Vol 3

Chronic Stress & Memory Erosion

The Bright Side of Stress?

Stress is a necessary human experience that keeps us alive.[1] It can be defined by the physical and mental responses we use to combat stressors experienced in our lives, such as threatening situations, insecurity, a tumultuous relationship or academic and work responsibilities.[2] We learn from previous stressors (e.g., avoiding sketchy alleyways we know of, or the signs of “red flags” in a relationship.) These adaptations are how short-term stress can beneficially inform our memory and subsequent learning. Stress-induced fears, anxieties and physiological signals cause us to react to danger or threats so that we know how to avoid a stressor again.

When the brain processes an imminent stressor, the sympathetic nervous system and hypothalamic-pituitary-adrenocortical (HPA) axis react to release adrenaline and glucocorticoids.[3] The sympathetic nervous system activates physiological responses for a fight or flight response. For example, pupils dilate and heart rate increases. The HPA axis regulates the stress response through structures such as the hypothalamus and hippocampus, an important structure for memory, via steroid hormones like cortisol.[4] By a negative feedback loop, the hippocampus’ cortical receptors are activated for the memory and biological learning of a stressful event.[5] As a result, memory is improved following an acute stress response so that our learning is improved for future similar stressful situations.[6,7] 

When Stress Becomes Problematic

While research indicates that short-term or acute stress can promote behavioral adaptations and improve spatial memory, in the same study by Lin et al. (2022), prolonged durations of stress led to behavioral and cognitive impairment in animal models.[8] Relatedly, in humans, long periods of stressful life events lead to cognitive and memory declines in older adults.[9] Additionally, prolonged (i.e., chronic) stress can increase risk of disease and mortality.[10,11] 

Chronic stress causes the body to be constantly out of balance (i.e., allostasis) in response to trying to restore balance (i.e., homeostasis) through energy expenditure.[12] The cumulatively created effect of chronic stress is referred to as allostatic load (when allostasis is repeatedly activated with a lack of adaptation or conclusion of the stress response.)[13] These chronic and repeated stress responses increase cortisol, which negatively affect components of memory (like navigation and long-term memory retention), and structurally damages neurons necessary for memory.[14,15] This leads the human body to be in a constant state of neurological disruption that is not restored, resulting in negative impacts on one’s memory.[16-22]  

Despite these negative health impacts, chronic stress remains an extremely common experience. According to the American Institute of Stress (2022), 94% of American workers say they are stressed at work while 55% of Americans report that they are stressed during any given day.[23] While some degree of stress in life is vital, an allostatic load can decrease well-being and cognition, and should be reduced to promote one’s health and overall life.

What Chronic Stress Looks Like

Chronic stress has particularly negative effects on the hippocampus (related to forming and sustaining memory), amygdala (related to emotional regulation) and neurons in the prefrontal cortex (related to problem-solving and planning).[24] Duman (2004) notes that by using physical restraints on rats, chronic stress was found to decrease neuron length and branching in the hippocampus.[25] Furthermore, increased glucocorticoid circulation leads to decreased neural plasticity (i.e., when neurons adapt and connect to process or establish information), and decreased growth of neurons in the hippocampus.[26] Brain-derived neurotrophic factor (BDNF) signaling, a marker of neural plasticity, is also reduced in the prefrontal cortex and hippocampus following chronic stress.[27] 

Chronic stress essentially impairs memory consolidation and retrieval, making reactivating and forming new information more difficult and less frequent.[28] Memory for spatial and navigating information was found to be impaired due to chronic stress, as well.[29] The body’s homeostatic regulation in response to a prolonged stressor additionally causes chronic neuroinflammation.[30] For these reasons, allostatic load leads to an increased risk of developing certain disorders such as post-traumatic stress disorder (PTSD), depression and neurodegeneration; these risks increase with age and cortisol levels.[31] 

Signs of chronic stress include:[32-34]

  • Emotional dysregulation

  • Decreased memory for events, general knowledge and navigation

  • Social withdrawal

  • Depressive symptoms

  • Increased anxiety and constant worrying

  • Fatigue or low energy

  • Immune system dysregulation and impaired disease resistance

  • High blood pressure

  • Digestive problems

 When chronic stress becomes persistently life-impairing, it can be a significant factor in several disorders, such as those involving anxiety, emotional disruption and cognitive problems. Stress-related cognitive impairment is found in several conditions and disorders:

  • PTSD symptom severity is associated with cognitive decline.[35] 

  • Chronic stress is a risk factor for dementia.[36]

  • In middle age, those with depression and high allostatic load have a higher risk of cognitive decline.[37] 

  • Childhood psychological stress (i.e., childhood poverty) is associated with a greater risk for anxiety-related symptoms and allostatic load in adolescence and adulthood with intensity relating to the duration of the allostatic load.[38] 

  • Impaired memory in depressed individuals is often attributed to chronic stress and its duration.[39]

Those with anxiety and mood disorders tend to experience psychological stress for lengthy periods. This is why high allostatic load is a factor for memory problems as the brain’s hippocampal neurons atrophy or degenerate and plasticity is disrupted by exhausted homeostatic energy expenditure. 

Perceptive Differences 

While individuals with mood or anxiety disorders are more vulnerable to chronic stress and memory impairment, stress responses can still vary by person and are not exclusive to those who experience such disorders. Chronic stress itself is also not a disorder, but a comorbid risk factor for memory impairment that can look different for everyone.

Internal beliefs vary per individual and are subjective, causing certain situations to be stressful to some and not to others, and leading to varied effects on memory. For example, students’ perceived high stress is found to be partially reliant on low self-efficacy (i.e., belief in self-success) and high emotional attention.[40] Additionally, high stress and cortisol levels lead to worsened memory performance such as declarative memory (i.e., memory for general knowledge and events), and cortisol is found to be in higher levels in females than males.[41,42] This is because cortisol levels are impacted by ovarian hormones such as estrogen.[43] Therefore, higher baseline cortisol levels may lead to high cortisol release when responding to stress.[44] For such reasons, cortisol administration is a way of inducing depression in animal models in addition to physical and social stressors due to chronic exposure. Other individual differences (such as age) may impact perceived stress as in older adults; egocentric stressors (e.g., self-health and financial stressors) were found to be detrimental to cognitive functioning as opposed to non-egocentric stressors.[45] 

Societal stressors may also impact the rate and intensity of the stressors that different groups face. For example, individuals of a sexual minority often experience increased impairment in psychosocial adaptation and overall quality of life likely due to negative stereotyping or stigma consciousness.[46] Menhinick & Sanders (2023) note that fear of violence is also an imminent physical stressor that many LGBTQ+ individuals and racial minorities experience, which can induce chronic stress, depression and PTSD.[47] 

Solutions to Mitigate and Overcome Chronic Stress

Several methods can be employed to tackle chronic stress. A social-psychological approach may look at the stressors that arise from social norms. From such a perspective, effortful social change can alleviate minority stress and threats, which removes the fault from the individual experiencing the neurological effects of stressors and targets the creation of the stressors themselves, such as violence and microaggressions arising from biases.[48] 

In terms of regenerating neurological functioning, Hernandez & Brinton (2022) found that allopregnanolone (a neurosteroid) may activate the GABA-chloride complex and can help to promote neurogenesis or the formation of neurons in the brain.[49] Relating to diet, Szala-Rycaj et al. (2023) found that chicory root insulin and topinambur powder, when supplemented long-term, can alleviate anxiety and cognitive disorder-like symptoms that were induced through chronic stress in animal models.[50] Additionally, Duman (2004) notes that antidepressants such as selective serotonin reuptake inhibitors (SSRIs) have been shown to reflect a reversal of neuron atrophy in the hippocampus and promote neural plasticity as well.[51] Note: it is important not to start or stop taking any medications or supplements without first discussing them with your physician and/or pharmacist.

Several evidence-based psychotherapies are effective at preventing and overcoming the effects of chronic stress. Acceptance and Commitment Therapy (ACT) is an approach that focuses on the awareness of mental states and thoughts with particular effectiveness for mood and anxiety disorders.[52] Mindfulness-Based Therapy (MBT) additionally reduces stress through attention to physical experiences and meditation.[53] This modality directly targets psychological stress reduction by promoting relaxation and building mindfulness skills. Cognitive Behavioral Therapy (CBT) is effective in treating stress-related disorders such as PTSD, anxiety, and depression by utilizing cognitive-restructuring of negatively-formed or maladaptive thoughts and behaviors that cause stress.[54] 

Due to the variety of potential stressors that one can experience and the individuality of perceived stress responses, it is possible that a combination of stressor-targeting and personal psychological support is necessary for both avoiding chronic stress and memory impairment, in addition to recovering from chronic stress. In everyday life, acute stress is beneficial for memory and the body, but chronic stress that takes both physical and psychological forms should be avoided as much as possible. Lowering chronic stress may further be promoted through prioritizing safety, relaxation, nutrition, time in nature, engaging in therapy to find ways to cope with stressors, and decreasing time on social media.[55] 

Moreover, this responsibility to avoid chronic stress is not always carried solely by the individual but is also held by a network of people that socially impact each other’s lives every day. In order to reduce the negative memory and health effects of chronic stress, both the individual and the environment by which they interact should be addressed. Stress and memory research continues to rapidly evolve, and may eventually be able to determine how to quantify, possibly by time and neural information, dangerous amounts of allostatic load on the brain and the processes of memory.  

If one is experiencing prolonged or chronic stress that is impacting daily life and overall well-being, please reach out to a licensed mental health professional (e.g., a psychotherapist, psychologist or psychiatrist) for guidance and support.

Contributed by: Phoebe Elliott

Editor: Jennifer (Ghahari) Smith, Ph.D.

