Sedentary Families Research Articles

‘If it is not too expensive, then you can send me sugar’: money matters among migrants and their families

Discussions about money among migrants and their families have long been a financial and emotional concern. Earning money, or more money, and securing a family’s present and future well-being were significant factors when men and women made the decision to immigrate abroad over the twentieth century. With postal services globally systemized, literally tons of letters crossed oceans and continents for migrants, their families, and others to remain in touch. Letters, as historians and other scholars note, provide a plethora of information and insight on the lives and experiences of migrants and non-migrants. These micro-narratives set against the backdrop of national and local macro-narratives, contribute to understanding the state of mind and the state of heart of correspondents whose reason for writing was directly linked to migration. In this paper, we examine issues that relate to money and its emotional underpinnings as conveyed by a number of migrants and their more sedentary families over the first half of the twentieth century. The letters we examine in our paper are part of the Digitizing Immigrant Letters Project collection housed at the University of Minnesota’s Immigration History Research Center (archives.ihrc.umn.edu/dil/index.html). The letters, originally written in Italian, Ukrainian, Russian, Slovak, Slovenian, Croatian, and Latvian, were translated into English as part of the Digitizing Immigrant Letters Project. Here, we examine migrant family letters using an interdisciplinary, comparative approach drawn from economic theory, social history and migration history. Some of the questions we explore are: What kind of monetary issues mattered and to whom? In what ways did these issues impact migrants and their families? How did money and familial intimacy intervene with processes of migration? What are some of the prominent links between money, family and migration discussed in migrant correspondence?

High mobility explains demand sharing and enforced cooperation in egalitarian hunter-gatherers.

‘Simple’ hunter-gatherer populations adopt the social norm of ‘demand sharing’, an example of human hyper-cooperation whereby food brought into camps is claimed and divided by group members. Explaining how demand sharing evolved without punishment to free riders, who rarely hunt but receive resources from active hunters, has been a long-standing problem. Here we show through a simulation model that demand-sharing families that continuously move between camps in response to their energy income are able to survive in unpredictable environments typical of hunter-gatherers, while non-sharing families and sedentary families perish. Our model also predicts that non-producers (free riders, pre-adults and post-productive adults) can be sustained in relatively high numbers. As most of hominin pre-history evolved in hunter-gatherer settings, demand sharing may be an ancestral manifestation of hyper-cooperation and inequality aversion, allowing exploration of high-quality, hard-to-acquire resources, the evolution of fluid co-residence patterns and egalitarian resource distribution in the absence of punishment or warfare.

Genomewide linkage scan of resting blood pressure: HERITAGE Family Study. Health, Risk Factors, Exercise Training, and Genetics.

The purpose of this study was to search for genomic regions influencing resting systolic (SBP) and diastolic (DBP) blood pressure (BP) in sedentary families (baseline), and for resting BP responses (changes) resulting from a 20-week exercise training intervention (post-training-baseline) in the Health, Risk Factors, Exercise Training, and Genetics (HERITAGE) Family Study. A genome-wide scan was conducted on 317 black individuals from 114 families and 519 white individuals from 99 families using a multipoint variance-components linkage model and a panel of 509 markers. Promising results were primarily, but not exclusively, found in the black families. Linkage evidence (P<0.0023) with baseline BP replicated other studies within a 1-logarithm of odds (LOD) interval on 2p14, 3p26.3, and 12q21.33, and provided new evidence on 3q28, 11q21, and 19p12. Results for several known hypertension genes were less compelling. For response BP, results were not very strong, although markers on 13q11 were mildly suggestive (P<0.01). In conclusion, these HERITAGE data, in conjunction with results from previous genomewide scans, provide a basis for planning future investigations. The major areas warranting further study involve fine mapping to narrow down 3 regions on 2q, 3p, and 12q that may contain "novel" hypertension genes, additional typing of some biological candidate genes to determine whether they are the sources of these and other signals, multilocus investigations to understand how and to what extent some of these candidates may interact, and multivariate studies to characterize any pleiotropy.

