Onset Of Disease In Adulthood Research Articles

Novel Filamin C Myofibrillar Myopathy Variants Cause Different Pathomechanisms and Alterations in Protein Quality Systems.

Myofibrillar myopathies (MFM) are a group of chronic muscle diseases pathophysiologically characterized by accumulation of protein aggregates and structural failure of muscle fibers. A subtype of MFM is caused by heterozygous mutations in the filamin C (FLNC) gene, exhibiting progressive muscle weakness, muscle structural alterations and intracellular protein accumulations. Here, we characterize in depth the pathogenicity of two novel truncating FLNc variants (p.Q1662X and p.Y2704X) and assess their distinct effect on FLNc stability and distribution as well as their impact on protein quality system (PQS) pathways. Both variants cause a slowly progressive myopathy with disease onset in adulthood, chronic myopathic alterations in muscle biopsy including the presence of intracellular protein aggregates. Our analyses revealed that p.Q1662X results in FLNc haploinsufficiency and p.Y2704X in a dominant-negative FLNc accumulation. Moreover, both protein-truncating variants cause different PQS alterations: p.Q1662X leads to an increase in expression of several genes involved in the ubiquitin-proteasome system (UPS) and the chaperone-assisted selective autophagy (CASA) system, whereas p.Y2704X results in increased abundance of proteins involved in UPS activation and autophagic buildup. We conclude that truncating FLNC variants might have different pathogenetic consequences and impair PQS function by diverse mechanisms and to varying extents. Further studies on a larger number of patients are necessary to confirm our observations.

Improving Diagnosis and Clinical Management of Acquired Systemic Autoinflammatory Diseases.

Systemic autoinflammatory diseases (SAID) are conditions caused by dysregulation or disturbance of the innate immune system, with neutrophils and macrophages the main effector cells. Although there are now more than 40 distinct, genetically defined SAIDs, the genetic/molecular diagnosis remains unknown for a significant proportion of patients with the disease onset in adulthood. This review focuses on new developments related to acquired/late onset SAID, including phenocopies of monogenic disorders, Schnitzler’s syndrome, Adult onset Still’s disease, VEXAS syndrome, and autoinflammatory complications associated with myelodysplastic syndrome.

Gene-based treatment in spinal muscular atrophy

The 5q-associated spinal muscular atrophy (SMA) affects ~80-120 newborns annually. The disease is characterized by progressive paresis involving the bulbar and respiratory musculatures. The phenotypes are very heterogeneous ranging from severe courses with early death in the first years of life to loss of gait in older age. There are now an increasing number of causally targeted therapies available that can either directly interfere with the transcription of the gene causing the disease or replace the homozygous loss of the SMN1 gene. This work aims to elucidate the current state of therapy in different groups of patients with SMA. Presentation of clinical trials and basic studies with afocus on patients with disease onset in adulthood. The clinical studies all show improvement or stabilization of motor function; however, in individual cases, the burden of the therapy for severely immobilized patients must be considered in addition to the efficacy in the treatment decision. Even if the drugs show agood safety profile, observations on the long-term efficacy and safety of the new substance classes are still lacking. The study landscape shows a good efficacy of the currently approved therapies across all degrees of severity and age groups. Due to the lack of comparative studies, the decision on the appropriate therapy should therefore be made according to an individual risk-benefit assessment.

Juvenile-Onset Huntington Disease Pathophysiology and Neurodevelopment: A Review.

ABSTRACTHuntington disease is an autosomal dominant inherited brain disorder that typically becomes manifest in adulthood. Juvenile‐onset Huntington disease refers to approximately 5% of patients with symptom onset before the age of 21 years. The causal factor is a pathologically expanded CAG repeat in the Huntingtin gene. Age at onset is inversely correlated with CAG repeat length. Juvenile‐onset patients have distinct symptoms and signs with more severe pathology of involved brain structures in comparison with disease onset in adulthood. The aim of this review is to compare clinical and pathological features in juvenile‐ and adult‐onset Huntington disease and to explore which processes potentially contribute to the observed differences. A specific focus is placed on molecular mechanisms of mutant huntingtin in early neurodevelopment and the interaction of a neurodegenerative disease and postnatal brain maturation. The importance of a better understanding of pathophysiological differences between juvenile‐ and adult‐onset Huntington disease lies in development and implementation of new therapeutic strategies. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

Ураження нирок при геморагічному васкуліті Шенлейна — Геноха, що почався в дитячому і дорослому віці

