Science Weekly podcast: AAAS 2011, drugs and the sound of the stars

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The highlights of this year’s AAAS science festival in Washington DC, professor David Nutt explains his latest research on reclassifying drugs; plus, the sound of the stars

Target Health and Ferring Pharmaceuticals Presenting on CTMS

Silvana Cappi, Executive Director Global Biometrics at Ferring International PharmaScience Center (Copenhagen) and Dr. Jules T. Mitchel, President of Target Health will be presenting at CBI’s 4th Annual Clinical Trial Management Systems (CTMS) meeting , March 24-25, 2011, Crowne Plaza, Philadelphia. Our session on “Analysis of the Decision Whether to Co-Develop a CTMS with an eCRO or to Buy an Existing Application”, provides the clinical operations and IT professional with insight into the development of a CTMS system that was not purchased off the shelf. FDA will also be speaking on “Understand Potential Regulatory Issues and Inspection Expectations.”

As the only forum dedicated solely to discussion regarding CTMS systems, this program offers the unique opportunity for industry collaboration among various CTMS stakeholders. Featuring industry case studies and perspectives from Sanofi-Aventis, Merck & Co., Inc., Millennium: The Takeda Oncology Company and GlaxoSmithKline, to name a few, this program offers a balanced perspective of the different types of CTMS systems utilized by the industry.

For more information about this meeting and/or 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. Target Health’s software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health website at:


King George VI after his coronation in 1937, with Queen Elizabeth
Photo Source: Agence France-Presse

In “The King’s Speech,” King George VI begins 1)  ______ at 4 and struggles with it throughout his life. His stutter is aggravated by stressful situations, like confronting his brother or addressing the public. He speaks better when playing with his daughters, singing words or inserting profanity, or when music blaring in his ears keeps him from hearing himself. These are complicated symptoms, but experts say these details, devised by a screenwriter who stuttered, mirror many aspects of actual stuttering.

Dispelling longstanding misconceptions that the underlying causes of stuttering are language problems or psychological problems like, 2)  ______ or 3.  ______. Researchers say stuttering is really a speech-production problem: a snag in the cascade of steps that our brains and bodies undertake to move the proper muscles to produce words.

Stuttering, which affects about 4)  ______ % of children, usually begins between age 2 and 6. While about 50% of stutterers have family members who stuttered, it is so far impossible to know who will develop it.

Anne Smith, a stuttering expert at Purdue University, says that “stuttering usually begins not with a child’s 5) ___ words and not even with two-word utterances like doggie bark, but when you’re starting with the grammar of the language, prepositions, adjectives, verbs and adverbs. The complexity of grammar, in fact, seems to be part of the hang-up. Dr. Smith has monitored the brain 6) ___ of children watching cartoons in which sentences with meaning errors (“Daddy puts the horse in his coffee”) and grammatical errors are inserted. Stutterers’ brains respond to meaning errors as normal speakers’ brains do, but have a much lower response to grammatical errors, she said.

For unclear reasons, 7) ______ are twice as likely to stutter, and up to four times as likely to continue stuttering into adulthood.

Scientists are finding some answers, though. By examining images of the brains of people who began stuttering as children and people who started stuttering after a stroke, It has been found that stutterers have excess activity in areas involved in speech motor control and coordination of the movements needed for speech. These brain areas may be working overtime because stutterers do not develop the “automatic pattern of speaking” that nonstutterers have, said Dr. Smith.

Genes almost certainly play a role for about half of all stutterers. Dennis Drayna, a scientist at the National Institute on Deafness and Other Communication Disorders, has identified gene mutations that appear to be associated with stuttering in a Pakistani family and others. But he and others say there are likely to be different mutations related to stuttering in other families.

As a child who stuttered badly, Gerald Maguire learned the tricks of coping. When called upon in class, he would sometimes answer in the voice of Elmer Fudd or Donald Duck because he didn’t stutter when imitating someone. He found easier-to-say synonyms for words that stymied him. And he almost never made phone calls because he stumbled over a phrase for which there was no substitute: his own name.

Now, Dr. Gerald Maguire, a psychiatrist at the University of California, Irvine, wants to cure the ailment that afflicts him and an estimated three million Americans. He is searching for a drug to treat stuttering, organizing clinical trials and even testing treatments on himself.

If the cause of stuttering has baffled scientists, so has its treatment. A 16th-century Italian physician prescribed 8) ______ to ”dehumidify” the brain. An American Indian tribe made stutterers spit through a hole in a board to drive the devil from their throats.

