Whatever the explanation, an immigration-related change in demographics does not seem to be it. When Komlos compared only non-Hispanic, non-Asian people who were born in the United States, Americans were still shorter than their Northern European counterparts.

Height is controlled by genetic programs that lead to the production of growth hormone and a c.o.c.ktail of other hormones in our bodies. Exactly how environmental factors influence growth is not well understood, but scientists have a pretty good idea of the mechanisms through which hormones exert their influence on height.

Growth hormone is produced by the pituitary gland-a tiny organ near the base of the brain. In about 1 in 20,000 people, the pituitary gland produces too much growth hormone. If this happens in children before p.u.b.erty, it can cause gigantism-excessive growth of the long bones in the limbs, as well as muscle and organ overgrowth.

Elongation of the bones in the arms and legs occurs at growth plates-regions near the ends of the bone consisting of cartilage. Stimulated by growth hormone, the cartilage cells reproduce, and the cartilage is later converted to compact bone. A variety of other hormones play a role in the proliferation and maturation of cartilage and the process by which it is removed and replaced with bone. Exercise also stimulates bone growth.

At p.u.b.erty, the s.e.x hormones (estrogen, testosterone) initially boost the release of growth hormone and lead to a growth spurt. Later, higher levels of s.e.x hormones close the growth plates by causing the cartilage-producing cells to die and be replaced with bone.

Therefore, after p.u.b.erty, an excess of growth hormone does not lead to gigantism. Instead, it can cause acromegaly-growth of soft features, resulting in enlarged feet, hands, and facial features.

Hair-raising Why is it when you get scared the hairs on your arms and legs stand up?

Hair standing on end goes by many names: the pilomotor reflex, horripilation, cutis anserina, or, simply, goose b.u.mps. It is part of the fight-or-flight reaction and is not unique to humans. You have probably seen a frightened feline a.s.sume a Halloween cat pose with fur puffed out, or a dog develop a bristling ruff when confronted by a rival.

Of course, humans are not particularly fuzzy mammals (with a few exceptions making an appearance on beaches and at poolside), and our pilomotor reflex does little to convince our enemies that we are bigger and should not be messed with. It may, in contrast, help us become consciously aware of our own fear response and make us more attentive to potential dangers in the environment.

Cold also causes our hair to stand on end. Again, this response works better for fuzzier mammals or birds. Lifting the hair or plumping feathers traps a layer of air close to the skin, which provides extra insulation.

Some people get goose b.u.mps when listening to beautiful music or in other pleasurable situations. Stress and strong emotions (good or bad) activate the sympathetic nervous system, which prepares the body to respond to the stress. The sympathetic nervous system causes the contraction of a tiny muscle-the arrector pili (also called the erector pili)-that is attached to each hair follicle, the elongated pit that contains the hair. When the muscle contracts, it elevates the hair follicle to form a goose b.u.mp.

Puny puckers How come we get goose b.u.mps on our arms and legs, but not on our face?

Goose b.u.mps can occur on the face. Facial hair follicles have arrector pili muscles that can elevate the follicle. But goose b.u.mps do seem to be less obvious on the face.

The explanation is not the size of the hair or follicle, because a study found that average hair diameter and follicle diameter were similar on the face and on the body.

It may be because hair follicles are much more numerous on the face and head than on the rest of the body. Since the skin puckers at the site of the goose b.u.mp, the skin surrounding the goose b.u.mp must be pulled tighter. If the hair follicles are close together, as they are on the face, as the arrector pili contracts to lift the hair, the tightening of the skin between the hair follicles would oppose the lifting and result in flatter, less noticeable goose b.u.mps. Facial skin is also thicker, and therefore more resistant to puckering, than skin on the forearms and calves, where goose b.u.mps are very noticeable.

Earplugs What are the source and purpose of earwax?

