Lutein is a carotenoid pigment found in many fruits and vegetables. In August
of 1996, lutein was also identified as having properties like a pterin
derivative: 2-amino-4hydoxy-6formyl-7, 8dihydropterin or more simply 7,8-dihydropterin-6-carboxaldehyde.
The pterin connection to autism has been elucidated through the research
into PKU, a disorder of tetrahydrobiopterinhydrofolic acid metabolism
which is listed as one of 5 conditions likely to precede an autism diagnosis.
Viral exposure and vaccine reactions are additional factors associated with
possibly leading to an autism diagnosis. Researching med-line and medical
journals led me to articles and notations which state that high levels of
cytokines (immune components which identify non-self pathogens) leads to
an increase in production of macrophage cells (the immune components which
engulf and remove pathogens) which produce antibodies to antigens. So an
increased reaction to vaccines and viruses could be a result of elevated
levels of macrophages, and identifying the reason for the elevated levels
of macrophages (cytokine reaction to a hapten) and the knowledge that pterins
can act as haptens (2)
leads to a scientific theory with supportable evidence for the removal
of specific dietary components to determine outcome. Another group of studies
show that elevated bilirubin in the infant is evidence for a later diagnosis
of autism spectrum disorders - again the connection to pigments is made,
as bilirubin, biliverdin, etc. are the body’s pigment waste products. Another
xanthine recently identified in annatto can act similarly to lutein.
Macular yellow is lutein
“A yellow component associated with human transthyretin has properties
like a pterin derivative, 7,8-dihydropterin-6-carboxaldehyde: Transthyretin
(TTR) in plasma is associated with yellow compounds. Their properties differ,
and in the chicken protein a major yellow compound has recently been identified
as a carotenoid, lutein, also called xanthophyll. We now show that the major
yellow component extracted from human TTR has properties like a pterin derivative,
7,8-dihydropterin-6-carboxyaldehyde (2-amino-4-hydroxy-6-formyl-7,8-dihydropteridine).
The human TTR derivative has chromatographic and spectral properties identical
to a yellow photochemical degradation product of biopterin and a spectrum
like that of the pterin aldehyde.” (3)
Another xanthine recently identified in annatto can act similarly to
lutein.
Historic perspectives
"Since 1782 there has been continuing controversy concerning the curious
central coloration referred to as "macular yellow," but no cumulative source
of information on the subject exists. This paper reviews the research efforts
of two centuries to determine the existence, nature, location, and function
of a specialized pigment in the foveal region. Using white-light illumination,
it is difficult to see a macular yellow spot in the living eye; it is best
observed and documented by red-free ophthalmoscopy and blue-light monochromatic
photography. Histologic, biochemical, and spectral absorption data suggest
that the yellow color is due to a xanthophyllic pigment, lutein, that is
distributed in all retinal layers internal to the outer nuclear layer, with
greatest concentration in the outer and inner plexiform layers. Clinically
absent in newborns, the pigment gradually accumulates from dietary sources
and appears to serve both as an optical filter, by absorbing blue light and
reducing chromatic aberration, and in a protective capacity, preventing actinic
damage. The absorption characteristics of the yellow pigment contribute to
the central dark spot seen during fluorescein angiography and to the risk
of photocoagulation near the fovea. Its apparent absence in albinos and
the reported functional improvement in certain degenerative retinopathies
following supplemental xanthophyll administration suggest a possible role
in hereditary or acquired maculopathies.” (4)
Lutein/zeaxanthin
To date the primary immune triggering pigmented foods identified in
our research are those that contain lutein/zeaxanthin. Foods highest in
lutein/ zeaxanthin are: kale, spinach, mustard greens, yellow corn, broccoli,
green peas, pumpkin, collard greens, summer (yellow) squash, carrot, brussels
sprouts, currants, green olive, green peppers, green bean (pod), chicken
fat, egg yolk, plums, peach, orange, tangerine, currants, avocado, kiwi fruit,
rhubarb, In many foods, the peel contains the majority of that foods
lutein content: cucumber, pear, pineapple. In other foods the dark
outer leaves contain lutein: Cabbage, lettuce, leek. Strawberry contains
a red form of lutein: vitello rubin. The lutein or carotenoid content of
the food depends on many factors including exposure to light, season, soil
and type. Many foods contain multiple pigments such as Oranges which have
been identified to contain at least 5 pigments including lutein/zeaxanthin.
Some foods which may not contain lutein or beta-carotene such as tomato
contain another pigment called lycopene which can be converted to lutein
or beta-carotene in the body. It appears that for some these non-lutein
foods can safely enter the body and the lycopene can reach systems which
benefit from lutein and the lycopene conversion will occur away from the
immune system interference resulting in bio-available lutein. Some foods
contain lutein only at some stages such as green pepper which does not contain
lutein as the pepper matures to its ripe red form. Animals consume foods
which contain lutein such as grass. These animals may then have lutein in
their blood products or stored in their fat. The highest lutein content
in the animal foods will come from blood products and meat fats. Some foods
have not been adequately studied for their pigment content such as grains,
nuts and legumes. (5) (6)
Betacryptoxanthin
It is most often that those who do not tolerate lutein/zeaxanthin foods
also do not tolerate the foods containing Beta-cryptoxanthin. Foods highest
in Betacryptoxanthin are: Orange juice, tangerine, papaya, peach, mango,
apple juice.
