Ketone bodies are not a danger signal in themselves. They are an alternative fuel your liver makes from fat whenever available glucose runs low — which happens during an ordinary overnight fast and on any low-carbohydrate diet. The difference between controlled nutritional ketosis and diabetic ketoacidosis is not the presence of ketones. It is the absence of insulin. Insulin is the brake that stops fat breakdown at a certain point; when it is missing, production runs without a ceiling until the blood itself turns acidic. That is why a ketone reading of 1.5 mmol/L can be completely ordinary in one person and a warning in another — the difference is their situation, not the number alone.
This article explains what a ketone meter actually measures, why a blood sugar reading alone can miss a genuine emergency, and what to do on a "sick day" — the day on which most serious episodes begin. This is general health education, not a substitute for your doctor's advice, and never a reason to change a medication on your own.
What are ketone bodies, and why does your body make them every night?
When available glucose falls, the body's primary fuel source shifts from sugar to fat. The StatPearls review Biochemistry, Ketogenesis, hosted by the U.S. National Library of Medicine, puts it plainly: "The primary energy source shifts from glucose to fat during periods of fasting or starvation, when carbohydrate intake is markedly reduced." The liver takes free fatty acids and converts them into ketone bodies.
There are three, practically speaking:
- Beta-hydroxybutyrate (BHB): the most abundant and the most clinically important. In severe ketoacidosis it "accounts for up to 75% of circulating ketones."
- Acetoacetate: which is precisely what a urine strip measures — a detail we will return to, because it matters more than it sounds.
- Acetone: a minor by-product formed by spontaneous decarboxylation of acetoacetate and "largely exhaled." This is the source of the "fruity-scented breath" that appears on every emergency symptom list.
And unlike long-chain fatty acids, "ketone bodies readily cross the blood–brain barrier and serve as an energy source for the brain" — during extended fasting they become "the principal alternative substrate for cerebral ATP production." In other words, ketones are a smart survival mechanism, not a malfunction.
The real difference: insulin is the brake, not carbohydrate
The most common misunderstanding here is the assumption that ketoacidosis simply means "far too many ketones from cutting carbs." The physiology says otherwise. The StatPearls review on adult diabetic ketoacidosis describes the mechanism this way: "Insulin deficiency and increased counterregulatory hormones also lead to the release of free fatty acids into circulation from adipose tissue (lipolysis), which undergo hepatic fatty acid oxidation to ketone bodies (beta-hydroxybutyrate and acetoacetate), resulting in ketonemia and metabolic acidosis."
Note the order: insulin deficiency first. The ketogenesis review names insulin explicitly as "the principal inhibitor" of the process. As long as there is enough insulin — as there is in the overwhelming majority of people following a low-carbohydrate diet — ketone production reaches a ceiling and stops there. The review describes the normal state as one in which ketone bodies "are produced in moderate amounts and efficiently utilized by peripheral tissues," and pathological ketoacidosis as what happens when "production surpasses the rate of peripheral utilization," overwhelming the blood's buffering capacity.
So diabetic ketoacidosis is not "too much fat burning." It is a missing brake. Which is why it happens first and foremost in people with an absolute or near-absolute insulin deficiency.
So what are the numbers?
Numbers help, as long as we remember they are read inside a clinical picture and never alone.
Nutritional ketosis: a 2021 review in the Cleveland Clinic Journal of Medicine states that "blood ketone levels ranging from 0.5 to 3.0 mmol/L are expected in nutritional ketosis, with the upper end (1.5−3.0 mmol/L) being optimal."
Diabetic ketoacidosis: StatPearls defines it by four elements together — "Blood glucose levels greater than 250 mg/dL, an arterial pH of less than 7.3, a serum bicarbonate level of less than 15 mEq/L, and the presence of ketonemia or ketonuria."
The decisive elements are the second and third: the acidity and the bicarbonate. Nutritional ketosis moves neither. That is why conflating the two states is a physiological error, not merely a difference of degree. Practically, Cleveland Clinic publishes an action table for blood ketone readings: below 0.6 mmol/L is "normal" with no action needed; 0.6–1.5 is "low to moderate risk — contact provider"; 1.6–2.9 is "high risk — visit ER"; and more than 3.0 mmol/L is "very high risk — visit ER." That table is aimed primarily at people with diabetes, which explains why a reading of 2.0 can be unremarkable for someone on a ketogenic diet and alarming for someone with type 1 diabetes: same number, entirely different context.
