Prediabetes: Signs, Diagnosis, and Treatment

Prediabetes is a condition in which blood sugar levels are higher than normal but not yet at the threshold for type 2 diabetes. It is not "mild diabetes," but a warning sign of an increased risk of progression to diabetes and cardiovascular disease. According to the American Diabetes Association (ADA), three validated tests are used to detect prediabetes: glycated hemoglobin, fasting plasma glucose, and a 2-hour oral glucose tolerance test. Each of these tests reflects different aspects of carbohydrate metabolism and can therefore identify different subtypes of the disorder. [1]

The practical value of diagnosis lies in timely intervention. Lifestyle changes, weight loss, regular exercise, and risk factor management can reverse the process or "freeze" it for a long time. Classic data from the Diabetes Prevention Program (DPP) show that behavioral interventions reduce the likelihood of diabetes over the long term; modern weight management medications (e.g., incretin agonists) provide additional protection in obese patients. [2]

Prediabetes is also important in children: childhood obesity and a family history delay the onset of carbohydrate metabolism disorders until adolescence. Children's guidelines emphasize risk-based screening: those with risk factors (overweight, family history, signs of insulin resistance) are screened. This allows for earlier adjustments to diet, activity, and sleep, preventing complications. [3]

Finally, prediabetes is a cardiometabolic marker: it is associated with dyslipidemia, hypertension, non-alcoholic (metabolically associated) fatty liver disease, and elevated inflammatory markers. This is why comprehensive strategies are so important: not only sugar, but also weight, blood pressure, lipids, sleep, and activity. Guidelines emphasize the need to consider the individual holistically, rather than "treating one test at a time." [4]

Code according to ICD-10 and ICD-11

The ICD-10-CM (USA) uses a group of codes under the section R73 "Impaired glucose tolerance". R73.03 (Prediabetes) is provided for prediabetes; next to it are R73.01 (Impaired fasting glucose) for impaired fasting glycemia and R73.02 (Impaired glucose tolerance) for impaired glucose tolerance. A number of countries outside the US still use the more general R73.09 (Other abnormal glucose); the choice of code depends on the local version of the classification and the wording of the conclusion. [5]

In ICD-11, prediabetes is classified as 5A40 "Intermediate hyperglycemia," which includes "prediabetes" and "impaired glucose regulation." If necessary, ICD-11 allows for post-coordination—the addition of codes for associated conditions (e.g., obesity, hypertension)—to more accurately describe a person's cardiometabolic profile. This approach better reflects reality: prediabetes rarely exists in isolation. [6]

Table 1. How to code prediabetes

Classification	Code	Name	When appropriate
ICD-10-CM	R73.03	Prediabetes	Prediabetes confirmed according to ADA criteria
ICD-10-CM	R73.01 / R73.02	Impaired fasting glucose/tolerance	When NGN or NTG is clearly documented
ICD-10 (other adaptations)	R73.09	Other abnormal glucose	If there is no specialized subcode
ICD-11	5A40	Intermediate hyperglycemia (including prediabetes)	Basic code; supplemented by post-coordination [7]

Epidemiology

Prediabetes is extremely common. The IDF Diabetes Atlas, 10th edition, estimates that approximately 541 million adults had impaired glucose tolerance in 2021—a surrogate for the "pool" of prediabetes (the proportions vary across countries due to methodologies and thresholds). In the 11th edition for 2025, the IDF focuses on the global rise in the burden of diabetes, reporting that nearly 1 in 9 adults already lives with diabetes; the "reservoir" of prediabetes is also growing. [8]

When converted to population estimates, this often amounts to 20-35% of adults, using the standard ADA thresholds and including all three criteria. The precise estimate depends on which tests predominate (glycated hemoglobin, fasting glucose, or 2-hour glucose): different tests identify different groups, which partially overlap. This explains why some countries have "more A1C prediabetes" and others "more IGT." [9]

Regional differences are significant. For example, in North America and the Caribbean, the IDF records high rates of diabetes (age-standardized prevalence of approximately 15%), and the proportion of undiagnosed individuals is up to 1 in 3; against this backdrop, prediabetes is naturally common. In developing regions, the problem of underdiagnosis is even more serious: people present to doctors already diagnosed with diabetes and complications, "skipping" the stage of early intervention. [10]

