The Golden Years: Traumatic Stress and Aging – An Interview with Joan Cook

Dr. Joan Cook is a clinical psychologist and Associate Professor in the Yale School of Medicine, Department of Psychiatry. She has specific expertise in the areas of traumatic stress and geriatric mental health. Dr. Cook has served as the principal investigator on four grants from the National Institute of Mental Health, as well as grants from the Agency for Healthcare Research and Quality and Patient-Centered Outcomes Research Institute. She is a member of the American Psychological Association (APA) Guideline Development Panel for PTSD and is the 2016 President of APA’s Division of Trauma Psychology.

 

Recently, I spoke with Dr. Cook about PTSD in older adults.

 

source: pexels
source: pexels

Dr. Jain: Can you comment on the unique methodological considerations for researchers doing PTSD research in the elderly?

 

Dr. Cook: There are a number of methodological considerations that researchers who want to study older traumatized individuals might want to think about beforehand. One issue in working with this current cohort of older (65 and above) adults is their potential denial or minimization of reporting of trauma and related symptoms. For some individuals in this current cohort, their traumas may have preceded the 1980 introduction of posttraumatic stress disorder (PTSD) into the official diagnostic classification. Thus they may associate more stigma or blame themselves for having experienced such event and/or having subsequent symptoms.

 

I think events such as the September 11th terrorist attacks, the wars in Iraq and Afghanistan, and Hurricane Katrina, have helped raise the national consciousness about trauma. But I still clinically come across older adults who lack an understanding of the potential effects of traumatic experiences or don’t accurately label such events as “traumatic.” In addition, there are also cognitive, sensory, and functional impairments that may affect the experience, impact, or reporting of trauma-related symptoms.

 

Dr. Steven Thorp, Heather Sonas and I (2011) provided some recommendations for conducting trauma and PTSD-related assessment and treatment with older survivors. This includes practical issues like the need for large, bold fonts in written assessment or therapy materials to increase readability and minimize frustration, using specific behaviorally anchored questions to assess for traumatic events, and the benefits of using more than one method of assessment (e.g., self-report, observation, caregiver report, and structured interviews).

 

source: pexels
source: pexels

Dr. Jain: Can you discuss the findings of Intimate Partner Violence (IPV) rates (and related PTSD) in older women versus younger women? How might these findings be explained (e.g. reporting bias, less public awareness, lack of resources to help older women)?

 

Dr. Cook: I’m so glad you asked this question! This is a topic that is near and dear to my heart. I’ve done a little research in this area but wish I had time and resources (grant support, interested collaborators) to do more.

 

In general, rates of IPV and related PTSD are lower in older as opposed to younger women. This may be due to more recent violent times in our society, for sure. But it also may be due to an interaction between reporting bias and cohort effects. The current cohort of older women may be less likely both to label IPV as such and to disclose such histories to health care providers. There also appears to be limited public awareness and fewer available services specifically designed for older IPV survivors compared to younger and middle-aged women.

 

A fairly recent systematic review that my colleagues and I conducted found that older women with IPV histories have greater psychological difficulties than older women who do not have these experiences. More specifically we also looked at data from a large nationally representative sample and found that one out of seven older women reported a history of physical or sexual assault, or both. And those who reported this type of traumatic history were generally more likely to meet criteria for past-year and lifetime PTSD, depression, or anxiety than those without such a history. Although IPV does not appear to be a widespread phenomenon in older women, it should not remain a “hidden variable” in their lives. I’d love to see more public attention, research, and clinical endeavors with older traumatized women.

 

Dr. Jain: Much of the studies of PTSD in older populations have been done in Veterans—do you think these findings are applicable to other populations of trauma exposed adults?

 

Dr. Cook: You’re right. The vast bulk of the empirical literature on older adult trauma survivors has been conducted on combat veterans and former prisoners of war. But there is a relatively decent sized research base on older adults who experienced Holocaust-related trauma earlier in their life and individuals who experienced natural or man-made disasters later in life. There is very little research on trauma in aging ethnic and racial minorities and, as explained above, less on physical and sexual abuse in older men and women.

 

I don’t think this means that the findings from the literature can never generalize. That would feel too extreme, right? But I think we need to sometimes exercise caution in our interpretation and recognize the limits of what we can and should say. I’m a researcher. I’m always looking to widen the representativeness of my samples (e.g., men/women, assessing for all types of trauma and a range of mental health and quality of life type outcomes, looking at people from varying SES, racial/ethnic backgrounds, and disability statuses) and to dive more into the nuances or intersectionality of those variables.

