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[2] [4] PRACTITIONERS’ SECTION epiphenomena. A specific cause for mental a group heritability of 0.49. The aetiology of retardation can be identified in approximately idiopathic mental retardation is usually 80% of people with SMR (IQ<50) and 50% of explained in terms of the ‘polygenic GENETICS OF MENTAL RETARDATION people with MMR (IQ 50–70). multifactorial model.’ The difficulty is that there A. S. AHUJA, ANITA THAPAR, M. J. OWEN are too few studies to provide sufficiently In this article, we will begin by considering precise estimates of the likely role of genes ABSTRACT what is known about the genetics of idiopathic and environment in determining idiopathic mental retardation and then move onto discuss mental retardation. Given the dearth of Mental retardation can follow any of the biological, environmental and psychological events that are capable of producing deficits in cognitive functions. specific genetic causes of mental retardation. published literature we are reliant on Recent advances in molecular genetic techniques have enabled us to understand attempting to draw conclusions from family and more about the molecular basis of several genetic syndromes associated with mental Search methodology twin studies, most of which are very old and retardation. In contrast, where there is no discrete cause, the interplay of genetic Electronic searching was done and the which report widely varying recurrence risks.[5] and environmental influences remains poorly understood. This article presents a relevant studies were identified by searching Recent studies of MMR have shown high rates critical review of literature on genetics of mental retardation. Medline, ClinPSYC, CINAHL, EMBASE, of chromosomal abnormalities and this raises PubMed and The Cochrane library using the the possibility that a proportion of individuals Key words: chromosomal abnormalities; genetic; mental retardation; X-linked. keywords: mental retardation, genetics, with idiopathic mental retardation may have learning disability, chromosomal abnormalities, undetected or unknown chromosomal Mental retardation is characterized by Early literature made a distinction between single-gene defect and X-linked mental aberrations or single-gene defects. Further significantly below average intellectual ‘pathological’ severe mental retardation (SMR) retardation. The references cited in the above advances in molecular genetics may find functioning existing concurrently with related and ‘familial’ (usually mild) mental retardation. studies were also searched in order to identify idiopathic mental retardation to be an impaired limitations in two or more of the More recently it has been customary to divide more studies. Also high yield journals related aetiologically heterogeneous group with some following applicable adaptive skills areas: it into two groups according to IQ. Those who to the topic were identified and were hand individuals showing retardation secondary to communication, self-care, home living, social show IQ scores between 50 and 70 are searched for relevant articles. specific genetic causes, others because of skills, community use, self-direction, health and categorized as having mild mental retardation environmental effects and the remainder due safety, functional academics, leisure and work, (MMR) and those with IQ scores of below 50 IDIOPATHIC MENTAL RETARDATION to multifactorial causes. manifest before the age of 18.[1] The term are considered as having moderate-severe mental retardation is not in itself a diagnosis, mental retardation (SMR).’ Idiopathic mental retardation refers to SINGLE-GENE DEFECTS as it does not inform about aetiology, individuals who show no evidence of gross prognosis, or specific treatments. Rather, it The impact of molecular genetics on our chromosomal defects or single-gene Single-gene defects account for only a small refers to a clinical state that is developmental understanding of disease processes has been anomalies. It is sometimes considered as proportion of mental retardation and are more in origin and which affects intellectual and enormous and is likely to increase even further. representing the lower end of the IQ likely to be seen in individuals with SMR. social functioning. The resurgence of interest in phenotypes distribution. IQ scores have been shown to These are well-recognized Mendelian combined with the new genetic techniques has have an average weighted correlation of 0.86 conditions and are characterized by autosomal for monozygotic twins and 0.61 for dizygotic recessive, autosomal dominant or X-linked Department of Psychological Medicine, Cardiff reduced the proportion of those with moderate/ Unive rsity, Heath Park, Cardiff, UK severe mental retardation in whom the cause twins and an average correlation between first- patterns of inheritance. Many single-gene is unknown to 20%. Genetic causes may be degree relatives of 0.4, suggesting an overall disorders are syndromic. Syndrome Correspondence hereditary or nonhereditary and may not produce heritability of 50%.