Familial aggregation of stroke volume and cardiac output during submaximal exercise: the HERITAGE Family Study.

Familial aggregation of stroke volume (SV) and cardiac output (Qc by CO2 rebreathing) at 50 Watts (W) and 60 % of maximal oxygen uptake (VO2max) as well as their changes in response to a 20-week endurance exercise training program was assessed in 99 Caucasian families who participated in the HERITAGE Family Study. In order to interpret familial influences independent of effects of age, sex, and body size (indexed by body surface area here), SV and Qc levels were adjusted for these primary parameters prior to genetic analysis within four sex-by-generation groups (the responses to training were additionally adjusted for their baseline values). Maximal heritabilities for baseline SV, Qc, and their changes in response to training during the two stages of submaximal exercise were estimated using a familial correlation model. At 50W, maximal heritabilities reached 41% and 42% for baseline SV and Qc, respectively, and were 29% and 38% for the respective responses to training. At 60% of VO2max, maximal heritabilities reached 46 % for baseline SV and Qc, and were 24% and 30% for the respective responses to training. Generally there were no meaningful differences between the maximal heritabilities at 50 W and 60% of VO2max. However, the maximal heritabilities for the baseline were slightly higher than the estimates for the changes in response to training. Based upon results arising from these non-obese, non-hypertensive, and sedentary families, we found that SV and Qc at 50 W and 60% of VO2max as well as their changes in response to the 20-week endurance exercise training were moderately heritable. Not only genetic determinants but also familial non-genetic factors might attribute to the observed patterns of familial aggregation of SV and Qc during submaximal exercise in the present study.

Familiality of triglyceride and LPL response to exercise training: the HERITAGE study.

The main purpose of the present investigation was to test whether and to what extent familial/genetic factors are involved in the changes of postheparin lipoprotein lipase (deltaPH-LPL) activity and triglyceride (deltaTG) levels in response to exercise training. Additional hypotheses were also tested as to whether there were familial/genetic factors shared by baseline and the corresponding response to exercise training (i.e., by baseline triglyceride (TG(B)) and deltaTG and by baseline postheparin lipoprotein lipase (PH-LPL(B)) and deltaPH-LPL activity). Serum TG and PH-LPL were measured in 459 subjects from 99 sedentary Caucasian families of the HERITAGE Family study before (baseline) and after completing a 20 wk (3 times per week) exercise training protocol. The training protocol had a target intensity of 75% of the heart rate associated with baseline VO2max during the last 6 wk. PH-LPL activity was measured in the study subjects. Both univariate and bivariate familial correlation analyses were applied to the baseline and response data. The maximal heritabilities for deltaTG and deltaPH-LPL activity were 22% and 15%, respectively. There were no common familial factors for TG(B) and deltaTG, nor were there any for PH-LPL(B) and deltaPH-LPL. However, we found that there were common familial factors underlying deltaTG and deltaPH-LPL; these familial factors seemed to differ across sex and generation groups. Although there were no common familial factors underlying the covariation between the baseline triglyceride and PH-LPL activity and the corresponding responses to exercise training (i.e., TG(B) with deltaTG or PH-LPL(B) with deltaPH-LPL), the deltaTG and deltaPH-LPL covariation apparently share some common familial determinants.

Segregation analysis of apolipoproteins A-1 and B-100 measured before and after an exercise training program: the HERITAGE Family Study.

