Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within 4 hours after a high carbohydrate meal in people who do not have diabetes.
The condition is related to homeostatic systems utilised by the body to control blood sugar levels. It is variously described as a sense of tiredness, lethargy, irritation, or hangover, although the effects can be less if one has undertaken a lot of physical activity within the next few hours after consumption.
The alleged mechanism for the feeling of a crash is correlated with an abnormally rapid rise in blood glucose after eating. This normally leads to insulin secretion (known as an insulin spike), which in turn initiates rapid glucose uptake by tissues either accumulating it as glycogen or utilizing it for energy production. The consequent fall in blood glucose is indicated as the reason for the "sugar crash".. A deeper cause might be hysteresis effect of insulin action, i.e., the effect of insulin is still prominent even if both plasma glucose and insulin levels were already low, causing a plasma glucose level eventually much lower than the baseline level.
Sugar crashes are not to be confused with the after-effects of consuming large amounts of protein, which produces fatigue akin to a sugar crash, but are instead the result of the body prioritising the digestion of ingested food.
The prevalence of this condition is difficult to ascertain because a number of stricter or looser definitions have been used. It is recommended that the term reactive hypoglycemia be reserved for the pattern of postprandial hypoglycemia which meets the Whipple criteria (symptoms correspond to measurably low glucose and are relieved by raising the glucose), and that the term idiopathic postprandial syndrome be used for similar patterns of symptoms where abnormally low glucose levels at the time of symptoms cannot be documented.
To assist diagnosis, a doctor can order an HbA1c test, which measures the blood sugar average over the two or three months before the test. The more specific 6-hour glucose tolerance test can be used to chart changes in the patient's blood sugar levels before ingestion of a special glucose drink and at regular intervals during the six hours following to see if an unusual rise or drop in blood glucose levels occurs.
According to the U.S. National Institute of Health (NIH), a blood glucose level below 70 mg/dL (3.9 mmol/L) at the time of symptoms followed by relief after eating confirms a diagnosis for reactive hypoglycemia.
Video Reactive hypoglycemia
Signs and symptoms
Symptoms vary according to individuals' hydration level and sensitivity to the rate and/or magnitude of decline of their blood glucose concentration. A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include:
The majority of these symptoms, often correlated with feelings of hunger, mimic the effect of inadequate sugar intake as the biology of a crash is similar in itself to the body's response to low blood sugar levels following periods of glucose deficiency.
Maps Reactive hypoglycemia
Causes
The NIH states: "The causes of most cases of reactive hypoglycemia are still open to debate. Some researchers suggest that certain people may be more sensitive to the body's normal release of the hormone epinephrine, which causes many of the symptoms of hypoglycemia. Others believe deficiencies in glucagon secretion might lead to reactive hypoglycemia.
Stomach surgery or hereditary fructose intolerance are believed to be causes, albeit uncommon, of reactive hypoglycemia. myo-Inositol or D-chiro-inositol withdrawal can cause temporary reactive hypoglycemia.
There are different kinds of reactive hypoglycemia:
- Alimentary hypoglycemia (consequence of dumping syndrome; it occurs in about 15% of people who have had stomach surgery)
- Hormonal hypoglycemia (e.g., hypothyroidism)
- Helicobacter pylori-induced gastritis (some reports suggest this bacteria may contribute to the occurrence of reactive hypoglycemia)
- Congenital enzyme deficiencies (hereditary fructose intolerance, galactosemia, and leucine sensitivity of childhood)
- Late hypoglycemia (occult diabetes; characterized by a delay in early insulin release from pancreatic ?-cells, resulting in initial exaggeration of hyperglycemia during a glucose tolerance test)
"Idiopathic reactive hypoglycemia" is a term no longer used because researchers now know the underlying causes of reactive hypoglycemia and have the tools to perform the diagnosis and the pathophysiological data explaining the mechanisms.
To check if there is real hypoglycemia when symptoms occur, neither an oral glucose tolerance test nor a breakfast test is effective; instead, a hyperglucidic breakfast test or ambulatory glucose testing is the current standard.