In adolescents, the prevalence of prediabetes is rising, following childhood obesity. ADA guidelines for children and adolescents strongly recommend risk-based screening in overweight and overweight groups with risk factors. Early detection is important not only because of the risk of diabetes but also because of associated conditions such as hypertension, dyslipidemia, and fatty liver disease. [11]

Reasons

The biological basis of prediabetes is insulin resistance and moderate pancreatic β-cell dysfunction. Energy excess and ectopic fat deposition in the liver and muscles disrupt insulin signaling; to maintain normal blood sugar levels, the body is forced to increase insulin secretion. Over time, the β-cells' ability to compensate declines, leading to fasting and/or post-exercise hyperglycemia. Modern standards view this as a continuum, not a "switch." [12]

Genetic predisposition increases the risk, but lifestyle plays a leading role. A high-calorie diet with an excess of ultra-processed foods, a sedentary lifestyle, lack of sleep, and chronic stress create "ideal conditions" for insulin resistance. Therefore, prevention and treatment are built around behavioral modification—interventions with the best benefit-to-cost ratio. [13]

In some people, the key triggers are medications (e.g., long-term glucocorticosteroid therapy), endocrine disorders (Cushing's syndrome), and obstructive sleep apnea. Early recognition and correction of these factors allows for the "release of the brakes" on carbohydrate metabolism and improvement without escalating therapy. [14]

In adolescents, the pubertal increase in insulin resistance is particularly significant, driven by weight gain, sedentary lifestyle, and family history. Here, early interventions to improve habits (family meals, sleep patterns, screen time, and physical activity) yield the greatest benefits—for both blood sugar and blood pressure/lipids. [15]

Risk factors

The main risk factors include obesity, especially abdominal obesity, low physical activity, and a family history of type 2 diabetes. The risk increases with age; however, prediabetes is increasingly being diagnosed in people under 40 years of age, due to lifestyle factors. Ethnic differences in risk are also important and are taken into account in screening recommendations. [16]

In women, a history of gestational diabetes and polycystic ovary syndrome are significant risk factors; in both sexes, obstructive sleep apnea, hypertension, and dyslipidemia are also significant risk factors. These conditions often occur together and mutually reinforce metabolic disturbances. [17]

A separate risk factor is medications (glucocorticosteroids, some antipsychotics), chronic inflammatory diseases, and liver disease. In pediatrics, signs include striae acanthosis nigricans, rapid weight gain, physical inactivity, and a family history of diabetes. [18]

Almost all risk factors are at least partially modifiable: a 5-10% weight loss, 150 minutes of moderate aerobic activity per week, and two strength training sessions significantly improve insulin sensitivity and metabolic profile. These are the basic "three pillars" of any prevention program. [19]

Table 2. Risk profile: what to pay attention to

Block	Adults	Children/teenagers
Anatomy	Abdominal obesity	Overweight/obesity, accelerated weight gain
Anamnesis	Familial type 2 diabetes, gestational diabetes, sleep apnea	Familial diabetes, physical inactivity
Related	Hypertension, dyslipidemia, hepatic steatosis	Acanthosis nigricans, hypertension
Medicines	GCS, atypical antipsychotics	Long-term GCS therapy (as indicated) [20]

Pathogenesis

Normally, insulin suppresses hepatic gluconeogenesis and helps muscles utilize glucose. In insulin resistance, these signaling pathways are disrupted: the liver continues to "release" glucose into the bloodstream, while the muscles are less able to uptake it. This leads to elevated fasting and postprandial blood sugar levels. Protein glycosylation (including hemoglobin) reflects average blood sugar levels over 2-3 months. [21]

Ectopic fat in the liver and muscles plays a key role: it triggers cascades of inflammation and endoplasmic reticulum stress, impairing insulin signaling. This explains the particular benefit of aerobic and strength training, which increases muscle "oxidative capacity" and reduces liver fat. [22]

