Down's Syndrome: Nutritional Intervention

Dr. Chris. M.
Reading,
C onsult an t P sy chi atr is t

*l t8

Suite 2a, 2nd Floor Pacific Medical Centre 8-12 Pacific Parade Dee Why, NSW 2099 Australin

ABSTRACT
Down's Slmdrome patients are known to be of short stature, prone to infections, autoi^^.r.," dir"ur", hypothyroidism, Ieukaemia, heart defects and later Alzheimer's disease.

They tend to have 6lder mothers, like Alzheimer's disease patients. The latter tend to have sibs'with either Down's Syndrome or lymphoma/leukaemia. Evidence, looking at 28 Down's Slmdrome patients,'suggests that muitiple food allergies, gluten-gliadin sensitivity or intolerance are Lausing u .6Ehu" diseaselike picture with a malabsorption state for essential vitamins, mineiils and severe autoimrnune disease. It is hoped that missed gluten-gliadin sensitivity or intolerance with or without coeliac disease will be considered Xr u .u,ir" of abnormal oogenesis and spermatogenesis resulting in trisorny 21 and other u"""ptoiai"r. The machanlsm most likely is l-ow nf interfering with sufficient release of cAMi, for normal meiosis. Alternatively exorphins and peptides from foods may suPPress p..J"gi""ai" ii synthesis, or food s6nsitivities may ilte. toic_ metal absorption mech'anismi which are ihought to play a role in the development of Alzheimer's disease. Adequate vitamin/mirieral suppiementation, especiat]y^nf , priol f9 conception and in the first triinester is recommendedior mothers at risk for DS, especially older mothers and a sluten free diet for those with coeliac disease or gluten-gliadin sensitivity/intolerance. - Hop"zuffy this will prevent conception of a DS chitd,-or prevent heart defects/stigmata if one id conc6ived. psthlldren shouid be investigated for the above and commence a food itt".gy free diet with relevant supplements to meet their needs as early as possible to allow maximum development.

INTRODUCTION
Down',s syndrome (DS) or Trisomy 2L, is the commonest form of chromosomal aberration known to cause mentai retardation. It occurs at a rate of about 1 in 600 live births (Stoller, 7971.; Pemose and Smith, 196L.) It accounts for 1V20Vo of the institutionalised mentally retarded population (Heller, 1969; Gibson,

In'I929,life expectancy was only 9 years (Penros-e, 7949.) It rose to 12-L5 by 1947 (Pnrose, ig4g; Benda 1969) by-.1982 the average lfe expecta,ncy was 35 years (Thase,1982,) The overall mq{ality rate-is more than 5 times that of the g"t"tui population (Ost"t et a1.,.1975). According to Thase (1982) there are incieasea specific moriality rates for respirato_ry diseas-e, congenital heart
years

1978.)

disease, leukaemia and neuroiogical disorders. The disordered immunglggy, particuiarly T-cell mediated, appdars to be related to the increased vulnerability' the perioils of highest risk ire: 1. Infancy (due to congenital heart disease, leukiemia and reslpiratory disorders); 2. Laie adulthood, when Alzheimer-type dementia (ATD) and declining immunological function are the problems (Thase,
1982).

91,

AETIOLOGY
The aetiology of Down's Syndrome remains a mystery. Several factors appear to increase the risk of conceiving a DS child: Tfie in'cide;c; ;f ;h;;;;{ifi"

increases with age of the mot"her. Mothers of _the 35 (Penrose 1951.)

ps ctritJr;"

;" ;;""lty ;;;,.

""a

p^re-gnancy (Fialkow et al,H{q::th{I:i{i:q . , 7977). Viral infeitions, such as'hepatitis

Other risk factors ut:'

Other reported factors are: Depression; Vomiting and fatigue in earlv preenancy; A history of-miscarriage. vaginal bleeding in the first"trimest"i, -6"iil3r production is usually less tha-n norfral.

