Lorazepam is not known to raise blood sugar in a clinically significant way. Hyperglycemia is not listed as a side effect on the FDA-approved label for Ativan (lorazepam), and no large studies have identified a direct, reliable blood-sugar-raising effect in people taking standard doses. That said, the relationship between benzodiazepines and glucose metabolism is more nuanced than a simple yes or no, especially if you have diabetes or are monitoring your blood sugar closely.
What the FDA Label Does and Doesn’t Say
The official prescribing information for lorazepam does not list high blood sugar, hyperglycemia, or any direct glucose-related disturbance among its adverse reactions. The metabolic side effects that are listed include changes in appetite, hyponatremia (low sodium), and changes in liver enzymes. This is notable because if lorazepam caused meaningful blood sugar spikes in a significant number of people, it would likely appear in post-marketing reports by now, given how widely the drug is prescribed.
So if you’re taking lorazepam occasionally for anxiety or a medical procedure and wondering whether it will throw off your glucose readings, the short answer is: it’s unlikely to cause a noticeable spike on its own.
How Benzodiazepines Interact With Insulin
Lab research does show that benzodiazepines can influence how the body handles sugar, though the effects are subtle and sometimes contradictory. In isolated pancreatic cells from rats, a natural compound that activates the same receptors benzodiazepines target was shown to inhibit insulin release in a dose-dependent way. Drugs that bind specifically to benzodiazepine receptors outside the brain (called peripheral receptors) reduced insulin secretion by slowing down cellular energy processes in those same lab studies.
However, lorazepam and similar drugs also relax muscles, and even brief reductions in muscle tension can change how efficiently your body clears sugar from the bloodstream. A clinical trial published in BMC Clinical Pharmacology that tested single doses of benzodiazepines in healthy volunteers noted this muscle-relaxant effect could theoretically alter insulin sensitivity and glucose disposal, though the researchers framed this as speculative rather than a proven clinical concern.
The takeaway from the lab data: benzodiazepines can nudge glucose metabolism in more than one direction. They may slightly reduce insulin release through one pathway while potentially improving glucose clearance through another. These opposing effects likely cancel each other out in most people at normal doses.
The Stress and Cortisol Connection
One indirect way lorazepam could affect blood sugar is through its impact on stress hormones. Cortisol, the body’s main stress hormone, signals the liver to release stored glucose. That’s why anxiety, poor sleep, and chronic stress can all push blood sugar higher, particularly in people with diabetes.
Lorazepam lowers cortisol output by calming the nervous system. Research published in Frontiers in Endocrinology found that lorazepam reduced overnight metabolic rate, likely by dampening cortisol secretion during sleep. For someone whose blood sugar runs high because of untreated anxiety or insomnia, this calming effect could actually help stabilize glucose levels rather than raise them.
This matters because the reason you’re taking lorazepam (anxiety, panic, insomnia) may itself be contributing more to blood sugar fluctuations than the medication does. Sustained anxiety keeps cortisol elevated, which keeps the liver dumping glucose into your blood. Treating the anxiety can sometimes improve glycemic control as a secondary benefit.
Masking Low Blood Sugar Symptoms
If you have diabetes, a more practical concern than high blood sugar is whether lorazepam could mask the warning signs of a low blood sugar episode. Hypoglycemia typically announces itself through trembling, a racing heart, sweating, and anxiety. Lorazepam suppresses several of these signals directly: it reduces tremor, slows heart rate, and blunts the anxious feeling that normally alerts you to dropping glucose.
Research published in Annals of Medicine and Surgery examined patients with benzodiazepine poisoning (overdose-level exposure, not normal doses) and found that these drugs can suppress the body’s normal adrenaline-driven response to falling blood sugar. One study of healthy adults showed that alprazolam, a related benzodiazepine, inhibited the hormonal alarm system that normally triggers a corrective sugar release when glucose drops too low. While this was studied with a different drug and at higher exposures, the mechanism is shared across the benzodiazepine class to varying degrees.
This doesn’t mean lorazepam at a normal prescribed dose will reliably mask hypoglycemia. But if you take insulin or medications that can cause low blood sugar, it’s worth being aware that your usual physical cues might be slightly dulled. Checking your glucose with a meter rather than relying solely on how you feel is a reasonable precaution.
What This Means if You Have Diabetes
For most people, lorazepam does not meaningfully raise blood sugar. It is not in the same category as medications with well-documented hyperglycemic effects, like corticosteroids or certain antipsychotics. You’re unlikely to see a dramatic change on your glucose monitor from a dose of lorazepam.
That said, individual responses vary. Some people with diabetes notice minor fluctuations when starting any new medication, partly because of changes in eating patterns, sleep quality, or physical activity that come along with it. If you track your blood sugar and notice a pattern after starting lorazepam, the explanation is more likely related to these secondary factors (sleeping more, eating differently, moving less due to sedation) than to a direct pharmacological effect on glucose.
The more relevant concern for people managing diabetes is the sedation itself. Lorazepam can make you drowsy enough to skip meals, delay snacks, or sleep through a scheduled glucose check, all of which matter more for day-to-day blood sugar management than the drug’s biochemistry.