Tag: Emotional Eating

Binge Eating Disorder Signs and Treatment in Adults and Kids

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Binge Eating Disorder, or BED, is one of the eating disorders I screen for most often in practice. Clinicians define it as repeated episodes of eating a large amount of food in a short period of time while feeling a loss of control during the episode. BED involves episodes that feel compulsive: the person cannot stop eating even when full or uncomfortable. This goes well beyond a second helping at dinner or an indulgent dessert.

The diagnostic criteria for BED require both that large amounts of food are consumed in a discrete time frame and that there is a sense of loss of control while eating. The episodes are also linked to behaviors such as eating more rapidly than normal, eating until uncomfortably full, eating when not hungry, eating alone because of embarrassment, and feeling disgusted or guilty afterward. At least three of those behaviors must be present. The episodes need to occur at least once a week for three months, cause distress, and they are not followed by purging behaviors like in bulimia.

Here’s a hypothetical that illustrates the pattern: someone sits down in the evening and works through an entire pizza and a half-gallon of ice cream in under two hours, not from hunger but because they can’t stop. They feel physically ill afterward. Ashamed, too. The cycle repeats weekly or more often. I’ve seen a real version of this on video visits. One of my patients was managing things with intermittent fasting, and it worked in the sense that the scale moved, but every time the eating window opened back up, they took in way more calories than they needed. The fast itself was setting up the binge.

Children complicate this picture. For kids under 12, researchers have proposed a related diagnosis called Loss of Control Eating Disorder, or LOC-ED (Tanofsky-Kraff et al., 2008). The issue is that children may not consume amounts of food that adults would consider objectively large, but they still experience the same loss of control. In this group, the definition focuses on the subjective sense of being unable to stop eating. The proposed criteria mirror those of BED but apply specifically to children younger than 12. The episodes still need to happen at least once a week for three months and cause distress.

Picture a hypothetical case in pediatrics: a 10-year-old who sneaks into the kitchen at night, eats snack foods quickly, and can’t stop once started. The amount might look modest by adult standards. For a child, it’s significant. What matters is the loss of control, not the portion size. Wrappers hidden in the trash. A refusal to eat breakfast the next morning. Those are often the only clues a parent gets.

Treatment is available for both BED and LOC-ED. For adults with BED, the most evidence supports cognitive behavioral therapy, which helps patients identify triggers, restructure eating patterns, and address guilt and shame. Interpersonal therapy has also been shown to help, especially when social stress is a driver. Some patients benefit from medications. SSRIs have modest benefit for binge frequency, and lisdexamfetamine is the only medication currently approved by the FDA for BED in adults. Nutritional counseling and structured meal planning are usually part of the approach.

I should be direct about where I actually fit into this picture. I don’t manage BED treatment myself. Real treatment leans heavily on behavioral health, and in my current telemedicine positions I don’t have the coordination with a therapist or eating-disorder specialist that this really requires. What I do is screen for it on video visits: ask the direct questions, name what I’m seeing, and refer out from there.

For children with LOC-ED, treatment recommendations are less formalized since the diagnosis itself is still considered research-based. The focus is often on family-based behavioral therapy, involving parents in setting up structured eating schedules and reducing situations where loss of control is most likely to occur. Addressing mood or anxiety symptoms is important, since these are often linked to eating episodes. Nutrition support is also key, both for the child and for parents trying to guide food choices. Medications are not first-line in children.

Recognizing BED or LOC-ED is important because both conditions are linked to higher rates of obesity, depression, and medical complications if untreated. Many people don’t come forward because of shame or because they don’t realize their pattern is a diagnosable disorder. Asking direct questions about eating behaviors, especially around loss of control, can uncover these conditions and open the door to treatment.

If this description fits you or someone you know, talk with a healthcare provider. Early recognition, especially in children, can change the trajectory and reduce the risk of chronic problems.

