Overexposed: The role of environmental toxicants on your brain

By Carlie Hoffman

It
is often said that we are products of our environment: who we are is
shaped by the things, people, and situations with which we surround
ourselves. However, whatever we may like to think, we are not in
control of every facet of our environment. In fact, we are unknowingly
and involuntarily exposed to dozens of man-made environmental chemicals,
called toxicants,
each day that can negatively alter our bodies and even our very brain
matter. In essence, we are becoming literal products of our environment.

Synthetic
chemicals and toxicants are ubiquitous within our surroundings. While some toxicants come from obvious
sources, like cigarette smoke and car exhaust, other sources of exposure
are more subtle. For instance, electrical equipment (like computers
and cell phones), beauty products (like makeup and shampoo), mattresses,
and furniture all contain flame retardants, chemicals used to reduce flammability [3, 13]. Bisphenol A (BPA) and phthalates,
chemicals used to harden plastics, can also be found in dental
sealants, cigarette filters, soda bottles, and the linings of canned
foods [4, 8, 12]. Additionally, dichlorodiphenyltrichloroethane (DDT),
a pesticide commonly used in the mid-1900s to combat outbreaks of
pests, malaria, and lice, was banned in 1972 in the US and yet is still currently present within both the environment and human tissues [12].

Pesticides not only harm insects, but certain doses can also have harmful effects on the human body.

The presence of chemicals within almost every facet of our society means we are
subjected to varying levels of environmental exposure throughout our lives– from the womb to the grave. A growing desire to
characterize the effects of this lifetime of exposure resulted in the
creation of a new concept: the “exposome.”
Defined in 2005 by Dr. Christopher Wild as “every exposure to which an
individual is subjected from conception to death,” this definition was
expanded by Dr. Gary Miller and Dr. Dean Jones
in 2014 to be “the cumulative measure of environmental influences and
associated biological responses throughout the lifespan, including
exposures from the environment, diet, behavior, and endogenous
processes” [9, 14, 15]. Indeed, some say the exposome profile may
tell a narrative about our individual lives with astounding accuracy–
including where we’ve traveled, what we’ve eaten, and trends in our
overall behavior.

As Dr. Wild stated, our environmental exposures, and our lives, begin in the womb. After this point, the developing fetus is subject to many
of the environmental chemicals and toxicants to which the mother is
(knowingly or unknowingly) exposed. A study described by CNN illustrated this point and found that pregnant mothers were exposed to pesticides and air
pollutants while engaging in everyday activities.  Some of these chemicals were also able to pass through the umbilical cord and enter into the bloodstream of the fetus, resulting in an average of 232 chemicals being found in the cord blood of 10 babies born over the course of the study.  Pregnant mothers were also exposed
to chemicals from unexpected sources, like taking a shower, cleaning the
house, and putting on makeup.  Some of these chemicals also made it into the fetus and were found in the fetal cord blood.  However, it
is important to note that the mere presence of such chemicals within the
blood is not necessarily harmful to human health. Instead, toxicity is
dependent upon the concentration and duration of exposure a person, or
fetus, is subjected to– meaning the presence of exposure does not always lead to the occurrence of detrimental health effects.



That
being said, certain types of environmental exposure can result in
numerous negative consequences for the brain. For instance, exposure to certain
amounts of air pollutants and pesticides during development has been associated with a
reduction in white matter volume in the brain, slower information
processing speed, behavioral problems, attention deficit/hyperactivity
disorder (ADHD) symptoms, and an alteration in mental and psychomotor
development [7, 10]. One study retrospectively examined a group of
adults in Cape Cod, Massachusetts who experienced prenatal and early
childhood exposure to drinking water contaminated with
tetrachloroethylene, a chemical solvent used in dry cleaning, and found
that early exposure was associated with impaired vision, increased
reports of impulsive behavior, and increased risks of developing bipolar
disorder and post-traumatic stress disorder (PTSD) in adulthood [1, 2,
6]. In addition, excessive prenatal exposure to BPA and phthalates has
been found to alter sexually dimorphic development of the brain and can also lead to alterations in anxiety, hyperactivity, and emotional control [4, 8, 12].  Thus, exposure to environmental chemicals can influence how our brains function, affect our mental health, and alter how we interact with the world around us.

