• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content

Loading…

Flash Player 9 (or above) is needed to view presentations.
We have detected that you do not have it on your computer. To install it, go here.

Like this presentation? Why not share!

Fetal programming

on

  • 2,126 views

fetal origins of adult diseases.............

fetal origins of adult diseases.............

Statistics

Views

Total Views
2,126
Views on SlideShare
2,126
Embed Views
0

Actions

Likes
0
Downloads
0
Comments
2

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel

12 of 2 previous next

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment
  • Speaker Notes: Prof.David Barker conducted studies in animals as early as the 1980’s to show that health during infancy has very high correlation to diseases that individuals developed as adults. This led him to develop the hypothesis of Early Programming and Foetal Origins of Adult diseases. This theory was given some weightage by the findings from the Dutch Famine Study. During the last 6 months of World War 2, an acute famine affected the western Netherlands. At the beginning of the famine the average daily ration was about 1800 calories until September 1944. This fell to about 1200 Calories in November and by the end of the year this was >800 Calories. By February this had become 580 Calories. This study showed that individuals that were exposed to famine in the last trimester of Pregnancy and the first 3-5 months of life had significantly lower obesity rate than that amongst unexposed controls. Incidence of obesity was a lot higher in individuals exposed to famine during the first and second trimesters of intratuterine life.
  • Speaker Notes: A number of studies have been done to test this hypothesis and many of these trials are prospective with follow up in adults. A classic example of this kind of study is the Pune Maternal nutrition Study conducted by Dr. Yajnik and his group in villages near Pune. We will discuss these in detail later in the presentation.
  • Speaker Notes: Evolution of non communicable disease in adult age start very early in life as early as pregnancy. Pregnancy is a critical window of opportunity where factors such as maternal size, metabolism, and nutrition affect fetal nutrition and growth which in turn affect the size at birth of the baby and his body composition. Post pregnancy the environmental factors that influence a child’s growth modify the risk that lead to development of adult risk factors, some morbidity and eventually premature mortality. In this whole sequence of events, maternal factors are the most important factors since a female child’s programming in utero, programs future generations resulting in intergenerational system of programming that results in epigenetic changes. Therefore, maternal nutrition is one of the most important environmental factors that influences fetal programming.
  • Speaker Notes: This chart has been taken from a review paper written by Dr. Caroline Fall and is a short summary of the effects of maternal undernutrition on her child. Maternal nutrition predisposes her child to developing diabetes and CVD early in life. What this theory implicitly states is that improving the status of girls and women could prevent common chronic diseases in future generation. The nutrients arriving at the placenta, and how they are transferred to the foetus, depend on maternal metabolism: her endocrine status, her partitioning of nutrients between storage, utilization or circulation, and her cardiovascular adaptations to pregnancy, such as plasma volume expansion which increases uterine blood flow. These are influenced by maternal nutrition in ways that are poorly understood. The link between maternal and foetal nutrition is thus indirect and explains why the full impact of maternal diet on foetal growth remains unclear
  • Speaker Notes: This slides elaborates on how the deficiency of many micronutrients such as Iron, Zinc, Vitamin A, Manganese, Calcium , folate etc results in epigenetic changes in gene regulation that restrict fetal growth and development. Hales and Barker (7) proposed that maternal or fetal malnutrition could affect fetal growth, metabolism, and vascular development.These changes could, in turn, affect the development of the kidneys; pancreatic b-cells; muscle, liver, or adipose tissue; or the hypothalamic-pituitary-adrenal (HPA) axis. This conceptual framework has been expanded to describe associations betweenmaternal micronutrient status, the role and mechanism for organ systems development, and the consequent functional outcomes in the offspring based on available evidence