ANSWERS: 1)  stuttering;  2)  anxiety;  3)  trauma;  4)  5;  5)  first; 6)  waves;  7)  boys;  8)  nosedrops

Medicine and the Law in the Ancient World

Close-up of the fingernail at top of the Stele, upon which is carved Hammurabi’s Code of Laws.  (Hammurabi, Babylonian Priest-King 1792-1750 BC)
One nearly complete example of the Code survives today, on a diorite stele in the shape of a huge index finger, 2.25 m or 7.4 ft tall.   The Code, consisting of 282 laws, is inscribed in the Akkadian language, using cuneiform script carved into the stele, today on display in the Louvre, in Paris.  The Code was also carved into clay tablets.

The establishment of the calendar and the invention of writing marked the dawn of recorded history. The clues to early knowledge are scanty, consisting of clay tablets bearing cuneiform signs and seals that were used by physicians of ancient Mesopotamia. In the Louvre there is preserved a stone pillar on which is inscribed the Code of Hammurabi, who was a Babylonian king of the 18th century BCE. This code includes laws relating to the practice of medicine, and the penalties for failure were severe. Law # 215 says, “If a physician operates on a man for a severe wound (or make a severe wound on a man) with a bronze lancet and save the man’s life; or if he open an abscess (in the eye) of a man with a bronze lancet and save that man’s eye, he shall receive ten shekels of silver (as his fee). And, law # 216 says, “If he be a freeman, he shall receive five shekels.”

Legal medicine is considered to be the field of study and accumulation of materials that deals with the application of medical knowledge to the administration of justice. Medicine and law have been related from the earliest times. The bonds that first united them were religion, superstition, and magic. The functions of the physician and the jurist were united in the priest, the intermediary between God and man. In early civilizations, primitive legal codes, religious doctrines, and social precepts were often ill distinguished, and laws with a medical content were often found within their context. Ecclesiastical courts and canon law were concerned with much that related not only to religious matters but also to medicine – for example, impotence, divorce, sterility, pregnancy, abortion, and period of gestation. The oldest of these written records, the Code of Hammurabi, includes legislation pertaining to the practice of medicine, dating back to the year 2200 BCE. It covered the topic of medical malpractice and set out for the first time the concept of civil and criminal liability for improper and negligent medical care. Penalties ranged from monetary compensation to cutting off the surgeon’s hand. Fees also were fixed. The Code discussed various diseases of a slave that would invalidate a contract. Also included were references to incest, adultery, and rape.

In ancient Egypt, the acts of the medical man were circumscribed by law. Stab wounds were differentiated in the 17th century BCE. The Egyptians had a thorough knowledge of poisons. There is evidence that priests made determinations regarding the cause of death and whether it was natural or not.

The Chinese published information about poisons, including arsenic and opium 3000 years BCE. In ancient Persia, wounds were put into one of seven classes, ranging from simple to mortal. In ancient Greece, there was a knowledge of poisons and laws against abortions. However, autopsies were not performed, since a dead body was regarded as sacred.

In Rome 600 years BCE, a law was passed requiring that a woman who died in confinement should be immediately “opened” to save the child. The investigators of murder were selected from the citizenry. When Julius Caesar was assassinated in 44 BCE (March 15), the physician Antistius examined his body and concluded that only one of the 23 stab wounds was mortal.

The legal code in ancient Greece (about 460 BCE) was very elaborate. In addition, it was a time of great advances in medicine. Though there is no clear evidence that medical knowledge was officially made use of in establishing proof in courts of law, it is known that Hippocrates and others discussed many genuine medicolegal questions. These questions included the relative fatality of wounds in different parts of the body, the average duration of pregnancy, the viability of children born before full term, and other matters. Moving across the Mediterranean, there is in existence a papyrus, found in Egypt and dated from pre-Christian times, in which a medical officer in Alexandria submitted a report on a suicide about which there had been some suspicion of murder.  Source: Cyril H. Wecht, MD, JD

Rare Gene Glitch May Hold Clues For Schizophrenia

Schizophrenia is known to have a strong genetic component – having a parent or sibling with the disorder increases one’s risk tenfold. Previous studies suggested that schizophrenia, might, in many cases, be rooted in different genetic causes in each affected individual, complicating prospects for cures. Based on an article published online in Nature (23 February 2011), the scientific world is now eyeing a rare genetic glitch for clues to improved treatments for some people with schizophrenia, even though the mutation was found in only one third of 1% of patients. In the study, schizophrenia patients were 14 times more likely than controls to have multiple copies of a gene on Chromosome 7. The mutations were in the gene for VIPR2, the receptor for vasoactive intestinal peptide (VIP) – a chemical messenger known to play a role in brain development. As schizophrenia affects about 1% of adults, discovery of the same genetic abnormality in even a small group of patients provides hope for progress in a field humbled by daunting complexity in recent years.

