ArticlePDF Available

Impact of nutrition on canine behaviour: Current status and possible mechanisms


Abstract and Figures

Each year, millions of dogs worldwide are abandoned by their owners, relinquished to animal shelters, and euthanised because of behaviour problems. Nutrition is rarely considered as one of the possible contributing factors of problem behaviour. This contribution presents an overview of current knowledge on the influence of nutrition on canine behaviour and explores the underlying mechanisms by which diet may affect behaviour in animals. Behaviour is regulated by neurotransmitters and hormones, and changes in the availability of their precursors may influence behaviour. Tryptophan, the precursor of serotonin, may affect the incidence of aggression, self-mutilation and stress resistance. The latter may also be influenced by dietary tyrosine, a precursor to catecholamines. As diet composition, nutrient availability and nutrient interactions affect the availability of these precursors in the brain, behaviour or stress resistance may be affected. PUFA, especially DHA, have an important role as structural constituents in brain development, and dietary supply of n-3 and n-6 PUFA could modify aspects of the dopaminergic and serotonergic system and, consequently, cognitive performance and behaviour. Finally, persistent feeding motivation between meals can increase stereotyped behaviour and aggression and decrease resting time. This feeding motivation may be altered by dietary fibre content and source. At present, few studies have been conducted to evaluate the role of nutrition in canine (problem) behaviour through the above mentioned mechanisms. Studies that explore this relationship may help to improve the welfare of dogs and their owners.
Content may be subject to copyright.
Impact of nutrition on canine behaviour: current status and possible
G. Bosch
*, B. Beerda
, W. H. Hendriks
, A. F. B. van der Poel
and M. W. A. Verstegen
Animal Nutrition Group, Animal Sciences Group, Wageningen University and Research Centre, PO Box 338,
6700 AH Wageningen, The Netherlands
Animal Production Division, Animal Sciences Group, Wageningen University and Research Centre, PO Box 65,
8200 AB Lelystad, The Netherlands
Each year, millions of dogs worldwide are abandoned by their owners, relinquished to animal
shelters, and euthanised because of behaviour problems. Nutrition is rarely considered as one of
the possible contributing factors of problem behaviour. This contribution presents an overview of
current knowledge on the influence of nutrition on canine behaviour and explores the underlying
mechanisms by which diet may affect behaviour in animals. Behaviour is regulated by
neurotransmitters and hormones, and changes in the availability of their precursors may influence
behaviour. Tryptophan, the precursor of serotonin, may affect the incidence of aggression, self-
mutilation and stress resistance. The latter may also be influenced by dietary tyrosine, a precursor
to catecholamines. As diet composition, nutrient availability and nutrient interactions affect the
availability of these precursors in the brain, behaviour or stress resistance may be affected. PUFA,
especially DHA, have an important role as structural constituents in brain development, and
dietary supply of n-3 and n-6 PUFA could modify aspects of the dopaminergic and serotonergic
system and, consequently, cognitive performance and behaviour. Finally, persistent feeding
motivation between meals can increase stereotyped behaviour and aggression and decrease
resting time. This feeding motivation may be altered by dietary fibre content and source. At
present, few studies have been conducted to evaluate the role of nutrition in canine (problem)
behaviour through the above mentioned mechanisms. Studies that explore this relationship may
help to improve the welfare of dogs and their owners.
Dogs: Food: Nutrients: Behaviour
The domestic dog (Canis familiaris) is believed to have
evolved from the grey wolf (C. lupis) as a separate species at
least 15 000 years ago and it is thought to be the first animal
species to be domesticated by humans
. At the present
time, as a result of selective breeding, approximately 400
distinct dog breeds are recognised worldwide, representing
a large variation in body size and weight, with the latter
ranging from 1 to 90 kg. Initial functions of dogs such as
hunting, shepherding and guarding have diminished
gradually in importance in favour of the dog’s role as a
companion to humans
. Though most human dog relation-
ships are fulfilling, each year a large number of animals are
abandoned by their owners or relinquished to animal
. Aggression toward people and animals, running
away, destructive behaviour, disobedience, house soiling
and excessive barking are unwanted behaviours that make
owners relinquish or abandon their dogs
. Although only
20 % of the dogs in the US shelters are assigned by their
owners for euthanasia
, a further 40 % of dogs admitted are
. Of the sheltered dogs that are purchased by new
owners, approximately 20 % are returned to shelters
and a
large proportion of these animals are euthanised
. The
number of dogs and cats euthanised annually in the USA is
estimated to be between 5 and 17 million
, with 3 6
million as a result of behaviour problems
. Strategies that
combat problem behaviours in dogs will greatly benefit
animal welfare. The behaviour of individual dogs is
controlled by numerous factors and from studies in humans
it can be derived that nutrition plays a role also. For
example, diets rich in vitamins and minerals may decrease
anti-social behaviour in schoolchildren
and supplemen-
tation of vitamins, minerals and essential fatty acids
Abbreviations: DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; GLP-1, glucagon-like peptide-1; ISF, insoluble fibre; LNAA,
large neutral amino acids; ME, metabolisable energy; PUFA, polyunsaturated fatty acid; PYY, peptide tyrosine tyrosine; SF, soluble fibre;
VFA, volatile fatty acids.
*Corresponding author: Ir G. Bosch, fax þ31 317 484260, email
Nutrition Research Reviews (2007), 20, 180–194
qThe Authors 2007
doi: 10.1017/S095442240781331X
decreased anti-social behaviour, including violence, of
young adult prisoners
. Dietary effects on behaviour have
been investigated for anti-social aspects, but also for
behavioural changes related to ageing and, in this, dogs have
been used as a model for humans. Dogs develop similar
cognitive deficits and neuropathology as can be seen in
ageing humans and elderly suffering from dementia
Milgram and co-workers initiated a series of experiments
with young and aged beagle dogs to study dietary
interventions on age-related cognitive decline. Results
showed that canine food enriched with antioxidants and
mitochondrial cofactors decreased the rate of cognitive
decline in aged beagle dogs under laboratory conditions and
improved age-related behavioural changes in older pet dogs
held in home situations (for reviews, see Roudebush et al.
and Zicker
). These findings demonstrate clearly that
canine behaviour can be influenced by dietary components.
The present review presents an overview of our current
knowledge on the influence of dietary macronutrient
composition on the behaviour of dogs and explores
the underlying mechanisms by which diet may affect
behaviour. Findings from food– behaviour studies in dogs
and other mammals are integrated to assess in what
way problem behaviour in dogs may be reduced through
dietary means.
Effects of dietary amino acids and protein content on
After ingestion, proteins are enzymically degraded and
absorbed in the small intestine mainly as tripeptides,
dipeptides and free amino acids. After hydrolysis of the
peptides in the enterocytes, the free amino acids are
transported through the portal vein to the liver. Amino acids
are important constituents required for the synthesis of
enzymes and other proteins, and used as precursors for the
synthesis of neurotransmitters and hormones
example, serotonin, catecholamines, acetylcholine and
histamine are metabolites from tryptophan, tyrosine, choline
and histidine, respectively
. These neurotransmitter pre-
cursors (except for choline) are amino acids and are natural
dietary constituents. Behaviour results from signal detec-
tion, transmission and processing in the (central) nervous
system, which is accomplished and modulated by chemical
messengers such as neurotransmitters and hormones.
Changes in neurotransmitter precursors such as tryptophan
and tyrosine are, therefore, likely to influence behaviour.
The amount and timing of food intake, diet composition and
digestibility are all factors that determine the availability of
different amino acids, i.e. precursors of chemical messen-
gers. Consequently, such factors may influence behaviour.
The effects of tryptophan and tyrosine on behaviour will be
discussed as these could be relatively potent modulators; for
similar reports on choline, histidine and threonine, we refer
to Young
Findings and mechanisms in different mammals
Tryptophan. A diet high in tryptophan has been shown to
reduce mouse killing by rats
, reduce aggression in
vervet monkeys
, enhance exploratory behaviour in female
silver foxes
and reduce self-injurious behaviour in rhesus
. In contrast to the observed reductions in
aggression in some experimental conditions, dietary
supplementation of tryptophan has also been shown to
increase territorial aggression in male mice
. Dietary
tryptophan may also influence the resistance or tolerance to
stress and, therefore, change the behavioural stress
response. Koopmans et al.
reported enhanced recovery
after social stress as measured by lower plasma cortisol and
noradrenaline concentrations in pigs fed a surplus of dietary
tryptophan compared with pigs fed diets containing a
‘normal’ concentration of tryptophan. In addition, sup-
plementation of dietary tryptophan reduced plasma cortisol
concentrations during a stress-inducing mental arithmetic
task in healthy stress-vulnerable humans
. It was, therefore,
suggested by Markus et al.
that tryptophan supplemen-
tation above normal dietary concentrations could improve
the ability of an individual to cope with stress. The effects of
dietary tryptophan on stress resistance involve different
pathways. In rats a variety of stressors, such as
immobilisation, foot shock, and hypothermia, increase
brain tryptophan and serotonin turnover
26 – 29
. Depressed
humans show decreased plasma tryptophan concentrations
in comparison with normal subjects
. It appears that
initially stressors stimulate serotonin turnover, which over
time may deplete serotonin (precursor) supplies and result in
decreased serotonin (precursor) concentrations.
Quantitatively the most important pathway for tryptophan
metabolism, after protein synthesis, is the kynurenine
pathway which is responsible for over 90 % of tryptophan
. In humans, normally 1 % of the available
tryptophan is converted to serotonin which is mainly present
in the gastrointestinal tract
. The first and rate-limiting step
in the synthesis of serotonin is the hydroxylation of
tryptophan to 5-hydroxytryptophan by the enzyme trypto-
phan hydroxylase (Fig. 1). Tryptophan hydroxylase is
normally about half saturated with tryptophan
. Conse-
quently, an increase in tryptophan in the brain, which
increases serotonin synthesis and serotonergic neurotrans-
, can maximally double serotonin synthesis. The
second step in the synthesis of serotonin is the
decarboxylation of 5-hydroxytryptophan to serotonin
which is stored in vesicles in the nerve terminal were it is
held before release. When serotonin is released into the
synaptic cleft, serotonin can bind to different subtype
receptors (for reviews, see Barnes & Sharp
and Hoyer
et al.
). Via binding to these different receptors, serotonin
can produce many different effects on post-synaptic cells
influencing various parts of the brain involved in controlling
a variety of physiological functions including hormone
releases, cardiovascular functioning, pain, appetite, and in
general mood and behaviour
35 – 37
Tryptophan transport across the bloodbrain barrier and
metabolism is in part affected by animal factors such as
, sex
, social status
, age
, activity
level of arousal
. The availability of dietary tryptophan to
the brain is largely dependent on the composition of
the ingested diet. Tryptophan is found in nearly all
protein-containing foods where it is found in a lower
concentration compared with the other large neutral amino
acids (LNAA) tyrosine, phenylalanine, leucine, isoleucine
Impact of nutrition on canine behaviour 181
and valine
. For access into the brain, tryptophan shares the
same carrier as other LNAA for transport across the blood
brain barrier
. Central tryptophan concentrations can either
be increased by increasing plasma tryptophan or by
lowering plasma concentrations of LNAA
. As trypto-
phan is normally present in only small concentrations in
dietary protein compared with other LNAA, the consump-
tion of a meal high in protein will decrease the ratio of
tryptophan to other LNAA
and thereby potentially lower
serotonin synthesis.
The fraction of unbound tryptophan as compared with
that bound to albumin is another factor that may influence
tryptophan availability to the brain
approximately 80 90 % of all tryptophan molecules in the
blood are bound to serum albumin
. It has been suggested
that the majority of the albumin-bound tryptophan is
available for passage across the blood– brain barrier
, but
possibly the concentration of circulating free tryptophan
may be especially important
. According to Chaouloff
three factors affect circulating free and bound tryptophan
concentrations: (i) the rate of lipolysis because blood non-
esterified fatty acids displace tryptophan from its binding to
; (ii) the activity of tryptophan 2,3-dioxygenase,
the rate-limiting enzyme in tryptophan detoxication through
the kynurenine pathway activation (inactivation) of this
enzyme decreases (increases) circulating blood tryptophan
; (iii) uptake into peripheral and central tissues.
Carbohydrate-induced insulin rises facilitate the uptake of
most LNAA into skeletal muscle, but not tryptophan bound
to albumin
. Consequently, the ratio of tryptophan
relative to LNAA increases. This results in a competitive
advantage of tryptophan over LNAA for uptake at the
blood brain barrier. However, as little as 2– 4 % of the
energy of a meal as protein seems to prevent this increased
availability of tryptophan
Tyrosine. In rats, a high-tyrosine diet prevents adverse
behavioural and neurochemical effects (for example,
immobility during a swim test, depletion of brain
noradrenaline) of various acute stressors including
, restraint and tail-shock
57 – 59
. Human studies
also suggest beneficial effects of tyrosine under conditions
of stress (for reviews, see Lieberman
and Young
Tyrosine, which can be synthesised from phenylalanine,
is the direct precursor for the catecholamines dopamine,
noradrenaline and adrenaline
. Dopamine can be
synthesised from tyrosine in neurons in two steps. The
first and rate-limiting step is the conversion of tyrosine to
dihydroxyphenylalanine by the enzyme tyrosine hydroxy-
lase. In rats, central tyrosine hydroxylase is approximately
75 % saturated with tyrosine
. In the second step,
dihydroxyphenylalanine is decarboxylated to dopamine
which can be used as an endproduct (neurotransmitter) in
neurons or further converted to noradrenaline or adrena-
. Like tryptophan, tyrosine competes with other
LNAA at the bloodbrain barrier for entry into the
and is taken up into skeletal muscle under the
influence of insulin
. In diets, tyrosine is typically
available in much higher concentrations compared with
tryptophan and high-protein meals will typically raise
tyrosine concentrations in the brain, but will lower the
concentration of tryptophan
. Catecholamines play a key
role in a variety of behavioural, neuroendocrine and
cardiovascular responses during stress
. Increases in
Fig. 1. Effects of dietary characteristics on tryptophan uptake by the central nervous system and synthesis of serotonin from brain tryptophan
(adapted from Grimmett & Sillence
with modifications). ( ), Factors that may ultimately decrease brain tryptophan; 5-HTP,
5-hydroxytryptophan; NEFA, non-esterified fatty acids.
