Homeless Scholar Blog ~ GLOBAL WARMING SO FAR

“As a dam built across a river causes a local deepening of the stream, so our atmosphere, thrown as a barrier across the terrestrial rays, produces a local heightening of the temperature at the Earth’s surface.” – John Tyndall, 1862

Even before John Tyndall’s experiments, the French scientist Joseph Fourier (also known for the Fourier transform, the math which makes the MRI coherent), realized that Earth’s atmosphere retains heat radiation, thus discovering the “greenhouse effect”. Fourier’s work was extended in the early 20th century by Svante Arrhenius, who was the first to make actual calculations of it.

The United States Geological Survey (USGS) which is part of the Dept. of the Interior, notes that global warming is just one part of climate change. The former “refers to the rise in global temperatures due mainly to the increasing concentrations of greenhouse gases in the atmosphere” and the latter “refers to the increasing changes in the measures of climate over a long period of time–including precipitation, temperature, and wind patterns.”

The Union of Concerned Scientists has listed 10 signs of global warming: Arctic sea ice extent is diminishing; ocean heat content is increasing; air temperature over ocean is increasing; sea surface temperature is increasing; global sea level is rising; humidity is increasing (causing more warming); temperature of the lower atmosphere is increasing; air temperature over land is increasing; snow cover is reduced, and snow is melting earlier; and glaciers are melting.

Increased evaporation from rising temperatures will lead to more storms as well as more drying of some land masses. “As a result,” says NASA, “storm-affected areas are likely to experience increases in precipitation and increased risk of flooding, while areas located far away from storm tracks are likely to experience less precipitation and increased risk of drought.”

While there are “climate skeptics” among scientists–arguing that current modeling is inaccurate, that natural (or unknown) causes are to blame and/or that global warming will have few consequences–the general consensus is that the planet is warming in an ominous way and that this has been caused by Homo sapiens. “Some scientific conclusions or theories,” wrote the United States National Research Council,” have been so thoroughly examined and tested, and supported by so many independent observations and results, that their likelihood of subsequently being found to be wrong is vanishingly small. Such conclusions and theories are then regarded as settled facts. This is the case for the conclusions that the Earth system is warming and that much of this warming is very likely due to human activities.”

In an attempt to set internationally binding emissions reduction targets, the Kyoto Protocol was adopted in 1997 and entered into force in 2005. The US withdrew from it in 2001, and Canada ten years later, but there are still 192 parties on board. The Paris Agreement (2015) may succeed because it allows individual countries to adjust their climate strategies, and there are no legally binding terms in it.

The Intergovernmental Panel on Climate Change is the United Nations body which assesses the science related to climate. Formed in 1988, it has published a series of reports on climate change, the most recent being one in 2018 on global warming of 1.5 degrees Centigrade. The IPCC has stated that “Climate-related risks to health, livelihoods, food security, water supply, human security, and economic growth are projected to increase with global warming of 1.5 degrees Centigrade [above pre-industrial levels] and increase further with 2 degrees C. (Although the Industrial Revolution dates back to the 18th century, the IPCC is using “pre-industrial” to refer to the latter half of the 19th century, when industrialization intensified.) If the rise in global temperature is not stabilized at a maximum of 1.5 deg C., by approximately 2030, climate scientists warn that the process will become uncontrollable, with widespread drought, floods,, and increases in extreme heat as well as in poverty. “As the report outlines,” notes the Climate Reality Project,  “if we want to hold the line at 1.5 degrees, we have to slash emissions by about 45% from 2010 levels by 2030. Then, we have to reach net-zero around 2050.”

(A word about albedo: This is the solar reflective power, the fraction of incident light or electromagnetic radiation that is reflected by a surface or body (as the moon, a planet, a cloud, the ground, or a field of snow). Its relevance to global warming is not hard to see. As icy surfaces decrease in area, less energy is reflected into space, and the earth will warm up even more, accelerating sea level rise. (This seems straightforward enough, but there are complex and even contradictory findings in albedo research, thus definite statements about the future with respect to the albedo effect cannot reliably be made at this time.))

In May 2019, the UN released a major report on biodiversity, stating that a million species of plants and animals are at risk of extinction due to deforestation, overfishing, pollution, and other human activities. “In parts of the ocean,” says National Geographic, ‘ little life remains but green slime.”

An ecologist at the University of California has stated that “we’re in the middle of the sixth great extinction, but it’s happening in slow motion.” A mass extinction event (also known as “biotic crisis”) occurs when the rate of extinction increases with respect to the rate of speciation. The oldest extinction was the Ordovician (445 million years), likely caused by an ice age. This was followed by the Devonian (375-360 million years ago; oceanic oxygen depletion); the Permian (252 million years ago; asteroid impact and volcanic activity; 95% of species were lost); Triassic (200 million years ago; probably also volcanos); Cretaceous (66 million years ago; asteroid; 75% lost). Arguably, a sixth mass extinction period has been underway for over 11,000 years. This is referred to as the Holocene (also Anthropocene) geological era, and is the result of human activity.

On its website, Extinction Rebellion describes itself as “an international movement that uses non-violent civil disobedience to achieve radical change in order to minimize the risk of human extinction and ecological collapse. Formed in the UK in May 2018, they have engaged in various acts of civil disobedience in an attempt to disrupt “business as usual” and heighten awareness of the emergency nature of the climate situation.

Certainly individuals can do their part to reduce their carbon footprint by, for example, eschewing air travel, driving fuel-efficient vehicles, insulating their homes efficiently, switching to energy-efficient lights and in general, not wasting electricity by keeping thing on needlessly. Also, as a community effort, they can buy carbon offsets to pay for reduction in greenhouse gases. But more important is governmental action; setting effective regulations to reduce carbon emissions. This will, of course, mean cracking down on corporate entities that cannot be expected to regulate themselves adequately. Transportation must end its reliance on fossil fuels. Hydro, wind, and solar electricity production must be greatly increased; agricultural practices must be better controlled (fewer fertilizers, less industrial beef production, more crop rotation and tilling of the soil); abolition of deforestation and irresponsible land use.

“We cannot solve a crisis without treating like a crisis,” says the prominent 16-year-old Swedish climate activist, Greta Thunberg, now famous for her (ongoing) school strikes. “If solutions within the system are so impossible to find, then maybe we should change the system itself.”

~ Wm. Doe, PhD – May 2019




Homeless Scholar Blog ~THE FILTHY RICH: TO SOAK or NOT TO SOAK?

