Tag: Mental Health

Do Weight Loss Apps and Devices Really Help?

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

Patients ask me whether weight loss apps and digital programs actually work. It is a fair question, and the honest answer has a lot of qualifiers in it. Traditional obesity care runs into limited visit time, cost, and a shortage of places to refer people. Technology, whether an app, a web platform, or a hybrid program with human coaching, routes around some of that.

Dr. Bonnie Spring at Northwestern has studied how eHealth, mHealth, and telehealth are reshaping obesity treatment. Her finding is that these tools extend reach, lower cost, and deliver feedback in real time. The difficulty is holding anyone’s attention long enough for that to matter.

The trends in the research are reasonably clear. Web-based programs on their own produce small losses, around 2 to 3 percent of body weight. Better than nothing, and well short of the 7 to 8 percent that structured in-person programs achieve (Wieland 2014; Raaijmakers 2015; Tang 2014). Roughly half of users drop out.

Mobile approaches do better. In a review of U.S. trials, about 63 percent of studies found meaningful weight loss with mHealth interventions (Burke, Ma, Spring 2015). Texting on its own moved very little; outcomes improved when coaching or app-based monitoring was layered on. The catch is that most people abandon apps almost immediately, with more than three quarters stopping within three days of downloading.

Spring’s Opt-In Study used the Multiphase Optimization Strategy to build something cost-effective: remote sessions, structured self-monitoring, goal setting, and a trained buddy for support. Participants targeted a 7 percent loss, the threshold known to reduce diabetes and cardiovascular risk. More than half got there, at under $500 per person. That is comparable to the Diabetes Prevention Program at a fraction of the cost.

The buddy component turned out to matter most. Having a friend or family member reinforcing the changes between formal sessions kept people going, which lines up with what we already knew: social support is among the strongest predictors of durable results.

Access remains uneven. Reliable internet and comfort with digital tools are not evenly distributed, even though weight loss apps are among the most downloaded health apps in the world (Nikolaou & Lean, 2017). Owning a smartphone is the easy part. Cultural fit, affordability, and whether someone finds the technology tolerable all matter as much.

In my practice I have seen patients do well with commercial programs like Omada or Noom, which pair app-based tracking with remote coaching. Others get further with something simpler, MyFitnessPal being the usual example. These run somewhere between $40 and $130 a month, which is its own barrier and worth asking about before recommending one.

Technology works when it carries evidence-based strategy inside it: goal setting, self-monitoring, timely feedback, social support. Without those it is a download that gets deleted on day three. Knowing which products have research behind them and which have marketing behind them is part of our job now, and steering a patient toward the right one is often what separates a few weeks of enthusiasm from an actual result.

Scott Rennie, D.O.

References

Spring B. Use of Technology in the Prevention and Treatment of Obesity. Northwestern University, 2024.

Wieland LS et al. Systematic Reviews. 2014.

Raaijmakers LGM et al. Obesity Reviews. 2015.

Tang J et al. Obesity Reviews. 2014.

Burke LE, Ma J, Spring BJ et al. Ann Behav Med. 2015.

Nikolaou CK, Lean MEJ. Int J Obes. 2017.

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.

How to Sleep Better: Practical Steps for Patients

On By Dr. Scott RennieIn Other Diseases and ConditionsLeave a comment

Sleep gets a fraction of the attention we give diet and exercise, and it should not. Research from Dr. Ari Shechter at Columbia University has shown that poor sleep feeds obesity, diabetes, hypertension, and heart disease. It costs people their daily functioning, and underneath that it is quietly setting long-term disease risk. It is not a secondary problem.

When I ask patients about sleep, I keep it practical. When did this start, and is it new or has it always been like this? What is the bedroom like, too warm or too bright or too loud? Do they snore, gasp, or stop breathing, which points toward apnea? Any crawling or tingling in the legs, which points toward restless legs? I ask about weekdays versus weekends, because an irregular schedule can look exactly like insomnia. And I ask about caffeine, alcohol, nicotine, and medications, which patients rarely volunteer.

Formal tools give the conversation structure. The Epworth Sleepiness Scale is quick for daytime sleepiness. The Pittsburgh Sleep Quality Index is broader. STOP-Bang and the Berlin questionnaire flag possible apnea. The Insomnia Severity Index tracks both severity and how much it is costing someone functionally.

For objective data, in-lab polysomnography remains the standard for apnea, limb movement disorders, narcolepsy, and REM sleep behavior disorder. Wrist actigraphy at home gives a more practical picture of sleep and wake patterns over time, which is often what I actually need.

