Saturday, November 8, 2014

Hiding from the Pain: Robin Williams's Autopsy

Robin Williams’s death on August 11 2014 generated a lot of interest because there were so many cues. Or cues that we strongly believe we need in order to be able to explain his suicide as “rational”. We are now learning that depression, anxiety, and Parkinson’s disease weren’t the only issues plaguing Robin Williams in the months before his death. According to a new autopsy and toxicology report his brain also showed signs of dementia. We have now “explained” the suicide as a biological fate accompli. Biological determinism. Dementia and Parkinson’s at the same time. What better reason to commit suicide.

But this is rubbish.

What neurologists think as the disease in the brain—the neuropathology—which in Alzheimer’s are the plaques and tangles—has never been validated. We see a lot of plaques and tangles in the brains of dementia or Alzheimer’s patients after they die. But there is not one study that shows that the plaques and the tangles CAUSE the disease. The same as a scab over a wound. The scab is an indication of a trauma, but it is not the trauma itself.

If we did an autopsy of you today it is very likely that you have some of the signs of dementia. In fact most older adults have these plaques and tangles. So much so that just under one in three of  older adults have as much disease as those with dementia but without expressing the disease. And it is not just older adults who have these neuronal damage. A study on young victims between the ages of 26 and 30 reported that more than one in five already had early stages of the disease.

What is stranger still is the observation that there are people with dementia who do not have the disease in their brain. There is a famous long-term study conducted by David Snowdon looking at nuns. Snowdon was one of the first to report such cases. There are inconsistencies in how we are trying—but failing—to define the cause of Alzheimer’s disease and dementia in general.

Diseases of the brain are not all that distinct. Although we have given names to specific diseases these are not as distinct in real life as neurologist would like them to be. We talk about Lewy Bodies dementia as though it is distinct from Alzheimer’s, but in fact they are on a sliding scale…more likely to look like Alzheimer’s or Lewy Bodies. There is also the vogue to call all types of dementia “Alzheimer’s”. Even Alois Alzheimer himself, more than 100 years ago, was confused by the distinction. And we remain confused today. Most of brain diseases share similar neurological deficits. Whether these are the cause or an expression of an underlying disease has not been determined.


With Robin Williams’s death we have to stop looking for simple answers. There is no greater answer to be found in biology. Our biological body is a balance—it is not a digital machine. As with cancer—and we all have cancer—it is how the body manages to keep it in balance. It is not whether there is a disease, but how we control and keep it in check. Evidence of dementia is no evidence. It is after-the-fact excuses to rationalize an individual’s pain and suffering as legitimate without understanding the pain and suffering.

© USA Copyrighted 2014 Mario D. Garrett

Saturday, October 25, 2014

Is Cancer the Cure for Alzheimer’s disease?

 In 2014 Ferrán Catalá-López and his colleagues from the University of Valencia in Spain reviewed the inverse association between cancer and neurological diseases including dementia. What they reported is that numerous studies have been showing that if you had one of these two diseases you are less likely to get the other. The first anecdotal evidence came more than fifty years ago when patients with Parkinson’s disease were reported to have a lower rate of cancers. More recently, this inverse relationship has also been documented for Alzheimer’s disease. In fact, this inverse relationships is most pronounced with Alzheimer’s disease and Huntington’s disease. While for cancer it is more pronounced for colorectal cancer and lung cancer.

If you have had cancer you are 50% less likely to get Alzheimer’s disease. While, if you have Alzheimer’s disease you are 60-70% less likely to get cancer. The same results do not exist for vascular dementia or Lou Gehrig's disease (ALS) and for some cancers such a melanoma, non-melanoma skin cancer and breast cancer.

There could be a number of reasons for this, and all could be working at the same time. It could be that once you are diagnosed with cancer or Alzheimer’s disease the focus of clinical care is on treatment and there might be less active interest in searching for additional diseases. However, this does not explain why it does not work with other diseases. It could be that the therapy for both diseases protects you from getting the other disease. Although plausible, it is unlikely. It could also be that the two diseases are separated by vulnerability in age and therefore if cancer kills you first you will not have the opportunity to get dementia. While being spared cancer you are then more likely get dementia. Although there are studies that dispel these arguments—some more conclusively than others—there is however a more subtle and persuasive argument.

There is a growing understanding of the chemical balance that is played in the body especially the process of generating energy for cells. The imbalance in this process—known as Glycolysis—of how the body converts sugar into fuel (pyruvate) for cells could be the balance that determines which of these two diseases you are likely to get. Too little fuel for cells—since neurons have such energy demands—and you get Alzheimer’s disease. Too much fuel, which feeds the erratic cells, and you get cancer.