The VIPR2 CNV is among the first to implicate a specific gene and neurobiological pathway in schizophrenia. CNVs previously identified, spanning dozens of genes, were too large to yield such clues. In the new genome-wide scan, the mutation was found in 29 of 8,290 patients (.35%) compared to only 2 of 7431 healthy controls. A few other schizophrenia-linked CNVs seen in previous studies were also detected. VIP and its receptor are known to play a role in regulating the growth of neurons and in learning and memory. They are also expressed in the immune and cardiovascular systems and in the gut – hence its name.

When VIP binds to the VIPR2 receptor on a neuron, it triggers a key relay chemical within the cell, called cyclic AMP. The study found that both VIP and cyclic AMP were overactive in blood cells of patients with the VIPR2 mutations.

Since the mutations lead to an overexpression of VIPR2, agents that block the receptor, which already exist, might hold potential for treatment development.

According to the authors, in addition to genetic screening of patients for such personalized medicine, there may be new opportunities for neuroimaging studies. Knowing where the VIPR2 gene is expressed in the human brain may point to specific regions where VIP activity levels may differ between people who carry this mutation and those who don’t.

Genetically Modified Fungi Kill Malaria-Causing Parasites in Mosquitoes

In a previous career, Dr. Mitchel, President of Target Health was involved in mosquito control programs and taught Tropical Medicine at Cornell Medical. His comments are that “While the following article is very important for control of malaria, there are additional options for mosquito control, which includes good water management to reduce the mosquito breeding sites.”

According to the World Health Organization (WHO), an estimated 225 million malaria cases occur worldwide annually, resulting in about 781,000 deaths. Although malaria is present in 106 countries, most cases occur in sub-Saharan Africa. Treating bed nets and indoor walls with insecticides is the main prevention strategy in developing countries, but the Anopheles mosquitoes that transmit malaria are slowly becoming resistant to these insecticides, rendering them less effective.

According to a new study published in the journal Science (2011;331:1074-1077), spraying malaria-transmitting mosquitoes with a genetically modified fungus, Metarhizium anisopliae, can kill the malaria parasite without harming the mosquito, potentially reducing malaria transmission to humans. Previous studies have found that this method nearly eliminates disease transmission when mosquitoes are sprayed soon after acquiring the malaria parasite. However, this strategy is not sustainable in the long term since if treating mosquitoes with the fungus kills them before they have a chance to reproduce and pass on their susceptibility to the spray, mosquitoes resistant to the fungus, which would reproduce normally, will soon become predominant and the spray will no longer be effective.

Because of this, the present study tried a more focused approach. Rather than developing fungi that rapidly kill the mosquito, they genetically modified M. anisopliae to block the development of the malaria parasite in the mosquito. The concept was that the genes added to the transgenic fungi would prevent the parasite from binding to the salivary glands of mosquitoes, so when a mosquito bites a human, the parasite is not transmitted.

For the evaluation of this approach, 11 days after feeding on blood infected by the malaria parasite, mosquitoes were divided into three groups and either sprayed with naturally occurring M. anisopliae fungi, genetically modified M. anisopliae fungi or not sprayed at all.

Results showed that two weeks post-treatment, the malaria parasite was found on the salivary glands of just 25% of the mosquitoes sprayed with the transgenic fungi, compared with 87% of those sprayed with the naturally occurring strain and 94% of unsprayed mosquitoes. The transgenic strain also reduced the density of parasites on the mosquitoes’ salivary glands by more than 95% compared with the unmodified strain.

Alcohol Consumption and Cardiovascular Disease

According to an article published in the British Medical Journal (2011;342:d671), a comprehensive systematic review and meta-analysis was conducted of studies assessing the effect of alcohol consumption on multiple cardiovascular outcomes. The data sources included Medline (1950 through September 2009) and Embase (1980 through September 2009) supplemented by manual searches of bibliographies and conference proceedings.

