Closer To The Ideal

I’ve read that some doctors are now attempting to treat cancer by taking various kinds of white blood cells from cancer patients, cloning the white blood cells, till there are billions of them, and then re-injecting them into the patient. The idea is to give a boost to the immune’s system’s effort to combat the cancer.

On a slightly different angle, I was just wondering why something similar could not be done for HIV patients. Especially if caught early, the patient would still have a lot of non-infected white blood cells. Why not take some of them, clone them, then store them in a refrigerator somewhere and inject some of it back into the patient every month? Every month the HIV would destroy a certain number of T-cells, and every month some of them could be put back via injection?

I realize there are important issues of variety, regarding the T-cells. One needs to keep the immune memory, somehow. But I’m skipping past the issues of implementation just now. I’m curious why this wouldn’t work in principle? Is it just too expensive, too time consuming?

I’m curious if this was ever tried, and if so, how did it turn out? If it was tried and it failed, I would be curious to know why it failed.

I’ve decided I’m going to cure cancer. Cancer isn’t really a biology problem, it is a programming problem (a problem with the code that runs the cells). However, where do I find the code?

For years I’ve heard hype about the Human Genome Project, which the US government funded. I just went to the website, and I am confused by how the data is laid out.

They have a gene database where you can look up any particular gene, but I am having trouble finding where I can find all the code, together, not chopped up into little pieces. They have assembled chromosomes here, but the data is in this form:

# Homo sapiens chromosome 7, alternate assembly (based on CRA_TCAGchr7v2)
#
# This file provides assembly instructions for sequence AC_000068
# included in alternate assembly of NCBI build 37 (CRA_TCAGchr7v2_chr7).
#
#chrom chr_start chr_stop part_no part_type comp_id/gap_len comp_type/gap_type comp_end/linkage orientation/empty
chr7 1 50000 1 N 50000 contig no
chr7 50001 62342 2 F AC097647.2 1 12342 +
chr7 62343 72220 3 F AC112517.1 1 9878 +
chr7 72221 83143 4 F AC097645.2 1 10923 +
chr7 83144 122470 5 F AC097646.2 1 39327 +
chr7 122471 135395 6 F AC093666.4 1 12925 +
chr7 135396 142640 7 F AC093627.4 1 7245 +
chr7 142641 690969 8 W CH236966.1 1 548329 +
chr7 690970 1168635 9 W CH236965.1 1 477666 +
chr7 1168636 4638969 10 W CH236953.1 1 3470334 +
chr7 4638970 4791006 11 F AC072054.10 1 152037 +

You can’t really read that as code. I really just want a straight list of the A, T, C and G amino acids that make up a human.

On the flip side, it is very cool that they give a tool for easily comparing the genomes of different species. The site offers a wealth of information, though I have not yet found the information that I am looking for now.

It is sort of fascinating the way biologists have looked for sequences. I want a list where I can run “grep someSequence | wc”. Though I am impressed with all the search tools they’ve made available.

On a different topic, does any think it is odd that they used 8 humans to come up with the “reference” DNA for all humans? Statistics is not my strong suit, but I find it hard to believe that 8 humans can be statistically representative of the 7 billion humans on Earth.

I am surprised to read how rare genes are:

Less than 2% of the genome codes for proteins.

A woman with cancer will have some cells in her body that are healthy and some cells in her body that are cancerous and both the healthy and cancerous cells will have the same genes – so the genes do not explain why some cells are cancerous. Rather, its the other 98% of the chromosomes, the part controls which genes express, that must be the driving force behind cancer. And that is why I am looking for a full map of human chromosomes, rather than a full map of human genes. Because it is the 98% of the chromosomes that are not genes that is of the most interest to me.

Reading over the site I am delighted at the wealth of information they make available. They have information on the differences between humans:

Scientists have identified about 1.4 million locations where single-base DNA differences (SNPs) occur in humans. This information promises to revolutionize the processes of finding chromosomal locations for disease-associated sequences and tracing human history.

I am interested to see this article about Venter’s genome sequence, but I do not see where I can download it.

Anyone know where I can find a straight list of the A, T, C and G of the human genome?

Obesity used to be so rare that people would pay money to see it.

