Does Depression Accelerate Aging?

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A clear association between depression, especially the major depressive disorder, oxidative stress, and accelerated aging is supported by research.

Depression, major depressive disorder more specifically, is one of the most striking problems of modern society. Millions of people worldwide suffer from depression, with many patients not experiencing relief from symptoms. Depression is associated with increased mortality from age-related conditions, such as cardiovascular disease and cancer. Researchers have suggested that depression is associated with increased oxidative stress and a disturbed immune response, which may accelerate aging and increase susceptibility to age-related disorders.

One of the proven indicators of cellular aging is the length of telomeres. Telomeres are nucleoprotein complexes that cap the end of chromosomal DNA and serve to protect chromosomal integrity. They become shorter with each round of replication and cell division, meaning that normally they become shorter with age. When telomeres reach a critically short length, the cells undergo apoptosis, i.e., programmed death. Leukocyte telomere length has been typically used in clinical studies as a marker of cellular aging. They shortening accelerates in the cells subjected to oxidative stress.

Multiple studies, including some meta-analysis, have questioned the association between leukocyte telomere length and major depressive disorder. For instance, one meta-analysis compared the length of telomeres between depressed and healthy individuals and found significantly shorter telomeres in groups with depression. A very recent prospective study including over 100 participants aged from 18 to 70 with or without major depressive disorder assessed telomere length at baseline and at two years follow-up. The authors concluded that individuals with major depressive disorder at baseline had significantly larger shortening of telomeres over the period of 2 years, supporting the association between depression and accelerated aging.

Major depressive disorder is typically classified as a mental illness, but its pathology is evident in cells throughout the body. According to some researchers, several biological mediators are deregulated in this disorder that contribute to accelerated aging. These changes affect levels of genetic and epigenetic mediators (i.e., the variants of genes), and biochemical mediators such as glucocorticoids and neurosteroids. This can alter immune functions, oxidative processes, and levels of factors regulating the metabolism of glucose and production of insulin.

It is evident that deregulation of some of these biological mediators leads to oxidative stress, which seems to be highly correlated with the aging process. Oxidative damage occurs when the body can’t cope with psychological and physical stressors. In other words, oxidative stress refers to the excessive production of free radicals that cannot be completely neutralized by the body’s antioxidative mechanisms. Elevated markers of oxidative stress, along with decreased antioxidant capacity, have been reported in subjects with depression.

Oxidative damage is associated with the aging process, while markers of oxidative stress correlate with the decreased activity of an enzyme called telomerase. This enzyme is responsible for extending the length of telomeres. When telomerase is absent, the telomeres shorten faster. Thus, the link between the depression and accelerated aging can partly be explained by an increased cellular oxidative stress.

Animal studies have also been conducted in order to elucidate the mechanisms underlying major depressive disorder-mediated accelerated aging. For instance, in one study, the researchers exposed rats to mild chronic stress in order to induce the symptoms of major depressive disorder. The animals that developed these symptoms were found to have shorter telomeres and decreased telomerase activity, along with an increase in oxidative damage and decreased antioxidant enzyme activity. In addition, damaged mitochondria and reduced mitochondrial DNA content were also reported in rats with depressive symptoms. This research provided clear cellular evidence of accelerated aging associated with major depressive disorder.

A group of researchers proposed that early treatment (i.e., in the first half of life) of psychiatric disorders, including depression, could extend life expectancy and significantly reduce the burden of age-related disorders (such as cardiovascular disease, cerebrovascular disease, and cancer). They demonstrated that the persistence of some psychiatric disorder from the ages of 11 to 38 years led to the dose-dependent shortening of telomere length by the age of 38. Analyses of blood samples collected at the age of 26 and 38 revealed an accelerated erosion of telomeric ends in males diagnosed with the psychiatric disorder such as depression. Interestingly, there was no such association in females with a psychiatric disorder in the interim assessment at the age of 26. This research points to the link between psychiatric disorders and accelerated biological aging, which may be particularly emphasized in men.

Recently, one study investigated the association between major depressive disorder and age-related changes of the basal ganglia. The basal ganglia are a set of subcortical structures involved in reward processing, which is often dysfunctional in subjects with major depressive disorder. Based on images from the brains of patients with depression and healthy controls, the authors assessed the grey matter volume of basal ganglia in their different parts. They found a negative correlation between the size of the putamen (a region of the basal ganglia located in the base of the forebrain) and age. Importantly, this association was twice as big in patients with major depressive disorder in comparison with healthy subjects. The finding of a greater age-related volume decrease in the depressed subjects, suggests that major depressive syndrome is clearly associated with accelerated aging.