Although this is an interesting avenue for biological and chemical research, there is an additional offshoot of this way of thinking…and that is the rejuvenation of the concept of homeostasis. That along a continuum of cancer or Alzheimer’s disease there is a balance. First described by Claude Bernard in 1865 and later coined by Walter Bradford Cannon in 1926, homeostasis requires three basis mechanisms. A sensor to detect changes, a mechanism that can modify that change, and a feedback connection between the sensor and a mechanism. The concept that homeostasis can determine Alzheimer’s disease has radical repercussions for psychologists because both the sensor and the mechanism can have psychological components. As an example, for the sensor being happy and content, tells the body that the system is in homeostasis, in balance while being stressed tells a different story. For the mechanism, being active, engaging and having tactile and sensory stimulation moderates and modulates our internal chemistry.

© USA Copyrighted 2014 Mario D. Garrett

Saturday, October 4, 2014

Is Having Children Detrimental to Longevity?

How can sleep deprivation, economic shocks, diminished disposable income, constant caregiving, incessant worrying, 24/7 responsibility, lack of privacy, and incessant crying be correlated with longer life?   But that is just what a new study from Denmark is reporting. Having children increases your life expectancy.

The study itself is simple.  The Dane Professor Esben Agerbo and his colleagues published a study in 2012 where they looked at 21,276 childless couples who in 1994 went to an in vitro fertilization clinic. All these women had problems conceiving. By 2005 a total of 96 women and 220 men died. Women who did NOT have a child were four times more likely to have died compared to those who did have a child. The inexplicable aspect of this study is that the same disadvantage also transferred to men. Men who remained childless in this study were twice as likely to die early.

How can this be explained? Gerontology theories predict that having children reduces your life expectancy--especially if you stop having sex afterwards--as most couple who have children tend to do. 

The theory of antagonistic pleiotropy argues that some genes have contradictory effects at different age. Genes which might enhance your reproductive success--genes that increase testosterone in men, resulting in more muscle mass and masculine secondary sexual characteristics; or estrogen and bigger breasts in women--may at the same time have detrimental effects on survival later on in life--elevated risk of cancer in men and larger cancer nodes in women. Natural selection tends to favor these kinds of genes because they maximize the ability to transfer your genes—termed as fitness--without due concern for later life mortality.  From this theory it follows that higher rates of reproduction comes at a cost of higher post-reproductive mortality.

As a complementary theory, the Disposable Soma Theory argues that there are metabolic trade-off between reproduction and longevity. Reproduction utilizes biological resources which could otherwise be used for physical maintenance. Having more children to bear and rear uses up limited physical resources that could have promoted better health and a longer life. In this view, higher reproduction is associated with a shorter life span.

These theories are supported by the numerous studies by demographers looking at nuns and monks. Overall, these studies have been showing reduced mortality of 31-11 percent among nuns and monks. An advantage that is generally larger for monks than for nuns. It is more a lifestyle that protects you from dying early (rather than promoting longer life.) In the real world, where people do not live in monasteries/nunneries and where they do not follow a regimented life, it is hard to separate what is causing people to die earlier.

In 2002, using data for a preindustrial Sami population in Finland, Samuli Helle and his colleagues showed that the number of sons--rather than the total number of children--affected women’s longevity. This association was also found in data from a 19th century Flemish village and confirmed the association between number of sons born contributing to their mother’s early age of death. However the effect was only evident among poorer women, and mainly for women whose sons survived to at least to age five. Leading to the conclusion that resource competition--rather than pregnancy--might be the main explanation. Having children is not only a biological event. There is also a financial cost associated between childbearing history and longevity.


Having four or five children shortened women’s life span after 50 by about 3.5 years compared to women with one child or less. However, this effect could only be found among the poorest women. No effect of number of children for more well-to-do women, or for men, could be found.

And the poorer you are the poorer your diet and the harder the competition for resources (both inside the womb and outside.) 

How can this Danish study show such different results? Could we explain the results that having children increased longevity because it is reflecting having less money?

In Denmark, the first three courses of IVF are given free-of-charge. Wealthier couples, who may be able to buy more IVF treatment sessions can increase their chances of pregnancy. So methodologically, there is a higher likelihood that those who conceived were a self selecting richer group making the results already biased. What helped to clarify this point further--that it is socio-economic status which is promoting longer life rather than bearing children--is the finding that researchers found it didn't matter if the women or men who had children had them biologically or through adoption for them to benefit from increased longevity. Being well off  is one of the main criteria for having successful adoption.