Adults should target 7 to 9 hours, and children and teenagers need more. Hours alone do not settle it. Timing, efficiency, and how someone feels the next day all matter. Patients tell me constantly that they are in bed for eight hours and wake up unrested. That is the point where efficiency and awakenings become the more useful thing to look at.

The consequences of chronic short sleep are well documented. It shifts ghrelin and leptin in the direction of more hunger and weight gain (Spiegel et al., 2004). It degrades glucose control and raises diabetes risk (Tasali et al., 2022). Hypertension, coronary disease, and stroke all track with insufficient sleep, and long-standing sleep problems are associated with cognitive decline and dementia risk (Vorster et al., 2024).

Causes are usually layered. Behavior contributes: irregular schedules, screens late, heavy meals and alcohol close to bed. So do physiologic and psychological factors: apnea, restless legs, anxiety, chronic pain.

Practical work starts with sleep hygiene. A consistent schedule resets circadian rhythm. Bedrooms should be cool, dark, and quiet. Bright light late interferes with sleep onset. Evening caffeine and alcohol come down. A wind-down routine, reading or stretching or a warm shower, makes the transition easier.

Daytime habits matter more than patients expect. Morning light anchors circadian rhythm. Even ten minutes of aerobic activity improves sleep depth. And for anyone waking in the night, what they do next shapes the rest of it: awake more than twenty minutes, get up and do something quiet in dim light rather than lie there getting frustrated.

The behavioral approach I use most is stimulus control. The principle is simple, which is rebuilding the association between the bed and sleep. Go to bed only when sleepy. Use the bed for sleep. Leave it if sleep is not coming. I have watched patients with years of insomnia retrain themselves this way. One had been scrolling his phone in bed for hours every night; once he started leaving the room when sleep would not come and only returning when he felt drowsy, his sleep onset shortened within a few weeks and the nightly frustration went with it.

Sleep is a medical necessity, and it belongs in routine care alongside everything else we screen for. Taking it seriously improves rest, and it also improves cardiometabolic health, mental health, and how people feel about their days.

Scott Rennie, D.O.

References

Shechter A. Improving Sleep in Your Patients. Columbia Cornell Obesity Medicine Course, 2024.

Spiegel K et al. Ann Intern Med. 2004.

Tasali E et al. JAMA Intern Med. 2022.

Markwald RR et al. PNAS. 2013.

Vorster A et al. Clin Transl Neurosci. 2024.

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.

Childhood Food Insecurity: What Doctors and Families Can Do

On By Dr. Scott RennieIn Other Diseases and ConditionsLeave a comment

Food insecurity means the lack of consistent access to enough food for a healthy, active life. Hunger is part of it. The rest reaches into development, school performance, behavior, and long-term health, and millions of children in this country live inside it.

In pediatrics it surfaces quietly. A child who can’t concentrate at school. A family that skips meals at the end of the month. A growth curve that looks off and doesn’t fit the usual explanations. Treating it as a clinical problem rather than a social one is where the work starts.

The scope is wide. In 2024, 13.7% of U.S. households experienced food insecurity at some point during the year, and among households with children the figure was 18.4% (1). That is up sharply from the 10.5% recorded in 2020. Children carry the heaviest burden. The literature links food insecurity to iron-deficiency anemia, delayed motor and cognitive development, poor school performance, and behavioral problems including depression and inattention (Cook et al., J Nutr, 2004; Casey et al., Pediatrics, 2006).

Food insecurity and obesity travel together, which surprises most parents. Economic pressure pushes families toward calorie-dense, low-cost food. Scarcity itself can trigger binge eating when food becomes available. Stress and parenting under pressure add another layer. Children get urged to clean their plates, or food becomes the tool for soothing. Children aged 10 to 15 in food-insecure households are more likely to carry higher BMI and adiposity (Tester et al., Curr Obes Rep, 2020).

Geography tells its own story. The Southeastern U.S. carries some of the highest rates of both food insecurity and childhood obesity. Mississippi, Arkansas, Louisiana, New Mexico, and Texas rank among the hardest hit for food insecurity. Mississippi, West Virginia, Kentucky, Alabama, and Oklahoma consistently report the highest pediatric obesity rates. The overlap is no coincidence. Rural areas, tribal lands, and parts of Appalachia function as food deserts, where grocery stores are scarce and convenience stores and fast food fill the gap. Poverty and underinvestment in health infrastructure compound it.

