Tag: weight loss

How Obesity and Nutrition Affect Cancer Risk

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

Nutrition tends to get treated as background noise in oncology, good for general health but peripheral to the actual treatment. That view is losing ground. Food behaves as information as much as fuel, shaping metabolism, influencing tumor biology, and affecting both cancer risk and outcomes.

Obesity is the clearest illustration. It is a metabolic state rather than a matter of extra weight. Higher BMI is linked to increased incidence and mortality across several cancers, breast, colon, and endometrial among them (Calle et al., NEJM, 2003). Excess adipose tissue alters hormones, raises inflammation, and activates growth pathways that hand tumors an advantage. Elevated insulin and IGF-1 drive proliferation. Leptin rises, adiponectin falls, and the balance tips toward growth. Adipose tissue also produces estrogen, which raises risk for the hormone-sensitive cancers (Schvartzman, 2023).

Cancer cell metabolism adds a layer. Rather than relying mainly on oxidative phosphorylation, many cancer cells run aerobic glycolysis, the Warburg effect, generating both energy and the building blocks for rapid division (PMID: 26232225). Which raises the obvious question of whether diet can be used to push back.

The evidence is mixed and growing. Ketogenic diets have shown potential for boosting immune responses against tumors (PMID: 27178315), while in renal cell carcinoma and BRAF-mutated melanoma they may promote growth instead (PMID: 28089569). Restricting amino acids such as methionine, or serine and glycine, slows tumor growth in preclinical work (PMID: 28425994, 32413275). High-dose vitamin C has shown promise in KRAS-mutant cancers (PMID: 26541605). And the gut microbiota, which diet shapes, appears to affect how well patients respond to immune checkpoint inhibitors (PMID: 29097494).

All of which points toward precision nutrition. What helps one cancer may do nothing for another, or worse. Tumor type, genetics, insulin sensitivity, concurrent treatment, and the microbiome all bear on it. So does whether a patient can actually live with the diet, because one that works in theory and not in practice has not helped anyone.

So what do I tell patients? Not to follow a cancer diet, because there is no such thing. I point them toward the findings that hold up consistently. Mediterranean-style eating and lower-carbohydrate patterns reduce inflammation and may lower recurrence risk (PMID: 28935150). Fiber supports the microbiome and helps hold metabolic balance (PMID: 29098294). Observational work links nuts, fish, olive oil, and coffee to lower cancer risk or mortality (PMID: 27436272, 29158191).

One patient I worked with had breast cancer and wanted to eat better without overhauling her life. We stayed with Mediterranean-style adjustments: more vegetables, legumes, fish, and olive oil, less in the way of processed food and added sugar. Her oncologist was on board. Through treatment she held her weight steady, had fewer energy crashes, and tolerated therapy better than she expected. None of that cured anything. It was a concrete thing she could do that supported the care she was getting, and it mattered to her that it was hers to do.

Obesity and nutrition influence cancer biology directly, through metabolic and inflammatory pathways we can measure. Nutrition is not a replacement for standard therapy and it should not be the last thing we get to either.

Scott Rennie, D.O.

References

Calle EE et al. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. NEJM. 2003;348(17):1625-1638. PMID: 12711737

Schvartzman JM. Metabolism, Nutrition, Obesity & Cancer. Columbia University Lecture, 2023.

Sullivan LB et al. Supporting aspartate biosynthesis is an essential function of respiration in proliferating cells. Cell. 2015. PMID: 26232225

Lussier DM et al. Enhanced immunity in a mouse model of malignant glioma is mediated by a therapeutic ketogenic diet. BMC Cancer. 2016. PMID: 27178315

Xia S et al. Prevention of dietary-fat-fueled ketogenesis attenuates BRAF V600E tumor growth. Cell Metab. 2017. PMID: 28089569

Maddocks ODK et al. Modulating the therapeutic response of tumours to dietary serine and glycine starvation. Nature. 2017. PMID: 28425994

Lien EC, Vander Heiden MG. Dietary approaches to cancer therapy. Cancer Cell. 2020. PMID: 32413275

Yun J et al. Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH. Science. 2015. PMID: 26541605

Routy B et al. Gut microbiome influences efficacy of PD-1-based immunotherapy against epithelial tumors. Science. 2018. PMID: 29097494

Farinetti A et al. Mediterranean diet and colorectal cancer: A systematic review. Nutrition. 2017. PMID: 28935150

Song M et al. Fiber intake and survival after colorectal cancer diagnosis. JAMA Oncol. 2018. PMID: 29098294

Song M et al. Marine ω-3 polyunsaturated fatty acid intake and survival after colorectal cancer diagnosis. Gut. 2017. PMID: 27436272

Hu Y et al. Association between coffee intake after diagnosis of colorectal cancer and reduced mortality. Gastroenterology. 2018. PMID: 29158191

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 Does Aging Change Your Metabolism? What Research Shows

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

Obesity, diabetes, cardiovascular disease, and frailty get treated as though they were the price of getting older. Work from researchers like Luigi Fontana points somewhere else. Decades of metabolic strain do most of this damage, and diet, activity, and the choices stacked on top of them shape how much strain accumulates.

The scale is hard to ignore. Chronic disease accounts for close to 90% of U.S. healthcare spending, most of it aimed at managing complications rather than preventing them (Martin et al., Health Affairs, 2021). Life expectancy in this country fell by more than two years between 2019 and 2021. Obesity now affects 40.3% of adults aged 20 and older, with 9.7% in the severe range (1). Excess adiposity drives hypertension, diabetes, fatty liver disease, and several cancers.

