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[Guest Alefshin]

Why the Miller–Urey research argues against abiogenesis

Dr Jerry Bergman

Summary

Abiogenesis is the theory that under the proper conditions life can arise spontaneously from non-living molecules. One of the most widely cited studies used to support this conclusion is the famous Miller–Urey experiment. Surveys of textbooks find that the Miller–Urey study is the major (or only) research cited to prove abiogenesis. Although widely heralded for decades by the popular press as ‘proving’ that life originated on the early earth entirely under natural conditions, we now realize the experiment actually provided compelling evidence for the opposite conclusion. It is now recognized that this set of experiments has done more to show that abiogenesis on Earth is not possible than to indicate how it could be possible. This paper reviews some of the many problems with this research, which attempted to demonstrate a feasible method of abiogenesis on the early earth.

Contemporary research has failed to provide a viable explanation as to how abiogenesis could have occurred on Earth. The abiogenesis problem is now so serious that most evolutionists today tend to shun the entire field because they are ‘uneasy about stating in public that the origin of life is a mystery, even though behind closed doors they freely admit that they are baffled’ because ‘it opens the door to religious fundamentalists and their god-of-the-gaps pseudo-explanations’ and they worry that a ‘frank admission of ignorance will undermine funding’.1

Abiogenesis was once commonly called ‘chemical evolution’,2 but evolutionists today try to distance evolutionary theory from the origin of life. This is one reason that most evolutionary propagandists now call it ‘abiogenesis’. Chemical evolution is actually part of the ‘General Theory of Evolution’, defined by the evolutionist Kerkut as ‘the theory that all the living forms in the world have arisen from a single source which itself came from an inorganic form’.3

Another reason exists to exaggerate abiogenesis claims—it is an area that is critical to proving evolutionary naturalism.4 If abiogenesis is impossible, or extremely unlikely, then so is naturalism.5–8

Darwin recognized how critical the abiogenesis problem was for his theory. He even conceded that all existing terrestrial life must have descended from some primitive life-form that was originally called into life ‘by the Creator’.9 But to admit, as Darwin did, the possibility of one or a few creations is to open the door to the possibility of many others! If God made one type of life, He also could have made many thousands of different types. Darwin evidently regretted this concession later and also speculated that life could have originated in some ‘warm little pond’ on the ancient earth.

The ‘warm soup’ theory

Although seriously challenged in recent years, the warm soup hypothesis is still the most widely held abiogenesis theory among Darwinists. Developed most extensively by Russian atheist Alexandr Ivanovich Oparin (1894–1980) in his book, The Origin of Life, a worldwide best seller first published in 1924 (the latest edition was published in 1965).10 Oparin ‘postulated that life may have evolved solely through random processes’ in what he termed a biochemical ‘soup’ that he believed once existed in the oceans. The theory held that life evolved when organic molecules that originally rained into the primitive oceans from the atmosphere were energized by forces such as lightning, ultraviolet light, meteorites, deep-sea hydrothermal vents, hot springs, volcanoes, earthquakes, or electric discharges from the sun. If only the correct mix of chemicals and energy were present, life would be produced spontaneously. Almost a half century of research and millions of dollars have been expended to prove this —so far with few positive results and much negative evidence.11

What sequence?

Oparin concluded that cells evolved first, then enzymes and, last, genes.12 Today, we recognize that genes require enzymes in order to function, but genes are necessary to produce enzymes. Neither genes nor cells can function without many complex structures such as ribosomes, polymerase, helicase, gyrase, single-strand–binding protein and scores of other proteins. Dyson concluded that Oparin’s theory was ‘generally accepted by biologists for half a century’ but that it ‘was popular not because there was any evidence to support it but rather because it seemed to be the only alternative to biblical creationism’.13

The Miller–Urey research

Haldane,14 Bernal,15 Calvin16 and Urey17 all published research in an attempt to support this model—each with little, if any, success. Then, in 1953 came what some then felt was a critical breakthrough by Harold Urey (1893–1981) of the University of Chicago and his 23-year-old graduate student, Stanley Miller (1930–). Urey came to believe that the conclusion reached by ‘many’ origin-of-life researchers that the early atmosphere was oxidizing must have been wrong; he argued instead that it was the opposite, namely a reducing atmosphere with large amounts of methane.18

