Ketogenesis vs Ketosis vs Ketoacidosis: Which One Is Dangerous, and What Each Does to Your Eyes

By the Rose Optometry optometrist team, Hamilton. General information only — it does not replace advice from your GP or diabetes team. Numbered references are listed at the end.

Three similar-sounding words get mixed up constantly. In short: ketogenesis is the process of making ketones, ketosis is the state of having raised ketones in your blood, and ketoacidosis is the dangerous one — a medical emergency. Neither ketogenesis nor nutritional ketosis is harmful in itself in a person who makes enough insulin.

The three terms side by side

Ketogenesis: the process

Ketogenesis is the process by which the liver converts fatty acids into ketone bodies, mainly beta-hydroxybutyrate and acetoacetate, with a little acetone. Ketones are always present in the blood, and their levels rise during fasting and prolonged exercise [1]. Most investigators define a normal blood ketone level as below 0.5 mmol/L [1].

Ketosis: the state

When ketone production rises enough for ketones to accumulate, you are in ketosis. Nutritional ketosis is usually described as blood ketones of about 0.5 to 3 mmol/L, with blood glucose and blood pH staying normal [2]. (That range originates from a clinical textbook cited in the review, not from a trial.)

Insulin is the brake: the enzymes that drive ketogenesis are tightly controlled by circulating insulin, which inhibits ketone production [1]. In people who make enough insulin, this keeps ketones well below DKA levels — ketone levels in DKA are some five to ten times higher than in nutritional ketosis [2]. That protection does not apply to people with type 1 diabetes, people with insulin-deficient type 2 diabetes, or anyone taking an SGLT2 inhibitor medicine.

Ketoacidosis: the dangerous one

In DKA there is too little insulin to apply that brake. The 2024 international consensus report defines DKA by three things together: diabetes or a glucose of 11.1 mmol/L or above; beta-hydroxybutyrate of 3.0 mmol/L or above (or urine ketones 2+ or more); and a blood pH below 7.3 and/or bicarbonate below 18 mmol/L [3].

About 10% of people with DKA have near-normal glucose (euglycaemic DKA), and SGLT2 inhibitors account for most of those cases [3,4]. Very-low-carbohydrate diets and prolonged fasting are recognised risk factors for DKA in people taking SGLT2 inhibitors [3], and DKA has been reported in a person who started a ketogenic diet while taking one [5]. An international consensus advises that SGLT inhibitors should not be used by people on low-carbohydrate or ketogenic diets [6].

Warning signs described in the consensus report [3]:

• Passing a lot of urine, intense thirst, dehydration and weight loss
• Nausea, vomiting and abdominal pain
• Deep, laboured breathing with a fruity smell on the breath
• Drowsiness or a change in alertness

DKA is an emergency. If you have diabetes and these symptoms, call 111 or go to an emergency department.

Home ketone readings if you have diabetes

Published cut-offs differ, and all were written for people with type 1 diabetes, not for people in diet-induced ketosis. One international consensus, for adults with type 1 diabetes taking SGLT inhibitors, uses: below 0.6 mmol/L normal; 0.6 to 1.5 mmol/L raised; 1.6 to 3.0 mmol/L impending DKA; above 3.0 mmol/L probable DKA, seek immediate medical attention [6]. An earlier guideline uses 1.0 mmol/L as the level needing action and above 3.0 mmol/L for medical review [7]. Both agree on the upper figure. Your own diabetes team's sick-day plan takes priority over any general table.

What each one does to your eyes

Ketogenesis

Ordinary metabolism. We found no evidence of any effect on the eye.

