Closer To The Ideal

Sexual Reproduction for Gay Couples. If you take genetic material from both parents, and then fertilize an egg with that material, then you get a child that is biologically descended from both of its gay parents (or, if we are talking about 2 women, take genetic material from one woman and use it to fertilize an egg in the other woman).

A big surprise, found with birds:

It was previously thought that sex chromosomes in birds control whether a testis or ovary forms, with sexual traits then being determined by hormones.

The researchers, however, identified differences between male and female cells that control the development of sexual traits. The scientists have named the phenomenon, cell autonomous sex identity (CASI).

I wonder if this is true for mammals as well?

This kind of thing really scares me:

They had a theory of the disease that made sense, fit the evidence, but was utterly wrong.

I am interested in cases where technology goes backwards and important scientific break throughs are forgotten, so this story about scurvy got my attention:

Now, I had been taught in school that scurvy had been conquered in 1747, when the Scottish physician James Lind proved in one of the first controlled medical experiments that citrus fruits were an effective cure for the disease. From that point on, we were told, the Royal Navy had required a daily dose of lime juice to be mixed in with sailors’ grog, and scurvy ceased to be a problem on long ocean voyages.

But here was a Royal Navy surgeon in 1911 apparently ignorant of what caused the disease, or how to cure it. Somehow a highly-trained group of scientists at the start of the 20th century knew less about scurvy than the average sea captain in Napoleonic times. Scott left a base abundantly stocked with fresh meat, fruits, apples, and lime juice, and headed out on the ice for five months with no protection against scurvy, all the while confident he was not at risk. What happened? …

This pattern of fresh meat preventing scurvy would be a consistent one in Arctic exploration. It defied the common understanding of scurvy as a deficiency in vegetable matter. Somehow men could live for years on a meat-only diet and remain healthy, provided that the meat was fresh.

This is a good example of how the very ubiquity of vitamin C made it hard to identify. Though scurvy was always associated with a lack of greens, fresh meat contains adequate amounts of vitamin C, with particularly high concentrations in the organ meats that explorers considered a delicacy. Eat a bear liver every few weeks and scurvy will be the least of your problems.

But unless you already understand and believe in the vitamin model of nutrition, the notion of a trace substance that exists both in fresh limes and bear kidneys, but is absent from a cask of lime juice because you happened to prepare it in a copper vessel, begins to sound pretty contrived.

Doctors of the era looked at this puzzling evidence and wondered. Other diseases had recently been shown to have their source in bacterial infection. The bacterial model was new, and had already had spectacular success in identifying and treating diseases like typhus, tuberculosis, and cholera. What if the cause of scruvy had also been misunderstood? What if instead of a deficiency disease, scurvy was actually a kind of chronic food poisoning from bacterial contamination of meat? Thus was born the ptomaine theory of scurvy, and Koettlitz became its enthusiastic backer

It is interesting that 2 people can look at the same thing and see such different things:

I don’t think it’s an accident that 7NC Luxury Cruises appeal mostly to older people. I don’t mean decrepitly old, but like fiftyish people for whom their own mortality is something more than an abstraction. Most of the exposed bodies to be seen all over the daytime Nadir were in various stages of disintegration. And the ocean itself turns out to be one enormous engine of decay. Seawater corrodes vessels with amazing speed—rusts them, exfoliates paint, strips varnish, dulls shine, coats ships’ hulls with barnacles and kelp and a vague and ubiquitous nautical snot that seems like death incarnate. We saw some real horrors in port, local boats that looked as if they had been dipped in a mixture of acid and shit, scabbed with rust and goo, ravaged by what they float in….

Here’s the thing: A vacation is a respite from unpleasantness, and since consciousness of death and decay are unpleasant, it may seem weird that the ultimate American fantasy vacation involves being plunked down in an enormous primordial stew of death and decay.

Or maybe the sea is abundant with life? Maybe some organisms die but are then eaten by other organisms which then grow? Things change, I won’t argue that, but if an 60 kilogram woman dies and becomes 60 kilograms of bacteria, then the world still has the same amount of life, merely in a different form. It works the other way too, of course, things die, get absorbed into the soil, get absorbed into some stalks of wheat, get turned into some bread that I eat, get absorbed into who I am, and thus allow me to type these words. The blog entry I linked to was called “Things fall apart”. But it seems describe as much life as death.

In 1994 I was living in Chapel Hill, North Carolina, and a friend of mine, a biologist, told me that it had been discovered that some viruses had receptors that allowed them to listen to the hormones that humans emit when under stress. That was my introduction to the idea that organisms listen to each other. Researchers have since discovered a great deal more:

But it’s Bjarnsholt’s latest discovery that reveals microbes’ gift for language: the bacteria aren’t just talking amongst themselves, but also quietly listening in on signals sent by their human host. So when a cavalry of white blood cells arrives to repel the invading bacteria, the entrenched biofilm senses their presence, and launches a coordinated counterattack (Microbiology, vol 155, p 3500). The microbes release deadly compounds called rhamnolipids, which burst the white blood cells, killing them before they can even take aim, says Bjarnsholt, who is at the University of Copenhagen in Denmark.

This of course suggests new kinds of treatments:

Then there’s our own immune system’s battle to prevent P. aeruginosa making itself at home in our lungs. Bjarnsholt is hunting for the signal P. aeruginosa uses to “listen out” for white blood cells, and ways to block it. He doesn’t think of the bacteria as being physically aware of their hosts. To them, the signals they detect are just foreign compounds they have to fend off. But it’s certainly a far more sophisticated take on the host-pathogen relationship than we’re used to, notes Atkinson. “Rather than the pathogen just piling into the host cell and taking over its DNA, it’s about signal production, interception – and maybe even coercion of the host to do something that it wouldn’t normally do.”

Of course, some bacteria is friendly to humans:

Many of the early examples of cross-kingdom communication that Atkinson and Williams catalogued are less than congenial, but there is also good evidence for cooperative interaction between bacteria and their hosts, says Atkinson – particularly between ourselves and our microbiome, the huge population of bacteria that live in us and on us.

These days we’re all well acquainted with the millions of microbes lining our insides. Yogurt adverts have taught us nothing if not to love the friendly bacteria which line our guts, helping to keep nastier bugs at bay. Microbes don’t just make themselves at home in the intestines, however. They’re in your mouth, up your nose, and covering your skin, all the while releasing a cacophony of quorum-sensing signals.

Atkinson thinks our own cells exploit this same signalling system to monitor and cajole our personal population of microbes, just as they eavesdrop on and manipulate us. In other words, we don’t passively host this bacterial colony, but actively engage it in conversation. We’ve evolved together, he says. “We have to consider that we’re intrinsically linked.”

Since there are thousands, maybe tens of thousands, of words (chemicals) in use among these organisms, it is going to take a lot of work to learn this new vocabulary:

The team is using an imaging system based on mass spectrometry to detect swathes of signals at the same time. They grow their bacteria on a stainless steel plate, and use a laser to vaporise their signalling molecules, feeding these into a mass spectrometer to catalogue the molecules present.

