Reactive hypoglycemia

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Reactive hypoglycemia
Other namesPostprandial hypoglycemia, sugar crash
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A typical recommendation: Half the plate is filled with high-fiber vegetables, and the rest is divided between tuna fish and a single serving of ramen noodles.
Symptoms Clumsiness, difficulty talking, confusion, loss of consciousness, and other symptoms related to hypoglycemia
Usual onsetWithin 4 hours of a high carbohydrate meal
Causes Gastric bypass surgery, over-secretion of insulin
Diagnostic method Whipple criteria, blood glucose test during spontaneous occurrence of symptoms, HbA1c blood test, 6-hour glucose tolerance test
Differential diagnosis Alimentary hypoglycemia, factitious hypoglycemia, insulin autoimmune hypoglycemia, noninsulinoma pancreatogenous hypoglycemia syndrome, insulinoma, hereditary fructose intolerance
PreventionLow-carbohydrate diet, frequent small meals

Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within four hours [1] after a high carbohydrate meal in people with and without diabetes. [2] The term is not necessarily a diagnosis since it requires an evaluation to determine the cause of the hypoglycemia. [3]

Contents

The condition is related to homeostatic systems used by the body to control the blood sugar level. It is described as a sense of tiredness, lethargy, irritation, or hangover, although the effects can be lessened if a lot of physical activity is undertaken in the first few hours after food 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 storing it as glycogen or fat, or using it for energy production. The consequent fall in blood glucose is indicated as the reason for the "sugar crash". [4] Another 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. [5]

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. [6]

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 in diagnosis, a doctor may 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 Institutes 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. [1]

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.[ citation needed ]

A crash is usually felt within four hours of heavy carbohydrate consumption. Along with the symptoms of hypoglycemia, symptoms of reactive hypoglycemia include: [7] [8] [9]

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. [10]

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. [1]

Several other hormones are responsible for modulating the body's response to insulin, including cortisol, growth hormone and sex hormones. Untreated or under-treated hormonal disorders such as adrenal insufficiency (see also Addison's disease [11] ) or growth hormone deficiency [12] can therefore sometimes cause insulin hypersensitivity, and reactive hypoglycemia.

Stomach bypass surgery or hereditary fructose intolerance are believed to be causes, albeit uncommon, of reactive hypoglycemia. Myo-inositol or 1D-chiro-inositol withdrawal can cause temporary reactive hypoglycemia.[ citation needed ]

There are several kinds of reactive hypoglycemia: [13]

  1. Alimentary hypoglycemia (consequence of dumping syndrome; it occurs in about 15% of people who have had stomach surgery)
  2. Hormonal hypoglycemia (e.g., hypothyroidism)
  3. Helicobacter pylori -induced gastritis (some reports suggest this bacteria may contribute to the occurrence of reactive hypoglycemia) [14]
  4. Congenital enzyme deficiencies (hereditary fructose intolerance, galactosemia, and leucine sensitivity of childhood) [15]
  5. Late hypoglycemia (occult diabetes; characterized by a delay in early insulin release from pancreatic beta-cells, resulting in initial exaggeration of hyperglycemia during a glucose tolerance test) [16]

"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. [13]

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. [13] [17]

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. [18] 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. [19] 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.[ citation needed ]

Treatment

Reactive hypoglycemia can usually be relieved by dietary changes: [20]

Other tips to prevent sugar crashes include:

Low-carbohydrate diet and/or frequent small 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 absorbed 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. [13]

As it is a short-term ailment, a sugar crash that was not caused by injecting too much insulin 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. [24]

Acute (short-term) 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:

The anti-hypertensive class of medication known as calcium channel blockers could be useful for reactive hypoglycemia as inhibition of the calcium channels on beta islet cells can help prevent an overproduction of insulin after a meal is eaten. [26] [27]

Postprandial syndrome

If there is no hypoglycemia at the time of the symptoms, this condition is called idiopathic postprandial syndrome. It might be an "adrenergic postprandial syndrome" — blood glucose levels are normal, but the symptoms are caused through autonomic adrenergic counterregulation. [28] Often, this syndrome is associated with emotional distress and anxious behaviour of the patient. [13] This is often seen in dysautonomic disorders as well. Dietary recommendations for reactive hypoglycemia can help to relieve symptoms of postprandial syndrome.[ citation needed ]

See also

Related Research Articles

<span class="mw-page-title-main">Hypoglycemia</span> Health condition

Hypoglycemia, also called low blood sugar, is a fall in blood sugar to levels below normal, typically below 70 mg/dL (3.9 mmol/L). Whipple's triad is used to properly identify hypoglycemic episodes. It is defined as blood glucose below 70 mg/dL (3.9 mmol/L), symptoms associated with hypoglycemia, and resolution of symptoms when blood sugar returns to normal. Hypoglycemia may result in headache, tiredness, clumsiness, trouble talking, confusion, fast heart rate, sweating, shakiness, nervousness, hunger, loss of consciousness, seizures, or death. Symptoms typically come on quickly.

