13 Things That Do Not Make Sense
It is estimated that the number of protons in the universe is 10 to the 80th power.
Without geometry, life is pointless.
by Michael Brooks
The Placebo Effect
Don't try this at home. Several times a day, for several days, you induce pain in someone. You control the pain with morphine until the final day of the experiment, when you replace the morphine with saline solution. Guess what? The saline takes the pain away. This is the placebo effect: somehow, sometimes, a whole lot of nothing can be very powerful. Except it's not quite nothing.
When Fabrizio Benedetti of the University of Turin in Italy carried out the above experiment, he added a final twist by adding naloxone, a drug that blocks the effects of morphine, to the saline. The shocking result? The pain-relieving power of saline solution disappeared. So what is going on? Doctors have known about the placebo effect for decades, and the naloxone result seems to show that the placebo effect is somehow biochemical. But apart from that, we simply don't know. Benedetti has since shown that a saline placebo can also reduce tremors and muscle stiffness in people with Parkinson's disease (Nature Neuroscience, vol 7, p 587). He and his team measured the activity of neurons in the patients' brains as they administered the saline. They found that individual neurons in the subthalamic nucleus (a common target for surgical attempts to relieve Parkinson's symptoms) began to fire less often when the saline was given, and with fewer "bursts" of firing - another feature associated with Parkinson's. The neuron activity decreased at the same time as the symptoms improved: the saline was definitely doing something.
We have a lot to learn about what is happening here, Benedetti says, but one thing is clear: the mind can affect the body's biochemistry. "The relationship between expectation and therapeutic outcome is a wonderful model to understand mind-body interaction," he says. Researchers now need to identify when and where placebo works. There may be diseases in which it has no effect. There may be a common mechanism in different illnesses. As yet, we just don't know.
The Horizon Problem
Our universe appears to be unfathomably uniform. Look across space from one edge of the visible universe to the other, and you'll see that the microwave background radiation filling the cosmos is at the same temperature everywhere. That may not seem surprising until you consider that the two edges are nearly 28 billion light years apart and our universe is only 14 billion years old. Nothing can travel faster than the speed of light, so there is no way heat radiation could have travelled between the two horizons to even out the hot and cold spots created in the big bang and leave the thermal equilibrium we see now.
This "horizon problem" is a big headache for cosmologists, so big that they have come up with some pretty wild solutions. "Inflation", for example. You can solve the horizon problem by having the universe expand ultra-fast for a time, just after the big bang, blowing up by a factor of 1050 in 10-33 seconds. But is that just wishful thinking? "Inflation would be an explanation if it occurred," says University of Cambridge astronomer Martin Rees. The trouble is that no one knows what could have made that happen. So, in effect, inflation solves one mystery only to invoke another. A variation in the speed of light could also solve the horizon problem - but this too is impotent in the face of the question "why?" In scientific terms, the uniform temperature of the background radiation remains an anomaly.
Ultra-Energetic Cosmic Rays
For more than a decade, physicists in Japan have been seeing cosmic rays that should not exist. Cosmic rays are particles - mostly protons but sometimes heavy atomic nuclei - that travel through the universe at close to the speed of light. Some cosmic rays detected on Earth are produced in violent events such as supernovae, but we still don't know the origins of the highest-energy particles, which are the most energetic particles ever seen in nature. But that's not the real mystery. As cosmic-ray particles travel through space, they lose energy in collisions with the low-energy photons that pervade the universe, such as those of the cosmic microwave background radiation. Einstein's special theory of relativity dictates that any cosmic rays reaching Earth from a source outside our galaxy will have suffered so many energy-shedding collisions that their maximum possible energy is 5 × 1019 electronvolts. This is known as the Greisen-Zatsepin-Kuzmin limit. Over the past decade, however, the University of Tokyo's Akeno Giant Air Shower Array - 111 particle detectors spread out over 100 square kilometres - has detected several cosmic rays above the GZK limit. In theory, they can only have come from within our galaxy, avoiding an energy-sapping journey across the cosmos. However, astronomers can find no source for these cosmic rays in our galaxy. So what is going on?
One possibility is that there is something wrong with the Akeno results. Another is that Einstein was wrong. His special theory of relativity says that space is the same in all directions, but what if particles found it easier to move in certain directions? Then the cosmic rays could retain more of their energy, allowing them to beat the GZK limit. Physicists at the Pierre Auger experiment in Mendoza, Argentina, are now working on this problem. Using 1,600 detectors spread over 3,000 square kilometres, Auger should be able to determine the energies of incoming cosmic rays and shed more light on the Akeno results.
Alan Watson, an astronomer at the University of Leeds, UK, and spokesman for the Pierre Auger project, is already convinced there is something worth following up here. "I have no doubts that events above 1020 electronvolts exist. There are sufficient examples to convince me," he says. The question now is, what are they? How many of these particles are coming in, and what direction are they coming from? Until we get that information, there's no telling how exotic the true explanation could be.
Belfast Homeopathy Results
Madeleine Ennis, a pharmacologist at Queen's University, Belfast, was the scourge of homeopathy. She railed against its claims that a chemical remedy could be diluted to the point where a sample was unlikely to contain a single molecule of anything but water, and yet still have a healing effect. Until, that is, she set out to prove once and for all that homeopathy was bunkum. In her most recent paper, Ennis describes how her team looked at the effects of ultra-dilute solutions of histamine on human white blood cells involved in inflammation. These "basophils" release histamine when the cells are under attack. Once released, the histamine stops them releasing any more. The study, replicated in 4 different labs, found that homeopathic solutions - so dilute that they probably didn't contain a single histamine molecule - worked just like histamine. Ennis might not be happy with the homeopaths' claims, but she admits that an effect cannot be ruled out.
So how could it happen? Homeopaths prepare their remedies by dissolving things like charcoal, deadly nightshade or spider venom in ethanol, and then diluting this "mother tincture" in water again and again. No matter what the level of dilution, homeopaths claim, the original remedy leaves some kind of imprint on the water molecules. Thus, however dilute the solution becomes, it is still imbued with the properties of the remedy. You can understand why Ennis remains sceptical. And it remains true that no homeopathic remedy has ever been shown to work in a large randomised placebo-controlled clinical trial. But the Belfast study (Inflammation Research, vol 53, p 181) suggests that something is going on. "We are," Ennis says in her paper, "unable to explain our findings and are reporting them to encourage others to investigate this phenomenon." If the results turn out to be real, she says, the implications are profound: we may have to rewrite physics and chemistry.