Complex segregation analyses of apolipoproteins (apo) A-1 and B-100 were performed in a sample of 520 individuals from 99 white families who participated in the HERITAGE Family Study. In these sedentary families, plasma apo A-1 and B-100 concentrations were measured before and after a 20-week endurance exercise training program. Baseline apo A-1 and B-100 were adjusted for the effects of age (age-adjusted baseline apo A-1 and B-100) and for the effects of age and BMI (age-BMI-adjusted baseline apo A-1 and B-100). The change in response to training was computed as a simple Delta (posttraining minus baseline) and was adjusted for age and the baseline (age-baseline-adjusted apo A-1 and B-100 responses to training). In the present study, a major gene could not be inferred for baseline apo A-1. Rather, we found a major effect along with a multifactorial effect accounting for 8% to 9% and 51% to 56% of the variance, respectively. In addition, no clear evidence supported a major-gene effect for its response to training, whereas the transmission of a major effect from parents to offspring was ambiguous, ie, genetic in nature or familial environmental in origin. The major effect accounted for 15% of the variance, with an additional 21% and 58% of the variance being accounted for by a multifactorial effect in parents and offspring, respectively. It is interesting to have obtained evidence of a putative recessive major locus for baseline apo B-100, which accounted for 50% to 56% of the variance, with an additional 25% to 29% of the variance due to a multifactorial effect. In contrast, no major effect for its response to training was identified, although a multifactorial effect was found that accounted for 27% of the variance. The novel findings arising from the present study are summarized as follows. Baseline apo A-1 and its response to training were influenced by a major effect and a multifactorial effect. Baseline apo B-100 was influenced by a putative major recessive gene with a multifactorial component, but its response to training was influenced solely by a multifactorial component in these sedentary families.

A genetic study of dehydroepiandrosterone sulfate measured before and after a 20-week endurance exercise training program: The HERITAGE Family Study

Familial aggregation and possible major gene effects were evaluated for the baseline serum dehydroepiandrosterone sulfate (DHEAS) level and the change in DHEAS in response to a 20-week exercise training program in a sample of 481 individuals from 99 Caucasian families who were sedentary at baseline and who participated in the HERITAGE Family Study. Baseline DHEAS levels were not normally distributed, and were therefore logarithmically transformed and adjusted for the effects of age and sex prior to genetic analysis. The DHEAS response to training was computed as the simple difference, post-training minus baseline, and was adjusted for the baseline DHEAS level, age, and sex. Maximal (genetic and familial environmental) heritabilities (using a familial correlation model) reached 58% and 30% for the baseline and the response to training, respectively. Our estimate for the baseline is generally in agreement with previous reports, suggesting that the magnitude of the familial effect underlying this phenotype in these sedentary families is similar to that in the general population. However, segregation analysis showed no evidence for a multifactorial familial component in data for either the baseline or the response to training. Rather, a major additive gene controlling the baseline was found. For the response to training in the complete sample, transmission of the major effect from parents to offspring was ambiguous, but in a subset of 56 "responsive" families (with at least 1 family member whose response to training was greater than 1 standard deviation) this major effect was Mendelian in nature. The putative major genes accounted for 50% and 33% of the variance for the baseline and the response to training, respectively. The novel finding in this study is that the baseline DHEAS level and the change in DHEAS in response to training may be influenced by major gene effects.

Evidence of pleiotropic loci for fasting insulin, total fat mass, and abdominal visceral fat in a sedentary population: the HERITAGE family study.

To examine whether there is a major gene effect on fasting insulin and pleiotropic loci for fasting insulin, total fat mass (FM), and abdominal visceral fat (AVF). A major gene hypothesis for fasting plasma insulin levels was assessed using segregation analyses of data on 495 members in 98 normolipidemic sedentary families of white descent who participated in the HERITAGE Family Study. Segregation analyses were performed on insulin adjusted for age, on insulin adjusted for age and FM, and on insulin adjusted for age and AVF. Before adjustment for AVF and FM, a major gene effect on fasting insulin levels was indicated. The putative locus accounted for 54% of the variance under a recessive inheritance pattern, affecting 11% of the sample (i.e., allele frequency = 0.33). However, after adjusting for the effects of AVF or FM, neither a major effect alone nor a multifactorial component alone could be rejected, and support for a major gene was equivocal, i.e., neither the hypothesis of Mendelian tau values or that of the equal tau(s) were rejected and the equal tau model fit the data better than the Mendelian tau model. This pattern (i.e., major gene evidence for insulin before but not after adjustment for AVF or FM) suggests that there is a putative locus with pleiotropic effects on both insulin and FM and another pleiotropic locus for both insulin and AVF. Although these data do not directly support an additional major gene for insulin independent of AVF and FM, such support cannot be ruled out because there is still a significant major effect on FM- or AVF-adjusted insulin (albeit the Mendelian nature of this effect is ambiguous).