The longest person that ever lived, Jeane Lousie Clament had one daughter. But she also did not work, lived a life of leisure, smoked (until she was 117 years) and ate over a kilo of chocolate a week. If children should choose their parents wisely, then similarly parents need to make sure they can afford their children or else pay for it with their life.

© USA Copyrighted 2014 Mario D. Garrett

Wednesday, September 17, 2014

Is the Human Race Heading For Extinction?

We are looking at a childless future.

All industrialized countries are having fewer children. Not enough growth to maintain our current population size. With the exception of Africa, and certain small ethnic and religious communities, Total Fertility Rate—the number of children an average woman will have in her lifetime—is declining sharply. Government incentives cannot reverse this slide into a childless future.

Are we becoming less efficient at making babies?

In 1992, following a study by the Danish Elizabeth Carlsen showing worldwide decline by 50 percent in sperm density, there was a backlash of critical reports refuting these findings. Then in 1997 Shanna Swan and her colleagues from California Department of Health Services, performed a reanalysis of data from 61 studies. Their study supports a significant decline in sperm density since the 1950s in the United States and Europe. Although there are exceptions—and recent studies by Elizabeth Carlsen herself in 2012 has shown improvement in sperm count—there is still a large proportion of people who are compromised fertility.  As an example, Denmark, during 2002–2004 reported more than one in fifteen Danish children born with assisted reproduction and, in addition, many couples were adopting foreign children.

The decline in sperm involves numerous factors, but the finger is pointing towards the use of pesticides and hormones in our food chain. Such an interpretation is supported by the increasing occurrences of testicular cancer and possibly also of malformations of the genital tract.

On the other side of the spectrum is the ability and motivation of women to have children. Women are having children later in life and when they have two or more children they are delaying each birth. Education—both formal and informal—plays a role in determining that women don't get pregnant early and then have children in quick succession. There is also a declining ability of women to have children, known as fecundity—the capacity to bear children. Women are experiencing increasing problems with conceiving and maintaining pregnancies.

According to the National Survey of Family Growth, one in seven U.S. women reported impaired fecundity in 2002. However, across a lifetime, Arthur Greil, from Alfred University, New York, and his colleagues, reported that more than half of women aged 25 to 45 in 2011 reported an episode of infertility at some point in their lives.

Although women are starting families later in life, which by itself reduces their success rate, there is an additional worry about declining fecundity. The Dutch researcher Boukje Zaadstra and her colleagues reported in 1993 that increasing obesity, specifically the waist-hip ratio, reduces the chances of conception more then age or overall obesity. So certain type of fat—stomach fat—effectively reduces fecundity among women. With an obesity epidemic reaching to all countries in the world, this has negative reproductive consequences. And it is the lower waist/hip ratio (WHR) rather than despite increasing BMI.  Compared to women with high WHR, women with a low WHR have fewer irregular menstrual cycles (Van Hooff et al., 2000), optimal sex hormone profiles (Jasienska, Ziomkiewicz, Ellison, Lipson, & Thune, 2004), ovulate more frequently (Moran et al., 1999), and have lower endocervical pH, which favors sperm penetration (Jenkins, Brook, Sargeant, & Cooke, 1995). Low WHR is also an independent predictor of pregnancy in women attending an artificial insemination clinic (Zaadstra et al., 1993) and in women attempting in vitro embryo fertilization transfer (Waas, Waldenstrom, Rossner, & Hellberg, 1997).

Paul Ehrlich’s 1968 sensational book “The Population Bomb” was such a good work of fiction that programs to limit fertility were put in place worldwide. There are so many emperors without clothes nowadays that we are virtually a nudist colony.

© USA Copyrighted 2014 Mario D. Garrett

Is Our Population Sustainable?