Earwax, or cerumen, is produced in the outer third of the ear, in the auditory ca.n.a.l. It is a mixture of secretions from the sebaceous or oil-producing glands and from modified apocrine or sweat glands. Cerumen lubricates the ear and prevents it from getting dry and itchy. It has antimicrobial properties and traps dust and debris.

Earwax also helps clean the ear because the skin in the auditory ca.n.a.l migrates out of the ear very slowly (about 1 millimeter every couple of weeks), carrying the wax that adheres to the skin, along with the dirt trapped in the wax.

Itchy and scratchy When you have an itch on your back, and you or someone else scratches it, why does the itchy spot seem to move from one spot to another? Sometimes scratching makes your entire back itchy. Why?

Detection and alleviation of itchiness involve nerve pathways for itch, tickle, and pain. The pathways are distinct, but each involves receptors in the skin to detect the sensation, nerves to relay the information to the brain, and nerves to relay information from the brain back to the skin.

Scratching reduces itchiness by removing whatever is causing the itch, such as a hair or an insect. If the cause of the itch cannot be removed-for example, because the skin has launched an allergic reaction to the saliva in a mosquito bite-we may find ourselves scratching until it hurts. The pain signal occupies the central nervous system so that it "forgets" about the itch signal, at least temporarily. The sting of rubbing alcohol also helps soothe the itch of an insect bite for this reason.

When someone else scratches you, the receptors for tickle can be activated. When we touch our own bodies, inhibitory signals from the brain suppress the tickle response. Inhibitory signals from the brain also kick in to shut down the itch response when a large area of the skin is scratched or rubbed, so it may feel like you need to scratch your entire back to make the itch go away.

Scratching can sometimes make the situation worse, because scratching may cause mast cells in the skin to release histamine, which causes inflammation and itchiness. Scratching is more likely to stimulate the release of histamine if someone is already experiencing an allergic reaction or has very dry skin.

Heart-stopping Does your heart stop when you sneeze?

No. The heart's rhythm is controlled by a natural pacemaker-the sinoatrial node, a group of cells located in the right atrium of the heart. These cells create an electrical impulse by pumping charged particles out of the cell and then allowing them to flow back in. Conducting cells transmit the electrical impulse to all parts of the heart to initiate muscle contraction. Sneezing does not stop this electrical activity.

On the other hand, the nervous system and circulating hormones, such as adrenalin, alter the rate of the electrical activity in the sinoatrial node to increase or decrease heart rate. Just as exercise increases the heart rate, sneezing works many muscles; therefore, it is possible for a "sneeze attack" to increase the heart rate.

Sneeze grimace Why can't you sneeze with your eyes open?

A close relationship exists between the protective reflexes of the nose and eyes. When something like pollen irritates the mucous membranes in the nose, the trigeminal nerve is stimulated, and it relays the message to a sneeze integration center in the medulla at the base of the brain.

The sneeze center is mission control for the sneeze reflex, and it coordinates three simultaneous actions. It commands the respiratory muscles to produce an explosive inspiration and then expiration. It causes the glands in the nose to produce mucous, and it triggers facial muscles to close the eyes and grimace.

Photon allergy Why do I always sneeze when I step into bright sunlight?

You have a photic sneeze reflex, also known as ACHOO Syndrome. If you want to impress your friends, ACHOO stands for autosomal dominant compelling helio-ophthalmic outburst. (I'm not sure why it's not ADCHOO, but at least sneeze scientists have a sense of humor.) About one-quarter of the population has this reflex, and it is thought to be genetic. The reflex varies in strength, with some people affected only in bright sunlight and others affected by camera flashes or other light sources.

The number of sneezes initiated in bright light varies among individuals. And some people even have a sneeze reflex when they rub the corner of their eye, pluck their eyebrows, or comb their hair.

Scientists are not exactly sure what causes ACHOO Syndrome. It is known that the sneezing integration center at the base of the brain receives neural inputs from other parts of the brain as well as the nose.