Given
these documented detrimental health effects, we should seek to avoid
excessive environmental exposures. However, while we can limit our
interaction with known sources of environmental
chemicals, such as by avoiding areas that have recently been sprayed
with pesticides or not living in areas subjected to large amounts of car
exhaust, how do we protect ourselves from environmental toxicants coming from largely unknown and unavoidable sources?  And why are chemicals are being added to
commonly-used household items in the first place when such substances
have the potential to negatively alter our brains and neurodevelopment?

The
answer to this latter question can be traced to the years surrounding
the Great Depression and World War II. In this era, the fields of human
industry and farming began to employ synthetic chemicals for numerous
beneficial purposes, like controlling pest populations, reducing
flammability, and acting as additives in paints and wood finishes. These
potential useful applications led to the quick introduction of such
compounds to widespread use without thorough examination of their
possible negative impacts on human health. The reason for rapidly adding
these chemicals was described in the 1930s by the president of
the Halowax Corporation: “The problem so far as the chemical
manufacturer is concerned is a question of timing… should we take a
product of which you have developed, say, 5 or 10g and spend $50,000 on
research to determine whether or not it is toxic, or should you wait
until you have determined whether you have a market for it?...You can
see that would run into box car numbers in the way of dollars and cents
until you ever sold any” [12]. Essentially, adequate chemical testing
was not performed because it was not cost-effective, resulting in the
public remaining largely unaware of the adverse health effects that could arise from excessive exposure to these added chemicals.

Unfortunately, this cost-driven lack of investigation still describes how chemical research is performed today.  An article in The New England Journal of Medicine
stated that only 200 of the 80,000 chemicals added to products sold
within the US in 2011 were sufficiently tested for carcinogenicity, not to mention the number of chemicals that were inadequately tested for other, non-cancer-related negative outcomes arising from excessive exposure [5].

EPA

This mass-production of chemicals without adequate toxicity testing continues in part because of the vague chemical testing regulations that govern chemical companies in the United States. According to
the Environmental Protection Agency’s (EPA) chemical testing policy,
chemical companies are responsible for determining whether their
substances “may present an unreasonable risk of injury to health or the
environment.” The nebulous wording of this regulation, the lack of a
precise definition of “unreasonable risk,” and the increased cost
associated with increased research has resulted in many chemical
companies simply testing their chemicals for acute toxicity (which
involves giving experimental animals large doses of a chemical and
checking for a decrease in lifespan or the presence of illness), instead
of performing long-term testing (which involves giving experimental
animals small doses of a chemical over a long period of time). Thus,
the effects of gradual exposure, as would be experienced through daily
contact with a chemical over the course of a lifetime, are not examined
and the effects of such gradual exposure are only determined as people
are exposed to these chemicals for many years.

Thankfully,
this problem of non-consensual daily exposure to toxic chemicals is not
one without a solution– though working toward this solution will not be
easy. One of the first steps toward a less-polluted and more hospitable future is to
continue characterizing the human exposome. Several organizations
within the United States and Europe, including the HERCULES
exposome research center at Emory University, operate under this goal.
These organizations seek to develop a better understanding of the role
of the environment on brain disease onset and progression, to discover
chemicals that cause disease, and to remove or diminish exposures to
such chemicals [11]. More stringent regulations on chemical testing and
increased collaboration between chemical companies and neuroscientists
will also move chemical testing in the right direction, helping to
elucidate the long-term effects of environmental chemicals on the brain
and leading to more detailed chemical toxicity characterization.
Unfortunately, increased chemical testing is often viewed as an
unnecessary hindrance and is perceived as being less cost-effective than
rapidly mass-producing a chemical. However, more thorough testing and
increased chemical regulation will result in an improved quality of
life, better brain development, and an increase in human liberties for
individuals throughout our society and the world– and that is priceless.