G. Bosch et al.182
brain tyrosine have little or no effect on catecholamine
, but the situation may be different during
stress when brain noradrenaline turnover increases and
noradrenaline concentrations decrease
. An enhanced
noradrenergic activity is part of a normal adaptive stress
. In stressed rats (tail-shock), ingestion of a
high-tyrosine diet reversed the post-stress decline in brain
noradrenaline and attenuated behaviour changes, i.e.
decreased locomotion, standing on hind legs, hole-poking
in a novel open field
. This suggests that a high-tyrosine
diet may be beneficial during severe stress, as it prevents
depletion of the substrate required for catecholamine
synthesis in times of high catecholaminergic activity and
Findings in dogs
Studies on the effects of tryptophan or tyrosine on behaviour
in dogs seem to be limited to one. DeNapoli et al.
formulated diets with high or low protein content
(approximately 310 or 190 g crude protein/kg, respectively)
and with or without tryptophan supplementation (1·45 g/kg)
in order to provide varying tryptophan contents and
tryptophan:LNAA ratios (Table 1). Each of the four diets
was fed in random order for 1 week to thirty-three privately
owned dogs that displayed a high territorial aggression,
dominance aggression or hyperactivity. There was no effect
of dietary protein or tryptophan content on the behavioural
scores within each group of problem behaviour. However,
when the groups of dogs were analysed as one study
population a lower territorial aggression score was obtained
for dogs fed the high-tryptophan diet compared with dogs
fed the low-tryptophan diet, but only when fed a low-protein
diet. In addition, dogs fed the high-protein diet without
tryptophan supplementation showed a higher dominance
aggression score compared with dogs on the other dietary
Three studies in literature have reported that low-protein
diets decreased aggression in dogs, though these were not
performed under controlled experimental conditions. In a
study with seven aggressive golden retrievers held at in-
home living conditions, incidences of aggression as reported
by their owners immediately decreased after the introduc-
tion of a low-protein diet (1518 % of total energy)
Unfortunately, neither the composition of the experimental
diet nor the composition(s) of the diet(s) before the dietary
intervention were reported. The reduction in aggressive
incidences, however, was only sustained in three dogs; two
dogs deteriorated again in their behaviour and contact
was lost with the remaining two clients. In another study,
twelve dogs that exhibited either high territorial aggression,
dominance aggression or hyperactivity and fourteen control
dogs were fed each of three diets varying in protein content
(180, 250 and 310 g crude protein/kg DM) for 2 weeks at
in-home living situations
. The low-protein diet and
medium-protein diet decreased territorial aggression scores
compared with the high-protein diet. No effects of dietary
protein content in dogs with dominance aggression or
hyperactivity were found. Additional behavioural analysis
of the group of dogs demonstrating territorial aggression
revealed that five of these dogs showed dominance-related
Table 1. Effect of dietary protein and tryptophan (TRP) content on canine behaviour
Authors Dogs and design Diets* Results
Seven aggressive golden retrievers at in-home living
situations. Measurements were not reported
15 –18 % protein of total dietary energy
based on approximately 20 % meat
and 80 % boiled rice
Seven dogs improved of which three sustained the improvement,
two worsened, and contact was lost with two clients
et al.
Twelve territorial aggressive, twelve dominance aggressive,
twelve hyperactive and fourteen control dogs
(age .1 year) fed each diet (Latin square) at
in-home living situations for 14 d. Each day, owners
scored their dogs for territorial aggression, dominance
aggression, excitability and fearfulness
(1) 180 g protein/kg; 1·0 g TRP/kg;
0·024:1 TRP:LNAA
(2) 250 g protein/kg; 1·6 g TRP/kg;
0·024:1 TRP:LNAA
(3) 310 g protein/kg; 1·6 g TRP/kg;
0·021:1 TRP:LNAA
(a) Territorial aggressive dogs showed lower territorial aggression
scores when fed diets 1 and 2 compared with diet 3
(b) Seven territorial aggressive dogs were fearful and showed lower
territorial aggression scores when fed diets 1 and 2 compared
with diet 3; the remaining five territorial aggressive dogs tended
to be dominant which was not affected by dietary treatment
(c) No changes in behaviour scores of dogs within the dominance
aggressive, hyperactive and control groups
et al.
Eleven territorial aggressive, eleven dominance aggressive
and eleven hyperactive dogs (age .1 year) fed each
diet (at random) at maintenance level at in-home living
situations for 7 d. Each day, owners scored their dogs for
territorial aggression, dominance aggression, excitability,
fearfulness and hyperactivity
(1) 186 g protein/kg; 1·8 g TRP/kg;
0·044:1 TRP:LNAA
(2) 188 g protein/kg; 3·0 g TRP/kg;
0·073:1 TRP:LNAA
(3) 308 g protein/kg; 2·4 g TRP/kg;
0·035:1 TRP:LNAA
(4) 315 g protein/kg; 3·7 g TRP/kg;
0·054:1 TRP:LNAA
(a) No changes in behaviour within each behaviour group for any
dietary treatment
(b) When all dogs were combined, dominance aggression scores
were higher for dogs fed diet 3 compared with dogs fed
diets 1, 2 and 4
(c) When all dogs were combined, territorial aggression
scores were higher for dogs fed diet 1 compared
with dogs fed diet 2
LNAA, large neutral amino acids (tyrosine, phenylalanine, leucine, isoleucine, valine).
* Values are presented on a DM basis.
Impact of nutrition on canine behaviour 183
territorial aggression, whereas the other seven dogs
showed fear-related territorial aggression. In the latter
dogs, territorial aggression decreased when fed the low-
protein diet.
For adult dogs fed at maintenance, the minimal dietary
tryptophan requirements are currently set at
0·0669 g/1000 kJ (0·28 g/1000 kcal) metabolisable energy
(ME) with a tryptophan:LNAA ratio of 0·061 : 1 and for
tyrosine and phenylalanine the minimal dietary require-
ments are 0·3537 g/1000 kJ (1·48 g/1000 kcal) ME
. The
Association of American Feed Control Officials
has minimum dietary requirements for these
nutrients which are slightly higher (0·1099 and 0·4995 g/
1000 kJ (0·46 and 2·09 g/1000 kcal) ME, respectively) in
order to account for the lower digestibility and availability
of nutrients in commercial canine foods compared with
semi-synthetic diets. Nutritional guidelines for humans
and dogs rarely take behaviour into account as a response
criterion, something which has been criticised
. The
minimum quantity of tryptophan in a commercial canine dry
expanded diet that has passed a maintenance AAFCO
feeding protocol has been reported to be 0·0502 g/1000 kJ
(0·21 g/1000 kcal) ME
. The criteria for passing an
AAFCO maintenance feeding protocol however, do not
take into account animal behaviour. It is unknown if the
minimal amount of tryptophan in typical dog foods meets
the requirements of the wide variety of dogs, for example,
from emotionally stable to anxious individuals, under
different conditions, for example, from stress-free to
stressful. Both excessive intake and a deficiency of
tryptophan are detrimental to the health of an animal
and are likely to affect behaviour. In horses, a dose of
0·1 mg/kg body weight appears to be too low, causing mild
. In humans, the most common side effect of
overfeeding precursors of neurotransmitters has been
reported to be nausea
. There are currently no requirement
estimates for the maximum amount of tryptophan
in canine food and it remains to be determined how
high-tryptophan diets affect the health of dogs and their
behaviour in the long term.
Effects of dietary lipids on behaviour
Lipids have various functions, such as constituents of
cellular membranes, precursors for chemical messengers
(for example, steroid hormones) and their use as an energy
source or stored in the body as adipose tissue. After adipose
tissue, the central nervous system has the greatest
concentration of lipids
. The structural constituents in the
grey matter of the brain and retinal tissues in mammals are
derived from dietary linoleic acid (18 : 2n-6) and a-linolenic
acid (18 : 3n-3). Both are polyunsaturated fatty acids
(PUFA) and can be metabolised to long-chain PUFA by
sequential alternating enzymic desaturation and elongation.
Linoleic acid can be metabolised to arachidonic acid
(20 : 4n-6) which can be further metabolised to docosapen-
taenoic acid (22 : 5n-6). The enzymic desaturation and
elongation of a-linolenic acid yields eicosapentaenoic acid
(EPA) (20 : 5n-3) which can be further metabolised to
docosahexaenoic acid (DHA) (22 : 6n-3)
Findings and mechanisms in different mammals
There is ample scientific literature available in which the
effects of both dietary deficiency and supplementation of
PUFA on animal performance in cognitive or behavioural
tests are evaluated (for reviews, see Wainwright
McCann & Ames
). For example, the learning ability of
rodents decreased when fed n-3 fatty-acid-deficient
and increased when fed DHA-supplemented
compared with rodents fed diets adequate in n-3
fatty acid concentrations. Other studies, however, did not
find affects of dietary n-3 PUFA manipulation on learning
performance as tested with a Morris water-maze in rats
or mice
. Dietary PUFA seem to affect animal cognition
but can also cause behavioural changes. Rats fed n-3
PUFA-deficient diets showed increased aggression scores
in a resident intruder test
and increased expression of
stress-related behaviours during several stress tests
compared with male rats fed adequate amounts of n-3
PUFA. Similarly, anxiety was found to be increased in
mice fed a diet deficient in n-3 PUFA
, though others did
not observe any effects of dietary PUFA on anxiety in
or rats
The dopaminergic and serotonergic systems in the brain
are known to play important roles in learning, emotions, and
impulse control
37,86 – 90
, which makes it tempting to assume
that the effects of PUFA on behaviour run through these
systems. Indeed, both systems are known to be influenced
by PUFA. Rats deficient in n-3 PUFA compared with rats
fed diets with a-linolenic acid showed a reduction in
dopamine concentration in the frontal cortex
91 – 94
and an
increase in dopamine concentration in the nucleus
but no effects in the striatum
. In the
frontal cortex of these animals the rate of dopamine
synthesis and breakdown mediated by monoamine oxidase
was not affected
and the reduced concentrations may
have been linked to the reduced dopaminergic storage
. Changes in dopamine concentrations were
followed by changes in number of D
PUFA-deficient rats had a lower number of D
receptors in
the frontal cortex
but higher in the nucleus
. Rats fed diets supplemented with EPA
and DHA had an increased dopamine concentration and D
binding possibly as a result of a reduction in monoamine
oxidase activity in the frontal cortex compared with rats fed
adequate amounts of PUFA
As for dopamine concentrations, frontal cortex serotonin
concentrations were increased in rats fed diets sup-
plemented with n-3 PUFA
. In line with this, serotonin in
the frontal cortex was reduced in piglets fed n-3 and n-6
PUFA-deficient formula for 18 d from birth compared with
piglets fed formula supplemented with linoleic acid and a-
linolenic acid and/or arachidonic acid and DHA
. The
findings in the frontal cortex may not extrapolate to other
brain areas. For example, in the hippocampus of 2-month-
old rats fed an n-3 PUFA-deficient diet extracellular basal
serotonin concentrations were increased
probably due to reduced storage pools
, not due to
decreased activity of monoamine oxidase
. Such effects of
n-3 PUFA deficiency on serotonin concentrations are not
found in all studies (for example, Delion et al.
G. Bosch et al.184
In addition to the observed changes in the dopaminergic
and serotonergic systems in different brain regions, physical
properties (for example, fluidity, permeability) of cerebral
membranes may also mediate dietary effects on cognition
and behaviour
. For example, chronic dietary deficiency in
n-3 PUFA resulted in low concentrations of n-3 PUFA in the
rat brain
whereas diets high in EPA and DHA resulted in
high concentrations of EPA and DHA in the brain of
. In addition, dietary a-linolenic acid deficiency
induces a more pronounced reduction in DHA concen-
trations in the frontal cortex than in the striatum and
. Besides changes in brain PUFA compo-
sitions, dietary PUFA may alter properties of the neuronal
membrane, such as the activity of membrane-bound
enzymes, receptors and ion channels
. These alterations
may affect neurological functioning and may, therefore, also
contribute to the observed changes in cognitive functioning
and behaviour.
Findings in dogs
To the authors’ knowledge, there are at this moment no
scientific articles available regarding the influence of n-3 or
n-6 PUFA deficiency or enrichment on canine behaviour or
cognitive performance. Since DHA is essential for the
development and function of the brain and retina
, its
supply may affect neurological development in puppies. For
example, low dietary concentrations of DHA during the
gestation or lactation of bitches and dry diets for puppies
depressed their retinal sensitivity
. Although the
immediate connection between the cellular effects of
DHA and visual sharpness and cognitive abilities in
receiving dietary DHA still needs more support
, studies
seem to emphasise the importance of DHA in the diet of
bitches during gestation until weaning and the diet of
puppies in order to ensure optimal neurological develop-
ment. At present, there is no recommended allowance for
DHA for both bitches in gestation and lactation or puppies,
but the recommended allowance for a-linoleic acid is 3·35 g/
1000 kJ (0·8 g/1000 kcal) ME
. A diet high in a-linolenic
acid fed from breeding throughout lactation increased a-
linolenic acid concentration in milk but failed to do this for
. In a recent study, puppies converted a-linolenic
acid to DHA during the first month of weaning but little
conversion of a-linolenic acid to DHA occurs after
. It seems that the capacity of puppies to
synthesise DHA from dietary a-linolenic acid or other n-3
fatty acid precursors is active for only a short time during the
neonatal period and is decreased thereafter. The amount of
dietary a-linolenic acid for sufficient synthesis of DHA and
the amount of DHA required for optimal neurological
development in puppies still remain to be determined.
Whether the provision of sufficient DHA for optimal
neurological development in dogs also results in changes in
the dopaminergic and serotonergic systems and subsequent
effects in cognitive abilities or behaviour in later life remains
to be confirmed.
