Disease/Health/Hot topics/Spirituality

Unlinking Moral Failure and Mental Illness

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With one in every five Americans experiencing a mental illness at some point in their lives, how is it that the stigma surrounding mental illness remains so pervasive? Despite the high societal prevalence, according to National Alliance on Mental Illness (NAMI), almost 57% of adults with mental illness do not receive treatment and the average delay between symptom onset and treatment is eleven years. For Karen Ranus, Executive Director of NAMI-Austin, it comes down to a disconnect between viewing mental health conditions as medical conditions because parts of society view mental illnesses as “some character flaw or some kind of moral failing… a personality flaw.” Clearly, linking mental illness with moral failings contributes to and perpetuates the existing stigma surrounding mental health.

So, how do we begin unlinking mental illness and moral failures?

According to NAMI, talking openly about mental health and educating both yourself and others are two incredibly important ways to help decrease the stigma surrounding mental health. So, let’s take a quick dive into the brain and look at one of the biological risk factors for developing schizophrenia.

Inside the brain:

One of the ways that your body seeks to be more efficient is by having multiple copies of a gene arranged in sequence one right after another along the same strand of DNA. This is a really powerful way for your body to make multiple RNA copies of those genes by having RNA Polymerase, the molecular machine that transcribes DNA into RNA, simply bind at the beginning of that series of genes and work down the DNA strand at one time, rather than having to bind multiple times to the start of the gene to make the same number of RNA copies. After this process of transcription is completed, the RNA will be translated into proteins by another molecular pathway. While we won’t spend time on translation here, you should know that more copies of RNA transcripts usually result in more proteins being formed. (If you want to learn more about transcription and translation, click here.)

(image credit: Khan Academy)

Interestingly, the number of these gene copies can vary from person to person. This is called Copy Number Variation or CNV. Importantly, CNVs can be passed from parents to children. In schizophrenia, specific CNVs at different locations on chromosomes are associated with a higher risk of developing the illness. This is an exciting area of active research in genetics because we do not yet understand the exact molecular pathway between the genetic risk factor posed by the CNV and the development of schizophrenia symptoms. (Image Credit: National Institutes of Health)

Now that we understand one of the biological risk factors for schizophrenia development, what else should we do to help end the stigma surrounding mental illness? NAMI’s other recommendations are:

  • Be conscious of the language we use to describe mental health conditions
  • Encourage equality between physical and mental illness
  • Show compassion for those with mental illness
  • Choose empowerment over shame
  • Be honest about treatment
  • Let the media know when they’re being stigmatizing
  • Don’t harbor self-stigma

To learn more about mental health stigma and take NAMI’s StigmaFree pledge, click here.

 

Disease/Health

Infections During Pregnancy and Schizophrenia: Causation or Correlation?

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Neurological diseases and disorders are health deficits that many people fear at some point in their lives. Some neurological diseases and disorders do not begin to suppress the brain and nervous system until later in life, but others can come as a result of molecular interactions that occurred before birth. One of these disorders that can be caused before birth includes Schizophrenia.

What goes wrong in the brain?

Schizophrenia is a neurological disorder that negatively affects a person’ ability to think clearly, behave normally, feel normally, and perceive reality normally. A common molecular pathway that has been shown to be involved with schizophrenia is the Wnt signaling pathway. When the Wnt pathway is activated it induces a cascade of events that can effect nervous system functions including neural circuit formation and synaptic plasticity. This pathway can become disrupted in a multitude of ways, but those involved with schizophrenia include disruptions of the destruction complex. Disruption of this complex can cause increased activation of the protein complex GSK3beta. GSK3beta inhibits beta-catenin which is a necessary molecule for gene transcription. If beta-catenin is not able to attach to transcription factors, then nervous system functionality could be rendered.