In photic sneezers, bright light may directly or indirectly stimulate nerves that usually respond when something irritates your nose. This information gets sent to the sneezing integration center, which in turn sends signals to coordinate the diverse muscle groups needed for the sneeze.

Sleeping beauty What goes on in your body while you are sleeping?

Until the late 1950s, the dominant view was that sleep was simply an idling state. However, electroencephalograms (EEGs), which record fluctuations of electrical activity in groups of nerve cells in the brain, have shown that the sleeping brain is active and that sleep is composed of identifiable stages that occur in cycles throughout the night.

About 30 to 45 minutes after falling asleep, a person enters slow-wave sleep, which is characterized by slow-frequency brain waves. As a sleeper progresses through stages 1 to 4 of slow-wave sleep, the EEG records brain waves that are progressively slower frequency and higher voltage.

The muscles are relaxed during slow-wave sleep, but the sleeper shifts posture regularly. Heart rate and blood pressure decrease. Stage-4 sleep is the deepest and most difficult to interrupt. Someone awakened from stage-4 sleep feels groggy and confused.

By about 90 minutes after the initiation of sleep, the sleeper has progressed back through stages 4 to 1 of slow-wave sleep, and the EEG pattern changes abruptly. The EEG records low-voltage, high-frequency brain waves, similar to those observed in the waking state. This is rapid eye movement or REM sleep, and if awakened, most sleepers will recall dreaming. Sleepers awakened from slow-wave sleep may recall an image or emotion, but rarely a story-like dream.

The pons-an area at the base of the brain-keeps the body in a state of paralysis throughout REM sleep, although the muscles controlling eye movements and respiration are not inhibited. During REM sleep, the body even ceases to regulate its temperature.

Cats with damage to the pons appear to act out their dreams, such as stalking and pouncing as if they were chasing mice. People can also have "REM behavior disorder." One sleeper, who had been dreaming he was a football player charging an opponent, woke up with a gash on his head from tackling his dresser.

Depriving people of sleep right after they are trained to do a task interferes with learning, even when people are tested a week later, after recouping their sleep. Brain-imaging studies with animals reveal that the pattern of brain activity that occurs during the learning of a task, such as navigating a maze, is replayed during sleep. Greater replay during sleep translates into greater learning.

The exact mechanisms through which sleep facilitates learning and memory are not understood. However, certain genes known to play a role in changing connections between nerve cells are switched on in the brain during post-training sleep.

Yawning maw I have often wondered what triggers a yawn.

According to folk belief, we yawn because we are not breathing in enough oxygen. The deep inhalation that is a major feature of the yawn makes this idea appealing, but compelling evidence exists that this explanation is not entirely correct.

When people were made to breathe air with higher-than-normal levels of carbon dioxide, their respiration rate increased, but they did not yawn more than people breathing normal air. The number of yawns also did not change when people breathed pure oxygen. Therefore, respiration rate, rather than yawning, seems to regulate oxygen intake.

So why do we yawn? One possibility is that yawning stimulates us to stay awake. In support of this hypothesis, studies have shown that people yawn frequently in the hour before they go to bed but rarely yawn when they are trying to fall asleep. People also yawn frequently while driving. Zoo and laboratory animals yawn before their normal feeding time. Yawning seems to occur when it is important to stay awake.

How would yawning help us stay awake? Some scientists think yawning may dilate the arteries that bring blood to the brain, thereby increasing cerebral blood flow.

The exact trigger for the yawn remains elusive. Certain research suggests that an oxygen sensor, located in a part of the brain known as the hypothalamus, initiates the yawn in response to low levels of oxygen in the brain. Since blood carries oxygen, this research is consistent with the idea that yawning causes a jump in blood flow to the brain, but it does not explain why breathing air containing less oxygen does not induce yawning.

Many different brain chemicals can induce or inhibit yawning, but because the effects of these chemicals are often studied by injecting them into the brains of anesthetized animals, it is unclear which play a role under normal conditions.

