Author: lindadriscoll

I am a sales, education and marketing professional in the natural health and wellness industry. I have created this blog site to use as an online resume and partial portfolio. Thanks for stopping by!

Anthropological Perspectives on Schizophrenia: How Cultural Narrative Affects Prevalence, Course, and Outcome

by lindadriscoll

Western medical literature classifies schizophrenia (SZ) as a mental illness characterized by significant changes in thought processes and speech. Symptoms include delusions, such as false beliefs of control or persecution; hallucinations, such as hearing voices, having visions, or feeling bizarre physical sensations; reduced emotional intensity, flat affect, or catatonia; inappropriate social responses, such as spontaneous laughter or shouting; and sometimes, disturbances in motor behavior, such as repeated, aimless movement patterns.[1] According to the World Health Organization (WHO), hallucinations and false beliefs of control or persecution are the most frequently observed symptoms, found in about 70 percent of patients.[2]

SZ typically presents during late adolescence or early adulthood, between the ages of 16 and 30, yet earlier and later ages of onset are frequently noted. [3] Due to variable diagnostic models and lack of clinical data from developing nations, it is estimated that people with SZ represent as few as .46 percent and as many as 1 percent[4] of the global population, which is currently approximated at 7.4 billion people.[5] These point estimates translate into ~34,000,000 to ~76,000,000 people experiencing SZ at any given time. The highest incidence figures come from the United States; central and northern Europe, particularly among racially disadvantaged Afro-Caribbean communities in the U.K. [6]; and from marginalized populations within industrialized worlds, such as indigenous groups in Canada and Australia. It has been suggested that social disruption caused by the exposure to western lifestyles may increase risk in these groups.[7]

Developed vs. Developing Nations

While SZ is found all over the world, in both developed and developing nations, there are drastic differences in severity, course, and recovery outcomes depending on geographic region. A large body of research shows a more benign course and better outcomes in developing countries and a worse course/outcomes in industrialized nations.[8] A WHO 10-country study showed that the percentage of cases with full remission after a single “psychotic” episode ranged between 3 percent in the U.S., an industrialized nation, and 54 percent in India, a developing nation.[9]

The WHO believes that more favorable outcomes (in developing nations) are due to a combination of factors, such as greater tolerance of illness, more availability of suitable jobs, and better support from kinship groups and communities.[10] These findings have led anthropologists and medical professionals to focus their research on elucidating the many cultural factors that contribute to better outcomes in developing nations.

Anthropological Study of People With Schizophrenia

A large body of research shows that environment and level of social stigma surrounding mental illness play significant roles in both illness course and outcome.[11] Stigma is defined as, “a set of deeply discrediting attributes, related to negative attitudes and beliefs towards a group of people, likely to affect a person’s identity and thus leading to a damaged sense of self through social rejection, discrimination, and social isolation.”[12]

Level of societal stigma is rooted in cultural narratives, which help societies organize experiences so that they are recognizable, thus projecting past experiences into imagined futures. Cultural narratives and stigma exist in three realms: the larger community (generalized stigma), within mental health services (its own culture, which fosters segregation, dependency, and powerlessness), and as internalized negative self-perceptions held by people with SZ. Cultural narratives are particularly impactful for how medical professionals approach SZ because the narratives outline, “what story they [the doctors] are in, what they are likely to encounter, and what the resolution should look like.”[13]

Medical anthropologists and cultural psychiatrists research cultural narratives by investigating a person’s subjective experiences while gaining additional feedback from kinship groups and/or medical care teams. Anthropologists have found that cultural narratives dramatically impact how individuals, families, and communities support people with SZ, thus influencing the person’s ability to navigate the illness’ onset, make sense of their experience, and whether or not the person goes on to live a meaningful life and feel valued within society.

For example, Stanford anthropologist, Tanya Luhrmann, recently found that voice-hearing experiences of people with SZ are largely shaped by cultural context and that people with SZ in different cultures have different voice-hearing experiences. For this study, Luhrmann and her colleagues interviewed 60 adults diagnosed with SZ: 20 in San Mateo, California; 20 in Accra, Ghana; and 20 in Chennai, India. While all the study participants heard similar voices, many of the African and Indian subjects reported predominantly positive experiences, yet not one American did. The research team discovered notable differences between the study participants’ perception of voices, dependent on region.

Participants in San Mateo, California, were more likely to report their voices as violent, scary, and hateful. They were also less likely to develop personal relationships with their voices. Most of the Americans used clinical terms to describe themselves as “sick,” and 17 of the 20 participants self-identified as “schizophrenic.” This group was much more likely to attribute their voices to being little more than symptoms of a brain disease caused by genes or trauma, which accurately reflects the western biomedical model of SZ diagnosis and treatment.[14]

Participants in Chennai, India, were more likely to describe positive experiences with their voices, and many of them heard the voices of family members or deities. Overall, this group believed their voices to be more helpful, talking as relatives do; offering guidance and giving beneficial commands, such as reminders to complete domestic tasks. Overall, the Indian participants were more likely to associate the voices with social relationships and entertainment. Only four of the sample (of 20) said that the voices commanded them to do harm, and only four used the diagnostic term, “schizophrenia,” to describe their condition.[15]

Participants in Accra, Ghana, mostly spoke about the positive aspects of hearing voices, and 16 of the sample (of 20) said they heard God or another divinity speaking to them. Their culture accepts that there are “human-like, non-embodied spirits that can talk,”[16] which researchers believed, led participants to take on a more relaxed perception of their voices. Even when the voices were “bad,” people described being able to maintain a social relationship with them. Furthermore, only two of the 20 used the term, “schizophrenia” when describing their condition.[17]

What is behind these differences in experience? Psychological anthropological studies consistently find that European and American cultures place more emphasis on self-identity, whereas outside the west, people “imagine mind and self as interwoven with others and defined through relationships.”[18] The participants in Africa and India were better able to interpret their voices as relationships with the spirit world, rather than as the sign of a violated or “sick” mind, as the Americans did.

Differences in Cultural Narratives and Treatment of SZ: Developed vs. Developing Nations

In the west, where cultural emphasis is placed on self-sufficiency and capitalistic values, severe SZ makes it increasingly difficult—if not impossible—to survive without direct financial support from family and/or government assistance programs. As result, many people with SZ wind up isolated, worse off in their conditions, homeless, and/or incarcerated. SZ becomes an identity, rather than a temporary condition. Societal struggles are further compounded by social stigma, which exists (in part) due to the strict biomedical model of mental healthcare, lack of public health education, and limited access to affordable and effective care for those who suffer.

The media also plays a role in pushing negative cultural perceptions. From fictional crime shows to emotion-evoking pharmaceutical advertisements, western culture is bombarded with images that associate SZ with violence and danger, often sensationalized for profit. The truth is: In the west, people with severe mental illness are 11 times more likely to be the victims of violent crime than to perpetrate it. And, the greatest risk of harm is to oneself rather than another.[19] For example, people with SZ are 12 times more likely to complete suicide than the rest of the population.[20]

Social stigma and negative sense of self is perpetrated not only by western individualistic cultural values, but also how SZ is diagnosed and treated. Western doctors aggressively pursue explanations as to the biological causes of SZ. It is a commonly held belief that the condition is little more than a set of pathological “chemical imbalances” that can be corrected with pharmacological interventions. Antipsychotic medications are the go-to treatments of the west, often used in combinations (polypharmacy).