Take our best understanding of gravity, apply it to the way galaxies spin, and you'll quickly see the problem: the galaxies should be falling apart. Galactic matter orbits around a central point because its mutual gravitational attraction creates centripetal forces. But there is not enough mass in the galaxies to produce the observed spin. Vera Rubin, an astronomer working at the Carnegie Institution's department of terrestrial magnetism in Washington DC, spotted this anomaly in the late 1970s. The best response from physicists was to suggest there is more stuff out there than we can see. The trouble was, nobody could explain what this "dark matter" was.
And they still can't. Although researchers have made many suggestions about what kind of particles might make up dark matter, there is no consensus. It's an embarrassing hole in our understanding. Astronomical observations suggest that dark matter must make up about 90% of the mass in the universe, yet we are astonishingly ignorant what that 90% is. Maybe we can't work out what dark matter is because it doesn't actually exist. That's certainly the way Rubin would like it to turn out. "If I could have my pick, I would like to learn that Newton's laws must be modified in order to correctly describe gravitational interactions at large distances," she says. "That's more appealing than a universe filled with a new kind of sub-nuclear particle."
20 July 1976 - Gilbert Levin is on the edge of his seat. Millions of kilometres away on Mars, the Viking landers have scooped up some soil and mixed it with carbon-14-labelled nutrients. The mission's scientists have all agreed that if Levin's instruments on board the landers detect emissions of carbon-14-containing methane from the soil, then there must be life on Mars. Viking reports a positive result. Something is ingesting the nutrients, metabolising them, and then belching out gas laced with carbon-14. So why no party?
Because another instrument, designed to identify organic molecules considered essential signs of life, found nothing. Almost all the mission scientists erred on the side of caution and declared Viking's discovery a false positive. But was it? The arguments continue to rage, but results from NASA's latest rovers show that the surface of Mars was almost certainly wet in the past and therefore hospitable to life. And there is plenty more evidence where that came from, Levin says. "Every mission to Mars has produced evidence supporting my conclusion. None has contradicted it." Levin stands by his claim, and he is no longer alone. Joe Miller, a cell biologist at the University of Southern California in Los Angeles, has re-analysed the data and he thinks that the emissions show evidence of a circadian cycle. That is highly suggestive of life.
Levin is petitioning ESA and NASA to fly a modified version of his mission to look for "chiral" molecules. These come in left or right-handed versions: they are mirror images of each other. While biological processes tend to produce molecules that favour one chirality over the other, non-living processes create left and right-handed versions in equal numbers. If a future mission to Mars were to find that Martian "metabolism" also prefers one chiral form of a molecule to the other, that would be the best indication yet of life on Mars.
Four years ago, a particle accelerator in France detected 6 particles that should not exist. They are called tetraneutrons: 4 neutrons that are bound together in a way that defies the laws of physics. Francisco Miguel Marquès and colleagues at the Ganil accelerator in Caen are now gearing up to do it again. If they succeed, these clusters may oblige us to rethink the forces that hold atomic nuclei together. The team fired beryllium nuclei at a small carbon target and analysed the debris that shot into surrounding particle detectors. They expected to see evidence for 4 separate neutrons hitting their detectors. Instead the Ganil team found just one flash of light in one detector. And the energy of this flash suggested that 4 neutrons were arriving together at the detector. Of course, their finding could have been an accident: 4 neutrons might just have arrived in the same place at the same time by coincidence. But that's ridiculously improbable.
Not as improbable as tetraneutrons, some might say, because in the standard model of particle physics tetraneutrons simply can't exist. According to the Pauli exclusion principle, not even 2 protons or neutrons in the same system can have identical quantum properties. In fact, the strong nuclear force that would hold them together is tuned in such a way that it can't even hold 2 lone neutrons together, let alone 4. Marquès and his team were so bemused by their result that they buried the data in a research paper that was ostensibly about the possibility of finding tetraneutrons in the future (Physical Review C, vol 65, p 44006).
And there are still more compelling reasons to doubt the existence of tetraneutrons. If you tweak the laws of physics to allow 4 neutrons to bind together, all kinds of chaos ensues (Journal of Physics G, vol 29, L9). It would mean that the mix of elements formed after the big bang was inconsistent with what we now observe and, even worse, the elements formed would have quickly become far too heavy for the cosmos to cope. "Maybe the universe would have collapsed before it had any chance to expand," says Natalia Timofeyuk, a theorist at the University of Surrey in Guildford, UK. There are, however, a couple of holes in this reasoning. Established theory does allow the tetraneutron to exist - though only as a ridiculously short-lived particle. "This could be a reason for 4 neutrons hitting the Ganil detectors simultaneously," Timofeyuk says. And there is other evidence that supports the idea of matter composed of multiple neutrons: neutron stars. These bodies, which contain an enormous number of bound neutrons, suggest that as yet unexplained forces come into play when neutrons gather en masse.
The Pioneer Anomaly
This is a tale of two spacecraft. Pioneer 10 was launched in 1972. Pioneer 11 a year later. By now both craft should be drifting off into deep space with no one watching. However, their trajectories have proved far too fascinating to ignore. That's because something has been pulling - or pushing - on them, causing them to speed up. The resulting acceleration is tiny, less than a nanometre per second per second. That's equivalent to just one ten-billionth of the gravity at the earth's surface, but it is enough to have shifted Pioneer 10 some 400,000 kilometres off track. NASA lost touch with Pioneer 11 in 1995, but up to that point it was experiencing exactly the same deviation as its sister probe. So what is causing it?