(It is common among those who have behavioral and allergic response
to lutein/zeaxanthin/Beta-cryptoxanthin containing foods that most fish
and shell fish are also not tolerated. Reactions as severe as seizure has
been observed when fish was ingested.)
Beta-carotene
The second most common intolerance is to beta-carotene containing foods
and supplements. Foods highest in beta-carotene are: Apricot, cantaloupe,
kale, pumpkin, sweet potato, carrot. It is common that those who are intolerant
to beta-carotene also cannot tolerate alpha-carotene foods. The highest
food sources of alpha-carotene so far identified are: carrots, oranges, pumpkin,
and winter squash.
(note: there is no comprehensive work detailing the colored carotenoid
content of all the identified carotenoid pigments in foods.)
Bixen – Annatto
Used as a food coloring in commercial dairy products and dairy replacers
such as custard, butter, margarine, ice cream.
[NB: there is no comprehensive work detailing the colored carotenoid
content of all the identified carotenoid pigments in foods.]
References
1. Ernström, U., Pettersson, T., Jörnvall, H.; Department
of Neuroscience, Karolinska Institutet, Stokholm Sweden; FEBS Lett, 360:
2, 1995 Feb 27, 177-82.
2. Unconjugated Pterins in Neurobiology; Lovinberg, Levine; 1984.
3. A yellow component associated with human transthyretin has properties
like a pterin derivative, 7,8-dihydropterin-6-carboxaldehyde; Ernström,
U., Pettersson, T., Jörnvall, H.; Department of Neuroscience, Karolinska
Institutet, Stockholm, Sweden; FEBS Lett. 1995 Feb, 360:2, 177-82.
4. Historic perspectives. Macular yellow pigment. The first 200
years; Nussbaum, J.J., Pruett, R.C., Delori, F.C.; Retina, 1981, 1:4, 296-310.
5. Nutrient Composition Lab; “Gary Beecher, Ph. D. USDA-ARS”
6. “The development and application of a carotenoid database for
fruits, vegetables, and multicomponent foods” Jaspreet K. Chug-Ahuja; M.
S./ Joanne M. Holden, M. S. / Michele R. Forman, Ph. D. / Ann Reed Mangels,
Ph. D., R. D./ Gary R. Beecher, Ph. D./ Elaine Lanza, Ph. D. “Journal of
The American Dietetic Association” March 1993, Vol.93 #3
Additional references
1. "The pterins, neopterin and biopterin, occur naturally in body fluids
including urine. It is well established that increased neopterin levels
are associated with activation of the cellular immune system and that
reduced biopterins are essential for neurotransmitter synthesis. It has been
suggested that some autistic children may be suffering from an autoimmune
disorder. To investigate this further we performed high performance liquid
chromatography analyses of urinary pterins in a group of pre-school autistic
children, their siblings and age-matched control children. Both urinary neopterin
and biopterin were raised in the autistic children compared to controls
and the siblings showed intermediate values. This supports the possible
involvement of cell-mediated immunity in the etiology of autism." Urinary
levels of neopterin and biopterin in autism; Messahel S, Pheasant AE , Pall
H , Ahmed-Choudhury J , Sungum-Paliwal RS ,Vostanis P; School of Biochemistry,
University of Birmingham, UK.; Neurosci Lett 1998 Jan 23;241(1):17-20
2. De novo purine synthesis is increased in the fibroblasts of purine
autism patients; Page T; Coleman M; University of California, San Diego,
La Jolla 92093, USA; Adv Exp Med Biol, 1998, 431:, 793-6
3. "Unstable (CAG)n trinucleotide repeat microsatellites are hypothesized
to cause schizophrenia. The (CAG)n microsatellite of dominant spinal cerebellar
ataxia type 1 (SCA1) is a candidate schizophrenia gene. Autism results from
expansions of (CGG)n and (GAA)n trinucleotide repeat stretches at fragile
X syndrome (FRAXA), and the recessive Friedreich's ataxia (FA). Dominant
ataxia genes may cause schizophrenia and recessive ataxia genes may cause
autism. Syndromes with autism show purine synthesis defects (PSDs) and/or
pigmentation defects (PDs). Autism is caused by very lengthy expansions of
(CAG)n, smaller (CAG)n and (CGG)n repeat expansions." Expanded (CAG)n, (CGG)n
and (GAA)n trinucleotide repeat microsatellites, and mutant purine synthesis
and pigmentation genes cause schizophrenia and autism; Fischer KM;
Med Hypotheses, 1998 Sep, 51:3, 223-33
4. "When to suspect and thus investigate for inborn errors of purine
and pyrimidine metabolism is a dilemma for even the most observant investigator.
