Purpose: There is a growing body of evidence that income indicators and racial compositions of urban neighborhoods mediate access to food stores and healthy foods. The purpose of this study was to determine whether there were any differences in access (availability, quality and cost) to fruits and vegetables between two racially homogeneous regions, one considered low-income and the other middle-income, in the City of Atlanta, Georgia. Methods: This was a cross-sectional, exploratory study. A convenience sample of 56 food stores (convenience, grocery and supermarket) was assessed over a three-week period. The stores were surveyed using an instrument developed to capture availabilities of fresh items, the quality of these and the ability of the food stores to meet the Thrifty Food Plan (TFP) 2006 fruit and vegetable categories for a reference family of four. Each category had constraints (variety and weights), and lowest-cost items were identified to meet these. Store to 10,000 population ratios and percent median income required to fulfill the TFP fruits and vegetables were calculated. Fisher’s Exact Tests and Chi Square were used to analyze categorical data. ANOVA analyses were used to determine differences in costs between the regions for the complete TFP fruit and vegetable basket and for price differences for each fruit and vegetable category among stores within each region. Results: The food store to 10,000 ratios were 5.8 and 3.7, respectively, for the low-income region and middle-income region. The low-income region grocery store ratio was 2.7, compared to 0.9 for the middle-income. Access to fresh items, quality of these and numbers of stores meeting each category and the complete TFP basket were not significantly different between the regions. The low-income region had a significantly greater number of stores that met whole fruits (p=0.03) and the variety constraint for other vegetables, which was four types (p=0.05). The TFP category weights were difficult to achieve with most categories in deficits. The majority of the lowest-cost items identified were canned fruits and vegetables. There were no significant differences between the regions for the costs of each category. The low-income region had a significantly greater number of stores charging more than the mean ($52.91±14.85) for the complete TFP fruit and vegetable basket (p=0.04). Store types and not income was the significant factor contributing to the price differences between the regions for the complete TFP basket. Within region analyses indicated significant price differences for several categories among the store types. Typically, convenience stores and/or grocery stores charged significantly more for certain categories than did supermarkets. Conclusion: There were few differences in overall availability, quality and category comparisons. The low-income region potentially pays more for the TFP 2006 fruits and vegetables for a family of four. Cost has been cited as a barrier to complying with healthy diets. More research needs to be undertaken to aid in policy development in consideration of healthy food cost implications for low-income families. Further education efforts are required to guide low-income families on how the TFP can be met optimally on a budget.

Genetic predisposition to obesity presents a paradox: how do genetic variants with such a detrimental impact on human health persist through evolutionary time? Numerous hypotheses, for instance the thrifty genotype hypothesis, attempt to explain this phenomenon, yet fail to provide a satisfying answer to the modern obesity epidemic. In this critical review, I appraise existing theories explaining the evolutionary origins of obesity and explore novel biological and sociocultural agents of evolutionary change that may help explain the distribution of obesity and leanness predisposing variants in modern human populations. Gene pleiotropy and adaptations to diverse environmental niches may explain the rise and subsequent selection of obesity risk alleles. The regulation of gene expression by epigenetic mechanisms may serve as a stochastic factor affecting the manifestation of obesity phenotypes. Finally, exposure to malnutrition and disease epidemics in the wake of colonialism, culturally mediated notions of attractiveness and desirability, and diverse