Witness my Life: A Psychotherapist's Journey to Healing

Witness my Life: A Psychotherapist Journey to Healing

Why is it that people participate in research?

A new method of recording and documenting perspectives from a community perspective, called photovoice, has started generating interesting results. Photovoice is where community members are provided with a camera, video or voice recorder to document events at the community level. Photovoice was developed in 1992–by Caroline Wang of the University of Michigan, and Mary Ann Burris, at Women's Health at the Ford Foundation, Beijing, China--for rural women in Yunnan Province, China to advocate for new policies and programs. This method has been producing some amazing documentaries on homelessness among teenagers, illegal drug trade, as well as images of dementia. And the motivation for participating in this kind of documentation is that it seems we want someone to be a witness to our life. Not to judge it, or even be part of it, but just to witness our trials and tribulations. Perhaps an affirmation, that because someone sees our lives nearly as close to as we experience them, that somehow, then, we matter. Perhaps it is seen as some form of non-judgmental validation. All of those screaming social network sites are but another expression of this desire for others to witness our lives.  In this case of witnessing, it is a form of benevolent narcissism.

Albert Camus wrote about this in 1956, in one of his most understated novels, The Fall. This story tells of a confession to a stranger. It takes place in a bar called Mexico City in Amsterdam, by the protagonist of the story Jean-Baptiste Clamence. From his success as a wealthy Parisian defense lawyer culminating on an unidentified crisis which brings about a vague fall from grace. After making some broad and general confession to a stranger in a bar, Jean-Baptiste Clamence ventures out into the night one last time. We are meant to assume that his last act is suicide. Jumping off one of the may bridges in Amsterdam. But the point of the novel is that the only way to bring meaning to the suffering of living, without a god, without objective truth is if there is some recognition that we exist. 

Jean-Baptiste Clamence’s confidant, an unknown character, becomes his final witness to his life. The Fall was awarded the 1957 Nobel Prize in Literature and was Camus’ final piece of fiction until he died in a car crash. The book’s complexity allows for different interpretations and for me it has been the fact that we are ultimately responsible for everything. By your activity or inactivity, we choose to support an outcome. But such an interpretation is too shallow for a deeply complex and ambivalent story.  We might be responsible for our actions, but then there is no morality to pass final judgement. Our final judgement is to have a witness. Good or bad actions do not matter if there is no one to witness it.

Maria Arman with the Karolinska Institutet in Solna, Stockholm, Sweden, in her book, Bearing witness: An existential position in caring has one of the closest meaning to this interpretation of witness. That witnessing is part of the definition of who we are. As social beings, our awareness of self is influenced (if not completely defined) by what and how we think others are defining us.  A basic assumption in caring, or being empathic is to be present for the other person. To bear witness for someone, to share their awareness is to share their burden. But there is more to witnessing, because by sharing an awareness you are affirming their journey through life.

The philosopher Emmanuel Lévinas defines an encounter with another person as a privileged experience. The proximity of the other person is the acknowledgement of being real. In a world where images are held as real, and truth is negotiated, the idea that I matter is a consoling balm on the rawness of my ever changing world.

To be a witness you share a physical space and experience the same perspective with another person. You share, verbally, emotionally or spatially a mutual reality. There is a convergence where you become the other person as much they become you. This is the healing of witnessing. Developing such a relationship is a willful act on your part. Witnessing is an affirmation that we have passed through life. No judgment about good or bad outcomes. There is a validation of my presence, and my journey. A memorable tune, a remembered story, a shared intimacy. All experiences that when witnessed can assert my place in this world. That although there might be nothing else but my experiences, that for one brief moment, that internal and closed trove has been acknowledged.

Isn’t this what psychotherapy is all about? If Sigmund Freud in 1905, the father of psychotherapy, was not so misguided as to suggest that because learning stops at age 50, older adults are not good candidates for psychotherapy, perhaps we would be able to see the effect of witnessing in alleviating despair. As psychotherapists try to instill trust, the experience of witnessing remains the bedrock for affirmation of one life.

 © USA Copyrighted 2016 Mario D. Garrett

Witness my Life: A Psychotherapist's Journey to Healing

Witness my Life: A Psychotherapist Journey to Healing

Why is it that people participate in research?

