Question 1.

Primordial soup
Life on Earth began more than 3 billion years ago, evolving from the most
basic of microbes into a dazzling array of complexity over time. But how did
the first organisms on the only known home to life in the universe develop
from the primordial soup?

One theory involved a "shocking" start. Another idea is utterly chilling. And
one theory is out of this world!

Inside you'll learn just how mysterious this all is, as we reveal the different
scientific theories on the origins of life on Earth.

Electric Spark

Lightning may have provided the spark needed for life to begin.

Electric sparks can generate amino acids and sugars from an atmosphere
loaded with water, methane, ammonia and hydrogen, as was shown in
the famous Miller-Urey experiment reported in 1953, suggesting that
lightning might have helped create the key building blocks of life on Earth in
its early days. Over millions of years, larger and more complex molecules
could form. Although research since then has revealed the early atmosphere
of Earth was actually hydrogen-poor, scientists have suggested that volcanic
clouds in the early atmosphere might have held methane, ammonia and
hydrogen and been filled with lightning as well.

Community Clay

The first molecules of life might have met on clay, according to an idea
elaborated by organic chemist Alexander Graham Cairns-Smith at the
University of Glasgow in Scotland. These surfaces might not only have
concentrated these organic compounds together, but also helped organize
them into patterns much like our genes do now.

The main role of DNA is to store information on how other molecules should
be arranged. Genetic sequences in DNA are essentially instructions on how
amino acids should be arranged in proteins. Cairns-Smith suggests that
mineral crystals in clay could have arranged organic molecules into
organized patterns. After a while, organic molecules took over this job and
organized themselves.

Or maybe life began at the bottom of the sea. Keep going to learn how.

Deep-Sea Vents

The deep-sea vent theory suggests that life may have begun at submarine
hydrothermal vents spewing key hydrogen-rich molecules. Their rocky nooks
could then have concentrated these molecules together and provided
mineral catalysts for critical reactions. Even now, these vents, rich in
chemical and thermal energy, sustain vibrant ecosystems.

The next idea is a chilling thought. Read on!

Chilly Start

Ice might have covered the oceans 3 billion years ago, as the sun was about
a third less luminous than it is now, scientists say. This layer of ice, possibly
hundreds of feet thick, might have protected fragile organic compounds in
the water below from ultraviolet light and destruction from cosmic impacts.
The cold might have also helped these molecules to survive longer, allowing
key reactions to happen. [Related: The Ingredients of Life]

Understanding lifes origin may involve unravelling the mystery of DNA's

formation, as we explain next.

RNA World

Nowadays DNA needs proteins in order to form, and proteins require DNA to
form, so how could these have formed without each other? The answer may
be RNA, which can store information like DNA, serve as an enzyme like
proteins, and help create both DNA and proteins. Later DNA and proteins
succeeded this "RNA world," because they are more efficient.

RNA still exists and performs several functions in organisms, including acting
as an on-off switch for some genes. The question still remains how RNA got
here in the first place. And while some scientists think the molecule could
have spontaneously arisen on Earth, others say that was very unlikely to
have happened. Other nucleic acids other than RNA have been suggested as
well, such as the more esoteric PNA or TNA.

A study in 2015 suggests the missing link in this RNA puzzle may have been
found.

We have two last ideas to throw at you . . .

Simple Beginnings

Instead of developing from complex molecules such as RNA, life might have
begun with smaller molecules interacting with each other in cycles of
reactions. These might have been contained in simple capsules akin to cell
membranes, and over time more complex molecules that performed these
reactions better than the smaller ones could have evolved, scenarios dubbed
"metabolism-first" models, as opposed to the "gene-first" model of the "RNA
world" hypothesis.

The final theory is truly out of this world. Check out the next slide.

Panspermia

Perhaps life did not begin on Earth at all, but was brought here from
elsewhere in space, a notion known as panspermia. For instance, rocks
regularly get blasted off Mars by cosmic impacts, and a number of Martian
meteorites have been found on Earth that some researchers have
controversially suggested brought microbes over here, potentially making us
all Martians originally. Other scientists have even suggested that life might
have hitchhiked on comets from other star systems. However, even if this
concept were true, the question of how life began on Earth would then only
change to how life began elsewhere in space.

Oh, and if you thought all that was mysterious, consider this: Scientists admit
they don't even have a good definition of life!
The origin of life is a scientific problem which is not yet solved. There are plenty of ideas, but few
clear facts.[1]

It is generally agreed that all life today evolved by common descent from a single primitive lifeform.
[2]
We do not know how this early form came about, but scientists think it was a
natural process which took place perhaps 3,900 million years ago. This is in accord with
a philosophy called naturalism: only natural causes are admitted.

We do not know whether metabolism or genetics came first. The main hypothesis which supports
genetics first is RNA world hypothesis, and the one which supports metabolism first is Protein
world hypothesis.

Another big problem is how cells develop. All existing forms of life are built out of cells.[3]

The Nobel Prize in Chemistry winner Melvin Calvin wrote a book on the subject,[4] and so
did Alexander Oparin.[5] What links most of the early work on the origin of life was the idea that
before biological evolution began there must have been a process of chemical evolution. [6] Another
question which has been discussed by J.D. Bernal and others is the origin of thecell membrane. By
concentrating the chemicals in one place, the cell membrane performs a vital function. [7]

Fossil record[change | change source]

Earliest claimed life on Earth[change | change source]

The earliest claimed lifeforms are fossilized microorganisms (or microfossils). They were found in
iron and silica-rich rocks which were once hydrothermal vents in theNuvvuagittuq greenstone
belt of Quebec, Canada.

These rocks are as old as 4.28 billion years. The tubular forms they contain are shown in a report.
[8]
If this is the oldest record of life on Earth, it suggests "an almost instantaneous emergence of life"
after oceans formed 4.4 billion years ago.[9][10][11] According to Stephen Blair Hedges, "If life arose
relatively quickly on Earth then it could be common in the universe."[12]

Previous earliest[change | change source]

A scientific study from 2002 showed that geological formations of stromatolites 3.45 billion years old
contain fossilized cyanobacteria.[13][14] At the time it was widely agreed that stromatolites were oldest
known lifeform on Earth which had left a record of its existence. Therefore, if life originated on Earth,
this happened sometime between 4.4 billion years ago, when water vapor first liquefied,[15] and 3.5
billion years ago. This is the background to the latest discovery discussed above.

Earliest evidence of life comes from the Isua supercrustal belt in Western Greenland and from
similar formations in the nearby Akilia Islands. This is because a high level of the
lighter isotope of carbon is found there. Living things uptake lighter isotopes because this takes less
energy. Carbon entering into rock formations has a concentration of elemental 13C of about 5.5.
of 12C, biomass has a 13C of between 20 and 30. These isotopic fingerprints are preserved in the
rocks. With this evidence, Mojzis suggested that life existed on the planet already by 3.85 billion
years ago.[16]

A few scientists think life might have been carried from planet to planet by the transport of spores.
This idea, now known as panspermia, was first put forward byArrhenius.[17]

History of studies into the origin of life[change | change source]

Alexander Oparin (right) at the laboratory

Spontaneous generation[change | change source]

Until the early 19th century many people believed in the regular spontaneous generation of life from
non-living matter. This was called spontaneous generation, and was disproved by Louis Pasteur. He
showed that without spores no bacteria orviruses grew on sterile material.
Darwin[change | change source]

In a letter to Joseph Dalton Hooker on 11 February 1871,[18] Charles Darwin proposed a natural
process for the origin of life.

He suggested that the original spark of life may have begun in a "warm little pond, with all sorts
of ammonia and phosphoricsalts, lights, heat, electricity, etc. A protein compound was then
chemically formed ready to undergo still more complex changes". He went on to explain that "at the
present day such matter would be instantly devoured or absorbed, which would not have been the
case before living creatures were formed".[19]

Haldane and Oparin[change | change source]

No real progress was made until 1924 when Alexander Oparin reasoned that
atmospheric oxygen prevented the synthesis of the organic molecules. Organic molecules are the
necessary building blocks for the evolution of life. In his The Origin of Life,[20][21] Oparin argued that a
"primeval soup" of organic molecules could be created in an oxygen-less atmosphere through the
action of sunlight. These would combine in ever-more complex fashions until they formed droplets.
These droplets would "grow" by fusion with other droplets, and "reproduce" through fission into
daughter droplets, and so have a primitive metabolism in which those factors which promote "cell
integrity" survive, those that do not become extinct. Many modern theories of the origin of life still
take Oparin's ideas as a starting point.

Around the same time J.B.S. Haldane also suggested that the Earth's pre-biotic oceans, which were
very different from what oceans are now, would have formed a "hot dilute soup". In this soup, organic
compounds, the building blocks of life, could have formed. This idea was called biopoiesis, the
process of living matter evolving from self-replicating but nonliving molecules. [22]

Early conditions on Earth[change | change source]

There is almost no geological record from before 3.8 billion years ago. The environment that existed
in the Hadean era was hostile to life, but how much so is not known. There was a time, between 3.8
and 4.1 billion years ago, which is known as the Late Heavy Bombardment. It is so named because
many lunar craters are thought to have formed then. The situation on other planets, such as
Earth, Venus, Mercury and Mars must have been similar. These impacts would likely sterilizethe
Earth (kill all life), if it existed at that time.[23]

Several people have suggested that the chemicals in the cell give clues as to what the early seas
must have been like. In 1926, Macallum noted that the inorganiccomposition of the
cell cytosol dramatically differs from that of modern sea water: "the cell has endowments
transmitted from a past almost as remote as the origin of life on earth". [24] For example: "All cells
contain much more potassium, phosphate, and transition metals than modern ... oceans, lakes, or
rivers".[25] "Under theanoxic, CO2-dominated primordial atmosphere, the chemistry of inland basins
at geothermal fields would [be like the chemistry inside] modern cells". [25]

Temperature[change | change source]

If life evolved in the deep ocean, near a hydrothermal vent, it could have originated as early as 4 to
4.2 billion years ago. If, on the other hand, life originated at the surface of the planet, a common
opinion is it could only have done so between 3.5 and 4 billion years ago. [26]

Lazcano and Miller (1994) suggest that the pace of molecular evolution was dictated by the rate of
recirculating water through mid-ocean submarine vents. Complete recirculation takes 10 million
years, so any organic compounds produced by then would be altered or destroyed by temperatures
exceeding 300 C. They estimate that the development of a 100 kilobase genome of a DNA/protein
primitive heterotroph into a 7000 gene filamentous cyanobacterium would have required only 7
million years.[27]

History of Earth's atmosphere[change | change source]

Originally, the Earth's atmosphere had almost no free oxygen. It gradually changed to what it is
today, over a very long time (see Great Oxygenation Event). The process began with cyanobacteria.
They were the first organisms to make free oxygen by photosynthesis. Most organisms today need
oxygen for their metabolism; only a few can use other sources for respiration.[28][29]

So it is expected that the first proto-organisms were chemoautotrophs, and did not use aerobic
respiration. They were anaerobic.