mating systems – including forced copulation, consanguinity and polygamy – may play a role in shaping the human genome. In short, I posit that in order to explain ethnic variation in obesity susceptibility, we must examine the origin of physiological adaptations and understand the sociocultural experiences of individuals and populations. As an imperative first step towards the identification of important drivers of obesity gene evolution, this review will inform empirical research focused on testing evolutionary theories by way of population genetics and mathematical modelling. Ultimately, these data will promote a better understanding of the aetiology of obesity and are expected to guide the development of targeted management, treatment, and prevention strategies. / Thesis / Master of Science (MSc)

Die hier vorliegende Arbeit zeigt die molekulare Evolution des Melatoninrezeptor 1 B-Gens (MTNR1B) und des Fat Mass and Obesity Associated-Gens (FTO). Für beide Gene wurden in genomweiten Assoziationsstudien (GWAS) Varianten entdeckt, welche zu der Entwicklung einer Adipositas bzw. deren Folgeerkrankungen beitragen können. So wurde für Einzelbasenaustausche (SNPs) im MTNR1B (rs10830963, rs4753426) eine Verschlechterung der Nüchternglukose sowie der Insulinausschüttung gezeigt. Zudem wurde für die Allelfrequenz des rs4753426 C-Allels ein Zusammenhang mit der täglichen Sonnenscheindauer beschrieben. Im FTO wurde eine (tagging) Variante im ersten Intron identifiziert (rs9939609), welche einen erhöhten Körpermasseindex (BMI) zu vermitteln scheint und robust repliziert werden konnte. Zusätzlich konnte in den Sorben, einer in der Lausitz ansässigen Volksgruppe, eine Variante im dritten Intron (rs17818902) beschrieben werden, die ein zusätzliches, stärkeres Assoziationssignal mit einem erhöhten BMI zeigte. Dies führte zu der Fragestellung, ob MTNR1B und FTO einer Konservierung unterlegen sind. Zudem interessierten populationsspezifische Unterschiede, um die Untersuchungen in den Kontext der Hypothese des sparsamen Genotyps stellen zu können. Demnach haben Individuen mit einer genetischen Veranlagung, die ihnen eine effizientere Energiespeicherung ermöglicht, zu Zeiten von Nahrungsmangel einen Fitness-Vorteil gegenüber Nicht-Trägern. Die Konservierung zwischen den Spezies wurde mit Phylogenetic Analysis by Maximum Likelihood (PAML) betrachtet, eine Analyse die auf dem Verhältnis von nichtsynonymen zu synonymen Basenaustauschen innerhalb einer kodierenden Sequenz beruht. Die Selektion innerhalb bzw. zwischen menschlichen Populationen wurde anhand verschiedener populationsgenetischer Variablen näher beleuchtet. Sowohl für MTNR1B als auch für FTO konnte gezeigt werden, dass sie über die betrachteten Spezies im Durchschnitt stark oder sehr stark konserviert sind, was die physiologische Relevanz dieser Gene untermauert. Für MTNR1B zeigte sich zudem, dass es auf dem Ast zum Menschen nicht konserviert, sondern positiv selektioniert ist. Dies kann als Anzeichen für durch die Umwelt bedingte Einflüsse gedeutet werden. Essentielle Residuen des Rezeptors sind jedoch auch hier hochgradig konserviert. Die populationsgenetischen Variablen implizieren bei beiden Genen eine nicht-neutrale Selektion. Während sich beim MTNR1B insbesondere populationsspezifische Unterschiede anhand des Fixierungsindex Fst zeigten, konnten für FTO marginal signifikante Korrelationen zwischen der Konservierung der Haplotypen und der Stärke der Assoziation mit BMI in den Sorben gezeigt werden. Für beide Gene kann die Hypothese des sparsamen Genotyps nicht prinzipiell ausgeschlossen werden, allerdings sind weitere Untersuchungen diesbezüglich von Nöten.

Nepakankama mityba iki nėštumo ir per nėštumą gali lemti palikuonio svorio pokyčius, vėlesnę brandą ar lėtines neinfekcines ligas suaugus. Darbo tikslas: Įvertinti mitybos iki nėštumo ir per nėštumą įtaką žiurkių palikuonių fizinei būklei. Uždaviniai: 1. Nustatyti ir palyginti žiurkių palikuonių svorio kitimo tendencijas tarp pirmos ir antros palikuonių kartų. 