This one seems straight out of a science fiction story. Apparently there is a 17 year old girl who appears in every way to be an 11 month old infant.

In 1932, Bidder postulated that senescence results from “continued action of a (genetic) regulator (of development) after growth ceases (maturation occurs).” A 16-year-old girl who physically appears to be an infant has not been diagnosed with any known genetic syndrome or chromosomal abnormality. The subject’s anthropometric measurements are that of an 11-month-old. Coordinated development of structures for swallowing/breathing has not occurred resulting in dysfunctional digestive and respiratory systems. Brain structure, proprioception and neuroendocrine functions are infantile. Dental and bone ages are pre-teen, while telomere length and telomerase inactivity suggest a cellular age at least comparable to her chronological age. Sub-telomeric microdeletions known to be responsible for developmental delay and chromosomal imbalances are not present. Findings suggest that the subject suffers from “developmental disorganization” resulting from spontaneous mutation of Bidder’s putative “regulator” of development, thereby providing an opportunity to locate and identify developmental gene(s) responsible for ensuring integrated and coordinated change in form and function from conception to adulthood. If their continued expression beyond maturation erodes internal order to promote senescence then further study of her DNA and testing of homologous genes in animal models may provide clues to genetic determinants of aging and human life span.

What causes ageing?

Time passes, and suddenly we need reading-glasses; then comes the menopause (for women) and fat redistribution. Why do these events occur when they do? One possibility is that over time the level of a rate-of-ageing regulator falls, crossing thresholds that trigger various aspects of ageing. In C. elegans, genes whose expression changes with age have been identified, and many of these genes contain a consensus GATA-factor binding site94 that also binds DAF-16/FOXO29. DAF-16, in turn, is regulated during adulthood by a microRNA (lin-4), which also acts earlier to control developmental timing95. Could this microRNA (or something else) change DAF-16 or GATA factor levels over time, influencing the course of ageing? In yeast68 and mice96, sirtuin activity and sirtuin-dependent chromatin modifications decline with age, and in yeast at least, this change shortens lifespan. In mammals, circulating levels of Wnt signal proteins increase with age, and this increase triggers muscle stem-cell ageing97.

What other age-related events are triggered by changes in the levels of regulatory molecules? And what, in turn, changes the regulators? Their levels could change simply because of a decline in protein homeostasis caused by molecular damage. Alternatively, their levels could potentially be subject to the action of a temporal regulatory cascade, somewhat analogous to the per system for circadian rhythms. The per system is in fact a candidate for such a regulatory mechanism, as mice mutant for transcription factors involved in circadian rhythms age prematurely98.

Surprisingly, the speed at which mortality kicks in has not slowed, but the aging process has been delayed (if you are looking at graph, instead of being stretched out at the end, the same sudden chop off at the end is being pushed back a few years). In other words, when aging hits, it still hits relatively fast, but it is now hitting at a later date.

Senescence results from a cumulative imbalance between damage and repair57, 62. Progress in reducing damage (by means of public-health efforts to enhance living conditions and to prevent disease, for example) and progress in increasing repair (by medical interventions, for example) are the two fundamental causes of health improvement. It might be thought that such progress would slow the rate of deterioration such that the debilitation that used to occur between ages 70 and 80 would occur between ages 70 and 85 and the debilitation that used to occur between ages 80 and 90 would occur between ages 85 and 100. Remarkably, this does not seem to be the case. Indeed, the pace at which death rates increase with age accelerated somewhat over much of the twentieth century and has been roughly constant in recent decades17, 18, 19, 24, 25, 26, 27. The evidence suggests that deterioration, instead of being stretched out, is being postponed: levels of mortality and other indices of health that used to prevail at age 70 now prevail at age 80, and levels that used to prevail at age 80 now prevail at age 90. The various strands of demographic and epidemiological evidence reviewed above, and some intriguing animal studies64, have been reinforced by new evidence from a study of supercentenarians (that is, people 110 years old and older)73.

Most reported cases of a person being a centenarian — and to an even greater extent a supercentenarian — are erroneous73, 74. To verify reputed high ages, correct birth records have to be found. A meticulous research endeavour has yielded a remarkable finding: between the validated ages of 110 and 114, the annual probability of death is constant at a level of 50% per year73. The sparse observations of survival after age 114 are not inconsistent with the hypothesis that mortality stays at this level at all ages after 110. As explained in Box 1, this result implies that at least at advanced ages, human individuals deteriorate at the same rate.

