Treating GI Disease Begins with a GI Diet:
When to Consider GI Low Fat
When to Consider GI High Energy
Craig B. Webb, PhD, DVM, DACVIM
The foundation of treatment for the vast majority of gastrointestinal (GI) diseases in dogs and cats
begins with diet. In fact, in some cases, it ends with diet. At one end of the spectrum you have patients
with Food Intolerance and a single offending component, ingredient, or additive must be eliminated
from the patient’s diet. At the other end of the spectrum you have idiopathic Inflammatory Bowel
Disease (IBD), where in extreme cases, every imaginable antigen must be eliminated using an
extensively hydrolyzed diet.
1,2
This paper will examine the evidence and appropriate use of two of the
veterinary diets that fall in between these extremes: a low fat GI diet and a high energy GI diet.
Low Fat GI Diets
The definition of a “low fat” veterinary diet is somewhat arbitrary, and the fat content of a pet food diet
may be represented in a variety of ways. Reducing the fat content of a diet is the most effective way to
reduce that diet’s caloric content, so low fat diets are commonly used for weight loss. The use of a low
fat diet in GI disease is aimed at an entirely different target.
A minimum fat content and essential fatty acids are required for normal metabolic functions.
A diet with a fat content of less than 25g/1000 kcal (generally less than 8% fat content on a dry
matter basis) is considered a low fat diet.
The best assessment of dietary fat is the fat content based on metabolizable energy (ME), the
percentage of calories coming from fat versus protein and carbohydrate.
The digestion and absorption of fat is a complex process involving pancreatic enzymes, bile
acids, micelle formation, and chylomicron absorption.
It takes significant mucosal inflammation, gallbladder obstruction, exocrine pancreatic
insufficiency, or lymphatic dysfunction before significant fat appears in the stool (steatorrhea).
Dietary fat content is correlated with transit time through the stomach; the more fat, the longer a
meal remains in the stomach. This property makes fat content a “motility modifier.”
The following table is a small sample of commercially available products and homemade ingredients to
provide a general comparison of the fat content of various GI diets.*
*(from Dr. Sara Wennogle, with permission)
a
% metabolizable energy (ME)
b
Not complete and balanced, should not be fed exclusively for extended period of time without appropriate supplements
Low Fat GI Diets for Pancreatitis
Fat restricted diets are critical in the treatment of hyperlipidemia. Although not a GI disease,
hyperlipidemia is one cause of pancreatitis in humans and may be the cause, a contributing factor, or a
consequence of pancreatitis in dogs.
Humans with hyperlipidemia are at increased risk of developing acute, severe pancreatitis.
3,4
In these patients, dietary intervention is potentially the sole successful treatment for severe
hypertriglyceridemia.
3,4
Feeding a low fat diet is used to reduce the discomfort of chronic pancreatitis in human patients.
5
Hypertriglyceridemia also appears to be a risk factor for canine pancreatitis.
6,7,8
Pancreatitis is prevalent in Miniature Schnauzers and a number of other breeds with primary
hypertriglyceridemia.
9,10
Comparison of Select Diets Used in the Management of Gastrointestinal Disease in Dogs
Protein Source
% Fat Dry
a
% Fat Can
a
Royal Canin Veterinary Diet® Canine Hydrolyzed Protein Adult HP
Soy protein isolate
43
34
Royal Canin Veterinary Diet® Ultimino®
Hydrolyzed poultry by-
products aggregate
38
Royal Canin Veterinary Diet® Canine Hydrolyzed Protein Moderate
Calorie
Soy protein isolate
29
Royal Canin Veterinary Diet® Canine Selected Protein Adult KO
Kangaroo
29
Hills Prescription Diet® z/d® Canine
Chicken
32
31
Royal Canin Veterinary Diet® Canine Selected Protein Adult PV
Venison
29
41
Royal Canin Veterinary Diet® Canine Selected Protein Adult PW
Moderate Calorie
Whitefish
25
Purina® Pro Plan® Veterinary Diet HA Hydrolyzed®
Soy protein isolate
24
Hills Prescription Diet® i/d® Low Fat
Chicken, turkey, pork
17
20
Royal Canin Veterinary Diet® Gastrointestinal Low Fat LF
Chicken, pork
17
16
Purina® Pro Plan® Veterinary Diet EN Gastroenteric Low Fat ®
Chicken
16
20
Tilapia/sweet potato (weight ratio 2.5:1 baked tilapia: baked sweet
potato)
b
Tilapia
13
White tuna/potato (weight ratio 3:1 canned white tuna in water: boiled
potato)
b
Tuna
10
Although direct evidence to support the use of a low fat diet for the prevention or the treatment
of canine pancreatitis is lacking, preliminary work and expert opinion strongly favors this
approach.