2. Įvertinti morfologinius pirmos ir antros kartos palikuonių išvaizdos ir elgsenos pokyčius. Tyrime naudotos 12 motininių žiurkių patelių ir 121 palikuonis. Žiurkių maitinimas vyko nustatytomis eksperimento sąlygomis: I eksperimentinės grupės (N=5) žiurkės buvo 50 proc. ribotos maisto 1 mėnesį iki nėštumo ir per visą nėštumo laikotarpį, II eksperimentinės grupės (N=5) žiurkės buvo ribotos 50 proc. maisto 1 mėnesį iki nėštumo, III eksperimentinė grupė (N=2) – kontrolinė, buvo maitinama ad libitum (apie 20 g/p). Vėliau visų grupių žiurkės šertos ad libitum. Palikuonys sverti kartą per savaitę, vertinta metabolinį stresą patyrusių ir nepatyrusių žiurkių palikuonių išvaizda, elgsena ir kiti metabolinio streso požymiai: domėjimasis aplinka, bailumas, agresyvumas, nervingumas. Rezultatai: 1. ▪ Suaugę pirmos kartos iki nėštumo ir per nėštumą maisto medžiagų ribojimą patyrusių žiurkių vyriškos lyties palikuonys sveria reikšmingai daugiau už kitas grupes; ▪ Suaugę antros kartos tik iki nėštumo maisto medžiagų ribojimą patyrusių žiurkių vyriškos lyties palikuonys sveria reikšmingai daugiau nei kitų grupių palikuonys... [toliau žr. visą tekstą] / Unsufficient diet before pregnancy or in time of pregnancy can lead to inadequate weight of offspring, delayed maturation as well as obesity and greater risk of noncommunicable diseases in adulthood. The main objective of this study was to explore if there is a change in rat offspring’s body weight that can be attributed to maternal nutrition. Materials and methods. The animals were housed under standard conditions in the vivarium of the Institute of Biochemistry. All animal procedures are in accordance with the The State Food and Veterinary Service. The cohort of 12 mature female Wistar rats was divided into 3 groups with respect to nutritional restriction. The rats were fed either a control (1 group) or restricted diet (2 groups): one experimental group was food-restricted prior to pregnancy and the other - one month prior and through the pregnancy period. Both food-restricted rat groups received 50 percent less of the feed eaten in the control group. After 1 month maternal rats were mated. After weaning all pups were fed with control diet ad libitum. Pups were weighted weekly with the same, calibrated scales. After 4 months female offspring were mated following a standard above mentioned procedure. 2nd offspring generation was kept and weighted under the same standardized conditions. We also observed and evaluated offspring appearance, behavior and other signs of metabolic stress: interest in the environment, fear, aggressiveness, nervousness. Results show that 1... [to full text]

<p>This thesis outlined a novel operationalization and extension of the thrifty phenotype and fetal overnutrition hypotheses, two evolutionary developmental hypotheses stemming from the developmental origins of health and disease perspective, for developmental pathways from prenatal risk through child growth to early puberty. Support has accumulated for both, but previous studies have not clearly determined which hypothesis better predicts early puberty. Using the Fragile Families and Child Wellbeing Study (<i>n</i>=4898), the thrifty phenotype and fetal overnutrition pathways were tested against each other, separately by sex, and race/ethnicity for adrenal, and gonadal pubertal markers. Results indicated that in general, both hypotheses were supported. Contrary to hypotheses, the thrifty phenotype pathway did not predict perceived pubertal timing better in boys and the fetal overnutrition pathway did not predict perceived pubertal timing best in girls. Instead, both pathways predicted puberty equally well between girls and boys and the fetal overnutrition pathway stemming from maternal gestational weight gain was stronger than the pre-pregnancy BMI pathway. Individual paths of the hypothesized pathways were generally supported when analyzed by race/ethnicity group separately, but support for the entire pathways were sparse. Implications of this work are that pubertal timing may be similarly programmed by restrictive and overnutrition prenatal risks, both should be prioritized, and that interventions for maternal gestational weight should be prioritized over interventions for pre-pregnancy BMI for reducing rates of early puberty. </p>