[3] A recent study found twin recognition facilitates diagnosis and has Dr. AS Ahuja Department of Psychological Medicine, specific syndromes. Over 500 recognized concordances for mild mental impairment was allowed discrete phenotypes to be delineated. Cardiff University, Heath Park, syndromes involving a have 74% for monozygotic twins, 45% for same-sex It may be aided by the reference to a Cardiff CF14 4XN, UK E-mail: [email protected] now been isolated and many have behavioural and 36% for opposite sex dizygotic twins with dysmorphology database such as the London

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Dysmorphology Database-LDDB (http:// disorders causing mental retardation is the in- clinical phenotypes, depending on how the associated with mental retardation [Table 2]. dhmhd.mdx.ac.uk LDDB.html). The second born errors of metabolism, which have been affects the production and function of There are also a considerable number of X- database is the Online Mendelian Inheritance well documented by Scriver et al.[6] In some protein involved. This phenomenon is known linked nonsyndromic mental retardation in Man-OMIM (http://www.ncbi.nlm.nih.gov/ circumstances, different occurring as allelic heterogeneity. The majority of inborn syndromes, where certain clinical phenotypic Omim/). Another large group of single-gene within the same gene may cause different errors of metabolism follow an autosomal features are associated with learning recessive pattern of inheritance, with some difficulties.[7] Over 200 heritable X-linked Table 1: Single-gene defects causing mental retardation notable exceptions, e.g. . disorders associated with mental retardation Inheritance and are known and almost a third of these fall into Disorder Prevalence [Table 1] describes some of the common the category of nonspecific XLMR, with no Tuberous sclerosis 1 in 7000–1 Normal IQ to severe Autosomal dominant in 10 000 mental retardation, adenoma TSC1 9q34, single-gene defect disorders causing mental other features present apart from mental sebaceum, hypo pigmented patches, TSC2 16p13.3 [8] hamartomaClinical features gene of locationbrain, heart and kidneys, retardation. retardation. The commonest cause of XLMR hyperactivity, autistic spectrum disorders, is the . Manifesting females self-injurious behaviour Phenylketonuria Commonest inborn Mental retardation, Autosomal recessive X-linked mental retardation have been described in several of the XLMR of metabolism retarded growth, , Phenylalanine X-linked disorders are due to germline disorders. In some conditions, such as Coffin– (1 in 10 000) epilepsy, fair hair and skin, eczema, hydroxylase deficiency [9] hyperactivity, autistic features are common 12q24.1 mutations in genes on the X-chromosome and Lowry syndrome, females always manifest, Dihydropteridine characteristically affect males. Carrier women whereas in other disorders, carrier females are reductase deficiency 4p 15.31 Homocystinuria 1 in 300 000 Mental retardation, ectopia lentis, Cystathionine β-synthetase usually have few, if any, manifestations. The usually phenotypically normal but may skeletal abnormalities, fair, poor deficiency large contribution of X-linked genes to mental occasionally manifest symptoms as a result of peripheral circulation, thromboembolic 21q22.3 episodes, epilepsy, liver degeneration retardation is striking and estimated to occur altered Lyonization[10] or the presence of an X- Cornelia de Lange 1 in 100 000 Severe mental retardation, Autosomal dominant in about 1 in 600 male births. Many X-linked autosome translocation. In the latter case, the syndrome (Brachmann–de hypertricosis depressed Chromosome 3 Lange syndrome) nasal bridge, ocular anomalies, conditions with characteristic phenotypes are breakpoint on the X-chromosome affects the limb deformities, gastrointestinal abnormalities. Language deficits involving Table 2: X-linked disorders expressive speech, feeding difficulties, self-injurious behaviour