During the regime of that wild-eyed radical Dwight D. (“Ike”) Eisenhower, the marginal tax rate on the highest income bracket in the United States was 91% and stayed at or above 70% until 1981 when Ronald Reagan declared America to be “back”. Thus, Rep. Alexandria Ocasio-Cortez’s recent suggestion of a restoration of the 70% level should hardly seem extremist. The United States does not have a wealth tax at present, but one has been proposed by Senator Elizabeth Warren, based on research by economists Emmanuel Saez and Gabriel Zucman. (A wealth tax is basically a levy on total assets.) The plan is to impose a 2% tax on fortunes worth more than $50 million and a 3% tax on those worth more than one billion dollars. This would affect about 75,000 families (less than 0.1% of U.S. households, raising an estimated $2.75 trillion over a ten-year period. (There have been some concerns raised as to the constitutionality of the proposal, but the majority of experts appear to view it as constitutional.)

As they say on the radio, Let’s do the numbers: In the Great Depression, Franklin Roosevelt’s administration established a 94% maximum marginal income tax rate, which dropped, as noted, only to 91% during the Eisenhower years. John Kennedy maintained this with a 25% maximum long-term capital gains tax. Under Lyndon Johnson, the income tax rate dropped to 77% (for annual figure exceeding $400,000) and the LTCG increased by 2 points. Richard Nixon kept the maximum marginal income tax the same but pushed the capital gain tax up to 37%. Gerald Ford pushed it even higher, to 40%, with a 70% income tax rate on $200,000 and up. Ronald Reagan kept the income tax max about the same, dropped the CGT to 20%, but increased it later to 28%. George Bush, Sr. had the CGT at 28% with the income tax at 31% for $86K and up. Clinton kept the latter the same, but decreased the capital gains tax by 8 percentage points. George Bush, Jr. started the income tax at 39%, then dropped it to 35%, with the CG starting at 21% then dropping to its current rate of 15%. Under Barack Obama, the income tax was 35% for annual sum of $388,000 and up, with the CG unchanged. Finally, Donald Trump’s maximum marginal tax rate for $560K and up (an average of single and married filers) is 37%, with the maximum long-term capital gains tax as under the second term of Reagan: 20%.

Better known than Saez and Zucman is their colleague at UC Berkeley, Thomas Piketty, who in 2014 released the unlikely best-seller, Capital in the 21st Century, a fat, graph & math-packed tome purporting to demonstrate that capitalism is seriously dysfunctional, because of the accelerating economic inequality it has engendered and as a result, is a threat to democracy. Piketty starts with the idea expressed as r > g ; that is,  rate of return on capital (wealth in general) is exceeding economic growth as measured in income or output. Capital and the money it produces accumulates faster than economic growth, a phenomenon which has intensified in the last four decades with financial deregulation. However, shortly after the book was published he wrote in an article for the American Economic Review, “I do not view r>g as the only or even primary tool for considering changes in income and wealth in the 21st century. Institutional changes and political shocks…played a major role in the past, and probably will…in the future.” He then adds that the equation is not useful for dealing with the rising inequality of labor income.

Piketty has been criticized from across the political spectrum, on methodological as well as theoretical and practical grounds, but for me personally, as a leftist freethinker (for lack of a better term), the most serious criticism centers on why he thinks reformism will rein in the plutocrats at this late date when there is no nominally communist superpower to embolden a social democratic alternative.

Numerous countries have or had wealth tax, and the example of France has been in the news a lot in recent years. The French tax was introduced in 1982 by Francois Mitterand. Thirty years later, Francois Hollande imposed a 75% supertax on earnings of 1 million Euros and above. French courts reversed themselves on its constitutionality after a redraft, but what really sank it was capitalist flight. Emmanuel Macron (“the President of the rich”) scrapped the tax, replacing it with one much more favorable to the upper crust, one which mostly just covered real estate. More on Macron presently.

There are various arguments against a wealth tax but the one most often brought up is that of tax evasion and capital flight, i.e., the fat cats can always find a way around it, even if they have to do move to another country to achieve this. The research group, New World Wealth, reported that 10,000 millionaires left France for this reason in 2015; 12,000 left the following year.

How do the critical economists propose to deal with this problem?

More stringent penalties appears to be the answer (easier to do in the U.S. than in France because of different financial law). In America, there is already a punitive “exit tax” of 40% on the net worth about $50 million of any U.S. citizen who renounces their citizenship. Moreover, there is the Foreign Account Tax Compliance Act (FATCA) which legally obligates foreign financial institutions to identify accounts held by U.S. citizens and report details to the IRS. In their 2019 paper, “How Would a Progressive Wealth Tax Work”, Saez and Zucman wrote, ‘Just like for legal avoidance, illegal evasion depends on policies and can be reduced through proper enforcement. Key to reducing evasion are (i) the collection of comprehensive data; (ii) sanctions for the suppliers of tax evasion services (the countries and financial intermediaries that facilitate it); (iii) proper resources for auditing.” Of course, it is unrealistic to think the problem can be removed completely, but the hope is that it can be reduced to an acceptable level.

There is a side issue which I’ll just touch on here: viz., when should taxing begin, period? Last year, Ontario announced a coming tax exemption for low-income worker: those earning less than 30 K will no longer have to pay provincial income tax. One wonders: how could this be applied to the U.S. federal taxation system? As things stand now, in the U.S., $12,100 is a poverty line of sorts, below which one need not file. Should taxation kick in at $20,000? $30,000? There needs to be a national discussion about a new, higher cutoff. The lower working class is overtaxed; this can and should be remedied.

In recent months, there has been significant political fallout from Macron’s economic policies. Since last November, there have been weekly protests, sometimes violent, all over France from working class people fed up with increasing poverty and plutocracy. These are the so-called Gilets Jaunes (yellow vests), named after the colored jacket required for all cars in the interest of public safety in the event of an accident.) In a blog post from last December, Piketty wrote: “If Macron wants to save his five-year period in power, he must immediately re-instate the wealth and allocate the revenue to compensate those who are most affected by the rises in carbon tax, which must continue.” As of this writing, the wealth tax has not been re-instated.

Back to the American situation: to liberate money to shore up the social safety net and implement a strong climate change program, Congress should cut the bloated war budget down to a rational size. If this seems unrealistic, all the more reason to soak the filthy rich with both a wealth tax and a marginal income tax of at least a 70% rate, as well as strengthening the inheritance/estate tax. Starting at $10 million, as suggested by AOC, is reasonable. No multimillionaires will be knocked down into the middle class thereby.

In sum, the reforms should be threefold, leaving aside the aforementioned possible rise in zero taxing of the lower stratum: (1) an increase in the estate tax;  (2) 70-80% marginal income tax starting at $70K, or thereabouts; (3) and the wealth tax proposed by Saez and Zucman, but preferably higher.

