SCIENTIFIC
REFERENCES
Listed below are links to three key scientific papers
regarding effects of food additives and then relevant scientific papers
organised by additive group. The listing
is not exhaustive and is not intended to be repetitive, therefore it does not
contain, for instance, the references already given in the major CSPI
review.
If you take the time to examine the scientific
literature, we think you will agree that there has been enough science to
justify changing the basis on which additives are approved and to ensure
monitoring by review after release.
References for the DVD “Fed Up with Children’s
Behaviour”: 
KEY PAPERS
CSPI Review 1999
(PDF)
Swain et al 1985
(PDF)
Clarke et al
1996 (2MB PDF)
REFERENCES
Effects of food additives on behaviour, health and
learning
Abstracts for most of the articles listed
below are available on www.pubmed.com
In the US
in 1999, a quarter century review of 23 controlled studies
regarding diet and behaviour concluded that ’17 of the studies found evidence
that some children's behaviour significantly worsens after they consume
artificial colours or certain foods such as wheat or milk’ (Jacobson MF and
Schardt MS 1999) and ‘research with
electroencephalography (EEG) indicates that certain foods trigger physiological
changes in sensitive individuals’ (Uhlig, Merkenschlager et al. 1997). This
review can be easily downloaded from www.cspinet.org/reports/
A review commissioned by the US National Institutes of
Mental Health concluded that success of dietary management depends on the type
of diet used (
The Feingold diet introduced in the
In
In a trial of the LALS diet (low additive, low
salicylate), nearly 80% of 516 children improved significantly(Breakey, Hill et
al. 1991) and in an open trial of the Failsafe diet (free of additives, low in
salicylates, amines and flavour enhancers), 100% of 27 children who completed
2-3 weeks of their elimination diet improved significantly (Dengate and Ruben
2002).
Other diets that have been used successfully to reveal
the effects of food additives and other foods include the Few Foods or
oligoantigenic diet, and the ketogenic diet. The Few Foods diet, developed in
the UK, involves wholefood exclusion and has been used for children’s
behaviour, migraine, epilepsy, enuresis and a wide range of other food
intolerance symptoms although it is considered by many to be difficult to
follow (Bennett CPW, McEwen LM et al. 1998) (Egger, Carter et al. 1983; Carter,
Egger et al. 1985; Egger, Carter et al. 1985; Egger, Carter et al. 1989; Egger,
Carter et al. 1992; Carter, Urbanowicz et al. 1993; Schulte-Korne, Deimel et
al. 1996; Schmidt, Mocks et al. 1997; Pelsser and Buitelaar 2002).
The ketogenic (low carbohydrate) diet has been used
for eight decades to treat children’s epilepsy. More recently, behaviour, autism
and depression have been found to improve on this diet (Pulsifer, Gordon et al.
2001; Evangeliou, Vlachonikolis et al. 2003; Murphy, Likhodii et al. 2004;
Murphy, Likhodii et al. 2005). Since the ketogenic diet excludes many processed
foods as well as many fruits and vegetables, in practice it is a low additive,
low salicylate diet.
Adverse effects by additive
- Colours
Since Speer
reported six cases of childhood asthma related to food dyes in 1958(Speer
1958), artificial colours have been implicated in a wide range of adverse
reactions (Lockey 1959; Chafee and Settipane 1967; Settipane, Chafee et al.
1976; Freedman 1977; Swanson and Kinsbourne 1980; Weiss, Williams et al. 1980;
Rowe 1988; Boris and Mandel 1994; Rowe and Rowe 1994; Jacobson MF and Schardt
MS 1999; Bateman, Warner et al. 2004).
- Natural colour annatto E160b
Annatto is
the only natural colour to affect consumers at least as badly as artificial
colours (Mikkelsen, Larsen et al. 1978; Clarke L, McQueen J et al. 1996).
- Sorbates
Sorbates
are one of the preservatives identified by RPAH as implicated in a wide range
of food intolerance reactions (Rietschel 1978; Swain AR, Soutter VL et al.
2002). More references at the end of this file.
- Benzoates
Benzoate
preservatives have been implicated in a range of adverse reactions from children’s
behaviour to urticaria to asthma and most recently with preschoolers’ behaviour
(Freedman 1977; Petrus, Bonaz et al. 1996; Bateman, Warner et al. 2004).
- Sulphites
Sulphite
preservatives in both foods and medications have been associated with asthma
exacerbation in many countries over many years (Kochen J 1973; Freedman 1977;
Baker, Collett et al. 1981; Towns and Mellis 1984; Steinman and Weinberg 1986;
Friedman ME and Easton JG 1987; Timberlake, Toun et al. 1992; Steinman, Le Roux
et al. 1993; Gastaminza, Quirce et al. 1995; Hodge, Yan et al. 1996; American
Academy of Pediatrics Committee on Drugs 1997).
However,
the effects of food additives on children may have been underestimated. With
the realisation that children eat and drink significantly more than adults
proportional to their body weight and consequently take in more food additives,
the World Health Organisation (WHO) revised upward their estimate of prevalence
of sulphite sensitivity from 4% of the asthmatic population to 20-30% of asthmatic
children (Fifty-first meeting of the Joint FAO/WHO Expert Committee on Food
Additives). The main sulphite vectors for children are drinks (Steinman and
Weinberg 1986; Food Standards Agency (UK) 2004), sulphited meats such as
sausages and illegally sulphited mince (Scottish Food Co-ordination Committee;
Armentia-Alvarez, Fernandez-Casero et al. 1993), and potato products including
hot chips (Ministry of Agriculture Fisheries and Food 1993), due to the level
of sulphites used in these foods and the frequency of consumption. For those who eat them, dried fruit can be
the greatest sulphite vector especially for young children, with Australian
2-year-olds consuming 70 times more dried fruit than 12-year-olds (on average
21.5 compared to 0.3 grams/per day)(Australia New Zealand Food Authority 1996).
The Food Intolerance Network recently received a report of a two-year-old who
had regularly consumed 20 times the Acceptable Daily Intake for sulphites
through a very high intake of dried apricots and similar tree fruits (Rigg
1997). The anti-nutritional properties of sulphites may be a concern, since
sulphites can destroy thiamine (Vitamin B1) and folates in the body, even when
sourced from supplements (Studdert and Labuc 1991; Quattrucci and Masci 1992;
Steel 1997). Sulphites have been shown to be neurotoxic in the laboratory
(Baud, Laudenbach et al. 2001).
- Nitrates
Nitrates
are associated with a wide range of food intolerance reactions including
headaches, irritable bowel symptoms (Loblay RH and Swain AR) and children’s
behaviour (Swain, Soutter et al. 1985).
- Propionates
There is
little information in the medical literature about the effects of low doses of
propionates on humans (Joint FAO/WHO Expert Committee on Food Additives; Swain,
Soutter et al. 1985; Dengate and Ruben 2002). However, the association between
the very high levels of propionic acid seen in some metabolic diseases and
severe neurological problems is well recognised in paediatric medicine. In
addition, a number of studies on rats suggest that early administration of
propionic acid alters normal development and induces long-lasting behavioural
deficits and that administration of ascorbic acid can prevent the behaviour
alterations provoked by propionic acid (Brusque, Terracciano et al. 1998; Wyse,
Brusque et al. 1998; Brusque, Mello et al. 1999; Fontella, Pulrolnik et al.