Gradually, under chronic stress, β-cells lose their ability to compensate for insulin resistance—and this is the transition from prediabetes to diabetes. The rate of progression varies: in some people, prediabetes remains stable for years, while in others, it quickly progresses to diabetes—the rate is influenced by weight, activity, sleep, medications, and genetics. [23]

Adolescents experience the physiological effects of puberty, including insulin resistance and hormonal fluctuations, which increases vulnerability to excess calories and sedentary behavior. Therefore, family-based behavioral interventions are particularly effective during puberty. [24]

Symptoms

Most often, prediabetes is asymptomatic. A person feels normal until lab tests show "borderline" values. Occasionally, nonspecific complaints appear, such as fatigue, thirst, or frequent urination, but these are sufficient grounds to rule out the possibility of diabetes. This latent course is precisely what makes screening so important. [25]

Prediabetes is often "masked" by non-carbohydrate signs: elevated triglycerides, low high-density lipoprotein cholesterol, hypertension, and liver enlargement due to steatosis. These findings serve as a signal to check carbohydrate metabolism. [26]

In children, acanthosis nigricans is a marker—dark, velvety patches of skin in folds (neck, armpits), reflecting hyperinsulinemia. When combined with excess weight, these signs require laboratory confirmation of metabolic disorders. [27]

It's important to understand that a normal fasting glucose level does not rule out prediabetes if glycated hemoglobin or 2-hour post-exercise glucose are elevated. Therefore, if there is a suspicion, it is often necessary to combine tests to increase diagnostic sensitivity. [28]

Classification, forms and stages

Clinically, it is convenient to distinguish three "entrances" to prediabetes: elevated glycated hemoglobin (5.7-6.4%), impaired fasting glucose (100-125 mg/dL), and impaired glucose tolerance (2-hour OGTT 140-199 mg/dL). These subtypes overlap somewhat but are not completely identical; one person may have one criterion, another two, or all three. Each variant carries similar long-term risks. [29]

The stage can be described as a continuum: normal → prediabetes → diabetes. The speed of transition varies and depends on weight, activity, sleep, comorbid conditions, and interventions. For children and adolescents, the family and school environment are crucial – they determine whether healthy behavior will persist. [30]

Epidemiologically, prediabetes is often part of metabolic syndrome (obesity, hypertension, dyslipidemia, insulin resistance) and is also associated with fatty liver disease. Therefore, assessment and management are not limited to sugars; the entire cardiometabolic profile is considered. [31]

"Risk phenotypes" are sometimes used for clinical decision-making: a predominance of hepatic insulin resistance (high fasting glucose), muscle insulin resistance (high 2-hour glucose), or a mixed phenotype (elevated glycated hemoglobin). This can influence training and nutritional focus. [32]

Complications and consequences

The main threat of prediabetes is the development of type 2 diabetes mellitus with its micro- and macrovascular complications. However, risks begin already at the prediabetes stage: the likelihood of cardiovascular events, arterial hypertension, dyslipidemia, and hepatic steatosis increases. Therefore, delaying intervention "until diabetes sets in" is a strategy with predictably worse outcomes. [33]

DPP/DPPOS data show that even after 10-15 years, those participating in the behavioral program maintain a reduction in diabetes incidence; metformin also provides long-term benefit in some participants. Newer incretin-based weight management agents (e.g., tirzepatide) further reduce the likelihood of progression, especially in obese individuals. [34]

Prediabetes is associated with increased inflammation, coagulation disorders, and endothelial dysfunction—factors that directly impact vascular outcomes. This explains why managing blood pressure and lipids, smoking cessation, and sleep and activity are so important in prediabetes. [35]

In children, long-term prediabetes increases the risk of early-onset type 2 diabetes, hypertension, and fatty liver disease at a young age. Early family prevention is particularly effective and cost-effective in this area. [36]

When to see a doctor

All adults aged 35-70 who are overweight or obese should seek screening—this group is recommended for screening by the US Preventive Services Task Force (USPSTF, Class B). Screening is also warranted before age 35 in the presence of risk factors (family history, gestational diabetes, hypertension, dyslipidemia, sleep apnea). If the results are normal, a repeat screening is usually planned in 3 years. [37]