References

1 Hadany, L., Beker, T., Eshel, I., & Feldman, M. W. (2006). Why is stress so deadly? An evolutionary perspective. Proceedings. Biological sciences, 273(1588), 881–885. https://doi.org/10.1098/rspb.2005.3384

2 American Psychological Association. (2023). Stress. In APA Dictionary of Psychology. https://dictionary.apa.org/stress?amp=1 

3 Lenart-Bugla, M., Szcześniak, D., Bugla, B., Kowalski, K., Niwa, S., Rymaszewska, J., & Misiak, B. (2022). The association between allostatic load and brain: A systematic review. Psychoneuroendocrinology, 145, 105917. https://doi.org/10.1016/j.psyneuen.2022.105917

4 Peavy, G. M., Salmon, D. P., Jacobson, M. W., Hervey, A., Gamst, A. C., Wolfson, T., Patterson, T. L., Goldman, S., Mills, P. J., Khandrika, S., & Galasko, D. (2009). Effects of chronic stress on memory decline in cognitively normal and mildly impaired older adults. The American journal of psychiatry, 166(12), 1384–1391. https://doi.org/10.1176/appi.ajp.2009.09040461

5 Ibid.

6 Lenart-Bugla et al. (2022)

7 Peavy et al. (2009)

8 Lin, L., Zhang, J., Dai, X., Xiao, N., Ye, Q., & Chen, X. (2022). A moderate duration of stress promotes behavioral adaptation and spatial memory in young C57BL/6J mice. Brain Sciences, 12(8) doi:10.3390/brainsci12081081

9 Peavy et al. (2009)

10 Bobba-Alves, N., Juster, R. -., & Picard, M. (2022). The energetic cost of allostasis and allostatic load. Psychoneuroendocrinology, 146 doi:10.1016/j.psyneuen.2022.105951

11 Selye, H. (1950). Stress and the general adaptation syndrome. British medical journal, 1(4667), 1383–1392. https://doi.org/10.1136/bmj.1.4667.1383

12 Bobba-Alves et al. (2022)

13 Lenart-Bugla et al. (2022)

14 Akan, O., Bierbrauer, A., Kunz, L., Gajewski, P. D., Getzmann, S., Hengstler, J. G., Wascher, E., Axmacher, N., & Wolf, O. T. (2023). Chronic stress is associated with specific path integration deficits. Behavioural brain research, 442, 114305. https://doi.org/10.1016/j.bbr.2023.114305

15 Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life sciences, 58(17), 1475–1483. https://doi.org/10.1016/0024-3205(96)00118-x

16 Peavy et al. (2009)

17  Bobba-Alves et al. (2022)

18 Lenart-Bugla et al. (2022)

19 Prieto, S., Nolan, K. E., Moody, J. N., Hayes, S. M., Hayes, J. P., & Department of Defense Alzheimer’s Disease Neuroimaging Initiative (2023). Posttraumatic stress symptom severity predicts cognitive decline beyond the effect of Alzheimer's disease biomarkers in Veterans. Translational psychiatry, 13(1), 102. https://doi.org/10.1038/s41398-023-02354-0

20 Perlman, G., Cogo-Moreira, H., Wu, C. -., Herrmann, N., & Swardfager, W. (2022). Depression interacts with allostatic load to predict cognitive decline in middle age. Psychoneuroendocrinology, 146 doi:10.1016/j.psyneuen.2022.105922

21 Duman R. S. (2004). Neural plasticity: consequences of stress and actions of antidepressant treatment. Dialogues in clinical neuroscience, 6(2), 157–169. https://doi.org/10.31887/DCNS.2004.6.2/rduman

22 Kirschbaum et al. (1996)

23 The American Institute of Stress. (2022). What is Stress? https://www.stress.org/daily-life 

24 Lenart-Bugla et al. (2022)

25 Duman (2004)

26 Ibid.

27 Ibid. 

28 Lenart-Bugla et al. (2022)

29 Akan et al. (2023)

30 Craddock, T. J. A., Michalovicz, L. T., Kelly, K. A., Rice, M. A., Jr., Miller, D. B., Klimas, N. G., . . . Broderick, G. (2018). A logic model of neuronal-glial interaction suggests altered homeostatic regulation in the perpetuation of neuroinflammation. Frontiers in Cellular Neuroscience, 12 doi:10.3389/fncel.2018.00336 

31 Palego, L., Giannaccini, G., & Betti, L. (2021). Neuroendocrine response to psychosocial stressors, inflammation mediators and brain-periphery pathways of adaptation. Central Nervous System Agents in Medicinal Chemistry, 21(1), 2-19. doi:10.2174/1871524920999201214231243 

32 National Institutes of Health. (2022). Stress. In The National Center for Complementary and Integrative Health. https://www.nccih.nih.gov/health/stress 

33 Mariotti A. (2015). The effects of chronic stress on health: new insights into the molecular mechanisms of brain-body communication. Future science OA, 1(3), FSO23. https://doi.org/10.4155/fso.15.21

34 Yaribeygi, H., Panahi, Y., Sahraei, H., Johnston, T. P., & Sahebkar, A. (2017). The impact of stress on body function: A review. EXCLI journal, 16, 1057–1072. https://doi.org/10.17179/excli2017-480

35 Prieto et al. (2023)

36 Ibid.

37 Perlman et al. (2022)

38 De France, K., Evans, G. W., Brody, G. H., & Doan, S. N. (2022). Cost of resilience: Childhood poverty, mental health, and chronic physiological stress. Psychoneuroendocrinology, 144 doi:10.1016/j.psyneuen.2022.105872 

39 Dillon, D. G., & Pizzagalli, D. A. (2018). Mechanisms of Memory Disruption in Depression. Trends in neurosciences, 41(3), 137–149. https://doi.org/10.1016/j.tins.2017.12.006

40 Navarro-Mateu, D., Alonso-Larza, L., Gómez-Domínguez, M. T., Prado-Gascó, V., & Valero-Moreno, S. (2020). I’m not good for anything and That’s why I’m stressed: Analysis of the effect of self-efficacy and emotional intelligence on student stress using SEM and QCA. Frontiers in Psychology, 11 doi:10.3389/fpsyg.2020.00295

41 Kirschbaum et al. (1996)

42 Wolf, O. T., Schommer, N. C., Hellhammer, D. H., McEwen, B. S., & Kirschbaum, C. (2001). The relationship between stress induced cortisol levels and memory differs between men and women. Psychoneuroendocrinology, 26(7), 711–720. https://doi.org/10.1016/s0306-4530(01)00025-7

43 Edwards, K. M., & Mills, P. J. (2008). Effects of estrogen versus estrogen and progesterone on cortisol and interleukin-6. Maturitas, 61(4), 330–333. https://doi.org/10.1016/j.maturitas.2008.09.024

44 Wolf et al. (2001)

45 De France et al. (2022)

46 Dispenza, F. (2023). Chronic illness and disability among sexual minority persons: Exploring the roles of proximal minority stress, adaptation, and quality of life. Psychology of Sexual Orientation and Gender Diversity, doi:10.1037/sgd0000642

47 Menhinick, K. A., & Sanders, C. J. (2023). LGBTQ+ stress, trauma, time, and care. Pastoral Psychology, doi:10.1007/s11089-023-01073-z

48 Riggs, D. W., & Treharne, G. J. (2017). Decompensation: A novel approach to accounting for stress arising from the effects of ideology and social norms. Journal of Homosexuality, 64(5), 592-605. doi:10.1080/00918369.2016.1194116

49 Hernandez, G. D., & Brinton, R. D. (2022). Allopregnanolone: Regenerative therapeutic to restore neurological health. Neurobiology of Stress, 21 doi:10.1016/j.ynstr.2022.100502

50 Szala-Rycaj, J., Szewczyk, A., Zagaja, M., Kaczmarczyk-Ziemba, A., Maj, M., & Andres-Mach, M. (2023). The influence of topinambur and inulin preventive supplementation on microbiota, anxious behavior, cognitive functions and neurogenesis in mice exposed to the chronic unpredictable mild stress. Nutrients, 15(9) doi:10.3390/nu15092041

51  Duman (2004)

52 Wersebe, H., Lieb, R., Meyer, A. H., Hofer, P., & Gloster, A. T. (2018). The link between stress, well-being, and psychological flexibility during an Acceptance and Commitment Therapy self-help intervention. International journal of clinical and health psychology : IJCHP, 18(1), 60–68. https://doi.org/10.1016/j.ijchp.2017.09.002

53 Hofmann, S. G., Sawyer, A. T., Witt, A. A., & Oh, D. (2010). The effect of mindfulness-based therapy on anxiety and depression: A meta-analytic review. Journal of consulting and clinical psychology, 78(2), 169–183. https://doi.org/10.1037/a0018555

54 Hofmann, S. G., Asnaani, A., Vonk, I. J., Sawyer, A. T., & Fang, A. (2012). The Efficacy of Cognitive Behavioral Therapy: A Review of Meta-analyses. Cognitive therapy and research, 36(5), 427–440. https://doi.org/10.1007/s10608-012-9476-1

55 National Institutes of Health. (2022). Stress. In The National Center for Complementary and Integrative Health. https://www.nccih.nih.gov/health/stress

To Diagnose or Not to Diagnose: The Debate on Personality Disorders in Adolescence

The Intersectionality of PD in Adolescence 

The presentation of a personality disorder in adolescence is complicated by the ongoing debate of whether personality disorders should be diagnosed. Some licensed health professionals are hesitant to provide a diagnosis due to the belief that adolescence is a period of changing personality,[1] thus, it is not appropriate to judge if a personality is disordered. However, other health professionals argue for the benefits of early detection and treatment, leading to better health outcomes.[2] The impacts of the home environment, genetics and consequences of a diagnosis further complicate this debate.

Effects of Home Environment 

Childhood maltreatment (e.g., neglect, physical abuse) substantially increases the risk of developing a personality disorder.[3] The Minnesota Project by Sroufe et al. (2005) followed a group of high-risk children into adulthood and found that insecure attachment during childhood is strongly associated with the later development of personality disorders in adolescence.[4] Later studies on Borderline Personality Disorders (BPD) further supported the association of adverse childhood experiences as a risk factor for personality disorders. Marchetti et al. (2022) found that a history of childhood maltreatment was associated with higher levels of BPD in adolescents (average age 16).[5] Furthermore, studies by Xiao et al. (2023) found that adolescents with BPD had higher rates of all the assessed childhood traumas when compared to adolescents with non-disordered personalities; this was especially true for emotional neglect (the most commonly seen childhood trauma).[6]

Effects of Biological Factors

Adolescence is a time of biological change, including those that regulate one’s personality. Throughout adolescence, the brain continues to develop in term of myelination and the formation of synaptic networks; thus, the neural basis for many psychological regulatory systems are still in development.[7] Furthermore, the frontal, temporal and occipital lobes of the brain (which are responsible for response inhibition, emotion regulation, planning and organization) are still developing during adolescence, which may account for the increased impulsivity sometimes seen during this period.[8] The increased levels of sex hormones adolescents are exposed to during puberty also affect mood regulation.[9] Therefore, the developmental changes of adolescence can bring forth impulsivity and mood changes, similar to the changes brought by a personality disorder. 

However, studies by Xiao et al. (2023) have found that there are also biological differences in adolescents with personality disorders compared to non-disordered peers.[10] They found that adolescents with Borderline Personality Disorder showed increased Amplitude Low-Frequency Fluctuations in the limbic system (a measure of spontaneous neuronal activity related to the mood swings associated with BPD).[11] Thus, biological factors can also account for differences in the mood swings of adolescents with disordered personalities compared to non-disordered adolescents.