Concerning commercial dog food, it seems likely that in
dogs deficiencies of PUFA are rare as long as fat oxidation
during process and storage of the food is limited
. Levels
of PUFA, particularly the n-3 family, are nowadays higher in
commercial dog food compared to foods of several years
(Delton-Vandenbroucke et al., 1998). However, the
amount and ratio between n-6 and n-3 fatty acids may differ
considerably between commercially available diets. The
n-6:n-3 fatty acid ratio of twelve commercial dry dog foods
was found to differ considerably, ranging from 17:1 to
Effects of dietary carbohydrates on behaviour
Feeding of mammals is a discontinuous process in which
periods of food consumption are interspersed with periods
of non-eating
. Food intake behaviours are controlled by
feelings of hunger
and satiety
, but may be modulated
by psychological and social factors
. Numerous central
and peripheral signal molecules are involved in the
regulation of eating (for reviews, see Bray
, de Graaf
et al.
and Strader & Woods
). The rate and site of
degradation of nutrients largely determines the postprandial
physiological state of an animal and in this way the extent
and duration of satiety and, therefore, behaviour. There is a
wide variety of carbohydrates with different physical and
chemical properties. These properties can affect the rate and
site of degradation of these carbohydrates
. In single-
stomached animals, degradable carbohydrates may be
digested with endogenous enzymes in the first part of the
gastrointestinal tract, or fermented by micro-organisms that
colonise predominantly the last part of the gastrointestinal
tract. Products derived from digestible carbohydrates are
mainly monosaccharides. The digestion of starch and
absorption of monosaccharides are primarily responsible for
the fluctuations in the postprandial blood glucose concen-
trations that subsequently may modify tryptophan avail-
ability in the brain when protein intake is low (see section on
Findings and mechanisms in different mammals: Trypto-
phan), and influence mood in at least humans (for a review,
see Benton
). The indigestible carbohydrates are often
referred to as dietary fibre, which contains non-starch
polysaccharides, resistant starch and non-digestible oligo-
saccharides. The fermentation endproducts of dietary fibre
are volatile fatty acids (VFA; acetic, propionic and butyric
acid), lactate, alcohol and the gases methane, hydrogen and
carbon dioxide
. Apart from the fermentability, other
physical and chemical properties of dietary fibre include
solubility, ability to bind water and affect viscosity, and
possible interactions with the digestion and absorption of
starch, protein and fat. In addition, the duration of satiety
experienced by animals between meals may be affected by
carbohydrates, which in turn may reduce the behavioural
side effects of a high feed motivation.
Findings and mechanisms in different mammals
The effects of dietary carbohydrate sources (i.e. fibrous
ingredients) on animal behaviour have been relatively well
studied especially in pigs, where non-lactating sows were
fed energy-restricted diets in order to prevent excessive lipid
deposition and reduced reproduction performance. Com-
monly diets for sows are formulated to meet the daily
nutrient requirements for maintenance and reproduction.
However, the latter may not result in a sufficient level of
Impact of nutrition on canine behaviour 185
satiety between meals and is believed to be an important
reason for a persistent high feeding motivation throughout
the day contributing to the development of stereotyped
. In order to reduce stereotyped behaviour in
sows, diets high in fibrous ingredients (sugarbeet pulp, oat
hulls, soyabean hulls, wheat bran) can be fed
resulting in an increased time of sows laying down
increased resting time, less time spent on foraging and
and reduced posture changes 8 and 10 h after
. The latter authors compared sows fed a high-
and a low-fermentable carbohydrate diet (for further
examples, see Meunier-Salau
¨net al.
). The relationship
between dietary fibre content and stereotyped behaviour has
also been documented in horses. A large survey among
trainers of race horses in Sweden revealed a negative
correlation between the amount of roughage provided and
the incidence of stereotyped behaviour (cribbing or wind-
sucking, weaving, box-walking) or wood-chewing in
. Wood-chewing may be related to a ‘fibre
deficiency’ in the diet and represent attempts to increase
dietary fibre intake
126 – 128
. The effect of fibrous ingredients
on behaviour is not generic for all fibre sources; for
example, solvent-extracted coconut meal and soyabean
hulls as a dietary fibre source do not appear to affect
physical activity in pigs
, whereas sugarbeet pulp silage
. Since sows which are fed low amounts of feed were
shown to be more active compared with sows fed large
amounts of feed
it has been suggested that hunger is most
likely the cause of the increased physical activity
The variety in physical and chemical properties of
different fibrous ingredients results in differences between
these fibres in creating and maintaining satiety and
preventing feelings of hunger. The biological mechanisms
behind the satiating properties of dietary fibre are still not
fully understood, but several dietary fibre characteristics
seem to be important. First, fibres with a high water-binding
capacity may increase the volume and weight of the gastric
contents when liquids are available. The weight or volume
may stimulate stretch receptors that can induce gastric
signals of satiation
. Second, gastric emptying can be
affected either directly by dietary fibres high in intragastric
or indirectly through the stimulation of the
release of glucagon-like peptide-1 (GLP-1) (a potent
inhibitor of gastric emptying
). Stimulation of GLP-1
production can be mediated through carbohydrate fermenta-
tion in the distal part of the gastrointestinal track
through the production of VFA (mainly acetate) which
stimulates the release of peptide tyrosine tyrosine
137 – 139
. The effects of GLP-1 and PYY in delaying
gastric emptying are referred to as the ‘ileal brake
mechanism which results in a moderate and stable flow of
nutrients from the stomach into the small intestine
decrease in postprandial gastric-emptying rate will, conse-
quently, prolong gastric distension and gastric signals of
137 – 139
. This mechanism was studied by Moran
et al.
in rhesus monkeys where intramuscular injections
of PYY reduced gastric emptying and resulted in a decrease
in food intake. In addition, there are indications that PYY in
the brain reduces appetite in humans
, although this is still
a subject for debate
. Third, fibrous dietary ingredients
may increase small-intestinal transit time
, possibly also
by stimulation of PYY which is found to suppress intestinal
. An increase in small-intestinal transit time: (i)
prolongs contact between nutrients and intestinal receptors
involved in maintaining satiety
and postpones feelings
of hunger
; (ii) results in the slowing down of starch
digestion and subsequent absorption of glucose, thereby
maintaining more stable postprandial glucose and insulin
concentrations in the blood
. A transient decline in blood
glucose level preceded meal initiation in rats
and caused a delay in the decrease in blood
glucose concentrations. This may prolong satiety and
postpone hunger and meal initiation (for a review, see
Campfield & Smith
). Finally, fermentation of carbo-
hydrates may yield VFA which leads to a higher level of
satiety by (i) PYY-mediated reduction of gastric emptying
and (ii) becoming a source of energy (mainly acetate)
at times when glucose supply from the small intestine is
decreasing, which stimulates longer-term sati-
As suggested previously, hunger is most likely the cause
for the observed behavioural effects seen in sows
. Hunger
or appetite is correlated with the peripheral concentration of
, a twenty-eight amino acid peptide synthesised
predominantly in the stomach
. For example, a rise in
blood ghrelin concentration is associated with meal
initiation in humans
. Supplementation of short-chain
oligofructose (average degree of polymerization of 4·5) in a
diet for 3 weeks decreased energy intake and lowered
ghrelin concentrations in rats compared with rats fed the
control diet without fructan supplementation. However, rats
fed a diet supplemented with long-chain oligofructose
(average degree of polymerization of 25·0) showed a
decrease in energy intake but not in ghrelin concentrations
compared to rats fed the control diet
. It is suggested that
the lower blood ghrelin concentrations may contribute to a
decrease in appetite during fasting
. Whether these
results were accompanied with changes in behaviour (for
example, food-seeking behaviour) requires further
investigation. Fig. 2 shows the effects of dietary fibre on
Findings in dogs
‘When we are considering how a dog is behaving, we really
should be considering what is inside the stomach’
, p. 1046). Despite this statement, little
additional research has been conducted on the association
between canine behaviours and satiety or feeding
motivation between meals. To the authors’ knowledge,
three studies have investigated the effects of dietary fibre on
satiety and feeding motivation in dogs of which only one
also studied canine behaviour and another measured
ad libitum food intake of dogs fed diets varying in fibre
source and content (Table 2). Butterwick & Markwell
overweight dogs (.115 % ideal body weight) six different
moist diets varying in type and amount of fibre on an
energy-restricted basis (45 % restriction of calculated
maintenance energy requirements; ME (kJ) ¼461 £body
weight (kg)
). The four experimental high-fibre diets
formulated to vary in soluble fibre (SF) and insoluble fibre
(ISF), i.e. (g/kg DM) 40·8 SF and 13·6 ISF; 112·5 SF and
G. Bosch et al.186
37·5 ISF; 35·7 SF and 202·4 ISF; 24·8 SF and 310·6 ISF, were
compared with two dry control diets (36·5 SF and 14·6 ISF;
45·5 SF and 15·2 ISF). The authors found no differences in
time spent at behaviours related to feeding motivation (i.e.
cumulative time spent at feeding bowl and number of visits
to bowl 30 min after feeding, intake of a meal (canned diet)
provided 3 h after introduction of the test diets) between
dogs fed the different diets. In contrast, Jewell & Toll
find effects of fibre content on the satiety of dogs. Dogs with
ad libitum access to dry diets with a medium or high crude
fibre content (135·5 and 223·4 g/kg DM) decreased total ME
intake compared with dogs that had ad libitum access to
low-crude fibre diets (16·3 and 16·4 g/kg DM). When dogs
were offered a subsequent meal, 30 min after the end of the
last meal, energy and DM intake were lower in dogs fed the
high-fibre diet compared with dogs consuming the low-fibre
. Similarly, Jackson et al.
observed that a high-fibre
content in dry diets reduced energy intakes in dogs. These
authors fed dogs in the morning either a diet high in total
dietary fibre (26·7 SF, 263·7 ISF g/kg as fed) or low in total
dietary fibre (18·1 SF, 123·2 ISF g/kg as fed) followed 6 h
later by ad libitum access to a diet containing 23·2 SF, 123·5
ISF g/kg as fed. Average energy intake over the day was
lower (kJ/kg body weight) in the dogs fed the high-fibre diet
in the morning compared with the energy intake of the dogs
fed the low-fibre diet in the morning (273 v. 332 kJ (65·3 v.
79·4 kcal)/kg body weight). The difference in average daily
energy intake was the result of the energy intake in the
morning since there were no significant differences observed
in intake of the diet provided in the afternoon between
the high-fibre (181 kJ (43·2 kcal)/kg body weight) and low-
fibre (197 kJ (47·2 kcal)/kg body weight) groups. These
latter two studies showed that high levels of fibrous dietary
ingredients in dogs can increase satiety and reduce energy
intake. This, however, was not confirmed in a study
by Butterwick & Markwell
. The latter may be due to the
energy restriction and the large differences in DM content of
diets between studies. Energy restriction will result in an
increased feeding motivation in dogs to a level that nullifies
the possible effects of fibre on satiety
. DM content of the
moist diets fed to dogs in the study of Butterwick &
ranged between 132 and 168 g/kg whereas
Jewell & Toll
and Jackson et al.
fed dry diets with a
DM content between 908 and 923 g/kg. On an energy basis,
intake of a diet with a high DM content or high energy
density will result in lower weight of the digesta in the
stomach compared with a diet with similar nutrient
composition but lower DM content. A low dietary DM
content will therefore have a higher weight of digesta in the
stomach and will stimulate stretch receptors which affect
satiety in dogs
. Finally, food intake in g DM/kg body
weight was found to be lower in dogs with ad libitum access
to a diet with 15 g short chain fructo-oligosaccharides/kg
DM compared with dogs with ad libitum access to a diet
with 60 g cellulose/kg DM
. The authors suggested that
satiety between diets was altered because of the differences
in fermentability of the fibre sources included in the diets.
Unfortunately, no measurements were made in this study to
elucidate possible mechanisms underlying their observed
difference in food intake.
The mechanisms behind the observed effects of dietary
fibre on inducing and maintaining satiety in humans and
pigs (see previous section) have in part been also observed
in dogs. Stimulation of stretch receptors through infusion
of liquids or filling a balloon with water placed in the
stomach reduced sham feeding in dogs, indicating that
stimulation of stretch receptors induces satiety in dogs
Gastric emptying was reduced in dogs as fibre (for
example, psyllium, guar gum) content and viscosity of the
meal increased
, which will prolong gastric distension
Fig. 2. Effects of dietary fibre (DF) on satiety. ( ), Factors that may ultimately increase the residence time of digesta in the designated
segments of the gastrointestinal tract; WBC, water-binding capacity; VFA, volatile fatty acids; GLP-1, glucagon-like peptide-1; PYY, peptide
tyrosine tyrosine.
Impact of nutrition on canine behaviour 187
and gastric signals of satiation. In addition, a study of
Bueno et al.
in which dogs were fed different fibre
sources (wheat bran, cellulose, guar gum), both gastric
emptying and intestinal transit time were affected with the
effect depending on the fibre source included.
A delay in gastric emptying and thus an increase in
intestinal transit time by dietary fibre (alginate) results in
more stable blood glucose concentrations as observed by
Murray et al.