It seems that although various biochemical mediators are responsible for the clear association between depression and accelerated aging, oxidative stress is the largest contributor to this phenomenon. Thus, it is most likely that cellular oxidative damage caused by different psychological and physical stressors represents the underlying mechanism of depression-related accelerated aging.

References

Lin, P.Y., Huang, Y.C., Hung, C.F. (2016) Shortened telomere length in patients with depression: A meta-analytic study. Journal of Psychiatric Research. 76: 84-93. doi: 10.1016/j.jpsychires.2016.01.015

Vance, M.C., Bui, E., Hoeppner, S.S., et al. (2018) Prospective association between major depressive disorder and leukocyte telomere length over two years. Psychoneuroendocrinology. 90: 157-164. doi: 10.1016/j.psyneuen.2018.02.015

Wolkowitz, O.M., Reus, V.I., Mellon, S.H. (2011) Of sound mind and body: depression, disease, and accelerated aging. Dialogues in Clinical Neuroscience. 13(1): 25-39. PMID: 21485744

Xie, X., Chen, Y., Ma, L., Shen, Q., Huang, L., Zhao, B., Wu, T., Fu, Z. (2017) Major depressive disorder mediates accelerated aging in rats subjected to chronic mild stress. Behavioural Brain Research. 329: 96-103. doi: 10.1016/j.bbr.2017.04.022

Shalev, I., Moffitt, T.E., Braithwaite, A.W., et al. (2014) Internalizing disorders and leukocyte telomere erosion: a prospective study of depression, generalized anxiety disorder, and post-traumatic stress disorder. Molecular Psychiatry. 19(11): 1163-1170. doi: 10.1038/mp.2013.183

Sacchet, M.D., Camacho, M.C., Livermore, E.E., Thomas, E.A.C, Gotlib, I.H. (2017) Accelerated aging of the putamen in patients with major depressive disorder. Journal of Psychiatry and Neuroscience. 42(3): 164-171. PMID: 27749245

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Acupuncture and Pain

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Acupuncture is one of the oldest systems of traditional medicine. With roots in China, this medical system is more than 2000 years old. It differs from various other medical systems as it does not involve taking any herbs or substances. Instead, it involves inserting small needles at specific predefined points. From the 20th century onwards, it has continued to gain prominence in the Western world, although many remain skeptical about efficacy.

These days, researchers want to know the exact mechanism of action of any medical system. They only trust the therapy if it has been proven as effective in randomized placebo-controlled clinical trials. Acupuncture has been the subject of many such trials, and its usefulness has been established in certain pain-associated conditions, mood disorders, and even in some diseases of internal organs. This led to the recognition of this medical system by many healthcare providers and medical organizations. In the US, acupuncture is recognized as complementary medicine. The WHO also recommends it for a number of specific medical conditions.

Clinical evidence of efficiency

Hundreds of clinical trials provide evidence of the effectiveness of acupuncture in various medical conditions. Among the most relevant trials are the so-called German mega-trials named ARC, ART, COMP, and GERAC. The primary focus of these trials has been pain relief in various musculoskeletal conditions. GERAC and ART were high quality random clinical trials investigating low back pain. These trials compared real acupuncture with sham acupuncture and standard care. Sham acupuncture involved needling without the use of conventional acupuncture points. Whereas standard care included the use of physiotherapy, exercise therapy, and NSAIDs (non-steroidal anti-inflammatory drugs). Results were measured after three months, and the response was defined as adequate if there was an improvement of more than 33% on the pain scale (the Von Korff Chronic Pain Grade Scale). After 6-months, the response rate with real acupuncture was 47.6%, while it was 44.2% with sham acupuncture, and 27.4% with standard care. Though these trials clearly demonstrated the efficacy of acupuncture, they also showed the effectiveness of sham acupuncture. Researchers think that this phenomenon is linked to psychogenic factors involved with back pain.

Interestingly, similar results were also demonstrated in various trials in the US. Though these trials show the usefulness of acupuncture in painful conditions, they also illustrate the value of psychogenic factors. Therefore, it is not surprising that acupuncture had also proven its utility in treating mood disorders and sleep disorders.

In Chinese medicine, the use of acupuncture is not limited to pain-related conditions. Thus, there is need for more extensive trials across a diverse range of diseases. The existing data do indicate that acupuncture may be an alternative approach for many difficult to treat chronic ailments.

Possible mechanisms

One of the areas of debate regarding acupuncture has been the difficulty in explaining its mechanism of action. As per traditional explanation, acupuncture is used to correct the flow of energy (Qi) in the body. This life energy flows through the fixed paths or highways in our body called meridians. Practitioners of acupuncture believe that in disease conditions there is a blockade of energy highways or meridians. Acupuncture is about creating the balance between the internal forces called Yin and Yang. However, the trouble is that modern science is not able to demonstrate or even understand the concepts of Qi, Yin, Yang, and Meridians.

