Fit not Fat

Obesity and the Economics of Prevention
Fit not Fat
DOI:10.1787/9789264084865-en
This book examines the scale and characteristics of the obesity epidemic, the respective roles and influence of market forces and governments, and the impact of interventi…

Obesity and the Economics of Prevention

Fit not Fat

DOI:10.1787/9789264084865-en

This book examines the scale and characteristics of the obesity epidemic, the respective roles and influence of market forces and governments, and the impact of interventions.

Childhood Overweight and Obesity

The Consequences of Childhood Overweight and Obesity
Stephen R. Daniels

Journal: The Future of Children
Volume 16, Number 1, Spring 2006
pp. 47-67 | 10.1353/foc.2006.0004

The Consequences of Childhood Overweight and Obesity

Journal: The Future of Children
Volume 16, Number 1, Spring 2006
pp. 47-67 | 10.1353/foc.2006.0004

Obesity Among Swedish Men

No Country for Fat Men? Obesity, Earnings, Skills, and Health Among 450,000 Swedish Men Petter Lundborg Lund University School of Economics and Management; Tinbergen Institute; Institute for the Study of Labor (IZA) Paul Nystedt Linkoping University Dan-Olof Rooth University of Kalmar; Institute for the Study of Labor (IZA) IZA Discussion Paper No. 4775 Abstract: The […]


Petter Lundborg


Lund University School of Economics and Management; Tinbergen Institute; Institute for the Study of Labor (IZA)

Paul Nystedt


Linkoping University

Dan-Olof Rooth


University of Kalmar; Institute for the Study of Labor (IZA)

IZA Discussion Paper No. 4775
Abstract:

The negative association between obesity and labor market outcomes has been widely documented, yet little is known about the mechanisms through which the association arises. Using rich and unique data on 450,000 Swedish men enlisting for the military, we find that the crude obesity penalty in earnings, which amounts to about 18 percent, is linked to supply-side characteristics that are associated with both earnings and obesity. In particular, we show that the penalty reflects negative associations between obesity, on the one hand, and cognitive skills, non-cognitive skills, and physical fitness, on the other. Our results suggest that employers use obesity as a marker for skill limitations in order to statistically discriminate.

Number of Pages in PDF File: 41

Keywords: obesity, overweight, earnings, cognitive ability, non-cognitive ability, health, physical fitness

JEL Classification: I10, J10, J70

overweight and obesity are challenges among primary school children

Prevalence and Implications of Overweight and Obesity in Children’s Health and Learning Behavior: The Case of Kinondoni and Njombe Districts in Tanzania Kafyulilo, Ayoub Cherd Online Submission, M.A. Dissertation, University of Dar es Salaam The purpose of this study was to investigate the extent to which overweight and obesity are challenges among primary school children […]

Kafyulilo, Ayoub Cherd
Online Submission, M.A. Dissertation, University of Dar es Salaam
The purpose of this study was to investigate the extent to which overweight and obesity are challenges among primary school children in Kinondoni and Njombe districts. The study sought to investigate those aspects in terms of prevalence, causes and impacts on social, health as well as children learning behaviours and outcomes. Systematic random sampling was used to select schools while stratified sampling and simple random sampling were used in selecting pupils and teachers. Measurement of weights and height were done to determine Body Mass Index (BMI), measurements of skinfolds were also done to determine body fat percentage. Questionnaires, semi-structured interview schedule and focus group discussion guides were also used. Findings revealed an average of 13.5% children, were overweight and obese. Economy status, household occupations, nutrition and inactivity were significant causes of overweight and obesity. Hypertension, excessive sweating, teasing and peer rejection were common to obese children. In addition, overweight and obese children were reported to underperform in academic and physical activities. The study revealed that overweight and obesity were not friendly healthy conditions to children, thus a need to work it out. The study suggests for establishment of education programs through mass Medias, to raise people’s awareness on implications of obesity in children’s health, social, and learning behaviours and outcomes. Seven appendixes are included: (1) Pupils’ Questionnaires; (2) Pupils’ Focus Group Discussion Guide; (3) Teachers’ Interviews; (4) Number of Children and their Weight Status in both Rural and Urban Settings (BMI Results); (5) Percentage of Children According to their Weight Status and Performance Grades in the Classroom; (6) Factors Causing Overweight and Obesity among School Children and their Level of Significance; and (7) A Map of Kinondoni and Njombe Showing the Surveyed Schools. (Contains 12 tables and 11 figures.) [Funding for this study was provided by the Dar es Salaam University College of Education.]