Метою роботи стала порівняльна оцінка клініко-лабораторних і морфологічних проявів ниркової патології при геморагічному васкуліті Шенлейна — Геноха, що почався в дитячому та дорослому віці. Ураження нирок відзначено у 71 % від числа хворих (незалежно від віку пацієнтів у дебюті хвороби нефропатія зустрічалася з однаковою частотою), серед яких нефротичний синдром сформувався у 4 % випадків, хронічна хвороба нирок II, III, IV i V стадій — у 28 % спостережень (співвідношення 10 : 5 : 1 : 1), причому, за даними нефробіоптатів, у пацієнтів із трансформацією хвороби з ювенільної виявилися меншими ступені ураження ниркових артеріол, клубочків, канальців й строми, нижчими темпи прогресування ниркової недостатності, рівні артеріального тиску та периферійного судинного опору, а в цілому дебютний вік хворих впливає на подальшу частоту IV, V і VI класів генохівського гломерулонефриту, визначає рівень лімфогістіоцитарної інфільтрації судинних стінок й депозицій імуноглобулінів в клубочках та судинах.

Systemic lupus erythematosus in children and adults: A retrospective study in Brazilian patients.

Systemic lupus erythematosus (SLE) may have a different serological and clinical profile according to age of disease onset. To compare clinical presentation and serological data from patients with SLE onset in childhood (cSLE) with disease onset in adulthood (aSLE) in a sample of Brazilian patients. Retrospective study of 614 SLE patients from a single Rheumatology Unit from Brazil: 77 (12.5%) cSLE and 537 (87.4%) aSLE. Clinical and serological data were obtained from the charts. Comparisons of cSLE with aSLE in general and according to patient's gender were made. The comparison of whole sample showed that children had more malar rash (p = 0.04), seizures (p < 0.0001), psychosis (p = 0.02), glomerulonephritis (p = 0.001), anti-dsDNA (p = 0.008), anticardiolipin IgM (p = 0.04) but less discoid lesions (p = 0.01), anti-Ro (p < 0.0001) and anti-La antibodies (p = 0.007). When only the male sample was compared, no differences in glomerulonephritis and anti-dsDNA frequencies were found. Children had a higher frequency of severe manifestations (glomerulonephritis and central nervous system) than adults. The difference in glomerulonephritis occurrence disappeared when only males were compared.

The effects of assisted reproduction technologies on metabolic health and disease†.

The increasing prevalence of metabolic diseases places a substantial burden on human health throughout the world. It is believed that predisposition to metabolic disease starts early in life, a period of great susceptibility to epigenetic reprogramming due to environmental insults. Assisted reproductive technologies (ART), i.e., treatments for infertility, may affect embryo development, resulting in multiple adverse health outcomes in postnatal life. The most frequently observed alteration in ART pregnancies is impaired placental nutrient transfer. Moreover, consequent intrauterine growth restriction and low birth weight followed by catch-up growth can all predict future obesity, insulin resistance, and chronic metabolic diseases. In this review, we have focused on evidence of adverse metabolic alterations associated with ART, which can contribute to the development of chronic adult-onset diseases, such as metabolic syndrome, type 2 diabetes, and cardiovascular disease. Due to high phenotypic plasticity, ART pregnancies can produce both offspring with adverse health outcomes, as well as healthy individuals. We further discuss the sex-specific and age-dependent metabolic alterations reflected in ART offspring, and how the degree of interference of a given ART procedure (from mild to more severe manipulation of the egg) affects the occurrence and degree of offspring alterations. Over the last few years, studies have reported signs of cardiometabolic alterations in ART offspring that are detectable at a young age but that do not appear to constitute a high risk of disease and morbidity per se. These abnormal phenotypes could be early indicators of the development of chronic diseases, including metabolic syndrome, in adulthood. The early detection of metabolic alterations could contribute to preventing the onset of disease in adulthood. Such early interventions may counteract the risk factors and improve the long-term health of the individual.