. In dogs fed a diet with a high level of
fermentable fibres (sugarbeet pulp, gum arabic and
fructo-oligosaccharides), intestinal GLP-1 concentrations
were found to be increased compared with dogs fed a diet
with low-fermentable fibre (cellulose) levels
. GLP-1
slows down gastric emptying
and intestinal transit
which may result in prolonged gastric fill and delayed
nutrient digestion and absorption. In dogs, the ‘ileal
brake’ mechanism may also result from stimulation of
the release of PYY by fatty acids sufficient to delay gastric
emptying in dogs
As reported above, fermentation of carbohydrates
yields VFA
, which may lead to prolongation of satiety by
becoming a source of energy (mainly acetate) at times
when glucose supply from the small intestine is
. Although dogs have a relatively
small and simple large intestine, dogs are capable
of fermenting a significant quantity of dietary non-digestible
. Moreover, the faecal microflora of dogs
were found to give similar in vitro organic matter
disappearance results compared with the microflora from
humans, pigs and horses
. The latter indicates that
differences between these species in carbohydrate fermenta-
tion capacity are probably dependent on factors other than the
microbial population. The extent of fermentation in the
gastrointestinal tract in an animal largely depends on the time
available for microbial fermentation
. In dogs, a transit
time through the total gastrointestinal tract between 20 and
35 h is considered normal
. The large-intestinal transit of
digesta can take up to 90 % of the total gastrointestinal transit
, presenting a considerable time for large-intestinal
microflora to ferment undigested substrates entering from the
ileum. The VFA produced can be used by the hindgut bacteria
for protein synthesis, resulting in an increase in microbial
mass, or absorbed in the large intestine. The contribution of
large-intestinal VFA absorption towards the total energy
maintenance requirements of dogs has been reported to be
approximately 2 –7 %
Table 2. Effect of dietary fibre on food intake and canine behaviour
Authors Dogs and design Dietary fibre content or source* Results
Jewell &
Study 1, two groups of fifteen beagle
dogs were assigned to one of two
maintenance level for 14 d
On day 7, one of two diets was
provided 75 min after first meal. On
day 14, the other diet was offered
75 min after first meal. After 14 d,
the experimental design was
repeated but each group of dogs
received the other of the two diets
Study 2, identical as study 1 but
with different diets
(1) 16 g CF/kg (study 1)
(2) 136 g CF/kg (study 1)
(3) 16 g CF/kg (study 2)
(4) 223 g CF/kg (study 2)
(a) Energy intake of all dogs was
lower than energy on offer
(b) Dogs fed diets 2 and 4 had lower
daily energy intake than dogs fed
diets 1 and 3, respectively
(c) Energy intake of the second meal
75 min after first meal was lower
when dogs were fed diets 2 and 4
compared with dogs fed diets 1
and 3, respectively
Butterwick &
Six obese terrier dogs (.115 % of
ideal BW) were fed each of the six
wet diets (6 £6 Latin square) at
45 % of maintenance level for 12 d.
Number of visits to the bowl and
cumulative time spent at the bowl
were observed for 30 min from the
start of the meal. On day 7 and 10,
8 and 11, or 9 and 12, dogs had ad
libitum access to a wet diet that was
provided 180 min after the first
meal and food intake was
(1) 7 g CF/kg; 41g SF/kg; 14 g ISF/kg
(2) 13 g CF/kg; 113 g SF/kg; 38 g
(3) 143 g CF/kg; 36 g SF/kg; 202g
(4) 149 g CF/kg; 25 g SF/kg; 311g
(5) 15 g CF/kg; 37 g SF/kg; 15 g
(6) 8 g CF/kg; 46 g SF/kg; 15g ISF/kg
(a) No differences between diets in
daily energy intake
(b) No differences between diets in
observed behaviours
(c) No differences between diets in
food intake of the second meal
180 min after first meal
et al.
Two groups of fifteen miniature
schnauzers and toy poodles were
assigned to one of two dry diets fed
in the morning at 50 % of daily
intake and had ad libitum access to
a control diet in the afternoon
(approximately 6 h later) for 8 d
(1) 95 g CF/kg; 27 g SF/kg; 264 g
(2) 20 g CF/kg; 18 g SF/kg; 123 g
(3) 21 g CF/kg; 23 g SF/kg; 124 g
ISF/kg (control)
(a) Dogs fed diet 1 had lower morning
and daily energy intake/kg BW
than dogs fed diet 2
(b) There was no difference in food
intake of diet 3 in the afternoon
between dietary treatments
et al.
Twenty-eight adult beagle dogs were
stratified by BW and assigned at
random to one of four dry diets with
ad libitum access for 35 d
(1) 60 g cellulose/kg
(2) 15 g FOS/kg
(3) 60 g beet pulp/kg
(4) 60 g beet pulp/kg; 20 g gum
talha/kg; 15 g FOS/kg
(a) No differences between diets in
DM intake per d
(b) Dogs fed diet 2 showed lower DM
intake/d per kg body weight
compared with dogs fed diet 1
CF, crude fibre; BW, body weight; SF, soluble fibre; ISF, insoluble fibre; FOS, fructo-oligosaccharides.
* Values are presented on a DM basis except for the data of Jackson et al.
, which are as-fed.
G. Bosch et al.188
not to provide information on the way these values were
derived. In addition, the effect of production and absorption of
acetate as an energy source for body tissues on postprandial
satiety remains to be investigated. The work of Pouteau
et al.
on a method to evaluate acetate production and
metabolism using stable isotopes may be the starting point for
further exploration of the importance of carbohydrate
fermentation in the gastrointestinal tract and satiety in dogs.
To our knowledge, there is no information available in the
scientific literature regarding possible influences of dietary
fibre on ghrelin concentrations and behaviour in dogs.
However, when dogs are fed one scheduled meal per d,
ghrelin concentrations increase before and decrease rapidly
after the meal to remain relatively constant throughout the
rest of the day
, which may indicate little potency of
ghrelin concentrations to affect canine behaviour through-
out the day.
Nowadays, dry extruded diets for dogs may contain 30 %
or more carbohydrates of which starch is the major
component. Moreover, the non-digestible carbohydrate
fraction in diets can also make up a considerable
. As mentioned previously, fibres differing in
physical and chemical properties have diverse physiological
responses in animals. Nutrient digestion as well as transit
time through the gastrointestinal tract may be influenced by
the amount and source of fibre included in canine diets. In
the case of a reduction in nutrient digestibility when fibres
are included, it is necessary to increase the concentration of
some nutrients in order to ensure that the nutrient
requirements of the animals are met
. Future canine
research on the behavioural effects of dietary fibre should
account for the fact that different breeds may respond
differently (in terms of satiety). Gastric emptying rate is
inversely related to body weight in dogs of different sizes
Moreover, large-breed dogs have a longer large-intestinal
transit time and increased apparent total dietary fibre
, which may increase the production and the
use of VFA but may increase gastrointestinal discomfort as a
result of enhanced fermentation activity.
The degree of satiety in animals such as pigs has been
shown to affect behaviour, including aggressive and
stereotyped behaviour. Although likely, it is up till now
unknown whether canine behaviour can be affected by
degree of satiety and further research is required. Assuming
that behaviours in dogs are more favourable during times of
satiety than during times of hunger as observed in pigs (for
example, aggression), specific dietary fibres through their
potential to prolong satiety may assist in preventing
unwanted canine behaviours.
The present contribution provides an overview of current
knowledge on the influence of dietary macronutrient
composition on canine behaviour. It can be concluded that
little research has been conducted in this field although
research in other species indicates that there is potential to
modify behaviour in dogs through nutrition. There is
evidence that dietary composition can modulate animal and
human behaviour through different mechanisms. Dietary
protein may contain the precursors tryptophan and tyrosine
for the respective neurotransmitters serotonin and catechol-
amines. Since bioavailability of both tryptophan and
tyrosine in the brain are dependent on the dietary protein
content and amino acid composition, dietary composition
may have an impact on the behaviour and wellbeing of dogs
under specific circumstances (for example, stress). How-
ever, before application and extrapolation of the evidence
found in mostly rodent laboratory studies into commercial
canine diets is undertaken, research is required to identify
the optimal and safe dietary inclusion level in combination
with behavioural tests to study the magnitude of effects on
(problem) canine behaviour. The n-3 PUFA have an
important role in the development of the brain, and the
supply of essential fatty acids such as DHA could affect
aspects of the dopaminergic and serotonergic system and,
consequently, cognitive performance and behaviour as
observed in rodents. Most canine studies and dietary n-3
PUFA have been mainly focused on the effect of maternal
intake of different dietary n-3 PUFA during gestation and
lactation on n-3 PUFA in the milk and/or n-3 PUFA intake
on retinal function of puppies. It would be of interest to
examine the DHA required for optimal neurological
development and whether this leads to alterations in
cognitive abilities or behaviour later in life of dogs. In the
literature, studies have been reported which show that,
depending on the physical and chemical properties, certain
dietary fibres induce satiation or prolongation of satiety after
a meal. However, there have been no studies conducted in
which the effect of dietary fibre on physiological satiety
parameters, behaviour (for example, activity) and/or feeding
motivation were studied in dogs. If dietary fibre has short-
term effects that result in prolongation of satiety and a
reduction of hunger between meals, it may help to prevent
unwanted canine behaviours and also promote long-term
weight control.
1. Vila
`C, Savoleinen P, Maldonado JE, Amorim IR, Rice JE,
Honeycutt RL, Crandall KA, Lundeberg J & Wayne RK
(1997) Multiple and ancient origins of the domestic dog.
Science 276, 16871689.
2. Savolainen P, Zhang Y-P, Luo J, Lundeberg J & Leitner T
(2002) Genetic evidence for an East Asian origin of
domestic dogs. Science 298, 16101613.
3. Hart BL (1995) Analysing breed and gender differences in
behaviour. In The Domestic Dog: Its Evolution, Behaviour
and Interactions with People, pp. 65 77 [J Serpell, editor].
Cambridge, UK: Cambridge University Press.
4. Marston LC & Bennett PC (2003) Reforging the bond
towards successful canine adoption. Appl Anim Behav Sci
83, 227245.
5. Salman MD, Hutchison J, Ruch-Gallie R, Kogan L, New JC
Jr, Kass PH & Scarlett JM (2000) Behavioral reasons for
relinquishment of dogs and cats to 12 shelters. J Appl Anim
Welf Sci 3, 93– 106.
6. Patronek GJ, Glickman LT, Beck AM, McCabe GP & Ecker
C (1996) Risk factors for relinquishment of dogs to an
animal shelter. J Am Vet Med Assoc 209, 572581.
7. Houpt KA, Honig SU & Reisner IR (1996) Breaking the
human-companion animal bond. J Am Vet Med Assoc 208,
Impact of nutrition on canine behaviour 189
8. Carter CN (1990) Pet population control: another decade
without solutions? J Am Vet Med Assoc 197, 192 195.
9. Rowan A (1992) Shelters and pet overpopulation: a
statistical black hole. Anthrozoo
¨s5, 140143.
10. Dodman NH & Shuster L (1998) Preface. In Psychophar-
macology of Animal Behavior Disorders, pp. vii– xi [NH
Dodman and L Shuster, editors]. Malden, MA: Blackwell
11. Schoenthaler SJ & Bier ID (2000) The effect of vitamin-
mineral supplementation on juvenile delinquency among
American schoolchildren: a randomized, double-blind
placebo-controlled trial. J Altern Complement Med 6, 7 – 17.
12. Gesch CB, Hammond SM, Hampson SE, Eves A &
Crowder MJ (2002) Influence of supplementary vitamins,
minerals and essential fatty acids on the antisocial
behaviour of young adult prisoners. Randomised, placebo-
controlled trial. Br J Psychiatry 181, 22 28.
13. Studzinski CM, Araujo JA & Milgram NW (2005) The
canine model of human cognitive aging and dementia:
pharmacological validity of the model for assessment of
human cognitive-enhancing drugs. Prog Neuropsychophar-
macol Biol Psychiatry 29, 489 498.
14. Roudebush P, Zicker SC, Cotman CW, Milgram NW,
Muggenburg BA & Head E (2005) Nutritional management
of brain aging in dogs. J Am Vet Med Assoc 227, 722 728.
15. Zicker SC (2005) Cognitive and behavioral assessment in
dogs and pet food market applications. Prog Neuropsycho-
pharmacol Biol Psychiatry 29, 455 459.
16. Massey KA, Blakeslee CH & Pitkow HS (1998) A review of
physiological and metabolic effects of essential amino
acids. Amino Acids 14, 271300.
17. Young SN (1996) Behavioral effects of dietary neurotrans-
mitter precursors: basic and clinical aspects. Neurosci
Biobehav Rev 20, 313323.
18. Gibbons JL, Barr GA, Bridger WH & Leibowitz SF (1979)
Manipulations of dietary tryptophan: effects on mouse
killing and brain serotonin in the rat. Brain Res 169,
19. Kantak KM, Hegstrand LR, Whitman J & Eichelman B
(1980) Effects of dietary supplements and a tryptophan-free
diet on aggressive behavior in rats. Pharmacol Biochem
Behav 12, 173179.
20. Chamberlain B, Ervin FR, Pihl RO & Young SN (1987) The
effect of raising or lowering tryptophan levels on aggression
in vervet monkeys. Pharmacol Biochem Behav 28,
21. Rouvinen K, Archbold S, Laffin S & Harri M (1999) Long-
term effects of tryptophan on behavioural response and
growing-furring performance in silver fox (Vulpes vulpes).
Appl Anim Behav Sci 63, 6577.
22. Weld KP, Mench JA, Woodward RA, Bolesta MS, Suomi SJ
& Higley JD (1998) Effect of tryptophan treatment on self-
biting and central nervous system serotonin metabolism in
rhesus monkeys (Macaca mulatta). Neuropsychopharma-
cology 19, 314321.
23. Lasley SM & Thurmond JB (1985) Interaction of dietary
tryptophan and social isolation on territorial aggression,
motor activity, and neurochemistry in mice. Psychophar-
macology 87, 313321.
24. Koopmans SJ, Ruis M, Dekker R, van Diepen H, Korte M &
Mroz Z (2005) Surplus dietary tryptophan reduces plasma
cortisol and noradrenaline concentrations and enhances
recovery after social stress in pigs. Physiol Behav 85,
25. Markus CR, Olivier B, Panhuysen GE, Van Der Gugten J,
Alles MS, Tuiten A, Westenberg HG, Fekkes D,
Koppeschaar HF & de Haan EE (2000) The bovine protein
a-lactalbumin increases the plasma ratio of tryptophan to
the other large neutral amino acids, and in vulnerable
subjects raises brain serotonin activity, reduces cortisol
concentration, and improves mood under stress. Am J Clin
Nutr 71, 15361544.
26. Morgan WW, Rudeen PK & Pfeil KA (1975) Effect of
immobilization stress on serotonin content and turnover in
regions of the rat brain. Life Sci 17, 143 150.
27. Milakofsky L, Hare TA, Miller JM & Vogel WH (1985) Rat
plasma levels of amino acids and related compounds during
stress. Life Sci 36, 753761.
28. Okuda C, Saito A, Miyazaki M & Kuriyama K (1986)
Alteration of the turnover of dopamine and 5-hydroxytryp-
tamine in rat brain associated with hypothermia. Pharmacol
Biochem Behav 24, 79 83.
