Large glucose spikes following a meal, known as postprandial hyperglycemia (PPH), have emerged as an important risk factor not just for the development of type 2 diabetes, but also for cardiovascular disease risk, organ damage, impaired brain function, and all-cause mortality. A number of recent publications have pointed to an independent risk associated with PPH, i.e., one not dependent on other variables such as fasting plasma glucose or HbA1c, yet it is often overlooked because it is not as easily measured. This brief overview of recent research describes PPH’s clinical impact as well as strategies to mitigate its harm.
PPH affects both people with type 2 diabetes and people without obvious indicators of impaired glucose regulation, and often goes undetected in both. For example, in a large cohort of people with diabetes, episodes of PPH (defined in the study as >160 mg/dl, 2 hours postprandial) occurred in 84% within a one-week period (3 days of which had pre- & post-meal testing, for 9 total meals). Among people considered to have good metabolic control, nearly 40% had PPH following at least 4 of the 9 meals evaluated, indicating that it’s quite a frequent event even with well-controlled diabetes.
An important question is to what degree PPH contributes to overall HbA1c levels. One study attempted to quantify this and found that the relative contribution of post-meal glycemia to HbA1c levels among diabetics is more important than fasting glucose in people with well-controlled diabetes, contributing more (nearly 70%) at lower HbA1c levels (and still contributing 30% at the highest HbA1c quintile). Additionally, it’s clear that the peaks and nadirs of blood glucose may not be captured by HbA1c, a measure of average glucose levels.
Among people without diabetes, 2-hour postprandial increases have been linked with roughly a 2-fold increase in both higher cardiovascular and overall mortality in a large U.S. (NHANES) representative population. And reducing PPH appears to pay off among people with such spikes, especially before the onset of diabetes. In one multicenter randomized trial, people with impaired glucose tolerance (but not diabetes) who achieved normal glucose tolerance, with either medication or lifestyle changes, reduced their risk of MACE (all-cause death, non-fatal MI, or unplanned coronary revascularization) by 56% over a 10-year follow-up.
PPH can be defined differently, depending on the population. For example, among people with diabetes, it’s often defined as glucose levels > 180 mg/dL within 1-2 hours of a meal, while levels of 140–160 mg/dL (or a rise of 30–50 mg/dL from baseline) generally apply to non-diabetic populations. The International Diabetes Federation (IDF) Position Statement suggests a threshold of 155 mg/dL at one hour following a meal among people with normal glucose tolerance (during an oral glucose tolerance test), citing the risk for diabetes development, liver disease, macro and microvascular complications, and mortality. This threshold has been considered an early marker for dysglycemia, as well as a cluster of lipid abnormalities, kidney dysfunction, NAFLD, etc.
There are a number of lifestyle interventions that help mitigate postprandial spikes. While previous research highlighted the benefits of a 30-minute walk following meals, the journal Scientific Reports recently published results of a randomized crossover trial comparing the effect of a 10-minute walk immediately following a meal to a 30-minute walk initiated 30 minutes after the meal. This study emphasized the timing as particularly important, considering that while both groups reduced their blood glucose levels compared to a control, the peak levels were significantly lower with only the 10-minute walk (not the 30-minute walk). This and previous studies suggest that while walks of a longer duration reduce postprandial glucose to a greater degree than shorter ones, if timed immediately following a meal, even short walks at a comfortable pace can be effective.
Food choices and also food order appear to matter; in a randomized and controlled crossover trial, eating vegetables followed by protein and saving carbohydrates last reduced postprandial spikes compared to simultaneous consumption of the same meal. Although these studies are generally small, several have been conducted demonstrating an advantage of eating more fibrous vegetables and protein first, which blunts the glucose spikes (and insulin response) to the carbohydrate portion of a meal. Several studies have also found that premeal protein (whey) consumption (15-30g) also mitigates PPH in several populations, including women with gestational diabetes, with some evidence that β-cell function is increased and insulin clearance reduced (i.e., more efficient insulin function). A number of studies also point to the “second-meal effect,” which refers to the impact (either positive or negative) of one meal on the postprandial glucose levels of subsequent meals. And while limited to mostly small studies, adding a small amount (30mL) of vinegar to higher glycemic load meals may help.
Several nutrients have also been associated with benefits. Supplementation with berberine has been shown to reduce 2-hour postprandial glucose levels by a mean of 28 mg/dL in 8 clinical trials. However, among people with higher baseline glucose levels, the effect was even greater, approaching 45 mg/dL. Among people with prediabetes and low magnesium levels, supplementation with ~400 mg per day improved post-load glucose, as well as HOMA-IR, triglycerides, and fasting glucose. Identifying PPH is a good first step, with many interventions to help get it under control.