The biology is familiar. Oxidative stress, inflammation, and insulin resistance sit underneath most of these conditions (Fontana & Partridge, Cell, 2015). Abdominal fat is active tissue rather than storage. It fuels insulin resistance and chronic inflammation, and it also activates bone marrow. In the PESA cohort of 745 apparently healthy adults imaged with FDG-PET, bone marrow activation tracked with every component of metabolic syndrome, and the activated group carried metabolic syndrome at 22.2% versus 6.7% (Devesa et al., Eur Heart J, 2022). Obesity changes the terrain of the body long before symptoms show up.

Calorie restriction without malnutrition is the clearest intervention we have. The animal data are strong. In rhesus monkeys, long-term restriction slowed age-related brain atrophy (Colman et al., Science, 2009), preserved muscle and function (Colman et al., J Gerontol, 2008), and lowered frailty and chronic disease burden (Yamada et al., J Gerontol, 2018).

This literature gets oversold, and the primate data are where it happens. The 2017 joint reanalysis of the two big studies found a survival benefit in the Wisconsin animals and no significant survival effect in the National Institute on Aging cohort (Mattison et al., Nat Commun, 2017). Health measures improved in both. Lifespan did not reliably follow. That is a more honest summary than the one usually quoted.

Human data are thinner but point the same direction. CALERIE tested roughly a 25% calorie reduction over two years and found improvements in blood pressure, cholesterol, glucose, inflammatory markers, heart rate variability, and insulin sensitivity (Meydani et al., Aging, 2016; Stein et al., Aging Cell, 2012; Weiss et al., Am J Clin Nutr, 2006). Even the more realistic reduction people actually achieved, closer to 12%, produced meaningful metabolic change (Kraus et al., Lancet Diabetes Endocrinol, 2019).

Calories are one variable. Nutrient quality and timing matter too. Studies in mice suggest high-protein diets may shorten lifespan, while restricting methionine or branched-chain amino acids improves metabolic health and longevity markers (Solon-Biet et al., Cell Metab, 2014). A trial in men with prostate cancer found that a single month of protein restriction lowered fat mass, cholesterol, and insulin (Fontana et al., Cell Rep, 2016). Protein source appears to matter as well, with plant-based sources holding an advantage over animal-based ones.

Timing has drawn its own attention. Intermittent fasting, whether through time-restricted eating or alternate-day fasting, extends lifespan in animal studies and protects against age-related disease including diabetes and cancer (Mattson et al., PNAS, 2014). Human studies suggest benefits on body fat, insulin sensitivity, and metabolic markers (Tosti et al., Aging Biology, 2022).

The gut microbiome adds a layer underneath all of it. Diet shapes microbial diversity and function, which in turn shapes inflammation, immunity, and metabolism (Thorburn et al., Immunity, 2014; Griffin et al., Cell Host Microbe, 2017). Fiber, protein type, and eating pattern all shift that balance. Nutrition never acts alone. It works through microbial partners.

What Fontana and others argue is that the real challenge lies less in treating diseases once they appear and more in holding metabolic integrity across a lifespan. That means healthcare built around prevention rather than reaction. Whole-food, plant-predominant eating. Fewer excess calories. Less reliance on protein-heavy patterns. Fasting strategies where they fit the patient. Attention to gut and immune health.

Aging isn’t a disease. Metabolic dysfunction is. Treat it early and seriously, through diet, lifestyle, and the interventions that have evidence behind them, and the curve bends toward years worth having.

Scott Rennie, D.O.

References:

1. National Center for Health Statistics. Prevalence of Overweight, Obesity, and Severe Obesity Among Adults Age 20 and Older: United States, 1960–1962 Through August 2021–August 2023. https://www.cdc.gov/nchs/data/hestat/obesity-adult-17-18/obesity-adult.htm

2. Martin AB, et al. Health Affairs. 2021.

3. Fontana L, Partridge L. Promoting health and longevity through diet: from model organisms to humans. Cell. 2015;161(1):106-118. https://pubmed.ncbi.nlm.nih.gov/25815989/

4. Fontana L, Kennedy BK, Longo VD, Seals D, Melov S. Medical research: treat ageing. Nature. 2014;511(7510):405-407. https://pubmed.ncbi.nlm.nih.gov/25056047/

5. Devesa A, et al. Bone marrow activation in response to metabolic syndrome and early atherosclerosis. Eur Heart J. 2022;43(19):1809-1828. https://pubmed.ncbi.nlm.nih.gov/35567559/

6. Colman RJ, et al. Science. 2009;325(5937):201-204.

7. Colman RJ, et al. J Gerontol A Biol Sci Med Sci. 2008;63(6):556-559.

8. Yamada Y, et al. J Gerontol A Biol Sci Med Sci. 2018;73(3):273-278.

9. Mattison JA, et al. Caloric restriction improves health and survival of rhesus monkeys. Nat Commun. 2017;8:14063. https://pubmed.ncbi.nlm.nih.gov/28094793/

10. Weiss EP, et al. Am J Clin Nutr. 2006;84(5):1033-1042.

11. Meydani SN, et al. Aging (Albany NY). 2016;8(7):1416-1431.

12. Stein PK, et al. Aging Cell. 2012;11(4):644-650.

13. Kraus WE, et al. Lancet Diabetes Endocrinol. 2019;7(9):673-683.

14. Solon-Biet SM, et al. Cell Metab. 2014;19(3):418-430.

15. Fontana L, et al. Cell Rep. 2016;16(2):520-530.

16. Mattson MP, et al. Proc Natl Acad Sci USA. 2014;111(47):16647-16653.

17. Tosti V, et al. Aging Biology. 2022.

18. Thorburn AN, et al. Immunity. 2014;40(6):833-842.

19. Griffin NW, et al. Cell Host Microbe. 2017;21(1):84-96.

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 Parents Influence a Child’s Weight and Eating

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

Childhood obesity has little to do with a child’s willpower. Biology, environment, and daily routine shape it. Genetics matter. So does the household, and that is where parents hold real leverage: how they feed, how they structure the day, what they model.

