, including ourselves, will develop some form of a degenerative brain disorder like LBD which is what really killed Robin Williams.

IT’S TIME FOR A NEW SCIENCE OF DEATH

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Is there life after death? That’s a question folks have asked since the dawn of humanity. Historically, the answer has been faith-based. But today, modern science is closer to the truth following a major medical discovery at the University of Michigan. However, it depends on what your definition of life is. And your definition of death.

In 2014, a 24-year-old woman collapsed at home. She was taken to Emergency at U of M medical center where staff were unable to regain her consciousness. They moved her to the Intensive Care Unit (ICU), and she remained in ICU for four days while hooked to an electroencephalograph (EEG) to monitor her brain function. It showed she was in “brain death”.

Despite being on organic life support, (heart-lung machine) she flatlined on the electrocardiogram (ECG) monitor and went into cardiac arrest with her respiration ceasing — “clinical death” as it’s commonly called. Because her physical death seemed inevitable during the four days, her family had signed a Do Not Resuscitate (DNR) order. The woman remained in her bed, not breathing nor beating, and was still connected to the EEG for some time before she was removed to the morgue.

That was the end of this woman’s bodily life. Her physical life. But it wasn’t the end of her conscious life. In 2022, a researcher at the U of M reviewed the woman’s EEG charts and found that, astonishingly, at the moment of clinical death the woman’s brain came back to life—in fact into a hyperdrive in activity in the regions associated with consciousness. According to the researcher, “Something happened in that brain that makes no sense at all.”

We’ll closely examine what took place in that ward where Patient One, as she’s now known in the medical research community, physically passed away. And we’ll look at what consciousness, as that term applies to living human beings, might be. First, let’s review the definitions of death as they apply to clinical death and brain death, which are two separate deals. And see if it’s time for a new science of death.

I found a great death explanation resource at the United States National Library of Medicine. At their National Center for Biotechnology Information (NCBI) section there’s a multi-part series, one of which is titled Definitions of Death: What and When is Death? Interestingly, they divide it into two aspects. One is biological death. The other is social death.

To quote them. “The commonplace notion of death is to characterize it as an end state: being dead. Nevertheless, being dead is not the same as the event of death or the dying process.

Biological death can be understood as:

  1. A final event.
  2. An absolute state: being dead.
  3. Part of the dying process.

The absolute state of being dead is synonymous with the idea of medical or clinical death—where an individual has sustained irreversible cessation of circulatory and respiratory functions or irreversible cessation of all functions of the entire brain, including the brain stem.

Social death is a relational change in the meaning of a human life. It involves a change in the narrative identity of persons that either still biologically exist or have once existed.”

Biological death and social death, as set out in the NCBI paper, is broader coverage than what’s usually weighed in the mainstream medical community, such as physicians and coroners would use. From my experience in the death investigation business, we almost always relied on the clinical death measurement rather than the brain death evaluation. That’s because very few deaths are recorded on EEGs, and there is no brain activity to monitor. Therefore, the declaration of death usually refers to the standard definition of clinical death which is:

The cessation of blood circulation and breathing; the two criteria necessary to sustain human life.

Brain death is a different matter—the classic definition being:

The complete and irreversible loss of brain function to the point where there is no return.

So, is it possible to be dead and alive at the same time? Apparently, yes, as in the case of Patient One whose circumstances we’ll examine shortly. Before that, let’s look at the Florida Boy case as reported in the NCBI literature.

Florida Boy is a legal precedent of a boy who spent 14 years in an ICU connected to a heart-lung machine after an initial diagnosis of complete and total brain failure. He showed no EEG activity at all during that time. His parents demanded that he be artificially ventilated, fed, and hydrated in the hospital.

Over the 14 years, the boy biologically grew into a man as if he were normal—except in total death as in any form of consciousness. Interestingly, as his thorax and abdomen organ cellular activity functioned normally, his brain cells gradually replaced themselves and became a “grey goo of ghost-like tissues”. Apparently, without brain activity, the entire cerebral system decomposes. Not so with the neck-down region. The boy-turned-man was eventually disconnected via a court order, and he completed his clinical death cycle.