In utero infections correlating to schizophrenia

As stated previously, the molecular abnormalities that are thought to be involved with schizophrenia can begin before one is even born.  These in utero abnormalities can be caused by infection during pregnancy. Infections causing risk include influenza, viral infections, toxoplasmosis, rubella, and genital-reproduction infections (STDs). When a pregnant person becomes infected, their immune system becomes activated which can cause inflammation. When inflammation occurs, the body can recruit inflammation-induced cytokines.  There has been research that shows mothers who have birthed children who later are diagnosed with schizophrenia have been noted to have an elevation by nearly twofold of cytokine family molecules. Specifically, the most common cytokine family molecules that have been studied are interleukin-8 (IL8), interleukin-6 (IL6), tumor necrosis factor alpha (TNFalpha), as well as others. These molecules are soluble peptides that can cause decrease brain development and behavior abnormalities, and they have been correlated to decrease cerebral cortical neuron survival especially during brain development.

Preventative actions

The good news to this information is that infections can be treated as well as prevented. It is extremely important to decrease the amount of time the infection is present and the immune system is activated. Luckily, many bacterial infections can be treated with antibiotics. Antibiotics that are considered safe to take during pregnancy include penicillins (amoxicillin or ampicillin), cephalosporins, erythromycin, and clindamycin. These antibiotics can treat genital reproductive infections which have been noted to increase a baby’s risk of schizophrenia. Infections of this realm such as STDs can also be prevented by using barrier contraceptives. As for influenza, it is possible to prevent infection by receiving the influenza vaccine. Although, it is not recommended to receive the vaccine during pregnancy since it can put the fetus at risk for cytokine response exposure. Toxoplasmosis can be prevented through altered hygienic approaches. These approaches including limiting exposure to cat litter and gardening, as well as when cooking with meats, poultry, and fish to be sure to cook thoroughly to ensure that if there is any T. gondii oocytes, they are killed and will not entire the mothers body through ingestion. Taking all of the precautions and treatments stated above are extremely important during pregnancy and even before pregnancy.

Since there are many variables that can attribute to diseases and disorders of a child, it becomes extremely difficult to avoid all of them during pregnancy. But, the more science tells us, the more we can do to prevent exposure to environmental and molecular risk factors.

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Treating Schizophrenia with the Drug that has Stood the Test of Time

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Whether you learned about it in school or from the movies, schizophrenia is known about in pop culture for its wild symptoms. As a schizophrenic, being able to conjure up a person so vividly that they think they are seeing a real person that they can have a conversation with was bound to end up in a movie executives lap at some point. Having hallucinations such as these are part of the “positive” symptoms, or things that have been added on to normal everyday, schizophrenic life. There are also negative symptoms, which are a lack of doing something, such as depression or a lack of facial emotivity. Both of these kinds of symptoms have been hallmarks of the disorder for well over a century, and so treatment has also been experimented on for about as long. 

Lithium (yes, the element, in pill form) has been used as a treatment for schizophrenia since at least the late 19th century. It didn’t become a scientifically-based treatment until 1949, and then took another 20 years to get approval from the FDA. The fact that it wasn’t scientifically recognized didn’t stop it from being an effective treatment well before 1949 though, and amazingly, it is still used to this day as one of the most effective treatments for schizophrenia.

This speaks to one of two things. We as a society have either lagged behind in research and development and haven’t been able to adequately come up with, discover, or create a better treatment than lithium, or we luckily discovered one of the best treatments possible for schizophrenia patients early on (way before a lot of medicinal updates) and so to this day it still works as an adequate treatment option that works well. The truth is closer to the second one, of course we’ve come up with more treatment options; we’ve been able to create synthetic antipsychotics that certainly do their job, all thanks to modern medicine. Lithium however, has stood the test of time, continuing to be one of the most effective, responsive treatments for schizophrenia. 

Wnt signalling, a pathway for gene transcription among other things, is influenced by lithium. Lithium works to inhibit GSK3β, which is one of the principal problems discovered within schizophrenia. Overactive GSK3β means a lessened TCF/LEF-transcription factor output, of which lithium can mediate to increase transcription and alleviate the severity of schizophrenic symptoms. This is the mechanism by which lithium acts, but what are some of the other treatments for lithium, and what makes it so effective?