Current models[change | change source]

There is no "standard model" on how life started. Most accepted models are built on molecular
biology and cell biology:

1. Because there are the right conditions, some basic small molecules are created. These are
called monomers of life. Amino acids are one type of these molecules. This was proved by
the MillerUrey experiment by Stanley L. Miller and Harold C. Urey in 1953, and we now
know these basic building blocks are common throughout space. Early Earth would have
had them all.
 2. Phospholipids, which can form lipid bilayers, a main component of the cell membrane.

3. Nucleotides which might join up into random RNA molecules. This might have resulted in
self-replicating ribozymes (RNA world hypothesis).

4. Competition for substrates would select mini-proteins into enzymes. The ribosome is critical
to protein synthesis in present-day cells, but we have no idea as to how it evolved.

5. Early on, ribonucleic acids would have been catalysts, but later nucleic acids are specialised
for genomic use.

The origin of the basic biomolecules, while not settled, is less controversial than the significance and
order of steps 2 and 3. The basic chemicals from which life is thought to have formed are:

Methane (CH4),

Ammonia (NH3),

Water (H2O),

Hydrogen sulfide (H2S),

Carbon dioxide (CO2) or carbon monoxide (CO), and

Phosphate (PO43-).

Molecular oxygen (O2) and ozone (O3) were either rare or absent.

Three stages[change | change source]

Stage 1: The origin of biological monomers

Stage 2: The origin of biological polymers

Stage 3: The evolution from molecules to cells

Bernal suggested that evolution may have commenced early, some time between Stage 1 and 2.

Origin of organic molecules[change | change source]

There are three sources of organic molecules on the early Earth:

 1. organic synthesis by energy sources (such as ultraviolet light or electrical discharges).

2. delivery by extraterrestrial objects such as carbonaceous meteorites (chondrites);

3. organic synthesis driven by impact shocks.

Estimates of these sources suggest that the heavy bombardment before 3.5 billion years ago made
available quantities of organics comparable to those produced by other energy sources. [30]

Miller's experiment and the primordial soup[change | change source]

Main page: MillerUrey experiment

In 1953 a graduate student, Stanley Miller, and his professor, Harold Urey, performed an experiment
that showed how organic molecules could have formed on early Earth from inorganic precursors.

The now-famous MillerUrey experiment used a highly reduced mixture of gases

methane, ammonia and hydrogen to form basic organic monomers, such asamino acids.[31] We
do know now that for more than the first half of the Earth's history its atmosphere had almost no
oxygen.

Fox's experiments[change | change source]

In the 1950s and 1960s, Sidney W. Fox studied the spontaneous formation of peptide structures
under conditions that might have existed early in Earth's history. He demonstrated that amino acids
could by itself form small peptides. These amino acids and small peptides could be encouraged to
form closed spherical membranes, called microspheres.[32]

Special conditions[change | change source]

Some scientists have suggested special conditions which could make cell synthesis easier.

Clay world[change | change source]

A clay model for the origin of life was suggested by A. Graham Cairns-Smith. Clay theory suggests
complex organic molecules arose gradually on a pre-existing non-organic platform,
namely, silicate crystals in solution.[33]
Deep-hot biosphere model[change | change source]

In the 1970s, Thomas Gold proposed the theory that life first developed not on the surface of the
Earth, but several kilometers below the surface. The discovery in the late 1990s
of nanobes (filamental structures that are smaller than bacteria, but that may contain DNA in deep
rocks) [34] might support Gold's theory.

It is now reasonably well established that microbial life is plentiful at shallow depths in the Earth (up
to five kilometers below the surface)[34] in the form ofextremophile archaea, rather than the better-
known eubacteria (which live in more accessible conditions).

Gold asserted that a trickle of food from a deep, unreachable, source is needed for survival because
life arising in a puddle of organic material is likely to consume all of its food and become extinct.
Gold's theory was that the flow of food is due to out-gassing of primordial methane from the Earth's
mantle.

Self-organization and replication[change | change source]

Self-organization and self-replication are the hallmark of living systems. Non-living molecules
sometimes show those features under proper conditions. For example, Martin and Russel showed
that cell membranes separating contents from the environment and self-organization of self-
contained redox reactions are the most conserved attributes of living things. They argue that
inorganic matter like that would be life's most likely last common ancestor.[35]

Theories[change | change source]

RNA world hypothesis[change | change source]

In this hypothesis, RNA is said to work both as an enzyme and as a container of genes. Later, DNA
took over its genetic role.

The RNA world hypothesis proposes that life based on ribonucleic acid (RNA) pre-dates the current
world of life based on deoxyribonucleic acid (DNA), RNA and proteins. RNA is able both to store
genetic information, like DNA, and to catalyze chemical reactions, like an enzyme. It may have
supported pre-cellular life and been a major step towards cellular life.

There are some pieces of evidence which support this idea:

1. There are some RNAs which work as enzymes.

 2. Some viruses use RNA for heredity.

3. Many of the most fundamental parts of the cell (those that evolve the slowest) require RNA.
Metabolism and proteins[change | change source]

This idea suggests that proteins worked as enzymes first, producing metabolism. After
that DNA and RNA began to work as containers of genes.

This idea also has some evidences which supports this.

1. Protein as enzyme is essential for today's lives.

2. Some amino acids are formed from more basic chemicals in the Miller-Urey experiment.
Some deny this idea because Proteins cannot copy themselves.
Lipids[change | change source]

In this scheme membranes made of lipid bilayers occur early on. Once organic chemicals are
enclosed, more complex biochemistry is then possible. [36]

Panspermia[change | change source]

This is the idea suggested by Arrhenius,[37][38] and developed by Fred Hoyle,[39] that life developed
elsewhere in the universe and arrived on Earth in the form of spores. This is not a theory of how life
began, but a theory of how it might have spread. It may have spread, for example, by meteorites.[40]

Some propose that early Mars was a better place to start life than was the early Earth. The
molecules which combined to form genetic material are more complex than the "primordial soup" of
organic (carbon-based) chemicals that existed on Earth four billion years ago. If RNA was the first
genetic material, then mineralscontaining boron and molybdenum could assist its formation. These
minerals were much more common on Mars than on Earth.[41]

Question no. 2
MAJOR PERSONALITY STUDY
FINDS THAT TRAITS ARE
MOSTLY INHERITED
By DANIEL GOLEMAN
Published: December 2, 1986
THE genetic makeup of a child is a stronger influence on
personality than child rearing, according to the first study
to examine identical twins reared in different families. The
findings shatter a widespread belief among experts and
laymen alike in the primacy of family influence and are
sure to engender fierce debate.
The findings are the first major results to emerge from a
longterm project at the University of Minnesota in which,
since 1979, more than 350 pairs of twins have gone
through six days of extensive testing that has included
analysis of blood, brain waves, intelligence and allergies.
The results on personality are being reviewed for
publication by the Journal of Personality and Social
Psychology. Although there has been wide press coverage
of pairs of twins reared apart who met for the first time in
the course of the study, the personality results are the first
significant scientific data to be announced.
For most of the traits measured, more than half the
variation was found to be due to heredity, leaving less than
half determined by the influence of parents, home
environment and other experiences in life.
The Minnesota findings stand in sharp contradiction to
standard wisdom on nature versus nurture in forming
adult personality. Virtually all major theories since Freud
have given far more importance to environment, or
nurture, than to genes, or nature.
Even though the findings point to the strong influence of
heredity, the family still shapes the broad suggestion of
personality offered by heredity; for example, a family
might tend to make an innately timid child either more
timid or less so. But the inference from this study is that
the family would be unlikely to make the child brave.
The 350 pairs of twins studied included some who were
raised apart. Among these separately reared twins were 44
pairs of identical twins and 21 pairs of fraternal twins.
Comparing twins raised separately with those raised in the
same home allows researchers to determine the relative
importance of heredity and of environment in their
development. Although some twins go out of their way to
emphasize differences between them, in general identical
twins are very much alike in personality.
But what accounts for that similarity? If environment were
the major influence in personality, then identical twins
raised in the same home would be expected to show more
similarity than would the twins reared apart. But the study
of 11 personality traits found differences between the kinds
of twins were far smaller than had been assumed.
''If in fact twins reared apart are that similar, this study is
extremely important for understanding how personality is
shaped,'' commented Jerome Kagan, a developmental
psychologist at Harvard University. ''It implies that some
aspects of personality are under a great degree of genetic
control.''
The traits were measured using a personality
questionnaire developed by Auke Tellegen, a psychologist
at the University of Minnesota who was one of the
principal researchers. The questionnaire assesses many
major aspects of personality, including aggressiveness,
striving for achievement, and the need for personal
intimacy.
For example, agreement with the statement ''When I work
with others, I like to take charge'' is an indication of the
trait called social potency, or leadership, while agreement
with the sentence ''I often keep working on a problem,
even if I am very tired'' indicates the need for achievement.
Among traits found most strongly determined by heredity
were leadership and, surprisingly, traditionalism or
obedience to authority. ''One would not expect the
tendency to believe in traditional values and the strict
enforcement of rules to be more an inherited than learned
trait,'' said David Lykken, a psychologist in the Minnesota
project. ''But we found that, in some mysterious way, it is
one of traits with the strongest genetic influence.''
Other traits that the study concludes were more than 50
percent determined by heredity included a sense of well-
being and zest for life; alienation; vulnerability or
resistance to stress, and fearfulness or risk-seeking.
Another highly inherited trait, though one not commonly
thought of as part of personality, was the capacity for
becoming rapt in an aesthetic experience, such as a
concert.
Vulnerability to stress, as measured on the Tellegen test,
reflects what is commonly thought of as ''neuroticism,''
according to Dr. Lykken. ''People high in this trait are
nervous and jumpy, easily irritated, highly sensitive to
stimuli, and generally dissatisfied with themselves, while
those low on the trait are resilient and see themselves in a
positive light,'' he said. ''Therapy may help vulnerable
people to some extent, but they seem to have a built-in
susceptibility that may mean, in general, they would be
more content with a life low in stress.''
The need to achieve, including ambition and an inclination
to work hard toward goals, also was found to be genetically
influenced, but more than half of this trait seemed
determined by life experience. The same lower degree of
hereditary influence was found for impulsiveness and its
opposite, caution.
The need for personal intimacy appeared the least
determined by heredity among the traits tested; about
two-thirds of that tendency was found to depend on
experience. People high in this trait have a strong desire
for emotionally intense realtionships; those low in the trait
tend to be loners who keep their troubles to themselves.
''This is one trait that can be greatly strengthened by the
quality of interactions in a family,'' Dr. Lykken said. ''The
more physical and emotional intimacy, the more likely this
trait will be developed in children, and those children with
the strongest inherited tendency will have the greatest
need for social closeness as adults.''
No single gene is believed responsible for any one of these
traits. Instead, each trait, the Minnesota researchers
propose, is determined by a great number of genes in
combination, so that the pattern of inheritance is complex
and indirect.
No one believes, for instance, that there is a single gene for
timidity but rather a host of genetic influences. That may
explain, they say, why previous studies have found little
connection between the personality traits of parents and
their children. Whereas identical twins would share with
each other the whole constellation of genes that might be
responsible for a particular trait, children might share only
some part of that constellation with each parent.
That is why, just as a short parent may have a tall child, an
achievement-oriented parent might have a child with little
ambition.
The Minnesota findings are sure to stir debate. Though
most social scientists accept the careful study of twins,
particularly when it includes identical twins reared apart,
as the best method of assessing the degree to which a trait
is inherited, some object to using these methods for
assessing the genetic component of complex behavior
patterns or question the conclusions that are drawn from
it.
Further, some researchers consider paper-and-pencil tests
of personality less reliable than observations of how people
act, since people's own reports of their behavior can be
biased. ''The level of heritability they found is surprisingly
high, considering that questionnaires are not the most
sensitive index of personality,'' said Dr. Kagan. ''There is
often a poor relationship between how people respond on
a questionnaire and what they actually do.''
''Years ago, when the field was dominated by a
psychodynamic view, you could not publish a study like
this,'' Dr. Kagan added. ''Now the field is shifting to a
greater acceptance of genetic determinants, and there is
the danger of being too uncritical of such results.''
Seymour Epstein, a personality psychologist at the
University of Massachusetts, said he was skeptical of
precise estimates of heritability. ''The study compared
people from a relatively narrow range of cultures and
environments,'' he said. ''If the range had been much
greater - say Pygmies and Eskimos as well as middle-class
Americans - then environment would certainly contribute
more to personality. The results might have shown
environment to be a far more powerful influence than
heredity,'' he said.
Dr. Tellegen himself said: ''Even though the differences
between families do not account for much of the unique
attributes of their children, a family still exercises
important influence. In cases of extreme deprivation or
abuse, for instance, the family would have a much larger
impact -though a negative one - than any found in the
study. Although the twins studied came from widely
different environments, there were no extremely deprived
families.''
Gardner Lindzey, director of the Center for Advanced
Studies in the Behavioral Sciences in Palo Alto, Calif., said
the Minnesota findings would ''no doubt produce
empassioned rejoinders.''
''They do not in and of themselves say what makes a given
character trait emerge,'' he said, ''and they can be disputed
and argued about, as have similar studies of intelligence.''
For parents, the study points to the importance of treating
each child in accord with his innate temperament.
''The message for parents is not that it does not matter
how they treat their children, but that it is a big mistake to
treat all kids the same,'' said Dr. Lykken. ''To guide and
shape a child you have to respect his individuality, adapt to
it and cultivate those qualities that will help him in life.
''If there are two brothers in the same family, one fearless
and the other timid, a good parent will help the timid one
become less so by giving him experiences of doing well at
risk-taking, and let the other develop his fearlessness
tempered with some intelligent caution. But if the parent
shelters the one who is naturally timid, he will likely
become more so.''
The Minnesota results lend weight and precision to earlier
work that pointed to the importance of a child's
temperament in development. For instance, the New York
Longitudinal Study, conducted by Alexander Thomas and
Stella Chess, psychiatrists at New York University Medical
Center, identified three basic temperaments in children,
each of which could lead to behavioral problems if not
handled well.
''Good parenting now must be seen in terms of meeting the
special needs of a child's temperament, including dealing
with whatever conflicts it creates,'' said Stanley Grossman,
a staff member of the medical center's Psychoanalytic
Institute.
graph of degree to which eleven key traits of personality
are estimated to be inherited (NYT)