~ Wm. Doe, PhD – April, 2019





Homeless Scholar Blog ~ RENT CONTROL and the U.S. HOUSING CRISIS

“…There is no political reward in helping the poor. But what makes you think that the man who sits in judgment between the landlord and the tenant must have the mentality of a rent collector?” – Judge Sam Heller, who presided over L&T court during the Depression in Chicago *

Because of poverty, I lost my apartment in the last semester of a Ph.D. program and was forced to sleep in my friend’s rented garage. As with homeless shelters (which I’ve known from my more distant past), I had to clear out first thing in the morning as he came in early to prepare the copper for his roofing jobs. To urinate, I had to carefully descend rickety wooden steps to use a moldy, abandoned shower stall in the basement. I took showers at a homeless services center. Occasionally, some random individual from the alley would try to open the garage door in the middle of the night.

I slept there for three years, until my name came up on the public housing wait list. Some homeless people probably die before their number comes up.

Unaffordable housing continues to be a crisis, and unregulated landlords are a large part of the problem. In a market-intensive society like America, landlords pretty much rule. There’s little regulation, less rent control than there’s been in decades. Moreover, a growing number of landlords refuse to honor Section 8 vouchers. Some states and cities ban housing discrimination against the poor, a ban that should be extended nationwide. And tales of slumlords abound, of course, but I’m less interested in the “bad actors” narrative than in out-of-control private property ownership…However, the social philosophy and ethics of property ownership is beyond the scope of this article. Given the constraints of capitalism, landlords as a class cannot be swept away and entirely replaced by a state housing function or a radical communitarian arrangement. In this article, the landlords will be dealt with through the issue of rent control and more generally, that of (un)affordable housing.

Efforts to control rent governmentally go back several decades earlier, but the modern era of rent control started in 1943 with rent ceilings, also known as “vacancy control”, that is, rent restrictions remain in place when the unit re-rents. (With “vacancy decontrol,” rent restrictions turn off when there’s a new tenant.) Most so-called rent control is actually vacancy decontrol: landlords can raise rents considerably after a vacancy, and they are allowed to pass on maintenance costs. RC laws enacted in the 1970s exempted newly constructed buildings from control. The New York City Metropolitan Council on Housing states in a fact sheet that controls are “not the sweet deal that is often portrayed in the media and by landlords intent on ending rent protections. Most rent-controlled tenants pay a 7.5% increase each year, the median income is under $22,000 a year, and the majority pay well over 1/3 of their income towards rent.”

Soft rent control laws became widespread in the 1970s, as a result of tenant rights’ activism, but were hardly punishing to the property owners, who were given financial and legal breaks. However, despite these moderate provisions, landlords vigorously opposed all forms of rent control. Politically, the Zeitgeist turned conservative, and the tenants’ movement weakened. Rent control was defeated in Massachusetts in a 1994 referendum numerous legal scholars considered unconstitutional. This resulted in a doubling of median rents and the number of homeless in the Boston area. Five years later in California, rent control was significantly weakened statewide.

The ’94 Mass. Referendum is an interesting case study in political corruption. As mentioned, it was deemed unconstitutional by some legal experts. Instead of the referendum question asked only of residents in Boston, Cambridge, and Brookline, the areas to which it pertained, the property owners associations got in a back room with the State Attorney General and made it statewide to include the conservative western part of Massachusetts. Even so, the landlord lobby only narrowly won.

More recently, there was a major defeat of rent control in California: the Proposition 10 referendum of 2018. This measure would have repealed the Costa-Hawkins Rental Housing Act, a 1995 law forbidding cities from capping prices when a unit becomes vacant and from imposing rent control on single family homes. Needless to say, rent is largely out of control, and property owner associations want to keep it that way. They spread misinformation throughout the media and outspent rent control proponents 3 to 1 to deliver their message. And in Chicago, a struggle continues to vote in RC measures but this has been only ward by ward. The ultimate goal is to get the General Assembly to repeal the Rent Control Preemption Act of 1997, which prohibits any Illinois municipality from adopting rent control programs.

Oregon is positioned to be the first state to enact statewide RC, but many progressives are critical, as the bill’s limits on what landlords will be able to do are perceived as rather lenient: the limit on rent increases is generous (7%), there is an exemption for buildings less than 15 years old, and landlords can still push tenants to leave if the former intend to make substantial renovations. New York State Senator Julia Salazar has submitted a “good cause” eviction bill to protect tenants from being thrown out when the landlords jack the rent up. The annual increase cap proposed is 3.3%. A similar bill has already been signed into law in Philadelphia.

The Nolo legal group says in a fact sheet that 32 states have laws prohibiting local rent control ordinances.

“In the end,” notes the International Encyclopedia of the Social Sciences, “landlords are able, through the setting of high initial rents, to do just as well under tenancy rent control as in an unregulated market and therefore supply is not affected.” The combination of rent control, higher wages, and expanded public housing would work together to solve the affordable housing problem.

 Low-cost housing is disappearing from the market, and America isn’t building enough homes. The issue of widespread housing unaffordability is naturally linked to the greater issue of declining social spending. The United States spends considerably less on social welfare than do European nations. According to the Social Expenditure Database of the Organisation for Economic Co-operation and Development (OECD), the U.S. ranks 21st in social welfare spending as a percentage of GDP (the top countries being France, followed by Finland, Belgium, Italy, and Denmark. This is based on 2016 data.) In the ranking for per capita social welfare spending (2013 data), the U.S. is 13th (the top countries being Luxembourg, followed by Norway, Denmark, Austria, and Belgium).

In 2000, the rank of the U.S. for social spending as a percentage of GDP was even lower, and in the following year, a group of American economists (Alberto Alesina of Harvard et al.) addressed the question of why there is not a European-style welfare state in America. They concluded that “European countries are much more generous to the poor relative to the US level of generosity…The differences appear to be the result of…racial animosity [which] makes redistribution to the poor, who are disproportionately black, unappealing to many voter.”  Aside from the cultural, political explanations are advanced. America’s lack of proportional representation, they claim, prevented the growth of a socialist party. Moveover, “America has strong courts that have routinely rejected popular attempts at redistribution, such as the income tax or labor regulation. The European equivalents of these courts were swept away as democracy replaced monarchy and aristocracy.” **

In 2018, the Joint Commission at Harvard University released a report on the state of the nation’s housing and noted the following: Millennials and immigrants help drive household growth; housing demand is shifting from renting to owning; the single-family housing market tightened to historically low levels in 2017; and there has been a slowdown in rental demands.

More importantly, the following challenges were highlighted: “Cost burden” has significantly increased; that is, nearly a third of all households paid more than 30 percent of their income in 2016. Nearly half of renter households are cost-burdened, and more than half of these households pay over 50 percent of their income for housing. For the lowest income quartiles, this meant a drop in post-rent income from $730 in 2007 to $590 and only $490 for households with children. “The national median rate,” states the report, “rose 20 percent faster than overall inflation between 1990 and 2016, and the median home price rose 41 percent faster.” Income inequality played a major role in these increased housing costs. Only 1 in 4 very low-income households received rent assistance; the number of poorest households rose from 6 million in 2005 to 8.3 million 2015. Moreover, homelessness increased in 2017, and although 1.4 million is the figure cited in the report, the number is almost certainly larger in reality, as undercounting is a well-known factor in this problem.