None of what follows is about blame. It is about where the leverage actually sits.

The clearest example starts in infancy. Responsive feeding means reading hunger and fullness cues instead of pressuring or ignoring them, and it has been linked to healthier eating patterns and weight gain matched to a child’s needs (Ventura, Adv Nutr, 2017). A parent who notices a baby turning away from the bottle and respects that signal is teaching self-regulation. The “clean your plate” approach many of us grew up with does the opposite. It overrides the signal and sets up overeating later (Johnson & Birch, Pediatrics, 1994).

Breastfeeding is where the popular version of this claim outruns the evidence. Observational studies associate exclusive and longer breastfeeding with lower obesity risk, with reductions sometimes quoted around 24%. The review most often cited for that number argues the observational literature is heavily confounded by socioeconomic status, maternal weight, and the feeding practices that travel alongside breastfeeding, and that randomized and sibling-comparison designs show a far weaker effect (Woo & Martin, Curr Obes Rep, 2015). Breastfeeding is worth supporting on its own merits. Promising parents it will prevent obesity goes past what the data support.

Parents also teach by example. A child who regularly sees a parent eating vegetables or trying something unfamiliar is more likely to do it. Repeated exposure paired with parental modeling makes children more willing to accept foods they would otherwise refuse. Using food as a reward runs the other way. Saying “you can have dessert if you eat your broccoli” teaches a child that sweets are the prize and broccoli is the toll (Newman & Taylor, J Exp Child Psychol, 1992).

The home environment does quiet work. Fruit and vegetables visible and easy to grab, energy-dense snacks harder to reach, and children drift toward the better option without a rule being enforced. Family meals matter too. The link to diet quality is consistent even where the direct effect on weight is murkier. They add structure and cut down on distracted eating.

Sleep and activity belong in the same conversation. Short sleep and heavy screen time in early childhood both raise obesity risk. Parents who hold bedtimes, encourage active play, and set limits on screens are shaping energy balance in ordinary daily ways.

Some strategies backfire. Restriction is the main one. In a well-known experiment, restricting children’s access to a particular snack increased both their desire for it and how much they ate when it became available, compared with an unrestricted food (Fisher & Birch, Appetite, 1999). Using food to soothe emotion has a similar problem. It builds an association between eating and comfort that persists into adult life.

Genetics play their part. Some children are more sensitive to food cues and less attuned to satiety, and twin studies put real numbers on that heritability (Wardle, Carnell & Plomin, Am J Clin Nutr, 2008). Even so, a supportive home makes a measurable difference in children carrying that predisposition. Responsive feeding, structure, and consistent modeling buffer inherited risk.

For families already struggling, family-based behavioral treatment has trial evidence behind it. The model runs on collaborative goal-setting, structured monitoring, and positive reinforcement, and it improves child weight outcomes in ways that hold up over time (Wilfley et al., JAMA Pediatr, 2017). Parent-only versions of the same treatment perform comparably to parent-and-child versions, which matters for families who can’t get everyone to an appointment (Boutelle et al., Appetite, 2021).

Parents don’t cause obesity. They do hold leverage points that matter, from infancy through adolescence, in how food, sleep, stress, and activity get managed at home.

Scott Rennie, D.O.

References:

1. Ventura AK. Does Breastfeeding Shape Food Preferences? Links to Obesity. Adv Nutr. 2017;8(1):149-150.

2. Johnson SL, Birch LL. Parents’ and children’s adiposity and eating style. Pediatrics. 1994;94(5):653-661. https://pubmed.ncbi.nlm.nih.gov/7936891/

3. Woo JG, Martin LJ. Does Breastfeeding Protect Against Childhood Obesity? Moving Beyond Observational Evidence. Curr Obes Rep. 2015;4(2):207-216. https://pubmed.ncbi.nlm.nih.gov/26100032/

4. Newman J, Taylor A. Effect of a means-end contingency on young children’s food preferences. J Exp Child Psychol. 1992;53(2):200-216. https://pubmed.ncbi.nlm.nih.gov/1578198/

5. Fisher JO, Birch LL. Restricting access to foods and children’s eating. Appetite. 1999;32(3):405-419. https://pubmed.ncbi.nlm.nih.gov/10336797/

6. Wardle J, Carnell S, Haworth CM, Plomin R. Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment. Am J Clin Nutr. 2008;87(2):398-404. https://pubmed.ncbi.nlm.nih.gov/18258631/

7. Wilfley DE, et al. Dose, Content, and Mediators of Family-Based Treatment for Childhood Obesity. JAMA Pediatr. 2017;171(12):1151-1159. https://pubmed.ncbi.nlm.nih.gov/29084318/

8. Boutelle KN, et al. Appetite. 2021.

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.

