Diabetes Does Not Begin When It Is Diagnosed. It Begins Years Earlier, as Prediabetes.

Case

Let us call him Markus. A 44-year-old father of two with an office job. He came to the appointment complaining of fatigue that did not go away even during holidays. In the afternoons, about an hour after lunch, his eyes would begin to close during meetings. He had put it down to work, sleep debt, and age: “I suppose this is normal at this age.”

There were other things too, but he had not even thought to mention them aloud: he began craving sweets in the afternoons, and hunger returned surprisingly soon after a meal. Over a couple of years, his waist had increased by one trouser size, even though his weight on the scale looked almost the same. Darker, slightly velvety skin had appeared in the fold at the back of his neck and in his armpits. He thought it was dirt that would not come off when washed.

None of these was alarming. That is precisely the problem with prediabetes: it does not hurt, it does not prevent you from living your life, and every symptom has an everyday explanation.

The Disease and Its Progression

Behind Markus’s fatigue was insulin resistance, and by the time it was measured, already prediabetes.

Insulin is a hormone that works like a key: it opens the doors of the cells so that the sugar circulating in the blood can enter the cells to be used as energy. In insulin resistance, the locks have become stiff. The key no longer turns properly, so the pancreas has to produce more and more insulin to open the same door.

This explains Markus’s symptoms one by one. Afternoon fatigue and sugar cravings: a rapid rise and fall in blood sugar after a meal can drain alertness and trigger hunger again. These symptoms are non-specific and do not prove anything on their own. An increasing waist circumference at the same weight: fat accumulates around the internal organs, which does not always show on the scale but worsens insulin resistance. Darkened, velvety skin folds (acanthosis nigricans): elevated insulin accelerates the growth of skin cells in the folds, and this is a recognised sign of insulin resistance [1]. It is more common in darker skin, which is why it is not always associated with glucose metabolism.

The most essential part of the story is the timeline. Insulin resistance does not develop overnight, nor does it correct itself. It develops slowly, often over many years, and the pancreas compensates by producing more insulin. As long as the compensation is sufficient, blood sugar remains normal and an ordinary blood sugar measurement reveals nothing [2]. Only when the pancreas becomes exhausted does fasting blood sugar begin to rise, and at that point the person is already at the threshold of prediabetes and then diabetes. If left untreated, prediabetes progresses to type 2 diabetes at an estimated rate of approximately 5–10% per year [3], and diabetes, in turn, damages the blood vessels, kidneys, retinas, and nerves over the years.

How, then, can prediabetes be distinguished from diabetes that has already developed? The honest answer is: not by symptoms. They overlap because they are the same process at different stages. The more severe symptoms that many people associate with diabetes—intense thirst, frequent urination, and unexplained weight loss—do not appear until blood sugar has already risen to the diabetic range and begins to spill into the urine [4]. In other words, by the time you feel them, you have often already crossed the threshold. Prediabetes and early type 2 diabetes are usually asymptomatic and are found through a blood test, not necessarily through sensations or symptoms [4]. The only way to know which side of the threshold you are on is therefore to measure it. This is precisely why subtle clues—fatigue, an increasing waist circumference, and skin changes—should be taken seriously even when they seem insignificant.

In Finland, approximately 424,000 people have type 2 diabetes, and approximately 24,000 new cases are diagnosed every year [5]. Behind these figures is an even larger group of people in the prediabetes stage, many of them without knowing it. Most concerningly, an increasing number of those developing the disease are under the age of 40 [5].

The Window

This is the core of the entire article, and it is good news: prediabetes is not a sentence but a reversible condition. Impaired glucose metabolism can return to normal. And here is an important addition: reversibility does not end abruptly at the threshold of diabetes. According to current knowledge, even type 2 diabetes that has already developed can go into remission, particularly at an early stage and with sufficient weight loss [6], [7]. It is therefore more a continuum than a wall: the earlier action is taken, the easier and more complete the recovery. Prediabetes is the easiest point on that continuum: a window lasting several years during which the disease is not merely stopped in its tracks but can be turned backwards.