2000; Trindade, Brusque et al. 2002). While the propionic acid doses used were
around four times higher than might be expected from bread alone in the average
diet for a child in Australia, the effects were marked. It is extraordinary
that this widely used substance has not been tested more extensively in humans,
especially as neurological presentation is not always associated with metabolic
crises (Nyhan, Bay et al. 1999).
- Antioxidants: gallates, TBHQ, BHA, BHT
According
to Additive Code Breaker (Hanssen 2002), additives in this class are known to
cause gastric or skin irritation in some consumers; TBHQ has been associated
with ‘nausea, vomiting, ringing in the ears, suffocating feelings and
collapse’; BHA is known to promote forestomach cancers in rats and BHT is
associated with pulmonary inflammation and various tumours. None are permitted
in foods intended specifically for infants and young children, yet are widely eaten
because they are frequently used in commercially prepared and frozen hot chips.
Under the 5% labelling loophole, these additives are not always listed on the
label, for example, in frozen hot chips. Gallates (310-312), TBHQ (319) and
particularly BHA and BHT (320-321) have been associated with a wide range of
food intolerance reactions including asthma and children’s learning and
behaviour problems (Loblay RH and Swain AR; Fisherman EW and Cohen G 1973;
Schoenthaler, Doraz et al. 1986) .
- Flavour enhancers
When
reviewing double blind placebo controlled MSG studies, it is important to
ascertain whether the study was industry funded (Samuels 1999). MSG has been
associated with children’s behaviour (Swain, Soutter et al. 1985), asthma
(Allen, Delohery et al. 1987; Moneret-Vautrin 1987; Hodge, Yan et al. 1996) and
a range of other food intolerance symptoms including migraines (Loblay RH and
Swain AR).
Food
Intolerance Network researchers have been unable to find any evidence that
flavour enhancers 627 (disodium guanylate), 631 (disodium inosinate) and 635
(ribonucleotides – a mixture of 627 and 631) have ever been tested for adverse
effects on either humans or animals before approval. FSANZ was unable to provide any scientific
evidence. Although we have received numerous reports of itchy skin rashes,
swelling of lips and tongue (angio-edema), and behaviour problems in children
and adults associated with these additives, we have been unable to report these
adverse effects to any authority because there is no post-approval monitoring
in Australia or New Zealand.
- Artificial flavours
In 1968,
Feingold reported adverse respiratory, skin, gastrointestinal, neurological and
arthralgia symptoms associated with synthetic flavours, more recently reported
by others (Feingold 1968; Clarke L, McQueen J et al. 1996).
The references
Allen DH,
Van Nunen S, et al. (1984). "Adverse reactions to food." Med J
Aust 141 (Suppl): 37-42.
Allen, D.
H., J. Delohery, et al. (1987). "Monosodium L-glutamate-induced
asthma." J Allergy Clin Immunol 80(4): 530-7.
Ingested
chemicals, including aspirin and sulfites, are becoming increasingly recognized
as provokers of acute severe asthma. In order to investigate the
asthma-provoking potential of the widely used flavor enhancer, monosodium
L-glutamate (MSG), we challenged 32 subjects with asthma, a number of whom gave
histories of severe asthma after Chinese restaurant meals or similarly spiced
meals. The subjects received an additive-free diet for 5 days before challenge
and were challenged in hospital, after an overnight fast, with 500 mg capsules
of MSG. They were challenged in a single-blind, placebo-controlled fashion with
increasing doses of MSG from 0.5 gm to 5.0 gm. Thirteen subjects reacted. Seven
subjects (group 1) developed asthma and symptoms of the Chinese restaurant
syndrome 1 to 2 hours after ingestion of MSG. Six subjects (group 2) did not
develop symptoms of Chinese restaurant syndrome, and their asthma developed 6
to 12 hours after ingestion of MSG. These challenge studies confirm that MSG
can provoke asthma. The reaction to MSG is dose dependent and may be delayed up
to 12 hours, making recognition difficult for both patient and physician.
American
Academy of Pediatrics Committee on Drugs (1997). ""Inactive"
ingredients in pharmaceutical products." Pediatrics 99(2): 268-78.
Because
of an increasing number of reports of adverse reactions associated with
pharmaceutical excipients, in 1985 the Committee on Drugs issued a position
statement recommending that the Food and Drug Administration mandate labeling
of over-the-counter and prescription formulations to include a qualitative list
of inactive ingredients. However, labeling of inactive ingredients remains
voluntary. Adverse reactions continue to be reported, although some are no
longer considered clinically significant, and other new reactions have emerged.
The original statement, therefore, has been updated and its information
expanded.
Armentia-Alvarez,
A., A. Fernandez-Casero, et al. (1993). "Residual levels of free and total
sulphite in fresh and cooked burgers." Food Addit Contam 10(2): 157-65.
Forty
samples of fresh and fried burgers were analysed. A habitual use and often
abuse of sulphites was detected. In the case of the uncooked samples, 62.5%
contained residual levels of total SO2 above 450 micrograms/g. The frying
process was found to lead to a mean reduction of 36.8 +/- 11.1% in the case of
free sulphite and of 40.9 +/- 12.6% for total sulphite. This reduction was
independent of the concentration of sulphite present and did not seem to be
related to the type of meat used. Most burgers cooked in restaurants were found
to contain sulphites, sometimes at elevated levels. The HPLC analytical method
for the determination of sulphite contents in burgers, previously applied to
fresh sausages, was compared with the optimized Monier-Williams method. The
results obtained with both methods in the determination of total SO2 were found
to have the same precision although there were significant differences in the
contents of additive (p < 0.05).
Arnold, L.
E. (1999). "Treatment alternatives for Attention-deficit/hyperactivity
disorder." Journal of Attention Disorders 3(1):30-48.
Australia
New Zealand Food Authority (1996). 1994 Australian Market Basket Survey.
Canberra, Australian Government Publishing Service.
Baker, G.
J., P. Collett, et al. (1981). "Bronchospasm induced by
metabisulphite-containing foods and drugs." Med J Aust 2(11): 614-7.
Bateman,
B., J. O. Warner, et al. (2004). "The effects of a double blind, placebo
controlled, artificial food colourings and benzoate preservative challenge on
hyperactivity in a general population sample of preschool children." Arch
Dis Child 89(6): 506-11.
AIMS:
To determine whether artificial food colourings and a preservative in the diet
of 3 year old children in the general population influence hyperactive
behaviour. METHODS: A sample of 1873 children were screened in their fourth
year for the presence of hyperactivity at baseline (HA), of whom 1246 had skin
prick tests to identify atopy (AT). Children were selected to form the
following groups: HA/AT, not-HA/AT, HA/not-AT, and not-HA/not-AT (n = 277).
After baseline assessment, children were subjected to a diet eliminating
artificial colourings and benzoate preservatives for one week; in the
subsequent three week within subject double blind crossover study they
received, in random order, periods of dietary challenge with a drink containing
artificial colourings (20 mg daily) and sodium benzoate (45 mg daily) (active
period), or a placebo mixture, supplementary to their diet. Behaviour was
assessed by a tester blind to dietary status and by parents' ratings. RESULTS:
There were significant reductions in hyperactive behaviour during the
withdrawal phase. Furthermore, there were significantly greater increases in
hyperactive behaviour during the active than the placebo period based on
parental reports. These effects were not influenced by the presence or absence
of hyperactivity, nor by the presence or absence of atopy. There were no
significant differences detected based on objective testing in the clinic.
