King George III

 

King of Great Britain and Ireland later, King of the United Kingdom and of Hanover – Portrait by Allan Ramsay, 1762

 

 

 

George III (George William Frederick; 4 June 1738 – 29 January 1820) was King of Great Britain and King of Ireland from 25 October 1760 until the union of these two countries on 1 January 1801, after which he was King of the United Kingdom of Great Britain and Ireland until his death. George was the third British monarch of the House of Hanover, but unlike his two Hanoverian predecessors he was born in Britain, spoke English as his first language,and never visited Hanover.

 

His life and reign, which were longer than those of any previous British monarch, were marked by a series of military conflicts involving his kingdoms, much of the rest of Europe, and places farther afield in Africa, the Americas and Asia. Early in his reign, Great Britain defeated France in the Seven Years’ War, becoming the dominant European power in North America and India. However, many of its American colonies were soon lost in the American War of Independence. He played a minor role in the wars against revolutionary and Napoleonic France from 1793, which concluded in the defeat of Napoleon at the Battle of Waterloo in 1815.

 

George III was extremely popular in Britain.The British people admired him for his piety, and for remaining faithful to his wife.He was fond of his children, and was devastated at the death of two of his sons in infancy in 1782 and 1783 respectively.Nevertheless, he set his children a strict regimen. They were expected to attend rigorous lessons from seven in the morning, and to lead lives of religious observance and virtue.When his children strayed from George’s own principles of righteousness, as his sons did as young adults, he was dismayed and disappointed.

 

In the later part of his life, George III suffered from recurrent, and eventually permanent, mental illness. Medical practitioners were baffled by this at the time, although it has since been suggested that he suffered from the blood disease porphyria. Historical analysis of George III’s life has gone through a “kaleidoscope of changing views” that have depended heavily on the prejudices of his biographers and the sources available to them.Until re-assessment in the latter half of the 20th century, his reputation in America was one of a tyrant and in Britain he became “the scapegoat for the failure of imperialism”.He is often remembered as “The Mad King” and “The King Who Lost America”.

 

A study of samples of the King’s hair published in 2005 revealed high levels of arsenic, a possible trigger for the disease. The source of the arsenic is not known, but it could have been a component of medicines or cosmetics.The King may have suffered a brief episode of disease in 1765, but a longer episode began in the summer of 1788. At the end of the parliamentary session, he went to Cheltenham Spa to recuperate. It was the furthest he had ever been from London – just short of 100 miles (150 km) – but his condition worsened. In November, he became seriously deranged, sometimes speaking for many hours without pause, causing him to foam at the mouth and making his voice hoarse.With his doctors largely at a loss to explain his illness, spurious stories about his condition spread, such as the claim that he shook hands with a Plane (Sycamore) tree in the mistaken belief that it was the King of Prussia*.Treatment for mental illness was primitive by modern standards, and the King’s doctors, who included Francis Willis, treated the King by forcibly restraining him until he was calm, or applying caustic poultices to draw out “evil humors”

 

In late 1810, at the height of his popularitybut already virtually blind with cataracts and in pain from rheumatism, George III became dangerously ill. In his view the malady had been triggered by the stress he suffered at the death of his youngest and favorite daughter, Princess Amelia.By the end of 1811, George III had become permanently insane and lived in seclusion at Windsor Castle until his death at Windsor Castle on 29 January 1820.

 

 

 

*German composer, George Frederick Handel, who adopted England as his home, received a stipend from King George II and King George III.  In Handel’s great opera, Xerxes, the opening aria, “Ombra mai fu“, is sung by Persian (not Prussian) King, Xerxes to his Plane tree.

 

Handel – Xerxes – Ombra mai fu

By counter-tenor David Daniels, now singing in “The Enchanted island” at the MetOpera in NYC

 

 

32 Million Americans Have Autoantibodies That Target Their Own Tissues

 

 

The body’s immune system makes large numbers of proteins called antibodies to help the body fight off infections. In some cases, however, antibodies are produced that are directed against one’s own tissues. These are referred to as autoantibodies. Earlier studies have shown that antinuclear antibodies (ANA) can actually develop many years before the clinical appearance of autoimmune diseases, such as type 1 diabetes, lupus, and rheumatoid arthritis. ANA are frequently measured biomarkers for detecting autoimmune diseases, but the presence of autoantibodies does not necessarily mean a person will get an autoimmune disease. Other factors, including drugs, cancer, and infections, are also known to cause autoantibodies in some people.

