Does High Blood Sugar Increase Blood Viscosity?
Yes, elevated blood glucose levels directly increase blood viscosity, with this effect observable even within normal glucose ranges and becoming progressively more pronounced as glucose levels rise into prediabetic and diabetic ranges. 1
Evidence for the Glucose-Viscosity Relationship
Direct Correlation in Non-Diabetic and Prediabetic Populations
The relationship between blood glucose and viscosity exists on a continuum, not just in overt diabetes:
Blood viscosity increases progressively across normal glucose ranges, with subjects having fasting glucose 100-125 mg/dL (prediabetes) showing significantly higher blood viscosity compared to those with glucose <90 mg/dL, even when blood pressure, lipids, fibrinogen, and plasma viscosity are similar. 1
Blood glucose correlates directly with blood viscosity measurements at all shear rates (r = 0.131-0.162), and this relationship persists even within glucose values traditionally considered "completely normal." 1
Blood viscosity at high shear rate (225 s⁻¹) is independently associated with blood glucose levels, suggesting glucose itself—not just associated metabolic factors—drives viscosity changes. 1
Mechanism: Hematocrit-Mediated Effects
The primary mechanism appears to involve glucose-induced changes in red blood cell properties:
Glucose causes red blood cell swelling when transported into cells via GLUT-1, leading to increased hematocrit and subsequently elevated blood viscosity at low shear rates. 2
This effect is specific to D-glucose (the biologically active form); L-glucose, which cannot be transported into red cells, produces no viscosity changes. 2
The process is reversible upon removal of excess glucose, indicating an acute osmotic effect rather than permanent cellular damage. 2
Impact of Glycemic Control
Improving diabetes control directly reduces blood viscosity:
Patients achieving better glycemic control (HbA1c decreasing from 12.6% to 9.1%) demonstrated significant reductions in plasma viscosity (1.31 to 1.25, p<0.001) and whole blood viscosity at both low (22.8 to 20.2, p<0.01) and high shear rates (3.4 to 3.1, p<0.01). 3
Plasma fibrinogen levels decreased with improved control (4.1 to 3.7 g/L, p<0.01), contributing to the viscosity reduction. 3
Hyperviscosity in diabetes appears strongly related to hyperglycemia and is influenced by the quality of diabetic control, not just the presence of diabetes itself. 3
Clinical Implications for Morbidity and Mortality
Cardiovascular Risk
The glucose-viscosity relationship has direct implications for cardiovascular outcomes:
Increased blood viscosity is considered a major cardiovascular risk factor and may contribute to vascular complications in diabetes. 4
Postprandial hyperglycemia is an independent predictor of cardiovascular risk, though the mechanism may be more complex than simple viscosity changes during the postprandial period. 4
Hyperglycemia is associated with poor outcomes after ischemic stroke, including among patients treated with thrombolytic agents, with persistent hyperglycemia (blood glucose ≥200 mg/dL) during the first 24 hours independently predicting expansion of stroke volume and poor neurological outcomes. 5
Microvascular Complications
The viscosity-glucose relationship may contribute to diabetic organ damage:
Blood and plasma viscosity are significantly elevated in diabetic patients with major organ complications (nephropathy and leg ulceration) but not in those without complications or with only microalbuminuria. 6
This suggests viscosity elevation occurs later in the disease process rather than contributing early to pathogenesis, though the progressive nature of viscosity changes from normal glucose ranges suggests cumulative effects over time. 6
Acute Metabolic Decompensation
Severe hyperglycemia compounds viscosity-related risks:
Hyperglycemia with volume depletion (common in diabetic ketoacidosis) creates a particularly dangerous combination, as both factors independently increase blood viscosity. 5
Patients with hyperglycemia and nausea/vomiting require immediate evaluation for DKA, which represents a life-threatening emergency demanding urgent intervention. 7
Important Clinical Caveats
Postprandial Dynamics
The viscosity response to glucose varies by metabolic state:
In healthy individuals, blood viscosity actually decreases during the postprandial period, whereas in type 2 diabetic patients it remains unchanged despite elevated postprandial glucose. 4
This suggests alterations in haemorheological regulation in diabetes beyond simple glucose-viscosity effects, indicating the relationship is more complex in established disease. 4
Glycosylation vs. Acute Effects
Not all glucose-related changes affect viscosity:
- Glycosylation of hemoglobin (HbA1c up to 8%) does not directly alter hemoglobin solution viscosity, indicating the viscosity effects are primarily mediated through cellular and plasma factors rather than protein glycosylation. 2
Practical Management Implications
Optimizing blood glucose control should be prioritized not only for traditional microvascular and macrovascular risk reduction but also for reducing blood viscosity and its associated thrombotic and perfusion risks. 3
Even modest improvements in glycemic control produce measurable reductions in blood viscosity, suggesting that any degree of glucose optimization provides rheological benefits. 3
In acute settings (stroke, critical illness, surgery), maintaining glucose between 4-10 mmol/L (72-180 mg/dL) is essential, as acute hyperglycemia directly impairs outcomes through multiple mechanisms including viscosity effects. 5, 7