Effect Of Parental History Research Articles

19-OR: Maternal Diabetes Is Associated with Adverse Diabetes Characteristics and Accelerated Onset of Complications in Youth with Type 2 Diabetes (T2D) in TODAY

Background: Prenatal exposures, including parental nutrition and diabetes (DM) status, are increasingly viewed as risk factors for future cardiometabolic health. There are currently no data on effects of parental DM on disease progression or complications in youth-onset T2D. Aims: To analyze effects of parental history of DM on glycemic outcomes and complications in the TODAY study. Methods: Participants (n=699) aged 10-14 yr with newly diagnosed T2D were enrolled at 14 U.S. centers and followed for up to 15 yr. Subjects had negative islet autoantibodies and BMI >= 85th %. Information about DM diagnosis in mothers of participants was available for 621 participants [Never (MN) =301; During pregnancy (MD) =218; After pregnancy (MA)=102)] and in biological fathers in 519 (No DM=352; Paternal DM=167). Results: Maternal, but not paternal, DM was associated with accelerated loss of glycemic control, defined as HbA1c >8% for over 6 months (p < 0.0001). Participants whose mothers had diabetes had 60% higher risk of loss of glycemic control [MD vs. MN hazard ratio (HR): 1.58 (1.28, 1.95), p < 0.0001; MA vs. MN HR: 1.57 (1.20, 2.04), p = 0.0009]. Similarly, maternal, but not paternal, diabetes was associated with glomerular hyperfiltration [MD vs. MN HR: 1.58 (1.18-2.1), p = 0.0021; MA vs. MN HR: 1.56 (1.08, 2.24), p = 0.0170;], diabetic retinopathy (MD: 50.0%; MA: 59.7%; MN: 41.8%, p=0.0439), and pulse wave velocity indices reflecting heart rate variability, including SD of normal R-R interval [(SDNN), MD: 42 ± 26 ms; MA: 41 ± 26 ms; MN: 54 ± 31 ms; p = 0.0005] and proportion of successive NN intervals greater than 50 ms [(pNN50%), MD: 14.1 ± 19.4; MA: 16.2 ± 21.5; MN: 21.9 ± 23.5; p = 0.0069], after 10 to 15 yr of follow-up. Associations were maintained after adjusting for multiple confounders. Conclusions: Maternal, but not paternal, diabetes is associated with adverse diabetes outcomes and accelerated onset of complications in their offspring with T2D in TODAY. Disclosure E. M. Isganaitis: None. M. A. Van name: None. R. Shah: None. S. Chernausek: None. R. M. Farrell: Stock/Shareholder; Self; Tandem Diabetes Care. M. Geffner: Advisory Panel; Self; Daiichi Sankyo, Novo Nordisk, Pfizer Inc., Consultant; Self; Gilead Sciences, Inc., Other Relationship; Self; Ascendis Pharma A/S, McGraw-Hill, UpToDate, Research Support; Self; Novo Nordisk. J. Keady: None. M. M. Kelsey: Other Relationship; Self; Boehringer Ingelheim (Canada) Ltd., Daiichi Sankyo, Janssen Pharmaceuticals, Inc., Merck Sharp & Dohme Corp. B. Tesfaldet: None. J. B. Tryggestad: None. Funding National Institute of Diabetes and Digestive and Kidney Diseases (U01DK61212, U01DK61230, U01DK61239, U01DK61242, U01DK61254)

Parental and child factors associated with inhalant and food allergy in a population-based prospective cohort study: the Generation R Study

