10/25/2002

• Disordered Eating

• Hypertensive Disorders

• Gestational Diabetes

• Adolescence

Disordered Eating & Pregnancy

• Few data on prevalence of disordered eating in pregnancy

• Difficult to adequately capture this information from women

• No good, prospective studies • Results of published studies are confusing -

some find improvement with pregnancy - others find increased symptoms


Women may have needs for secrecy and denial so information about history of eating disorders is often not given to health care providers during pregnancy.

Developmental tasks of pregnancy are often about the same issues that arise in some women with eating disorders

Body changes Alterations in roles Concerns about a woman’s own mothering and

needs for psychological separation.


• Many women experience concerning food and body image behaviors in pregnancy

Attitudes to body weight, weight gain and

eating behavior in pregnancy, (Abraham et al J Psychosom Obstet Gynecol, 1994)

• N=100, exclusions were no hx of drug use or major psychiatric illness, baby not in ICU

• Questionnaires completed at 3 days pp.

Attitudes to body weight, weight gain and

eating behavior in pregnancy, (Abraham et al J

Psychosom Obstet Gynecol, 1994)

Did you: % Before preg. % Duringpreg.

% Worse inpreg.

Watch your weight 65 71 34

Preoccupation withfood/weight

42 52 23

Binge eating 37 44 22

Feel out of controlof eating/weight

30 30 20

Use weight controlmethods

81 76 -

Methods of Weight Control Used (Abraham et

al J Psychosom Obstet Gynecol, 1994)

% Before Preg % During Preg.

"Dieting" 82 37

Avoiding certain foods 56 42

Compulsive/excessiveexercise

15 4

Diet drugs 15 1

Fasting or fluid only diet 13 3

Smoking cigarettes 14 4

Pregnancy and Eating Disorders: A review and clinical Implications (Franko and Walton, Int.J. Eating Disorders,

1993) British report on 6 of 327 women who had

attended eating disorder clinic and got pregnant

Median BMI was 16.8 (range 14.9-18.1) Median length of time with AN was 15 years

(range 11-17) Average weight gain was 8 kg (range 5-14) -

recommendations for low BMI are 13-18 Poor third trimester fetal growth was found in all

5 babies who were monitored Babies had some catch up in infancy

Pregnancy Outcome and Disordered Eating (Abraham et al J Psychosom Obstet Gynecol, 1994)

• 24 women reported previous problems with disordered eating.

• These women had higher rates of antenatal complications such as IUGR, PIH, edema, GDM, vaginal bleeding (p<0.05)

• These women also were more likely to have infants with birthweights < 25th % ile (p<0.02)

Reported complications of pregnancy and eating disorders: Anorexia Nervosa

Maternal Complications Infant/Birth Complications

Inadequate Weight Gain Miscarriage Vaginal bleeding Decreased uterine size Hyperemesis

Low Birth Weight Delayed Development Premature Birth Prenatal death

Reported complications of pregnancy and eating disorders: Bulemia Nervosa

Maternal Complications Infant/BirthComplications

Increased symptoms Excessive exercise Low and high weight gain Miscarriage Hypertension

Stillbirth Low birth weight Low apgar scores Breech delivery Cleft palate

Postpartum eating and Body Image for all Women

• It is of note that in a general population of postpartum women, eating disorder behaviors increase markedly in the first 3 months post-partum and remain high for the next 9 months.

• Some women actually first experience clinical eating disorders during this time.

Eating Habits and Attitudes in the Post

Partum Period (Stein et al. Psychosomatic Med., 1996)

• N=97, prospective cohort study of primip. women followed during pregnancy and at 3 and 6 mos pp.

• Eating Disorder Examination (EDE): restraint, eating concern, shape concern, weight concern and global scores about state over last 28 days

• Repeated measures ANOVA indicated that changes in eating disorder pathology pp were largely due to changes in body weight.