Poor compliance with SZ medication is common due to high prices and negative side effects. Medication adjuncts such as psychosocial support and personal case management are sometimes implemented as well. Regardless of the modality, western interventions primarily focus on symptom reduction.[21] In the west, science has disregarded spirit and those experiencing SZ are rarely encouraged to “make peace” with their voices, let alone develop relationships with them. American clinicians tend to “treat the voices heard by people with psychosis as if they are the uninteresting byproducts of disease which should be ignored.”[22]

Western clinicians hold firm to the belief that SZ is a disease like any other; that those with SZ have a “brain disease” due to biological aberrations or genetics. On the surface, this viewpoint seems helpful, as if it removes causal blame from the person with SZ. However, this industrialized cultural narrative may unintentionally change SZ experiences and outcomes for the worse.

Does the Biomedical Narrative Increase Compassion and Improve Self-Esteem?

Psychology professor, Sheila Mehta, conducted a Milgram-like experiment (involving electric shock), to test whether the “brain disease” narrative increased compassion. She found that it did not and that people who were given the label of “brain disease” were treated more harshly by their peers. Reflecting on the study results, she told The New York Times Magazine:

The problem, it appears, is that the biomedical narrative about an illness like schizophrenia carries with it the subtle assumption that a brain made ill through biomedical or genetic abnormalities is more thoroughly broken and permanently abnormal than one made ill though life events. Viewing those with mental disorders as diseased sets them apart and may lead to our perceiving them as physically distinct. Biochemical aberrations make them almost a different species.[23]

The western agenda of biomedical “mental health literacy” is being pushed on the rest of the world as well. The “disease model” has spread through globalization, affecting layperson perceptions as well as medical training in developing nations. While research shows that stigmatizing attitudes have reduced in developing nations such as Pakistan, Nigeria, and Sri Lanka, physicians who adopted the biomedical model in Nigeria thought of people with SZ as more dangerous and unpredictable and wanted less contact with them.[24] It is clear that cultural narratives shape the experience and depth of suffering of those with SZ. Instead of a condition that can be navigated with the support of community, SZ often becomes a new identity—one with very little value or purpose in society. There are, however, western physicians who are encouraging cultural paradigm shifts in regards to the value and purpose of SZ symptoms.

Schizophrenia as a Gift

Joseph Polimeni, a cultural psychiatrist and author of Shamans Among Us, studies the commonalities between the western biomedical model of SZ symptoms and the traits of traditional shamans throughout time, dating back tens of thousands of years. He believes that traditional shamans are/were people with SZ “symptoms” that were given purpose by their kinship group and thus, were able to hone their innate skills to benefit society.

Dr. Polimeni believes that shamanistic behaviors are “spontaneous reflexes” that initially emerged to help hunter and gatherer societies solve complex evolutionary problems. As we understand, humans naturally produce task specialists, or “roles that seem to be written in the genes.”[25] Polimeni says that shamanism represents a form of task specialization in egalitarian, small-scale cultures that “helped ancient tribal societies outmaneuver other competing tribes.”[26]

By studying old anthropological literature, he found that regardless of geographic location, shamans were/are given similar designations, such as medicine man, diviner, sorcerer, witch doctor, magician, exorcist, or medium. The commonality between these roles is the ability to serve as a conduit to the spiritual world beyond the observable realm. He believes that SZ symptoms and shamanism are intrinsically bound, and he advocates the cultural importance of people who experience hallucinations and delusions. In a video connected to his book, he says:

Shamans were considered the religious leaders of their communities and would involve themselves with specific tribal activities. For example, they would lead rituals involving rites of passage, such as birth, coming of age, marriage and death. They also endeavored to heal the sick. Shamans often lead divining rituals, which focused on the tribe’s procurement of food and water, such as rain dances or predicting the movements of animals of prey. Shamans were also routinely consulted about matters of war. It should be noted that most shamans were probably not grossly psychotic and some may have never been psychotic at all. However, in most traditional societies, those persons who were overcome by hallucinations in young adulthood were more often than not destined to become shamans.[27]

There is evidence of spiritual purpose for people with SZ symptoms throughout time and in cultures all over the world. For example, The State Oracle of Tibet, or Nechung kuten, is a spirit medium who is dedicated to protecting the health and safety of the Dalai Lama. The kuten also helps make political decisions and predicts future harvest conditions, weather, and events.[28] Thupten Ngodup, the current kuten, recalled an SZ-like experience just before being identified as the (14th) State Oracle to serve the Dalai Lama:

In the period before I was possessed at the Nêchung Monastery, in March, 1987, I became seriously ill, felt unusual emotions, exhibited odd behaviors. I did things that were out of character for me, but I could not control myself. Then, while on pilgrimage to Bodhgaya [the site where Buddha Shakyamuni attained enlightenment, in Bihar, in eastern India] I started bleeding from the mouth and nose. Doctors were unable to stop the flow of blood, which continued for two days. My colleagues feared for my life. During this time of great difficulty, I lost consciousness and had repeated vivid visions of Nêchung.[29]

Upon return to the Nechung Monastary in Dharamsala, Ngodup was “seized” by the Nechung god as the monks were reciting texts. He remembered, “losing motor functions, seeing a bright flash of light, and falling into unconsciousness.”[30] After this experience, Thebten Ngodup began specialized ritual training with mentors to ripen and stabilize his abilities. He was later appointed head lama at the monastery and given the high position of Deputy Minister in the Tibetan government in exile, a role with great responsibility and prestige.[31] Instead of being shunned, Ngodup was looked up to and nurtured, for he had special gifts to contribute.

The Importance of Cultural Acceptance in SZ Outcomes

Developing nations may experience better outcomes in SZ recovery because these groups help people make sense of symptoms by applying a meaningful narrative while keeping the person bound to the kinship group vs. isolated. Anthropologist Juli McGruder witnessed this first-hand as she studied families of schizophrenics in Zanzibar.

McGruder found that although the population is primarily Muslim, the people still believe in traditional Swahili spirit-possession, which is used to explain the actions of anyone behaving outside of social norms. Communities in Zanzibar keep the ill person safe and secure within the kinship group, rather than isolating them. In this culture, the entire community rallies around the person, offering small acts of kindness—song, dance, food, and gifts—to coax the spirit from the body. This type of treatment helps the person feel valued throughout the course of their illness, allowing them to recover and return to their societal responsibilities faster. Perhaps most importantly, McGruder believes that because the illness is viewed as caused by outside forces, the person was not as likely to take on the symptoms as “their identity.”[32]

Conclusion

While the biomedical model of the west satisfies scientific curiosity, it leaves much to be desired in terms of cultural and spiritual support for people living with SZ. Human beings have lived in small, egalitarian groups for many thousands of years. Guidance and reassurance from the spirit world has helped navigate human experience for equally as long. Unfortunately, modern medicine and western psychiatry—as institutions—do not fully utilize the power of spirituality and community when addressing patients’ physical health and emotional wellness; thus affecting cultural narratives and perhaps public policy as well. An ongoing point of research, stemming from this inquiry, should include evidence of “the placebo effect,” which measures the power of human will, intention, and belief, to certain degrees.