Their ‘breakthrough’ resulted in front-page stories across the world that usually made the sensational claim that they had ‘accomplished the first step toward creating life in a test tube’.19 Carl Sagan concluded, ‘The Miller–Urey experiment is now recognized as the single most significant step in convincing many scientists that life is likely to be abundant in the cosmos.’20 The experiment even marked the beginning of a new scientific field called ‘prebiotic’ chemistry.21 It is now the most commonly cited evidence (and often the only evidence cited) for abiogenesis in science textbooks.22

Miller’s experiment13

The Miller–Urey experiments involved filling a sealed glass apparatus with the gases that Oparin had speculated were necessary to form life—namely methane, ammonia and hydrogen (to mimic the conditions that they thought were in the early atmosphere) and water vapour (to simulate the ocean). Next, while a heating coil kept the water boiling, they struck the gases in the flask with a high-voltage (60,000 volts) tungsten spark-discharge device to simulate lightning. Below this was a water-cooled condenser that cooled and condensed the mixture, allowing it to fall into a water trap below.23

Within a few days, the water and gas mix produced a pink stain on the sides of the flask trap. As the experiment progressed and the chemical products accumulated, the stain turned deep red, then turbid.24 After a week, the researchers analyzed the substances in the U-shaped water trap used to collect the reaction products.25 The primary substances in the gaseous phase were carbon monoxide (CO) and nitrogen (N2).21 The dominant solid material was an insoluble toxic carcinogenic mixture called ‘tar’ or ‘resin’, a common product in organic reactions, including burning tobacco. This tar was analyzed by the latest available chromatographic techniques, showing that a number of substances had been produced. No amino acids were detected during this first attempt, so Miller modified the experiment and tried again.20,26

In time, trace amounts of several of the simplest biologically useful amino acids were formed—mostly glycine and alanine.20 The yield of glycine was a mere 1.05%, of alanine only 0.75% and the next most common amino acid produced amounted to only 0.026% of the total—so small as to be largely insignificant. In Miller’s words, ‘The total yield was small for the energy expended.’27 The side group for glycine is a lone hydrogen and for alanine, a simple methyl (–CH3) group. After hundreds of replications and modifications using techniques similar to those employed in the original Miller–Urey experiments, scientists were able to produce only small amounts of less than half of the 20 amino acids required for life. The rest require much more complex synthesis conditions.

Oxygen: enemy of chemical evolution

The researchers used an oxygen-free environment mainly because the earth’s putative primitive atmosphere was then ‘widely believed not to have contained in its early stage significant amounts of oxygen’. They believed this because ‘laboratory experiments show that chemical evolution, as accounted for by present models, would be largely inhibited by oxygen’.28 Here is one of many examples of where their a priori belief in the ‘fact’ of chemical evolution is used as ‘proof’ of one of the premises, an anoxic atmosphere. Of course, estimates of the level of O2 in the earth’s early atmosphere rely heavily on speculation. The fact is, ‘We still don’t know how an oxygen-rich atmosphere arose.’29

It was believed that the results were significant because some of the organic compounds produced were the building blocks of much more complex life units called proteins—the basic structure of all life.30 Although widely heralded by the press as ‘proving’ that life could have originated on the early earth under natural conditions (i.e. without intelligence), we now realize the experiment actually provided compelling evidence for exactly the opposite conclusion. For example, without all 20 amino acids as a set, most known protein types cannot be produced, and this critical step in abiogenesis could never have occurred.

In addition, equal quantities of both right- and left-handed organic molecules (called a racemic mixture) were consistently produced by the Miller–Urey procedure. In life, nearly all amino acids that can be used in proteins must be left-handed, and almost all carbohydrates and polymers must be right-handed. The opposite types are not only useless but can also be toxic (even lethal) to life.31,32

Was there a methane–ammonia atmosphere?