<span class="mw-page-title-main">Insulin pump</span> Medical device to administer insulin

An insulin pump is a medical device used for the administration of insulin in the treatment of diabetes mellitus, also known as continuous subcutaneous insulin therapy. The device configuration may vary depending on design. A traditional pump includes:

The following is a glossary of diabetes which explains terms connected with diabetes.

<span class="mw-page-title-main">Glucose tolerance test</span> Medical test of how quickly glucose is cleared from the blood

The glucose tolerance test is a medical test in which glucose is given and blood samples taken afterward to determine how quickly it is cleared from the blood. The test is usually used to test for diabetes, insulin resistance, impaired beta cell function, and sometimes reactive hypoglycemia and acromegaly, or rarer disorders of carbohydrate metabolism. In the most commonly performed version of the test, an oral glucose tolerance test (OGTT), a standard dose of glucose is ingested by mouth and blood levels are checked two hours later. Many variations of the GTT have been devised over the years for various purposes, with different standard doses of glucose, different routes of administration, different intervals and durations of sampling, and various substances measured in addition to blood glucose.

<span class="mw-page-title-main">Hyperglycemia</span> Too much blood sugar, usually because of diabetes

Hyperglycemia is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/L (200 mg/dL), but symptoms may not start to become noticeable until even higher values such as 13.9–16.7 mmol/L (~250–300 mg/dL). A subject with a consistent range between ~5.6 and ~7 mmol/L is considered slightly hyperglycemic, and above 7 mmol/L is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average, however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time.

<span class="mw-page-title-main">Diabetic coma</span> Medical condition

Diabetic coma is a life-threatening but reversible form of coma found in people with diabetes mellitus.

<span class="mw-page-title-main">Blood sugar level</span> Concentration of glucose present in the blood (Glycaemia)

Glycaemia, also known as blood sugar level, blood sugar concentration, or blood glucose level is the measure of glucose concentrated in the blood of humans or other animals. Approximately 4 grams of glucose, a simple sugar, is present in the blood of a 70 kg (154 lb) human at all times. The body tightly regulates blood glucose levels as a part of metabolic homeostasis. Glucose is stored in skeletal muscle and liver cells in the form of glycogen; in fasting individuals, blood glucose is maintained at a constant level at the expense of glycogen stores in the liver and skeletal muscle.

<span class="mw-page-title-main">Ketoacidosis</span> Medical condition

Ketoacidosis is a metabolic state caused by uncontrolled production of ketone bodies that cause a metabolic acidosis. While ketosis refers to any elevation of blood ketones, ketoacidosis is a specific pathologic condition that results in changes in blood pH and requires medical attention. The most common cause of ketoacidosis is diabetic ketoacidosis but can also be caused by alcohol, medications, toxins, and rarely starvation.

Hyperinsulinemic hypoglycemia describes the condition and effects of low blood glucose caused by excessive insulin. Hypoglycemia due to excess insulin is the most common type of serious hypoglycemia. It can be due to endogenous or injected insulin.

<span class="mw-page-title-main">Dumping syndrome</span> Medical condition

Dumping syndrome occurs when food, especially sugar, moves too quickly from the stomach to the duodenum—the first part of the small intestine—in the upper gastrointestinal (GI) tract. This condition is also called rapid gastric emptying. It is mostly associated with conditions following gastric or esophageal surgery, though it can also arise secondary to diabetes or to the use of certain medications; it is caused by an absent or insufficiently functioning pyloric sphincter, the valve between the stomach and the duodenum.

Diabetes mellitus is a chronic disease in cats whereby either insufficient insulin response or insulin resistance leads to persistently high blood glucose concentrations. Diabetes affects up to 1 in 230 cats, and may be becoming increasingly common. Diabetes mellitus is less common in cats than in dogs. Eighty to ninety-five percent of diabetic cats experience something similar to type 2 diabetes but are generally severely insulin dependent by the time symptoms are diagnosed. The condition is treatable, and if treated properly the cat can experience a normal life expectancy. In type 2 cats, prompt effective treatment may lead to diabetic remission, in which the cat no longer needs injected insulin. Untreated, the condition leads to increasingly weak legs in cats and eventually to malnutrition, ketoacidosis and/or dehydration, and death.