Preconception Late pregnancy 3 mos pp 6 mos pp

Concern aboutshape***

0.91 1.14 1.34 1.08

Concern aboutweight****

0.96 0.80 1.34 1.63

Concern abouteating**

0.13 0.04 0.15 0.09

Dietaryrestraint*

0.94 0.90 1.08 0.90

GlobalEDE***

0.60 0.58 0.79 0.77

** = p <0.05, ***= p< 0.01, ****=p<0.001

Number Meeting DSM-IV Diagnostic Criteria for Clinical Eating Disorder NOS (Stein et al. Psychosomatic Med., 1996)

Preconception Earlypregnancy

Latepregnancy

3 mos pp 6 mos pp

3 3 4 4 4



• No cases of bulimia nervosa or anorexia nervosa

• No women who met criteria before pregnancy were cases during pregnancy

• All cases during pregnancy were do novo - but two had history of bulimia nervosa

• At postpartum, three cases were de novo

An observational study of mothers with eating disorders and their infants ( Stein et al., J Child Psychol Psychiat, 1994)

• 2 groups of primips:• Index group, women who had met EDE criteria

for disordered eating during pp period, n=34• Control group, balanced for SES, age, and

child’s gender, n=24• At one year:

• EDE• Child’s growth• Structured observation of child and mother at

task and mealtime

Mealtime Behaviors ( Stein et al., J Child Psychol Psychiat, 1994)

Index Control

Negative Expressedemotion toward child

3.27 0.90**

Intrusiveness 8.91 1.20**

% of maternalcontrollingstatements

27.3% 26.11%

** p<0.01

Play Behaviors ( Stein et al., J Child Psychol Psychiat, 1994)

Index Control

Negative Expressedemotion toward child

0.47 1.34

Intrusiveness 16.23 5.83**

% of maternalcontrollingstatements

51.23 44.5*

* p< 0.05, ** p<0.01

Discussion ( Stein et al., J Child Psychol Psychiat, 1994)

• Index mothers were more intrusive than control mothers

• About 1/3 of the index infants and one of the control infants had growth faltering

• Regression analysis models to predict infant weights were best fit when included:

– maternal height,– infant birthweight– conflict during meals – mothers concern about own body shape

www.anred.com

• You could become depressed and frantic because of weight gain during pregnancy. You might feel so out of control of your life and body that you would try to hurt yourself or the unborn baby. You might worry and feel guilty about the damage you could be causing the baby.

• Some women with eating disorders welcome pregnancy as a vacation from weight worries. They believe they are doing something important by having a baby and are able to set aside their fear of fat in service to the health of the child. Others fall into black depression and intolerable anxiety when their bellies begin to swell. Most fall somewhere between these two extremes.

• You might underfeed your child to make her thin, or, you might overfeed her to show the world that you are a nurturing parent. Power struggles over food and eating often plague families where someone has an eating disorder. You could continue that pattern with your child.

• Motherhood is stressful. If you are not strong in your recovery, you will be tempted to fall back on the starving and stuffing coping behaviors that are so familiar to you. Ideally, as you begin raising a family, you will already have learned, and will have had practice using, other more healthy and effective behaviors when you feel overwhelmed.

• Also, eating disordered women make poor role models. Your influence could lead your daughters to their own eating disorders and your sons to believe that the most important thing about women is their weight.

Clinical Implications

• Careful screening and monitoring• Possible use of self administered,

computer assisted screening tool• Psychotherapy may be indicated• Interventions are not evidence based at

this time, but based on case studies & individual counselor’s experiences

Clinical Interventions: Psychosocial

• Making the fetus as real as possible to the patient very early.

• Empathetically addressing fears of weight gain and feelings of being out of control

• Assurance about normal weight gain and patterns of pp weight loss

• Education of significant others

Clinical Interventions: Nutrition

• Discuss and provide materials about nutrients and food in pregnancy

• Design individual food plan• Determine optimal range of weight gain• Discuss hydration shifts in pregnancy

and need for fluid

Clinical Interventions: Exercise

• Assess exercise level

• Suggest joining exercise groups and new mothers groups to normalize experience of weight concerns