So how do we find it? Most pediatric settings use the Hunger Vital Sign, a two-question screener drawn from the USDA’s 18-item scale and endorsed by the American Academy of Pediatrics. Against the full scale it runs 97% sensitive and 83% specific (Hager et al., Pediatrics, 2010; AAP Council on Community Pediatrics, Pediatrics, 2015). It asks families to respond to two statements:

“We worried whether our food would run out before we got money to buy more.”

“The food we bought just didn’t last, and we didn’t have money to get more.”

An answer of “often true” or “sometimes true” to either one signals risk. It is short, it embeds cleanly in an EMR, and it has been validated across languages. Longer tools exist, including the USDA’s full 18-item module, its 6-item short form, and the 9-item youth survey, but the time cost usually rules them out.

Screening is harder to implement than it sounds. Time, competing priorities, and plain discomfort discussing money are real barriers. Self-administered forms, EMR prompts, and universal framing all help. Telling every family “we ask everyone about food, because it’s central to health” takes the sting out of the question. When a screen comes back positive, the referral pathway has to already exist, whether that means SNAP and WIC enrollment, food pantries, or school meal programs.

Federal nutrition programs remain the strongest safety net. SNAP provides grocery support. WIC offers food vouchers, nutrition education, and breastfeeding support. The National School Lunch and School Breakfast Programs cover the school year, and the Summer Food Service Program covers the gap when school is out. The evidence doesn’t support the worry that these programs worsen obesity risk. WIC participation tracked with a decline in obesity among children aged 2 to 4 across 2010 to 2016 (Pan et al., MMWR, 2019). Stable SNAP benefits reduce the time children spend with obesity compared with non-participants (Au et al., J Nutr, 2019).

For clinicians the task splits in two: identify and connect. Screening is the first half. The impact comes from linking families to something real, which might mean a referral list built into the EMR, a relationship with a local enrollment center, or a standing partnership with a community food bank. Even asking “would it help if I connected you with resources that provide healthy food?” moves something.

Food insecurity is a health problem, and it shows up in front of us constantly. Naming it, screening for it, and acting on it protects children from consequences that reach a long way forward.

Scott Rennie, D.O.

References:

1. Rabbitt MP, et al. Household Food Security in the United States in 2024. USDA Economic Research Service, ERR-358, December 2025. https://www.ers.usda.gov/publications/pub-details?pubid=113622

2. Cook JT, et al. Food insecurity is associated with adverse health outcomes among human infants and toddlers. J Nutr. 2004;134(6):1432-1438. https://pubmed.ncbi.nlm.nih.gov/15173408/

3. Casey PH, et al. Child health-related quality of life and household food security. Pediatrics. 2006;118(5):e1406-e1413. https://pubmed.ncbi.nlm.nih.gov/17079542/

4. Hager ER, et al. Development and validity of a 2-item screen to identify families at risk for food insecurity. Pediatrics. 2010;126(1):e26-e32. https://pubmed.ncbi.nlm.nih.gov/20595453/

5. Council on Community Pediatrics, Committee on Nutrition. Promoting Food Security for All Children. Pediatrics. 2015;136(5):e1431-e1438. Reaffirmed 2021. https://publications.aap.org/pediatrics/article/136/5/e1431/33896/

6. Tester JM, Rosas LG, Leung CW. Food Insecurity and Pediatric Obesity. Curr Obes Rep. 2020;9(4):562-570.

7. Au LE, et al. J Nutr. 2019;149(9):1642-1650.

8. Pan L, et al. Trends in Obesity Among Participants Aged 2 to 4 Years in WIC, United States, 2010 to 2016. MMWR Morb Mortal Wkly Rep. 2019;68(45):1057-1061. https://www.cdc.gov/mmwr/volumes/68/wr/mm6845a2.htm

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.

Childhood Obesity: How It’s Prevented and Treated

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

Childhood obesity is a chronic disease affecting roughly 14.7 million children and adolescents in the United States, and growth charts and BMI percentiles are the least interesting part of it. The American Academy of Pediatrics said as much in its 2023 Clinical Practice Guideline, which reframes obesity as a condition deserving the same urgency and structure we bring to any other chronic disease.

The guideline is built around 13 key action statements plus a set of consensus recommendations. The message running through all of them is that waiting doesn’t work. Early, structured intervention does.