For children and adolescents, testing is recommended based on their risk profile: if they are overweight or have at least one risk factor (familial diabetes, signs of insulin resistance, ethnic factors, hypertension, or dyslipidemia). The choice of test and its frequency should be discussed with a pediatrician/endocrinologist. [38]

Seek immediate medical attention if you experience symptoms of hyperglycemia, such as thirst, polyuria, blurred vision, or unexplained weight loss. This could indicate progression to diabetes and requires laboratory confirmation. Also discuss evaluation if fatty liver disease, resistant hypertension, or sudden weight gain are detected. [39]

Reasons for an unscheduled visit include changes in medications (for example, starting glucocorticosteroids), as well as pregnancy and its planning: gestational diabetes increases the lifelong risk of prediabetes and diabetes. [40]

Diagnostics

Step 1. Who to test. Adults aged 35-70 who are overweight or obese are required; those under 35 and adolescents with risk factors. At the initial appointment, the doctor collects a family history, assesses body weight, waist circumference, blood pressure, and signs of insulin resistance (e.g., acanthosis nigricans). [41]

Step 2. Which tests to choose. Three equivalent approaches are acceptable: glycated hemoglobin, fasting plasma glucose, and a 2-hour glucose level after a standard 75-g oral glucose tolerance test. The choice depends on availability, clinical objectives, and patient characteristics (for example, if A1C results are inconclusive, an OGTT may be appropriate). [42]

Step 3. How to interpret the results. ADA prediabetes limits: A1C 5.7-6.4%, fasting glucose 100-125 mg/dL, 2-hour glucose 140-199 mg/dL. If the results are borderline, repeat testing on a different day or using a different method is recommended. Different tests detect different phenotypes, so discrepancies between them are not uncommon. [43]

Step 4. What else to check. Lipid profile, blood pressure, liver function (for steatosis), sleep assessment (screening for apnea) - all this helps to form a comprehensive plan. In obesity, non-invasive markers of liver fibrosis are discussed; in adolescents - behavioral factors and family habits. [44]

Table 3. Diagnostic thresholds for prediabetes (according to ADA)

Test	Norm	Prediabetes	Diabetes
Glycated hemoglobin	< 5.7%	5.7-6.4%	≥ 6.5%
Fasting glucose	< 100 mg/dL	100-125 mg/dL	≥ 126 mg/dL
2-hour glucose (OGTT)	< 140 mg/dL	140-199 mg/dL	≥ 200 mg/dL [45]

Differential diagnosis

Not all "borderline" hyperglycemia is prediabetes. Drug-induced hyperglycemia (glucocorticosteroids) can temporarily increase blood sugar; discontinuing or adjusting the dose sometimes results in normalization. Endocrinopathies (Cushing's syndrome, acromegaly) and rare genetic conditions can also mimic prediabetes and require specialist evaluation. [46]

Impaired glucose tolerance should be distinguished from established diabetes: if symptoms and high values are present, diabetes is immediately confirmed with an alternative test. In questionable cases, the test is repeated or an alternative method is used (for example, an OGTT for a "gray zone" A1C). [47]

It is important to consider anemias and hemoglobinopathies that can distort A1C, as well as conditions with accelerated red blood cell turnover (pregnancy). In such situations, relying on plasma glucose and OGTT is preferable. [48]

In adolescents, type 1 (autoimmune) and monogenic forms (MODY) should be considered if there is an atypical clinical presentation, sudden weight loss, ketosis/ketoacidosis, or a significant family history of early diabetes - in these cases, the tactics and prognosis are different. [49]

Treatment

The basis of treatment remains lifestyle changes: a calorie deficit, a predominantly whole food diet, and limiting ultra-processed foods and sugary drinks. A realistic goal is a 5-10% weight loss over 6-12 months. Even such a moderate reduction significantly improves insulin resistance, lipids, and blood pressure. The key is not a "perfect diet," but sustainable habits integrated into real life. [50]