 

Footnotes

[1]. Angelo Barbato, “Schizophrenia and Public Health.” (World Health Organization), 4.

[2]. Ibid., 4.

[3]. “Schizophrenia.” (National Institute of Mental Health), 1.

[4]. Dinesh Bhugra, “The Global Prevalence of Schizophrenia.” (PLoS Medicine 2, no. 5), 0372.

[5]. “U.S. and World Population Clock,” (Population Clock by Census.gov), single page.

[6]. Angelo Barbato. “Schizophrenia and Public Health.” (World Health Organization), 6.

[7]. Ibid., 7.

[8]. Ibid., 8.

[9]. Ibid., 8.

[10]. Ibid., 8.

[11]. Ibid., 8.

[12]. Angelo Barbato, “Schizophrenia and Public Health.” (World Health Organization, 1998), 13.

[13]. Andrew R. Hatala, James B. Waldram, and Tomas Caal. “Narrative Structures of Maya Mental Disorders.” (Culture, Medicine, and Psychiatry 39, no. 3, 2015), 452.

[14]. Tanya Luhrmann, et. al, “Differences in Voice-hearing Experiences of People with Psychosis in the USA, India and Ghana: Interview-based Study.” (The British Journal of Psychiatry 206, no. 1, 2014), 2.

[15]. Ibid., 2.

[16] Ibid., 3

[17] Ibid., 3

[18] Stanford University. “Stanford Researcher: Hallucinatory ‘voices’ Shaped by Local Culture. (Stanford News. July 16, 2014), accessed online, included interviews with the researchers, 3.

[19]. R.J. Frances. “Crime Victimization in Adults With Severe Mental Illness: Comparison With the National Crime Victimization Survey.” (Yearbook of Psychiatry and Applied Mental Health, 2007), 1.

[20]. Angelo Barbato, “Schizophrenia and Public Health.” (World Health Organization), 12.

[21]. “Schizophrenia.” (National Institute of Mental Health), single page.

[22]. Stanford University. “Stanford Researcher: Hallucinatory ‘voices’ Shaped by Local Culture. (Stanford News. July 16, 2014), accessed online, included interviews with the researchers.

[23]. Ethan Watters, “The Americanization of Mental Illness.” (The New York Times. January 09, 2010), 4.

[24]. Jajadisha Thirthalli, et. al, “Stigma and Disability in Schizophrenia: Developing Countries’ Perspective,” (International Review of Psychiatry 24, no. 5, 2012), Table 3, 428.

[25]. Shamanism and the Evolutionary Origins of Schizophrenia. Performed by Dr. Joseph Polimeni. (YouTube), a video-summarization of his book, which was not accessible.

[26]. Ibid., 16:50 to 18:00.

[27]. Ibid., 19:05 to 21:14.

[28]. Homayun Sidky. “The State Oracle of Tibet, Spirit Possession, and Shamanism. (Numen 58, no. 1, 2011), 81.

[29]. Ibid., 84.

[30]. Ibid., 84.

[31]. Ibid., 84.

[32]. Juli H. McGruder, “Madness in Zanzibar: An Exploration of Lived Experience.” (Schizophrenia, Culture, and Subjectivity), 275.

Bibliography

Barbato, Angelo. “Schizophrenia and Public Health.” World Health Organization. 1998. http://www.who.int/mental_health/media/en/55.pdf.

Bhugra, Dinesh. “The Global Prevalence of Schizophrenia.” PLoS Medicine 2, no. 5 (2005). doi:10.1371/journal.pmed.0020151

Dein, Simon, and Kamaldeep Singh Bhui. “At the Crossroads of Anthropology and Epidemiology: Current Research in Cultural Psychiatry in the UK.” Transcultural Psychiatry 50, no. 6 (2013): 769-91. doi:10.1177/1363461513498618.

Fabrega, H. “The Self and Schizophrenia: A Cultural Perspective.” Schizophrenia Bulletin 15, no. 2 (1989): 277-90. doi:10.1093/schbul/15.2.277.

Frances, R.j. “Crime Victimization in Adults With Severe Mental Illness: Comparison With the National Crime Victimization Survey.” Yearbook of Psychiatry and Applied Mental Health 2007 (2007): 108-09. doi:10.1016/s0084-3970(08)70405-5.

Hatala, Andrew R., James B. Waldram, and Tomas Caal. “Narrative Structures of Maya Mental Disorders.” Culture, Medicine, and Psychiatry 39, no. 3 (2015): 449-86. doi:10.1007/s11013-015-9436-9.

Luhrmann, T. M., R. Padmavati, H. Tharoor, and A. Osei. “Differences in Voice-hearing Experiences of People with Psychosis in the USA, India and Ghana: Interview-based Study.” The British Journal of Psychiatry 206, no. 1 (2014): 41-44. doi:10.1192/bjp.bp.113.139048.

Mcgruder, Juli H. “Madness in Zanzibar: An Exploration of Lived Experience.” Schizophrenia, Culture, and Subjectivity: 255-81. doi:10.1017/cbo9780511616297.013.

Moreira-Almeida, Alexander, and Joan D. Koss-Chioino. “Recognition and Treatment of Psychotic Symptoms: Spiritists Compared to Mental Health Professionals in Puerto Rico and Brazil.” Psychiatry: Interpersonal and Biological Processes 72, no. 3 (2009): 268-83. doi:10.1521/psyc.2009.72.3.268.

“Schizophrenia.” National Institute of Mental Health. February 2016. https://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml.

Shamanism and the Evolutionary Origins of Schizophrenia. Performed by Dr. Joseph Polimeni. YouTube. September 25, 2013.

Sidky, Homayun. “The State Oracle of Tibet, Spirit Possession, and Shamanism.” Numen 58, no. 1 (2011): 71-99. doi:10.1163/156852711×540096.

Thirthalli, Jagadisha, and Chennaveerachari Naveen Kumar. “Stigma and Disability in Schizophrenia: Developing Countries Perspective.” International Review of Psychiatry 24, no. 5 (2012): 423-40. doi:10.3109/09540261.2012.703644.

University, Stanford. “Stanford Researcher: Hallucinatory ‘voices’ Shaped by Local Culture.” Stanford News. July 16, 2014. Accessed November 27, 2017. https://news.stanford.edu/2014/07/16/voices-culture-luhrmann-071614/.

“U.S. and World Population Clock Tell Us What You Think.” Population Clock by Census.gov. Accessed November 26, 2017. https://www.census.gov/popclock/.

Watters, Ethan. “The Americanization of Mental Illness.” The New York Times. January 09, 2010. Accessed November 26, 2017. http://www.nytimes.com/2010/01/10/magazine/10psyche-t.html.

Psychiatry Should Consider MTHFR Gene Polymorphisms

by lindadriscoll

Linda Driscoll Powers

December 2016

Psychiatry Should Consider MTHFR Gene Polymorphisms

Mental health issues are extremely common, to the extent that fourteen percent of the global disease burden can be attributed to neuropsychiatric disorders. Twenty-five percent of adults in the U.S. currently suffer from a mental illness, and at least half will develop one or more mental illnesses in their lifetime (Gardner). In addition to emotional strain, mental illness places significant economic burden on individuals, families, and communities. According to The National Institute of Mental Health (NIMH), the annual costs of mental disorders exceed the costs of diabetes, respiratory disorders, and cancers combined (Insel).