What Brain Scans Show About Appetite and Overeating

On By Dr. Scott RennieIn Weight Loss & Metabolic Health1 Comment

Patients say a version of the same thing constantly: “I know what I should eat, but I still crave the wrong things.” That gap between knowledge and behavior is what pushed researchers toward the brain. Functional MRI has shown that appetite runs on circuits that defend fat mass and respond to food cues, and that willpower is a small part of the story.

For years we leaned on BMI as the working definition of obesity. A BMI over 30 got the label, and the number explained nothing about why weight gain happened or why some patients struggle far more than others. Schwartz and colleagues reframed it in 2017 as “a disorder of energy homeostasis, characterized by the defense of an elevated body fat mass” (Schwartz et al., Endocr Rev, 2017). That definition earns its keep. It says the body is working to hold fat stores high, and that when weight comes off, biology answers with stronger hunger signaling, slower metabolism, and shifted hormones.

The gut-fat-brain conversation sits at the center. Leptin, ghrelin, insulin, GLP-1, and PYY all shape hunger and satiety, and fMRI shows how those signals land. High-calorie food cues light up the amygdala, striatum, medial orbitofrontal cortex, and ventral tegmental area, all reward and craving territory (Schur et al., Int J Obes, 2009; Melhorn et al., Am J Clin Nutr, 2018). After weight loss, that reward response doesn’t fade, which is a large part of why relapse is the rule. Interventions do move it. Leptin replacement, intranasal insulin, GLP-1 agonists, and bariatric surgery all reduce this activation (Holsen et al., Int J Obes, 2018; van Bloemendaal et al., Diabetes, 2014).

One finding deserves more attention than it gets: looking at pictures of calorie-dense food predicts what people actually eat. In studies where participants later chose from a buffet, those with higher reward activation to food images selected more high-fat, high-calorie items. The brain response translated into behavior at the table.

That has treatment implications. Patients with persistent reward-driven responses may get the most from GLP-1 agonists like semaglutide. For others, agents acting on central insulin or leptin signaling may fit better. Bupropion-naltrexone targets reward pathways directly and may suit patients where hedonic eating is the main driver. Obesity is a brain-based condition, and it needs brain-aware treatment.

Inflammation belongs in this picture too. Valdearcos and colleagues showed that rodents on a high-fat diet developed hypothalamic gliosis, an inflammatory response in the brain, before they gained significant weight (Valdearcos et al., Cell Metab, 2017). Human MRI findings line up. Individuals with obesity are more likely to show signs of hypothalamic gliosis (Schur et al., Obesity, 2015; Kreutzer et al., Diabetes, 2017). Inflammation may disrupt appetite regulation early, helping drive the defense of elevated fat mass.

For clinicians, this changes the posture. Blaming patients for “failing” when weight returns misreads the physiology. Their biology is built to resist fat loss. Medications acting on appetite centers belong in long-term care rather than short courses. Diet quality may matter for brain inflammation as well as calorie balance. And as with any other chronic disease, the expectation should be continuous management rather than a one-time fix.

Framing obesity as a chronic brain and inflammatory disease does something useful for the room. It takes stigma out of it. Patients are living with a condition in which the brain defends fat mass through powerful signals, and that framing replaces shame with something we can actually treat.

Scott Rennie, D.O.

References:

1. Schwartz MW, Seeley RJ, Zeltser LM, et al. Obesity Pathogenesis: An Endocrine Society Scientific Statement. Endocr Rev. 2017;38(4):267-296. https://pubmed.ncbi.nlm.nih.gov/28898979/

2. Schur EA, et al. Activation in brain energy regulation and reward centers by food cues varies with choice of visual stimulus. Int J Obes (Lond). 2009;33(6):653-661. https://pubmed.ncbi.nlm.nih.gov/19365394/

3. Melhorn SJ, et al. Am J Clin Nutr. 2018;107(4):574-582.

4. Holsen LM, et al. Int J Obes (Lond). 2018;42(4):785-793.

5. van Bloemendaal L, et al. GLP-1 receptor activation modulates appetite- and reward-related brain areas in humans. Diabetes. 2014;63(12):4186-4196. https://pubmed.ncbi.nlm.nih.gov/25071023/

6. Valdearcos M, et al. Microglial Inflammatory Signaling Orchestrates the Hypothalamic Immune Response to Dietary Excess and Mediates Obesity Susceptibility. Cell Metab. 2017;26(1):185-197.e3. https://pubmed.ncbi.nlm.nih.gov/28683286/

7. Kreutzer C, et al. Hypothalamic Inflammation in Human Obesity Is Mediated by Environmental and Genetic Factors. Diabetes. 2017;66(9):2407-2415. https://pubmed.ncbi.nlm.nih.gov/28576837/

8. Schur EA, et al. Radiologic evidence that hypothalamic gliosis is associated with obesity and insulin resistance in humans. Obesity (Silver Spring). 2015;23(11):2142-2148. https://pubmed.ncbi.nlm.nih.gov/26530930/

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.

Doctor Supervised Weight Loss: What Works Long Term

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

Telling patients to eat less and move more doesn’t cut it. Obesity is a chronic disease, and progress requires structured, ongoing, individualized care. The hardest part clinically is making sure the weight that comes off is fat rather than muscle.

Losing muscle costs more than strength. It costs independence, recovery capacity, and eventually survival. Older adults and patients with low baseline activity are the most exposed. Poorly managed weight loss produces sarcopenia, the loss of muscle mass and function. Layer excess fat on top and you get sarcopenic obesity, where a patient looks heavy and is functionally weak and metabolically compromised at the same time.