Let’s return to Patient One. Dr. Jimo Borjigin is a professor of neurology at the University of Michigan. As a project of interest, she investigated reports of Near Death Experiences (NDE) reported by resuscitated patients. Her studies expanded into those who were officially ‘brain dead” as in EEG monitored while still clinically alive. She stumbled upon the Patient One records and found an anomaly never before seen in medical experience.

Here’s Dr. Borjigin’s account:

—   —

In the moments after Patient One was taken off oxygen, there was a surge of activity in her dying brain. Areas that had been nearly silent while she was on life support suddenly thrummed with high-frequency electrical signals called gamma waves. In particular, the parts of the brain that scientists consider a “hot zone” for consciousness became dramatically alive. In one section, the signals remained detectable for more than six minutes. In another, they were 11 to 12 times higher than they had been before Patient One’s ventilator was removed.

As she clinically died, Patient One’s brain was functioning in a kind of hyperdrive. For about two minutes after her oxygen was cut off, there was an intense synchronization of her brain waves, a state associated with many cognitive functions, including heightened attention and memory. The synchronization dampened for about 18 seconds, then intensified again for more than four minutes. It faded for a minute, then came back for a third time.

In those same periods of dying, different parts of Patient One’s brain were suddenly in close communication with each other. The most intense connections started immediately after her oxygen stopped and lasted for nearly four minutes. There was another burst of connectivity more than five minutes and 20 seconds after she was taken off life support.

In particular, areas of her brain associated with processing conscious experience—areas that are active when we move through the waking world, and when we have vivid dreams—were communicating with those involved in memory formation. So were parts of the brain associated with empathy. Even as she slipped irrevocably deeper into death, something that looked astonishingly like life was taking place over many minutes in Patient One’s brain.

Those glimmers and flashes of something like life contradict the expectations of almost everyone working in the field of resuscitation science and near-death studies. The predominant belief—expressed by Greyson, the psychiatrist and co-founder of the International Association of Near Death Studies, in the Netflix series Surviving Death—was that as soon as oxygen stops going to the brain, neurological activity falls precipitously. Although a few earlier instances of slight and fading brain waves had been reported in dying human brains, nothing as detailed and complex as what occurred in Patient One had ever been detected.

Given the levels of activity and connectivity in particular regions of her dying brain, I believe it’s likely that Patient One had a profound near-death experience with many of its major features: out-of-body sensations, visions of light, feelings of joy or serenity, and moral re-evaluations of one’s life. Of course, Patient One did not recover, so no one can prove that the extraordinary happenings in her dying brain had experiential counterparts.

—   —

Near Death Experiences. NDEs. Are these events of total imagination? Or are they completely real?

We’ve all heard the stories—the familiar kitsches of NDEs. Being elevated from the operating table. Floating toward an immense light. Traveling down a tunnel. Complete bliss and harmony. Being beckoned by an infinite intelligence. Meeting dead relatives. And not wanting to return to normal life.

While these NDE experiences can be simulated by taking a hero’s worth of ketamine, almost all reports come from rational and sober people who clearly felt they went through something extraordinary. Some say paranormal. Others say supernatural.

This brings us to that mysterious and mostly unknown subject of consciousness. Almost nothing is solidly understood about what consciousness really is. Partly, that’s because no one has found a way to isolate and measure consciousness—it’s very difficult (almost impossible) to fund studies that can’t be isolated and measured.

Dr. David Chalmers is a world-leading consciousness researcher. (I wrote a blog post on Chalmers and his consciousness theories a few years ago. You can read it here.) Dr. Chalmers posits that consciousness may be a fundamental property of the human brain and that consciousness may be a universal entity of the cosmos that sends signals to us. Chalmers breaks consciousness into two arenas—the easy problem of recognizing that it exists and the hard problem of explaining how it operates. Or what it is.

All of us experience at least two consciousness forms. One is our awake state, which you’re in at the present. The other is our asleep state, also known as the subconscious. As long as we’re “alive”, both states exist and are vital to our function and survival.

So, what gives with someone like Patient One? Why was she clinically dead—according to the standard description—after she flatlined in the ICU—yet came fully alive in her once-thought-dead brain? The answer seems to be that death, clinical and brain, is not a precise time point. Rather, both are processes that can take extensive linear time to complete.