Every cockroach is beautilful to the eyes of his mother? Parent’s perception of child’s BMI

Abstract Background Childhood obesity is becoming a social health problem in the western world and an important goal is to analyze and correct risk factors. Part of the problem could be determined by a different perception of the weight. We aim to determine the association between children's BMI and the parent's perception of their Health Status. Methods In October 2019 we conduced a cross sectional study in which a questionaire was administrated to the parents of primary and secondary schools children in South-East Tuscany, Italy. Eating habits, lifestyle and biometric data were collected from children and their parents. 4324 persons were included. We used Stata for descriptive and inferential analysis. Cohen's Kappa was used to find the correlation between variables. Results Analysis was carried out on 1421 complete questionnaires. We found that most of parents have a wrong perception of weight's children. 88.3% of parents who have obese children belive that his child is normal weight or only “a little overweight” and only 11.7% have a perception of their child's obesity. 67.6% of parents who have overweight children, belive that their child is normal weight. While among underweight children, 74.3% of parents belive that their child is normal weight. Cohen's kappa show poor agreement between real and perceived BMI (K = 0.26; p = 0.0001). Conclusions Our results show, among the overweight children, there is a misperception in the weight of the child by the parents, uniformly with the data present in the literature. Acquisition of healty behavior during childhood is extremely important for the state of health in adulthood and for avoiding the onset of associated diseases. Therefore, food education becomes a crucial objective for the future of our country: an essential goal is to create prevention programs addressed to children and parents to increase consciousness of the correct weight and the diseases that can result from bad nutrition. Key messages Many parents have a misperception of the weight of their children. It is crucial to educate parents to control their children's weight to avoid the onset of metabolic diseases. Increase consciousness in children and parents of the correct weight should become extremely important to avoid the onset of disease in adulthood.

Differences of In-School Moderate to Vigorous Physical Activity among Fourth Grade Urban Youth

ABSTRACT There is a clear and well-documented link between physical activity (PA) and health. However, many youth do not participate in the recommended levels of PA in order to gain health benefits. Given the health disparities among urban youth, specifically among African American youth, and mindful of the lack of data for Arab Americans, the purpose of this study was to determine if in-school PA levels differed between European American, African American and Arab American urban elementary school children. The pilot study consisted of a sample that included 266 (107 males; M age = 9.36) fourth grade students whose in-school PA data was collected using an ActiGraph GT3X+ for six school days. Results showed male students were more active than female students, while African American and European American students were more physically active than their Arab American counterparts. This study highlights the difference of in-school PA levels of urban-minority students and discusses how urban schools should be intervening with Comprehensive School Physical Activity Programs designed for urban youth in order to prevent the onset of disease in adulthood. Health and physical educators should consider creating programs that are culturally relevant in order to increase PA levels of all youth.

Herpesvirus trigger accelerates neuroinflammation in a nonhuman primate model of multiple sclerosis

Pathogens, particularly human herpesviruses (HHVs), are implicated as triggers of disease onset/progression in multiple sclerosis (MS) and other neuroinflammatory disorders. However, the time between viral acquisition in childhood and disease onset in adulthood complicates the study of this association. Using nonhuman primates, we demonstrate that intranasal inoculations with HHV-6A and HHV-6B accelerate an MS-like neuroinflammatory disease, experimental autoimmune encephalomyelitis (EAE). Although animals inoculated intranasally with HHV-6 (virus/EAE marmosets) were asymptomatic, they exhibited significantly accelerated clinical EAE compared with control animals. Expansion of a proinflammatory CD8 subset correlated with post-EAE survival in virus/EAE marmosets, suggesting that a peripheral (viral?) antigen-driven expansion may have occurred post-EAE induction. HHV-6 viral antigen in virus/EAE marmosets was markedly elevated and concentrated in brain lesions, similar to previously reported localizations of HHV-6 in MS brain lesions. Collectively, we demonstrate that asymptomatic intranasal viral acquisition accelerates subsequent neuroinflammation in a nonhuman primate model of MS.

Two approaches reveal a new paradigm of \u2018switchable or genetics-influenced allele-specific DNA methylation\u2019 with potential in human disease

Imprinted genes are vulnerable to environmental influences during early embryonic development, thereby contributing to the onset of disease in adulthood. Monoallelic methylation at several germline imprints has been reported as DNMT1-dependent. However, which of these two epigenetic attributes, DNMT1-dependence or allelic methylation, renders imprinted genes susceptible to environmental stressors has not been determined. Herein, we developed a new approach, referred to as NORED, to identify 2468 DNMT1-dependent DNA methylation patterns in the mouse genome. We further developed an algorithm based on a genetic variation-independent approach (referred to as MethylMosaic) to detect 2487 regions with bimodal methylation patterns. Two approaches identified 207 regions, including known imprinted germline allele-specific methylation patterns (ASMs), that were both NORED and MethylMosaic regions. Examination of methylation in four independent mouse embryonic stem cell lines shows that two regions identified by both NORED and MethylMosaic (Hcn2 and Park7) did not display parent-of-origin-dependent allelic methylation. In these four F1 hybrid cell lines, genetic variation in Cast allele at Hcn2 locus introduces a transcription factor binding site for MTF-1 that may predispose Cast allelic hypomethylation in a reciprocal cross with either C57 or 129 strains. In contrast, each allele of Hcn2 ASM in J1 inbred cell line and Park7 ASM in four F1 hybrid cell lines seems to exhibit similar propensity to be either hypo- or hypermethylated, suggesting a ‘random, switchable’ ASM. Together with published results, our data on ASMs prompted us to propose a hypothesis of regional ‘autosomal chromosome inactivation (ACI)’ that may control a subset of autosomal genes. Therefore, our results open a new avenue to understand monoallelic methylation and provide a rich resource of candidate genes to examine in environmental and nutritional exposure models.