The European Working Group on Sarcopenia in Older People sets out how to catch it early. It starts with loss of strength, measured by grip strength or a chair-stand test. DXA or BIA can confirm low muscle mass. Poor strength plus low mass plus reduced physical performance defines severe sarcopenia. These definitions give us a framework to act before decline becomes permanent (Cruz-Jentoft et al., Age Ageing, 2019).

Muscle mass predicts survival on its own. Appendicular Lean Mass Index, lean tissue in the arms and legs divided by height squared, is a reliable measure, and people in the top quartile carry substantially lower all-cause mortality than those in the lowest, even after adjusting for BMI and comorbidities (Srikanthan & Karlamangla, Am J Med, 2014). Put plainly, a patient with stronger arms and legs has better odds of living longer regardless of what the scale says.

Strength testing matters as much as mass. Low grip strength tracks with higher mortality from cardiovascular disease, cancer, and respiratory illness. Poor lower-body strength, showing up as slower gait speed or difficulty rising from a chair, tracks with frailty, hospitalization, and long-term disability.

Both measures are cheap and fast, and both are underused. Grip strength needs a dynamometer and a hand to put it in, which rules it out of any remote encounter. The 30-second sit-to-stand doesn’t. A hard chair, arms crossed over the chest, as many stands as the patient can complete in thirty seconds, counted by whoever is watching. It works over video as well as it works in a room, and it yields a number worth tracking across visits. One usable functional measure beats a chart full of weights.

Nutrition is the cornerstone of preserving muscle during weight loss. The baseline protein RDA of 0.8 g/kg/day is inadequate for many adults, particularly older patients and anyone in a calorie deficit. The evidence supports closer to 1.2 to 1.6 g/kg/day, and up to 2.0 g/kg/day in some medically supervised cases (Paddon-Jones et al., Am J Clin Nutr, 2015; Bauer et al., J Am Med Dir Assoc, 2013). Spacing intake across meals rather than loading it at dinner sustains muscle protein synthesis better. Whey and casein, soy, eggs, and blended plant sources all work.

Calculating a target in patients with obesity is genuinely awkward. Actual body weight overshoots. Ideal body weight undershoots. Adjusted body weight is the usual compromise, and reasonable clinicians disagree about which to use. For a 5’6″ patient, a target weight around 73 kg at 1.5 g/kg puts the daily goal near 110 grams, which is a number a patient can actually work with.

Exercise has to include both resistance and aerobic work. Resistance training protects and builds lean mass. Aerobic activity improves cardiovascular and metabolic health. A 2022 systematic review and meta-analysis found the combination conferred the greatest mortality risk reduction, and notably found that weight training alone wasn’t associated with lower mortality among people doing no aerobic exercise (Shailendra et al., Am J Prev Med, 2022). For a patient that translates to brisk walking or cycling most days plus two or three weekly strength sessions using bands, weights, or bodyweight.

Think of muscle like a retirement account. Build it and hold it early, so it is there when it is needed. A patient in their seventies who lands in the hospital with pneumonia can lose a large fraction of their reserve to a few days of immobility and poor intake. If the reserve was thin going in, the decline may be permanent, and it shows up later as falls, fractures, and lost independence. Investing ahead of time changes that trajectory.

Medication is a real adjunct, and it has to be paired with strategies that protect lean tissue. GLP-1 receptor agonists produce substantial weight loss, and a meaningful fraction of that loss is lean mass. Adequate protein and resistance training are the mitigation strategies with actual evidence behind them, and body composition deserves monitoring wherever it is available rather than weight alone.

As clinicians, we need to screen past BMI. Ask about physical activity. Get a functional measure. Consider dietary adequacy. Refer to dietitians, physical therapists, or trainers where it helps, and even a single session with a trainer improves safety and confidence with resistance work. Set goals patients can hold: one to two pounds a week of fat loss while protecting muscle.

Obesity treatment is chronic care. The point is helping patients hold strength, mobility, and independence while metabolic health improves, and preserving muscle sits at the center of that.

Scott Rennie, D.O.

References:

1. Cruz-Jentoft AJ, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019;48(1):16-31. https://pubmed.ncbi.nlm.nih.gov/30312372/

2. Srikanthan P, Karlamangla AS. Muscle mass index as a predictor of longevity in older adults. Am J Med. 2014;127(6):547-553. https://pubmed.ncbi.nlm.nih.gov/24561114/

3. Paddon-Jones D, et al. Protein and healthy aging. Am J Clin Nutr. 2015;101(6):1339S-1345S. https://pubmed.ncbi.nlm.nih.gov/25926511/

4. Bauer J, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013;14(8):542-559. https://pubmed.ncbi.nlm.nih.gov/23867520/

5. Shailendra P, et al. Resistance Training and Mortality Risk: A Systematic Review and Meta-Analysis. Am J Prev Med. 2022;63(2):277-285. https://pubmed.ncbi.nlm.nih.gov/35599175/

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.

What Is MASLD? The New Name for Fatty Liver Disease

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

Liver disease is showing up more often, and it tracks closely with rising rates of obesity, diabetes, and metabolic syndrome. What many of us trained calling “fatty liver” or NAFLD has been renamed and reframed. The term now is MASLD, metabolic dysfunction-associated steatotic liver disease, and it reflects a better understanding of what actually drives the condition.