As proof of principle, Dorrestein and Straight have mapped the interactions between two species of soil-dwelling bacteria (Nature Chemical Biology, vol 5, p 885). Even in this simple case, the instrument detected as many as 100 different signalling molecules fired off by the two bacteria, only 10 of which the team managed to match to known molecules. Despite the huge scale of the problem, the team is already starting to translate their work into inter-kingdom studies, probing the interactions between bacteria and cells of the human immune system. By imaging cross-talk between different species, they even hope to identify inhibitors for Staphylococcus aureus, the hospital superbug that has evolved to defend itself against whole groups of our most effective antibiotics.

I’d guess that before the year 2100 humans will figure out ways of living for very long periods. By then, it seems likely we will unravel the puzzle of the tortoise and figure out what metabolic strategies are in use in long-lived species, and which of these might also be usable in humans. I was interested to read that last year a drug was found that does seem to extend life-span in some mammals:

One of 2009’s most significant breakthroughs in biogerontology (or in any field; q.v. Science, WIRED) last year was the announcement that the macrolide drug rapamycin can extend longevity in mice.

More specifically, rapamycin can accomplish this when administered to adult, wildtype mice. In other words, no genetic modification or early-life intervention is necessary, making rapamycin one of the first compounds that meets the criteria for an anti-aging drug that could be used for people who are already alive and well down the road toward aging themselves.

The lifespan extension achieved is modest (~10%), but this is more impressive in light of the fact that the mice were quite old at the time treatment began, and the study used only a single dose rate. Future studies will undoubtedly seek to optimize the dose and regimen with the goal of achieving greater enhancement of lifespan.

One thing I note about long-lived species is that they keep growing. The rule seems universal – trees, tortoises, some types of fish – every species that has an exceptionally long life span also keeps growing in size. There is no fixed, final form that one can associate with adulthood. For humans, of course, our size is fairly fixed – nearly all adults are between 5 feet and 6 feet, 6 inches. Perhaps if we just kept growing, we’d live to be 200. But then, I suspect, we’d end up with some terrible spinal pain and injuries. Humans are not designed to be 10 feet tall. Maybe long-life is reserved for those species who have a structure that can comfortably keep growing.

I see this article about how cells repair double-strand breaks in the DNA:

Humans utilize at least two major pathways to repair DNA double-strand breaks (DSBs): homologous recombination (HR) and non-homologous end joining (NHEJ), and there are at least two genetically discrete sub-pathways of NHEJ: classical-NHEJ (C-NHEJ) and alternative-NHEJ (A-NHEJ). Since the products generated by each of these three repair (sub)pathways differ substantially from one another, it is biologically critical that certain DSBs are repaired by certain DSB repair pathways. How this pathway choice is made in human cells was unclear. In this study, knockout human cell lines that are defective in core C-NHEJ factors were generated. These cell lines are by-and-large extremely deficient in DSB repair, proving that C-NHEJ is the major DSB repair pathway in human cells. Unexpectedly, cell lines reduced for the C-NHEJ factors Ku70 or Ku86, carried out proficient DSB repair because of hyperactive A-NHEJ. In published work we have also demonstrated that Ku suppresses HR throughout the genome and at telomeres. Collectively, these data imply that Ku ensures that C-NHEJ is the major DSB repair pathway by two mechanisms: i) enabling C-NHEJ and ii) by actively suppressing HR and A-NHEJ. Thus, Ku is the critical regulator of pathway choice in human somatic cells.

Since double strand breaks can lead to cell senescence, then Ku factors must play a role in how people ages. If I was a biology researcher, I’d follow up on this to find the connection between Ku and senescence.

Interesting:

This year 2.25 million Americans will get married—and a million will get divorced. Could birth control be to blame for some of these breakups? Recent research suggests that the contraceptive pill—which prevents women from ovulating by fooling their body into believing it is pregnant—could affect which types of men women desire. Going on or off the pill during a relationship, therefore, may tempt a woman away from her man.

It’s all about scent. Hidden in a man’s smell are clues about his major histocompatibility complex (MHC) genes, which play an important role in immune system surveillance. Studies suggest that females prefer the scent of males whose MHC genes differ from their own, a preference that has probably evolved because it helps offspring survive: couples with different MHC genes are less likely to be related to each other than couples with similar genes are, and their children are born with more varied MHC profiles and thus more robust immune systems.

This is also the main reason that monogamy is rare in the animal kingdom. There are only a few dozen species that practice true monogamy. For females, there is the drive to get diversity of MHC in their children, therefore there is a drive to have children with different males. Only in those rare cases where the task of raising a child faces extra special challenges (like the brutal cold of Antarctica, for penguins, or the extremely prolonged immaturity of human children, due to their huge brains) do males and females team up to raise the child together.

Interesting article on viruses influencing the human genome. . By the way, see the lovely blue shades in the photo of the viruses? I only recently learned that, basically, all photos of viruses use false color. That is because viruses are smaller than the wavelengths that we think of as the visible light spectrum (visible to humans, that is):

Oddly, a lot of people do not want to give coffee to 8 year olds, but they will give Ritalin to 8 year olds, even though Ritalin is a stronger drug than caffeine. I think if I had a child who was having trouble concentrating, I would start off giving them coffee, and I’d only switch to harder drugs if the coffee didn’t help them. Any stimulant helps concentration to some extent, but why not start off with the milder stimulant? What is the justification for starting off with the stronger drug?

Andrew Wakefield is the guy who started the hoax that autism was caused by vaccines. His panic he started lead to many parents making poor choices for the health of their children. The full extent of the harm that he has done will never be know. Happily, his career is now coming to an end, and he is facing the dishonor that he deserves.

Twelve years after his now discredited claim in The Lancet that injections of the MMR vaccine against measles, mumps and rubella might cause autism and bowel disorders in children, Andrew Wakefield is closer than ever to being banned from practising as a doctor.

Publication of his claims panicked parents into abandoning the shots, which had peaked in uptake at 92 per cent of UK children in 1995, falling to a trough of just 81 per cent in 2004.

A panel appointed by the UK General Medical Council – which regulates and monitors British doctors – concluded today that there’s now no factual impediment to Wakefield and two of the co-authors on his paper facing charges of professional misconduct.

…The GMC panel also affirmed irregularities in the way Wakefield recruited and managed the 12 children involved in the study.

At least four of the 12 lacked the history of gastrointestinal symptoms and so did not constitute the “routine referrals to the gastroenterology department” that had been stated in the paper. “The panel concluded that your description of the referral process as ‘routine’, when it was not, was irresponsible and misleading and contrary to your duty as a senior author,” it says. “The panel is satisfied that your conduct in this regard was dishonest and irresponsible.”