11-15
It has not yet been demonstrated that fat restriction is an important component in the prevention
or treatment of feline pancreatitis. With the decrease in caloric density and increase in
carbohydrate content of low fat diets, these are not considered necessary or appropriate for cats
with pancreatitis.
16-18
Low Fat GI Diets for Lymphangiectasia
Intestinal lymphangiectasia is, by definition, a malabsorption of lipids through the lymphatic system of
the GI tract. The lymphatic vessels are dilated, often to the point of being visible on gross endoscopic
examination, and dysfunctional, resulting in chronic diarrhea.
19
This condition is often severe enough to
result in a protein-losing enteropathy. Lymphangiectasia may be a primary GI problem, as seen in
Yorkshire terriers, or it may be an important component of the more commonly diagnosed condition,
IBD.
20
It is critical that dogs diagnosed with intestinal lymphangiectasia be treated with a low fat GI
diet. This is, in fact, the foundation of treatment in these cases.
21
A low fat diet is especially important in dogs with lymphangiectasia that fail treatment with
glucocorticoids. In fact, an argument can be made for treating canine lymphangiectasia with a
low fat diet before instituting steroid therapy.
21
Because lymphatic dilation is frequently observed as part of the histopathology of biopsy reports
that conclude with a diagnosis of IBD, instituting a low fat or even anultra-low fat” diet
(between 14 and 20 grams/1000 kcal) may be an important therapeutic trial in IBD dogs that fail
glucocorticoid and hypoallergenic dietary treatment.
22
Use of a Low Fat GI Diet for Gastric Motility Modification
In assessing the effect of dietary fat on gastric and intestinal function in humans, it has been shown that
a high fat diet will alter pyloric pressure, delay gastric emptying, decrease intestinal transit time, and
increase gastroduodenal reflux.
23,24
Diet modification, i.e. increased fiber and decreased fat, is used as one intervention to help
prevent gastroesophageal reflux disease (GERD) and reduce clinical symptoms of gastroparesis
in humans.
25,26,27
GERD in dogs and cats is most commonly recognized in association with anesthesia but can be
demonstrated (e.g. using fluoroscopy) in a number of cases as a component of esophageal or
gastric dysmotility.
28,29,30
Although pharmacologic intervention with gastric acid reducers is the most common approach to
GERD in veterinary patients, it would appear sensible to have these patients on a low fat GI diet.
A similar argument might be made for any condition where it would be beneficial to move
gastric contents in an aboral direction relatively quickly: chronic vomiting, regurgitation, GDV,
bloat, etc.
High Energy GI Diets
The basic premise of a High Energy GI Diet is to provide a high caloric density formula with ingredients
that are “GI friendly,” i.e. highly digestible and very palatable to the patient. GI diets will frequently
contain prebiotics, omega-3 fatty acids and/or antioxidants to directly enhance the health and function of
the GI mucosa. These high energy GI diets are most commonly seen in the critical care setting or in pets
recovering from diseases associated with hyporexia – a patient population that frequently requires a
feeding tube where small volume-high kcal, highly digestible feedings are ideal.
The following table highlights several of the high energy diets used predominantly in critical care
patients.
*These cans are often mixed with water to produce a formula that approximates 1-2 kcal/ml for use through a feeding tube.
The caloric content can be further increased by blending the canned diet with CliniCare.
Comparison of Select Diets Used in the Management of Critical Care Patients Metabolizable Energy (ME)
Kcal/can*
% Fat
% Protein
Royal Canin Veterinary Diet® Feline & Canine Recovery® RS
183
59
37
Purina® Pro Plan® CN Critical Nutrition®
211
63
28
Hills Prescription Diet® Urgent Care a/d®
183
33
44
Although currently there is a paucity of literature or clinical trials in this area, in theory the use of a high
energy GI diet may have a number of benefits in a more diverse, non-critically ill patient population.
Dogs consuming a high volume of food are at increased risk for gastric dilatation-volvulus
(GDV).
31
GDV is most prevalent in large and giant breed dogs, where the daily caloric
requirement might necessitate feeding a large volume of food. One solution is multiple small
meals per day, but another strategy would be to feed smaller amounts of a higher caloric density
GI diet.
Maintaining an optimal weight is an important component of the quality of life for dogs and cats
with cardiac disease or cancer.