29. Dunn AJ (1988) Changes in plasma and brain tryptophan
and brain serotonin and 5-hydroxyindoleacetic acid after
footshock stress. Life Sci 42, 18471853.
30. Branchey L, Branchey M, Shaw S & Lieber CS (1984)
Depression, suicide, and aggression in alcoholics and their
relationship to plasma amino acids. Psychiatry Res 12,
31. Sainio E-L, Pulkki K & Young SN (1996) L-Tryptophan:
biochemical, nutritional and pharmacological aspects.
Amino Acids 10, 2147.
32. Rodwell VW (1979) Protein & amino acid metabolism:
conversion of amino acids to specialized products. In
Review of Physiological Chemistry, pp. 430– 439 [HA
Harper, VW Rodwell and PA Mayes, editors]. Los Altos,
CA: Lange Medical Publications.
33. Carlsson A & Lindqvist M (1978) Dependence of 5-HT and
catecholamine synthesis on concentrations of precursor
amino-acids in rat brain. Naunyn-Schmiedebergs Arch
Pharmacol 303, 157164.
34. Fernstrom JD & Wurtman RJ (1972) Brain serotonin
content: physiological regulation by plasma neutral amino
acids. Science 178, 149152.
35. Barnes NM & Sharp T (1999) A review of central 5-HT
receptors and their function. Neuropharmacology 38,
36. Hoyer D, Hannon JP & Martin GR (2002) Molecular,
pharmacological and functional diversity of 5-HT receptors.
Pharmacol Biochem Behav 71, 533 554.
37. Lucki I (1998) The spectrum of behaviors influenced by
serotonin. Biol Psychiatry 44, 151162.
38. Bagshaw CS, Ralston SL & Fisher H (1994) Behavioral and
physiological effect of orally administered tryptophan on
horses subjected to acute isolation stress. Appl Anim Behav
Sci 40, 112.
39. Henry Y, Seve B, Mounier A & Ganier P (1996) Growth
performance and brain neurotransmitters in pigs as affected
by tryptophan, protein, and sex. J Anim Sci 74, 2700 2710.
40. Raleigh MJ, Brammer GL, McGuire MT & Yuwiler A
(1985) Dominant social status facilitates the behavioral
effects of serotonergic agonists. Brain Res 348, 274282.
41. Mench JA & Shea-Moore MM (1995) Moods, minds and
molecules: the neurochemistry of social behavior. Appl
Anim Behav Sci 44, 99118.
42. Peremans K, Audenaert K, Blanckaert P, et al. (2002)
Effects of aging on brain perfusion and serotonin-2A
receptor binding in the normal canine brain measured with
single photon emission tomography. Prog Neuropsycho-
pharmacol Biol Psychiatry 26, 13931404.
43. Chaouloff F, Laude D, Guezennec Y & Elghozi JL (1986)
Motor activity increases tryptophan, 5-hydroxyindoleacetic
acid, and homovanillic acid in ventricular cerebrospinal
fluid of the conscious rat. J Neurochem 46, 1313– 1316.
G. Bosch et al.190
44. Trulson ME & Jacobs BL (1979) Raphe unit activity in
freely moving cats: correlation with level of behavioral
arousal. Brain Res 163, 135150.
45. Spring B, Chiodo J & Bowen DJ (1987) Carbohydrates,
tryptophan, and behavior: a methodological review. Psychol
Bull 102, 234256.
46. Yuwiler A, Oldendorf WH, Geller E & Braun L (1977)
Effect of albumin binding and amino acid competition on
tryptophan uptake into brain. J Neurochem 28, 1015– 1023.
47. Leathwood PD (1987) Tryptophan availability and seroto-
nin synthesis. Proc Nutr Soc 46, 143– 156.
48. Chaouloff F (1993) Physiopharmacological interactions
between stress hormones and central serotonergic systems.
Brain Res Rev 18, 132.
49. Fuller RW & Roush BW (1973) Binding of tryptophan to
plasma proteins in several species. Comp Biochem Physiol
B46, 273276.
50. Pardridge WM (1998) Blood– brain barrier carrier-mediated
transport and brain metabolism of amino acids. Neurochem
Res 23, 635644.
51. McMenamy RH (1965) Binding of indole analogues to
human serum albumin. Effects of fatty acids. J Biol Chem
240, 42354243.
52. Badawy AA (1977) The functions and regulation of
tryptophan pyrrolase. Life Sci 21, 755 768.
53. Pozefsky T, Felig P, Tobin JD, Soeldner JS & Cahill GF Jr
(1969) Amino acid balance across tissues of the forearm in
postabsorptive man. Effects of insulin at two dose levels.
J Clin Invest 48, 2273– 2282.
54. Fernstrom JD & Wurtman RJ (1972) Elevation of plasma
tryptophan by insulin in rat. Metabolism 21, 337 342.
55. Benton D & Donohoe RT (1999) The effects of nutrients on
mood. Public Health Nutr 2, 403409.
56. Rauch TM & Lieberman HR (1990) Tyrosine pretreatment
reverses hypothermia-induced behavioral depression. Brain
Res Bull 24, 147150.
57. Lehnert H, Reinstein DK, Strowbridge BW & Wurtman RJ
(1984) Neurochemical and behavioral consequences of
acute, uncontrollable stress: effects of dietary tyrosine.
Brain Res 303, 215223.
58. Reinstein DK, Lehnert H, Scott NA & Wurtman RJ (1984)
Tyrosine prevents behavioral and neurochemical correlates
of an acute stress in rats. Life Sci 34, 2225 2231.
59. Reinstein DK, Lehnert H & Wurtman RJ (1985) Dietary
tyrosine suppresses the rise in plasma corticosterone
following acute stress in rats. Life Sci 37, 21572163.
60. Lieberman HR (1994) Tyrosine and stress: human and
animal studies. In Food Components to Enhance Perform-
ance: an Evaluation of Potential Performance-Enhancing
Food Components for Operational Rations, pp. 277 299
[BM Marriott, editor]. Washington, DC: National Academy
61. Fernstrom JD & Fernstrom MH (1994) Dietary effects on
tyrosine availability and catecholamine synthesis in the
central nervous system: possible relevance to the control of
protein intake. Proc Nutr Soc 53, 419– 429.
62. Wurtman RJ, Hefti F & Melamed E (1980) Precursor
control of neurotransmitter synthesis. Pharmacol Rev 32,
63. Brady K, Brown JW & Thurmond JB (1980) Behavioral and
neurochemical effects of dietary tyrosine in young and aged
mice following cold-swim stress. Pharmacol Biochem
Behav 12, 667674.
64. Yeghiayan SK, Luo S, Shukitt-Hale B & Lieberman HR
(2001) Tyrosine improves behavioral and neurochemical
deficits caused by cold exposure. Physiol Behav 72,
65. DeNapoli JS, Dodman NH, Shuster L, Rand WM & Gross
KL (2000) Effect of dietary protein content and tryptophan
supplementation on dominance aggression, territorial
aggression, and hyperactivity in dogs. J Am Vet Med
Assoc 217, 504508.
66. Mugford RA (1987) The influence of nutrition on canine
behaviour. J Small Anim Pract 28, 1046– 1055.
67. Dodman NH, Reisner IR, Shuster L, Rand WM, Luescher
UA, Robinson I & Houpt KA (1996) Effect of dietary
protein content on behavior in dogs. J Am Vet Med Assoc
208, 376379.
68. National Research Council (2006) Nutrient Requirements of
Dogs and Cats. Washington, DC: National Academy Press.
69. Association of American Feed Control Officials (2004)
Official Publication of the Association of American Feed
Control Officials. Atlanta, GA: AAFCO.
70. Lieberman HR (1999) Amino acid and protein require-
ments: cognitive performance, stress and brain function. In
The Role of Protein and Amino Acids in Sustaining and
Enhancing Performance, pp. 289– 307 [Committee of
Military Nutrition Research and Institute of Medicine,
editor]. Washington, DC: National Academy Press.
71. Reeds PJ (2000) Dispensable and indispensable amino acids
for humans. J Nutr 130, S1835 S1840.
72. Carrie
´I, Clement M, de Javel D, France
`s H & Bourre JM
(2000) Specific phospholipid fatty acid composition of brain
regions in mice. Effects of n-3 polyunsaturated fatty acid
deficiency and phospholipid supplementation. J Lipid Res
41, 465472.
73. Lauritzen L, Hansen HS, Jørgensen MH & Michaelsen KF
(2001) The essentiality of long chain n-3 fatty acids in
relation to development and function of the brain and retina.
Prog Lipid Res 40, 1– 94.
74. Wainwright PE (1992) Do essential fatty acids play a role in
brain and behavioral development? Neurosci Biobehav Rev
16, 193205.
75. McCann JC & Ames BN (2005) Is docosahexaenoic acid, an
n-3 long-chain polyunsaturated fatty acid, required for
development of normal brain function? An overview of
evidence from cognitive and behavioral tests in humans and
animals. Am J Clin Nutr 82, 281 295.
76. Bourre JM, Francois M, Youyou A, Dumont O, Piciotti M,
Pascal G & Durand G (1989) The effects of dietary a-
linolenic acid on the composition of nerve membranes,
enzymatic activity, amplitude of electrophysiological
parameters, resistance to poisons and performance of
learning tasks in rats. J Nutr 119, 1880 1892.
77. Moriguchi T, Greiner RS & Salem N Jr (2000) Behavioral
deficits associated with dietary induction of decreased brain
docosahexaenoic acid concentration. J Neurochem 75,
78. Lim S & Suzuki H (2001) Changes in maze behavior of
mice occur after sufficient accumulation of docosahexae-
noic acid in brain. J Nutr 131, 319 324.
79. Wainwright PE, Xing HC, Ward GR, Huang YS, Bobik E,
Auestad N & Montalto M (1999) Water maze performance
is unaffected in artificially reared rats fed diets sup-
plemented with arachidonic acid and docosahexaenoic acid.
J Nutr 129, 10791089.
80. Wainwright PE, Xing HC, Mutsaers L, McCutcheon D &
Kyle D (1997) Arachidonic acid offsets the effects on mouse
brain and behavior of a diet with a low (n-6) (n-3) ratio and
very high levels of docosahexaenoic acid. J Nutr 127,
81. DeMar JC Jr, Ma K, Bell JM, Igarashi M, Greenstein D &
Rapoport SI (2006) One generation of n-3 polyunsaturated
Impact of nutrition on canine behaviour 191
fatty acid deprivation increases depression and aggression
test scores in rats. J Lipid Res 47, 172 180.
82. Takeuchi T, Iwanaga M & Harada E (2003) Possible
regulatory mechanism of DHA-induced anti-stress reaction
in rats. Brain Res 964, 136 143.
83. Carrie
´I, Clement M, de Javel D, France
`s H & Bourre JM
(2000) Phospholipid supplementation reverses behavioral
and biochemical alterations induced by n-3 polyunsaturated
fatty acid deficiency in mice. J Lipid Res 41, 473 480.
84. France
`s H, Coudereau JP, Sandouk P, Cle
´ment M, Monier C
& Bourre JM (1996) Influence of a dietary a-linolenic acid
deficiency on learning in the Morris water maze and on the
effects of morphine. Eur J Pharmacol 298, 217225.
85. Chalon S, Delion-Vancassel S, Belzung C, Guilloteau D,
Leguisquet AM, Besnard JC & Durand G (1998) Dietary
fish oil affects monoaminergic neurotransmission and
behavior in rats. J Nutr 128, 2512 2519.
86. McEntee WJ & Crook TH (1991) Serotonin, memory, and
the aging brain. Psychopharmacology 103, 143149.
87. Graeff FG, Guimaraes FS, De Andrade TG & Deakin JF
(1996) Role of 5-HT in stress, anxiety, and depression.
Pharmacol Biochem Behav 54, 129 141.
88. Meneses A (1998) Physiological, pathophysiological and
therapeutic roles of 5-HT systems in learning and memory.
Rev Neurosci 9, 275– 289.
89. Missale C, Nash SR, Robinson SW, Jaber M & Caron MG
(1998) Dopamine receptors: from structure to function.
Physiol Rev 78, 189225.
90. Schultz W (1998) Predictive reward signal of dopamine
neurons. J Neurophysiol 80, 1– 27.
91. Delion S, Chalon S, Herault J, Guilloteau D, Besnard JC &
Durand G (1994) Chronic dietary a-linolenic acid
deficiency alters dopaminergic and serotoninergic neuro-
transmission in rats. J Nutr 124, 2466 2476.
92. Delion S, Chalon S, Guilloteau D, Besnard JC & Durand G
(1996) a-Linolenic acid dietary deficiency alters age-related
changes of dopaminergic and serotoninergic neurotrans-
mission in the rat frontal cortex. JNeurochem66,
93. Zimmer L, Delion-Vancassel S, Durand G, Guilloteau D,
Bodard S, Besnard JC & Chalon S (2000) Modification of
dopamine neurotransmission in the nucleus accumbens of
rats deficient in n-3 polyunsaturated fatty acids. J Lipid Res
41, 3240.
94. Zimmer L, Vancassel S, Cantagrel S, Breton P, Delamanche
S, Guilloteau D, Durand G & Chalon S (2002) The
dopamine mesocorticolimbic pathway is affected by
deficiency in n-3 polyunsaturated fatty acids. Am J Clin
Nutr 75, 662667.
95. Zimmer L, Delpal S, Guilloteau D, Aioun J, Durand G &
Chalon S (2000) Chronic n-3 polyunsaturated fatty acid
deficiency alters dopamine vesicle density in the rat frontal
cortex. Neurosci Lett 284, 25– 28.
96. de la Presa Owens S & Innis SM (1999) Docosahexaenoic
and arachidonic acid prevent a decrease in dopaminergic
and serotoninergic neurotransmitters in frontal cortex
caused by a linoleic and a-linolenic acid deficient diet in
formula-fed piglets. J Nutr 129, 20882093.