The first shift is consistent screening. Pediatricians should measure height, weight, and BMI annually for every child between 2 and 18. Once BMI reaches the 85th percentile, the number stops being the point and the evaluation begins: dyslipidemia, prediabetes, fatty liver disease, hypertension, sleep apnea. That workup includes history, physical examination, and a careful look at social and environmental context.

For children over 10 with obesity, the guideline recommends a fuller lab evaluation. Fasting glucose or A1c, a lipid panel, liver enzymes, and where indicated a sleep study or a PCOS evaluation in adolescent girls. Depression screening belongs in that set too. Obesity travels with comorbidities, and treating one while ignoring the others misses most of the disease.

Once the diagnosis is made, treatment starts. Not next visit. The model is family-centered and non-stigmatizing, and motivational interviewing sits at the center of it because it lets clinicians surface ambivalence, name barriers, and set goals with families rather than at them.

The cornerstone is Intensive Health Behavior and Lifestyle Treatment. IHBLT is structured and sustained in a way brief counseling never is. The evidence supports at least 26 hours of face-to-face individual or group contact over 3 to 12 months, delivered by a multidisciplinary team of physicians, dietitians, behavioral health providers, and exercise professionals. That threshold is where outcomes start to move, and it applies to children as young as 6.

Nutrition counseling focuses on limiting calorie-dense, nutrient-poor food and increasing fruit, vegetables, and lean protein. Activity goals scale by age, with 60 minutes of moderate-to-vigorous movement daily as the benchmark for school-aged children. Behavioral strategies cover self-monitoring, goal setting, and problem solving. Parental involvement is central rather than optional, and programs that engage parents in the behavior change itself see better outcomes.

For families, this looks nothing like being told to eat better and move more. The intensity and the support structure are what shift the needle.

Not every family can reach a program like that. Geography, insurance, and local capacity all get in the way. The guideline acknowledges it and asks providers to deliver the most comprehensive care available while advocating for expanded community-based IHBLT.

Pharmacologic therapy is the next tier. Adolescents 12 and older may be offered FDA-approved weight-loss medication as an adjunct to health behavior and lifestyle treatment, according to each drug’s indications, risks, and benefits. Twelve is the floor. Medications are adjuncts to behavioral treatment rather than replacements for it.

Metabolic and bariatric surgery is addressed as well. For adolescents 13 and older with severe obesity, defined as BMI at or above 120% of the 95th percentile, the guideline supports referral to a comprehensive pediatric surgical center for evaluation.

The guideline also spends real attention on social determinants. Families dealing with poverty, food insecurity, systemic inequity, or nowhere safe to play are facing barriers that have nothing to do with individual willpower. Effective treatment has to acknowledge that and work on it where it can.

For practicing clinicians the roadmap is short: treat when obesity is identified, use motivational interviewing, refer to or provide IHBLT, manage comorbidities in parallel, and advocate for families against stigma and structural barriers.

Sandra Hassink, who helped lead the work, put the central point plainly when the guideline was released: “There is no evidence that ‘watchful waiting’ or delayed treatment is appropriate for children with obesity.”

Scott Rennie, D.O.

References:

1. Hampl SE, Hassink SG, Skinner AC, et al. Clinical Practice Guideline for the Evaluation and Treatment of Children and Adolescents With Obesity. Pediatrics. 2023;151(2):e2022060640. https://publications.aap.org/pediatrics/article/151/2/e2022060640/190443/

2. Executive Summary: Clinical Practice Guideline for the Evaluation and Treatment of Children and Adolescents With Obesity. Pediatrics. 2023;151(2):e2022060641. https://publications.aap.org/pediatrics/article/151/2/e2022060641/190440/

3. American Academy of Pediatrics. Clinical Practice Guideline for the Evaluation and Treatment of Pediatric Obesity: resources and implementation tools. https://www.aap.org/obesitycpg

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.

Weight Loss Surgery Without Incisions: Bariatric Endoscopy

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

Obesity is one of the most common health problems we face, and treatment has never kept pace with the need. More than 100 million U.S. adults meet criteria for obesity. Roughly 1% of patients who qualify for metabolic and bariatric surgery actually undergo it in a given year. Lifestyle change and medication help, and plenty of patients either get insufficient benefit or can’t sustain them. That leaves a wide gap, particularly for people with moderate obesity and for those who don’t qualify for surgery.

Bariatric endoscopy is starting to fill it. These are minimally invasive outpatient procedures sitting between lifestyle and pharmacotherapy on one side and surgery on the other. No incisions, lower risk, same-day discharge for most patients. They are also repeatable or reversible, which gives patients and clinicians room to change course.