On another occasion, at his own son’s birthday party in 1999, he took blood from children who were there as guests and paid them each £5 for agreeing to this. He was accused by the panel of showing “callous disregard for the distress and pain that you knew, or ought to have known, the children would suffer.”

This is the rare article where every paragraph held a shock for me. There is a type of slug that absorbs organelles from algae and then uses the organelles to produce food:

It’s easy being green for a sea slug that has stolen enough genes to become the first animal shown to make chlorophyll like a plant.

Shaped like a leaf itself, the slug Elysia chlorotica already has a reputation for kidnapping the photosynthesizing organelles and some genes from algae. Now it turns out that the slug has acquired enough stolen goods to make an entire plant chemical-making pathway work inside an animal body, says Sidney K. Pierce of the University of South Florida in Tampa.

The slugs can manufacture the most common form of chlorophyll, the green pigment in plants that captures energy from sunlight, Pierce reported January 7 at the annual meeting of the Society for Integrative and Comparative Biology. Pierce used a radioactive tracer to show that the slugs were making the pigment, called chlorophyll a, themselves and not simply relying on chlorophyll reserves stolen from the algae the slugs dine on.

“This could be a fusion of a plant and an animal — that’s just cool,” said invertebrate zoologist John Zardus of The Citadel in Charleston, S.C.

Microbes swap genes readily, but Zardus said he couldn’t think of another natural example of genes flowing between multicellular kingdoms.

Pierce emphasized that this green slug goes far beyond animals such as corals that host live-in microbes that share the bounties of their photosynthesis. Most of those hosts tuck in the partner cells whole in crevices or pockets among host cells. Pierce’s slug, however, takes just parts of cells, the little green photosynthetic organelles called chloroplasts, from the algae it eats. The slug’s highly branched gut network engulfs these stolen bits and holds them inside slug cells.

Some related slugs also engulf chloroplasts but E. chlorotica alone preserves the organelles in working order for a whole slug lifetime of nearly a year. The slug readily sucks the innards out of algal filaments whenever they’re available, but in good light, multiple meals aren’t essential. Scientists have shown that once a young slug has slurped its first chloroplast meal from one of its few favored species of Vaucheria algae, the slug does not have to eat again for the rest of its life. All it has to do is sunbathe.

The article mentions that the slugs also steal the genetic material needed to keep the algae organelles going. For me this is proof that for almost every rule in biology, there is an exception.

Such a story allows for a completely new understanding of evolution:

Mixing the genomes of algae and animals could certainly complicate tracing out evolutionary history. In the tree of life, he said, the green sea slug “raises the possibility of branch tips touching.”

Branch tips touching would require a re-write of almost everything we think we know about the history of life on Earth.

All of the literature of computer science is devoted to the issues of arranging the state of the system in such a way that it can not be accidentally changed, or changed by 2 processes that need the state of the system to move in opposite directions. Programming has many catch-phrases to express these ideas:

information hiding

decoupling

small pieces, loosely joined

Apparently humans have trouble maintaining software that is written in a highly coupled way. And yet, our bodies appear to be highly coupled systems – failure of any one major part can lead to death for the whole. There are many global variables, such as body temperature, which effect the context in which all other variables operate (for instance, enzyme efficiency depends on body temperature). This leaves me curious – apparently nature has figured out how to build highly-coupled systems, systems which then last for 70 or 80 years (better than most computer systems can hope for). How is this done? Meta-programming? Processes that write macros that give rise to processes which can write macros? I suspect a close study of the ways cells program their activities will eventually lead to new strategies of programming software.

Interesting story about a woman who has built a fantastic career, despite having schizophrenia:

The first frank episode of psychosis happened when I was around 16, and I suddenly started walking home from school in the middle of the day. I began to feel the houses were getting weird; they were sending me messages: “You are special. You are especially bad. Now walk. Cries and whispers.” There were also some warning signs in college but I didn’t really “officially” break down until graduate school at Oxford.

….Subjectively, the best comparison I can make is to a waking nightmare. You have all the terror and confusion and the bizarre images and thoughts that you have in a nightmare. And then with the nightmare you sit bolt upright in bed in utter terror. Only with a nightmare you then wake up, while with psychosis you can’t just open your eyes and make it all go away.

When I was 16, I had maybe a dozen incidents where I woke up with what felt like a bad nightmare that would not stop, despite the fact that I was now awake. Most times I was able to fix the problem by going back to sleep and waking up maybe 15 minutes later. What I felt was similar to what she describes. It was a really awful sensation, the worst I’ve ever known. Reading her words, I have to wonder if I wasn’t skating along the edge of something serious.

Previous studies have suggested a link between creativity and depression. My experience among artists has left me aware how common drug use is among them, and how much that drug use goes toward treating their anxiety disorders. David Dobbs writes about new evidence suggesting a genetic explanation that may explain some of the link between creativity and mental illness:

Of special interest to the team was a new interpretation of one of the most important and influential ideas in recent psychiatric and personality research: that certain variants of key behavioral genes (most of which affect either brain development or the processing of the brain’s chemical messengers) make people more vulnerable to certain mood, psychiatric, or personality disorders. Bolstered over the past 15 years by numerous studies, this hypothesis, often called the “stress diathesis” or “genetic vulnerability” model, has come to saturate psychiatry and behavioral science. During that time, researchers have identified a dozen-odd gene variants that can increase a person’s susceptibility to depression, anxiety, attention-deficit hyperactivity disorder, heightened risk-taking, and antisocial, sociopathic, or violent behaviors, and other problems—if, and only if, the person carrying the variant suffers a traumatic or stressful childhood or faces particularly trying experiences later in life.

This vulnerability hypothesis, as we can call it, has already changed our conception of many psychic and behavioral problems. It casts them as products not of nature or nurture but of complex “gene-environment interactions.” Your genes don’t doom you to these disorders. But if you have “bad” versions of certain genes and life treats you ill, you’re more prone to them.

Recently, however, an alternate hypothesis has emerged from this one and is turning it inside out. This new model suggests that it’s a mistake to understand these “risk” genes only as liabilities. Yes, this new thinking goes, these bad genes can create dysfunction in unfavorable contexts—but they can also enhance function in favorable contexts. The genetic sensitivities to negative experience that the vulnerability hypothesis has identified, it follows, are just the downside of a bigger phenomenon: a heightened genetic sensitivity to all experience.

Steven Novellais is frustrated with the anti-vaccine bias of media:

At this time there are two slow panics spreading through the community – fear of the H1N1 “swine” flu pandemic, and fear of the vaccine to prevent H1N1 flu. Regarding the pandemic itself – this is a real threat, it is just not known at this time how severe it will turn out to be. So far it is looking like another seasonal flu in severity, but with some different features, such as a greater tendency to severely affect otherwise healthy individuals.