Clinical Intervention: Infant Feeding

• Offer assistance with parenting concerns

• Offer information about infant feeding:– infant’s ability to self regulate– attention to infant cues & signals– use of food as reward or control

mechanism

Hypertensive Disorders During Pregnancy

• Incidence

• Definitions

• Etiology/pathophysiology

• Nutritional Implications

WORKING GROUPREPORT ON HIGHBLOOD PRESSUREIN PREGNANCY

N A T I O N A L I N S T I T U T E S O F H E A L T HN A T I O N A L H E A R T , L U N G , A N D B L O O D I N S T I T U T E

July 2000

Incidence• Second leading cause of maternal

mortality in US• 15% of maternal deaths (abruptio placentae,

disseminated intravascular coagulation, cerebral hemorrhgae, hepatic failure, acute renal failure)

• Hypertensive disorders occur in 6 to 8% of pregnancies

• Contribute to neonatal morbitidy and mortality

High risk

First pregnancy and under age 17 or over 35 Family history of hypertension Multiple gestation Poor nutritional status Smoking Overweight Other health problems such as renal disease,

diabetes

Chronic Hypertension

• Known hypertension before pregnancy or rise in blood pressure to > 140/90 mm Hg before 20 weeks

• Hypertension that is diagnosed for the first time during pregnancy and that does not resolve postpartum is also classified as chronic hypertension.

Gestational Hypertension

Hypertension in pregnancy is present when diastolic BP is 90 or greater, systolic BP is 140 or greater

(the use of BP increases of 30 mm Hg systolic and 15 mm Hg diastolic has not been recommended - women in this group not likely to have increased adverse outcomes)

Preeclampsia

Preeclampsia is defined as the presence of hypertension accompanied by proteinuria– In the absence of proteinuria the disease is

highly suspect when increased blood pressure with headache, blurred vision, and abdominal pain, or with abnormal laboratory tests, specifically, low platelet counts and abnormal liver enzymes.

Proteinuria

• Proteinuria is defined as the urinary excretion of 0.3 g protein or greater in a 24-hour specimen.– This will usually correlate with 30 mg/dL (“1+

dipstick”) or greater in a random urine determination with no evidence of urinary tract infection.

• because of the discrepancy between random protein determinations and24-hour urine protein in preeclampsia it is recommended that the diagnosis be based on a 24-hour urine if at all possible

Findings that increase the possibility of Eclampsia and indicate need for FU

Dx of Superimposed Preeclampsia

Eclampsia

• Occurrence in a woman with preeclampsia, of seizures that can not be attributed to other causes

Etiology

• Not fully understood

• Characterized by:– Vasospasm– Activation of the coagulation system– Perturbations in systems related to volume

and blood pressure control

Pathogenic Mechanisms

Delivery is only known cure - research has focused on placenta– failure of the spiral arteries (terminal

branches of uterine artery) to remodel– alterations in immune response at the

maternal interface– increase in inflammatory cytokines in

placenta and maternal circulation, “natural killer” cells, and neutrophil activation

Pathophysiology

Decreased blood flow Decreased renal blood flow, decreased GFR, Na

retention Tissue hypoxia Damage to organs

Pathophysiology

Decreased blood volume Decreased placental blood flow may

occur 3-4 weeks before increased BP Hypoxia Decreased nutrient delivery

Outcomes

Increased LBW and IUGR for infant There is mounting evidence that children born

to mothers whose blood pressure was elevated during pregnancy are at greater risk for elevated blood pressure during childhood and adolescence

Also long term maternal health may be affected by consequences of maternal damage to renal and CV systems.

Focus of Possible Interventions

Smooth muscle contraction Prostaglandin synthesis

Calcium

Epi studies suggest inverse relation between dietary calcium and PIH

Intraerythrocyte calcium levels and intracellular calcium ion conc. increased in women with pre-eclampsia

HO: Ca supplementation reduced serum parathyroid hormone – reduced intracellular Ca conc. in vascular smooth muscle cells and reduces response to pressure stimuli

Several RCT have found reduced risk of PIH with Ca supplementation to prevent (not treat) PIH.

Calcium, cont.

Recent meta-analysis found Ca intake of 1.5-2 g associated with sig. reductions in systolic and diastolic BP without adverse effects.