Colman, 7969). Anaemia (Harlap,

1,973).

prior to conception or during early tSt-f%,

NUTRITIONAL DISORDER (see Tables 7 and 2) That deficiency in the ability to acquire or handle thiamin, vitamin 81, plavs a part in the causation of Ds was suggested by Reading asi6l. Bt-i;;;rj;" three male DS adults, carried out iiigzg, *"'r" .up*i3a'i" t6zs.-t""igiE, F. Schmid et aI. confirmed low vitamin 81 in.90 os pati5nts-They also in""rirgi"a vitamins 82 and 86. They established a disturbance of vitamin 81 metabolism, but not-(when compare-d io their controls) a deficiency of ir,tut". They suggested "disturbances in the phosphoryration or a cell menibr"";;;;r;;;'";;?a;il;
conceivable". GENERAL EFFECTS OF DISTURBED VITAMIN B1 METABOLISM 81 deficiency-can.cause.depression (Marks, rg7s,). simirarry, 81 deficiency can t* apathy, irritability, impairment oi -"-iry, concentration and motor l::,y]t lhese can respond sKrlls' to Bl thellpy; Harrel.(1946) measured th"

It is known that 81 deficien{z is not uncommon in pregnancv. In one survev pregnant women (Hellei et ar., 197-4,) zs-goz; #"i""r"""'a ,"'u";"o,l"t;a .599 with. respeo ,:erythrocyte transkeiolas" ,ut.r*tion. This pr;6.il; 1h."remained constant throughout gestation. In another ,.rrrr"y (Migaieni et i-., 197:) 428" of pregnant w6men aT frrlt term had nf J"fi.L..y. Chronic alcohorics are often 81 deficient lwooa u"J n"nnington, 1,974;wood., 1972') Chronic alcoholic mothers are known t" r,i"" .runio-fu.iui abnormalities, congenital heart defects and dermato;to'h. "r?rpting"witn abnormalities such as simian palmar creases (Jones et a1.,7973; hia,'t6iS.y fn"y _"t;r;-;; mentally retarded (foetal aliohol syndrome).
of

Half received 81 and half did not. Those treated with B1 12fi-,g daily;,lio;;;ilp;;; ement in acuity of vision,.skils at games, reaction tim"e, reiding, u.iih;iii.ur processes/ memory and intelligence tests.

tr;g;;;, in mental and physical skills of lz(i tnitar"" tiui"g'a an orphanage.

COMPARISON WITH DOWN'S SYNDROME The depression,, vomiting,,fatigue, anaemia and low oestriol production in DS wetl benefiilhe correction of a deficiency of ni equariy, ilr" nI Fj:g-T:%.:_uld tetus could well benefit from the correction of B1 deficiency in the nrdtir"rLike children of 81 deficient alcoholics, DS pauenis nurr" ..unlo-facial abnormay have heart defects, simian creises, short littt" rir,gerc ur-,J,.r".,tur :flla:"^r-:ld retardahonEFFECTS OF DOWN'S SYNDROME ON CHROMATIN

92

Jn DS, clumping of chromatin in the iris (of neural tube oriein) in the earlv foetus results in. Brushfield's spots (Ingalls et al., toiil ini"-r"'d;ii;;; can cause clumping or condensation of chromatin ir,."rtu#g?';rr,t""'."it

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TABLE

RESPONSE TO THIAMINE (81) TREATMENT IN 3 MALE DOWN'S SYNDROME PATIENTS, OBSERVED BY STAFF AND RELATIVES, AND BY INTERVIEWING

THE PATIENTS
Before commencing

On thiamine 50 mg

thiamine (81)

t.d.s. for ooer 18 mths

mths (before
thiamine)

Ot'f thiamine for ooer 6

recommenctnS

M1 Mood
(affect)

Depressed, prone to weeping spells often

Far more cheerful, spoke

Again became very depressed, quiet, shy

spontaneaously,

and withdrawn
Slow, unco-operative

weeping spells ceased

Workshop Sluggish, uncooperative skills Behaviour Negativistic. Refused to go home at weekends. Tended to isolate. Pale, anergic