The panic over the vaccine, however, is entirely manufactured, primarily by dedicated conspiracy theorists and anti-vaccinationists, and then aided by irresponsible media. There have been two stories in particular about alleged severe reactions following vaccines recently, one dealing with the HPV vaccine and the recent cased of what is being called dystonia following the seasonal flu vaccine. The young girl who died within hours of getting the HPV vaccine was found to have a heart defect, and her death had nothing to do with the vaccine, so that story was rather short-lived.

The new case making the rounds, however, appears to have some legs. It is getting international news attention, and I am being flooded with e-mail requests to analyze the case.

This is the story of Desiree Jennings, who is a 28 year old cheerleader who was apparently healthy until August when she received the seasonal flu vaccine. Ten days later she developed a severe respiratory illness, probably the flu, requiring hospitalization. She then developed an apparent neurological reaction in which she has difficulty speaking and walking, with involuntary muscle contractions and contortions. Her symptoms (including speech) are relieved, however, by walking backwards or by running. She also seems to have attacks of muscle contortions.

Several medical specialists are quoted, and he concludes:

It is therefore highly unlikely that whatever Jennings is suffering from now had anything to do with the flu vaccine she received in August. Unfortunately, this is not stopping irresponsible news coverage or exploitation by anti-vaccinationists. Further, Jennings is now in the hands of the Generation Rescue anti-vaccine quacks. I predict that they will be able to “cure” her, because psychogenic disorders can and do spontaneously resolve. They will then claim victory for their quackery in curing a (non-existent) vaccine injury.

There are elements in our society that prefer to react to rare dangers, rather than reacting to common dangers. It is an irrational preference. Novellais mentions the odds:

The medical community is always careful to point out that there are very rare reactions to vaccines. No one is claiming that they are 100% safe – no medical intervention is. But severe reactions are very rare. Meanwhile, about 36,000 people die each year in the US alone from the seasonal flu. That figure is likely to be higher this year, as seasonal strains are combined with the H1N1 strain to form a particularly bad flu season. We are fortunate that there are vaccines both for the seasonal flu and the H1N1 flu, which is particularly well targeted because we know the strain.

This type of irrationality is similar to the kind of irrationality that causes some people to prefer driving over flying, even though 34,000 Americans die each year on the roads, whereas the big headline on 1/12/2009 was Airlines go two years with no fatalities:

For the first time since the dawn of the jet age, two consecutive years have passed without a single airline passenger death in a U.S. carrier crash.

No passengers died in accidents in 2007 and 2008, a period in which commercial airliners carried 1.5 billion passengers on scheduled airline flights.

So for those 2 years, the death totals were roughly 70,000 versus 0. And yet I still know people who feel safer driving than flying. I suppose it is the illusion of control that driving one’s own vehicle gives. And, to be sure, there are airplane crashes in the future. I do not know when or where, but I am sure an airplane will crash at some point, causing deaths. There will always be some risk associated with flying. However, to believe that driving is safer than flying, you have to overlook all the risks of driving and only focus on the risks of flying. Likewise, to believe that taking a vaccine is more dangerous than not taking a vaccine, you either have to have a good reason for believing you will not be exposed to a particular pathogen, or you have to entirely overlooks the risks of not taking a vaccine, and focus only on the risk of taking the vaccine.

The CDC is serious about the issue of side-effects arising from vaccines. Helpfully, they have a page on their website that lists every known side-effect that doctors have been able to document, arising from any of the most common vaccines. As the page says in the introduction:

Any vaccine can cause side effects. For the most part these are minor (for example, a sore arm or low-grade fever) and go away within a few days. Listed below are vaccines licensed in the United States and side effects that have been associated with each of them. This information is copied directly from CDC’s Vaccine Information Statements, which in turn are derived from the Advisory Committee on Immunization Practices (ACIP) recommendations for each vaccine.

Remember, vaccines are continually monitored for safety, and like any medication, vaccines can cause side effects. However, a decision not to immunize a child also involves risk and could put the child and others who come into contact with him or her at risk of contracting a potentially deadly disease.

I’ll pick out one of the vaccines that I’ve personally been injected with: DTaP. This is the vaccine for tetanus. I’ve been injected with this vaccine 3 times, once in the 70s, once in the 80s, and once in the 90s (They say you should renew it once every 10 years, and I manage to either cut myself on rusty metal, or step on a rusty nail, once every 10 years). Here are the severe reactions:

Serious allergic reaction (less than 1 out of a million doses) Several other severe problems have been reported after DTaP vaccine. These include:

* Long-term seizures, coma, or lowered consciousness
* Permanent brain damage.

These are so rare it is hard to tell if they are caused by the vaccine.

Controlling fever is especially important for children who have had seizures, for any reason. It is also important if another family member has had seizures.

I’ve been lucky in that I’ve never had any side-effects at all, but even if I had, I understand the risk of serious side-effects is small compared to the risk of getting a tetnus infection. Consider the cost: a tetnus shot costs something around $45, but if you’ve never been vaccinated, and you get a tetnus infection, you will spend weeks on IV antibiotics, and the cost will be in the thousands. And the risk to your life will be much greater.

The CDC has a page caled Vaccine Safety Information for Parents that tries to remind parents of the balance of risks:

I suspect that the public will always be afflicted by some popular delusion regarding safety. It doesn’t help that some delusions have well-financed organizations promoting them, such as Jenny McCarthy’s organization Generation Rescue. (In case you don’t know, Jenny McCarthy’s child has autism, though McCarthy claims that, through the grace of God, her child is now healed.) This is anti-vaccine organization that promotes a narrative built around these 3 assertions:

1.)Neurological Disorders (NDs) in children are growing at a rate well in excess of population growth and are not the result of better diagnosis or widening diagnostic criteria.

2.) Children with NDs exhibit much higher levels of toxicity in their bodies.

3.) The ingredients in vaccines are neurotoxic and are capable of creating many of the medical issues children with NDs are suffering from.

When they speak of toxicity, they generally mean mercury, a dangerous heavy metal, which is found in thimerosal, a perservative used in vaccines. Here is the usual statement made against thimerosal:

You have probably seen your nurse insert a syringe into a large vial, extract some liquid, and then leave a substantial amount of vaccine in the original container. If you’ve witnessed this seemingly benign procedure, you’ve seen how vaccine manufacturers are saving money at the expense of public health. In order to store larger amounts of vaccine at a lower cost, companies began offering “multi-dose units” while adding preservatives to prevent contaminations. That way doctors can open and close a vaccine container, inviting germs into the once-sterile solution, while assuring the public that those contaminants are quickly killed by the preservative. Sound familiar? It’s the same story of corporate America’s love affair with preservatives. It saves them money, while posing an undue risk to your health. But like many toxic preservatives found in food, a vaccine preservative kills more than just bacteria and fungi; it can lead to extensive neurological damage in your children, and has even been implicated in autism.

However, the mercury is never free floating, but always bound, and humans ingest it just like they injest other deadly minerals – in bound form. For instance, no human being could safely swallow pure potassium, and yet we all eat food with bound potassium in it, and we would die if we did not get sufficient potassium.