<span class="mw-page-title-main">Diabetic hypoglycemia</span> Medical condition

Diabetic hypoglycemia is a low blood glucose level occurring in a person with diabetes mellitus. It is one of the most common types of hypoglycemia seen in emergency departments and hospitals. According to the National Electronic Injury Surveillance System-All Injury Program (NEISS-AIP), and based on a sample examined between 2004 and 2005, an estimated 55,819 cases involved insulin, and severe hypoglycemia is likely the single most common event.

Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterize said condition.

<span class="mw-page-title-main">Type 1 diabetes</span> Form of diabetes mellitus

Type 1 diabetes (T1D), formerly known as juvenile diabetes, is an autoimmune disease that originates when cells that make insulin are destroyed by the immune system. Insulin is a hormone required for the cells to use blood sugar for energy and it helps regulate glucose levels in the bloodstream. Before treatment this results in high blood sugar levels in the body. The common symptoms of this elevated blood sugar are frequent urination, increased thirst, increased hunger, weight loss, and other serious complications. Additional symptoms may include blurry vision, tiredness, and slow wound healing. Symptoms typically develop over a short period of time, often a matter of weeks.

Richard K. Bernstein is a physician and an advocate for a low-carbohydrate diabetes diet to help achieve normal blood sugars for diabetics. Bernstein has type 1 diabetes. His private medical practice in Mamaroneck, New York is devoted solely to treating diabetes and prediabetes.

<span class="mw-page-title-main">Blood sugar regulation</span> Hormones regulating blood sugar levels

Blood sugar regulation is the process by which the levels of blood sugar, primarily glucose, are maintained by the body within a narrow range. This tight regulation is referred to as glucose homeostasis. Insulin, which lowers blood sugar, and glucagon, which raises it, are the most well known of the hormones involved, but more recent discoveries of other glucoregulatory hormones have expanded the understanding of this process. The gland called pancreas secrete two hormones and they are primarily responsible to regulate glucose levels in blood.

An insulin tolerance test (ITT) is a medical diagnostic procedure during which insulin is injected into a patient's vein, after which blood glucose is measured at regular intervals. This procedure is performed to assess pituitary function, adrenal function, insulin sensitivity, and sometimes for other purposes. An ITT is usually ordered and interpreted by endocrinologists.

Rabson–Mendenhall syndrome is a rare autosomal recessive disorder characterized by severe insulin resistance. The disorder is caused by mutations in the insulin receptor gene. Symptoms include growth abnormalities of the head, face and nails, along with the development of acanthosis nigricans. Treatment involves controlling blood glucose levels by using insulin and incorporating a strategically planned, controlled diet. Also, direct actions against other symptoms may be taken This syndrome usually affects children and has a prognosis of 1–2 years.

Chronic Somogyi rebound is a contested explanation of phenomena of elevated blood sugars in the morning. Also called the Somogyi effect and posthypoglycemic hyperglycemia, it is a rebounding high blood sugar that is a response to low blood sugar. When managing the blood glucose level with insulin injections, this effect is counter-intuitive to people who experience high blood sugar in the morning as a result of an overabundance of insulin at night.