Why the change? NAFLD was a definition by exclusion. It told you the disease was not caused by alcohol without saying what it was. It also excluded patients with both alcohol and metabolic drivers, and the word “fatty” carried stigma that most patients felt immediately. In 2023 a multisociety Delphi process involving 236 panelists from 56 countries settled on the new nomenclature. Sixty-six percent of respondents found “fatty” stigmatizing and 61% said the same of “nonalcoholic.” The new definition requires at least one of five cardiometabolic risk factors, and it added MetALD for patients with metabolic dysfunction who also drink significantly (Rinella et al., J Hepatol, 2023).

MASLD is common. Roughly 30% of U.S. adults are affected. Among people with diabetes that figure climbs above 60%, and up to 15% carry advanced fibrosis (Le et al., Clin Mol Hepatol, 2022). Worldwide it is projected to overtake hepatitis C and alcohol as the leading cause of cirrhosis, hepatocellular carcinoma, and liver transplant.

The liver isn’t where most of these patients die. Cardiovascular disease is the leading cause of death in MASLD. The same inflammatory and metabolic pathways that damage the liver drive atherosclerosis. Diabetes worsens MASLD and MASLD worsens diabetes. The relationship runs in both directions.

One point matters more than any other: liver enzymes are a poor marker of severity. Normal ALT and AST are entirely compatible with advanced fibrosis. Fibrosis stage is what predicts progression, complications, and mortality. In a meta-analysis of 4,428 patients, all-cause mortality rose with each fibrosis stage, reaching a relative risk of 3.42 at stage 4 compared with stage 0, and liver-related mortality reached 11.13 (Taylor et al., Gastroenterology, 2020; Ekstedt et al., Hepatology, 2015). That is why guidelines now point everything at fibrosis assessment.

In primary care, FIB-4 is the practical first step. Age, AST, ALT, and platelet count. Under 1.3 suggests low risk and those patients can generally stay in primary care. Above 2.67 means high risk and warrants hepatology referral. Intermediate scores land in a gray zone that usually needs imaging such as FibroScan or a blood-based marker like the ELF test. FibroScan is fast and non-invasive but loses accuracy in patients with obesity, which is a real limitation given who has this disease. MR elastography is the most accurate option and the least available.

Treatment still starts with lifestyle. Weight loss of 5 to 10% improves steatosis and inflammation. The Mediterranean pattern is consistently associated with lower liver fat and better insulin sensitivity. Exercise at 150 minutes a week of moderate activity reduces liver fat even without weight loss, which is worth telling patients who are discouraged by the scale. Cutting sugar-sweetened beverages and limiting fructose is standard advice. Coffee earns its reputation here: a meta-analysis of observational studies found coffee consumption associated with 35% lower odds of significant fibrosis, with three or more cups a day the threshold most often cited, caffeinated or not (Hayat et al., Nutrients, 2021).

Medication options are expanding. Vitamin E has histologic benefit in non-diabetic patients with biopsy-proven MASH, though long-term safety concerns persist. Statins remain badly underused and are safe in MASLD, and they should be prescribed for cardiovascular risk reduction (Kargiotis et al., World J Gastroenterol, 2015). GLP-1 receptor agonists reduce liver fat and support weight loss.

In March 2024, resmetirom became the first FDA-approved drug for MASH with fibrosis. It is a liver-directed thyroid hormone receptor-beta agonist. In the phase 3 MAESTRO-NASH trial, MASH resolution without worsening fibrosis occurred in 25.9% of patients on 80 mg and 29.9% on 100 mg, against 9.7% on placebo, and both doses beat placebo on fibrosis improvement (Harrison et al., NEJM, 2024). It is approved for adults with non-cirrhotic MASH and stage F2 to F3 fibrosis. Those response rates are meaningful and they are also modest, and patients should hear both halves.

Endoscopic and surgical options matter too. Endoscopic sleeve gastroplasty and intragastric balloons reduce liver fat and improve fibrosis. Bariatric surgery remains among the most effective interventions available, with a systematic review and meta-analysis finding NASH resolution in roughly half of patients and fibrosis improvement in about a third (Lee et al., Clin Gastroenterol Hepatol, 2019).

MASLD management has moved well outside hepatology. It needs primary care, cardiology, endocrinology, nutrition, and gastroenterology working the same problem. Screen at-risk patients with FIB-4, particularly those with diabetes or obesity. Counsel on weight and diet. Prescribe statins when indicated. Refer for advanced assessment when fibrosis is suspected.

MASLD reframes liver disease as part of the broader cardiometabolic picture. Treating it means protecting the liver while cutting cardiovascular risk, improving glycemic control, and addressing systemic inflammation. That is where the impact lives.

Scott Rennie, D.O.

References:

1. Rinella ME, Lazarus JV, Ratziu V, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. J Hepatol. 2023;79(6):1542-1556. https://pubmed.ncbi.nlm.nih.gov/37364790/

2. Le MH, et al. Global incidence of non-alcoholic fatty liver disease. Clin Mol Hepatol. 2022;28(4):841-850. https://pubmed.ncbi.nlm.nih.gov/36117442/

3. Taylor RS, et al. Association Between Fibrosis Stage and Outcomes of Patients With Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis. Gastroenterology. 2020;158(6):1611-1625.e12. https://pubmed.ncbi.nlm.nih.gov/32027911/

4. Ekstedt M, et al. Fibrosis stage is the strongest predictor for disease-specific mortality in NAFLD after up to 33 years of follow-up. Hepatology. 2015;61(5):1547-1554. https://pubmed.ncbi.nlm.nih.gov/25125077/

5. Hayat U, et al. Effect of Coffee Consumption on Non-Alcoholic Fatty Liver Disease Incidence, Prevalence and Risk of Significant Liver Fibrosis: Systematic Review with Meta-Analysis of Observational Studies. Nutrients. 2021;13(9):3042. https://pubmed.ncbi.nlm.nih.gov/34578919/

6. Kargiotis K, et al. World J Gastroenterol. 2015;21(25):7860-7868.

7. Harrison SA, et al. A Phase 3, Randomized, Controlled Trial of Resmetirom in NASH with Liver Fibrosis. N Engl J Med. 2024;390(6):497-509. https://pubmed.ncbi.nlm.nih.gov/38324483/

8. Lee Y, et al. Complete Resolution of Nonalcoholic Fatty Liver Disease After Bariatric Surgery: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2019;17(6):1040-1060.e11. https://pubmed.ncbi.nlm.nih.gov/30326299/

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.

