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At least 19 recordsLinked to original sources
PubMed2003

A dual long-term effect of breastfeeding on atopy in relation to heredity in children at 4 years of age.

BACKGROUND: The long-term effect of early feeding on atopic sensitization is still unsolved. The aim of this study was to evaluate the long-term effect of breastfeeding on atopy in groups of 4-year-old children stratified by atopic heredity. METHODS: We collected four groups of 4-year-old children from a birth cohort: two groups with differing backgrounds of atopic heredity, all exclusively breast-fed for at least 3 months; and two groups with differing atopic heredity, but all fed with cow's milk-based formula during their first weeks. The data were collected with a questionnaire, skin prick testing, and measurement of serum total and allergen-specific IgE levels. RESULTS: Breastfeeding significantly decreased the risk of allergic rhino-conjunctivitis [odds ratio (OR) 0.41, 95% confidence interval (CI) 0.18-0.95] and sensitization to furred pets, as measured by skin prick results, in children with atopic heredity, whereas in children without atopic heredity, breastfeeding was related to an increased risk of symptomatic atopy (OR 2.57, 95% CI 1.16-5.70), and high serum IgE values. A significant interaction was found between heredity and breastfeeding. CONCLUSIONS: The long-term effect of breastfeeding was dual: in children with atopic heredity, breastfeeding protected against atopy, whereas in children without atopic heredity, it increased the risk of atopy.

Animals↗
PubMed1999

Heredity for hypertension influences intra-uterine growth and the relation between fetal growth and adult blood pressure.

OBJECTIVE: To study whether heredity for hypertension influences intra-uterine growth and the relationship between fetal growth and adult blood pressure. DESIGN: Five-year prospective follow-up study with retrospective collection of data on size at birth and gestational age from obstetric records. SETTING: Centre of preventive medicine in Malmo, Sweden. SUBJECTS: Thirty normotensive men with and 27 without heredity for hypertension were investigated in 1990, and the majority (n = 28 and n = 20, respectively) in 1995 also. MAIN OUTCOME MEASURES: Two measures of intra-uterine growth were compared between the groups and related to adult systolic blood pressure: the birth weight deviation from the expected birth weight based on ultrasonically derived intra-uterine growth curves, and the degree of thinness at birth (ponderal index = weight/length3). RESULTS: The birth weight deviation in men with heredity for hypertension differed significantly from that in men without such heredity (%) (-6.9+/-12.0 versus +7.3+/-18.4; P = 0.002). Ponderal index was somewhat lower in the men with than in those without heredity for hypertension, but the difference did not reach statistical significance (kg/m3) (25.9+/-2.6 versus 27.0+/-2.2; P = 0.08). In the group with heredity for hypertension, systolic blood pressure correlated inversely with ponderal index both in 1990 (r = -0.44; P = 0.01) and 1995 (r = -0.49; P = 0.009), and the 5-year increase in systolic blood pressure correlated inversely with the birth weight deviation (r = -0.38; P = 0.04). No such correlations were found in the group without heredity for hypertension. CONCLUSION: Our results suggest that genetic factors contributing to the development of hypertension may influence intra-uterine growth.

Adult↗
PubMed2002

The influence of heredity for psoriasis on the ILAR classification of juvenile idiopathic arthritis.

OBJECTIVE: To evaluate how heredity for psoriasis influences classification according to the International League of Associations for Rheumatology (ILAR). Heredity for psoriasis is currently both an exclusion and an inclusion criterion for different types of childhood arthritis according to ILAR classification criteria. METHODS: Twenty physicians in 5 Nordic countries prospectively collected data from the incident cases in their catchment areas over an 18 month period beginning July 1, 1997. Clinical and serological data from the first year of disease were collected. RESULTS: Of the 321 patients included who could be classified according to ILAR criteria for childhood arthritis, 50 (15.6%) patients were excluded from 55 classification events and fulfilled criteria for "other arthritis 1" i.e., did not fulfill criteria for any of the other classification categories, primarily because of heredity for psoriasis. If psoriasis in second degree relatives was disregarded as an exclusion criterion, only 8.7% of the patients remained in the "other arthritis 1" subgroup. For 20.6% of the whole group, heredity for psoriasis in a first or second degree relative (or both) and its distribution among arthritis subgroups did not differ except for juvenile psoriatic arthritis. CONCLUSION: We suggest that second degree heredity for psoriasis be withdrawn as an exclusion criterion from the ILAR criteria.