In the last few decades, practitioners of modern science have made various attempts to explain the mechanism of action of acupuncture, and they came up with multiple theories.

  • Measurable effects of acupuncture: One of the explanations is that needling does cause local changes and alterations in reflexes. It also has systemic effects, as it changes the working of the autonomous nervous system. Thus, acupuncture affects blood pressure, heart rate, levels of various hormones, and changes the levels of neurotransmitters. All of this results in pain relief and other beneficial effects.
  • Local mechanotransduction: This is a theory promoted by a French physician in 1961, who wrote that acupuncture points have lower local resistance when compared to surrounding skin. He wrote that while normal dry skin has a resistance of 200,000 to 2 million Ohms, acupuncture points have a resistance of just 50,000 Ohms. The believers in this theory say that acupuncture causes minute traumas at the points of needle insertion and thus stimulates survival mechanisms of the body. Needling stimulates homeostasis, anti-inflammatory responses, tissue regeneration, and much more.
  • Neurohumoral theory: it has been demonstrated that acupuncture is useful in pain relief, and naloxone blocks its analgesic effect. Thus, researchers propose that needling at specific points leads to the release of endogenous painkilling opiate-like substances such as enkephalins, endorphins, dynorphins and some other neurotransmitters like serotonin and noradrenaline.
  • Gate-control theory: This theory states that needling stimulates large myelinated nerve fibers. These fibers carry tingling sensations and feelings of warmth, and can inhibit the painful sensation that is transmitted to the brain by much smaller C-fibers via spinal tracts.
  • Postsynaptic inhibition: This is another explanation, which states that acupuncture results in the inhibition of pain through a central mechanism via disinhibition of RAF. This phenomenon typically works in cases of extreme trauma like loss of limb. This central mechanism has a role in protecting the body from extreme stress and pain.
  • Autonomous nervous system: Proponents of this theory suggest that acupuncture works by changing the balance of sympathetic and parasympathetic nervous system.
  • Morphogenetic singularity theory: This is one of the more complicated hypotheses that tries to explain the existence of meridians. Advocates of this theory explain the presence of non-neural communication pathways in the body. During embryonic development, when neurons are not yet formed, cells must communicate among themselves to direct development. Meridians are just the remains of these early communication paths, which are still present in the adult body.
  • Visualization: In recent years, fMRI methods have advanced a lot, and in many clinical studies it has been demonstrated that stimulation of various acupuncture points by needling results in activation of different brain centers, thus explaining the mechanism of action of acupuncture. It is believed that both the elements of morphogenetic singularity theory (meridians) and components of the neurohumoral response are involved in the stimulation of the brain.

It is obvious that various theories have been used to describe the mechanism of action of acupuncture, and most probably there is more than one mechanism is involved. Clinical trials do seem to indicate that acupuncture is beneficial in specific health conditions. But the way it works still remains a mystery.

References

Dong, B., Chen, Z., Yin, X., Li, D., Ma, J., Yin, P., … Xu, S. (2017. The Efficacy of Acupuncture for Treating Depression-Related Insomnia Compared with a Control Group: A Systematic Review and Meta-Analysis. BioMed Research International, 2017, 9614810. doi: 10.1155/2017/9614810

Kawakita, K., & Okada, K. (2014) Acupuncture therapy: mechanism of action, efficacy, and safety: a potential intervention for psychogenic disorders? Biopsychosocial Medicine, 8, 4. doi: 10.1186/1751-0759-8-4

White, A., & Ernst, E. (2004) A brief history of acupuncture. Rheumatology, 43(5), 662–663. doi: 10.1093/rheumatology/keg005

Wong MC, Shen HJ (2010) Science-based Mechanisms to Explain the Action of Acupuncture. Journal of the Association of Traditional Chinese Medicine (UK), 17(2), 5-10.

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How Self-Compassion Can Fight Perfectionism

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“Be kind to one another.”

You don’t need to be a die-hard Ellen DeGeneres fan to appreciate the value of that motto. And while we’re reminded how kindness goes a long way in our everyday interactions with others, we often forget to apply it to those who need it most: ourselves.

Whether it’s setting a personal weight-loss goal, or believing that we can ace a final exam—all of us are familiar with the experience of setting high standards. We’re even more familiar with the inevitable let-down that comes from not living up to those very standards.

Enter, the life of a perfectionist.

But, importantly, not all perfectionists operate the same. There are different types that are associated with different psychological outcomes.

On the one hand, if you strive to attain your ambitious goals and prevent yourself from being overly self-critical, you might be a personal strivings perfectionist. This isn’t so bad. In fact, this type of perfectionism is more likely to lead to relatively higher levels of self-esteem and decreased levels of negative affect.