 

According to an article published online in the journal Arthritis and Rheumatism (11 January 2012), more than 32 million people in the US have autoantibodies, which are proteins made by the immune system that target the body’s tissues and define a condition known as autoimmunity. The study looked at the prevalence of the most common type of autoantibody, known as ANA, and found that the frequency of ANA is highest among women, older individuals, and African-Americans. The study was conducted by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. Researchers in Gainesville at the University of Florida also participated.

 

According to the NIH, previous estimates of ANA prevalence have varied widely and were conducted in small studies not representative of the general population. Now, having this large data set that is representative of the general U.S. population which includes nearly 5,000 individuals, there is an accurate estimate of ANA and may allow new insights into the etiology of autoimmune diseases.

 

The study evaluated blood serum samples using a technique called immunofluorescence to detect ANA in 4,754 individuals from the 1994-2004 National Health and Nutrition Examination Survey (NHANES). The overall prevalence of ANA in the population was 13.8 percent, and was found to be modestly higher in African-Americans compared to whites. ANA generally increased with age and was higher in women than in men, with the female to male ratio peaking at 40-49 years of age and then declining in older age groups.

 

According to the authors, the peak of autoimmunity in females compared to males during the 40-49 age bracket is suggestive of the effects that the hormones estrogen and progesterone might be playing on the immune system. The study also found that the prevalence of ANA was lower in overweight and obese individuals than persons of normal weight. According to the authors, this raises the likelihood that fat tissues can secrete proteins that inhibit parts of the immune system and prevent the development of autoantibodies, but additional research is needed to understand the role that obesity might play in the development of autoimmune diseases.

ONCOLOGY

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Genetic Abnormality Predicts Benefit from Treatment for a Rare Brain Tumor

 

 

Oligodendrogliomas, a form of brain tumor, are characterized by tumors that form in the nerve tissue of the brain. Oligodendrogliomas occur primarily in adults, and the average age at diagnosis is 35. The tumors comprise 9.4% of all primary brain and central nervous system tumors.

 

A clinical trial has shown that addition of chemotherapy to radiation therapy leads to a near doubling of median survival time in patients with oligodendroglioma that carries a chromosomal abnormality called the 1p19q co-deletion. This abnormality is characterized by the simultaneous deletion of the short arm of chromosome 1 and long arm of chromosome 19. The presence of the chromosomal abnormality was associated with substantially better prognosis and marked improvements in survival in a treatment program of combined chemotherapy and radiation therapy compared to radiation therapy alone.

 

In the trial, 286 patients with aggressive oligodendrogliomas were randomly assigned to study groups of equal size to receive radiotherapy alone or radiotherapy plus PCV chemotherapy, which includes the drugs procarbazine, lomustine and vincristine. Tumor tissue from all patients was collected and stored for genetic tests. The analysis was performed when about half of the patients had been followed for just over 11 years.

 

For the entire study population, the median overall survival time for patients receiving radiotherapy alone or radiotherapy plus PCV chemotherapy was similar. However, the 126 patients with 1p19q co-deleted tumors had much longer median survival times than the 135 patients whose tumors did not carry the 1p19q co-deletion: 8.7 years versus 2.7 years. This observation suggests that patients whose tumors contain the chromosomal abnormality will live substantially longer than patients whose tumors don’t carry it, regardless of treatment. Even more impressive, however, was the finding that 1p19q co-deletion predicted the benefit from adding chemotherapy to radiotherapy. Patients with 1p19q co-deleted tumors who received PCV chemotherapy plus radiotherapy (59 patients) had a median overall survival time of 14.7 years, compared with only 7.3 years for patients with co-deleted tumors who received radiotherapy alone (67 patients). Patients whose tumors did not have the chromosomal abnormality did not show an improvement in survival from the addition of chemotherapy.

 

The study, known as RTOG 9402, was led by the Radiation Therapy Oncology Group (RTOG) with the participation of the North Central Cancer Treatment Group, the National Cancer Institute of Canada Clinical Trials Group, the Eastern Cooperative Oncology Group, and SWOG (formerly the Southwest Oncology Group).