Despite the frequency of mental health issues among the general population, psychiatric medicine is largely imprecise. Mental illnesses are difficult to diagnose and treat because the field lacks precise diagnostic tools that help create targeted pharmacological treatment plans, tailored to each individual. For the last forty years, clinicians have relied on a symptom cluster approach to diagnostics rather than tools such as imaging or physiological biomarkers obtained through laboratory tests, which are the mainstay of internal medicine. The DSM-5, a book referred to as the Bible of psychiatry, contains “a standard classification of mental disorders . . . and a listing of diagnostic criteria for every psychiatric disorder.” This guide, which focuses on observable symptoms rather than measurable biometric data, is viewed as the diagnostic gold standard (“American Psychiatric Association DSM-5 Development”).

Once symptoms are grouped together and a diagnosis is decided upon, psychiatric treatment primarily relies on pharmacological (medication) interventions, prescribed using a wait-and-see, trial-and-error approach. Unfortunately, this educated guesswork results in lower than desired success rates, and some medications do more harm than good. Each medication false start can result in months of suffering for patients. Research shows that fifty percent of patients suffering from depression do not respond to first-line therapies and/or experience severe adverse reactions or side effects to the medications prescribed by clinicians (Gardner).

While there are many commonalities in how mental health disorders present, every patient–and their illness–is unique and presents on a spectrum of severity. The field of psychiatry should leverage every available tool to improve the diagnostic process and better target treatments to the individual. Personal genomic data is one of these promising tools. In the case of MTHFR gene polymorphisms, looking at genomic data is critical for uncovering the biological underpinnings of mental illnesses.

 

EVOLVING BEYOND THE TRIAL-AND-ERROR APPROACH

When the most recent update to the DSM was released in 2013, The NIMH Director, Thomas Insel, MD, said that the updated manual is reliable, but lacks validity and that “patients with mental disorders deserve better” (Brauser). The NIMH recently announced their intention to take charge of evolving the way psychiatry is practiced with the Research Domain Criteria (RDoC) project, which will incorporate genetics, imaging, and other data into a new psychiatric classification system (Brauser). It is fantastic that the NIMH stands behind the clinical validity of genomic data in psychiatry, but a long waiting period is expected before the project becomes clinically useful. While the NIMH may eventually replace the current symptoms-focused diagnostic model, millions of people would benefit from more personalized approaches right now.

The heritability of mental health issues are widely known and accepted. Since the launch of the Human Genome Project in 2001, researchers have been looking for biomarkers that might advance predictive neuroscience and revolutionize psychiatric medicine. Thousands of studies and a few meta-analyses have made headway in determining underlying genetic factors, yet the resounding caveat is that more investigation is needed to confirm results. As with any field of scientific research, there are a wide range of variables to consider, such as: length of illness; lack of medication adherence monitoring; variable genetic phenotypes (differences in how genes are expressed from person to person); and epigenetic factors (how environmental influences such as stress, diet, inflammation, etc., affect gene expression) (Malhotra).

These ambiguous and unpredictable variables are the sticking point of frustration and confusion for researchers, resulting in hesitancy to announce the validity of genomic data in psychiatric care. In addition to the overwhelmingly complex variables, some psychiatrists are comfortable with the status quo and are flat-out resistant to changing the diagnostic and treatment models that they’re used to. In a branch of medicine with such high stakes, every possible resource should be used to improve treatment outcomes.

Plausable uses of genetic data in psychiatry. Many studies have shown a correlation between specific disease phenotypes and genetic mutations (polymorphisms) in more than 3,000 genes (Dubovsky). While controversial, there are a number of ways that mental health researchers are investigating genetic data in both laboratory and clinical settings. Examples of ongoing research include: pharmacogenetics (PGx) studies, drug transporter studies, pharmacodynamics studies, gene network studies, prospective treatment studies, and gene expression studies (Dubovsky). Of this list, PGx and gene expression are the most promising.

PGx primarily looks at detox genes to estimate how quickly a person will metabolize certain classes of drugs, in addition to whether negative side effects are likely (Daley). PGx has gotten the most attention in psychiatry, to the extent that new businesses have emerged to fill the gap in PGx testing and reporting tools that are available for clinical use. Much of the opposition to using genetic data in psychiatry is focused on dismantling PGx validity, since there are multiple genetic factors that can affect drug levels and disposition and drug interactions can be impossible to predict (Dubovsky). Therefore, the remainder of this essay will focus on gene expression, particularly the MTHFR gene and how its polymorphisms, or naturally-occurring variations, may impact mental health.

 

A PRIMER TO GENE EXPRESSION STUDIES – SNPs, GENOTYPE, AND PHENOTYPE

Before diving into the supportive MTHFR evidence, it will be helpful to explain how researchers work with genetic data: DNA information is essentially a code that is made up of four protein building blocks called nucleotide bases: adenine (A), guanine (G), cytosine (C), and thymine (T). Human DNA has around three billion bases, and more than ninety-nine percent of those bases are the same in all people. How the bases (A,G,C,T) are configured determines how information is “coded” for building and maintaining the body, similar to how letters of the alphabet appear in a certain order to form words and sentences (“What is DNA?”).  

SNPs. Single-nucleotide polymorphisms (SNPs) are the most common type of genetic dna2variation among people and are also the most studied. Each SNP represents a difference in a single DNA nucleotide building block. For example, refer to the image on the left (see fig. 1): a SNP section of DNA may replace the nucleotide building block cytosine with the nucleotide building block thymine. When certain SNPs, such as MTHFR are altered, the enzyme shape can become distorted, changing the enzyme’s ability to bind to the active site on a substrate and initiate a chemical reaction. It is similar to the grooves on a key: If the grooves are slightly different than the lock, the key may fit and turn the lock a little, but it does not unlock the door (Lynch).

 

While most SNPs have no effect on health, researchers have found that some SNPs serve as valuable predictors of health risk. For example, SNPs are widely accepted and used to track the inheritance of disease within families, such as breast cancer risk via the BRCA1 and BRCA2 genes (“What are single nucleotide polymorphisms (SNPs)?”). In terms of mental health, these nucleotide changes (polymorphisms) are particularly important when it comes to transcription of enzymes that affect neurotransmitter synthesis.

Genotype and phenotype. Genotype refers to a particular gene or set of genes, including inheritable SNP polymorphisms. Phenotypes are the harder-to-predict “wild cards” of genetic studies that are influenced by the genotype (hard-coding) along with epigenetic factors, or the unique circumstances that may alter the transcription of genes found in the genotype. Think of genotype as “nature” (the unique genome you carry), and phenotype and “nurture” (how environment, stress, diet, etc. can alter genetic expression) (“What is genotype?”).