CONCLUSIONS: There is a general adverse effect of artificial food colouring and
benzoate preservatives on the behaviour of 3 year old children which is
detectable by parents but not by a simple clinic assessment. Subgroups are not
made more vulnerable to this effect by their prior levels of hyperactivity or
by atopy.
Baud, O.,
V. Laudenbach, et al. (2001). "Neurotoxic effects of fluorinated
glucocorticoid preparations on the developing mouse brain: role of
preservatives." Pediatr Res 50(6):
706-11.
Prenatal
betamethasone (Celestene) therapy reduces the incidence of brain damage,
whereas prenatal or neonatal dexamethasone (Soludecadron) increases the risk of
brain lesions or neuromotor deficits. To determine whether this increase is
ascribable to the sulfites used as preservatives in Soludecadron, we
investigated the effects of 12 h of exposure to pure dexamethasone,
Soludecadron, pure betamethasone, Celestene, and sulfites on in vitro and in
vivo death of neurons cultured under basal conditions or with excitotoxic
agents (N-methyl-D-aspartate or (S)-5-bromowillardiine) or hypoxia. Apoptotic
features were quantitated using a fluorescent chromatin stain (Hoechst 33258).
Neuronal viability was unaffected by pure dexamethasone, pure betamethasone, or
Celestene. Soludecadron or sulfites significantly increased neuronal loss. Pure
dexamethasone or pure betamethasone produced a 40-50% decrease in neuronal
death induced by N-methyl-D-aspartate, (S)-5-bromowillardiine, or hypoxia,
whereas Soludecadron had no effect and sulfites significantly increased the
neurotoxicity of excitotoxic agents. In in vivo experiments involving terminal
deoxynucleotidyl transferase-mediated dUTP nick-end labeling after several i.p.
injections of fluorinated glucocorticoids, Soludecadron, but not pure
dexamethasone, significantly increased the number of terminal deoxynucleotidyl
transferase-mediated dUTP nick-end labeling-stained cells in neocortical layers
and thalamus. These experimental findings suggest that injectable dexamethasone
should be used with caution during the perinatal period.
Bennett
CPW, McEwen LM, et al. (1998). "The Shipley Project: treating food allergy
to prevent criminal behaviour in community settings." J Nutr Envir Med
8: 77-83.
Boris, M.
and F. S. Mandel (1994). "Foods and additives are common causes of the
attention deficit hyperactive disorder in children." Ann Allergy 72(5): 462-8.
The
attention deficit hyperactive disorder (ADHD) is a neurophysiologic problem
that is detrimental to children and their parents. Despite previous studies on
the role of foods, preservatives and artificial colorings in ADHD this issue
remains controversial. This investigation evaluated 26 children who meet the
criteria for ADHD. Treatment with a multiple item elimination diet showed 19
children (73%) responded favorably, P < .001. On open challenge, all 19
children reacted to many foods, dyes, and/or preservatives. A double-blind
placebo controlled food challenge (DBPCFC) was completed in 16 children. There
was a significant improvement on placebo days compared with challenge days (P =
.003). Atopic children with ADHD had a significantly higher response rate than
the nonatopic group. This study demonstrates a beneficial effect of eliminating
reactive foods and artificial colors in children with ADHD. Dietary factors may
play a significant role in the etiology of the majority of children with ADHD.
Breakey,
J., M. Hill, et al. (1991). "A report on a trial of the low additive, low
salicylate diet in the treatment of behaviour and learning problems in
children." Aust J Nutr Diet 48(3):
89-94.
Brusque, A.
M., C. F. Mello, et al. (1999). "Effect of chemically induced propionic acidemia
on neurobehavioral development of rats." Pharmacol Biochem Behav 64(3): 529-34.
High
levels of propionic acid (PPA) comparable to those of human propionic acidemia
were achieved in blood (1-5 mmol/l) and brain (1 micromol/g) of rats by
administering saline-buffered propionate (pH 7.4) subcutaneously twice a day
from the 6th to the 28th day of life. PPA doses ranged from 1.44 to 1.92
micromol/g body weight as a function of animal age. Control rats were treated
with saline in the same volumes. Growth and development of physical landmarks
were assessed by monitoring the following parameters daily: body weight, upper
incisor eruption, eye opening, and hair coat. Development of some reflexes was
also monitored, and a specific subset of motor skills was evaluated at days 14
and 21 of life by the free-fall righting test and the spontaneous alternation
test. Chronic PPA administration had no effect on body weight, cerebral cortex
weight, or cerebellum weight, but caused slight but significant delays in the day
of appearance of hair coat and eye opening, indicating an effect of PPA on the
development of physical parameters. Free-fall righting was impaired in
PPA-treated animals. On the other hand, PPA administration had no effect on the
performance of the animals in the spontaneous alternation tests. Long-term
effects of early PPA administration were investigated by assessing animal
performance in an aversive task (two-way shuttle avoidance task) and in a
nonaversive (open-field task) behavioral task at 60 days of age. PPA-treated
rats did not habituate to the open field, and presented a lack of retention of
the shuttle-avoidance task. Our results suggest that early postnatal PPA
administration to rats alters normal development and induces long-term
behavioral deficits in aversive and nonaversive tasks.
Brusque, A.
M., S. T. Terracciano, et al. (1998). "Chronic administration of propionic
acid reduces ganglioside N-acetylneuraminic acid concentration in cerebellum of
young rats." J Neurol Sci 158(2):
121-4.
Elevated
levels of propionate comparable to those of human propionic acidaemia were
achieved in the blood of young rats by injecting subcutaneously buffered
propionic acid (PPA) twice a day at 8-h intervals from the 6th to the 28th day
of life. A matched group of animals (controls) was treated with the same
volumes of saline. The animals were weighed and sacrificed by decapitation at
28, 35 or 60 days of age. Cerebellum and cerebrum were weighed and their
protein and ganglioside N-acetylneuraminic acid (G-NeuAc) contents determined.
Body, cerebral and cerebellar weights were similar in both groups, suggesting
that PPA per se neither alters the appetite of the rats nor causes
malnutrition. Brain protein concentration was also not affected by chronic
administration of PPA, in contrast to G-NeuAc concentration which was
significantly reduced in the cerebellum. Since ganglioside concentration is
closely related to the dendritic surface and indirectly reflects
synaptogenesis, our results of an important ganglioside deficit in the brain of
PPA-treated animals may be related to the neurologic dysfunction characteristic
of propionic acidaemic patients.
Carter, C.
M., J. Egger, et al. (1985). "A dietary management of severe childhood
migraine." Hum Nutr Appl Nutr 39(4):
294-303.
We
describe in detail a dietary treatment which has been shown to be effective in
most children with severe migraine. Potential adverse nutritional and allergic
effects are outlined; because of the diet should be undertaken only in those
ill enough to justify it. In the first stage very few foods are given, and if
the child responds to this oligoantigenic diet, foods are reintroduced one by
one at weekly intervals. In this way foods causing symptoms are identified and
eliminated. Research is urgently needed to establish simpler empirical diets
and diagnostic tests.
Carter, C.
M., M. Urbanowicz, et al. (1993). "Effects of a few food diet in attention
deficit disorder." Arch Dis Child 69(5): 564-8.