Why looking at your blood sugar is not enough
This is the most practically useful idea in the article, and the least widely known. The familiar rule is "very high sugar equals ketone risk" — but there is a recognised clinical state that breaks that rule completely: euglycemic diabetic ketoacidosis, a full ketoacidosis while the meter reading looks close to normal.
In 2015 Diabetes Care, the journal of the American Diabetes Association, published a paper with a striking title: "Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, and Preventable Safety Concern With SGLT2 Inhibitors." The state was originally defined as "DKA with plasma glucose levels <300 mg/dL."
The mechanism makes sense once explained. SGLT2 inhibitors, a class of diabetes medication, work by excreting glucose in the urine — "ranging 50–100 g/day." That lowers blood sugar, which is the intent, but it simultaneously reduces available carbohydrate, so insulin falls and glucagon rises, ketone production climbs, and blood glucose stays in a reassuring-looking range. The StatPearls review describes the same effect: these drugs "lower insulin requirements but can promote lipolysis, ketogenesis, and glucagon secretion while reducing renal ketone clearance, thereby increasing plasma ketone levels."
The U.S. Food and Drug Administration issued a warning about this on 15 May 2015 covering "all the approved sodium–glucose cotransporter 2 (SGLT2) inhibitors," based on "20 clinical cases requiring hospitalization captured between March 2013 and June 2014."
And the triggers the paper itself lists are ordinary life: "Intercurrent illness, reduced food and fluid intake, reduced insulin doses, and history of alcohol intake."
The paper's practical conclusion is explicit. Patients should be taught to monitor "ketonuria/ketonemia when unwell regardless of glucose levels," to maintain vigorous fluid and carbohydrate intake, to avoid reducing insulin doses on their own, and to seek prompt medical attention if symptoms appear.
Blood test or urine strip — and why the strip can mislead you
Here is a small technical detail with a large practical consequence. Conventional urine strips rely on the nitroprusside test, which — per StatPearls — "only detects acetoacetate in blood and urine." But in acute ketoacidosis "the ketone body ratio (3-beta-hydroxybutyrate: acetoacetate) increases from a reference range of 1:1 to as high as 10:1."
In other words, the strip measures precisely the fraction whose share is shrinking at the moment you most need accuracy. The 2024 paper "Update on Measuring Ketones" in the Journal of Diabetes Science and Technology spells out the two awkward consequences:
- Early in an episode, "the delayed increase in acetoacetate early in DKA can underestimate the severity" — false reassurance at the worst possible moment.
- As the episode resolves, beta-hydroxybutyrate converts back to acetoacetate, so the urine reading rises "when it is actually resolving" — false alarm.
The paper therefore calls "blood testing of beta-hydroxybutyrate the preferred test for monitoring ketones," and recommends a blood ketone meter specifically for: all youth with type 1 diabetes and their parents, adults with type 1 diabetes at risk of DKA, users of SGLT2 inhibitors, people following ketogenic diets, and anyone with a history of recurrent DKA.
Cleveland Clinic adds a useful timing distinction: a blood test gives you your level now, while a urine test "can't tell you your body's current ketone levels, but they can tell you what your ketone levels were within the last few hours."
Sick-day rules: the day most episodes begin
A "sick day" is not a footnote here — it is where all the previous threads converge. Mayo Clinic explains why: "An infection or other illness can cause the body to make higher levels of certain hormones, such as adrenaline or cortisol." Blood sugar rises — sometimes even when appetite is poor and you are barely eating. Which explains a trap many people fall into: "I haven't eaten anything today, so why would I need my medication?"
The American Diabetes Association states the same rule: "the illness and stress from it causes your body to release hormones that raise blood glucose (blood sugar) levels." Its key practical guidance for sick days:
- Check ketones on a schedule. The ADA recommends "testing for ketones every four to six hours when you're feeling sick."
- Do not stop your medication on your own. The ADA places "How to adjust your insulin or oral medication, if you need to" among the things to agree with your care team in advance — meaning any adjustment is a planned medical decision, not an improvisation made mid-illness.
- Fluids first. "Be sure you're getting enough water—so drink plenty of it. If you're having trouble keeping water down, have small sips every 15 minutes or so throughout the day."
- Simple carbohydrates have a role here. The ADA recommends keeping them handy — "Having simple carbs handy like regular soda, Jell-O, or popsicles will help keep your blood glucose up" if it falls. This is a specific therapeutic exception for illness, not general dietary advice.