Do Children Inherit Their Parents'

Personalities?
by SHARON PERKINS Last Updated: Oct 23, 2015

Children inherit their parents' physical attributes, but scientists know less about whether
they also inherit the personalities of their mother and father. Some personality traits
appear to have a genetic basis, but several genes, not just one, contribute to
personality. Environment also plays a part in the development of personality traits.
Although your child might have a genetic tendency toward certain personality traits, he
might develop them only if conditions in his environment work in conjunction with the
genes to produce them.

Genes and Personality

Researchers haven't isolated the genes that might carry markers for all personality traits. Since
genes work with one another and influence their expression, it might take several different
genetic combinations for a child to have a certain personality trait. Genes can switch on and off,
 sometimes because of environmental factors, other times because of other genetic influences.
Genes can affect chemical messengers such as seratonin and dopamine, which can have profound
effects on the brain and influence personality traits such as anxiety or shyness, according to the
Genome News Network.

Heredity Versus Environment

Around 40 percent of a person's personality traits stem from inherited genes, according to Dr.
David Funder, psychology professor at the University of California, Riverside, and author of
"The Personality Puzzle." This leaves room for considerable influence from environmental
factors. Environmental factors refer to more than where a person lives; cultural influences and
early life experiences and exposures can all impact personality. For example, notes Dr. Funder,
people who carry a certain gene that affects seratonin have a higher risk of depression and anti-
social behavior, but only if their childhood is marked by severe stress or maltreatment.
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Family Traits

Not even identical twins, who have the same genetic makeup, have identical personalities. While
they do have more behavioral characteristics in common than fraternal twins or non-twin
siblings, they share just 50 percent of several personality traits, child psychologist Dr. David
Shaffer notes in his book, "Social and Personality Development." Fraternal twins share around
30 percent of the same traits, while non-twin siblings share around 20 percent. Biologically
unrelated children raised in the same home share just 7 percent of traits.
Behavioral Disorders

Researchers have found that many behavioral disorders, such as schizophrenia, clinical
depression or bipolar disorder have a genetic basis, but that doesn't mean everyone who inherits
the gene develops the illness. If you have an identical twin with schizophrenia, for example, your
chance of having the same disorder is one in two, or 50 percent, even though you inherited the
same genes. But only 5 to 10 percent of children with one parent with schizophrenia also develop
schizophrenic symptoms, according to Dr. Shaffer.
Are Personality Traits Hereditary?
Blaming genes is no excuse when dealing with defiant adolescents.
Posted Oct 11, 2016

In one of my previous posts, some people, in the comments section, expressed

disagreement with my stance that parents are the primary influence in the lives of their
children. At least two commenters insisted that they are easy-going persons and that
thepersonality of their difficult children mirrored the personality of relatives related to the
children. One person stated her child was like the father, while the other stated the child
was like the fathers mother. This reminded me of a story about two parents who
returned their adopted son back to his orphanage about seven years after they had
adopted him. They had adopted him when he was a year old. The reasoning the couple
gave was that they believed the boy to be a psychopath and they had to return him
for fear of their safety. In an argument with someone about this issue, I took the stance
that the parents had wrongfully abandoned the boy, and the other person took the
stance that they had done the right thing given thatpsychopathy is hereditary.

So to the question, is it hereditary? First and foremost, I am not a geneticist, by any

stretch of the imagination. However, due to my work as a psychotherapist, I have
studied a lot of research about neuroscience and and the role of genes in human
behavior. The most important takeaway is that genes do not operate in isolation (Rutter
M. 2006.) Another way to put it is that there is always an interaction between the genes
of a person and the persons experience. So while personalities are certainly inherited,
the behavior of a child or teen is a result of how the childs personality interacts with his
or her daily experiences.

So if you identified ten children with personality traits indicating a strong-willed

character, their behaviors are not going to be consistent based on the influences of their
households. You can have one strong-willed child who habitually presents a defiant
attitude in one household, while you can have another strong-willed child who presents
a commitment to following through with all household rules so that he can work on
achieving excellence in an extracurricular activity.

A strong-willed child or teen who is habitually disrespectful in one household does not
necessary mean that he or she has been abused by the parent. It could be a matter of a
personality clash between the parents and child coupled with the parents not
knowing how to redirect the strong will of their child. It is not uncommon for parents to
raise one or two children with little or no conflict and then experience a mountain of
challenges with a subsequent child. Try as they might, these parents experience what
amounts to no progress with each strategy they implement. In truth,
most parenting strategies are effective in theory but the difference is the approach or
context in which the parenting strategy is used. In order to parent a child who presents
significant defiance towards you, you have to make adjustments in your lifestyle and
expectations in order for your strategies to be effective.

For example, if I am working with two adolescents who

present anger management issues, the messages I convey to both teens are the same,
but my approach in conveying the messages to both teens would be tailored to each of
their personality traits. This forces me to make compromises with my own attitude and
behaviors. I would have to reevaluate which boundaries are absolutely necessary and
which boundaries to relax for the teen. Down the road, once rapport has been
established, the less necessary boundaries can be shored up. This means that
adjustments parents make with themselves for the sake of the child dont have to be
permanent.

In conclusion, heredity is not a catch-all excuse when parenting defiant children. The
influence of each parent is not to be underestimated.
Character traits determined genetically? Genes may hold
the key to a life of success, study suggests
Date:

May 16, 2012

Source:

University of Edinburgh

Summary:

Genes play a greater role in forming character traits -- such as self-control, decision making
or sociability -- than was previously thought, new research suggests.

Identical twin boys. Genes play a greater role in forming character traits -- such as self-control,
decision making or sociability -- than was previously thought, new research suggests.
Credit: vgm6 / Fotolia
Genes play a greater role in forming character traits -- such as self-control,
decision making or sociability -- than was previously thought, new research
suggests.

A study of more than 800 sets of twins found that genetics were more influential in shaping key traits
than a person's home environment and surroundings.

Psychologists at the University of Edinburgh who carried out the study, say that genetically
influenced characteristics could well be the key to how successful a person is in life.

The study of twins in the US -- most aged 50 and over- used a series of questions to test how they
perceived themselves and others. Questions included "Are you influenced by people with strong
opinions?" and "Are you disappointed about your achievements in life?"

The results were then measured according to the Ryff Psychological Well-Being Scale which
assesses and standardizes these characteristics.

By tracking their answers, the research team found that identical twins -- whose DNA is [presumed to
be] exactly the same -- were twice as likely to share traits compared with non-identical twins.

Psychologists say the findings are significant because the stronger the genetic link, the more likely it
is that these character traits are carried through a family.

Professor Timothy Bates, of the University of Edinburgh's School of Philosophy, Psychology and
Language Sciences, said that the genetic influence was strongest on a person's sense of self-
control.
Researchers found that genes affected a person's sense of purpose, how well they get on with
people and their ability to continue learning and developing.

Professor Bates added: "Ever since the ancient Greeks, people have debated the nature of a good
life and the nature of a virtuous life. Why do some people seem to manage their lives, have good
relationships and cooperate to achieve their goals while others do not? Previously, the role of family
and the environment around the home often dominated people's ideas about what affected
psychological well-being. However, this work highlights a much more powerful influence from
genetics."

The study, which builds on previous research that found that happiness is underpinned by genes, is
published online in theJournal of Personality.

Do Children Inherit Their Parents

Personalities?
24 May 2016 / By Molly Owens

Categories: Personality Science, Relationships & Communication

The question of whether our genes influence our personality essentially boils down to
nature versus nurture, one of the oldest debates in the history of psychology. It has
dominated personality theory since Darwin noticed that survival meant passing on the
most capable of our genes to the next generation.

