After meal blood sugar spikes as a cause of vascular failure

This article is about the damaging effects of high blood sugar on the blood vessels after a meal.

Post Prandial Hyperglycemia

Post-prandial hyperglycemia (PPH) is the medical term for increased blood sugar after eating. It occurs if the blood sugar is 140 – 200 mg/dl two hours after eating.

PPH can damage the arteries. The inner lining of blood vessels, the endothelium, can correct the damage brought about by high blood sugar.

However, if the injury is repetitive, the blood vessels cannot repair themselves and deliver adequate blood to the whole body. That condition is called a vascular failure by the authors of Post-prandial hyperglycemia as an etiological factor in vascular failure.

Recurrent waves of oxidative stress from post-prandial hyperglycemia could eventually lead to a cardiovascular event like a stroke or a heart attack.

Source: Postprandial hyperglycemia as an etiological factor in vascular failure. Cardiovasc Diabetol. 2009 Apr 29;8:23

It is commonly known that if your blood sugar is controlled, as shown by the HbA1c, then your risk of a heart attack is low.

HbA1c is a blood test that averages the blood sugar level of the past two to three months. Patients with diabetes get this test every three months.

But that is not always the case. A heart attack can still happen in Type 2 diabetics even with acceptable HbA1cs.

The blood sugar spikes after meals predict atherosclerosis better than fasting blood sugar and hemoglobin A1c (HbA1c).

The Funagata Diabetes study showed that atherosclerosis is formed even if the fasting blood sugar is <90 mg/dl and HBA1c is within normal (4%-5.6%).[2]

A multicenter study by the Diabetic Epidemiology: Collaborative Analysis of Diagnosis Criteria in Europe (DECODE) showed a direct relationship between 2-hour post-load glucose levels and risk for cardiovascular death.

The increased risk of atherosclerosis correlates with blood sugar levels after eating. Even the lower limit of 140 mg at two hours post-meal is enough to raise atherosclerosis risk. Here is a quote from Node et al.

The risk for postload glycemia begins to increase at levels >80 mg/dl and by 140 mg/dl, the point at which patients are traditionally classified as having impaired glucose tolerance (IGT) or prediabetes, cardiovascular risk is already increased by 58%.

Source: Postprandial hyperglycemia as an etiological factor in vascular failure. Cardiovasc Diabetol. 2009 Apr 29;8:23.

This could explain why some people who do not have diabetes, those with prediabetes, and those with diabetes who have adequate blood sugar control still develop cardiovascular diseases like strokes and heart attacks.

It also means that even if the total cholesterol and LDL are good but if repetitive PPH exists, a heart attack can still happen.

It can be argued that blood sugar control, including post-prandial glycemia, predicts heart disease better than total cholesterol and LDL levels.

A meta-analysis of 27 trials published in the Journal of the American Medical Association about using statins to lower all-cause mortality, myocardial infarction, or stroke had the following conclusions.

The results of this meta-analysis suggest that the absolute risk reductions of treatment with statins in terms of all-cause mortality, myocardial infarction, and stroke are modest compared with the relative risk reductions, and the presence of significant heterogeneity reduces the certainty of the evidence.

A conclusive association between absolute reductions in LDL-C levels and individual clinical outcomes was not established, and these findings underscore the importance of discussing absolute risk reductions when making informed clinical decisions with individual patients.[5]

I credit the authors who used absolute risk reduction instead of relative risk, which is always higher and sells more drugs. That is how they sold the COVID shots to the unsuspecting masses. Remember the 96% effectiveness of the Pfizer shot? That’s relative risk. If you want to know more about the absolute risk reduction of the covid injections, please read:

Returning to the topic, what happens to the arteries if the blood sugar increases?

Nitric oxide, the molecule that vasodilates and maintains the smoothness of the arteries, decreases leading to endothelial dysfunction.

Endothelial dysfunction is the start of atherosclerosis. Once it starts, inflammation results from the produced free radicals and activated neutrophils, the most common type of white blood cells.

Oxidative stress from inflammation causes further damage to the endothelium and the mitochondria, which decreases ATP production.

The cells use adenosine triphosphate (ATP) for fuel to maintain the health of the arteries 24/7. If energy is lacking, cellular maintenance goes down the drain.

In summary, post-prandial hyperglycemia leads to the loss of the maintenance function of the endothelium or vascular failure.

If endothelial dysfunction continues, the muscle layer of the arteries gets calcified and stiff, and the lumen becomes narrower. Atherosclerosis will thicken to develop a plaque, and one day, the plaque will rupture to cause a heart attack or a stroke.

There are other nasty cardiovascular diseases like aortic dissection and aortic aneurysms. They are all life-threatening.

Solutions

Lifestyle changes can prevent endothelial dysfunction. One is avoiding excess sugar.

Another is rearranging the order of food intake. The proper order can slow sugar absorption and prevent an after-meal glucose spike by delaying gastric emptying and proactively increasing insulin.

Walking after meals can also help post-prandial high blood sugars. – Walk After Meals to Prevent Sky High Blood Sugars

Intermittent fasting is another way to repair vascular damage. Exercising after a meal can also lower after-meal blood sugar increases.

Next time, I will discuss studies about how intermittent fasting and exercise after eating helped prevent post-prandial hyperglycemia.

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References:

Node K, Inoue T. Post-prandial hyperglycemia as an etiological factor in vascular failure. Cardiovasc Diabetol. 2009 Apr 29;8:23. Doi: 10.1186/1475-2840-8-23. PMID: 19402896; PMCID: PMC2688503.
Tominaga M, Eguchi H, Manaka H, Igarashi K, Kato T, Sekikawa A. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study. Diabetes Care. 1999 Jun;22(6):920-4. doi: 10.2337/diacare.22.6.920. PMID: 10372242.
DECODE Study Group, European Diabetes Epidemiology Group. Is the current definition for diabetes relevant to mortality risk from all causes and cardiovascular and noncardiovascular diseases? Diabetes Care. 2003 Mar;26(3):688-96. doi: 10.2337/diacare.26.3.688. PMID: 12610023.
Sasso FC, Carbonara O, Nasti R, Campana B, Marfella R, Torella M, Nappi G, Torella R, Cozzolino D. Glucose metabolism and coronary heart disease in patients with normal glucose tolerance. JAMA. 2004 Apr 21;291(15):1857-63. doi: 10.1001/jama.291.15.1857. PMID: 15100204.
Byrne P, Demasi M, Jones M, Smith SM, O’Brien KK, DuBroff R. Evaluating the Association Between Low-Density Lipoprotein Cholesterol Reduction and Relative and Absolute Effects of Statin Treatment: A Systematic Review and Meta-analysis. JAMA Intern Med. 2022;182(5):474–481. doi:10.1001/jamainternmed.2022.0134