There are countless stories of people being resuscitated minutes and even hours after their hearts stopped beating and their lungs stopped breathing. Many events occurred in hypothermic conditions; temperature being a huge life-preservation factor. But bringing someone back from brain death? It’s never been recorded before Dr. Borjigin stumbled upon Patient One’s charts.

This seems to be because no one has looked at this angle before. Once a patient flatlines in a medical environment and there’s no resuscitation made, there’s no reason to review the EEG charts—if there even are recordings. It’s just shut things down, shroud them, send them downstairs, and move on to the next.

Makes me wonder how many people are written off for dead when they’re still very much alive.

Maybe it’s time for a new science of death.

THE SUDDEN (SUSPICIOUS?) DEATH OF U.S. PRESIDENT WARREN G. HARDING

One hundred years ago, on August 2nd, 1923, Warren G. Harding, the 29th President of the United States, suddenly died in a San Francisco hotel room. He was 57 years old. Immediately—due to no autopsy insisted upon by the ironclad demand from his wife, Florence Harding, and the fact that his body was embalmed one hour after death—suspicious rumors of foul play circulated. Conspirators came in many forms. Corrupt politicians, scandal cover-ups, quack physicians, and foreign operatives. But the most sinister accusation of all was Harding being intentionally poisoned by his wife.

The official cause of death released in press statements by the attending doctors was a “probable cerebral apoplexy”. In other words, President Harding had a stroke, a fatal brain event. There was no mention of any toxicity through poison nor any suggestion of a chronic cardiac condition, a heart attack.

Harding’s body was returned by train to Washington, DC, lay in state for two days, then was transported again by train to his hometown of Marion, Ohio where he was entombed in a marble crypt. His wife, Florence, died the following year of kidney failure and came to rest beside him. As the years passed, the truth of the Harding Administration emerged. It became known as America’s most scandalous presidency.

Extramarital lovers, illegitimate children, political corruption, cronies, bribes, payoffs, and even suicides emerged that painted a black mark on Harding’s history. The persistent suspicion of cover-up in his death failed to go away. Today, there’s a consensus as to what really happened in Harding’s death. We’ll get to that conclusion but, first, let’s look at who Warren Harding was, how he got to the White House, and how he came to die in that San Francisco hotel room.

Warren Gamaliel Harding was born on November 3rd, 1865—the year the Civil War ended—on his grandfather’s farm near Blooming Grove, Ohio. His father was a small-town physician with a small practice that earned little money. His mother was a devoutly religious homemaker with eight children to care for, including Warren who was the oldest. Harding was an average student but a very strong boy with even stronger work ethic.

Following grade school, Harding attended Ohio Central College graduating in 1882 with a B.S. degree (which grounded him as a later politician). Here he  gained experience editing and publishing the college paper. After college, Harding worked at various jobs such as a barn painter, a railroad laborer, and a horse team driver. It was in Marion, Ohio where Warren Harding got his first business break.

Harding had saved enough money to purchase a failing newspaper in Marion. He parlayed it into a profitable venture in which he wore all hats—reporter, editor, and publisher. These roles allowed Harding to get well connected and form the “Marion Gang” whom he nepotistically took with him through his political career, including placing some of these friends and allies in high-ranking service jobs in the United States federal government. That was to come back and haunt him.

In the late 1880s, Warren Harding met Florence Kling at a community dance. He became smitten with Florence who was the daughter of a banker and Marion’s richest man. Amos Kling did not approve of Warren Harding and warned Florence that Harding “would never amount to anything”. He refused to speak to Harding.

Florence Harding went to work in their newspaper business. She also got active in his political ambitions. “The only things I know are publishing and politics,” Florence was quoted as saying. She was especially good at politics.

History—now one hundred years after Harding’s death—records Harding to be an excellent speaker, very personable with a great memory for people, a driven man, but not too bright. Florence was smart, and she used her intelligence to make connections and pave roads for Harding to travel as he moved up the Ohio political ladder.

Warren Harding served as an Ohio State Senator from 1900 to 1904. From then to 1906 he was the Lieutenant Governor of Ohio, and in 1910 he ran as Ohio’s Governor but was defeated. Harding went back to the paper industry but in 1915 he entered federal politics and won a seat as a Senator for the State of Ohio. This opened doors in Washington.