Nutritional ketosis

We found no human clinical trial of ketosis or a ketogenic diet with eye outcomes. What exists:

• Animal research. In mice that spontaneously develop glaucoma, eight weeks of a ketogenic diet (0.1% carbohydrate) preserved more retinal ganglion cells and optic nerve axons than a control diet and partly preserved visual signalling to the brain, without changing eye pressure [8]. A companion study found less inflammation in the retina and optic nerve [9]. This is mouse data and cannot be assumed to apply to people.
• Human observational data. In three US cohorts totalling 185,638 people, low-carbohydrate diet scores were not associated with primary open-angle glaucoma (relative risk 1.13, 95% CI 0.91 to 1.39) [10]. This is not a test of ketosis: even the lowest-carbohydrate group took 37 to 43% of their energy from carbohydrate, and ketones were not measured [10].

So we do not recommend ketosis as a treatment for any eye condition, and we found no evidence that nutritional ketosis harms the eye.

Two practical points apply if a change of diet brings down glucose that has been high for a long time. Neither has been studied with ketogenic diets specifically; both come from studies of glucose-lowering treatment:

• Your glasses prescription can shift for weeks to months. In adults whose very high glucose was corrected, a temporary long-sighted shift appeared within about a week, peaked at around ten days (range 4 to 28), averaged about 1.5 dioptres (up to 3.75), and took 14 to 84 days to return to baseline [11]. In adolescents with newly diagnosed diabetes, recovery took up to 94 days [12]. The authors of the adult study note that glasses made during this period will not suit one or two months later [11]. The leading explanation, still a hypothesis, is fluid and sorbitol changes in the lens [11,12].
• Existing diabetic retinopathy can worsen temporarily. In the DCCT trial of type 1 diabetes, early worsening of retinopathy occurred in 13.1% of people on intensive treatment versus 7.6% on conventional treatment, with about half recovering by 18 months. The main risk factors were a higher starting HbA1c and a larger fall in it over the first six months. Lowering glucose more gradually was not shown to reduce the risk, and the long-term benefits of good control greatly outweighed the early worsening [13]. Over 6.5 years, intensive treatment cut the risk of developing retinopathy by 76% in people who started with none [14]. The practical step is a retinal check before, and in the months after, a major improvement in control [13,15].

Ketoacidosis

• Blurred vision around an episode. Blurred vision is not listed as a symptom of DKA itself in the consensus report [3]. Blur relates to the high glucose and its correction: the temporary long-sighted shift above follows treatment [11,12], while blur during high glucose is not always explained by a measurable change in focus [16].
• Temporary cataract, rarely. Sudden lens clouding, sometimes reversible, has been documented during treatment of DKA and hyperosmolar hyperglycaemia. The evidence is a small number of case reports, mostly in children and young adults [17].
• A link with later retinopathy, not proven to be causal. In a Taiwanese cohort of people with type 2 diabetes, those who had had DKA had a higher later risk of diabetic retinopathy (hazard ratio 1.64, 95% CI 1.34 to 2.01) [18]. The study had no HbA1c data, so poor long-term control may explain both. In 230 people with childhood-onset type 1 diabetes followed for about 20 years, ketoacidosis at diagnosis did not predict later retinopathy; lifetime HbA1c and duration of diabetes did [19]. Either way, anyone who has had DKA should have their retinal screening up to date.
• A rare, serious fungal infection. In a review of 929 reported cases of mucormycosis, 337 (36%) were in people with diabetes; ketoacidosis was documented in 48% of those with type 1 and 34% of those with type 2 diabetes, and 145 of the 337 had rhinocerebral disease, which starts in the sinuses [20]. In a review of 145 people with rhino-orbital-cerebral mucormycosis, 60% had diabetes and 30% had ketoacidosis. Among those with eye findings recorded, 67% had paralysis of the eye muscles, 65% reduced vision, 64% a bulging eye and 43% swelling around the eye; swelling around the eye or face and reduced vision were each present within the first three days in about a third [21]. Survival fell when treatment started more than six days after symptoms began [21]. In DKA, high glucose and acidity impair the white cells that fight the fungus, and acidosis frees iron that it uses to grow [22]. This applies to diabetic ketoacidosis and poorly controlled diabetes; none of this research links it to nutritional ketosis. New swelling or pain around one eye, a bulging eye, double vision or reduced vision in someone with poorly controlled diabetes needs same-day hospital assessment.