Prevalence of Obesity and Trends in the Distribution of Body Mass Index Among US Adults, 1999-2010

 

 

Between 1980 and 1999, the prevalence of adult obesity (body mass index [BMI] >30) increased in the United States and the distribution of BMI changed. More recent data suggested a slowing or leveling off of these trends. As a result, a study published online in the Journal of the American Medical Association (17 January 2012) was performed to estimate the prevalence of adult obesity from the 2009-2010 National Health and Nutrition Examination Survey (NHANES) and compare adult obesity and the distribution of BMI with data from 1999-2008. NHANES includes measured heights and weights for 5,926 adult men and women from a nationally representative sample of the civilian non-institutionalized US population in 2009-2010 and for 22,847 men and women in 1999-2008.

The main outcome measures were the prevalence of obesity and mean BMI.

 

Results showed that in 2009-2010 the age-adjusted mean BMI was 28.7 for men and also 28.7 for women. The age-adjusted prevalence of obesity was 35.7% among adult men and 35.8% among adult women. Over the 12-year period from 1999 through 2010, obesity showed no significant increase among women overall (age- and race-adjusted annual change in odds ratio, 1.01; P=0.07), but increases were statistically significant for non-Hispanic black women (P =0.04) and Mexican American women (P =0.046). For men, there was a significant linear trend (1.04; P < .001) over the 12-year period. For both men and women, the most recent 2 years (2009-2010) did not differ significantly (P =0.08 for men and P = 0.24 for women) from the previous 6 years (2003-2008). Trends in BMI were similar to obesity trends.

 

According to the authors, in 2009-2010, the prevalence of obesity was 35.5% among adult men and 35.8% among adult women, with no significant change compared with 2003-2008.

TARGET HEALTH excels in Regulatory Affairs. Each week we highlight new information in this challenging area.

 

 

FDA Approves Voraxaze To Treat Patients With Toxic Methotrexate Levels

 

 

Methotrexate is a commonly used cancer chemotherapy drug normally eliminated from the body by the kidneys. However, patients receiving high doses of methotrexate may develop kidney failure.

 

The FDA approved Voraxaze (glucarpidase) to treat patients with toxic levels of methotrexate in their blood due to kidney failure. Voraxaze is an enzyme that rapidly reduces methotrexate levels by breaking the chemotherapy drug down to a form that can be eliminated from the body. Voraxaze is administered directly into a patient’s vein (intravenously).

 

Voraxaze has an orphan drug designation, given to therapies indicated for rare or specific disease populations. A single clinical study of 22 patients evaluated the effectiveness of Voraxaze. All patients received Voraxaze treatment. The study considered treatment a success if the methotrexate level fell below a critical level within 15 minutes and stayed below the critical level for eight days. Ten of the 22 patients achieved this standard. Although not all patients experienced this result, Voraxaze eliminated 95% of the methotrexate in all patients. A separate clinical study evaluated the safety of Voraxaze in 290 patients experiencing problems clearing methotrexate from their blood.

 

The most common side effects observed in greater than 1% of patients in the clinical study were low blood pressure (hypotension), headache, nausea, vomiting, flushing, and abnormal sensation (paraesthesia). Voraxaze is marketed by BTG International Inc., West Conshohocken, Pa.

Discovery Could Lead to an Exercise Pill

 

Technology Review

 

 

A newly identified hormone acts like a workout, and transforms bad fat into good

 

 

MIT Technology Review, January 16, 2012, by Karen Weintraub  —  Researchers have discovered a natural hormone that acts like exercise on muscle tissue—burning calories, improving insulin processing, and perhaps boosting strength. The scientists hope it could eventually be used as a treatment for obesity, diabetes, and, potentially, neuromuscular diseases like muscular dystrophy.

In a paper published online today by the journal Nature, the scientists, led by Bruce Spiegelman at the Dana-Farber Cancer Institute in Boston, showed that the hormone occurs naturally in both mice and humans. It pushes cells to transform from white fat—globules that serve as reservoirs for excess calories—into brown fat, which generates heat.

Because the hormone is present in both mice and humans, Spiegelman speculates that it may have served as an evolutionary defense against cold by triggering shivering. He named it irisin, after the Greek messenger goddess Iris, who allowed humans to communicate with the gods in Greek mythology, because exercise appears to “talk” to various tissues in the body via irisin.

Mice given irisin lost a few grams in the first 10 days after treatment, the study shows, and certain genes involved in powering the cell were turned on. Irisin also appeared to reduce the damage done by a high-fat diet, protecting mice against diet-induced obesity and diabetes, according to the paper, whose first author is postdoctoral fellow Pontus Boström.