On the one side, there's the notion that the apple doesn't fall far from the tree
("nature"). Children inherit eye color, skin pigmentation and vulnerability to specific
illnesses from one or other parent, and they inherit specific personality traits in the
same way. Personality is wired in, and no quirks of upbringing will change it.
In the opposing corner stands the theory of nurture. Nurture argues that the human
mind is a tabula rasa (blank slate), and it's the sum total of your environment, learning
and experiences that shape you to be the person you are today.

So, who's wrong? Who's right? Let's take a closer look.

Nature Versus Nurture in Psychology

The nature versus nurture debate is an on-going one and one that reflects the popular
culture of the time. Back in Darwin's day, for example, the psychologist and eugenicist
Francis Galton (himself a cousin of Charles Darwin) was convinced that intelligence
was hereditary and that society could be improved through "better breeding."

Freud changed the popular thinking. He believed that personality was shaped by
conflicts resolved in childhood and how an individual learned to navigate their physical
environment. Throughout much of the 20th century, this behaviorist or nurture approach
dominated psychology. It was commonly believed that human personality was primarily
influenced by their environment and could be changed through social conditioning. It
was during this time that Bandura conducted his famous Bobo doll experiment to
show that aggression could be learned through imitation and thousands of Americans
hit the psychotherapy couch to talk about their childhood.

Today, research into the human genome has given scientists a much better
understanding of how traits and certain behavioral characteristics are passed from
parent to child. Recent research on twins reveals that genetics have a stronger
influence on the development of certain personality traits than previously thought, and
may even play a larger role than child rearing.

The Twin Studies

For 20 years, researchers at the University of Minnesota studied 350 pairs of twins,
some of whom were raised in different families. The landmark study was the first of its
kind to compare twins raised independently with those raised in the same environment.
This allowed researchers to assess the relative influence of heredity and of upbringing
in their development.

During the study, participants were put through a series of personality tests which
broadly followed theBig-5 personality test . Big-5 measures test-takers against five
core personality traits, as well as various sub-traits. These are:

O - Openness to experience (your level of curiosity)

C - Conscientiousness (your level of work ethic)

E - Extraversion (your level of sociability)

A - Agreeableness (your level of kindness)

N - Neuroticism (your level of anxiety or shame).

The results are fascinating. For most of the traits measured, more than half the
variation between the twins was shown to be genetic. Among the traits found most
strongly determined by heredity were ambition, vulnerability to stress (neuroticism),
leadership, risk-seeking, a sense of well-being and, surprisingly, respect for authority.
The genetic factor for these traits was found to run somewhere in the region of 50 to 60
percent.

Jim Lewis and Jim Springer , the most astounding raised-apart twin set in the
Minnesota study, were shown to be so similar in the personality variables of tolerance,
flexibility and conformity that it was almost impossible to tell them apart.

Do Parents Still Matter?

Even though the twin studies demonstrate the strong influence of nature, family
influence still matters.More recent studies , for example, have shown that the
personality trait of conscientiousness has a far lower genetic correlation than the other
personality traits. This suggests that a parent or educator might equip an inherently
spontaneous child with the tools she needs to show duty and self-discipline, and thus
influence the development of her personality.

It's not just family influence that matters, either. In a recent British study , researchers
found that, on average, 60 percent of the variation in a child's unruly behavior in school
was down to their genes. But in London and other global hotspots, environment played
a far greater role. The researchers concluded that issues such as deprivation, housing,
education and even pollution levels could all influence how your DNA expresses itself
as personality.

This brings us to another fascinating conclusion drawn by the Minnesota twin studies.
Researchers found that raised-apart identical twins are more similar than identical twins
that are raised together. That's because together-twins have the opportunity to
recognize their similarities and deliberately change their behavior so they might be
different from their sibling - effectively turning off their genes.

All of which seems to suggest that, even if we do inherit certain parts of our
personalities, we're not forever stuck with them. There's a strong possibility that we can
change our disposition simply by changing our environment, or possibly even through
sheer force of will.

Summing It Up

The current thinking is pretty clear - our personalities are shaped by biology and
upbringing, and it is almost impossible to hold an all-or-nothing view. Instead of asking
whether personality is down to nature or nurture, the question should be, how much?
How much of our personalities is down to nature and how much can we control and
change over time? And can we even put a figure on something that has so many
variables?
So if you're looking at your child and thinking, "Where did that personality come from?"
the answer is, at least a little bit from you. But with multiple personality dimensions to
look at, and two parents, this won't result in an exact type match very often. Our
personality type code is shorthand for a hugely complex system of thought processing.
Until we can map the specific gene code for each individual personality trait, we're
going to have to embrace the mystery of our personalities and how our own unique
character came to be.

If I were to ask you the simple question,"Do you think that genes influence
yourpersonality?" the first thing you might think is that I'm asking you a stupid
question. After all, nearly all our lay beliefs about the world include beliefs that some of
our genetic material influences who we become as people. And though we do believe,
to varying degrees, that our experiences shape who are, I'm sure we can't think of all
that many people who believe, like Aristotle, that we are a tabula rasa (blank slate). As
well, if you believe in evolution then you must have an implicit belief that genes
influence who we are. If evolution has taught us anything, it is that survival means
passing on the fittest of our genes to the next generation.

So, you come to this post with the implicit belief that your personality is most certainly
influenced by your genes. What if I told that this is not what the most recent research in
behavioral genetics would suggest?

Genes and Personality: The Early Years

In the early years examining the links between genes and personality, it was typical for
a study to examine self-reports of personality and compare the self-reports between
fraternal twinswho share roughly 50% of their genesto those of identical twins, who
share 100% of their genes. In these early twin studies, very consistent effects emerged
that suggested one thing: when it comes to personality, genes matter.
In that work, researchers calculated heritability estimatesin lay terms, the amount of
variation in personality that is explained by genesby examining personality similarity
between twin pairs. For identical twins, heritability estimates hovered around 46%, and
23% for fraternal twins (a heritability of 1.00 means that all variance is genetic; Jang et
al., 1996). Together, this early work was very clear in its suggestion that there are some
genetic influences on personality. The next question, was of course, which genes would
be the biggest players in the gene-to-personality pathways?

Candidate Genes
The early work in twins is suggestive of the possibility that eventually, with enough
knowledge about human DNA, scientists will be able to discover a specific gene for,
well, for anything related to personality, preferences, intelligence, or physical
characteristics. That's a potentially exciting domain of future research, and one that
researchers have examined very vigorously in the last 15 years or so. In this work,
affectionately referred to as "gene for" studies by one of my colleagues, researchers
looked for specific small repeating sections of genes (single nucleotide polymorphisms
or SNPs) that identified a version of a specific gene. The SNPs usually were related to
the specific production or reception of neuropeptides implicated in any number of social
behaviors in non-humans. One really famous SNP is the APOE4 genetic polymorphism,
which has been linked to increased risk for Alzheimer's Disease in humans. Another one
is the GG variant of the oxytocin receptor gene rs53576, which is associated with
increased oxytocin receptors in the brain.

The critical point in these "gene for" studies is that, if we know what parts of personality
that a specific neuropeptide influences, then its genetic variants should predict behavior
in a similar fashion. More specifically, knowing how oxytocin influences
personality (although oxytocin's influence on behavior is still in question) would suggest
that knowing variations in specific SNPs on the oxytocin receptor gene should help us
predict personality.

In the subsequent "gene for" research, many researchers were left disappointed
Specifically, for every breakthrough finding linking a specific SNP to a personality
characteristic, there was a null replication. Several of the most promising candidate
genes, such as the MAOA gene which has been linked to antisocial behavior in past
research (Caspi et al., 2002), have failed to replicate in subsequent work, according to
several meta-analyses (De Moor et al., 2010).

Question no. 3

Zika virus (ZIKV) is a member of the virus family Flaviviridae.[3] It is spread by daytime-
active Aedes mosquitoes, such as A. aegypti and A. albopictus.[3] Its name comes from the Zika
Forest of Uganda, where the virus was first isolated in 1947.[4] Zika virus is related to
the dengue, yellow fever, Japanese encephalitis, and West Nile viruses.[4] Since the 1950s, it has
been known to occur within a narrow equatorial belt from Africa to Asia. From 2007 to 2016, the virus
spread eastward, across the Pacific Ocean to the Americas, leading to the 201516 Zika virus
epidemic.

The infection, known as Zika fever or Zika virus disease, often causes no or only mild symptoms,
similar to a very mild form ofdengue fever.[3] While there is no specific
treatment, paracetamol (acetaminophen) and rest may help with the symptoms.[5]As of 2016, the
illness cannot be prevented by medications or vaccines.[5] Zika can also spread from a pregnant
woman to her fetus. This can result in microcephaly, severe brain malformations, and other birth
defects.[6][7] Zika infections in adults may result rarely in GuillainBarr syndrome.[8]

In January 2016, the United States Centers for Disease Control and Prevention (CDC) issued travel
guidance on affected countries, including the use of enhanced precautions, and guidelines for
pregnant women including considering postponing travel.[9][10] Other governments or health agencies
also issued similar travel warnings,[11][12][13] while Colombia, the Dominican Republic, Puerto Rico,
Ecuador, El Salvador, and Jamaica advised women to postpone getting pregnant until more is
known about the risks.[12][14] Zika is pronounced /zik/ or /zk/.[15][16]

The Zika virus belongs to the Flaviviridae family and the Flavivirus genus, and is thus related to
the dengue, yellow fever,Japanese encephalitis, and West Nile viruses. Like other flaviviruses, Zika
virus is enveloped and icosahedral and has a nonsegmented, single-stranded, 10 kilobase positive-
sense RNA genome. It is most closely related to the Spondweni virusand is one of the two known
viruses in the Spondweni virus clade.[17][18][19][20][21]
Cross-section of Zika virus, showing the viral envelope composed of envelope proteins (red) and membrane
proteins (purple) embedded in the lipid membrane (white).The capsid proteins (orange) are shown interacting
with the RNA genome (yellow) at the center of the virus. [22]

A positive-sense RNA genome can be directly translated into viral proteins. As in other flaviviruses,
such as the similarly sized West Nile virus, the RNA genome encodes seven nonstructural proteins
and three structural proteins.[23] One of the structural proteins encapsulates the virus. This protein is
the flavivirus envelope glycoprotein, that binds to the endosomal membrane of the host cell to initiate
endocytosis.[24] The RNA genome forms a nucleocapsid along with copies of the 12-kDa capsid
protein. The nucleocapsid, in turn, is enveloped within a host-derived membrane modified with two
viral glycoproteins. Viral genome replication depends on the making of double stranded RNA from
the single stranded positive sense RNA (ssRNA(+)) genome followed by transcription and replication
to provide viral mRNAs and new ssRNA(+) genomes.[25][26]

There are two Zika lineages: the African lineage and the Asian lineage.[27] Phylogenetic studies
indicate that the virus spreading in the Americas is 89% identical to African genotypes, but is most
closely related to the Asian strain that circulated in French Polynesia during the 20132014
outbreak.[27][28][29]

