Our weekly Family Caregiver Support Group meets tonight, 7:00-8:00 PM ET. Join us on Zoom tonight at 7:00 PM ET: https://us02web.zoom.us/j/81284915200?pwd=UaA7f0AL0cQh8uXmMbqONkw4UDv9fU.1 Theme: making a daily plan that bends. Bring your Caregiver Daily Plan Checklist if you've tried it, or just bring yourself. 👉 https://www.skool.com/carecfa-community-7806/calendar Camera on or off. All members welcome. 💛

"Sick-day rules" center on never stopping insulin, more frequent glucose and ketone monitoring, aggressive hydration/carbohydrate intake, and temporarily holding certain oral/injectable agents that risk dehydration, AKI, lactic acidosis, or euglycemic DKA. The overarching principle for insulin-treated patients—especially type 1 diabetes—is that basal insulin must never be discontinued even when the patient is not eating, because counter-regulatory stress hormones drive hyperglycemia and ketogenesis regardless of oral intake.[1][2] Monitoring during illness - Check capillary glucose every few hours (roughly every 2-4 h, or every 6 h at minimum), and check blood or urine ketones at least twice daily in ketosis-prone patients.[1][3] - Maintain adequate fluids and carbohydrate intake; if unable to eat solids, substitute carbohydrate-containing fluids.[2][1] - Seek urgent care for persistent vomiting, inability to keep fluids down, reduced consciousness, significant ketosis, tachycardia, or hypotension—these signal impending DKA or volume depletion.[4][1] Insulin adjustment - Never stop basal insulin in type 1 diabetes (and insulin-requiring type 2), even with poor oral intake.[1][2] - For hyperglycemia/ketosis, increase insulin: consensus guidance recommends raising basal and bolus insulin by 10-20% based on glucose trends, with supplemental correction (rapid-acting) doses for ketones.[4][5] - For GI upset with reduced intake but feeling otherwise well, the prandial/bolus component may need reduction to avoid hypoglycemia while continuing basal.[5][2]

Stress raises blood glucose and worsens glycemic control in people with diabetes through both physiological and behavioral pathways, and chronic stress is also an independent risk factor for developing type 2 diabetes. Physiological mechanism. Acute stress activates the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis, releasing epinephrine and cortisol. Epinephrine increases hepatic glucose production and inhibits insulin secretion, while cortisol mobilizes energy stores, drives gluconeogenesis, reduces muscle glycogen synthesis, and suppresses insulin secretion — effects that onset within minutes and can last several hours.[1][2] In diabetes, the underlying insulin deficiency or insulin resistance prevents the normal return to glucose homeostasis, so these adaptive responses produce sustained hyperglycemia.[1] Glucocorticoids specifically induce insulin resistance across multiple tissues: upregulating hepatic gluconeogenic enzymes (PEPCK, G6Pase), impairing GLUT4-mediated glucose uptake in muscle and fat, and impairing β-cell function and GLP-1 insulinotropic effects.[3][4][5] Both hyper- and hypoglycemia risk. The ADA Standards of Care 2026 note that stressful events (illness, trauma, surgery) increase the risk of both hyperglycemia and hypoglycemia, and in severe cases may precipitate life-threatening hyperglycemic crises (DKA, hyperosmolar states) — particularly in patients with clinical complexity and polypharmacy.[6] Acute stress in the inpatient setting. Acute stress impairs glucose control in both type 1 and type 2 diabetes, and stress-related dysglycemia (hyper- or hypoglycemia) in the hospital predicts short- and long-term morbidity and mortality in critical illness.[7]

https://sinclair.hms.harvard.edu/research

https://docs.google com/document/d/1rB3ZapY1cKSj0hXAeFbo0gPEc1jr8cWM/edit?usp=sharing&ouid=118181092252632675507&rtpof=true&sd=true