Weight Loss Surgery Risks and How to Lower Them

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

Bariatric surgery has become one of the most effective treatments for obesity and its complications. Roux-en-Y gastric bypass and sleeve gastrectomy are performed more often now as safety has improved and demand has grown. Surgery is still surgery, and the risks are worth knowing in detail.

The numbers are encouraging. In the LABS Consortium multicenter prospective study, 30-day mortality was 0.3% across 4,776 patients, and major adverse events including venous thromboembolism, reoperation, or extended hospitalization occurred in 4.3% (LABS Consortium, NEJM, 2009). For context, that mortality rate sits below several common major operations. Vigilance still matters, particularly in patients with prior VTE, untreated sleep apnea, poor functional status, or very high BMI.

Among early complications, leaks are what surgeons and patients fear most. Anastomotic leaks occur in about 1% of gastric bypass patients and 2 to 5% after sleeve gastrectomy (Sakran et al., Surg Endosc, 2013; Rosenthal et al., Surg Obes Relat Dis, 2012). Median time to diagnosis is around a week, which usually means the patient is already home. Treatment ranges from drainage and stents to reoperation. Endoscopic vacuum therapy is a newer approach with reported success rates up to 90% (Markus et al., Langenbecks Arch Surg, 2022).

Thrombosis is the other serious early risk. Deep vein thrombosis and pulmonary embolism account for a large share of postoperative deaths, and 70 to 80% of cases occur after discharge (O’Connor et al., Surg Obes Relat Dis, 2021). That timing is the whole problem. There is no universal agreement on extended prophylaxis, and weight-based dosing with enoxaparin is often considered for high-risk patients. Portal vein thrombosis is less common and has been reported almost exclusively after sleeve gastrectomy. These patients present with abdominal pain and are treated with anticoagulation (Parikh et al., Surg Obes Relat Dis, 2017).

Obstruction is a particular concern in bypass patients. Small bowel obstruction can follow adhesions, hernias, or clots, and internal hernias are the tricky ones. Symptoms may be vague, intermittent pain or nausea, or they may present as a full obstruction. Missing it leads to bowel ischemia. A high index of suspicion is the only real defense.

Nutritional problems arrive later and cause real harm when overlooked. Thiamine deficiency can produce Wernicke’s encephalopathy with confusion, ataxia, and nystagmus, and it develops in patients with vomiting or poor intake. Deficiencies in iron, calcium, vitamin D, and B12 are common. Routine supplementation and lab monitoring at three months, six months, and annually thereafter are the standard for good reason (Makarewicz et al., Obes Surg, 2007).

Weight regain is a reality rather than a failure. Roughly one in five patients regains some weight after gastric bypass. Sometimes the cause is behavioral, sometimes anatomical. Either way it is a signal to look more closely, and revisional surgery can be appropriate depending on anatomy and history.

For clinicians, the practical question is when to send a patient back to their bariatric team. Persistent abdominal pain, food intolerance, unexplained weight regain, or concerning deficiencies should all prompt referral. Imaging, endoscopy, or revision may follow.

Bariatric surgery can transform a patient’s life and substantially improve comorbidities. The benefits come attached to responsibilities: careful preoperative evaluation, surgical expertise, and long-term follow-up. Patients do best when both they and their providers understand what can go wrong and stay alert for the early signs.

Scott Rennie, D.O.

References:

1. Longitudinal Assessment of Bariatric Surgery (LABS) Consortium. Perioperative safety in the longitudinal assessment of bariatric surgery. N Engl J Med. 2009;361(5):445-454. https://pubmed.ncbi.nlm.nih.gov/19641201/

2. Sakran N, et al. Surg Endosc. 2013;27(1):240-245.

3. Rosenthal RJ, et al. International Sleeve Gastrectomy Expert Panel Consensus Statement. Surg Obes Relat Dis. 2012;8(1):8-19. https://pubmed.ncbi.nlm.nih.gov/22248433/

4. O’Connor EA, et al. Surg Obes Relat Dis. 2021;17(7):1218-1225.

5. Parikh M, et al. Surg Obes Relat Dis. 2017;13(11):1835-1839.

6. Markus PM, et al. Langenbecks Arch Surg. 2022;407(3):1039-1047.

7. Makarewicz W, et al. Wernicke’s syndrome after sleeve gastrectomy. Obes Surg. 2007;17(5):704-706. https://pubmed.ncbi.nlm.nih.gov/17658034/

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 Options for Obesity Explained

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

Weight loss surgery, also called bariatric or metabolic surgery, is one of the most effective treatments available for severe obesity. Gastric bypass and sleeve gastrectomy are safer now than they have ever been, and demand keeps climbing. Surgery carries risk and requires a long-term commitment, and both belong in the conversation from the first visit.