Arguments in favor of a diagnosis

The argument in favor of a diagnosis appeals to the benefits of early diagnosis, specifically: better health outcomes. Paris et al. (2013) report that conditions such as antisocial personality disorders begin in childhood, and as a result of the early onset, psychopathology is more likely to continue.[12] An analysis of personality trait dimensions also supports the early establishment of personality. Studies by Shiner et al. (2009) suggest a continuity from child to adult personality based on findings that certain personality traits (e.g., openness, conscientiousness, extroversion, agreeableness, neuroticism) in childhood predicted later behaviors.[13] Klimstra et al. (2009) distinguish that personality traits change considerably at the ages of 10-15 years old and then stabilize at the ages of 16-21 years.[14] However, according to Cicchetti et al. (2009), since personality disorders (PD) do not begin in adulthood, early investigation is necessary to develop a lifespan model for treatment.[15] Schmeck (2022) further supports the need for early intervention in personality disorders, arguing that early diagnosis rids the stigma associated with PD and lessens the possibility of long-lasting impairments and disability by facilitating the transition into adulthood.[16] 

These benefits of early diagnosis may have been considered by the Diagnostic and Statistical Manual of Mental Disorders (DSM) since the most recent version of the guide to diagnosing mental disorders has changed its age requirements for diagnosing PD. While earlier versions of the DSM did not allow someone under 18 to be diagnosed, the DSM-5 (the most recent version) allows the diagnosis of a personality disorder in someone under 18 if symptoms are present for at least one year.[17] 

Arguments against diagnosis

A study by Laurenssen et al. (2013) found that 57.8% of psychologists working with adolescents acknowledged the existence of personality disorders in this age group; however, only 8.7% of them actually made formal PD diagnoses in the adolescents.[18] The majority of psychologists are reluctant to diagnose adolescents based on the idea that personality is fluid and still developing.[19] Dijk et al. (2021) argue that while personality traits (e.g., openness, conscientiousness, extroversion, agreeableness, neuroticism) are structurally similar between adolescents and adults, there are developmental differences; for example, adolescents appear to be less conscientious.[20] Some psychologists also argue that an early diagnosis is stigmatizing since personality pathology can often be viewed as being unmodifiable.[21,22] Furthermore, according to Adshead et al. (2012), a misdiagnosis of a personality disorder in adolescence can focus attention away from interventions to improve the caregiving environment, particularly if neglect or abuse are present.[23] Perhaps taking the drawbacks of diagnosis into account, the American Psychiatric Association webpage, as of now, states that diagnosis of personality disorders is only applicable to individuals 18 and older (It is important to note that the American Psychiatric Association oversees the DSM-5).[24]

Treatment of PD in adolescence

Personality disorders vary in the ways they impact an individual’s thoughts and ways of expressing themselves, however, they align in their need for treatment to go away.[25] In adults certain psychotherapies (e.g., Dialectical Behavior Therapy (DBT), Cognitive Behavioral Therapy (CBT), Group Therapy, Psychoanalytic) have shown to be effective for treating personality disorder.[26] If an adolescent is diagnosed with a personality disorder, their treatment plans may differ slightly from adults. Adolescent treatment plans are complex due to a current need for more evidence if adult interventions also work for adolescents.[27] Furthermore, these treatment plans are unique as they often incorporate the adolescent’s school and parents.[28]

If you believe you or your child may have a personality disorder, please reach out to a licensed mental health professional (e.g., a psychotherapist, psychologist or psychiatrist) for guidance and support.

Contributed by: Maria Karla Bermudez

Editor: Jennifer (Ghahari) Smith, Ph.D.

References

1 Adshead, G., Brodrick, P., Preston, J., & Deshpande, M. (2012). Personality disorder in adolescence. Advances in Psychiatric Treatment, 18(2), 109-118. doi:10.1192/apt.bp.110.008623

2 Cicchetti, D., & Crick, N. R. (2009). Precursors and diverse pathways to personality disorder in children and adolescents. Development and Psychopathology, 21(3), 683-685. doi:https://doi.org/10.1017/S0954579409000388

3 Adshead et al. (2012)

4 Sroufe, A, Egeland, B, Carlson, E et al (2005) The Development of the Person: The Minnesota Study of Risk and Adaptation from Birth to Adulthood. Guilford Press

5 Marchetti, D., Musso, P., Verrocchio, M., Manna, G., Kopala-Sibley, D., De Berardis, D., . . . Falgares, G. (2022). Childhood maltreatment, personality vulnerability profiles, and borderline personality disorder symptoms in adolescents. Development and Psychopathology, 34(3), 1163-1176. doi:10.1017/S0954579420002151

6 Xiao, Q., Yi, X., Fu, Y., Jiang, F., Zhang, Z., Huang, Q., Han, Z., & Chen, B. T. (2023). Altered brain activity and childhood trauma in Chinese adolescents with borderline personality disorder. Journal of affective disorders, 323, 435–443. https://doi.org/10.1016/j.jad.2022.12.003

7 Adshead et al. (2012)

8 Ibid. 

9 Ibid. 

10 Xiao et al. (2023)

11 Ibid. 

12 Paris, Joel. “Personality disorders begin in adolescence.” Journal of the Canadian Academy of Child and Adolescent Psychiatry = Journal de l'Academie canadienne de psychiatrie de l'enfant et de l'adolescent vol. 22,3 (2013): 195-6. doi:10.1007/s00787-013-0389-7

13 Shiner, R (2009) The development of personality disorders: perspectives from normal development. Development and Psychopathology 4: 715–34

14 Klimstra, TA, Hale, WW, Raaijmoken, QA (2009) Maturation of personality in adolescence. Journal of Personality, Society & Psychology 96: 898–912

15 Cicchetti et al. (2009)

16 Schmeck, K. (2022, March 17). Debate: Should CAMHS professionals be diagnosing ... - wiley online library. ACAMH. https://acamh.onlinelibrary.wiley.com/doi/10.1111/camh.12553

17 Personality disorders: Diagnosis. CAMH. (n.d.). https://www.camh.ca/en/professionals/treating-conditions-and-disorders/personality-disorders/personality-disorders---diagnosis#:~:text=According%20to%20DSM%2D5%2C%20features,for%20at%20least%20one%20year.

18 Laurenssen, E. M., Hutsebaut, J., Feenstra, D. J., Van Busschbach, J. J., & Luyten, P. (2013). Diagnosis of personality disorders in adolescents: a study among psychologists. Child and adolescent psychiatry and mental health, 7(1), 3. https://doi.org/10.1186/1753-2000-7-3

19 Paris (2013)

20 van Dijk, I., Krueger, R. F., & Laceulle, O. M. (2021). DSM-5 alternative personality disorder model traits as extreme variants of five-factor model traits in adolescents. Personality disorders, 12(1), 59–69. https://doi.org/10.1037/per0000409

21 Cicchetti et al. (2009)

22 Adshead et al. (2012)

23 Ibid. 

24 What are personality disorders?. Psychiatry.org - What are Personality Disorders? (2022, September). https://www.psychiatry.org/patients-families/personality-disorders/what-are-personality-disorders#:~:text=Diagnosis%20of%20a%20personality%20disorder,their%20personalities%20are%20still%20developing.

25 Ibid.

26 Ibid.

27 Adshead et al. (2012)

28 Ibid.

Inherited Memories: Current Research & Popular Misunderstandings

Memory Transmission & Monarch Butterflies

Carl Jung (1875-1961)[1] used the term “collective unconscious” to describe inherited wisdom and intuition from the past.[2] Evidence of the intergenerational effects of trauma have been found in populations affected by subjugation, genocide, racism and war.[3] This raises the question of how these memories are transmitted and whether there are biological mechanisms that enable the transmission of this information beyond environmental upbringing.

In nature, an example of inherited memory might be seen in monarch butterflies who take three generations to return from Mexico to Canada; the last generation knowing the route without any living members having previously been there.[4] Whether the inherited memories that have been demonstrated in cells, worms and butterflies can be extended to mammals has become a growing area of interest to researchers in recent decades.[5] In 2013, researchers at Emory University showed that mice are capable of passing the fear of a specific scent (a smell similar to a cherry blossom) down to future generations, via their sperm.[6] This process (which takes place through a mechanism referred to as “transgenerational epigenetic inheritance,”)  has led many scientists to jump to exciting conclusions as to how this research might be applied to the transmission of memories between generations of humans.[7] Yet researchers are still working to understand the intertwined relationship between epigenetics and genetics.[8]

Transgenerational Epigenetic Inheritance

There are a growing number of studies indicating that trauma may be able to be passed down through epigenetics,[9] which is the study of how the environment and people’s behavior can change the way genes work.[10] In genetic research, however, the environment is used as a general term to refer to anything other than genetics (which may include a person’s actions, the actions of others and the general, physical world).[11]

The term epigenetics is commonly used to refer to two concepts:[12]

1) The ways that packaging or modification of DNA results in the transmission of information within a group of cells (a theory widely accepted by science).

2) The ways that packaging or modifications of DNA might result in transmitting information from one generation to the next (a newer theory not as well established).

Epigenetic changes are reversible (unlike genetic changes) and they do not change a DNA sequence, but rather how the body reads the DNA sequence.[13] In epigenetics, the gene is not changed or damaged, instead the mechanisms of expression (when a gene is converted into functioning proteins) is altered.[14] These changes can affect gene expression by turning genes “on” and “off.”[15] Such molecular pathways with the potential to act epigenetically include histone modifications, DNA methylation, small RNAs and protein-protein interactions.[16]

It is believed that modifications to genetic expression may help an organism to respond to a changing environment and also help its descendants increase their likelihood of surviving.[17] When discussing how information is passed through generations, intergenerational change refers to changes that take place in one generation, whereas transgenerational changes are inherited from two or more generations.[18] Epigenetic transgenerational inheritance therefore refers to inheritance from an environmental exposure (e.g., the effects of an endocrine disruptor such as BPA or DDT) that alters the genetic programming of the germline with the changes transmitted between generations in the absence of direct exposure.[19]

Nonhuman Examples

In nonhuman species, research supports the notion that memories may be transmitted through multiple generations. Erickson (2020) found that the eggs of chickens originally domesticated in the red jungle fowl of Southeast Asia over 4,000 years ago (that later biologically adapted to the higher elevations of Tibet 1,200 years ago) were able hatch eggs when incubated in the lowland environment of their ancestral past unlike a control group of eggs that did not show the same adaptability.[20] Research on worms has also shown specific genes called the Modified Transgenerational Epigenetic Kinetics (MOTEK) are involved with turning epigenetic transmissions through RNA on or off.[21] Similarly, plants also appear to be particularly prone to transgenerational epigenetic inheritance through heritable changes in DNA methylation.[22] These findings raise the question as to whether comparable results can be found in mammals.