An enigmatic feature of yawning is that it appears to be contagious. Perhaps you have yawned while reading this answer. Seeing someone yawn, and reading about and thinking about yawning, can cause humans to yawn.

Although nearly all vertebrates (even fish, frogs, and birds) yawn, until recently humans were the only species known to yawn contagiously. However, recent research has shown that chimps yawned more when watching a video of other chimps yawning. Images of grinning chimps did not have the same effect. Not all the chimps were susceptible to contagious yawning, but neither are all humans.

The fact that yawning is contagious has led researchers to suggest that it may have evolved as a way of synchronizing the social behavior of groups. College lecture halls are a good place to observe vestiges of this evolutionary mechanism.

Smells good Everything in our world has a scent. Has anyone ever been able to identify how many scents and odors exist in our world?

If we humans were to count all the scents in the world, we would come up with a different number than the other members of the animal kingdom. Dogs, for instance, can detect odors at concentrations almost 100 million times lower than humans can.

There is also much variation among humans in how well we can smell: Some people are unable to perceive certain smells, women generally have a more sensitive sense of smell than men, and as we age we lose our ability to discriminate between smells.

You get a whiff of something because small, volatile molecules from that thing have become airborne, and you have breathed them in. New paint smells because molecules in the paint are evaporating and dissolving in the mucus that lines your nasal pa.s.sages. When all the volatile molecules have evaporated, paint loses its smell.

At the top of your nasal pa.s.sages are two postage stamp-sized patches of cells that contain olfactory, or scent, receptors. Estimates of the number of olfactory receptor cells vary widely. Humans likely have somewhere in the range of 10 million of these cells, while scent-tracking bloodhounds have about a billion.

Your brain finds out about a smell when molecules bind to the olfactory receptors in your nose. Scent molecules activate different receptors, with each type of receptor thought to respond to no more than a handful of different smells. The pattern of activation of olfactory receptors seems to work something like a bar code from which the brain determines the smell's ident.i.ty.

Some controversy exists among scientists about just how olfactory receptors become activated, but currently the most compelling explanation is that smell molecules activate receptors into which they fit, like a key in a lock.

Of the five senses, smell remains the most difficult for scientists to explain. Coffee, bacon, and cigarette smoke all have hundreds of volatile molecules, yet we do not detect the individual components. But we can detect the distinct fragrances of coffee, bacon, and cigarette smoke when all three are mixed together.

Previously scientists estimated that we should be able to distinguish 10,000 different smells. However, from our current understanding of smell discrimination, in theory we should be able to distinguish an almost infinite number of smells.

One of the most enigmatic features of smell is how the mere hint of an aroma can conjure up powerful memories. For example, the smell of apple pie might take you back to your grandmother's kitchen. This is because information about smell is sent to the hippocampus, a part of the brain concerned with emotion, motivation, and certain kinds of memory.

Tip of the tongue Please explain this apparently common phenomenon. You are trying to remember the name of someone you knew a long time ago. Despite earnest and repeated attempts to recall the name, it eludes you. When you are no longer trying to think of it, the name suddenly pops into your brain.

The very mechanisms that help us concentrate can cause thoughts to shy away from us like skittish horses, only to return when we have stopped pursuing them.

To make knowledge more accessible, our brains suppress conceptual distractions through a process known as retrieval-induced forgetting. Researchers have most commonly studied this active process of forgetting using word retrieval tests.

For instance, people learn lists of categoryexemplar pairs (fruitsapple, fruitsplum, fruitsbanana) for several categories (fruits, sports, cars, dog breeds). They then practice retrieving some of the exemplars when cued with the category and the first two letters of the exemplar (fruitspl__). Later, they are given the categories and asked to recall all the exemplars from each category.

As expected, retrieval practice improves recall of the reviewed material. Surprisingly, recall of the categoryexemplar pairs that were not practiced is worse than it is when people do not practice retrieving any of the categoryexemplar pairs at all. In other words, the recall of one memory causes the suppression of related memories.

