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Technical Briefs |
We studied 73 otherwise healthy adults (47 women, 26 men), ages 40–81
years (mean 52.0 years; SD, 9.1 years), who visited physicians'
offices for a medical health check-up. None of the patients
showed signs of inflammatory bowel disease or any other chronic or
infectious diseases, and none was receiving medication. No vitamin
supplements were taken because this was an exclusion criterion. Blood
samples were collected after an overnight fast. Breath
H2 content was measured with a Bedfont
gastrolizer (Bedfont) (6)(7). A baseline
H2 breath test was performed after a 12-h
overnight fast. An oral dose of 50 g of fructose was given in 250
mL of tap water. All tests were performed between 0800 and 0830,
and body weight and height were measured. After the fructose load,
H2 exhalation was monitored in 30-min intervals
for at least 2 h. Maximum H2
exhalation after fructose load was registered, and the
differences from baseline (
H2) were
calculated. Fasting plasma samples were drawn into a 5-mL EDTA syringe,
and folic acid was measured by an immunoassay (Elecsys System 2010;
Boehringer Mannheim) according to the manufacturer's instructions.
The cutoff point for the diagnosis of fructose malabsorption was an
increase in breath H2 >20 µL/L above
baseline (1)(8). Subjects with increases in
breath H2 
20 µL/L above baseline were
considered normal fructose absorbers.
In 46 patients (17 men and 29 women; ages 51.7 ± 9.3 years,
mean ± SD), breath H2 concentrations
increased >20 µL/L above baseline fasting values; they were
therefore classified as fructose malabsorbers. The remaining 27
subjects (9 men and 18 women, ages 52.4 ± 9.1 years) were normal
fructose absorbers (H2 <20 µL/L). Plasma
folic acid was significantly lower in fructose malabsorbers (7.14
± 2.2 µg/L, mean ± SD) than in normal fructose absorbers
(9.1 ± 3.7 µg/L; P <0.01, Student
t-test; P <0.02, nonparametric Mann–Whitney
U-test; Fig. 1
.). The lower plasma folic acid concentration in fructose
malabsorption was independent of sex or age.
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Low plasma folic acid concentrations may be attributable to dietary deficiency or malabsorption of folic acid. Another cause may be an unfavorable bacterial composition in the gut because folic acid derived from colonic bacterial metabolism is a major source of resorbed folic acid. Because malnutrition is highly unlikely in our study population, the lower folic acid concentrations in fructose malabsorbers compared with normals are probably attributable to malabsorption of alimentary folic acid or changes in intestinal bacterial colonization. Fructose malabsorption is known to accelerate gastrointestinal transit when patients are exposed to fructose, thus reducing the contact time that is necessary for the absorption of (micro)nutrients. On the other hand, fructose malabsorption leads to a profound change in bacterial colonization, especially in the colon. Because a substantial amount of folic acid derives from intestinal bacteria, it seems reasonable that a change in the population of gastrointestinal bacteria could lead to a change in the plasma concentrations of folic acid. Fructose malabsorption can be seen in approximately one-third to one-half of the Western European population; therefore, fructose malabsorption could be a major cause of lower folic acid status.
Folic acid deficiency, like vitamin B6 and B12 deficiencies, may increase concentrations of homocysteine (9), which is known to be an additional risk factor for cardiovascular disease (10). Further studies are needed to determine whether fructose malabsorption is indeed associated with increased plasma homocysteine concentrations. In addition, folic acid deficiency has also been shown to increase the risk for development of neural tube defects in newborns (11)(12), and folic acid supplementation was found to reduce the relative risk for the development of colon carcinoma (13). These findings suggest that fructose malabsorption could be a risk factor in the development of these diseases.
Because bacterial metabolism alters folic acid status and intestinal bacterial colonization is altered by nutritional factors and carbohydrate malabsorption syndromes, dietary measurements should not rely solely on folic acid supplementation but should also consider carbohydrate malabsorption syndromes, especially fructose malabsorption. It is suggested that fructose malabsorption be considered in the elderly with folic acid deficiency. Further studies will be necessary to compare not only folic acid concentrations but also homocysteine, vitamin B12, and hematological indices in patients with and without fructose malabsorption.
References
The following articles in journals at HighWire Press have cited this article:
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  M. Ledochowski, B. Widner, C. Murr, and D. Fuchs Decreased Serum Zinc in Fructose Malabsorbers Clin. Chem., April 1, 2001; 47(4): 745 - 747. [Full Text] [PDF]
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