Lessons from Mice

In mice, studies have shown that a traumatic event could alter sperm that may affect the behavior of future generations.[23] Dias & Ressler (2014) found that by exposing mice to an odor and associating it with fear before conceiving the next generation of mice, the following two generations showed increased behavioral sensitivity to the same odor.[24] Similar initial research conducted by Gapp (2018) indicated that inheritance of specific trauma symptoms can be transmitted through alterations to long RNA in sperm through several generations in mice.[25] Mukherjee et al. (2018) evaluated five immediate-early genes in mice after memories were stored of either a positive or negative experience and found that the expressions were so unique for each that they could predict which experience the mouse had undergone by simply looking at the gene expression; suggesting the activation profile for each gene can contain information about experiences they have undergone.[26] These examples provide a framework of how environmental information could potentially be passed down through generations at the epigenetic, behavioral and neuroanatomical levels.[27]

To evaluate whether epigenetic changes resulting from environmental exposures could be reversed, Aoued et al. (2019) established fear in mice through olfactory cue-based fear conditioning and then sought to reverse the effects.[28] They did this by training the first generation of mice to associate the odors of either acetone or Lyral with mild foot shocks. They then extinguished this fear by providing odor-only exposure without the presentation of electric shocks. The results showed that first generation offspring did not show behavior sensitivity to the two odors. These findings provide hope for potential therapies in the future that may provide methods for reversing the influence of parental stress in both offspring and the parental germline.[29]

Human Applications

Though environmentally-induced changes passed from one generation to the next are observed relatively often in plants, it has remained elusive in mammals and even more difficult to find in humans.[30] The working memory that human beings, jumping spiders, archerfish and honeybees all possess involve similar genes that are believed to be inherited from the last common ancestor over 600 million years ago.[31] However, the study of transgenerational epigenetic inheritance in humans is difficult to isolate due to the confounding of ecological, genetic and cultural inheritance.[32] Since parental trauma is sometimes linked to childhood emotional abuse, it can be difficult for researchers to disentangle whether the experiences of parents are transferred to offspring as a result of genetics or through lived experiences.[33] With a newly sparked interest on whether epigenetics explains generational trauma, research has been conducted on descendants of abused prisoners from the American Civil War, children in the womb during the Dutch Hunger Winter, and Holocaust survivors.[34] However, within any traumatic situation, the effects may depend on the severity of the trauma, the age of an individual during the event, and whether the trauma was an isolated event or a reoccurring one.[35]

When discussing intergenerational memories in humans, it is important to differentiate between the concepts of transgenerational epigenetically inherited memories and collective memories. Collective memories are the shared remembrance or interpretation of facts about social groups which a person belongs (such as the person’s ethnic group or country) and may range from a national to a global level.[36] However, collective memories have been shown to change with time based on societal perception (e.g., older Americans alive during World War II remember the bombing of Hiroshima as a positive event that ended the war whereas younger Americans view it as a negative event because thousands of innocent civilians were killed).[37] Epigenetic transgenerational memories would be affected by different mechanisms and would not necessarily reflect the same changes as collective memories.

Lessons From Survivors and Their Descendants

To determine whether the epigenetic mechanisms of intergenerational transmission of stress effects can be found in humans, Yehuda et al. (2015) analyzed a specific gene encoding (epigenetic changes in FKBP5 methylation) in Holocaust survivors and their offspring with comparable parent/offspring control groups.[38] Their work found epigenetic alterations in both the exposed parent and offspring that were associated with preconception parental trauma. These findings were believed to be the first evidence in humans of an association between preconception stress effects and epigenetic changes in exposed parents and their adult offspring. Researchers believe these findings may contribute to an increased risk for psychopathology in the offspring of highly traumatized individuals.[39]

Alterations to the sperm of adult men has already been found to take place due to diet, alcohol, smoking, age and toxic exposure.[40] Costa et al. (2018) conducted research looking at children born after the Civil War who survived to age 45, comparing those whose fathers were POWs compared to those whose fathers were non POW veterans of the war. They also compared children born before and after the war in the same family by paternal ex-POW status. Though they did not find any impact of POW status on daughters, they found that sons of ex-POWs who experienced the camps during the harshest conditions were 1.11 times more likely to die than the sons of non POWs even after accounting for family structure, socioeconomic status, quality of marriage, maternal effects, and father-specific survival traits concluding that the findings were most consistent with an epigenetic explanation. However, they were not able to disentangle whether these epigenetic results were due to the stress of captivity or the effects of starvation.[41]

Future Research and Challenges

The University of Zurich’s Laboratory for Neuroepigenetics, run by Professor Isabel Mansuy, conducts research focused on determining molecular and cellular processes underlying how life experiences may influence physical and mental health across generations.[42] The laboratory not only conducts original research pioneering an understanding of transgenerational epigenetic inheritance in mice, but also conducts collaborative studies with clinicians in Europe and Asia to research the relevance as it relates to trauma patients in humans.[43] Professor Mansuy explains that trauma not only affects a person’s brain but also their reproductive system, which could cause depression or borderline personality disorder to be a trait inherited from parents.[44]

Challenges to studying environmentally-induced inheritance in humans include the nonexistence of four generations of human epidemiological cohorts and the ethical considerations of human experimentation.[45] A female fetus growing in the mother’s womb already contains the full complement of eggs, which means the DNA of future grandchildren is already present in a pregnant mother, so that it could take up to four generations to study true trans-generational inheritance in females.[46] In males, these changes could be seen in the next generation, since sperm is continually being produced.[47]

In terms of evolution, the transmission of epigenetic information in a fast-producing animal population could assist that species in rapidly adapting to a new environment, but this could become a maladaptive practice if the actual environment does not match that which was anticipated.[48] This may be one reason that the trait is not observed as much in humans who may come across multiple environments in their lifetimes.[49]

Research Riddled With Controversy

While the implications of epigenetic research have been met with enthusiasm by the press and public, there are scientists who heavily contest both the findings and their presentation. The research conducted by Yahuda et al. on Holocaust survivors was heavily criticized by Professor Ewan Birney, Director of the EMBL-European Bioinformatics Institute, for its small sample size (32 people and 8 controls), the tiny subset of genes used and the possibility of other potential causes for the findings.[50]

Similarly, Kevin Mitchell, a neurogeneticist known for speaking up against “neuro-bollocks,” in an interview with Claire McKenna (2020) explained his belief that there will never be accurate biomarkers (e.g., bloodwork, brain scans) for psychiatric or neurological conditions because the conditions are defined at the level of human behavior explaining, “Even if there’s a dynamic neural state that underpins some aspects of psychosis that we both share, the way that state looks in your brain may be very different from the way it looks in my brain…”[51] Mitchell does not find the transmission of trauma through epigenetic mechanisms plausible because it overly simplifies the relationship between psychological traits and genes explaining that a person’s experiences are expressed through changes in neuroanatomy instead of gene expression.[52]

In his blog, Wiring the Brain, Mithell also wrote an entry on May 29, 2018, reviewing what he believed to be the most prominent research on this topic at the time, and provided detailed information on each study as to why he believed them to be invalid (often small sample sizes and lack of predefined hypotheses).[53] In response, Jill Esher (a research philanthropist who funds pilot studies on exposure-induced nongenetic inheritance) posted a rebuttal on Germline Exposure’s website stating, among other things, that Mitchell cherry-picked the human studies he cited and then countered his argument by citing eleven studies illustrating transgenerational effects in humans and over 30 studies of intergenerational nongenetic inheritance in mammals.[54]

Mosche Szys, a professor of pharmacology at McGill University, similarly supported published findings on epigenetic research in mice telling the New York Times (2018) that dismissals of epigenetic theory are premature by explaining that, “The effects we’ve found have been small, but remarkably consistent and significant….This is the way science works. It is imperfect at first and gets stronger the more research you do.”[55]

Yehuda et al. (2018) (authors of the holocaust research criticized above) sought to clarify misconceptions by explaining that sensational media was oversimplifying their findings, obscuring the boundaries between fact and hypothesis and making inferences with implications far beyond the original findings; citing an example from Teen Vogue that cited their study and warned “You can get PTSD from your ancestors.”[56] They also warn that often articles claiming to debunk the notion that trauma is inherited are citing limitations written into the original research paper by the research team and are in fact debunking an over-interpretation of earlier journalists as opposed to the research itself. This led to an additional warning of inaccurately teaching the public that scientists are debunking one another rather than collaborating through the process of critique and correction.[57]

Potential Applications

Professor Mansuy explained during an interview with Jean Mary Zarate (2023), a senior editor at the journal Nature Neuroscience, that modifications to reproductive cells from traumatic experiences may transmit some of the effects of the exposure to children and research in this field could further our understanding of how inheritance can potentially affect psychiatric disorders including depression, anxiety and borderline personality disorder.[58] She explains there is a lot of work to be done in this field before it can be used to help people directly, but understanding that complex diseases like depression may be inherited from parents directly, instead of being related to something a person has done, would be important for psychiatrists and medical practitioners to know.[59]

This field is a budding new area of research and while the potential implications may excite the public, and at times become exaggerated in the media, the science is not yet understood well enough to be applied in the therapeutic setting. Though in the future, as more research emerges, it may be possible to incorporate these findings into techniques such as cognitive behavior therapy (CBT) or acceptance and commitment therapy (ACT) as a multi-pronged approach for addressing the root cause.

While progress in this field may be slow to produce answers, the current lack of understanding of epigenetic transgenerational inheritance does not minimize the reality of generational trauma and collective memories that can be passed down through a variety of other pathways. In addition to the potential for traumatic events that occur through transgenerational epigenetic inheritance, descendants of traumatized individuals may also be affected by the prenatal state of an anxious/symptomatic mother, or trauma affecting a parent’s behavior.[60] If you or someone you know is struggling to process generational trauma, please reach out to a licensed mental health professional (e.g., a psychotherapist, psychologist or psychiatrist) for guidance and support. 

Contributed by: Theresa Nair

Editor: Jennifer (Ghahari) Smith, Ph.D.

REFERENCES

1 Fordham F, Fordham M. Carl Jung | biography, archetypes, books, collective unconscious, & theory | Britannica. Britannica Web site. https://www.britannica.com/biography/Carl-Jung. Updated 2023. Accessed Jun 8, 2023.

2 Treffert D. Genetic memory: How we know things we never learned. Scientific American Blog Network Web site. https://blogs.scientificamerican.com/guest-blog/genetic-memory-how-we-know-things-we-never-learned/. Updated 2015. Accessed May 11, 2023.

3 Yehuda R, Lehrner A, Bierer LM. The public reception of putative epigenetic mechanisms in the transgenerational effects of trauma. Environ Epigenet. 2018;4(2):dvy018. doi: 10.1093/eep/dvy018.

4 Treffert (2015)

5 Fisher AG, Brockdorff N. Epigenetic memory and parliamentary privilege combine to evoke discussions on inheritance. Development. 2012;139(21):3891-3896. doi: 10.1242/dev.084434.

6 Gallagher J. 'Memories' pass between generations. BBC News. -12-01 2013. Available from: https://www.bbc.com/news/health-25156510. Accessed May 11, 2023.