Works Cited



1.
Aschengrau, A, Weinberg, JM, Janulewicz, PA, Romano, ME, Gallagher, LG,
Winter, MR, Martin, BR, Vieira, VM, Webster, TF, White, RF, &
Ozonoff, DM (2011) Affinity for risky behaviors following prenatal and
early childhood exposure to tetrachloroethylene (PCE)-contaminated
drinking water: a retrospective cohort study. Environ Health 10: 102.
doi: 10.1186/1476-069x-10-102



2. Aschengrau, A,
Weinberg, JM, Janulewicz, PA, Romano, ME, Gallagher, LG, Winter, MR,
Martin, BR, Vieira, VM, Webster, TF, White, RF, & Ozonoff, DM (2012)
Occurrence of mental illness following prenatal and early childhood
exposure to tetrachloroethylene (PCE)-contaminated drinking water: a
retrospective cohort study. Environ Health 11: 2. doi:
10.1186/1476-069x-11-2



3. Ballesteros-Gomez, A, de
Boer, J, & Leonards, PE (2014) A novel brominated triazine-based
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Getz, KD, Janulewicz, PA, Rowe, S, Weinberg, JM, Winter, MR, Martin,
BR, Vieira, VM, White, RF, & Aschengrau, A (2012) Prenatal and early
childhood exposure to tetrachloroethylene and adult vision. Environ
Health Perspect 120: 1327-1332. doi: 10.1289/ehp.1103996



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Rodriguez-Barranco, M, Ballester, F, Rebagliato, M, & Hernandez, AF
(2014) A systematic review of neurodevelopmental effects of prenatal and
postnatal organophosphate pesticide exposure. Toxicol Lett 230:
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8. Lin, CY,
Shen, FY, Lian, GW, Chien, KL, Sung, FC, Chen, PC, & Su, TC (2015)
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chemical in plastic containers, and carotid artery intima-media
thickness in adolescents and young adults. Atherosclerosis 241: 657-663.
doi: 10.1016/j.atherosclerosis.2015.06.038



9. Miller,
GW, & Jones, DP (2014) The nature of nurture: refining the
definition of the exposome. Toxicol Sci 137: 1-2. doi:
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10. Peterson, BS, Rauh, VA,
Bansal, R, Hao, X, Toth, Z, Nati, G, Walsh, K, Miller, RL, Arias, F,
Semanek, D, & Perera, F (2015) Effects of prenatal exposure to air
pollutants (polycyclic aromatic hydrocarbons) on the development of
brain white matter, cognition, and behavior in later childhood. JAMA
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Rappaport, SM, Barupal, DK, Wishart, D, Vineis, P, & Scalbert, A
(2014) The blood exposome and its role in discovering causes of disease.
Environ Health Perspect 122: 769-774. doi: 10.1289/ehp.1308015



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Rosner, D, & Markowitz, G (2013) Persistent pollutants: a brief
history of the discovery of the widespread toxicity of chlorinated
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13. Venier, M, Salamova,
A, & Hites, RA (2015) Halogenated Flame Retardants in the Great
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outstanding challenge of environmental exposure measurement in molecular
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10.1158/1055-9965.epi-05-0456



15. Wild, CP (2012) The exposome: from concept to utility. Int J Epidemiol 41: 24-32. doi: 10.1093/ije/dyr236





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Hoffman, C. (2015). Overexposed: The role of environmental toxicants on your brain. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2015/09/overexposed-role-of-environmental.html

Unintentional discrimination in clinical research: Why the small decisions matter

by Arthur T. Ryan, M.A. and Elaine F. Walker, Ph.D.



Arthur Ryan is a graduate student in clinical psychology at Emory University. His research focuses on understanding the etiology and neuropathology underlying severe mental illness.



Elaine Walker is a Professor of Psychology and Neuroscience in the Department of Psychology at Emory University and is the Director of the Development and Mental Health Research Program, which is supported by the National Institute of Mental Health. Her research is focused on child and adolescent development and the brain changes that are associated with adolescence. She is also a member of the AJOB Neuroscience editorial board.

Arthur Ryan, M.A.

Over the past several decades, there has been a significant effort to minimize bias against individuals based on ethnicity and other demographic factors through the creation of seemingly impartial and objective criteria across a host of domains. For example, when the United States Federal Sentencing Guidelines were created in the 1980’s, one of their primary goals was to alleviate “...unwarranted disparity among offenders with similar characteristics convicted of similar criminal conduct” [1]. Unfortunately, even well-intentioned efforts such as this one can still have a disparate negative impact upon historically marginalized groups, such as the well-documented disproportionate sentencing of black individuals due to differing rules governing offenses committed with crack vs. powdered cocaine [2]. Concerns about such inadvertent bias are not limited to the legal domain. Agencies that fund clinical investigations are paying greater attention to demographic representativeness and access to participation in health-related research.