 

GENE EXPRESSION AND MTHFR POLYMORPHISMS

One SNP in particular, MTHFR, pops up over and over in mental health research. The 5,10-methylenetetrahydrofolate reductase (MTHFR) gene plays a central role in folate metabolism by converting food folate and supplemental folic acid into the usable form within the body, 5-methylenetetrahydrofolate. (Note that both the gene and the enzyme it codes for are called MTHFR.) The methylated form of folate does some very important things in the body and brain, such as recycling the inflammatory amino acid, homocysteine; synthesizing biopterin (BH4), a major cofactor for neurotransmitter synthesis; synthesizing DNA and tRNA; and helping to build red and white blood cells, and platelets (Lynch). Methyl-folate also donates a methyl group to homocysteine to make SAMe (the brain’s main methyl donor), which is responsible for the formation of phospholipids, glutathione, myelin, coenzyme q10, carnitine, and creatine. SAMe also helps to build the monoamine neurotransmitters of mood, motivation, and pleasure: serotonin, norepinephrine, and dopamine (Marano, Gilbody).

Folate methylation is fundamentally critical to healthy cell function, and folate’s connections to neurological health and psychiatric disorders are well documented (Gillbody). Folate is so important to human health that the USDA requires that refined, bleached flours are enriched with folic acid, while doctors communicate the importance of folic acid to expecting mothers (think neural tube defects). It is important to note that methyl-folate does not work alone. The vitamins B2, B6, and B12, plus other cofactors such as magnesium, are necessary to support optimal methylation cycle function in the body (Brogan).

The methylation cycle is disturbed by many factors, such as lack of the aforementioned cofactors, antacid medications, and MTHFR polymorphisms (Lynch). Furthermore, psychiatric disorders such as depression, schizophrenia, and bipolar disorder have been positively linked to low folate levels, defective folate metabolism, and MTHFR polymorphisms (Gilbody). Research has shown that disorders such as schizophrenia correlate with abnormally high homocysteine levels, a clinical symptom of a low-functioning MTHFR gene (Kevere).

There are two common (inherited) polymorphisms of the MTHFR gene, where replacements of single nucleotides may result in reduced enzyme activity at SNPs C677T and A1298C. Both SNPs affect nucleotide synthesis and DNA methylation, forming a “plausible biologic explanation for potential associations between genetic variation in folate metabolism and both depression and schizophrenia” (Gillbody).

MTHFR C677T SNP polymorphism. One base change (CT) on C677T equates to a forty percent loss in MTHFR enzyme function, and two base changes (TT) equates to an astounding seventy percent loss of function. The C677T polymorphism has been studied the most in psychiatry and has been positively correlated with “a reduction in the bioavailability of folate and folate metabolites, ‘mimicking’ low dietary folate intake” (Gillbody). The C677T polymorphism commonly produces issues with cardiovascular health, mental health, the ability to conceive and/or carry pregnancy to term, high homocysteine levels, DNA regulation, and low methylfolate levels (“Methylation and MTHFR Defects”).

A 2006 meta-review focused on MTHFR polymorphisms and psychiatric disorders demonstrated a strong association between the C677T variant and depression, schizophrenia, and bipolar disorder (Gillbody). For patients who had the C677T polymorphism in heterozygotic form (one base pair change – CT), a more serious pace of schizophrenia illness was observed (Gillbody). The meta-review also showed that the highest levels of homocysteine were observed in patients with severe paranoid schizophrenia and were credibly higher in those with the CT genotype (1 base change) rather than the common “wild type” (CC), where methylation functions optimally (Kevere). Yet another meta-analysis involving ten studies showed that there was an increased risk of depression and schizophrenia among persons with the homozygous variant TT genotype involving 2 base changes at the C677T SNP (Gillbody). As reminder, the homozygous TT base changes on the C677T SNP are said to reduce MTHFR activity by as much as seventy percent (Gillbody). In other words, the MTHFR research matches the clinical findings reported in the aforementioned clinical studies involving actual patients and their lab tests.

MTHFR A1298C SNP polymorphism. This polymorphism is the lesser studied of the two, but no less important. Polymorphisms of A1298C have been implicated in altering neurological health by primarily reducing the production of two critical mood-balancing neurotransmitters, serotonin and dopamine, while inhibiting the breakdown of ammonia (Lynch). This polymorphism is more controversial than C677T due to challenges with finding a biochemical explanation of how the defect is working. Regardless, MTHFR A1298C polymorphisms are commonly found alongside C677T polymorphisms. When both copies of the A1298C SNP are mutated, it is estimated that thirty percent of the gene’s function is lost. If polymorphisms are found on both the C677T and A1298C SNPs, there is a high likelihood that the conversion of folic acid into methyl-folate is significantly hampered (Lynch).

MTHFR and treatment-resistant depression. Genetic testing is especially important in cases of treatment-resistant depression, where selective serotonin reuptake inhibitors (SSRIs) have proven ineffective. People with MTHFR polymorphisms may have a hard time getting relief with SSRIs. This is why: The serotonin that the body makes is broken down in the receptor, so it is only used for a short time. A SSRI prevents the breakdown and reuptake of serotonin, so the brain gets more use out of the serotonin that is naturally released. The SSRI does not help the body build more serotonin; it simply helps get prolonged use from the serotonin that naturally exists. The issue for people with MTHFR polymorphisms is that there may not be adequate levels of serotonin available for use due to methylation issues that slow neurotransmitter synthesis, so SSRIs won’t be as effective (or effective at all). Some people are prescribed very high doses of SSRIs but don’t get results, while still getting the side effects (Neuzil). MTHFR polymorphisms are a plausible explanation for this situation, yet these polymorphisms are rarely considered.

MTHFR and addiction. MTHFR has an interesting connection to alcohol and drug addiction as well. According to Amy Neuzil, ND, addictions are common in the family trees of people with MTHFR polymorphisms. She says that people with reduced MTHFR enzyme tend to process alcohol less efficiently and therefore have a lower tolerance. In addition, there is more addictive potential due to the associated neurotransmitter deficiency issues. While there is a great deal of willpower stigma in addiction issues, the truth is that addictions are used as self-medication. People with addictions are trying to “fix” a problem that exists, be it unhealed trauma, neurotransmitter deficiency, or both! With MTHFR polymorphisms, the neurotransmitters are less available, so people are prone to looking for substances that make them feel better in whatever way possible (Neuzil).

MTHFR polymorphism prevalence. MTHFR polymorphisms are quite common. This table, showing MTHFR polymorphism frequency by race (and thus genetic makeup), was taken from a presentation that Lynch created in 2012 (see fig. 2). MTHFR polymorphisms may be affecting a significant portion of the population in one way or another. With such high prevalence, it is unfortunate that conventional family physicians and psychiatrists do not look for and address MTHFR polymorphisms proactively.  

mthfr-chart2

 

PSYCHIATRY MUST BEGIN CONSIDERING MTHFR POLYMORPHISMS

When MTHFR polymorphisms cause problems with neurotransmitter synthesis, no amount of SSRI or antipsychotic is going to help balance the brain, because the specific mechanisms of action do not address foundational serotonin deficits. MTHFR experts suggest that anyone with mental health issues, especially treatment-resistant depression, carry out a $200 genetic test through 23andme.com, measure homocysteine levels via blood, and exercise caution with folic acid supplementation, since it may not be converted to methyl-folate optimally (Lynch).

