Early Intervention in Schizophrenia

Preventative Psychiatry:  Early Intervention in Schizophrenia

It is well accepted that for someone with Schizophrenia, the disorder can lead to a decline in functioning across both interpersonal and occupational domains and on a larger level is a public health concern (Lieberman, J. & Fenton, W., 2000).

Prior to the onset of symptoms diagnostic of schizophrenia is a “premorbid” phase of slight social and cognitive impairment (Keshavan, M. & Amirsadri, A., 2007).  This is followed by a “prodromal” period” characterized by vague behaviors that often cannot be differentiated from other mental and behavioral experiences (Lieberman, J. & Fenton, W., 2000).  This includes “subtle psychotic-like symptoms” and social withdrawal (Keshavan, M. & Amirsadri, A., 2007). This prodromal period and the first episode of the disorder are viewed as “critical therapeutic” opportunities (Lieberman, J. & Fenton, W., 2000).

So if someone appears to be in a prodromal state of a potentially devastating illness and has risk factors for developing the illness, is there a way to prevent it from progressing?  Over the last decade, there is increasing interest in early intervention for Schizophrenia; however, questions remain as to who and when to treat, as many symptoms characteristic of the prodromal period are also characteristic of other mental disorders and life transitions (Keshavan, M. & Amirsadri, A., 2007).  These questions have to be weighed against well-established evidence associating a longer time to treatment with a worse prognosis (Keshavan, M. & Amirsadri, A., 2007).

There has been an increasing focus on early intervention programs that aim to identify and treat psychotic disorders sooner with the goals of improving patient prognosis and easing the financial burden of the illness on the healthcare system (Francey, S. et al., 2010).  One such program is the Specialized Treatment Early in Psychosis (STEP) program at Yale, which is composed of an interdisciplinary team approach to providing “comprehensive care for individuals who are early in the course of a psychotic illness in order to prevent symptoms from becoming disabling” (Yale School of Medicine, 2015).

Preliminary data suggests that early intervention models, like the one described above, result in fewer hospital admissions, fewer relapses, improved functional outcomes, as well as financial advantages on a societal level (Francey, S. et al., 2010).   Controversy exists concerning who should be referred to early intervention programs as well as what treatment modalities should be utilized.  Many individuals with prodromal-like behaviors, even those in the age group most at risk for developing schizophrenia (adolescence or early adulthood), do not develop the disease (Lieberman, J. & Fenton, W., 2000).  There are benefits though to assessing and treating an illness like Schizophrenia early as earlier stages of the illness appear to be more treatment responsive (Francey, S. et al., 2010).  Furthermore, starting psychotropic medication has also been shown to slow the structural brain changes correlated with the illness (Francey, S. et al., 2010).  However, the benefits of beginning pharmacological treatment have to be weighed against less intensive treatments with fewer side effects such as therapy alone.

One could argue that not everyone who receives a vaccine would have contracted the illness he or she is being protected against.  Preventative medicine is well accepted across many specialties such as vaccination or the use of sunscreen and even when it comes to more invasive measures such as mastectomies.  However, it appears to be either less accepted or less known in psychiatry and perhaps this is related to the lack of concrete diagnostic tests such as a blood test or a biopsy.  While we know Schizophrenia is more treatment responsive in earlier stages, how do we even know this is going to turn into Schizophrenia?  As of now we really do not, leading to those ethical questions with regard to starting medications known to cause serious side effects.

About one half of patients with early psychosis will actually develop chronic schizophrenia and not all individuals with prodromal features will become psychotic (Keshavan, M. S., Berger, G., Zipursky, R., Wood, S., & Pantelis, C., 2005).

Currently referral into an early intervention program is based on both having prodromal tendencies as well as being deemed “at risk”.  This includes things like age, family psychiatric history, and trauma.  One study looked at neurodevelopmental elements of the illness from a trauma perspective highlighting similarities between the effects of trauma on the developing brain and the structural brain changes in those diagnosed with schizophrenia.  This included overactivity of the hypothalamic-pituitary-adrenal axis, ventricular enlargement, and cerebral and hippocampal atrophy (Read, J., Perry, B., Moskowitz, A., & Connolly, J., 2001).  However, another analysis found significant hipoocampi volume reductions in first episode patients but an insignificant reduction in hippocampi volume in those deemed high-risk for psychosis, even in the high-risk individuals whom later developed psychosis (Copolov et al., 2000).