A new method of recording and documenting perspectives from a community perspective, called photovoice, has started generating interesting results. Photovoice is where community members are provided with a camera, video or voice recorder to document events at the community level. Photovoice was developed in 1992–by Caroline Wang of the University of Michigan, and Mary Ann Burris, at Women's Health at the Ford Foundation, Beijing, China--for rural women in Yunnan Province, China to advocate for new policies and programs. This method has been producing some amazing documentaries on homelessness among teenagers, illegal drug trade, as well as images of dementia. And the motivation for participating in this kind of documentation is that it seems we want someone to be a witness to our life. Not to judge it, or even be part of it, but just to witness our trials and tribulations. Perhaps an affirmation, that because someone sees our lives nearly as close to as we experience them, that somehow, then, we matter. Perhaps it is seen as some form of non-judgmental validation. All of those screaming social network sites are but another expression of this desire for others to witness our lives.  In this case of witnessing, it is a form of benevolent narcissism.

Albert Camus wrote about this in 1956, in one of his most understated novels, The Fall. This story tells of a confession to a stranger. It takes place in a bar called Mexico City in Amsterdam, by the protagonist of the story Jean-Baptiste Clamence. From his success as a wealthy Parisian defense lawyer culminating on an unidentified crisis which brings about a vague fall from grace. After making some broad and general confession to a stranger in a bar, Jean-Baptiste Clamence ventures out into the night one last time. We are meant to assume that his last act is suicide. Jumping off one of the may bridges in Amsterdam. But the point of the novel is that the only way to bring meaning to the suffering of living, without a god, without objective truth is if there is some recognition that we exist. 

Jean-Baptiste Clamence’s confidant, an unknown character, becomes his final witness to his life. The Fall was awarded the 1957 Nobel Prize in Literature and was Camus’ final piece of fiction until he died in a car crash. The book’s complexity allows for different interpretations and for me it has been the fact that we are ultimately responsible for everything. By your activity or inactivity, we choose to support an outcome. But such an interpretation is too shallow for a deeply complex and ambivalent story.  We might be responsible for our actions, but then there is no morality to pass final judgement. Our final judgement is to have a witness. Good or bad actions do not matter if there is no one to witness it.

Maria Arman with the Karolinska Institutet in Solna, Stockholm, Sweden, in her book, Bearing witness: An existential position in caring has one of the closest meaning to this interpretation of witness. That witnessing is part of the definition of who we are. As social beings, our awareness of self is influenced (if not completely defined) by what and how we think others are defining us.  A basic assumption in caring, or being empathic is to be present for the other person. To bear witness for someone, to share their awareness is to share their burden. But there is more to witnessing, because by sharing an awareness you are affirming their journey through life.

The philosopher Emmanuel Lévinas defines an encounter with another person as a privileged experience. The proximity of the other person is the acknowledgement of being real. In a world where images are held as real, and truth is negotiated, the idea that I matter is a consoling balm on the rawness of my ever changing world.

To be a witness you share a physical space and experience the same perspective with another person. You share, verbally, emotionally or spatially a mutual reality. There is a convergence where you become the other person as much they become you. This is the healing of witnessing. Developing such a relationship is a willful act on your part. Witnessing is an affirmation that we have passed through life. No judgment about good or bad outcomes. There is a validation of my presence, and my journey. A memorable tune, a remembered story, a shared intimacy. All experiences that when witnessed can assert my place in this world. That although there might be nothing else but my experiences, that for one brief moment, that internal and closed trove has been acknowledged.

Isn’t this what psychotherapy is all about? If Sigmund Freud in 1905, the father of psychotherapy, was not so misguided as to suggest that because learning stops at age 50, older adults are not good candidates for psychotherapy, perhaps we would be able to see the effect of witnessing in alleviating despair. As psychotherapists try to instill trust, the experience of witnessing remains the bedrock for affirmation of one life.