Those with compromised methylation can take pre-methylated forms of folate (methylfolate) and its most critical cofactor, B-12 (methylcobalamin), together to overcome the methylation issues (Lynch). All MTHFR polymorphism treatment protocols are best carried out under the supervision of an MTHFR-literate Integrative or Functional Medicine practitioner. Although MTHFR polymorphisms are likely to impair methylation status and potentially disrupt neurotransmitter synthesis, clinicians cannot make assumptions and must carefully consider all factors (including patient-reported symptoms) during the diagnostic and treatment process.

 

WHERE DO WE GO FROM HERE?

Although controversial, a recent study found that physicians in the psychiatric departments of three different academic institutions endorsed the use of genetic testing and found it to be most useful in cases of treatment resistant depression and medication intolerance (Gardner). The demand for genetic testing in psychiatry is evident, and there will certainly be more research to establish widespread clinical validity. Until then, I am hopeful that pioneering psychiatrists will embrace the current research, pursue further education, and push against status quo, insurance-directed treatment methods to better detect the underlying causes of poor neurotransmitter synthesis, such is the case with MTHFR polymorphisms.

Medication is not the end-all-be-all cure for mental health disorders. Seeking out and addressing the underlying biological factors that contribute to mental dysfunction is where the field of psychiatry must turn. Certain genetic data can—and should—be brought into the current model of care, especially when patients show little-to-no improvement using standard pharmacological approaches. The MTHFR gene and its polymorphisms are but one facet of the complex genomic gem—yet one that can be used to nudge psychiatry closer to personalized, targeted, timely, and overall more effective mental health treatment.

Of course, no clinician should use genetic data in a vacuum, and all genomic data-related decisions should be carefully weighed against the individual’s treatment history and current evidence-based standards of care. However, if spending a few more minutes with patients, running a few hundred dollars worth of lab tests, learning how to interpret the results, and prescribing methylated forms of nutrients could help even a small percentage of patients feel better faster, it is worth every penny and every second.

It is high time that the field of psychiatry is brought out of the dark ages and is allowed to blossom in the light of recent scientific discoveries. To do so, mental health clinicians must remain steadfast in pursuing ongoing education and push status quo boundaries in effort to improve patient outcomes. The millions of psychiatric patients in the U.S. and around the world deserve the opportunity to view their illnesses as what they really are: problems with brain biology rather than character defects. It is the duty of psychiatrists and mental health clinicians to help patients step away from cycles of despair, stigma, and ineffective treatments, so they may live longer, fuller, and more satisfying lives; a mission that is better realized using every tool available.

 

Works Cited

“American Psychiatric Association DSM-5 Development.” About DSM-5, APA. May 2013, http://www.dsm5.org/about/pages/default.aspx.

Brauser, Deborah. “NIMH, APA Clash Over Upcoming DSM-5.” Medscape, 7, May 2013, http://www.medscape.com/viewarticle/803752.

Brogan, MD Kelly. “Folate and You: Perfect Together.” Kelly Brogan MD, 2 July 2015, kellybroganmd.com/folate-perfect-together/.

Dubovsky, Steven L. “The Limitations of Genetic Testing in Psychiatry.” National Center for Biotechnology Information, U.S. National Library of Medicine, 5 Apr. 2016, DOI: 10.1159/000443512

Gardner, Kathryn R., et al. “The Potential Utility of Pharmacogenetic Testing in Psychiatry.” Hindawi Publishing Corporation, 17 Dec. 2014, www.hindawi.com/journals/psychiatry/2014/730956/.

Gillbody, Simon et al. “Methylenetetrahydrofolate Reductase (MTHFR) Genetic Polymorphisms and Psychiatric Disorders: A HuGE Review.” Am. J. Epidemiol., 30 Oct. 2006, Academic Search Premier, DOI: kwj347v1.

Insel, Thomas. “Mental Health Awareness Month: By the Numbers.” National Institutes of Health, U.S. Department of Health and Human Services, 15 May 2015, https://www.nimh.nih.gov/about/directors/thomas-insel/blog/2015/mental-health-awareness-month-by-the-numbers.shtml

Kevere, Laura, et al. “Homocysteine And MTHFR C677T Polymorphism In Children And Adolescents With Psychotic And Mood Disorders.” Nordic Journal Of Psychiatry, 68.2 (2014): 129-136, Academic Search Premier, DOI: 10.3109/08039488.2013.782066.

Lynch, Ben. “What is MTHFR? Learn What the MTHFR Gene is. – MTHFR.net.” MTHFRNet, 4 Nov. 2011, mthfr.net/what-is-mthfr/2011/11/04/.

Malhotra, A K, et al. “Pharmacogenetics In Psychiatry: Translating Research Into Clinical Practice.” Molecular Psychiatry 17.8 (2012): 760-769. Academic Search Premier. DOI: 10.1038/mp.2011.146

Marano, Hara Estroff. “The SAM-e Story.” Psychology Today, 1 Mar. 2002, http://www.psychologytoday.com/articles/200203/the-same-e-story.

“Methylation and MTHFR Defects,” director. Dr. Ben Lynch, 25 Apr. 2012, http://www.youtube.com/watch?v=qrhif2avpvw.

Neuzil, Amy. “MTHFR with Dr. Amy Neuzil ND.” BlogTalkRadio RSS Main, www.blogtalkradio.com/erinchamerlik/2016/09/22/mthfr-with-dr-amy-neuzil-nd.

“What is DNA? – Genetics Home Reference.” U.S. National Library of Medicine, National Institutes of Health, https://ghr.nlm.nih.gov/primer/basics/dna.

“What Is Genotype? What Is Phenotype?” PgEd.org, Personal Genetics Education Project, pged.org/what-is-genotype-what-is-phenotype/.

 

My New Dance Fitness Website!

by lindadriscoll

It’s been a year in the making, but my dance fitness website, DanceFitFun.com, is LIVE!

Did you know that I’ve been a lifelong dancer? It’s true!

Along with loads of traditional dance classes during my childhood, I spent 20+ years dancing my heart out in the electronic dance community. THIS is where I realized the therapeutic power of moving meditation. I left the nightlife culture years ago, but the love for dance was still in my heart, itching to be shared. I was called to share the therapeutic power of dance with others during daylight hours, free from the draining energy of intoxicants.

I now carry out this inspiration as a dance fitness instructor, blending international music and dance styles with soulful and funky house music to move bodies, hearts and minds.

Please check out my new website and attend one of my classes! (Occurring in the Boulder, Colorado area). Thank you!

Click here: DanceFitFun.com

Junk food shouldn’t be used as reward or incentive within public schools (or at home!)

by lindadriscoll

We have a severe health crisis on our hands here in United States.

 

Over the last 30 years, obesity rates have more than doubled in children and have quadrupled in adolescents.

30 percent of children age 6-19 are currently overweight or obese, and that figure climbs to as high as 50 percent in lower-income school districts (Lee & Sprague 1). Of course, an obese child is 69 percent more likely to become an obese adult, which significantly increases their risk for developing over 30 chronic health issues[i] (AOTA). Obesity-related health care costs are now at 169 billion per year: a hefty financial burden that strains the resources of families, taxpayers, and government-funded services (Obesity Society).
 

In addition, there has been a significant increase in neurologically based learning disabilities[ii] among children and adolescents over the same time span.