Drugs that treat schizophrenia are often overlapped with bipolar disorder, because the drugs work for both disorders. Comparing the 4 drugs that are commonly used for both, which include lithium, Valproate, Olanzapine, and Quetiapine, lithium can be found to display several benefits. Effective treatment of schizophrenia can be characterized by the ability to take the drug for as long as possible without the downsides of the side effects outweighing the benefits of the drug itself. When a drug is stopped due to this effect, it’s known as treatment failure. Lithium, when compared to the other 3 drugs here, had the longest treatment failure times. It also appeared to be the most effective treatment to prevent relapse or recurrence of bipolar disorder and may prolong the time before complimentary prescribing is necessary.

On that note, a meta-analysis was done on 20 different studies that looked at the effectiveness of lithium and found that as a sole agent, lithium wasn’t as effective as when prescribed with another drug for treating schizophrenia. This is referred to as lithium augmentation, and although some sources disagree, most confirm that this method is the best way to treat either of these disorders. 

There are almost no other drugs that can be said to have been the most effective drug for a disorder for over 150 years, but lithium is in that category. 

 

Health

Western Society’s Toxic Role on Hallucinogens

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Hallucinogens have been a controversial recreational drug type that has “plagued” Western nations for decades. However, hallucinogens have shown to have innumerable research and religious applications. Therefore, Western usage of hallucinogens has created a negative connotation on a significant resource.

ON RELIGION

Hallucinogens have been a long-standing tradition in Hindu religious practices, dating all the way back to the Vedic period. The idea of using hallucinogens and other recreational drugs is to transcend the mortal realm and reach a deeper sense of darsan, or mutual gaze with a deity. One way to transcend via hallucinogens is to drink the juice from the soma plant. Since Hinduism is considered to be very spiritual and lived-in experience, the idea of a mutual gaze with a god or goddess can increase a Hindu’s good karma and be able to break out of their reincarnation cycle, or samsara. All Hindus end goal is to break out of samsara and be able to be absorbed into a god or goddess that person is most devoted to.

With current Abrahamic traditions and Western perspectives seeming to colonize what is right and wrong in today’s world, Hindu practices seem extreme and almost illegal to some. If we continue to view hallucinogens as hazardous in recreational use and work to abolish them, an entire religion may lose a close connection to their gods and goddesses.

ON RESEARCH

Hallucinogens also offer a new form research outlook on schizophrenia research. The origin of schizophrenia is still unknown even though the diagnostic criterion was first written into the DSM-III in 1980. Nestler (2013) discussed the best “guess” of schizophrenia origin. Though the severity and variation of schizophrenia is vast, most researchers believe there is to some extent a dysregulation of Wnt signaling via GSK3b, b-catenin, and Akt, which is involved in healthy neurodevelopment in infants. Also, too high of dopamine signaling, lack of b-catenin transcription, and overactive GSK are all considered to cause developmental delays.

Unfortunately, the most common medication for Schizophrenia is lithium. This medication has been used for nearly two centuries. Lithium inhibits GSK and directly activates Wnt signaling to combat hallucinations experienced in Schizophrenia. However, a medication lasting as top choice in mental health disorder treatment for two centuries is overly concerning. Therefore, it is more important than ever to conclude the origin of schizophrenia. One complication researchers are facing is how to create a schizophrenia model in animals, such as rodents. Hallucinogens, such as LSD and PCP, all bind to serotonin, 5-HT2A, receptors. Serotonin binding in the ventral striatum and the ventral tegmental area, or VTA, are both associated with causing psychosis if a dysregulation is present. This binding is also perceived to be present in schizophrenic hallucinations. The primary distinction between hallucinations in both scenarios is that hallucinogens produce altered perceptions of reality and the person is aware these hallucinations are not real. Those who are diagnosed with schizophrenia that experience hallucinations believe they are real and appear seemingly out of nowhere. Both cases, however, can experience hallucinations in a tactile, auditory, or visual way. Therefore, disregarding the “real/not real” distinction, hallucinogens can mimic schizophrenic-like hallucinations in animal models.

In conclusion, hallucinogens are continually regarded as toxic and dangerous in Western recreational use. However, if we remove ourselves from our traditional viewpoints, we can see the innumerable roles hallucinogens play in research and religious practices. Therefore, it is important to educate ourselves beyond one use to fully gain an opinion on hallucinogens role in the modern world.