“We are hopeful, though we have no evidence, that this hormone may embody some of the other benefits of exercise, perhaps in the neuromuscular system,” Spiegelman says. If so, it could also be used to treat disorders like muscular dystrophy and muscle wasting.

Researchers still have to figure out how much benefit irisin could provide someone with diabetes or other health problems, says Spiegelman, also a professor of cell biology and medicine at Harvard Medical School. “I’m optimistic,” he says. “I just don’t want to overpromise and underdeliver.”

Harvard Medical School’s Dean Jeffrey Flier, an endocrinologist, says he is quite enthusiastic about the new hormone. The study, he says, “opens up a completely new approach to understanding the links between exercise, body weight, and diabetes.”

Flier believes irisin offers strong therapeutic potential. “Though much remains to be learned about the action of irisin, and its status in humans with various diseases, this work has the potential to be a game-changer in the field of metabolic disease.”

Last month, Spiegelman formed a Boston-based company named Ember Therapeutics to develop his brown-fat research projects, including irisin. The company raised $34 million in series A financing, and is backed by Third Rock Ventures of Boston.

Harvey Lodish, a professor of biology and bioengineering at MIT, and a member of the Whitehead Institute for Biomedical Research, says it may be harder to make irisin into a drug than Spiegelman anticipates. Lodish tried for years to make adiponectin, a hormone he discovered in the mid-1990s, into a similar drug, but never succeeded.

The concentration of both hormones in the blood is already so high that manufacturing enough to make a difference in health is quite challenging, he says. Maybe irisin will be easier to produce, he says, or maybe it could be delivered via gene therapy, in a modified version of the delivery system Spiegelman used in his research—but Lodish is dubious.

However, of Spiegelman’s new research, he says, “It’s very nice, it’s very elegant.”

 

Device Brings $1,000 Genome Within Reach

 

Sequence machine: The Ion Proton Sequencer chip
Life Technologies

 

 

Ion Torrent introduced its new tabletop sequencer at CES this week.

 

 

MIT Technology Review, January 16, 2012, by Erica Westly  —  Thanks to advances in chemistry and software, researchers can soon sequence a human genome for $1,000 in a day.

Back in July, Jonathan Rothberg, CEO of the Connecticut-based biotech company Ion Torrent, predicted that by 2013 his company would develop a chip that could sequence an entire human genome.

This week, the company surpassed that prediction with a new tabletop sequencer called the Ion Proton. The company introduced the device at the Consumer Electronics Show in Las Vegas on Tuesday, although the sequencer is only available to researchers at this point.

At $149,000, the new machine is about three times the price of the Personal Genome Machine, the sequencer that the company debuted about a year ago. But the DNA-reading chip inside it is 1,000 times more powerful, according to Rothberg, allowing the device to sequence an entire human genome in a day for $1,000—a price the biotech industry has been working toward for years because it would bring the cost down to the level of a medical test.

“The technology got better faster than we ever imagined,” Rothberg says. “We made a lot of progress on the chemistry and software, then developed a new series of chips from a new foundry.” The result is a technology progression that has moved faster than Moore’s law, which predicts that microchips will double in power roughly every two years.

Ion Torrent’s semiconductor-based approach for sequencing DNA is unique. Currently, optics-based sequencers, primarily from Illumina, a San Diego-based company, dominate the human genomics field. But, while the optics-based sequencers are generally considered more accurate, these machines cost upwards of $500,000, putting them out of reach for most clinicians. Meanwhile, at Ion Torrent’s price, “you can imagine one in every doctor’s office,” says Richard Gibbs, director of Baylor College of Medicine’s human genome sequencing center in Houston, which will be among the first research centers to receive a Proton sequencer.

The new Ion Torrent sequencer will also allow researchers to buy a chip that sequences only exons, the regions of the genome that encode proteins. Exons only account for about 5 percent of the human genome, according to the National Human Genome Research Institute, but they are where most disease-causing mutations occur, making so-called exome sequencing a faster and potentially cheaper option for many researchers. Although it’s the same price as the genome chip, the Ion Torrent exome chip can sequence two exomes at a time, bringing the per-sequence cost down to $500.

“Some researchers want to sequence single genes, others want to do exomes, and others—for example, cancer researchers—will want to sequence whole genomes, so all three are going to coexist,” says Rothberg. “It’s about finding the right tool for the problem.”

