The role of specific neurotransmitters and neurotransmitter circuits in decision making is being explored in a variety of ways. Dopamine appears to have significant research support for a key role in making decisions related to reward.
The role of serotonin in decision making is less well studied but also appears to be important. Robert Rogers, Ph.D. recently presented some of his lab's research at the Warren Frontiers in Neuroscience lecture in Tulsa, Oklahoma. (Additionally, I have reviewed and placed a link to a recent research manuscript from Dr. Rogers related to topic below.)
Dr. Rogers noted the relationship between serotonin, depression and social function include these research findings:
Social isolation is a known risk factor for major depression
Serotonin appears important in developing nourishing social contacts
Social isolation found in anxiety and depression may be mediated by serotonin mechanisms
Serotonin mechanisms in human research is aided by the safe ability to modulate brain serotonin levels. Brain serotonin can be temporarily depleted using a amino acid drink deficient in the serotonin precursor L-tryptophan. Humans without mood or anxiety disorders show an increase in brain serotonin after a week of administration of any of commonly used selective serotonin reuptake inhibitors.
Depleting serotonin or augmenting serotonin can be combined with a variety of behavioral and brain imaging techniques. Dr. Rogers note his lab has recently documented several findings in adult control subjects without current or past anxiety or depression:
Tryptophan depletion decreased measures of cooperative interaction in a resource management game known as the Prisoner's dilemma
Tryptophan depletion appears to impair the ability of individuals to learn from a social cooperation task
When working on a resource decision task, trytophan depletion changed decision-making behavior in women but not in men
The antidepressant citalopram reversed the decision making behavior changes found in women with tryptophan depletion
The brain medial prefrontal cortex is activated when individual observe the social decision-making behavior of others
When working in groups on a resource harvesting task, tryptophan depletion produces a tendency to revert to the mean behavior in the group, even when this results in an earlier adverse group outcome
Dr. Rogers notes that these findings support more research in clinical populations suffering from a mood or anxiety disorders. Serotonin dysregulation found in depression and other psychiatric disorders may go hand-in-hand with deficits in initiating social interaction, impaired learning from social interaction experience and making adverse decisions in social situations.
Photo of Coopers Hawk from the author's private collection.
Rogers RD (2011). The roles of dopamine and serotonin in decision making: evidence from pharmacological experiments in humans. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 36 (1), 114-32 PMID: 20881944
Today I will review a study that provides some insight into potential genetic contributions to hoarding behavior. Of interest, this genetic link also appears to carry some increased risk for obesity.
Timpano from the University of Miama along with colleagues at Florida State University and the National Institute of Mental Health Intramural programs have recently published a study of 301 subjects with obsessive compulsive disorder (OCD).
In previous posts it was noted that hoarding can occur in the context of OCD but that not all hoarders will meet criteria for OCD. In the Timpano et al study, subjects started with a diagnosis of OCD and then were grouped into those with hoarding and those without hoarding behaviors.
The hoarding classification status was assigned based upon the subject response to two items found on the Yale Brown Obsessive Compulsive Scale (YBOCS). One item queried about tending to save objects and second item queried about difficulty discarding objects. Hoarding subjects were required to endorse both items.
The research team then looked at the subjects and the brain-derived neurotrophic factor (BDNF) status. BDNF has been a genetic region of interest in a variety of clinical neuroscience conditions including schizophrenia, anxiety and aggression. Additionally it appears to be involved in memory function and variants of BDNF have been linked to higher rates of obesity.
BDNF appears to serve a role as a central neurological system plasticity factor and modulates both serotonin and glutamatergic neurotransmitter systems. The BDNF gene codes for a protein that can vary in an region in status of two amino acids valine and methionine. At this regions, individuals can be assigned one of three genetic types: Val/val, val/met or met/met.
The Timpano et al team found the following key findings:
About 25% of those with OCD met criteria for being hoarders
The BDNF val/val genotype was found in 77% of the hoarding group versus only 60% of the non-hoarding OCD group
The BDNF val/val genotype correlated with increased hoarding symptom severity and BMI
45% of the hoarding group met criteria for obesity (BMI >30) versus only 21% of the OCD only group
The authors note that there are animal models of hoarding where hoarding behaviors have been linked to dysregulation of feeding behaviors. When humans begin to hoard objects, there may also be a overlapping drive to hoard (and consume) food. The authors note there may be a complex gene mechanism whereby individuals display hoarding, increased body weight and psychopathology as evidence of a "thrifty gene" strategy that may have survival and evolutionary manifestations.
It would be informative to examine the BDNF gene status of hoarders without a diagnosis of OCD. The authors note that interaction between BDNF and serotonergic function may partially explain some other the BDNF-hoarding-obesity triad.
There role of serotonin in OCD has received significant research attention. In the next post, I will look at the potential for selective serotonergic antidepressants pharmocotherapy in the treatment of hoarding behaviors.
The molecular model of BDNF above is in the public domain from a Creative Commons Attribution-ShareAlike 3.0 file (Wikepedia) authored by Microswitch.