  • Speaker Notes: We have discussed in detail the role that maternal nutrition plays in causing life style related disorders in her offspring. However that is not the only thing that is influenced by maternal nutritional status. Maternal undernutrition also affects the cognitive development since perinatal time is the biggest window of opportunity for nutritional optimization of brain development
  • Speaker Notes: However data from preterm births has shown that there are structural changes in the brain which results in significant cognitive and motor development – all of them were the result of early nutrition. For e.g. an inadequate supply of iodine during gestation results in damage to the fetal brain that is irreversible by mid-pregnancy. Animal studies have demonstrated that even mild to moderate maternal hypothyroxinemia may result in suboptimal neurodevelopment, and increase the risk for neurological disabilities in offspring.
  • Speaker Notes: Even data from MRI dones on children show that early nutrition has a significant role to play in the cognitive development of the child as it has multiple effects on the structure of the brain. In animals, documented effects of early undernutrition on brain structure include changes incell number, growth of the cerebral cortex, and dendriticarborization. In humans there are marked changes in cortical folding, myelination, and gray-matter distribution. Consistent with these findings, it has been demonstrated that nutritional interventions that lasted only a few weeks had large, long-term, and likely permanent effects on cognitive function in infants who were born preterm and in whom interventions took place ex utero but before the equivalence of term. It has been shown that shown that nutritional interventions affect brain macrostructure.
  • Speaker Notes: Studies done on monozygotic twins show that there was a relationship between a within-pair difference in birth weight and a subsequent within pair-difference in VIQ scores. This relationship differed according to the degree of discrepancy in birth weight. However, the mean advantage for the heavier twin can be as large as half an SD in verbal IQ scores.
  • Speaker Notes: Studies in twins have further added to this body of evidence. In twins, for each 1 kg reduction in birth weight there was a 13 point loss in verbal IQ
  • Speaker Notes: Maternal undernutrition has also indirect effects on the brain development of the fetus. Poor nutrient intake may affect the immune system of the mother making her susceptible to infections. Maternal infections such as influenza or respiratory infections are associated with increased risk of schizophrenia in the children. This information is based on data collected from over 12,000 mothers and these findings are supported by an association between elevated cytokines or anti-influenza antibodies in maternal serum and Schizophrenia in the offspring.
  • Speaker Notes: Based on his study in Pune, Dr. Yagnik proposed the theory of the “Indian Thin-Fat Baby”. This chart on the left compares the anthropometric data from Indian babies with anthropometric data from caucasian babies. The 0 line represents the weight of the caucasian baby. As you can see from the chart the Indian babies are 2.5 SD lighter than the caucasian baby. However, the subscapular measurement was very similar in the two babies indicating that the amount of fat is much higher in the Indian baby even though it is much lighter in weight. This showed that the thin fat phenotype is present at birth. The picture on the right shows the levels of insulin, leptin and adiponectin in the cord blood of Indian babies at much higher levels than in the blood of caucasian babies. 3 endocrine abnormalities associated with a future risk of diabetes