 © USA Copyrighted 2016 Mario D. Garrett

If Alzheimer’s disease was Treated like Cancer

The 2016 Cancer Moonshot, headed by Vice-President Joe Biden, the most potentially funded-health research enterprise in the USA just issued a set of 10 recommendations for cancer research. The Blue Ribbon Panel of expert advisers suggested basic steps in research that are very similar to the steps we should be taking in dementia research if we are serious about a cure. What would these Blue Ribbon Panel of expert advisers advise on dementia? Perhaps something along the following lines below:

1. Establish a network for direct patient involvement; engage patients to contribute their comprehensive dementia profile data to expand knowledge about what therapies work, in whom, and in which types of dementia.
2. Establish a dementia immunotherapy clinical trials network devoted exclusively to discovering and evaluating immunotherapy approaches.
3. Develop ways to overcome dementia’s resistance to therapy, through studies that determine the mechanisms of misfolded proteins, in addition to the Beta Amyloid and Tau Protein.
4. Create a national ecosystem for sharing and analyzing dementia data so that researchers, clinicians, and patients will be able to contribute data, which will facilitate efficient data analysis.
5. Intensify research on the major drivers of early onset dementia; improve understanding of the genetic component of early onset and use new preclinical models to develop inhibitors that target them.
6. Minimize dementia treatment's debilitating side effects; accelerate the development of guidelines for routine monitoring and management of patient-reported symptoms to minimize debilitating side effects of dementia and its treatment.
7. Reduce dementia risk and dementia health disparities through approaches in development, testing, and broad adoption of proven prevention strategies.
8. Mine past patient data to predict future patient outcomes; predict response to standard treatments through retrospective analysis of patient specimens.
9. Create dynamic three-dimensional maps of human dementia evolution to document the genetic lesions and cellular interactions of each neuropathological event  as it evolves from a preclinical to advanced dementia.
10. Develop new enabling dementia technologies to characterize neuropathology and test therapies.

For a complete summary of the faults with Alzheimer’s research and why we need a similar Blue Ribbon Panel of expert advisers of Alzheimer’s disease:

Garrett MD & Valle R (2016) A Century of Confusion in Researching Alzheimer’s Disease. Dementia: The International Journal of Healthcare 2(2), 13-22.

Garrett MD, Valle R (2015) A New Public Health Paradigm for Alzheimer’s Disease Research. SOJ Neurol 2(1), 1-9.

Garrett MD & Valle RJ (2016).A Methodological Critique of The National Institute of Aging and Alzheimer’s Association Guidelines for Alzheimer’s disease, Dementia and Mild Cognitive Impairment. Dementia: The International Journal of Social Research and Practice,15(2) 239–254. DOI: 10.1177/1471301214525166

Garrett MD (2015) Politics of Anguish: How Alzheimer's disease became the malady of the 21st century. Createspace. USA

© USA Copyrighted 2016 Mario D. Garrett

The Death of Biological Determinism

In May 2016, in a short eight-page report in Nature Biotechnology, Rong Chen, Stephen Friend and Eric Schadt from the Icahn School of Medicine at Mount Sinai, New York, and their colleagues reversed our ideas about genetic determinism. This small revolution proved to be radical because by association, this also unhinges biological determinism—the belief that biology determines all your traits.

What they did is to apply scientific methods to commonly held beliefs about disease. Usually genetic investigations focus on a group with disease by trying to find genes that are different in this group from the rest of the population. By comparing this group with a control group they hope to single out the gene that causes this difference. Sometimes geneticists hit lucky and find only one gene that is different between the two groups. In such circumstances this single gene follows Mendelian laws in how it affects people. Mendelian laws are named after the monk Gregor Johann Mendel.

Between 1856 and 1863--before genes were discovered in the early 1900s--Mendel was working on cultivating some 29,000 pea plants. He noticed that peas seem to acquire their characteristics from both parents in a mathematical fashion, with some traits being more dominant than others. Mendel discovered the mathematics of heritability.

He defined for every characteristic—a phenotype, an expressed genetic trait—there are two parts determining how that characteristic is expressed. Now we know that two alleles compose a gene that determine a physical trait. Mendel’s observations developed three basic laws:

·      Alleles can be either dominant or recessive, with the dominant allele always imposing its influence over the recessive.

·      Alleles separate during cell formation so that recessive and dominant allleles are received by different cells.

·      Alleles have different and unique characteristics that are unrelated to other elleles.