 

Dr. Jain: Can you talk about the correlation between PTSD and dementia? How robust are these findings? What other causal factors may be involved? What about the reverse—how does having dementia impact PTSD symptoms?

 

Dr. Cook: This is a hard one for me to answer. It’s intriguing data for sure, but there’s so much we don’t know. We know that older adults with PTSD perform more poorly across a range of cognitive measures, particularly processing speed, learning, memory, and executive functioning compared to older adults without PTSD.

 

Over the years there have been several case reports indicating that dementia may exacerbate existing PTSD symptoms. However in the past few years data from two recent large veteran datasets relatively indicate some evidence for a link between PTSD and dementia. In a sample of 181,000 veterans age 55 and over, those with PTSD were more than twice as likely to develop dementia over a six-year follow-up. In another study, almost 10,000 veterans age 65 and older were categorized according to PTSD status (yes or no) and having received a Purple Heart medal (yes or no). There was a greater incidence and prevalence of dementia in the older veterans with PTSD.

 

Some, however, believe that PTSD and dementia may share a third variable, intelligence, which may account for the link.

 

Dr. Jain: With regards to PTSD and older adults—what do you think are the top 5 questions/priorities for researchers to address in the coming 10-20 years?

 

Dr. Cook: The older adult population is increasing rapidly, and that changing demographic landscape will likely translate to an increased need for mental health services for older adults. Most randomized controlled trials investigating psychotherapy or pharmacotherapy for adults with PTSD do not typically include older individuals or sufficient numbers of them to examine age comparisons. A recent systematic review on psychotherapy for PTSD with older adults identified 13 case studies and seven treatment outcome studies. But this literature is disappointing in some ways. It has significant methodological limitations, including non-randomized research designs, lack of comparison conditions, and small sample sizes. One conclusion from this review was that select evidence-based interventions validated in younger and middle-aged populations appear efficacious with older adults. But while a number of the studies reported that older adults experienced a reduction of PTSD, depression, and anxiety symptoms, few experienced complete remission. It’s currently unclear if those treatments were not delivered in sufficient dose (i.e., intensity and frequency) to produce full benefit or if chronic, severe PTSD is harder to treat in older as opposed to younger adults.

 

Over the past decade there have been several epidemiological studies both in the United States and in several industrialized countries using representative samples of community dwelling adults and examining the prevalence and impact of traumatic experiences and PTSD with sufficient numbers of older adults to examine late-life age effects. Needless to say, this is very exciting and a significant advancement for both the traumatic stress and geriatric mental health fields. Now that we’ve done that I’d love to see more on the experience of trauma and expression of any related distress in the least healthy and potentially most “vulnerable” older adults—those with, physical, emotional, or cognitive impairment; those who are homebound; and long-term care residents.

 

Although the prevalence of full PTSD appears to be relatively low, there is some evidence to suggest that older adults may have clinically important PTSD symptoms. I think it would be great if we could invite subthreshold PTSD in the older adult population as well as trauma-related depression. There is a very robust literature on depression in older adults and only a handful of articles that look at the connection between depression and trauma.

 

Though older adulthood encompasses at least a 30-year age range, the vast majority of studies on older adult trauma survivors lump all of them into a generic older adult group. Ideally I would like to see more fine-grained analyses (even if they are exploratory) on young-old (65–74 years), middle-old (75–84 years) and old-old (85 years and older). This seems to be fairly low hanging fruit that most investigators could try to do.

 

I’ve also included other things in my wish list above.

Is risk of Alzheimer’s Disease reduced by taking a more positive attitude toward aging?

Unwarranted claims that “modifiable” negative beliefs cause Alzheimer’s disease lead to blaming persons who develop Alzheimer’s disease for not having been more positive.

Lesson: A source’s impressive credentials are no substitute for independent critical appraisal of what sounds like junk science and is.

More lessons on how to protect yourself from dodgy claims in press releases of prestigious universities promoting their research.

If you judge the credibility of health-related information based on the credentials of the source, this article  is a clear winner:

Levy BR, Ferrucci L, Zonderman AB, Slade MD, Troncoso J, Resnick SM. A Culture–Brain Link: Negative Age Stereotypes Predict Alzheimer’s Disease Biomarkers. Psychology and Aging. Dec 7 , 2015, No Pagination Specified. http://dx.doi.org/10.1037/pag0000062

alzheimers
From INI

As noted in the press release from Yale University, two of the authors are from Yale School of Medicine, another is a neurologist at Johns Hopkins School of Medicine, and the remaining three authors are from the US National Institute on Aging (NIA), including NIA’s Scientific Director.