Image Sourced From: Livescience.com

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Nature, Nurture, Ghost

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Schizophrenia: The Nature, The Nurture, The Ghosts

Ghosts

While sitting on a bench at the park enjoying the lovely weather, you notice a stranger sitting a couple of benches down from yours. They appear to be conversing with someone, but this person is out of your line of sight. After a couple more minutes of peaceful rest, you stand up to continue on with your day and to tend to the other responsibilities and events you have planned. You look over once more at the stranger who still appears to be in a conversation, but this time with a clear view you notice there doesn’t seem to be anyone near this individual besides yourself. You think back to an article you recently read describing the condition of schizophrenia.

Schizophrenia is a relatively common neurological disorder affecting an individual’s psyche. An exact cause for this condition remains elusive, but it is believed that there are strong genetic components and or altered brain chemistry or structures along with environmental factors in a percentage ratio of roughly 70:30 respectively contributing to the development of this disorder. The condition of schizophrenia is characterized by disconnected thoughts or experiences with reality. The most recognized and well-known symptoms fall under the category of positive symptoms (hallucinations, delusions, scrabbled thoughts, disorganized speech, movement irregularities) which are falsely believed to have a more debilitating effect on schizophrenics when in reality it’s the negative symptoms (lack of motivation, pleasure, emotion, inattention to cognitive input) that have a greater crippling effect.

Nature

One mechanism by which schizophrenia may occur is through malfunctions within the Wnt and GSK3 signaling pathways within the brain. The Wnt pathway functions to regulate the activity of an important molecule called Beta-catenin. In short, when the Wnt pathway is active within the brain, Beta-catenin is being produced which causes the cell to create proteins that are important for cellular functions. When the Wnt signaling pathway is off, the Beta-catenin is actively destroyed through the signaling of GSK3 which is another molecule within the Wnt signaling pathway. Schizophrenia occurs when there is insufficient Beta-catenin transcription. So, in simple terms:

  • active Wnt = Beta-catenin = no schizophrenia
  • high Beta-catenin = transcription of proteins = no schizophrenia
  • low Beta-catenin = schizophrenia
  • active GSK3 = destroyed Beta-catenin = schizophrenia

There are a number of factors that interplay with the Wnt signaling pathway making the study of schizophrenia and its cause complex. Drugs such as lithium show effects of increasing Wnt signaling pathway activation and inhibiting GSK3 which prevents GSK3 from destroying the needed Beta-catenin. Antipsychotic medications also regulate the production of Beta-catenin by interacting with the Dopamine pathway and Dopamine receptors which interlink with molecules within the Wnt pathway such as GSK3. Typically, Dopamine pathways activate GSK3, but antipsychotic medications block the dopamine pathways preventing the activation of GSK3 which also leads to an increase in Beta-catenin. Because of the significant factors of GSK3 and Wnt in the development of schizophrenia, it’s thought that inactivity of the Wnt pathway or overstimulation of GSK3 can lead to the development of schizophrenia.

Nurture

There are numerous details and complexities within cellular signaling which we could further explore, but it’s also important to consider the contributions of environmental factors as well. Proper prenatal care can significantly decrease the risk of developing schizophrenia. Factors such as illness, infection, and drug use while pregnant can put the child at risk of development. While pregnant, diabetes can increase the risk of a child’s development of the condition by 800% and a vitamin D deficiency can increase the risk by 4-fold. Proper management of diabetes, immunization of women prior to pregnancy, and other similar precautions can decrease the risk of development by 30%. Outside of prenatal care, complications in labor, urbanicity such as living in regions with populations of a million or more, increase risk by 500% and sexual abuse between the ages of 5 and 6 drastically increase the risk of development. The contributions from both the complex signaling pathways and the environmental factors make schizophrenia a challenging condition to study and even more so to fully understand. Further research is needed to illuminate the mysteries of this condition.

Sources

https://onlinelibrary.wiley.com/doi/full/10.1111/cge.12111

https://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml

https://www.mdedge.com/psychiatry/article/66140/schizophrenia-other-psychotic-disorders/negative-symptoms-schizophrenia-how#:~:text=Negative%20symptoms%20include%20blunting%20of,to%20social%20or%20cognitive%20input.