and autistic Disorder features Fragile X syndrome Macrocephaly, large ears, long face and Inactivation of FMR-1 gene at Xq 27.3 Noonan syndrome 1 in 1500 Mild mental retardation, short stature, Autosomal dominant (1 in 4425–6045 males, macro-orchidism,Clinical Genefeatures location speech and language problems, due to CGG base repeats with high gene nuchal oedema/webbing, pulmonary Unknown chromosome 12 1 in 8000 females) attention deficit, hyperactivity and autistic features methylation plus subsequent reduced stenosis, cryptorchidism, poor communication FMRIP (Fragile X protein) skills and autistic features Treacher collins 1 in 40 000 Mild to moderate mental retardation, Autosomal dominant [1 in 10 000–1 in 15 000 females Normal development followed by regression, Causal association with a gene syndrome maxillary mandibular syndrome, hypoplasia, 5q31–33 acquired microcephaly, hand wringing, MECP2 at the Xq28 site absent or malformed external ears, hyperventilation downslanting palpebral fissures (incidence)] autistic features, seizures, self-injurious behaviour, Hurler syndrome 1 in 100 000 Gradual deterioration, coarse facies, Autosomal recessive hyperventilation and sleep difficulties stiff joints, skeletal abnormalities IDUA 4p16.3 Chen syndrome Moderate to severe mental retardation, Autosomal recessive truncal obesity, joint hypermobility, Lesch-Nyhan syndrome Attacks of hypertonia spasticity, ataxia, Congenital deficiency of hypoxanthine pigmentary retinopathy, cheerful, [1 in 10 000–1 in 380 000 involuntary movements such as choreoathetosis, phosphoribosyl transferase, short arm of social disposition live births (incidence) males] moderate to severe mental retardation, seizures, chromosome Xq26–27 verbal and physical aggression, self-injurious Seckel syndrome 1 in 40 000 Moderate to severe mental retardation, Autosomal recessive behaviours (biting of lips and fingers, thumping of severe microcephaly (bird head), Gene location unknown ears and face, and head banging) beaked nose, extreme short stature Coffin–Lowry syndrome Coarse face, hypertelorism, tapering fingers RSK2 Xp22 Bardet-Biedl Unknown Mild mental retardation, post-axial Autosomal recessive polydactyly, obesity, hypogonadism, BBS 1,2,3, etc Aicardi’s syndrome Mental retardation, agenesis of , Xp22 pigmentary retinopathy chorioretinopathy, micropthalmia, seizures, Apert’s syndrome 1 in 150 000 Mild to severe mental retardation, Autosomal dominant lethal in males coronal craniosynostosis, ‘tower skull’, FGFR2 10q Lowe’s syndrome Severe mental retardation, vitamin D resistant Xq26.1 shallow orbits, trapezoid mouth, rickets, cataracts, , dome-shaped head mitten hands and feet Norrie’s syndrome Cataracts, blindness, epilepsy, hearing impairment Xp11.4

Indian J Med Sci, Vol. 59, No. 9, September 2005 Indian J Med Sci, Vol. 59, No. 9, September 2005 INDIAN JOURNAL OF MEDICAL SCIENCES 411 412 GENETICS OF MENTAL RETARDATION function of the XLMR gene concerned. Some responsible for the characteristic clinical always cause syndromes of multiple congenital maternal age at the time of conception. forms of XLMR, which follow an X-linked features of fragile X syndrome.[15] ‘Anticipation’ anomalies and mental retardation.[22] The Approximately 94% of the cases are caused dominant pattern of inheritance, affect females occurs when premutations often expand to full commonest autosomal abnormalities are by trisomy 21, 3.5% by translocation and 2.5% exclusively and usually, lead to lethality in mutations while transmitted by female carriers trisomies, particularly involving chromosomes by mosaicism. The majority of individuals have males. Perhaps the best example of such a and the clinical severity of the disease 13, 18 and 21 and these are all associated moderate to SMR and some of those with a disorder is Rett syndrome, a with increased maternal age. The most increases with each successive generation. A milder phenotype have been shown to have a neurodevelopmental disorder that occurs common aneusomy in live newborns is trisomy milder form of mental retardation expressed as mosaic karyotype. The critical region for the almost exclusively in females. [16] 21 (Down syndrome), which is invariably FRAXE occurs by FMR-2 mutation. Down syndrome phenotype is in the region of associated with mental retardation. Almost all bands 21q21.3–21q22.