97. Kodas E, Galineau L, Bodard S, Vancassel S, Guilloteau D,
Besnard JC & Chalon S (2004) Serotoninergic neurotrans-
mission is affected by n-3 polyunsaturated fatty acids in the
rat. J Neurochem 89, 695– 702.
98. Delion S, Chalon S, Guilloteau D, Lejeune B, Besnard JC &
Durand G (1997) Age-related changes in phospholipid fatty
acid composition and monoaminergic neurotransmission in
the hippocampus of rats fed a balanced or an n-3
polyunsaturated fatty acid-deficient diet. J Lipid Res 38,
99. Kitajka K, Sinclair AJ, Weisinger RS, Weisinger HS,
Mathai M, Jayasooriya AP, Halver JE & Puska
´s LG (2004)
Effects of dietary omega-3 polyunsaturated fatty acids on
brain gene expression. Proc Natl Acad Sci USA 101,
100. Bourre JM, Bonneil M, Dumont O, Piciotti M, Nalbone G &
Lafont H (1988) High dietary fish oil alters the brain
polyunsaturated fatty acid composition. Biochim Biophys
Acta 960, 458461.
101. Bourre JM, Bonneil M, Dumont O, Piciotti M, Calaf R,
Portugal H, Nalbone G & Lafont H (1990) Effect of
increasing amounts of dietary fish oil on brain and liver fatty
composition. Biochim Biophys Acta 1043, 149 152.
102. Yehuda S, Rabinovitz S & Mostofsky DI (1999) Essential
fatty acids are mediators of brain biochemistry and
cognitive functions. J Neurosci Res 56, 565– 570.
103. Heinemann KM, Waldron MK, Bigley KE, Lees GE &
Bauer JE (2005) Long-chain (n-3) polyunsaturated fatty
acids are more efficient than (-linolenic acid in improving
electroretinogram responses of puppies exposed during
gestation, lactation, and weaning. J Nutr 135, 1960 1966.
104. Bauer JE, Heinemann KM, Lees GE & Waldron MK (2006)
Retinal functions of young dogs are improved and maternal
plasma phospholipids are altered with diets containing long-
chain n-3 polyunsaturated fatty acids during gestation,
lactation, and after weaning. J Nutr 136, S1991 S1994.
105. Bauer JE, Heinemann KM, Bigley KE, Lees GE & Waldron
MK (2004) Maternal diet a-linolenic acid during gestation
and lactation does not increase docosahexaenoic acid in
canine milk. J Nutr 134, S2035 S2038.
106. Bauer JE, Heinemann KM, Lees GE & Waldron MK (2006)
Docosahexaenoic acid accumulates in plasma of canine
puppies raised on a-linolenic acid-rich milk during suckling
but not when fed a-linolenic acid-rich diets after weaning.
J Nutr 136, S2087S2089.
107. Biagi G, Mordenti AL, Cocchi M & Mordenti A (2004) The
role of dietary omega-3 and omega-6 essential fatty acids in
the nutrition of dogs and cats: a review. Prog Nutr 6,
108. Delton-Vandenbroucke I, Maude MB, Chen H, Aguirre GD,
Acland GM & Anderson RE (1998) Effect of diet on the
fatty acid and molecular species composition of dog retina
phospholipids. Lipids 33, 11871193.
109. Ahlstrøm Ø, Krogdahl A, Vhile SG & Skrede A (2004)
Fatty acid composition in commercial dog foods. J Nutr
134, S2145S2147.
110. Blundell J (1991) Pharmacological approaches to appetite
suppression. Trends Pharmacol Sci 12, 147– 157.
111. Rowland NE, Morien A & Li BH (1996) The physiology
and brain mechanisms of feeding. Nutrition 12, 626 639.
112. Read NW (1992) Role of gastrointestinal factors in hunger
and satiety in man. Proc Nutr Soc 51, 7– 11.
113. Bray GA (2000) Afferent signals regulating food intake.
Proc Nutr Soc 59, 373– 384.
114. de Graaf C, Blom WA, Smeets PA, Stafleu A & Hendriks
HF (2004) Biomarkers of satiation and satiety. Am J Clin
Nutr 79, 946961.
115. Strader AD & Woods SC (2005) Gastrointestinal hormones
and food intake. Gastroenterology 128, 175– 191.
116. Cummings JH, Roberfroid MB, Andersson H, Barth C,
Ferro-Luzzi A, Ghoos Y, Gibney M, Hermansen K,
James WP, Korver O, Lairon D, Pascal G & Voragen AG
(1997) A new look at dietary carbohydrate: chemistry,
physiology and health. Eur J Clin Nutr 51, 417 423.
G. Bosch et al.192
117. Benton D (2002) Carbohydrate ingestion, blood glucose and
mood. Neurosci Biobehav Rev 26, 293– 308.
118. Bergman EN (1990) Energy contributions of volatile fatty
acids from the gastrointestinal tract in various species.
Physiol Rev 70, 567590.
119. Lawrence AB & Terlouw EM (1993) A review of behavioral
factors involved in the development and continued
performance of stereotypic behaviors in pigs. J Anim Sci
71, 28152825.
120. Ramonet Y, Meunier-Salau
¨n MC & Dourmad JY (1999)
High-fiber diets in pregnant sows: digestive utilization and
effects on the behavior of the animals. J Anim Sci 77,
121. Bergeron R, Bolduc J, Ramonet Y, Meunier-Salau
Robert S (2000) Feeding motivation and stereotypies in
pregnant sows fed increasing levels of fibre and/or food.
Appl Anim Behav Sci 70, 2740.
122. Robert S, Matte JJ, Farmer C, Girard CL & Martineau GP
(1993) High-fibre diets for sows: effects on stereotypies and
adjunctive drinking. Appl Anim Behav Sci 37, 297309.
123. Danielsen V & Verstergaard E-M (2001) Dietary fibre for
pregnant sows: effect on performance and behaviour. Anim
Feed Sci Technol 90, 71 80.
124. de Leeuw JA, Jongbloed AW & Verstegen MWA (2004)
Dietary fiber stabilizes blood glucose and insulin levels and
reduces physical activity in sows (Sus scrofa). J Nutr 134,
125. Meunier-Salau
¨n MC, Edwards SA & Robert S (2001) Effect
of dietary fibre on the behaviour and health of the restricted
fed sow. Anim Feed Sci Technol 90, 5369.
126. Redbo I, Redbo-Torstensson P, O
¨dberg FO, Hedendahl A &
Holm J (1998) Factors affecting behavioural disturbances in
race-horses. Anim Sci 66, 475481.
127. Willard JG, Willard JC, Wolfram SA & Baker JP (1977)
Effect of diet on cecal pH and feeding behaviour of horses.
J Anim Sci 45, 87 93.
128. Krzak WE, Gonyou HW & Lawrence LM (1991) Wood
chewing by stabled horses: diurnal pattern and effects of
exercise. J Anim Sci 69, 1053 1058.
129. Rijnen MM, Verstegen MWA, Heetkamp MJ & Schrama
JW (2003) Effects of two different dietary fermentable
carbohydrates on activity and heat production in group-
housed growing pigs. J Anim Sci 81, 1210 1219.
130. Rijnen MM, Verstegen MW, Heetkamp MJ, Haaksma J &
Schrama JW (2003) Effects of dietary fermentable
carbohydrates on behavior and heat production in group-
housed sows. J Anim Sci 81, 182 190.
131. Spoolder HAM, Burbidge JA, Edwards SA, Simmins PH &
Lawrence AB (1995) Provision of straw as a foraging
substrate reduces the development of excessive chain and
bar manipulation in food restricted sows. Appl Anim Behav
Sci 43, 249262.
132. de Leeuw JA, Zonderland JJ, Altena H, Spoolder HAM,
Jongbloed AW & Verstegen MWA (2005) Effects of levels
and sources of dietary fermentable non-starch polysacchar-
ides on blood glucose stability and behaviour of group-
housed pregnant gilts. Appl Anim Behav Sci 94, 15 29.
133. van Leeuwen P, van Gelder AH, de Leeuw JA & van der
Klis JD (2006) An animal model to study digesta passage in
different compartments of the gastro-intestinal tract (GIT)
as affected by dietary composition. Curr Nutr Food Sci 2,
134. Guerin S, Ramonet Y, LeCloarec J, Meunier-Salau
¨n MC,
Bourguet P & Malbert CH (2001) Changes in intragastric
meal distribution are better predictors of gastric emptying
rate in conscious pigs than are meal viscosity or dietary fibre
concentration. Br J Nutr 85, 343 350.
135. Anvari M, Paterson CA, Daniel EE & McDonald TJ (1998)
Effects of GLP-1 on gastric emptying, antropyloric motility,
and transpyloric flow in response to a nonnutrient liquid.
Dig Dis Sci 43, 1133 1140.
136. Cani PD, Dewever C & Delzenne NM (2004) Inulin-type
fructans modulate gastrointestinal peptides involved in
appetite regulation (glucagon-like peptide-1 and ghrelin) in
rats. Br J Nutr 92, 521 526.
137. Brown AJ, Goldsworthy SM, Barnes AA, Eilert MM,
Tcheang L, Daniels D, Muir AI, Wigglesworth MJ, Kinghorn
I, Fraser NJ, Pike NB, Strum JC, Steplewski KW, Murdock
PR, Holder JC, Marshall PH, Szekeres PG, Wilson S, Ignar
DM, Foord SM, Wise A & Dowell SJ (2003) The Orphan G
protein-coupled receptors GPR41 and GPR43 are activated
by propionate and other short chain carboxylic acids. The
Journal of Biological Chemistry 278, 1131211319.
138. Le Poul E, Loison C, Struyf S, Springael JY, Lannoy V,
DecobecqME, Brezillon S, Dupriez V, VassartG, VanDamme
J, Parmentier M & Detheux M (2003) Functional character-
ization of human receptors for short chain fatty acids and their
role in polymorphonuclear cell activation. The Journal of
Biological Chemistry 278, 25481–25489.
139. Karaki S, Mitsui R, Hayashi H, Kato I, Sugiya H, Iwanaga T,
Furness JB & Kuwahara A (2006) Short-chain fatty acid
receptor, GPR43, is expressed by endoroendocrine cells and
mucosal mast cells in rat intestine. Cell and Tissue Research
324, 353600.
140. Holt S, Heading RC, Carter DC, Prescott LF & Tothill P
(1979) Effect of gel fibre on gastric emptying and
absorption of glucose and paracetamol. Lancet 1, 636 639.
141. Moran TH, Smedh U, Kinzig KP, Scott KA, Knipp S &
Ladenheim EE (2005) Peptide YY(3-36) inhibits gastric
emptying and produces acute reductions in food intake in
rhesus monkeys. Am J Physiol 288, R384 R388.
142. Batterham RL, Cowley MA, Small CJ, Herzog H, Cohen MA,
Dakin CL, Wren AM, Brynes AE, Low MJ, Ghatei MA,
Cone RD & Bloom SR (2002) Gut hormone PYY(3-36)
physiologically inhibits food intake. Nature 418, 650–654.
143. Woods SC (2005) Signals that influence food intake and
body weight. Physiol Behav 86, 709 716.
144. Bueno L, Praddaude F, Fioramonti J & Ruckebusch Y
(1981) Effect of dietary fiber on gastrointestinal motility
and jejunal transit time in dogs. Gastroenterology 80,
145. Lundberg JM, Tatemoto K, Terenius L, Hellstrom PM, Mutt
V, Hokfelt T & Hamberger B (1982) Localization of peptide
YY (PYY) in gastrointestinal endocrine cells and effects on
intestinal blood flow and motility. Proc Natl Acad Sci USA
79, 44714475.
146. Houpt KA (1982) Gastrointestinal factors in hunger and
satiety. Neurosci Biobehav Rev 6, 145 164.
147. Lin HC, Zhao XT, Chu AW, Lin YP & Wang L (1997) Fiber-
supplemented enteral formula slows intestinal transit by
intensifying inhibitory feedback from the distal gut. Am J
Clin Nutr 65, 1840 1844.
148. Roberfroid M (1993) Dietary fiber, inulin, and oligofruc-
tose: a review comparing their physiological effects. Crit
Rev Food Sci Nutr 33, 103 148.
149. Louis-Sylvestre J & Le Magnen J (1980) A fall in blood
glucose level precedes meal onset in free-feeding rats.
Neurosci Biobehav Rev 4, 13– 15.
150. Campfield LA, Brandon P & Smith FJ (1985) On-line
continuous measurement of blood glucose and meal pattern
in free-feeding rats: the role of glucose in meal initiation.
Brain Res Bull 14, 605 616.
Impact of nutrition on canine behaviour 193
151. Campfield LA, Smith FJ, Rosenbaum M & Hirsch J (1996)
Human eating: evidence for a physiological basis using a
modified paradigm. Neurosci Biobehav Rev 20, 133– 137.
152. Campfield LA & Smith FJ (2003) Blood glucose dynamics
and control of meal initiation: a pattern detection and
recognition theory. Physiol Rev 83, 25– 58.
153. Cherbut C (2003) Motor effects of short-chain fatty acids
and lactate in the gastrointestinal tract. Proc Nutr Soc 62,
154. Bleiberg B, Beers TR, Persson M & Miles JM (1992)
Systemic and regional acetate kinetics in dogs. Am J Physiol
262, E197E202.
155. Re
´rat A (1996) Influence of the nature of carbohydrate
intake on the absorption chronology of reducing sugars and
volatile fatty acids in the pig. Reprod Nutr Dev 36, 319.
156. Wren AM, Seal LJ, Cohen MA, Brynes AE, Frost GS,
Murphy KG, Dhillo WS, Ghatei MA & Bloom SR (2001)
Ghrelin enhances appetite and increases food intake in
humans. J Clin Endocrinol Metab 86, 5992 5995.
157. Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H &
Kangawa K (1999) Ghrelin is a growth-hormone-releasing
acylated peptide from stomach. Nature 402, 656– 660.
158. van der Lely AJ, Tscho
¨p M, Heiman ML & Ghigo E (2004)
Biological, physiological, pathophysiological, and pharma-
cological aspects of ghrelin. Endocr Rev 25, 426 457.
159. Cummings DE, Purnell JQ, Frayo RS, Schmidova K, Wisse
BE & Weigle DS (2001) A preprandial rise in plasma
ghrelin levels suggests a role in meal initiation in humans.