Included in the analysis were prospective cohort studies on the association between alcohol consumption and overall mortality from cardiovascular disease, incidence of and mortality from coronary heart disease, and incidence of and mortality from stroke. Of 4,235 studies reviewed for eligibility, quality, and data extraction, 84 were included in the final analysis.

Results showed that the pooled adjusted relative risks for alcohol drinkers relative to non-drinkers in random effects models for the outcomes of interest were 0.75 for cardiovascular disease mortality (21 studies), 0.71 for incident coronary heart disease (29 studies), 0.75 for coronary heart disease mortality (31 studies), 0.98 for incident stroke (17 studies), and 1.06 for stroke mortality (10 studies).

Dose-response analysis revealed that the lowest risk of coronary heart disease mortality occurred with 1-2 drinks a day, but for stroke mortality it occurred with <1 drink per day. Secondary analysis of mortality from all causes showed lower risk for drinkers compared with non-drinkers (relative risk 0.87).

According to the authors, light to moderate alcohol consumption is associated with a reduced risk of multiple cardiovascular outcomes.

TARGET HEALTH excels in Regulatory Affairs and Public Policy issues. Each week we highlight new information in these challenging areas.

Goings On In Wisconsin

Major current events often provide valuable lessons for those willing to probe beneath the surface and detect emerging trends. Watching the turmoil over retirement and health care benefits for public employees in the American Midwest offers valuable insights about evolving trends in health care & health spending to those engaged in discovering, developing and marketing health care products and services (e.g. Target Health Clients). These insights are valuable strategically and therefore warrant consideration irrespective of anyone’s view about which side has the more compelling arguments in the controversy.

Examining the healthcare-related proposals reveals policy initiatives reciprocating widely adopted (and not especially novel) approaches to health coverage in the private sector. Specifically, the design of private sector benefit programs has evolved to increasingly shift costs to individuals. This is accomplished through multiple mechanisms, among these increased premiums, deductibles and “co-pays”, tiered pharmaceutical benefits, and restricted provider networks with high out of pocket payments for services from non-network providers. The common theme is to “off load” costs (and thus some of the financial risk) to individual patients. Wisconsin appears to be moving tentatively in a similar direction.

In addition to the obvious cost savings for employers, a stated goal of newer plans is to increase the cost sensitivity of patients, making the market for medical care reminiscent of more conventional consumer markets. Accomplishing this responsibly requires providing patients with accurate and actionable information about the products and services among which they will be obligated to choose from. The hypotheses are that 1. consumer choice will result in a more efficient market for medical services, and 2. With the engagement of decision-making by individual patients, cost-containment will be achieved.

For developers and marketers of medicines and devices, this means that the value of these products and services will increasingly need to be transparent to multiple users: physicians, payers and patients. An additional competitive advantage will accrue to firms able to rapidly communicate enhanced value effectively and accurately to this array of constituencies.

Bluntly, if patients are asked to pay an increasingly larger percentage of health costs out of pocket, they will seek value – and bargains – just as they do when making other major purchases. Patients will not, however, be willing to be sold a “bill of goods” and assume the brunt of out-of control healthcare costs. Whether this can be achieved at an acceptable “cost” and with no negative impact on patient care is uncertain, but there is no question that the competitive landscape is shifting in favor of products and services with compelling and effectively communicated data. By Mark L. Horn, MD, CMO, Target Health Inc.

For more information about our expertise in Medical Affairs, contact Dr. Mark L. Horn. For Regulatory Affairs, please contact Dr. Jules T. Mitchel or Dr. Glen Park.

The figure above was kindly provided by Dr. Bruno Pichler at The National Institute for Medical Research in London.

Dr. Jeffrey H. Toney is an educator and a scientist whose career has spanned academia and the pharmaceutical industry. He serves as the dean of the College of Natural, Applied and Health Sciences at Kean University. He is dedicated to strengthening public appreciation of the beauty and impact of science in our daily lives. His news media publications include The Star Ledger, The New York Times as well as regular blogs at NJ Voices, OpEdNews and The Huffington Post; he has published more than 60 peer-reviewed scientific publications and holds six US patents., February 24, 2011  —  Anyone with a young daughter knows about “bedazzled.” When I first saw these images of intact, single neurons capable of generating electrical signals, “bedazzled” came to mind.