Recent literature has focused on neuroimaging using MRI’s to show structural changes that are specific to the prodromal period.  These findings have important clinical implications as beginning treatment is more justifiable if one can say that these prodromal tendencies coupled with these brain changes will become Schizophrenia.

Previous research in the area of Schizophrenia has shown a relationship between prolonged untreated psychosis and loss of gray matter and enlarged cerebral ventricles in patients with an established diagnosis of the disorder (Keshavan, M. & Amirsadri, A., 2007). More relevant to early intervention services, is the progression of this gray matter loss.   In first-episode patients, there are fewer brain abnormalities whereas in follow-up studies, these patients have more prominent gray-matter loss after several years (Keshavan, M. & Amirsadri, A., 2007).

In a study of 75 prodromal individuals, 23 of whom later became psychotic, those who developed psychosis had less gray matter in the right medial temporal, lateral temporal, and inferior frontal cortex and bilaterally in the cingulate cortex.  This shows that disease progression may be occurring while one is “transitioning” into psychosis (Keshavan, M. & Amirsadri, A., 2007).  A study completed in an early intervention program measured gray matter loss in participants at risk for developing psychosis and in participants with first-episode psychosis as well as in a control group.   Results showed gray matter loss in temporal, orbitofrontal, and cingulate areas in those that had developed psychosis with a “progressive process” occurring in the superior temporal gyrus preceding a psychotic episode (Takahashi, T. 2009). This possible identification of a structural brain change occurring prior to the onset of psychosis is significant when considering pharmacological treatment in an early-intervention setting.  Another area of interest is brain metabolism, specifically in membrane phospholipids in the early stage of the illness (Keshavan, M. S., Berger, G., Zipursky, R., Wood, S., & Pantelis, C., 2005).  While there is not yet a clear picture of any one structural brain change that is definitive in the development of a future psychotic disorder, the literature does point to indicative progressive changes.  Described consistently in the literature is the benefit of early intervention in schizophrenia and the need for more neurobiological research with specific regard to the prodromal period of the illness.


Copolov, D., Velakoulis, D., McGorry, P., Mallard, C., Yung, A., Rees, S…Pantelis, C. (2000).  Neurobiological Findings in Early Phase Schizophrenia.  Elsevier:  Brain Research Reviews, 31(2-3): 157-165.  DOI:  10.1016/S0165-0173(99)00033-8.

Francey, S., Nelson, B., Thompson, A., Parker, A., Kerr, M., Macneil, C… Fraser, R.(2010).  Who Needs Antipsychotic Medication in the Earliest Stages of Psychosis?  A reconsideration of Benefits, Risks, Neurobiology, and Ethics in the Era of Early Intervention.  Elsevier:  Schizophrenia Research, 119, 1-10.  DOI:  10.1016/j.schres.2010.02.1071.

Keshavan, M. S., Berger, G., Zipursky, R., Wood, S., & Pantelis, C. (2005).  Neurobiology of Early Psychosis.  The British Journal of Psychiatry, 187, s8-s18. DOI:  10.1192/bjp.1987.48.s8.

Keshavan, M. & Amirsadri, A. (2007).  Early Intervention in Schizophrenia:  Current and Future Perspectives.  Current Psychiatry Reports, 9: 325-328.  Http://link.springer.com/article/10.1007/s11920-007-0040-8#page-1.

Lieberman, J. & Fenton, W. (2000).  Delayed Detection of Psychosis:  Causes, Consequences, and Effect on Public Health.  Psychiatry Online, 157 (11): 1727-1730.  Http://psychiatryonline.org/doi/full/10.1176/appi.ajp.157.11.1727.

Read, J., Perry, B., Moskowitz, A., & Connolly, J. (2001).  The Contribution of Early Traumatic Events to Schizophrenia in Some Patients:  A Traumagenic Neurodevelopmental Model.  Psychiatry, 64(4): 319-345.