 

Disease/Health

Schizophrenia and Estrogen: An Unexpected Relationship

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What is schizophrenia and how does it manifest?

Schizophrenia is a form of chronic mental illness that plagues around 20 million people worldwide, often intruding on an individual’s ability to function normally in social, educational, and occupational settings. Symptoms of schizophrenia are categorized into two types, positive and negative. Positive symptoms encompass the presence of ideas and perceptions that are not visible to others without the disorder. These symptoms can include hallucinations, delusions, disorganized thought and speech, movement disorders, and attention and memory difficulties. The negative symptoms are the symptoms that result due to an absence of normal cognitive, behavioral, and perceptual functioning. Negative symptoms can include hopelessness, social withdrawal, absence of pleasure or excitement, and a lowered ability to function at a normal standard in various settings within one’s life.

What is the science behind schizophrenia?

As the symptoms of schizophrenia can undoubtedly reduce the quality of an individual’s life, there is a great demand for expanded research and experimentation that explores the etiology, genetic and environmental risk factors, and potential treatments of this mental disorder. In the literature article titled, “An emerging role for Wnt and GSK3 signaling pathways in schizophrenia,” authors Jacques L. Michaud and Olivier Pourquie discuss the role of various pathways in the brain and how disruption of these pathways can lead to the development of schizophrenia. An example of a disrupted pathway is the overactivation of the dopamine pathway and its ability to potentiate the development and effects of schizophrenia. In this context, the neurotransmitter dopamine binds to its inhibitory receptor, called a D2 receptor, in the brain. When dopamine binds to the D2 receptor, the enzyme glycogen synthase kinase 3 (GSK3) is activated and destroys a protein called beta-catenin. This protein is responsible for the initiation of the transcription process of key developmental genes that aid in cognitive and social functioning. However, when excess dopamine binding results in the destruction of this beta-catenin protein and a lack of transcription of important developmental genes, schizophrenia and its associated symptoms can arise. Therefore, the dopamine pathway plays a primary target for antipsychotics and other treatments in the hopes of minimizing the symptoms of schizophrenia.

So, where does estrogen come in?

Through the use of animal studies, it has been shown that the reproductive hormone estrogen plays a role in the regulation of these dopaminergic pathways. The findings of these experiments showed that estrogen reduced both the levels and activity of D2 receptors in the nucleus accumbens and caudate nucleus regions of the brain. Without lowered levels of D2 receptor activation by way of estrogen, GSK3 is active and consequently results in beta-catenin protein degradation. This event leads to the lack of transcription of key developmental genes, resulting in some of the cognitive deficits found in schizophrenia, as mentioned above.

Estrogen levels are low during various biological events, including the menstrual phase of the menstrual cycle, postpartum period, and throughout menopause. During these times, women are therefore more likely to experience more severe psychotic episodes of schizophrenia due to the lack of sufficient estrogen in its action of blocking dopamine receptors. As a result, estrogen therapy is emerging as a promising option for treatment of schizophrenia in both men and women, as it has shown to reduce the severity of symptoms. Supplemental estrogen has also been shown to increase the effectiveness of antipsychotic drugs, as many of these drugs also result in the inhibition of the dopaminergic pathway.

Men and estrogen?

An interesting and potentially controversial finding is that men who have been diagnosed with schizophrenia have lower levels of estrogen than men without the disorder. Estrogen therapy is therefore a legitimate form of treatment for men as well as women. However, it seems unlikely that all men would view estrogen therapy as a treatment option they would consider, as there is a common misconception that this supplemental estrogen would promote the development of female characteristics in men. However, estrogen therapy for schizophrenia is administered at a far lower dose than the estrogen used for the development of secondary female characteristics. Despite scientific evidence that proves that estrogen as a treatment in the context of schizophrenia will not promote “feminisation” of men, it is quite difficult to convince men to utilize this form of treatment due to this unfortunate myth. 