Whether Ion Torrent’s new technology will be enough to make it the dominant supplier of these tools remains to be seen. A day after the company debuted the Proton sequencer, Illumina also announced that it, too, had reached the $1,000 genome milestone.

“It’s a volatile field, and there’s no sentiment to keep researchers from switching to new technologies,” says Gibbs. Still, Ion Torrent clearly has the price advantage. For researchers who already have Illumina’s latest sequencer, the price to upgrade will be only $50,000, but the retail price will be $740,000, which will likely scare off most newcomers.

 

Target Health Presentations 2012

 

 

Target Health is pleased to announce that it will be presenting at the following meetings this year. Details to follow as we get closer:

 

1. Risk-Based Approaches to Clinical Investigation – April 10-12 – Philadelphia

2. Encouraging Development of Therapeutics for Neglected Diseases – May 12-13 – Philadelphia

3. DIA Annual Meeting – June 25-27 – Philadelphia

4. Disruptive Innovations – Boston – September 13-14

 

For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at www.targethealth.com

 

 

On the Hunt for Universal Intelligence

 

On the hunt for the universal intelligence test. (Credit: SINC)

 

 

 

How do you use a scientific method to 1) ___ the intelligence of a human being, an animal, a machine or an extra-terrestrial? So far this has not been possible, but a team of Spanish and Australian researchers have taken a first step towards this by presenting the foundations to be used as a basis for this method in the journal Artificial Intelligence, and have also put forward a new intelligence test.

 

We have developed an “anytime” intelligence 2) ___, in other words a test that can be interrupted at any time, but that gives a more accurate idea of the intelligence of the test subject if there is a longer time available in which to carry it out,” José Hernandez-Orallo, a researcher at the Polytechnic University of Valencia (UPV), said. This is just one of the many determining factors of the universal 3) ___ test. “The others are that it can be applied to any subject — whether biological or not — at any point in its development (child or adult, for example), for any system now or in the future, and with any level of intelligence or speed,” points out Hernández-Orallo.

 

Orallo, along with his colleague David L. Dowe of the Monash University, Clayton (Australia), has suggested the use of 4) ___ and computational concepts in order to encompass all these conditions. The study forms part of the “Anytime Universal Intelligence” project, in which other scientists from the UPV and the Complutense University of Madrid are taking part.

 

The authors have used interactive 5) ___exercises in settings with a difficulty level estimated by calculating the so-called “Kolmogorov complexity” (they measure the number of computational resources needed to describe an object or a piece of information). This makes them different from traditional psychometric tests and artificial intelligence tests (Turing test).

 

Use in Artificial Intelligence

 

The most direct application of this study is in the field of 6) ___ intelligence. Until now there has not been any way of checking whether current systems are more intelligent than the ones in use 20 years ago, “but the existence of tests with these characteristics may make it possible to systematically evaluate the progress of this discipline,” says Hernández-Orallo. And what is even “more important” is that there were no theories or tools to evaluate and compare future intelligent systems that could demonstrate intelligence greater than 7) ___ intelligence.

 

The implications of a universal intelligence test also impact on many other disciplines. This could have a significant impact on most cognitive sciences, since any discipline depends largely on the specific techniques and systems used in it and the mathematical basis that underpins it. The authors conclude that “The universal and unified evaluation of intelligence, be it human, non-human animal, artificial or extraterrestrial, has not been approached from a 8) ___ viewpoint before, and this is a first step.”

 

ANSWERS: 1) measure; 2) test; 3) intelligence; 4) mathematical; 5) exercises; 6) artificial; 7) human; 8) scientific

Evolution Is Written All Over Your Face

 

 

Primates from Central and South America. (Credit: Image courtesy of University of CaliforniaLos Angeles)

 

 

Why are the faces of primates so dramatically different from one another? UCLA biologists working as “evolutionary detectives” studied the faces of 129 adult male primates from Central and South America, and they offer some answers in research published on 11 January 2011, in the early online edition of the journal Proceedings of the Royal Society B. The faces they studied evolved over at least 24 million years.