This was also interesting:

With rising age, women make up an increasing share of the population. In Sweden in 2008, almost 52% of births were boys and, despite higher male death rates, men outnumbered women up to age 60. There were three women for every two men by age 80 and six women for every man among centenarians. In terms of various indices of health and disability, however, older men generally do better than coeval women. This is the health–survival paradox: men seem to be healthier than women, but they die younger69. Social and biological factors interact to determine the prevalence of frail females and dead males, but the relative importance of specific mechanisms is not well understood69, 70, 71. Males tend to believe their health is better than it actually is and do not seek medical care as frequently as females: they have fewer appointments with general practitioners but require emergency treatment more often69. Females seem to be better able to survive with poor health72. Males tend to engage in reckless behaviour. This tendency may be partly genetic in origin, having its basis in the different reproductive opportunities males face in comparison with females70, 71.

Our germ line is immortal. And, in an experiment done in worms, suppressing a type of insulin lead to an increase of longevity, due to genes from germ cells being expressed in somatic cells:

The first pathway shown to influence ageing in animals was the insulin/IGF-1 pathway19. In C. elegans, mutations that decrease the activity of daf-2, which encodes a hormone receptor similar to the insulin and IGF-1 receptors, more than double the lifespan of the animal, and mutations affecting the downstream phosphatidylinositol 3-kinase (PI(3)K)/AKT/PDK kinase cascade extend lifespan as well. The most remarkable thing about these (and many other) long-lived mutants is that they remain young long after normal worms look old25, 26. (Imagine yourself, in your thirties, learning that your attractive young dinner date is actually 70.) Inhibiting insulin/IGF-1 signalling changes lifespan through changes in gene expression: through DAF-16, a FOXO transcription factor; the heat-shock transcription factor HSF-1; and SKN-1 (ref. 27), a Nrf-like xenobiotic-response factor. These transcription factors, in turn, upregulate or downregulate diverse genes that act cumulatively to produce large effects on lifespan. Downstream genes shown to be functionally significant include stress-response genes such as catalases, glutathione S-transferases and metallothioneins, as well as genes encoding antimicrobial peptides, chaperones, apolipoproteins, lipases28 and channels. Surprisingly, genes normally expressed in the germ line are misexpressed in the somatic tissues of daf-2 mutants, where they contribute to longevity29. This is intriguing because the germline lineage (traced from fertilized egg to fertilized egg) is immortal. However, unfertilized germ cells that express these germline genes do age, along with the rest of the animal, in a daf-2-dependent manner25. Thus, germline genes account for some, but not all, of the longevity mechanism. More generally, each downstream longevity gene has its own story, often completely unknown. Together, these genes constitute a treasure trove of discovery for the future. For example, some genes double their activity in a long-lived mutant; what would happen if their activity were increased tenfold?

Interesting bit on how diversity of genes is important to species survival. A conflict of genetic interests is healthy for the long term.

The genes that are most beneficial to males are the most disadvantageous for females, and vice versa. However, this genetic conflict between the sexes is important in maintaining genetic variation within a species, researchers at Uppsala University have shown in a study on fruit-flies published in the open access journal

Males and females of many species often look quite different from one another. These differences are thought to have evolved because the sexes often have needs and strategies that do not coincide. For example, in fruit-flies, females may do best by concentrating their efforts in acquiring resources to lay more eggs, while males benefit by increasing their mating and fertilization success.

Such differences generate a sexual “conflict of interests,” and since as a general rule each characteristic of an organism is regulated by the same set of genes in the two sexes, this conflict takes place at the genetic level. Using a combination of behavioral studies and genomic technology, researchers Paolo Innocenti and Ted Morrow have succeeded in getting a first insight into which genes are influenced by this type of sexual conflict.

An odd thing I learned today:

Mutations in the same gene can cause dramatically different effects in humans from those seen in other species. For instance, mutations in the RB1 gene are associated with eye cancer in humans but cause worm genitalia to develop in the wrong place.