Takashashi, T., Wood, S., Yung, A., Soulsby, B., McGorry, P., Suzuki, M…Pantelis, C. (2009).  Progressive Gray Matter Reduction of the Superior Temporal Gyrus During Transition to Psychosis.  Arch Gen Psychiatry, 66(4): 366-376. DOI:10.1001/archgenpsychiatry.2009.12.

Yale School of Medicine (2015).  Specialized Treatment Early in Psychosis.  Retrieved from: http://medicine.yale.edu/psychiatry/step/index.aspx.


Diet Sticks: Nicotine and Appetite Suppression

A recent NPR article highlights how scientists at Yale discovered the appetite suppression effects of nicotine on mice during a drug trial for depression. The drug compound was similar to nicotine, and one member of the team noted that the mice treated with cytisine did not eat as much as the other mice who were not on the same drug. This attention to detail on the mice and their eating behavior, led the scientists to look at cells in the hypothalamus, where appetite regulation occurs. Initially they found that the nicotine activated the Proopiomelanocortin (POMC) cells (which suppress appetite), however they wanted to research a little deeper. The team found that the same receptors involved in the “fight-or-flight” response also sustained appetite suppression effects. Now they are looking to develop safe weight-loss agents, based on their research. Positive momentum has been made to develop agents from the laburnum plant, which has a similar chemical make-up as nicotine.

NPR Article – The Skinny on smoking: Why Nicotine Curbs Appetite

Smoking cigarettes has been associated with causing various cancers, strokes, chronic headaches Alzheimer’s disease, and exacerbating symptoms in many other undesirable conditions. In the 1960s, there was some speculation that cigarettes helped with weight loss and cigarettes were being used as diet sticks. At this time it was not yet known that there was a concrete association between nicotine and appetite suppression. Big Tobacco capitalized on this speculation, by advertising the addition of tartaric acid to cigarettes to further help reduce appetite in smokers.


Source: http://www.smokernewsworld.com/tobacco-advertising-research-assignment/

Despite health warnings concerning cigarettes, many people enjoyed, and still do enjoy, smoking due to its association with appetite suppression, alteration of feeding patterns and subsequent reduced body weight (Miyata, G.,1999). But what happens when people reach their ideal body weight and decide to quit smoking? Unbeknownst to many, smoking cessation generally triggers an increased appetite (hyperphagia) and, thus, 70-80% who quit smoking, especially women, tend to experience rebound weight gain (Jo, Y., Talmage, D. A., & Role, L. W., 2002). Smokers typically weigh less than non-smokers, thus, adolescent women continue to heavily use cigarettes as a steady form of weight regulation.

Appetite Suppression

So why exactly have cigarettes been used successfully as diet sticks for the masses? Researches are still debating the exact neuroscience behind this phenomenon, but there is increasing evidence that the POMC nuerons are major factors. POMC neurons help regulate appetite by decreasing the impulse to eat. Nicotine helps mediate satiety, by increasing the activation rate of POMC neurons (Picciotto, M. R., 2013). POMC undergoes the process of cleaving to produce another food-intake subduer named α- melanocyte-stimulating hormone (α –MSH). α –MSH works with the melanocortin (MC) receptors, MC3R and MC4R, which are strongly indicated in the hypothalamus (Higgins & George, 2013). To recap: nicotine stimulates POMC neurons, which decrease one’s desire to eat and, as a bonus, produce other appetite suppressing hormones, which have a strong presence in the hypothalamus. The hypothalamus is the part of the brain, which helps regulate homeostatic processes, including, reproduction, thermoregulation and feeding.

Now let us talk about the lateral hypothalamus. This is where pathological lesions have caused adverse outcomes such as temporary aphagia (inability or refusal to swallow), adipsia (absence of thirst) and a decrease in body weight, which contributes to appetite regulation (Jo, Y., Talmage, D. A., & Role, L. W., 2002). Nicotine is heavily associated with the lateral hypothalamus and works with endogenous cholinergic systems in the control of normal feeding behavior. Also, “nicotine regulates dopamine and serotonin release, from extrinsic projections to the lateral hypothalamus and it modulates GABA and glutamate transmission within the lateral hypothalamus” (Jo, Y., Talmage, D. A., & Role, L. W., 2002). With all of this neurological activity stimulated by nicotine, it is no wonder users have experienced appetite suppression.