Intragastric balloons are the simplest example. The device occupies space in the stomach, and patients feel full on less food. Studies consistently show 10 to 15% total body weight loss over six months alongside improvements in insulin resistance and liver health. In a prospective study of patients with NASH and early fibrosis who underwent balloon placement with paired liver biopsies, every patient who lost 10% or more of their weight showed a reduction in NAFLD activity score, 90% had resolution of NASH, and 45% showed fibrosis regression (Bazerbachi et al., Clin Gastroenterol Hepatol, 2021). Small study, striking numbers.

Endoscopic sleeve gastroplasty is the more durable option. An endoscopic suturing device reduces stomach volume, mimicking a surgical sleeve without incisions. MERIT, the first randomized trial of the procedure, compared ESG plus lifestyle modification against lifestyle alone in class 1 and 2 obesity and found the procedure safely induced and maintained weight loss with improvement in metabolic comorbidities (Abu Dayyeh et al., Lancet, 2022). Five-year data from a single-center cohort show mean total body weight loss around 16%, with roughly three-fifths of patients holding 10% or more (Sharaiha et al., Clin Gastroenterol Hepatol, 2021). Compared with surgery it means fewer complications, faster recovery, and preserved native anatomy.

Endoscopic revision is gaining traction too. Transoral outlet reduction addresses weight regain after gastric bypass by tightening the gastrojejunal anastomosis and the pouch, restoring restriction (Jirapinyo & Thompson, Endoscopy, 2018). For patients demoralized by regain, it is a far less invasive option than surgical revision.

Duodenal interventions work differently. Duodenal mucosal resurfacing and duodenal-jejunal bypass sleeves act less on restriction and more on metabolic signaling, with early data showing HbA1c reductions and weight loss in the 9 to 15% range. This is the least mature part of the field and should be described that way to patients.

Safety looks good. Serious adverse events run in the 0.2 to 4% range depending on the procedure. Most problems, nausea and abdominal discomfort, are mild and short-lived. FDA clearance of endoscopic suturing platforms reflects the accumulating evidence on both safety and efficacy.

So who are the candidates? Typically patients with BMI 30 to 50 who haven’t gotten results from diet and exercise alone. It is also an option for people who aren’t ready for surgery or not eligible. Patients who have regained weight after bariatric surgery may benefit, especially from TORe. Comorbidities like diabetes and MASLD factor in, since weight reduction directly improves their course.

The thing to stress is that bariatric endoscopy is a tool rather than a cure, and it doesn’t replace surgery or medication. Outcomes are best when procedures are combined with pharmacotherapy and lifestyle change, which is the same lesson obesity keeps teaching. It is a chronic, relapsing disease and it needs long-term management.

Scott Rennie, D.O.

References:

1. Bazerbachi F, et al. Intragastric Balloon Placement Induces Significant Metabolic and Histologic Improvement in Patients With Nonalcoholic Steatohepatitis. Clin Gastroenterol Hepatol. 2021;19(1):146-154.e4. https://pubmed.ncbi.nlm.nih.gov/32360804/

2. Abu Dayyeh BK, et al. Endoscopic sleeve gastroplasty for treatment of class 1 and 2 obesity (MERIT): a prospective, multicentre, randomised trial. Lancet. 2022;400(10350):441-451. https://pubmed.ncbi.nlm.nih.gov/35908555/

3. Sharaiha RZ, et al. Five-Year Outcomes of Endoscopic Sleeve Gastroplasty for the Treatment of Obesity. Clin Gastroenterol Hepatol. 2021;19(5):1051-1057.e2. https://pubmed.ncbi.nlm.nih.gov/32683103/

4. Jirapinyo P, Thompson CC. Endoscopic bariatric and metabolic therapies: surgical analogues and mechanisms of action. Endoscopy. 2018;50(4):371-377.

5. Ponce J, et al. Surg Obes Relat Dis. 2015;11(4):874-881.

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.

Eating Disorders in People With Obesity: Combining Care

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

Working with patients who struggle with obesity, I see how often excess weight and disordered eating overlap. The two get treated as separate problems, sometimes as opposites. Plenty of people live at the intersection, and ignoring that connection makes treatment less effective and occasionally harmful.

Eating disorders are psychiatric conditions in which eating patterns or related behaviors disrupt health or functioning (APA, DSM-5-TR, 2022). They affect people across all ages, genders, and body sizes. The DSM-5-TR describes anorexia nervosa, bulimia nervosa, binge eating disorder, avoidant or restrictive food intake disorder, and others. Each has distinct features. All carry real medical and psychological risk.