Die hier vorliegende Arbeit zeigt die molekulare Evolution des Melatoninrezeptor 1 B-Gens (MTNR1B) und des Fat Mass and Obesity Associated-Gens (FTO). Für beide Gene wurden in genomweiten Assoziationsstudien (GWAS) Varianten entdeckt, welche zu der Entwicklung einer Adipositas bzw. deren Folgeerkrankungen beitragen können. So wurde für Einzelbasenaustausche (SNPs) im MTNR1B (rs10830963, rs4753426) eine Verschlechterung der Nüchternglukose sowie der Insulinausschüttung gezeigt. Zudem wurde für die Allelfrequenz des rs4753426 C-Allels ein Zusammenhang mit der täglichen Sonnenscheindauer beschrieben. Im FTO wurde eine (tagging) Variante im ersten Intron identifiziert (rs9939609), welche einen erhöhten Körpermasseindex (BMI) zu vermitteln scheint und robust repliziert werden konnte. Zusätzlich konnte in den Sorben, einer in der Lausitz ansässigen Volksgruppe, eine Variante im dritten Intron (rs17818902) beschrieben werden, die ein zusätzliches, stärkeres Assoziationssignal mit einem erhöhten BMI zeigte. Dies führte zu der Fragestellung, ob MTNR1B und FTO einer Konservierung unterlegen sind. Zudem interessierten populationsspezifische Unterschiede, um die Untersuchungen in den Kontext der Hypothese des sparsamen Genotyps stellen zu können. Demnach haben Individuen mit einer genetischen Veranlagung, die ihnen eine effizientere Energiespeicherung ermöglicht, zu Zeiten von Nahrungsmangel einen Fitness-Vorteil gegenüber Nicht-Trägern. Die Konservierung zwischen den Spezies wurde mit Phylogenetic Analysis by Maximum Likelihood (PAML) betrachtet, eine Analyse die auf dem Verhältnis von nichtsynonymen zu synonymen Basenaustauschen innerhalb einer kodierenden Sequenz beruht. Die Selektion innerhalb bzw. zwischen menschlichen Populationen wurde anhand verschiedener populationsgenetischer Variablen näher beleuchtet. Sowohl für MTNR1B als auch für FTO konnte gezeigt werden, dass sie über die betrachteten Spezies im Durchschnitt stark oder sehr stark konserviert sind, was die physiologische Relevanz dieser Gene untermauert. Für MTNR1B zeigte sich zudem, dass es auf dem Ast zum Menschen nicht konserviert, sondern positiv selektioniert ist. Dies kann als Anzeichen für durch die Umwelt bedingte Einflüsse gedeutet werden. Essentielle Residuen des Rezeptors sind jedoch auch hier hochgradig konserviert. Die populationsgenetischen Variablen implizieren bei beiden Genen eine nicht-neutrale Selektion. Während sich beim MTNR1B insbesondere populationsspezifische Unterschiede anhand des Fixierungsindex Fst zeigten, konnten für FTO marginal signifikante Korrelationen zwischen der Konservierung der Haplotypen und der Stärke der Assoziation mit BMI in den Sorben gezeigt werden. Für beide Gene kann die Hypothese des sparsamen Genotyps nicht prinzipiell ausgeschlossen werden, allerdings sind weitere Untersuchungen diesbezüglich von Nöten.

Master of Science / Department of Human Nutrition / Mary Meck Higgins / Because of the ever-changing nature of the economy and the food environment, research as recent as 2010 may not be relevant to today’s discussion on food insecurity, food deserts, obesity rates, and nutritional quality in the U.S. population’s diet. Today, people of low socioeconomic status in the U.S. are at risk for overweight, obesity, and chronic illnesses such as type 2 diabetes, hypertension, and certain cancers. In this report, I investigate published research about low-income populations in the U.S. relative to the food environment and describe implications for healthcare professionals implementing interventions with these populations, discussed in the following categories: Dietary Intake Quality and Socioeconomic Status; Food Insecurity; Barriers to Quality Food Access in the U.S. Food Environment; Communities Alleviating Food Insecurity; Food-Related Perceptions, Attitudes, and Behaviors; Homelessness and Food-Related Behaviors; Why Do People Buy What They Buy?; Nutrition Assistance Programs and Policies; Current U.S. Food Costs; and Comparing the Nutritional Value Versus Price of Foods. Although the literature on the subject of low-income diet quality is thorough, much of it needs to be updated with current data on food prices, food environments, and U.S. diet quality. For this purpose, I compiled the most recent data from the National Bureau of Labor & Statistics on food prices to discuss the elevated food prices of healthful foods as opposed to less healthful foods. I also created a one-month menu based on the U.S. Department of Agriculture’s Thrifty Food Plan budget allowance in order to follow a healthful diet in this harsh economic climate utilizing the Dietary Guidelines for Americans 2010 and the Affordable Nutrients Index.