Let us consider a hypothetical example, drawn from the authors’ own field of research in a US context, of how seemingly objective research design choices can results in biases in access to research participation. There is increasing evidence that inflammatory factors may play an important role in the etiology of schizophrenia and other psychotic illnesses [3]. One thing researchers do when attempting to understand a complex system like the human brain is to minimize external sources of variance. One readily identifiable correlate of inflammatory markers is body mass index (BMI) [4]. Schizophrenia itself is also correlated with BMI, such that patients tend to have a higher BMI than healthy individuals [5]. So a hypothetical researcher might reasonably say to herself, “Let me compare inflammatory markers in individuals with and without schizophrenia who have a BMI below 25 (BMIs of 25 or greater are considered to be medically overweight). That way, if I find a difference between the groups, I can more strongly conclude that the difference has to do with schizophrenia’s underlying pathology and was not due to individuals with schizophrenia being medically overweight.”

Elaine Walker, Ph.D.

Our hypothetical researcher’s experimental design choice is scientifically defensible and seemingly innocuous, but her decision may have unintended negative consequences. In a study of patients at the Grady Medical Clinic, an Atlanta primary care clinic serving inner city residents, 80% of black American women had a BMI of ≥ 25 [6]. Of particular note, the Grady Health System and its patients regularly participate in mental health research, including our own clinical studies, and the vast majority of those patients— around 85% [7]— are African American. So if our hypothetical researcher had unknowingly gone ahead with her BMI exclusion criterion and was recruiting from a similar population, she would effectively be excluding four out of five black American women from participating in her research, despite the disproportionately high number of black patients served. This would be more than a minor unfairness or lost opportunity for the individual women who could not participate: given the growing research literature showing that various biological and genetic risk markers have differential predictive utility across racial and ethnic groups, this hypothetical study might produce findings that are invalid for minority individuals. Because rates of schizophrenia seem to be similar across various racial groups and nationalities when measured by well-controlled studies, such an omission is not acceptable. If the study yielded results valid largely for one racial group, our hypothetical researcher would also be compromising one of her ethical obligations described under the Belmont Report, which requires that researchers avoid creating unjust patterns in the “...overall distribution of the burdens and benefits of research” [8]. The report explicitly extends this principle to research involving racial minorities and other historically exploited groups.

To reiterate, the preceding example was hypothetical and no such exclusionary criterion was employed in our own work. However, the possibility of research design choices having a discriminatory impact is no hypothetical hazard. In a 2006 review of randomized controlled drug trials, only 24% of participants were women [9], while a 2008 review of trials funded by the National Heart, Lung, and Blood Institute showed a mean female participation rate of 27% [10]. Even non-human females are underrepresented in research, with male-animal-only studies outnumbering female-animal-only studies at a roughly 5 : 1 ratio in neuroscience and pharmacology [11]. Such exclusion is even more notable considering that some conditions may be experienced at higher rates by those left out of such trials. For example, major depression affects women at an approximately 2:1 ratio [12]. So, theoretically, it would be particularly egregious to exclude women from antidepressant medication trials—and any research that sought to create a representative sample should include women at that same 2:1 ratio.

So why do male-only studies still predominate? Because it is cheaper and easier to conduct male-only studies. With less variance among individuals, experimental effects are easier to detect. In addition, male hormones fluctuate less over time and including women in drug trials necessitates extra experimental protections to prevent harm should one of the participants become pregnant. Again, this practice is not simply an unfairness to the individual women who would otherwise want to participate in medical research. FDA studies have shown that drug concentrations in blood and tissue can vary by as much as 40% between men and women, with similar variations in side effect profiles [13]. This shouldn’t be surprising as gene expression may vary between males and females by more than 50% in liver, fat, and muscle tissue [14]. It is clear that such a systematic policy of excluding women from research, even if it lacked any conscious discriminatory intent, could have serious, even life-threatening, consequences for women receiving medical treatment for years to come.

There is no way to completely prevent unintentional discriminatory sequelae of research design choices. And it would be naïve to believe that there will never be genuine tradeoffs that need to be weighed when designing research studies. Sometimes researchers will need to decide between sample representativeness and experimental control. The important point here is that if researchers make their decisions in a reflective and intentional manner, always considering the downstream consequences of their study design choices, they are more likely to identify and mitigate secondary negative consequences of their work. In doing so, they are increasing the scientific value of their work, as well as fulfilling their ethical obligations to promote beneficence and justice with their research.