Point #1 above raises the point that autism seems to be increasing in the population. I think this has been well-documented at this point. Strangely, Jenny McCarthy’s organization seems to think that this fact helps their cause, though in fact it undermines it. Thimerosal was introduced into vaccines in the 1930s. If it was going to cause an epidemic of autism, then the epidemic would have happened in the 1930s.

There is even better evidence. The theory that there is a link between thimerosal and autism is clearly disproven by the experience of Denmark, which banned the use of thimerosal back in 1992 – and yet the rate of autism kept increasing, demonstrating that there was no link between thimerosal and autism. Here is the conclusion of one study that looked at the experience of banning thimerosal in Denmark:

Conclusions. The discontinuation of thimerosal-containing vaccines in Denmark in 1992 was followed by an increase in the incidence of autism. Our ecological data do not support a correlation between thimerosal-containing vaccines and the incidence of autism.

All the same, the United States followed the lead of Denmark and banned the use of thimerosal in 2001:

Thimerosal is a mercury-containing preservative used in some vaccines and other products since the 1930s. There is no convincing scientific evidence of harm caused by the low doses of thimerosal in vaccines, except for minor reactions like redness and swelling at the injection site. However, in July 1999, the Public Health Service agencies, the American Academy of Pediatrics, and vaccine manufacturers agreed that thimerosal should be reduced or eliminated in vaccines as a precautionary measure.

Since 2001, with the exception of some influenza (flu) vaccines, thimerosal is not used as a preservative in routinely recommended childhood vaccines.

This ban had no effect on the rate of autism, which continues to increase. Clearly there is no link between thimerosal and autism.

Incidentally, 2 weeks ago I had a conversation with a researcher who’d investigated a type of mycoplasma that infects people’s genitals but which causes no symptoms and therefore is usually undetected. But, using primates as a test specicies, he found that the mycoplasma (when found in pregnant females) was associated with a lack of purkinje cells in the cerebellum of new babies. The primary physical symptom of Autism is a lack of purkinje cells in the cerebellum. Therefore, it was possible that the current epidemic of autism is actually caused by a previously unknown species mycoplasma, and therefore the epidemic of autism might be ended by liberal use of antibiotics in women who test positive. He pointed out that other bacterial infections of the mother, such as syphillis, are known to cause mental defects in children (for instance, syphillis in the mother is associated with the eventual development of schizophrenia in the child).

As to the benefits of vaccines, Brent Simmons has an interesting point to make, about his own, unusually bad, case of Chicken Pox:

It was just a thing. We thought we were modern because it was just chicken pox — not polio or smallpox or one of those scarier diseases that had been conquered.

But now there is a vaccine, and I wish like crazy there had been a vaccine when I was a kid.

…I remember vomiting so much that the vomiting itself didn’t even bother me any more. I started crying out of frustration. Just when I started to feel a little better, a little cooler, and hungry and thirsty, I’d try the smallest sip of water, and whatever was left in me to come up would come back up. It just went on and on.

…But I was looking at someone else’s paper. Because I couldn’t see the chalkboard anymore and I couldn’t read the questions to copy them down.

…It was a few weeks before news got to my parents and they took me for an eye exam.

Chicken pox had ruined my eyesight.

…Which brings me back to the subject of vaccines. And, you know, I thought I was going to, but I don’t really need to state the obvious.

Because he had such a bad case, he will likely suffer episodes of awful pain throughout his adult life:

I later got shingles when I was 20. I won’t be surprised to get it again, but I sure hope not. Shingles hurts.

The organizations, such as Jenny McCarthy’s, that are devoted to spreading misinformation about vaccines are doing real harm to the overall health of the public. Why do such organizations, and their irrational agendas, flourish? John Gruber quotes a recent article from Wired, about parents who skip vaccine shots for their children:

The rejection of hard-won knowledge is by no means a new phenomenon. In 1905, French mathematician and scientist Henri Poincaré said that the willingness to embrace pseudo-science flourished because people “know how cruel the truth often is, and we wonder whether illusion is not more consoling.” Decades later, the astronomer Carl Sagan reached a similar conclusion: Science loses ground to pseudo-science because the latter seems to offer more comfort. “A great many of these belief systems address real human needs that are not being met by our society,” Sagan wrote of certain Americans’ embrace of reincarnation, channeling, and extraterrestrials. “There are unsatisfied medical needs, spiritual needs, and needs for communion with the rest of the human community.”

Looking back over human history, rationality has been the anomaly. Being rational takes work, education, and a sober determination to avoid making hasty inferences, even when they appear to make perfect sense. Much like infectious diseases themselves — beaten back by decades of effort to vaccinate the populace — the irrational lingers just below the surface, waiting for us to let down our guard.

There is also this:

Current public opinion about childhood vaccinations sometimes seems to be influenced less by science and more by Jenny McCarthy. But here’s something that rarely gets discussed: the threat posed by the nonvaccinated to children who are immunosuppressed. Last year, while searching for child care for our 2-and-a-half-year-old son, my husband and I thought we had we found the perfect arrangement: an experienced home day care provider whose house was an inviting den of toddler industriousness. Under her magical hand, children drifted calmly and happily from the bubble station to the fairy garden to the bunnies and the trucks, an orchestrated preschool utopia. But when I asked: “Are any of the children here unvaccinated?” the hope of my son’s perfect day care experience burnt to a little crisp. As it turned out, one child had a philosophical or religious exemption—a convenient, cover-all exemption that many doctors grant, no questions asked, when a parent requests one. (I still do not understand how the state can allow one to attribute his or her fear of vaccines and their unproven dangers to religion or philosophy. But that’s a question for another day.)

Ordinarily I wouldn’t question others’ parenting choices. But the problem is literally one of live or don’t live. While that parent chose not to vaccinate her child for what she likely considers well-founded reasons, she is putting other children at risk. In this instance, the child at risk was my son. He has leukemia.

By middle age, people are riddled with cancer cells:

But knowing more about how tumors develop and sometimes reverse course might help doctors decide which tumors can be left alone and which need to be treated, something that is now not known in most cases.

Cancer cells and precancerous cells are so common that nearly everyone by middle age or old age is riddled with them, said Thea Tlsty, a professor of pathology at the University of California, San Francisco. That was discovered in autopsy studies of people who died of other causes, with no idea that they had cancer cells or precancerous cells. They did not have large tumors or symptoms of cancer. “The really interesting question,” Dr. Tlsty said, “is not so much why do we get cancer as why don’t we get cancer?”

The earlier a cell is in its path toward an aggressive cancer, researchers say, the more likely it is to reverse course. So, for example, cells that are early precursors of cervical cancer are likely to revert. One study found that 60 percent of precancerous cervical cells, found with Pap tests, revert to normal within a year; 90 percent revert within three years.

But if you think about it, it is tough to imagine a model whereby this situation comes about suddenly in middle age. What is more likely is that everyone has cancer cells from a young age. What declines over time is the ability of the body to manage those cancer cells.