  • Speaker Notes: After demonstrating that Indian babies have a body composition and endocrine profile at birth that predisposes them to diabetes later in life. Dr. Yajnik started to look for determinants of this phenotype. They looked at maternal nutrition and found that conventional measurements such as calories, protein and fat were not very strongly predictive of birth size. In fact the maternal frequency of intake of fruits, green leafy vegetables and milk-foods that are powerhouses of micronutrients are more accurately predictive of birth size. The more often the mother ate these foods the higher the birthweight of her baby. They measured the red blood cell folate level and found that it was strongly predictive of birthsize.
  • Speaker Notes: Dr. Yagnik then embarked on the evaluation of the biochemical parameters that might contribute to this phenotype of Indian babies. Indians have high levels of homocysteine.A 40 year old Indian has twice as much homocysteine as that of the Caucasian. However high levels of homocysteine in Caucasians is due to a low intake of folate whereas in Indians high homocysteine levels are due to low intake of vitamin B12. Low Vitamin B12 intakes may be due to high degree of vegetarianism in India. They compared the levels of homocysteine in the preserved blood of mother to the size of her baby and found that high levels of homocysteine were strongly correlated with SGA at birth.
  • Speaker Notes: When they measured these children at 6 years of age they saw that Maternal nutrition and nutrient intake was strongly correlated with the body composition of their children even at 6 years of age. Children born to mothers with higher B12 had lower BMI. Mothers with higher levels of folate had children with more adiposity and higher levels of insulin at 6 years of age. This was particularly true for mothers with low B12 concentrations. This is the first prospective study where maternal nutritional status during pregnancy has been linked risk of diabetes in the children.
  • Speaker Notes: Gestational diabetes in the mother exposes the fetus to a state of hyperinsulinemia in-utero. This programs the fetus to develop a disposition towards obesity, diabetes Mellitus and Metabolic Syndrome. In the case of the female offspring it changes the phenotype such that the fetus when grows to adulthood and becomes pregnant is also predisposed to obesity and IGT during pregnancy.
  • Speaker Notes: Thus the epigenetic susceptibility, combined in precipitating factors that are lifestyle related accelerated by glucotoxicity and lipotoxicity that arises out of the small rise in the levels of these nutrients results in Multiphasic Malnutrition related diabetes Mellitus.
  • Speaker Notes: Programming for CVD risk in later life continues to happen even after birth. Dr. Lucas and Dr. Singhal have conducted a number of studies in both animals and humans and their findings suggest that a high-nutrient diet in infancy adversely programmes the principal components of the metabolic syndrome by promoting growth acceleration(upward centile crossing). This suggestion raises the concept that relative undernutrition and slower infant growth benefits later CVD and its risk factors. Breastfed infants show slower growth than those fed formula (especially in the early weeks when breastfeeding is not fully established), and subsequently have lower risk of CVD, hypercholesterolaemia,obesity, NIDDM, and high blood pressure. Reduced early growth due to a lower nutrient intake is the potential link between breastfeeding and reduced CVD later in life.
  • Speaker Notes: There has been a lot of evidence for this body of research
  • Speaker Notes: The pregnancy diet needs to be such that is it meets the nutrient needs for adequate brain development and growth of the baby, supports mother’s immunity and healthy digestion since pregnancy may be accompanied with constipation.
  • Speaker Notes: Where pregnancy has generally been approached as a maternal stage with temporal additional nutritional requirements, evidence in the post-genome medical arena increasingly suggests that the prenatal period may constitute a critical time for postgestational short- and long-term maternal health and well-being, and that nutrition provides essential design factors for the lifelong health and functioning of mother and child.