References



1. United States Sentencing Commission. An Overview of the United States Sentencing Commission.

2. NPR. High Court Rules on Drug Sentencing Disparities.

3. Miller, B. J., Buckley, P., Seabolt, W., Mellor, A. & Kirkpatrick, B. Meta-Analysis of Cytokine Alterations in Schizophrenia: Clinical Status and Antipsychotic Effects. Biol. Psychiatry 70, 663–671 (2011).

4. Festa, A. et al. The relation of body fat mass and distribution to markers of chronic inflammation. Int. J. Obes. 25, 1407–1415 (2001).

5. Homel, P., Casey, D. & Allison, D. B. Changes in body mass index for individuals with and without schizophrenia, 1987–1996. Schizophr. Res. 55, 277–284 (2002).

6. Jacobson, T. A., Morton, F., Jacobson, K. L., Sharma, S. & Garcia, D. C. An assessment of obesity among African-American women in an inner city primary care clinic. J. Natl. Med. Assoc. 94, 1049–1057 (2002).

7. Saunders, S. P. & Campbell, C. L. The Word on the Street: Performing the Scriptures in the Urban Context., (Wipf and Stock Publishers, pp.23, 2006).

8. The National Commission for the Protection of Human Subjects of Biomedical and Behavioral Research. The Belmont Report: Ethical principles and guidelines for the protection of human subjects of research. (1979)

9. Geller, S. E., Adams, M. G. & Carnes, M. Adherence to Federal Guidelines for Reporting of Sex and Race/Ethnicity in Clinical Trials. J. Womens Health 15, 1123–1131 (2006).

10. Kim, E. S. H., Carrigan, T. P. & Menon, V. Enrollment of Women in National Heart, Lung, and Blood Institute-Funded Cardiovascular Randomized Controlled Trials Fails to Meet Current Federal Mandates for Inclusion. J. Am. Coll. Cardiol. 52, 672–673 (2008).

11. Beery, A. K. & Zucker, I. Sex Bias in Neuroscience and Biomedical Research. Neurosci. Biobehav. Rev. 35, 565–572 (2011).

12. Kessler, R. C. Epidemiology of women and depression. J. Affect. Disord. 74, 5–13 (2003).

13. Anderson, G. D. Sex and racial differences in pharmacological response: where is the evidence? Pharmacogenetics, pharmacokinetics, and pharmacodynamics. J. Womens Health 2002 14, 19–29 (2005).

14. Yang, X. et al. Tissue-specific expression and regulation of sexually dimorphic genes in mice. Genome Res. 16, 995–1004 (2006).





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Ryan, A and Walker, E. (2015). Unintentional discrimination in clinical research: Why the small decisions matter. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2015/09/unintentional-discrimination-in.html.

Ethics and suicide: Are we paying attention to the important issues?

by Victoria Saigle and Eric Racine, Ph.D.

Eric Racine, Ph.D.

Victoria Saigle is a graduate student at the Institut de recherches cliniques de Montréal's Neuroethics Research Unit. She is a completing her MSc in Experimental Medicine at McGill University through the Biomedical Ethics Unit. 

Dr. Eric Racine is the director of the Neuroethics Research Unit at the Institut de recherches cliniques de Montréal and holds academic appointments in the Department of Medicine and the Department of Social and Preventive Medicine at Université de Montréal and in the Department of Neurology and Neurosurgery, the Department of Medicine, and the Biomedical Ethics Unit at McGill University. He is also a member of the AJOB Neuroscience Editorial Board.

Discussing suicide can be difficult in clinical, public, and academic settings because many people have strong intuitions about which, when, and whether voluntary death is appropriate. However, discussions about suicide are largely absent from bioethics scholarship. Considering that suicide is among the ten most common causes of death worldwide and the second leading cause of death for individuals aged 15-29 (World Health Organization, 2014), it is surprising that more attention is not devoted to this topic.

Victoria Saigle

Ethical dilemmas related to suicide intersect with important questions in research ethics, clinical ethics, and public health ethics. However, we discovered in recent work that the majority of ethics scholarship on voluntary death focuses either entirely on physician-assisted dying (PAD – a term we are using here to describe many different acts in which a physician helps to hasten death at a patient’s request) or consists of philosophical arguments about the acceptability or rationality of suicide. Though interesting, these topics do little to address the challenges and lived experiences of suicidal individuals, their families, suicide researchers, or health professionals. Below, we will delineate aspects of suicide that deserve more attention.