Progesterone

Progesterone (abbreviated as P4), also known as pregn-4-ene-3,20-dione,[5][6] is an endogenous steroid and progestogen sex hormone involved in the menstrual cycle, pregnancy, and embryogenesis of humans and other species.[7] It belongs to a group of steroid hormones called the progestogens,[7] and is the major progestogen in the body. Progesterone is also a crucial metabolic intermediate […]

Progesterone (abbreviated as P4), also known as pregn-4-ene-3,20-dione,[5][6] is an endogenous steroid and progestogen sex hormone involved in the menstrual cycle, pregnancy, and embryogenesis of humans and other species.[7] It belongs to a group of steroid hormones called the progestogens,[7] and is the major progestogen in the body. Progesterone is also a crucial metabolic intermediate in the production of other endogenous steroids, including the sex hormones and the corticosteroids, and plays an important role in brain function as a neurosteroid.[8]

It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system.[9]

Barbara McClintock

Barbara McClintock (June 16, 1902 – September 2, 1992) was an American scientist and cytogeneticist who was awarded the 1983 Nobel Prize in Physiology or Medicine. McClintock received her PhD in botany from Cornell University in 1927. There she started her career as the leader in the development of maize cytogenetics, the focus of her […]

Barbara McClintock (June 16, 1902 – September 2, 1992) was an American scientist and cytogeneticist who was awarded the 1983 Nobel Prize in Physiology or Medicine. McClintock received her PhD in botany from Cornell University in 1927. There she started her career as the leader in the development of maize cytogenetics, the focus of her research for the rest of her life. From the late 1920s, McClintock studied chromosomes and how they change during reproduction in maize. She developed the technique for visualizing maize chromosomes and used microscopic analysis to demonstrate many fundamental genetic ideas. One of those ideas was the notion of genetic recombination by crossing-over during meiosis—a mechanism by which chromosomes exchange information. She produced the first genetic map for maize, linking regions of the chromosome to physical traits. She demonstrated the role of the telomere and centromere, regions of the chromosome that are important in the conservation of genetic information. She was recognized among the best in the field, awarded prestigious fellowships, and elected a member of the National Academy of Sciences in 1944.

During the 1940s and 1950s, McClintock discovered transposition and used it to demonstrate that genes are responsible for turning physical characteristics on and off. She developed theories to explain the suppression and expression of genetic information from one generation of maize plants to the next. Due to skepticism of her research and its implications, she stopped publishing her data in 1953.

Later, she made an extensive study of the cytogenetics and ethnobotany of maize races from South America. McClintock’s research became well understood in the 1960s and 1970s, as other scientists confirmed the mechanisms of genetic change and genetic regulation that she had demonstrated in her maize research in the 1940s and 1950s. Awards and recognition for her contributions to the field followed, including the Nobel Prize in Physiology or Medicine, awarded to her in 1983 for the discovery of genetic transposition; she is the only woman to receive an unshared Nobel Prize in that category.[1]

Evolution

Microevolution happens on a small scale (within a single population), while macroevolution happens on a scale that transcends the boundaries of a single species. Despite their differences, evolution at both of these levels relies on the same, establish…

Microevolution happens on a small scale (within a single population), while macroevolution happens on a scale that transcends the boundaries of a single species. Despite their differences, evolution at both of these levels relies on the same, established mechanisms of evolutionary change:

Epigenetics

Epigenetics (from Ancient Greek επί/epi = ‘upon’, ‘over’, ‘above’ and γενετικός/genetikos = ‘genitive’ > γενεά/genea = ‘generation’ > γεννώ/geno = ‘birth to’ > γένεσις/genesis = ‘origin’) is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external orenvironmental factors that switch genes on and off and […]

Epigenetics (from Ancient Greek ???/epi = ‘upon’, ‘over’, ‘above’ and ?????????/genetikos = ‘genitive’ > ?????/genea = ‘generation’ > ?????/geno = ‘birth to’ > ???????/genesis = ‘origin’) is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external orenvironmental factors that switch genes on and off and affect how cells read genes instead of being caused by changes in the DNA sequence.[1][2] Hence, epigenetic research seeks to describe dynamic alterations in the transcriptional potential of a cell. These alterations may or may not be heritable, although the use of the term “epigenetic” to describe processes that are not heritable is controversial.[3] Unlike genetics based on changes to the DNA sequence (the genotype), the changes in gene expression or cellular phenotype of epigenetics have other causes, thus use of the prefix epi-(Greek: ???– over, outside of, around).[4][5]