- Know when to call. Contact your doctor "if you are vomiting or have diarrhea more than three times over 24 hours or have had a fever over 101° for 24 hours."
Mayo Clinic adds a direct preventive note: "When you're ill or stressed, test your urine for extra ketones with a urine ketones test kit."
The signs that mean "get help now"
Mayo Clinic lists the symptoms of ketoacidosis roughly as they appear: "Being very thirsty. Urinating often. Feeling a need to throw up and throwing up. Having belly pain. Being weak or tired. Being short of breath. Having fruity-scented breath. Being confused."
It advises contacting a professional immediately if "You're throwing up and can't keep down food or liquid," if blood sugar stays high despite home treatment, or if urine ketones are moderate or high. Emergency care is warranted when blood sugar stays above 300 mg/dL, when ketones are present and no professional is reachable, or when several symptoms occur together.
Cleveland Clinic puts it more bluntly: "Go to the nearest hospital" for moderate or large ketone levels.
And to keep the risk in proportion without alarm: ketoacidosis is a genuine emergency, but a very treatable one. StatPearls notes that the discovery of insulin, together with antibiotics, "has led to a drastic decrease in mortality with DKA, down to 1%," while remaining higher ("greater than 5%") in older adults and those with concurrent life-threatening illness. The message is not fear. It is earliness.
The Saudi picture: the leading cause is preventable
In 2022, Annals of Saudi Medicine published "Diabetic ketoacidosis in Saudi Arabia: factors precipitating initial admission and readmission," a medical record review of 176 patients at a tertiary care centre in Jeddah covering January 2018 through December 2020.
The findings deserve a pause:
- The leading precipitant of a first admission was treatment nonadherence, at 55.1%, followed by infections and wounds at 31.8%, diet nonadherence at 25.6%, and a first presentation of diabetes at 16.5%.
- The readmission rate was 32.4%, with a median of 12 weeks between admissions.
- Among readmissions, insulin nonadherence rose to 73.7%.
The authors concluded: "Treatment nonadherence is the leading precipitating factor of DKA in our region. Patient education and counseling play a major role in addressing this preventable complication."
That is a rare sentence in medicine: the leading cause is not a gene or bad luck, but a dose not taken. Which is exactly what gives an article like this real practical value.
Who should pay closer attention?
- People with type 1 diabetes: the highest-risk group. Mayo Clinic identifies the greatest risk in those who "Have type 1 diabetes" and "Often miss insulin doses."
- Anyone taking an SGLT2 inhibitor: because blood sugar may not warn you. Checking ketones when unwell — regardless of the glucose reading — is the explicit recommendation.
- Anyone with diabetes considering a ketogenic diet: the Cleveland Clinic Journal of Medicine review is clear here. SGLT2 inhibitors should be "discontinued" before starting a ketogenic diet, while metformin is "generally considered safe to continue" and GLP-1 agonists "can be continued with close monitoring." It also warns that "euglycemic DKA is possible while following a ketogenic diet," and stresses that "diligent and more frequent blood glucose monitoring should be a mainstay." None of this is an argument against a ketogenic diet — it is precisely why, in someone with diabetes, it should be medically supervised.
- Pregnancy, prolonged vomiting or diarrhoea, and severe food restriction: Cleveland Clinic lists pregnancy, prolonged vomiting/diarrhoea, eating disorders and starvation among the causes of raised ketones.
Important: nothing here replaces your doctor's judgement. Do not start a ketogenic diet, and do not stop or adjust any medication — least of all insulin or an SGLT2 inhibitor — except on a decision from your care team.
Where does Bakery 8 fit into this?
No bread prevents ketoacidosis. We will say it plainly: this is a medical condition caused by insulin deficiency, its prevention and treatment are purely medical decisions, and no food — ours or anyone's — performs that role. There is no product that "lowers ketones" or "protects against acidosis."
There is exactly one honest thing we can say. For someone who has chosen — as a medical decision — a low-carbohydrate pattern, the difference between following it steadily and following it in bursts of deprivation is usually made by having alternatives whose ingredients they actually know. In our bread range, almond-flour samoli remains a daily option; our keto granola is a breakfast with a fixed ingredient list; and our sugar-free desserts cover the occasional gathering.