Binge eating disorder matters most in this conversation. It is the most common eating disorder in the United States. Patients describe episodes of eating large amounts with a loss of control, followed by guilt, shame, or depression, without the vomiting or other compensatory behaviors seen in bulimia. Lifetime prevalence runs around 0.85% of U.S. adults, with 12-month prevalence near 0.44% (Udo & Grilo, Biol Psychiatry, 2018; Hudson et al., Arch Gen Psychiatry, 2007). Among patients seeking behavioral weight loss treatment, roughly one in ten meet criteria (Chao et al., Obesity, 2017). Among adults presenting for bariatric surgery, meta-analytic estimates using DSM-5 criteria put it near 14% (Hilbert et al., Int J Eat Disord, 2020).

Why does this matter? Untreated binge eating disorder makes weight loss programs harder to sustain. Patients drop out more often, regain faster, and carry higher rates of depression, anxiety, and substance use. The metabolic toll shows up as more diabetes and hypertension. Identifying it early lets us adapt care, often by starting with cognitive behavioral therapy or another evidence-based treatment before any weight loss effort.

Eating disorders leave physical findings, and a fair number of them are visible on a video call. Dry skin, thinning hair, and the fine body hair of anorexia are all things a patient can show on camera. Parotid enlargement in bulimia is visible. Dental enamel erosion isn’t, and neither are the electrolyte abnormalities that matter most, which is where labs and a low threshold for in-person referral come in. Severe cases can develop life-threatening arrhythmias. Binge eating disorder is more often associated with metabolic changes, elevated liver enzymes and worsening insulin resistance. Psychiatric comorbidity is frequent across the whole spectrum, including depression, anxiety, PTSD, and ADHD (Hilbert et al., Psychol Med, 2014).

It is a mistake to think only thin patients have eating disorders. Many patients with obesity have restrictive patterns, obsessive food thoughts, or emotional eating cycles. I have seen patients try extreme diets, binge during periods of stress, then spiral into weight cycling. Others present with nutrient deficiencies despite high calorie intake. Body size rules an eating disorder neither in nor out.

Screening is where this gets caught. The SCOFF questionnaire and the Eating Disorder Screen for Primary Care are short and practical. Even plain questions about body image, eating patterns, or feeling out of control with food will surface problems. When the psychiatric history includes depression, trauma, or substance use, suspicion should go up.

Treatment requires integration. For binge eating disorder, first-line options include cognitive behavioral therapy, interpersonal therapy, and dialectical behavior therapy (Brownley et al., Ann Intern Med, 2016; Grilo et al., Curr Obes Rep, 2023). Lisdexamfetamine, SSRIs, and topiramate help some patients. These approaches reduce binge episodes and rarely produce significant weight loss, which is worth saying to patients directly so nobody is disappointed by a treatment that is working. Obesity care gets layered in once eating behaviors stabilize. Dietitians, primary care, psychiatry, and behavioral health need to be working the same case. Heavy emphasis on BMI or food rules can backfire by reinforcing disordered thinking.

Sequencing depends on the condition. In anorexia, the priority is weight restoration and psychiatric treatment, never weight reduction. For bulimia, obesity treatment waits until binge-purge behaviors are controlled. In binge eating disorder, obesity treatment can follow once episodes are reduced and things are stable. For ARFID, individual assessment guides the approach. In every case the eating disorder comes first while symptoms are active. Starting weight loss treatment too early worsens the disorder, damages trust, and blocks recovery (Mehler et al., J Eat Disord, 2011).

Recognizing that obesity and eating disorders coexist changes how we practice. It moves the focus from weight to whole-person health. Patients need care addressing both the physical and psychological sides, which means helping them repair their relationship with food and body while long-term medical outcomes improve.

Scott Rennie, D.O.

References:

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). 2022.