The term also refers to the changes themselves: functionally relevant changes to the genome that do not involve a change in the nucleotide sequence. Examples of mechanisms that produce such changes are DNA methylation and histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA. These epigenetic changes may last through cell divisions for the duration of the cell’s life, and may also last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism;[6] instead, non-genetic factors cause the organism’s genes to behave (or “express themselves”) differently.[7]

One example of an epigenetic change in eukaryotic biology is the process of cellular differentiation. During morphogenesis, totipotent stem cells become the various pluripotentcell lines of the embryo, which in turn become fully differentiated cells. In other words, as a single fertilized egg cell – the zygote – continues to divide, the resulting daughter cells change into all the different cell types in an organism, including neurons, muscle cells, epithelium, endothelium of blood vessels, etc., by activating some genes while inhibiting the expression of others.[8]

Chimpanzee Genome Project

The Chimpanzee Genome Project is an effort to determine the DNA sequence of the Chimpanzee genome. It is expected that by comparing the genomes of humans and other apes, it will be possible to better understand what makes humans distinct from other species from a genetic perspective. Human and chimpanzee chromosomes are very similar. The […]

The Chimpanzee Genome Project is an effort to determine the DNA sequence of the Chimpanzee genome. It is expected that by comparing the genomes of humans and other apes, it will be possible to better understand what makes humans distinct from other species from a genetic perspective.

Human and chimpanzee chromosomes are very similar. The primary difference is that humans have one fewer pair of chromosomes than do other great apes. Humans have 23 pairs of chromosomes and other great apes have 24 pairs of chromosomes. In the human evolutionary lineage, two ancestral ape chromosomes fused at their telomeres, producing human chromosome 2.[3] There are nine other major chromosomal differences between chimpanzees and humans: chromosome segment inversions on human chromosomes 1, 4, 5, 9,12, 15, 16, 17, and 18. After the completion of the Human genome project, a common chimpanzee genome project was initiated. In December 2003, a preliminary analysis of 7600 genes shared between the two genomes confirmed that certain genes such as theforkhead-box P2 transcription factor, which is involved in speech development, are different in the human lineage. Several genes involved in hearing were also found to have changed during human evolution, suggesting selection involving human language-related behavior. Differences between individual humans and common chimpanzees are estimated to be about 10 times the typical difference between pairs of humans.[4]

About 600 genes have been identified that may have been undergoing strong positive selection in the human and chimp lineages; many of these genes are involved in immune system defense against microbial disease (example: granulysin is protective against Mycobacterium tuberculosis [8]) or are targeted receptors of pathogenic microorganisms (example: Glycophorin C and Plasmodium falciparum). By comparing human and chimp genes to the genes of other mammals, it has been found that genes coding fortranscription factors, such as forkhead-box P2 (FOXP2), have often evolved faster in the human relative to chimp; relatively small changes in these genes may account for the morphological differences between humans and chimps. A set of 348 transcription factor genes code for proteins with an average of about 50 percent more amino acid changes in the human lineage than in the chimp lineage.

Six human chromosomal regions were found that may have been under particularly strong and coordinated selection during the past 250,000 years. These regions contain at least one marker allele that seems unique to the human lineage while the entire chromosomal region shows lower than normal genetic variation. This pattern suggests that one or a few strongly selected genes in the chromosome region may have been preventing the random accumulation of neutral changes in other nearby genes. One such region on chromosome 7 contains the FOXP2 gene (mentioned above) and this region also includes the Cystic fibrosis transmembrane conductance regulator (CFTR) gene, which is important for ion transport in tissues such as the salt-secreting epithelium of sweat glands. Human mutations in the CFTR gene might be selected for as a way to survivecholera.[9]

Another such region on chromosome 4 may contain elements regulating the expression of a nearby protocadherin gene that may be important for brain development and function. Although changes in expression of genes that are expressed in the brain tend to be less than for other organs (such as liver) on average, gene expression changes in the brain have been more dramatic in the human lineage than in the chimp lineage.[10] This is consistent with the dramatic divergence of the unique pattern of human brain development seen in the human lineage compared to the ancestral great ape pattern. The protocadherin-beta gene cluster on chromosome 5 also shows evidence of possible positive selection.[11]

Results from the human and chimp genome analyses should help in understanding some human diseases. Humans appear to have lost a functional caspase-12 gene, which in other primates codes for an enzyme that may protect against Alzheimer’s disease.