Transmission

The vertebrate hosts of the virus were primarily monkeys in a so-called enzootic mosquito-monkey-
mosquito cycle, with only occasional transmission to humans. Before the current pandemic began in
2007, Zika "rarely caused recognized 'spillover' infections in humans, even in highly enzootic areas".
Infrequently, however, other arboviruses have become established as a human disease and spread
in a mosquitohumanmosquito cycle, like the yellow fever virus and the dengue fever virus (both
flaviviruses), and the chikungunya virus (a togavirus).[30] Though the reason for the pandemic is
unknown, dengue, a related arbovirus that infects the same species of mosquito vectors, is known in
particular to be intensified by urbanization andglobalization.[31] Zika is primarily spread by Aedes
aegypti mosquitoes,[32] and can also be transmitted through sexual contact[33] or blood transfusions.
[34]
The basic reproduction number (R0, a measure of transmissibility) of Zika virus has been
estimated to be between 1.4 and 6.6.[35]

In 2015, news reports drew attention to the rapid spread of Zika in Latin America and the Caribbean.
[36]
At that time, the Pan American Health Organization published a list of countries and territories that
experienced "local Zika virus transmission" comprising Barbados, Bolivia, Brazil, Colombia, the
Dominican Republic, Ecuador, El Salvador, French Guiana, Guadeloupe, Guatemala, Guyana, Haiti,
Honduras, Martinique, Mexico, Panama, Paraguay, Puerto Rico, Saint Martin, Suriname, and
Venezuela.[37][38][39] By August 2016, more than 50 countries (list and map) had experienced active
(local) transmission of Zika virus.[40]

Mosquito[edit]

Zika is primarily spread by the female Aedes aegypti mosquito, which is active mostly in the daytime.
[41][42]
The mosquitos must feed on blood in order to lay eggs.[43]:2 The virus has also been isolated from
a number of arboreal mosquito species in the Aedes genus, such as A. africanus, A.
apicoargenteus, A. furcifer, A. hensilli, A. luteocephalus and A. vittatus, with anextrinsic incubation
period in mosquitoes of about 10 days.[20]

The true extent of the vectors is still unknown. Zika has been detected in many more species
of Aedes, along with Anopheles coustani, Mansonia uniformis, and Culex perfuscus, although this
alone does not incriminate them as a vector.[42]

Transmission by A. albopictus, the tiger mosquito, was reported from a 2007 urban outbreak in
Gabon where it had newly invaded the country and become the primary vector for the
concomitant chikungunya and dengue virus outbreaks.[44] There is concern
for autochthonous infections in urban areas of European countries infested by A. albopictus because
the first two cases of laboratory-confirmed Zika infections imported into Italy were reported
from viremic travelers returning from French Polynesia.[45]

The potential societal risk of Zika can be delimited by the distribution of the mosquito species that
transmit it. The global distribution of the most cited carrier of Zika,A. aegypti, is expanding due to
global trade and travel.[46] A. aegypti distribution is now the most extensive ever recorded across all
continents including North America and even the European periphery (Madeira, the Netherlands,
and the northeastern Black Sea coast).[47] A mosquito population capable of carrying Zika has been
found in a Capitol Hill neighborhood of Washington, D. C., and genetic evidence suggests they
survived at least four consecutive winters in the region. The study authors conclude that mosquitos
are adapting for persistence in a northern climate.[48] The Zika virus appears to be contagious via
mosquitoes for around a week after infection. The virus is thought to be infectious for a longer period
of time after infection (at least 2 weeks) when transmitted via semen. [49][50]

Research into its ecological niche suggests that Zika may be influenced to a greater degree by
changes in precipitation and temperature than Dengue, making it more likely to be confined to
tropical areas. However, rising global temperatures would allow for the disease vector to expand
their range further north, allowing Zika to follow.[51]

Sexual[edit]

Zika can be transmitted from men and women to their sexual partners; however, most cases involve
transmission from symptomatic men to women.[52][33][53] As of April 2016, sexual transmission of Zika
has been documented in six countries Argentina, Chile, France, Italy, New Zealand, and the United
States during the 2015 outbreak.[8]

Since October 2016, the CDC has advised men who have traveled to an area with Zika should use
condoms or not have sex for at least six months after their return, even if they never develop
symptoms, because the virus is transmissible in semen.[54]

Pregnancy[edit]

The Zika virus can spread by vertical (or "mother-to-child") transmission, during pregnancy or at
delivery.[55][6]

Blood transfusion[edit]

As of April 2016, two cases of Zika transmission through blood transfusions have been reported
globally, both from Brazil,[34] after which the US Food and Drug Administration (FDA) recommended
screening blood donors and deferring high-risk donors for 4 weeks.[56][57] A potential risk had been
suspected based on a blood-donor screening study during the French Polynesian Zika outbreak, in
which 2.8% (42) of donors from November 2013 and February 2014 tested positive for Zika RNA
and were all asymptomatic at the time of blood donation. Eleven of the positive donors reported
symptoms of Zika fever after their donation, but only three of 34 samples grew in culture. [58]

Pathogenesis[edit]

Zika virus replicates in the mosquito's midgut epithelial cells and then its salivary gland cells. After 5
10 days, the virus can be found in the mosquitos saliva. If the mosquitos saliva is inoculated into
human skin, the virus can infect epidermal keratinocytes, skin fibroblasts in the skin and the
Langerhans cells. The pathogenesis of the virus is hypothesized to continue with a spread to lymph
nodes and the bloodstream.[17][59] Flaviviruses replicate in the cytoplasm, but Zika antigens have been
found in infected cell nuclei.[60]

Zika fever[edit]

Main article: Zika fever

Rash on an arm due to Zika

Zika fever (also known as Zika virus disease) is an illness caused by the Zika virus. [61] Most cases
have no symptoms, but when present they are usually mild and can resemble dengue fever.[61]
[62]
Symptoms may include fever, red eyes, joint pain, headache, and a maculopapular rash.[61][63]
[64]
Symptoms generally last less than seven days.[63] It has not caused any reported deaths during the
initial infection.[62] Infection during pregnancy causes microcephaly and other brain malformations in
some babies.[6][7] Infection in adults has been linked to GuillainBarr syndrome (GBS).[62]

Diagnosis is by testing the blood, urine, or saliva for the presence of Zika virus RNA when the
person is sick.[61][63]

Prevention involves decreasing mosquito bites in areas where the disease occurs, and proper use of
condoms.[63][65] Efforts to prevent bites include the use of insect repellent, covering much of the body
with clothing, mosquito nets, and getting rid of standing water where mosquitoes reproduce.[61] There
is no effective vaccine.[63] Health officials recommended that women in areas affected by the 201516
Zika outbreak consider putting off pregnancy and that pregnant women not travel to these areas. [63]
[66]
While there is no specific treatment, paracetamol (acetaminophen) and rest may help with the
symptoms.[63]Admission to hospital is rarely necessary.[62]

Vaccine development[edit]

Effective vaccines have existed for several viruses of the flaviviridae family, namely yellow fever
vaccine, Japanese encephalitis vaccine, and tick-borne encephalitis vaccine, since the 1930s, and
dengue fever vaccine since the mid-2010s.[67][68][69] World Health Organization(WHO) experts have
suggested that the priority should be to develop inactivated vaccines and other non-live vaccines,
which are safe to use in pregnant women and those of childbearing age. [70]

As of March 2016, 18 companies and institutions internationally were developing vaccines against
Zika but a vaccine was unlikely to be widely available for about ten years. [70][71] In June 2016 the FDA
granted the first approval for a human clinical trial for a Zika vaccine.[72]

History[edit]

See also: Zika fever Epidemiology, and Zika virus outbreak timeline

Countries that have past or current evidence of Zika transmission (as of January 2016) [73]

Spread of Zika[29][74][75]
Spread of Zika in Africa and Asia, based on molecular sequence data

Virus isolation in monkeys and mosquitoes, 1947[edit]

The virus was first isolated in April 1947 from a rhesus macaque monkey that had been placed in a
cage in the Zika Forest of Uganda, near Lake Victoria, by the scientists of the Yellow Fever
Research Institute.[76] A second isolation from the mosquito A. africanus followed at the same site in
January 1948.[77] When the monkey developed a fever, researchers isolated from
its serum a "filterable transmissible agent" that was named Zika in 1948.[78]

First evidence of human infection, 1952[edit]

Zika was first known to infect humans from the results of a serological survey in Uganda, published
in 1952.[79] Of 99 human sera tested, 6.1% had neutralizing antibodies. As part of a 1954 outbreak
investigation of jaundice suspected to be yellow fever, researchers reported isolation of the virus
from a patient,[80] but the pathogen was later shown to be the closely related Spondweni virus.
[81]
Spondweni was also determined to be the cause of a self-inflicted infection in a researcher
reported in 1956.[82]

Spread in equatorial Africa and to Asia, 19511983[edit]

Subsequent serological studies in several Africa and Asian countries indicated the virus had been
widespread within human populations in these regions.[78] The first true case of human infection was
identified by Simpson in 1964,[83] who was himself infected while isolating the virus from mosquitoes.
[78]
From then until 2007, there were only 13 further confirmed human cases of Zika infection from
Africa and Southeast Asia.[84]

Micronesia, 2007[edit]
Main article: 2007 Yap Islands Zika virus outbreak

In April 2007, the first outbreak outside of Africa and Asia occurred on the island of Yap in the
Federated States of Micronesia, characterized by rash, conjunctivitis, and arthralgia, which was
initially thought to be dengue, chikungunya, or Ross River disease.[85] Serum samples from patients
in the acute phase of illness contained RNA of Zika. There were 49 confirmed cases, 59
unconfirmed cases, no hospitalizations, and no deaths. [86]

20132014[edit]
This section needs
expansion.You can help
 by adding to it. (February 2016)

Main article: 20132014 Zika virus outbreaks in Oceania

Between 2013 and 2014, further epidemics occurred in French Polynesia, Easter Island, the Cook
Islands, and New Caledonia.[16]

Americas, 2015present[edit]
Main article: 201516 Zika virus epidemic

As of early 2016, a widespread outbreak of Zika was ongoing, primarily in the Americas. The
outbreak began in April 2015 in Brazil, and has spread to other countries in South America, Central
America, North America, and the Caribbean. Isolations of Zika were reported in Singapore and
Malaysia in Aug 2016,[87] but the virus in Singapore was shown to be the same as strains present
since the 1960s and not recently imported from South America.[88] In January 2016, the WHO said
the virus was likely to spread throughout most of the Americas by the end of the year; [89] and in
February 2016, the WHO declared the cluster of microcephaly and GuillainBarr syndrome cases
reported in Brazil strongly suspected to be associated with the Zika outbreak a Public Health
Emergency of International Concern.[4][90][91][92] It is estimated that 1.5 million people have been infected
by Zika in Brazil,[93] with over 3,500 cases of microcephaly reported between October 2015 and
January 2016.[94]