How to know which state you are in

You cannot tell by how you feel. A finger-prick blood ketone meter is the test to use if you are unwell. A continuous ketone monitor shows the trend through the day and night — see our guide to continuous ketone monitors; we stock the KS1 Continuous Ketone Monitor in our wearables range. A wearable sensor is for tracking patterns; it is not a tool for diagnosing or ruling out DKA. For the diet itself, see our keto diet guide, and for eye checks, diabetic retinopathy and diabetes eye checks.

Common questions

Is ketosis the same as ketoacidosis?

No. In nutritional ketosis blood pH and glucose stay normal [2]. In ketoacidosis the blood is acidic, by definition [3].

Can a keto diet cause ketoacidosis?

In people who make enough insulin, insulin restrains ketone production [1,2]. The documented risk is in people taking SGLT2 inhibitors [3,5,6] and in people who are insulin-deficient, who should not start a ketogenic diet without their diabetes team.

Is a keto diet good for your eyes?

That has not been tested in people. The supportive findings are from mice [8,9], and a large human study found no link between lower-carbohydrate eating and glaucoma risk [10].

How long should I wait for new glasses after my glucose changes?

Until your prescription is stable on repeat testing. In the studies above that took from two weeks to about three months [11,12].

References

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2. Gershuni VM, Yan SL, Medici V. Nutritional ketosis for weight management and reversal of metabolic syndrome. Curr Nutr Rep. 2018;7(3):97-106 (corrected 2025). doi:10.1007/s13668-018-0235-0
3. Umpierrez GE, Davis GM, ElSayed NA, et al. Hyperglycemic crises in adults with diabetes: a consensus report. Diabetes Care. 2024;47(8):1257-1275. doi:10.2337/dci24-0032
4. Peters AL, Buschur EO, Buse JB, et al. Euglycemic diabetic ketoacidosis: a potential complication of treatment with sodium-glucose cotransporter 2 inhibition. Diabetes Care. 2015;38(9):1687-1693. doi:10.2337/dc15-0843
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8. Harun-Or-Rashid M, Pappenhagen N, Palmer PG, et al. Structural and functional rescue of chronic metabolically stressed optic nerves through respiration. J Neurosci. 2018;38(22):5122-5139. doi:10.1523/JNEUROSCI.3652-17.2018
9. Harun-Or-Rashid M, Inman DM. Reduced AMPK activation and increased HCAR activation drive anti-inflammatory response and neuroprotection in glaucoma. J Neuroinflammation. 2018;15(1):313. doi:10.1186/s12974-018-1346-7
10. Hanyuda A, Rosner BA, Wiggs JL, et al. Low-carbohydrate-diet scores and the risk of primary open-angle glaucoma: data from three US cohorts. Eye (Lond). 2020;34(8):1465-1475. doi:10.1038/s41433-020-0820-5
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13. Diabetes Control and Complications Trial Research Group. Early worsening of diabetic retinopathy in the Diabetes Control and Complications Trial. Arch Ophthalmol. 1998;116(7):874-886. doi:10.1001/archopht.116.7.874
14. Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329(14):977-986. doi:10.1056/NEJM199309303291401
15. Bain SC, Klufas MA, Ho A, Matthews DR. Worsening of diabetic retinopathy with rapid improvement in systemic glucose control: a review. Diabetes Obes Metab. 2019;21(3):454-466. doi:10.1111/dom.13538
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19. Salardi S, Porta M, Maltoni G, et al. Ketoacidosis at diagnosis in childhood-onset diabetes and the risk of retinopathy 20 years later. J Diabetes Complications. 2016;30(1):55-60. doi:10.1016/j.jdiacomp.2015.10.009
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