Bringing Neuroscience Into the Therapy Session
By Ralph Carson, PhD
The anorectic’s brain is a complicated structure that is influenced by genetics and the environment. This duality epitomizes the loaded-gun theory, in that who our parents are (genetics) provides the ammunition and how we live our life (starvation) pulls the trigger. Numerous adolescents go on very-low-calorie diets every year, but less than 1 percent continue to progress on to anorexia allowing them to maintain an extremely low weight for years (Bulik, Slof-Op’t Landt, van Furth, & Sullivan, 2007; Hudson et al., 2007). The genetic vulnerability may remain latent for the first decade of life until it is precipitated by circumstances (puberty, social media, peer pressure) and perpetuated by severe food restriction, starvation, and weight loss. Anorexia can be considered a biopsychosocial condition whereby a physiological change is brought on by an emotional response.
Fifty to seventy percent of the risk of developing an eating disorder is genetic (Bulik et al., 2007; Cui et al., 2013). Though identifying a single gene would simplify early identification, the fact remains that multiple genes interact to produce a wide spectrum of symptoms and behaviors. A genetic mouse model (BDNF val66met) has been useful in conducting research to elucidate further understanding of the disorder that may contribute to treatment efficacy (Madra & Zeltser, 2016). The genes themselves are activated to produce proteins that are encoded into neural processes. Starvation turns on genetic transcription factors that initiate the course of events leading to anorectic behaviors. Pre-existing genetic traits define the individual’s temperaments, character qualities, and personalities that profile the anorectic and persist after recovery (Cloninger et al., 1993, 1994).
Starvation, malnutrition, and weight restoration must be addressed during the acute stages of recovery. Depression, irritability, food obsessions, rituals, difficulty concentrating, mental fatigue, memory decline, apathy, and hopelessness are manifestations of starvation (van der Zee, 1998; Keys et al., 1950). When the body is appropriately nourished and weight is restored to 90 percent of ideal, many of the psychiatric symptoms can be reversed. Lack of food and immense stress can cause cellular loss, but, fortunately, the brain is malleable and the damage can be reversed with appropriate dietary intervention. Many in the treatment field argue that the order or priority in the treatment of anorexia should be: “First we eat, then we talk.” Thought processes and commitment to change are not responsive to therapy until the brain is fully engaged, which entails replacing lost brain tissue (Zakzanis et al., 2010; Lauer et al., 1999). Starvation is a state condition, and the disturbances attributed to that state are normalized after weight restoration (Marzola et al., 2013).
Constructing a visual picture of healing and recovery instills confidence in the treatment and, thereby, increases the likelihood of successful outcomes. Brain scans from those struggling with anorexia show brain cell loss similar to that seen with dementia (Alzheimer’s). Observing the return of gray matter volume can provide encouragement that one can get all of his or her brain substance and function back (Zakzanis et al., 2010; Lauer et al., 1999).
It is beyond the scope of this paper to explain neuroscientifically the multitude of symptomology, behaviors, and traits associated with anorexia nervosa. Following is a brief summary to explain the various differences (as opposed to calling them deficits) through the language of neuroscience (Halmi et al., 1991, 2000, 2004; Kaye et al., 1996, 1998, 1999a, b, c, 2001, 2002, 2003, 2005, 2008a, b, 2009, 2011; Lask et al., 2005, 2011; Cloninger, 1986; Cloninger, Svrakic, & Przybeck, 1993; Fassino et al., 2002; Liu, 1979, 2007; Klump et al., 2004; Roberts & Pomerantz, 2004; Roberts et al., 2007, 2010; Tchanturia et al., 2007; Lopez et al., 2004):
- Anhedonia: Increased binding by D2D3 receptors in the anterior ventral striatum
- Ascetism: Increased binding by D2D3 receptors in the dorsal striatum
- Impaired set shifting and persistence: Increased thalamic D2 binding and alterations in the rostral and dorsal anterior cingulate cortex
- Perfectionism: Over-activation of the dorsolateral prefrontal cortex and hyperfunction of the ventromedial prefrontal cortex
- Harm avoidance and anxiety: Enhanced 5-HT1A binding in the amygdala and hypothalamus; reduced 5-HT2A binding in the amygdala and cortex