Anorexic Mechanism

As an appetite suppressant, nicotine displays an anorexic mechanism, which sometimes features altered leptin signaling. The anorexic mechanism of nicotine parallels that of leptin and appears to involve both common and distinct cellular targets that may inhibit the feeding desire by increasing leptin levels and/or by enhancing step(s) along the leptin-receptor-mediated signaling cascade (Jo, Y., Talmage, D. A., & Role, L. W., 2002). “Nicotine binds with a subunit of the nicotine acetylcholine receptors on the POMC neurons, which leads to reduced food intake and weight loss. This receptor subunit may be accessible to pharmacologic manipulation turning on one benefit of smoking without the toxic effects” (H&G, 2013, p 156). Nicotine activates POMC. POMC is activated by high levels of leptin. Lower levels of leptin inhibit POMC. Leptin was one of the first markers for adiposity and the following neurotransmitters or hormone genes, code for leptin, to help regulate appetite and body weight: NPY, orexin or hypocretin, melanocortin 4 receptors for melanocyte-stimulating hormone (MC4-Rs), cocaine and amphetamine regulated transcript (CART), cholecystokinin (CCK), corticotropin-releasing hormone (CRH), and uncoupling proteins (UCP-1, -2, and -4). The aforementioned play a vital role as appetite inhibitors, except for NPY and orexin, which stimulate food consumption (Li, M. D., 2000).

As we have read above, there is a beneficial, albeit controversial, reason many people do not wish to quit smoking. Along with potentially becoming comfortable with the weight regulation smoking provides, nicotine users may also be addicted, making it difficult to quit. Additionally, we now know that many people gain weight after smoking cessation, and thus do not want to quit smoking for fear of additional unwanted poundage. Although it is generally healthier to be physically fit, which often implies being slender, using smoking as a means to stay slim is not recommended. Some would recommend titrating down from smoking cigarettes, using a nicotine patch and then decreasing the usage of the patch to stop completely. Due to the addictive nature of nicotine, however, some prescribers may be weary about issuing a patch and would prefer smokers to try to stop on their own accord. This article does not promote smoking as a form of dieting, rather it serves solely to inform about the association between nicotine and appetite suppression.



Gonseth, S., Jacot-Sadowski, I., Diethelm, P. A., Barras, V., & Cornuz, J. (2012). The tobacco industry’s past role in weight control related to smoking. European Journal of Public Health, 22, 234-237. doi:10.1093/eurpub/ckr023

Higgins, E., & George, M. (2013). The neuroscience of clinical psychiatry. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. P 154-156

Jo, Y., Talmage, D. A., & Role, L. W. (2002). Nicotinic receptor-mediated effects on appetite and food intake. Journal of Neurobiology, 53, 618-632. doi:10.1002/neu.10147

Li, M. D. (2000). Regulation of feeding-associated peptides and receptors by nicotine. Molecular Neurobiology, 22, 143; 143-166; 166.

Miyata, G. (1999). Nicotine’s effect on hypothalamic neurotransmitters and appetite regulation. Surgery, 126, 255; 255-263; 263.

Picciotto, M. R. (2013). Nicotine, food intake, and activation of POMC neurons. Neuropsychopharmacology (New York, N.Y.), 38, 245; 245-245; 245.

Traumatic brain injury and psychosis

During my clinical rotation in the  Emergency Department, I encountered a patient whose case has continued to fascinate me months later. He was a pleasant young man in his mid-20s, cooperative despite his frustration and confusion about being in the ED. I noticed nothing strange about him during the interview, and also struggled to figure out why he had been brought to us. Police notes simply stated that he’d had a fight with his father and needed to be evaluated. I figured we would let him cool off for a bit and send him on his way. A bit later, I returned to his room to let him know two visitors had arrived.