Nobody knows. Some possible explanations have already been ruled out, including software errors, the solar wind or a fuel leak. If the cause is some gravitational effect, it is not one we know anything about. In fact, physicists are so completely at a loss that some have resorted to linking this mystery with other inexplicable phenomena. Bruce Bassett of the University of Portsmouth, UK, has suggested that the Pioneer conundrum might have something to do with variations in alpha, the fine structure constant (see #12 below: "Not So Constant Constants"). Others have talked about it as arising from dark matter - but since we don't know what dark matter is, that doesn't help much either. "This is all so maddeningly intriguing," says Michael Martin Nieto of the Los Alamos National Laboratory. "We only have proposals, none of which has been demonstrated." Nieto has called for a new analysis of the early trajectory data from the craft, which he says might yield fresh clues. But to get to the bottom of the problem what scientists really need is a mission designed specifically to test unusual gravitational effects in the outer reaches of the solar system. Such a probe would cost between $300 million and $500 million and could piggyback on a future mission to the outer reaches of the solar system (www.arxiv.org). "An explanation will be found eventually," Nieto says. "Of course I hope it is due to new physics - how stupendous that would be. But once a physicist starts working on the basis of hope he is heading for a fall." Disappointing as it may seem, Nieto thinks the explanation for the Pioneer anomaly will eventually be found in some mundane effect, such as an unnoticed source of heat on board the craft.
It is one of the most famous, and most embarrassing, problems in physics. In 1998, astronomers discovered that the universe is expanding at ever faster speeds. It's an effect still searching for a cause - until then, everyone thought the universe's expansion was slowing down after the big bang. "Theorists are still floundering around, looking for a sensible explanation," says cosmologist Katherine Freese of the University of Michigan, Ann Arbor. "We're all hoping that upcoming observations of supernovae, of clusters of galaxies and so on will give us more clues." One suggestion is that some property of empty space is responsible - cosmologists call it dark energy. But all attempts to pin it down have fallen woefully short. It's also possible that Einstein's theory of general relativity may need to be tweaked when applied to the very largest scales of the universe. "The field is still wide open," Freese says.
The Kuiper Cliff
If you travel out to the far edge of the solar system, into the frigid wastes beyond Pluto, you'll see something strange. Suddenly, after passing through the Kuiper belt, a region of space teeming with icy rocks, there's nothing. Astronomers call this boundary the Kuiper Cliff, because the density of space rocks drops off so steeply. What caused it? The only answer seems to be a 10th planet. We're not talking about Quaoar or Sedna: this is a massive object, as big as the earth or Mars, that has swept the area clean of debris.
The evidence for the existence of "Planet X" is compelling, says Alan Stern, an astronomer at the Southwest Research Institute in Boulder, Colorado. But although calculations show that such a body could account for the Kuiper Cliff (Icarus, vol 160, p 32), no one has ever seen this fabled 10th planet. There's a good reason for that. The Kuiper belt is just too far away for us to get a decent view. We need to get out there and have a look before we can say anything about the region. And that won't be possible for another decade, at least. NASA's New Horizons probe, which will head out to Pluto and the Kuiper belt, is scheduled for launch in January 2006. It won't reach Pluto until 2015, so if you are looking for an explanation of the vast, empty gulf of the Kuiper cliff, be patient.
The Wow Signal
It was 37 seconds long and came from outer space. On 15 August 1977 it caused astronomer Jerry Ehman, then of Ohio State University in Columbus, to scrawl "Wow!" on the printout from Big Ear, Ohio State's radio telescope in Delaware. And 28 years later no one knows what created the signal. "I am still waiting for a definitive explanation that makes sense," Ehman says. Coming from the direction of Sagittarius, the pulse of radiation was confined to a narrow range of radio frequencies around 1420 megahertz. This frequency is in a part of the radio spectrum in which all transmissions are prohibited by international agreement. Natural sources of radiation, such as the thermal emissions from planets, usually cover a much broader sweep of frequencies. So what caused it?
The nearest star in that direction is 220 light years away. If that is where is came from, it would have had to be a pretty powerful astronomical event - or an advanced alien civilisation using an astonishingly large and powerful transmitter. The fact that hundreds of sweeps over the same patch of sky have found nothing like the Wow signal doesn't mean it's not aliens. When you consider the fact that the Big Ear telescope covers only one-millionth of the sky at any time, and an alien transmitter would also likely beam out over the same fraction of sky, the chances of spotting the signal again are remote, to say the least. Others think there must be a mundane explanation. Dan Wertheimer, chief scientist for the SETI@home project, says the Wow signal was almost certainly pollution: radio-frequency interference from earth-based transmissions. "We've seen many signals like this, and these sorts of signals have always turned out to be interference," he says. The debate continues.
In 1997 astronomer John Webb and his team at the University of New South Wales in Sydney analysed the light reaching the earth from distant quasars. On its 12-billion-year journey, the light had passed through interstellar clouds of metals such as iron, nickel and chromium, and the researchers found these atoms had absorbed some of the photons of quasar light - but not the ones they were expecting. If the observations are correct, the only vaguely reasonable explanation is that a constant of physics called the fine structure constant, or alpha, had a different value at the time the light passed through the clouds. But that's heresy. Alpha is an extremely important constant that determines how light interacts with matter - and it shouldn't be able to change. Its value depends on, among other things, the charge on the electron, the speed of light and Planck's constant. Could one of these really have changed?
No one in physics wanted to believe the measurements. Webb and his team have been trying for years to find an error in their results. But so far they have failed. Webb's are not the only results that suggest something is missing from our understanding of alpha. A recent analysis of the only known natural nuclear reactor, which was active nearly 2 billion years ago at what is now Oklo in Gabon, also suggests something about light's interaction with matter has changed. The ratio of certain radioactive isotopes produced within such a reactor depends on alpha, and so looking at the fission products left behind in the ground at Oklo provides a way to work out the value of the constant at the time of their formation. Using this method, Steve Lamoreaux and his colleagues at the Los Alamos National Laboratory in New Mexico suggest that alpha may have decreased by more than 4% since Oklo started up (Physical Review D, vol 69, p 121701).
There are gainsayers who still dispute any change in alpha. Patrick Petitjean, an astronomer at the Institute of Astrophysics in Paris, led a team that analysed quasar light picked up by the Very Large Telescope (VLT) in Chile and found no evidence that alpha has changed. But Webb, who is now looking at the VLT measurements, says that they require a more complex analysis than Petitjean's team has carried out. Webb's group is working on that now, and may be in a position to declare the anomaly resolved - or not - later this year. "It's difficult to say how long it's going to take," says team member Michael Murphy of the University of Cambridge. "The more we look at these new data, the more difficulties we see." But whatever the answer, the work will still be valuable. An analysis of the way light passes through distant molecular clouds will reveal more about how the elements were produced early in the universe's history.