If you want the wider picture, our article on net carbs and how to count them covers the arithmetic side, and our article on the dawn phenomenon addresses another common question about morning glucose readings.
Frequently asked questions
Does a ketogenic diet cause ketoacidosis?
No — not in a person whose insulin secretion is intact. Nutritional ketosis typically sits between 0.5 and 3.0 mmol/L and does not change blood pH, whereas a diagnosis of ketoacidosis requires a pH below 7.3 and bicarbonate below 15 alongside high glucose and ketones. The difference is the absence of insulin, not the reduction of carbohydrate. The picture is different for someone with type 1 diabetes or on an SGLT2 inhibitor, which is why those cases are managed medically.
What is the difference between a blood ketone test and a urine strip?
A urine strip measures acetoacetate; a blood meter measures beta-hydroxybutyrate — the more abundant ketone in acute ketoacidosis, where the ratio rises from 1:1 to as high as 10:1. Blood testing is therefore the preferred method for monitoring, while a urine strip can give false reassurance at the start of an episode and false alarm as it resolves.
I have diabetes, I have a cold, and I'm not eating. Should I stop my medication?
That decision belongs to your doctor alone and should never be made on your own. What matters is knowing that blood sugar can rise during illness even when you eat little, because the body releases hormones such as adrenaline and cortisol that raise glucose. This is exactly why a sick-day plan — including any medication adjustment — is written with your care team in advance, not improvised during the illness.
Can my blood sugar be normal while I'm in ketoacidosis?
Yes. This is euglycemic diabetic ketoacidosis, originally defined by a plasma glucose below 300 mg/dL. It is associated mainly with SGLT2 inhibitors, and the U.S. FDA issued a warning about it in May 2015. That is precisely why guidance says to check ketones when unwell regardless of the glucose reading.
When does a ketone reading mean I should go to the emergency room?
Per Cleveland Clinic's table for people with diabetes: below 0.6 mmol/L needs no action; 0.6–1.5 means contact your provider; 1.6 and above means visit the emergency room. And with any fruity-scented breath, shortness of breath, or confusion, do not wait for a number.
What is the commonest cause of ketoacidosis in Saudi Arabia?
In the 2022 Jeddah study of 176 patients, the leading precipitant was treatment nonadherence at 55.1%, followed by infection at 31.8%. Among readmissions, insulin nonadherence rose to 73.7%. In other words, the most common cause is entirely preventable.
The practical takeaway
Ketones are not the enemy; they are a natural back-up fuel. What turns them dangerous is the absence of the insulin that caps their production. And because a blood sugar number may not warn you — especially on an SGLT2 inhibitor — the three habits that matter most are: know what your own normal ketone reading looks like, check it when you are ill regardless of your glucose, and have your sick-day plan written down with your doctor before you get sick.
And if a low-carbohydrate pattern is part of your plan, having everyday alternatives whose ingredients you know makes sticking to it easier. Browse Bakery 8 — healthy and delicious, from Riyadh, Saudi Arabia.
References
- Lizzo JM, Waseem M, et al. Adult Diabetic Ketoacidosis. StatPearls, NCBI Bookshelf, U.S. National Library of Medicine.
- Dhillon KK, Gupta S. Biochemistry, Ketogenesis. StatPearls, NCBI Bookshelf, U.S. National Library of Medicine.
- Cleveland Clinic. Ketones: What They Are, Function, Tests & Normal Levels.
- Cleveland Clinic. Ketones in Urine: Causes, Symptoms & Treatment.
- Cleveland Clinic Journal of Medicine. Ketogenic diets in the management of type 1 diabetes: Safe or safety concern? 2021;88(10):547.
- Taylor SI, Blau JE, Rother KI. Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, and Preventable Safety Concern With SGLT2 Inhibitors. Diabetes Care. 2015;38(9):1638.
- U.S. Food and Drug Administration. Drug Safety Communication on SGLT2 inhibitors and ketoacidosis, 15 May 2015 (as reported in the reference above).
- American Diabetes Association. Diabetes and Planning for Sick Days.
- Mayo Clinic. Diabetic ketoacidosis — Symptoms and causes.
- Huang J, Yeung AM, Bergenstal RM, et al. Update on Measuring Ketones. Journal of Diabetes Science and Technology. 2024.
- Alharbi AS, et al. Diabetic ketoacidosis in Saudi Arabia: factors precipitating initial admission and readmission. Annals of Saudi Medicine. 2022;42(2):119.
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