Great article on the origins of life, before the first cells formed.

I’m just thinking out loud here.

If the cell was like a computer, it would need a processor, and it would need RAM. The nucleus would be the processor, and the endoplasmic reticulum would be the RAM (the Golgi Apparatus would be something like the network router, making sure proteins get sent to the correct places). Processes might be initiated in the nucleus, but some processes would be multi-step, requiring processes and callbacks to be registered in the endoplasmic reticulum. The need to conserve protein would force the adoption of paging (whatever the next process is could recycle protein from the last process). The need for protein conservation would probably also force the adoption of lightweight scripting languages (I mean lighter weight than base 4 DNA). DNA might be the machine language of living things, but a paging system that conserved protein (through re-use) would perhaps use larger molecules that worked at more than base 4. Evolution would encourage a system that was fast enough yet conserved protein.

There would have to be a garbage collector (as in the Java language – something that takes care of cleaning up variables, resources and processes after they are finished). For single celled organisms, the garbage collector would not have to be very good, so long as there was some kind of complete integrity check when the cell divided. Maybe the cell would forget to unregister a callback (or, in real-life, the forgotten unfolded protein), but why would it matter? After 30 minutes of eating, the single-celled organism divides, and undergoes some process that offers a real integrity check. The endoplasmic reticulum starts out clean again in the new cell. This is like a PHP script – no need to be terribly efficient about cleaning up the RAM while the script processes, because it is only going to run for 60 seconds. When it is done, all its variables will cease to exist, all the RAM it was using will be properly reclaimed. But problems arise for multi-celled organism that hope to live a long time. They need cells to stay in place and maintain a certain structure for a long time. The inefficient garbage collector that worked reasonably well for single celled organisms spells death for multi-celled organisms. And why wasn’t this problem addressed? Because rebooting is cheaper than building a perfect garbage collector that can last forever. It is cheaper for a multi-celled organism to have children than for that multi-celled organism to figure out how to be perfect in its use of its resources.

I recall when I was young I asked my dad why people got older, and he said it was because of genetic damage that builds up over time. That was the standard answer back then. My science teacher said the same thing. But of course, that can not be true. A 30 year old male and a 30 year old female can combine to create a child that is 0 years old. That is not possible if aging is a result of genetic damage. Assuming the egg cell and the sperm cell are exposed to the same genetic damage as the rest of the body, then the baby would be 30 years old the moment it is born, since it would be born with whatever genetic damage the male and the female had accumulated. No, to explain aging, we need a mechanism that allows two 30 year olds to give birth to a baby that is 0 years old. This article on aging raises the point:

How exactly does random damage to macromolecules translate into the reproducible and recognizable organismic phenotype we call “aging”? This issue was first raised in 1959 (2), but it still remains unsolved (3). Most often, free radicals or other noxious agents will damage macromolecules in a very stochastic, idiosyncratic fashion. It is difficult to understand how such a random process can lead to the significant and reproducible loss in tissue function observed during aging.

Aging can not simply arise from random accidents, otherwise the incidence of aging would appear as a bell curve, and on the extreme tips of that bell curve would be some individual humans who looked as if they had some age other than their chronological age. There would be the 20 year old with gray hair, dementia and osteoporosis, and there would be the 60 year old who is still able to play pro NFL football, because their body is really 20 years old. And, anyway, no one seriously suggests that the changes in the body of a 3 year old, as it becomes a 4 year old, arise simply from accidental genetic damage. There is clearly a process at work.

Reading on this issue, I get the impression that biologists currently have a model aging that goes like this:

1.) Senescence is used to end an individuals initial growth phase. Only some cells are suppose to enter senescence.

2.) Genetic damage causes other cells to undergo senescence.

3.) Once the body has largely stopped growing, cell death leads to loss of function, as the dying cells are no longer replaced.

About damage, the above article says:

Thus, we propose that aging ensues only when damage is extensive enough, and of a type capable of inducing a cellular response, which often results in either cell senescence or apoptosis.

But this really just moves the question: if aging is caused by senescence, then why does senescence cause aging? Why can’t the cells just live forever, and therefore why can’t the multi-celled organism (for instance, us humans) live forever? This bit is interesting:

There are considerable data indicating that, if a cellular response to damage is not activated, then cells can withstand a significant amount of damage to DNA without the organism showing signs of premature aging (10). Indeed, in most of the mouse models where caretaker functions have been inactivated, an increased level of DNA mutations has been observed as expected, but the mice fail to display an accelerated aging phenotype. For example, Xpc–/– mice accumulate up to 30-fold higher levels of DNA mutations than do their wild-type counterparts, yet there is no effect on their life span (11). A similar, though less dramatic result has been observed in the case of scavenging proteins. … There is a considerable accumulation of unrepaired mutations that has no deleterious effect on life span. … In contrast, mouse models in which the activity of gatekeepers (including telomerase, Wrn, Blm, ATM, or p53) has been manipulated do generally display an accelerated aging phenotype (16–20). In the cases of telomerase, Wrn, Blm, and others, the gene knockout results in generalized genomic instability, including not only double-stranded breaks, but also telomere shortening and/or stalled replication or transcription complexes, both of which appear to be interpreted by the cell as an unrepaired double-stranded break. As previously mentioned, this type of damage leads to activation of a response that culminates in cellular senescence or apoptosis (4). From these data, we must conclude either that genomic instability (but not mutations) plays a role in aging, or that longevity is related to the cellular response of the cell to such DNA damage.

So the cell can take a lot of genetic damage, with no impact on life span, but a few key gatekeepers are needed to watch over things.

Most cells can only reproduce a limited number of times, even when you remove them from the body and cultivate them under ideal circumstances in a petri dish:

Cells divide vigorously and can often be subcultivated in a matter of a few days. Eventually, however, cells start dividing slower, which marks the beginning of Phase III. Eventually they stop dividing at all and may or not die (reviewed in Hayflick, 1985; Hayflick, 1994). Hayflick and Moorhead noticed that cultures stopped dividing after an average of fifty cumulative population doublings (CPDs). This phenomenon is known as Hayflick’s limit, Phase III phenomenon, or, as it will be called herein, replicative senescence (RS).

The limit depends on the type of cell and the species it is from:

Early results suggested a relation between the number of CPDs cells undergo in culture and the longevity of the species from which the cells were derived. For example, cells from the Galapagos tortoise, which–as described–can live over a century, divide about 110 times (Goldstein, 1974), while mouse cells divide roughly 15 times (Stanley et al., 1975; Rohme, 1981).

But some cells are immortal:

Exceptions exist and certain cell lines never reach RS. These are said to be “immortal” and include embryonic germ cells and most cell lines derived from tumors, such as HeLa cells (Brunmark et al., 1986; Chen and Yu, 1994; Pera et al., 2000). Some types of rat cells have also been claimed as capable of evading RS (Mathon et al., 2001; Tang et al., 2001).