On the other hand, if you constantly believe that you are not good enough, if you judge yourself by your shortcomings, and if you are constantly worried that other people won’t approve of you, then you might be more on the side of maladaptive perfectionism. This form of perfectionism has been linked to depressive symptoms in both adolescents and adults.

It’s no wonder then that researchers are curious to know more about interventions that help buffer against this maladaptive perfectionism. In one recent study, researchers examined the possibility that self-compassion can protect us against the negative effects of maladaptive perfectionism. The questions is, can self-directed kindness increase our chances of living a full, healthy life? Can it combat the symptoms of depression that come from this less ideal version of perfectionism?

Understanding self-compassion

You may ask, “What exactly is self-compassion? And is it something that can be cultivated by anyone, or is a skill that is only available to some of us?” To shed some light on these questions, researchers have broken down self-compassion into three main components: self-kindness, common humanity, and mindfulness.

While the first component is self-explanatory, the other two require careful consideration. When something terrible happens to us, often the initial reaction is to sit and wallow in our grief and self-pity. We convince ourselves that no one else is going through similar problems in their lives. But that is simply not true. Statistically speaking, it’s an erroneous judgment.

In order to be more accepting of ourselves, we need to realize that we are never as alone and isolated as we think we are. This is at the heart of common humanity.

At the same time, many of us are prone to over-analyzing painful experiences, or trying to avoid negative feelings altogether. Mindfulness then, is about acknowledging our thoughts, feelings, and emotions without judgement, and accepting them as part of the common human experience.

Back to our study. Taking into account these three sub-components, the researchers in the present investigation set out to predict that self-compassion would weaken the relationship between perfectionism and depression in both adolescent and adult populations.

The study

541 adolescents from grades 7 to 10 were recruited for the first study. Participants were asked to complete three online questionnaires during school hours, as part of a larger well-being intervention study. The questionnaires tapped into perfectionism, mood/feelings, self-worth and self-esteem, as well as reported self-compassion.

As predicted, self-compassion was found to moderate, or weaken, the relationship between maladaptive perfectionism and depression in this sample of adolescents. Next, the researchers wanted to see if the results would hold for adults.

515 adults from the general population were recruited through online advertisements. Again, participants were asked to complete the same questionnaires. Once again in line with the researchers’ predictions, self-compassion was found to weaken the relationship between perfectionism and depression in the adult sample. What was true for teens was also true for adults later on in life.

Why it matters

It seems that more than anything, today’s culture values perfection. Parents and teachers may push us towards excellence at school, our friends may judge us by how we dress and act in their company, and perhaps worst of all, our social media accounts constantly fool us into thinking that there are people out there who actually have perfect lives.

Good news, bad news. The bad news is that we can’t completely eradicate perfectionistic thoughts. Good news is that we can try to change our relationship to those thoughts through self-compassion. If we learn to cultivate self-kindness, connection, and mindfulness as we strive toward achieving our goals, any setback we face along the way will be met with greater resilience and mental strength. As a result, we are less likely to fall victim to the debilitating effects of depression, and more likely to live a happy, balanced life.

So, as Ellen DeGeneres reminds us, always be kind to others. But before you do, be sure to look after yourself first. In this case, it’s okay to be a little selfish.

References

Ferrari, M., Yap, K., Scott, N., Einstein, D., & Ciarrochi, J. (2018). Self-compassion moderates the perfectionism and depression link in both adolescence and adulthood. PLOS ONE, 13(2), e0192022. doi: 10.1371/journal.pone.0192022

Hill, R., Huelsman, T., & Araujo, G. (2010). Perfectionistic concerns suppress associations between perfectionistic strivings and positive life outcomes. Personality And Individual Differences, 48(5), 584-589. doi: 10.1016/j.paid.2009.12.011

NEFF, K. (2003). The Development and Validation of a Scale to Measure Self-Compassion. Self And Identity, 2(3), 223-250. doi: 10.1080/15298860309027

Stoeber, J., & Otto, K. (2006). Positive Conceptions of Perfectionism: Approaches, Evidence, Challenges. Personality And Social Psychology Review, 10(4), 295-319. doi: 10.1207/s15327957pspr1004_2

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How Misreading Bodily Signals Causes Anxiety

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It’s 9 AM Monday morning. You’ve just pulled into work and are ready to pitch your presentation to the senior management team. Your PowerPoint slides are damn near perfect and you’ve gone over the script dozens of times. You’ve got this.