7 Ibid.

8 Spinney L. Epigenetics, the misunderstood science that could shed new light on ageing. The Guardian Web site. https://www.theguardian.com/science/2021/oct/10/epigenetics-the-misunderstood-science-that-could-shed-new-light-on-ageing. Updated 2021. Accessed June 2, 2023.

9 Henriques M. Can the legacy of trauma be passed down the generations? BBC Future Web site. https://www.bbc.com/future/article/20190326-what-is-epigenetics. Updated 2019. Accessed May 26, 2023.

10 Center for Disease Control and Prevention, (CDC). What is epigenetics? | CDC. Centers for Disease Control and Prevention Web site. https://www.cdc.gov/genomics/disease/epigenetics.htm. Updated 2022. Accessed May 26, 2023.

11 Birney E. Why I'm sceptical about the idea of genetically inherited trauma. The Guardian Web site. https://www.theguardian.com/science/blog/2015/sep/11/why-im-sceptical-about-the-idea-of-genetically-inherited-trauma-epigenetics. Updated 2015. Accessed June 1, 2023.

12 Ibid.

13 CDC (2022)

14 Benedict C. Can we really inherit trauma? The New York Times Web site. https://www.nytimes.com/2018/12/10/health/mind-epigenetics-genes.html. Updated 2018. Accessed May 26, 2023.

15 CDC (2022)

16 Sarkies P. Molecular mechanisms of epigenetic inheritance: Possible evolutionary implications. Semin Cell Dev Biol. 2020;97:106-115. https://www.sciencedirect.com/science/article/pii/S1084952118301484. doi: 10.1016/j.semcdb.2019.06.005.

17 Lacal I, Ventura R. Epigenetic inheritance: Concepts, mechanisms and perspectives. Frontiers in molecular neuroscience; Front Mol Neurosci. 2018;11:292. doi: 10.3389/fnmol.2018.00292.

18 Sarkies (2020)

19 Skinner MK. Epigenetic transgenerational inheritance. Nature Reviews Endocrinology. 2016;12(2):68-70. https://doi.org/10.1038/nrendo.2015.206. doi: 10.1038/nrendo.2015.206.

20 Erickson J. Past is prologue: Genetic ‘memory’ of ancestral environments helps organisms readapt. University Wire. 2020. Available from: https://www.proquest.com/docview/2405486117?pq-origsite=primo#. Accessed May 14, 2023.

21 Javelosa J. Scientists have discovered how memories are inherited. World Economic Forum Web site. https://www.weforum.org/agenda/2018/12/memories-can-be-inherited-and-scientists-may-have-just-figured-out-how/. Updated 2018. Accessed May 11, 2023.

22 Quadrana L, Colot V. Plant transgenerational epigenetics. Annu Rev Genet. 2016;50:467-491. doi: 10.1146/annurev-genet-120215-035254.

23 Gallagher (2013)

24 Dias BG, Ressler KJ. Parental olfactory experience influences behavior and neural structure in subsequent generations. Nat Neurosci. 2014;17(1):89-96. Accessed May 24, 2023. doi: 10.1038/nn.3594.

25 Gapp K, van Steenwyk G, Germain PL, et al. Alterations in sperm long RNA contribute to the epigenetic inheritance of the effects of postnatal trauma. Mol Psychiatry. 2020;25(9):2162-2174. https://www.nature.com/articles/s41380-018-0271-6. Accessed May 30, 2023. doi: 10.1038/s41380-018-0271-6.

26 Sagar V, Kahnt T. Genetic signatures of memories. eLife. 2018;7:e36064. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5862524/. Accessed May 12, 2023. doi: 10.7554/eLife.36064.

27 Dias & Ressler (2014)

28 Aoued HS, Sannigrahi S, Doshi N, et al. Reversing behavioral, neuroanatomical, and germline influences of intergenerational stress. Biol Psychiatry. 2019;85(3):248-256. doi: 10.1016/j.biopsych.2018.07.028.

29 Ibid.

30 Birney (2015)

31 Earl B. Humans, fish, spiders and bees inherited working memory and attention from their last common ancestor. Frontiers in psychology; Front Psychol. 2023;13:937712. doi: 10.3389/fpsyg.2022.937712.

32 Horsthemke B. A critical view on transgenerational epigenetic inheritance in humans. Nature Communications. 2018;9(1):2973. https://doi.org/10.1038/s41467-018-05445-5. doi: 10.1038/s41467-018-05445-5.

33 Yehuda R, Daskalakis NP, Bierer LM, et al. Holocaust exposure induced intergenerational effects on FKBP5 methylation. Biol Psychiatry. 2015;80(5):372-380. doi: 10.1016/j.biopsych.2015.08.005.

34 Benedict (2018)

35 Byrne D. How trauma’s effects can pass from generation to generation. Nature. 2023. https://www.nature.com/articles/d41586-023-01433-y. Accessed May 30, 2023.

36 Roediger H, DeSoto K. The power of collective memory. Scientific American Web site. https://www.scientificamerican.com/article/the-power-of-collective-memory/. Updated 2016. Accessed May 24, 2023.

37 Ibid.

38 Yehuda et al. (2015)

39 Ibid.

40 Costa DL, Yetter N, DeSomer H. Intergenerational transmission of paternal trauma among US civil war ex-POWs. Proc Natl Acad Sci U S A. 2018;115(44):11215-11220. doi: 10.1073/pnas.1803630115.

41 Ibid.

42 University of Zurich (UZ). Laboratory of neuroepigenetics | isabelle mansuy. University of Zurich Web site. http://www.hifo.uzh.ch/en/research/mansuy.html. Accessed May 30, 2023.

43 Ibid.

44 Byrne (2023)

45 Escher J. No convincing evidence? A response to kevin mitchell’s reckless attack on epigenetic inheritance. Germline Exposures Web site. http://www.germlineexposures.org/1/post/2018/07/no-convincing-evidence-a-response-to-kevin-mitchells-reckless-attack-on-epigenetic-inheritance.html. Updated 2018. Accessed Jun 2, 2023.

46 Birney (2015)

47 Ibid.

48 Horsthemke (2018)

49 Ibid.

50 Birney (2015)

51 McKenna C. Kevin mitchell. BJPsych Bull. 2020;44(2):81-83. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7283122/. doi: 10.1192/bjb.2020.18.

52 Ibid.

53 Mitchell K. Grandma’s trauma – a critical appraisal of the evidence for transgenerational epigenetic inheritance in humans. . 2018. http://www.wiringthebrain.com/2018/05/grandmas-trauma-critical-appraisal-of.html. Accessed Jun 5, 2023.

54 Escher (2018)

55 Benedict (2018)

56 Yehuda et al. (2018)

57 Ibid.

58 Byrne (2023)

59 Ibid.

60 Yehuda et al. (2018)

When Does Dissociation Become Unhealthy?

Physically I’m Here… Mentally I’m Far, Far Away

Dissociative experiences can be a harmless and even euphoric part of life. This can look like getting lost in your favorite song, watching a beautiful sunset in complete awe or being so engaged in a meditation session that nothing else matters to you in that moment. On the other end of the spectrum, however, maladaptive dissociation can have detrimental impacts on a person’s wellbeing and functionality if left untreated and misunderstood.

Dissociation can severely impair peoples’ ability to effectively integrate their thoughts, memories and emotions with their experience of reality and perception of their identity.[1] The result in such extreme cases is often a highly fragmented sense of life and self-identity that can lead to mental health problems such as depression, anxiety and suicidal thoughts. Understanding the difference between so-called “healthy” and “unhealthy” dissociation is a critical first step for determining whether someone should seek help.

What is “Healthy” Dissociation?

Compared to other psychological defenses, dissociation is unique in that milder versions can be invoked voluntarily. For example, the ability of absorption to be consciously learned and applied combined with its psychological defensive capacity makes it an ideal therapeutic strategy.[2] Absorption consists of disconnecting from one’s current circumstances (both external and psychological) and becoming immersed in another focus. Absorption in music, nature and other positive foci can relieve emotional distress when a person is experiencing emotional or even physical pain.[3] While absorption itself involves some degree of dissociation, it is not indicative of pathological dissociation and can have many advantageous effects. 

In her book, Everyday Music Listening: Absorption, Dissociation and Trancing, Ruth Herbert describes absorption in music as a therapeutic practice that may involve “multi-sensory blending” and “heightened awareness”.[4] She argues that everyday listening can be not only pleasurable or relaxing, but transcendent in a way that is comparable to religious rituals and mindfulness meditation — all of which frequently prompt a state of dissociation. The multitude of ways in which individuals can remold, reinterpret or redirect their own consciousness through absorption in positive foci certainly exemplifies the human brain as a powerful tool in constructing our reality. Healthy dissociation — that is, when one can control it and choose when to do it — has incredible promise in both therapeutic approaches and consciousness research more broadly. So… How can dissociation become a chronic or even debilitating problem, characteristic of the dissociative disorders?

A Very Fine Line

Milder forms of dissociation often provide a defensive function which dislocates affect from ideas, diminishing the impact of disturbing emotional states.[5] For example, a dissociative episode may help foster a state of indifference or neutrality towards a stressful situation. Up to 75% of people experience at least one depersonalization/derealization episode in their lives, with only 2% meeting the full criteria for chronic episodes.[6] Yet, most clinically-noted dissociative episodes typically involve severely dysfunctional behavior, perpetuating the notion that dissociation is not applicable to the overall population.[7]

Upon examining typical manifestations of dissociation as defense mechanisms conducive to survival, we see that dissociation is the “freeze” part of the flight, fight and freeze emergency systems. Taken alone, this is a completely natural mental response to discomfort, stress and adversity. However, the tendency to rely on this “freeze” reaction can be the birthplace of dissociative disorders. Once individuals have learned to use dissociation to cope with an aversive event, dissociation can presumably become automatized and invoked on a habitual basis in response to even minor stressors.[8] Thus, even seemingly isolated experiences of dissociation can become chronic manifestations characteristic of dissociative disorders. It is therefore important that researchers and therapists take note of this link as to not overlook acute, nonpathological episodes in a clinical framework.

The Trauma-Dissociation Link

At some point in life, most people will endure some degree of heartbreak and loss. However, to live through true trauma is a completely different experience. The physical and mental shock of trauma elicits the brain’s immediate survival instincts — one of which being dissociation.[9] The vast majority of people who develop dissociative disorders have experienced repetitive, overwhelming trauma in childhood. Those who have experienced physical and sexual abuse in childhood are at increased risk of dissociative identity disorder (DID). Among people with dissociative identity disorder in the United States, Canada and Europe, roughly 90 percent had been the victims of childhood abuse and neglect.[10] 

Severely dissociative symptoms are manifestations of an automatic defense mechanism that serves to mitigate the impact of highly aversive or traumatic events. The idea of dissociation serving a defensive function can be traced back to Pierre Janet’s 1889 pioneering investigations of dissociative phenomena.[11] In the context of trauma, dissociation can be one of the ways your brain protects us in the face of adversity – both in the present moment and for the future. In a traumatic situation where someone might need to react quickly and instinctively to escape danger, dissociation serves as a way to mentally “check out” so that stress and fear does not overwhelm their mind. Also taking preventative measures, our brains do not want us to relive the shock of a traumatic experience, so it leaps into survival mode, taking steps to conceal or numb what happened. But… If dissociation is a natural response meant to protect us from trauma, how does it become something disordered that requires treatment?