[23] chromosomal aneuploidies, which involve an FRAGILE X SYNDROME The key clinical characteristics of fragile X alteration in the amount of chromosome syndrome are mental retardation, large ears Those with Down syndrome have Fragile X syndrome is the most common material, are associated with mental and a long face and macro-orchidism. In some characteristic clinical features including short inherited cause of mental retardation and retardation. It is not certain whether this is due adults, there is a characteristic facial stature, round skull, brachycephaly, neonatal originally derived its name from the to dosage effects of specific genes within the appearance, with a large forehead with supra hypotonia, a flat occiput, flat facial profile, small characteristic nonstaining band or fragile site on duplicated or deleted segments, or to a more orbital fullness, long face, long nose, simply formed ears, protrusion of the tongue, the X-chromosome. It affects approximately 1 general effect of aneuploidy per se. It is prominent jaws, high-arched palate and large high arched palate and typical eye signs (e.g. in 4425 to 6045 males and causes mental certainly true that individuals with ears with a bat-eared appearance. Eye mongoloid slope of the palpebral fissures, retardation in 1 in 8000 females. This syndrome chromosomal aneuploidy share some abnormalities such as pale irises may be a epicanthic fold, Brushfield spots, premature accounts for half of all the X-linked mental nonspecific features in common such as poor [17] retardation cases and around 0.6% of the subtle finding in some cases. Epilepsy is growth, microcephaly, epicanthic folds and cataracts, myopia, nystagmus, strabismus, population who show mental retardation. The reported in about 25% of the cases. unusual palmar creases, in addition to features etc.). Common abnormalities seen in the limbs mean IQ scores in Fragile X males seems to more specific to the chromosomes involved. include a single-palmar crease (simian crease), decline with increasing age, a phenomenon also Many affected individuals show higher rates of incurved fifth fingers, syndactyly (webbed [11] described in people with Down syndrome. A speech and language problems, attentional Some chromosome abnormalities occur in the fingers) and a wide gap between the first and curvilinear relationship exists between the difficulties and hyperactivity and autistic-like mosaic form (where some cells show the second toes (sandal gap). Congenital heart length of CGG repeat (the mutation) and the features such as gaze avoidance and hand normal 46 chromosomes and others have an defects (e.g. atrial or ventricular septal defect, level of intelligence in Fragile X adults.[12] flapping.[18,19] The observation of this type of extra chromosome) and for disorders, which mitral valve prolapse, patent ductus arteriosus) behavioural phenotype in conjunction with are usually seen in the full form, mosaicism will occur in 40% of infants and are a common In normal individuals between 6 and 54 CGG early reports of increased rates of Fragile X in confer a milder phenotype. However, there are repeats are expected with an average of 30 cause of death. There is predisposition to autism led to interest in the relationship some conditions, which are lethal in the full repeats. The mutation for Fragile X is a Hirschprung’s disease, hypothyroidism and between Fragile X and autism. form and are therefore found only in the heritable unstable sequence of trinucleotide leukaemia and the early onset of Alzheimer’s mosaic form in surviving individuals. The CGG repeats ranging from 230 to over disease. CHROMOSOMAL ABNORMALITIES common chromosomal abnormalities 1000.[13,14] The full mutation, when the repeat associated with mental retardation are Microdeletion syndromes sequence reaches a critical length of about summarized in Table 3. Chromosomal abnormalities account for 35– Recent advances in cytogenetic analysis 200 copies, is associated with [20,21] 40% of SMR and 10% of MMR. techniques such as high resolution hypermethylation of the repeat and adjacent Down syndrome Chromosomal aneusomies (loss or excess of chromosome banding and fluorescent in situ region. This results in the failure of FMR1 It is the most common cause of mental chromosomal material) cause a gene dosage hybridization (FISH) together with microsatellite transcription and an absence of the FMR1 difference for a large number of genes and the retardation and affects approximately 1 in 1000 analysis[24,25] have enabled the detection of gene protein product (FMRP), which is phenotypic effect is pleiotropic; therefore, they live births. The incidence rises with advancing increasingly small chromosomal abnormalities.

