Maintaining healthy glucose balance is critical. When blood sugar is out of range, either too high or too low for too long, serious damage can be done to the body, including irreversible damage to various tissues, falling into a coma or even death. The body has intelligent internal mechanisms such as neurotransmitters, hormones and specific organ systems in place that normally prevent these complications through carefully monitoring and balancing the blood sugar. The main organ that monitors and maintains glucose levels is the pancreas which secretes Insulin when sugar levels get too high.
We take in glucose daily through our diet, but it is also synthesised by the liver through a process known as Hepatic blood sugar production. Excess dietary glucose is stored in the liver as glycogen. Glucose is released from glycogen in a process known as glycogenolysis. Another critical mechanism for glucose production in the liver is when glucose is newly synthesised from precursors; this process is known as hepatic gluconeogenesis. During gluconeogenesis, the liver converts certain amino acids or metabolites, such as alanine, glycerol, and lactate into glucose.
Frequently Asked Questions
- 1What is hypoglycaemia?
- 2What are the symptoms of hypoglycaemia?
- 3How is hypoglycaemia diagnosed?
- 4What are possible causes, triggers and risks associated with hypoglycaemia?
- 5What is the conventional treatment of hypoglycaemia?
- 6How is hypoglycaemia managed through diet?
- 7What supplements can be given?
Hypoglycaemia is the term given to describe very low blood sugar. Anything under 3.3mmol/l is considered low, with 2.5mmol/l being severe and can cause significant, acute, life-threatening consequences if not treated immediately.
Reactive hypoglycaemia is the exaggerated drop in blood sugar level, also know as a “crash” that occurs when there is an overly exaggerated insulin spike following eating carbohydrates, this then causes a reactive plunge in blood sugar levels which produces the symptoms.
Low blood sugar levels in the range of 3.3mmol/l-2.5mmol/l can cause a variety of symptoms ranging from:
- fast heart rate,
- confusion and
Below 2.5mmol/l it causes worsening of the symptoms but can also lead to unconsciousness or in severe cases, even coma and death.
The diagnostic criteria for hypoglycaemia are is called Whipple’s Triad. They are:
- Symptoms clinically known or likely to be caused by low blood sugar especially after fasting or heavy exercise.
- A low plasma glucose measured at the time of the symptoms, usually confirmed though a finger prick test.
- Relief of symptoms when the glucose is raised to normal.
- Treatment related or “iatrogenic” hypoglycaemia occurs in people being treated for type 1 Diabetes using Insulin are the highest risk for developing hypoglycaemia as a result of aggressive pharmaceutic treatment of the disease.
- Type 2 diabetics can also develop hypoglycaemia as a result of over treatment with glucose-lowering drugs, in particular the class of drugs known as sulfonylureas.
- Reactive hypoglycaemia (or postprandial hypoglycaemia) is a phenomenon in which blood sugar levels drop suddenly a few hours after eating. Typically, reactive hypoglycaemia strikes people who are not diabetic but still have less than optimal glucose control (eg, individuals with prediabetes or insulin resistance).
- Excess alcohol, if consumed while fasting, can cause hypoglycaemia, as can several medications such as Quinine. Certain antibiotics are known to cause hypoglycaemia. For example, the fluoroquinolone enhances insulin secretion by a mechanism similar to sulfonylureas and induces hypoglycemia.
- Alpha lipoic acid can also cause hypoglycaemia if used in conjunction with other blood sugar lowering medications.
- Reactive hypoglycaemia is also more common in people who have undergone gastric bypass surgery for severe obesity.
- Cortisol is an anti-inflammatory hormone produced by the adrenal glands that also helps sustain glucose levels during stressful events. When there is insufficient cortisol produced the condition is known as Addison’s disease, patients with Addison’s often develop hypoglycaemia along with their other symptoms.
- Polycystic ovary syndrome (PCOS) is associated with obesity and an exaggerated insulin response. Reactive hypoglycaemia is more prevalent in PCOS sufferers than in the general population.
- Fasting-induced hypoglycaemia is associated with a number of congenital disorders, many of which are diagnosed in childhood and remain in adulthood. Some examples of conditions in this group are glycogen storage or fatty acid metabolism diseases and gluconeogenesis disorders.
- Exercise-induced hypoglycaemia is caused by insulin hyper secretion in response to anaerobic exercise, specifically during anaerobic exercise because pyruvate in the blood is increased by the high intensity activity. Another cause of exercise-induced hypoglycaemia is hypoglycaemia-associated autonomic failure (HAAF), which may be caused by an exaggerated endorphin response to exercise.
- The less common causes of hypoglycaemia are live and kidney disease, hypopituitarism, sepsis elsewhere in the body and some auto immune diseases .
Conventional management of hypoglycaemia includes:
- Immediately restoring glucose levels in a patient who presents with severe hypoglycaemia,
- Taking steps to help stabilize long-term glucose control and prevent additional episodes of hypoglycaemia.
The Health Renewal doctors suggest that most healthy people strive to maintain fasting glucose levels between 3.5mmol/l and 5.0mmol/l . Minor changes in dietary habits can help stabilize glucose levels and achieve these goals for many people.
Fibre reduces the speed at which carbohydrates and sugars are absorbed. This can be accomplished by eating more whole fruits and vegetables.
A more direct way to reduce the glycemic impact of the diet is to consume fewer carbohydrates. Typical dietary suggestions for reactive hypoglycaemia include:
- Avoid refined carbohydrates (eg, white rice, white flour).
- Eat several small meals and snacks throughout the day (6 small meals or in-between meal snacks).
- Avoid excess alcohol while fasting (or at least consume food while drinking alcohol).
- Eat foods with a lower glycemic index. These are foods that raise blood sugar levels more slowly (eg, lean protein, high-fibre foods).
- Fiber: Fructooligosaccharides (FOS) or Glucomannan may help stabilise glucose after eating by prolonging carbohydrate absorption.
- Chromium: This 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.
- Green Coffee Bean Extract is an antioxidant-rich mixture from un-roasted coffee beans that may regulate glucose after eating. Chlorogenic acid, a compound derived from green coffee extract, has been shown to reduce glucose absorption in healthy volunteers.
- White bean extract (Phaseolus vulgaris) and Irvingia gabonensis are powerful blockers of the enzyme alpha-amylase, which is secreted by the pancreas. 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. White bean extract slows the digestion of starch and 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.
- Extracts from kelp (Ascophyllum nodosum) and bladderwrack (Fucus vesiculosus) have been demonstrated to inhibit the digestive enzymes alpha-amylase and alpha-glucosidase which interferes with the digestion of dietary starches and may reduce or slow the absorption of high glycemic carbohydrates.
- L-arabinose: By blocking the metabolism of sucrose, L-arabinose inhibits the spike in blood sugar and fat synthesis that would otherwise follow a meal high in sugars or carbohydrates.