Work output
increased, more motivated
Far less stubborn, and negativistic. Far more alert & able to stay in

Unco-operative. Tended to isolate

group activities. Happy to go home

Far less depressed, spoke more spontaneously, not
weePy

M2 Mood
(affect)

Depressed, tearful

Very weepy,
depressed

Workshop Very hard to get him to Far more motivated work. Slow and uncoskills operative Behaviour Very attention seeking behaviour. Negativistic. Hypochondriacal (headaches and abdominal pain) Far less attention seeking behaviour and much less negativistic

Refused to work,

most unco-operative Tended to isolate.

Attention seeking
behaviour predominant

M3 Mood
(affect)

Mood swings. Euphoric, paranoid auditory hallucinations

calling him monkey face, overactive, depressed at times

Cheerful, talked
spontaneously

Depressed, paranoid.

Mood swings,
euphoric at times

Workshop Would refuse to work Motivated to work and Refused to work in the afternoons. in the afternoon. Very output increased skills Lacked motivation reluctant to work in the

morning
Cooperative, friendly, Behaviour Very negativistic at times refused to go on no violent outbursts. No psychotic episodes outings or weekend leave home. Violent to staff and patients

Very negativistic. Violent at times, punching staff

* Low in 86 as well. For the trial period had there been minimal or no improvement on 81, then 86 would have been added. (Reading, et al., 1979)

94

(Manocha, 7972). The addition of cAMP to certain cells can cause diffuse dispersal of chromatin (Kano et al., 1972). This is the oPPosite of chromatin clumping and condensation. 81 deficiency can upset cAMP release. This occurs at

a
the adrenal cortex in response to ACTH thereby upsetting the steroidogenic action of ACTH (Meikle et al., 1972). Normal ooryte meiosis is dependent on cAMP (Koch et al., 1974). It is no^t known wheth6r 81 deficiency is the cause of meiotic nondisjunction in D.S' However, if 81 deficiency interferes with the release of cAMP by ovarian cells in response to luteinizinf hor*one (Ll! _ just as it can upset release of cAMP
at the'adrenal cortex in r6sponse to ACTH

meiotic nondisjunction miy result. The amount of cAMP released from the adrenal cortex under the iniluence of ACTH and from ovarian tissue under the influecne of LH, is of the same order. Certainly B1 deficiency may re'sult in anovulation and ovarian atrophy and thereby blGht the {eveloping fetal ovary The daughter ir [h"tt at-risk bf rriving.D-S.children,-esggcially ;;; "*yi"s- over 35 years of age and becomes 81 -deficient herself, The 81 is when she J"ii.l""Vaumaged oo.yt"r muy t"h"r, be selected for ovulation rather than the normal ot"t. VVo*et ott"t 35 iend to shed more damaged ova' It is of interest that leukaemia occurs more commonly in DS (Schuler ef al', 1972) and, that trisomy 2I can occur in bone marrow cells alone; this latter .""f,iti"n is pre-leuka6mic. (It is not kl9-l at this s_tage whether these cells are 81 deperident as in DS.)'It is possible that 81 deficiency is also the factor Ufighti"g fhe foetal bone marrow development and can, therefore, cause vacuoli,ui'1o1. oTbot marrow and iris cells in such conditions as B1-dependent Leigh's " Svndrome (Simopoulos et a1.,1972;Howard and Albert, 1972).It 81 deficiency .i.r proa.t.L preileukaemia then, if it_persists, lt-may indu.ce frank leukaemia as is sometim^es seen in DS children at 6irth or with aneuploidy of bone marlow
cells.

