FODZYME®’s fructan hydrolase is the only enzyme that can target the broad spectrum of fructans. But did you know it is also effective in breaking down the disaccharide sucrose? Read on to learn more.
The most common disaccharides in the American diet are sucrose and lactose. Disaccharidases are enzymes found in the intestinal brush border that are responsible for the breakdown of these disaccharides into monosaccharides, which is necessary for absorption in the intestinal tract.
Sucrase-Isomaltase (SI) is an enzyme complex located along the small intestinal brush border. Sucrase metabolizes sucrose to its constituent monosaccharides - glucose and fructose. In addition, isomaltase targets oligosaccharides from starch breakdown, with help from sucrase and glucoamylase, to generate constituent monosaccharides. These monosaccharides are fairly quickly absorbed and metabolized (1, 2).
SI deficiency can result in increased osmotic load from malabsorbed sugars in the small intestine which can contribute to watery diarrhea (Fig 1). Subsequent fermentation of undigested sucrose by colonic bacterial microflora can release gas, causing further symptoms like bloating and abdominal pain. SI deficiency symptoms can thus mimic the symptoms commonly reported by patients with Disorders of Gut-Brain Interaction (DGBI) such as Irritable Bowel Syndrome (IBS) (3).
Fig 1: Effect of fermented sugars in disaccharidase deficient patients compared to healthy individuals (Ref: Vishwanathan L et al doi: 10.1007/s11894-023-00870-z.)
Disaccharidase deficiencies have been fairly well documented in young children to explain chronic abdominal pain (4). However, it has recently become evident that disaccharidase deficiencies in adults are more common than previously thought (5).
Specifically, Congenital sucrase-isomaltase deficiency (CSID), characterized by complete abrogation of SI enzyme function, typically manifests in infancy or early childhood and was historically considered to be a rare disorder (6). However, newer research has identified several mutations in the human sucrase gene which can result in an array of SI variants with different enzymatic activity ranging from absent to almost normal activity, referred to as adult partial SI deficiency (SID). With SID symptoms present later in life with varying severity. It is currently estimated that 2–9 % of Americans of European descent may be affected, suggesting that SI deficiency has been greatly under-recognized (3).
Secondary or acquired SI deficiency has also been recently described, often in association with damage to the enteric brush-border membrane secondary to infection or autoimmune disorders. Given the increasing awareness of genetic SI variants and their association with a spectrum of gastrointestinal symptom severity, researchers suggest a better term: genetic sucrase-isomaltase deficiency (GSID) (7). Overall, SI enzyme deficiency may be an important and overlooked cause of unexplained GI symptoms.
SI deficiency symptoms can often be improperly attributed to IBS as the two present very similarly. In fact, SID should be considered in the differential diagnosis of patients presenting with abdominal pain, diarrhea, or bloating. In a 2020 study, SID was found in 35% of patients with presumed IBS-D/M (10).
Further, functional SI gene variants have been associated with poorer symptom response to a low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) diet in IBS-D (11, 12). The low FODMAP diet does not limit sucrose or starch so if a patient does not respond to FODMAP restriction, SI may be suspected.
There is also accumulating evidence that partial SI deficiency is associated with increased risk of IBS in the general population (13, 14). Thus genetic defects in the SI gene may explain abdominal symptoms in some patients with IBS.
At its core, CSID/SID/GSID symptoms result from impaired hydrolysis of sucrose and certain starches, leading to maldigestion, osmotic diarrhea, and secondary symptoms. Hence standard management strategies for SI deficiency include:
Despite these approaches, many patients remain underserved, highlighting a need for additional, easier-to-access non-prescription enzymatic tools to help normalize sucrose and starch digestion.
Fructans are long chains (polymers) of fructose (monomer), typically with a sucrose (fructose + glucose) molecule at one end. FODZYME®’s patent-pending fructan hydrolase is known for its ability to cleave β-linked fructosyl residues in dietary fructans (e.g., inulin, fructo-oligosaccharides). But that’s not all. It also has notable sucrase (disaccharidase) activity, cleaving sucrose into its constituent monosaccharides - glucose and fructose.
The dual catalytic capacity of FODZYME®’s fructan hydrolase has been demonstrated in vitro assays.
This enzymatic versatility opens a new possibility: supporting sucrose digestion.
Habitual sucrose intake ranges between 20-25 g per day (9). Equally divided into 3 daily meals - this would amount to an average intake of 6-7 g sucrose per meal. Under standard assay conditions, FODZYME®’s fructan hydrolase has a sucrose degrading capacity of up to 40 g sucrose. Thus the fructan hydrolase in FODZYME® can readily tackle typical sucrose amounts present in a regular meal, as well as the occasional, indulgent sucrose-heavy meal.
Clinical implication: fructan hydrolase could support better digestion of sucrose when consuming sucrose-containing foods.
Disaccharidase deficiencies often present as defects in more than one enzyme. This can often be the case with secondary or acquired SI deficiency. 20% of abnormal disaccharidase levels in adults stem from a defect in all 4 important disaccharidases located at the intestinal brush border - maltase, sucrase, isomaltase and lactase (8). Along with its sucrase activity, FODZYME®’s formula can also provide the much needed lactase activity to target the abundant dietary disaccharide lactose.
Poor tolerance to disaccharides may be more common than previously suspected. FODZYME®’s fructan hydrolase targets not only fructans, but sucrose as well. For clinicians, this represents an exciting potential addition to support better digestion of common carbohydrate triggers - one that may help expand food options and support digestive flexibility, making it easier to enjoy a wider variety of meals.