The Republican national convention was deadlocked in the 1920 presidential selection race. Ultimately, the delegates chose Warren Harding as a compromise candidate. He went on to represent the Republicans as a moderate in the November 1920 presidential election. Together with running mate Calvin Coolidge, they won a landslide victory over the Democrats.

Warren G. Harding was inaugurated as the 29th United States President on March 4th, 1921. He ran on the slogan “Return to Normalcy” which fit his leadership style. America was only two years past the end of WWI and the public longed for a return to pre-war normal. The country was in a financial recession with what many Americans thought was unnecessary ties still with foreign countries.

Harding focused on a protectionist America by lowering taxes, increasing foreign tariffs, and getting the country out of the League of Nations process that dynamited Woodrow Wilson’s presidency. In one year after taking off, the country rebounded and began prosperity never seen before. It was the Roaring Twenties.

Warren Harding was a hands-off president. He appointed people he thought he could trust into high office and let them loose to do their jobs. His error was not holding them accountable and, given human nature, even his closest friends began to abuse their positions for personal gain.

Harding’s other error—his vice and weakness—was womanizing, drinking, and gambling. Rumors put him having secret tunnels under the White House where he would smuggle his girls in and ply them with illegal alcohol. (Remember, this era was the start of Prohibition.) Harding’s poker games were legendary as well as a well-known fact that he supported mistresses and had at least one illegitimate daughter. Warren and Florence were childless.

Among the brewing political and criminal crises was what’s known as the Teapot Dome Scandal. This involved an oil-producing region in Wyoming that held reserves set apart for the U.S. Navy. Harding had appointed his close Marion Gang friend, Albert B. Fall, as Secretary of the Interior who oversaw the federal lands at Teapot Dome and had the power to award oil production contracts. Fall pocketed hundreds of thousands of payoff money for preferential treatment. This scandal (among others), which Harding knew about, had the potential to have President Harding impeached.

It was under this stressful black cloud that Warren Harding departed Washington on his “Voyage of Understanding” cross-country train and ship tour in June of 1923. Members of Harding’s staff observed his health rapidly deteriorating. A once vibrant man with the world’s best handshake was notably nervous and privately conferring with advisors about how to diffuse the runaway in the Marion Gang.

“I can take care of my enemies all right. But my damn friends… they’re the ones that keep me walking the floor at night,” Harding said to one aide. To another, “If you knew of a great scandal in our administration, would you for the good of the country and the party expose it publicly, or would you bury it?”

President Harding’s tour took him across the west and up to Alaska. He spoke before hundreds of thousands of common folks in places like St. Louis, Kansas City, Denver, Salt Lake City, Helena, and Spokane. He went to a small Alaskan village called Metlakatla, then did a by-stop in Vancouver, Canada before heading straight for San Francisco and checking into the Palace Hotel with an extensive entourage including the future president Herbert Hoover who was his Secretary of Commerce.

Harding’s health had been going downhill since leaving Washington. The stress of his job and unfolding issues gave him a malady then diagnosed as neurasthenia which is an overly nervous condition where the sufferer is unable to relax. Compounding this condition, including non-recognizing many presenting symptoms of bad physical health, was the president’s personal doctor.

Charles E. Sawyer was part of the Ohio Gang. Sawyer wasn’t a trained physician. He was an odd, self-taught homeopath who prescribed plants and birds and rocks and things (not sure about sand and hills and rings) as substitutes for accepted medical practices. But Sawyer was a likable, down-homey Oh-Hi-Yo officially forehead-stamp-approved by Mrs. Harding who saw Sawyer as a 1920s genuine guru teaching them a better way.

Harding also traveled with a real doctor—Joel T. Boone. Dr. Boone knew Harding was critically ill and telegrammed ahead from Alaska to San Francisco, having two of the country’s leading cardiology specialists standing by. These were Dr. Ray Lyman Wilbur, the president of the American Medical Society, and Dr. Charles Cooper, the leading cardiac surgeon in the USA.