Arthritis, Juvenile↗
PubMed1979

T lymphocytes and blood eosinophils in early infancy in relation to heredity for allergy and type of feeding.

T lymphocytes in 50 one-month-old infants were determined and correlated to heredity for allergy, blood eosinophil counts, and type of feeding. It was found that infants with heredity for atopy had significantly lower relative numbers of T lymphocytes than infants without heredity (p less than 0.05). This difference was particularly obvious in heredity for asthma on the paternal side (p equals 0.001). There was an inverse correlation between T lymphocyte counts and blood eosinophil counts in infants who were cow's milk-fed; i.e., low T lymphocyte counts were associated with high blood eosinophil counts (r = -0.59, p less than 0.01). T lymphocyte counts were not correlated to the type of feeding, whereas blood eosinophils were significantly higher in the cow's milk-fed than in the breast-fed group (p less than 0.01). The results suggest that atopic allergy may be associated with a genetically determined lymphocyte defect.

Asthma↗
PubMed2001

Influence of atopic heredity on IL-4-, IL-12- and IFN-gamma-producing cells in in vitro activated cord blood mononuclear cells.

Several reports have claimed that there is a greater risk for a child with an atopic mother to develop allergy as compared to a child with an atopic father. This suggests that the fetal environment during pregnancy might be of importance for the development of atopic disease. Both proliferative and cytokine responses have been detected in cord blood mononuclear cells (CBMC) after stimulation with allergens, suggesting allergen priming already in utero. The aim of this study was to investigate whether the atopic status of the mother influences cytokine production by CBMC. We compared interleukin (IL)-4, IL-12 and interferon (IFN)-gamma-producing CBMC from children with double atopic heredity (dh), maternal atopic heredity only (mh) or no atopic heredity (nh). CBMC were stimulated in vitro with allergens (birch, ovalbumin and cat), phytohaemagglutinin (PHA) or purified protein derivative (PPD) and cytokine-producing cells were measured by the enzyme-linked immunospot assay. In response to PHA, the frequency of IL-4-producing cells, as well as the ratio of IL-4/IFN-gamma-producing cells, were significantly higher in the dh group compared to the nh group. High numbers of IL-12-producing cells in response to allergens were detected, significantly highest in the nh group, followed by the dh and mh groups. Our results suggest that there is a stronger Th2 bias after in vitro stimulation of CBMC from children with atopic heredity, as reflected by higher IL-4/IFN-gamma ratios in response to PHA, and lower numbers of IL-12-producing cells after allergen stimulation. Whether these differences influence later allergy development will be evaluated when the atopic status of the children is assessed at 2 years of age.

Adult↗
PubMed1981

[The cardiovascular risk profile in patients with disorders of glucose tolerance (borderline diabetes) dependent on the heredity of the diabetes].

In the statement of the profile of the cardiovascular risk of 1,780 persons evaluable data on a probable heredity of diabetes of 1st degree were got. Taking into consideration the same age groups no differences could be found concerning the heredity of diabetes between persons with carbohydrate tolerance lying in the borderline region (oral glucose tolerance test in the modification of the European study group for epidemiology of diabetes) and newly detected diabetics, whereas normal persons showed significantly more infrequently an occurrence of diabetes in near relatives. Taking into consideration the same age and sex of the comparative couples (150 biostatistic twins each) borderline diabetics with and without heredity of diabetes had an identical profile of risk with restriction to 5 generally accepted cardiovascular sizes of influence (overweight, hypertension, hypertriglyceridaemia, hypercholesterolaemia and hyperuricaemia). An existing heredity of diabetes does not increase the signs of risk associated with the carbohydrate intolerance.

Cardiovascular Diseases↗
PubMed1997

Some history of heredity-vs-environment, genetic inferiority at Harvard (?), and The (incredible) Bell Curve.

This article discusses some historical and intellectual roots of American behaviorism in psychology and its anti-heredity, environmentalist bias, as well as the early 'justification' for pure line theory in genetics and some interrelations between the two fields. Next, I discuss the heritability concept, its promotion, its critique and the importance of distinguishing it from, rather than confusing or conflating it with, the heredity concept. Then, briefly I consider some of the history and problems associated with the intelligence concept, as well as the capital importance of biological controls in studies of human heredity. And finally, I document the incredibility of the The Bell Curve and the appalling inadequacy of its reception.

Environment↗
PubMed1986

The cyclic AMP second messenger system in man: the effects of heredity, hormones, drugs, aluminum, age and disease on signal amplification.