Trapped in Limbo Between Past and Present

Binks & Ferguson (2013) note that while at the moment of the traumatic event dissociation is highly adaptive and protects the psyche from pain and feelings of helplessness and humiliation, individuals who cope with trauma by dissociating are vulnerable to using this method to cope with future stressors.[12] This becomes especially problematic in cases of childhood/adolescent trauma, as these time periods are integral junctures in the development of more persistent personality pathology.[13] Exposure to trauma during these critical periods exacerbates the likelihood of establishing dissociation as a habitual coping mechanism for the rest of life.

Dissociation is paradoxical in that it can relieve trauma survivors of the immediate pain they are in, but can also become a danger in, and of, itself. In the long-run, habitual dissociation established as a standardized defense mechanism early in life produces detrimental consequences. An account of dissociation from the perspective of a childhood trauma survivor illustrates why: “Dissociation makes surviving the abuse much easier… But it also makes living as an adult so much harder.”[14] Contorting the timeline of when trauma is experienced, dissociation keeps someone trapped in a sort of limbo between past and present. It challenges their ability to fully heal and transcend childhood levels of emotional maturity. In turn, dissociation threatens the agency a person has over their own life and, ultimately, the beauty of actually living as opposed to merely surviving.

The Double-Edged Sword

There are many promising avenues for future research in the realm of therapeutic dissociation, keeping in mind that dissociation in the context of mindfulness is vastly different from habitual dissociation evoked as the primary response to trauma. This distinction lies in the agency we have over the dissociation – that is, choosing to dissociate to enhance the experience of living vs. dissociating merely to survive. In this way, dissociation is a double-edged sword, possessing a great potential in encouraging wellbeing when we can control it, but perhaps an even greater potential for danger when it controls us.

If you feel you may be dissociating at unhealthy levels and/or in a way that is interfering with fully living your life, please reach out to a licensed mental health professional (e.g., a psychotherapist, psychologist or psychiatrist) to discuss possible therapeutic options and treatment modalities. Cognitive behavioral therapy (CBT) and dialectical behavioral therapy (DBT) are both common forms of psychotherapeutic treatment for all dissociative disorders.[15] To learn more about types of dissociative disorders and effective treatments, feel free to refer to our encyclopedia entry on dissociation.

Contributed by: Sara Wilson

Editor: Jennifer (Ghahari) Smith, Ph.D.

REFERENCES

1 American Psychiatric Association. (2022, October). What are Dissociative Disorders? Psychiatry.org. Retrieved 27 May, 2023, from https://www.psychiatry.org/patients-families/dissociative-disorders/what-are-dissociative-disorders

2  Bowins, B. E. (2012). Therapeutic Dissociation: Compartmentalization and Absorption. Counseling Psychology Quarterly, 25(3), 307-317.

3 Ibid.

4  Becker, J. (2014). [Review of Everyday Music Listening: Absorption, Dissociation and Trancing, by R. Herbert]. Ethnomusicology Forum, 23(2), 266–268. http://www.jstor.org/stable/43297432.

5  Bowins (2012)

6  National Alliance on Mental Illness. (2023). Dissociative Disorders. Retrieved 27 May 2023, from https://www.nami.org/About-Mental-Illness/Mental-Health-Conditions/Dissociative-Disorders.

7  Bowins (2012)

8  Giesbrecht, T., Lynn, S. J., Lilienfeld, S. O., & Merckelbach, H. (2008). Cognitive Processes in Dissociation: An Analysis of Core Theoretical Assumptions. Psychological Bulletin, 134(5), 617-647. https://doi.org/10.1037/0033-2909.134.5.617.

9  Gillette, H. (2021, August 3). Trauma-Related Dissociation: Symptoms, Treatment, Coping, and More. Psych Central. https://psychcentral.com/pro/coping-with-trauma-through-dissociation.

10  American Psychiatric Association.

11  Giesbrecht et. al., (2008)

12  Binks, E., & Ferguson, N. (2013). Religion, trauma and non-pathological dissociation in northern ireland. Mental Health, Religion & Culture, 16(2), 200-209. https://doi.org/10.1080/13674676.2012.659241.

13 Shiner, R. (2023, April 4). Emergence of Personality Disorder in Adolescence: New Findings and Their Implications for Treatment. YouTube. https://www.youtube.com/watch?v=K00Xdcjd7_E&t=416s.

14 Beauty After Bruises. (2023, April 21). Dissociation and Survival vs. Living: A Survivor’s Story. Beauty After Bruises. https://www.beautyafterbruises.org/blog/survivorstory.

15  Cleveland Clinic. (2022, October 24). Dissociative Disorders: Causes, Symptoms, Types & Treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/17749-dissociative-disorders.

Marijuana: The “Band-Aid Strategy” That May Not Heal Wounds of Anxiety

The ABC’s of THC & CBD

Produced in the form of lotions, candles, candies and oils, Cannabidiol (CBD) products have built their popular reputation as a treatment for anxiety relief. These CBD products are shown to have the ability to ease pain and induce relaxation, ultimately relieving stressful symptoms of anxiety. Some may believe that if CBD, the second most active ingredient in marijuana, is capable of bringing about anxiety relief, then marijuana as a whole substance can relieve anxiety as well. However, the presence of Tetrahydrocannabinol (THC), which is the major psychoactive ingredient in marijuana, complicates the idea that marijuana is a solely “relaxing” drug.

Cannabis is the world’s most widely-used illicit drug, with continually increasing prevalence. Despite this high prevalence, little attention has been given to the potential risk of developing mood and anxiety disorders due to regular marijuana use - especially for users later in life. A 2019 systematic review of 11 studies involving 23,317 individuals by researchers at McGill University, however, found that cannabis use during adolescence is associated with increased odds of developing anxiety in young adulthood. In addition, the risk of depression and suicidality has also been shown to increase with the usage of marijuana during adolescence. This is especially problematic, as US individuals aged 18 to 29 years who reported cannabis use roughly doubled from 2001 to 2013, from 10.5% to 21.2%. Though we’ve known the mood-elevating properties of cannabis for a long time, it may be time to delve more deeply into the long-term negative effects that cannabis can induce in terms of mental health, and especially anxiety.[1]

While marijuana may have some short-term anxiety-relieving benefits, studies have shown that a long-term use of THC at high doses will actually increase anxiety. Over the past decade, marijuana usage has significantly increased in the United States, especially since many states have legalized marijuana use in some form. Notably, the marijuana being produced has resulted in higher THC content, while the CBD content has gradually decreased. This is potentially problematic because whileas THC in its purest form can decrease anxiety at low doses, it has been shown to actually increase anxiety at high doses, and decrease anxiety at low doses. Conversely, CBD in its purest form has been shown to decrease anxiety at all doses tested.[2]

EFFECTS OF MARIJUANA INTOXICATION

Marijuana intoxication is known to have a broad range of effects, including:[3]

  • Euphoria 

  • Sense of calm

  • Synesthesia/blending of the senses (e.g., you may be listening to music, but seeing shapes simultaneously) 

  • Craving sweet/salty foods

  • Belief of arriving at a transcendent insight 

  • Enhanced perception

  • Impaired shifting focus

  • Lack of attention 

  • Short-term memory loss

  • Poor decision-making

  • Paranoia

  • Decreased motor activity 

  • Lack of motivation

THE ENDOCANNABINOID SYSTEM 

The endocannabinoid system in the brain is responsible for processing feelings of anxiety, fear, and stress responses. Marijuana intoxication is often associated with calmness and being content, which increases cannabinoid and oxytocin receptor activation, and increases dopamine levels. However, once the frequent and chronic user is not intoxicated, cannabis withdrawal is mediated with stress hormone release and reduced dopamine levels. It is important to note that the endocannabinoid system plays a role in anxiety, especially because endocannabinoids modulate highly interactive stress and reward networks that create balance between pain and well-being. This means that in the long-term, the positive emotional effects of marijuana intoxication may be outweighed by negative emotional effects brought about by marijuana withdrawal.[4] 

Other factors associated with the risk of increased anxiety when consuming cannabis include:[5]

  • Genetic vulnerability

  • Female gender

  • High usage frequency

  • High dosage

  • High THC/low CBD content

  • History of anxiety

CANNABINOID RECEPTORS

The psychoactive effects of marijuana are related to the cannabinoid receptor CB1, while the non-psychoactive effects are related to the cannabinoid receptor CB2. THC is the main psychoactive component of marijuana, while CBD has no psychoactive effects. The CB1 receptor is strongly expressed in the brain and central nervous system (CNS). The CB2 receptor is more pertinent in peripheral immune cells and tissues. The explanation for lack of benefit derived from THC in terms of mental health could be that chronic regular use of marijuana builds a tolerance in the user. The rise in tolerance leads to the eventual downregulation of the CB1 receptor, which means some of the negative symptoms of THC that are usually felt are exacerbated even when the user is not intoxicated.[6] 

The CB1 receptor is also responsible for inhibiting the release of excitatory amino acids and GABA, which regulates other transmitter releases, such as the release of acetylcholine, dopamine, histamine, serotonin and opioid peptides. Inhibitory interneurons (GABAergic) contain high levels of CB1 receptors, while excitatory terminals (glutamatergic) contain lower levels of CB1 receptors. Dopamine receptors, which play a specific important role in emotional behavior and psychiatric disorders, also contain lower levels of CB1 receptors. THC activates the CB1 receptor to induce feelings of euphoria and even heighten negative emotions, such as anxiety. On the other hand, CBD has been shown to function as a negative allosteric regulator of CB1 receptor activation, but it does not play a role as a complete antagonist.[7] This indicates that CBD plays an inhibitory role in CB1 activation, preventing the elevated emotions that THC induced through CB1 activation. However, CBD does not completely eliminate the effects of THC when both substances are present and interacting with the CB1 receptor. 