Dr. Boone knew what was happening.  President Harding was presenting these symptoms:

  • Severe abdominal and thoracic pains as in a crushing weight on the chest
  • Pain radiating down both arms
  • Shortness of breath
  • Dyspnoea at night
  • Nausea
  • Severe bouts of indigestion
  • Off and on fever—chills & sweats
  • Exhaustion after little energetic effort
  • Foul acetonic breath

Dr. Boone knew President Harding was suffering congestive heart failure and likely experienced a series of myocardial infarctions where his enlarged heart muscles were quickly failing. Boone knew Harding’s heart was likely to stop, and that he would suddenly die.

That happened at 7:20 pm on August 2nd, 1923. President Harding was in his hotel suite with his wife and two nurse care aids. Florence was reading a favorable column in the Saturday Evening Post. Harding remarked, “That is good. Go on.”

Florence continued when, with only a shudder and not a sound, the President of the United States stiffened, laid back on the bed, and instantly died.

President Harding’s staff came into the room. That included Herbert Hoover and Doctors Sawyer, Boone, Wilbur, Cooper, and another cardiac expert, Hubert Work. These medical practitioners debated the primary cause of death.

They knew the American public would immediately want to know what happened to their Commander-in-Chief and be assured nothing illegal, conspirator, or dark was behind the president’s sudden and unexpected death—especially when the official reports released to the following press during the Voyage of Understanding assured that Warren Harding was a man fit to competently hold office and guide the nation.

The doctors knew, under the circumstances, that no conclusive cause of death could be established without a complete and thorough autopsy. To this, Florence Harding was fiercely opposed. As Doctor Wilbur put it in his notes written the next day, “We shall never know exactly the immediate cause of President Harding’s death since every effort that was made to secure an autopsy was met with complete and final refusal by Mrs. Harding.”

Knowing that the public must be notified of the president’s death as soon as possible and that they would demand to know what happened—what the true cause of death was—the team of five physicians signed this statement:

Realizing their rush to judgment without medical evidence (and strongly suspecting a myocardial infarction or a heart attack), they released this second statement twenty minutes later:

Stroke of Cerebral Apoplexy. Myocardial Infarction. Let’s look at what these medical terms mean.

So how did the 1923 American public and folks over the last one hundred years go from accepting that President Warren G. Harding died of natural causes to a conspirator suspicion that he was murdered—possibly by his wife?

I think a few reasons. One is the president’s staff poorly handled the president’s health information. One day the president was strong as an ox. The next day he died.

There was no autopsy. His body was embalmed an hour after death. And this was through an ironclad order from the wife, Florence Harding, who knew full well of her husband’s infidelity and unwinding scandals.

Note: I cannot find anything in historical notes to determine if there was a San Francisco coroner having jurisdiction and the authority to hold the body while an independent autopsy was done. Or if any other authorities like the SF police were notified.

The other factor was the collective doctors’ stick handling of the “probable cause of death.” They were aware of the public backlash for knowing how serious the president’s medical condition and the perception of them not being seen to do something about it and prevent his death, but they first wrote it off as an unpredictable and unpreventable stroke, not a preventable heart attack. From Dr. Wilbur’s notes:

“In the aftermath, we were belabored and attacked by the newspapers antagonistic to Harding, and by the cranks, quacks, antivisectionalists, nature healers, the Dr. Albert Abrams electronic-diagnostic group, and many others. We were accused of starving the president, overfeeding him to death, of assisting in slowly poisoning him, and plying him to death with pills and purgatives. We were accused of being abysmally ignorant, stupid and incompetent, and even of malpractice. We were said to have forced our way to Harding’s bedside “through political pull and for political reasons.”

But the craziest theory of them all came from a book written by Gaston B. Means in 1930 titled The Strange Death of President Harding. Means claimed that Florence Harding murdered her presidential husband with poison. Without a shred of evidence, Means suggested two motives. One was because of her husband’s cheating. The other was to save him the embarrassment of the scandals. Gaston Means, by the way, went to jail over a con job in scamming the Charles Lindberg baby homicide case.

One hundred years have passed since United States President Warren G. Harding passed. There’s no doubt Harding had a fatal heart attack. That’s life, but the fallout from living the presidential life sucks. Here are lines from Herbert Hoover while dedicating a memorial to President Harding:

We saw him gradually weaken not only from physical exhaustion but from mental anxiety. Warren Harding had a dim realization that he had been betrayed by a few of the men whom he trusted, by men whom he believed were his devoted friends. That was the tragedy of the life of Warren Harding.