From a research ethics standpoint, multiple studies have reported the challenges of conducting research with individuals who are, or who were previously, suicidal. Likewise, recruiting the loved ones of someone who has died by suicide can be difficult

(Mishara & Weisstub, 2005; Moore, Maple, Mitchell, & Cerel, 2013; Omerov, Steineck, Dyregrov, Runeson, & Nyberg, 2014). While it is important to exercise great care and sensitivity when involving these individuals in research, efforts should be made within ethics scholarship to examine what factors contribute to suicide research challenges and to develop solutions when possible. Not doing so risks building barriers to research in an area in need of more evidence. Complications posed by the involvement of suicidal individuals and their families in research should be addressed, rather than ignored.

Similarly, suicidality in clinical settings raises a wide range of ethical issues that deserve attention. For example, health professionals may not have received adequate training to deal with suicidal individuals (Osteen, Jacobson, & Sharpe, 2014) or they may be unsure whether breaking confidentiality is appropriate if their patients disclose suicidal ideations (Barrett, 1997). This can lead to unsettling situations in places like emergency departments, where uncertainty is the norm and time is in short supply. Knowing how to respond to repeated attempts of suicide or to situations where there is evidence that the decision to commit suicide was preplanned may also be challenging for clinicians, whose training teaches them to prevent harm. Protecting the well-being of clinicians who interact with suicidal populations, examining organizational responses to suicide disclosure in clinical settings, and ensuring that the interactions between health care professionals and their suicidal patients are appropriate are all examples of issues that could be addressed within clinical ethics.

Finally, further attention should be paid to the strategies used to detect, address, and prevent suicide at a national level. Many people view suicidality to be a symptom of mental disorders, and it is estimated that roughly 90% of individuals who die by suicide have an underlying mental illness (Turecki, 2014). This presumption that the wish to end one’s life and mental illness are related is not novel. In fact, some have suggested that ethical dilemmas in suicide research are often unaddressed because researchers believe that suicidality is a symptom of mental illness that can be removed by curing the underlying disorder (Stanley, 1986). At the moment, treating the presumed mental illness is the most predominant public health strategy for suicide prevention (Mishara & Chagnon, 2011). However, different ways of conceiving of the linkage between mental illness and suicide can lead to the adoption of different prevention strategies. For example, if it is assumed that mental illness causes suicidality directly, treating the mental illness may be the primary method of suicide prevention. If, on the other hand, suicidality is seen as the result of complications one endures due to a mental illness (e.g. unemployment, social problems), then education and efforts to reduce stigma about mental disorders may become the primary strategy (Mishara & Chagnon, 2011). It is important to consider if more than one prevention method should be used and/or if the emphasis on curing mental illness as the sole form of suicide prevention further stigmatizes the act and makes it harder for those experiencing suicidal ideation to seek help (Mishara & Chagnon, 2011).

In sum, it seems that ethics scholarship about suicide neglects many practical ethical issues that are raised by suicide. Our purpose here is not to pass judgment on whether suicide is always right or wrong, moral or immoral, but to draw attention to the fact that these discussions sometimes eclipse more common issues that deserve more attention than they currently receive.

References

Barrett, N. A. (1997). The medical student and the suicidal patient. Journal of Medical Ethics, 23(5), 277–281.

Mishara, B. L., & Chagnon, F. (2011). Understanding the Relationship between Mental Illness and Suicide and the Implications for Suicide Prevention. In R. C. O'Connor, S. Platt, & J. Gordon (Eds.), International Handbook of Suicide Prevention: Research, Policy and Practice: John Wiley & Sons, Ltd.

Mishara, B. L., & Weisstub, D. N. (2005). Ethical and legal issues in suicide research. Int J Law Psychiatry., 28(1), 23-41.

Moore, M., Maple, M., Mitchell, A. M., & Cerel, J. (2013). Challenges and opportunities for suicide bereavement research: the experience of ethical board review. Crisis, 34(5), 297-304.

Omerov, P., Steineck, G., Dyregrov, K., Runeson, B., & Nyberg, U. (2014). The ethics of doing nothing. Suicide-bereavement and research: ethical and methodological considerations. Psychological Medicine, 44(16), 3409-3420.