Brain imaging has shown that retrieval-induced forgetting is adaptive because it reduces the demands on the cognitive control mechanisms needed to recall one of the competing memories.

Unfortunately, it also trips us up when we are searching for that less-used memory. It has even been shown to be responsible for what can seem like deliberate lapses of native-language words in novices after immersion in a foreign language.

Retrieval-induced forgetting shuts off when we are no longer trying to actively recall a memory. The thread of a related memory can then lead us to the forgotten memory. Memories are more like spiderwebs than file folders, because different aspects of a memory (such as someone's name or image or an event involving the individual) are stored in different parts of the brain.

Mood also affects forgetting and recall. Studies have shown that positive moods enhance retrieval-induced forgetting, and negative moods inhibit it. This is because positive moods encourage global processing of information and connections between related ideas (connections that can lead to suppression of a memory during active attempts at retrieval), whereas negative moods encourage item-specific processing. Later though, when one is no longer trying to recall something and it is no longer being actively suppressed, a positive mood can enhance retrieval by making it more likely that a connection will be forged to the elusive memory.

A particularly intriguing insight into recall comes from people with synesthesia-a mixing of the senses. In one form of synesthesia, lexical-gustatory synesthesia, hearing, seeing, saying, or thinking about a word leads to specific, detailed food experiences, as well as activation of the brain region responsible for the perception of taste. For example, for one lexical-gustatory synesthete, the word "part" tasted like chicken noodle soup. When they have a word on the tip of their tongues, lexical-gustatory synesthetes can taste the word before they can retrieve it. This is consistent with the notion that memories have many components and connections, and access to an individual component can be blocked without affecting other connections.

5. Pesky pathogens

Bundle up

Do you get a cold from being cold? I sat in an unheated library yesterday, and today my nose is streaming.

Modern virology textbooks reject the idea that being cold makes one catch a cold. The standard explanation of why colds are more prevalent in the winter than in the summer is that people spend more time indoors in contact with each other in the winter, which facilitates the spread of the viruses that cause colds.

Still, the folklore surrounding the relationship between cold exposure and the common cold is so longstanding and widespread that a number of researchers have considered it worthy of further exploration. Their studies suggest that Mom's advice to "Keep warm so that you don't catch a cold" may not have been off the mark after all.

One study of populations in seven countries in Europe, from Finland to Greece, showed that there were fewer deaths from respiratory diseases in regions where people tended to take protective measures against the cold. These included heating their homes, wearing protective clothes, and being physically active, rather than standing and shivering, when outdoors.

In the study, a given fall in temperature claimed more lives in regions with mild winters, and people in these regions were less likely to bundle up and heat their homes. For example, at the same outdoor temperature, 45 degrees Fahrenheit (7 degrees C), only 13 percent of people in Athens wore hats, whereas 72 percent of people in south Finland wore them. In addition, average living room temperatures were 4 degrees Fahrenheit (2.2 degrees C) warmer in southern Finland than in Athens.

Experimental studies on the effect of cold exposure have been mixed. One hypothesis to explain this inconsistency is that getting chilled makes a difference if a person not only has been exposed to one of the more than 200 cold viruses but also is already in the process of fighting the infection. In other words, cold exposure can turn an asymptomatic infection into full-fledged, nose-tooting misery.

Being cold may lead to the release of stress hormones, which suppress the body's immune system. Low temperatures also cause the blood vessels in the nose and upper airways to constrict, possibly reducing the access of blood cells responsible for attacking invaders. In addition, cold air damps the action of cilia-tiny moving hairs that help eliminate contaminants in the airways.

So while doctors' advice to wash your hands and avoid sick people will help you stay healthy, taking precautions against getting chilled may also help you fight the good fight against those insidious germs.