Looking ahead

Estrogen therapy in a clinical setting proves itself to be an encouraging option in the future of treatment for schizophrenia. Estrogen supplementation in low doses undermines the intense severity of many of the symptoms of schizophrenia, without causing the potentially damaging side effects that arise with traditional antipsychotic drug use. However, myths and stereotypes regarding the “feminisation” of men continue to serve as an obstacle in the treatment of men using this hormone. Continued research and experimentation will be extremely helpful in both minimizing the prevalence of the myths surrounding estrogen therapy in men and understanding the potential of estrogen to increase the quality of life for those struggling with schizophrenia. 

Abstract/Featured Image created by S. Wiger 

 

Community/Disease

Schizophrenia and Autism: More Alike Than You’d Think

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Distinct differences, striking similarities

Schizophrenia and Autism Spectrum Disorder (ASD) are both well-known developmental disorders involving the brain. At first glance, the two seem strikingly different: when we think of symptoms of schizophrenia, we may think of hallucinations, delusions, or loss of speech and movement. With ASD, we may think of interrupted social and communication skills or repetitive behaviors. ASD is typically evident and diagnosed in childhood, while schizophrenia often doesn’t show up for several decades of a person’s life. However, the two disorders arise from similar molecular causes and even their symptoms are more alike than you might realize.

Both disorders have a genetic component (meaning that children can inherit them from their parents) and an environmental component (meaning the circumstances a person grows up in from conception to adolescence influence their likelihood of developing the disorder). Let’s dive into the genetic and molecular component of these two disorders.

Schizophrenia on the brain

First, let’s look at the way schizophrenia is caused in the brain. It is a developmental disorder, meaning that the brain differences resulting in schizophrenia occur as the brain develops in the womb (even though symptoms usually don’t come about until later in life).

In a non-schizophrenic brain, an important signaling pathway (a cascade of events in a cell) known as the canonical Wnt pathway causes a protein called β-catenin to form and accumulate in neurons (brain cells). When there are high levels of this protein in a neuron, it causes certain target genes to be expressed. This means that the DNA of those target genes is copied and the proteins that the genes code for are made. The genes that are affected by β-catenin are important mostly during development, so the brain doesn’t need them to be at high levels all the time. A protein called GSK3 helps break down and recycle β-catenin so it doesn’t lead to gene expression all the time.

That was a lot of neurochemistry! If you’re interested in reading more, this paper by K. Singh dives even deeper into the pathway and its role in schizophrenia. If not, the big takeaway is that β-catenin is an important molecule during brain development, and GSK3 makes sure there isn’t too much of it. In schizophrenia, GSK3 is too active. This means that it breaks down more β-catenin than it should, so the genes making proteins needed for development aren’t expressed and the brain doesn’t form the way it’s supposed to.

What about ASD?

In ASD, the developmental disruptions resulting in brain changes are very similar. Even the exact same molecule is involved in the same way: β-catenin levels are too low, so genes that should be expressed during development aren’t, resulting in brain abnormalities. In ASD the lack of β-catenin is due to other interruptions to the signaling pathway, but the result is similar.

Can someone have both schizophrenia and ASD?

Yes; and it’s fairly common. When two disorders are frequently present together, the disorders are said to have high comorbidity. An individual’s official diagnosis could more likely be something like “ASD with psychosis”, but they would often display sufficient symptoms to be diagnosed with both disorders.

Additionally, studies have shown that individuals diagnosed with schizophrenia but not ASD still have higher levels of autistic symptoms than control groups. Symptoms of schizophrenia that are less-well known are often similar to characteristics of ASD: social withdrawal and exhibiting lower levels of emotion are two shared symptoms. These schizophrenia symptoms that are more similar or identical to ASD symptoms are called negative symptoms, not because they’re inherently bad, but because they exhibit a lack of something that is expected to be there, like emotional expression. The more well-known symptoms of schizophrenia like hallucinations and delusions are called positive symptoms because they’re adding something that doesn’t exist.

Conclusion

Despite very similar molecular causes involving a lack of the protein β-catenin during development, the differences between schizophrenia and ASD from age of onset to symptoms remain significant. However, knowing the similarities between molecular causes of the developmental disorders may help scientists in diagnosing and treating individuals exhibiting symptoms of both disorders in the future.