 

“If you look at New World primates, you’re immediately struck by the rich diversity of faces,” said Michael Alfaro, a UCLA associate professor of ecology and evolutionary biology and the senior author of the study. “You see bright red faces, moustaches, hair tufts and much more. There are unanswered questions about how faces evolve and what factors explain the evolution of facial features. We’re very visually oriented, and we get a lot of information from the face.” Some of the primate species studied are solitary, while others live in groups that can include dozens or even hundreds of others.

 

Each face was divided into 14 regions; coded the color of each part, including the hair and skin; studied the patterns and anatomy of the faces; and gave each a “facial complexity” score. The authors studied how the complexity of primate faces evolved over time and examined the primates’ social systems. To assess how facial colors are related to physical environments, they analyzed environmental variables, using the longitude and latitude of primates’ habitats as a proxy for sun exposure and temperature. They also used statistical methods to analyze the evolutionary history of the primate groups and when they diverged from one another.

 

“We found very strong support for the idea that as species live in larger groups, their faces become more simple, more plain,” said lead author Sharlene Santana, a UCLA postdoctoral scholar in ecology and evolutionary biology and a postdoctoral fellow with UCLA’s Institute for Society and Genetics. “We think that is related to their ability to communicate using facial expressions. A face that is more plain could allow the primate to convey expressions more easily.

 

The finding that faces are more simple in larger groups came as a surprise. “Initially, we thought it might be the opposite,” Santana said. “You might expect that in larger groups, faces would vary more and have more complex parts that would allow one individual to identify any member of that group. That is not what we found. Species that live in larger groups live in closer proximity to one another and tend to use facial expressions more than species in smaller groups that are more spread out. Being in closer proximity puts a stronger pressure on using facial expressions.”

 

“This finding suggests that facial expressions are increasingly important in large groups,” said co-author Jessica Lynch Alfaro, associate director of the UCLA Institute for Society and Genetics. “If you’re highly social, then facial expressions matter more than having a highly complex pattern on your face. ” The authors also found that when primates live in environment with more species that are closely related, their faces are more complex, regardless of their group size. This finding is consistent with their need to recognize individuals of other closely related species that live in the same habitat to avoid interbreeding, Santana said.

 

The study presented the first quantitative evidence linking social behavior to the evolution of facial diversity and complexity in primates, and how ecology controls aspects of facial patterns. As species live closer to the equator, the skin and hair around their eyes get darker. It was also found that regions of the face around the nose and mouth get darker when species live in humid environments and denser forests and that facial hair gets longer as species live farther from the equator and the climate gets colder, which may be related to regulating body temperature.

 

In the future, the authors may use computer facial-recognition software to help quantify the faces in a more sophisticated way. They also plan to study the faces of carnivores, including big cats. Previous studies have found that primate species with moustaches and beards tend to look poker-faced; they don’t move their faces much when they communicate, compared with other species.

 

The authors also devised a way to test a theory that has been in the biological literature for decades but had never been tested before. As a lineage diverges and species accumulate, a series of changes in facial coloration and body coloration emerges. The theory suggests that once a species evolves to have a certain color, such as hair color, the change is irreversible and it cannot evolve back to a previous color in its lineage. This theory was found to be wrong.

 

Lessons for human faces?

 

The findings do suggest that an important factor in shaping human faces is the premium on making unambiguous facial expressions. “Humans don’t have all these elaborate facial ornamentations, but we do have the ability to communicate visually with facial expressions,” Alfaro said. “Does reduced coloration complexity create a blank palate for visual expressions that can be conveyed more easily? That is an idea we are testing.”

 

The nature and origins of hominid intelligence is a much-studied and much-debated topic, of natural interest to humans as the most successful and intelligent hominid species. There is no universally accepted definition of intelligence, one definition is “the ability to reason, plan, solve problems, think abstractly, comprehend ideas and language, and learn.” The evolution of hominid intelligence can be traced over its course for the past 10 million years, and attributed to specific environmental challenges.

 

It is a misunderstanding of evolutionary theory, however, to see this as a necessary process, and an even greater misunderstanding to see it as one directed to a particular outcome. There are primate species which have not evolved any greater degree of intelligence than they had 10 million years ago: this is because their particular environment has not demanded this particular adaptation of them. Intelligence as an adaptation to the challenge of natural selection is no better or worse than any other adaptation, such as the speed of the cheetah or the venomous bite of the cobra. It is, however, the only adaptation which has allowed a species to establish complete domination over the rest of the natural world.

 

Whether our species has yet acquired sufficient intelligence to manage this responsibility is a matter for debate.

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