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What is lutein?

c. Max & Sandra Desorgher 1999-2002
 
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