The prevalence of allergic diseases in children is markedly increasing to epidemic proportions. The aim of this study is to describe the presence and examine associated parental and child characteristics of allergic sensitization and physician-diagnosed allergy in Dutch children at age 10 years. This study among 5471 children was performed in a population-based prospective cohort from fetal life onwards. Allergic sensitization was measured by skin prick tests. Physician-diagnosed allergy and parental and child characteristics were collected by questionnaires. In children aged 10 years, inhalant and food allergic sensitization was present in 32.2% and 7.1%, and physician-diagnosed inhalant and food allergy in 12.4% and 2.3%. Maternal and paternal history of allergy, eczema or asthma was associated with increased risks of physician-diagnosed inhalant allergy (aOR (95% CI) 1.44 (1.23–1.70) and 1.59 (1.30–1.94), respectively), but not with food allergy. Asthma and eczema ever at age 10 years were associated with increased risks of physician-diagnosed inhalant allergy (4.60 (3.55–5.96) and 2.42 (1.94–3.03), respectively). Eczema ever at age 10 years was associated with an increased risk of physician-diagnosed food allergy (5.78, 3.04–9.52), with the highest risk of cashew (7.36, 3.20–16.94) and peanut (5.58, 3.08–10.10) food allergy.Conclusions: We found strong effects of parental history of allergy, eczema or asthma on the presence of physician-diagnosed inhalant allergy in children at age 10 years. Eczema ever at age 10 years was a strong risk factor for the development of physician-diagnosed inhalant and food allergy.What is Known:• The prevalence of allergic diseases in children has markedly increased.• Early-life influences are critically important in the development of allergic diseases.What is New:• Maternal and paternal history of allergy, eczema or asthma is associated with increased risks of physician-diagnosed inhalant allergy but not with food allergy.• Eczema ever at age 10 years is associated with an increased risk of physician-diagnosed food allergy, with the highest risk for cashew and peanut food allergy.

Prospective investigation of psychological and affective pathways from childhood trauma to psychosis-like experiences in a UK birth cohort

with childhood maltreatment and sex on the risk for alcohol dependence. Using national data with extensive measures, we address these issues: (1) Do childhood sexual abuse, physical abuse, emotional abuse, physical neglect, and emotional neglect predict adult lifetime DSM-IV alcohol dependence, controlling for co-occurring maltreatments and other childhood traumas? (2) Are these relationships synergistically modified by parental alcoholism history? Method: Face-to-face interviews of 27 712 adult participants in the National Epidemiological Survey on Alcohol and Related Conditions were conducted. Results: Childhood physical, emotional, and sexual abuse, and physical neglect were associated with alcohol dependence (P b .001), controlling for demographics, co-occurring maltreatments, and other childhood trauma. A significant (P b .05) synergistic relationship between parental history and physical abuse was found in the entire sample (AP, 0.21), and between parental history and sexual abuse (AP, 0.31) and emotional neglect (AP, 0.26) in women. In other words, the risk of alcohol dependence given both parental history and the maltreatment was higher than what would be expected given the additive effect of each alone. Conclusions: Childhood maltreatments independently increased the risk of alcohol dependence, underscoring the importance of early identification and prevention and suggesting the need to develop and incorporate alcohol preventative components, such as cognitive restructuring, in maltreatment interventions. Importantly, the effect of physical abuse on alcohol dependence may depend on genetic vulnerability as suggested by the effect of parental history of alcoholism, whereas the effects of sexual abuse and emotional neglect may depend on this vulnerability among women. Thus, maltreatment may have a long-term negative impact, which may depend on genetic vulnerability and sex. Findings can be used to guide genetic studies and intervention development.

Cardiovascular haemodynamic response to repeated mental stress in normotensive subjects at genetic risk of hypertension: evidence of enhanced reactivity, blunted adaptation, and delayed recovery.

