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.]

Theory of Change

The Center for Theory of Change is a non-profit organization established to promote quality standards and best practice for the development and implementation of Theory of Change, with a particular focus on its use and application in the areas of … Continue reading

The Center for Theory of Change is a non-profit organization established to promote quality standards and best practice for the development and implementation of Theory of Change, with a particular focus on its use and application in the areas of international development, sustainability, education, human rights and social change.

Theory of Change (ToC) is a specific type of methodology for planning, participation, and evaluation that is used in the philanthropy, not-for-profit and government sectors to promote social change. Theory of Change defines long-term goals and then maps backward to identify necessary preconditions.[1]

Theory of Change explains the process of change by outlining causal linkages in an initiative, i.e., its shorter-term, intermediate, and longer-term outcomes. The identified changes are mapped –as the “outcomes pathway” – showing each outcome in logical relationship to all the others, as well as chronological flow. The links between outcomes are explained by “rationales” or statements of why one outcome is thought to be a prerequisite for another.[2]

The innovation of Theory of Change lies (1) in making the distinction between desired and actual outcomes, and (2) in requiring stakeholders to model their desired outcomes before they decide on forms of intervention to achieve those outcomes. A common error in describing Theory of Change is the belief that it is simply a methodology for planning and evaluation.[3] Theory of Change is instead a form of critical theory that ensures a transparent distribution of power dynamics. Further, the process is necessarily inclusive of many perspectives and participants in achieving solutions.

Theory of Change can begin at any stage of an initiative, depending on the intended use. A theory developed at the outset is best at informing the planning of an initiative. Having worked out a change model, practitioners can make more informed decisions about strategy and tactics. As monitoring and evaluation data become available, stakeholders can periodically refine the Theory of Change as the evidence indicates. A Theory of Change can be developed retrospectively by reading program documents, talking to stakeholders and analyzing data. This is often done during evaluations reflecting what has worked or not in order to understand the past and plan for the future.

Scared Straight

Doing What Doesn’t Work Why Scared Straight Programs Are a Waste of Taxpayer Dollars Research shows that Scared Straight programs, which bring at-risk teens to prisons in an effort to deter them from potential criminal behavior, have no positive effect … Continue reading

Doing What Doesn’t Work

Why Scared Straight Programs Are a Waste of Taxpayer Dollars

Research shows that Scared Straight programs, which bring at-risk teens to prisons in an effort to deter them from potential criminal behavior, have no positive effect and can actually lead to a greater likelihood of offending actions.

Court Orders Act of 2016 (CCOA)

“This draft bill is the most ludicrous, dangerous, technically illiterate tech policy proposal of the 21st century so far.” – Kevin Bankston, director of New America’s Open Technology Institute.1 Last week, privacy advocates and security experts widely denounced draft encryption … Continue reading

“This draft bill is the most ludicrous, dangerous, technically illiterate tech policy proposal of the 21st century so far.” – Kevin Bankston, director of New America’s Open Technology Institute.1

Last week, privacy advocates and security experts widely denounced draft encryption legislation leaked to The Hill newspaper as a radical assault on privacy that would make the American people less safe.2, 3

The Compliance with Court Orders Act of 2016 (CCOA) would undermine Americans’ privacy, make encryption illegal and force companies to weaken the security of their products and services. We need to make sure this dangerous legislation doesn’t gain any traction in Congress.

Sign the petition: Stop the Burr-Feinstein attack on privacy and security. Click here to sign the petition.

The CCOA, which is being drafted by Senate Intelligence Committee Chair Richard Burr (R-AL) and Ranking Member Dianne Feinstein (D-CA), is bad policy for a number of reasons. It would:

  • Make end-to-end encryption illegal by requiring companies to provide “information or data” to the government “in an intelligible format” anytime they are served with a court order. It would also require companies to decrypt secure communications “in a timely manner” or give technical assistance to law enforcement agencies attempting to do so. As Sen. Ron Wyden said in a statement, “for the first time in America, companies who want to provide their customers with stronger security would not have that choice – they would be required to decide how to weaken their products to make you less safe.”4
  • Undermine Americans’ privacy by increasing the risk that their private information and information entrusted to businesses is accessed by criminals, hackers and government entities, both domestically and abroad.
  • Make American technology companies less competitive by making it illegal for them to offer secure communications protected by end-to-end encryption, which is currently relied upon by Google, Apple, Facebook, WhatsApp and countless other companies.6 Foreign companies would not be bound by this constraint. As the executive director of a trade group that represents thousands of app developers put it, “the senators might as well take a hatchet to the entire Internet economy.”7
  • Force platforms to censor applications by requiring license distributors to ensure that all “products, services, applications or software” they distribute are able to provide the content of communications to law enforcement agencies “in an intelligible format.” This would put Apple, Google and any other company that operates a platform for software applications in the untenable position of vetting every app to make sure they aren’t secure, and censoring those that are secure.8

Tell Congress: Reject legislation that would undermine our privacy and security. Click here to sign the petition.

As we saw with the FBI’s recent attempt to force Apple to create a backdoor to access San Bernardino shooter Syed Farook’s iPhone, law enforcement agencies are determined to undermine Americans’ privacy and security, and gain access to encrypted communications. The Obama administration’s sudden reversal in that case in March – which came only after it said a third party had helped it access the content of the phone without Apple’s help – doesn’t change its desire to force companies to weaken the security of their own products. Indeed, in an April 8 letter to a district court judge presiding over a separate case, the Department of Justice maintained that “the government continues to require Apple’s assistance in accessing the data that it is authorized to search by warrant.”9

As this debate continues to play out over the coming weeks and months, we need to forcefully reject the dangerous language in the draft Burr-Feinstein bill and any other legislation that would put Americans’ privacy and security at risk by undermining encryption.

Sign the petition to Congress: Stop the Burr-Feinstein attack on privacy and security. Click here to sign the petition.

Thanks for fighting to protect our privacy and security.

Josh Nelson, Campaign Manager
CREDO Action from Working Assets

Add your name:

Sign the petition ?
  1. Anti-Encryption Bill from Senators Burr and Feinstein Would Be Disastrous for Cybersecurity, Tech Economy,” Open Technology Institute, March 31, 2016.
  2. Cory Bennett, “Senate encryption bill draft mandates ‘technical assistance’,” The Hill, April 7, 2016.
  3. Jenna McClaughlin, “Bill That Would Ban End-to-End Encryption Savaged by Critics,” The Intercept, April 8, 2016.
  4. Wyden Statement on Draft Bill Requiring Companies to Undermine Strong Encryption,” April 8. 2016.
  5. Max J. Rosenthal, “Tech and Privacy Experts Erupt Over Leaked Encryption Bill,” Mother Jones, April 8, 2016.
  6. Andy Greenberg, “The Senate’s Draft Encryption Bill Is ‘Ludicrous, Dangerous, Technically Illiterate’,” Wired, April 8 2016.
  7. Dawn Chmielewski, “The New Encryption Bill Isn’t Finished and Silicon Valley Already Hates it,” Recode, April 6, 2016.
  8. Andy Greenberg, “The Senate’s Draft Encryption Bill Is ‘Ludicrous, Dangerous, Technically Illiterate’,” Wired, April 8 2016.
  9. Julian Chokkattu, “Apple vs. U.S. isn’t over yet; Feinstein-Burr ‘encryption bill’ draft surfaces,” Digital Trends, April 8, 2016.

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]