Obesity affects more than 100 million U.S. adults, roughly 40.3% of the adult population, with 9.7% in the severe range (NCHS, NHANES August 2021 to August 2023). Type 2 diabetes, cardiovascular disease, cancer, and early death all track with excess weight. Lifestyle programs and medications help, and for many patients the results don’t hold. That is the gap surgery fills. The Swedish Obese Subjects study followed patients for over a decade and found surgery produced durable weight loss and lower mortality (Sjöström et al., NEJM, 2007), and a retrospective cohort found a 40% reduction in all-cause mortality after gastric bypass (Adams et al., NEJM, 2007).

So who qualifies? Under the 2022 ASMBS and IFSO guidelines, surgery is recommended for people with BMI over 35 regardless of comorbidity, and for BMI 30 to 34.9 in patients with metabolic disease that has not responded to medical therapy (Eisenberg et al., Surg Obes Relat Dis, 2022). That is a meaningful loosening from the 1991 NIH thresholds most clinicians still carry in their heads. There is no strict age cutoff, though surgeons approach adolescents and older adults with extra care.

Before surgery, patients go through a thorough workup: nutrition and psychology evaluations, cardiac and pulmonary assessment, sometimes a sleep study and endoscopy. Smoking cessation is required. Most insurers still ask for documentation of six months of supervised weight management, a requirement with no good evidence behind it that delays care for people who need it. That time does get used for preparation and education, which is the one argument in its favor.

Several procedures are available. Sleeve gastrectomy is the most common worldwide. About 80% of the stomach is removed, limiting intake and changing hunger hormones. Patients typically lose 55 to 60% of excess weight. The operation is shorter than bypass and hospital stays run one to two days. Worsening reflux is the main downside (Peterli et al., JAMA, 2018).

Roux-en-Y gastric bypass has decades of long-term data behind it. A small pouch connects to the small intestine, bypassing part of the digestive tract. Average weight loss runs 60 to 70% of excess weight, diabetes remission rates are high, and reflux often improves. Risks include vitamin deficiencies, marginal ulcers, and internal hernias (Higa et al., Surg Obes Relat Dis, 2011).

One anastomosis gastric bypass simplifies the technique and shows promising results for weight and comorbidities, with higher risk of bile reflux and deficiencies. Duodenal switch and SADI combine a sleeve with intestinal rerouting. These are the most powerful options for diabetes remission and weight loss and they demand the most careful long-term monitoring. Gastric banding is now rare. It once looked appealing because it was reversible and low-risk, and the weight loss proved modest while long-term reoperation rates ran high (Genco et al., Surg Obes Relat Dis, 2016).

The randomized evidence is strong. Trials by Mingrone, Schauer, and Ikramuddin all demonstrated higher diabetes remission with surgery than with medical therapy alone, and the Schauer and Mingrone cohorts held those differences out to five and ten years (Schauer et al., NEJM, 2012 and 2017; Mingrone et al., Lancet, 2015 and 2021; Ikramuddin et al., JAMA, 2018).

Weight regain happens. About one in five patients regains some weight after bypass, from changes in anatomy or lapses in eating and activity. Surgeons can offer revision: re-sleeving, converting sleeve to bypass, or tightening pouches. These get tailored to the individual.

Long-term success depends on follow-up. Regular labs, nutrition counseling, ongoing team support. Lifelong vitamin and mineral supplementation is required rather than optional. Behavioral support matters, because habits carry as much weight as anatomy over years.

Weight loss surgery is one of the most powerful tools we have for a disease that is otherwise progressive and difficult to manage. With careful preparation, modern technique, and sustained follow-up, patients see improvements in weight, health, and quality of life that few other interventions produce.

Scott Rennie, D.O.

References:

1. National Center for Health Statistics. Prevalence of Overweight, Obesity, and Severe Obesity Among Adults Age 20 and Older: United States, August 2021–August 2023. https://www.cdc.gov/nchs/data/hestat/obesity-adult-17-18/obesity-adult.htm

2. Sjöström L, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med. 2007;357(8):741-752. https://pubmed.ncbi.nlm.nih.gov/17715408/

3. Adams TD, et al. Long-term mortality after gastric bypass surgery. N Engl J Med. 2007;357(8):753-761. https://pubmed.ncbi.nlm.nih.gov/17715409/

4. Eisenberg D, et al. 2022 American Society for Metabolic and Bariatric Surgery (ASMBS) and International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO) Indications for Metabolic and Bariatric Surgery. Surg Obes Relat Dis. 2022;18(12):1345-1356. https://pubmed.ncbi.nlm.nih.gov/36280539/

5. Schauer PR, et al. N Engl J Med. 2012;366(17):1567-1576; and N Engl J Med. 2017;376(7):641-651.

6. Mingrone G, et al. Lancet. 2015;386(9997):964-973; and Lancet. 2021;397(10271):293-304.

7. Ikramuddin S, et al. JAMA. 2018;319(3):266-278.

8. Peterli R, et al. Effect of Laparoscopic Sleeve Gastrectomy vs Laparoscopic Roux-en-Y Gastric Bypass on Weight Loss in Patients With Morbid Obesity: The SM-BOSS Randomized Clinical Trial. JAMA. 2018;319(3):255-265. https://pubmed.ncbi.nlm.nih.gov/29340679/

9. Higa K, et al. Surg Obes Relat Dis. 2011;7(4):516-525.

10. Genco A, et al. Surg Obes Relat Dis. 2016;12(10):1783-1788.

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.