After 16 years, it's back. In fact, cold fusion never really went away. Over a 10-year period from 1989, US navy labs ran more than 200 experiments to investigate whether nuclear reactions generating more energy than they consume - supposedly only possible inside stars - can occur at room temperature. Numerous researchers have since pronounced themselves believers. With controllable cold fusion, many of the world's energy problems would melt away: no wonder the US Department of Energy is interested. In December, after a lengthy review of the evidence, it said it was open to receiving proposals for new cold fusion experiments.
That's quite a turnaround. The DoE's first report on the subject, published 15 years ago, concluded that the original cold fusion results, produced by Martin Fleischmann and Stanley Pons of the University of Utah and unveiled at a press conference in 1989, were impossible to reproduce, and thus probably false. The basic claim of cold fusion is that dunking palladium electrodes into heavy water - in which oxygen is combined with the hydrogen isotope deuterium - can release a large amount of energy. Placing a voltage across the electrodes supposedly allows deuterium nuclei to move into palladium's molecular lattice, enabling them to overcome their natural repulsion and fuse together, releasing a blast of energy. The snag is that fusion at room temperature is deemed impossible by every accepted scientific theory. That doesn't matter, according to David Nagel, an engineer at George Washington University in Washington DC. Superconductors took 40 years to explain, he points out, so there's no reason to dismiss cold fusion. "The experimental case is bulletproof," he says. "You can't make it go away."
Source: newscientist.com 19 March 2005
What Do You Believe Is True Even Though You Cannot Prove It?
This was the question posed to scientists, futurists and other creative thinkers by John Brockman, a literary agent and publisher of Edge, a Web site devoted to science. The site asks a new question at the end of each year. Here are excerpts (the ones I agreed with, of course) from the responses posted at edge.org.
I do not believe that people are capable of rational thought when it comes to making decisions in their own lives. People believe they are behaving rationally and have thought things out, of course, but when major decisions are made - who to marry, where to live, what career to pursue, what college to attend, people's minds simply cannot cope with the complexity. When they try to rationally analyse potential options, their unconscious, emotional thoughts take over and make the choice for them.
For me, this is an easy question. I believe that animals have feelings and other states of consciousness, but neither I nor anyone else has been able to prove it. We can't even prove that other people are conscious, much less other animals. In the case of other people, though, we at least can have a little confidence since all people have brains with the same basic configurations. But as soon as we turn to other species and start asking questions about feelings and consciousness in general we are in risky territory because the hardware is different.
Because I have reason to think that their feelings might be different than ours, I prefer to study emotional behaviour in rats rather than emotional feelings. There's lots to learn about emotion through rats that can help people with emotional disorders. And there's lots we can learn about feelings from studying humans, especially now that we have powerful function imaging techniques. I'm not a radical behaviourist. I'm just a practical emotionalist.
I feel that I know something that will turn out to be correct and eventually proved to be true beyond doubt.
That our ability to perceive signals in the environment evolved directly from our bacterial ancestors. That is, we, like all other mammals including our apish brothers detect odours, distinguish tastes, hear bird song and drumbeats and we too feel the vibrations of the drums. With our eyes closed we detect the light of the rising sun. These abilities to sense our surroundings are a heritage that preceded the evolution of all primates, all vertebrate animals, indeed all animals.
Mine would be a fairly simple, straightforward case of an unjustifiable belief, namely that there is no god(s) or such a thing as a soul (whatever the religiously inclined of the right persuasion mean by that word). ...
I'm taken with religious folks who argue that you not only can, but should believe without requiring proof. Mine is to not believe without requiring proof. Mind you, it would be perfectly fine with me if there were a proof that there is no god. Some might view this as a potential public health problem, given the number of people who would then run damagingly amok. But it's obvious that there's no shortage of folks running amok thanks to their belief. So that wouldn't be a problem and, all things considered, such a proof would be a relief - many physicists, especially astrophysicists, seem weirdly willing to go on about their communing with god about the Big Bang, but in my world of biologists, the god concept gets mighty infuriating when you spend your time thinking about, say, untreatably aggressive childhood leukemia.
I believe that consciousness and its contents are all that exists. Space-time, matter and fields never were the fundamental denizens of the universe but have always been, from their beginning, among the humbler contents of consciousness, dependent on it for their very being. The world of our daily experience - the world of tables, chairs, stars and people, with their attendant shapes, smells, feels and sounds - is a species-specific user interface to a realm far more complex, a realm whose essential character is conscious. It is unlikely that the contents of our interface in any way resemble that realm. Indeed the usefulness of an interface requires, in general, that they do not. For the point of an interface, such as the Windows interface on a computer, is simplification and ease of use. We click icons because this is quicker and less prone to error than editing megabytes of software or toggling voltages in circuits.
Evolutionary pressures dictate that our species-specific interface, this world of our daily experience, should itself be a radical simplification, selected not for the exhaustive depiction of truth but for the mutable pragmatics of survival. If this is right, if consciousness is fundamental, then we should not be surprised that, despite centuries of effort by the most brilliant of minds, there is as yet no physicalist theory of consciousness, no theory that explains how mindless matter or energy or fields could be, or cause, conscious experience.
I believe that human consciousness is a conjuring trick, designed to fool us into thinking we are in the presence of an inexplicable mystery. Who is the conjuror and why is s/he doing it? The conjuror is natural selection, and the purpose has been to bolster human self-confidence and self-importance - so as to increase the value we each place on our own and others' lives.
I believe that the prison guards at the Abu Ghraib Prison in Iraq, who worked the night shift in Tier 1A, where prisoners were physically and psychologically abused, had surrendered their free will and personal responsibility during these episodes of mayhem. But I could not prove it in a court of law. These 8 Army reservists were trapped in a unique situation in which the behavioural context came to dominate individual dispositions, values and morality to such an extent that they were transformed into mindless actors alienated from their normal sense of personal accountability for their actions - at that time and place.
The "group mind" that developed among these soldiers was created by a set of known social psychological conditions, some of which are nicely featured in Golding's Lord of the Flies. The same processes that I witnessed in my Stanford Prison Experiment were clearly operating in that remote place: deindividuation, dehumanization, boredom, groupthink, role-playing, rule control and more.