Osteen, P., Jacobson, J. & Sharpe, T. (2014) Suicide Prevention in Social Work Education: How Prepared Are Social Work Students?, Journal of Social Work Education, 50:2, 349-364

Stanley, B. (1986). Ethical considerations in biological research on suicide. Ann N Y Acad Sci., 487, 42-46. 

Carter v. Canada (Attorney General), 2015 SCC 5, (2015). Retrieved from: https://scc-csc.lexum.com/scc-csc/scc-csc/en/item/14637/index.do

Turecki, G. (2014). The molecular bases of the suicidal brain. Nat Rev Neurosci, 15(12), 802-816.

World Health Organization. (2014). Preventing suicide: A global imperative (pp. 1-92). Switzerland: World Health Organization.

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Saigle, V. and Racine, E. (2015). Ethics and suicide: Are we paying attention to the important issues? The Neuroethics Blog. Retrieved on Retrieved on , from http://www.theneuroethicsblog.com/2015/09/ethics-and-suicide-are-we-paying.html

Is trauma in our genes? Ethical implications of epigenetic findings

by Neil Levy



Neil Levy is professor of philosophy at Macquarie University, Sydney and deputy director of the Oxford Centre for Neuroethics. He is the author of 7 books, including Neuroethics (2007) and Consciousness and Moral Responsibility (2014), and edits the journal Neuroethics. He is also a member of the AJOB Neuroscience board.



A recent study by Rachel Yehuda et al. in Biological Psychiatry provided further evidence for the genetic transmission of acquired characteristics, by showing that Holocaust survivors passed certain acquired genetic markers to their children. The idea that acquired characteristics can be genetically transmitted is (roughly) equivalent to the doctrine of Lamarckism, and was long considered a heresy in biology. [Editor's note: see also Ryan Purcell's 2014 post for this blog on the relationship between Lamarckism and epigenetics.] According to the Darwinian orthodoxy, traits change because randomly occurring mutations confer a relative fitness advantage on some organisms, not because they change their behaviour, and that change then comes to be encoded in the genes. But the orthodoxy has long been shattered. Scientists now recognize that the story is a lot more complex than that.





This new study is of central interest to neuroethics for many reasons. One is that the trait in question is psychological, or at least very plausibly underlies a disposition to certain psychological responses, given the right circumstances. Children of Holocaust survivors are themselves at higher risk for stress disorders: a propensity to stress disorders is inherited. How does the inheritance work? One possibility is that their parents behave differently, due to the trauma they experienced, and this difference in how they treat their children causes the difference in susceptibility. Another possibility is that the trauma caused an alteration in the genes of the parents, and this alteration was then transmitted biologically – in the DNA or cytoplasm – to children. Of course, these are not exclusive possibilities – its very likely that people who have been massively traumatized have persisting psychological problems that affect their parenting. The new study strongly suggests that in addition to any such transmission of a vulnerability to stress disorders, there is also biological transmission. In effect, the children of Holocaust survivors were born with bodies “prepared” for stress. What might have been (somewhat) protective, had their world been as massively awful as their parents’, proved instead to be maladaptive.

Buchenwald concentration camp, WWII

Studies like this show that many of the subdisciplinary boundaries we are wont to draw – bioethics or even genethics versus neuroethics, for instance – do not mark boundaries that nature respects. While it is a mistake, I think, to identify the mind with the brain, the mind is nevertheless dependent on and realized by entirely physical properties: it falls within the province of those studying the body and how it is constructed. Equally, bioethics doesn’t have an exclusive right to the somatic: in order to understand the mind, we need to be able to understand the somatic too.



The study has an upshot, too, for one of the most cherished distinctions in genethics: between ‘germline’ and ‘somatic’ interventions. Many bioethicists think it is permissible for adults to make changes in themselves so long as they limit those changes to cells that will not be transmitted to future generations. But epigenetic effects, which are only just beginning to be understood, make this distinction extremely hard to draw. In fact, interventions may be transmissible in indirect and unsuspected ways: people may change their environment, which changes their cells in ways that are then transmitted. The very idea that germline interventions are more problematic may be a product of a mistaken view about genes as especially powerful and uniquely segregated units of reproduction. In fact, we transmit all kinds of things to future generations, by all kinds of causal routes, from shared culture to built environment to ideas to DNA and other cellular resources. All these factors are inextricably intertwined and none are causally privileged as the dominant cause of the resulting people.