In the matter of social goods and services involving human rights (e.g., food, shelter, health care, education), it is the legitimate function of the government to be strongly involved. Since third parties in the US are structurally not permitted to wield significant influence, short of revolution (highly improbable here), the only way forward seems to be a radical working-class mass movement, like that of the Gilets Jaunes in France, to act as an unavoidable pressure on the political class to take action for economic justice.


*from a 1971 interview with Studs Terkel



~ Rylan Dray, PhD – March 2019


Homeless Scholar Blog ~ AGITATED DEPRESSION

The stereotypical image of a depressed person is one of persistent sadness, lack of energy and loss of usual interests, often including food; social isolation, and statements/feelings of helplessness, hopelessness, or self-denigration. By contrast, agitated depression (AD) is characterized by, among other things, extreme irritability, anger, restlessness, racing thoughts and incessant talking, outbursts of complaining or shouting, pacing, and picking at the skin. Causes and triggers or the disorder include traumatic events, long-term stress, hormone imbalances, bipolar and anxiety disorders. Suicide is a definite risk with this syndrome.

According to the DSM-V, at least one episode of major depression is required for the diagnosis. Also required are at least two of the following: psychomotor agitation, or physical symptoms of agitation and restlessness; racing and crowded thoughts; psychic agitation, or intense inner tension. An Italian study noted as far back as 2004 that AD was common in depression outpatients, and emphasized the importance of getting the subtyping right, as certain antidepressants might increase agitation. (This resonates with my own personal experience with the alarmingly stimulating Prozac, even at a very low dose.) This study defined AD as a major depressive episode with four or more hypomanic symptoms.

Considering the phenomenon of agitation per se, it should be remembered that the disorder may not be of psychiatric origin. A recent commentary in the Annals of Emergency Medicine notes the many different possible medical causes for agitation in a patient: hypoglycemia, hypoxia, delirium, intracranial injuries, and encephalitis, to name just a few. (Occasionally, the problem can be easily solved by simply asking why the patient is agitated. De-escalation, when it can be done safely, should always be tried, as opposed to immediately jumping to more extreme measures. “A turkey sandwich,” the authors observe, “has been known on occasion to de-escalate a smoldering patient.”) Often, though, physical restraints are necessary; however, patients can be injured by fighting against them. Proper method is essential, as is proper choice of drug therapy. Antipsychotics and benzodiazepines are both good options. The “B-52” (Benadryl, 5 mg. of haloperidol, and 2 mg. of lorazepam) is often used, but it can potentially prolong the QT-interval. Ketamine can be effective in rapidly controlling an acute and potentially violent patient. An example is the patient with excited delirium who is “violent, shouting, hyperactive, and hyperthermic, [has] unexpected strength, and may progress to sudden cardiopulmonary arrest, even with intervention.”

Melancholia, a term going back to antiquity and lasting well into the 19th century, assumed many forms, some of which would correspond to mixed states like agitated depression today. Koukopoulos & Koukopoulos (1999) include a history of this various phenomenon in order to shed light on the complexity of the contemporary diagnosis of AD. By the mid-19th century, “a significant number of melancholias became a component of a more complex disease entity and lost their nosological independence. This…led eventually to the creation of ‘manic-depressive insanity’ by Kraepelin in 1899 and the definitive substitution of the concept of melancholia with that of depression,” Again, from the practical standpoint, understanding the distinction between AD and the more “standard”, sad and lethargic form of depression is essential to avoid psychopharmacological errors which sometime lead to suicide attempts (Healy, 2004).

Psychotherapy is often indicated, which may be psychodynamic in nature, or more likely, cognitive-behavioral therapy. The patient will need to learn coping skills, especially, the ability to detect triggers and how to prevent them from setting off the pathological behaviors.

Regarding drug treatment, good results have been obtained with typical and atypical antipsychotics, anticonvulsants, and benzodiazepines, with olanzapine being particularly rapid and effective. Lithium is occasionally useful and severe cases may call for shock therapy.

Koukopoulos & Koukopoulos (1999) make a distinction between agitated depression and depressive anxiety, with the former often responding to antidepressants. They note, “The anxiety observed in AD is inherent in the agitation itself…The despair, the undirected and groundless rages and the violent, suicidal impulses of the more mundane agitated depression of today, seem to be caused by that ominous, dark force…so violent that it cannot be anything but manic in nature.” To treat such an agitation with SSRIs-as-usual (or any antidepressant) can lead, and has led, to disaster.

~ Wm. Doe, Ph.D., CPhT – February 2019


F. Benazzi (2004). Agitated depression: A valid depression subtype? Progress in Neuropharm & Biol Psychiatry, 28.

D. Healy (2004). Let Them Eat Prozac: The Unhealthy Relationship between the Pharmaceutical Industry and Depression. New York: NYU Press.

A. Koukopoulos & A. Koukopoulos (1999). Agitated depression as mixed state and the problem of melancholia. Psychiatric Clinics of North America, 22 (3).

J. Mason et al (2018). Agitation crisis control. Annals of Emergency Medicine, 72 (4).

Homeless Scholar Blog ~ ICU-induced PTSD

Post-traumatic stress disorder is increasingly reported in ICU survivors (Broomhead & Brett, 2002). PTSD is an anxiety disorder developing in some people after such traumatic events as combat, crime, accidents, or natural disasters and characterized by nightmares, flashbacks, intrusive memories and avoidance. Despite its crucial role in enabling many critically ill patients to survive, the ICU can be a stressful environment for patients, who may experience/suffer iatrogenic distress, both physical and mental: pain, respiratory insufficiency, ICU-induced physical limitations. ICU survivors experience prolonged weakness, sleep disturbances, and impairments of memory, attention, and concentration.  (Generally, the severity of the illness itself is not predictive of PTSD.) Compared with non-ICU patients, survivors of ICU are almost four times more likely to experience PTSD. Using a questionnaire called the Experience After Treatment in Intensive Care 7 Item Scale, researchers have shown that intensive care treatment is a contributing factor to the development of post-traumatic stress. There may be avoidance of clinics and hospitals (and media depictions of them); hypervigilant preoccupation with somatic symptoms, large or small; preoccupation with thoughts of ‘delusional memories’ from ICU hospitalization; claustrophobia related to memories of being restrained or held down in the ICU; reactivity related to noises similar to those occurring in an ICU, such as ‘beeping’ sounds.

An example of a serious mental condition that may cause psychological trauma as a result of ICU stay is subarachnoid hemorrhage (SAH), which is bleeding into the space between the inner and middle later of the meninges, the tissues which cover the brain. The most common cause is the rupture of an arterial aneurysm, which usually causes a sudden, severe headache, vomiting, and photophobia. This is often followed by a brief loss of consciousness. Complications such as myocardial stunning, neurogenic pulmonary edema, thromboembolus and infection can prolong the ICU stay. (Naturally, it is difficult to separate the adverse of the ICU stay with those of the medical condition itself, but it seems reasonable to assume that the iatrogenic component is often an aggravating factor, especially since, as with SAH, it is known that the sequelae include a misinterpretation of normal physiological sensations as indicating imminent danger.)

