Targeted Natural Interventions
Stabilization of glucose levels following a meal may help avert reactive hypoglycemia. Several natural interventions may help reduce post-meal glycemic variability.
Supplementation of the diet with fiber such as fructooligosaccharides (FOS) or propolmannan (a type of glucomannan) may help stabilize post-meal glucose levels by prolonging carbohydrate absorption (Wursch 1997; Sabater-Molina 2009; Gietl 2012; Hopman 1988). This may be beneficial for people prone to reactive hypoglycemia.
Fructooligosaccharides (FOS) are fermentable prebiotic fibers found in plant foods such as onion, garlic, chicory, asparagus, artichokes, and bananas (Sabater-Molina 2009; Gietl 2012). A study found that supplementation with 20 g of FOS daily for two weeks in people with reactive hypoglycemia resulted in significantly improved blood glucose profiles and fewer episodes of hypoglycemia (Sorensen 2010).
Glucomannan and propolmannan are types of dietary fiber that form a gel-like substance within the gastrointestinal tract, which delays carbohydrate absorption. In one study on subjects who had undergone gastric surgery and had reactive hypoglycemia, the addition of glucomannan to a carbohydrate-rich meal resulted in improved post-meal glucose dynamics. This effect was found to be dose-dependent in that 2.6 g of glucomannan raised post-meal glucose levels from 41 to 59 mg/dL, and 5.2 g of glucomannan raised levels from 41 to 73 mg/dL. Supplementation with glucomannan also restrained post-meal spikes in glucose levels, which are responsible for the exaggerated insulin response and subsequent hypoglycemia (Hopman 1988).
Chromium is an essential trace mineral that plays a significant role in sugar metabolism. Chromium supplementation helps control blood sugar levels in type 2 diabetes and improves metabolism of carbohydrates (Ghosh 2002; Jovanovic 1999). A small, double-blind, crossover trial assessed the effects of chromium on 8 women with symptoms of reactive hypoglycemia. Supplemental chromium, at a daily dose of 200 mcg for 3 months, led to improvements in both blood sugar metabolism parameters and hypoglycemic symptoms such as sweating, trembling, and blurred vision (Anderson 1987).
Green Coffee Bean Extract
Green coffee bean extract, an antioxidant-rich mixture from unroasted coffee beans, may temper post-meal spikes in glucose (Nagendran 2011). Chlorogenic acid, a compound derived from green coffee extract, has been shown to reduce glucose absorption in healthy volunteers (Thom 2007). One compelling study showed that people not taking green coffee extract had glucose levels of 130 mg/dL one hour after sugar ingestion. In this same study, , glucose levels of subjects taking 400 mg of green coffee extract dropped to 93 mg/dL after sugar ingestion (Nagendran 2011).
Chlorogenic acid may reduce postprandial hyperglycemia both by shutting down excess liver glucose production and also stimulating glucose uptake into skeletal muscle (Ong 2012; Ong 2013). Another means by which chlorogenic acid acts to suppress post-meal glucose surges is by inhibiting alpha-glucosidase. This intestinal enzyme breaks apart complex sugars and enhances their absorption into the blood (Pusztai 1998). Slowing the absorption of common sugars (including sucrose) limits after-meal glucose spikes (Alonso-Castro 2008).
White Bean Extract (Phaseolus vulgaris) and Irvingia Gabonensis
White bean extract (Phaseolus vulgaris) and Irvingia gabonensis are powerful blockers of the enzyme alpha-amylase, which is secreted by the pancreas (Mosca 2008; Obiro 2008). Alpha-amylase breaks down long-chain, complex starch molecules into simple sugars and short-chain oligosaccharides for absorption in the small intestine. Blocking alpha-amylase inhibits the metabolism of starches and slows the rate at which free sugars are absorbed (Udani 2004; Celleno 2007; Oben 2008; Ngondi 2009).
In one double-blind, placebo-controlled study of obese but otherwise healthy adults, one month of supplementation with Irvingia gabonensis produced a 5.3% body weight loss in supplemented patients compared with only a 1.3% loss in the control group (Ngondi 2005). These individuals also saw significant improvement in their lipid profiles. Additional studies confirm these findings, demonstrating significant reductions in body fat waist circumference, blood sugar levels, and markers of fat tissue regulation (Oben 2008; Ngondi 2009).
White bean extract shows enormous potential for preventing the blood sugar and insulin spikes associated with many chronic health disorders (Preuss 2007). Slowing starch digestion prolongs the amount of time it takes for the stomach to empty its contents, reducing the amount of carbohydrate calories released at any one time into the intestine (Layer 1986).
White bean extracts operate along numerous overlapping pathways in multiple, related physiological systems. Laboratory research shows that supplementation with white bean extract promotes weight loss in obese animals, with dramatic reduction in fat accumulation without loss of muscle mass (Santoro 1997; Pusztai 1998). Plasma insulin levels also dropped substantially following a high-carbohydrate meal including white bean extract in pre-clinical studies, reflecting a much more gradual rise in blood sugar levels (Pusztai 1998).
Extracts from kelp (Ascophyllum nodosum) and bladderwrack (Fucus vesiculosus) have been demonstrated to inhibit the activity of the digestive enzymes alpha-amylase and alpha-glucosidase (Paradis 2011). Inhibition of these enzymes interferes with the digestion of dietary starches and may reduce or slow the absorption of high glycemic carbohydrates (Preuss 2009).
Sucrose (table sugar) is composed of 2 simple sugar molecules, glucose and fructose. It is poorly absorbed in the intestine in this form. In order to be utilized, it must first be broken down by the digestive enzyme sucrase. Blocking the enzymatic action of sucrase therefore reduces uptake of sucrose. Researchers have identified a potent sucrase inhibitor called L-arabinose. L-arabinose, an indigestible plant compound, cannot be absorbed into the blood. Instead, it remains in the digestive tract and is eventually excreted (Seri 1996; Osaki 2001). By blocking the metabolism of sucrose, L-arabinose inhibits the spike in blood sugar and fat synthesis that would otherwise follow a sugar-rich meal (Osaki 2001).