Seventy-eight
children, referred to a diet clinic because of hyperactive behaviour, were
placed on a 'few foods' elimination diet. Fifty nine improved in behaviour
during this open trial. For 19 of these children it was possible to disguise
foods or additives, or both, that reliably provoked behavioural problems by
mixing them with other tolerated foods and to test their effect in a placebo
controlled double blind challenge protocol. The results of a crossover trial on
these 19 children showed a significant effect for the provoking foods to worsen
ratings of behaviour and to impair psychological test performance. This study
shows that observations of change in behaviour associated with diet made by
parents and other people with a role in the child's care can be reproduced
using double blind methodology and objective assessments. Clinicians should
give weight to the accounts of parents and consider this treatment in selected
children with a suggestive medical history.
Chafee, F.
H. and G. A. Settipane (1967). "Asthma caused by FD&C approved
dyes." J Allergy 40(2):
65-72.
Clarke L,
McQueen J, et al. (1996). "The dietary management of food allergy and food
intolerance in children and adults." Australian Journal of Nutrition
and Dietetics 53(3): 89-94.
Dengate, S.
and A. Ruben (2002). "Controlled trial of cumulative behavioural effects
of a common bread preservative." J Paediatr Child Health 38(4): 373-6.
OBJECTIVE:
Many anecdotes and one scientific report describe cumulative behavioural
effects of bread preservative on children. METHODOLOGY: Twenty-seven children,
whose behaviour improved significantly on the Royal Prince Alfred Hospital
diet, which excludes food additives, natural salicylates, amines and
glutamates, were challenged with calcium propionate (preservative code 282) or
placebo through daily bread in a double-blind placebo-controlled crossover
trial. RESULTS: Due to four placebo responders, there was no significant
difference by ANOVA of weighted placebo and challenge Rowe Behaviour Rating
Inventory means, but a statistically significant difference existed in the
proportion of children whose behaviours 'worsened' with challenge (52%),
compared to the proportion whose behaviour 'improved' with challenge (19%),
relative to placebo (95% confidence intervals 14-60%). CONCLUSIONS:
Irritability, restlessness, inattention and sleep disturbance in some children
may be caused by a preservative in healthy foods consumed daily. Minimizing the
concentrations added to processed foods would reduce adverse reactions. Testing
for behavioural toxicity should be included in food additive safety evaluation.
Egger, J.,
C. H. Carter, et al. (1992). "Effect of diet treatment on enuresis in
children with migraine or hyperkinetic behavior." Clin Pediatr (Phila)
31(5): 302-7.
Twenty-one
children with migraine and/or hyperkinetic behavior disorder which was
successfully treated with an oligoantigenic (few-foods) diet also suffered from
nocturnal and/or diurnal enuresis. On diet, the enuresis stopped in 12 of these
children and improved in an additional four. Identification of provoking foods
was by sequential reintroduction of the foods that were avoided on the
oligoantigenic diet. In eight of the 12 children who recovered on the
oligoantigenic diet and in the four who improved, reintroduction of one or more
foods provoked a reproducible relapse of the enuresis. Nine children were
subjected to a placebo-controlled, double-blind reintroduction of provoking
foods. Six children relapsed during testing with incriminated foods; none
reacted to placebo. Enuresis in food-induced migraine and/or behavior disorder
seems to respond, in some patients, to avoidance of provoking foods.
Egger, J.,
C. M. Carter, et al. (1985). "Controlled trial of oligoantigenic treatment
in the hyperkinetic syndrome." Lancet 1(8428): 540-5.
76
selected overactive children were treated with an oligoantigenic diet, 62
improved, and a normal range of behaviour was achieved in 21 of these. Other
symptoms, such as headaches, abdominal pain, and fits, also often improved. 28
of the children who improved completed a double-blind, crossover,
placebo-controlled trial in which foods thought to provoke symptoms were
reintroduced. Symptoms returned or were exacerbated much more often when
patients were on active material than on placebo. 48 foods were incriminated.
Artificial colorants and preservatives were the commonest provoking substances,
but no child was sensitive to these alone.
Egger, J.,
C. M. Carter, et al. (1989). "Oligoantigenic diet treatment of children
with epilepsy and migraine." J Pediatr 114(1): 51-8.
We
studied the role of oligoantigenic diets in 63 children with epilepsy; 45
children had epilepsy with migraine, hyperkinetic behavior, or both, and 18 had
epilepsy alone. Of the 45 children who had epilepsy with recurrent headaches,
abdominal symptoms, or hyperkinetic behavior, 25 ceased to have seizures and 11
had fewer seizures during diet therapy. Headaches, abdominal pains, and
hyperkinetic behavior ceased in all those whose seizures ceased, and in some of
those whose seizures did not cease. Foods provoking symptoms were identified by
systematic reintroduction of foods, one by one; symptoms recurred with 42
foods, and seizures recurred with 31; most children reacted to several foods.
Of 24 children with generalized epilepsy, 18 recovered or improved (including 4
of 7 with myoclonic seizures and all with petit mal), as did 18 of 21 children
with partial epilepsy. In double-blind, placebo-controlled provocation studies,
symptoms recurred in 15 of 16 children, including seizures in eight; none
recurred when placebo was given. Eighteen other children, who had epilepsy
alone, were similarly treated with an oligoantigenic diet; none improved.
Egger, J.,
C. M. Carter, et al. (1983). "Is migraine food allergy? A double-blind
controlled trial of oligoantigenic diet treatment." Lancet 2(8355): 865-9.
93%
of 88 children with severe frequent migraine recovered on oligoantigenic diets;
the causative foods were identified by sequential reintroduction, and the role
of the foods provoking migraine was established by a double-blind controlled
trial in 40 of the children. Most patients responded to several foods. Many
foods were involved, suggesting an allergic rather than an idiosyncratic (metabolic)
pathogenesis. Associated symptoms which improved in addition to headache
included abdominal pain, behaviour disorder, fits, asthma, and eczema. In most
of the patients in whom migraine was provoked by non-specific factors, such as
blows to the head, exercise, and flashing lights, this provocation no longer
occurred while they were on the diet.
Evangeliou,
A.,
A
pilot prospective follow-up study of the role of the ketogenic diet was carried
out on 30 children, aged between 4 and 10 years, with autistic behavior. The
diet was applied for 6 months, with continuous administration for 4 weeks,
interrupted by 2-week diet-free intervals. Seven patients could not tolerate
the diet, whereas five other patients adhered to the diet for 1 to 2 months and
then discontinued it. Of the remaining group who adhered to the diet, 18 of 30
children (60%), improvement was recorded in several parameters and in
accordance with the Childhood Autism Rating Scale. Significant improvement
(> 12 units of the Childhood Autism Rating Scale) was recorded in two
patients (pre-Scale: 35.00 +/- 1.41[mean +/- SD]), average improvement (>
8-12 units) in eight patients (pre-Scale: 41.88 +/- 3.14[mean +/- SD]), and
minor improvement (2-8 units) in eight patients (pre-Scale: 45.25 +/- 2.76
[mean +/- SD]). Although these data are very preliminary, there is some
evidence that the ketogenic diet may be used in autistic behavior as an
additional or alternative therapy.
Feingold,
B. F. (1968). "Recognition of food additives as a cause of symptoms of
allergy." Ann Allerg 26(309-13).
