HypoglycemiaLife Extension Suggestions
Understanding Glycemic Control
Maintaining glucose balance is critical. When blood sugar is too high for too long (chronic hyperglycemia), irreversible damage can be done to various tissues. On the other hand, severe hypoglycemia may cause a person to become comatose or even die. To prevent these complications, the body has adopted a variety of mechanisms to maintain plasma glucose levels within certain values, a process known as homeostasis, which is controlled by a symphony of interrelated checks and balances within the body, including neurotransmitters, hormones, and organ systems (Klement 2012).
Blood glucose is mainly derived from two sources: diet and synthesis in the liver via a process known as hepatic blood sugar production (Boden 2004). Excess dietary glucose can be stored in the liver as glycogen. Glucose can be released from glycogen in a process known as glycogenolysis. Another critical mechanism for glucose production in the liver is when glucose is newly synthesized from precursors; this process is known as hepatic gluconeogenesis (Cersosimo 2011). During gluconeogenesis, the liver converts certain amino acids or metabolites, such as alanine, glycerol, and lactate into glucose (Watford 2006).
Islets are specialized clusters of hormone-secreting cells in the pancreas. Within the islets are alpha cells that secrete glucagon and beta cells that secrete insulin. The major effect of glucagon is to stimulate glycogenolysis and gluconeogenesis in the liver, which results in an increase in the blood levels of glucose (Lee 2012). During carbohydrate ingestion, insulin inhibits glucagon and stimulates glucose uptake primarily in skeletal muscle, effectively lowering the blood glucose concentration (Lee 2011; Roth 2007).
Glucagon, as well as growth hormone, cortisol, and epinephrine all oppose the action of insulin and are known as “counter-regulatory hormones” (Lager 1991).
In the absence of dietary carbohydrate, (eg, during starvation) hepatic glucose production by gluconeogenesis and glycogenolysis guards against hypoglycemia (Rothman 1991; Cahill 2006). Upon carbohydrate ingestion, hepatic glucose production is reduced and blood glucose levels are maintained by dietary glucose absorbed through the gastrointestinal tract.
Dietary Contribution to Glucose Levels
The contribution of diet to glucose levels is relatively straightforward: dietary carbohydrates are broken down into glucose and absorbed through the gastrointestinal tract after ingestion. Thus, eating a meal containing large amounts of carbohydrate contributes to a rapid elevation of blood glucose levels. Ingestion of a pure glucose solution causes detectable elevations in blood glucose levels in as little as 15 minutes (Shrayyef 2010). On the other hand, the more complex or “fibrous” the carbohydrates ingested are, the slower the subsequent glucose elevations. Moreover, the addition of fats and proteins to a meal can also slow glucose absorption (Gemen 2011; Bajorek 2010; Riccardi 1991). This is why a high-fiber diet with moderate amounts of slowly-digested carbohydrate, good quality protein, and healthy fats (eg omega-3 fatty acids from fish) is recommended for people with impaired glucose control, such as those with type 2 diabetes.
With regard to hypoglycemia, the contribution of diet is somewhat counterintuitive. If too much rapidly-digested carbohydrate is consumed and absorbed quickly, an ensuing hypoglycemic episode can follow if the body generates an exaggerated insulin response to bring post-meal glucose levels back down (Kuipers 1999). This is called reactive hypoglycemia (Bell 1985). Thus, interventions aimed at reducing the rapid absorption of dietary carbohydrate can help avoid the reactive drop in blood sugar following an overly exaggerated insulin spike.
Regulation of Glucose Levels Following a Meal
Once glucose is absorbed from the gastrointestinal tract into the bloodstream, the body must keep blood sugar from rising to levels above normal since too much glucose in the blood can damage tissues and contribute to inflammation and vascular stress (Averill 2009). The process of controlling after-meal glucose levels is a complex interplay of several organs, hormones, and neurotransmitters (Shrayyef 2010).
When glucose levels rise following a meal, the pancreas releases the hormone insulin. Insulin triggers numerous tissues throughout the body to initiate the breakdown and/or storage of glucose, thus bringing blood glucose levels back down. Insulin stimulates the uptake of glucose from the blood into muscle and fat tissue, where it can either be stored or broken down and used to meet cellular energy demands. Insulin also suppresses the release of glucose from the liver, a significant source of glucose between meals (Shrayyef 2010).