Sustainability, the “characteristic of a process or state that can be maintained at a certain level indefinitely,” cannot be applied to our population because we are already changing.
The main event that will ensure change is population aging. Population aging is where the number and proportion of older adults are increasing. This is happening at such speed and magnitude that the United Nations has identified aging as unprecedented, enduring, pervasive and profound. This is happening faster in developing countries. Although it took France over 110 years to become an aging country—one of the side effects of a declining TFR, from 7% to 14% of the population being 65 years and older—most developing countries will experience this within two decades. And all countries are reducing the number of children born. 
Population aging will ensure that we will never see such a young population again among our species. Our population will be changed permanently.
This is a living experiment. The main push is not that we are living longer but that we are having fewer children. This seems strange at first, but people are not living much older at old age, they are surviving better from childhood.
In the United States, an older adult at 65 increased their life expectancy by only 5.7 years. What this means is that in 2000 a 65-year-old was expected to live an additional 5.7 years more than someone who was 65 in 1900, a hundred years ago. As strange as this sounds, gains in our aging population are occurring among children.
For the first time in the history of our species, we are seeing a decline in the number of births. The decline in births is the primary cause of aging, it lowers the proportion of younger adults and it enhances the survival rate of children so that they have a better chance of reaching older age.
Around the 1950s and '60s, birth rates in most of the developed world started to decline. The primary reason for this is that after the Second World War, women for the first time had access to employment, education and contraception, which resulted in delaying pregnancy, extending the period between pregnancies and stopping having children at an earlier age.
All these factors determined a decline in the birth rate. Once this process of having fewer children started, it proved to be irreversible.
All developed countries, including the United States, have a fertility rate that is lower than that required to replace existing population (i.e., without immigration the population will decline). Without our healthy immigration, the United States will be experiencing severe pressures on our health and social services similar to what European countries are experiencing now.
Despite incentives in some European countries for couples to have more children, there is no indication that we can reverse this process. By itself this is of some concern, but there are also the findings that as a species we are loosing our ability to have children.
Since 1992 researchers at Copenhagen University have reported a decline in sperm counts around the world. We have been seeing this trend continue. In addition, by retarding the age of first pregnancy, women are also reducing their fecundity (their ability to become pregnant).
At the other end of the spectrum, the older adult population is increasing at a rate that we have not seen before. Helped by slightly better life expectancy, but fueled mainly by the sheer number of people, the fastest-growing group is that of centenarians (those 100 years of age and older).
Recent surveys estimate that there are 450,000 centenarians worldwide (about 50,000 in the United States). However daunting this great success is, if we look at super-centenarians (those over 110 years of age), we find that this figure drops to 30.
As a species, our life span (the longest that we have ever lived) was defined by the Frenchwoman Jeanne Calmert who lived to 122 years. There is evidence that indicates that we, as a species, are reaching this outer limit of life.
How sustainable is our lifestyle if we have a scenario where there are fewer children being born and where most older adults are pushing survival up to the life span (100 years plus).
Harry Dent has long maintained that our demography is destiny and that our economic market is held hostage to this powerful changing foundation. This profound change is already having pervasive repercussions on many aspects of our lives.
We are experiencing the beginning of these effects on our economy with declining savings and investment and diminishing demand for infrastructure such as highways, housing and schools. The recent realty collapse is just one (major) effect of the aging of the baby boomers.
However, the biggest fear of all, as expressed by former Federal Reserve Chairman Alan Greenspan, is Medicare. Unlike Social Security, which is a known quantity, because of the spiraling cost of medical procedures and advancing surge of medical technology, Medicare remains an ever-increasing and variable liability that will dwarf all other federal expenditures. By 2024, Medicare spending is expected to exceed Social Security spending and will continue to escalate thereafter.
The only way that our demography does not determine our destiny is to ensure that there is enough political will to address these issues. Are we making that commitment?

Tuesday, September 9, 2014

Is Castration the Answer to Longevity?

Genetic studies by Cynthia Kenyon—at the Hillblom Center for the Biology of Aging at the University of California San Francisco—with flatworms, and Richard Miller—at the Geriatrics Center of the Medical School, University of Michigan—with mice, show that having a diminished growth hormone production (or reception) seems to increase longevity. Having stunted growth increases longevity. The body seems to know that it needs to live longer to pass on its genes since its growth is stunted.

Which is exactly what happens with Michael Rose’ s experiments—at the Department of Ecology and Evolutionary Biology at the University of California, Irvine—with flies. Collecting eggs produced by older mothers produces offspring that lived longer.

There seems to be an expiration date stamped on our genes.  If we are stunted in growth or our parents delayed producing us, then our body seems to know that it needs to live longer in order to pass on its genes.  The best way to explain this is through the disposable soma theory. This theory which was first developed in 1977 by a biologist named Thomas Kirkwood—who now heads The Institute for Ageing and Health in its School of Clinical Medical Sciences, at Newcastle University—states that the body protects itself just enough so that we are able to pass on our genes.