Feingold,
B. F. (1977). "Behavioral disturbances linked to the ingestion of food
additives."
Feingold,
B. F. (1979). "Dietary management of nystagmus." J Neural Transm
45: 107-115.
Fifty-first
meeting of the Joint FAO/WHO Expert Committee on Food Additives "Safety
Evaluation of Certain Food Additives: sulfur dioxide and sulfites; evaluation
of national assessments of intake of benzoates; evaluation of national
assessments of intake of butylated hydroxyanisole (BHA); evaluation of national
assessments of intake of butylated hydroxytoluene.
Fisherman
EW and Cohen G (1973). "Chemical intolerance to butylated-hydroxyanisole
(BHA) and butylated-hydroxytoluene (BHT) and vascular response as an indicator
and monitor of drug intolerance." Ann Allerg 31: 126-33.
Fontella,
F. U., V. Pulrolnik, et al. (2000). "Propionic and L-methylmalonic acids
induce oxidative stress in brain of young rats." Neuroreport 11(3): 541-4.
The
in vitro effects of propionic and L-methylmalonic acids on some parameters of
oxidative stress were investigated in the cerebral cortex of 21-day-old rats.
Chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS) and total
radical-trapping antioxidant capacity (TRAP) were measured in brain tissue
homogenates in the presence of propionic or L-methylmalonic acids at
concentrations ranging from 1 to 10mM. Both acids significantly increased
chemiluminescence and TBA-RS and decreased TRAP, indicating a simulation of
lipid peroxidation and a reduction of tissue antioxidant potential. Other organic
acids tested which accumulate in some organic acidemias (suberic, sebacic,
adipic, 3-methylglutaric and 4-hydroxybutyric acids) did not affect these
parameters. This study provides evidence that free radical generation may
participate in the neurological dysfunction of propionic and methylmalonic
acidemias.
Food
Standards Agency (
Freedman,
B. J. (1977). "Asthma induced by sulphur dioxide, benzoate and tartrazine
contained in orange drinks." Clin Allergy 7(5): 407-15.
Of
272 patients with asthma, thirty (11%) gave a history of exacerbations
occurring after ingestion, solutions of orange orange drinks. Fourteen of these
were given provocation tests by drinking, on separate occasions of sulphur
dioxide, sodium benzoate and tartrazine, which are present in all orange
drinks. Eight reacted to sulphur dioxide with a fall in FEV1, four to sodium
benzoate and one to tartrazine, and four did not react to any of these agents.
Three of the benzoate patients were also sensitive to sulphur dioxide. The
sulphur dioxide sensitive patients were predominantly young, with extrinsic
asthma. The benzoate sensitive patients were predominantly middle-aged and the
proportion with intrinsic asthma was higher. Prior inhalation of sodium
cromoglycate by four patients inhibited the reaction to these substances.
Friedman ME
and
Gastaminza,
G.,
BACKGROUND:
Asthma elicited by sulfite ingestion has been mainly described in
steroid-dependent and in non-atopic asthmatics. We have studied a group of 18
young extrinsic asthmatics who presented with asthma attacks immediately after
eating pickled onions. OBJECTIVE: The aim of this study is to ascertain if
these asthma attacks are elicited by sulfites contained in pickled onions and
the influence of the dose and pH of onions. METHODS: The bronchial
hyperreactivity of the patients was assessed by a methacholine challenge test.
Oral challenge tests were performed with sodium metabisulfite (MSB) diluted in
lemon juice at pH 4.2 and at pH 3.3 (only in patients who did not react with pH
4.2). Two types of pickled onions, Spanish and Dutch pickled onions, were used
for oral challenge in seven of the patients. The Monier-Williams method was
used to measure the SO2 concentration in pickled onions. RESULTS: The oral
provocation test with MBS, pH 4.2, elicited a positive response in six patients
(33.3%) and the test at pH 3.3 was positive in three out of 12. No significant
difference in PD20 values was found between these groups. Three of the seven
patients challenged with Spanish pickled onions had a positive reaction but had
no reaction with Dutch pickled onions. The SO2 concentration in Spanish pickled
onions varied between 765 and 1182 ppm while in Dutch pickled onions were 200
ppm; this exceeded the permitted level (100 ppm). SO2 release in Spanish
pickled onion samples was nearly 2.5 times higher when the pH of the sample
decreased from 4.2 to 3.3. CONCLUSION: High levels of SO2 in Spanish pickled
onions, and their low pH (3.3) would be the responsible factors of the
asthmatic outbreaks after ingestion of Spanish pickled onions by these
patients.
Hanssen, M.
(2002). Additive Code Breaker. Melbourne, Lothian.
Hodge, L.,
K. Y. Yan, et al. (1996). "Assessment of food chemical intolerance in
adult asthmatic subjects." Thorax 51(8): 805-9.
BACKGROUND:
Identification of food chemical intolerance in asthmatic subjects can be
reliably assessed by changes in the forced expiratory volume in one second
(FEV1) in response to double blind, placebo controlled challenges on a strict
elimination diet. However, this method is cumbersome and time consuming. A
study was undertaken to determine whether changes in bronchial responsiveness
to histamine following food chemical challenge without an elimination diet
might be a faster, more convenient method. METHODS: Eleven adult asthmatic
subjects were challenged twice with metabisulphite, aspirin, monosodium
glutamate, artificial food colours, sodium nitrite/ nitrate, 0.5% citric acid
solution (placebo), and sucrose (placebo) on separate days. During the first
set of challenges subjects consumed a normal diet. Bronchial responsiveness to
histamine was assessed 90 minutes after each challenge. A greater than twofold
increase in bronchial responsiveness was considered positive. For one month
prior to and during the second set of challenges subjects followed a strict
elimination diet and FEV1 was monitored during and for two hours after each
challenge. A fall in FEV1 of 20% or more was considered positive. RESULTS: Of
the 77 food chemical challenges performed on an unmodified diet, 20 were
positive (six placebo responses). In two subjects it was not possible to
perform a histamine test after one of the chemical challenges because of poor
spirometric function. Of the 77 food chemical challenges performed on an
elimination diet, 11 were positive (no placebo responses). Excluding the two challenges
in which there were no corresponding histamine tests, only on two occasions did
the positive responses in both methods coincide, giving the unmodified diet
method a sensitivity of 22%. CONCLUSIONS: Strict dietary elimination and
measurement of FEV1 after double blind food chemical challenge remains the most
reliable method for the detection of food chemical intolerance in asthmatic
subjects.
Jacobson MF
and Schardt MS (1999). Diet, ADHD and behaviour: a quarter-century review.
Joint
FAO/WHO Expert Committee on Food Additives "Propionic acid and its
calcium, potassium and sodium salts. World Health Organization,
Kochen J
(1973). "Sulfur dioxide, a respiratory tract irritant, even if
ingested." Pediatrics 52(1):
145-6.
Loblay RH
and
Lockey, S.
D. (1959). "Allergic reactions due to F D and C Yellow No. 5, tartrazine,
an aniline dye used as a coloring and identifying agent in various
steroids." Ann Allergy 17:
719-21.
Mikkelsen,
H., J. Larsen, et al. (1978). "Hypersensitivity reactions to food colours
with special reference to the natural colour annatto extract (butter
colour)." Arch Toxicol Suppl(1): 141-3.