Using this method, scientists have identified 584 Mendelian diseases: where one gene causes a specific disease. Most of genetic studies are based on this methodology. But such methodology remains flowed in reasoning. Just because a group had a specific gene, and a control did not, does not define a causal relationship. The syllogism is wrong. Just because all As have Bs does not mean that all Bs have As.

Such fault in reasoning in our genetic understanding of Mendelian diseases was exposed by Rong Chen and his colleagues who performed a comprehensive screen of 874 genes in 589,306 genomes—individuals—with 874 implicated genes. This comprehensive study led them to identify 15,597 candidates where their genes did not match the expression of the disease. After rigorous elimination of candidates for various technical and theoretical reasons, a final list of 13 candidates remained. All these individuals had either both pairs of a recessive gene, or one of a dominant gene that causes one of eight type of Mendelian disease. These Mendelian childhood disorders would normally be expected to cause severe disease before the age of 18 years: cystic fibrosis, Smith-Lemli-Opitz syndrome, familial dysautonomia, epidermolysis bullosa simplex, Pfeiffer syndrome, autoimmune polyendocrinopathy syndrome, acampomelic campomelic dysplasia and atelosteogenesis.

There are three possible interpretations of this outcome. That the Mendelian diseases identified were in fact incorrectly defined and there might be other genes involved. Secondly, that these individuals are resilient—in ways unknown--to the disease. The third possibility being that there are other factors—including genetic factors as well as epigenetic influence--that determine whether genes express into a disease--genotype expresses into a phenotype.

The overarching outcome of this study is however the importance of logic/reasoning and the scientific method. Science is nothing but method. The results of scientific work are always incomplete since science is not about the outcomes but about the method. In gerontology this study contributes to a continuing appreciation of how genetics might be the road map, but we are in fact the drivers of our journey through life.

Reference:

Chen, R., Shi, L., Hakenberg, J., Naughton, B., Sklar, P., Zhang, J., ... & Sleiman, P. (2016). Analysis of 589,306 genomes identifies individuals resilient to severe Mendelian childhood diseases. Nature biotechnology.

© USA Copyrighted 2016 Mario D. Garrett

How Mild is "Mild Cognitive Impairment"?

As we get older, we start having a constant fear that our lapses in memory are the beginning of Alzheimer’s disease. After cancer, Alzheimer's disease has taken hold as the number one fear among Americans.  We all have memory lapses, at any age. But when we are older we tend to be more aware of these lapses in memory and we become more fearful when we forget.  We try and add humor in order to alleviate this fear. We say things like it’s a senior moment, a brain fart, a mental hiccup, misfiring neuron, and my favorite synaptic lapse. Despite the humor the fear persists.

The problem is that although all those with Alzheimer’s disease started off experiencing memory loss, not all those that have memory loss will develop into Alzheimer’s disease. In fact even with documented memory impairment you are more likely to have some other underlying condition than Alzheimer's disease. Unfortunately what we call Mild Cognitive Impairment (MCI), the term used to refer to these bouts of memory lapses, is itself not well understood.

There are problems measuring memory loss using MCI. When we refer to “cognitive” we should be referring to our mental processes that should include perception, judgment, reasoning, AND memory. However, MCI is most often just limited to memory. So if you have a failing memory then it is assumed that the rest of your cognitive abilities are similarly diminished. This is not only not true but also simplistic. The second issue with this method of defining your mental capacities is the assumption that there is an average or normal level of memory and that this level is stable. This is of course not true. From experience we know that we have good days and bad days, at any age. Memory is not a static library but an active engaging process that is vulnerable to many external factors, particularly emotional trauma. Memory can become compromised during episodes of grief, retirement, an upcoming medical operation or divorce among many other situations that distracts our ability to remember past events.. This is made worse by lack of sleep, which accompanies stressful times, and is one of the biggest issues with older adults.

In addition, being retired means that you can take little naps during the day. But this results in not feeling sleepy at night, or getting up in the early hours of the day. Sleep deprivation not only affects your memory but also changes your mood, balance and appetite.  In some cases, sleep disorders are due to changes in our brain, such as the reduction in melatonin, but we can do something about this, as we will discuss later on.