What if we cheated our body? As in these experiments cheating the body into thinking that it is developing really slowly and therefore needed more time. What if we were castrated? The Cumming Manuscript Collection of the New York Academy of Medicine Library contains more than 1200 references, abstracts, and documents concerning the early history of human castration.

But the first time that eunuchs—boys who had their testicles and sometimes their penis removed surgically—featured in longevity debates was with the observation by Serge Abrahamovitch Voronoff in the early 1900s.  And it was not a positive observation.

Voronoff—a French surgeon of Russian—worked at a hospital in Cairo from 1896 to 1910 where he had the opportunity to observe eunuchs. He noted their obesity, lack of body hair, and broad pelvises, as well as their flaccid muscles, lethargic movements, memory problems, and lowered intelligence. He concluded that the absence of testicles was responsible for aging and that their presence should prompt bone, muscle, nerve, and psychological development. He saw aging as the result of the lack of substance from the testicles and ovaries. This is all before we knew about hormones. Voronoff gained fame for his technique of grafting monkey testicle tissue on to the scrotum of men for anti-aging purposes. Voronoff and his predecessor and mentor Charles-Édouard Brown-Séquard—although ridiculed at the time—developed the field of endocrinology, the study of hormones. 

Coming back to the observation about eunuchs, Voronoff observations was that castration had retarding effects.

But then a new study in 2012 by Kyung-Jin Min from the Inha University, and his Korean colleagues, reversed this finding. In their study the authors reported that during Chosun Dynasty between 14th to early 20th centuries Korean eunuchs lived 14 to 19 years longer than other (intact) men. Researchers were able to identify 81 eunuchs, who were castrated as boys, and determined that they lived to an average age of 70, significantly longer than other men of similar social status. Three of the eunuchs lived to 100. This is a centenarian rate that's far higher than would be expected today.

Historically, and as recent as the 19th century, eunuchs were common across the world. Castrati boys—castrated before puberty—were among the most prized singers especially in catholic churches in Italy (the Sistine Chapel retained the last of the castrati singers) and Opera houses in Vienna. Elsewhere eunuchs were hired staff in harems and imperial palaces in China, Korea, Japan, and the rest of Asia and the Middle East. As well as in Europe and Russia.

In the 18th century there was a Christian sect called the Skoptzy, also called the White Doves, whose male members—in order to attain their ideal of sanctity—subjected themselves to castration. They believed that the Messiah would not come until the Skoptsy numbered 144,000 (Rev. 14:1,4).

Further East, in China, eunuchs played a more central role in government The emperor maintained approximately 2,000 in his service, the imperial princes and princesses each had about 30, and various family members were allowed 10 or so eunuchs each. Although in this context, castration was mostly as a punishment, some subjected themselves to the procedure in order to gain employment. At the same time, during the Ottoman period, especially from the 16th century on, black eunuchs from Ethiopia or Sudan were in charge of the harem in the Ottoman court. Many of these boys were castrated at a monastery in Upper Egypt by Coptic priests. The practice was pervasive and endemic.

In 1999 Jean Wilson and Claus Roehrborn investigated the long-term effects of castration. These included the enlargement of the pituitary gland, especially among those with an earlier castration. Skeletal changes included thinning of the bones of the skull and decreased bone mineral density. Although an increased incidence of fractures does not appear to have been reported in the eunuchs. Some reported growth of breasts in the Ottoman court eunuchs, which is also evident in photographs of Skoptzy men and Chinese eunuchs. Shrinkage of the prostate was common among eunuchs. However the authors could not resolve whether life span differed in their study.

A study on life span difference was done earlier in 1969, by James Hamilton and Gordon Mestler from the Department of Anatomy, State University of New York College of Medicine. They studied the mortality of patients in a mental institution with a population of 735 intact White males, 883 intact White females, and 297 White eunuchs. It was common practice to castrate mentally challenged children at the turn of the century, part of the eugenics movement. They reported that survival was significantly better in eunuchs than in intact males and females. This survival advantage started at age 25 years and continued throughout their life. The life expectancy for eunuchs was 69.3 years compared to 55.7 years in intact males. Males castrated at 8-14 years of age—before sexual maturation—were longer lived than males castrated at 20-39 years of age—after sexual maturation. Castration reduced the age of death by 0.28 years for every year of castration from age 39 and younger.

There are many changes that happen as a result of castration. The world was very different 600 years ago, or even 100 years age. In most cases it was a very violent world where men suffered early mortality through wars, famine, and daily trauma.  Eunuchs, because of their demeanor might have escaped all of that onslaught of violence. They might also have had more nurturing qualities that extended to looking after themselves better. We will never know.

