The causes and consequences of fat malabsorption Skip to content

The causes and consequences of fat malabsorption

Essential fatty acids are indispensable building blocks of human health

Fatty acids are derived from medium-chain triglycerides (MCTs) and long-chain triglycerides (LCTs). When hydrolyzed, LCTs yield omega-3 fatty acids, which benefit human health. LCTs are an important source of omega-3 fatty acids.1

Omega-3 fatty acids strengthen the development and functioning of:


Brain + Retina

Have highly specialized functional roles in normal signal transduction, neurotransmission, and neurogenesis2,3,4



Help lower blood pressure and improve blood vessel function5



Play a key role in numerous metabolic processes in addition to acting as a source of energy1,6



Are released from membranes by phospholipases for conversion to mediate immune function, platelet aggregation, and lipid homeostasis1,3

Omega-3 fatty acids can ease inflammation before it causes widespread damage to the body.2

  • Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may have clinically important anti-inflammatory effects in a variety of conditions associated with fat malabsorption.2
  • A balanced ratio of omega-6 to omega-3 fatty acids has been shown to reduce the risk of many chronic diseases and is beneficial in maintaining normal development and overall health.7
  • Fats can increase caloric uptake and, when compared with proteins and carbohydrates, are a greater source of calories (9 kcal/gram vs 4 kcal/gram for proteins and carbohydrates).8

Fat malabsorption has devastating consequences

Gastrointestinal (GI) symptoms associated with fat malabsorption:9

  • Diarrhea
  • Steatorrhea
  • Abdominal pain
  • Nausea
  • Bloating
  • Constipation

Overall short- and long-term health impacts are multisystemic and varied:10,11,12

  • Weight loss or an inability to gain weight
  • Intestinal obstructions
  • Diabetes
  • Respiratory issues
  • Chronic infections
  • Impaired bone health (vitamin K deficiency)
  • Even death

In critically ill patients in the ICU, an inflammation-modulating diet enriched with eicosapentaenoic acid (EPA) and γ-linolenic acid gamma-linolenic acid (GLA) resulted in:13


83% risk reduction of developing new organ failures


60% risk reduction of 28-day in-hospital all-cause mortality


~5 fewer days on mechanical ventilation


~4 fewer days in the ICU

Exocrine Pancreatic Insufficiency (EPI)

Fat malabsorption is associated with exocrine pancreatic insufficiency (EPI), a health condition where the body does not produce enough digestive enzyme or produces digestive enzymes that do not work properly. Children are most vulnerable to the consequences of untreated EPI and a delayed diagnosis often results in growth and developmental delays in addition to poor quality of life.14

Deficiency of pancreatic lipase

  • Pancreatic lipase is essential to break down fats into fatty acids and accounts for a majority of fatty acid digestion.15,16
  • As pancreatic insufficiency progresses, lipid malabsorption causes many clinical symptoms and nutritional deficiencies while protein and starch digestion are usually maintained at a normal physiologic level.17
  • Patients with compromised pancreatic output have a higher risk for fatty acid deficiencies, which may result in adverse cellular responses to metabolic processes, such as inflammation, gene expression in the cell, and cellular protein production.18
  • Among patients with cystic fibrosis, fat malabsorption is associated with low BMI and poor outcomes that can have an impact on digestive symptoms, nutritional status, physical functioning, treatment burden, body image, and pain.19.20

Conditions commonly associated with fat malabsorption and EPI:21,22

  • Cystic fibrosis
  • Acute/chronic pancreatitis
  • Pancreatic cancer
  • Crohn’s disease
  • Celiac disease
  • Other inflammatory bowel diseases
  • Short bowel syndrome
  • Other cancers
  • Abdominal surgery
  • Trauma/critical care

RELiZORB is formulated for enteral nutrition

Enteral formulas contain a type of fat called triglycerides. Triglycerides are more stable and do not spoil as quickly as other types of fats, but some triglycerides are not absorbed by the body without first being broken down, resulting in fat malabsorption.

Pancreatic enzyme replacement therapy, or PERTs, are capsules containing the digestive enzymes the body would normally produce, but PERTs are designed to be taken orally and are not intended to be crushed or added to enteral formula.

RELiZORB connects directly to the feeding tube and is the only enzyme product designed to break down fats in enteral formula. The iLipase in RELiZORB is able to break down the triglycerides into absorbable forms (fatty acids and monoglycerides) during enteral feeding, before entering the body.

feeding tube

Pancreatic enzyme replacement therapy (PERT) capsules are not indicated for enteral feeding systems

PERT capsules are indicated for oral use only and are not intended to be crushed or added to enteral feeding regimens.23 PERT capsules have been shown to result in clogged feeding tubes.24

The enteric-coated microspheres in PERTs may separate from meal contents in the stomach and not adequately mix during delivery to the small intestine25 and some unprotected enzymes may fail due to prolonged exposure to gastric acid.26

RELiZORB hydrolyzes fats prior to ingestion and is the only FDA-cleared enzyme product to hydrolyze fats in enteral formula.