The number of children receiving services for learning disabilities nearly doubled between 1975 and 2011. Approximately 5 percent of students enrolled in public schools have a neurological disability diagnosis—not to mention the number of children left undiagnosed and untreated, struggling to learn (NCLD 12). These higher disability rates threaten the financial stability of future generations and current generations as we continue to age; disabled children grow into disabled adults who may or may not have the ability to work and pay taxes. According to the State of Learning Disabilities 2014 report, poor nutrition is a major contributing factor to the higher incidences of learning disabilities among low-income families (3).
 

To shift these health epidemics in a more positive direction, new strategies focused on prevention and early-life intervention are of prime focus. 

As an overwhelming body of literature demonstrates, both obesity and neurological dysfunction are either supported or exacerbated by nutrition and lifestyle habits.

Children are influenced by multiple factors. Some factors, such as media advertisements and peer interactions are more difficult for parents to control, so it is critical that children receive health-supportive modeling and messaging from adults and society as a whole. Many people believe that this health behaviors modeling should rest solely on the shoulders of parents, yet nutritionists and public health experts believe that schools–the place where children spend the bulk of their time–play an equally large role in helping children adopt and maintain healthy eating and physical activity habits (CDC 5).
 

While very basic nutrient standards and sugar limits exist for U.S. school lunch programs, many school districts still allow high-sugar junk food rewards and incentives to be used within the classroom.

This practice, often downplayed by sugar-loving school administrators, negatively impacts the physical and cognitive health of school-age children and puts them at risk for lifelong eating issues, such as eating to reward themselves or to simply “feel better.”

According to a study of middle school teachers in the mid-2000s:

  • A whopping 73 percent of teachers surveyed used candy as rewards and incentives within the classroom
  • 34 percent used candy to incentivize students at least 2-3 times per month.
  • Other commonly used items were cookies/donuts (37 percent), sweetened drinks (35 percent), and pizza (28 percent) (Kubic 343).

 

The overarching goal of this essay is to explore the health implications of using high-sugar/fat, non-nutritive junk food as rewards and/or incentives within public schools.

 

In addition, I will demonstrate how the practice undermines the healthy modeling that children receive at home, while directly contributing to poor health: physically, cognitively, and psychologically.

While this essay covers a number of causative and contributing factors, it is not intended to provide an exhaustive exploration of the topic, and further essays are sure to follow. To accomplish these initial goals, I have organized this essay into four main sections, one of which has sub-sections.

  1. The first section explores societal underpinnings that have led to the acceptance of junk food rewards.
  2. The second section, which includes sub-sections, discusses the myriad physical and psychological consequences of using junk food rewards and incentives with school-aged children.
  3. The third section proposes alternatives and solutions to help educators and parents move beyond the practice.
  4. The fourth section provides a summary of the common sense factors discussed in the paper, in addition to a call to action for government funded programs that influence the health and wellbeing of children.

 

WHY ARE JUNK FOOD REWARDS USED IN THE FIRST PLACE?

The consumption of non-nutritive, processed junk food has become a socially acceptable practice in modern day society. Sugar-laden celebrations are considered the norm, as is “using food to feel better” (like a drug) after a hard or stressful day. These behaviors are adopted during childhood and are directly related to parental or caregiver modeling during formative years (Epel et al. 12). Many adults, classroom teachers included, grew up within these societal norms and expectations, and therefore believe that high-sugar/fat foods qualify as an acceptable form of praise, motivation or demonstration of love for the children they care for.

To compound the issue, teachers in public school systems receive very little funding to support learning motivation and often purchase extrinsic incentives out-of-pocket. Teachers with limited-resources tend to choose sugary, non-nutritive food rewards because they are easy, inexpensive, and may bring about short-term behavior change.
 

THE CONSEQUENCES OF USING JUNK FOOD REWARDS AND INCENTIVES IN SCHOOLS

Junk foods compromise cognitive function and good decision-making. Processed foods that are high in sugar and refined carbohydrate flours cause large spikes and dips in blood sugar. For people of all ages, the dips often lead to or exacerbate restlessness, irritability, reduced ability to focus on tasks at hand, and greater likelihood of making poor food choices in the future (Amen 55). These effects are particularly enhanced in children with ADD/ADHD, the most common neurobehavioral disorder of childhood (Schnoll, Burshteyn, and Cea-Aravena 67).

Junk food overconsumption results in ill health and obesity. Policy-makers, and even some dieticians, believe that people who are overweight simply need to “stop being lazy and exercise more.” We have been duped into believing that all calories are equal, regardless of the source, how they’re delivered and the other types of molecules they’re bound to when ingested. The blame and shame of obesity has been conveniently shifted away from food manufacturers and public health regulations and on to consumers, with little regard as to the biochemical processes that occur during digestion, absorption and assimilation. Infants as young as 6 months old are now being diagnosed with obesity (McCormick et al. 1). Are these infants just lazy, too? Hardly.

Consider this: 200 calories from nuts is not the same as 200 calories from candy, a soda, or a donut. In addition to calories, nuts contain fiber, protein, and healthy fats. These molecules metabolize much slower than sugar, trigger very little insulin release, and contribute to a longer-lasting feeling of satiety (fullness). Conversely, 200 calories from sugar comes with little to no protein, fiber, or healthy fat, so this “food” is metabolized very quickly, triggering a rush of insulin—the hormone behind fat storage and diabetes. When sugar is digested without protein, fiber, and healthy fats, it is unlikely that a person will feel satisfied for very long, which results in feeling hungry and eating more within a shorter period of time (along with many other harmful effects, which will be discussed below).

Sugar dysregulates the brain’s reward center, similar to illicit drugs. Recent neuroscience shows that sugar disrupts the biochemical balance within the brain’s reward center by reducing the amount of dopamine—the “feel-good” neurotransmitter of satiety and motivation—circulating in the brain after just 3 weeks of habitual exposure; due to down-regulating the number of dopamine receptors within synapses. Like every other drug of abuse—nicotine, cocaine, alcohol, cannabis, morphine—sugar triggers hedonia, tolerance, and withdrawal symptoms (UCTV-1). When looking at the biochemical processes involved in addiction, sugar and alcohol (ethanol) are almost identical and carry most of the same long-term health risks (Lustig, Schmidt, and Brindis 28). For children with a genetic predisposition to addiction, junk food can quickly become a stimulating, dopamine-triggering drug of abuse (UCTV-2).

Junk foods rewards undermine the healthy behaviors taught in school health classes. Schools are designed to teach and model appropriate behaviors and skills to children. The health and nutrition principles taught by schools are meaningless if contradicted by rewarding children with candy and junk foods.

Rewarding children with unhealthy foods in school undermines our efforts to teach them about good nutrition. It’s like teaching children a lesson on the importance of not smoking, and then handing out ashtrays and lighters to the kids who did the best job listening. –Marlene Schwartz, Ph.D., Deputy Director, Rudd Center for Food Policy an Obesity, Yale University (Connecticut).

 

Junk foods rewards undermine the healthy behaviors taught by parents at home. For parents who do not advocate the use of junk food rewards at home, the undermining of healthy behavioral modeling without expressed consent can become a source of conflict and frustration. For most children, no amount of healthy eating at home will stop them from eating junk food in school—where they spend the bulk of their day. The temptation is simply too great. For children with food allergies or children who’s parents take a stand against junk food in school and send “special treats” instead, there are myriad psychological implications that arise for the child as result of being left out of food-sharing celebrations, including bullying from peers, anger due to exclusion and lying or stealing to ingest the sugar anyway.