Another disorder that may develop in the ICU is delirium,  which is characterized by an acute change in cognition and a disturbance of consciousness, usually resulting from an underlying medical condition or from medication or drug withdrawal. It affects 10 to 30 percent of hospitalized patients with medical illness. ICU delirium is associated with increased mortality and cognitive disorders after discharge.

One group of researchers has proposed that “the development of acute PTSD-related symptoms may be related more to recall of delusions alone and that even relatively unpleasant memories for real events during critical illness may give some protection from anxiety and the later development of PTSD-related symptoms when memories of delusions are prominent (Jones et al, 2001).

The connection between ICU delirium and PTSD should be investigated further. There are 4 key characteristics of delirium: altered level of consciousness, inattention, disorganized thinking, and a fluctuating course. Iatrogenic/environmental risk factors for the development of ICU delirium are: sedative, analgesic, and anticholinergic agents; epidural use; central venous catheter; rectal/bladder catheter; use of physical restraints; sleep deprivation; excessive noise; absence of diurnal light variation. The Confusion Assessment Method (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC) can evaluate the severity of the above characteristics. A 2018 study by anesthesiologists notes that “ICU delirium is associated with increased mortality, prolonged hospitalization, prolonged mechanical ventilation…and the occurrence of cognitive disorders after discharge from the unit.” (Kotfis, 2018)

“Intensive care unit admission,” concludes a longitudinal cohort study of 300 patients in a British hospital, “is associated with a high mortality rate, a poor physical quality of life, and a low quality adjusted life-years-gained compared to the general population for 5 years after discharge.” However, specifically in reference to PTSD, its true prevalence in ICU survivors has not yet been determined since numerous methodological deficiences have plagued the effort, such as: lack of true prospective data, failure to employ appropriate comparison groups, sampling bias, measurement issues, and statistical problems. Recently, some rehabilitation psychologists have questioned the traumatic effect of the ICU and that the literature on the subject has not taken into account differential risk and resilience factors. (These risk/resilience factors are said to be: demographics, psychiatric history, psychobiology, social support, coping behaviors, personality, optimism, cognitive appraisal, and emotion regulation/regulatory flexibility.) These psychologists argue that future research needs to establish just who is at risk and why (McGiffin et al, 2016).

~ Wm. Doe, Ph.D., CPhT – January 2019


L.R. Broomhead & S.J. Brett (2002). Intensive care follow-up: What has it told us? Critical Care, 6: 411-417.

Kotkis, K. & A. Marra (2018). ICU delirium–A diagnostic and therapeutic challenge in the intensive care unit. Anesthesiology Intensive Therapy, 50(2), 128-40.

E. Berry (1998). Post-traumatic stress disorder after subarachnoid hemorrhage. Br J Clin Psychol, 37: 365-7.

J.N. McGiffin et al (2016). Is the intensive care unit traumatic? What we know and don’t know about the ICU and post-traumatic stress responses. Rehabilitation Psychology, 61(2): 120-131.

J.E. Tedstone & N. Tarrier (2003). Post-traumatic stress disorder following medical illness and treatment. Clin Psychol Rev, 23: 409-448.

C. Jones, R.D. Griffiths et al. (2001). Memory, delusions, and the development of acute post-traumatic stress disorder-related symptoms after intensive care. Crit Care Med, 29(3), 573 ff.






Homeless Scholar Blog ~ NEUROPLASTICITY

Neural plasticity–a more general term than neurogenesis (the regrowth of injured neurons)–refers to the brain’s ability to reorganize itself by rewiring connections, the ability of the nervous system to change in response to experience or environmental stimulation. Santiago Ramon y Cajal (1852-1934), “the father of neuroscience”, was already using the term, “neuronal plasticity”. In the late 1960’s electron microscopy studies demonstrated an “anatomical reorganization” of the neurophil in the septal nuclei of adult rats after a selective lesion to axons which terminate on the neurons in those nuclei. Long-term potentiation (LTP) is a well-known form of functional neuroplasticity., the long-lasting enhancement in signal transmission between two neurons after synchronous stimulation. Work with absorbed carbon-14 in the atmosphere after nuclear bomb tests has shown hippocampal neurogenesis. Clinical applications for the regrowth of the injured neurons is obvious, although the adult brain is less plastic than the developing one….


…It was long a dogma that nerve cells could not be added after birth. However, research in the late 20th century showed that new neurons can form in two brain areas: the olfactory bulb and the hippocampus. Despite the limitations of such putative neurogenesis, it has been widely held to be an empirically verifiable phenomenon.

Unfortunately, more recently, research at UCSF has concluded that hippocampal neurogenesis drops sharply in children to undetectable levels in adults. “Recruitment of young neurons to the primate hippocampus,” write the authors, “decrease rapidly during the first years of life, and neurogenesis in the dentate gyrus does not continue, or is extremely rare, in adult humans.” (S.F. Sorrells et al (2018). Human hippocampus neurogenesis. Nature, 555(7696).)

The UCSF study has been criticized by many neuroscientists who have declared the methodology unreliable. Molecular markers used to indicate presence of new neurons were not employed in living brains, and the critics claim that within a few hours after death, degradation of the markers renders the data dubious. Thus, while neuroplasticity is a generally accepted phenomenon, neural regeneration remains controversial.

~ Wm. Doe, Ph.D., CPhT – December 2018



Homeless Scholar Blog ~ RESILIENCE

“Although meant to counteract preoccupations in psychology with such characteristics as low self-esteem and assertiveness and high depression, anxiety and anger, the emphasis on happiness [in positive psychology] is problematic in that it does not fully appreciate the inherently stressful nature of living well.” – Salvatore Maddi, “Hardiness: The Courage to Be Resilient”

The concepts of resilience and hardiness are obviously related, but a title search of Pub Med for each shows much more research interest in the former. Hardiness is a presumed characteristic of an individual, whereas resilience is more of a behavioral outcome, a description of the tendency to rebound quickly from the  adverse effects of stress. An important research question is the extent to which people can cultivate resilience capability psychologically, thereby controlling susceptibility to mental disorders and even physical illness. Outcomes associated with high resilience include strong coping skills, a strong support network, and lower rates of depression. Positive physical outcomes include independence in daily activities, faster cardiovascular recovery, and lower mortality risk (MacLeod, 2016). Biomedically, the construct of resilience can be expressed as “physiological reserve” or “intrinsic capacity.”