RELiZORB vs. oral PERT for continuous overnight enteral feeding

RELiZORB is intended to provide continuous fat hydrolysis during overnight enteral feeding*
Oral PERT is active in the GI tract for about 45-60 minutes after administration[CFF]

*Timing is based on volume and flow rate. A single RELiZORB cartridge can be used for up to 500mL of formula at a rate of 10-120 mL/hr. A tandem RELiZORB cartridge configuration can be used for over 500mL and up to 1000mL of formula at a rate of 24-120 mL/hour. Please see additional details in the Instructions for Use.

  1. National Institutes of Health Website. Omega-3 fatty acids: fact sheet for professionals. Accessed October 16, 2017.
  2. Calder PC. Omega-3 fatty acids and inflammatory processes. Nutrients. 2010;2(3):355-374.
  3. Abedi E, Sahari MA. Long-chain polyunsaturated fatty acid sources and evaluation of their nutritional and functional properties. Food Sci Nutr. 2014;2(5):443-463.
  4. Uauy R, Mena P, Rojas C. Essential fatty acids in early life: structural and functional role. Proc Nutr Soc. 2000;59(1):3-15.
  5. Harvard School of Public Health Website. The Nutrition Source. Omega-3 fatty acids: an essential contribution. Accessed October 16, 2017.
  6. Prentice AM, Paul AA. Fat and energy needs of children in developing countries. Am J Clin Nutr. 2000;72(5 Suppl):1253S-1265S.
  7. Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002 Oct;56(8):365-79.
  8. Cleveland Clinic Website. Fat and calories. Accessed October 16, 20.
  9. Blaauw R. Malabsorption: causes, consequences, diagnosis and treatment. S Afr J Clin Nutr. 2011;24(3):125-127.
  10. Mayo Clinic Website. Cystic fibrosis: symptoms and causes. symptoms-causes/dxc-20211893. Accessed October 16, 2017.
  11. Kalnins D, Wilschanski M. Maintenance of nutritional status in patients with cystic fibrosis: new and emerging therapies. Drug Des Devel Ther. 2012;6:151-161.
  12. Dominguez-Munoz JE. Pancreatic exocrine insufficiency: diagnosis and treatment. J Gastroenterol Hepatol. 2011;26(2):12-16.
  13. Pontes-Arruda, A, et al. The use of an inflammation-modulating diet in patients with acute lung injury or acute respiratory distress syndrome: a metaanalysis of outcome data. JPEN. 2008;32(6)596-605.
  14. Sankararaman S, Schindler T, and Sferra TJ. Management of Exocrine Pancreatic Insufficiency in Children. Nutrition in Clinical Practice. 2019;34(1):S27-S42.
  15. Whitcomb DC, Lowe ME. Human pancreatic digestive enzymes. Dig Dis Sci. 2007;52:1-17.
  16. Carriere F, Barrowman JA, Verger R, Laugier R. Secretion and contribution of lipolysis of gastric and pancreatic lipases during a test meal in humans. Gastroenterology. 1993;105:876-888.
  17. Fieker A, Philpott J, Armand M. Enzyme replacement therapy for pancreatic insufficiency: present and future. Clin Exp Gastroenterol. 2011;4:55-73.
  18. Mogensen KM.Essential Fatty Acid Deficiency. Practical Gastroenterology. 2017;41(6):37-44.
  19. Bodnar R, Kadar L, Holics K, et al. Factors influencing quality of life and disease severity in Hungarian children and young adults with cystic fibrosis. Ital J Pediatr. 2014;2:40-50.
  20. Sawiki GS, Rasouliyan L, McMullen AH, et al. Longitudinal assessment of health-related quality of life in an observational cohort of patients with cystic fibrosis. Pediatr Pulmonol. 2011;46(1):36-44.
  21. Singh VK, Haupt ME, Geller DE, Hall JA, Quintana Diez PM. Less common etiologies of exocrine pancreatic insufficiency. World J Gastroenterol. 2017; 23(39): 7059-7076.
  22. MedLinePlus Website. Accessed October 7, 2021.
  23. Berry AJ. Pancreatic enzyme replacement therapy during pancreatic insufficiency. Nutr Clin Pract. 2014;29(3):312-321.
  24. Ferrie S, Graham C, Hoyle M. Pancreatic enzyme supplementation for patients receiving enteral feeds. Nutr Clin Pract. 2011;26(3):349-351.
  25. Trang T, Chan J, Graham DY. Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency in the 21st century. World J Gastroenterol. 2014;20(33):11467-11485.
  26. Kalnins D, Wilschanski M. Maintenance of nutritional status in patients with cystic fibrosis: new and emerging therapies. Drug Des Devel Ther. 2012;6:151-161.
  27. Cystic Fibrosis Foundation. Accessed April 19, 2018.