then abnormal oocytic meiosis and

The above findings and correlative evidence suggest that a 81 deficient state in the mother prio"r to conception, or at conceptiol, induces chromosomal chanses such as DS and then continues to act on vulnerable tissues at critical p"rio?i- foetul derrelopment. Thus children with an abnormal karyotype (extra 'chro-ororne) and ,t"ty f"* stigmata may have Jrad adequate nutrition (in particular their B-groui vitamin"needs may have been met).especially during iurty pr"gnun.y. 1bS dhildt"., can be born"with no heart defects and minimal ;;;il'd"fi"ge.iSi*itarty a 81 deficient state in pregnancy mav result in a child with heart iefects, *etttul retardation, and DS facies with a normal karyotype' CORRECTION OF 81 DEFICIENCY/METABOLISM In1979,I concluded that correction of 81 deficiency: A. Prior to conception and oaulation may result in:- 1. Ovulation of normal_o_ocytes 2. Normal ir-rot preferential selection of 81 damaged.ggWteg for ovulation); oocviic maturation and non meiotic no-n-dislunction; 3. Far fewer DS births.

B. Ouiing

(especially) and throughoyt pr:4nar.tcA Tuy T".s:lt.il'; of foetal 6varies (so that the daughter hasn't blighted 1. Noinal development ovaries (oocytes) and is not at risk to have children with DS many years later). Z.' Normit bone marrow development (no-t,trisoTy Zt and_ other pre-a DS child with minimal-stigmata, leukaemic changes). 3. The birth of heart iefects and mental retardation. 4. Fewer DS children being especially bo'rn with leukaemia (B1 supplements may prevent the leukaemic change in the preJeukaemic trisomy 21 cells). C. Aftei birth and throughoui life in p,esple with DS:- 1. Will help the.normal

the

first trimester

maturation of the Ientral'nervous system. 2' Improve motor skills and behaviour. 3. Help prevent early senescence. (B1 requirements increase with age. DS people utL'*ot" prone to dementia such as Alzheimer's disease')
7979
95

by smithells and Tolarova strongly .:"PPgtts th.e view that precbnceptual suppiementation with vitamins, especially folic acid,

work subsequent to

helps prevent recurrence of cleft lip and other neural tube defects (Tolarova 1982; Smithells ef al., \980, 7981,1983) (see Table 3).
TABLE
3

SOME EVIDENCE THAT VITAMIN SUPPLEMENTS HELP IN THE PREVENTION OF CONGENITAL ABNORMALITIES

(1) Periconceptional supplementation with vitamins and folic acid to prevent recurrence of cleft lip
(Tolarova, 1982) - 85 pregnancies fully supplemented - one recurrence - acting as control, 212 pregnancies not supplemented ended in 15

(2) Prevention of neural tube defects by periconceptional vitamin

supplementation (SmithelIs, et al., 1980, 1987, 1983). There were 2 NTD
recurrences in 254 vitamin

supplemented mothers. Significantly fewer than 11 NTD recurrences in 219 unsupplemented mothers.

Sufficient supplementation of relevant vitamins/minerals should prevent conception resulting in DS and where conception has already taken place, prevent the stigmata. It was not known in1979 why the mother of a DS child should be 81 dependent/ deficient or why a DS child should be so, but there are great sirnilarities between DS children and children with coeliac disease (short stature, proneness to infections, etc were noted in both instances. New areas of research were considered.) Could DS children have gluten/gliadin sensitivity/intolerance with malabsorption for B1,, B,6, etc? Could this be the case with their mothers or fathers? In about 20o/o of DS patients, the extra chromosome 21 originates from the father and not the mother - more males being born when the error was maternal, and more females when the error was paternal (Mikkelsen, 1982).
FURTHER RESEARCH

An investigation was undertaken with 28 DS patients (14 male and 14 female, aged from 372 months to 21 years.) Vitamin and mineral deficiencies, food
allergies, autoimmune disease (including gluterValpha gliadin sensitivity/intolerance) and cow's milk allergy/intolerance were looked at.
Methodology