Fetal programming Fetal programming Presentation Transcript

  • POGS ORATION18TH DEC 2011DR NARENDRA MALHOTRA
  • NARENDRA MALHOTRA M.D., F.I.C.O.G., F.I.C.M.C.H President FOGSI (2008), Dean of I.C.M.U. (2008) Director Ian Donald School of Ultrasound National Tech. Advisor for FOGSI-G.O.I.—Mc Arthur Foundation EOC Course Editor SAFOG journal,chair AOFOG publication & YGAA committee Hon Prof Ob Gyn at DMIMS,Sawangi,Advisor ART unit at MAMC & SMS Jaipur Practicing Obstetrician Gynecologist at Agra. Special Interest in High Risk Obs., Ultrasound, Laparoscopy and Infertility, ART & Genetics Member and Fellow of many Indian and international organisations FOGSI Imaging Science Chairman (1996-2000) Awarded best paper and best poster at FOGSI : 5 times, Ethicon fellowship, AOFOG young gyn. award, Corion award, Man of the year award, Best Citizens of India award Over 30 published and 100 presented papers Over 50 guest lectures given in India & Abroad.Presented 13 orations. Organised many workshops, training programmes, travel seminars and conferences Editor 8 books, many chapters, on editorial board of many journals Editor of series of STEP by STEP books Revising editor for Jeatcoate’s Textbook of Gynaecology (2007) Very active Sports man, Rotarian and Social worker MALHOTRA HOSPITALS 84, M.G. Road, Agra-282 010 Phone : (O) 0562-2260275/2260276/2260277, (R) 0562-2260279, (M) 98370-33335; Fax : 0562-2265194 E-mail : mnmhagra10@dataone.in / mnmhagra3@gmail.com Website : www.malhotrahospitals.com Consultant for IVF at jalandhar,ludhiana,ambala,bhiwani,gwalior,allahabad,gorakhpur,udaipur,bariely,jaipur,delhi Neapal & Bangladesh
  • Fetal Origins of Adult Diseases narendra malhotra jaideep malhotra neharika malhotra www.malhotrahospitals.com
  • Early life origins of human helath and disease Compelling evidence that many of the risks leading to chronic adulthood diseases,originate in the earliest stages of life Adverse intrauterine enviornment and infancy leads to negative health effects in adulthood There is evidence on the developmental origins of diabetes,cancers and obesity Genetic and epigentic pathways of development are affected by nutrition and pollution Enviornmental insult not only affects the individual ,but also the future generations Preventive intrauterine nutritional measures can be applied.
  • fetal origins of adult disease Adult Disease
  • Fetal origins of adult diseases It is now widely accepted that the risks of a number of chronic diseases in adulthood such as diabetes mellitus, hypertension and coronary heart disease may have their origins before birthRef:Effect of In Utero and Early-Life Conditions on Adult Health and Disease; Peter D. Gluckman et.al; N Engl J Med 2008;359:61-73. The early life origins of asthma and related allergic disorders J O Warner Correspondence to: Prof. J O Warner Professor of Child Health, Allergy & Inflammation Sciences, Division of Infection, Inflammation & Repair, School of Medicine, University of Southampton, UK; jow@soton.ac.uk
  • Early Programming and Fetal origins of adult diseases Developmental plasticity: Ability of an organism to develop in various ways, depending on the particular environment or setting Developmental programming is defined as the response by the developing mammalian organism to a specific challenge during a critical time window that alters the trajectory of development with resulting persistent effects on phenotypeRef: Prenatal origins of adult disease; Current Opinion in Obstetrics and Gynecology 2008, 20:132–138 Peter D. Gluckman, et.al, N Engl J Med 2008;359:61-73
  • History of Early Programming Barker’s in 1980’s reveals:  High correlation between infant and adult mortality  Association between low birth weight and adult ischemic heart disease This lead to his ‘fetal Origin of Adult Diseases’ and to the Early programming hypothesis.Ref: Ravelli GP et al N Eng J Med 1976, 12;295(7) 349-53; Lucas A, Adv Exp Med. Biol 2005, 569:13-5: PMID 934222, 1613710
