Coming back to: Renal impairment: what the labelling says about dose

For anyone arriving from a search: the marked solution above is the direct answer, and the replies underneath it add the caveats that make it safe to use.

Hepatic impairment: less is known about dosing in significant liver disease than in kidney disease. Extreme caution applies because the liver metabolises a large fraction of many medications.

Disordered eating history: a history of anorexia nervosa, bulimia, or other eating disorders changes the risk-benefit calculation because appetite suppression might trigger relapse. This population requires specialist input.

On post #14 — agreed on the reasoning, with one qualification.

Hypoglycemia risk: in people already on insulin or sulfonylureas, adding a GLP-1 agonist requires insulin dose reduction and close monitoring for hypoglycemia. This is manageable with attention.

This follows post #16 rather than contradicting it.

Pregnancy and planning: these compounds are not approved for use in pregnancy. Planning windows (how long to wait before attempting pregnancy) are not formally established. Conservative approaches wait several months to allow clearance.

Renal impairment: the compounds are cleared renally to some degree. Dose adjustments might be needed in severe renal impairment. Consulting with a clinician familiar with renal dosing is prudent.

Older adults: sarcopenia risk is higher, polypharmacy is common, and the clinical trials did not enroll many people over 75. Extrapolating to very old people is extrapolating beyond the data.

Pancreatitis history: the compounds can rarely trigger pancreatitis. A history of pancreatitis makes monitoring for recurrence more important during titration.

Worth separating two things that post #19 runs together.

Practical note that does not fit anywhere else. Whatever you conclude from this topic, write down what you did and when. The single most useful thing in your own records is not any individual result; it is that they are dated and consecutive.

post #23 is right about the mechanism and I think understates the practical bit.

Medullary thyroid carcinoma history: an absolute contraindication because of the preclinical findings in rodent toxicology. The history (personal or family, especially multiple endocrine neoplasia type 2) is an important screening question.

Coming back to post #23, because the follow-up matters more than the original answer.

Gastroparesis: pre-existing severe delayed gastric emptying can worsen with compounds that slow it further. Discussion with a clinician is prudent if this history exists.

Disordered eating history: a history of anorexia nervosa, bulimia, or other eating disorders changes the risk-benefit calculation because appetite suppression might trigger relapse. This population requires specialist input.

Gastroparesis: pre-existing severe delayed gastric emptying can worsen with compounds that slow it further. Discussion with a clinician is prudent if this history exists.

post #27 answers the question as asked. The question underneath it is different.

Medullary thyroid carcinoma history: an absolute contraindication because of the preclinical findings in rodent toxicology. The history (personal or family, especially multiple endocrine neoplasia type 2) is an important screening question.

I read post #27 twice before replying, because I had assumed the opposite.

Pancreatitis history: the compounds can rarely trigger pancreatitis. A history of pancreatitis makes monitoring for recurrence more important during titration.

This follows post #27 rather than contradicting it.

For anyone arriving from a search: the marked solution above is the direct answer, and the replies underneath it add the caveats that make it safe to use.