Vitamin assaus: The patients were fasted for 12 hours overnight and 20-40m1 renuus blocid was collected in heparinized test tubes (Readiig et aI., 1979). Food allergies Tnere looked at using: 7. The RAST (IgE mediated immediate reation type I). 2. Bryan's Cytotoxic Test (BCFT) which is IgMiIgA/IgG/IgD (but not IgE) mediated. (The relevance of this test for ingested food allergies/intolerancei hypersensitivity was discussed by me in my addresss to the Schizophrenia Association of Creat Britain's Conference, April 22, 7982. Also by others (Fenneil, 1983; Downing, 1983). Clinical Immunology: Autoantibodies (Unsworth, 1981), complements C3, C4, CH50, immunoglobulins were looked at. Routine biochemistry was undertaken (minerals; trace elements; fasting blood sugar, etc.).
Vitamin leuels: Males (see Tables (i) and
(ii))

96

Vitamin A Retinol and Caroteniods: Of 14 patients none was low in vitamin A Retinol but one supplemented patient (M14) had a slightly raised level. 3 pati-

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ents had low total carotenoids. Two were low despite supplementation; 1 (M7)extremely low. Vitamin E; Five were low (4 despite supplementation). M3 was very low despite supplementation. Vitqmin C: One patient was low and not supplemented. 1 patient was high (2.34mg7o - Normal range 0.7-2mg%) but was mistakenly given 500m9 of the vitamin before the test. Vitamin 81: Two patients (M5 & M13), both unsupplemented, showed increased TPP activity and were thus 81 deficient. On ETKA test and ETKA+TPP/ seven patients were low in vitamin 81 despite 5 being supplemented. This supports what was noted by me and by others (Reading et aI., 1979 - reporting findings of 7973; Schmid et al., 1975). Folic Acid: No patient had low levels but two, supplemented, had raised levels. Vitamin 83: Only two assays were done. One was high and supplemented. The other was low despite supplementation. Vitamin 82: No patient was low but 9 out of 12 were supplemented. Vitamin 86: By the P5P test, no patient was low. On the EGOT+PSP test, two patients (M4 & M10) were low in 86. Vitamin 812: One patient (supplemented) had raised B12 levels; 5 were in the lower quarter range (below 276) (Serum levels are not a measure of tissue
stores).

under 2years of age and at risk of juvenile pernicious M1 already has parietal cell antibodies 1.:20. M4, M6, M8, M10 were already supplemented. M10 and M13 have latent pernicious anaemia - M10 with parietal cell antibodies 1:40 and intrinsic factor antibodies 1:2. M13 had parietal cell antibodies L:40 and intrinsic factor antibodies 1:4 (Thomas and lewell, 1979).
3 cases (M1, M4 & M6) are

anaemia

Vitamin Leaels: Femsles (see Tables 5(i) and 5 (ii))

Vitamin A Retinol E Caroter.oids: Of 74 patients two were low in total caroteniods despite supplements. One (F12) was borderline low. Vitamin E: Three patients were low - 2 (F5 & F12) seriously low. A further 9 were borderline low including one (F7) supplemented with 100mg vitamin E per day. F1, a supplemented patient, had a slightly raised vitamin E. Vitamin C: F1 had raised levels but supplements had been given on the morning of the test. Despite supplements, F3 was seriously low whilst F8 and F11 were borderline low (the latter despite 1000mg the day before the test). Vitqmin 81: No patient had low B1 on TPP. Four showed low BL on ETKA and ETKA+TPP (three received supplements.) Three patients (F8, F10, F13) were borderline low, despite supplementation. Folic Acid: One patient (F12) was low. Vitamin 83: Two patients only were assessed. Although one was supplemented both had low 83 levels. Vitamin 86: One patient was low by P5P test (increased activity) six were low in 86 on the EGOT and EGOT*PSP tests (4 were supplemented); Vitamin 8L2: Two patients (F4 & F12) had seriously low B12 levels and thus pernicious anaemia, despite vitamin supplementation. F4 had parietal cell antibodies 1:20, but not intrinsic factor antibodies. F12 had thyroglobulin antibodies, but not parietal cell antibodies. F5 had borderline low B12 and already had parietal cell antibodies 1:20. Two patients, both supplemented, had raised B12 Ievels. Tables 6 andT summarise vitamin levels in both male and female patients: 23 out of 27 (85.2'/') had one deficiency, 13 out of 27 (48.1.o/o) had two deficiencies, 6 99 out of 27 (22.2%) had three deficiencies.