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Table 3: Chromosomal abnormalities associated with mental retardation ordination deficits are common, intelligence is behaviour particularly in the form of skin Syndrome Prevalence Clinical features Behavioural phenotype Chromosomal abnormality usually in the normal range. picking and obsessional behaviour are Down syndrome 1 in 1000 Short stature, flat occiput, The stereotype of being happy, Approximately 94% of the live births epicanthic folds, oval face, good tempered and placid cases are caused by trisomy frequently observed.[32] Brushfield spots, large tongue, has not been validated. No one 21, 3.5% by translocation, hypotonia, clinodactyly, particular behavioural phenotype and 2.5% by mosaicism Prader–Willi syndrome simian crease Rubinstein–Taybi 1 in 125 000 Broad thumbs, broad great toes, Sociable, distractible, poor Autosomal dominant The region of chromosome 15q11–13 is Angelman syndrome syndrome live births persistent foetal finger pads, short concentration labile mood, stature, generalised hirsuitism, self-injurious behaviour, Microdeletion 16p13.3 subject to the phenomenon known as genomic A deletion in the maternally derived long arm congenital heart disease, seizures expressive language difficulties imprinting. The genetic information of maternal of chromosome 15 (q11–q13) will give rise to Velocardofacial 1 in 5000 Cardiac abnormalities, cleft palate Mild mental retardation, Microdeletion of and paternal origin is manifested differently in the symptoms of Angelman syndrome. It is syndrome (Di (incidence) speech and swallowing difficulties, language and motor chromosome 22q11 [30] George facial abnormalities, developmental delay, this region. The individuals who have a also known as the ‘happy puppet syndrome’. syndrome) hypocalcaemia, hypotonia psychotic features microdeletion of 15q11–13 manifest different It affects between 1 in 20 000 and 1 in 30 000 Williams 1 in 55 000 Infantile hypercalcaemia, Moderate to severe mental Microdeletion of chromosome syndrome live births supravalvular aortic stenosis, retardation, superficially fluent 7q11 characteristics depending on whether the people and is characterized by ataxia, jerky elfin-like face verbal skills, over-friendly, overactive, socially disinhibited deletion is maternal or paternal in origin. A limb movements and abnormal gait, absent Smith 1 in 25 000 Subtle facial abnormalities Mental retardation, self-abusive Microdeletion 17p11 paternal deletion gives rise to features of the speech and SMR. Typical facial features Magenis behaviours, sleep disturbance, [29] syndrome tendency to self-hugging Prader–Willi syndrome and a maternal consist of a long face and prominent jaw, a Prader–Willi 1.2–1.3 per Neonatal hypotonia, hyperphagia, Temper tantrums, self-injurious Microdeletion on chromosme deletion gives rise to features of Angelman wide mouth with widely spaced teeth, thin syndrome 10 000 obesity, hypogonadism, short behaviour (skin picking) and 15, paternal origin at the locus stature, mild to moderate mental obsessional behaviour Abnormalities 15q11-13 syndrome.[30] These conditions can also arise upper lip, mid facial hypoplasia, deep set blue retardation, bitemporal narrowing & of speech and sleep are common. almond shaped palpebral fissures Good visuo–spatial abilities and from maternal and paternal uniparental disomy eyes, blonde hair and microcephaly. Other long-term memory for chromosome 15 leading to Prader–Willi characteristic features include epilepsy (about Angelman 1 in 20 000 to Seizures, ataxia, jerky limb Happy social disposition (happy Microdeletion on chromosome syndrome 1 in 30 000 movements, abnormal gait, puppet syndrome), inappropriate 15, maternal origin at the locus syndrome and Angelman syndrome, 86%) and/or an abnormal EEG, inappropriate absent speech and severe mental bouts of laughter 15q11–13 retardation respectively. bouts of laughter, tongue thrusting movement, Cri-du-chat 1 in 50 000 Characteristic cry, facial Mental retardation, hyperactivity Deletion 5p mouthing behaviour and a happy, social syndrome abnormalities, spasticity Prader–Willi syndrome is also known as HHHO disposition. The microdeletions are usually small- (4 kb) or described are ventricular septal defect, (H, hypotonia; H, hypogonadism; H, hypomentia; less- and encompass multiple genes, which tetralogy of Fallot, interrupted aortic arch, O, obesity). It is a rare condition with a Sex chromosome anomalies may all contribute to the phenotype. Those pulmonary atresia and truncus arteriosus.[27] prevalence of 1.2–1.3 per 10 000. It is Abnormalities in the number of sex microdeletions, which are observed most Hypotonia is present in half of the patients. characterized by neonatal hypotonia, chromosomes are generally less devastating commonly, tend to have similar breakpoints, Relatively slender hands with hypotonic and hyperphagia (over eating), obesity, in their effects than aneuploidies in the occurring in regions of the chromosome where hyperextensible fingers are not uncommon. hypogonadism, short stature and mild to autosomes. Sex chromosome anomalies occur there is a repetitive DNA sequence. [33] The facies are dysmorphic with a broad nasal moderate mental retardation. Feeding difficulties in roughly 1 in 400 live births. These bridge, narrow alae nasae that are often such as absence of swallowing and sucking abnormalities cause mild decreases in IQ (5– Di George syndrome (velocardiofacial notched, small mouth and chin and overfolded reflexes are common in the initial stages. The 15 points) in relation to the family’s mean IQ. syndrome) helices. The features vary considerably from hands and feet are often small and the facies are These anomalies are commonly due to person to person, with the speech and distinctive, with bitemporal narrowing and chromosomal nondisjunction, the risk of which It is the commonest microdeletion syndrome swallowing difficulties being the most almond-shaped palpebral fissures. increases with maternal age. The most and involves a deletion of chromosome 22q11. consistent features. There is an excess of common include Turner’s syndrome (45,XO), It has an estimated incidence of 1 in 5000. psychotic disorders in these individuals. The Abnormalities in speech, sleep and behaviour Klinefelter’s syndrome (47XXY) and the 47XXX Multiple anomalies are seen including a cleft most recent study found that more than one are common. A remarkable area of cognitive and 47 XYY karyotypes. All four are associated palate, velo-pharyngeal insufficiency (causing quarter fulfilled diagnostic criteria for strength is their visual–spatial integration as with a slight decrease in IQ, as evidenced by feeding difficulties), hypocalcaemia and schizophrenia.[28] Although language and motor they may show unusual skill with jigsaw comparison with siblings and by their higher [26] immunodeficiency. Cardiac malformations [31] [34] developmental delay and persistent co- puzzles. Temper tantrums, self-injurious frequency in mentally retarded populations.