The intracellular effects of a number of hormonal signals are mediated by the cyclic AMP second messenger system in man and the ubiquitous distribution of hormone-stimulated adenylate cyclase suggests the importance of this enzyme complex in normal aging and pathophysiological states. Various vectors including heredity, endogenous catecholamines, steroid hormones, and drugs affect the activity of hormone-stimulated adenylate cyclase in man. The effect of heredity was studied using lymphocytes obtained from monozygotic twin pairs and age and sex-matched sib pairs. Only for forskolin-stimulated activity is a significant proportion of individual variance attributable to heredity, suggesting the relative stability of the catalytic subunit. Beta-adrenergic and prostaglandin E-1 activity are "state" characteristics and their activities are controlled by environmental parameters. A significant reduction in isoproterenol-stimulated cyclic AMP accumulation between the menses and luteal phase of the menstrual cycle is observed in lymphocytes obtained from 11 female subjects. The lowest level of beta-adrenergic receptor activity is associated with the highest levels of progesterone and estradiol hormone levels in blood. Lithium at therapeutic concentrations markedly inhibits adenylate cyclase activity in platelet membranes. Moreover, marked individual differences are observed in sensitivity to lithium as determined by Dixon plot derived Ki values for 9 normal, healthy subjects. Human adenylate cyclase obtained from platelets and lymphocytes is activated by micromolar amounts of aluminum in the presence of NaF. Irreversible activation of adenylate cyclase by aluminum is suggested as a possible mechanism of this metal's neurotoxicity. The biochemical basis for the age-associated decline in beta-adrenergic responsiveness in man is discussed. Several investigations suggest a deficit at two levels in the adenylate cyclase complex: an impaired coupling of the receptor/N protein subunits and an additional lesion distal to the receptor at the level of N/C coupling. Perfusion studies with salbutamol suggest that the decline in beta-adrenergic sensitivity is general and not restricted to lymphocytes. Possible abnormalities in cyclic AMP signal amplification and recognition in various disease states is discussed. Increased prostaglandin E-1-stimulated cyclic AMP accumulation is observed in lymphocytes obtained from patients with Alzheimer's disease compared to age-matched controls and correlated with severity of the disease state.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenylyl Cyclases↗
PubMed2001

Francis Galton on twins, heredity and social class.

In 1875 Francis Galton was the first to study twins as a test of the relative strenght of heredity and environment. This paper examines Galton's work on twins, using his surviving working papers. It shows that his enquiry was larger and more systematic than previously realized. Galton issued several hundred questionnaires to parents of twins, with the aim of establishing how far the similarities and differences between twins were affected by their life experiences. The paper also discusses Galton's study in relation to his understanding of the physiology of twinning and his theory of heredity. The modern concept of monozygotic twins had not yet been established, and the similarity between Galton's work and modern twin studies should not be overstated. While Galton's work was important as a pioneering study, in some respects his conclusions went beyond his evidence. The paper finally examines whether Galton's twin studies influenced his position on the links between social class, heredity and social mobility, and surveys the evidence for his views on these issues.

Genetics↗
PubMed1999

The development of Francis Galton's ideas on the mechanism of heredity.

Galton greeted Darwin's theory of pangenesis with enthusiasm, and tried to test the assumption that the heredity particles circulate in the blood by transfusion experiments on rabbits. The failure of these experiments led him to reject this assumption, and in the 1870s he developed an alternative theory of heredity, which incorporated those parts of Darwin's theory that did not involve the transportation of hereditary particles throughout the system. He supposed that the fertilized ovum contains a large number of hereditary elements, which he collectively called the "stirp," a few of which are patent, developing into particular cell types, while the rest remain latent; the latent elements can be transmitted to the next generation, while the patent elements, with rare exceptions, cannot since they have developed into cells. The problem with this theory is that it does not explain the similarity between parent and child unless there is a high correlation between latent and patent elements. Galton probably came to realize this problem during his subsequent statistical work on heredity, and he quietly dropped the idea that patent elements are not transmitted in Natural Inheritance (1889). Galton thought that brothers and sisters had identical stirps, and he attributed differences between them to variability in the choice of patent elements from the stirp, that is to say to developmental variability. He attributed the likeness of monozygotic twins to the similarity of their developmental environment. Galton's twin method was to track the life history changes of twins to see whether twins who were similar at birth diverged in dissimilar environments or whether twins who were dissimilar at birth converged in similar environments. It is quite different from the modern twin method of comparing the similarities between monozygotic and dizygotic twins, on the assumption that monozygotic twins are genetically identical whereas dizygotic twins are not. It has been argued that Galton foreshadowed Weismann's theory in the continuity of the germ-plasm, but this is only true in a weak sense. They both believed that the inheritance of acquired characters was either rare or impossible, but Galton did not forestall the essential part of Weismann's theory, that the germ-plasm of the zygote is doubled, with one part being reserved for the formation of the germ-cells.

