Between normal blood sugar and type 2 diabetes lies a grey zone where the disease is not yet installed but the machinery is already running. It is called prediabetes, and it concerns an estimated ten million people in France alone, most of them unaware. This is the phase where everything can still tip in either direction: towards declared diabetes, or back to normal glycaemia. The article on Xiao Ke and established diabetes covers the declared disease; this one stops at the window before it, the most profitable to work.
The continuum: from prediabetes to diabetes, without a break
Type 2 diabetes does not start at diagnosis. It starts ten to fifteen years earlier, when the pancreas begins compensating for a nascent resistance by producing more insulin. Fasting glycaemia stays normal at first because the compensation suffices. Then it climbs slowly: between 1.10 and 1.25 g/L fasting, or an HbA1c between 5.7 and 6.4 %, the panel falls into the prediabetic zone. The pancreas is then exhausting itself compensating, and diabetes sets in when it can no longer keep up.
This continuum explains why the diagnostic boundary is artificial: the same process (insulin resistance, fatty overload, low-grade inflammation) runs the whole way through; only the final number changes. It is also what makes the prediabetic phase precious: as long as the pancreas is not exhausted, the process remains reversible.
The early markers the standard panel misses
Fasting glucose alone arrives too late: it only rises once the compensation is already faltering. Three measurements precede it.
Fasting insulin and HOMA-IR. The HOMA-IR score (fasting insulin × fasting glucose ÷ 22.5) measures resistance before glucose has moved: a pancreas producing a lot to maintain a normal glycaemia is already in trouble. High fasting insulin with normal glucose is the first signal, years before prediabetes.
Postprandial glycaemia. The peak an hour and a half after a meal is often the first to overflow, while fasting glucose is still clean. A reading above 1.40 g/L two hours after a standard meal deserves attention, even with fasting glucose in range.
The triglyceride/HDL ratio. This simple ratio, available on any lipid panel, is a reliable proxy for insulin resistance: above 2 (in mmol/L), the odds that insulin is resisting are high. Triglycerides climbing while cholesterol stays put often tell the start of prediabetes.
Lipotoxicity: the mechanism that blocks insulin
Insulin resistance is not a mysterious exhaustion: it is a congestion. When subcutaneous fat cells overflow, free fatty acids drift towards organs not designed to store them: liver, muscle, pancreas. This ectopic fat (lipotoxicity) produces ceramides and diacylglycerols that physically jam the insulin signalling cascade inside the cell. Insulin knocks at the door, but the lock mechanism is gummed up by fat.
The liver is hit first: non-alcoholic fatty liver disease (the metabolic “foie gras”) precedes diabetes by years, and the article on fatty liver as Liver Damp-Heat describes that stage in detail. The TCM reading of the same process speaks of Spleen deficiency that engorges then inflames: insulin resistance read as Spleen deficiency is exactly this phase, before the Heat of Xiao Ke is lit.
Remission is possible: what DiRECT proved
In 2018, the British DiRECT trial changed the picture: putting recently diagnosed type 2 diabetics on a tightly controlled diet producing 10 to 15 kg of weight loss, nearly half the participants entered remission (normalised glycaemia off medication) at one year, and 70 % among those who had lost more than 15 kg. Remission corresponds to defatting the liver and pancreas: once lipotoxicity is lifted, insulin secretion resumes and sensitivity is restored.
The lesson of the protocol is clear: the more recent the diabetes, the earlier and larger the weight loss, the likelier remission. Prediabetes, sitting ten years upstream of that window, responds even better: the pancreas has not yet sustained lasting damage, and correcting the terrain alone suffices.
The dietary strategy: defat the liver, regulate the Centre
The nutritional approach to prediabetes is nothing exotic: simple discipline applied in the window where it pays most.
Reduce the real glycaemic load. Fast sugars (soft drinks, juices, refined bakery, puffed cereals) give way to slow-digesting foods: pulses, whole unrefined grains, vegetables, whole fruit. The glycaemic index provides the reading grid.
Separate the meals. Every snack relaunches an insulin surge that keeps the pancreas under pressure. Three clear meals, no grazing, then a twelve-to-fourteen-hour overnight window form the most effective rhythm. Intermittent fasting formalises that rhythm when it suits the terrain.
Cook, warm, regularise. In the TCM reading, prediabetes is a Spleen deficiency that is clogging: cooked and warm food (soups, congees, gentle stews) spares the digestive fire, and regular meal times stabilise the Centre’s Qi. Frankly reducing the cold-iced, the concentrated sweet and alcohol is the first gesture.
Walk after meals. A fifteen-minute post-prandial walk measurably lowers the glycaemic peak: the simplest gesture in the whole protocol, and one of the most effective. TCM would frame it as moving the Centre’s Qi downwards through gentle movement.
Frequently asked questions about prediabetes
Does prediabetes have to become diabetes?
No. The major intervention trials (Diabetes Prevention Program, DiRECT) show that progression is not a fate: a 5 to 7 % weight loss combined with 150 minutes of weekly activity more than halves the transition to diabetes, and full remission is possible. The prognosis depends on when you act.
What are the exact prediabetes thresholds?
Per WHO and ADA: fasting glucose between 1.10 and 1.25 g/L (6.1 to 6.9 mmol/L), or HbA1c between 5.7 and 6.4 %, or a 2-hour glucose between 1.40 and 1.99 g/L after a 75 g load. Below that, glycaemia is normal; above, it is diabetes.
Can you be prediabetic while slim?
Yes, and this is the “TOFI” phenotype (thin outside, fat inside): fat lodges in the liver and around the organs without thickening the silhouette. Waist circumference and the triglyceride/HDL ratio spot it where the scales miss it. Slimness is not a certificate of insulin sensitivity.
Does Xiao Ke correspond to prediabetes?
No: Xiao Ke describes declared diabetes with its three dissipations. Prediabetes corresponds in TCM to the earlier phase: the Spleen deficiency that is engorging, before Heat has consumed the Yin. This is the phase where Centre dietetics is most effective.
The window where the terrain still listens
Prediabetes is the only stage of the continuum where the disease can be entirely sent back by diet alone. Neither medication nor spectacular gestures: reduce the glycaemic load, separate meals, walk after eating, cook warm, and support the clogging Spleen. It is also the phase where Chinese dietetics of Spleen deficiency has most to offer, since the terrain is still functional. Once the threshold is crossed, you treat; before it, you correct.
In the Yin Shi app, the food sheets give each product’s glycaemic load and thermal nature: barley and mung bean tick the boxes of the engorging Centre, the post-meal walk those of Qi that must descend.
Further reading: insulin resistance read as Spleen deficiency, type 2 diabetes as Xiao Ke, the glycaemic index and the sweet flavour, inflammatory obesity, and intermittent fasting in TCM.
To go further
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