  • Science of early programming  Numerous examples of early programming in animals and humans  Some trails have prospective follow-up well into adult lifeRef: Fall C. Indian J Med Res 2009;130:593-599
  • Effects of programmingProgramming involves structural changes in Important organs, altered cell number, imbalance in distribution of different cell types within the organ, and altered blood supply or receptor numbers.Ref: Mark J. Nijland et.al; Current Opinion in Obstetrics and Gynecology 2008, 20:132–138
  • Fetal Origins of Adult Disease MATERIAL ENVIRONMENT + fetal MATERIAL & Environment PLACENTAL + GENOME IntrauterineEnv PHYSIOLOGY U –Placental Unity Alterations: Responses to adverse environments: •fetal growth1. Accelerated maturation ( G- corticoid level) •Interaction pre-and-1. Keeps nutrients post natal environments ( growth & nutrition)3. Pregnancy termination (abortion, prematurity) FETAL ORIGIN OF DISEASE
  • Umbilical Chorionic vessels Chorionic plate Amnion vessels Normal Placental Development Placental Spiral septumUteroplacental Basal artery veins plate Sadler TW Lagman’s Medical Embryology 1990
  • The Supply Line to the Human FetusCuningham FG, MacDonald PC, Leveno K, Gant NF, Gilstrap LC II Williams Obstetrics 1993
  • Fetal Origins of Adult DiseaseHow does the fetus respond an adverseenvironment – e.g.: nutritional? By makingirreversible changes in its development Abnormal insulin Type II Diabetes secretion/action Reduced vascularity Hypertension Reduced nephron number CV Disease
  • Pregnancy – a critical window of opportunity Maternal size fetal Nutrition and Birth Size and Childhood Environment Risk factors Metabolism Growth Body Composition And Morbidity Nutrition Growth MortalityRef: Dr.Niva Shapira,Women’s Health,2008;4(6)-639-656 Yajnik CS, Deshmukh U, 2009
  • Programming Effects ofMaternal Undernutrition
  • Effects of undernutrition Maternal Uteroplacentral Placentral Fetal diet blood flow transfer genome Nutrient demand exceeds supply FETAL UNDERNUTRITION Brain sparing Down regulation Early Altered of growth Maturation body composition ↓ Insulin/IGF-1 Impaired development: Secretion and Cortisol Muscle ↓ bloodvessels,liver, sensitivity kidneys,pancreas. Hyperlipidaemia Central Insulin Hypertension obesity resistance Type 2 diabetes and CHDRef: Maternal nutrition: Effects on health in the next generation Caroline Fall; Indian J Med Res 130, November 2009, pp 593-599
  • Conceptual frameworks for how maternal diet and micronutrients status may affect the development of chronic disease in the offspring Maternal micronutrient deficiency Hormonal adaptations Epigenetic gene Fe,Zn,Ca regulation •Increased stress hormones Folate ,Vitamin B-12 •Decreased somatotrophic hormones(GF,Insulin) Restricted foetal growth and development Renal function Cardiovascular function Pancreas / β –cell Body composition Primary Function Fe, Zn,Vitami n A foalte Fe,Zn,Viatmin A folate function Mg,Zn,folate,Vitamin Vitamin A,Vitamin D •Impaired •Impaired Fe,Zn,folate,Vitamin B-12 •Reduced bronchial nephrogenesis/ vascularization B-12 •Reduced lean body branching & alveoli Reduced •Malformations •Reduction in mass •Reduced elastin nephronendowment •Cardiac hpertrophy number and area of •Altered fat deposition •Reduced VEGF •Reduced GFR β - cell or metabolism •Chronic respiratory •Increased sodium •Sedentary behaviour infections sensitivity •Altered appetite •Reduced lung •regulation capacity Hypertension Insulin resistance and β – cell dysfunction Cardio metabolic riskRef: Stewart CP, J Nutr 2010 140(10): 437-445 PMID 20071652
  • Nutritional Programming of the Brain Brain Development
  • Perinatal period is a “BrainTime”:A window of opportunity forNutritional optimization ofbrain development andfuture health and performance
  • Maternal Nutrition and Cognition in offspring Permanent, large cognitive and motor effects of early nutrition – with structural changes in the brain
  • MRI Brain mapping Suggests cognitive effects of early nutrition related to multiple effects on brain structureRef: Edmonds CJ et al. Pediatrics 2010;126:e1095–e1101