Source: nytimes.com 4 January 2005
The Infection Connection
by Harriet Washington
Psychology has long held that mental illness is born of adverse experiences. More recently, research has pointed the finger at flawed genes. Now a third culprit may be emerging: invasion by bacteria and viruses.
Eight-year-old Seth broke from the grasp of Jane, his harried mother, for the third time in 10 minutes. Tearing across the emergency room, he stopped short, transfixed by a piece of paper lying on the floor. His red-rimmed eyes seemed to bulge from their sockets and his mouth twitched violently, as if he were in pain. Indifferent to Jane's pleas to stop, he proceeded to pick up from the floor every piece of paper, no matter how filthy, with hands that were reddened and raw. It was the state of his hands that had precipitated the trip to the hospital: Seth had spent most of the night in the bathroom, washing them over and over. With his head jerking spasmodically and his fingers pecking at pieces of paper and cigarette butts, the boy resembled some strange overgrown bird. Then, suddenly terrified, he flew back to Jane and began pulling on her arm. "Mommy, Mommy, let's leave!" he whimpered. "They're going to kill us. They're coming!"
Jane tried her best to calm him, but she too was beginning to panic. Two days before, Seth had been a perfectly normal little boy whose most serious health problems were the occasional cold or sore throat. He had become mentally ill overnight. What caused Seth's anxiety, his tics, his obsessive-compulsive behaviour? Astonishingly, it was probably that minor sore throat, his doctors concluded. Today, scientists are increasingly coming to recognise that the bacteria and viruses that frequently invade our bodies and cause sore throats and other minor ailments may also unleash a host of major mental and emotional illnesses, including anorexia, schizophrenia and obsessive-compulsive disorder.
It is a theory sharply at odds with earlier views of the genesis of psychological illness. Followers of Freud long held that mental and emotional trouble is primarily the result of poor parenting, especially by mothers. Indeed, until about 30 years ago, psychoanalysts frequently placed the blame for schizophrenia on "schizophrenogenic" mothers. Obsessive-compulsive disorder, also, was put at Mom's door. "It was thought to be the result of harsh toilet training," observes Susan Swedo, MD, chief of pædiatrics and developmental neuropsychiatry at the National Institutes of Mental Health. But such theories, which added immeasurable guilt to the burdens of parents with mentally ill offspring, have turned out to have little evidence to back them up, most experts now agree.
Instead, in recent years, the focus has shifted to genes as the main source of mental illness. Faulty DNA is thought to be at least partly responsible for, among other problems, anxiety and panic disorders, schizophrenia, manic depression and antisocial personality disorder, which is characterised by impulsive, excessively emotional and erratic patterns of interpersonal behaviour. Yet genetics doesn't appear to wholly account for the occurrence of major psychiatric ailments. If heredity alone were to blame, identical twins would develop schizophrenia with a high degree of concordance, but in fact in only 40% of cases in which one identical twin has the disease does the other twin have it as well. Autism, though it has been observed to run in families, also strikes five of every 10,000 children apparently arbitrarily. Nor can depression and other affective disorders be completely explained by damaged DNA. Says Ian Lipkin, Phd, a neuroscientist and microbiologist at the University of California at Irvine: "Genetics doesn't hold the key to understanding how to fit these square pegs into round holes."
Bacteria and viruses may be that key, but scientists have been slow to grasp the idea. Consider the case of syphilis, which is caused by the bacterium Treponema pallidum. In its final, or tertiary, stage, the disease can precipitate psychiatric problems like dementia, mania, depression, delusions and Tourette's like tics. Though some scientists suspected a connection between infection with the bacterium and the mental disturbances that may take 3 to 5 decades to emerge, the link became widely accepted only in the 1940s after the introduction of the antibiotic penicillin as a treatment for syphilis. In the interim, patients with syphilis who later developed psychiatric problems were often institutionalised as crazy. But even with the link established, Freud's theories were in ascendance and few scientists were willing to consider that microbes might be a common source of other mental illness.
Now, decades later, infection has emerged as a prime suspect in psychological illnesses. The inadequacy of genetic and experiential explanations has prompted scientists to look elsewhere - and their gaze has come to rest on physical ailments, such as heart disease, cancers and ulcers, that in some cases have an infectious origin. Could the same be true, they wonder, for mental and emotional ills? Improved technology has made it easier to find out.
Since active only when inside other living creatures, microbes are notoriously hard to grow, and therefore study, in the lab, but scientists' ability to do so has increased steadily over the last few decades. Other tools have allowed researchers to see their quarry more clearly. For about a decade, microbiologists have used a technique called polymerase chain reaction, or PCR, to replicate a small piece of genetic material over and over until it forms a quantity large enough to study - and large enough to show the lingering traces of an infection. A new variant of PCR, called representational difference analysis, introduced in 1994, allows scientists to go one step further and compare the differences between two separate pieces of DNA (including healthy and diseased segments, for instance). And the refinement of electron microscopes has permitted researchers to follow the "footprints" left by infection in patients' cerebrospinal fluid.
The introduction of CAT scans in the early 1970s has been another leap forward. Before then, only an X-ray - or an autopsy - could reveal damage to the brain, and then only in its grossest form. CAT scans show subtle changes that can be tracked over time, giving researchers a more accurate sense of a microbe's impact. MRI, developed in the early 1980s, has added 3-dimensionality to pictures of the brain, and PET scans, invented soon after, have added motion. Now bacteria and viruses can be caught red-handed. Still, teasing out the tie between microbes and psychological problems has proved a difficult task, in no small part because of the cunning and guile of the pathogens themselves, which have many ways of attacking our bodies and brains.
T pallidum, syphilis' causative bacterium, proceeds in straightforward fashion: it attacks and kills brain cells. After entering the body - usually through sexual intercourse, or through the mother's placenta into her fœtus - the bacterium travels along the lymph system until it arrives at the brain. Once it lodges there, it spares few structures, inflaming some neurons and stripping the myelin, or insulation, from others. (Without myelin, nerve impulses are slowed or stopped altogether.) Other microbes are more devious. The human immunodeficiency virus, for example, which can cause anxiety, delirium, psychosis and suicidal impulses, uses a Trojan horse strategy. Instead of directly attacking brain cells, it infects macrophages, the immune-system enforcers that roam the bloodstream, engulfing foreign cells that may pose a threat to the body. After hitching a macrophage ride into the brain, HIV cranks out cytokines, protein peptides that kill off neurons. The virus Chlamydia pneumoniae may use a similar trick - slipping into the brain and manufacturing cytokines - to cause Alzheimer's disease.