Cross-trait familial resemblance for resting blood pressure and body composition and fat distribution: The HERITAGE family study.

Cross-trait familial resemblance between resting blood pressure (BP) and body composition and fat distribution was examined in 98 Caucasian families participating in the HERITAGE Family Study by using a multivariate familial correlation model assessing both intraindividual and interindividual cross-trait correlations. The 520 family members were sedentary at baseline examination, and both resting systolic (SBP) and diastolic (DBP) BP were cross-analyzed with each of the following 10 indications of body composition and fat distribution: percent body fat (%BF), abdominal visceral fat (AVF), body mass index (BMI), fat-free mass (FFM), fat mass (FM), sum of eight skinfolds (SF), total abdominal fat (TAF), ratio of trunk-to-extremity skinfolds (TER), waist circumference (WAIST), ratio of waist-to-hip circumferences (WHR). Five of the variables were also corrected for fat mass (AVFf, TAFf, TERf, WAISTf, WHRf) to index these measures independent of total degree of adiposity. In general, the results suggested strictly intraindividual cross-trait resemblance, with occasional spouse cross-trait resemblance, but few or no sibling or parent-offspring cross-trait correlations. This pattern is largely consistent with nongenetic specific environmental determinants for the BP-body composition and fat distribution covariation, with possibly some common environmental influence between spouses and negligible genetic effects. The only findings suggesting any familial cross-trait resemblance were significant sibling correlations for DBP-FFM and DBP-WHR, although the parent-offspring correlation was not significant. These findings suggest that the observed BP-body composition and fat distribution cross-trait correlations in these sedentary families are probably not due to multifactorial effects such as polygenic and/or common familial environmental effects. Whether or not other factors such as nonadditive effects are involved warrants further investigation using other methods. Am. J. Hum. Biol. 12:32-41, 2000. Copyright 2000 Wiley-Liss, Inc.

Evidence of a major locus for lipoprotein lipase (LPL) activity in addition to a pleiotropic locus for both LPL and fasting insulin: results from the HERITAGE Family Study

A major gene hypothesis for heparin releasable plasma lipoprotein lipase (PH-LPL) activity was assessed using segregation analyses of data on 495 members in 98 normolipidemic sedentary families of Caucasian descent who participated in the HERITAGE Family Study. Segregation analyses were performed on PH-LPL adjusted for age, and on PH-LPL activity adjusted for age and fasting insulin. Prior to adjustment for insulin, neither a major gene effect nor a multifactorial component could be rejected, and support for a major gene was equivocal i.e. neither the Mendelian transmission nor the no transmission (equal τs) models were rejected. However, after adjusting for the effects of insulin, a major gene effect on PH-LPL activity was unambiguous. The putative locus accounted for 60% of the total phenotypic variance, and the homozygous recessive form affected 10% ( q 2)of the sample (i.e. gene frequency ( q)=0.31), and led to a low PH-LPL value. The lack of a significant multifactorial effect suggested that the familial etiology of PH-LPL activity adjusted for insulin was likely to be primarily a function of the major locus. In conclusion, the present study is the first to report segregation analyses on PH-LPL activity prior to and after adjusting for insulin, and suggests that there is an indication of a pleiotropic genetic effect on PH-LPL activity and insulin, in addition to a major gene effect on PH-LPL activity alone.