The results of the chimpanzee genome project suggest that when ancestral chromosomes 2A and 2B fused to produce human chromosome 2, no genes were lost from the fused ends of 2A and 2B. At the site of fusion, there are approximately 150,000 base pairs of sequence not found in chimpanzee chromosomes 2A and 2B. Additional linked copies of the PGML/FOXD/CBWD genes exist elsewhere in the human genome, particularly near the p end of chromosome 9. This suggests that a copy of these genes may have been added to the end of the ancestral 2A or 2B prior to the fusion event. It remains to be determined if these inserted genes confer a selective advantage.

  • PGML. The phosphoglucomutase-like gene of human chromosome 2. This gene is incomplete and may not produce a functional transcript.[12]
  • FOXD. The forkhead box D4-like gene is an example of an intronless gene. The function of this gene is not known, but it may code for a transcription control protein.
  • CBWD. Cobalamin synthetase is a bacterial enzyme that makes vitamin B12. In the distant past, a common ancestor to mice and apes incorporated a copy of a cobalamin synthetase gene (see: Horizontal gene transfer). Humans are unusual in that they have several copies of cobalamin synthetase-like genes, including the one on chromosome 2. It remains to be determined what the function of these human cobalamin synthetase-like genes is. If these genes are involved in vitamin B12 metabolism, this could be relevant to human evolution. A major change in human development is greater post-natal brain growth than is observed in other apes. Vitamin B12is important for brain development, and vitamin B12 deficiency during brain development results in severe neurological defects in human children.
  • CXYorf1-like protein. Several transcripts of unknown function corresponding to this region have been isolated. This region is also present in the closely related chromosome 9p terminal region that contains copies of the PGML/FOXD/CBWD genes.
  • Many ribosomal protein L23a pseudogenes are scattered through the human genome.

Benzodiazepines (BZD)

Benzodiazepines (BZD), sometimes called “benzos“, are a class of psychoactive drugs whose core chemical structure is the fusion of a benzene ring and a diazepine ring. The first such drug, chlordiazepoxide (Librium), was discovered accidentally by Leo Sternbach in 1955, and made available in 1960 by Hoffmann–La Roche – which, since 1963, has also marketed […]

Benzodiazepines (BZD), sometimes called “benzos“, are a class of psychoactive drugs whose core chemical structure is the fusion of a benzene ring and a diazepine ring. The first such drug, chlordiazepoxide (Librium), was discovered accidentally by Leo Sternbach in 1955, and made available in 1960 by Hoffmann–La Roche – which, since 1963, has also marketed the benzodiazepinediazepam (Valium).[1] In 1977 benzodiazepines were globally the most prescribed medications.[2]

Benzodiazepines enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor, resulting insedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties. High doses of many shorter-acting benzodiazepines may also cause anterograde amnesia and dissociation.[3] These properties make benzodiazepines useful in treating anxiety, insomnia, agitation, seizures, muscle spasms, alcohol withdrawal and as a premedication for medical or dental procedures.[4] Benzodiazepines are categorized as either short-, intermediate-, or long-acting. Short- and intermediate-acting benzodiazepines are preferred for the treatment of insomnia; longer-acting benzodiazepines are recommended for the treatment of anxiety.[5]

Benzodiazepines are generally viewed as safe and effective for short-term use, although cognitive impairment and paradoxical effects such as aggression or behavioral disinhibition occasionally occur. A minority of people can have paradoxical reactions such as worsened agitation or panic.[6] Long-term use is controversial because of concerns about adverse psychological and physical effects, decreasing effectiveness, and physical dependence and withdrawal.[7][8] As a result of adverse effects associated with the long-term use of benzodiazepines, withdrawal from benzodiazepines, in general, leads to improved physical and mental health.[9][10]The elderly are at an increased risk of suffering from both short- and long-term adverse effects,[9][11] and as a result, all benzodiazepines are listed in the Beers List of inappropriate medications for older adults.[12]

There is controversy concerning the safety of benzodiazepines in pregnancy. While they are not major teratogens, uncertainty remains as to whether they cause cleft palate in a small number of babies and whether neurobehavioural effects occur as a result of prenatal exposure;[13] they are known to cause withdrawal symptoms in the newborn. Benzodiazepines can be taken in overdoses and can cause dangerous deep unconsciousness. However, they are much less toxic than their predecessors, the barbiturates, and death rarely results when a benzodiazepine is the only drug taken; however, when combined with other central nervous system (CNS) depressants such as ethanol and opioids, the potential for toxicity and fatal overdose increases.[14] Benzodiazepines are commonly misused and taken in combination with other drugs of abuse.[15][16][17]