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101

TABLE 7 TOTAL NUMBER OF PATIENTS WITH VITAMIN DEFICIENCIES

MaIe
E Female
7a

Total

Vo

(a) One deficiency

r2lt3
6113

92.3
46.1

rU4
7t14 4lL4

(b) Two deficiencies

(c) Three deficiencies
Food Allergies (see Table 8)

78.6 50.0
28.6

2t13

15.4

23127 13127 6127

85.2
48.1.

22.2

female patients with DS aged 1-11 years were examinedby the RAST and Bryan's Cyiotoxic tests. 40% had low IgE. One patient. G1a) had raised IgE but stiil did not show food allergies. However, food allergies can occur with low IgE (as F2, allergic to cow's milk).
1-2

-Bryan',s Cytotoxic test looked at up to 108 foods at a time while the RAST test iooked at between 3 & 16. The cytotoxic tests detected more positive_ reactions for cow's milk, wheat, egg and positives for a far greater variety of foods.

FooD ALLERGIES IN 22 DowN't tfrBkt"$E pArIENrs (11FEMALE,

USING RAST AND BRYAN'S CYTOTOXIC TEST. (i) B.C.F.T. (BRYAN',S CYTOTOXIC TEST)
Female
1.1

11 MALE)

Male 11 assayed
6 4

TotaI

assayed
4

22 assayed
10
8 6 5

Corn Cow's Milk Wheat

Peanut Bakers yeast Barley

45%
36%
27Vo

4
2 2
1 1
1.

4
J

22.SVo
13Vo

2
1 1

J 2
2

Malt Ry"
Soyabean Egg

0
1 1
1

2
L

2
1

9% 9% 9% 9%
97a 4.SVo

2
1

Oat

(ii) R.A.s.T.
Female

Male
10 assayed 0 0
1

Total 19 assayed
3
2

9 assayed

Cow's milk
Wheat Chicken

157
L0Vo 1.0%

2
1 1 1

2
1 1
1

Ry"
Egg Soyabean

0
0
1

5%
5Vo

5%

(iii)

cow,s MILK, WHEAT,

CORN ALLERGY/INTOLERANCE IN 24 DOWN',S SYNDROME PATIENTS POSITIVE ON RAST AND/OR B.C.F.T.

Female

Male

TotaI

No. positive
Cow's milk 102
Wheat Corn
5

No. positive
4

No. positive
9 8 10

37.5%
33.3Vo 41..6%

4
6

12 male DS patients, aged 3Yz months to 2\ years,.were subject to similar tests. RAST was positive for 2 foods in only one out of 12 patients. BCFT gave many positives with tt out of 12 cases (one case was not tested).
Clinical lmmunology (see Table 9)

Patients were examined for antibodies associated with autoimmune disease. The antibodies in question were for reticulin, bile duct, smooth muscle, parietal cells, gluten/alphagliadin, pancreatic duct and thyroid. 12 male patients and 14 Table 9 is a summary of ihe overall autoimmune disease in the 26 patients: 78o/o were positive for r-eticulin antibodies; 69oh for bile duct antibodies; 58% for parietal celi antibodies;47o/o for smooth muscle and gluten antibodies; 43o/o for agliadin antibodies; 35o/o for thyroglobulin antibodies; 33o/o for ANF; 3oo/o for pincreatic duct antibodies; 17o/o for microsomal thyroid antibodies'
Minerals and Blood Sugar (see Table 10) ' females

with DS were assessed.