  • Key cognitive educational performance & motor skills influenced by early nutritionRef: Edmonds CJ et al. Pediatrics 2010;126:e1095–e1101
  • For each 1kg reduction in birth weight (compared to other twin) there was a 13 Point loss in verbal IQRef: Edmonds CJ et al. Pediatrics 2010;126:e1095–e1101
  • Maternal immune activation alters foetal brain development through interleukin-6  Birth in winter/spring is an accepted risk factor for schizophrenia, mostly associated with influenza (Tochigi et al, 2004)  Second-trimester respiratory infection increases the risk for schizophrenia in the offsprings by 3-7 fold.  14-21% of schizophrenia cases are assumed to have been caused by maternal infection.  Cytokines that drive that innate immune response, i.e Interleukin (IL-6), assumed to affect brain health.Ref: Stephen E.P Smith, The Journal of Neuroscience, 3 October 2007, 27(40): 10695-10702
  • theperiod of prior to fullterm is a very sensitiveone for NutritionalProgramming of thebrain
  • Programming for Diabetes:Undernutrition and Overnutrition Type2 Diabetes
  • Dual - Teratogenesis Undernourished Altered fuels (small) motherfetal fetal adiposity &undernutrition islet dysfunction Pregestational and gestational Undernutrition Postnatal under Overnutrition hyperglycemia nutrition Small baby (Thin-fat) Macrosomia Obesity and Insulin resistance hyperglycemia Postnatal over nutrition Nutrient-mediated (Urbanisation) Fuel-mediated teratogenesis teratogeneis Ref: Yajnik CS, Deshmukh U, 2009
  • Pune Maternal Nutrition Study2006-08 Children & parents Size, body 12Y Composition IR CVD risk markers Cognition 690/722 (95%) Children & parents Size, body Composition IR CVD risk markers2000-03 6Y 698/723 (96%) Postnatal Growth every 6 months 7431994-96 Birth Size Phenotype 770 Maternal Size Nutrition Metabolism Paternal size Metabolic variables Intrauterine fetal growth (USG) 814 1993 Preconception Maternal Size Hemoglobin 2675 Ref: Indian J Med Res 130, Caroline Fall ,November 2009, pp 593-599
  • Indian Thin-Fat Baby (vs. white Caucasian) 1.5 Neonatal Cord 1 blood 0.5Maternal Anthropometry 0 -0.5 -1 -1.5 -2 -2.5 W B A Ch Bi H M He Tr S T C H G I L Ad eig MI bd rth eig id -A ad ice ubs rigl hol DL luc nsul ept ht om est we h t ps ca yc es os in in ipon en rm p er t e ec igh t id erol tin esYajnik et al, Int J Ob, 2003 Yajnik et al, JCEM, 2002 Lubree et al, Paed Res 2005
  • Maternal Nutrition & offspring birth size Mean Calories 2800 Fat2800 P>0.05 P>0.05 2726 2700 Mean 26712700 2663 2668 2657 2654 2628 2617 260026002500 25002400 2400 < 1336 kcal <1638 kcal <1978 kcal 1978 kcal+ <23g <30g <39g 39g+ 2800 p<0.005 GLV 2735 2700 2655 Mean 2631 Also fruits & milk 2600 2584 & E-folate adjusted for gestation, 2500 sex, and maternal size 2400 Never <once/wk once/wk every other day
  • Maternal tHcy & Risk of SGA B12 defi 65% 4 Folate defi 0.2% 3.2 ** Risk of SGA High Hcy 33% 3 High MMA 90% 2 1.6 1.2 1.1 1.3 1 8 9 10 11 12 13 14 SGA : gestation and gender specific <10th C tHcy (µmol/L)
  • Maternal Folate, Vitamin B12& Childhood Adiposity& Insulin Resistance(fetal Programming) 3.5 14 13.9 3.4 6y Fatmass (kg) 13.8 6y BMI (kg/m2) 13.7 3.3 13.6 P=0.01 P=0.002 3.2 13.5 13.4 3.1 13.3 3 13.2 13.1 2.9 13 2.8 <103 <135 <175 >175 Vitamin B12 (pmol/L) <734 <961 <126  1269 9 Red cell folate (nmol/L) Adjusted for sex,age and fat %: maternal adiposity , Ref: Rao S, et al, J Nutr, 2001 Yajnik CS et al, Diabetologia 2008 protein intake,birth size, vitamin B12 Pune Maternal Nutrition Study
  • Pune Maternal Nutrition Study: Conclusions First demonstration that maternal micronutrient nutrition influences risk of diabetes in the offspring Vegetarianism determines the B12 and folate status of Indians.
  • Matrenal obesity and perinatal risks
  • Maternal obesity and perinatal risks “Maternal obesity is associated with increased risk of almost all pregnancy complications: GDM, PIH, LGA, congenital defects”. “A child of an obese mother suffer from suboptimal in utero environment may extend the risk to adulthood”. Optimizing pre-pregnancy weight could prevent upto 40% of childhood overweight (11y)