The puns are annoying, but I basically agree with his point:

Communication “experts” tell me that in order to have any success in vanquishing people’s irrational beliefs, one has to fill the void left by said vanquishment with something else. I have, in the past (and will continue in the future), to be very critical of the new field of evolutionary psychology based advice. This advice ranges from business marketing to relationships. What it boils down to is attempting to exploit the evolved stimulus response behaviors of individuals in order to manipulate them like a meat puppet. Sort of a neurolinguistic programming light. The evolutionary psychology relationship advice in particular boils down to attempting to fake having higher fitness in the hopes that other people will want to commit reproductive acts with them. Classy.

Much of so-called “evolutionary psychology” amounts to unprovable stories that people tell to justify whatever they want. If you want to argue that people are greedy, or women want monogamy, or men are hunters, or why do people love the fat and sugar in the meals served at McDonalds, then you can come up with a simple, but unprovable, story, using evolution as a narrative. People who do this are “hyper adaptationist” – they think every observed behavior about humans should have some evolutionary explanation. (Such people have trouble with issues like homosexuality and art – both of which are hard to explain in evolutionary terms.)

Josh Witten says it well:

Biologists have the bad habit of trying to explain every trait in terms of a natural selection narrative. Stephen Jay Gould strongly criticized this hyperadaptationist tendency, a point on which this rugbyologist and notable evolutionary biologist Michael Lynch have both agreed with Gould. The public face of the field of evolutionary psychology unfortunately fully embraces the hyperadaptationist world view.

…While I was reading the Guardian article … I noticed a link to their evolutionary psychology advice column. The shtick of “evolutionary agony aunt” Carol Jahme is to provide all your standard “Dear Abby” advice, but through the perspective of evolutionary psychology. Essentially, Carol is going to explain either how your perceived problem 1) was caused by natural selection in a pre-modern environment, or 2) can be solved by exploiting the formerly adaptive tendencies of others.

There are two problems with this approach. First, there is very little evidence to support the adaptive stories of evolutionary psychology for humans. There is not necessarily contrary evidence, but adaptation is not our null hypothesis. They are not right or wrong. Grain of salt time folks. Second, this presupposes that evolutionary psychology has the answer to every question. Reading Jahme’s column would make you think

And it leads to things like this:

I. . .have applied your guidance to my search for a suitable mate. My profile on a certain online dating site has been written to emphasise my evolutionary advantages (height, intelligence, employment status, alpha-male potential, physical fitness and social skills) and has proved to be successful at attracting attention from females of breeding age and, after carefully sifting out unsuitable candidates, converting that attention into a first date. . .Despite choosing neutral locations with convivial atmospheres and ensuring I am well groomed, I have been unable to secure a second date. . .
-from Valentine’s Day Dating Tips (emphasis mine)

Yo, dog, let me channel some Randy Jackson at you and break this down for you. Your problem is not your application of evolutionary psychology. Your problem is that you are dick who treats women like puppets you can manipulate. And, you probably stink. I for one do not have to make sure I am well groomed before i leave the domicile for a social encounter. Allow me to recommend that you get into the inescapable habit of devoting the first 30 minutes after you wake each day to placing your phenotype in an advantageous state.

You see, fitness (W) can be really hard to define, especially in large animals with long generation times. Its like pornography, one cannot define high fitness, but one knows it when one sees it.4 W is hard to fake, which is essentially what you are trying to do, which the use of the word “convivial” makes completely obvious.

In short, you can’t fake alpha-male potential.

I’ve always wondered why there are such large gaps between species. Check out the order of Caniformia: dogs, bears, pandas, raccoons, weasels, etc. All these animals started out with a single pair of common ancestors, with a particular male and female who mated and had children. How many differences had to accumulate in the children (and children of children, etc, all through the generations) before the children lost the ability to have sex with each other (or rather, with other children of parents of the same generation as that original male and female) and produce children of their own? What is the exact point when descendants of a particular female end up belonging to different species?

I’ve always assumed there had to be some mechanical reason why the gaps between species tends to be large, and so I’m interested to see that biologists are closing in the exact mechanics of the matching of chromosomes that must occur during reproduction:

The research also casts some interesting light on how species form in plants. CENH3 plays the same crucial role in cell division in all plants and animals. Usually, such important genes are highly conserved — their DNA is very similar from yeast to whales. But instead, CENH3 is among the fastest-evolving sequences in the genome.