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Mental retardation: estimates that over one billion people are Eastern Mediterranean and Africa, where clinical findings of children with 47XXY, 47XYY genetic findings, clinical implications and research overweight globally, and that if current trends cardiovascular disease-related deaths are and 47XXX karyotypes. In: Stewart DA, editor. continue, that number will increase to 1.5 agenda. J Child Psychol Psychiatr 1996;37:259- predicted to rise by over 25%. Birth Defects: Original Article Series, Alan Liss billion by 2015. This warning comes in WHO welcomes and supports this year’s World 80. Inc: New York; 1982. advance of World Heart Day on 25 September. Heart Day, taking place on Sunday, 25 34. de la Chapelle A. Sex chromosome abnormalities. 39. Mandoki MW, Sumner GS, Hoffman RP, Riconda Overweight and obesity are important risk September 2005, which draws attention to this In: Emery AEH, Rimoin DL, eds. Principles and DL. A review of Klinefelter’s syndrome in children factors for cardiovascular disease, which is the problem and focus on the importance of Practice of Medical Genetics. Churchill and adolescents. J Am Acad Child Adol Psychiatr number one cause of death and accounts for maintaining Healthy Weight, Healthy Shape. Livingstone: Edinburgh; 1990. p. 273-300. 1991;30:167-72. over 17 million deaths every year. Once “The real tragedy is that overweight and considered a problem only in wealthy obesity, and their related chronic diseases, are countries, WHO estimates show that largely preventable,” said Dr Robert overweight and obesity are now dramatically Beaglehole, WHO Director of Chronic on the rise in low and middle income countries. Diseases and Health Promotion. This is due to a number of factors, including a “Approximately 80% of heart disease, stroke, global shift in diet towards increased energy, and type 2 diabetes, and 40% of cancer could fat, salt and sugar intake, and a trend towards be avoided through healthy diet, regular decreased physical activity due to the physical activity and avoidance of tobacco sedentary nature of modern work and use.” transportation, and increasing urbanisation. The WHO Global Strategy on Diet, Physical According to WHO estimates, more than 75% Activity and Health and the WHO Framework of women over the age of 30 are now Convention on Tobacco Control describe the overweight in countries as diverse as actions needed to reduce tobacco use and Barbados, Egypt, Malta, Mexico, South Africa, support the adoption of healthy diets and Turkey, and the United States. Estimates are regular physical activity. similar for men, with over 75% now overweight Additional important risk factors, disability, in, for example, Argentina, Germany, Greece, death and economic projections for heart Kuwait, New Zealand, Samoa, and the United disease, stroke and other chronic diseases will Kingdom. Notably, the Western Pacific islands be released by the World Health Organization of Nauru and Tonga have the highest global in its forthcoming publication, Preventing prevalence of overweight where nine out of Chronic Diseases: A Vital Investment, due to every 10 adults are overweight. be launched later this year. The report will “The sheer magnitude of the overweight and present the latest scientific information and obesity problem is staggering,” said Dr make the case for urgent action to turn back Catherine Le-Galès Camus, WHO Assistant the growing global threat of chronic diseases. Director-General of Noncommunicable Source: http://www.who.int/mediacentre/news/ Diseases and Mental Health. “The rapid releases/2005/pr44/en/index.html

Indian J Med Sci, Vol. 59, No. 9, September 2005 Indian J Med Sci, Vol. 59, No. 9, September 2005