But perhaps the biggest culprit that affects our memory is medication. Medication among older adults is perhaps the single most significant cause of problems. Such iatrogenic diseases--problems caused by bad medical practices--remains a hidden problem among older adults. Medication can have drastic effects on memory. Even if you have been taking the same medication for some time, your body processes chemicals differently as you age. Especially if you have recently started taking additional medications or substances. In particular, nearly all sleeping pills, over-the-counter antihistamines, anti-anxiety medications and antidepressants can have negative effects on memory. Medications that you might be taking for other existing conditions can also start having negative effects on your memory such as some medications used to treat schizophrenia, and pain medicines used after surgery.

Identifying the cause of your memory lapses is important because it means that you can reverse these problems. Some memory problems can also be related to vitamin B1 and B12 deficiency, easily checked with a blood test. Some health issues, such as thyroid, kidney, or liver disorders also can lead to memory loss. In addition, some herbal medicines, recreational drugs and also the use of alcohol will negatively effect memory.

These are all likely culprits for why your memory has gotten worse. Rather than jumping to the conclusion that you have Alzheimer’s disease. Unfortunately, nearly all websites that offer advice on memory loss--despite the caveat that not all memory loss leads to Alzheimer's disease--invariably end up with a definition of Alzheimer's disease. It is important to think of these other ways that your health can be changed rather than resigning yourself to saying that it is Alzheimer’s. Especially since Alzheimer's disease is so passive a disease. At least by approaching it as a lifestyle issue  you retain control, you can change your condition.

A recent study by Dale Breseden from southern California has successfully reversed clinically diagnosed Alzheimer’s disease. Breseden did this not with some magic potion or a new drug, but with some simple behavior strategies, involving diet, exercise and social/physical activities. This recent study reported how an intervention included:

Cutting out all simple carbohydrates and reducing wheat products and processed foods, while increasing consumption of vegetables, fruits and non-farmed fish;
Fasting 12 hours before bedtime and 3 hours between dinner and bedtime;
Yoga and meditation for 20 minutes a day;
Exercising for at least 30 minutes a day, 4-6 days a week;
Taking melatonin each night (used to ease insomnia), and increasing sleep to 7-8 hours;
Taking methylcobalamin (a form of vitamin B), vitamin D3, fish oil and CoQ10 supplements each day; and,
Increasing oral hygiene through use of an electric flosser and electric toothbrush.

Using this comprehensive life-style change, Bredesen saw nine out of the 10 patients improve within 3‐6 months. These improvements were sustained for two-and-one‐half years from initial treatment. The one person who did not improve was because their dementia was so great that he forgot to carry out the exercises. Not surprisingly, this life-style change was found to have a positive impact on multiple other chronic illnesses in addition to Alzheimer’s disease. Memory loss is unlikely to be due to Alzheimer’s disease, but use this as an indication that you need to address some of your life-style patterns and aim to live a healthier life. There is nothing mild about Mild Cognitive Impairment but it does not mean its a death knell.

© USA Copyrighted 2016 Mario D. Garrett

Reversible Alzheimer’s Disease: The role of normal-pressure hydrocephalus

Between 9 and 13 percent of residents in nursing homes and assisted living facilities are likely mis-diagnosed with Alzheimer’s disease and can be cured. Anthony Marmarou with the Virginia Commonwealth University Medical Center, Richmond, Virginia and his colleagues investigated how common it is to find buildup of fluid in the brain among clients in assisted-living and extended-care facilities. [1]  Known as idiopathic (unknown cause) normal-pressure hydrocephalus (iNPH), this condition mimics the behavior of Alzheimer’s disease. Normal-pressure hydrocephalus occurs when there is a restriction in the spaces that hold fluid deep inside the brain, resulting in pressure build-up. The pressure compresses the soft tissues of the brain restricting its function. The authors found that out of 147 patients between 9 to 14% had NPH depending on the diagnostic criteria used. Among these 17 patients, 11 received shunts and seven of these showed either transient or sustained improvement a year later. Although they were likely diagnosed with Alzheimer’s disease, a year later most were cured.