Community/Disease/Spirituality

The Voices in My Head: Friends or Foes?

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In America, when we think of hearing voices, most people’s immediate reaction is to think well, that’s crazy! And while auditory hallucinations are certainly a sign of abnormal functioning in the brain, some societies think of them in a different manner: as a gift, magic, or as a sign from a higher being. With this in mind, we will dive deeper into why these hallucinations come to be and how interpretation may be a much more crucial component than we think.

But what causes these voices?

Most commonly, auditory hallucinations are tied to a diagnosis of schizophrenia. In short, schizophrenia occurs as a result of a lack of b-catenin transcription, going hand-in-hand with too much dopamine or too little Wnt signaling. Wnt signaling is a crucial component of development, so it’s a major concern when it isn’t working properly. These differences ultimately result in chemical variations in our neurotransmitters, which are essential for communication within the brain. Taken together, there are neurochemical, genetic, and environmental risk factors/implications associated with a schizophrenia diagnosis, ultimately manifesting as the voices people hear in their head.

How are the voices expressed?

To a patient with schizophrenia, these auditory hallucinations—voices—are as real as their mother and father’s voices. In many cases, the voices cause people to do things typically out of their character and are quite troubling, often encouraging their host to perform violent acts. The voices can lead to trouble keeping jobs and maintaining relationships, resulting in difficulty with “normal” societal functioning.

This understanding of voices in one’s head is what we Westerners commonly associate with auditory hallucinations. Think of movies you’ve seen about individuals with schizophrenia: in most movies, auditory hallucinations are commonly portrayed as a negative, insulting, troublesome, and sometimes dangerous aspect of the patient’s life.

What’s incredibly interesting, though, is that this all may depend on cultural context.

What if the voices aren’t bad?

While other cultures’ understanding of schizophrenia may be wildly different, the symptom expression can be almost the exact same—beside one crucial aspect: interpretation. These individuals still have the same major psychotic disorder, but don’t understand the visual hallucinations in the same manner. To Westerners, the voices are most often hostile and scary, but different cultures see those voices as friendly and possibly even magical.

What this suggests, Stanford researcher Tanya Luhrmann says, is that “the way people pay attention to their voices alters what they hear their voices say” (see article below). This is an incredible thought. Essentially, interpretation may have a much bigger role in the voices’ manifestation than we ever considered. In Luhrmann and colleagues’ study, the results showed that while individuals from California, Ghana, and India all reported prevalence of both good and bad voices, not one American reported predominantly positive experiences with the voices, where the majority of the others did. The Americans were more likely to describe violent voices, whereas the Indians and Africans said their voices reminded them of friends and family—more of a companion than an outsider.

What does this mean?

This early research may suggest another method for treating schizophrenia: encouraging patients to develop relationships with their voices to have a more tolerable experience. Because there is no outright cure for schizophrenia, there is still much more to understand and study in order to improve patients’ quality of life. Thinking of auditory hallucinations as friends rather than foes may be the new “drug” of choice for schizophrenia.

Continue reading →

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Anxiety and The Hippocampus

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Role of Hippocampus:

The hippocampus is a region in the brain located between the inner folds of the temporal lobe. This region plays an especially important role in the formation of two specific types of memories. These include spatial relationship and declarative memories. Spatial relationship memories help us derive directions whereas declarative memories are related to the facts and events. These two types of memories help transform short term memories into long term memories and then they will be stored elsewhere. More information on the role of the hippocampus and memory can be found at https://www.positivemed.com/2018/06/02/role-of-the-hippocampus/.

How the Hippocampus Relates to Anxiety:

The hippocampus is an important area to look at when studying anxiety. When an individual undergoes chronic anxiety, they have an increase in glucocorticoids which are hormones that contribute to the flight or fight response. This increase in glucocorticoids causes a raise in cortisol levels which ultimately impairs the fragile hippocampus.

One major impairment to the hippocampus from chronic anxiety is the decrease in this regions size. Many studies have proven that individuals undergo a shrinkage of their hippocampus if they are under sever anxiety. Decreasing of size in any area of the brain is not ideal and, in this case, memory formation becomes extremely hard. When one loses volume in their hippocampus, that means they also lose storage space for all the memories that are within the spatial relationship and declarative memory categories. These memories are often used to pull certain events together and create a memory. Less volume equals less memories formed.