- Impulse control and crossover to bulimia nervosa: Interconversion of the long and short alleles of the 5-HTTLPR (serotonin transporter-linked polymorphic region)
- Reduced appetite (anorexia): Reduced interoceptive response (anterior insula) with diminished awareness and an unresponsive ventral striatum
- Body image impairment: Insular dysfunction; allocentric lock and an inability to update body image
- Problems with central coherence: Visuospatial difficulties stemming from increased parietal activity
- Compulsive exercising (foraging and hoarding behavior): Unmasking NPY2
- Hyperactivity (excessive exercise) and rituals: Serotonin deficits
- Low reward dependence: Norepinephrine dysregulation
Anorexic patients also can struggle with the following:
Recognizing the severe consequences that are associated with anorexia, one questions how a genetic predisposition to anorexia would survive in the gene pool over time to the present. The adaptive flee hypothesis attempts to explain this condition as an evolutionary instinct for helping primitive man cope with famine (Guisinger, 2003; Kersting, 2004). In Paleolithic times, there were numerous survival threats that influenced the availability of food (climatic conditions, including droughts and freezing winters, as well as pestilence and predators). The ensuing starvation brought on extreme hunger, weakness, and fatigue that prohibited the searching and energy necessary to secure a source of food. However, these stark conditions activated genes in a select few that were unfazed by starvation and capable to forage for food when others were incapacitated. These unique individuals were not only equipped with the energy to find food, but also demonstrated remarkable restraint to refuse consumption in order to feed others. Once food became plentiful, the family or clan would refeed the foragers enough to reproduce and pass on their genes to future generations.
This strategy for times of hardship when famines were imminent was duplicated during the Dutch starvation winter of 1945 (van der Zee, 1998). Nearing the end of World War II, the Hitler regime punished the Dutch for their siding with the Allies by providing them with limited food rations. It was reported that individuals traveled considerable distances on foot or on bikes at great physical expense to forage for food. These same volunteers refused to eat what they found, despite starving themselves. This behavior reflects a form of hoarding, but also characteristic behavior of those with anorexia (Ammar et al., 2000; Bair, 2006; Bartness, Keen-Rhinehart, Dailey, & Teubner, 2011; Beaumont, 1996; Cabanac & Swiergiel, 1989).
Researchers have identified an increase level of NPY1 (neuropeptide Y) in the arcuate nucleus of the hypothalamus (feeding center of the brain) that normally turns on the drive for food. However, during times of famine, NPY2 is unasked which contrarily inhibits the consumption of food and directs attention only to food acquisition (Ammar et al., 2000; Baird, Gray, & Fischer, 2006; Bartness et al., 2011; Beaumont, 1996; Cabanac & Swiergiel, 1989). This may be an explanation as to what occurs when starvation turns on the gene in anorectics during times of extreme food restriction.
It would be natural to conclude that recovery is at the mercy of our genes over which we have no control because we can’t choose our parents. Fortunately, heredity is not destiny (Kagan & Snidman, 2004; Kagan, 2010; LeDoux, 1996, 2001). Traits are not a pure category in that they differ in degree and fall on a continuum. They are only one dimension of our personality. Genes do not directly affect our traits, but they direct cells to synthesize proteins that shape our nervous systems (Cozolino, 2010; Tryon, 2014; Dharani, 2014). Our brains are forgiving, and cognitive flexibility is possible through therapy and medical intervention (Saxena & Feursner, 2006; Simpson & Campbell, 2013). The instruments of change at the disposal of the healing brain are epigenetics, resilience, collateral repair, neuroregeneration, and neuroplasticity. Each of these neurological mechanisms is activated by various therapeutic interventions. Some of the more familiar therapeutic interventions include cognitive behavioral therapy (CBT), dialectical behavioral therapy (DBT), acceptance and commitment therapy, and exposure response prevention. Additional tools include medication, surgery, nutrition, activity, and sleep hygiene to enhance, accelerate, and ensure complete recovery.