  • Primary prevention Maternal Diabetes Intrauterine mellitus during growth retardation pregnancy (‘low birth weight’) fetal and / or early postnatal over nutrition fetal and / or early postnatal hyperinsunilism Permanent malprogramming of the ‘neuro-endocrine-immune-system’ (particularly of hypothalamic regulatory centers of food intake, body weight & metabolism) Perinatally acquired disposition to obesity, diabetes mellitus, and the metabolic Syndrome X Maternal phenotype of female offspring during their pregnancy : overweight and impaired glucose tolerance
  • Recommended weight during pregnancy Weight gain per Recommended total weight gain week after 12 weeks First 12 weeks [88] 0.9 – 1.8 Kg (2-4 lb) After 12 weeks [88] BMI < 19.8 12.5 to 18 Kg (28 – 40 lb) o.5 Kg (-1 lb) BMI of 19.8 to 26.0 11.5 to 16 Kg (25 – 35 lb) 0.4 Kg (- 1 lb) BMI > 26.0 TO 29.0 7 to 11.5 Kg (15 – 25 lb) 0.3 Kg (0.7 lb) BMI >29.0 7 to 11.4 Kg ( 15 – 25 lb) Multiple pregnancy [92] BMI < 19.8 22.7- 28.1 Kg ( 50 – 62 lb) BMI of 19.8 to 26.0 18.1 – 24.5 Kg (40 – 54 lb) BMI > 26.0 TO 29.0 17.2-21.3 Kg (38- 47 lb) BMI >29.0 13.2 – 17.2 Kg (29-38 lb) Twin pregnancy[88] 15.9 – 20.4 Kg (34 – 45 lb) 0.7 Kg (3lb) Twin pregnancy[88] >16.2 Kg at 24 weeks [91] 22.7 Kg (50 lb) overall Adolescent Pregnancy[93] Upper end of ≤ 16 years old Upper end of recommendations recommendations Similar to adult > 16 – 19 years old Similar to adult women women
  • Perinatal diabetogenic risks Maternal GDM increases T2DM risk upto 70% within 10y Even borderline Glycemia increases risk of LGA, earlier adiposity rebound, MetS, Increased energy intake, BMI, and BF% and reduced EE Rapid growth (foetal and post-natal) contribute to hyper-insulinism high BP, BMI and MetSRef: Davey, 2005;Wang et al, 2007;Boney et al, 2005
  • Diet Analysis and lipid profiel in urban Asian Indian adolescents- young adults- I  Subjects: n-1236 (607 M, 629 F) aged 17.6 y 193-25 y), BMI- 198.8  RESULTS: carbohydrates 53% Kcal, protein 11%, total fat 34%, SFAs 11%, MUFA 10%, PUFA 9% (n- 31%, n-6.8%), trans-fat 0.3%  Fat intake 84+/-29 g/d M, 72+/- g/d F-4-fold DRI of Asian Indian (20-22 g/d)  CONCLUSIONS: High total fat and SFA with low n-3 PUFA could contribute to increasing obesity and insulin resistance in urban Indians.Ref: Gulati S, et al. J Am Coll Nutr 2010 Apr, 29(2): 81-9 PMID 20679142
  • T2D, Multiphasic MRDM Precipitating factors AcceleratingSusceptibility (Obesogenic) factors T2DM• Genetics • Lifestyle related • Glucotoxicity• foetal programming - Nutrition • Lipotoxicity(Epigenetic) - Inactivity - Psychosocial stress • Rapid childhood growth • Inflammation Post-reproductive diabetes prevention ?
  • Programming in humans- Risk of CVD
  • Programming of CVD risk Beneficial Adverse
  • 40 years of animal andhuman studies show early nutritionis a key factor for health and majorbiological and social implications
  • Traditional View of Disease Genetic Component Environment Factors© 2006 VR
  • Personalized Medicine Paradigm “It will be possible to ascertain the genetic predisposition to disease of a given individual orpopulation and then implement behavioral and/orpharmacological interventions to delay or prevent disease or to improve treatment” Collins F and Guttmacheer AE. JAMA 2001;286:2332.
  • Fetal Origins of Adult Disease
  • The nutritional statusof pregnant women in India
  • Current scenario in India 18% of pregnant women consumed < 50% of calories 34% of pregnant women consumed <50% of protein 85% of pregnant women consumed <50% iron 57% of pregnant women consumed <50% b-caroten - relative to theirRef: Indian Pediatrics 1999; 36: 991-998 RDA(recommended dietary allowance)