Timpano, K., Schmidt, N., Wheaton, M., Wendland, J., & Murphy, D. (2011). Consideration of the BDNF gene in relation to two phenotypes: hoarding and obesity. Journal of Abnormal Psychology DOI: 10.1037/a0024159
Selective serotonin reuptake inhibitors frequently produce significant gastrointestinal side effects. Nausea was reported by up to 26% of subjects and diarrhea in up to 30% of subjects in a recent review of the new antidepressant vilazodone. Gastrointestinal side effects tend to be seen with the initiation of antidepressant drugs commonly followed by a period of improved tolerability.
The mechanism for this gastrointestinal effect is poorly understood. The gut is known to have serotonin receptors. Some gastrointestinal therapeutic agents target the serotonin receptor as their mechanism of action. For example, the antinausea drug ondansetron appears to act through it's antagonism of the 5HT (serotonin) 3 receptor. This results in inhibition of gastric activity while components of activity of the small intestine remain functional.
To better understand the effects of serotonin on GI motility, Janssen and colleagues from the University of Leuven conducted a novel experiment. Twenty healthy subjects were studied in a GI motility study following administration of placebo and the selective serotonin reuptake inhibitor citalopram.
The authors found that administration of citalopram significant reduced the gastrointestinal transit time compared to that found at baseline and placebo (see chart).
Upper gastrointestinal transit time is composed of three separate phases known as the migrating motor complex of MMC. Citalopram appeared to reduce the duration of phase 1 and phase 2 while the time spent in phase 3 was unchanged.
The authors attribute the change in transit time to a direct effect of citalopram on GI serotonin receptors although a central CNS effect could not be ruled out. The speculate this effect may be potentially therapeutic in individuals with constipation predominant irritable bowel syndrome.
This study did not directly address the issue of GI side effects associated with the SSRI antidepressants. Nevertheless, it suggests acute increased GI transit times with SSRIs may be a mechanism that contributes to GI side effects of nausea, diarrhea, cramping and pain.
Further studies of this effect are needed looking at a longer time frame. Since most GI side effects improve with prolonged administration, it is possible a receptor compensation mechanism may be involved in changes in side effects over time.
Graph of gastrointestinal transit times is an original graph produced by the author from data in the manuscript.
Janssen P, Vos R, & Tack J (2010). The influence of citalopram on interdigestive gastrointestinal motility in man. Alimentary pharmacology & therapeutics, 32 (2), 289-95 PMID: 20456311
Parents with children who have autism commonly report significant sleep problems. Clinicians commonly encounter complaints by parents about the child’s sleep problem and consider behavioral or pharmacologic interventions. Now a study informs parents and clinicians about the type of sleep abnormalities found in children with autism.
Buckley et al conducted sleep studies using polysomnography in a series of children with the diagnosis of autism between the ages of 2 and 13. Sleep architecture variables were examined compared to controls as well as a group of children with developmental delay without autism. This second control group is quite helpful as it helps identify whether sleep abnormalities in autism might be due to generally to a developmental delay.
The autism group had significant cognitive impairment with a mean IQ of 57. Here are the key statistically significant findings with results presented for autism, typical controls and developmentally delayed controls:
Total sleep time: 7.7 hours, 8.8 hours, 9.2 hours
Slow wave sleep %: 21.5%, 18.6%, 13.7%
REM sleep %: 14.5%, 22.6%, 25.0%
REM sleep latency: 109 min, 64 min, 69 min
So autism sleep architecture is characterized by less total sleep with more time spent in stage 3 sleep (slow wave sleep) and less time in REM (dream-related) sleep. The investigators note this pattern might inform us on some of the neurotransmitter abnormalities in autism. REM sleep control is a complex system that involves:
GABA
Glutamate
Serotonin from the cells in the brain dorsal raphe
Epinephrine in the locus ceruleus
Acetylcholine
The authors note that acetylcholine is a particular driver of slow wave sleep as well as REM sleep. They note “A more global (not just in the pontine brainstem where REM is orchestrated) cholinergic deficiency would predict a more permissive environment for slow-wave generation and could conceivably be represented by a higher percentage of this state”.
The authors note their study provides some insight into potential drug strategies in treating children with autism and sleep problems. Additionally, this pattern deserves additional research and an “objective biomarker for identification of infants at risk for autism”.
Buckley AW, Rodriguez AJ, Jennison K, Buckley J, Thurm A, Sato S, & Swedo S (2010). Rapid eye movement sleep percentage in children with autism compared with children with developmental delay and typical development. Archives of pediatrics & adolescent medicine, 164 (11), 1032-7 PMID: 21041596
First of all, man am I glad to be back home. New York City was awesome this trip, and I’ll be writing about my food adventures there at http://180kitchen.wordpress.com/ very soon. But all in all it felt like a competition to see how much caffeine, alcohol, sugar, nitrates, and vegetable oil I could get into my system. I’m more than ready for a breather from that. I’ve never been so glad to see ground beef, coconut oil, sweet potatoes, and spinach. In fact, the burger I ate for breakfast this morning was so large I started singing “Everybody Wants Some.” I actually filmed it below. Any resemblance to a young John Cusack is purely coincidental.