A number of countries have issued travel warnings, and the outbreak is expected to significantly
impact the tourism industry.[4][95] Several countries have taken the unusual step of advising their
citizens to delay pregnancy until more is known about the virus and its impact on fetal development.
[14]
With the 2016 Summer Olympic Games hosted in Rio de Janeiro, health officials worldwide have
voiced concerns over a potential crisis, both in Brazil and when international athletes and tourists,
who may be unknowingly infected, return home and possibly spread the virus. Some researchers
speculate that only one or two tourists may be infected during the three week period, or
approximately 3.2 infections per 100,000 tourists.[96] In November 2016, the World Health
Organization declared that the Zika virus was no longer a global emergency while noting that the
virus still represents "a highly significant and a long-term problem".[97]

Other cases[edit]

On 22 March 2016 Reuters reported that Zika was isolated from a 2014 blood sample of an elderly
man in Chittagong in Bangladesh as part of a retrospective study.[98] Zika is also occurring in
Tanzania as of 2015/2016.[99]
In 2017, Angola reported two cases of Zika virus.[100]

Zika virus infection induces mitosis abnormalities and apoptotic

cell death of human neural progenitor cells

Zika virus (ZIKV) infection has been associated with severe

complications both in the developing and adult nervous system. To
investigate the deleterious effects of ZIKV infection, we used human
neural progenitor cells (NPC), derived from induced pluripotent stem
cells (iPSC). We found that NPC are highly susceptible to ZIKV and the
infection results in cell death. ZIKV infection led to a marked
reduction in cell proliferation, ultrastructural alterations and induction
of autophagy. Induction of apoptosis of Sox2 + cells was demonstrated
by activation of caspases 3/7, 8 and 9, and by ultrastructural and flow
cytometry analyses. ZIKV-induced death of Sox2 + cells was prevented
by incubation with the pan-caspase inhibitor, Z-VAD-FMK. By confocal
microscopy analysis we found an increased number of cells with
supernumerary centrosomes. Live imaging showed a significant
increase in mitosis abnormalities, including multipolar spindle,
chromosome laggards, micronuclei and death of progeny after cell
division. FISH analysis for chromosomes 12 and 17 showed increased
frequency of aneuploidy, such as monosomy, trisomy and polyploidy.
Our study reinforces the link between ZIKV and abnormalities in the
developing human brain, including microcephaly.

Yale team discovers how Zika virus causes fetal brain

damage
By Bill Hathaway

Infection by the Zika virus diverts a key protein necessary for neural cell division in the
developing human fetus, thereby causing the birth defect microcephaly, a team of Yale
scientists reported Aug. 24 in the journal Cell Reports.

The findings suggest that Zika virus might be susceptible to existing antiviral drugs that
may prevent disruption to the developing nervous system, said the researchers.
One of the frightening side-effects of Zika virus infection in pregnant women is the risk of
fetal microcephaly, in which babies are born with abnormally small brains. The
multidisciplinary collaboration of Yale scientists revealed that Zika virus kills stem cells in the
brain and disrupts the process of creating brain cells. An analysis shows that the virus
diverts a form of the protein TBK1 from its primary job of organizing cell division to the
mitochondria, the cells power pack, where it helps initiate an immune response. Lacking the
protein at the site of cell division, cells die instead of forming new brain cells, resulting in
microcephaly. The data suggest this mechanism may also contribute to microcephaly
associated with other common congenital viral infections.

Researchers note that an existing FDA-approved drug, Sofosbuvir, showed promise in

preventing Zika virus infection of neural stem cells in laboratory culture and also seems to
keep phospho-TBK1 involved in cell division. More study needs to be conducted to prove the
efficacy of the drug as a medical therapy for Zika virus, the authors said.

There is an urgent need to identify therapeutic approaches to halt Zika infection, especially
in pregnant women, said Marco Onorati, co-first author of the paper and researcher in the
lab of senior author Nenad Sestan, professor of neuroscience, comparative medicine,
genetics, and psychiatry. In the interim, we hope these findings can lead to therapies that
might minimize the damage caused by this virus.

Co-first authors of the paper are Zhen Li, Fuchen Liu, and Andre M.M. Sousa of Yale. Tamas
L. Horvath and Brett Lindenbach, also of Yale, are co-senior authors of the work.

The mitotic spindle: linking teratogenic effects of

Zika virus with human genetics?
Abstract

Go to:

Background

The Zika virus (ZIKV) is an arbovirus of the flaviviridae family with a single-stranded RNA
genome of approximately 10,000 nucleotides (GenBank: KU647676.1, GenBank: KU509998.1,
GenBank: KU501215.1). It is vertically transmitted by mosquitoes of the Aedes family (Aedes
spec.). Accordingly, spreading of the virus will coincide primarily with the geographical
distribution of mosquitoes of this family as e.g. Aedes aegypti. On the other hand, some recent
cases of ZIKV infections suggest sexual transmission of the virus by semen as well.
Quite recently, in Brazil microcephaly [1] and chorioretinopathy [2, 3] as well as signs of in
utero growth restriction [4] were found to be epidemiologically associated with either clinically
suspected maternal ZIKV infections during pregnancy and/or positive qualitative RT-PCR tests
for ZIKV in maternal blood, urine or both. The association between ZIKV infection and
microcephaly was deduced also from a recent more detailled case report: In a pregnant women
who has had a febrile illness with rash at the end of the first trimester of her pregnancy,
ultrasonography at the 29th gestational week showed microcephaly with calcifications in the
fetal brain and placenta. After termination of the pregnancy, the presence of ZIKV was
demonstrated in the fetal brain and the whole genome of ZIKV was recovered by using next
generation sequencing [4], (GenBank deposition numberKU527068). A causal relationship has
been presumed [5, 6] and this association was the major reason that prompted the WHO to
declare a Public Health Emergency of International Concern (PHEIC). While public health
authorities advised pregnant travellers to consider avoiding travel to an area where active Zika
transmission is being reported(see: https://www.gov.uk/guidance/zika-virus), proof for a causal
relationship between the infection and the neurotopic teratogenic effects has not been established
yet and possible underlying mechanisms remain to be elucidated.

An interesting aspect of the nearly endemic occurrence of microcephaly in Brazil is its

coincidence with ocular abnormalities. As reported in a study from Salvador, Brazil, out of
twenty-nine infants diagnosed with microcephaly having a presumed diagnosis of ZIKV
infection of their mothers based on clinical signs during pregnancy, ten presented with ocular
abnormalities that were bilateral in seven cases. Mostly they revealed focal pigment mottling of
the retina and chorioretinal atrophy (11/17 eyes) and optic nerve abnormalities (8/17 eyes) [7].
Similar findings are reported in a study from Recife, Brazil [2].

Go to:

Hypothesis generation

In order to understand the possible causal relationship between the viral infection and
microcephaly, we looked for genetic disorders showing the same coincidence of microcephaly
with ocular abnormalities as reported from Brazil. As to severe congenital microcephaly in
general, a large number of cases can be correlated with inherited gene mutations. Of these, those
causing mitotic dysfunctions can be assumed to play a major role in the development of
microcephaly. In addition to microcephaly associated with other syndromic features, most of the
genetic causes of primary developmental microcephaly are known to be associated with
dysfunction of centrosomal proteins controlling the mitotic spindle assuring normal cell
proliferation during mitosis [8]. Akin to isolated microcephaly, the combination of microcephaly
with chorioretinal abnormalities also seems to be related to mutations of genes involved in
proper spindle function:

As for autosomal-dominant inheritance, a phenotypic overlap can be noted between two

syndromes i.e. MLCRD (microcephaly, primary lymphedema, and chorioretinal dysplasia)
syndrome (MIM 152950, OMIM) and CDMMR (chorioretinal dysplasia, microcephaly, and
mental retardation) syndrome (MIM 156590) [9, 10]. In MLCRD the main ocular abnormalities
are bilateral chorioretinopathy, but optical nerve abnormalities do occur as well [11].
Interestingly, in both syndromes heterozygous mutations of the KIF11 (Kinesin Family Member
11) gene encoding EG5, a spindle motor protein of the kinesin-5 family were found [10]. One
possible explanation for families with either MLCRD or CDMMR where no variants in the
coding region of KIF11 were detected [10] is that they represent phenocopies of the syndromes.
While Eg5 is essential for the organization and maintenance of mitotic and meiotic spindles in
dividing cells [12, 13] by acting during poleward movement [14] Ferhat et al. [15] were able to
demonstrate the relevance of EG5 for neuronal development in postmitotic cells as well.
Remarkably, viral proteins are able to interact with EG5. Liu et al. [16] recently demonstrated
that Tat, the transactivation factor of human immunodeficiency virus type 1 interacts with Eg5 by
allosterically modulating the ATPase activity of Eg5.

Autosomal recessive forms of microcephaly with chorioretinopathy are caused by mutations of

the genes of the master regulator of centriole duplication, the PLK4 kinase (MCCRP2, MIM
616171) [17], and their substrates TUBGCP4 (MCCRP3, MIM 616335) [18] and TUBGCP6
(MCCRP1, MIM 251270) [17]. As essential components of the spindle formation, all three
proteins are also involved in the proper mitotic function.

Considering possible ZIKV-related birth defects as phenocopies of the syndromes described

above and taking into account that viruses are able to interfere with the mitotic spindle
[16, 19, 20], we would like to advance the hypothesis that ZIKV, either directly or indirectly,
exerts its teratogenic effects by interacting with proteins engaged in the assembly of the mitotic
apparatus. The hypothesis is supported by the findings that cytopathogenic effects of ZIKV
infections in cell culture seem to depend on the cell line used, that ZIKV is able to infect neural
stem cells, hampering cell growth and interrupting the cell division cycle, and that viral proteins
could be detected in the nucleus of infected cells [2123].

Go to:

Testing the hypothesis

To test this hypothesis, well-known cytogenetic and molecular-cytogenetic methods to evaluate

function, maintenance and establishment of the mitotic spindle poles can be applied on infected
cells. E.g. they can be tested for the formation of micronuclei, chromosomal lagging, and the
number of centrosomes. Also, proteins encoded by genes involved in inherited syndromes with
microcephaly and occular findings resembling those in presumed cases of intrauterine ZIKV
infection should be tested for possible interaction with viral proteins.

Vice versa, as a straightforward approach one might also consider testing newborns with
microcephaly that may be associated with maternal ZIKV infection for germline mutations of the
genes mentioned but the rarity of these syndromes makes such an explanation unlikely.

Go to:

Implications of the hypothesis

With regard to ZIKV infection, there is a considerable lack of knowledge on basic mechanisms
of the virus interaction with host cells. Accordingly, it may take months or even years to test
whether or not ZIKV infection has a teratogenic potential. We have proposed a hypothesis that
allows for a targeted approach into mechanisms of possible relevance.

How does Zika infect cells?

Once Zika virus particles are in the human body, they must
enter individual cells in order to replicate and make more
viruses. Cell entry is possible because a Zika virus particle
carries specific proteins on its outer envelope that interact
with receptor proteins on human cells. When the viral
proteins bind to cell receptors, they trick the cells into
taking up the viral particle^{13}13start superscript, 13, end
superscript.
Image modified from "Zika virus: Genome, by ViralZone, Swiss Institute of
Bioinformatics (CC BY-NC 4.0).