14 female patients with DS and L3 male patients were assessed_ for copper, zinc, iron, ialcium, magnesium and aluminium. In addition their fasting blood elucose was measured. The results are set out in Table L0: 1,6.6% had low Ealcium; 73.60/o had low iron, 12.5o/o had low copper and 8.3% had low zinc (despite supplementation). Two female patients had hair analysis (see Table 11); one showed toxic levels of aluminium,-cadmium and lead and high levels of calcium, magnesium and sodium with low levels of chromium, coppel and selenium. The second patient showed low calcium, iron, manganes, nickel, zinc, selenium and vanadiurn. T2o/o of patients examined had low blood glucose.

DISCUSSION
These assessments indicate that patients with DS are likely to be:- 1. Low in despite supplementation. 2. Low in certain minerals/trace certain vitamins despite supplementation. They have a marked tendency !9 a low elements fasting blood sugar level. 3. At risk for non-IgE mediated food allergies/ intoleiance/hypersensitivity as disclosed by Bryan's Cytotoxic test (IgM/IgA/ IgG/IgD medlated). This is in accord with tests for autoimmune disease with clinical immunology. 4. Highly at risk"for autoimmune disease. (a) Especially that seen with wheat/giains/gluten/agliadin intolerance/sensitivity, and commonly associated with coeliac disease. (b) Pemicious anaemia/gastritis. (c) Collagen disease, including juvenile SLE. (d) Autoimmune thyroiditis. (e) Chronic active hepitis. The bile duct antibodies and pancreatic duct antibodies strongly support impaired hepatic and pancreatic function interfering with normal digestion. Coeliacs tend to have low trypsin and chymotrypsin. There is also some evidence that DS patients are likely to have high levels of

toxic metals. Supplementation with too much copper could render this state worse. If iron levels are too high this could also be deleterious. Harrel and collegues (1981), under double blind conditions showed that with vitamin/mineral supplementation plus thyroid hormone, three quarters of the DS children gained between 10 and 25 units in IQ. Their physical appearance changed notably during the study; there was fluid loss in faces and extremities. One nine year old child with cataract had the condition arrested. The supplemented group gained more height than controls, over four months' There was also generalimprovement in school work. The observers also noted healthier hair, skin and nail texture in six cases and cessation of hyperactive behaviour in six cases. During the trial, all parents were asked to restrict the patients intake of less nutritibus, sugary, foods and soft drinks, and to supply fruit and

milk

freely.

103

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a
TABLE 11 HAIR ANALYSIS RESULTS IN 2 FEMALE DOWN'S SYNDROME PATIENTS
Patient 1 Aged 6 Yrs Normal
Range

Patient 2
Aged 2 Yrs 92.5 0.8 0.64 8.24 L9.5 0.02
44.3

Normal
Range

Calcium

155*

375-920

Chromium
Cobalt Copper

Iron

Lithium
Magnesium
Manganese

0.33 0.16 17" 4g* 0.34

0.4-1.6 0.1-0.4
18-50
19-6.1.

r2g*
1.5 0.22 1.3
r1.2

Molybdenum Nickel
Phosphorus
Potassium

0.1-1.3 4+-98 0.6-2.8 0.1-0.8

0.15-2.0

0.39

0.17
0.27
221.

200-600 0.5-1.50 0.04-1.00 12-35 20-50 0.02-0.80 25-75 1.00-10.00 0.10-0.70 0.30-1.00
100-170
75-1.80

92-r65

147

Selenium Sodium Vanadium

3VI75
0.9+-5.75 85-385

126
0.1.2 281.
0.7'1.

0.10
528 0.33 175*
ZJ

3.00-6.00
150-350

Zinc

0.1-0.6
125-2s4

Aluminium
Arsentic Cadmium
Lead

150

1.00-2.00 760-240
10.00-20.00

<15

7.93
J.4J

0.39 4.5

<2.0
<7.6 <18

2-5
1.00-2.00 20-30 2.50-5.00

t9
0.10

2.6r Serum Levels were normal - See F7. Patient 2 tested on hair analysis only. Note: Selenium and Copper were low in both patients.