Interaction of genes and environment shapes brain circuits (Rutten et al., 2013; Stewart-Knox et al., 2012; Presnell et al., 2007; Franklin et al., 2006). The process whereby there are changes in gene expression that do not involve changes to the underlying DNA sequence is called epigenetics. It is a complicated mechanism that occurs when a gene is modified by histone variants and methylation of DNA bases. These modifiers are the clothing that governs the pattern of gene expression and tells the gene to switch on or off. All this is to say that genes can change as a consequence of the environment in which they are expressed, and as such, dysfunctional behaviors are capable of being altered and reprogrammed. Our experiences govern the patterns of gene expression as to whether certain genes are turned on or off (Dupont, 2009).
Neurogenesis is the process during which lost nerve cells are replenished (Spalding et al., 2013; Dennis, Suh, Rodriguez, Kril, & Sutherland, 2016; Nyberg, 2012; Gorio, 1992). This is not a version of the familiar mitotic division of pre-existing neurons. Deep within the limbic system are the hippocampus and periventricular areas from which de novo cells are generated. Here lies a collection of stem cells or amplified progenitor cells that are stimulated by different thoughts and beliefs to proliferate and migrate to various cognitive areas of the neocortex to replace lost neurons. This replenishment contributes to the way we think, reason, and learn. It is logical to assume that these undifferentiated cells transform into active neurons that produce new memories, thoughts, emotions, feelings, and, subsequently, behaviors. Awareness that comes from being in the present through mindfulness practices, such as DBT, can ensure such neuroregeneration is accomplished both expediently and efficiently.
The brain functions not solely on the activation of specific locations within the brain, but involves multiple regions that form a complex integrated circuit throughout the brain. Often the brain evolves to be wired in a pattern that produces dysfunctional behaviors. Therapeutic interventions can improve on the original design through a process called neuroplasticity (Doidge, 2006; Arden, 2010; Jacobs, 2014; Raskin, 2011). This rewiring involves redirecting the connections (axonal guidance) and making new and stronger connections to other neurons (dendritic arborization). The strength of these new connections is dependent on synaptogenesis, which involves neurotransmitter concentrations and receptor sensitivity. The rewiring can be envisioned as a habit loop that manifests in new behaviors and is effectively orchestrated by CBT or behavior modification. Adjunctive interventions such as exercise and meditation can accelerate the process by adding growth factors such as brain-derived neurotrophic factor (BDNF).
Resilience contributes to recovery in that it transforms the frightened victim into one capable of surviving during times of duress. This involves the process of adapting well in the face of adversity, whereby one bends but does not break. It is about flexibility and change when the old ways no longer work and invokes the ability to bounce back when one is faced with stress or pressure. Deliberate and consistent practice has been shown to reconfigure and increase the number and strength of connections in the resilience circuit (amygdala; medial, ventromedial, lateral, dorsolateral prefrontal cortex; anterior cingulate cortex; and nucleus accumbens) (Southwick & Charney, 2012; Graham, 2013; Davidson & Begley, 2013; Botvinick, Braver, Barch, Carter, & Cohen, 2001; Amodio, Jost, Master, & Yee, 2007). Neurochemical changes include an elevation of dopamine and BDNFs with reduction in serotonin and glutamate in specific areas of the brain (Husseini et al., 2001).
It is entirely possible that brain locations designed for specific functions can transform into areas that serve a similar but alternative purpose. Take, for example, the location for sight that is found at the rear of the brain in an area called the occipital lobe. For a blind person, there is no activation when his or her eyes look at the pages of a book. However, while interpreting the writing by touch (Braille), brain imaging demonstrates that the occipital lobe is activated in the visual word-form area (Reich et al., 2011; Cohen, Scherzer, Viau, Voss, & Lepore, 2011; Bar-Cohen, 2009; Merabet et al., 2004). A change in function brought about by learning alternative processes in lieu of lost function would be an example of collateral repair.
This capacity to change is elucidated in the orchid hypothesis (Dobbs, 2012; Belsky, Bakermans-Kranenburg, & van IJzendoorn, 2007; Belsky & Pluess, 2009; Conley, Rauscher, & Siegal, 2013; Pluess et al., 2010; Ellis & Boyce, 2008; Aron, Aron, & Jagiellowicz, 2012). A dandelion is known to thrive in any environment. In contrast, the orchid wilts easily but grows magnificently in the proper environment. Applying this to humans, genes and traits may underlie our greatest weakness, but also underlie our strength and resilience if nurtured properly.
