Journal of Pediatric Gastroenterology and Nutrition
38:237–238 © March 2004 Lippincott Williams & Wilkins, Inc., Philadelphia
News and Views
News and Views Editors:
ESPGHAN
Yigael Finkel, M.D., Ph.D.
A Critical Perspective on Trophic Feeding
Trophic feeding is a concept viewed with an almost religious
fervor in some nurseries, intensive care units and surgical
wards. Indeed, the determination to give trophic feedings oc-
casionally approaches fanaticism. Having just been told by a
dietician that a neonate with a recent intestinal resection would
experience rapid atrophy of his remaining 16 cm of small
bowel if he didn’t get immediate trophic feedings, I thought
some perspective on this misunderstood concept was war-
ranted.
The generally accepted definition of trophic feeding is a
small volume of balanced enteral nutrition insufficient for the
patient’s nutritional needs but producing some positive gastro-
intestinal or systemic benefit. The volume of feeding consid-
ered trophic in most neonatal nurseries is 10–12 cc/Kg/d or
1cc/h. If more than 25% of the patient’s nutritional needs are
administered enterally, the feeding should no longer be con-
sidered trophic. The commonly identified benefits of trophic
feeding in the intact intestine are maturation of neonatal intes-
tinal digestive, absorptive, motor and immune function; im-
proved neonatal feeding tolerance and eating behavior; main-
tenance of intestinal function during starvation and catabolic
states; and prevention of intestinal bacterial overgrowth and
bacterial translocation.
There is an extensive literature on the importance of luminal
nutrition in promoting mucosal hypertrophy after intestinal re-
section. It may be semantic, but this kind of nutrition is not
trophic either in volume or caloric content. Most animal ex-
periments of post resection intestinal adaptation have used the
maximum enteral feeding the animal can tolerate, generally
more than 30% of nutritional needs. To date, no studies of
post-resection intestinal adaptation in response to strictly de-
fined trophic feedings have been performed. Part of the dieti-
cian’s anxiety over the failure to institute enteral feedings
quickly was her concern that there was a critical time beyond
which intestinal adaptation would not occur. This is a miscon-
ception. The potential for hypertrophy of residual bowel in
response to luminal nutrition is always there, ready to start up
in response to luminal feedings even if they are delayed for
months (or years?) after resection.
There are problems with the attractive concept of trophic
feedings. First, the presumed benefits are poorly defined. For
example, trophic feedings are said to promote intestinal im-
mune function or intestinal maturation, both of which are in-
credibly complex processes. Animal and human studies on the
role of trophic feedings in promoting these complex functions
are inadequate to isolate a unique contribution of trophic feed-
237
NASPGHAN
Robert D. Baker, Jr., M.D., Ph.D.
Philip Rosenthal, M.D.
Philip M. Sherman, M.D., F.R.C.P.C.
ings. Second, the catabolic impact of starvation on the organ-
ism and on the gastrointestinal tract is often not considered in
the selection of controls in such studies. If the negative impact
of withholding trophic feedings from the intestine is to be iso-
lated from the catabolic impact of undernutrition or the absence
of an essential luminal nutrient, then adequate nutrition by the
parenteral route must be part of any human or animal study.
Animal Studies
Pythons eat huge meals and then fast for long periods during
which intestinal villous atrophy develops. Histologic abnor-
malities, mucosal mass and mucosal nutrient transport all im-
prove rapidly in the python when small, balanced, nutritionally
inadequate feedings are given enterally, but not when glucose,
lipid, bile or saline alone are given (Secor SM et al. Am J
Physiol Gastrointest Liver Physiol 2002;283:G1298). In pig-
lets, who experience very modest mucosal atrophy with fasting,
it requires the enteral administration of at least 40% of the daily
nutritional to produce any increase in villous height in the
jejunum and 60% of daily needs to produce mucosal prolifera-
tion in the ileum (Basu R, et al. Am J Clin Nutr 2000;71:1603)
This suggests that mucosal atrophy is a reflection of general
undernutrition and not a result of the absence of trophic feed-
ings since it is only reversed by a large enteral intake. In en-
terally fasted puppies nourished by total parenteral nutrition
(TPN), it likewise takes an enteral feeding of at least 30% of
daily nutritional needs to produce mucosal growth above that of
controls. There does appear to be a more rapid development of
mature motor activity in the stomach and upper small bowel of
puppies receiving trophic feedings plus TPN than is observed
in pups on TPN alone (Owens L et al. J Nutr 2002;132:2717).
Some claim that trophic feedings will prevent cholestasis or
other liver injury associated with parenteral nutrition. The
mechanisms for this benefit are said to be the prevention of
bacterial overgrowth, bacterial translocation and enterotoxin
absorption or the augmentation of intra and extrahepatic biliary
excretion via positive impacts on mucosal integrity, motor
function and hormone release. The animal data to support these
assumptions is weak. One study in adult rats receiving TPN for
7 days showed that there was more glutathione in the liver of
animals who received “targeted” trophic feedings of alanine
when compared to animals receiving saline. Hepatic sensitivity
to exogenously administered endotoxin was less in the animals
who received alanine (Dzakovic A et al. J Pediatr Surg
2003;38:844). Alanine would not fit most people’s definition of
trophic feeding. It is more an essential precursor. The appro-
238 NEWS AND VIEWS
priate control would be an animal receiving extra alanine by
vein. There is very little information about the impact of trophic
feedings on biliary flow and gall bladder function.