This is not wishful thinking but measured science, and some of the decisive evidence is Finnish. In the Finnish Diabetes Prevention Study (DPS), more than 500 people with prediabetes were assigned either to conventional follow-up or to intensive lifestyle guidance. In the lifestyle group, the risk of developing diabetes decreased by 58% [8], and the benefit remained more than a decade later [9]. The same result has since been repeated in several countries and confirmed in recent meta-analyses [10]. In the Finnish FIN-D2D programme, a sustained weight loss of just 5% reduced the risk by approximately 69% [11].

And, importantly, recovery itself is protective. In a large follow-up study, those whose glucose metabolism returned to normal even once later developed diabetes 56% less often than those who remained at the prediabetes level, regardless of how the normal level was achieved [12]. More recent research has gone even further and begun to speak of remission of prediabetes as a treatment goal: when weight and, in particular, the fat accumulated around the internal organs decrease, insulin sensitivity is restored and glucose metabolism can normalise [13]. The goal is therefore concrete and measurable: a return to normal, and reaching that point is worthwhile even if it does not always last.

Three Concrete Things to Do if You Recognise Yourself in Markus

Measure the right thing at the right time. Ask your doctor for fasting blood glucose and HbA1c, or long-term blood sugar. If you have risk factors—abdominal obesity, diabetes in the family, or high blood pressure—these should be monitored regularly, not only once symptoms appear [4].

Strengthen your muscles: an underestimated but effective lever. Muscle is the body’s largest storage site for sugar. When muscles are used and developed, they take glucose from the bloodstream even without insulin, and insulin sensitivity improves. This has also been demonstrated in prediabetes [14]. Even a short brisk walk after a meal reduces the post-meal blood sugar spike [15]. The single greatest lever in studies is nevertheless weight loss; muscular work supports it.

The most surprising factor: sleep. Even a single poorly slept night weakens the body’s insulin sensitivity the following day [16]. Chronic sleep deprivation and untreated sleep apnoea are associated with impaired insulin sensitivity, so the cause of fatigue should also be sought at night, not only in blood sugar.

In-Depth Section

This section goes further than is usually possible during a 15-minute appointment, not because the basic formula is wrong, but because time is limited. These are additional perspectives to discuss with your own doctor.

Conventional screening looks at sugar. The problem is that sugar rises only late, when the pancreas has already begun to become exhausted. Insulin resistance may have developed silently for years before fasting blood sugar or HbA1c changes, because the pancreas compensates by producing more insulin [2]. The practical conclusion is not some new miracle measurement but early action: if diabetes runs in the family or the waist has increased, the values should be checked while you still feel well, not only after symptoms appear.

The use of fasting insulin and the HOMA-IR calculated from it as an early marker is also discussed in the research world. They are not included in official screening recommendations, and their reference values have not been standardised, so they should not be interpreted in isolation. However, they describe the same phenomenon: insulin reacts before sugar does.

Waist circumference instead of the scale. The most metabolically dangerous fat is visceral fat around the internal organs, which does not always show in body weight. A measuring tape often reveals more about insulin resistance than a scale.

The ethnic risk perspective. If your family roots are in South Asia, the risk is substantially higher and begins at a lower weight and at a younger age [17].

Note: Markus is a fictional example patient. The patient stories in the text are composites of typical situations encountered in medical practice and do not describe any single real person. The article provides general health information and does not replace a personal medical assessment.

References

The numbers refer to the citations in the text, in order of appearance.