Physical activity is the number one medicine. A minimum of 150 minutes of moderate aerobic exercise per week and two days of strength training are recommended. Strength training improves insulin sensitivity independent of weight loss; the combination with aerobics works better than either modality alone. A good starting point is walking and bodyweight exercises, then gradually progress. [51]

Sleep and stress are hidden regulators of blood sugar. Sleep deprivation and obstructive sleep apnea increase insulin resistance; if apnea is suspected (snoring, pauses in breathing, daytime sleepiness), screening and treatment (e.g., CPAP) are indicated. Sleep hygiene (7-9 hours, regular sleep) maintains glycemic control and enhances the effects of exercise and nutrition. These are inexpensive but effective interventions. [52]

For some patients, metformin is a suitable medication—a traditional option for people with prediabetes and high risk (obesity, young adults, women with a history of gestational diabetes). It reduces hepatic glucose production and improves insulin sensitivity; long-term benefit in reducing diabetes risk has been demonstrated in DPP continuation studies. Prescription is discussed individually, taking into account tolerability. [53]

Incretin drugs for weight control have been a significant breakthrough. Glucagon-like peptide 1 receptor agonists and dual agonists (such as tirzepatide) not only reduce weight in people with obesity and prediabetes but also dramatically reduce the risk of progression to diabetes. In three-year data, patients with prediabetes and obesity had a roughly 94% lower risk of progression compared to placebo, and nearly 99% remained diabetes-free—with adequate tolerance. This is not a "magic wand," but it is a powerful tool in high-risk patients. [54]

Dietary patterns are tailored to the individual. The Mediterranean diet is suitable for long-term adherence and improves cardiometabolic health; moderately low-carbohydrate plans may be useful for some people for appetite and weight control. Eating patterns vary widely across time periods; it is important that the chosen approach is sustainable and does not impair sleep and physical activity. [55]

Comorbidities are treated aggressively: target blood pressure and lipid levels, smoking cessation, and correction of fatty liver disease. This reduces cardiovascular risk independently of sugar levels. In real-world practice, it is the "combination" approach (weight + activity + blood pressure/lipids + sleep) that yields the greatest overall benefit. [56]

In people with severe obesity and failure of conservative therapy, metabolic surgery is considered. It improves glycemia and reduces the risk of developing diabetes by influencing weight, gut hormones, and insulin resistance. The decision is made by a multidisciplinary team with a benefit/risk assessment and mandatory long-term follow-up. [57]

Digital programs and group interventions (DPP models, feedback apps) help maintain motivation and discipline. They don't replace face-to-face contact, but they improve adherence—especially during the habit-forming phase. For adolescents, family and school involvement is critical: when the environment is supportive, results are better. [58]

Finally, the treatment plan must be reviewed every 3-6 months. If weight, lipids, blood pressure, and sugar levels do not improve, the strategy is adjusted: the volume/type of activity and diet are changed, weight control medications are discussed, sleep and medications that interfere with glycemia are monitored. A timely "reset" prevents disappointment and progression. [59]

Table 4. What each strategy provides

Approach	Expected effect	The key to success
-5-10% of body weight	Improvement of insulin resistance, lipids, and blood pressure	Realistic deficit, family support
150 min/week + 2 strength	↑ insulin sensitivity, ↓ liver fat	Step-by-step progression, enjoyment of the process
Metformin (as indicated)	Modest reduction in diabetes risk	Tolerability, regular monitoring
Incretins/tirzepatide (obesity)	Significant weight loss and risk of progression	Selection according to indications, monitoring of adverse events [60]

Prevention

Primary prevention is simple in its formula and complex in everyday life: move more often, eat more simply, sleep better. Add 20-30 minutes of walking per day and two strength training sessions per week, and you'll already be reducing insulin resistance and improving lipids and blood pressure. This program is especially effective when family involvement is involved: when household habits change, the results are easier to maintain. [61]

The "small steps" principle works: reduce portion sizes, replace sugary drinks with water, add vegetables to every meal, wear a pedometer, and increase your average daily steps. Any activity is better than no activity; start with something accessible and enjoyable (walking, cycling, swimming), and then gradually increase the difficulty. [62]