“It may be that centromere differences create barriers to breeding between species,” Chan said. Ravi and Chan plan to test this idea by crossing closely-related species.

So gross. Here is a study that says when we take a shower any drugs and chemicals we may be using, help to cause water pollution:

“We’ve long assumed that the active ingredients from medications enter the environment primarily as a result of their excretion via urine and feces,” said Dr. Ruhoy. She directs the Institute for Environmental Medicine at Touro University in Henderson, Nev., and did the research with Christian Daughton, Ph.D., of the U.S. Environmental Protection Agency’s National Exposure Research Laboratory in Las Vegas. “However, for the first time, we have identified potential alternative routes for the entry into the environment by way of bathing, showering, and laundering. These routes may be important for certain APIs found in medications that are applied topically, which means to the skin. They include creams, lotions, ointments, gels, and skin patches.”

From the point of view a computer programmer, this is an overly obvious conversation:

Our genes may not be the basis for human individuality, according to new studies in Science and Nature. The key may actually lie in the sequences that surround and control our genes.

The interaction of those sequences with a class of proteins, called transcription factors, can vary significantly between two people and are likely to affect our appearance, our development and even our predisposition to certain diseases.

I might write, sarcastically, it’s almost as if the software that allows us to exist has a working state in which you can record variables that hold different values. On a more serious note, the comparison seems so obvious to me, I’m unclear why this seems like a surprise for geneticists. What is their working model of what goes on in the chromosomes?

The tone of surprise has me imagining some scene such as some geneticist sitting down next to some dude who plays Halo a lot. The geneticist asks how its going and the Halo gamer says “Pretty good. I lost the last game but this game I’m winning and I just got more grenades and more ammo” and the geneticist says “But that’s impossible. Microsoft hasn’t changed the software since the last time you played. If the source code is still the same, then whatever happened to you last time should also happen to you this time.”

In 2008 I recall reading that a group cloned pigs were growing up with as much diversity as any group of pigs. Which makes me think this idea should have been settled a long time ago.

I find it interesting that they might be close to figuring how if() statements are written in DNA:

“We developed a new approach which enabled us to identify cases where a protein’s ability to turn a gene on or off can be affected by interactions with another protein anchored to a nearby area of the genome,” Korbel explains. “With it, we can begin to understand where such interactions happen, without having to study every single regulatory protein out there.”

DNA, combined with the proteins that make up our chromosomes, resembles a solid state computer, in that the software and the working memory share the same medium. The genes make up the “software” that begins the process of creating us, but the rest of our DNA is given over to recording the working state of who we are:

A group of scientists led by Jan Korbel at EMBL and Michael Snyder initially at Yale and now in Stanford were the first to compare individually sequenced human genomes to look for what caused differences in gene regulation amongst ten different people. They focused on non-coding regions – stretches of DNA that lie between genes and, unlike genes, don’t hold the instructions for producing proteins. These DNA sequences, which may vary from person to person, can act as anchors to which regulatory proteins, known as transcription factors, attach themselves to switch genes on or off.

Korbel, Snyder, and colleagues found that up to a quarter of all human genes are regulated differently in different people, more than there are genetic variations in genes themselves. The scientists found that many of these differences in how regulatory proteins act are due to changes in the DNA sequences they bind to. In some cases, such changes can be a difference in a single letter of the genetic code, while in others a large section of DNA may be altered. But surprisingly, they discovered even more variations could not be so easily explained. They reasoned that some of these seemingly inexplicable differences might arise if regulatory proteins didn’t act alone, but interacted with each other.

Here is an oddly conservative statement:

Finally, Korbel, Snyder and colleagues compared the information on humans with that from a chimpanzee, and found that with respect to gene regulation there seems to be almost as much variation between humans as between us and our primate cousins – a small margin in which may lie important clues both to how we evolved and to what makes us humans different from one another.

In a study published online in Nature yesterday, researchers led by Snyder in the USA and Lars Steinmetz at EMBL in Heidelberg have found that similar differences in gene regulation also occur in an organism which is much farther from us in the evolutionary tree: baker’s yeast.