Familial aggregation of resting blood pressure and heart rate in a sedentary population: The heritage family study

The familial aggregation of resting systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) was assessed in 98 white families, who participated in the HERITAGE Family Study, and were selected to be sedentary, and primarily nonobese and normotensive. In the present study, 522 family members were sedentary at baseline examination, and resting SBP, DBP, and HR measured during this examination were investigated. If physical activity level is a potent environmental factor, then we expected that the relative contribution of environmental factors to the familial aggregation of blood pressure (BP) would be somewhat reduced, because activity was controlled for in this study. Using a familial correlation model, maximal heritabilities were estimated to be 54%, 41%, and 32% for resting SBP, DBP, and HR, respectively, in these families; and they were 51%, 42%, and 34% for resting SBP, DBP, and HR, respectively, when the data were adjusted for body mass index. The estimates are somewhat higher for BP but similar for HR to those reported in previous family studies, suggesting that the distribution of the underlying etiologic factors in these sedentary families may be similar to those in the general population. There was substantial spouse resemblance in this study, which may be explained by a higher concordance for correlated lifestyle factors including diet, similar activity levels, or by assortative mating for relative weight or dietary preferences.

Familial clustering of insulin and abdominal visceral fat: the HERITAGE Family Study.

Abdominal visceral fat (AVF) is an obesity-related phenotype thought to be associated with insulin resistance, diabetes mellitus, and atherosclerosis. Significant genetic influences on both AVF and insulin levels have been reported. However, information is lacking as to whether common genetic influences on AVF and insulin levels exist. AVF was assessed by computed tomography scan, and fasting insulin was measured by RIA in 512 members of 98 sedentary Caucasian families participating in the HERITAGE Family Study. Baseline data, collected before exercise training, were used in the present investigation. A bivariate familial correlation model was applied to evaluate whether there are familial influences that are common to insulin and AVF before and after adjustment for total fat mass (FM), and to assess the overall heritability of insulin and AVF. The maximal heritability for AVF, before and after adjustment for total FM, was 42% and 50%, respectively; and for insulin, it was 21%. Interestingly, 29% of the familial influences on insulin were also common to AVF, whereas 14% of the familial influences on AVF were shared by insulin. Furthermore, after AVF was adjusted for total FM, these common familial influences were increased to 48% and 20%. Genes and/or familial nongenetic factors with pleiotropic effects seem to influence both AVF and plasma insulin levels to a certain degree. Genes involved in the regulation of lipid storage and mobilization in the abdominal fat depot are potential candidates for these genetic pleiotropic effects.

Segregation analysis of abdominal visceral fat: the HERITAGE Family Study.

A major gene hypothesis for abdominal visceral fat (AVF) level, both before and after adjustment for total body fat mass, was investigated in 86 white families who participated in the HERITAGE Family Study. In this study, sedentary families were tested for a battery of measures (baseline), endurance exercise trained for 20 weeks, and then remeasured again. The baseline measures reported here are unique in that the variance due to a potentially important environmental factor (activity level) was limited. AVF area was assessed at L4 to L5 by the use of computerized tomography scan, and total body fat mass was assessed with underwater weighing. For fat mass, a putative locus accounted for 64% of the variance, but there was no evidence of a multifactorial component (i.e., no polygenic and/or common familial environmental effects). For AVF area, both a major gene effect accounting for 54% of the variance and a multifactorial component accounting for 17% of the variance were significant. However, after AVF area was adjusted for the effects of total level of body fat, the support for a major gene was reduced. In particular, there was a major effect for fat mass-adjusted AVF area, but it was not transmitted from parents to offspring (i.e., the three transmission probabilities were equal). The importance of this study is twofold. First, these results confirm a previous study that suggested that there is a putative major locus for AVF and for total body fat mass. Second, the findings from the HERITAGE Family Study suggest that the factors underlying AVF area in sedentary families may be similar to those in the population at large, which includes both sedentary and active families. Whether the gene(s) responsible for the high levels of AVF area is the same as that which influences total body fat content remains to be further investigated.