The unexpected truth about dates and hypoglycemia : Journal of Family and Community Medicine

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The unexpected truth about dates and hypoglycemia

Yasawy, Mohammed I.

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Journal of Family and Community Medicine 23(2):p 115-118, May–Aug 2016. | DOI: 10.4103/2230-8229.181008
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The date fruit is one of the oldest cultivated trees, numerous varieties of which are widely grown in Saudi Arabia. In many ways, dates may be considered as an ideal food to provide a wide range of essential nutrients and potential health benefits.[1]

Antioxidant and anti-inflammatory assays confirm bioactive compounds in Ajwa dates.[2] Their content of natural sugars depends on the variety. As the date fruit dries, the sugar becomes concentrated. Total sugar may be about 70%, mainly in the form of glucose and fructose with small fractions of maltose and sucrose. Chemical composition of different types of dates is shown in Table 1.[3] In patients with heredity fructose intolerance (HFI) which is a rare hereditary disorder, the presence of significant amount of fructose in dates can lead to symptoms and complications. Table 2 provides a list of other foods (including honey) which have high content of fructose.[4]

Table 1:
Chemical Composition of various types of dates in Saudi Arabia
Table 2:
Some foods with high fructose content

The term of fructose intolerance is a general term that describes two possible conditions.

Hereditary fructose intolerance

This is a rare autosomal recessive genetic disorder that results from a deficiency of fructose-1-phosphate aldolase in the liver, intestines, and kidneys. The estimated incidence is one in 20,000 live births,[5] but the prevalence of HFI in adults is difficult to estimate since the majority of patients are asymptomatic and affected people may simply avoid the ingestion of most or all sweets.

The clinical symptoms were first described by Chambers and Pratt in 1956.[6] Affected individuals fail to metabolize fructose completely in the liver, kidney, and intestines because of aldolase enzyme deficiency, and the ingestion of fructose causes symptoms such as abdominal pain and vomiting with hypoglycemia. In the early and mid-20th century, death from fructose infusion was frequently reported in Europe in this group of population.[7] If fructose intake is restricted and its intravenous (IV) administration is strictly avoided, serious life-threatening complications can be prevented. Continuous use of oral fructose intake may lead to renal failure and liver cirrhosis.[89]

Fructose malabsorption

Patients have difficulty in absorbing fructose because of the deficiency of co-transporters in the small intestine. This is a less serious disorder because it does not result in liver or kidney damage but can cause abdominal pain, bloating, gas, and diarrhea. Fructose malabsorption (FM) is not a rare condition and is found in up to 30% of the population.[1011]

Because of the similarity of symptoms between HFI and FM and the similar type of diets causing the problems, HFI may be confused with FM. An easy way to differentiate the two is by performing fructose intolerance test (FIT) and fructose breath test (FBT). FIT is positive in HFI while positive FBT indicates FM. Other diagnostic tests include intestinal, kidney, or liver biopsy to assess aldolase enzyme deficiency and DNA analysis for mutated gene in suspected cases for the confirmation of HFI.[1213]


This report is based on three patients, from the same family, who live in a date growing region of the Kingdom of Saudi Arabia (KSA). The patients had visited several medical centers without any definite answer or diagnosis being made. These patients were then referred to the Gastroenterology Clinic of the King Fahd Hospital of the University, Al-Khobar, KSA. The data were obtained by taking careful history and laboratory investigations, and a final diagnosis of HFI was made after an FIT.


The first patient was a 32-year-old male who was a well-educated government employee from the eastern region of KSA. He was also known to have ulcerative colitis and was well controlled on treatment. He was referred to the Gastroenterology Clinic of the King Fahd Hospital of the University, Al-Khobar, KSA, for the evaluation of episodic nonspecific abdominal pain with easy fatigability and sweating. He reported that his symptoms were associated with possible ingestion of dates but had no problem with the usual amounts of dairy products. He also mentioned that he is allergic to honey which makes him slow, tired, shivery, and sleepy (symptoms of hypoglycemia). He could not recall if his parents had any similar problem. The other two patients were the younger sisters of this patient, who also suffered from similar problems after the intake of dates and honey. They had made frequent visits to many peripheral clinics. Unfortunately, only one of the sisters was able to take the test.

They neither had any abnormal physical finding nor suffered from anemia, kidney, or liver problem. Thyroid function test and insulin level were reported normal. Repeated stool analysis, percutaneous abdominal ultrasound, and upper gastrointestinal endoscopy were performed, and all were normal.

Hydrogen breath test for fructose malabsorption did not show any positive results. During repeated follow-up visits, they always referred again and again to their experiences with the intake of dates and the symptoms of hypoglycemia. A question of adult HFI was, therefore, raised. They were offered fructose infusion test; however, after they were given detailed descriptions of the test, they refused IV fructose infusion. However, they agreed to take the FIT, one of the diagnostic tests for HFI that required the ingestion of a specific amount of fructose followed by periodic measurements of sugar levels in the blood.

They were given 1 g of fructose of per kg body weight. The tests revealed gradual decrease in the blood glucose levels, from about 100 mg/dl to about 60 mg/dl at 150 min [Table 3]. The patients also developed significant hypoglycemic symptoms which were controlled with dextrose infusion after completion of the test. The patients were discharged after being stabilized. Based on the results of FIT and aforementioned symptoms, the patients were diagnosed as adult HFI. They were referred to a dietitian who advised fructose-free diet. The patients felt well and were free of symptoms.