Inside the cell, the RNA genome of the virus is released into
the cytoplasm, or fluid-filled main compartment, of the cell.
There, the RNA molecule is read (translated) by enzymes in
the cell to make a long protein, which is chopped up into a
number of smaller proteins (see image at left). Some of these
proteins are the structural components needed to make new
viral particles, such as capsid and envelope proteins. Other
 viral proteins copy and process the RNA genome ^{13, 14}
13,14start superscript, 13, comma, 14, end superscript.

Viral proteins and copies of the RNA genome assemble at the

surface of the endoplasmic reticulum (ER), a membrane
compartment thats part of the cells export system. New
viral particles bud off into the interior of the ER, taking a
small patch of ER membrane along with them. This "stolen"
membrane will form the viral envelope. The particles then
travel through another structure, the Golgi apparatus, where
they undergo more processing before release at the cell
surface^{13,14}13,14start superscript, 13, comma, 14, end
superscript. Released viral particles can infect other cells,
continuing the infection cycle.

QUESTION 4

Type 2 diabetes and

genetics
Key points
1. If both of your parents have type 2 diabetes, you
have a 50 percent chance of developing the disease.
2. Having a hereditary risk doesnt mean youll
definitely develop the condition.

3. If youre at increased risk for type 2 diabetes, your

doctor can help you find ways to reduce your risk.

Diabetes is a complex condition. Several

factors must come together for you to
develop type 2 diabetes. For example,
obesity and a sedentary lifestyle play a role.
Genetics can also influence whether youll
get this disease.

If youve been diagnosed with type 2

diabetes, theres a good chance that youre
not the first person with diabetes in your
family. According to the American
Diabetes Association, your risk of
developing type 2 diabetes is:
1 in 7 if one of your parents was
diagnosed before the age of 50
1 in 13 if one of your parents was
diagnosed after the age of 50
 1 in 2, or 50 percent, if both your
parents have diabetes
Several gene mutations have been linked to
the development of type 2 diabetes. These
gene mutations can interact with the
environment and each other to further
increase your risk.
Part 2 of 6

The role of genetics in

type 2 diabetes
Type 2 diabetes is caused by both genetic and environmental
factors.

Scientists have linked several gene mutations to a higher

diabetes risk. Not everyone who carries a mutation will get
diabetes. But many people with diabetes do have one or
more of these mutations.

It can be difficult to separate genetic risk from environmental

risk. The latter is often influenced by your family members.
For example, parents with healthy eating habits are likely to
pass them on to the next generation. On the other hand,
 genetics plays a big part in determining weight. Sometimes
behaviors cant take all the blame.

Part 3 of 6

Identifying the genes

responsible for type 2
diabetes
Studies of twins suggest that type 2 diabetes might be linked
to genetics. These studies were complicated by the
environmental influences that also affect type 2 diabetes risk.

To date, numerous mutations have been shown to affect type

2 diabetes risk. The contribution of each gene is generally
small. However, each additional mutation you have seems to
increase your risk.

In general, mutations in any gene involved in

controlling glucose levelscan increase your risk of type 2
diabetes. These include genes that control:

production of glucose
production and regulation of insulin
how glucose levels are sensed in the body
Genes associated with type 2 diabetes risk include:
 TCF7L2, which affects insulin secretion and glucose
production
ABCC8, which helps regulate insulin
CAPN10, which is associated with type 2 diabetes risk in
Mexican-Americans
GLUT2, which helps move glucose into the pancreas
GCGR, a glucagon hormone involved in glucose
regulation
Part 4 of 6
Genetic testing for type
2 diabetes
Tests are available for some of the gene mutations associated
with type 2 diabetes. The increased risk for any given
mutation is small, however. Other factors are far more
accurate predictors of whether youll develop type 2
diabetes, including:

body mass index

family history
high blood pressure
high triglyceride and cholesterol levels
history of gestational diabetes
being of certain ethnicity, such as Hispanic, African-
American, or Asian-American

Part 5 of 6
 Tips for prevention
The interactions between genetics and the environment
make it difficult to identify a definite cause of type 2
diabetes. That doesnt mean you cant reduce your risk
through changing your habits.

The Diabetes Prevention Program, a large study of

people at high risk for diabetes, suggests that weight
loss and increased physical activity can prevent or delay
type 2 diabetes. Blood glucose levels returned to normal
levels in some cases. Other international studies have
reported similar results.

Here are some things you can start doing today to reduce
your risk for type 2 diabetes:

Start an exercise program

Slowly add physical activity into your daily routine. For
example, take the stairs instead of the elevator, or park
further away from building entrances. You can also try going
for a walk during lunch.

Once youre ready, you can start adding light weight-training

and other cardiovascular activities to your routine. Aim for 30
minutes of exercise each day. If you need ideas for how to get
started, check out this list of14 cardio exercises to get you
moving.
 Create a healthy meal plan
It can be hard to avoid extra carbohydrates and calories
when youre dining out. Cooking your own meals is the
easiest way to make healthy choices. Come up with a weekly
meal plan that includes dishes for every meal. Stock up on all
the groceries youll need, and do some of the prep work
ahead of time.

You can ease yourself into it, too. Start by planning your
lunches for the week. Once youre comfortable with that, you
can plan out additional meals.

Learn more: 7-day type 2 diabetes meal plan

Choose healthy snacks

Stock up on healthy snack options so you arent tempted to
reach for a bag of chips or candy bar. Here are some healthy,
easy-to-eat snacks you may want to try:

carrot sticks and hummus

apples, clementines, and other fruits
a handful of nuts, though be careful to keep an eye on
serving sizes
air-popped popcorn, but skip adding lots of salt or butter
whole-grain crackers and cheese

Part 6 of 6

Outlook
Knowing your risk for type 2 diabetes can help you make
changes to prevent developing the condition.

Tell your doctor about your family history with type 2

diabetes. They can decide if genetic testing is right for you.
They can also help you reduce your risk through lifestyle
changes.

Your doctor may also want to regularly check your glucose

levels. That can help them detect any blood sugar
abnormalities or warning signs for type 2 diabetes earlier.
Early treatment can have a positive impact on your outlook.

Type 2 Diabetes Causes

Genetics and Lifestyle Choices Play a Role

Written by Lisa M. Leontis RN, ANP-C and Amy Hess-Fischl MS, RD, LDN, BC-ADM, CDE

ype 2 diabetes has several causes: genetics and lifestyle are the most important
ones. A combination of these factors can cause insulin resistance, when your body
doesnt use insulin as well as it should. Insulin resistance is the most common cause of
type 2 diabetes.

Genetics Play a Role in Type 2 Diabetes

Type 2 diabetes can be hereditary. That doesnt mean that if your mother or father has
(or had) type 2 diabetes, youre guaranteed to develop it; instead, it means that you
have a greater chance of developing type 2.

Researchers know that you can inherit a risk for type 2 diabetes, but its difficult to
pinpoint which genes carry the risk. The medical community is hard at work trying to
figure out the certain genetic mutations that lead to a risk of type 2.
 Lifestyle Is Very Important, Too
Genes do play a role in type 2 diabetes, but lifestyle choices are also important. You
can, for example, have a genetic mutation that may make you susceptible to type 2, but
if you take good care of your body, you may not develop diabetes.
Say that two people have the same genetic mutation. One of them eats well, watches
their cholesterol, and stays physically fit, and the other is overweight (BMI greater than
25) and inactive. The person who is overweight and inactive is much more likely to
develop type 2 diabetes because certain lifestyle choices greatly influence how well
your body uses insulin.

Lifestyle choices that affect the development of type 2 diabetes include:

Lack of exercise: Physical activity has many benefitsone of them being that it
can help you avoid type 2 diabetes, if youre susceptible.
Unhealthy meal planning choices: A meal plan filled with high-fat foods and
lacking in fiber (which you can get from grains, vegetables, and fruits) increases the
likelihood of type 2.
Overweight/Obesity: Lack of exercise and unhealthy meal planning choices can
lead to obesity, or make it worse. Being overweight makes it more likely that youll
become insulin resistant and can also lead to many other health conditions.
Insulin Resistance
That combination of factorsgenetic susceptibility and lifestyle choicesleads to
insulin resistance. If your body is insulin resistant, it doesnt use insulin properly.

Your body may produce enough insulin to transport the glucose to the cells (you can
read more about how insulin works in our article oninsulin), but unfortunately, the body
resists that insulin.

Glucose builds up in the blood when you are insulin resistant, leading to the symptoms
associated with type 2 diabetes.

In type 2 diabetes, genetics and lifestyle play a role in causing your body to become
insulin resistant.

Type 2 Diabetes Isnt Always Caused by Insulin Resistance

Insulin resistance is the most common cause of type 2 diabetes, but it is possible to
have type 2 and not be insulin resistant. You can have a form of type 2 where you body
simply doesnt produce enough insulin; thats not as common. Researchers arent sure
what exactly keeps some people from producing enough insulin, but thats another thing
theyre working hard to figure out.

Type 2 Risk Factors

There are risk factors that have been linked to type 2, and you can learn more about
them (and see if youre at risk) in our type 2 diabetes risk factors article.
Genetics of Diabetes
You've probably wondered how you developed diabetes. You may worry that
your children will develop it too.

Unlike some traits, diabetes does not seem to be inherited in a simple

pattern. Yet clearly, some people are born more likely to develop diabetes
than others.

What Leads to Diabetes?

Type 1 and type 2 diabetes have different causes. Yet two factors are
important in both. You inherit a predisposition to the disease then something
in your environment triggers it.

Genes alone are not enough. One proof of this is identical twins. Identical
twins have identical genes. Yet when one twin has type 1 diabetes, the other
gets the disease at most only half the time.

When one twin has type 2 diabetes, the other's risk is at most 3 in 4.

Type 1 Diabetes

In most cases of type 1 diabetes, people need to inherit risk factors from
both parents. We think these factors must be more common in whites
because whites have the highest rate of type 1 diabetes.

Because most people who are at risk do not get diabetes, researchers want
to find out what the environmental triggers are.

One trigger might be related to cold weather. Type 1 diabetes develops more
often in winter than summer and is more common in places with cold
climates.
Another trigger might be viruses. Perhaps a virus that has only mild effects
on most people triggers type 1 diabetes in others.

Early diet may also play a role. Type 1 diabetes is less common in people
who were breastfed and in those who first ate solid foods at later ages.

In many people, the development of type 1 diabetes seems to take many

years. In experiments that followed relatives of people with type 1 diabetes,
researchers found that most of those who later got diabetes had certain
autoantibodies in their blood for years before.

(Antibodies are proteins that destroy bacteria or viruses. Autoantibodies

are antibodies 'gone bad,' which attack the body's own tissues.)

Type 2 Diabetes

Type 2 diabetes has a stronger link to family history and lineage than type 1,
although it too depends on environmental factors.

Studies of twins have shown that genetics play a very strong role in the
development of type 2 diabetes.

Lifestyle also influences the development of type 2 diabetes. Obesity tends

to run in families, and families tend to have similar eating and exercise
habits.