Scott Rennie, D.O.
Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

References:

Allison KC, Tarves EP. Treatment of night eating syndrome. Psychiatr Clin North Am. 2011;34(4):785-796. doi:10.1016/j.psc.2011.08.002

McCuen-Wurst C, Ruggieri M, Allison KC. Disordered eating and obesity: associations between binge-eating disorder, night-eating syndrome, and weight-related comorbidities. Ann N Y Acad Sci. 2018 Jan;1411(1):96-105. doi: 10.1111/nyas.13467. PMID: 29044551; PMCID: PMC5788730

Tanofsky-Kraff M, Marcus MD, Yanovski SZ, Yanovski JA. Loss of control eating disorder in children age 12 years and younger: proposed research criteria. Eat Behav. 2008;9(3):360-365. doi:10.1016/j.eatbeh.2008.03.001

Does Chronic Stress Cause Weight Gain? A Doctor Explains

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Obesity gets described as a balance of diet and exercise, and stress plays a far larger role in it than most people are told. I have seen patients who eat well and stay active and still lose ground the moment their stress rises. Research from Dr. Rajita Sinha at Yale explains a good deal of why. Chronic stress produces measurable biological change, well past anything you would call a mood.

Stress acts on the brain circuits governing emotion, motivation, and self-control. Those circuits overlap with the ones handling food reward and craving, particularly for calorie-dense processed food (Sinha et al., 2022). Cortisol climbs under chronic stress. Ghrelin rises with it while leptin falls. What you end up with is a body primed to eat more, in an environment where high-calorie food is always within reach.

Calling that emotional eating undersells it. In Sinha’s lab work, people exposed to stress through guided imagery ate more snack food afterward, and participants who were already overweight were the most affected. Their cravings and calorie intake tracked with measured increases in cortisol and ghrelin. The stress reached past how they felt and changed how their brains and bodies handled food.

The pandemic ran this experiment at national scale. Nearly half of U.S. adults gained weight over that period, with worse effects among people who already had higher BMIs (Khubchandani et al., 2022). Children were not spared; CDC data showed the rate of BMI increase doubling against pre-pandemic years (Lange et al., 2021). The predictors of gain were emotional distress, having children at home, and how long it had been since someone last weighed themselves.

Work outside the pandemic points the same way. In one community study, people with higher baseline cortisol and greater insulin resistance were more likely to gain weight over the following six months (Chao et al., 2017). Those markers did more than correlate with obesity. They predicted it.

That has pushed researchers past the eat-less-move-more framing toward treatments aimed at the stress itself. Mindfulness-based stress reduction lowers food cravings, perceived stress, and blood pressure in people with obesity (Tuit et al., 2011). There is even evidence in parenting: a small study of low-income mothers found mindful parenting reduced parental stress and was associated with healthier BMI outcomes in their children (Jastreboff et al., 2018).

Medical and surgical treatment still matter, and the evidence suggests they perform best alongside strategies that reduce stress reactivity and support executive function. Stress management belongs in the treatment plan rather than tacked onto the end of it.

I have seen patients who feel defeated because they are certain the weight they gained under stress was a personal failure. The science says otherwise. Stress reshapes brain pathways, moves hormone levels, and changes eating behavior in ways we can measure. None of that makes change impossible. It does mean compassion is not optional in this conversation, and that treating stress as part of the disease moves the discussion off blame and onto something we can actually act on.

Scott Rennie, D.O.

References

Sinha R. Chronic Stress and Obesity. Yale School of Medicine, Columbia Obesity ABOM Virtual Course, 2022.

Chao A et al. High Cortisol and Insulin Resistance Predict Weight Gain. Obesity. 2017.

Khubchandani J et al. Depression and Anxiety Predict Weight Gain During the COVID-19 Pandemic. Diabetes & Metabolic Syndrome. 2022.

Lange SJ et al. Body Mass Index Increase in Children During COVID-19. MMWR Morb Mortal Wkly Rep. 2021.

Tuit K et al. Mindfulness and Stress Reduction in Obesity. Appetite. 2011.