2. Udo T, Grilo CM. Prevalence and Correlates of DSM-5-Defined Eating Disorders in a Nationally Representative Sample of U.S. Adults. Biol Psychiatry. 2018;84(5):345-354. https://pubmed.ncbi.nlm.nih.gov/29859631/

3. Hudson JI, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2007;61(3):348-358. https://pubmed.ncbi.nlm.nih.gov/16815322/

4. Chao AM, et al. Obesity (Silver Spring). 2017;25(4):713-720.

5. Hilbert A, et al. Meta-analysis on the long-term effectiveness of psychological and medical treatments for binge-eating disorder. Int J Eat Disord. 2020;53(9):1353-1376. https://pubmed.ncbi.nlm.nih.gov/32583527/

6. Hilbert A, et al. Psychol Med. 2014;44(15):3239-3250.

7. Brownley KA, et al. Binge-Eating Disorder in Adults: A Systematic Review and Meta-analysis. Ann Intern Med. 2016;165(6):409-420. https://pubmed.ncbi.nlm.nih.gov/27367316/

8. Grilo CM, et al. Curr Obes Rep. 2023.

9. Mehler PS, et al. J Eat Disord. 2011.

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.

How Obesity in Pregnancy Affects the Baby and Placenta

On By Dr. Scott RennieIn Menopause & Women's Health, Weight Loss & Metabolic HealthLeave a comment

As healthcare providers, we’ve long recognized the importance of maternal health in shaping pregnancy outcomes. What’s become clearer in recent years is the role of epigenetics, changes in gene expression that don’t alter DNA itself but influence how genes are turned on or off.

When we look at pregnancies complicated by obesity, DNA methylation patterns in the placenta are altered, with increased methylation suppressing genes that matter for nutrient transport and fetal growth. DNA hydroxymethylation, usually tied to active gene expression, tends to drop at the same time. One study found a 21 percent increase in methylated regions and a 31 percent decrease in hydroxymethylated regions in placentas from obese pregnancies compared with lean ones (Mitsuya K, Parker AN, Liu L, Ruan J, Vissers MCM, Myatt L. PLOS ONE. 2017, 12(10):e0186115).

These changes show up directly in the structure and function of the placenta. Inflammatory changes are common, disrupting hormonal signals and communication between maternal and fetal systems, while lipid buildup in placental cells interferes with normal function and impaired blood vessel development slows villous maturation, reducing the placenta’s ability to exchange oxygen and nutrients efficiently (Saben J, Lindsey F, Zhong Y, et al. Placenta. 2014, 35:171-177).

Mitochondrial function also suffers. Placental cells from obese pregnancies generate less ATP through oxidative phosphorylation. Less energy available means nutrient transport and other vital processes get compromised, which can directly affect fetal growth and development (Mele J, Muralimanoharan S, Maloyan A, Myatt L. Am J Physiol Endocrinol Metab. 2014, 307:E419-E425).

The clinical consequences are real. Growth restriction at one extreme, excessive growth at the other. Both ends of that spectrum carry a higher risk of metabolic problems later in life, including insulin resistance and obesity (Ornoy A. Reprod Toxicol. 2011, 32:205-212).

In practice, weight and metabolic health before and during pregnancy matter more than we once realized. Supporting women to reach a healthier weight before conception can reduce risks. During pregnancy, balanced diets built around whole foods, healthy fats, and complex carbohydrates can help improve metabolic stability. For women with metabolic dysfunction, medications such as metformin may play a role in improving insulin sensitivity.

Regular follow-up lets us track maternal health and fetal growth, and adjust care as needed. The goal reaches past the pregnancy itself. Reducing the child’s long-term risk of obesity and metabolic disease matters just as much.

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.

Sources:

  • 1. Mitsuya K, Parker AN, Liu L, Ruan J, Vissers MCM, Myatt L. Alterations in the placental methylome with maternal obesity and evidence for metabolic regulation. PLOS ONE. 2017;12(10):e0186115. https://pubmed.ncbi.nlm.nih.gov/29045485/
  • 2. Saben J, Lindsey F, Zhong Y, et al. Maternal obesity is associated with a lipotoxic placental environment. Placenta. 2014;35(3):171-177. https://pubmed.ncbi.nlm.nih.gov/24484739/
  • 3. Mele J, Muralimanoharan S, Maloyan A, Myatt L. Impaired mitochondrial function in human placenta with increased maternal adiposity. Am J Physiol Endocrinol Metab. 2014;307(5):E419-E425. https://pubmed.ncbi.nlm.nih.gov/25028397/
  • 4. Ornoy A. Prenatal origin of obesity and their complications: gestational diabetes, maternal overweight and the paradoxical effects of fetal growth restriction and macrosomia. Reprod Toxicol. 2011;32(2):205-212. https://pubmed.ncbi.nlm.nih.gov/21620955/

Managing Insomnia and Sleep Problems: A Physician’s Perspective

On By Dr. Scott RennieIn Other Diseases and ConditionsLeave a comment

Insomnia is one of the most common problems I deal with. A few bad nights bleed into everything: work, mood, patience, appetite. Patients usually open the visit asking about pills or supplements, and I understand why. Sleep feels like something that should have a switch. Most of the time the answer is duller than a prescription and works better, which is a hard sell at nine at night when someone has been staring at the ceiling for a week.