Often parents of affected children, or a history involving siblings, can
provide valuable clues. The recognition of new purine and pyrimidine disorders
requires skill and serendipity. But even identifying known disorders
can prove difficult, since they cover a broad spectrum of illnesses, can
have more than one symptom, or lead to early death. This problem is compounded
by the fact that they are relatively recently described and therefore often
little known, either in the clinic or laboratory. The considerable heterogeneity
in clinical expression within families as well as between families means
that asymptomatic homozygotes may not be recognized or can present at any
time from early childhood through adolescence up to their eighth decade.
Consequently, all siblings should be screened. These disorders should be suspected
in any case of unexplained anaemia, failure to thrive, susceptibility to
recurrent infection, or neurological deficits with no current diagnosis, including
autism, cerebral palsy, delayed development, deafness, epilepsy, self-mutilation,
muscle weakness, the inability to walk or talk, and-unusual in children and
adolescents-gout, sometimes with renal disease. Some disorders present with
radiolucent kidney stones, in acute or chronic renal failure, alone or with
any of the above, or as an intolerance/sensitivity to therapy (e.g. 5-fluorouracil
in malignancies or azathioprine immunosuppression in organ transplantation),
often with life-threatening consequences. Several parameters need to be evaluated
to ensure correct diagnosis. Pitfalls which can mask diagnosis using only
a single test are renal failure, blood transfusion, diet or drugs." When
to investigate for purine and pyrimidine disorders. Introduction and review
of clinical and laboratory indications; Simmonds HA; Duley JA; Fairbanks
LD; McBride MB Purine Research Laboratories, UMDS, Guy's Hospital, London
Bridge, UK. J Inherit Metab Dis, 1997 Jun, 20:2, 214-26
5. "Previously, we demonstrated an enhancement of in vitro antibody
(Ab) production in response to T-dependent antigens (TD-Ag) by astaxanthin,
a carotenoid without vitamin A activity. The effects of beta-carotene, a
carotenoid with vitamin A activity, and lutein, another carotenoid without
vitamin A activity, on in vitro Ab production were examined with spleen cells
from young and old B6 mice. In addition, the in vivo effects of lutein, astaxanthin,
and beta-carotene on Ab production were studied in young and old B6 mice.
Lutein, but not beta-carotene, enhanced in vitro Ab production in response
to TD-Ags. The depletion of T-helper cells prevented the enhancement of
Ab production by lutein and astaxanthin. In vivo Ab production in response
to TD-Ag was significantly enhanced by lutein, astaxanthin, and beta-carotene.
The numbers of immunoglobulin M- and G-secreting cells also increased in
vivo with the administration of these carotenoids when mice were primed with
TD-Ags. Antibody production in response to TD-Ags in vivo and in vitro was
significantly lower in old than in young B6 mice. Astaxanthin supplements
partially restored decreased in vivo Ab production in response to TD-Ags in
old B6 mice. Lutein and beta-carotene also enhanced in vivo Ab production
in response to TD-Ags in old B6 mice, although to a lesser extent than did
astaxanthin. However, none of the carotenoids had an effect on in vivo or
in vitro Ab production in response to T-independent antigen. These results
indicate significant immunomodulating actions of carotenoids for humoral
immune responses to TD-Ags and suggest that carotenoid supplementation may
be beneficial in restoring humoral immune responses in older animals." Immunomodulating
actions of carotenoids: enhancement of in vivo and in vitro antibody production
to T-dependent antigens; Jyonouchi H; Zhang L; Gross M; Tomita Y Department
of Pediatrics, University of Minnesota, Minneapolis 55455; Nutr Cancer, 1994,
21:1, 47-58
6. "The purpose of this article is to review basic and clinical investigations
that elucidate the relationship between the CNS and the immune system. An
activation of the immune system in schizophrenia and depressive disorders
has repeatedly been described. Cytokines, actively transported into the
CNS, play a key role in this immune activation. It was recently observed
that cytokines activate astrocytes and microglia cells, which in turn produce
cytokines by a feedback mechanism. Moreover, they strongly influence the dopaminergic,
noradrenergic, and serotonergic neurotransmission. There are indications
that the cascade of cytokines can be activated by neuronal processes. These
findings close a theoretical gap between stress and its influence on immunity.
Psychomotor, sickness behavior and sleep are related to IL-1; disturbances
of memory and cognitive impairment are to IL-2, in part also to TNF-alpha.
The hypersecretion of IL-2 is assumed to have a prominent influence on schizophrenia,
and IL-6, on depressive disorders. A characteristic pattern of cytokine
actions in the CNS, including influences of the cytokines on the blood-brain
barrier, seems to play a role in psychiatric disorders. This may have therapeutic
implications for the future." Psychoneuroimmunology and the cytokine action
in the CNS: implications for psychiatric disorders; Muller N , Ackenheil
M psychiatric Hospital, Ludwig Maximilian-University, Munich, Germany; Prog
Neuropsychopharmacol Biol Psychiatry 1998 Jan;22(1):1-33