The symptoms of normal-pressure hydrocephalus are very similar to Alzheimer’s disease. When identified as a distinct disease it is known as the “wet, wild, and wobbly.”  Characterized by urinary incontinence (wet), dementia (wild), and gait dysfunction (wobbly). It is estimated that 1.6–5.4% of those with dementia are affected by iNPH.[2]  If the condition is left untreated—most of these cases are overlooked as Alzheimer’s disease—chronic iNPH patients share overlapping characteristics with Alzheimer’s disease in 75% of the time. It becomes increasingly difficult to differentiate the two the longer that iNPH is left untreated since the NPH syndrome will become Alzheimer’s disease.

Although there is no community-wide study looking at how common NPH is, there are some small sample studies that indicates that it is likely to be very common among older adults 65 years older. [3]  Among older adults in the community, the prevalence is around 1.3%, higher in assisted-living and extended-care residents with 11.6%. A small proportion of patients (2%) show permanent improvement after releasing the pressure in the brain using a shunt. The problem is that there are no easy indicators—including brain imaging—for distinguishing iNPH and Alzheimer’s disease. The images must still be interpreted with clinical features, blood measurements, CSF biomarker measurements, tap test, and CSF drainage results.

Because it is hard to diagnose, iNPH remains under recorded. Many studies report an association between hypertension, vascular disease and iNPH—with strokes and heart attacks being common precursors—so there is a need to look at any vascular disease as a precursor to Alzheimer’s. And the problem is that Alzheimer’s disease is so broad a category that most things that affect the brain and cause behavior changes are likely to be diagnosed Alzheimer’s disease even though it is likely not, such as amyloid deposition, CSF biomarker content, and presence of vasculature diseases. [4] A diagnosis of Alzheimer’s disease is a prescription for lost hope, whereas vascular disease is more likely to be amenable to therapy.

Vascular dementia—where the plaques and tangles are caused by a lack of blood flow in the brain (called cerebral perfusion)—is confused with Alzheimer’s disease most often because both share the same biomarkers and have the same expression. They look the same to the inexperienced clinician. Cerebrovascular disease among adults over 75 years of age is a common condition—36 percent overall, 25 percent for coronary, 58 percent hypertension, and 11 percent for stroke. [5]  It seems likely that because of these co-morbidities, vascular dementia contributes to, and is sometimes mis-diagnosed as Alzheimer’s disease. The silent issue is recognizing how frequently vascular disease promotes dementia.  Contemporary neuroscience still lacks a thorough understanding of exactly what contribution cerebrovascular disease makes to cognitive impairment. [6]

The answer is to move away from the practice of calling anything that disturbs cognition as Alzheimer’s disease.[7] Clinicians need a strategy, a roadmap to differentiate all these different type of diseases because they have different causes. Knowing the cause is the first step to formulating a cure. That is, if we are truly serious about finding a cure for Alzheimer’s disease.

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[1] Marmarou A, Young HF & Aygok GA (2007) Estimated incidence of normal-pressure hydrocephalus and shunt outcome in patients residing in assisted-living and extended-care facilities. Neurosurgical Focus, 22(4); 1-8.

[2] Gallia GL, Rigamonti D, Williams MA (2006) The diagnosis and treatment of idiopathic normal pressure hydrocephalus. Nat Clin Pract Neurol 2, 375-381.

[3] Martín-Láez, R., Caballero-Arzapalo, H., López-Menéndez, L. Á., Arango-Lasprilla, J. C., & Vázquez-Barquero, A. (2015). Epidemiology of Idiopathic Normal Pressure Hydrocephalus: A Systematic Review of the Literature.World neurosurgery, 84(6), 2002-2009.

[4] Di Ieva, A., Valli, M., & Cusimano, M. D. (2014). Distinguishing Alzheimer's disease from normal pressure hydrocephalus: a search for MRI biomarkers.Journal of Alzheimer's Disease, 38(2), 331-350.

[5] Schiller J.S., Lucas J.W. & Peregoy J.A. (2012.) Summary health statistics for U.S. adults:National Health Interview Survey, 2011. National Center for Health Statistics. Vital Health Stat, 10(256).

[6] Jellinger K.A. (2008). Morphologic diagnosis of 'vascular dementia' - a critical update. J Neurol Sci, 270: 1-12

[7] Garrett MD (2015) Politics of Anguish: How Alzheimer's disease became the malady of the 21st century. Createspace. USA

© USA Copyrighted 2016 Mario D. Garrett

Early Emotional Cascade and Alzheimer’s disease