How Much Sleep Do We Need

Seven to nine hours suits most adults. Under six on a regular basis carries real risk, and routinely running past nine is its own signal that something else is going on. The exact number moves from person to person, and I put more weight on how someone functions at four in the afternoon than on the number they report.

What Sleep Actually Does

Sleep is repair time. It consolidates memory, sharpens focus, and steadies the emotional baseline, which is why a rested person absorbs a bad day and a chronically tired one doesn’t. It supports immune function, cardiovascular health, and metabolic balance. The long-run associations with longevity and lower rates of chronic disease are consistent enough that I treat sleep as a vital sign rather than a lifestyle detail.

The Cost of Short Nights

Chronic sleep loss shows up in obvious ways and quiet ones. Fatigue, irritability, work that slips. Those are the complaints people bring. What they usually do not connect to sleep are the things that accumulate over years: hypertension, diabetes, heart disease, obesity. Immunity weakens, which is why the poor sleepers in a household tend to be the ones who catch everything going around. Anxiety and depression travel with chronic insomnia in both directions, each making the other worse. Cognitive decline is the long-horizon concern, and it is the one patients ask about most once they hear it.

Medications for Insomnia

Short-term use can help. None of these drugs are free of risk, and I’d rather say so plainly than bury it at the end of a list.

Zolpidem (Ambien) helps with both falling asleep and staying asleep, though daytime drowsiness and the odd nighttime behaviors are well documented. Zaleplon (Sonata) is shorter acting and suits the patient whose whole problem is sleep onset. Eszopiclone (Lunesta) covers onset and maintenance, and the metallic taste is a common enough complaint that I mention it before someone calls about it. Temazepam (Restoril) is a benzodiazepine, still prescribed, and carries the most dependence risk of the group.

Shortest effective course, every time. These work best as a bridge while the behavioral changes take hold, not as the plan itself.

Supplements

Melatonin is the one everybody has already tried. It earns its place in circadian problems, delayed sleep phase and jet lag especially, and sometimes in mild insomnia. One to five milligrams is the usual range, and timing matters more than dose, which is the part most people get wrong. Magnesium is worth considering in patients who are actually deficient. Leafy greens and nuts are good sources. Supplements are gentler than prescription hypnotics, and they won’t touch the underlying driver of chronic insomnia.

Sleep Hygiene

In my opinion, the most effective and lasting treatment is better sleep hygiene. Patients who hold a consistent schedule, same bedtime and same wake time seven days a week, often notice a difference within a few weeks. Cool, dark, quiet. Screens and blue light in the last hour before bed work against the transition.

Routine matters more than people expect. Reading, stretching, meditation, anything repeated nightly trains the body to wind down on cue. Caffeine, nicotine, and alcohol all interfere and are best kept well away from evening. Daylight exercise helps; a hard workout an hour before bed usually doesn’t.

One small change that pays out more than it should: turn the clock away from the bed. Patients who wake at three and check the time start doing arithmetic about how much sleep is left, and the arithmetic keeps them up longer than the original waking would have.

Keeping a Sleep Diary

When insomnia persists, a diary earns its keep. Bedtimes, wake times, awakenings, caffeine, stress, exercise. Two weeks of honest entries usually surfaces a pattern nobody had noticed, and reviewing it together tends to point at a small, specific change rather than a large vague one.

When to Seek Help

If the problem holds after the schedule and the environment have genuinely been addressed, it needs a proper evaluation. Sleep apnea, restless leg syndrome, anxiety, and depression all hide behind a complaint of insomnia. Treating the thing underneath is what fixes the sleep.

Scott Rennie, D.O.

Sources

National Institutes of Health Office of Dietary Supplements. Magnesium Fact Sheet for Health Professionals. https://ods.od.nih.gov/factsheets/Magnesium

National Sleep Foundation. How Much Sleep Do We Really Need? https://www.thensf.org

Centers for Disease Control and Prevention. Sleep and Sleep Disorders. https://www.cdc.gov/sleep

American Academy of Sleep Medicine. Clinical Practice Guideline for the Pharmacologic Treatment of Chronic Insomnia in Adults. J Clin Sleep Med. 2017;13(2):307-349.

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.