Jastreboff AM et al. Mindful Parenting and Childhood Obesity Prevention. Journal of Pediatrics. 2018.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Food Addiction and Obesity: How the Brain Is Involved

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

The human brain gets described as an engineering marvel. Like any product, it ships with vulnerabilities. Evolution built a system for surviving scarcity, and we now run that system in an environment of constant stimulation and engineered food. The mismatch explains a great deal about why obesity and addiction share so much ground.

One useful way to frame it is in terms of failure modes. Sometimes the design itself creates the problem. Sometimes development goes off track. And sometimes a perfectly good brain breaks down under conditions no brain was built for.

Take the design. We evolved to crave calorie-dense food because it was scarce and it kept us alive. Sugar and fat are now everywhere, and those old drives get hijacked. Food companies understand how to exploit them, the same way addictive substances exploit the same reward circuitry. The biology has not changed. The environment has.

Development matters too. Prenatal nutrition, early childhood adversity, and other disruptions shape how the brain handles reward and stress. Analysis of roughly 2,700 children in the NIH-funded ABCD Study found that higher BMI was associated with thinner cortex, particularly in prefrontal regions, and with lower working memory on list-sorting tasks (Laurent et al., 2020). Brain development itself appears alterable in the setting of poor diet and excess weight.

Then there are the extreme conditions. Trauma, chronic stress, and social adversity overwhelm coping systems, and food and drugs become the fallback. Calling that a failure of willpower misses what is happening. The brain is adapting, badly, to circumstances it can’t otherwise handle. It also helps explain why obesity and addiction cluster in groups facing economic hardship and unstable environments.

Dopamine sits at the center of both. Dopamine does more than produce pleasure. It teaches the brain what to attend to and what to repeat. Eat sugar, dopamine surges, the brain takes note. Use a drug, same signal. With repeated exposure, dopamine receptors downregulate (Volkow et al., 2013). Tolerance builds. Soon more sugar or more drug is needed to reach baseline.

Refined sugar is unusually effective in this loop. It spikes glucose fast, drives dopamine release, and slips past satiety signaling. Animal studies show sugar producing binge-like intake patterns and withdrawal signs on removal (Avena et al., Neurosci Biobehav Rev, 2008). In humans, high sugar intake has been linked to memory problems, greater inflammation, and impaired hippocampal function (Kendig, Appetite, 2014). Which is why cutting sugar feels less like breaking a habit and more like breaking an addiction.

So what helps? Supporting the brain at each stage. Protecting the developing brain through prenatal nutrition and limiting early sugar exposure. Teaching children coping skills, protecting sleep, and building activity, all of which strengthen the prefrontal cortex that reins in impulse. Reducing ultra-processed food at home and in schools.

Medications now target this signaling directly. GLP-1 receptor agonists act on satiety hormones in the gut and on brain pathways that regulate appetite. They reset the system rather than substituting for resolve.

Research is moving toward brain-based interventions: neurofeedback, brain stimulation, digital tools that reinforce healthier behavior in real time. The underlying message has not changed. Obesity and addiction are brain-based conditions shaped by biology, environment, and lived experience. Recognizing that changes how we treat and support the people in front of us, without letting anyone off the hook for their own care.

Scott Rennie, D.O.

References:

1. Laurent JS, et al. Associations Among Body Mass Index, Cortical Thickness, and Executive Function in Children. JAMA Pediatr. 2020;174(2):170-177. https://pubmed.ncbi.nlm.nih.gov/31816020/

2. Volkow ND, Wang GJ, Tomasi D, Baler RD. Obesity and addiction: neurobiological overlaps. Obes Rev. 2013;14(1):2-18. https://pubmed.ncbi.nlm.nih.gov/23016694/

3. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39. https://pubmed.ncbi.nlm.nih.gov/17617461/

4. Kendig MD. Cognitive and behavioural effects of sugar consumption in rodents: a review. Appetite. 2014;80:41-54. https://pubmed.ncbi.nlm.nih.gov/24816323/

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.