Pragmatically we know that sex, and the activity surrounding sex, increases longevity. Howard Friedman and Leslie Martin in the Longevity Project longitudinal study provided our first glimpse into female orgasms and longevity. The study which was begun by Lewis Terman of Stanford University, California in 1921 on 1548 children with high intelligence born around 1910 was continued after his death in 1958. Now in their nineties, the study morphed into a gerontological study. One of the interesting and pertinent findings was that women who had a higher frequency of orgasm tended to live longer than their less fulfilled sisters.

No data on men was collected from this study. But a separate study in in the town of Caerphilly in South Wales, England, provided evidence for males as well.  George Davey Smith from Department of Social Medicine, University of Bristol,, England, and his colleagues interviewed nearly 1,000 men in six small villages about their sexual frequency,, then followed up on their death records ten years later. The authors determined that men who had two or more orgasms a week had died at a rate half that of the men who had orgasms less than once a month. And importantly there was a dose effect, where the more times these men had orgasms the longer they lived.

These observations have been replicated in Sweden and in the USA for both male and female.

The most conclusive evidence however comes from the masters of longevity themselves—centenarians. In the Blue Zones the cluster of centenarians teach us about the pragmatisms of living longer and sexual activity is a significant part of their life. In some cases they also carried out extra marital affairs.


Perhaps there are better ways to cheat the body to tell it that it is not quite finished yet. Perhaps if you behave like you are still sowing seeds, the body will still support your endeavors. It is likely then that you do not need to cheat the body. It seems that enjoying its great capacity, in all its wondrous glory, is enough to increase longevity. Castration might cheat the body to stay around longer, but sex will make it want to stay longer. 

© USA Copyrighted 2014 Mario D. Garrett

Monday, August 25, 2014

Grieve Alone, Your Way.

Despite older adults having more experience with grief, the classic grief study that has determined grief counseling was developed for children.

Most everyone knows of the Swiss physician Elizabeth Kubler-Ross stages of grief. Based on earlier work by the psychologists Bowlby and Parkes, Kubler-Ross crystalized the stages in her 1969 book On Death and Dying. What was unique is focusing on communication during grieving. She singlehandedly overturned how physicians were treating dying patients—as medical failures to be ignored until they expired. 

The theory states that we go through a series of stages before we come to accept the loss. Kubler-Ross defines five stages starting with an initial short period of Denial (D) that it could not happening, moving into Anger (A) when the loss is taken personally, followed by a series of Bargaining (B) strategies to try and reverse the outcome, and then once the realization of the loss is seen as permanent, Depression (D) and eventually, at the end of the grief there is Acceptance (A) that we cannot change these events. DABDA model of stages of dying morphed into stages of grief.

It is the only grief theory discussed in psychology training. The stage theory of grief is also part of the medical curricula and part of the grief education at the National Cancer Institute.  It has been accepted widely across the globe. It is the script provided to grieving relatives and has even entered into product market research to understand the reaction to the “death” of iPhone 4 in favor of iPhone 5.  It is a pervasive theory.

Despite its popularity, how accurate is it for older adults?

George Bonanno with Columbia University, New York, has been the main counterpoint for these stages.  Bonanno takes a diametrically apposing approach.  He argues that there are no stages. In fact having no stages is healthy. In 2002 Bonanno studied elderly bereaving spouses and nearly half showed no signs of shock, despair, anxiety or intrusive thoughts six months after their loss. This he termed as Resilience. Suggesting that grief stages are not prescriptive, dispelling "grief work hypothesis."

This idea of expressing grief in order to cope was also dispelled by the Dutch husband-and-wife Dutch research team Wolfgang and Margaret Stroebe of Utrecht University. They found that widows who avoided confronting their loss were not any more depressed than widows who "worked through" their grief—talking or writing about the experience. More recently, in 2008, Mark Seery from State University of New York and his colleagues studying reactions to the attacks of September 11, 2001, reported similar findings. There are no stages. It is not prescriptive to healthy coping.


But what these stages have done is that it allowed grieving to be accepted as healthy. It is the first time since Victorian times that grief is validated. Because there were assumed stages, people felt more comfortable to allow others express their grief—thinking, this is only a stage, it will pass. Although there are many valid criticisms, focused on the meaning of constructs and the therapeutic value of expressing loss, one outcome has been that we are discussing grief. And that is healthy, because grief is real and painful.

 © USA Copyrighted 2014 Mario D. Garrett