Streptococcal bacteria, like those that cause strep throat, take yet a different tack. As they invade the body, they automatically trip the body's defense alarm, calling up the immune system's antibody soldiers. But once the skirmish begins, the bacteria camouflage themselves within that very immune system. Like a wolf in sheep's clothing, they disguise themselves through molecular mimicry, cloaking themselves in proteins that imitate the body's own proteins, and thereby elude attack. For reasons scientists don't yet understand, the antibodies of some people - perhaps those with a genetic predisposition - then turn on their bodies' own tissues, assailing neurons the basal ganglia. These structures, located between the more primitive lower brain and the higher cortical centers, help interpret information from the senses and are key to healthy emotions and behaviour.
The self-destruction instigated by streptococcal bacteria can be particularly dangerous to young children. Because their immune systems are naïve, or underdeveloped, "their bodies mount a vigourous response to streptococci, but it is not terribly effective, and their antibodies wind up injuring their own neurons instead of the bacteria," explains Swedo. She believes that such self-induced damage leads some children to develop obsessive-compulsive disorder. In an experiment conducted earlier this year, Swedo replaced the blood plasma of 28 children who suffered from OCD (and who had elevated levels of streptococcus antibodies) with healthy donor plasma, reasoning that such a switch would remove the trouble-making antibodies. Within a month, the incidence of ties declined by half, and their other OCD symptoms were reduced by 60%. "That was really gratifying," says Swedo. "It means that OCD is a medical illness, and if you catch it before there is scarring in the brain, you can cure it."
OCD isn't the only mental illness associated with streptococcus. Though anorexia nervosa has been tied to a distorted body image, societal pressure to be thin, discomfort with developing sexuality, and other emotional and cultural factors, doctors have also noted that the eating disorder sometimes appears or worsens after a case of strep throat. Streptococcus has been implicated as well in Tourette's syndrome and in Sydenhams chorea, which makes the arms and legs of those afflicted jerk in a manner often likened to dancing.
Researchers think that the seeds of yet other mental illnesses may be planted while a fœtus is still in the womb, when the pregnant mother-to-be becomes infected. Flu epidemics have been followed a generation later by waves of schizophrenia in England, Wales, Denmark, Finland and other countries, and a recent study published in the New England Journal of Medicine reports higher rates of schizophrenia among children born in crowded areas in cold weather - conditions hospitable to respiratory ailments. Scientists suspect that in such cases a virus, such as the one that causes influenza or a newer candidate, the Borna virus, may insinuate itself into the fœtal brain at a crucial stage of development. The microbe then subtly deranges the brain's neural connections in a process that becomes apparent only as the brain reaches full maturity, in early adulthood. In people with schizophrenia, parts of the brain - the cortex, thalamus, limbic system and basal ganglia - shrink, while crevices and fluid-filled spaces enlarge by as much as half, and the brain's chemical balance shifts. Such changes might well be the terrible legacy of a prenatal virus.
Microbes that cause mental illness can also enter the body another way - on one's fork. In the mid-1990s, an outbreak of Creutzfeldt-Jakob disease struck fear into meat-eaters, especially in England, where 35 people died after eating infected beef. While alive, the victims of what was dubbed "mad cow disease" exhibited bizarre symptoms such as continual screaming, inappropriate laughter, failure to bathe and compulsive walking. Scientists theorised that the "mad cows" became infected because they were fed on sheep afflicted with the disease known as scrapie, but a similar infection endemic to cows may be to blame. (Scrapie in sheep, bovine spongiform encephalitis in cows and Creutzfeldt-Jakob disease in humans are all believed to be caused by what's known as a prion, or infectious protein, which acts in a manner similar to a virus.) Contaminated human growth hormone, corneal transplants and surgical instruments have also been suspected of communicating the disease to humans. Earlier this year, the British medical journal The Lancet reported that multiple surgeries and living on a farm are risk factors for CJD. Though the disease is considered rare, Yale neuropathologist Laura Manueldis, MD, who thinks that the causative agent is actually a small virus rather than a prion, suspects that CJD is more common than we believe, and is often misdiagnosed as Alzheimer's.
Why doesn't every child with a strep throat develop an anxiety disorder? Or dementia strike every adult with syphilis? Our bodies protect us from most invasions by unfriendly microbes, but the vulnerable - those with poor health, weakened immune systems or, perhaps, genetic susceptibility - are less equipped to fend off the viruses and bacteria that may eventually cause mental illness. Continuing research is likely to bring more effective vaccines and antibiotics, but prevention and treatment will have to be every bit as shrewd as the infectious agents themselves, which spread and reproduce in seemingly countless ways. More worrisome is the fact that illness-causing organisms may be outwitting our antimicrobial strategies. With the development of antibiotics and antivirals, researchers had hoped to vanquish viruses and bacteria once and for all. But they underestimated the wily ingenuity of these microbes, which soon produced strains resistant to the new miracle medicines.
Likewise, scientists at one time believed that infectious agents evolved to become less potent, if only to ensure their own survival: the longer an infected host stays alive, after all, the greater the number of people who can be exposed to the pathogen, and the more likely the microbe is to reproduce itself. But recent research has turned up a less reassuring reality: under some conditions, microbes can flourish with increased virulence in crowded modern cities. These densely populated areas can maintain dangerous pathogens that otherwise might whip through a community and then have nowhere else to go.
To fight these pathogens successfully, doctors will have to tailor the treatments to the specific disease. Sometimes, for example, they may want to relieve an infected patient's fever and inflammation; at other times, fever must be left alone to kill off heat-sensitive viruses. Syphilis can be cured with penicillin, and doctors have had some success in prescribing antibiotics to people with anorexia. Other illnesses require more involved treatment, such as Swedo's plasma replacement for children with OCD, and some ailments cannot be helped much at all. The only way to treat HIV dementia, for example, is to try to slow the replication of the virus itself. No current therapy does this permanently, and many HIV-positive patients still suffer psychiatric symptoms. (In fact, suicide is a leading cause of death among the HIV-infected.) There's no treatment for Creutzfeldt-Jakob disease beyond palliative care, and by the time influenza-induced schizophrenia becomes apparent, the neurological damage is already done.