CBD VS. THC AS AN ANXIETY TREATMENT 

Current data suggests that CBD is associated with anxiolytic activity, with acute doses having been found to reduce or manage anxiety. Anxiolytic activity indicates that this drug can be used to treat symptoms of anxiety by blocking certain chemicals in the nervous system that may be triggered as a reaction to stress. CBD’s anxiolytic effects have been studied in various animal models of generalized anxiety disorder, social phobia, panic disorder, and post-traumatic stress disorder (PTSD) in humans. The anxiolytic effects have been established in people with generalized social anxiety disorder (SAD), and other anxiety disorders, with a heavy influence on the limbic and paralimbic areas of the brain.[8] Higher doses of CBD did not prove to have anxiogenic effects (i.e., anxiety inducing), however, higher doses of THC in clinical human studies have shown to demonstrate common effects of anxiety. This is the reason why CBD is heavily incorporated in hemp and medicinal products.[9] 

Smith & Randall (2022) note that it can be more risky to administer THC-based medical marijuana treatments for anxiety disorders since the results for this treatment are more ambiguous than CBD-based treatments. This means that some may experience an increase in symptoms of anxiety with THC-dominant products, while some patients have experienced initial feelings of anxiety with use of these products.[10]

A placebo controlled, randomized study performed by researchers at Maastricht University in 2022 focused on 26 healthy recreational cannabis users to compare the effects of THC-dominant, CBD-dominant, THC/CBD-equivalent, and placebo cannabis products on anxiety. The State-Trait Anxiety Inventory (STAI) was utilized to assess the state levels of anxiety amongst these users, along with a computer-based emotional Stroop task, questionnaire, and visual analogue scale. Some of the most significant findings were that:

  • THC-induced anxiety based on the STAI was independent of baseline anxiety.

  • THC/CBD-equivalent products result in lower state anxiety levels than THC-dominant, alone.

  • In comparison to the placebo product, both the THC and THC/CBD products increased state level anxiety significantly.

  • It was also found that at low baseline states of anxiety, the CBD-dominant product was able to entirely counteract THC-induced anxiety.

  • However, at a high baseline state of anxiety, the CBD-dominant product was not able to counteract THC-induced anxiety.[11]

Thus, it would appear that CBD (without the presence of THC) would work best to mitigate one’s anxiety.

BAND-AID STRATEGY

It is not uncommon for people with anxiety and mood disorders to seek medical or recreational marijuana for symptom relief, and in the short-term, users may even experience the desired symptom relief. However, the long-term effects of such usage tend not to be as positive. Mammen et al. conducted a systematic review of 12 longitudinal studies on a total of 11959 patients with a range of anxiety disorders in 2018. The researchers found that for each diagnosis, frequent cannabis users had more-severe symptoms and lower rates of remission (i.e., the total disappearance of symptoms of anxiety) than less-frequent and non-users. Some of the studies even showed that there is a link between stopping marijuana usage and symptom improvement. So while individuals with anxiety disorders may use marijuana as a temporary strategy to improve acute symptoms, the results of these studies have shown this method to actually worsen symptoms in the long run. This temporary fix is what is referred to as the “Band-Aid Strategy.”[12]

If one has been using or has previously used marijuana, and is experiencing feelings of heightened anxiety, it is crucial to contact a licensed mental health professional for guidance on how to decrease anxiety symptoms and prevent possible worsening of mental health. Before beginning to take any products with THC and/or CBD, it's also important to speak with your doctor or pharmacist to address any potential health risks.

Contributed by: Ananya Udyaver

Editor: Jennifer (Ghahari) Smith, Ph.D.

References

1 Su, M., Luo, Y., & Wang, Y. (2021). The association between cannabis use and suicidal behavior: A systematic review and meta-analysis. Journal of Affective Disorders, 294, 256-263. doi:10.1016/j.jad.2021.07.083

2 Stoner, A. (2017) Effects of Marijuana on Mental Health: Anxiety Disorders. Alcohol and Drug Abuse Institute: University of Washington. https://adai.uw.edu/pubs/pdf/2017mjanxiety.pdf

3 Ibid.

4 Ibid.

5 Ibid.

6 Ibid.

7 Graczyk, M., Łukowicz, M., & Dzierzanowski, T. (2021). Prospects for the use of cannabinoids in psychiatric disorders. Frontiers. https://www.frontiersin.org/articles/10.3389/fpsyt.2021.620073/full 

8 Ibid.

9 Berenbaum, H., & Connelly, J. (2020). The effect of cannabis use on mood and anxiety disorders: Clinical implications. Current Psychiatry Reports, 22(12), 78. doi:10.1007/s11920-020-01219-z 

10 Smith, K. P., & Randall, C. L. (2022). Anxiety disorders and cannabis use: A review. Substance Abuse and Rehabilitation, 13, 1361-1379. doi:10.2147/sar.s326480

11 Hutten, N. R. P. W., Arkell, T. R., Vinckenbosch, F., Schepers, J., Kevin, R. C., Theunissen, E. L., Kuypers, K. P. C., McGregor, I. S., & Ramaekers, J. G. (2022). Cannabis containing equivalent concentrations of delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) induces less state anxiety than THC-dominant cannabis. Psychopharmacology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9584997

12 Mammen, G., Reuda, S., Roerecke, M., Bonato, S., Rev-Lan, S., & Rehm, J. (2018). Association of cannabis with long-term clinical symptoms in anxiety and mood disorders: a systematic review of prospective studies. The Journal of Clinical Psychiatry. 79(4). https://doi.org/10.4088/JCP.17r11839

When Past Happiness is Skewed: How Accurate are Childhood Memories?

Capturing the Past

A mother and daughter swirl steaming coffee, reminiscing about their Ocean City vacation ten years ago. The mother pictures her daughter gleefully building sandcastles, eating sandwiches by the shore and begging not to leave at the end of the trip. The daughter stares at her mother in disbelief, recalling a completely different version of the story. She remembers getting sunburned to the point of peeling, slicing her foot on a sharp shell and being chased by an aggressive seagull who wanted her chips. What causes two people to remember the happiness of past experiences differently over time? It is possible that the mother initially misinterpreted her child as being happy, when she was not - but new research indicates there may also be other factors at play.

Current Life Satisfaction & Past Perspectives

One reason happiness can appear elusive is that memories of past well-being can be influenced by one’s current feelings.[1] In the classic test to determine whether someone is an optimist or a pessimist, a person evaluates a glass of liquid and is asked to state whether the glass is half-empty or half-full. In terms of recalling happiness, it may be helpful to reconsider this question from a different perspective: “Is the glass filling up or is it draining?” A person’s assessment of past well-being may tie into the perception of their overall life trajectory by placing the past in context of current levels of life-satisfaction and projected expectations of future happiness.[2]

Is the glass filling up or is it draining?

Whether a person is an optimist or a pessimist may have an impact on their perception of past events. To analyze the relationship between past perceptions of happiness and current mood, Prati & Senik (2022) evaluated data from four surveys (three publicly available national surveys and one commercial survey) including 260,000 surveys from more than 60,000 individuals in Germany, Britain, France, and the United States.[3] The results showed that happy people tended to remember their lives as progressively becoming better while those who were unhappy tended to view their happiness as deteriorating.[4]

One potential explanation for these findings is that a person’s experience of current happiness may inherently be dependent on feeling better than yesterday.[5] A person who is happy in their present life may therefore need to remember their past as slightly less happy to feel that they are making progress, while a person who is unhappy now may view the past as happier in order to justify current feelings.[6] These misconceptions may cyclically alter an individual’s future behavior leading happy people (who perceive their situation as continually improving) more open to new experiences, while unhappy people (who perceive their situation to be getting worse) to perceive a higher risk associated with change and taking chances.[7]

Those who struggle with severe depression may also experience additional skews in memory. Comparing 30 individuals with major depressive disorder (MDD) to 46 healthy individuals in a control group, Kim & Yoon (2020) found that those with MDD experienced more sadness when recalling their saddest memories and less happiness associated with their happiest memories, which may lead to hindering mood regulation and perpetuate a negative cycle.[8]

What Makes a Memory Happy or Sad?

Neuroscientists recently discovered that one specific molecule determines whether an event is stored as a good or bad memory.[9] As the brain assesses an experience to be categorized as positive or negative, neurons adjust the release of neurotensin (a small peptide molecule) which sends the information through different neural pathways.[10] Hao Li, postdoctoral researcher at the Salk Institute for Biological Studies in California, explained to Quanta Magazine that conditions such as anxiety or addiction may be the result of breakdowns in this process that result in “too much negative processing.”[11] From an evolutionary perspective, this process assisted in avoiding things that produced negative memories (e.g., a dangerous animal dwelling in a certain area or a food that made a person sick).[12] This process still helps people today to assess whether a situation is safe or dangerous by associating items with happy or sad memories.

Storing Memories of Emotions

While the above explanation accounts for generally categorizing a memory as positive or negative, there is a simultaneous belief that the intensity of emotions can’t be stored in the form of memories. To illustrate this concept, Wilson et al. (2003) gave the example that people cannot go on vacation just one time and continually live that happiness through memories; they need to repeatedly go on vacation to enjoy the experience once again.[13] Memories of emotions fade over time and people later rely on additional information to reconstruct their feelings which may erroneously lead to incorporating experiences and knowledge gained after the initial event.[14] This idea is further reinforced by research conducted by Kaplan et al. (2016) which interviewed participants to determine how they felt about election results both immediately after the election and one-month later following the 2008 and 2012 presidential elections.[15] Their analysis showed that the intensity of emotion diminished over time, which corresponds with a diminishing appraisal of the importance of the election as time passed.[16]

However, the inaccurate report of memories does not always present in the form of diminished feelings. Wilson et al. (2003) describes one type of change in memory due to emotions as “retrospective impact bias,” which leads people to overestimate their reactions to past events which can then potentially impact their ability to accurately recall information (e.g., the emotional impact that a fan will experience if their favorite sports team wins).[17] The incorrect recollection of memories is supported by an analysis of data collected from 1997-2009 through the British Household Panel Survey (BHPS) which found that 90% of participants incorrectly recalled their own self-reported levels of past happiness at least one time.[18] Similarly, a study conducted by Safer, Levine and Drapalski (2002) found that the recollection students had of how anxious they were before taking an exam was influenced by the grade they later received on the exam.[19]

Memory Engrams

Accurate recollection of memories involves multiple parts of the brain and may be affected by a variety of factors. A memory engram refers to the enduring changes (chemical or physical) that take place in brain networks when new information is learned representing acquired memory information.[20] Research conducted by Roy et al. (2022) supports the unified engram complex hypothesis for memory storage which proposes that each specific memory is stored in cell ensembles that are functionally connected and distributed widely across multiple brain regions.[21] Reactivating these neurons is believed to give rise to the recall of a specific memory.[22] However, the requirement of activating neurons in multiple regions of the brain may can potentially lead to the development of false memories.[23]

Selective Memories

Dating back to 1976, research conducted by Mischel, Ebbesen and Zeiss found that individuals exposed to both positive and negative descriptions of their personalities were more likely to remember the positive information.[24] Using this idea as a catalyst, Chew & Zhao (2020) evaluated three types of positive memory errors:[25]

  • Positive delusion - fabricating the memory of a positive event that did not happen