Anyway, time to discuss what is a huge and extremely prevalent problem in the modern world – emotional eating.
As discussed in many prior posts, food triggers a response in the pleasure centers in the human brain, acting on pleasure neurotransmitters like serotonin and dopamine. It is no surprise that when many people feel a sense of chronic stress, anxiety, shame, guilt, and so on – food becomes not just a way to fuel oneself, but a form of psychoactive medication. And in general, what provides the highest pleasure response is…
1) Rapidly-absorbed foods like white flour and liquid sugars 2) Sweets, whether natural as in honey, refined as in sucrose, or non-caloric 3) Calorie dense foods – like French fries, pizza, brownies, ice cream, or cheesecake 4) Alcohol and caffeine-containing drinks and substances 5) Foods with flavor enhancers like MSG found in most fast food and highly-flavored stuff like Cheetos or Doritos 6) Foods with low water content – that are therefore very calorie dense (butter, oils, nuts, dried fruit, chips, crackers, cookies, bread) 7) High-calorie liquids such as soft drinks, fruit juices, whole milk, half n’ half 8) Large quantities of food in general, of any kind
This is a 2-way street, as eating some of these foods, particularly those with the highest capability of triggering a pleasure center response like a fast food meal with a large sugary drink and a dessert all mixed together in one hit, can in turn cause massive emotional fluctuations. First a high, followed by a crash, which is addiction pathology 101 and can be caused by anything that is unusually, and unnaturally, pleasurable.
It works the other way as well. Chronic stresses such as the loss of a loved one, self-esteem issues, relationship problems, being in an abusive situation, financial stresses, and other problems that are of a chronic nature have a tendency to activate the same hormonal changes that a famine is capable of inducing. That is, an increase in cortisol production as well as synthesis in fat cells themselves. Hypercortisolemia, induced by any form of chronic stress from famine (the reason we are designed to have this fat storage response to stress in the first place – marked by a drop in metabolism, reduction in fat burning, increased production of fat storage enzymes, increased appetite, increased cravings) to depression to sleep deprivation can all trigger an increased appetite for the things on the above list.
This is why calorie restriction combined with a huge exercise load has the following impacts on a typical person…
1) Increased alcohol, sugar, and caffeine cravings – along with foods with very high calorie density and huge quantities of overall food in general 2) Increased appetite 3) Reduced body temperature 4) Increased risk of infection 5) Decreased desire for physical activity (as well as sex and other calorie-burning activities) 6) And so on
Likewise, following the guidelines laid out in the THIS FREE EBOOK brings about the exact opposite set of changes.
Anyway, ending emotional eating is not difficult. In fact, most people have emotional eating issues to begin with because of chronic dieting, undernourishment, insufficient sleep, and excessive stress in the first place. It all starts with feeding yourself well as the FREE EBOOK explains.
Helpful tips include eating a diet that keeps you even keel emotionally. No one ever could have convinced me of the power of eating a well-balanced, calorically-sufficient, whole foods diet without excessive exercise and adequate sleep on emotions until I actually tried it religiously. Like Jon Gabriel mentions in this fantastic interview, “there are no more good days and bad days.” You are more or less anti-dieting at that point.
Another helpful hint is to eliminate substances you know you are addicted to WHILE EATING WELL and RESTING WELL. Eliminating addictive or problem foods that have been a target of emotional eating binges for years does not work if you are depriving yourself of anything. Otherwise you will increase your cravings for those “problem” foods as each day passes. With the right set of nourishment and minimal stress from intense exercise regimens – as well as plenty of time for rest and relaxation, there is simply no low serotonin and dopamine state occurring in your brain that causes the outrageous cravings to eat foods that spike those feel good neurotransmitters into the stratosphere.
By keeping yourself even keel with consistent sleep patterns, regular mealtimes, no skipped meals (or at the very least not skipping meals when you are hungry), and plenty of calories at each feeding to leave you feeling satisfied – there is simply no low state in need of medicating with food and drugs.
The real problem is that people are under all kinds of emotional stress, work stress, lack of sleep, and more while at the same time thinking it’s healthy to eat as little as possible, or at the very least go to war with fat, carbohydrates, or animal products while exercising as much as they can stand to.
This is what CAUSES emotional eating in the first place, exacerbated of course by the halo of guilt that a person experiences after eating junk food and the shame and loss of self-esteem that they feel over whatever excess fat they carry after each episode.
In short, emotional eating is caused by being at war with yourself and asking much more of your body and mind than you give in return. The big picture answer to emotional eating is to end that war.
Would you try to raise a healthy baby by depriving it of food, making it feel constantly scared, torturing it, yelling at it for being fat, weak-willed, and lazy, not letting it sleep, and forcing it to do a lot of exercise? No. Then why are you pursuing health by trying to do that to yourself?
Physical, emotional, and mental health is obtained by obeying your physical, emotional, and mental needs – not ignoring them and then beating yourself up over your cravings, fatigue, depression, and body fat.