Langerhans Cell Histiocytosis with Atypical Intervertebral Disc and Sacroiliac Joint Involvement Mimicking Osteoarticular Tuberculosis in an Adult.

Langerhans cell histiocytosis (LCH), typically found in children, is a rare single or multisystem disorder with a wide range of clinical and radiological manifestations. Unusual presentations of LCH are occasionally encountered and it may be difficult to distinguish LCH from an infection or a benign or malignant tumor. A 35-year-old female presented with pain in her back and left buttock, malaise, and weight loss, with a duration of several months. Her laboratory test results were within the normal ranges except for the levels of acute phase reactants, which were elevated. Magnetic resonance imaging and computed tomography revealed a unilateral destructive sacroiliac lesion, and multiple vertebral lesions with adjacent discal involvement and extensive soft tissue extensions. She was initially misdiagnosed with multifocal osteoarticular tuberculosis. An open biopsy and joint curettage was performed. Histopathological examination showed that she had LCH. To the best of our knowledge, this is the first case of LCH associated with a destructive unilateral sacroiliac lesion, discal involvement, and involvement of the adjacent vertebrae, in an adult patient; the LCH mimicked osteoarticular tuberculosis. Disease onset in adulthood is rare, and this can potentially delay diagnosis. Familiarity with the imaging features of unusual LCH manifestations is necessary to ensure accurate diagnosis and appropriate treatment.

Protective effect of early prenatal stress on the induction of asthma in adult mice: Sex-specific differences

Adversities faced during the prenatal period can be related to the onset of diseases in adulthood. However, little is known about the effects on the respiratory system. This study aimed to evaluate the effects of prenatal stress in two different time-points during pregnancy on pulmonary function and on the inflammatory profile of mice exposed to an asthma model. Male and female BALB/c mice were divided into 3 groups: control (CON), prenatal stress from the second week of pregnancy (PNS1) and prenatal stress on the last week of pregnancy (PNS2). Both PNS1 and PNS2 pregnant females were submitted to restraint stress. As adults, fear/anxiety behaviors were assessed, and animals were subjected to an asthma model induced by ovalbumin. Pulmonary function, inflammatory parameters in bronchoalveolar lavage (BAL) and histology were evaluated. There was a significant decrease in the number of entries and time spent in the central quadrant on the open field test for the PNS1 animals. Females (PNS1) showed improved pulmonary function (airway resistance, tissue damping and pulmonary elastance), significant increase in the percentage of neutrophils and lymphocytes and a decrease in eosinophils when compared to controls. There was a significant decrease in inflammatory cytokines in BAL of both males (IL-5 and IL-13) and females (IL-4, IL-5 and IL-13) from PNS1 and PNS2 when compared to the CON group. Prenatal stress starting from the beginning of pregnancy reduces the impact of asthma development in adult female mice, showing an improved pulmonary function and a lower inflammatory response in the lungs.