Mercury

0.84 5.36

<3.0

CONCLUSION

It is hoped that the aboveJinding.s will be considered in the primary, secondary and tertiary_prevention of Down's Syndrome patients.
Table 12 shows the similarities between coeliic disease and Down's Svndrome using some of the findings. It explains many of the features of Down's Syndrome and associated conditions in their parents.

{igtt" 1 shows how normal meiosis disjunction trisomy 21 of DS.

Figyp
and-

may be upset resulting in meiotic non-

2 attempts-to explain the links between increasing maternal/paternal age Down's syndrome and why Down's syndrome patients ute mote at risk f6r Alzheimer's disease and leukaemia and why Alkheim-er's disease patients tend to have siblings with Down's syndrome and leukaemia. The corn-on factor is coeliac disease or gluten/gliadin sensitivity/intolerance with low 81, 83, 86, etc.

106

TABLE 12 SIMILARITIES BETWEEN COELIAC DISEASE AND DO\\A]'S SYNDROME

Coeliac Disease

Down's Syndrome Present 47%

Immunology

aGliadin Antibodies
Reticulin Antibodies Parietal Cell Antibodies Thyroid Antibodies
C3, C4, GI5O

Gluten Antibodies

+ + + + +
Low + Low or High Low or High +

(N:26)

+ + + +

43o/o
78o/o

58o/o 35o/o

Immune Complexes IgM

IgA Vitamin Deficiencies

Mineral Deficiencies
Female

+
Prone to spontaneous abortion/miscarriage

Low + Low or High Low or High + + Present in mothers of DS patients prior to conception
and with DS pregnanry. DS sexual dysfunction Fathers of DS children have? missed/untreated coeliac disease or gluten/. gliadin intolerance (especially with
increasing age). DS have male

infertility
Male

Prone to infertility hypogonadism impaired hypothalmic

pituitary
regulation Stature Lynnphoma Leukaemia risk Prone to infections Prone to food allergies Prone to atopies Short Small head
Circumference

hypogonadism inf ertility

Same

+ + +

+ +
+

+
+ +

Low ETKA
Fissured Tongue

+ + +

107

{a)

Nomal

}leiosis'

Adequate B6' D3 Vit C; Ils' Ihr'

Zi\c

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s-

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t, 81 is 1oD, made Horse by

loN calciw. ? opioid
PGEI can """ cAJ'tP lou. make

pePtides (exorPhins) can depre66 PGD] and thus

cAuP.

Figure 1. If the mother or father of a DS child has coeliac disease, they could have low 81, 83, 86-, Vitamin C, Mg, Mn, zinc upsetting oogenesis in the mother or spennatogenesis in the

father and result in Down's Syndrome.

VITH MISSED COELIAC

OLDER I.ATHER

OI,DER MOr}{ER

DISEASE

G, GLI,TEN/CCLIADIN SENSITIVI?Y DISTI'RBED TTYPOTHAI.A.},IO

AND RISK T'@ COELIAC DISDASE

(

on r,lteilr)

AINORMAL OOCYIIC MATURATION

(t)lca-llP due to low 81' biotin' ca and PGEI (z)trcr2 due to low PGEI due to low vit c, zn, Mnr UB + 6uPPr6ssLon of PGE1 by glutonr a8lLadin' othr prolamln ftactlons or exorphins uith opiaie actlwlty. (1)

_lPcar LEuruE}cc J
tiltK-a.El1rA
LYMPHC[,IA

cIrANcE

(z) srns

oLDER MOIHDRS

IJITH DS AND LYMPHOt4A

DOLNTS STNDRO'ID ( PATHoLGY oF

i orr-r,rc orso.lsn

To)(IC EFFECT PER SE OF GLITTEN, AGLIADIN, EXGPIiINS

THER PROLA.I{IN FRAC?IONS

108

Figure 2. Links between Down's Syndrome, L}'rnphonal Leukaemia, Alzheimer's Disease and older mothers and fathers.

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