As everyone gathers in the room, you’re suddenly flooded with a hit of adrenaline. The bad kind. In a flash you become acutely aware of what your body is doing: beads of sweat forming on your brow, a dry mouth that no amount of water can fix, and a steadily increasing heart rate thumping inside your chest.

This ability to perceive the signals of your body is known as interoceptive accuracy (IAc). There are, as the example demonstrated, different psychosomatic cues that you pick up within yourself during states of anxiety. But above all, a beating heart is the hardest one to ignore.

It’s for this reason that heartbeat perception, as brain scientists call it, is a direct proxy for measuring people’s IAc and reported anxiety and stress levels.

IAc and a beating heart

Having the ability to accurately detect your own heartbeat is critical for reappraising your anxiety on a moment to moment basis. We know that anxiety is as much in the body as it is in the mind, and that a (mis)perception of a fast heart rate can easily contribute to the catastrophization of a panicked state.

It’s why some of the most effective anxiety-related therapies, like progressive muscle relaxation and deep breathing, tend to focus on muting a physiological response followed by a cognitive reappraisal technique.

Now in terms of IAc, the longstanding view was that it is an inherited trait, similar to eye color or height. Your IAc is immutable, unchanging. But now there’s new evidence suggesting that the situation matters just as much as the person: While some people may have inherently bad interoceptive ability, we can’t ignore the influence of the broader context. And this, if it turns out to be true, is a definite win for anyone looking to reverse a certain anxiety-based predisposition.

The study and findings

A team of researchers led by Martin F. Whittkamp out of the University of Luxembourg  set out to investigate just how much of a role the environment plays in determining our ability to self-reflect on accurate biofeedback.

The researchers relied on two methods to measure IAc via heartbeat perception. The first, called the counting task is simply a comparison between actual measures of your heartbeat with your self-reported measures. Another method, called the heartbeat discrimination task, measures how accurately you can rate whether or not your heartbeat is in sync with an external stimulus such as a blinking light on a computer screen.

The team in this newest study compared the results of both a heartbeat counting task and discrimination task in two conditions: a resting state and a stress state. Mental stress was induced by having participants match the color of a flashing light bulb with a corresponding button as fast and accurately as possible. If this wasn’t stressful enough, the experimenter also chimed in with a few verbal cues urging the participant to perform better so as to not ruin the entire experiment.

In addition to comparing stress state IAc with resting state IAc, the researchers also designed a number of computational models. These models aimed to measure how much of one’s interoceptive accuracy is owed to individual ability versus the situation.

The results found that about 40% of a person’s IAc can be explained by his/her individual traits, while around 30% can be explained by the changing situation, leaving the remaining 30% to measurement error.

What this says is that your ability to detect and therefore modulate your bodily responses during an anxious state is not fixed. These signals are amenable to change. You can learn to more accurately perceive your beating heart in a high-stress environment. You can apply reappraisal techniques in mitigating your anxiety.

The findings of this study have the potential to inform research on stress and anxiety management. For example, having a general idea of how much your IAc is dependent on biological predisposition could provide leeway to pharmaceutical interventions to help combat debilitating responses to stressful situations.

For now there’s therapeutic power in knowing you can improve your IAc and work towards minimizing your anxiety.

References

Feldman, G., Greeson, J., & Senville, J. (2010). Differential effects of mindful breathing, progressive muscle relaxation, and loving-kindness meditation on decentering and negative reactions to repetitive thoughts. Behaviour Research And Therapy, 48(10), 1002-1011. doi: 10.1016/j.brat.2010.06.006

Knoll, J., & Hodapp, V. (1992). A Comparison between Two Methods for Assessing Heartbeat Perception. Psychophysiology, 29(2), 218-222. doi: 10.1111/j.1469-8986.1992.tb01689.x

Richter, D., Manzke, T., Wilken, B., & Ponimaskin, E. (2003). Serotonin receptors: guardians of stable breathing. Trends In Molecular Medicine, 9(12), 542-548. doi: 10.1016/j.molmed.2003.10.010

Wittkamp, M., Bertsch, K., Vögele, C., & Schulz, A. (2018). A latent state-trait analysis of interoceptive accuracy. Psychophysiology, 55(6), e13055. doi: 10.1111/psyp.13055

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Why We Don’t Remember Early Childhood?

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Although early experiences are important for personal development and future life, as adults we recall nothing or very little of those early formative events, such as making first steps or learning first words. In fact, when adults are asked about their first memories they usually don’t recall events before the age of 2-3, with only fragmented recollection of events that happened between the age of 3 and 7. This phenomenon is often called childhood or infantile amnesia. It represents an inability of both children and adults to recall episodic memories (i.e., memories for particular events or stimuli that occur in a particular context) from infancy and early childhood, before the age 2-4.