Globally, the prevalence of Type 2 diabetes is rising. The most affected populations are those that have undergone recent and rapid transition towards a Western lifestyle, characterised by energy-dense diets and physical inactivity.¶ Two major hypotheses have attempted to explain the variation in diabetes prevalence, both between and within populations, beyond the contributions made by adult lifestyle. The thrifty genotype hypothesis proposes that some populations are genetically well adapted to surviving in a subsistence environment, and are predisposed to develop diabetes when the dietary environment changes to one that is fat and carbohydrate rich. The programming hypothesis focuses on the developmental environment, particularly on prenatal and early postnatal conditions: nutritional deprivation in utero and early postnatal life, measured by low birthweight and disrupted child growth, is proposed to alter metabolism permanently so that risk of diabetes is increased with subsequent exposure to an energy-dense diet. Both hypotheses emphasise discord between adaptation (genetic or developmental) and current environment, and both now put forward insulin resistance as a likely mechanism for predisposition.¶ Diabetes contributes significantly to morbidity and mortality among Australia’s Indigenous population. Indigenous babies are more likely to be low birthweight, and typical patterns of child growth include periods of faltering and rapid catch-up. Although there have been numerous studies in other populations, the programming hypothesis has not previously been tested in an Australian Indigenous community. The framework of the programming hypothesis is thus expanded to consider exposure of whole populations to adverse prenatal and postnatal environments, and the influence this may have on diabetes prevalence.¶ The present study took place in Cherbourg, a large Aboriginal community in southeast Queensland with a high prevalence of diabetes. Study participants were adults with diagnosed diabetes and a random sample of adults who had never been diagnosed with diabetes. Data were collected on five current risk factors for diabetes (general and central obesity, blood pressure, age and family history), in addition to fasting blood glucose levels. A lifestyle survey was also conducted. Participants’ medical records detailing weight growth from birth to five years were analysed with regard to adult diabetes risk to determine whether childhood weight and rate of weight gain were associated with subsequent diabetes. Adult lifestyle factors were xiialso explored to determine whether variation in nutrition and physical activity was related to level of diabetes risk.¶ Approximately 20% of adults in Cherbourg have diagnosed diabetes. Prevalence may be as high as 38.5% in females and 42% in males if those who are high-risk (abnormal fasting glucose and three additional factors) are included. Among those over 40 years, total prevalence is estimated to be 51% for females and 59% for males.¶ Patterns of early childhood growth may contribute to risk of diabetes among adults. In particular, relatively rapid weight growth to five years is associated with both general and central obesity among adult women. This lends some qualified support to the programming hypothesis as catch-up growth has previously been incorporated into the model; however, although the most consistent association was found among those who gained weight more rapidly, it was also found that risk is increased among children who are heavier at any age.¶ No consistent associations were found between intrauterine growth retardation (as determined by lower than median birthweight and higher than median weight growth velocity to one and three months) and diabetes risk among women or men. A larger study sample with greater statistical power may have yielded less ambiguous results.¶ Among adults, levels of physical activity may be more important than nutritional intake in moderating diabetes risk, although features of diet, such as high intake of simple carbohydrates, may contribute to risk in the community overall, especially in the context of physical inactivity. A genetic component is not ruled out. Two additional areas which require further investigation include stress and high rates of infection, both of which are highly relevant to the study community, and may contribute to the insulin resistance syndrome.¶ Some accepted thresholds indicating increased diabetes risk may not be appropriate in this population. Given the relationship between waist circumference and other diabetes risk factors and the propensity for central fat deposition among women even with low body mass index (BMI), it is recommended that the threshold where BMI is considered a risk be lowered by 5kg/m2 for women, while no such recommendation is made for men.¶ There are a number of social barriers to better community health, including attitudes to exercise and obesity, patterns of alcohol and tobacco use and consumption of fresh foods. Some of these barriers are exacerbated by gender roles and expectations.¶