Alzheimer’s Disease and Anxiety:

Following the chain of events within anxiety we can trace our way to Alzheimer’s disease. Individuals with Alzheimer’s disease struggle with memory formation and retrieval. To no surprise the hippocampus is playing a large role in this disease. Those with Alzheimer’s also show a decrease in volume to their hippocampus. It is no coincidence then that individuals with anxiety are more likely to develop Alzheimer’s.

 

Can You Grow What Has Been Lost?

After reading about the negative impacts anxiety has on the hippocampus region of your brain, one questions the possibility of healing. When chronic anxiety levels have become so high that physical volume in your brain starts to decrease, what can one do to help? Although treatments are subjective to the individual, researchers passionately believe that you can slowly grow volume size back. Through Exercise one can start to create new hippocampus neurons which ultimately leads to increase of size. Exercising with the balance of a good diet will help increase the hippocampus. Studies also show that challenging yourself with brain training will also help memory function and increase volume in the brain region. More information of the explanation of these “treatments” can be found at https://www.growthengineering.co.uk/train-your-hippocampus/.

 

Conclusion:

Overall, it is evident the severe complications anxiety can cause. With the increase of glucocorticoid and cortisol levels, the hippocampus Is proven to shrink. Shrinkage in this region of the brain leads to memory formation issues which later on can cause further complications such as Alzheimer’s disease. Trying to avoid the difficulties of anxiety can be very tough but one can help themselves which some daily changes.

 

 

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Over the Edge

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Your heart rate spikes and yet you experience a shortness of breath. Your mind is overwhelmed with fear-filled stimulus. Your chest resists expansion and your lungs burn as your muscles ache for oxygen. An unbearable sense of dread floods your entire being. You may be experiencing an anxiety attack, one of many anxiety disorders. These include panic attacks, obsessive-compulsive disorder (OCD), and post-traumatic stress disorder (PTSD). Let’s take a step over the edge into the depths of anxiety.

Ground Level

Anxiety is a result of Intense psychological stress which may induce physical/behavioral alterations as a result of changes in hippocampal brain function brought about by complex molecular signaling pathways.

There are interconnections between stress, behavior, and memory where stress plays an important role in long-term memory formation. Because memory and its formation are critical for our interactions with our environment and crucial to our survival (such as remembering a terrifying experience with peanut allergies from your past), stressful events induce the formation of long-lasting memories. These memories then influence our behaviors within our environment such as avoiding the peanut-butter and jelly sandwich a stranger handed you.

The Depths

Through the usage of rodent models and well-established stress-inducing experiments, the molecular mechanisms governing the observed changes related to stress and memory have been explored.

To briefly summarize the detailed pathways and mechanisms leading to anxiety and the formation of associated long-term memories, these events are closely related to glucocorticoids, MAPK, NMDA, and GABA, neural signaling pathways, which are all related to stress, behavioral changes, and long-term memory.

Recap

Subjection of individuals to traumatic or hyper stressful situations specifically early on in their development makes them more likely to develop anxiety disorders especially PTSD and is a result of an inability to properly cope with intense stresses. The link between stress, behavioral response, and memory is revealed, as aforementioned, through the interactions of glucocorticoids, NMDA, MAPK, and Gabaergic driven neural pathways in the regulation of gene transcription within the limbic system. Any disruptions to these pathways can result in stress-related disorders including PTSD. To summarize, a cascade of molecular interactions between several proteins and their effectors results in an increased Histone mark (H3S10pK14ac) which then encourages the stress induced transcription of two genes fos and erg1 which produces proteins important in the process of memory formation.

Relief

Further exploration and a deeper understanding of these mechanisms could lead to therapeutic treatments for stress-related disorders and shed light on the complex mechanisms that govern the link between stress, behavior, and memory.  the link between psychological stress, the changes in behavior, and the effects on memory is an important subject of investigation as it could yield potential therapeutics with intentions of relieving individuals of their symptoms or the disorder completely.

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