Still, science continues to offer hope that one day such infectious agents will be controlled or even eliminated. That day can't come too soon for Swedo, a pædiatrician by training. "When I practiced medicine at Memorial Hospital in Chicago, I saw parents suffer horribly when they lost their children to leukemia," she says. "When I came to the NIMH, I began to see parents lose their children to OCD and schizophrenia. These parents' grief is so much more profound. The fact that their children's illnesses are socially unacceptable makes their pain almost unbearable." Now that we know many psychiatric ills begin with a microbe, rather than a suffocating mother or remote father, "we can start treating mentally ill people without the shame and blame. We can treat them medically."
What You Can Do
Since we know so little about the viruses and bacteria that cause some types of mental illness, it makes sense to avoid them when you can. Here, advice on preventing infection from leading scientists (much of which sounds uncannily like Mom's):
Case File: Mystery of the Black Death
Photo by Arlo Bryan Guthrie. Modelled by Re'chard Atwater. Source: ahleman.com
in the secluded English village plague broke out. To prevent the outbreak from spreading throughout the region, the whole town was quarantined - no one was allowed in or out. Outsiders assumed that the plague would simply wipe out the entire village. But they were wrong. 350 years later, Dr Stephen O'Brien, a geneticist from the National Institutes of Health in Washington, DC delved into the reasons why some individuals managed to survive while others died around them.
No one knows exactly why, but in the late 1320s or early 1330s, the plague spread through Italy and across the European continent. (Which plague is a bit controversial - see article below.) By the following spring, it had reached as far north as England, and within 5 years had killed 25 million people - 1/3 of Europe.
The plague first spread to Britain in 1348, travelling from Bristol to Oxford and London in several days. In 1665, perhaps the worst of the English epidemics broke out in London. That summer, the nobility and clergy fled the city, as some 7,000 people died each week. As many as 100,000 lives were lost before the epidemic tapered off. Contemporary medicine could provide no explanation for the sickness, and most doctors were afraid to offer treatment. In an attempt to keep from being infected, the few physicians who did risk exposure wore leather masks with glass eyes and a long beak filled with herbs and spices that were thought to ward off the illness. Even one person in a household showing plague-like symptoms was enough to mandate a 40-day quarantine for the whole home - a virtual death sentence for everyone living in it.
In September 1665, George Viccars, a tailor in the small, central England village of Eyam, came down with the plague and died 4 days later. By the end of the month, 5 more villagers had succumbed. The entire village was quarantined to prevent spreading throughout the region. It seemed like suicide. A year later, the first outsiders ventured into Eyam, expecting a ghost town. Yet, miraculously, half the town had survived. How did so many villagers live through the most devastating disease known to man?
Local Eyam lore tells befuddling stories of plague survivors who had close contact with sufferers but never caught the disease. Elizabeth Hancock buried 6 children and her husband in a week, but never became ill. The village gravedigger handled 100s of plague-ravaged corpses, but survived as well. Could these people have somehow been immune to the Black Death?
Dr Stephen O'Brien of the National Institutes of Health in Washington DC suggests they were. His work with HIV and the mutated form of the gene CCR5, called "delta 32," led him to Eyam. In 1996, research showed that delta 32 prevents HIV from entering human cells and infecting the body. O'Brien thought this principle could be applied to the plague, which affects the body in a similar manner. To determine whether the Eyam plague survivors may have carried delta 32, he tested the DNA of their modern-day descendents. He feels that the mutated CCR5 gene, delta 32, may have prevented the plague from being able to enter its host's white blood cells.
Knowing who died and who lived through the early years of the plague is somewhat problematic. Deaths among the general English population were not recorded in the 14th Century, and most communities did not begin recording parish registers until around 1538. Fortunately, Eyam began keeping a parish register in 1630. Thus historian John Clifford began by examining the register, noting everyone who was alive in 1665, the year the plague came to Eyam. He searched for evidence of life through the year 1725 - marriages, baptisms, burials that took place years after the plague had left the village. Deleting the names of those lost during the plague period, he was able to determine who the survivors were.
DNA samples could only be collected from direct descendents of the plague survivors. Eyam resident Joan Plant, for instance, may have inherited the delta 32 mutation from one of her ancient relatives. Plant could trace her mother's lineage back 10 generations to the Blackwell siblings, Francis and Margaret, who both lived through the plague to the turn of the century. The next step was to harvest a DNA sample from Joan and the other descendants. After 3 weeks of testing at University College in London, delta 32 had been found in 14% of the samples. This was a genetically significant percentage, yet what, really, did it mean? Could the villagers have inherited delta 32 from elsewhere, residents who had moved to the community in the 350 years since the plague? Was this a higher percentage than elsewhere? To find out, O'Brien assembled an international team of scientists to test for the presence of delta 32 around the world. "Native Africans did not have delta 32 at all," O'Brien says, "and when we looked at East Asians and Indians, they were also flat zero." In fact, the levels of delta 32 found in Eyam were only matched in regions of Europe that had been affected by the plague and in America, which was, for the most part, settled by European plague survivors and their descendents.
Meanwhile, recent work with another disease strikingly similar to the plague, AIDS, suggests O'Brien was on the right track. HIV, the virus that causes AIDS, tricks the immune system in a similar manner as the plague, targeting and taking over white blood cells. Virologist Dr Bill Paxton at the Aaron Diamond AIDS Research Center in New York City noticed, "the centre had no study of people who were exposed to HIV but who had remained negative." He began testing the blood of high-risk, HIV-negative individuals like Steve Crohn, exposing their blood to 3,000 times the amount of HIV normally needed to infect a cell. Steve's blood never became infected. Paxton began studying Crohn's DNA, and concluded there was some sort of blocking mechanism preventing the virus from binding to his cells. Further research showed that that mechanism was delta 32.