Sigmund Freud was the first researcher to develop the theory of infantile amnesia, as he had observed that his patients rarely had been able to recall memories of events that took place during the first years of life. He believed that childhood memories are being repressed and thus forgotten. Still, modern theories focus on cognitive and social development as an important predictor of childhood amnesia. One possible explanation of childhood amnesia is the lack of neurological development, i.e., the development of brain parts that are in charge of storage and retrieval of episodic memories. For instance, some researchers believe that the development and functioning of the prefrontal cortex (cortex area at the front of the brain) is crucial for the creation of contextualized memories. Moreover, the prefrontal cortex and hippocampus are assumed to be crucial for the development of autobiographical memories. Importantly, these two brain structures develop around the age of 3 or 4.

The lack of neurological maturation, i.e., maturation of brain structures required for creation, storage, and recall of memories during infancy and early childhood might explain the phenomenon of childhood amnesia. According to this explanation, childhood amnesia occurs not due to the loss of memories over time (the forgetting explanation), as Freud had suggested, but rather due to the lack of storing of these memories in the first place. The lack of stored memories, according to this theory, is due to brain immaturity.

Some evidence has suggested that amnesia for events taking place in early childhood (before the age of 2) could be at least partly explained by difficulties with verbally recalling memories that were encoded before language acquisition. In line with this is the fact that the majority of words (the vocabulary) are acquired between the age of 2 years and 6 months and 4 years and 6 months. This is the time period that the earliest memories can be recalled.

Childhood amnesia seems not to be an exclusively human phenomenon. Indeed, some researchers have observed something like infantile amnesia in animals (for instance, rodents). The discovery of amnesia in animals has pointed to the possibility of investigating the underlying mechanisms of childhood amnesia, such as neurological events, by using animal models. The animal studies have addressed the importance of some parts of brain and their development in relation to the childhood amnesia. For instance, they have indicated that high rate of neurogenesis in hippocampus as observed in infancy might explain the accelerated forgetting of contextual fear memories. It seems that integrating of new neurons into the existing circuit might destabilize and weaken the existing memories.

Some researchers believe that it is unclear whether childhood amnesia occurs due to the failure of memory retrieval or failure of their storage. Forgetting might be described as a linear function of the time passing since the event. Since there is a long time span between the early events and recall in adulthood, it might be assumed that early events are simply forgotten. Still, some researchers disagree. This is because they have found that subjects recall far less memories for events occurring between the age of 6 and 7 as would be expected by simply extrapolating the forgetting curve. Thus, forgetting could not completely explain the phenomenon of childhood amnesia. This is why a neurogenic hypothesis of childhood amnesia has been developed.

According to its inventors, a neurogenic hypothesis explains childhood amnesia through the continuous adding of new neurons (neurogenesis) in the hippocampus, as already mentioned above. According to this hypothesis, high levels of postnatal neurogenesis (which occurs in both humans and some animals) in the hippocampus prevents the creation of long-lasting memories. This hypothesis has been experimentally tested in animal models (mouse and rat). The findings emerging from these models have proposed that high levels of neurogenesis jeopardize the formation of long-term memories, possibly by replacement of synapses in pre-existing memory circuits. In addition, the same findings indicate that the decline in hippocampal neurogenesis corresponds with the emerging ability to form stabile memories.

Thus, according to these animal studies, the theory of neurogenesis appears to be a logical explanation for childhood amnesia.

Although the early theory regarding the forgetting or repressing of memories might look like a good explanation of childhood amnesia, more recent findings demonstrate that something else is happening in our brain that contributes to this phenomenon. Whether this is the lack of development in some brain parts, or the continuous synthesis of new neurons, or both, remains to be further investigated. Childhood amnesia cannot be explained by simple forgetting.

References

Newcombe, N., Drummey, A., Fox, N., Lai, E., Ottinger-Alberts, W. (2000) Remembering Early Childhood: How Much, How, and Why (or Why Not). Current Directions in Psychological Science. 9 (2): 55–58.

Hayne, H., Jack, F. (2011) Childhood amnesia. Wiley Interdisciplinary Reviews. Cognitive Science. 2(2): 136-145. doi: 10.1002/wcs.107

Simcock, G., Hayne, H. (2003) Age-related changes in verbal and non-verbal memory during early childhood. Developmental Psychology. 39: 805–814. PMID: 12952395

Madsen, H.B., Kim, J.H. (2016) Ontogeny of memory: An update on 40 years of work on infantile amnesia. Behavioural Brain Research. 298(Pt A):  4-14. 10.1016/j.bbr.2015.07.030

Wetzler, S.E., Sweeney, J.A. (1986) Childhood amnesia: An empirical demonstration. In Autobiographical memory (ed. DC Rubin), pp. 191–201. Cambridge University Press, New York, NY.