“T. and S. are here to see you,” I told him. “Are they your parents?”

Suddenly, he became confused and furrowed his brow. He crossed his arms across his chest, frowning.

“Yeah I guess so,” he said. He was guarded when pressed, but finally burst out: “I just have so many of them! They’re always changing. Wearing wigs, trying to confuse me. There are at least four S’s, and those are just the ones I know of!”

I got a far more detailed picture when I met with his parents. Three years ago, he had been in a severe motor vehicle accident during which he sustained head trauma, among other injuries. Prior to the accident, he had been living on his own for some time, had recently been promoted at work, and had a steady girlfriend. Gradually though, his parents started noting changes in his behavior. He complained about people spying on him: co-workers, neighbors, even his girlfriend. He eventually lost his job after getting into a fight with his boss, the girlfriend left him, and he moved back home with his parents.

Always friendly and caring, he became volatile. He had angry outbursts, and began threatening his parents with violence. He spent most of the day sitting in the dark in his room. When his Mother entered his room to do laundry, she found spoiled food hidden in his closet: he was afraid the imposters who had taken the place of his parents were poisoning him. He often stayed up all night, and woke up his parents screaming at them to quiet down and stop laughing so loudly. He had been brought to the ED after holding a knife to his father’s throat, demanding to know where his real father was.
This case has stayed with me not because it is particularly unique in terms of a psychotic presentation, but because the timing of his symptoms so closely aligned with his head injury. I wondered whether a traumatic brain injury (TBI) could cause this type of frank psychosis. As I dug into the literature, I found that TBI is indeed closely correlated with a range of neuropsychiatric issues, psychosis among them. In fact, about 40% of TBI victims experience at least two psychiatric disorders and a literature review by Vashnavi, et. al., shows that between 3% and 8% of those with TBI develop psychotic symptoms (2009).

So what is it that underlies these troubling symptoms? Like most other psychiatric disorders, the exact cause is unknown, and in the case of the psychiatric consequences of TBI, sufficient research is still scarce. However, there are some neuroanatomical correlates that have been found. Multiple studies have concluded that while the severity of the TBI does not directly correlate with the likelihood of developing psychosis, the location of the injury may be directly related (Vashnavi 2009).

Fujii and Fujii offer the most comprehensive review of studies of psychotic disorders due to TBI (PD-TBI) reported in psychiatry and neurology journals (2012). What I found most interesting in their review was some of the ways PD-TBI can be differentiated from schizophrenia in terms of brain dysfunction:

PD-TBI is more likely to show positive findings on MRI/CT than schizophrenia (70% vs. 12%-35%). For PD-TBI, findings are more focal in nature, with frontal (74%) and temporal (47%) lesions the most prevalent. By contrast, schizophrenia is most commonly associated with whole-brain and hippocampal atrophy and enlarged ventricles. On PET/SPECT scans, PD-TBI demonstrates abnormalities in both temporal (46%) and frontal areas (38%), whereas, in schizophrenia, hypo- frontality is the most common finding, and temporal areas are generally normal. EEG abnormalities are more prevalent in PD-TBI (77%) versus schizophrenia (20%–60%). The most common EEG finding in PD-TBI is temporal spiking or slowing, whereas schizophrenia is associated with general slowing (Fujii and Fujii 2012: 283).

The frontal lobe is a major center of brain activity, involved in motor function, judgment, executive processing, emotional regulation, language, memory, among many other things. Damage to this area can cause a wide range of issues, and unfortunately, the frontal lobe is particularly vulnerable to injury given its location at the very front of our heads. The temporal lobe has more distinct functions; it is associated with processing auditory input, interpreting visual stimuli, and memory, as well as comprehension and naming. It would make sense that lesions in each of these areas could indeed cause many of the auditory and perceptual disturbances associated with PD-TBI, as well as much of the cognitive dysfunction and behavioral dysregulation.

While all these differences are fascinating from a neuroscientific standpoint, they are unlikely to be useful in clinical practice. What is more interesting from a clinical standpoint is the difference in presentation between PD-TBI and schizophrenia. Compared to those with schizophrenia, people with PD-TBI are much less likely to show negative symptoms (14% versus 25-84%). Of the positive symptoms typically associated with schizophrenia, PD-TBI patients most commonly present with persecutory delusions (22%-80%) and auditory hallucinations (47%-84%) (Fujii and Fujii 2012).