It
is well known that synthetic food colours especially some azo dyes can provoke
hypersensitivity reactions such as urticaria, angioneurotic oedema, and astma
(Michaelsson and Juhlin, 1973, Granholt and Thune, 1975). Natural food colours
are scarcely investigated with respect to potential allergic properties.
Annatto extract, a commonly used food colour in edible fats e.g. butter, has
been tested in patients. Among 61 consecutive patients suffereing from chornic
urticaria and/or angioneurotic oedema 56 patients were orally provoked by
annatto extract during elimination diet. Challenge was performed with a dose
equivalent to the amount used in 25 grammes of butter. Twentysix per cent of
the patients reacted to this colour 4 hours (SD: 2,6) after intake. Similar
challenges with synthetic dyes showed the following results: Tartrazine 11%,
Sunset Yellow FCF 17%, Food Red 17 16%, Amaranth 9%, Ponceau 4 R 15%,
Erythrosine 12% and Brillant Blue FCF 14%. The present study indicates that
natural food colours may induce hypersensitivity reactions as frequent as
synthetic dyes.
Ministry of
Agriculture Fisheries and Food (1993). Dietary intake of food additives in the
Moneret-Vautrin,
D. A. (1987). "Monosodium glutamate-induced asthma: study of the potential
risk of 30 asthmatics and review of the literature." Allerg Immunol (
Monosodium
glutamate is a physiological nutrient, and food additive used as a taste
enhancer. Several cases of intolerance to MSG in patients with asthma and with a
Chinese Restaurant Syndrome have been published. A high dose of 2.5 g was
tested in 6 healthy controls and 30 asthmatics (7: allergic asthma; 15:
intrinsic asthma with intolerance to aspirin; 8: intrinsic asthma with aspirin
intolerance, intolerance to alcohol or to food additives). Two patients
presented with a mild bronchospasm, occurring 6 to 10 hours after the
ingestion. Different mechanisms are discussed. A cholinergic mechanism might be
incriminated, either due to stimulation of the synthesis of acetylcholine, or
due to a vagal reflex elicited by a reflux esophagitis. However, a high vagal
hyperreactivity seems to be needed for the occurrence of asthma. It is
concluded that a very small subset of patients with intrinsic asthma might
present with an intolerance to MSG if high doses are consumed.
Murphy, P.,
BACKGROUND:
The ketogenic diet is used to treat epilepsy refractory to anticonvulsant
medication. Individuals with epilepsy often have behavioral problems and
deficits in attention and cognitive functioning. The ketogenic diet has been
found to effect improvements in these domains. It has also been suggested that
the ketogenic diet may act as a mood stabilizer. METHODS: The present research
used the Porsolt test, an animal model of depression, to determine whether the
ketogenic diet has antidepressant properties. Porsolt test scores of rats on
the ketogenic diet were compared with those of rats on a control diet. RESULTS:
The rats on the ketogenic diet spent less time immobile, suggesting that rats
on the ketogenic diet, like rats treated with antidepressants, are less likely
to exhibit "behavioral despair." CONCLUSIONS: It is concluded that
the ketogenic diet may have antidepressant properties.
Murphy, P.,
S. S. Likhodii, et al. (2005). "Effect of the ketogenic diet on the
activity level of Wistar rats." Pediatr Res 57(3): 353-7.
Children,
adolescents, and adults with epilepsy often also show symptoms associated with
attention-deficit/hyperactivity disorder (ADHD). The ketogenic diet, which is
administered to children with epilepsy refractory to drug therapy, seems to
improve behavior in individuals with symptoms of ADHD. The basis for this
improvement is unknown, although it seems to be unrelated to seizure control.
The present research was designed to investigate the effect of two ketogenic
diets on the behavior of normal adult male rats. Two experiments were
conducted. In experiment 1, 36 subjects were placed on one of three diets: a
control diet, a 6.3:1 ketogenic diet, and a 4:1 ketogenic diet. In experiment
2, 20 subjects were placed either on a control diet or on a 4:1 ketogenic diet.
The activity level of each subject was measured using an open field test. Time
spent immobile, grooming, and in exploratory behavior was measured for 600 s.
Subjects were tested once before initiation of the diets and once while on the
diets. No significant group differences were found in activity level before
initiation of the diets. After initiation of the diets, subjects in both
ketogenic groups showed a significantly lower activity level than the rats on
the control diet. The ketogenic diet decreases activity level in an animal
model. This behavioral change may relate to the improved behavior seen when
children with symptoms of ADHD are placed on the diet.
Nyhan, W.
L., C. Bay, et al. (1999). "Neurologic nonmetabolic presentation of
propionic acidemia." Arch Neurol 56(9): 1143-7.
BACKGROUND:
Patients with propionic acidemia usually present in the neonatal period with
life-threatening ketoacidosis, often complicated by hyperammonemia. It was
thought that the neurologic abnormalities seen in this disease were exclusively
the consequences of these acute crises. Experience with 2 patients with
propionic acidemia indicates that this disease may present first with prominent
neurologic disease without the life-threatening episodes of ketoacidosis that
usually serve as the alerting signals for a diagnosis of an organic acidemia.
OBJECTIVE: To examine the clinical and metabolic aspects of 2 patients with a
phenotype that suggested disease of the basal ganglia. DESIGN: Examination of
patterns of organic acids of the urine and enzyme assay for propionyl-CoA
carboxylase in fibroblasts and lymphocytes. SETTING: Referral population to a
biochemical genetics laboratory. PATIENTS: Two patients whose prominent
features were hypotonia followed by spastic quadriparesis and choreoathetosis.
Both had seizures. One patient was mildly mentally retarded but grew normally
physically. The other had profound mental retardation and failure to thrive; he
also self-mutilated his lower lip. Self-injurious behavior has not been
reported in this disease. MAIN OUTCOME MEASURES: Clinical description, blood
ammonia levels, organic acid levels in the urine, and enzyme activity. RESULTS:
Excretion of metabolites, including methylcitrate, was typical. Residual
activity of propionyl-CoA carboxylase approximated 5% of the control in each
patient. CONCLUSIONS: Propionic acidemia can present as a pure neurologic
disease without acute episodes of massive ketoacidosis. Hyperammonemia may
occur after infancy in some patients, presenting as Reye syndrome.
Parker, G.
and T. Watkins (2002). "Treatment-resistant depression: when
antidepressant drug intolerance may indicate food intolerance." Aust N
Z J Psychiatry 36(2): 263-5.
Pelsser, L.
M. and J. K. Buitelaar (2002). "[Favourable effect of a standard elimination
diet on the behavior of young children with attention deficit hyperactivity
disorder (ADHD): a pilot study]." Ned Tijdschr Geneeskd 146(52): 2543-7.
OBJECTIVE:
To determine whether a standard elimination diet can decrease the ADHD-symptoms
in a heterogeneous group of young children with ADHD. DESIGN: Open,
descriptive. METHOD: 40 children, 36 boys and 4 girls, aged 3-7 (average 4.8
years), who met the DSM-IV-criteria for ADHD, followed their usual diet for two
weeks and thereafter for two weeks an elimination diet, based on the few foods
diet (rice, turkey, pear and lettuce). The behaviour of the child was evaluated
at study entry, after the baseline period and at the end of the diet. Parents
completed the 10-item Conners list, the ADHD Rating Scale and a physical
complaints list. The teachers completed the 10-item Conners list and the ADHD
Rating Scale twice, at the beginning and at the end of the diet. RESULTS:
According to the parent-ratings, 25 children (62%) showed an improvement in
behaviour of at least 50% on both the Conners list and the ADHD Rating Scale at
the end of the elimination diet. Nine children (23%) withdrew from the study
because the parents were unable to stick to the diet or because the child fell
ill. Among the 15 children with both parent and teacher ratings, 10 responded
both at home and in school. CONCLUSION: In young children with ADHD an
elimination diet can lead to a statistically significant decrease in symptoms.