And, of course, in recent years, scientists have figured out ways to roll back specialized cells and make them more like embryonic stem cells.

As things stand now, if one of your cells suffers a certain kind of damage, it will become senescent, and then it becomes a risk for cancer. If it accumulates more damage of a certain type, it will eventually develop into cancer. So why does the body allow such cells to exist? Why not kill all such cells? The most obvious answer to that is that, once the body has stopped generating a lot of new cells, it can not afford to kill off all of its existing cells. It needs to hang on to them, with the hope that you, damaged as you are, can live long enough to raise children.

Here is an avenue I’d like to research (perhaps some day I will switch careers): what if all senescent cells in your body were forced to die, and your body was allowed to grow new cells? This assumes that science develops a reliable method for getting particular genetic commands to one’s cells – but there are experiments with using genetically engineered viruses that are getting closer to that goal.

I’ve read that senescence is unique to vertebrates. To put that another way, senescence is unique to creatures that have central nervous systems. Lately I’ve been wondering if the nervous system is the main reason our bodies do not already do what I’m suggesting – why not kill off all the senescent cells and replace them with younger cells? While it would be great to have new muscle cells and new bone cells and new kidney cells and new colon cells and new skin cells, it generally would not be a good thing to casually kill off nerve cells. That is where vertebrates store everything they’ve learned. Tadpoles spend several days learning how to swim, no doubt it would be suicide for an adult frog to suddenly forget how to swim in water – evolution will not allow the emergence of a vertebrate that loses crucial skills as an adult. But humans are in a unique situation. We can afford to retire from life – we already do so. We could retire from life for 4 or 5 years, and be helpless, and have nurses take care of us. We could afford to forget how to walk and talk and eat – some already do this when they are old. But the way things work now, when humans reach that point, they usually only go a few more years and then they die. It is fascinating to think where we will be when we know how to order our cells to die off and then renew. Then we would retire from life for a few years, relearn skills, and then return to life, made young again. We would not die, though there would be a sorrow like death, as we would probably suffer massive amnesia, depending on how many of our nerve cells renewed. Our friends would regret the disappearance of the person they knew and loved. They would have to learn to live with the fact that the soul is transitory and does not last, even as the body lives on forever.

I’ve been reading John C. Bogle’s book, Enough. He makes the argument that we live in an era where our business leaders have forgotten what enough is. However much they have, they need more: more cars, more jets, more yachts, more homes, more money. Bogle feels that the ethical lapses we’ve seen in recent years were facilitated by the loss of the concept of enough. It is a good book. People who are interested in questions of business ethics should read it.

On a related note, today the news page over at YCombinator pointed to this old article “How Much Scratch is Enough?” written by Ryan D’Agostino.

Okay, let’s see. Say I give myself eight years—no, better make it ten. Just to be safe. I figure I’ll definitely want a great apartment in Manhattan. Near Central Park. Plus a summer house in, say, the Carolinas. Nothing too big, but nice. Also, enough to put a couple of kids through college. Prep school too. Oh, and Colorado. A condo, on the slopes. Gotta have a nice set of wheels—Beemer—and an SUV (to get around Colorado). Then maybe I’ll open up a little cafe somewhere, or get a boat. Yeah, a boat would be cool. Ten years. Figure $15 million. I think I can do it. But then I’m out. Definitely. Out for good. Just sailing around on my boat.

This is how it starts: with a pledge. A promise to yourself that you will make a certain amount of money—that you will hit your number—by a certain age, and that you will, upon reaching that carefully calculated goal, get out. Go sail your boat. Or open your bookstore or your bed and breakfast, or be a philanthropist or whatever. You won’t have to worry about money. You’ll invest a big, juicy nugget and live off the interest, which will be more than enough.

For some people, though, that word becomes a stumbling block: enough. It makes the calculations tricky, and sometimes, it changes the plan. Enough creeps slowly but steadily upward, like ivy spreading imperceptibly over an entire side of a house, and once it does you can’t picture what the house looked like before. At first, you aim high—way into the millions—and while part of you knows that chances are you won’t really end up with that much, part of you knows there’s a chance you will. You see the number in big, block numerals in your mind, and the corners of your mouth curl up into a little smile, just for a second, when you picture yourself hitting the mark.

Bogle and D’Agostino are both criticizing consumption (cars, houses, jets, etc). I’ve no problem with that. I’m critical of consumption too. But I think it is odd that they both write as if consumption is the only thing that a person might want money for.

For my part, I will never have enough money.

I have in my head an unlimited number of ideas for new businesses. Some are web-based, and of these, some are content sites and some offer a software service. But also, some of the businesses I’d like to pursue have nothing to do with the web. I’ve some software ideas to help biologists and, in particular, to help people learn biology (I’ve just been studying biology myself, so I’m aware of things that could help me learn it better). Some of these ideas are simple, such as a calculator that allows certain kinds of very easy programming (easier than Matlab). And having only recently started studying advanced math, I’m aware that people who take up math as adults, and who are self-taught, may have a set of questions that are different than what high school students ask. And I’ve various creative endeavors I’d like pursue. For instance, I’ve been writing a screenplay for a movie loosely based on the events that occurred at Enron.

The various ideas I’ve got in my head right now could keep me busy for 40 years, and I could easily burn through $200 million pursing them all. I really doubt that I’m going to succeed at all of these endeavors, and I seriously doubt I’ll ever have anything like that kind of money, but I figure I might as well just give it a try and see how far I get. And if a miracle happens, and I end up with $200 million, I’m very certain that by that time my overall goals will have expanded to the point that I’ll need a billion to fund my further ambitions.

I will never have enough money.

D’Agostino suggests that when you finally get the millions of dollars that you’ve been aiming for, you smile: “You see the number in big, block numerals in your mind, and the corners of your mouth curl up into a little smile, just for a second, when you picture yourself hitting the mark.”

I think the opposite is true: the most exciting part of launching a new business is the first dollar that you get. The first few dollars bring a huge thrill, even though the numbers are trivial:

“Our first $100 dollars!”

And then:

“Out first $1,000 dollars!”

And then:

“OMIGOD! Our first $10,000 dollars!”

After awhile the thrill starts to fade. No one celebrates when a new business reaches the $30,000 mark. I assume there is some satisfaction to reaching a $1,000,000 (never been there myself) but I have trouble imagining it is as exciting as the first few dollars that come in, those early dollars that give you your first clue that maybe you’ve a product or service that people will actually want to give you money for.

I do not need multiple cars, houses, jets or yatchs. 10 years from now, I’ll be happy if I have a small apartment in New York City, my current Volvo, which I hope to keep going despite some body rust, and $100,000,000 of software projects that are all going well.

In his fictional scenario (I assume it is fictional) D’Agostino says: “But then I’m out. Definitely. Out for good. Just sailing around on my boat.”

I can’t imagine ever wanting to get out. The thrill of launching and running a business is the most fun thing I’ve yet discovered. If I got out, what would I do? I’d simply get back in.