Question remains: does lowering BP have effect on pathophysiology of PIH?

Cochrane: Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems

• Nine studies met criteria

• Modest reduction in hbp and risk of preeclampsia with Ca supps.

• Effect greatest in those with high risk of htn and those with low baseline Ca intake.

Cochrane: Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems

Reviewer’s conclusions:

“Calcium supplementation appears to be beneficial for women at high risk of gestational hypertension and in communities with low dietary calcium intake.”

Omega-3 Fatty Acids In Maternal Erythrocytes and Risk of Preeclampsia (Williams et al, Epidemiology, 1995)

• Theory:– Ratio of omega 6 and omega 3 fa may

modify processes related to PIH such as platelet and leukocyte reactivity, vasodilation, and inflammatory processes.

• Study design: – small case control, n=22 cases, 40 controls– adjusted for parity and pre-pregnancy BMI

Omega-3 Fatty Acids In Maternal Erythrocytes

and Risk of Preeclampsia (Williams et al, Epidemiology, 1995)

• Results:– Women with the lowest tertile of n-3 in

erythrocytes had odds ratio of 7.6 (95% CI=1.4-40.6) for developing preeclampsia.

Other Nutrition Related Factors

Na: Pregnant women with proteinuric hypertension have lower plasma volume Na. restriction is associated with accelerated volume depletion – not recommended

Mg: Not found beneficial in prevention, unclear about benefits in treatment

Energy and Protein intake: increases not found to be useful

Weight reduction or limited gain in pregnancy: not found to be useful

Report of the Canadian Hypertension Society Consensus Conference: Non pharmacologic management and prevention of hypertensive disorders

in pregnancy (Can Med Assoc J., 1997) • A normal diet without salt restriction is

advised.

• Promising preventive interventions may include:

• Calcium supplementation (2g/d)• Fish oil supplementation and low-dose

acetylsalicylic acid therapy, particularly in women at high risk for early-onset gest. htn.

Canadian Consensus Report: Calcium

• Calcium supplementation of 2 g/d is associated with a reduction of blood pressure in gestational hypertension with or without proteinuria in both low and high risk women

• There is no apparent effect on the prevention of more severe gestational hypertension in women with established gestational hypertension.

Canadian Consensus Report: Fish Oil

• “Trials with larger samples of Canadian women are required to assess reliably the potential benefits or adverse effects of fish oil supplementation during pregnancy.”

• “Fish oil supplementation potentially prevents proteinuric gestational hypertension.”

2002 Working Group Report - Current Knowledge of Nutrients and

Hypertensive Disorders of Pregnancy

• Calcium supplements only beneficial for prevention in high risk women

• Magnesium not effective for prevention• Fish oil not effective for prevention• Studies of vitamins C and E encouraging, but

needs further work

Position StatementGestational Diabetes Mellitus

American Diabetes Association2002

Definition

• Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. The definition applies whether insulin or only diet modification is used for treatment and whether or not the condition persists after pregnancy. It does not exclude the possibility that unrecognized glucose intolerance may have antedated or begun concomitantly with the pregnancy.

Prevalence

• 7% of all pregnancies are complicated by GDM in US

• more than 200,000 cases annually in US

• prevalence may range from 1 to 14% of all pregnancies, depending on the population studied and the diagnostic tests employed.

Diagnosis

• Assess risk at first visit• If high risk (marked obesity, personal

history of GDM, glycosuria, or a strong family history of diabetes) GTT ASAP

• Women of average risk should have testing undertaken at 24–28 weeks of gestation

• Low-risk status requires no glucose testing

Low Risk Criteria

• Age <25 years

• Weight normal before pregnancy

• Member of an ethnic group with a low prevalence of GDM

• No known diabetes in first-degree relatives

• No history of abnormal glucose tolerance

• No history of poor obstetric outcome

Non GTT dx

• A fasting plasma glucose level >126 mg/dl (7.0 mmol/l) or a casual plasma glucose >200 mg/dl (11.1 mmol/l) meets the threshold for the diagnosis of diabetes, if confirmed on a subsequent day, and precludes the need for any glucose challenge

One-step Approach

• Perform a diagnostic oral glucose tolerance test (OGTT) without prior plasma or serum glucose screening

• May be cost-effective in high-risk patients or populations (e.g., some Native-American groups).