45. Clinical and electrophysiological non-SPG4 spectrum of HSP

SPG clinical spectrum of “pure” and “complicated” HSP is wide, including visual pathways and retina involvement, motor neuron and extrapyramidal syndromes. Two females (sporadic cases) and one male patient have been studied. (1) Disease onset in early childhood: mild mental retardation with learning disability, skeletal deformity and speech impairment have been related to complicated delivery with cyanosis and hypoxia with need to ICU support. The occurrence of progressive spastic paraparesis addressed to diagnostic evaluation by MRI and neurophysiological investigation. Abnormalities of MEPs, mild polyneuropathy support the hypothesis of AR-HSP. DNA sample analysis confirmed mutations in SPG11 gene. Gait was still possible. (2) Disease onset in early childhood: progressive muscle weakness and distal atrophy; at 24 years old age, she was wheelchair-bound. Neurophysiological assessment pointed out a peripheral motor neuron damage and abnormalities of MEPs; delayed visual evoked potentials with a normal elecroretinogram (both to luminance and contrast variations) was suggestive for the occurrence of optic neuropathy without retina involvement. Direct sequencing of SPG11 identified 2 heterozygous mutations. (3) Disease onset in adulthood: progressive paraparesis and pain in the lower limbs with pyramidal signs. There was a family history of paraparesis. Spine MRI was normal. Neurophysiological assessment showed normal peripheral motor conduction, normal VEPs and delayed MEPs. Direct sequencing of SPG 7 identified heterozygous mutation missense and splicing. Diverse clinical features have been reported with SPG mutations, including diversity in presentation and clinical course: comprehensive electrophysiological testing disclosed a more widespread affection of nervous system and could reflect different underlying pathomechanisms of HSP.

Dietary supplementation with polyunsaturated fatty acid during pregnancy modulates DNA methylation at IGF2/H19 imprinted genes and growth of infants (1120.3)

Epigenetic regulations of imprinted genes are highly plausible explanation for the associations of dietary exposures in early life and the onset of diseases in adulthood. We tested whether prenatal dietary supplementation with docosahexaenoic acid (DHA) during pregnancy may modulate epigenetic states at birth in a randomized intervention trial among Mexican pregnant women supplemented daily with 400 mg of DHA or a placebo from 18 to 22 week of gestation to parturition. We applied quantitative profiling of DNA methylation states at IGF2 promoter 3 (IGF2 P3), IGF2 DMR and H19 DMR in cord blood mononuclear cells of the DHA‐supplemented group (n=131) and the control group (n=130).There were no significant differences between the DHA and the control groups for DNA methylation levels at imprinted genes; however in stratified analyses, we observed a positive association between DNA methylation levels and maternal BMI; IGF2 DMR methylation was higher in the DHA than the control groups in infants from overweight mother (p=0.03) and H19 DMR, methylation levels were significantly lower in the DHA than control groups in infants from normal weight mothers (p=0.01). Prenatal DHA supplementation modulated IGF2/H19 methylation in infants and methylation levels at IGF2/H19 imprinted regions were related with maternal BMI. Epigenetic mechanism may be modulated by DHA with potential impacts on growth and development of children.Grant Funding Source: NIH‐NICHHD (RO1HD058818), NIH (RO1HDO43099) and CONACYT Mexico (SALUD‐2008‐01‐87121)

Burden of disease in adolescents and young people in Spain

ObjectiveThis article analyses the burden of disease in adolescents and young people in Spain in 2008. Materials and methodsA cross-sectional population-based study. We estimated disability-adjusted life years (DALYs) by sex and cause for subjects aged 15-29 years. Data sources were used: (1) National death records by age, sex and cause; (2) population data (both in July 2008); and (3) estimates of the disability pattern for European countries with very low mortality. ResultsIn 2008, adolescents and young people lost 786,479 DALYs (414,346 in males). Non-communicable diseases generated 661,282 DALYs (84% of the total). The main specific causes of disease burden were: unipolar depression (16% of DALYs), alcohol use disorders (11%), migraine (9%), bipolar disorder (7%), schizophrenia (6%), road traffic accidents (5%) and drug addiction disorders (5%). ConclusionsThe burden of disease expressed in DALYs can define the loss of health in adolescents and young people. At these ages, health promotion and protection are essential to prevent the onset of disease in adulthood.

Carga de enfermedad en adolescentes y jóvenes en España

This article analyses the burden of disease in adolescents and young people in Spain in 2008.A cross-sectional population-based study. We estimated disability-adjusted life years (DALYs) by sex and cause for subjects aged 15-29 years. Data sources were used: 1) National death records by age, sex and cause; 2) Population data (both in July 2008); and 3) Estimates of the disability pattern for European countries with very low mortality.In 2008, adolescents and young people lost 786,479 DALYs (414,346 in males). Non-communicable diseases generated 661,282 DALYs (84% of the total). The main specific causes of disease burden were: unipolar depression (16% of DALYs), alcohol use disorders (11%), migraine (9%), bipolar disorder (7%), schizophrenia (6%), road traffic accidents (5%) and drug addiction disorders (5%).The burden of disease expressed in DALYs can define the loss of health in adolescents and young people. At these ages, health promotion and protection are essential to prevent the onset of disease in adulthood.

