Case Spotlight

Great question. We have a pretty standard, stepwise approach to obesity in our practice:

1. Step one is to screen for binge eating disorder (https://psychology-tools.com/binge-eating-scale/). In addition to psychotherapy, the FDA has approved Vyvanse at a starting dose of 30 mg daily and a max dose of 70 mg daily for “moderate to severe” (18 or higher on the binge eating scale). I send these patients to a local psychologist who specializes in eating disorders and follow her advice on who might benefit from drugs in addition to psychotherapy. 
2. Step two is to modify or eliminate other medications that may be contributing to weight gain. The Endocrine Society lists glucocorticoids, beta-blockers, and antihistamines as nearly universally obesogenic, along with selected antidepressants, antipsychotics, diabetes meds, and progestin-only contraceptives. 
3. Step three is to screen for sleep disorders or other medical issues that may be contributing. OSA, in particular, is not only a consequence of weight gain but can itself contribute significantly to weight gain. An Epworth scale, STOP-Bang, or a sleep study are well worth it. If any signs at all of Cushing’s are present, like weight redistribution, skin thinning, or muscle weakness, it might be worthwhile to screen. The best screening tests are either a bedtime salivary cortisol level (worrisome threshold >145 ng/dl) or a 24-hour urine free cortisol level. A 1 mg overnight dexamethasone suppression (1 mg dex at bedtime, followed by a first-morning serum cortisol level, with a normal AM cortisol suppressed to <1.8 mcg/dL) is also an option, but it has more false negatives than the other tests. The dex suppression can’t be used if the patient is on an OCP due to the effects of estrogen on cortisol-binding globulin. Now that we have an FDA-approved med (Imcivree; setmelanotide) for Bardet-Biedl syndrome and POMC, PCSK1, or LEPR gene mutations, some advocate for more aggressively screening for those mutations in patients who have been morbidly obese since toddlerhood. Testing is available in some “panels,” like at https://blueprintgenetics.com/tests/panels/endocrinology/monogenic-obesity-panel/. But it’s so early I don’t have a great handle on how well different insurers cover this kind of testing. If your patient was not obese as a toddler, I would not order the testing. And Tesomet (Tesofensine + metoprolol) is now available as an orphan drug for hypothalamic obesity, but that diagnosis is generally pretty obvious post-CVA or head injury.
4. Step four is to determine if the patient qualifies for a program. For instance, if the patient has a fasting glucose of 100-125 mg/dl and/or an A1c level of 5.7-6.4% in conjunction with a BMI over 25.0 kg/m2, they qualify for the diabetes prevention program, a one-year behavioral program that’s pretty effective. The directory of CDC-recognized programs can be found here: https://nccd.cdc.gov/ddt_dprp/registry.aspx. The program has been shown to reduce the risk of progression to diabetes in pre-diabetic patients by roughly 60%, which is roughly twice as effective as metformin. If a patient doesn’t have binge eating or another medical condition predisposing to weight gain, has optimized their other medications, and doesn’t appear to qualify for the DPP, we advise the judicious use of meal replacements, avoidance of processed meats and sugar, incorporation of the Mediterranean diet, and a minimum of 150 minutes per week of physical activity at a target heart rate of 70% of predicted maximum HR (you can calculate the predicted max heart rate by 220-age). I’ve mostly moved away from low-carb diets, primarily because dietary fiber seems to be so important to the microbiome and diabetes risk. Instead, I’ve pivoted toward a diet composed primarily of foods in Group 1 of the NOVA Food Classification System (see: https://educhange.com/wp-content/uploads/2018/09/NOVA-Classification-Reference-Sheet.pdf). This strategy eliminates harmful, highly processed carbs while leaving fiber in the diet. Finally, it is worth determining if your patient is a good candidate for bariatric surgery. It’s the only intervention that improves mortality in obese patients; it reduces all-cause mortality by at least a third and probably more. Medicaid covers bariatric surgery for most people with a BMI >40 kg/m2 and anyone with a BMI >35 kg/m2 with at least one major comorbid condition, such as CHF, OSA or Pickwickian syndrome, HTN, pseudotumor cerebri, type 2 diabetes, CVD or PVD, pulmonary HTN, dyslipidemia resistant to meds, recurrent skin ulcerations, GERD, or OA. Many private payers have started covering procedures, too. I would not advocate for gastric banding; RYGB or gastric sleeve would be much preferred. Weight loss drugs are almost universally costly and only modestly effective (weight loss of 3.5-10%), so I’m less excited by them, but they’re still probably under-prescribed. Furthermore, people need to understand that we use weight medications just as we treat hypertension or dyslipidemia: with no expectation that the problem will spontaneously resolve and stop needing medications. There is no such thing as “kick-starting” weight loss. But if the patient understands that, we now have six FDA-approved meds for weight loss: Qsymia (phentermine/topiramate), Contrave (naltrexone/bupropion), Xenical (orlistat), Wegovy (high-dose semaglutide, the same molecule as Ozempic), Saxenda (high-dose liraglutide), and Plenity (cellulose and citric acid, which is arguably more of a device). Each has its plusses and minuses, and all are expensive, but again, I think they’re probably under-utilized overall. Let me know if I can help choose one for your patient. I hope that’s helpful. Please message me back if any of this is unclear or incomplete or if new issues come up with your patient’s care.