My experience with my patient seems to mirror these findings. While his affect might have been described as somewhat blunted, for the most part negative symptoms were not the major issue. Rather, his delusions of persecution and auditory hallucinations were at the root of his distress. Though it would be a stretch to rule out a first psychotic break associated with schizophrenia, it is clinically interesting to consider these differences when approaching his treatment. Witnessing how devastating this situation was for his family, I can only hope that future research will provide more guidance about early interventions for victims of head injury that may prevent TBI from progressing to serious psychiatric disorders.


Fujii, D., Ahmed, I, & Hishinuma, E. (2004). A Neuropsychological Comparison of Psychotic Disorder Following Traumatic Brain Injury, Traumatic Brain Injury Without Psychotic Disorder, and Schizophrenia. The Journal of Neuropsychiatry and Clinical Neurosciences, 16, 306–314.

Fujii, D. & Fujii, D. (2012). Psychotic Disorder Due To Traumatic Brain Injury: Analysis of Case Studies in the Literature. The Journal of Neuropsychiatry and Clinical Neurosciences, 24, 278–289.

Vaishnavi, S., Rao, V., & Fann, R. (2009). Neuropsychiatric Problems after Traumatic Brain Injury: Unraveling the Silent Epidemic. Psychosomatics, 50, 198-205.

Zapping Appetite Away?

Vagus Nerve Stimuation – not just for depression anymore….

Although the hypothalamus has long been considered the control center for weight maintenance and appetite, recent research has focused on the signals the brain receives from the GI tract as a potential site of intervention in the battle against obesity. Vagus nerve stimulation, long used for both epilepsy and treatment-resistant depression, and shown to have the serendipitous effect of inducing weight loss, has now been utilized in the “first FDA-approved obesity device since 2007” (FDA press release, 2015).

What Does the Vagus Do?

The vagus nerve (CN X, mixed sensory-motor) projects to various visceral organs, and is the major highway system carrying signals between the GI tract and the brain, with as much as 80% of neural traffic traveling in the “gut to brain” direction (Higgins & George, 2013). Containing both chemoreceptors and mechanoreceptors, the vagus nerve detects both “mechanical” stretch in the stomach (distention from food intake) as well as neurotransmitters released from the GI tract that induce satiety, such as cholecystokinin (CCK) (Berthoud, 2008). Food interacts with sensors all along the alimentary canal to provide the brain with information related to its composition, energy content, and beneficial effect (Berthoud, 2008).

After eating a meal, chemical and mechanical signals from the gut activate vagal afferents that project up to the brain, going to the nodose ganglion – the structure containing the cell bodies of vagal afferent neurons (Berthoud, 2008). Afferent signals then travel to the medulla where they synapse with the nucleus of the solitary tract (NST) which relays the information to the hypothalamus satiety and feeding center (Owyang & Heldsinger, 2011) The paraventricular nucleus of the hypothalamus (PVN) modulates vagal digestive motor functions via oxytocinergic projections to the nucleus of the solitary tract (NST) and dorsal motor nucleus of the vagus (DMV) (Rinaman, 1998). The release of oxytocin from the hypothalamus, traveling back down the vagus nerve, leads to a sensation of satiety.



The Vagus and Obesity

Due to its vital role in signaling satiety, it’s no wonder the vagus nerve has been researched as a potential site to control and reverse obesity. Bariatric surgery is currently the most effective treatment for morbid obesity and the number of procedures has dramatically increased over the last 10 years, with the most common procedure involving surgery that leaves the patient with a small gastric pouch about 5% the size of the original stomach (Berthoud, 2008). In terms of gut innervation, both branches of the vagus nerve (ventral and dorsal) are cut by the gastrostomy procedure; although not well understood, it has been hypothesized that this could play a role in the weight loss seen after bariatric surgery (Berthoud, 2008). In addition to bariatric surgery, vagotomy surgery has been around since the 1940s, discovered by accident when it was found that obese patients getting the procedure done for ulcers were found to lose weight (Shekhar, 2008). However, this procedure is a drastic and permanent one, for once the vagus nerve is cut there is no going back.