  • Calcium and Vitamin D Status in India  Indian RDA for non-pregnant women- 600 mg/day.  Over 50% of women, are not meeting this number  There is evidence of calcium depletion, measured by bone mineral density, particularly in women after repeated pregnancy and lactation  Vitamin D deficiency exists in Indian adults -based on 25 hydroxy Vitamin D2  Vit D status of children - very low in both urban and rural populations  Pregnant women and their new born had low vitamin D status  Dietary calcium supplementation had positive effect on 25(OH)D levelsRef: JAPI, 2009; (57):40-48
  • Pregnancy – importance of nutrients There are periods before and during pregnancy in which specific nutrients are required for optimal development. There is growing evidence that adequate intake of nutrients, like iodine, docosahexaenoic acid (DHA), choline, and folate, is necessary during pregnancy and lactation Ref: Am J Clin Nutr 2009;89(suppl):685S–7S
  • Pregnancy Diet – 4 Pillars of development
  • Diet  Starting a healthy diet before pregnancy  Diet - Quantity and quality  Basic and extra nutrients for • Maintenance of maternal health • Needs of growing fetus • Strength and vitality required during labour • Successful lactationRef: http://www.acog.org/publications/patient_education/bp001.cfmDutta D.C. Text book of obs, 2004
  • Planning healthy meals Include all food groups in diet • Vegetables & fruits • Milk and dairy foods • Cereals & Grains • Meat, beans, and eggs • Fats and oils
  • Supplementary nutrition Personal food preferences, lifestyle habits and special needs may affect the intake of nutrients Essential vitamins lacking in diet or destroyed during cooking Nutritional supplements are one of the ways to fill the nutritional gap that may be arising due to improper diet It fills the gap by providing the vitamins, minerals, and other substances that may be missing out
  • Maternal supplementation affects both the mother and newbornRef: Resmussen KM, J Nutr 2010,Feb140(2): 402—6; Epub 2009 Dec 23 PMID 20032480
  • Lactation : Role of Nutrients
  • Vital nutrients in breast milk Breast milk provides all the nutrients a baby needs to grow well for the first six months of life. The key nutrients in breast milk support the optimal growth and development of the baby and all organs and systems. Breast milk contains: • DHA and AA - building blocks of brain & eye development • Taurine & choline - support overall mental development & functioning. • Calcium and vitamin D for bone development • Many protective factors that protect the infant from infections • Fat, protein and carbohydrate, which are easily digested and absorbed
  • Mother’s nutrition influences the composition andquality of breast milk The nutritional needs of a breastfeeding mother is high - increased demand for Energy, Vitamins C, B12 • Nutrients consumed by mother is transferred to the growing baby to support its growth and development. • Nutritional deficiencies may develop during this period and affect both mothers and infants Maintaining a diet of fruits, vegetables, whole grains, lean meats, and dairy products regularly will help to meet nutritional needs
  • Gestation is a critical opportunity for future health  Gestation is a most critical period for future maternal and infant health, wellbeing, performance and diseases.  Maternal undernutrition/obesity increases risk for pregnancy complications, and future health.  Transitional diets (i.e westernization) add risk of imbalance and deficiencies, especially vs. increased calorie-dense foods and the obesity epidemic.  Multiparous women represent especially relevant target population for nutritional support.
  • Gestation is a critical opportunity for future health  fetal “programming” affect also immunity, brain health and development, future taste and eating habits.  A variety of local, seasonal, low calorie, and high nutrient dense foods and well planned meals are important for satisfying increased perinatal requirements, for metabolic balance and for health protection.  Healthy eating in pregnancy, together with food modification, fortification and supplementation as required.
  • AIMS OF OBSTETRICAL CARE ISso both are safe and Happy
  • A fetal programmed baby of the future……………………..
  • Thank you members of POGS for this invitation