 

Junk Food Rewards Contribute to Unhealthy Behaviors in Adulthood. “I did good, now I get a cookie!” neural pathways are laid down in childhood. If these behaviors are practiced and reinforced over and over, systematically strengthened by emotional response, they often stick for life. Several studies have shown that using highly palatable food as a reward during childhood dramatically increases the risk for developing eating disorders, such as binge eating and emotional eating in adulthood (Epel et al. 12).

 

Using food as a reward or as a punishment can undermine the healthy eating habits that you’re trying to teach your children. Giving sweets, chips, or soda as a reward often leads to children overeating foods that are high in sugar, far, and empty calories. Worse, it interferes with kids’ natural ability to regular their eating, and it encourages them to eat when they’re not hungry to reward themselves. –Yale Medical Group (Fedewa, Courtney, and Hinds 4).

 

SOLUTIONS

Schools can help promote healthy behaviors by offering a variety of zero-and-low-cost reward alternatives, such as: sitting by friends, reading or eating lunch outdoors, receiving “no homework” passes, playing computer games, listening to music, physical activity brain breaks, stickers, pencils, flash cards, or “mystery packs” with a notebook, folder, sports cards, etc. (Michigan 2). For these alternatives to work, a level playing field must be established where all children receive the same rewards, vs. only select children receiving junk food alternatives.

For more ideas on effective, non-food classroom rewards, read the white paper: The Use of Food as a Reward in Classrooms: The Disadvantages and the Alternatives. A link to the white paper can be found in the Works Cited section at the end of this essay (Fedewa, Courtney, and Hinds).

 

CONCLUSION

Parents assume that children will not be exposed to toxic water or air at school, and the same should hold true for food: the source of fuel for developing brains and bodies. Public schools are funded by public tax dollars. Therefore, it is the responsibility of schools to create and enforce policies that serve the long-term health and wellbeing of students from a public health perspective that considers long-term factors such as economic repercussions.

Public education is an essential government function, yet many U.S. public schools are underfunded and perpetually budget-strapped. Knowing this, every effort should be made to optimize learning effectiveness using healthy, cost-effective methods. Non-nutritive, high-sugar/fat junk “foods” (although I am hesitant to even use the word “food”) such as candy, soda, donuts and pizza are not the answer. The use of junk foods to reward and incentivize students is an undeniably unhealthy practice. Although many administrators and teachers may be addicted to sugar themselves, this is not an acceptable reason to jeopardize the health of students; especially when doing so undermines parental modeling.

By disallowing the use of junk food rewards and incentives in the classroom, schools have the power to shift long-term health trends, including brain health and learning capacity, in a more positive direction. Taking small, incremental steps to improve healthy behavior modeling at school, where children spend the bulk of their time, will help future generations become healthier, happier, and more successful taxpaying adults who contribute to social service funds, rather than drain them.

Researched and Written By: Linda Driscoll Powers, student of Integrative Mental Health Nursing, Colorado – 5.2015

Learn more about Linda at her professional website: lindadriscoll.wordpress.com

— Footnotes —

[i] Obesity puts individuals at risk for more than 30 chronic health conditions: type 2

diabetes, high cholesterol, hypertension, gallstones, heart disease, fatty liver disease, sleep apnea, GERD, stress incontinence, heart failure, degenerative joint disease, birth defects, miscarriages, asthma and other respiratory conditions, and numerous cancers (Obesity Society).

[ii] Learning disabilities arise from neurological differences in brain structure and function and affect a child’s ability to receive, store, process, retrieve, or communicate information. Common learning disabilities include: ADD, ADHD, Auditory Processing Disorder Dyslexia, Dyscalculia, Dysgraphia, Executive Functioning Deficit, and Visual Processing Deficit (NCLD).

— Works Cited —

Amen M.D., Daniel G. “Change Your Brain, Change Your Body.” Irvine: MindWorks Press. 2009. Book.

AOTA. “Obesity Basics, Childhood Obesity.” American Obesity Treatment Association. (n.d.) Web. 25 Apr. 2015.

CDC. “The Role of Schools in Preventing Childhood Obesity.” The State Education Standard. Dec. 2004. Centers for Disease Control. Web. 25 Apr. 2015.

Connecticut State Department of Education. “Alternatives to Food Rewards.“ May 2005, revised Nov. 2011. Healthymeals.nal.usda.gov. Web. 25 Apr. 2015.

Epel, Elissa S., et al. “The Reward-Based Eating Drive Scale: A Self-Report Index Of Reward-Based Eating.” Plos ONE 9.6 (2014): 1-8. Academic Search Premier. Web. 25 Apr. 2015.

Fedewa, Alicia, Courtney, Anita, Hinds, Casey. “The Use of Food as a Reward in Classrooms: The Disadvantages and the Alternatives.” n.p. 2014. Kyhealthykids.com. Web. 25 Apr. 2015.

Kubik, Martha Y. “Food Related Beliefs, Eating Behavior and Classroom Food Practices of Middle School Teachers.” Journal of School Health. Oct 2002, Vol. 72 Issue 8, p339. 7p. Academic Search Premier. Web. 2 Apr. 2015

Lee , Deborah, Sprague, Nancy. “Point: Public Schools Should not be Permitted to Sell Junk Food to Students.” Points of View: Junk Food in Schools (2015): 2. Points of View Reference Center. Web. 2 Apr. 2015.

Lustig, Robert H., Laura A. Schmidt, and Claire D. Brindis. “Public Health: The Toxic Truth About Sugar.” Nature 482.7383 (2012): 27-29. Academic Search Premier. Web. 25 Apr. 2015.

Mayo Clinic Staff. “Diseases and Conditions, Sleep Apnea, Definition.” Mayo Clinic. 24 Jul. 2012. Web. 25 Apr. 2015.

Michigan State University. “Alternatives to using Food as a Reward.” Michigan State University. n.d. Michigan.gov. Web. 25 Apr. 2015.

NCLD. “The State of Learning Disabilities: Facts, Trends and Emerging Issues.” The National Center for Learning Disabilities. 2014. LD.org. Web. 25 Apr. 2015.

McCormick DP et al. “Infant obesity: are we ready to make this diagnosis?” Journal of Pediatrics 2010 July: 157(1) PubMed. Web. 23 Apr. 2015.

Obesity Society. “What is Obesity.” Obesity Society. Oct. 2014. Web. 25 Apr. 2015.

Schnoll, Roseanne, Dmitry Burshteyn, and Juan Cea-Aravena. “Nutrition In The Treatment Of Attention-Deficit Hyperactivity Disorder: A Neglected But Important Aspect.” Applied Psychophysiology & Biofeedback 28.1 (2003): 63-75. Academic Search Premier. Web. 25 Apr. 2015.

UCTV-1. ” Sugar – The Bitter Truth.” Online video. YouTube, University of California Television. 30 July 2009. Web. 23 Apr. 2015

UCTV-2. “The Skinny on Obesity (Ep. 4): Sugar – A Sweet Addiction.” Online video clip. YouTube, University of California Television. 3 May 2012. Web. 24 Apr. 2015