The press release Negative beliefs about aging predict Alzheimer’s disease in Yale-led study declared:

“Newly published research led by the Yale School of Public Health demonstrates that                   individuals who hold negative beliefs about aging are more likely to have brain changes associated with Alzheimer’s disease.

“The study suggests that combatting negative beliefs about aging, such as elderly people are decrepit, could potentially offer a way to reduce the rapidly rising rate of Alzheimer’s disease, a devastating neurodegenerative disorder that causes dementia in more than 5 million Americans.

The press release posited a novel mechanism:

“We believe it is the stress generated by the negative beliefs about aging that individuals sometimes internalize from society that can result in pathological brain changes,” said Levy. “Although the findings are concerning, it is encouraging to realize that these negative beliefs about aging can be mitigated and positive beliefs about aging can be reinforced, so that the adverse impact is not inevitable.”

A Google search reveals over 40 stories about the study in the media. Provocative titles of the media coverage suggest a children’s game of telephone or Chinese whispers in which distortions accumulate with each retelling.

Negative beliefs about aging tied to Alzheimer’s (Waltonian)

Distain for the elderly could increase your risk of Alzheimer’s (FinancialSpots)

Lack of respect for elderly may be fueling Alzheimer’s epidemic (Telegraph)

Negative thoughts speed up onset of Alzheimer’s disease (Tech Times)

Karma bites back: Hating on the elderly may put you at risk of Alzheimer’s (LA Times)

How you feel about your grandfather may affect your brain health later in life (Men’s Health News)

Young people pessimistic about aging more likely to develop Alzheimer’s later on (Health.com)

Looking forward to old age can save you from Alzheimer’s (Canonplace News)

If you don’t like old people, you are at higher risk of Alzheimer’s, study says (RedOrbit)

If you think elderly people are icky, you’re more likely to get Alzheimer’s (HealthLine)

In defense of the authors of this article as well as journalists, it is likely that editors added the provocative titles without obtaining approval of the authors or even the journalists writing the articles. So, let’s suspend judgment and write off sometimes absurd titles to editors’ need to establish they are offering distinctive coverage, when they are not necessarily doing so. That’s a lesson for the future: if we’re going to criticize media coverage, better focus on the content of the coverage, not the titles.

However, a number of these stories have direct quotes from the study’s first author. Unless the media coverage is misattributing direct quotes to her, she must have been making herself available to the media.

Was the article such an important breakthrough offering new ways in which consumers could take control of their risk of Alzheimer’s by changing beliefs about aging?

No, not at all. In the following analysis, I’ll show that judging the credibility of claims based on the credentials of the sources can be seriously misleading.

What is troubling about this article and its well-organized publicity effort is that information is being disseminated that is misleading and potentially harmful, with the prestige of Yale and NIA attached.

Before we go any further, you can take your own look at a copy of the article in the American Psychological Association journal Psychology and Aging here, the Yale University press release here, and a fascinating post-publication peer review at PubPeer that I initiated as peer 1.

Ask yourself: if you encountered coverage of this article in the media, would you have been skeptical? If so what were the clues?

spoiler aheadcure within The article is yet another example of trusted authorities exploiting entrenched cultural beliefs about the mind-body connection being able to be harnessed in some mysterious way to combat or prevent physical illness. As Ann Harrington details in her wonderful book, The Cure Within, this psychosomatic hypothesis has a long and checkered history, and gets continually reinvented and misapplied.

We see an example of this in claims that attitude can conquer cancer. What’s the harm of such illusions? If people can be led to believe they have such control, they are set up for blame from themselves and from those around them when they fail to fend off and control the outcome of disease by sheer mental power.

The myth of “fighting spirit” overcoming cancer that has survived despite the accumulation of excellent contradictory evidence. Cancer patients are vulnerable to blaming themselves for being blamed by loved ones when they do not “win” the fight against cancer. They are also subject to unfair exhortations to fight harder as their health situation deteriorates.

onion composite
                                                        From the satirical Onion