Sleep-related eating disorder versus sleepwalking: A controlled study

Sleep-related eating disorder (SRED) may have some common clinical features with sleepwalking and with eating behavior disorders. The objective of this study was to compare clinical, sleep, and eating behavior measures in patients with SRED vs. sleepwalkers and controls. Overall, 15 patients with SRED, 21 sleepwalkers, and 20 age- and sex-matched healthy volunteers underwent interviews, completed sleep, anxiety, depression, and eating behavior scales, and had a night-time videopolysomnography. Patients with SRED were mainly women, had disease onset in adulthood, suffered nightly episodes and insomnia, and had more frequent eating problems in childhood and higher current anorexia scores than sleepwalkers and controls. Unlike controls, they shared several commonalities with sleepwalkers, including a high frequency (66%) of past or current sleepwalking, a similar timing of parasomnia episodes during the first half of the night, numerous arousals from stage N3, and a similarly altered level of daytime sleepiness and anxiety, but higher awareness during parasomnia episodes. Conversely, only 10% of sleepwalkers ate during their sleepwalking episodes. On videopolysomnography, the eating episodes occurred mostly within 1min after awakening from stage N2 (n=9) or stage N3 (n=6). The frequencies of restless legs syndrome, periodic leg movements, and sleep apnea were similar across the three groups. Patients with SRED share several clinical commonalities with sleepwalkers (although their level of awareness is higher) plus former or current eating behavior problems. It suggests that they have specialized a former sleepwalking behavior toward sleep-related eating because they are more vulnerable to eating behavior problems during the daytime.

Early Life Origins of Adult Disease and Maternal Smoking During Pregnancy

Johnson and Shoeni examined the relation between low birth weight (LBW) and childhood family socioeconomic disadvantage and disease onset in adulthood.1 They report that LBW independently predicted asthma, hypertension, diabetes, and cardiovascular diseases by age 50 years. Disease prevalence was influenced also by childhood socioeconomic (SES) status. They conclude that these findings are consistent with the fetal origins hypothesis, which posits that adverse in utero influences increases the risk of disease later in life. We would like to stress the likely mediating effect of maternal smoking during pregnancy. In the study by Johnson and Shoeni, the smoking variable, parental smoking, increased disease risk in adulthood in univariate but not in multivariate analyses probably because it lacks specification (i.e., it did not distinguish which parent was a smoker and whether the mother smoked or not during her pregnancy). Maternal smoking during pregnancy is known to be associated with negative prenatal and birth consequences and LBW.2,3 Maternal smoking during pregnancy is an independent risk factor for obesity,4–6 type 2 diabetes mellitus,4 high blood pressure,7 and smoking,2 all known risk factors for cardiovascular disorders. Intrauterine exposure to maternal smoking is also associated with asthma even in offspring of nonsmoking mothers but who themselves were exposed in utero to maternal smoking,8 suggesting that smoking may induce genotoxicity. Moreover, maternal smoking during pregnancy dose-dependently increases the likelihood of psychiatric disorders and all cause mortality up to age 20 years.9 In addition, smoking, and in particular smoking during pregnancy, is known to be associated with low SES.10 Maternal smoking during pregnancy is the most important modifiable adverse fetal exposure risk.3 It is likely to mediate a significant part of the relation between LBW and disease onset in adulthood that was reported by Johnson and Schoeni.1 Full eradication of smoking among pregnant women may reduce the onset of several diseases in the next generation.

Early-Life Origins of Adult Disease: National Longitudinal Population-Based Study of the United States

We examined the relation between low birth weight and childhood family and neighborhood socioeconomic disadvantage and disease onset in adulthood. Using US nationally representative longitudinal data, we estimated hazard models of the onset of asthma, hypertension, diabetes, and stroke, heart attack, or heart disease. The sample contained 4387 children who were members of the Panel Study of Income Dynamics in 1968; they were followed up to 2007, when they were aged 39 to 56 years. Our research design included sibling comparisons of disease onset among siblings with different birth weights. The odds ratios of having asthma, hypertension, diabetes, and stroke, heart attack, or heart disease by age 50 years for low-birth weight babies vs others were 1.64 (P < .01), 1.51 (P < .01), 2.09 (P < .01), and 2.16 (P < .01), respectively. Adult disease prevalence differed substantially by childhood socioeconomic status (SES). After accounting for childhood socioeconomic factors, we found a substantial hazard ratio of disease onset associated with low birth weight, which persisted for sibling comparisons. Childhood SES is strongly associated with the onset of chronic disease in adulthood. Low birth weight plays an important role in disease onset; this relation persists after an array of childhood socioeconomic factors is accounted for.