If you have a family history of type 2 diabetes, it may be difficult to figure

out whether your diabetes is due to lifestyle factors or genetic susceptibility.
Most likely it is due to both. However, dont lose heart. Studies show that it
is possible to delay or prevent type 2 diabetes by exercising and losing
weight.

- See more at: http://www.diabetes.org/diabetes-basics/genetics-of-diabetes.html?

referrer=https://www.google.com.ph/#sthash.dguXKsEr.dpuf

Type 1 Diabetes: Your Child's Risk

In general, if you are a man with type 1 diabetes, the odds of your child
developing diabetes are 1 in 17.
If you are a woman with type 1 diabetes and your child was born before you
were 25, your child's risk is 1 in 25; if your child was born after you turned
25, your child's risk is 1 in 100.

Your child's risk is doubled if you developed diabetes before age 11. If both
you and your partner have type 1 diabetes, the risk is between 1 in 10 and 1
in 4.

There is an exception to these numbers. About 1 in every 7 people with type

1 diabetes has a condition called type 2 polyglandular autoimmune
syndrome. In addition to having diabetes, these people also have thyroid
disease and a poorly working adrenal gland. Some also have other immune
system disorders. If you have this syndrome, your child's risk of getting the
syndrome including type 1 diabetes is 1 in 2.

Researchers are learning how to predict a person's odds of getting diabetes.

For example, most whites with type 1 diabetes have genes called HLA-DR3
or HLA-DR4. If you and your child are white and share these genes, your
child's risk is higher. (Suspect genes in other ethnic groups are less well
studied. The HLA-DR7 gene may put African Americans at risk, and the HLA-
DR9 gene may put Japanese at risk.)

Other tests can also make your child's risk clearer. A special test that tells
how the body responds to glucose can tell which school-aged children are
most at risk.

Another more expensive test can be done for children who have siblings with
type 1 diabetes. This test measures antibodies to insulin, to islet cells in
the pancreas, or to an enzyme called glutamic acid decarboxylase. High
levels can indicate that a child has a higher risk of developing type 1
diabetes.

Type 2 Diabetes: Your Child's Risk

Type 2 diabetes runs in families. In part, this tendency is due to children

learning bad habits eating a poor diet, not exercising from their
parents. But there is also a genetic basis.

More Information on Genetics

If you would like to learn more about the genetics of all forms of diabetes,
the National Institutes of Health has published The Genetic Landscape of
Diabetes. This free online book provides an overview of the current
knowledge about the genetics of type 1 and type 2 diabetes, as well other
less common forms of diabetes. The book is written for health professionals
and for people with diabetes interested in learning more about the disease.

- See more at: http://www.diabetes.org/diabetes-basics/genetics-of-diabetes.html?

referrer=https://www.google.com.ph/#sthash.dguXKsEr.dpuf
Diagram based on "The flavivirus life cycle," by Ted Pierson ^{15}15start superscript,
15, end superscript.

What are the symptoms and effects of

Zika?
In most cases, the symptoms of Zika infection are very mild.
According to the CDC, only 1 in 5 people infected with Zika
will get sick at all, and typical symptoms may include rash,
fever, conjunctivitis (irritation of the eyes), and joint
pain^{16}16start superscript, 16, end superscript. These
symptoms generally resolve, and most people do not
experience any lasting effects from Zika.

Pregnant women and their unborn fetuses are at higher risk

for harmful effects from Zika^{17}17start superscript, 17,
end superscript. Specifically, there is a link between Zika
infection during pregnancy and a condition called
microcephaly (small head) in newborns. Microcephaly may
involve neurological problems or developmental delays, but
these effects vary greatly from person to person ^{18}18
start superscript, 18, end superscript. Health authorities are
encouraging women who are (or might become) pregnant to
take steps to avoid Zika exposure^{19}19start superscript,
19, end superscript.

In a very small fraction of cases, Zika may be linked with

neurological problems, such as Guillain-Barr syndrome.
Guillain-Barr syndrome is an autoimmune condition that
causes paralysis, which is usually temporary (lasting for
weeks or a few months in most cases). An increased
frequency of Guillain-Barr syndrome has been reported in
areas with active Zika infections, but researchers are still
investigating whether there is a causal connection ^{20}20
start superscript, 20, end superscript.

What can be done about Zika?

In the short term, health authorities have recommended that
people protect themselves from Zika by avoiding exposure to
mosquitos in areas where the virus is active. For people in
high-risk groups, such as pregnant women, this might mean
postponing travel to areas known to harbor Zika virus ^{21}
21startsuperscript, 21, end superscript. For others who live in
areas where Zika is active, avoiding exposure might mean
remaining indoors, using mosquito repellents and mosquito
nets, and removing sources of standing water (which provide
a breeding ground for mosquitoes)^{22}22start superscript,
22, end superscript.

In the longer term, a vaccine against Zika could provide more

durable protection. Encouragingly, a vaccine against dengue,
a flavivirus related to Zika, was recently approved for use in
Brazil. This vaccine was built off an inactive version of yellow
fever, another related flavivirus, and its possible that a
similar strategy could be used for a Zika vaccine ^{23}23
start superscript, 23, end superscript. Recently, promising
initial results in mice were reported for one Zika vaccine
candidate^{24}24start superscript, 24, end superscript.
However, many more tests will be needed to establish
whether this and other potential vaccines are safe and
effective in humans.

Genetic causes of diabetes mellitus type 2

From Wikipedia, the free encyclopedia

Most cases of diabetes mellitus type 2 involved many genes contributing small amount to the overall
condition.[1] As of 2011 more than 36 genes have been found that contribute to the risk of type 2
diabetes.[2] All of these genes together still only account for 10% of the total genetic component of the
disease.[2]

There are a number of rare cases of diabetes that arise due to an abnormality in a single gene
(known as monogenic forms of diabetes).[1] These include maturity onset diabetes of the
young (MODY), Donohue syndrome, and Rabson-Mendenhall syndrome, among others.[1] Maturity
onset diabetes of the young constitute 15% of all cases of diabetes in young people. [3]

Polygenic[edit]
Genetic cause and mechanism of type 2 diabetes is largely unknown. However, single nucleotide
polymorphism (SNP) is one of many mechanisms that leads to increased risk for type 2 diabetes. To
locate genes and loci that are responsible for the risk of type 2 diabetes, genome wide association
studies (GWAS) was utilized to compare the genomes of diabetic patient group and the non-diabetic
control group.[4] The diabetic patients genome sequences differ from the controls' genome in specific
loci along and around numerous genes, and these differences in the nucleotide sequences
alter phenotypic traits that exhibit increased susceptibility to the diabetes. GWAS has revealed 65
different loci (where single nucleotide sequences differ from the patient and control group's
genomes), and genes associated with type 2 diabetes,
including TCF7L2, PPARG, FTO, KCNJ11,NOTCH2, WFS1, IGF2BP2, SLC30A8, JAZF1, HHEX, D
GKB, CDKN2A, CDKN2B, KCNQ1, HNF1A,HNF1B MC4R, GIPR, HNF4A, MTNR1B,
PARG6, ZBED3, SLC30A8, CDKAL1, GLIS3, GCKR, among others.[4][5][6][7]KCNJ11 (potassium
inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium
channel Kir6.2, and TCF7L2 (transcription factor 7like 2) regulates proglucagon gene expression
and thus the production of glucagon-like peptide-1.[8] In addition, there is also a mutation to the Islet
Amyloid Polypeptide gene that results in an earlier onset, more severe, form of diabetes. [9]
[10]
However, this is not a comprehensive list of genes that affects the proneness to the diabetes.

Most SNPs that increase the risk of diabetes reside in noncoding regions of the genes, making the
SNPs mechanism for increasing susceptibility largely unknown. However, they are thought to
influence the susceptibility by altering the regulation of those gene expressions. Only few genes
(PARG6, KCNJ11-ABCC8, SLC30A8, and GCKR) have SNPs in the open reading frame (ORF).
 These SNPs in ORFs result in altering of the protein function, and the altered function and
[4]

therefore compromise the performances of the protein product causes increased susceptibility to the
type 2 diabetes.

One of the examples of gene regulation in non-ORF SNPs that influences susceptibility is the
changes in nucleotide sequence in microRNA (miRNA) binding site. miRNAs regulate gene
expression by binding to the target mRNAs and physically block translation. SNPs on the miRNA-
binding site can result in faulty levels of gene expression as miRNA fails to bind to the corresponding
mRNA effectively, leading to excess amount of protein product overall. Although the protein structure
of the genes with SNPs are identical to that of the normal gene product, due to their faulty level of
expressions, those genes increase risk. Genes such as CDKN2A, CDKN2B, and HNF1B exhibit
increase the risk phenotype with SNPs in their 3' UTR miRNA binding sites. As CDKN2A and B
regulate the pancreatic beta-cellreplication,[11] and HNF1B is homeodomain containing transcription
factor that regulates other genes,[12] faulty regulations of those genes increase the risk of diabetes.

Another example of faulty gene regulation that influence the susceptibility is the SNPs
in promoter regions of the genes. Gene like APOM and APM1 increase the risk of type 2 diabetes
when there are SNPs in their proximal promoter regions. Promoters are sequences of DNA that
allows proteins such as transcription factors to bind for gene expression, and when the sequences
are modified, the proteins no longer bind as effectively, resulting in depressed level of gene
expression. APOM is partly responsible for producing pre beta-high-density lipoprotein and
cholesterol,[13] and APM1 is responsible for regulating glucose level in blood and fatty acid.
[14]
Decreasing the level these gene products reduce the body's ability to handle glucose, which leads
to the increased risk of diabetes.

It is important to note that those discovered genes do not determine susceptibility to diabetes for all
people or cases. As the risk of diabetes is combination of the gene regulations and the interplay
between those gene products, certain genes may not pose a threat to increase the susceptibility.
TCF7L2 is one of the well-studied genes for diabetes susceptibility in most populations. However,
SNPs in TCF7L2 that would normally increase the risk of diabetes does not affect the susceptibility
for Pima Indians. However, this gene is associated with regulating the BMI for Pima Indian
population.[15]

Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's
ataxia. Wolfram's syndrome is an autosomal recessiveneurodegenerative disorder that first becomes
evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness,
hence the acronym DIDMOAD.[16]

While obesity is an independent risk factor for type 2 diabetes that may be linked to lifestyle, obesity
is also a trait that may be strongly inherited.[17] Other research also shows that type 2 diabetes can
cause obesity as an effect of the changes in metabolism and other deranged cell behavior attendant
on insulin resistance.[18]

However, environmental factors (almost certainly diet and weight) play a large part in the
development of type 2 diabetes in addition to any genetic component. Genetic risk for type 2
diabetes changes as humans first began migrating around the world, implying a strong
environmental component has affected the genetic-basis of type 2 diabetes. [19][20] This can be seen
from the adoption of the type 2 diabetes epidemiological pattern in those who have moved to a
different environment as compared to the same genetic pool who have not. Immigrants to Western
developed countries, for instance, may be more prone to diabetes as compared to its lower
incidence in their countries of origins.[21] Such developments can also be found in environments
which have had a recent increase in social wealth, increasingly common throughout Asia.