Often our thoughts and behaviors become locked, making change quite challenging. Stuck in our ways is analogous to a computer on which one is assigned to type a letter in Arial (font) 10 (point size). Initially, the type appears as Times Roman, 12 point, and one must manually pull down the appropriate font and size to continue the task at hand. No matter how many times we return to the computer to type a message, it will continue to first show up in the default mode. The only way to change this permanently is to go into the computer and adjust the hard drive. Antipsychotic drugs, deep-brain stimulation, and repetitive transcranial magnetic stimulation (rTMS) have all demonstrated effectiveness in improving cognitive flexibility and are analogous to changing the brain’s hard drive (Pittenger et al., 2005, 2006, 2008, 2011; Ho et al., 2011; Bloch et al., 2006; Konradi & Heckers, 2001; Torres, 2013; Poeppl et al., 2014; Greenberg et al., 2008, 2010; Malone Jr. et al., 2009). One might imagine these interventions as applying WD-40 to the brain that enables therapy to be more effective in changing the way one thinks. Oxytocin reduces the likelihood of food obsessions, such as anxiously fixating on high-caloric foods, body shape, and negative emotions (Kim, 2014a, b, c). A dopamine agonist (olanzapine; Zyprexa®) might prove to be helpful for weight gain and anxiety reduction (Bissada, Tasca, Barber, & Bradwejn, 2008). Cognitive control over compulsive features of anorexia (i.e., feeling fat, rigid decision making, urges to restrict) might be reduced by magnetic pulses (rTMS) stimulating the dorsal left prefrontal cortex (McClelland et al., 2016a, b; Jay et al., 2016).
Anorectic patients highly value their cognitive function (intelligence) and can be motivated to pursue a legitimate course of treatment if they trust and believe in the process (Helgoe, 2008, 2011). Having insight into the neuroscience goes a long way in helping them understand their symptoms, accept treatment interventions, and utilize coping strategies. Those with anorexia can also find strength in those same traits that got them into trouble when they realize they can alternatively be a source of encouragement that can be projected as beneficial to their recovery. As deep and persistent thinkers, they possess analytical skills that integrate and process complex concepts and make them better at handling information overload (Cain, 2011, 2012). Though they take pride in their ability to lose weight, control their size, and manage their food intake; it is imperative that they connect with other accomplishments to redefine self and achieve personal fulfillment.
Critical to change is how the anorectic perceives the interventions to be effective. The psychoeducation that neuroscience brings forth has the potential to place them in their comfort zone. It is a nonthreatening way to address the disorder such that, by knowing the facts, they are better able to succeed. Presenting a neural map can construct a visual path of recovery and uncover biomarkers that predict outcomes. This helps the recovering anorectic feel more in control and in ownership of the disorder, which is necessary to stay with the program plan. Neuroscience allows the patients and treatment team to identify solutions for recovery and warnings of relapse (Guisinger, 2003; Kardum et al., 2008).
About the author:
Dr. Carson has been involved in the clinical treatment of obesity, addictions, and eating disorders for over 40 years. His unique background in health science and medicine (BS Duke University and B. H. S. Duke University Medical School) coupled with nutrition and exercise (BS Oakwood College, Ph.D. Auburn University) has prepared him to integrate neuropsychobiological intervention and proven psychotherapeutic treatment. Dr. Carson has honed his skills in communication and often-complicated science into enjoyable, practical and informative workshops. He is currently Vice President of Science and Innovation for the Eating Recovery Center’s & CORE Program for eating disorders treatment for people of higher weight in Denver, CO and consultant for the Pinegrove Behavioral Health and Addiction Center in Hattiesburg, MS. Ralph Carson, Ph.D. has consulted with numerous addiction and eating disorder treatment centers throughout the country, as well as being a highly sought after speaker at various conferences and workshops. Additionally, Dr. Carson has set up several eating disorder programs and corporate wellness programs. He is an active board member of the International Association of Eating Disorder Professionals (IAEDP). Working with Academy Medical Systems, he developed workshops for professional groups throughout the U. S. on topics such as exercise therapy, sports nutrition, eating disorders, and childhood obesity. He authored several popular books on nutrition, lifestyle practices, good health, and the brain: Harnessing the Healing Power of Fruits and the recently published The Brain Fix: What’s the Matter with Your Gray Matter?
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