Diabetes 50, 17141719.
160. Delzenne NM, Cani PD, Daubioul C & Neyrinck AM
(2005) Impact of inulin and oligofructose on gastrointestinal
peptides. Br J Nutr 93, S157 S161.
161. Butterwick RF & Markwell PJ (1997) Effect of amount and
type of dietary fiber on food intake in energy-restricted
dogs. Am J Vet Res 58, 272 276.
162. Jewell DE & Toll PW (1996) Effects of fiber on food intake
in dogs. Vet Clin Nutr 3, 115 118.
163. Jackson JR, Laflamme DP & Owens SF (1997) Effects of
dietary fiber content on satiety in dogs. Vet Clin Nutr 4,
164. Pappas TN, Melendez RL & Debas HT (1989) Gastric
distension is a physiologic satiety signal in the dog. Dig Dis
Sci 34, 14891493.
165. Howard MD, Kerley MS, Sunvold GD & Reinhart GA
(2000) Source of dietary fiber fed to dogs affects nitrogen
and energy metabolism and intestinal microflora popu-
lations. Nutr Res 20, 1473 1484.
166. Russell J & Bass P (1985) Canine gastric emptying of fiber
meals: influence of meal viscosity and antroduodenal
motility. Am J Physiol 249, G662– G667.
167. Murray SM, Patil AR, Fahey GC Jr, Merchen NR, Wolf BW,
Lai C-S & Garleb KA (1999) Apparent digestibility and
glycaemic responses to an experimental induced viscosity
dietary fibre incorporated into an enteral formula fed to dogs
cannulated in the ileum. Food Chem Toxicol 37, 47– 56.
168. Massimino SP, McBurney MI, Field CJ, Thomson AB,
Keelan M, Hayek MG & Sunvold GD (1998) Fermentable
dietary fiber increases GLP-1 secretion and improves
glucose homeostasis despite increased intestinal glucose
transport capacity in healthy dogs. JNutr128,
169. Daniel EE, Anvari M, Fox-Threlkeld JE & McDonald TJ
(2002) Local, exendin-(9-39)-insensitive, site of action of
GLP-1 in canine ileum. Am J Physiol 283, G595 G602.
170. Kumar D, Phillips SF & Brown ML (1988) Reflux from
ileum to colon in the dog. Role of external ligamentous
attachments. Dig Dis Sci 33, 345 352.
171. Pappas TN, Debas HT, Chang AM, Taylor IL & Peptide YY
(1986) Peptide YY release by fatty acids is sufficient to inhibit
gastric emptying in dogs. Gastroenterology 91, 1386– 1389.
172. Fahey GC Jr, Flickinger AE, Grieshop CM & Swanson KS
(2004) The role of dietary fibre in companion animal
nutrition. In Dietary Fibre: Bio-active Carbohydrates for
Food and Feed, pp. 295– 328 [JM Kamp, NG Asp, J Miller
and G Schaafsma, editors]. Wageningen, The Netherlands:
Wageningen Academic Publishers.
173. Sunvold GD, Hussein HS, Fahey GC Jr, Merchen NR &
Reinhart GA (1995) In vitro fermentation of cellulose, beet
pulp, citrus pulp, and citrus pectin using fecal inoculum
from cats, dogs, horses, humans, and pigs and ruminal fluid
from cattle. J Anim Sci 73, 3639 3648.
174. Butine TJ & Leedle JA (1989) Enumeration of selected
anaerobic bacterial groups in cecal and colonic contents of
growing-finishing pigs. Appl Environ Microbiol 55,
175. Williams BA, Bosch M, Houdijk JGM & Van der Camp Y
(1997) Differences in fermentative capabilities of flora from
different areas of porcine GIT. In Proceedings of the 48th
EAAP Meeting, p. 133. Rome: European Association of
Animal Production.
176. Diez M & Istasse L (1997) Fibres alimentaires chez le chien:
II. Effets sur la vidange gastrique et le transit gastro-intestinal
(Food fibres in the dog II. Effects on gastric draining and
gastrointestinal transit). Ann Me
´t141, 27– 37.
177. Iwanaga Y, Wen J, Thollander MS, Kost LJ, Thomforde
GM, Allen RG & Phillips SE (1998) Scintigraphic
measurement of regional gastrointestinal transit in the
dog. Am J Physiol 275, G904G910.
178. Bruce SJ, Guilford WG, Hedderley DI & McCauley M
(1999) Development of reference intervals for the large
intestinal transit of radiopaque markers in dogs. Vet Radiol
Ultrasound 40, 472476.
179. Bugaut M (1987) Occurrence, absorption and metabolism of
short chain fatty acids in the digestive tract of mammals.
Comp Biochem Physiol B 86, 439 472.
180. Stevens EC & Huma ID (1998) Contributions of microbes in
vertebrate gastrointestinal tract to production and conserva-
tion of nutrients. Physiol Rev 78, 393427.
181. Pouteau E, Nguyen P, Ballevre O & Krempf M (2003)
Production rates and metabolism of short-chain fatty acids
in the colon and whole body using stable isotopes. Proc Nutr
Soc 62, 8793.
182. Pouteau E, Frenais R, Dumon H, Noah L, Martin L & Nguyen
P (2005) Colonic fermentation of inulin increases whole-body
acetate turnover in dogs. JNutr135, 28452851.
183. Yokoyama M, Nakahara K, Kojima M, Hosoda H, Kangawa
K & Murakami N (2005) Influencing the between-feeding
and endocrine responses of plasma ghrelin in healthy dogs.
Eur J Endocrinol 152, 155 160.
184. Diez M, Hornick JL, Baldwin P, Eenaeme CV & Istasse L
(1998) The influence of sugar-beet fibre, guar gum and
inulin on nutrient digestibility, water consumption and
plasma metabolites in healthy beagle dogs. Res Vet Sci 64,
185. Bourreau J, Hernot D, Bailhache E, Weber M, Ferchaud V,
Biourge V, Martin L, Dumon H & Nguyen P (2004) Gastric
emptying rate is inversely related to body weight in dog
breeds of different sizes. J Nutr 134, S2039 S2041.
186. Weber MP, Hernot D, Nguyen PG, Biourge VC & Dumon
HJ (2004) Effect of size on electrolyte absoprtion rates and
fermentative activity in dogs. J Anim Physiol Anim Nutr 88,
187. Grimmett A & Sillence MN (2005) Calmatives for the
excitable horse: a review of l-tryptophan. Vet J 170, 2432.
G. Bosch et al.194
... In addition, an incomplete and unbalanced diet can negatively affect the behaviour of dogs. Since behaviour is regulated by hormones and neurotransmitters, changes in the availability of their precursors in the brain can affect dogs' behaviour (BOSCH et al., 2007;VERSTEgEN, 2017). The availability of hormone and neurotransmitter precursors is conditioned by the availability of nutrients and their interaction in the diet. ...
... The availability of hormone and neurotransmitter precursors is conditioned by the availability of nutrients and their interaction in the diet. Some behavioural disorders, such as aggressiveness and self-mutilation, and stress resistance may be affected by tryptophan -the precursor of serotonin, or by tyrosine -the precursor of the catecholamines dopamine, noradrenaline and adrenaline (BOSCH et al., 2007;VERSTEgEN, 2017). VESTERgEN (2017) explained that stress, anxiety and compulsive problems may potentially be linked to the quality of foods. ...
... Tryptophan supplementation may be helpful in reducing dominance and territorial aggression. Some undesirable behaviours are caused by a lack of satiety due to dietary fibres and their fermentability (BOSCH et al., 2007). Further, the activity level of dogs may also be regulated by the fermentability of dietary fibres, energy restriction and, indirectly, by energy surplus. ...
The importance of nutrition for the welfare of dogs is highlighted in this review. Malnutrition can be the cause of many health disorders, including behavioural disorders. On the other hand, dietary interventions and modifications, and nutritional enrichment can be used for the treatment of certain health problems and improving welfare in dogs. The paper focuses on data collected from the literature on omissions in the diet of dogs for which owners, food producers, veterinarians and/or animal welfare societies are responsible. Manufacturers are responsible for the composition, quality and safety of commercially available dog food. They are also responsible for the clarity of the feeding guidelines that are provided on the labels. Owners are expected to know what type of food is most suitable for their dogs in terms of any particular allergies or intolerances they may have, as well the quality and quantity of food they should feed their dogs. It is especially important for owners to be aware of the risks of using raw food in dog nutrition. Due to the special social status that dogs have in their owners’ families, owners are increasingly interested in the quality and safe nutrition of their companions. This should be a challenge for veterinarians to master the necessary knowledge of pet nutrition, and to develop and provide advice and consulting services in this area within their practice. Owners’ interest in good quality and safe dog nutrition should also be a challenge for animal welfare societies to include information on nutrition in general dog ownership education.
... The latter may also be affected by dietary tyrosine levels, which is a precursor to catecholamines. Since diet composition influences nutrient availability and interactions, the presence of these precursors in the brain may influence behaviour or stress resistance (Bosch et al., 2007). In rats, a tyrosine-rich diet can prevent adverse behavioural and neurochemical effects caused by acute stressors, including hypothermia, restraint, and tail-shock. ...
... In stressed rats (tail-shock), ingestion of a high-tyrosine diet reversed the post-stress decline in brain noradrenaline and attenuated behaviour changes, i.e. decreased locomotion, standing on hind legs, and hole-poking in a novel open field (Lehnert et al., 1984;Rauch and Lieberman, 1990). This suggests that a tyrosine-rich diet may be beneficial during periods of severe stress as it prevents depletion of the substrate required for catecholamine synthesis during high catecholaminergic activity and demand (Bosch et al., 2007). ...
... The aetiology of fur chewing has not been conclusively established, but it may be related to long-term stress, which can lead to the development of repetitive behaviours induced by frustration, repeated attempts to cope, and/or a central nervous system dysfunction known as impulsive-compulsive disorder (Łapiński et al., 2014). The present study, as well as previous research concerning the effects of dietary tyrosine on the neurochemical and behavioural consequences of stress (Lehnert et al., 1984;Rauch and Lieberman, 1990;Bosch et al., 2007) suggest that feeding chinchillas with impulsivecompulsive disorders with increased Tyr and Phe doses may be justified. ...
... Fibers (nondigestible carbohydrates) potently promote satiety too, at least in humans (Wanders et al., 2011) and pigs (De Leeuw et al., 2008). This involves various underlying mechanisms (for a review see Bosch et al., 2007) that relate to the formation of gels in the stomach (e.g. alginate; Paxman et al., 2008) and small intestine (e.g. ...
... Dietary proteins and fibers promote satiety (Bosch et al., 2007;Morrison et al., 2012) and are thus expected to reduce food motivation. We tested whether protein and fiber levels in 12 commercial foods explained variation in motivation for food. ...
... Dietary fermentable fibers reduced appetite in various species including humans (Korczak and Slavin, 2018), dogs (Bosch et al., 2009a,b) and pigs (Souza da Silva et al., 2012) and various underlying appetiteregulating mechanisms have been described (for a review see e.g. Bosch et al., 2007). The large intestine of cats is relatively short and non-sacculated, but it hosts an active microbial community that is capable of fermenting fibers, including inulin (Sunvold et al., 1995;Bosch et al., 2017), and potentially stimulating mechanisms that promote satiety. ...
Full-text available
Overweight and obesity are common in global pet cat populations which makes it important to understand how properties of food affect appetite (food motivation). In four experiments, we studied this by using a model of operant conditioning for assessing appetite in which cats could press a lever for food rewards. There was no effect of protein status on motivation for protein, when evaluated in a cross-over design with cats receiving low protein (LP) or high protein (HP) foods for 14 days. Cats obtained similar numbers of HP and LP rewards, irrespective of whether their daily food was HP or LP (mixed-effects model, P=0.550 for food × reward, P=0.151 for reward). High dietary protein reduced food motivation when we regressed protein levels in 12 commercial foods (12.0 to 27.4 g crude protein/MJ metabolizable energy; P=0.022) fed for 2 days and tested at 5 h postprandially on the third day whereas fiber levels were without effect (3.8 to 17.8 g non-starch polysaccharides/MJ; P=0.992). Dietary fiber may reduce appetite depending on its physicochemical properties and we tested the effect of a gelling fiber (alginate), viscous fiber (psyllium) and a fermentable fiber (inulin). Cats received test foods as well as control foods for 3 days and were tested on the third day at 3 h (alginate), 5 h (psyllium) or 8 h (inulin) postprandially. Enriching the food with alginate (P=0.379) or psyllium (P=0.153) did not affect the number of rewards obtained, but the feeding of the inulin-enriched food did make the cats obtain fewer rewards than when they received the control food (P=0.001). Finally, cooking or grinding of dietary meat increased the number of rewards obtained by cats, on day 3 at 3 h postprandial, without evidence for additive effects of these treatments (P=0.014 for grinding × cooking). This study shows that dietary content of protein or fiber, and the grinding or cooking of meat, all affect appetite in cats as expected, though some predicted effects remained undetected and clearly details regarding food properties matter. These and future findings can guide the designing of foods that promote satiety and prevent over-eating in meal-fed cats.
... Through changes in diet, it is possible to modify the composition and function of the intestinal microbiome and the behaviour of the host indirectly [38,39]. Administering a special diet in dogs with behavioural abnormalities altered their neuroendocrine serum parameters, including neurotransmitters which are associated with stress and anxiety [38]. ...
... Administering a special diet in dogs with behavioural abnormalities altered their neuroendocrine serum parameters, including neurotransmitters which are associated with stress and anxiety [38]. The supplementation of ω-3 and ω-6 fatty acids in pigs and rodents caused changes in the serotonergic and dopaminergic system, with a secondary effect on their behaviour and cognition [39]. A direct modification of the microbiome can be achieved by using prebiotics, probiotics, psychobiotics (probiotics that influence host behaviour), synbiotics, faecal microbiota transplantation (FMT) and bacteriotherapy [40][41][42]. ...