32,33
These patients often have decreased appetites and experience
nausea for a variety of reasons, e.g. medications, stress, metabolic changes, intestinal perfusion
and motility abnormalities, etc.
Although cardiac patients may have a number of specific dietary requirements, maintaining
optimal weight with a high caloric density GI diet may be appropriate in a number of cases.
Cancer cachexia results from alterations in metabolism and can impact quality of life, treatment
schedules and success, and, ultimately, life expectancy. As with cardiac disease, there may be a
number of specific dietary or supplementation requirements, but a high caloric density GI diet
may be beneficial in a number of these cases.
Feline hepatic lipidosis is a unique condition of anorectic cats where the foundation of successful
treatment is getting nutrition in to these patients. Feeding energy dense diets high in protein is
critical and does not promote increased hepatic lipid accumulation.
34
Part of the treatment for many esophageal motility disorders, megaesophagus, and regurgitation
involves labor-intensive modifications in the frequency, volume, pace, and positioning of
patients during feedings. This places a premium on getting as many kcal as possible into as small
a volume of food as possible.
The following table highlights several of the high energy GI diets available for use in non-critically ill
patients.
Conclusion
The increased understanding and ongoing diversification of veterinary nutrition has greatly expanded the
potential use of GI diets as both diagnostic and therapeutic tools. Although the veterinary practitioner
cannot be expected to double as a nutritionist, they can and will be called upon to make informed
decisions (and educated guesses!) regarding the optimal dietary strategy for a variety of GI signs and
diseases. There are huge gaps in our knowledge, and in order to make evidence-based decisions our
profession is in dire need of well-designed clinical investigations. In the interim, it will benefit our
patients if we make the effort to base dietary recommendations on thoughtful consideration of the
patient’s problem, and the dietary possibilities.
Comparison of Select Diets Used in the Management of non-Critical Care Patients Metabolizable Energy (ME)
Kcal/can or cup
% Fat
% Protein
Royal Canin Veterinary Diet® Canine GI High Energy® Can
424
51
27
Royal Canin Veterinary Diet® Canine GI High Energy® Dry
394
44
22
Royal Canin Veterinary Diet® Feline GI High Energy® Can
180
51
30
Royal Canin Veterinary Diet® Canine GI High Energy® Dry
441
48
29
Purina® Pro Plan® EN Gastroenteric Canine Formula® Can
405
38
32
Purina® Pro Plan® EN Gastroenteric Canine Formula® Dry
397
29
25
Purina® Pro Plan® EN Gastroenteric Feline Formula® Can
151
44
40
Purina® Pro Plan® EN Gastroenteric Feline Formula® Dry
610
38
47
References:
1. Mandigers P, German AJ. Dietary hypersensitivity in cats and dogs. Tijdschr Diergeneeskd.
2010;135:706-10.
2. Gaschen FP, Merchant SR. Adverse food reactions in dogs and cats. Vet Clin North Am Small
Anim Pract. 2011;41:361-79.
3. Adiamah A, Psaltis E, Crook M, Lobo DN. A systematic review of the epidemiology,
pathophysiology and current mamangement of hyperlipidaemic pancreatitis. Clin Nutr
2017;[Epub ahead of print]
4. Rawla P, Sunkara T, Thandra KC, Gaduputi V. Hypertriglycertidemia-induced pancreatitis:
updated review of current treatment and preventive strategies. Clin J Gastroenterol 2018;[Epub
ahead of print]
5. Gachago C, Draganov PV. Pain management in chronic pancreatitis. World J Gastroenterol
2008;14:3137-48.
6. Xenoulis PG, Steiner JM. Canine hyperlipidemia. J Sm Anim Pract 2015;56:595-605.
7. Xenoulis PG, Cammarata PJ, Wooten K, et al. Serum triglyceride and cholesterol concentrations
and lipoprotein profiles in dogs with naturally occurring pancreatitis and healthy control dogs. J
Vet Intern Med (Abstract) 2011;25:1488
8. Verkest KR, Fleeman LM, Rand JS, et al. Subclinical pancreatitis is more common in
overweight and obese dogs if peek postprandial triglyceridemia is >445 mg/dL (Abstract) J Vet
Intern Med 2008:22;804.
9. Xenoulis PG, Suchodolski JS, Ruaux CG, Steiner JM. Association between serum triglyceride
and canine pancreatic lipase immunoreactivity concentrations in miniature schnauzers. J Am
Amin Hosp Assoc 2010;46:229-43.