Genetics↗
PubMed1981

An overview of a multifactor-system theory of personality and individual differences: III. Life span development and the heredity-environment issue.

In Part III of this three-part series on multifactor-system theory, multivariate, life-span development is approached from the standpoint of a quantitative and qualitative analysis of the ontogenesis of factors in each of the six systems. The pattern of quantitative development (described via the Gompertz equation and three developmental parameters) involves growth, stability, and decline, and qualitative development involves changes in the organization of factors (e.g., factor differentiation and convergence). Hereditary and environmental sources of variation are analyzed via the factor gene model and the concept of heredity-dominant factors, and the factor-learning model and environment-dominant factors. It is hypothesized that the sensory and motor systems are heredity dominant, that the style and value systems are environment dominant, and that the cognitive and affective systems are partially heredity dominant.

Genotype↗
PubMed2000

Influence of heredity for obesity on adipocyte lipolysis in lean and obese subjects.

OBJECTIVE: To evaluate a possible influence of a hereditary trait for obesity on the regulation of adipocyte metabolism in vitro in subcutaneous fat cells in obese and non-obese subjects. DESIGN: A biopsy from abdominal subcutaneous fat was obtained from consecutive subjects with or without a family trait for obesity. A positive family history of obesity was considered present if one or more of the first degree relatives had a BMI of 27 kg/m2 or more. SUBJECTS: 67 non-obese and 60 obese subjects, age 19-60 y. A family trait for overweight was present in 42 of the lean subjects and in 50 of the obese subjects. MEASUREMENTS: Fat cells were isolated and incubated in vitro with isoprenaline (a non-selective beta-adrenoceptor agonist), forskolin (activates the adenylyl cyclase) and dibutyryl cyclic AMP (stimulates the protein kinase hormone-sensitive lipase complex). Glycerol release was measured and used as lipolytic index. RESULTS: Maximal lipolytic response per g triglycerides was about 50% lower in obese subjects both with and without a positive heredity and in non-obese subjects with a family trait for obesity as compared to non-obese subjects without such trait (P=0.0001). Fat cell volume was twice as high in obese as compared to lean subjects. Drug-induced maximal glycerol release per fat cell in the obese subjects, regardless of family history of obesity, reached a similar level, but did not exceed that of the lean group without heredity. CONCLUSIONS: Obesity is associated with catecholamine resistance with a relatively ineffective lipolysis in fat cells, and presence of a family history of obesity was not associated with a further suppression of lipolysis. In the lean subjects, heredity for obesity significantly influenced lipolysis to similar low levels as in the obese subjects.

Adipocytes↗
PubMed2001

Fetal exposure, heredity and risk indicators for cardiovascular disease in a Swedish welfare cohort.

BACKGROUND: The overall aim was to test whether low birthweight (LBW) in newborns is associated with the risk indicators for cardiovascular disease in early middle age, even in a welfare society. Further, a possible interaction of LBW and heredity for myocardial infarction or stroke was investigated. METHODS: Overall, subjects were identified as newborns in a local birth register, and as adult participants, in the Västerbotten Intervention Program (n = 7876). Outcome measures such as systolic (SBP) and diastolic blood pressures (DBP), body mass index (BMI), cholesterol, triglycerides and anthropometrics were investigated (at age 29-41 years) in relation to LBW. RESULTS: Low birthweight was associated with increased SBP and DBP. Triglycerides were elevated among women with LBW and total cholesterol was elevated in men with LBW. Heredity for myocardial infarction or stroke interacted with LBW, and indicated a synergistic effect on the level of SBP. The BMI did not differ between LBW and normal birthweight subjects. CONCLUSIONS: Our interpretation is that the 'fetal origins' hypothesis' is valid for middle-age subjects who grow up in a welfare society. The population attributable proportions that result from different exposures to LBW were relatively small overall; from a public health perspective, heredity was more important than LBW for elevated SBP.

Adult↗