The body requires a relatively constant input of glucose, a sugar produced upon digestion of carbohydrates, for normal functioning. Glucagon and insulin are among the hormones that ensure a normal range of glucose in the human body. Upon consumption of a meal, blood sugar normally rises, which triggers pancreatic cells to produce insulin. This hormone initiates the absorption of the just-digested blood glucose as glycogen into the liver for metabolism or storage, thereby lowering glucose levels in the blood. In contrast, the hormone glucagon is released by the pancreas as a response to lower than normal blood sugar levels. Glucagon initiates uptake of the stored glycogen in the liver into the bloodstream so as to increase glucose levels in the blood. Sporadic, high-carbohydrate snacks and meals are deemed the specific causes of sugar crashes. The "crash" one feels is due to the rapid increase and subsequent decline of blood sugar in the body system as one begins and ceases consumption of high-sugar foods. More insulin than is actually needed is produced in response to the large, rapid ingestion of sugary foods.
Treatment
To relieve reactive hypoglycemia, the NIH recommends taking the following steps:
- Avoiding or limiting sugar intake;
- Exercising regularly; exercise increases sugar uptake which decreases excessive insulin release
- Eating a variety of foods, including meat, poultry, fish, or nonmeat sources of protein, foods such as whole-grains, fruits, nuts, vegetables, and dairy products;
- Choosing high-fiber foods.
Other tips to prevent sugar crashes include:
- Avoiding eating meals or snacks composed entirely of carbohydrates; simultaneously ingest fats and proteins, which have slower rates of absorption.
- Consistently choosing longer lasting, complex carbohydrates to prevent rapid blood-sugar dips in the event that one does consume a disproportionately large amount of carbohydrates with a meal
- Monitoring any effects medication may have on symptoms.
Low-carbohydrate diet and/or frequent small split meals is the first treatment of this condition. The first important point is to add small meals at the middle of the morning and of the afternoon, when glycemia would start to decrease. If adequate composition of the meal is found, the fall in blood glucose is thus prevented. Patients should avoid rapidly absorbable sugars and thus avoid popular soft drinks rich in glucose or sucrose. They should also be cautious with drinks associating sugar and alcohol, mainly in the fasting state.
As it is a short-term ailment, a sugar crash does not usually require medical intervention in most people. The most important factors to consider when addressing this issue are the composition and timing of foods. Acute low blood sugar symptoms are best treated by consuming small amounts of sweet foods, so as to regain balance in the body's carbohydrate metabolism. Suggestions include sugary foods that are quickly digested, such as:
- Dried fruit
- Soft drinks
- Juice
- Sugar as sweets, tablets or cubes.
Postprandial syndrome
If there is no hypoglycemia at the time of the symptoms, this condition is called "postprandial syndrome." It might be an "adrenergic postprandial syndrome" -- blood glucose levels are normal, but the symptoms are caused through autonomic adrenergic counterregulation. Often, this syndrome is associated with emotional distress and anxious behaviour of the patient. This is often seen in dysautonomic disorders as well. Dietary recommendations for reactive hypoglycemia can help to relieve symptoms of postprandial syndrome.
See also
- Spontaneous hypoglycemia
- Refeeding syndrome
References
External links
- Overview at Mayo Clinic
- How to Get Diagnosed [Broken Link]
- Dumping Syndrome Overview at Mayo Clinic
- Article about hypoglycemia at eMedicine
- Research about reactive hypoglycemia [Broken link]
- Research about suspected reactive hypoglycemia associated with B-adrenergic hypersensivity and emotional distress [Broken link]
- Açbay O, Celik AF, Kadio?lu P, Göksel S, Gündo?du S (1999). "Helicobacter pylori-induced gastritis may contribute to occurrence of postprandial symptomatic hypoglycemia". Dig. Dis. Sci. 44 (9): 1837-42. doi:10.1023/A:1018842606388. PMID 10505722.
- Classification and possible causes of reactive hypoglycemia (article of 1972; may not be in accord with current medical practice)
Source of the article : Wikipedia
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