Josselyn, S.A., Frankland, P.W. (2012) Infantile amnesia: a neurogenic hypothesis. Learning and Memory. 19(9): 423-433. doi: 10.1101/lm.021311.110

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Facebook Science: How Facebook Breaks Effect Stress and Wellbeing

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Inadvertently, in the wake of recent Facebook data harvesting scandals, Elon Musk and Brian Acton spurring on Facebook users to #DeleteFacebook in past weeks and the resulting Facebook breaks could (potentially) do some good for the average users stress levels. While differences between being deleted, deactivated, or abandoned have yet to be explored, new research is the first to report that the average user can relieve physiological measures of stress by taking a break from Facebook—at least in the short-term.

Findings from a 2013 survey in the Pew Research Center’s Internet & American Life Project, posit that 61% of current Facebook users reported taking a “Facebook vacation,” in which they voluntarily stopped using Facebook for several weeks or more. Moreover, 20% of adults reported having once used Facebook but that they no longer did so.

In a study that was just published in the Journal of Social Psychology, researchers in Australia investigated how taking a Facebook break (i.e., abstaining from using Facebook) effects stress and wellbeing. They recruited 138 active Facebook users and split them into two groups: the Facebook use as normal and five-day Facebook break groups.

Taking a break from Facebook lowered levels of salivary cortisol (a stress biomarker) after just five days. Yet despite this physiologically stress-relieving effect, users taking a Facebook break reported feeling lower levels of life satisfaction and wellbeing than users that continued Facebook use as normal (as measured by subjective reports from the users).

These seemingly contradictory effects are consistent with the general love-hate feelings about Facebook that may typify most active users, exemplified by “I’m done with Facebook” posts one minute and regular selfies and check-ins the next—its a super social tool with tonnes of obvious benefits, but often feels taxing, addictively time-wasting, forces social comparison, lowers self-esteem, and can be an information overload.

Its important to remember that Facebook users in this study were not users that had reached Facebook breaking point and desired a Facebook vacation themselves. They were essentially “cut off” from Facebook for the purpose of the experiment, with the researchers reasoning that subjective feelings of life-satisfaction and well-being were lowered by removing a currently desired means of contact and connection with others, despite the break lowering stress levels by other means.

At first glance, two other Facebook break studies may seem to contradict the reduced wellbeing observed from taking a Facebook break. They reported that subjects reported feeling increased wellbeing when taking a Facebook break over a one-week (study 1) or two-week (study 2) period, particularly for the heaviest Facebook users.

The 5-day break in the newly published cortisol study was perhaps too short to observe the decline in subjective wellbeing previously reported from longer periods of regular Facebook use. Moreover, the Facebook break was also over a weekend, which is typically a wellbeing booster and may have counteracted negative effects of regular Facebook use.

It is also important to note that the participants were recruited based on a willingness to give up Facebook for five days (and not naturally occurring Facebook vacations), and may have over-selected for people already overburdened by Facebook and seeking a good reason to have a Facebook break. However, this didn’t seem to be the case as only a handful of users reported that they expected the Facebook break to be a pleasant experience—the majority of the participants did not think a Facebook break would be a nice experience. As one participant speculated:

I will probably feel…upset as my social life will be totally stopped if I cannot use Facebook and
cannot find my friends in Facebook, I will also feel like left behind as I will not be able to know
what has happened with my Facebook friends in the coming five days.

Many participants (unprompted) expressed happiness that they could get back onto Facebook again because they felt so cut off. Naturally occurring Facebook breaks, on the other hand, may come with better improvements in stress levels that coincide with improved wellbeing because the break is truly desired and needed.

This may also be why the self-reports of stress were not significantly affected (statistically speaking), despite a trend towards reporting lower stress, where their negative perceptions about being cut off from Facebook (e.g., “I’m disconnected!”) influenced their perceived stress.

Additionally, a moderator effect was found when participants were divided on the basis of Dunbar’s number, 150—the number of individuals with whom Dunbar suggested that any one person can maintain stable relationships with. Those with 150 or fewer friends showed a decline in cortisol, whether they took a break or continued to use Facebook as usual. However, the small number of participants who actually had fewer than 150 friends prevented them from having sufficient power to fully test these effects.

To really get to the bottom of all this, researchers should be asking what happens to cortisol levels (and subjective stress and wellbeing) when people are disconnected from Facebook for much longer periods (e.g., months), the mechanisms involved, and to what extent naturally occurring cyclical patterns of Facebook activity occur (where stress from Facebook builds, users disconnect and go cold turkey, and then return as their desire to feel connected again builds).