Table 3:
Results of oral fructose intolerance test (1 g of fructose of per kg body weight)


Fructose is a sugar found naturally in many fruits (including dates) and honey. It is absorbed from the small intestine by active transport, metabolized primarily in the liver and kidney and partially in the small intestine and adipose tissue.[812]

Deficiency in aldolase B in the above-mentioned areas causes fructose intolerance.[1415] After ingestion, fructose rapidly enters the hepatocytes where fructose is phosphorylated to fructose-1-phosphate. Because of the deficiency of enzyme fructose-1-phosphate aldolase in HFI, which splits fructose-1-phosphate into glyceraldehydes and dihydroxy-acetones-phosphate, the accumulation of fructose-1-phosphate results in the inhibition of other enzymes namely phosphorylase, liver fructose 1–6 bisphosphate aldolase, and fructose kinase. This results in impaired glycogenolysis and gluconeogenesis and induced hypoglycemia,[1516] which can lead to further life-threatening complications such as hepatorenal damage and death.[91718] Further, a series of cases of fatalities due to intravenous fructose infusion has been reported in some European hospitals.[51314] The cause of severe hepatic dysfunction remains unknown but may be a manifestation of focal cytoplasmic degeneration and cellular fructose toxicity. Hypoglycemia and acidosis may act together to cause organ damage, shock, or coma. Mortality may result from any or all of the above conditions.[71519]

Fortunately, most of the patients start gradually avoiding diets that contain fructose due to the previous undesirable experiences so are saved from severe complications and side effects as was mentioned in an earlier case report of a 50-year-old German woman.[13] Definitive therapy simply consists of avoidance of fructose-containing diet. Continuous intake of fructose in the diet can lead to complications. Eliminating fructose early in the course of the disease totally restores the affected child's health. The prognosis is excellent for infants who are rapidly diagnosed and are fructose-containing diet avoided sooner. In such individuals, life expectancy remains normal.


Dates contain high amounts of sugar. So it's unusual to lead to hypoglycemia. But If incase that happens, one should consider a rare condition i.e,., hereditary fructose intolerance.

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Conflicts of interest

There are no conflicts of interest.


We thank Professor Mohammad Akram Randhawa for his review.


1. Al-Shahib W, Marshall RJ. The fruit of the date palm: Its possible use as the best food for the future? Int J Food Sci Nutr. 2003;54:247–59
2. Zhang CR, Aldosari SA, Vidyasagar PS, Nair KM, Nair MG. Antioxidant and anti-inflammatory assays confirm bioactive compounds in Ajwa date fruit J Agric Food Chem. 2013;61:5834–40
3. Alkaabi JM, Al-Dabbagh B, Ahmad S, Saadi HF, Gariballa S, Ghazali MA. Glycemic indices of five varieties of dates in healthy and diabetic subjects Nutr J. 2011;10:59
4. . USDA National Nutrition Database Foods with high fructose content. Release. 2007
5. Gitzlmann R, Baerlocher K. Vorteil und Nuchteile der Fructose in der Nahrung Padiatr Fortbidk Praxis. 1973;37:40–55
6. Chambers RA, Pratt RT. Idiosyncrasy to fructose Lancet. 1956;271:340
7. Cox TM. Iatrogenic deaths in hereditary fructose intolerance Arch Dis Child. 1993;69:413–5
8. Froesch ER. Disorders of fructose metabolism Clin Endocrinol Metab. 1976;5:599–611
9. Ananth N, Praveenkumar GS, Rao KA, Vasanthi, Kakkilaya S. Two cases of hereditary fructose intolerance Indian J Clin Biochem. 2003;18:87–92
10. Rao SS, Attaluri A, Anderson L, Stumbo P. Ability of the normal human small intestine to absorb fructose: Evaluation by breath testing Clin Gastroenterol Hepatol. 2007;5:959–63
11. Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ Modern Nutrition in Health and Disease. 2009 Baltimore, MD Lippincott Williams and Wilkins
12. Hers HG, Joassin G. Anomaly of hepatic aldolase in intolerance to fructose Enzymol Biol Clin (Basel). 1961;1:4–14
13. Yasawy MI, Folsch UR, Schmidt WE, Schwend M. Adult hereditary fructose intolerance World J Gastroenterol. 2009;15:2412–3
14. Cox TM, O'Donnell MW, Camilleri M, Burghes AHCowett RM. Isolation and characteristics of a mutant liver aldolase in adult hereditary fructose intolerance Principles of Perinatal - Neonatal Metabolism. 2012 Heidelberg, Germany Springer Science & Business Media
15. Devlin TM Textbook of Biochemistry with Clinical Correlations. 2015 Philadelphia John Wiley & Sons
16. Cox TM. Hereditary fructose intolerance Baillieres Clin Gastroenterol. 1990;4:61–78
17. Burmeister LA, Valdivia T, Nuttall FQ. Adult hereditary fructose intolerance Arch Intern Med. 1991;151:773–6
18. Jamar S, Evenepoel P, Kuypers D, Maes B, Vanrenterghem Y. A young patient with unexplained acute hepatorenal dysfunction Nephrol Dial Transplant. 2003;18:1220–2
19. Ali M, Rosien U, Cox TM. DNA diagnosis of fatal fructose intolerance from archival tissue Q J Med. 1993;86:25–30

Dates; heredity fructose intolerance; hypoglycemia

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