Two-step approach

• Initial screening by measuring the plasma or serum glucose concentration 1 h after a 50-g oral glucose load

• Diagnostic OGTT on that subset of women exceeding the glucose threshold value on the GCT

Table 1— Diagnosis of GDM with a 100-g oral glucose load

Two or more of the venous plasma concentrations must be met or exceeded for a positive diagnosis. The test should be done in the morning after an overnight fast of between 8 and 14 h and after at least 3 days of unrestricted diet ( 150 g carbohydrate per day) and unlimited physical activity. The subject should remain seated and should not smoke throughout the test.

mg/dl mmol/l

Fasting 95 5.3

1-h 180 10.0

2-h 155 8.6

3-h 140 7.8

Infant Concerns in GDM

• Higher risk of:• neural tube defects• birth trauma• hypocalcemia• hypomagnsemia• hyperbilirubinemia• prematurity syndromes• subsequent childhood and adolescent obesity

and risk of diabetes

Infant Concerns, cont.

– Macrosomia in infant due to high glucose levels from mother and fetal insulin response leading to increased fat deposition, associated with complications at delivery.

– Hypoglycemia of infant following delivery due to high fetal insulin levels at delivery and sudden withdrawal of maternal glucose transfer

Maternal Concerns

• Higher risk of: – hypertension– preeclampsia– urinary tract infections– cesarean section– future diabetes

Nutritional Therapy in GDM

• Goals:– prevent perinatal morbidity and mortality by

normalizing the level of glycemia– prevent ketosis– provide adequate energy and nutrients for

maternal and fetal health • dependent on maternal body composition

Monitoring

• Daily self-monitoring of blood glucose (SMBG)

• Urine glucose monitoring is not useful in GDM. Urine ketone monitoring may be useful in detecting insufficient caloric or carbohydrate intake in women treated with calorie restriction.

Monitoring

• Blood pressure and urine protein monitoring to detect hypertensive disorders.

• Increased surveillance for pregnancies at risk for fetal demise is appropriate

• Assessment for asymmetric fetal growth by ultrasonography to assess need for insulin

Nutrition Management

• All women with GDM should receive nutritional counseling, by a registered dietitian when possible

• For obese women (BMI >30 kg/m2), a 30–33% calorie restriction (to 25 kcal/kg actual weight per day) has been shown to reduce hyperglycemia and plasma triglycerides with no increase in ketonuria

• Restriction of carbohydrates to 35–40% of calories has been shown to decrease maternal glucose levels and improve maternal and fetal outcomes

Insulin

• Insulin therapy is recommended when MNT fails to maintain self-monitored glucose at the following levels: – Fasting whole blood glucose 95 mg/dl (5.3 mmol/l) – Fasting plasma glucose 105 mg/dl (5.8 mmol/l) – 1-h postprandial whole blood glucose 140 mg/dl (7.8 mmol/l) – 1-h postprandial plasma glucose 155 mg/dl (8.6 mmol/l) – 2-h postprandial whole blood glucose 120 mg/dl (6.7 mmol/l) – 2-h postprandial plasma glucose 130 mg/dl (7.2 mmol/l)

• Oral glucose-lowering agents have generally not been recommended during pregnancy

Exercise

• Programs of moderate physical exercise have been shown to lower maternal glucose concentrations in women with GDM

Long Term• Reclassification of maternal glycemic status

should be performed at least 6 weeks after delivery

• If glucose levels are normal post-partum, reassessment of glycemia should be undertaken at a minimum of 3-year intervals

• education regarding lifestyle modifications that lessen insulin resistance, including maintenance of normal body weight through MNT and physical activity.

Long Term

• Avoid medications that worsen insulin resistance (e.g., glucocorticoids, nicotinic acid)

• Seek medical attention if develop symptoms suggestive of hyperglycemia.

• Use family planning to assure optimal glycemic regulation from the start of any subsequent pregnancy

10/25/2002

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