Do they simply not understand what they are looking at? Are they unaware that software has both code and state? As a point of comparison, If a friend of mine is playing a game of Halo, and Microsoft suddenly gave me the complete source code to Halo, would I know what was happening to my friend in the game? Of course not – how many times he’s been killed, how much ammo he has left, that would all be state, that would all be recored in working memory, it wouldn’t be in the source code. Or, another example, if I’m given the complete source code for Adobe Photoshop, I still know nothing about what images people, all across the world, might be editing at any given moment. Having source code doesn’t tell me state.

Why is this obvious to me and yet seemingly confusing to the biologists?

Boltzmann did a great deal to introduce statistics to science but most scientists of his generation fought against the idea and insisted that Newton’s mechanical view of the universe was correct. The true era of statistics began on December 14th of 1900, when Max Plank first presented the Planck postulate. Since that time, statistics have conquered science. If you were to list things that were dominant motifs of the 20th century, you might include skyscrapers, airplanes, rockets, penicillin and statistics.

Nevertheless, statistics are not the truth about our universe. They are a useful tool, but as a world view, they take us no closer to the truth than Newton’s mechanical universe. As I write these words, I’m thinking of what Kuhn said, that science adopts a new paradigm, not because it is a better representation of reality, but because it is useful to the work that scientists are now doing.

For these reasons, it is important to remember the many problems that science faces when relying on statistical methods:

Statistical problems also afflict the “gold standard” for medical research, the randomized, controlled clinical trials that test drugs for their ability to cure or their power to harm. Such trials assign patients at random to receive either the substance being tested or a placebo, typically a sugar pill; random selection supposedly guarantees that patients’ personal characteristics won’t bias the choice of who gets the actual treatment. But in practice, selection biases may still occur, Vance Berger and Sherri Weinstein noted in 2004 in ControlledClinical Trials. “Some of the benefits ascribed to randomization, for example that it eliminates all selection bias, can better be described as fantasy than reality,” they wrote.

Randomization also should ensure that unknown differences among individuals are mixed in roughly the same proportions in the groups being tested. But statistics do not guarantee an equal distribution any more than they prohibit 10 heads in a row when flipping a penny. With thousands of clinical trials in progress, some will not be well randomized. And DNA differs at more than a million spots in the human genetic catalog, so even in a single trial differences may not be evenly mixed. In a sufficiently large trial, unrandomized factors may balance out, if some have positive effects and some are negative. (See Box 3) Still, trial results are reported as averages that may obscure individual differences, masking beneficial or harm ful effects and possibly leading to approval of drugs that are deadly for some and denial of effective treatment to others.

“Determining the best treatment for a particular patient is fundamentally different from determining which treatment is best on average,” physicians David Kent and Rodney Hayward wrote in American Scientist in 2007. “Reporting a single number gives the misleading impression that the treatment-effect is a property of the drug rather than of the interaction between the drug and the complex risk-benefit profile of a particular group of patients.”

Another concern is the common strategy of combining results from many trials into a single “meta-analysis,” a study of studies. In a single trial with relatively few participants, statistical tests may not detect small but real and possibly important effects. In principle, combining smaller studies to create a larger sample would allow the tests to detect such small effects. But statistical techniques for doing so are valid only if certain criteria are met. For one thing, all the studies conducted on the drug must be included — published and unpublished. And all the studies should have been performed in a similar way, using the same protocols, definitions, types of patients and doses. When combining studies with differences, it is necessary first to show that those differences would not affect the analysis, Goodman notes, but that seldom happens. “That’s not a formal part of most meta-analyses,” he says.

Meta-analyses have produced many controversial conclusions. Common claims that antidepressants work no better than placebos, for example, are based on meta-analyses that do not conform to the criteria that would confer validity. Similar problems afflicted a 2007 meta-analysis, published in the New England Journal of Medicine, that attributed increased heart attack risk to the diabetes drug Avandia. Raw data from the combined trials showed that only 55 people in 10,000 had heart attacks when using Avandia, compared with 59 people per 10,000 in comparison groups. But after a series of statistical manipulations, Avandia appeared to confer an increased risk.

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.