Full-text available
Background: Epilepsy is the most common chronic neurological disease in dogs. More than two-thirds of these patients suffer from associated behavioural comorbidities. The latter could have their origin in partially overlapping pathomechanisms, with the intestinal microbiome as a potential key link between them. The current arsenal of drugs for epilepsy management remains limited. Most canine patients continue to have seizures despite treatment and the occurrence of comorbidities is not sufficiently addressed, limiting quality of life of affected dogs and owners. Therefore, novel additional epilepsy management options are urgently needed. The microbiome-gut-brain axis may serve as a new target for the development of innovative multimodal therapeutic approaches to overcome current shortcomings in epilepsy management. Methods: A six-month prospective, randomised, double-blinded, placebo-controlled, crossover, dietary trial was designed to investigate the potential of the psychobiotic Bifidobacterium longum on behavioural comorbidities in canine epilepsy. Seizure semiology will be evaluated as a secondary outcome measure. Thirty-four privately owned dogs are planned to be included in the ongoing study meeting the following inclusion criteria: Dogs displaying increased anxiety/fear behaviour since the start of the idiopathic epilepsy. Tier II confidence level of the International Veterinary Epilepsy Task Force for the diagnosis of idiopathic epilepsy, with a maximum seizure interval of 3 month and a minimum of three generalised seizures within that period and chronically treated with at least one antiseizure drug without improvement in seizure frequency Each dog will receive the allocated supplement (probiotic vs. placebo) alongside its normal diet for a 3-month period. After a three-week wash out period, the second phase starts by administering the respective other supplement for another 3 months. Discussion: The current study considers modern high-quality standards for epilepsy medication trials. Common biasing effects should be limited to a possible minimum (regression-to-the mean effect, placebo effect, observer effect), ensuring a high validity and accuracy of the acquired results, thus enabling a representative nature of the efficacy of Bifidobacterium longum as add-on supplement for dogs suffering from epilepsy and its comorbidities. This publication should provide a description of the study procedure and data acquisition methods, including prognosed statistical analysis.
... Digestibility and nutrient availability are important parameters when estimating the nutritional quality of pet food (3). The diet composition, nutrient availability, and their interaction also regulates the cognition and behavior of canines (4,5). ...
Full-text available
Digestibility and nutrient availability are important parameters when estimating the nutritional quality of pet food. We have developed a simulated semi-dynamic in vitro canine digestion model to evaluate the digestibility of dry extruded canine food. Canine food was assessed for digestible energy, dry matter digestibility, protein digestibility, non-fibrous carbohydrate (NFC) digestibility, and total antioxidant capacity (TAC) in the absence and presence of an enzyme blend (DigeSEB Super Pet). Enzyme blend supplementation in canine food was found to increase the dry matter digestibility (18.7%, p < 0.05), digestible energy (18.1%, p < 0.05), and protein digestibility (11%, p < 0.1) and reducing sugar release (106.3%, p < 0.005). The release of low molecular weight peptides (48.7%) and essential amino acids (15.6%) increased within 0.5 h of gastrointestinal digestion due to enzyme blend supplementation. Furthermore, the TAC of the digesta was also increased (8.1%, p < 0.005) in the canine food supplemented with enzyme blend. Overall, supplementation of enzyme blend in canine food is an effective strategy to enhance the food digestibility and nutrient availability for absorption.
... Although levels of chronic malnutrition are lower in smaller families, several other studies did not get different findings (Wong and al., 2014). Also, it should be noted that the presence of more than two children under five in a household is negatively correlated with the child's nutritional status (Bosch, 2007). The nutritional status of children is affected in a household hosting more children under five to feed with a reduced income. ...
Full-text available
During the first two years of a child's life, nutritional status is crucial for his or her well-being and growth. This study explains the risk factors of chronic malnutrition during the first two years of life in south west Benin. The methodological approach uses the construction of Food Consumption Score (FCS), Reduced Coping Strategies Index (rCSI), Household Dietary Diversity Score (HDDS), and Livelihood Coping Strategies (LCS). The Chi2 test helps to examine the dependency between the variables. The simple binary logit model is used to explore the effects of the explanatory variables on the dependent variable. The results show that about 27% of children aged 6-23 months are chronically malnourished. The age range of the child, the type of union, the average monthly income of the head of the household, the food consumption score, and the size of the family determine the chronic malnutrition. During difficult times, households rely on atypical coping strategy mechanisms by disposing of their productive assets. 20.3% of households can marginally cover their minimum food needs using crisis or emergency coping strategy mechanisms.
... Although levels of chronic malnutrition are lower in smaller families, several other studies did not get different findings (Wong and al., 2014). Also, it should be noted that the presence of more than two children under five in a household is negatively correlated with the child's nutritional status (Bosch, 2007). The nutritional status of children is affected in a household hosting more children under five to feed with a reduced income. ...
Full-text available
During the first two years of a child's life, nutritional status is crucial for his or her well-being and growth. This study explains the risk factors of chronic malnutrition during the first two years of life in south west Benin. The methodological approach uses the construction of Food Consumption Score (FCS), Reduced Coping Strategies Index (rCSI), Household Dietary Diversity Score (HDDS), and Livelihood Coping Strategies (LCS). The Chi2 test helps to examine the dependency between the variables. The simple binary logit model is used to explore the effects of the explanatory variables on the dependent variable. The results show that about 27% of children aged 6-23 months are chronically malnourished. The age range of the child, the type of union, the average monthly income of the head of the household, the food consumption score, and the size of the family determine the chronic malnutrition. During difficult times, households rely on atypical coping strategy mechanisms by disposing of their productive assets. 20.3% of households can marginally cover their minimum food needs using crisis or emergency coping strategy mechanisms.
... In rodents magnesium deficiency, and manganese toxicity in people also cause aggression. In dogs, tryptophan and tyrosine, omega-6 and omega-3 fatty acids have been hypothesised to be associated with aggression and other behavioural changes [36]. In a thesis and literature review [37] canine aggressive behaviour was reported to be decreased by a low protein diet and tryptophan supplements. ...
... In veterinary medicine, dietary manipulations have attracted increasing consideration as an alternative approach to managing seizure activity and behaviour in dogs with idiopathic epilepsy (IE) (11,38,39). In 2015, Law et al. compared an MCT kibble diet (test formula contained 5.5 % MCT; 10% of the total formula calories from C8, C10, C12) to a standardised placebo diet on its seizure-controlling effects in 21 chronically nonresponsive ASD-treated dogs with IE in a crossover trial design (39). ...
Full-text available
Consumption of medium-chain triglycerides (MCT) has been shown to improve seizure control, reduce behavioural comorbidities and improve cognitive function in epileptic dogs. However, the exact metabolic pathways affected by dietary MCT remain poorly understood. In this study, we aimed to identify changes in the metabolome and neurotransmitters levels relevant to epilepsy and behavioural comorbidities associated with the consuming of an MCT supplement (MCT-DS) in dogs with idiopathic epilepsy (IE). Metabolic alterations induced by a commercial MCT-DS in a population of 28 dogs with IE were evaluated in a 6-month multi-centre, prospective, randomised, double-blinded, controlled cross-over trial design. A metabolic energy requirement-based amount of 9% MCT or control oil was supplemented to the dogs' stable base diet for 3 months, followed by the alternative oil for another 3 months. A validated, quantitative nuclear magnetic resonance (NMR) spectroscopy platform was applied to pre- and postprandially collected serum samples to compare the metabolic profile between both DS and baseline. Furthermore, alterations in urinary neurotransmitter levels were explored. Five dogs (30%) had an overall reduction in seizure frequency of ≥50%, and were classified as MCT-responders, while 23 dogs showed a ≤50% reduction, and were defined as MCT non-responders. Amino-acid metabolism was significantly influenced by MCT consumption compared to the control oil. While the serum concentrations of total fatty acids appeared similar during both supplements, the relative concentrations of individual fatty acids differed. During MCT supplementation, the concentrations of polyunsaturated fatty acids and arachidonic acid were significantly higher than under the control oil. β-Hydroxybutyric acid levels were significantly higher under MCT supplementation. In total, four out of nine neurotransmitters were significantly altered: a significantly increased γ-aminobutyric acid (GABA) concentration was detected during the MCT-phase accompanied by a significant shift of the GABA-glutamate balance. MCT-Responders had significantly lowered urinary concentrations of histamine, glutamate, and serotonin under MCT consumption. In conclusion, these novel data highlight metabolic changes in lipid, amino-acid and ketone metabolism due to MCT supplementation. Understanding the metabolic response to MCT provides new avenues to develop better nutritional management with improved anti-seizure and neuroprotective effects for dogs with epilepsy, and other behavioural disorders.
... This waste, which represents a huge cost for companies, is a rich source of compounds with a high nutritional value as well as of secondary metabolites that remain in the squeezing residue. In particular, the unsaponifiable fraction of HSO and HSM, which until now received very little attention by researchers, represents the true inherent potential of industrial hemp products for their possible use in the nutraceutical field [20,21]. ...
Full-text available
Recently, there has been a growing interest in the recovery of agri-food waste within the circular economy perspective. In this study, the nutritional, phytochemical, and biological features of the cold-pressed hempseed oil (HSO) and hempseed meal (HSM) of two industrial hemp varieties (USO 31 and Futura 75, THC ≤ 0.2%) were evaluated. The HSOs showed a high total phenols and flavonoid content, which were confirmed by LC-DAD-ESI-MS analysis, with rutin as the most abundant compound (56.93–77.89 µg/100 FW). They also proved to be a rich source of tocopherols (81.69–101.45 mg/100 g FW) and of a well-balanced ω-6 to ω-3 fatty acid ratio (3:1) with USO 31, which showed the best phytochemical profile and consequently the best antioxidant activity (about two times higher than Futura 75). The HSMs still retained part of the phytochemicals identified in the HSOs (polyphenols, tocopherols, and the preserved ω-6/ω-3 fatty acids ratio) and a modest antioxidant activity. Furthermore, they showed a very interesting nutritional profile, which was very rich in proteins (29.88–31.44 g/100 g FW), crude fibers (18.39–19.67 g/100 g), and essential and non-essential amino acids. Finally, only a restrained amount of anti-nutritional factors (trypsin inhibitors, phytic acid, and condensed tannins) was found, suggesting a promising re-use of these byproducts in the nutraceutical field.
Here, we compared the traditional nutritional definition of the dispensable and indispensable amino acids for humans with categorizations based on amino acid metabolism and function. The three views lead to somewhat different interpretations. From a nutritional perspective, it is quite clear that some amino acids are absolute dietary necessities if normal growth is to be maintained. Even so, growth responses to deficiencies of dispensable amino acids can be found in the literature. From a strictly metabolic perspective, there are only three indispensable amino acids (lysine, threonine and tryptophan) and two dispensable amino acids (glutamate and serine). In addition, a consideration of in vivo amino acid metabolism leads to the definition of a third class of amino acids, termed conditionally essential, whose synthesis can be carried out by mammals but can be limited by a variety of factors. These factors include the dietary supply of the appropriate precursors and the maturity and health of the individual. From a functional perspective, all amino acids are essential, and an argument in favor of the idea of the critical importance of nonessential and conditionally essential amino acids to physiological function is developed.
This review is part of a series intended for nonspecialists that will summarize evidence relevant to the question of whether causal relations exist between micronutrient deficiencies and brain function. Here, we focus on experiments that used cognitive or behavioral tests as outcome measures in experimental designs that were known to or were likely to result in altered brain concentrations of the n−3 fatty acid docosahexaenoic acid (DHA) during the perinatal period of “brain growth spurt.” Experimental designs reviewed include observational breastfeeding studies and randomized controlled trials in humans and studies in rodents and nonhuman primates. This review is based on a large number of expert reviews and commentaries and on some 50 recent studies in humans and animals that have not yet been included in published reviews. Expert opinion regarding the strengths and weaknesses of the major experimental systems and uncertainties associated with interpreting results is summarized. On the basis of our reading of this literature, we conclude that evidence from several types of studies, particularly studies in animals, suggests that, within the context of specific experimental designs, changes in brain concentrations of DHA are positively associated with changes in cognitive or behavioral performance. Additional experimental information required to conclude that a causal association exists is discussed, as are uncertainties associated with applying results from specific experimental designs to the question of whether infant formula should be supplemented with DHA.
Conference Paper
Ileal proglucagon gene expression and postprandial plasma concentrations of proglucagon-derived peptides are reported to change with the type and quantity of dietary fiber ingested by rats. Within the intestine, proglucagon encodes several proglucagon-derived peptides known to modulate intestinal absorption capacity and pancreatic insulin secretion. To determine whether the chronic ingestion of fermentable dietary fiber regulates the expression and synthesis of proglucagon-derived peptides in the distal intestine to modulate glucose homeostasis, the following study was conducted: 16 adult dogs (23 +/- 2 kg) were fed isoenergetic, isonitrogenous diets containing a mixture of high fermentable dietary fibers (HFF) or low fermentable (LFF) wood cellulose for 14 d in a randomized cross-over design. Food was withheld for 16 h before an oral glucose tolerance test was conducted supplying 2 g of glucose/kg body wt, and peripheral blood was collected via a hind-leg catheter at 0, 15, 30, 45, 60, 90 and 120 min for plasma glucose, insulin and glucagon-like peptide-1(7-36)NH, (GLP-1) analyses. Intestinal samples were collected after the second dietary treatment. Ileal proglucagon mRNA, intestinal (GLP-1) concentrations and the integrated area under the curves (AUC) for plasma GLP-1 and insulin were greater and plasma glucose AUC was reduced when dogs were fed the HFF diet compared to the LFF diet (P < 0.05). Intestinal villi heights, brush border and basolateral glucose transporter protein abundance and jejunal transport capacities were significantly greater when dogs were fed the HFF diet than when fed the LFF diet. In conclusion, improvements in glucose homeostasis are observed in healthy dogs when they ingest fermentable fibers.
The aim of this second review is to summarize data on the duration of gastric emptying and on the transit time in the gastrointestinal tract of healthy dogs. An overview of the investigation techniques is also given. The incorporation of fibres in the diet is one of many other factors which influence the mechanisms of emptying in the gastrointestinal tract. The effect of dietary fibres is also discussed in other monogastric species.