Cervical vagus nerve stimulation, increasingly used to treat epilepsy, pain, and intractable depression, has been shown to cause weight loss in obese patients (Pardo et al., 2007). In one study, 14 patients were treated over two years with cervical VNS as adjunctive therapy for severe, treatment-resistant depression. The study reported that patients experienced gradual, highly significant weight loss despite the patients’ reports of not dieting or exercising (Pardo et al., 2007). Findings like this encouraged researchers and medical device companies to further investigate the relationship.

Last week, the FDA approved the VBLOC vagal blocking device for certain obese adults, “the first weight loss treatment device that targets the nerve pathway between the brain and the stomach that controls feelings of hunger and fullness” (FDA press release, 2015). The device generates an electrical pulse in the vagus nerve, perhaps blocking or confusing communication between the brain and the stomach (Bruzek, 2015). However, the device will be limited in who is approved to use it. Patients must be over 18 and have tried, unsuccessfully, other weight loss programs; they must also have a BMI of 35-45 and have an additional obesity-related illness (press release). In a clinical trial, published in the September 2014 issues of JAMA, the device did not help people lose 10 percent more excess weight than the control group, which was the study’s target (Ikramuddin et al., 2014). However, the FDA approved it anyway, stating that the benefits were still significant enough to use in patients meeting the specific criteria. Although the long-term side effects and efficacy of using such devices has yet to be seen, vagal blocking may be an important component of obesity treatment – although habit and lifestyle change continue to be the most holistic and healthiest methods available.

Vagal Block Animation: https://www.youtube.com/watch?v=GcW_-I0Rjco


Berthoud, H. (2008). The vagus nerve, food intake and obesity. Regulatory Peptides, 149(1-3), 15-25. doi:10.1016/j.regpep.2007.08.024

Bruzek, A. (2015). A Weight-Loss Device Aims To Curb H

unger By Zapping A Nerve. NPR.org. Retrieved 17 January 2015, from http://www.npr.org/blogs/health/2015/01/16/377428448/a-weight-loss-device-aims-to-curb-hunger-by-zapping-a-nerve

Fda.gov. (2015). FDA approves first-of-kind device to treat obesity. Retrieved 18 January 2015, from http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm430223.htm

Higgins, E., & George, M. (2007). The neuroscience of clinical psychiatry. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Ikramuddin, S., Blackstone, R., Brancatisano, A., Toouli, J., Shah, S., & Wolfe, B. et al. (2014). Effect of reversible intermittent intra-abdominal vagal nerve blockade on morbid obesity. JAMA, 312(9), 915. doi:10.1001/jama.2014.10540

Owyang, C., & Heldsinger, A. (2011). Vagal control of satiety and hormonal regulation of appetite. Journal Of Neurogastroenterology And Motility, 17(4), 338-348. doi:10.5056/jnm.2011.17.4.338

Pardo, J., Sheikh, S., Kuskowski, M., Surerus-Johnson, C., Hagen, M., & Lee, J. et al. (2007). Weight loss during chronic, cervical vagus nerve stimulation in depressed patients with obesity: an observation. Int J Obes Relat Metab Disord, 31(11), 1756-1759. doi:10.1038/sj.ijo.0803666

Rinaman, L. (1998). Oxytocinergic inputs to the nucleus of the solitary tract and dorsal motor nucleus of the vagus in neonatal rats. J. Comp. Neurol., 399(1), 101-109. doi:10.1002/(sici)1096-9861(19980914)399:1<101::aid-cne8>3.0.co;2-5

Sabatier, N., Leng, G., & Menzies, J. (2013). Oxytocin, feeding, and satiety. Front. Endocrinol., 4. doi:10.3389/fendo.2013.00035

Shekhar, C. (2008, June 9). Nervy approach to fighting fat. Los Angeles Times. Retrieved from http://articles.latimes.com/2008/jun/09/health/he-implant9