Invader individuality During cold season, we are told that antibiotics will not kill viruses and that colds are caused by a virus. What is the difference between viruses and bacteria, and why is it so hard to come up with a medicine to kill viruses?

Bacteria are single-celled organisms that contain the machinery needed to grow and replicate. Antibiotics inhibit various life processes in bacteria. Penicillin and related compounds interfere with the systems that build the cell walls of bacteria. Tetracyclines, as well as erythromycin and its relatives, block the bacterial cell's machinery for making new proteins. Other antibiotics prevent bacteria from duplicating DNA, or from using or making essential nutrients.

Viruses are smaller than bacteria and basically consist of genetic material (RNA or DNA) packaged in a protein sh.e.l.l. Viruses cannot provide their own energy or replicate on their own. To reproduce, viruses must hijack the cellular machinery of another organism. Since antibiotics and antivirals must target processes that are unique to the infectious agents to avoid harming the cells of the infected organism, the simplicity of viruses means that they have fewer Achilles' heels than bacteria. Also, viruses can hide within cells, in some cases for many years.

Thirty years ago, just three antiviral drugs were available. Genome sequencing and the study of the replication cycle of viruses have since led to major advances because antiviral drugs must be tailored to the viruses they attack. Knowledge of the structures and functions of the viral enzymes, or catalysts, guides the design of drugs that specifically block those enzymes. A similar procedure is used to develop antibiotics, although some-broad-spectrum antibiotics-are effective against a range of bacteria.

More than 40 drugs for the treatment of viral infections have now been approved, about half of which are used to treat HIV infections. One example of an antiviral medication is AZT, which inhibits an enzyme used by HIV to copy its genes into the genetic material of the cells it infects. Other antiviral medications prevent viruses from getting into cells, and still others prevent the finished virus particles from leaving cells and spreading elsewhere in the body.

Viruses and bacteria both mutate and become resistant to the drugs designed to fight them. Like the Red Queen in the sequel to Alice's Adventures in Wonderland Alice's Adventures in Wonderland-running as fast as possible just to stay in place-researchers must continually develop new strategies to overcome drug resistance.

Moving target Influenza viruses are known to mutate into new, sometimes more virulent forms, which explains why some of us periodically get sick. Why is it that the same is not true for other known viruses, such as the polio and smallpox viruses?

Influenza viruses do evolve particularly quickly. Vaccine strains used against influenza must be changed at least every two to three years, because the proteins on the virus surface keep changing, thereby disguising it from the immune system. Vaccines against polio and many other human viruses have been stable for decades.

Part of what determines how fast a virus mutates is the type of genetic material it uses. Some viruses have genomes consisting of DNA. A chemically similar molecule, RNA, serves as the genetic material for other viruses. Another type of virus, the retrovirus, has RNA as its genetic material but copies RNA into DNA within an infected cell.

As a general rule, DNA viruses mutate more slowly than retroviruses, which mutate more slowly than RNA viruses. The fastest-mutating RNA virus has a mutation rate about 100,000 times faster than the slowest-mutating DNA virus. This range reflects the accuracy and proofreading ability of the machinery used to copy the different types of genetic material.

The genome of the variola (smallpox) virus is DNA, and a comparison of 45 virus samples from around the world during the 30 years prior to the eradication of smallpox revealed little sequence diversity. Yet genetic spellchecking is not the whole story, because polio, measles, and influenza are all caused by RNA viruses.

The mutation rate in viruses is also influenced by their generation time, genomic architecture (how the DNA or RNA is folded and whether it is single- or double-stranded), viral and host enzymes, and opportunities for virus particles to exchange genetic material with one another.

Yet higher mutation rates do not always enhance evolution. In an experiment in which the mutation rate of poliovirus was artificially increased by a factor of 10, the production of the virus decreased 1,000-fold, probably the result of an error catastrophe. In fact, increasing mutation rates to a lethal level is the mechanism of some antiviral drugs, such as ribavirin, a treatment for hepat.i.tis C.