Clinical decision support that reasons like a nutrologist: diagnose malnutrition by GLIM, feed the refeeding-risk patient without harm, ladder obesity from lifestyle to GLP-1 to surgery, and choose enteral over parenteral when the gut works — with the decision rule and exactly what would change it. Built for verified physicians.
Two real nutrology questions, each reasoned the way HeyHippocrates answers: the skills fire, the answer is cited, the decision rule is explicit, and what's missing is flagged. Scroll to each.
A severely malnourished patient — BMI 14, almost no intake for two weeks — about to start nutrition — how do I feed safely?
This patient is at high risk of refeeding syndrome, so feed low and slow. Give thiamine before or with the first calories and continue it, and check and correct phosphate, potassium and magnesium at baseline. Start at a low caloric target — around ten kilocalories per kilogram per day — and advance gradually over several days while monitoring electrolytes daily. A falling phosphate is the hallmark; replace it aggressively and do not chase full calories early. Rushing to full feeds can be fatal.
Decision ruleRefeeding risk (severe malnutrition, low intake) → thiamine first + correct phosphate/potassium/magnesium; start low (~10 kcal/kg/day) and advance slowly over days; monitor electrolytes daily; falling phosphate is the hallmark, replace aggressively.
Not established from this alone — the degree of malnutrition, the electrolytes and the comorbidity change the rate.
A patient with a BMI of 34 and type 2 diabetes, lifestyle change alone insufficient — the next step?
This is obesity with a weight-related comorbidity, so add pharmacotherapy to a structured lifestyle program. An incretin-based agent is first-line and especially fitting with type 2 diabetes — a GLP-1 receptor agonist such as semaglutide, or the GLP-1/GIP agent tirzepatide — titrated with attention to gastrointestinal tolerance. Consider referral for metabolic surgery at a BMI of 35 or more with a comorbidity, or 40 or more without. Set metabolic and functional goals, and monitor rather than target a number alone.
Decision ruleObesity + comorbidity → structured lifestyle + pharmacotherapy; incretin first-line (GLP-1 like semaglutide, or GLP-1/GIP tirzepatide), apt with type 2 diabetes; metabolic surgery referral at BMI 35+ with comorbidity or 40+; goals metabolic and functional, monitor.
Not established from this alone — the comorbidity, the BMI and the tolerance change the agent and the referral.
Illustrative simulations. The physician always decides.
The exact questions your field searches for — answered in the format the knowledge base speaks: the answer, the decision rule, what's missing, and the source.
Screen every at-risk patient with a validated tool such as NRS-2002 or MUST, then diagnose with the GLIM criteria: at least one phenotypic criterion — unintentional weight loss, low body-mass index, or reduced muscle mass — plus one etiologic criterion — reduced intake or absorption, or disease-related inflammation. Grade the severity, and act, because malnutrition worsens every clinical outcome. Then build a nutrition-support plan matched to the route and the needs.GLIM · ESPEN
Decision ruleScreen (NRS-2002 / MUST) → GLIM diagnosis: one or more phenotypic (weight loss, low BMI, low muscle mass) + one or more etiologic (reduced intake/absorption, inflammation); grade severity; build a route-matched support plan.
Missing data: the screening score, the weight history and the inflammation change the diagnosis.
Identify the high-risk patient — very low body-mass index, little or no intake for days, prior low electrolytes, or chronic alcohol or diuretic use. Before feeding, give thiamine and correct phosphate, potassium and magnesium. Start feeding at a low caloric rate and advance slowly over days, monitoring electrolytes and replacing them as they fall — the drop in phosphate as insulin drives it intracellularly is the defining feature. Never withhold feeding entirely; feed cautiously and correct in parallel.NICE · refeeding
Decision ruleHigh risk (very low BMI, prolonged low intake, low electrolytes, alcohol/diuretics) → thiamine + correct phosphate/potassium/magnesium first; start low calories, advance slowly, monitor and replace daily; the phosphate drop defines it.
Missing data: the risk factors, the baseline electrolytes and the intake history change the plan.
Treat obesity as a chronic disease along a ladder. Everyone gets a structured lifestyle intervention — nutrition, physical activity and behavior. Add pharmacotherapy for a body-mass index of 30 or more, or 27 or more with a weight-related comorbidity, favoring the incretin agents (GLP-1 receptor agonists and GLP-1/GIP), which give the largest and most durable loss. Refer for metabolic and bariatric surgery at a body-mass index of 35 or more with a comorbidity, or 40 or more, which remains the most effective durable treatment. Match therapy to comorbidity and goals.obesity guidelines
Decision ruleLifestyle for all → pharmacotherapy at BMI 30+ (or 27+ with comorbidity), incretins preferred (GLP-1, GLP-1/GIP); metabolic surgery at BMI 35+ with comorbidity or 40+; match to comorbidity + goals.
Missing data: the BMI, the comorbidity and the response change the step.
When the gut works, use it: enteral nutrition is preferred whenever the gastrointestinal tract is functional and accessible, because it preserves gut integrity and carries fewer infectious and metabolic complications than parenteral. Reserve parenteral nutrition for a non-functioning or inaccessible gut — obstruction, short bowel, severe malabsorption or intolerance of adequate enteral feeding. Start nutrition support early in the at-risk patient, meet protein and energy targets progressively, and watch for refeeding when malnutrition is present.ASPEN
Decision ruleFunctional accessible gut → enteral (preferred, fewer complications, preserves gut); parenteral only for non-functioning or inaccessible gut (obstruction, short bowel, severe malabsorption, enteral intolerance); start early, advance to targets, watch refeeding.
Missing data: the gut function, the access and the tolerance change the route.
Your whole practice, one specialist brain — grounded in champion-authored, cited knowledge.
A generalist nutrology colleague across malnutrition, nutrition support, obesity, micronutrients, disease-specific nutrition and the metabolic patient — cited, non-directive, always with the decision rule.
Deep specialist agents for clinical nutrition support, obesity and metabolic medicine, micronutrient and deficiency medicine, and disease-specific nutrition — each its own soul and knowledge base — plus your own uploaded materials.
From the refeeding rate to the obesity agent the margin is thin. Only one of these reasons like a nutrology colleague whose every claim you can trace.
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Leave your name and work email. We'll reach out the moment nutrology opens — with your Founding Nutrologist offer.
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It reasons in the frameworks you use — the GLIM criteria, the refeeding-syndrome protocol, the obesity ladder and the enteral-versus-parenteral rule — and always shows the reasoning, the decision rule and what would change it. The decision always stays your call.
Both. Residents use it to pressure-test a plan and learn the decision rule; attendings use it as a fast, cited second opinion on the ward and in clinic. Access is gated to verified physicians.
Clinical nutrition support, obesity and metabolic medicine, micronutrient and deficiency medicine, and disease-specific nutrition each have their own deep specialist agent on the Pro plan, on top of the full nutrology scope on Basic.
No. It is physician-facing clinical decision support — a cited thinking partner. It does not diagnose, does not treat, and gives no patient-facing advice. The decision always stays with you.
Every answer is grounded only in champion-authored, cited nutrology knowledge — traceable, not hallucinated — and always states the decision rule plus what data is missing, instead of a confident guess.