According to the paper in Nature Neuroscience:
(on which Dr. Bruno Pichler is an author) Single-cell genetic manipulation is expected to substantially advance the field of systems neuroscience. However, existing gene delivery techniques do not allow researchers to electrophysiologically characterize cells and to thereby establish an experimental link between physiology and genetics for understanding neuronal function. In the mouse brain in vivo, we found that neurons remained intact after ‘blind’ whole-cell recording, that DNA vectors could be delivered through the patch-pipette during such recordings and that these vectors drove protein expression in recorded cells for at least 7 d. To illustrate the utility of this approach, we recorded visually evoked synaptic responses in primary visual cortical cells while delivering DNA plasmids that allowed retrograde, monosynaptic tracing of each neuron’s presynaptic inputs. By providing a biophysical profile of a cell before its specific genetic perturbation, this combinatorial method captures the synaptic and anatomical receptive field of a neuron.

Figure 3: Multiple gene delivery.

(a) Native fluorescence images of a layer 5 neuron in somatosensory cortex 3 d after patching with pCAGGS-Cerulean (top right) and pCAGGS-tdTomato (50 ng μl−1 each, bottom right). Scale bars, 824 μm (left) and 20 μm (right). (b) Gallery of native fluorescence images for a layer 2/3 cell in somatosensory cortex 5 d after recording with pCAGGS-DsRed2, pCAGGS-Venus and pCAGGS-ChR2-Cerulean. Scale bar, 20 μm.

Breakthrough in Neuroscience – new method allows characterization of neuronal networks on single-cell level

An international team led by neuroscientist Troy Margrie has developed a new method, which will shape the future of cellular neuroscience. The researchers from MRC National Institute for Medical Research in London, Columbia University in New York and Max-Planck-Institute for Medical Research in Heidelberg succeeded in determining the function of individual nerve cells in the brain and identify those neurons from which a given cell receives its signals. “The new method enables us for the first time to identify a neuronal networks on the level of individual cells and characterize it functionally”, explains Ede Rancz. This study is now published in Nature Neuroscience.

A genetically modified rabies virus leads the way

The scientists combined two existing methods, “whole-cell patch clamp recording” and “monosynaptic retrograde virus tracing”. They use the patch-clamp technique to determine the exact stimuli to which a given brain cell responds. Through the glass micropipette, which is used to record electrical signals, they simultaneously inject plasmid DNA into this cell. In the vicinity of the cell they later inject a rabies virus, which is lacking proteins necessary for entering a cell and spreading through neuronal pathways. These missing proteins are provided by the plasmid DNA injected previously into the cell. Therefore, the virus can only infect this single cell and then spread across synapses to only those neurons which are exactly one step upstream in the signaling chain. There it stops because these presynaptic cells do not contain the necessary plasmid DNA, which the modified virus needs for spreading.

Cellular networks in the living organism
The plasmid DNA and the virus both produce fluorescent proteins, which are then visualized through specialized microscopes. In this way, the functionally characterized cell as well as its connected ‘neighbours’, from which the cell receives information – let them be in close proximity or in a different brain area -can be identified. As this technique can be used in a living organism, cellular networks can be identified and then subjected to further experiments. The researchers are convinced that this method opens up the door for answering a plethora of very important but previously unapproachable questions.

The original paper is available online:
Short video clips of original microscopy images are available at:


Prof. Troy Margrie
The Division of Neurophysiology
The National Institute for Medical Research
Mill Hill
London NW7 1AA

Security,, February 24, 2011, byAndy Greenberg  —  Ray Kurzweil may be the world’s most prominent techno-optimist. The 63-year old futurist and artificial intelligence guru believes, famously, that by 2045 humans will build a computer capable of replicating and storing the human mind–what he calls the “singularity”–essentially allowing our mental selves to live on indefinitely.

So perhaps it’s no surprise that Kurzweil takes an equally sunny view of cybersecurity,  in contradiction to the prevailing gloom around the threat of cyberwar and the futile arms race against cybercriminals. In fact, Kurzweil believes that the information security industry should serve as a model for addressing the sort of pandemic diseases that may result from our globalized society and the looming problem of bioterrorism. Just as the antivirus industry constantly detects new threats, takes them apart, and distributes a “cure,” he argues that our biological antivirus systems need to work in the same networked fashion at a comparable speed.

While interviewing Kurzweil last week about topics closer to his usual fare–immortality and the progress of artificial intelligence–I slipped in a question about this information security idea, which Kurzweil mentioned in passing at a talk promoting the singularity-focused film Transcendent Man earlier this month in New York.