  • Positive amnesia - forgetting a negative event

  • Positive confabulation - distorting the memory of a past negative event into a positive event

Their research (which included 701 participants in Singapore and 669 from Beijing participating in both phases of the trial) found that individuals who answered questions regarding their performance on an IQ test (both immediately following the test and several months later) found considerable incidence of positive delusion (64.12%), amnesia (33.95%) and confabulation (10.63%).[26] These results show participants were more likely to forget their inaccuracies and exhibit positive false memories than negative false memories.[27]

Perceptions of Happiness Throughout One’s Lifespan

Age is also believed to be a factor in skewing a person’s view of past happiness. Hyman (2014) analyzed qualitative interviews of 26 adults from different regions of the United Kingdom and found that older adults (aged 60 and above) were more likely to view the past as happier, both in their personal lives as well as in society as a whole.[28] It was also found that happiness in the present could be gained by reminiscing about the past.[29]

Lachman et al. (2008) examined the responses of 3,793 participants, aged 24 to 74 at baseline, who provided retrospective, prospective and present ratings on two different occasions 8-10 years apart.[30] Their results showed that individuals over 65 found the past and present to be equally satisfying, though there was some belief that the future may not be equally so. Conversely, younger individuals felt their lives in the present were more satisfying than they were in the past.[31] These findings support the life-span motivational interpretation of recalling memories, reiterating that the stage of a person’s life may impact recollections of happiness.[32] In other words, those who are older are more likely to see their future as declining while those who are younger tend to see their future as improving. Since perceptions of the past may inherently be dependent on an individual’s perceived current and future perceptions of happiness, those who are younger may be more likely to minimize past happiness in hopes of a brighter future to look forward to while older individuals may remember the past fondly if they expect a diminished amount of happiness in the future.

How Memories Change

People not only have a tendency to change perceptions of past happiness, but sometimes memories can be entirely fabricated. Hugo Munstenberg first started studying the psychology of false memories in 1906 when a farmer’s son confessed to murdering a woman whose body was found in Chicago - despite having a valid alibi. Each retelling of the story added more details that were sometimes contradictory.[33] This raised the question of suggestibility and whether police officers may have been influencing a confession, though it would be decades before the topic was studied in further detail.[34]

In addition to outside influence skewing a person’s memories, sometimes the brain’s recollection process can be the culprit. Northwestern University’s Feinberg School of Medicine (2012) conducted research showing that every time a person recalls a memory the brain network changes in a way that can alter how the event is later recalled.[35] The memory can potentially become less precise every time it is remembered, eventually becoming a completely false memory.[36] Each person out of the 70 studied showed this effect.[37]

This year, new research also emerged revealing false memories may generate more quickly than previously believed. Experiments funded by the European Research Council (2023) showed the creation of false memories can occur within seconds.[38] The 534 participants were shown an initial set of letters from the western alphabet on a slide (in either mirrored or original orientation) with some participants shown a second slide intended to scramble the original memory.[39] When asked to recall a target letter from the first slide, within 500 milliseconds, 20% of participants formed an illusory memory of the target letter with the number increasing to 30% after 3 seconds.[40] Researchers believe this was the result of human brains altering occurrences based on what it expects to see, which can be difficult to process when there is an unexpected change, such as seeing a letter backwards.[41]

Benefits of Nostalgia

Nostalgic memories are also believed to positively skew our perceptions of the past. People sometimes feel nostalgic over things they did not like at the time such as a song they once found annoying or difficult class.[42] These memories may be induced by merely smelling a specific scent or sound (e.g., the smell of summer grass producing memories of playing outside as a child),[43] but the question can be raised as to whether reliving the past is psychologically healthy. FioRito and Routledge (2020) proposed that nostalgia is actually a future-oriented emotional experience instead of a retrospective event because it involves reflection on past behavior and experiences in order to prepare for future decisions.[44] Nostalgia is viewed by experts as a defense response that can alleviate sadness, strengthen social bonds, improve mood and increase spirituality.[45] It has been described as a redemptive sequence in which the feelings of loss and longing lead to the positive feelings of hope, happiness and gratitude.[46] By increasing a sense of meaning, nostalgia may help motivate individuals to pursue important life goals.[47]

While the subjectivity of past happiness may be impacted by a variety of factors, it can be helpful to take a deep breath and put memories into perspective. Though evidence indicates that memories are impacted by our current emotional state,[48] modern psychology teaches us that these changes are not inherently negative and that some changes to memories can be beneficial for helping individuals process the past and make more informed choices.[49] Speaking with others about shared events or keeping a journal about current experiences are ways to assess the accuracy of past memories.

However, if a person feels confused about the past and is having trouble sorting out truth from fiction or is having difficulty processing distressing memories from their past, it may be helpful to speak with a licensed mental health professional.

Contributed by: Theresa Nair

Editor: Jennifer (Ghahari) Smith, Ph.D.

REFERENCES

1 Association for Psychological Science (APS). Was I happy then? our current feelings can interfere with memories of past well-being. ScienceDaily Web site. https://www.sciencedaily.com/releases/2022/11/221109124402.htm. Updated 2022. Accessed Apr 25, 2023.

2 Lachman ME, Röcke C, Rosnick C, Ryff CD. Realism and illusion in americans' temporal views of their life satisfaction: Age differences in reconstructing the past and anticipating the future. Psychol Sci. 2008;19(9):889-897. doi: 10.1111/j.1467-9280.2008.02173.x.

3 Prati A, Senik C. Feeling good is feeling better. Psychol Sci. 2022;33(11):1828-1841. doi: 10.1177/09567976221096158.

4 APS (2022)

5 Ibid.

6 Prati & Senik (2022)

7 Ibid.

8 Kim D, Yoon KL. Emotional response to autobiographical memories in depression: Less happiness to positive and more sadness to negative memories. Cogn Behav Ther. 2020;ahead-of-print(-):1-11. doi: 10.1080/16506073.2020.1765859.

9 Li H, Namburi P, Olson JM, et al. Neurotensin orchestrates valence assignment in the amygdala. Nature. 2022;608(7923):586-592. https://doi.org/10.1038/s41586-022-04964-y. doi: 10.1038/s41586-022-04964-y.

10 Ibid.

11 Saplakoglu Y. A good memory or a bad one? one brain molecule decides. Quanta Magazine Web site. https://www.quantamagazine.org/a-good-memory-or-a-bad-one-one-brain-molecule-decides-20220907/. Updated 2022. Accessed May 4, 2023.

12 Ibid.

13 Wilson TD, Meyers J, Gilbert DT. "How happy was I, anyway?" A retrospective impact bias. SOC COGNITION. 2003;21(6):421-446. doi: 10.1521/soco.21.6.421.28688.

14 Ibid.

15 Kaplan, R. L., Levine, L. J., Lench, H. C., & Safer, M. A. Forgetting feelings: Opposite biases in reports of the intensity of past emotion and mood. Emotion. 2016;16(3):309–319. doi: 10.1037/emo0000127

16 Ibid.

17 Wilson et al. (2003)

18 Prati & Senik (2022)

19 Wilson et al. (2003)

20 Josselyn SA, Tonegawa S. Memory engrams: Recalling the past and imagining the future. Science. 2020;367(6473):eaaw4325. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7577560/. Accessed May 22, 2023. doi: 10.1126/science.aaw4325.

21 Roy DS, Park Y, Kim ME, et al. Brain-wide mapping reveals that engrams for a single memory are distributed across multiple brain regions. Nature Communications. 2022;13(1):1799. https://doi.org/10.1038/s41467-022-29384-4. doi: 10.1038/s41467-022-29384-4.

22 Josselyn & Tonegawa (2020)

23 Ortega-de San Luis C, Ryan TJ. Understanding the physical basis of memory: Molecular mechanisms of the engram. J Biol Chem. 2022;298(5):101866. doi: 10.1016/j.jbc.2022.101866.

24 Mischel, W., Ebbesen, E. B., & Zeiss, A. M. (1976). Determinants of selective memory about the self. Journal of Consulting and Clinical Psychology. 1976; 44(1), 92–103. Doi: 10.1037/0022-006X.44.1.92

25 Chew SH, Huang W, Zhao X. Motivated false memory. The Journal of political economy. 2020;128(10):3913-3939. doi: 10.1086/709971.

26 Ibid.

27 Ibid.

28 Hyman L. Happiness and memory: Some sociological reflections. SOCIOL RES ONLINE. 2014;19(2):1-9. doi: 10.5153/sro.3268.

29 Ibid.

30 Lachman et al. (2008)

31 Ibid.

32 Ibid.

33 Starr D. Remembering a crime that you didn’t commit. The New Yorker Web site. https://www.newyorker.com/tech/annals-of-technology/false-memory-crime. Updated 2015. Accessed May 12, 2023.

34 Dodgson L. Our brains sometimes create 'false memories' — but science suggests we could be better off this way. Business Insider Web site. https://www.businessinsider.com/science-of-false-memories-2017-12. Updated 2017. Accessed May 7, 2023.

35 M. Your memory is like the telephone game. Northwestern Now Web site. https://news.northwestern.edu/stories/2012/09/your-memory-is-like-the-telephone-game. Updated 2012. Accessed May 5, 2023.

36 Ibid.

37 Ibid.

38 . Otten M, Seth AK, Pinto Y. Seeing Ɔ, remembering C: Illusions in short-term memory. PLOS ONE. 2023;18(4):e0283257. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0283257. Accessed May 22, 2023. doi: 10.1371/journal.pone.0283257.

39 Nelson F. Your brain can create a false memory quicker than you think. ScienceAlert Web site. https://www.sciencealert.com/your-brain-can-create-a-false-memory-quicker-than-you-think. Updated 2023. Accessed May 4, 2023.

40 Otten et al. (2023)

41 Nelson (2023)

42 Brooks AC. Nostalgia is a shield against unhappiness. The Atlantic Web site. https://www.theatlantic.com/family/archive/2023/03/nostalgia-defense-unhappiness-happy-memories/673320/. Updated 2023. Accessed May 3, 2023.

43 Ibid.

44 FioRito TA, Routledge C. Is nostalgia a past or future-oriented experience? affective, behavioral, social cognitive, and neuroscientific evidence. Frontiers in psychology. 2020;11:1133. https://search.proquest.com/docview/2424436969. doi: 10.3389/fpsyg.2020.01133.

45 Brooks (2023)

46 Routledge C. The surprising power of nostalgia at work. Harvard Business Review. 2021. https://hbr.org/2021/04/the-surprising-power-of-nostalgia-at-work. Accessed May 3, 2023.

47 Ibid.

48 APS (2022)

49 Dodgson L. Our brains sometimes create 'false memories' — but science suggests we could be better off this way. Business Insider Web site.  https://www.businessinsider.com/science-of-false-memories-2017-12. Updated 2017. Accessed May 22, 2023.