There are numerous instruments for testing resilience, at least 15, of which the Connor-Davidson Scale, the Resilience Scale for Adults, and the Brief Resilience Scale have received the best psychometric ratings. A 2011 methodological review found no current “gold standard” (Windle, 2011). In Connor and Davidson’s original paper on their scale, 25 descriptors of the construct are listed, for example: “Able to adapt to change; not easily discouraged by failure; think of self as strong person; humor in the face of stress; strong sense of purpose; know where to turn for help….” The authors conclude that “the scale demonstrates that resilience is modifiable and can improve with treatment.”

An early study of a 25-item resilience scale using principal components factor analysis with 810 community-dwelling older adults as sample boiled down to “personal competence” and “acceptance of self and life”. The results supported the internal consistency reliability and concurrent validity of the scale for the measure of resilience (Wagnill & Young, 1993).

A more recent study of the Resilience Scale is critical, but still asserts that its use “can help identify older adults low in resilience and expose these individuals to interventions to improve resilience and facilitate successful aging” (Resnick & Inquito, 2011). The authors recommend the use of more qualitative studies.

Applications of the resilience concept have been fairly wide in both medical and psychological literature. For example, a recent article investigated the relationship between psychological hardiness and resilience with depression in women with breast cancer, concluding that there is a need for training courses and counseling services for these women in order to improve their mental health status. Research into burnout, especially among nurses, continues to be of interest to researchers. A 2016 study of resilience and burnout status among oncology nurses using the RS Scale for Adults and Maslach’s Burnout Inventory, states that information on the relationship between burnout and resilience can be used to plan interventions supporting these workers. A 2018 investigation of the moderating effects of resilience on the relationship between emotional labor and burnout among hospital workers in geriatrics in South Korea urged that management interventions should be developed based on the recognition that emotional labor should be seen as a significant mental health issue. Another 2018 study focused on  resilience among the homeless population and still another on how engagement in creative art was associated with high resilience among Holocaust survivors.

The American Psychological Association has published an information sheet on resilience, including ten ways to build it, viz., making social connections; avoiding seeing crises as insurmountable problems; accepting that change is a part of living; moving toward one’s goals; taking decisive actions; looking for opportunities for self-discovery; nurturing a positive view of oneself; keeping things in perspective (big picture); maintaining a hopeful outlook; and general self-care.

A British work earlier this year synthesized the available evidence on interventions designed to improve individual resilience, assessing the methodological rigor of each included study. Programs were stratified into one of three categories: (a) cognitive-behavioral-based interventions; (b) mindfulness; (c) a combinations of the two. A meta-analysis led to the conclusion that resilience interventions based on a combination of the two techniques had a positive impact on individual resilience.

Being mindful of maladaptive cognitions leading to emotions which reinforce a self-defeating response to the environment can lead to engendering the courage required to build ongoing resilience.

~ Wm. Dray, Ph.D., CPhT – November 2018


MacLeod, S. et al. (2016). The impact of resilience among older adults. Geriatric Nursing, 37: 266-272.

Windle, G. et al. (2011). A methodological review of resilience measurement scales. Health & Quality Life Outcomes, 9:8.

Connor, K.M. & Davidson, J.R. (2003). Development of a new resilience scale: the CD-RISC. Depression and Anxiety, 18: 76-82.

Resnick, B.A., Inquito, P.L. (2011). The Resilience Scale: Psychometric properties and clinical applicability in older adults. Archives of Psychiatric Nursing, 25 (1): 11-20.

Joyce, S., Shand, F. et al. (2018). Road to resilience: A systematic review and meta-analysis of resilience training programmes and interventions. BMJ Open, 8: e017858.



“The problem of anxiety is the nodal point of many important issues. By solving this problem, you can reveal the whole mental life of a human.” – Sigmund Freud

Anxiety may be functional or pathological, and the latter type comes in various forms: social, panic, obsessive-compulsive, post-traumatic stress, and so on. Generalized anxiety disorder (GAD) was originally viewed as a residual construct, but today it is more often considered distinctive. The central feature of the disorder is worry, but unlike ordinary worry, the worry of GAD is uncontrollable, pervasive, i.e., free-floating. (Secondary symptoms include restlessness, fatigue, sleep disturbances, and difficulty concentrating.)

Freud conceived of the precursor of the syndrome, “anxiety neurosis,” back in  1894, and the term was standard until 1980 when the radical DSM-III was published. In the DSM-II, GAD was still referred to as “anxiety neurosis”. A power struggle in psychiatry came to a head with the publication of the third edition, with the result that Dr. Robert Spitzer & Co. had managed to purge psychoanalytic/psychodynamic theory from the tome in the interests of being “atheoretical”. This meant, of course, that unconscious mental forces are left out of the picture, obviously good for the cognitive-behavioral therapists, among others. (However, this assumed that no cases of such anxiety required depth psychology which, in my opinion, was presumptuous. From the empirical work of Howard Shevrin to the Implicit Association Test, there is evidence of unconscious mental processes, and that should have been taken into account in later revisions of the manual. In the DSM-V, for example, there is no mention made of the unconscious mind as a potential source of anxiety, generalized or otherwise.)

In addition to worry, avoidance has been posited as a key feature of GAD. Borkovec’s Avoidance Model asserts that worry is a verbal activity which inhibits vivid mental imagery and associated somatic and emotional activation. This prevents the emotional processing of fear. Insecure attachment from childhood may also play a part in the maintenance of the disorder.

Compared to depression, there is poor physician recognition of generalized anxiety disorder. Among people with GAD, there is high health care utilization, and these patients often present with pain, insomnia, and other physical symptoms, including cardiac and gastrointestinal. (Obviously, though, in the latter cases, a clinician cannot afford to assume psychogenic causation for fear of missing serious heart and gut conditions.) To deal with the problem of GAD in the primary care setting, Roy-Byrne and Wagner (2004, p. 20) have stated, “The collaborative care approach is designed to overcome [treatment] barriers. With this approach, the patient is provided with additional educational materials, physicians are supported by physician extenders [nurses, social workers, or expert consultants) who provide case-based feedback, follow-up, extra visits, and telephone calls to patients.”

Instead of “hypochondriasis”, the DSM-V utilizes the terms, Somatic Symptom Disorder and, in a minority of cases, Illness Anxiety Disorder (“if the patient has extensive worries about health but no or minimal somatic symptoms”).

The propensity to react negatively to everyday uncertainties has been associated with generalized anxiety, obsessive-compulsive disorder, social anxiety and panic disorders, depression, and anorexia/bulimia. This tendency has been referred to as Intolerance of Uncertainty.