 What I saw when I skimmed the press release and the article

  • The first alarm went off when I saw that causal claims were being made from a modest sized correlational study. This should set off anyone’s alarms.
  • The press release refers to this as a “first ever” d discussion section of the article refer to this as a “first ever” study. One does not seek nor expect to find robust “first ever” discoveries in such a small data set.
  • The authors do not provide evidence that their key measure of “negative stereotypes” is a valid measure of either stereotyping or likelihood of experiencing stress. They don’t even show it is related to concurrent reports of stress.
  • Like a lot of measures with a negative tone to items, this one is affected by what Paul Meehl calls the crud factor. Whatever is being measured in this study cannot be distinguished from a full range of confounds that not even being assessed in this study.
  • The mechanism by which effects of this self-report measure somehow get manifested in changes in the brain lacks evidence and is highly dubious.
  • There was no presentation of actual data or basic statistics. Instead, there were only multivariate statistics that require at least some access to basic statistics for independent evaluation.
  • The authors resorted to cheap statistical strategies to fool readers with their confirmation bias: reliance on one tailed rather than two-tailed tests of significance; use of a discredited backwards elimination method for choosing control variables; and exploring too many control/covariate variables, given their modest sample size.
  • The analyses that are reported do not accurately depict what is in the data set, nor generalize to other data sets.

The article

The authors develop their case that stress is a significant cause of Alzheimer’s disease with reference to some largely irrelevant studies by others, but depend on a preponderance of studies that they themselves have done with the same dubious small samples and dubious statistical techniques. Whether you do a casual search with Google scholar or a more systematic review of the literature, you won’t find stress processes of the kind the authors invoke among the usual explanations of the development of the disease.

Basically, the authors are arguing that if you hold views of aging like “Old people are absent-minded” or “Old people cannot concentrate well,” you will experience more stress as you age, and this will accelerate development of Alzheimer’s disease. They then go on to argue that because these attitudes are modifiable, you can take control of your risk for Alzheimer’s by adopting a more positive view of aging and aging people

The authors used their measure of negative aging stereotypes in other studies, but do not provide the usual evidence of convergent  and discriminant validity needed to establish the measure assesses what is intended. Basically, we should expect authors to show that a measure that they have developed is related to existing measures (convergent validity) in ways that one would expect, but not related to existing measures (discriminate validity) with which it should have associations.

Psychology has a long history of researchers claiming that their “new” self-report measures containing negatively toned items assess distinct concepts, despite high correlations with other measures of negative emotion as well as lots of confounds. I poked fun at this unproductive tradition in a presentation, Negative emotions and health: why do we keep stalking bears, when we only find scat in the woods?

The article reported two studies. The first tested whether participants holding more negative age stereotypes would have significantly greater loss of hippocampal volume over time. The study involved 52 individuals selected from a larger cohort enrolled in the brain-neuroimaging program of the Baltimore Longitudinal Study of Aging.

Readers are given none of the basic statistics that would be needed to interpret the complex multivariate analyses. Ideally, we would be given an opportunity to see how the independent variable, negative age stereotypes, is related to other data available on the subjects, and so we could get some sense if we are starting with some basic, meaningful associations.

Instead the authors present the association between negative age stereotyping and hippocampal volume only in the presence of multiple control variables:

Covariates consisted of demographics (i.e., age, sex, and education) and health at time of baseline-age-stereotype assessment, (number of chronic conditions on the basis of medical records; well-being as measured by a subset of the Chicago Attitude Inventory); self-rated health, neuroticism, and cognitive performance, measured by the Benton Visual Retention Test (BVRT; Benton, 1974).

Readers get cannot tell why these variables and not others were chosen. Adding or dropping a few variables could produce radically different results. But there are just too many variables being considered. With only 52 research participants, spurious findings that do not generalize to other samples are highly likely.

I was astonished when the authors announced that they were relying on one-tailed statistical tests. This is widely condemned as unnecessary and misleading.

Basically, every time the authors report a significance level in this article, you need to double the number to get what is obtained with a more conventional two-tailed test. So, if they proudly declare that results are significant p = .046, then the results are actually (non)significant, p= .092. I know, we should not make such a fuss about significance levels, but journals do. We’re being set up to be persuaded the results are significant, when they are not by conventional standards.

So the authors’ accumulating sins against proper statistical techniques and transparent reporting: no presentation of basic associations; reporting one tailed tests; use of multivariate statistics inappropriate for a sample that is so small. Now let’s add another one, in their multivariate regressions, the authors relied on a potentially deceptive backwards elimination:

Backward elimination, which involves starting with all candidate variables, testing the deletion of each variable using a chosen model comparison criterion, deleting the variable (if any) that improves the model the most by being deleted, and repeating this process until no further improvement is possible.