I conclude from animal studies that intestinal mucosal atro-
phy may accompany enteral fasting in some species with (pups,
rats and piglets) or without (pythons) adequate IV nutrition and
that feeding a mixed meal of significant caloric magnitude
stimulates mucosal growth and function. There does not appear
to be any impact of feedings providing less than 30% of daily
nutritional needs except in the area of neonatal gastroduodenal
motility.
Human Studies
Does mucosal atrophy actually occur in humans from whom
enteral nutrition is withheld with or without IV nutritional sup-
port? Alpers reports that there at most a 10% decrease in the
adult bowel wall thickness during catabolic states in the inten-
sive care setting (Alpers DH. Curr Opin Clin Nutr Metab Care
2002;5:697). According to Alpers, reversal of this modest at-
rophy with trophic feedings has not been documented. Alpers
feels, after a review of the adult ICU literature, that mucosal
atrophy is simply a manifestation of a catabolic state as is
muscle wasting and fat store depletion, which can be prevented
by adequate IV nutrition with no unique contribution from
trophic feeding.
In the 1980s several good studies evaluated trophic feedings
in premature neonates. The primary objective was to see wheth-
er early small enteral feedings increased the incidence of nec-
rotizing enterocolitis. Most studies confirmed that they did not.
The unexpected result of these studies was that babies given
adequate IV nutrition plus balanced minimal enteral feedings
progressed faster to full enteral nutrition. Feeding behavior and
tolerance were better and babies were discharged from the hos-
pital faster than those not receiving minimal enteral feedings. In
one study, hospital discharge was 22 days earlier than controls.
Peak direct bilirubin was lower in premature neonates receiving
trophic feedings (.7mg/dL vs 2.5mg/dL) and fewer days of
phototherapy were required for indirect hyperbilirubinemia
(6.8days vs 9.5 days) as well (Dunn L et al. J Pediatr 1988;
112:622–9). Voluntary energy intake was better in babies re-
ceiving early minimal enteral feedings even briefly, a result
attributed to overall better feeding behavior. One study found
that the weight of premature neonates who had received only 7
days of trophic feeding was 225g over birth weight at 30 days
of age while the body weight of those receiving no trophic
feedings was only 95g above birth weight. The average caloric
intake of these babies was identical for the 30 days. Somato-
medin levels were the same in the two groups, suggesting that
maturation of hormone secretion was not the cause of better
growth (Troche B et al. Biol Neonate 1995;67:172–81). The
authors wondered whether efficiency of absorption was better
in the neonates who got trophic feedings thus increasing their
actual calorie intake. As in puppies, the use of minimal enteral
nutrition in neonates is associated with an earlier appearance of
a mature antro-duodenal motility pattern. Saline perfused con-
trols have not been studied, so the impact of volume as opposed
J Pediatr Gastroenterol Nutr, Vol. 38, No. 3, March 2004
to luminal nutrient cannot be assessed (Berseth CL et al. Pe-
diatrics 2003;111:529).
Trophic feedings are said to promote maturation of intestinal
absorptive function, but hard data are scanty. One study has
shown indirectly that absorption of leucine is better in preterms
receiving trophic feedings (Saenz de Pipaon M et al. Ped Res
2003;53:281). There are very few other studies that have as-
sessed the impact of minimal enteral nutrition on any aspect of
digestive or absorptive function.
The claims for improved immunity in infants and adults
receiving trophic feedings are weak, because of the complexity
of the process and the inadequate scope of the outcome mea-
sures used. In one study of infants on TPN, bactericidal activity
of neutrophils against coagulase positive staph and release of
TNF␣ was better after 7 days of trophic feedings but neither
function approached the level of enterally fed controls. The
incidence of septic events in infants with and without trophic
feedings is the same (Ocada Y et al. J Pediatr Surg 1998;
33:16). There are no studies evaluating intestinal responses to
infectious agents, the development of food allergy or the nature
of the intestinal immune function in infants receiving trophic
feedings.
The Cochrane group reviewed the human literature on tro-
phic feedings (defined as less than 25 calories /Kg for more
than 5 days). They agreed that total hospital stay, days to
achieve full enteral nutrition and days feedings were withheld
because of intolerance were fewer in neonates who received
trophic feedings. In all other clinical studies, they concluded
that methodologic problems prevented the conclusion that tro-
phic feedings had any other benefits and that enteral fasting
until the child was ready for “real feedings” was still an ap-
propriate clinical approach (Tyson JE et al. Cochrane Database
Syst Rev 2: CD 000504,2000).
It would facilitate management planning in many clinical
situations if the confusion between the three concepts of lumi-
nal nutrition, specific luminal nutrients essential for enterocyte
function and trophic feeding were clarified and if words like
atrophy and hypertrophy were used with more precision. Most
of the supposed benefits of trophic feedings still require con-
firmation by good clinical studies. These studies are doable. I
submit that assessing intestinal absorptive function is tedious
but possible. Assessing the biochemical and histologic evi-
dence of liver injury should be easy. Evaluating histologic
changes before and after trophic feedings is possible in care-
fully selected situations, for example by monitoring the biop-
sies of the easily accessible distal small intestine in infants with
ileostomies. The measures of immune function must be more
carefully selected since endpoints like infection rate are too
insensitive to reveal possible differences. The challenge to pe-
diatric gastroenterology is evaluate the unconfirmed benefits of
trophic feeding before insisting on its use in fragile patients
who might be better off fasting and supported by TPN until
truly ready to feed.
Judith M. Sondheimer, M.D.
Section of Gastroenterology, Hepatology and Nutrition,
University of Colorado Health Sciences Center and The
Children’s Hospital, Denver, CO