Lately I’ve become interested in chaos theory. My friend Lark Davis pointed me in the direction of Leonard Smith’s book, Chaos, A Very Short Introduction. It is a short, somewhat technical book, and it dives into the details fast.

I took a step back from it and decided to re-read James Gleick’s book, Chaos, Making A New Science. It is aimed at a popular audience. I read it back in the 90s, though apparently I never understood it. All this time I’ve been thinking there are random elements in any chaotic system, and of course, the whole point of chaos theory is that you can get chaotic outcomes from deterministic equations.

This bit (starting on page 63) says it well:

An ecologist imagining real fish in a real pond had to find a function that matched the crude realities of life – for example, the reality of hunger, or competition. When the fish proliferate, they start to run out of food. A small fish population will grow rapidly. An overly large population will dwindle (they will starve).

…In the Malthusian scenario of unrestrained growth, the linear growth function rises forever upward. For a more realistic scenario, an ecologist needs an equation with some extra term that restrains growth when the population becomes large. The most natural function to choose would rise steeply when the population is small, reduce growth to near zero at intermediate values,and crash downward when the population is very large. By repeating the process, an ecologist can watch a population settle into its long-term behavior – presumably reaching some steady state. A successful foray into mathematics for an ecologist would let them say something like this: Here’s an equation; here’s a variable representing the reproductive rate; here’s a variable representing the natural death rate; here’s a variable representing the additional death rate from starvation or predation; and look – the population will rise at this speed until it reaches that level of equilibrium.

How do you find such a function? Many different equations might work, and possibly the simplest modification of the linear, Malthusian version is this:

x[next] = rx(1-x)

x[next] is the population next year.

Again, the parameter r represents a rate of growth that can be set higher or lower. The new term, 1-x, keeps the growth within bounds, since as x rises, 1-x falls. Anyone with a calculator could pick some starting value, pick some growth rate, and carry out the arithmetic to derive next year’s population.

For convenience, in this highly abstract model, “population” is expressed as a fraction between zero and one, zero representing extinction, one representing the greatest possible population of the pond.

So begin: Choose an arbitrary value for r, say, 2.7, and a starting population of .02. One minus .02 is .98. Multiply by 0.02 and you get .0196. Multiply that by 2.7 and you get .0529. The very small starting population has more than doubled. Repeat the process, using the new population as the seed, and you get .1353. The population rises to .3159, then .5835, then .6562 – the rate of increase is slowing. Then, as starvation overtakes reproduction, .6092. Then .6428, then .6199, then .6362, then .6249. The numbers seem to be bouncing back and forth, but closing in on a fixed number: .6328, .6273, .6312, .6285, .6304, .6291, .6300, .6294, .6299, .6295, .6297, .6296, .6296, .6296, .6296, .6296, .6296. Success!

[skipping to page 69]

Robert May was a biologist. His interests at first tended toward the abstract problems of stability and complexity, mathematical explanations of what enables competitors to coexist. But he soon began to focus on the simplest ecological questions of how single populations behave over time.

…Once, in fact, on a corridor blackboard he wrote the equation out as a problem for the graduate students. It was starting to annoy him. “What the Christ happens when lambda gets bigger than the point of accumulation?” What happened, that is, when a population’s rate of growth, its tendency toward boom and bust, passed a critical point. By trying different values of this nonlinear parameter, May found that he could dramatically change the system’s character. Raising the parameter meant raising the degree of nonlinearity, and that changed not just the quantity of the outcome, but also it quality. It affected not just the final population at equilibrium, but also whether the population would reach equilibrium at all.

When the parameter was low, May’s simple model settled at a steady rate. When the parameter was higher, the steady state would break apart, and the population would oscillate between two alternating values. When the parameter was very high, the system – the very same system – seemed to behave unpredictably. Why? What exactly happened at the boundaries between the different kinds of behavior? May couldn’t figure it out. (Nor could the graduate students.)

May carried out a program of intense numerical exploration into the behavior of this simplest of equations… It seemed incredible that its possibilities for creating order and disorder had not long since been exhausted. But they had not. He investigated hundreds of different values of the parameter, setting the feedback loop in motion and watching to see where – and whether – the string of numbers would settle down to a fixed point. He focused more and more closely on the critical boundary between steadiness and oscillation. It was as if he had his own fish pond, where he could wield fine mastery over the “boom-and-bustiness” of the fish. Still using the logistic equation x[next] = rx(1-x), May increased the parameter as slowly as he could. If the parameter was 2.7, then the population would be .6292. As the parameter rose, the final population rose slightly too, making a line that rose slightly as it moved left to right on the graph.

Suddenly, though, as the parameter passed 3, the line broke in two. May’s imaginary fish population refused to settle down to a single value, but oscillated between 2 points in alternating years. Starting at a low number, the population would rise and then fluctuate until it was steadily flipping back and forth. Turning up the knob a bit more – raising the parameter a bit more – would split the oscillation again, producing a string of numbers that settled down to four different values, each returning every fourth year. Now the population rose and fell on a regular four-year schedule. The cycle had doubled again – first from yearly to every two years, and now to four. Once again, the resulting cyclical behavior was stable; different starting values for the population would converge on the same four year cycle.

With parameters of 3.5, say, and a starting value of .4, then May would see a string of numbers like this:
.4000, .8400, .4704, .8719,
.3908, .8332, .4862, .8743,
.3846, .8284, .4976, .8750,
.3829, .8270, .4976, .8750,
.3829, .8270, .5008, .8750,
.3828, .8269, .5009, .8750,
.3828, .8269, .5009, .8750,
.3828, .8269, .5009, .8750.

As the parameter rose further, the number of points doubled again, then again, then again. It was dumbfounding – such a complex behavior, and yet so tantalizingly regular. “The snake in the mathematical grass,” as May put it. The doublings themselves were bifurcations, and each bifurcation meant that the pattern of repetition was breaking down a step further. A population that had been stable would alternate between different levels every other year. A population that had been alternating on a two year cycle would now vary on the third and fourth years, thus switching to period 4.

These bifurcations would come faster and faster – 4, 8, 16, 32… – and suddenly break off. Beyond a certain point, the “point of accumulation,” periodicity gives way to chaos, fluctuations that never settle down at all. Whole regions of the graph are completely blacked in. If you were following an animal population governed by this simplest of nonlinear equations, you would think the changes from year to year were absolutely random, as though blown about by environmental noise. Yet in the middle of this complexity, stable cycles suddenly return. Even though the parameter is still rising, meaning that the nonlinearity is driving the system harder and harder, a window will suddenly appear with a regular period: an odd period, like 3 or 7. The pattern of changing population repeats itself on a three year or seven year cycle. Then period doubling bifurcations begin again, at a faster rate, rapidly passing through cycles of 3, 6, 12… or 7, 14, 28…, and then breaking off once again to renewed chaos.