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Levy, N. (2015). Is trauma in our genes? Ethical implications of epigenetic findings. The Neuroethics Blog. Retrieved on Retrieved on , from http://www.theneuroethicsblog.com/2015/09/is-trauma-in-our-genes-ethical.html

Brain devices: Navigating collaborations between industry, government, and researchers

by Paul J. Ford, PhD



Dr. Ford is Director of the NeuroEthics Program at the Cleveland Clinic. He is an active clinical ethicist, and teaches ethics to medical students, residents, and fellows. His publications have appeared in Science, The Hastings Center Report, Neurology, Neuromodulation, and Journal of Medical Ethics. He is also a board member for AJOB Neuroscience.



This spring (June 3-4, 2015) the National Institutes of Health (NIH) as part of the BRAIN Initiative convened an eclectic group of individuals in hopes of encouraging more investigator initiated studies of currently approved neuromodulation and neuro recording devices for new indications (agenda, session videos, and program goals available here). The participants, both on the program and in the audience, specifically included industry, researchers, universities, and governmental agencies. I was delighted to participate in the workshop and was impressed by the number of sincerely interested parties across the spectrum of roles. Within these conversations it was apparent that there existed many shared values and goals as well as complex challenges for protecting particular interests. It beautifully highlighted the complexities of interactions among varied stakeholders.





Among the group there was a broad interest in performing due diligence in discharging their various duties to their constituents. At its heart, the meeting was a good faith effort to realize a desire to see innovations develop to the point of helping clinical populations, i.e. real people who suffer. This aspect of the BRAIN initiative recognizes the current significant logistical barriers to exploring new uses of existing devices within a research context. Too often the current system in the United States with respect to devices encourages off-label use with retrospective review data, rather than small prospective trials. There are numerous disincentives within the system, some of which are bureaucratic and legalistic in nature (see Kelly et al. discussion.) In developing new ways for investigators to create partnerships with industry, the June meeting announced opportunities that would allow easier access to letters for “right of reference” (a specific type of permission needed from intellectual property owners to allow use of previously submitted safety and engineering data. Kelly et al. discusses this further) as well as standardized intellectual property agreements as part of a streamline for some types of NIH funded research. In addition, the dialogue between industry, researchers, universities, regulators, and funders creates an opportunity to standardize approaches to some of the most difficult ethics challenges in brain implant research, such as long-term access to implant upgrades.



Much of the June meeting itself was dedicated to understanding the mechanisms for collaboration, addressing the challenges of negotiating intellectual property, as well as the need for further aggregation of data across research studies. However, the organizers also dedicated a session specifically to ethics, in which I participated as a panelist. The session included a brief presentation by Joseph Fins, MD followed by panel comments by Christine Grady, MSN, PhD, Scott Kim, MD, PhD, Helen Mayberg, MD, and me. A diverse set of practical ethical issues were addressed relating to both research ethics in general and specific ethical issues in neuromodulation. Scott Kim particularly highlighted the opportunity for neuroethics research that could be undertaken in parallel to the other science conducted during further neurological device studies. This model of integrating ethical investigation in tandem with the initial clinical research provides an opportunity to fully appreciate the research participants’ perspective.



A second session of particular interest to the neuroethics community was a presentation by a Public-Private enterprise, Medical Device Innovation Consortium (MDIC) developed in collaboration with the FDA. This organization “aims to advance regulatory science in the medical device industry.” In particular it has various industry, non-profit, and governmental members. This past spring, they released a report on a framework for use in demonstrating to the FDA whether a risk benefit balance is appropriate from a patient perspective (draft release May 2015). The FDA released a companion draft guideline regarding how patient preferences could be used in the approval process. These draft guidance documents provide an opportunity to include neuroethics research into clinical trials of neurological devices. Scott Kim’s comment regarding the need for rigorous methods to be applied in undertaking the type of ethics research nicely resonates with the intention of the MDIC document to provide guidance of methods.



The initiatives and conversations that occurred during this June 2015 meeting is well worth paying attention to for their long reaching implications on how neurological device research is approached and the ethics opportunities that are available.



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Ford, P.J (2015). Brain devices: Navigating collaborations between industry, government, and researchers. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2015/09/brain-devices-navigating-collaborations.html