Obesity prevalence continues to increase worldwide, yet few safe and effective treatment options are available suggesting there needs to be a greater emphasis on preventing rather than treating obesity. This research investigated the association of obesity predisposing SNPs and a gene score with nutrient consumption patterns including total energy intake and macronutrient distribution in a European ancestry population as well as discussing an evolutionary perspective on eating disorders using current epidemiological evidence to identify genes which may be involved. The association of two of the 14 obesity predisposing SNPs and the gene score with BMI was confirmed in the EpiDREAM population. Novel associations between two SNPs located in or near BDNF (rs6265 and rs1401635) were found with total fat, MUFA, and PUFA intake. Rs1401635 was also associated with total energy and trans fat intake. Novel associations of rs6235 (PCSK1) and the gene score were found with total energy intake. The novel associations found indicate that food related behaviours are one of the mechanisms of action through which obesity predisposing SNPs cause obesity and therefore warrant further investigation. The lack of association among all genes and the modest association of the gene score show that mechanisms other than food consumption are important. The investigation of the evolutionary history of eating disorders revealed that the adapted to flee famine hypothesis is a plausible theory explaining anorexia nervosa while the thrifty genotype hypothesis provides a possible explanation for bulimia nervosa and binge eating disorder. These evolutionary theories can be applied to identify new candidate genes as well as phenotypic traits to investigate to better understand the genetic architecture of eating disorders. Understanding genes associated with disordered eating patterns may highlight future areas for obesity prevention. / Thesis / Master of Science (MSc) / A large percentage of the risk of developing obesity or an eating disorder (anorexia nervosa, bulimia nervosa, and binge eating disorder) is determined by genetics. For obesity, many genes have been identified as influencing risk, but the mechanisms through which the genes work are largely unknown. For eating disorders, gene identification efforts have been mostly unsuccessful and no mechanisms of action have been determined. In the first component of this thesis we found an association between previously identified obesity risk genes and food intake, specifically the total number of calories consumed per day and the percentage of calories from total fat and fat subtypes. These results support that food related behaviours are possible mechanisms of action which need to be further investigated. In the second half of the thesis we viewed eating disorder behaviours from an evolutionary perspective. We concluded that there are theories that possibly explain eating disorder behaviours including being able to live off of small quantities of food as well as binging. These evolutionary theories can be applied to identify new genes to study in the context of eating disorders as well as different definitions of eating disorders.

The hand has the highest surface area-to-volume ratio of any body part. This property offers the potential for the hand to serve an important function in thermoregulation through radiative heat loss. Theoretically, the capacity for heat loss may be influenced by hand and digit proportions, but the extent to which these proportions influence the hand's radiative properties remains under-investigated. Although hand morphology is highly constrained by both integration and functional dexterity, phenotypic variation in hand and digit proportions across human populations shows broad ecogeographic patterns. These patterns have been associated with climate adaptation. However, the theory linking climate adaptation to such ecogeographic patterns is based on underlying assumptions relating to thermodynamic principles, which have not been tested in vivo. This study sought to determine the influence of hand and digit proportions on heat loss from the hands directly, the additional anthropometric factors that may affect this relationship, and the impact of variation in hand proportions on dexterity in the cold. The relationship between hand proportions and thermoregulation was tested through both laboratory-based investigation and a field study. The laboratory investigation assessed the relationship between hand proportions and heat loss, the influence of body size and composition on this relationship, and the effect of morphological variation on manual dexterity. Participants (N=114; 18-50 years of age), underwent a 3-minute ice-water hand-immersion. Thermal imaging analysis was used to quantify heat loss. Hand and digit proportions were quantified using 2D and 3D scanning techniques; body size and composition were measured using established anthropometric methods and bio-impedance analysis. After accounting for body size, hand width, digit-to-palm length ratio, and skeletal muscle mass were significant predictors of heat loss from the hand, whilsthand length and fat mass were not. A separate set of participants (N=40) performed a Purdue pegboard dexterity test before and after the immersion test, which demonstrated that digit width alone negatively correlated with dexterity. The field study tested whether phenotypic variation in upper limb proportions could be attributed to cold adaptation or selection for dexterity in living populations exposed to significant energetic stress. Upper limb segment lengths were obtained from participants (N=254; 18-59 years of age), from highland and lowland regions of the Nepalese Himalayas using established anthropometric methods, and relative hand proportions were assessed in relation to severe energetic stress associated with life at high altitude. Relative to height, hand length and hand width were not reduced with altitude stress, whilst ulna length was. This indicates that cold adaptation is not shaping hand proportions in this case, although phenotypic variation in other limb segments may be attributed to cold adaptation or a thrifty phenotype mechanism. The current study provides empirical evidence to support the link between surface area-to-volume ratio, thermodynamic principles and ecogeographical patterns in human hand morphology. However, this research also demonstrates the complexity of the hand's role in thermoregulation; not only do other factors such as muscularity affect heat loss from the hand, but hand morphology is also highly constrained by integration and dexterity.