Scientists studying HIV first learned about the gateway-blocking capacity of the CCR5 mutation in 1996. Several drug companies, then, quickly began exploring the possibility of developing pharmaceuticals that would mimic delta 32 by binding to CCR5 and blocking the attachment of HIV. Previous methods of treatment interfered with HIV's ability to replicate after the virus has already entered a cell. This new class of HIV treatment, called early-inhibitor - or fusion-inhibitor - drugs seek to prevent the virus from ever attaching at all. These pharmaceuticals are still in relatively early stages of development, but certainly stand as a hopeful new method of approaching HIV treatment.
The mutation of the CCR5 gene - "delta 32" in its mutated form - has no adverse effect - in fact, possessing delta 32 could save your life, and the lives of your children. "The non-mutated form is what's called a chemokine receptor," says O'Brien. Chemokines are protein distress calls released by an injured region of your body. "The normal function of the CCR5 gene is to act as a retriever of the chemokine distress signal from these bruises, which will then be alleviated by the chemokines." Delta 32 is a powerful mistake. HIV, the virus that causes AIDS, attacks the human immune system, infecting the white blood cells sent to destroy it. The delta 32 mutation, however, effectively blocks the crucial gateway into human cells the virus needs. In the case of Steve Crohn, whose partner was the 5th person known to die from AIDS, possessing the CCR5 mutation has prevented him from contracting the virus.
O'Brien explains further, "In order to have total resistance to HIV, you have to carry two doses of the mutated gene - one from each parent. If you get only one dose, you will not be resistant. However, you may be able to delay the onset of HIV once you become infected. That's because, in patients with one copy of the mutation, the amount of "portals" that HIV can use is reduced by about 50%. That slows down virus replication, which is the most important factor in AIDS progression."
O'Brien's work on AIDS led him to another disease that delta 32 could prevent, the plague. "They both, upon entering the body, infect the microphages, which are the first line of defense against infections," he says. "Over the course of evolution, many bugs and pathogens have become extinct because the body learned how to defend itself against them. So the ones that are around today, like HIV and the plague, are pretty savvy - HIV, for example, specifically attacks and kills the very cells that are designed to kill it. Both these pathogens have developed very clever ways around our immunological defenses." The results of the Eyam study suggest that delta 32 may have helped save Europe from at least one type of plague pandemic. Delta 32 seems to be a formidable defense the human body has developed in response to ages of pathogenic exposure. And though we may just be getting acquainted with it, delta 32 has been protecting humans for ages. O'Brien suspects the mutation has been around since long before the Black Death. "There have been human remains dug up from graves in Scandinavia - bodies 3,000 and 4,000 years old - in which they actually found the mutation, through DNA typing. So there are all kinds of pieces in this puzzle that are coming together."
How Many Different Kinds of Plagues Were There and What Caused Them?
Recent scientific and historical investigations have led researchers to doubt the long-held belief that Black Death was an epidemic of bubonic plague.
In 1984, Graham Twigg published The Black Death: A Biological Reappraisal, where he argued that the climate and ecology of Europe and particularly England made it nearly impossible for rats and fleas to have transmitted bubonic plague. Combining information on the biology of R rattus, R norvegicus and the common fleas X cheopis, and P irritans with modern studies of plague epidemiology, particularly in India, where the R rattus is a native species and conditions are nearly ideal for plague to be spread, Twigg concludes that it would have been nearly impossible for Y pestis to have been the causative agent of the beginning of the plague, let alone its explosive spread across all of Europe and England. Twigg also shows that the common theory of entirely pneumonic spread does not hold up. He proposes, based on a reexamination of the evidence and symptoms, that the Black Death may actually have been an epidemic of pulmonary anthrax caused by B anthracis.
Scott and Duncan, 2001
In 2001, epidemiologists Susan Scott and Christopher Duncan from Liverpool University proposed the theory that the Black Death might have been caused by an Ebola-like virus, not a bacterium. Their rationale was that this plague spread much faster and the incubation period was much longer than other plagues confirmed to be caused by Yersinia pestis. A longer period of incubation will allow carriers of the infection to travel farther and infect more people than a shorter one. When the primary vector is humans, as opposed to birds, this is of great importance. Studies of English church-records indicate an unusually long incubation period in excess of 30 days which could account for the rapid spread, topping at 5 km/day. The plague also appeared in areas of Europe where rats were uncommon like Iceland. Epidemiological studies suggest the disease was transferred between humans (which happens rarely with Yersinia pestis), and some genes that determine immunity to Ebola-like viruses are much more widespread in Europe than in other parts of the world.
In a similar vein, historian Norman F Cantor, in his 2001 book In the Wake of the Plague, suggests the Black Death might have been a combination of pandemics including a form of anthrax, a cattle murrain. He cites many forms of evidence including: reported disease symptoms not in keeping with the known effects of either bubonic or pneumonic plague, the discovery of anthrax spores in a plague pit in Scotland, and the fact that meat from infected cattle was known to have been sold in many rural English areas prior to the onset of the plague. See ISBN 0060014342
Gunnar Karlsson (Iceland's 1100 Years: The History of a Marginal Society) points out that the Black Death killed between half and two thirds of the population of Iceland, although there were no rats in Iceland at this time. Rats were accidentally introduced in the 19th century, and have never spread beyond a small number of urban areas attached to seaports. In the 14th century there were no urban settlements in Iceland. Iceland was unaffected by the later plagues which are known to have been spread by rats.
Counterarguments have been drawn in defense of the bubonic plague theory.
However - tooth pulp tissue from a 14th century plague cemetery in Montpelier tested positive for Y pestis DNA. However, such a finding has never confirmed in any other cemetery. In September 2003, a team of researchers from Oxford University tested 121 teeth from 66 skeletons found in 14th century mass graves. The remains showed no genetic trace of Yersinia pestis, and the researchers suspect that the Montpelier study was flawed.
I read an article recently that said a researcher believed the Ashkenazi Jews, who often suffer from Tay=Sachs disease, were the victims/beneficiaries of a genetic mutation that made them carriers of genetic mutations that both made them more prone to certain kinds of disease - but also made them more intelligent - 27% of Nobel prizes have been won by Ashkenazis...
Inventions the World Still Needs
Source: I can't find the source for the list above, but I believe it was a group of junior-high students from several years ago. Some of the things on the list (for example DNA gun) are currently available - although maybe not exactly in a form the authors had in mind....
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