The amounting evidence supports that taking short breaks from Facebook could be beneficial to both mental and physical health due to the significant role of stress and the HPA axis in mental and physical disorders. This is particularly beneficial for people who heavily use the platform or experience too much social comparison and envy that harms their wellbeing.

Soon, research will likely tell us how long the breaks should be and how often and under what circumstances they should occur to get the most out of being both connected and disconnected from Facebook and perhaps social media use in general. Science can’t yet say with confidence the ways that deleting facebook and the #DeleteFacebook movement could impact users health and wellbeing, but it certainly suggests taking a #FacebookBreak if your #donewithfb. Maybe consider taking a Facebook break for lent next year.

References

Kross, E., Verduyn, P., Demiralp, E., Park, J., Lee, D. S., Lin, N., Shablack, H., Jonides, J., & Ybarra, O. (2013). Facebook use predicts declines in subject well-being in young adults. PLOS ONE, 8(8), e69841-e69841. doi:10.1371/journal.pone.0069841

Pew Internet and American Life Project (2013). What teens said about social media, privacy, and online identity. Pew Internet. https://ift.tt/2HlOwCh, accessed on January 5, 2017.

Tromholt, M. (2016). The Facebook experiment: Quitting Facebook leads to higher levels of well-being. Cyberpsychology, Behavior, and Social Networking, 19, 661-666.

Vanman, E., Baker, R., & Tobin, S. (2018). The burden of online friends: the effects of giving up Facebook on stress and wellbeing. The Journal Of Social Psychology. doi:10.1080/00224545.2018.1453467

Image via geralt/Pixabay.

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Finding the Right Way to Use Ketamine for Depression

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Many studies have shown ketamine to be a promising treatment for those suffering from severe depression, but figuring out how to safely administer the drug has been a challenge for researchers. One hopeful delivery method was a nasal spray device because of its ease-of-use and the fact that it is less invasive than other methods such as injection.

But a new Australian study published in the Journal of Psychopharmacology reveals some unexpected problems with the nasal spray method. In particular, the study shows the unpredictable nature of intranasal ketamine tolerance from one person to the next.

Lead author Professor Colleen Loo at the University of New South Wales (UNSW), who is based at Black Dog Institute, states:

It’s clear that the intranasal method of ketamine delivery is not as simple as it first seemed. Many factors are at play when it comes to nasal spray ketamine treatments. Absorption will vary between people and can fluctuate on any given day within an individual based on such things as mucous levels in the nose and the specific application technique used.

The pilot trial aimed to analyze the effectiveness of repeated doses of ketamine through an intranasal device amongst 10 volunteers with severe depression, ahead of a larger randomized controlled trial.

First, the participants were given extensive training in proper self-administration techniques before receiving either a course of eight ketamine treatments or an active control over a period of four weeks, under supervision at the study center.

Following the observation of each patients’ initial reaction to the nasal spray, the dosages were adjusted to include longer time intervals between sprays.

However, the trial had to be put on hold after testing with five participants resulted in unexpected problems with tolerability. Side effects included high blood pressure, psychotic-like effects, and motor incoordination which left some participants unable to continue to self-administer the spray.

Professor Colleen Loo commented:

Intranasal ketamine delivery is very potent as it bypasses metabolic pathways, and ketamine is rapidly absorbed into the bloodstream. But as our findings show, this can lead to problems with high peak levels of ketamine in some people causing problematic side effects. Other recent studies have questioned whether changes to ketamine’s composition after being metabolised into derivative compounds may actually deliver useful therapeutic effects. It remains unclear whether ketamine nasal sprays can be safely relied upon as a treatment for patients with severe depression.

Previous research led by Loo last year revealed the success of ketamine’s antidepressant effects in elderly patients when delivered in repeated doses, which were adjusted on an individual basis and given by the subcutaneous method (injections under the skin):

Our prior research has shown that altering the dose on an individual patient basis was important. However, we wanted to see if a simpler approach using a set dose of ketamine for all people and administered by nasal spray could work just as well in this latest pilot. More research is needed to identify the optimal level of ketamine dosage for each specific application method before nasal sprays can be considered a feasible treatment option.

The researchers are now recruiting participants for the world’s largest independent trial of ketamine to treat depression, to determine the safety and effects of repeated dosing using subcutaneous injections.

This guest article appeared on PsychCentral.com: Ketamine Nasal Spray for Depression Runs Into Problems and was originally posted on Psych Central by Traci Pedersen.

References

Gálvez V, Li A, Huggins C et al. Repeated intranasal ketamine for treatment-resistant depression – the way to go? Results from a pilot randomised controlled trial. Journal of Psychopharmacology. 2018;32(4):397-407. doi:10.1177/0269881118760660.

Image via ThorstenF/Pixabay.

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