The relation of fetal length, ponderal index and head circumference to blood pressure and the risk of hypertension in adult life

1992 ◽  
Vol 6 (1) ◽  
pp. 35-44 ◽  
Author(s):  
D.J.P. Barker ◽  
K.M. Godfrey ◽  
C. Osmond ◽  
A. Bull
PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 446-453
Author(s):  
Alistair G.S. Philip

Sixty-three term newborn infants with fetal growth retardation were evaluated within three days of birth. They were classified by length and head circumference. In group 1, both length and head circumference were less than the tenth percentile; in group 2, either length or head circumference was less than the tenth percentile; and in group 3, both length and head circumference were greater than the tenth percentile. Ponderal index (weight/length ratio), anterior fontanel size, and amount of epiphyseal ossification were also determined. Significantly lower birth weights and decreased ossification were found when groups 1 or 2 were compared separately with group 3. These differences were most marked when the weight/length ratio was less than 2.25. When the ponderal index was less than 2.0, epiphyseal ossification was usually absent (suggesting a chronic process). Epiphyseal ossification was positively correlated with birth weight and length but was unrelated to anterior fontanel size. Ossification was more often absent in males than in females. There was a negative (inverse) correlation between birth weight and anterior fontanel size. Follow-up of 32 of these infants at age 1 year showed marked individual variations, but there were significant differences in incremental linear growth between groups 1 and 3, a finding which supports results of animal studies showing that catch-up growth may be related to skeletal immaturity. Physical measurements at birth in the individual baby with fetal growth retardation do not reliably predict subsequent growth.


2018 ◽  
Vol 5 (3) ◽  
pp. 1019
Author(s):  
Mohandas Nair ◽  
Gireesh S. ◽  
Rubeena Yakoob ◽  
Cheriyan N. C.

Background: Low birth weight is the major determinant of mortality, morbidity and disability in infancy and childhood and has a long-term impact on health outcome in adult life. The objectives of this study were to study the relationship between maternal anemia and birth weight of babies and to study anthropometric measures of babies born to anemic and non-anemic mothers and to correlate the timing of anemia with birth weight of babies.Methods: Term babies born in Institute of Maternal and Child Health, Government Medical College, Kozhikode from November 2014 to October 2016 fulfilling the criteria were divided into 2 groups, cases (term babies with birth weight <2500g) and controls (term babies with weight >2500g) and studied and their maternal hemoglobin values were compared.Results: Maternal anaemia in all three trimesters was found to be more in cases compared to controls. Mean 1st trimester hemoglobin of cases was 10.68 g/dl which was significantly lower when compared to controls. Mean 2nd trimester hemoglobin of cases was 10.36 g/dl compared to 11.47 g/dl in controls. Mean 3rd trimester hemoglobin of cases was 10.42 g/dl which was also significantly lower compared to 11.32 g/dl in controls. SGA babies were also found to be more in cases, 89%, compared to 18% in controls. The difference in head circumference between two groups was not statistically significant. Mean length of babies were higher in controls compared to cases. Mothers with anemia at any time during pregnancy was found to have 4.3 times higher risk of giving birth to low birth weight babies compared to non-anemic mothersConclusion: Anemia during pregnancy is a risk factor for low birth weight and SGA, independent of the trimester. Length of babies born to anaemic mothers is also low. But it does not have a significant effect on head circumference of babies.


2008 ◽  
Vol 295 (2) ◽  
pp. R543-R549 ◽  
Author(s):  
Analía Lorena Tomat ◽  
Felipe Inserra ◽  
Luciana Veiras ◽  
María Constanza Vallone ◽  
Ana María Balaszczuk ◽  
...  

Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. After weaning, male offspring of each group of mothers were fed low or control zinc diet. Systolic blood pressure, creatinine clearance, proteinuria, renal morphology, renal apoptosis. and renal oxidative stress state were evaluated after 60 days. Zinc deficiency during pre- and postweaning growth induced an increase in systolic blood pressure and a decrease in the glomerular filtration rate associated with a reduction in the number and size of nephrons. Activation of renal apoptosis, reduction in catalase activity, glutathione peroxidase activity, and glutathione levels and increase in lipid peroxidation end products could explain these morphometric changes. Zinc deficiency through pre- and postweaning growth induced more pronounced renal alteration than postweaning zinc deficiency. These animals showed signs of renal fibrosis, proteinuria, increased renal apoptosis, and higher lipid peroxidation end products. A control diet during postweaning growth did not totally overcome renal oxidative stress damage, apoptosis, and fibrosis induced by zinc deficiency before weaning. In conclusion, zinc deficiency during a critical period of renal development and maturation could induce functional and morphological alterations that result in elevated blood pressure and renal dysfunction in adult life.


2020 ◽  
Vol 33 (8) ◽  
pp. 695-702
Author(s):  
Chukwuemeka R Nwokocha ◽  
Enitome E Bafor ◽  
Olutayo I Ajayi ◽  
Anthony B Ebeigbe

Abstract Malaria etiologies with pathophysiological similarities to hypertension currently constitute a major subject of research. The malaria-high blood pressure hypothesis is strongly supported by observations of the increasing incidence of hypertension in malaria-endemic, low- and middle-income countries with poor socioeconomic conditions, particularly in sub-Saharan African countries. Malnutrition and low birth weight with persistent symptomatic malaria presentations in pregnancy correlate strongly with the development of preeclampsia, gestational hypertension and subsequent hypertension in adult life. Evidence suggest that the link between malaria infection and high blood pressure involves interactions between malaria parasites and erythrocytes, the inflammatory process, effects of the infection during pregnancy; effects on renal and vascular functions as well as effects in sickle cell disease. Possible mechanisms which provide justification for the malaria-high blood pressure hypothesis include the following: endothelial dysfunction (reduced nitric oxide (NO) levels), impaired release of local neurotransmitters and cytokines, decrease in vascular smooth muscle cell viability and/or alterations in cellular calcium signaling leading to enhanced vascular reactivity, remodeling, and cardiomyopathies, deranged homeostasis through dehydration, elevated intracellular mediators and proinflammatory cytokine responses, possible genetic regulations, activation of the renin–angiotensin–aldosterone system mechanisms and renal derangements, severe anemia and hemolysis, renal failure, and end organ damage. Two key mediators of the malaria-high blood pressure association are: endothelial dysfunction (reduced NO) and increased angiotensin-converting enzyme activity/angiotensin II levels. Sickle cell disease is associated with protection against malaria infection and reduced blood pressure. In this review, we present the state of knowledge about the malaria-blood pressure hypothesis and suggest insights for future studies.


2015 ◽  
Vol 7 (3) ◽  
pp. 306-313 ◽  
Author(s):  
S. Sandboge ◽  
C. Osmond ◽  
E. Kajantie ◽  
J. G Eriksson

Previous studies suggest that the inverse association between birth weight and adult blood pressure amplifies with age. Rapid childhood growth has also been linked to hypertension. The objective of this study was to determine whether the association between childhood growth and adult blood pressure amplifies with age. The study comprised 574 women and 462 men from the Helsinki Birth Cohort Study who attended a clinical study in 2001–2004 and a follow-up in 2006–2008. Mean age at the clinic visits was 61.5 and 66.4 years, respectively. Blood pressure was measured at both occasions. Conditional growth models were used to assess relative weight gain and linear growth. We studied the associations between conditional growth and blood pressure as well as the presence of hypertension. Relative weight gain and linear growth between ages 2 and 11 years were inversely associated with systolic blood pressure at mean age 66.4 years, after adjustment for sex, blood pressure at mean age 61.5 years, as well as other covariates. A one s.d. increase in linear growth between 2 and 11 years was associated with an OR of 0.61 for hypertension at mean age 66.4 years. Contrary to previous studies, we have shown an inverse association between childhood growth and adult blood pressure. There were, however, no associations between childhood growth and systolic blood pressure at mean age 61.5 years indicating that the beneficial effects of a more rapid than expected childhood growth might become more apparent with increasing age.