Petrus, M.,
S. Bonaz, et al. (1996). "Asthmé et intolérance aux benzoates." Arch
Pédiatr 3(10): 984-7.
BACKGROUND:
Some foods and drug additives may induce allergic reactions. CASE REPORT: A
girl with a family history of asthma in both parents developed asthma in her
early life. She was successfully given continuous bronchodilator therapy until
the age of 7 years. At that time, she had more frequent and severe
exacerbations (8 within 10 months) despite reinforced continuous treatment.
Oral challenges with bisulfite and sodium benzoate, both additives abundantly ingested
by the patient, revealed heightened sensitivity to administration of sodium
benzoate. Avoidance of this additive was followed by complete and prolonged
disappearance of episodes of coughing and wheezing. CONCLUSION: Adverse
reactions to benzoate in this patient required avoidance of some drugs, some of
those classically prescribed under the form of syrups in asthma.
Pulsifer,
M. B., J. M. Gordon, et al. (2001). "Effects of ketogenic diet on
development and behavior: preliminary report of a prospective study." Dev
Med Child Neurol 43(5): 301-6.
The
ketogenic diet is increasingly used for the management of difficult-to-control
seizures in children. Here, we describe the first prospective study of the
effects of the diet on development, behavior, and parenting stress.
Participants were 65 children (36 males, 29 females) with intractable seizures,
ages 18 months to 14 years 6 months, enrolled in a prospective study at the
Quattrucci,
E. and V. Masci (1992). "Nutritional aspects of food preservatives." Food
Addit Contam 9(5): 515-25.
Despite
the benefits attributed to food preservatives, some concern still remains
regarding their safety and possible influence on nutrients. Surprisingly, there
is quite a lack of scientific knowledge in this field. In order to describe a
few examples, the effects of the extensively used sulphite on thiamine,
folates, pyridoxal and other nutrients have been reported. Among its
antibrowning effects, inhibition of ascorbic acid browning is also considered.
As far as sorbic acid is concerned, notwithstanding its easy reaction with
protein, probably the acid environment of the stomach determines the breakdown
of the sorbic-protein adducts. Detoxication of nitrite by tocopherol and
ascorbic acid leads, in the last case, to dehydroascorbic acid and its
oxidative products with loss of vitamin activity. Any oxidizing substance
destroys ascorbic acid, vitamin E and free vitamin A. Phosphates are largely
used with different aims, including preservation, in food processing. Their
antimicrobial activity is due to both a direct effect and an interaction with
other antimicrobials. Sequestering capacity of phosphates and its nutritional
implications are discussed. Also mechanisms of action of organic acids are
reported, focusing on sorbic acid effects on single amino acids and proteins.
Finally, the little information available about the potential impact of food
preservatives on nutritional functions is presented.
Rietschel,
R. L. (1978). "Contact urticaria from synthetic cassia oil and sorbic acid
limited to the face." Contact Dermatitis 4(6): 347-9.
A
patient with contact urticaria with skin and respiratory symptoms was found to
be sensitive to both sorbic acid and synthetic oil of cassia. The contact
urticaria was only elicitable on intact skin of the face by open testing. The
source of the patient's contactants was her shampoo and toothpaste.
Rigg, A.
(1997). "Sulphur dioxide in sausages and other products. ACT Health
services. Food survey reports, www.health.act.gov."
Rowe, K. S.
(1988). "Synthetic food colourings and 'hyperactivity': a double-blind
crossover study." Aust Paediatr J 24(2): 143-7.
Of
220 children referred for suspected 'hyperactivity', 55 were subjected to a 6
week trial of the Feingold diet. Forty (72.7%) demonstrated improved behaviour
and 26 (47.3%) remained improved following liberalization of the diet over a
period of 3-6 months. The parents of 14 children claimed that a particular
cluster of behaviours was associated with the ingestion of foods containing
synthetic colourings. A double-blind crossover study, employing a
single-subject repeated measures design was conducted, using eight of these
children. Subjects were maintained on a diet free from synthetic additives and
were challenged daily for 18 weeks with either placebo (during lead-in and
washout periods) or 50 mg of either tartrazine or carmoisine, each for 2
separate weeks. Two significant reactors were identified whose behavioural
pattern featured extreme irritability, restlessness and sleep disturbance. One
of the reactors did not have inattention as a feature. The findings raise the
issue of whether the strict criteria for inclusion in studies concerned with
'hyperactivity' based on 'attention deficit disorder' may miss children who
indicate behavioural changes associated with the ingestion of food colourings.
Moreover, for further studies, the need to construct a behavioural rating
instrument specifically validated for dye challenge is suggested.
Rowe, K. S.
and K. J. Rowe (1994). "Synthetic food coloring and behavior: a dose
response effect in a double-blind, placebo-controlled, repeated-measures
study." J Pediatr 125(5
Pt 1): 691-8.
OBJECTIVE:
To establish whether there is an association between the ingestion of synthetic
food colorings and behavioral change in children referred for assessment of
"hyperactivity." PARTICIPANTS: From approximately 800 children
referred to the Royal Children's Hospital (
Samuels, A.
(1999). "The toxicity/safety of processed free glutamic acid (MSG): a
study in suppression of information." Account Res 6(4): 259-310.
Schmidt, M.
H., P. Mocks, et al. (1997). "Does oligoantigenic diet influence
hyperactive/conduct-disordered children--a controlled trial." Eur Child
Adolesc Psychiatry 6(2): 88-95.
A
crossover 'placebo'-controlled, double-blind design was used to examine the
effectiveness of an oligoantigenic diet in 49 children with
hyperactive/disruptive behavior disorder. Effects of diet were compared with
those yielded by stimulant medication (methylphenidate). The study was
conducted in an inpatient unit at the Department of Child and Adolescent
Psychiatry, Central Institute of Mental Health,
Schoenthaler,
S., W. Doraz, et al. (1986). " The impact of a low food additive and
sucrose diet on academic performance in 803
Schulte-Korne,
G., W. Deimel, et al. (1996). "[Effect of an oligo-antigen diet on the
behavior of hyperkinetic children]." Z Kinder Jugendpsychiatr
Psychother 24(3): 176-83.
The
influence of an oligoantigenic diet on different dimensions of the behavior of
21 children diagnosed as having attention-deficit hyperactivity disorder (ADHD)
was examined. Treatment effects were assessed with three subjective measures
(two questionnaires and an interview) and three objective measures (two
attention tests and actometer). The study was divided into three phases: baseline,
diet and provocation, each lasting three weeks. A crossover design was used. A
significant effect was found for the subjective measures, but not for the
objective measures. The results are discussed in terms of possible types of
effects, e. g. rater effects and environmental effects. It may be that the
oligoantigenic diet influences only certain dimensions of hyperactivity.