Sleep is a strategic goal of prevention. Regular 7-9 hours of sleep, consistent bedtimes and wake-up times, and control of evening light and screen time all make appetite and blood sugar regulation more predictable. If you snore or experience drowsiness, be sure to check for sleep apnea—sleep correction enhances the effects of nutrition and activity. [63]

Prevention in children is a family project: shared walks, limiting sugary drinks, access to sports at school and in the community, and routine medical checkups. The earlier habits are formed, the lower the risk of prediabetes and early diabetes in adulthood. [64]

Forecast

Without intervention, some people with prediabetes progress to type 2 diabetes within a few years. However, with weight loss, increased activity, and improved sleep, the prognosis is favorable: the risk of progression decreases, and the cardiometabolic profile improves. The first 3-6 months are the "golden window" for establishing sustainable habits. [65]

Long-term observations of DPP confirm the enduring benefits of behavioral programs, and modern weight management medications significantly enhance their effectiveness in people with obesity and high risk. This does not negate the importance of lifestyle: medications work better when combined with physical activity and mindful eating. [66]

In adolescents, the prognosis is determined by the degree of family involvement and school/community support. In this group, it is especially important to avoid stigma and "prohibitory" approaches—sustainable change comes from collaborative, realistic steps. [67]

Even small victories—minus 2-3 kg, an extra 30 minutes of walking a day—already shift risks in the right direction. It's not the "perfect diet" that makes the difference, but consistency and maintenance. [68]

FAQ

Is prediabetes diabetes?
No. It's a "threshold" condition with an increased risk of diabetes and vascular disease. But it's at this stage that interventions are most effective – diabetes can be delayed for a long time or even prevented altogether. [69]

Which test is best for screening?
The ADA recognizes three equivalent tests: glycated hemoglobin, fasting plasma glucose, and 2-hour glucose after OGTT. Different tests detect different phenotypes, so when in doubt, it's best to combine them. [70]

Is it possible to "cure" prediabetes without medication?
Yes. Weight loss, exercise, and normalizing sleep often lead to normoglycemia. For high-risk individuals, metformin is considered, as are modern weight control medications, which further reduce the risk of progression in obesity. [71]

How often should I retest if I'm currently at risk?
Typically, every 1-3 years if the risk is low, and annually if there are multiple risk factors or if there's progression of weight, blood pressure, or lipids. This decision is individualized with your doctor. [72]

Table 5. Algorithm of actions (briefly)

Step	What to do	For what
1	Assess risk (age, weight, medical history, blood pressure, lipids, sleep)	Determine the need for screening
2	Select a test (A1C, fasting, OGTT) and confirm at the “borderline”	Improve the accuracy of diagnosis
3	Create a plan: nutrition, activity, sleep, smoking cessation	Reduce insulin resistance
4	Consider pharmacotherapy for high risk/obese	Reduce the risk of progression
5	Control after 3-6 months and adjustments	Capture lasting changes [73]

Table 6. Who should receive special attention?

Group	Why
Women after gestational diabetes	High lifetime risk of prediabetes/diabetes
People with obesity and sleep apnea	Sleep increases insulin resistance
Adolescents with a family history	Early onset of disorders, environmental influences
Patients on GCS/atypical antipsychotics	Drug-induced hyperglycemia [74]

Table 7. What to monitor besides sugar

Parameter	Target
Body weight and waist circumference	-5-10% weight loss, waist reduction
Pressure	Achieving target values
Lipids (TG, HDL, LDL)	Normalization of the profile, therapy if necessary
Liver (steatosis/enzymes)	Early correction of MASLD risk factors [75]

Table 8. Codes and clinical thresholds

Block	Meaning
ICD-11	5A40 - intermediate hyperglycemia (prediabetes)
ICD-10-CM	R73.03 - prediabetes; R73.01 - NGN; R73.02 - NTG
ADA thresholds	A1C 5.7-6.4%; NGN 100-125 mg/dl; IGT 140-199 mg/dl
USPSTF Screening	35-70 years old if overweight/obese; then according to risk [76]