[1] Kahn CR, Flier JS, Bar RS, et al. The syndromes of insulin resistance and acanthosis nigricans. Insulin-receptor disorders in man. N Engl J Med 1976;294(14):739–745. https://doi.org/10.1056/NEJM197604012941401 (PMID 176581) – original description: acanthosis nigricans as a sign of insulin resistance (elevated insulin → IGF-1 → keratinocyte growth). More recent confirmation alongside it: Acanthosis Nigricans. StatPearls [Internet], NCBI Bookshelf NBK431057 (updated 2023). https://www.ncbi.nlm.nih.gov/books/NBK431057/

[2] Tabák AG, et al. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet 2009;373:2215–2221. https://pubmed.ncbi.nlm.nih.gov/19515410/

[3] Tabák AG, Herder C, Rathmann W, Brunner EJ, Kivimäki M. Prediabetes: a high-risk state for diabetes development. Lancet 2012;379(9833):2279–2290. https://doi.org/10.1016/S0140-6736(12)60283-9

[4] Current Care Guideline: Type 2 Diabetes (updated 2024). The Finnish Medical Society Duodecim. https://www.kaypahoito.fi/khp00066

[5] Finnish Institute for Health and Welfare: Diabetes / Finnish Diabetes Register (2025). https://thl.fi/data-ja-tilastot/sairaudet-ja-hoidon-laatu/diabetes

[6] Riddle MC, Cefalu WT, Evans PH, et al. Consensus Report: Definition and Interpretation of Remission in Type 2 Diabetes (international expert group, ADA). Diabetes Care 2021;44(10):2438–2444. https://doi.org/10.2337/dci21-0034

[7] Lean MEJ, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): open-label, cluster-randomised trial. Lancet 2018;391:541–551 (2-year follow-up Lancet Diab Endocrinol 2019; 5-year extension 2024). https://pubmed.ncbi.nlm.nih.gov/29221645/

[8] Tuomilehto J, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001;344(18):1343–1350. https://doi.org/10.1056/NEJM200105033441801

[9] Lindström J, et al. Improved lifestyle and decreased diabetes risk over 13 years: long-term follow-up of the DPS. Diabetologia. https://pubmed.ncbi.nlm.nih.gov/23093136/

[10] Wang Y, et al. Effectiveness of Different Intervention Modes in Lifestyle Intervention for the Prevention of Type 2 Diabetes and the Reversion to Normoglycemia in Adults With Prediabetes: Systematic Review and Meta-Analysis of RCTs. J Med Internet Res. https://doi.org/10.2196/63975

[11] FIN-D2D: Long-term outcomes of lifestyle intervention in primary health care. 2021. https://www.sciencedirect.com/science/article/pii/S1751991821000425

[12] Perreault L, et al. Effect of regression from prediabetes to normal glucose regulation on long-term reduction in diabetes risk (DPPOS). Lancet 2012;379(9833):2243–2251. https://pubmed.ncbi.nlm.nih.gov/22683134/

[13] Sandforth A, et al. Mechanisms of weight loss-induced remission in people with prediabetes: post-hoc analysis of the Prediabetes Lifestyle Intervention Study (PLIS). Lancet Diabetes Endocrinol 2023;11(11):798–810. https://doi.org/10.1016/S2213-8587(23)00235-8

[14] Exercise training modalities in prediabetes: systematic review and network meta-analysis. Front Endocrinol. https://doi.org/10.3389/fendo.2024.1308959

[15] Engeroff T, Groneberg DA, Wilke J. After Dinner Rest a While, After Supper Walk a Mile? A Systematic Review with Meta-analysis on the Acute Postprandial Glycemic Response to Exercise Before and After Meal Ingestion. Sports Med 2023;53(4):849–869. https://doi.org/10.1007/s40279-022-01808-7

[16] Donga E, et al. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. J Clin Endocrinol Metab 2010;95(6):2963–2968. https://pubmed.ncbi.nlm.nih.gov/20371664/

[17] Caleyachetty R, Barber TM, Mohammed NI, et al. Ethnicity-specific BMI cutoffs for obesity based on type 2 diabetes risk in England: a population-based cohort study. Lancet Diabetes Endocrinol 2021;9(7):419–426. https://doi.org/10.1016/S2213-8587(21)00088-7