10. Xenoulis PG, Levinski MD, Suchodolski JS, et al. Serum triglyceride concentrations in
Miniature Schnauzers with and without a history of probable pancreatitis. J Vet Intern Med
2011;25:20-25
11. Xenoulis PG, Suchodolski JS, Steiner JM, et al. Effect of a low-fat diet on serum triglyceride,
cholesterol, and pancreatic lipase immunoreactivity concentrations in Miniature Schnauzers with
hypertriglyceridemia. (Abstract) J Vet Intern Med 2011;25:687
12. Kerl ME, Johnson PA. Nutritional plan: Matching diet to disease. Clin Tech Small Anim Pract
2004;19:9-21.
13. Zoran D. Nutritional management of gastrointestinal disease. Clin Tech Small Anim Pract
2003;18:211-217.
14. Mansfield C, Beths T. Management of acute pancreatitis in dogs: a critical appraisal with focus
on feeding and analgesia. J Sm Anim Pract 2015;56-27-39.
15. Hernandez J, Pastor J, Simpson K, et al. Main pitfalls in the management of pancreatitis. Vet
Focus 2010;Special Issue:20-27.
16. Michel KE. Dietary management of canine and feline pancreatitis. In: Proceed Atlantic Coast
Vet Conf, Atlantic City, 2002: www.vin.com
17. Zoran DL. Pancreatitis in cats: diagnosis and management of a challenging disease. J Am Anim
Hosp Assoc 2006;42:1-9.
18. Armstrong PJ, Williams DA. Pancreatitis in cats. Top Comp An Med 2012;27:140-47.
19. García-Sancho M, SAinz A, Villaescusa A, et al. J Vet Sci 2011;12:165-9.
20. Simmerson SM, Armstrong PJ, Wűnschmann A, et al. Clinical features, intestinal
histopathology, and outcome in protein-losing enteropathy in Yorkshire Terrier dogs. J Vet
Intern Med 2014;28:331-37.
21. Okanishi H, Yoshioka R, Kagawa Y, et al. The clinical efficacy of dietary fat restriction in
treatment of dogs with intestinal lymphangiectasia. J Vet Intern Med 2014;28:809-17.
22. Wennogle SA, Stockman J, Webb CB. Clinical effect of a dietary change in ten dogs with
steroid-resistant inflammatory bowel disease and protein-losing enteropathy. (Manuscript in
preparation).
23. Boyd KA, O’Donovan DG, Doran S, et al. High-fat diet effects on gut motility, hormone, and
appetite response to duodenal lipid in healthy men. Am J Physiol Gastrointest Liver Physiol
2003;284:G188-96.
24. Clegg ME, McKenna P, McClean C, et al. Gastrointestinal transit, post-prandial lipaemia and
satiety following 3 days high-fat diet in men. Eur J Clin Nutr 2011;65:240-6.
25. Festi D, Scaioli E, Baldi F, et al. Body weight, lifestyle, dietary habits and gastroesophageal
reflux disease. World J Gastroenterol 2009;15:1690-701.
26. Sethi S, Richter JE. Diet and gastroesohageal reflux disease: role in pathogenesis and
management. Curr Opin Gastroenterol 2017;33:107-11.
27. Parkman HP. Upper GI disorders: pathophysiology and current therapeutic approaches. In:
Greenwood-Van Meerveld B. (eds) Gastrointestinal Pharmacology. Handbook of Experimental
Pharmacology, vol 239. Springer, Cham. Gastrointestinal Pharmacology 2017 pp. 17-37.
28. Muenster M, Hoerauf A, Vieth M. Gastro-oesophageal reflux disease in 20 dogs (2012 to 2014).
J Small Anim Pract 2017;58:276-83.
29. Garcia RS, Belafsky PC, Della Maggiore A, et al. Prevalence of gastroesophageal reflux in cats
during anesthesia and effect of omeprazole on gastric pH. J Vet Intern Med 2017;31:734-42.
30. Shaver SL, Barbur LA, Jimenez DA, et al. Evaluation of gastroesophageal reflux in anesthetized
dogs with brachycephalic syndrome. J Am Anim Hosp Assoc 2017;53:24-31.
31. Raghavan M, Glickman N, McCabe G, et al. Diet-related risk factors for gastric dilatation-
volvulus in dogs of high-risk breeds. J Am Anim Hosp Assoc 2004;40:192-203.
32. Freeman LM. Interventional nutrition for cardiac disease. Clin Tech Small Anim Pract
1998;13:232-7.
33. Ogilvie GK. Interventional nutrition for the cancer patient. Clin Tech Small Anim Pract
1998;13:224-31.
34. Center SA. Feline hepatic lipidosis. Vet Clin Small Anim 2005;35:225-69.