Hypertension ◽  
2012 ◽  
Vol 60 (6) ◽  
pp. 1393-1399 ◽  
Author(s):  
Susan Cheng ◽  
Vanessa Xanthakis ◽  
Lisa M. Sullivan ◽  
Ramachandran S. Vasan

BMJ ◽  
1993 ◽  
Vol 306 (6875) ◽  
pp. 422-426 ◽  
Author(s):  
D J Barker ◽  
C Osmond ◽  
S J Simmonds ◽  
G A Wield

2012 ◽  
Vol 4 (1) ◽  
pp. 12 ◽  
Author(s):  
Oke Rina Ramayani

BACKGROUND: Uric acid is the end product of purine metabolism. Hyperuricemia can occur because of decreased excretion, increased production and/or a combination of both mechanisms. Elevation of uric acid in the blood (>5.5 mg/dL) in children is associated with the occurrence of essential hypertension. The relevance of pediatric hyperuricemia into adult hypertension have been widely studied.CONTENT: The high percentage of children and adolescents with metabolic syndrome who had an elevated concentration of uric acid could be of great concern if it were concluded that uric acid was an independent risk factor for cardiovascular disease. The minimum age that has shown blood pressure is significantly associated with adult life is unknown. There are a number of possible explanations for the phenomenon of blood pressure tracking, including hyperuricemia. Several pathophysiological mechanisms increase uric acid with cardiovascular damage through proliferation of vascular smooth muscle cells, stimulate inflammatory path, and then prothrombotic effects triggered by the activation of platelets. Once vascular lesion has appeared, then arises the sodium-sensitive hypertension, although uric acid levels have returned to normal. Persistant mechanism of sodium sensitivity is caused by renal ischemia that leads to activation of the renin-angiotensin system, renal vasoconstriction and increased reabsorption of salt. This supports better understanding of the link between childhood hyperuricemia and adulthood hypertension.SUMMARY: Childhood hyperuricemia is an independent risk factor of hypertension and is ‘linked to’ adult blood pressure.KEYWORDS: uric acid, hyperuricemia, primary hypertension, children, adult


2018 ◽  
Vol 48 (3) ◽  
pp. 954-965 ◽  
Author(s):  
Nikkil Sudharsanan

Abstract Background There are few estimates of the potential gains in adult mortality from population-level improvements in systolic blood pressure (SBP) in a major low-and-middle income country (LMIC). Using nationally representative cohort data from Indonesia—the third most populous LMIC— I estimated the gains in adult life expectancy from improving SBP control among adults ages 40 and above and assessed the benefits among richer and poorer subpopulations. Methods I used longitudinal data from 10 085 adults ages 40 and above (75 288 person-age observations) enrolled in the 2007 and 2014/15 waves of the Indonesian Family Life Survey. Next, I used Poisson-regression parametric g-formulas to directly estimate age-specific mortality rates under different blood pressure control strategies and constructed period life expectancies using the observed and counterfactual mortality rates. Results Fully controlling SBP to a population mean of under 125 mmHg was associated with a life expectancy gain at age 40 of 5.3 years [95% confidence interval (CI): 3.2, 7.4] for men and 6.0 years (95% CI: 3.6, 8.4) for women. The gains associated with blood pressure control were similar for both rich and poor subpopulations. The life expectancy gains under scenarios with imperfect blood pressure control and coverage were more modest in size and ranged between 1 and 2.5 years for a large fraction of the scenarios. Conclusions In Indonesia, elevated SBP carries a large mortality burden, though the results suggest that realistic efforts to address hypertension will likely produce more modest gains in life expectancy. Comparing improvements from different strategies and identifying the most cost-effective ways to introduce and scale up hypertension interventions is a critical focus for both research and policy.


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