GAD has as its defining feature a “free-floating” worry that can affix to almost anything. Thus, it is distinguished from specific obsessions. This worry is not necessarily irrational, just “amplified” out of proportion to what would normally be considered appropriate. In the case of everyday ambiguity, a GAD sufferer will fixate on this as a disturbing aspect of life and wonder why others are nonchalant about such maddening uncertainty. Attachment theory has explanatory value here in that one can easily see how a small child who was insecurely attached to its parents could develop to see the uncertainty as distressing, even threatening. A good example is ACOA: the child of alcoholic parents often does not know what to expect from them from day to day or sometimes even hour to hour. “If parental responses are unstable or inconsistent, a child may not learn to adequately regulate distress,” writes Canadian psychologist Magdalena Zdebik (2017). “Insecurely attached children are more likely to process or interpret ambiguous information or situations as threatening, hostile, or negative than securely attached children.” Frank personality changes in the parent are especially psychically disruptive and, if the situation is severe or prolonged, could actually make the child entertain thoughts of “body-snatching”.

The standard treatment for GAD is the combination of counseling/psychotherapy and an appropriate medication. Until recently, the favored drug was a benzodiazepine–and some physicians still prefer benzos for their fast-acting effectiveness–but this choice has fallen out of favor due to the addiction potential. Sometimes, buspirone is used in its place, but more often the substitute is a selective serotonin reuptake inhibitor (SSRI). (For a skeptical view of this off-label practice, see Healy (2004, p. 281). When supportive therapy is deemed inadequate, cognitive behavioral therapy (CBT) is the usual choice. However, in a minority of cases, a better method would be psychodynamic (derived from psychoanalysis), which can be done as brief therapy. This would be for those patients who have deeper issues generating the anxiety, unconscious conflicts which CBT is too superficial to address.

It seems that Freud is not quite dead yet.

~ Wm. Doe, Ph.D., October 2018


E. Behar et al (2009). Current theoretical models of generalized anxiety disorder. J Anx Disord, 23: 1011-1023.

Healy, D. (2004). Let Them Eat Prozac: The Unhealthy Relationship Between the Pharmaceutical Industry and Depression. New York: NYU Press.

Roy-Byrne, P. & A. Wagner (2004). Primary care perspectives on generalized anxiety disorders. J Clin Psychiatry: 65 [suppl 13]: 20-26.

Zdebik, M.A. (2017). Childhood attachment and behavioral inhibition: Predicting intolerance of uncertainty in adulthood. In Development and Psychopathology. Cambridge University Press.

Homeless Scholar Blog ~ FORENSIC ENTOMOLOGY

“The absence of significant numbers of blowfly larvae and lack of evidence of their feeding in the natural orifices or gunshot wounds on the corpse suggested that the body had been kept elsewhere, probably indoors, for several months and only recently placed on the site where it was found…Subsequent confession by the murderer established that the victim had been shot and kept in a sauna room for five months, then dumped at the edge of the woods where the body was found.” – K.G.V. Smith (1986)

The use of insects in death investigations goes back as least as far as the 13th century when one Sung Tzu (also known as Song Ci) described a homicide in which flies landing on a sickle retaining invisible traces of blood, indicated that it was the murder weapon and led to the perpetrator’s capture. The first formal case documentation, though, is that of a Dr. Bergeret who, in an autopsy of a child found hidden in the wall of a house in 1850, discovered flesh-fly larvae deposits that had to have occurred in 1848, the year before the occupants in question moved in. Another interesting case–hard to choose as there are so many worth nothing–involved a Hungarian ferryboat captain in the 1960s who arrived at work one September evening at 6 p.m., shortly after which the body of postmaster was found on board. The captain, protesting that he was innocent, was sentenced to life imprisonment for murder. Eight years later, the case was re-opened. A forensic entomologist noted the fact that no sarcophagous flies, such as were found in the autopsy the following day, are active in Hungary at 6 p.m. in the month of September. This and other insect data from the entomologist’s experiments, led to the conclusion that the flies’ eggs must have been laid before 6 p.m. on the day of the crime, i.e., before the captain even boarded the vessel. The data on oviposition were verified, and the captain was exonerated.

Why use insects in medicolegal investigations? Several reasons: First, they are usually the earliest creatures to find a decomposing corpse, and their reproduction information can serve as the basis for estimating the post-mortem interval (PMI), i.e., the time between death and corpse discovery. Second, there is predictability in  the changes and succession of arthropod fauna in and around the body. Also, arthropods in the general vicinity can provide valuable data which is sometimes ignored by investigators.

“Not only do insects swarm over an exposed corpse in great numbers,” writes physician K. V. Iverson in a morbid but informative and entertaining volume, “but they also arrive in a very precise sequence, depending upon the body’s location and condition. British Columbia scientists, for example, have found a markedly different insect succession than has been reported for other areas….”

Flies arrive first, then are replaced by beetles, which are replaced in turn by spiders, mites, and millipedes. The flies and beetles are necrophages, feeding on the corpse tissue per se. Parasites and predators eat not only that, but the necrophages as well. Omnivores will eat, in addition to corpse tissue, any flies or beetles still around as well as ants and wasps. Finally, there are incidentals (e.g., spiders and centipedes) which use the dead body as an extension of their environment.

(A quick definition of terms: Strictly speaking, insects are a class of the phylum Arthopoda and characterized by 3 distinct body divisions, 3 pairs of jointed legs, tracheas, and usually two pairs of wings. Arthropoda also include crustaceans, arachnids, and similar forms. It is the largest animal phylum, containing over 900,000 species.  Instar refers to any one of the various stages of insect development; and myiasis is basically the infestation by the larvae (maggots) of flies.)

Many techniques have recently been developed for FE use. Scanning electron microscopy (SEM) can identify key morphological features in eggs and maggots and distinguish species on the basis of shape and length as well as the presence or absence of anastomosis (connected blood vessels).

However, the high cost of the SEM equipment is a disadvantage, as is the time it takes to use; thus, it is not optimal for field study. A faster, less expensive technique is potassium permanganate staining. Slides can be used with any light microscope and can demonstrate key morphological differences for species identification. When structural differences prove difficult to descry, the mitochondrial DNA method can be used to identify characteristics at certain life stages.

Scientists in Germany (Zoologische Staatsammlung Munchen) have established a DNA reference library of potentially forensic relevant arthropod species, essentially using a form of barcoding. “DNA barcoding,” they write, “uses a short genetic sequence of the mitochondrial cytochrome c oxidate 1 gene (CO1-5′) as a unique identifier to differentiate between species.” Also, mock crime scenes using pig carcasses have been used frequently in the training of entomologists. The carcass serves as a surrogate for a human body and is used to illustrate various environmental effects relevant to crime investigation with insects. Finally, there are gene expression studies, in which the age of an egg is determined based on the expression of particular genes. Sometimes developmental stages are not evident by changes in size of the egg or pupa. The use of such genetic analysis can determine size changes, which data can then render the PMI more accurate.