Scottish
Food Co-ordination Committee "A survey of the level of sulphur dioxide
preservatives in minced meat in
Settipane,
G. A., F. H. Chafee, et al. (1976). "Significance of tartrazine
sensitivity in chronic urticaria of unknown etiology." J Allergy Clin
Immunol 57(6): 541-6.
Of
38 patients with chronic urticaria of unknown etiology who were evaluated for
food and drug additive sensitivity, 53% (20/38) had urticaria for 1 yr or more.
Total eosinophil counts were not elevated in most patients, and the frequency
of atopy was found to be similar to that in a general population. Of these 38
patients, 10 (26%) had a personal history of aspirin intolerance, but
elimination of aspirin did not relieve the urticaria. In a double-blind
crossover challenge with 0.22 mg of tartrazine and a control, tartrazine
sensitivity was found in 8% (3/38) of patients with chronic urticaria and 20%
(2/10) of patients with aspirin intolerance.
Speer, S.
(1958). Management of Childhood Asthma.
Steel, R.
J. (1997). "Thiamine deficiency in a cat associated with the preservation
of 'pet meat' with sulphur dioxide." Aust Vet J 75(10): 719-21.
A
cat with allergic dermatitis was fed a diet of fresh meat and a multi-vitamin
supplement for 38 days to exclude food allergy as a cause of its dermatopathy.
The cat died as a result of acute thiamine deficiency, which was caused by
inactivation of thiamine by the preservative, sulphur dioxide. The continuing
undeclared usage of sulphites in the Australian pet food industry is discussed.
Steinman,
H. A., M. Le Roux, et al. (1993). "Sulphur dioxide sensitivity in South
African asthmatic children."
Steinman,
H. A. and E. G. Weinberg (1986). "The effects of soft-drink preservatives
on asthmatic children."
Sulphites,
used extensively as preservatives in foods and soft drinks, are known to
precipitate asthma attacks in 5-10% of susceptible children. Among children
attending the Allergy Clinic at the Red Cross War Memorial Children's Hospital,
Studdert,
V. P. and R. H. Labuc (1991). "Thiamin deficiency in cats and dogs
associated with feeding meat preserved with sulphur dioxide." Aust Vet
J 68(2): 54-7.
Thiamin
deficiency was diagnosed in cats and dogs being fed fresh minced meat, which
contained sulphur dioxide as a preservative and less than 0.5 mg/kg thiamin.
Thiamin in the meat and in added dietary ingredients, including a supplementary
vitamin mixture, was destroyed by the sulphur dioxide.
Swain, A.,
V. Soutter, et al. (1985). "Salicylates, oligoantigenic diets, and
behaviour." Lancet 2(8445):
41-2.
Swain AR,
Soutter VL, et al. (2002). Friendly Food.
Swanson, J.
M. and M. Kinsbourne (1980). "Food dyes impair performance of hyperactive
children on a laboratory learning test." Science 207(4438): 1485-7.
Forty
children were given a diet free of artificial food dyes and other additives for
5 days. Twenty of the children had been classified as hyperactive by scores on
the Conners Rating Scale and were reported to have favorable responses to
stimulant medication. A diagnosis of hyperactivity had been rejected in the
other 20 children. Oral challenges with large doses (100 or 150 milligrams) of
a blend of FD & C approved food dyes or placebo were administered on days 4
and 5 of the experiment. The performance of the hyperactive children on
paired-associate learning tests on the day they received the dye blend was
impaired relative to their performance after they received the placebo, but the
performance of the nonhyperactive group was not affected by the challenge with
the food dye blend.
Timberlake,
C. M., A. K. Toun, et al. (1992). "Precipitation of asthma attacks in
Melanesian adults by sodium metabisulphite." P N G Med J 35(3): 186-90.
Seven
Melanesian asthmatic patients were challenged with substances that have been
shown to precipitate asthma attacks in asthma patients in developed countries.
Patients were challenged in a double-blind fashion using placebo and active
substances. The active substances were tartrazine, sodium metabisulphite,
aspirin and betel nut. All 7 patients were challenged with tartrazine and
sodium metabisulphite; 5 were challenged with aspirin also, but only 2 were
challenged with betel nut. Asthma attacks were precipitated by sodium
metabisulphite in 3 patients. No other substances precipitated asthma. As
sodium metabisulphite is a common food additive, these results suggest that
processed foods introduced into developing countries may have an important role
in precipitating asthma attacks in susceptible persons.
Towns, S.
J. and C. M. Mellis (1984). "Role of acetyl salicylic acid and sodium
metabisulfite in chronic childhood asthma." Pediatrics 73(5): 631-7.
The
role of a commonly ingested food additive, the preservative sodium
metabisulfite (MBS), and aspirin (ASA), in chronic asthma has been studied in
29 children. After 1 week on a strict elimination diet, all 29 children were
challenged, in a single-blind fashion, in the pulmonary function laboratory on
three consecutive days with placebo, MBS (capsule form and solution), and ASA.
Children with a positive response to MBS were prescribed a diet that excluded
foods containing MBS. Patients with a positive response to ASA were prescribed
a diet excluding medications containing aspirin and natural salicylates. After
3 months on these restricted diets, the children were reassessed to determine
whether there had been any therapeutic response. There was a 66% (19/29)
incidence of positive challenge (greater than 20% decrease in forced expiratory
volume in one second) with MBS and a 21% (6/29) incidence of positive challenge
with ASA. None of the children reacted to MBS in capsule form (maximum dose =
100 mg), but 19/29 reacted to MBS in solution with 30 mL of 0.5% citric acid.
After 3 months on the restricted diet, four of 19 children on the MBS-free diet
and one of six on the salicylate-free diet had objective signs of improvement,
namely, reduction in asthma medications and/or improvement in lung function.
Unfortunately, compliance with the restrictive diet during this 3-month period
was poor, particularly with the ASA-sensitive children.(ABSTRACT TRUNCATED AT
250 WORDS)
Trindade,
V. M., A. M. Brusque, et al. (2002). "Ganglioside alterations in the
central nervous system of rats chronically injected with methylmalonic and
propionic acids." Metab Brain Dis 17(2): 93-102.
Neurological dysfunction and structural cerebral abnormalities are commonly found in patients with methylmalonic and propionic acidemia. However, the mechanisms underlying the neuropathology of these disorders are poorly understood. We have previously demonstrated that methylmalonic and propionic acids induce a significant reduction of ganglioside N-acetylneuraminic acid in the brain of rats subjected to chronic administration of these metabolites. In the present study, we investigated the in vivo effects of chronic administration of methylmalonic (MMA) and propionic (PA) acids (from the 6th to the 28th day of life) on the distribution and composition of gangliosides in the cerebellum and cerebral cortex of rats. Control rats were treated with the same volumes of saline. It was first verified that MMA and PA treatment did not modify body, cerebellum, or cortical weight, nor the ganglioside concentration in the cerebral cortex of the animals. In contrast, a significant reduction in total ganglioside content in the cerebellum of approximately 20-30% and 50% of control levels occurred in rats injected with MMA and PA, respectively. Moreover, chronic MMA and PA administration did not interfere with the ganglioside pattern in the cerebral cortex, whereas the distribution of individual gangliosides was altered in the cerebellum of MMA- and PA-treated animals. Rats injected with MMA demonstrated a marked decrease in GM1 and GD3, whereas chronic PA treatment provoked a significant reduction of all ganglioside species, with the exception of an increase in GM2. Since gangliosides are