The authors assembled their candidate control/covariate variables and used a procedure that checks them statistically and drop some from consideration, based on whether they fail to add to the significance of the overall equation. This procedure is condemned because the variables that are retained in the equation capitalize on chance. Particular variables that could be theoretically relevant are eliminated simply because they fail to add anything statistically in the context of the other variables being considered. In the context of other variables, these same discarded variables would have been retained.

The final regression equation had fewer control/covariates then when the authors started. Statistical significance will be calculated on the basis of the small number of variables remaining, not the number that were picked over and so results will artificially appear stronger. Again, potentially quite misleading to the unwary reader.

The authors nonetheless concluded:

As predicted, participants holding more-negative age stereotypes, compared to those holding more-positive age stereotypes, had a significantly steeper decline in hippocampal volume

The second study:

examined whether participants holding more negative age stereotypes would have significantly greater accumulation of amyloid plaques and neurofibrillary tangles.

The outcome was a composite-plaques-and-tangles score and the predictor was the same negative age stereotypes measure from the first study. These measurements were obtained from 74 research participants upon death and autopsy. The same covariates were used in stepwise regression with backward elimination. Once again, the statistical test was one tailed.

Results were:

As predicted, participants holding more-negative age stereotypes, compared to those holding more-positive age stereotypes, had significantly higher composite-plaques-and-tangles scores, t(1,59) = 1.71 p = .046, d = 0.45, adjusting for age, sex, education, self-rated health, well-being, and number of chronic conditions.

Aha! Now we see why the authors commit themselves to a one tailed test. With a conventional two-tailed test, these results would not be significant. Given a prevailing confirmation bias, aversion to null findings, and obsession with significance levels, this article probably would not have been published without the one tailed test.

The authors’ stirring overall conclusion from the two studies:

By expanding the boundaries of known environmental influences on amyloid plaques, neurofibrillary tangles, and hippocampal volume, our results suggest a new pathway to identifying mechanisms and potential interventions related to Alzheimer’s disease

pubpeerPubPeer discussion of this paper [https://pubpeer.com/publications/16E68DE9879757585EDD8719338DCD ]

Comments accumulated for a couple of days on PubPeer after I posted some concerns about the first study. All of the comments were quite smart, some directly validated points that I been thinking about, but others took the discussion in new directions either statistically or because the commentators knew more about neuroscience.

Using a mechanism available at PubPeer, I sent emails to the first author of the paper, the statistician, and one of the NIA personnel inviting them to make comments also. None have responded so far.

Tom Johnstone, a commentator who exercise the option of identifying himself noted the reliance on inferential statistics in the absence of reporting basic relationships. He also noted that the criterion used to drop covariates was lax. Apparently familiar with neuroscience, he expressed doubts that the results had any clinical significance or relevance to the functioning of the research participants.

Another commentator complained of the small sample size, use of one tailed statistical tests without justification, the “convoluted list of covariates,” and “taboo” strategy for selecting covariates to be retained in the regression equation. This commentator also noted that the authors had examined the effect of outliers, conducting analyses both with and without the inclusion of the most extreme case. While it didn’t affect the overall results, exclusion dramatically change the significance level, highlighting the susceptibility of such a small sample to chance variation or sampling error.

Who gets the blame for misleading claims in this article?

dr-luigi-ferrucciThere’s a lot of blame to go around. By exaggerating the size and significance of any effects, the first author increases the chance of publication and also further funding to pursue what is seen as a “tantalizing” association. But it’s the job of editors and peer reviewers to protect the readership from such exaggerations and maybe to protect the author from herself. They failed, maybe because exaggerated findings are consistent with the journal‘s agenda of increasing citations by publishing newsworthy rather than trustworthy findings. The study statistician, Martin Slade obviously knew that misleading, less than optimal statistics were used, why didn’t he object? Finally, I think the NIA staff, particularly Luigi Ferrucci, the Scientific Director of NIA  should be singled out for the irresponsibility of attaching their names to such misleading claims. Why they do so? Did they not read the manuscript?  I will regularly present instances of NIH staff endorsing dubious claims, such as here. The mind-over-disease, psychosomatic hypothesis, gets a lot of support not warranted by the evidence. Perhaps NIH officials in general see this as a way of attracting research monies from Congress. Regardless, I think NIH officials have the responsibility to see that consumers are not misled by junk science.

This article at least provided the opportunity for an exercise that should raise skepticism and convince consumers at all levels – other researchers, clinicians, policymakers, and those who suffer from Alzheimer’s disease and those who care from them – we just cannot sit back and let trusted sources do our thinking for us.