Here’s what he told me:

If we sat back and hoped no one put out a destructive software virus, the Internet wouldn’t last very long. We have a system between all the security protocols and the antivirus software and cybersecurity companies where we’re constantly scouting for new threats. When one’s found, it’s reverse engineered, partly with human intelligence and partly witih computer intelligence, an antidote is coded, and it’s distributed virally, getting the patches to the antiviral programs. The whole system gets more sophisticated in parallel with the predators, the viruses.

It’s never something we can cross off our list. We’ll always have computer viruses. But despite the negative perception of Internet security, it’s something that works very well. No one’s taken down the Internet for any meaningful period of time.

We need a system for biological viruses that can do the same thing. And we’re working on putting one into place. I’ve been on the Army science advisory group, and involved in this issue. The U.S. Army is responsible for bioterrorism protection. They protect us from anthrax, from small pox. But what about the specter of a bioengineering lab that engineers a new virus, adds some genes to the flu virus to make it deadlier, more communicable, more stealthy?

Today we have some techniques to deal with this like rapid sequencing. We can sequence a virus in a day, while HIV took us five years. We can create an RNA-interference medication or a antigen-based vaccine very quickly. It can be tested in-silico if the FDA accepts that sort of testing. There are these ideas that could go into a rapid response system. It would never be finished. The risks would get more and more sophisticated. But thats’ the approach.

On the Internet, a virus can spread in seconds. It’s a little easier in the biological world. It takes days or weeks to spread in a meaningful way, as we saw with swine flu. That could give you time to ship these [antidotes] around the world, just as we ship the antivirus update around the Internet.

It’s a system that’s not in place yet, but it’s feasible.

Here’s the edited interview: Ray Kurzweil and Andy Greenberg…………..

For 30 years Ray Kurzweil has been preaching the artificial intelligence gospel. As computers drive cars and play Jeopardy!, are we on track to reach his cybertopia?

Andy Greenberg: You’ve predicted that by 2045 accelerating progress in technology means we’ll build a computer–the so-called singularity–powerful enough to let us upload and replicate our brains, essentially becoming immortal. Are we on schedule?

Ray Kurzweil: With regard to artificial intelligence, we’re very much on schedule. Just look at the actual tasks that AI is performing that weren’t possible three years ago. Driving a car in a busy urban situation with no driver: Google’s driverless cars have logged 140,000 miles.

IBM’s Jeopardy!-playing supercomputer Watson plays at about the level of the best human players. I predicted in the early ’80s that a computer would defeat the world chess champion by 1998. It happened in ’97. Now people say, “Of course computers can play chess. But they’ll never be able to do something as human as understand language.” Watson is harder to dismiss.

AG: You also predicted we’d have a computer capable of 20 petaflops of processing by 2009, and we’re still less than a tenth of the way there.

RK: That computer is being built now. In 2011 there will be a 20 petaflop computer, the IBM Sequoia. So on that point we’re slightly behind schedule.

AG: What do you think about the fact that China, not the U.S.,has the fastest supercomputer in the world currently?

RK: I’m not overly concerned. It’s not a zero-sum game. We all benefit from the advance of knowledge.

AG: You talk about a certain inevitability of progress toward the singularity. What drives that progress? Is it business?

RK: Money plays an important role. It’s an enabling factor, like clay to a sculptor. But we’re programmed by biological evolution to innovate. Technological innovation just continues a process that started with biological evolution.

AG: So you’d say innovation drives business more than business drives innovation?

RK: That’s definitely true.

AG: You’ve been accused of unscientific optimism.

RK: The curve of computational progress that I’ve charted since the 1890 census until now is amazingly smooth. World War I and II, the Great Depression and the recent recession, none of these things can perturb it. That’s a powerful argument, both theoretically and empirically. But optimism is more than just an attitude about the future, it’s also a self-fulfilling prophecy.

AG: You’re 63, and I’ve read you take more than 200 pills a day to extend your life in hopes of reaching the singularity. Do you still believe you’ll live forever?

RK: Well, it’s tough to ever win that bet and say, “I’ve lived forever.” It’s never forever. But we’ll get to a point fairly soon, within 15 years, where we’ll reach a tipping point, what [gerontologist] Aubrey de Grey calls “longevity escape velocity.” Life expectancy will increase faster than time passes. I’d be irrational to say that I’m sure I’ll get to the stage where I can back myself up, which is the key point that one would need to reach to live forever. That’s maybe four decades away. In general, life expectancy is a statistical phenomenon. You can still be hit by a truck tomorrow.

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