To identify unique cardiovascular responses to stressors in a population at genetic risk of hypertension, we studied haemodynamic responses in initial reactivity to, subsequent adaptation to, and final recovery from repeated active mental stress in young, normotensive individuals stratified by hypertension parental history (PH). Two groups (n=21/group) of normotensive white males underwent stress testing. One group (N+PH) had a hypertensive parent, while the other group (N-PH) did not. Cardiovascular response was measured before, during, and after repeated serial-subtraction math. Initial reactivity was measured as the difference between baseline and initial stress response, subsequent adaptation as the difference in response to repeated trials, and final recovery was assessed by the difference between baseline and postbaseline levels. The influence of PH on reactivity, adaptation, and recovery was assessed by repeated measures ANOVA for stroke volume, cardiac output, pre-ejection period, total peripheral resistance, mean successive heartbeat time difference, blood pressure, and heart rate. Multivariate analysis of variance (MANOVA) determined the effect of PH on overall reactivity, adaptation, and recovery. As compared to the N-PH group, initial reactivity was higher in the N+PH group for cardiac index (P<0.05) and pre-ejection period (P<0.05). Subsequent adaptation in the N+PH group was significantly slower for pre-ejection period (P=0.03). Finally, the N+PH group showed delayed recovery in heart rate (P=0.03), diastolic blood pressure (P<0.05), and pre-ejection period (P=0.007). In conclusion, the heightened reactivity, lack of adaptation, and delayed recovery occur in the sympathetic system of normotensive subjects at genetic risk of hypertension, specifically in beta-adrenergic responses (pre-ejection period). The parasympathetic response (mean successive heartbeat time difference) was not different. Increased cardiac output reactivity in the N+PH group (P<0.05) thus precedes any difference in blood pressure reactivity (P<0.99). Delayed recovery of diastolic blood pressure is also found in the N+PH group (P<0.05), which suggests lower baroreceptor sensitivity. Since delayed recovery in heart rate (P=0.03), and diastolic blood pressure (P<0.05) occur in N+PH subjects even before the corresponding changes in reactivity (P>0.10) or adaptation (P>0.07) are seen, these recovery impairments may be among the earliest precursors to the development of essential hypertension in this population. Finally, PH group haemodynamic differences suggest that these traits (reactivity, adaptation, and recovery) may constitute early 'intermediate' phenotypes in the pathogenesis of hypertension.

Course of DSM‐IV Alcohol Dependence in a Community Sample: Effects of Parental History and Binge Drinking

The role of positive family history in the etiology of alcohol dependence has been demonstrated repeatedly but little is known about the effect of this risk factor on the chronicity of alcohol dependence once it has begun. We studied the effects of parental and sibling history in conjunction with frequency of binge drinking in a sample of 169 community residents who met criteria for DSM-IV alcohol dependence at the baseline interview. Subjects were re-interviewed approximately 1 year later and the status of their alcohol-dependence disorders (remitted or chronic) was determined. Parental history of alcoholism was significantly related to chronicity of alcohol dependence, as was frequency of binge drinking. Failure to find an effect for family history on chronicity would have suggested that the effect was transient, perhaps interacting with time-limited environmental vulnerability. The finding of a positive relationship between family history and chronicity suggests that the relationship between familial/ genetic background and alcohol dependence is stable.

Course of DSM-IV Alcohol Dependence in a Community Sample: Effects of Parental History and Binge Drinking

Course of DSM-IV Alcohol Dependence in a Community Sample: Effects of Parental History and Binge Drinking

Effects of parental history of hypertension and urbanization on blood pressure in zimbabweans

The increasing prevalence of essential hypertension is a growing public health concern for Zimbabwe and other African countries. Two important risk factors for hypertension are urbanization and parental history of hypertension. The relations among parental history of hypertension, urbanization, and blood pressures (BPs) are poorly understood. The objective of this study is to clarify these relations in a population of urbanized, African, young adults. The relation between parental history of hypertension and urbanization on resting BP's and Bp responses to a mental arithmetic stressor was examined in a group of normotensive, Black medical students with (n = 36) and without (n = 34) a parental history of high BP, and with (n = 49) and without (n = 19) a parental history of urbanization. Results indicate that those with a positive parental history counterparts. Further, those with parents residing in urban areas had higher resting SBPs than those with parents residing in rural areas. However, no reactivity differences were apparent between the urban and rural parent groups. These data suggest that although parental history for hypertension influences both resting and reactivity BP's parental history of urbanization may influence only resting BP.

Parental history of alcoholism and probability of marriage.

Personal interview data for 16,795 U.S. adults 18-39 years of age were analyzed to assess the effect of positive parental history of alcoholism on the probability of ever having been married. The data were collected as part of the 1988 National Health Interview Survey. The effects of parental history were estimated using logistic regression models that adjusted for age, race, gender, and respondent history of alcohol problems. Nonblack adults who lived with one or more alcoholic parents when growing up were 50% more likely ever to have been married than those with no parental history. The effect was of the same magnitude regardless of whether the alcoholic parent was the mother or the father, but was larger if both parents were reported to be alcoholics. Among blacks, positive parental history of alcoholism did not affect the odds of marriage. The greater likelihood of early marriage among children of alcoholics may help explain their excess risk of marital disruption.