Although this subfield of forensic pathology has powerful investigative methods, there are certain pitfalls and limitations to this approach. The post-mortem interval can easily be underestimated in numerous ways. For example, the wrapping of the corpse, low temperature, rain, burial, or the inactivity of most flies at night can lead to a delay in colonization, and hence, inaccurate measurements. Where the body is discovered might not be the scene of death. Also, infestations on a body might have begun before, not since, death. Drugs and toxins which affect maggots might be overlooked. Variations in the developmental biology of local populations could throw things off. All in all, the calculation of insect activity as it relates to the cadaver can be quite complex and fraught with pitfalls. However, despite these concerns, forensic entomology remains “the most reliable method for establishing the minimum time since death in the first weeks post-mortem” (Amendt & Richards, 2011).

~ Wm. Doe, PhD, CPhT – September 2018


Kenneth G.V. Smith (1986). A Manual of Forensic Entomology. London: The Trustees of the British Museum (Natural History). [opening quote: pp. 66-7]

E.P. Catts & M. L. Goff (1992). Forensic entomology in criminal investigations. Annu Rev Entomol, 37: 253-272.

J. Amendt & C.S. Richards (2011). Forensic entomology: Applications and limitations. Forensic Sci Med Pathol, 7: 379-392.

C. Chimeno, J. Moriniere, et al. (2018). DNA barcoding in forensic entomology–Establishing a reference library of potentially forensic-relevant arthropod species. J. Forensic Sci. [online]

K. V. Iserson (2001). Death to Dust: What Happens to Dead Bodies. Tucson, AZ: Galen Press; p. 388



Homeless Scholar Blog ~ SUDDEN DEATH

“Although the vast majority of these deaths may be ascribed to coronary atherosclerosis, there are many other potential causes of sudden cardiac death, such as cardiomyopathies, which are more frequently encountered in people aged less than 35 years.” – Oliva & Pascali, (2010), “Sudden Death in Forensic Pathology,” p. 108

A while back, I wrote a general article on the electricity of heart function, but in this post I am focusing on the specific problem of sudden cardiac death (SCD), news of which often comes as a surprise, especially when it occurs in the young and apparently healthy.

A widely accepted definition of SCD is: “A natural death due to cardiac causes heralded by abrupt loss of consciousness, within one hour after the onset of acute symptoms, or an unwitnessed, unexpected death of someone seen in a stable medical condition less than 24 hours previously with no evidence of a non-cardiac cause.” The term, “non-sudden cardiac death” would be used if resuscitation is initially effective but the patient dies somewhat later (Koene, 2017).

In younger individuals, such incidents are usually related to athletic activity. The leading cardiac causes of sudden death in athletes are cardiomyopathies, coronary artery abnormalities, myocarditis, channelopathies (muscle diseases causes by congenital defects in the cell membrane proteins that move ions in and out of the cell), valvulopathies, coronary artery disease, and aortic stenosis. (But there are also NON-cardiac causes: hypothermia (including heat stroke), use of illicit drugs, acute pulmonary diseases, acute cerebral diseases (including stroke), sickle cell disease, and rhabdomyolysis (an acute, sometimes fatal disease characterized by destruction of skeletal muscle).

For the general population, in industrialized countries, myocardial ischemia from advanced atherosclerosis is the most common cardiac cause of sudden death. The non-arrhythmic forms of SCD include aortic dissection, pulmonary embolism, cardiac tamponade (accumulation of excess fluid in the pericardium), and atrial myxoma (tumor in an upper chamber of the heart). An important warning symptom of SCD following syncope (fainting) is dyspnea, exceeded in risk only by a history of prior lifetime syncope or presyncope.

Sudden cardiac death accounts for 50% of all cardiovascular deaths. Key factors are atherogenesis, plaque destabilization, onset of ischemia and arrhythmias. Current estimates for out-of-hospital SCDs are 390,000 per year in the U.S.; in-hospital: 200,000. Ventricular tachycardia accounts for about two-thirds of all SCD attributed to arrhythmias. (Other causative arrhythmias are ventricular fibrillation, Torsade de Pointes (very rapid ventricular tachycardia that may turn into ventricular fibrillation), and pulseless electrical activity, including bradyarrhthmias.) But sudden death is not always mediated by arrhythmias. One of the greatest risk factors for out-of-hospital cardiac arrest is congestive heart failure. Contributing pathological factors of SCD in heart failure fall into two categories: endogenous (so-called “substrate development”: hypertrophy; left ventricle dilation/remodeling: scar formation/fibrosis; conduction pathway changes): and acute environmental triggers (electrolyte imbalances; sympathetic activation; ischemia; hemodynamic changes) (Weeks, 2016).

For decades, cardiovascular scientists have been trying to identify vulnerable atherosclerotic plaque in patients, with the hope of preventing disaster. Rupture of such plaque can be detected in victims of sudden death with the use of post-mortem CT coronary angiography (Moss, 2018). However, although rupture-prone plaques have been visualized even in living patients, risk prediction has been disappointing. In fact, it has been argued that the concept of vulnerable plaque is a “myth” hindering future research and that the focus should be not on individual plaques, but on arteriosclerotic disease burden (Arbab-Zadeh & Fuster, 2015).

The contingency of the human condition is such that any recommendation for prevention of SCD, especially in vulnerable individuals, must needs be a matter of probability. Nevertheless, certain factors can be mentioned based on documented medical cases. (Despite the earlier emphasis on young athletes, most people who suffer sudden cardiac death have a history of coronary heart disease.) Modifiable risk factors include cholesterol intake, smoking, glucose intolerance, hypertension, and obesity. The standard medical interventions are antiarrhythmic agents and implantable cardioverter-defibrillators. But public access to automated external fibrillators (AED) is hampered by the public’s limited ability to locate them quickly. Most people do not recognize the international sign and do not know what AED stands for. An American cardiologist has suggested that a better, more uniform sign design be employed and perhaps a better name as well (Otto, 2016). Also important for prevention is the exercise stress test, which can assess both ischemia and susceptibility to sustained ventricular tachyarrhythmias.

~ Wm. Doe, PhD, CPhT – August 2018


Koene, R. J. et al. (2017). Syncope and the risk of sudden cardiac death: Evaluation, management, and prevention. Journal of Arrhythmia, 33.

Brugada, R. (Ed.) (2010). Clinical Approach to Sudden Cardiac Death Syndrome. London: Springer-Verlag.

Moss, A.J. et al. (2018). Vulnerable plaque detection in sudden cardiac death: Post-mortem CT coronary angiography. BMJ Heart, 104 (Suppl. 5).

Arbab-Zadeh, A. & V. Fuster (2015). The myth of the “vulnerable plaque.” J. Am. Coll. Cardiol., 65 (8).

Weeks, P.A., A. Sieg, et al. (2016). The role of pharmacotherapy in the prevention of sudden cardiac death in patients with heart failure. Heart Fail Rev, 21.

Otto, C.M. (2016). Heartbeat: Prevention of sudden cardiac death. Heart, 102: 729-30.