References

  1. 1 2 3 "Hypoglycemia." It can also be referred to as "sugar crash" or "glucose crash." National Diabetes Information Clearinghouse, October 2008. http://diabetes.niddk.nih.gov/dm/pubs/hypoglycemia/ Archived February 8, 2015, at the Wayback Machine Archived version at https://web.archive.org/web/20180415102429/https://www.niddk.nih.gov/health-information/diabetes/overview/preventing-problems/low-blood-glucose-hypoglycemia
  2. ↑ "Hypos After Eating - Reactive Hypoglycemia" . Retrieved September 8, 2018.
  3. ↑ Service, FJ; Vella, A (June 11, 2018). "Postprandial (reactive) hypoglycemia". UpToDate. Retrieved September 8, 2018.
  4. 1 2 Hendrickson, Kirstin. "Side Effects of a Sugar Overdose". Demand Media, Inc. Retrieved November 8, 2011.
  5. ↑ Wang, Guanyu (October 15, 2014). "Raison d'être of insulin resistance: the adjustable threshold hypothesis". J R Soc Interface. 11 (101): 20140892. doi:10.1098/rsif.2014.0892. PMC   4223910 . PMID   25320065.
  6. ↑ "The Truth about Tryptophan". WebMD.
  7. ↑ "Hypoglycemia". National Diabetes Information Clearinghouse. U.S. Department of Health and Human Services. Archived from the original on February 8, 2015. Retrieved November 8, 2011.
  8. ↑ "Hypoglycemia". Mayo Foundation for Medical Education and Research. Mayo Clinic. Retrieved November 8, 2011.
  9. ↑ Simpson, Jamie. "Causes of Low Blood Sugar". Demand Media. Retrieved November 8, 2011.
  10. ↑ "Diabetes". American Dietetic Association. Retrieved November 11, 2011.
  11. ↑ Turner, Edward L. (November 1, 1933). "Inverted sugar tolerance curves in a case of Addison's Disease". Endocrinology. 17 (6): 699–702. doi:10.1210/endo-17-6-699.
  12. ↑ Pia A, Piovesan A, Tassone F, Razzore P, Visconti G, Magro G, Cesario F, Terzolo M, Borretta G (December 2004). "A rare case of adulthood-onset growth hormone deficiency presenting as sporadic, symptomatic hypoglycemia". J. Endocrinol. Invest. 27 (11): 1060–4. doi:10.1007/BF03345310. PMID   15754739. S2CID   1411317.
  13. 1 2 3 4 5 Brun JF, Fedou C, Mercier J (November 2000). "Postprandial reactive hypoglycemia". Diabetes Metab. 26 (5): 337–51. PMID   11119013.
  14. ↑ Açbay O, Celik AF, Kadioğlu P, Göksel S, Gündoğdu 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. S2CID   22096584.
  15. ↑ Hamdy O, Srinivasan V, Snow KJ. "Hypoglycemia". Medscape. WebMD LLC. Retrieved July 6, 2007.-Updated March 2018
  16. ↑ Umesh Masharani (2007). "Postprandial Hypoglycemia (Reactive Hypoglycemia)". The Hypoglycemic states - Hypoglycemia. Armenian Medical Network.
  17. ↑ Berlin I, Grimaldi A, Landault C, Cesselin F, Puech AJ (November 1994). "Suspected postprandial hypoglycemia is associated with beta-adrenergic hypersensitivity and emotional distress". J. Clin. Endocrinol. Metab. 79 (5): 1428–33. doi:10.1210/jcem.79.5.7962339. PMID   7962339.
  18. ↑ "How the Body Controls Blood Sugar". Web MD Diabetes. Healthwise Incorporated. Retrieved November 8, 2011.
  19. ↑ "Hypoglycemia". Hormonal and Metabolic Disorders. Merck Sharp & Dohme Corp. Retrieved November 8, 2011.
  20. 1 2 3 4 5 6 7 8 "Healthy Eating for Reactive Hypoglycemia". National Health Service (3rd ed.). UK. 2017. NHS Trust Docs ID: 10513 (Review date: 2020-06-11).
  21. ↑ Kenrose, S. The Reactive Hypoglycemia Sourcebook, 2009. ISBN   978-0-557-07407-5"
  22. ↑ Gregory, Justin M.; Muldowney, James A.; Engelhardt, Brian G.; Tyree, Regina; Marks-Shulman, Pam; Silver, Heidi J.; Donahue, E. Patrick; Edgerton, Dale S.; Winnick, Jason J. (September 2, 2019). "Aerobic exercise training improves hepatic and muscle insulin sensitivity, but reduces splanchnic glucose uptake in obese humans with type 2 diabetes". Nutrition & Diabetes. 9 (1): 25. doi:10.1038/s41387-019-0090-0. ISSN   2044-4052. PMC   6717736 . PMID   31474750.
  23. ↑ Gibala, Martin J; Little, Jonathan P (September 15, 2010). "Just HIT it! A time-efficient exercise strategy to improve muscle insulin sensitivity". The Journal of Physiology. 588 (Pt 18): 3341–3342. doi:10.1113/jphysiol.2010.196303. ISSN   0022-3751. PMC   2988497 . PMID   20843832.
  24. ↑ Collazo-Clavell, Maria. "Reactive Hypoglycemia". Mayo Foundation for Medical Education and Research. Retrieved November 11, 2011.
  25. ↑ "Hypoglycemia (Low Blood Sugar) in People Without Diabetes". Diabetes Health Center. WebMD, LLC. Retrieved November 8, 2011.
  26. ↑ Sanke, T; Nanjo, K; Kondo, M; Nishi, M; Moriyama, Y; Miyamura, K (October 1986). "Effect of calcium antagonists on reactive hypoglycemia associated with hyperinsulinemia". Metabolism: Clinical and Experimental. 35 (10): 924–7. doi:10.1016/0026-0495(86)90055-7. PMID   3762399.
  27. ↑ Guseva, Nina; Phillips, David; Mordes, John (January 2010). "Successful Treatment of Persistent Hyperinsulinemic Hypoglycemia with Nifedipine in an Adult Patient". Endocrine Practice. 16 (1): 107–111. doi:10.4158/EP09110.CRR. PMC   3979460 . PMID   19625246.
  28. ↑ "Postprandial Hypoglycemia" . Retrieved November 29, 2011.

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