According to many researchers today, an even more serious problem is the fact that the atmosphere of the early earth was very different from what Miller assumed. ‘Research has since drawn Miller’s hypothetical atmosphere into question, causing many scientists to doubt the relevance of his findings.’33 The problem was stated as follows:

   ‘… the accepted picture of the earth’s early atmosphere has changed: It was probably O2-rich with some nitrogen, a less reactive mixture than Miller’s, or it might have been composed largely of carbon dioxide, which would greatly deter the development of organic compounds.’34

A major source of gases was believed to be volcanoes, and since modern-day volcanoes emit CO, CO2, N2 and water vapour, it was considered likely that these gases were very abundant in the early atmosphere. In contrast, it is now believed that H2, CH4 and NH3 probably were not major components of the early atmosphere. Furthermore, many scientists now believe that the early atmosphere probably did not play a major role in the chemical reactions leading to life.20

Although the composition of the atmosphere of the early earth is now believed to have consisted of large amounts of carbon dioxide, this conclusion still involves much speculation. Most researchers also now believe that some O2 was present on the early earth because it contained much water vapour, and photodissociation of water in the upper layers of the atmosphere produces oxygen.35 Another reason is that large amounts of oxidized materials exist in the Precambrian geological strata.36

Yet another reason to conclude free oxygen existed on the early earth is that it is widely believed that photosynthetic organisms existed very soon after the earth had formed, something that is difficult for chemical evolutionary theories to explain. A 2004 paper argues from uranium geochemistry that there were oxidizing conditions, thus photosynthesis, at 3.7 Ga.37 But according to uniformitarian dating, the earth was being bombarded by meteorites up to 3.8 Ga. So even granting evolutionary presuppositions, this latest research shows that life existed almost as soon as the earth was able to support it, not ‘billions and billions of years’ later. Even if the oxygen were produced by photodissociation of water vapour rather than photosynthesis, this would still be devastating for Miller-type proposals.

The dilution problem

Urey also speculated that the oceans in the ancient earth must have consisted of about a 10% solution of organic compounds that would be very favourable for life’s origin.38 This level of organic matter would equal a concentration about 100 times higher than a modern American city’s sewer water. The total amount of extant organic compounds on the earth today could not produce even a fraction of that needed to achieve a concentration this high in the oceans.

Early hopes not realized

Modern replications of the Miller–Urey experiment using a wide variety of recipes, including low levels of O2, yield even lower amounts of organic compound than the original experiment.39 To solve this problem, some researchers have speculated that small, isolated pools of water achieved the required level of concentration. The same problem remains: No feasible method exists to account for this source. Some even speculate that ‘submerged volcanoes and deep-sea vents—gaps in the earth’s crust where hot water and minerals gush into deep oceans—may have provided the initial chemical resources’.40

To duplicate what might have happened in a primordial soup billions of years ago, scientists would need to mix the chemicals currently believed to be commonly found on the early earth, expose them to likely energy sources (usually speculated to be heat or radiation), and see what happens. No-one has performed this experiment, because we now know that it is impossible to obtain relevant biochemical compounds by this means. The Miller–Urey experiment held great hopes for the materialists, which have now given way to pessimism:

   ‘Soon after the Miller–Urey experiment, many scientists entertained the belief that the main obstacles in the problem of the origin of life would be overcome within the foreseeable future. But as the search in this young scientific field went on and diversified, it became more and more evident that the problem of the origin of life is far from trivial. Various fundamental problems facing workers in this search gradually emerged, and new questions came into focus … . Despite intensive research, most of these problems have remained unsolved.

   ‘Indeed, during the long history of the search into the origin of life, controversy is probably the most characteristic attribute of this interdisciplinary field. There is hardly a model or scenario or fashion in this discipline that is not controversial.’41

Some of these major problems will now be reviewed.

Functional proteins can exist only in very narrow conditions

To produce even non-functional amino acids and proteins, researchers must highly control the experiment in various ways because the very conditions hypothesized to create amino acids also rapidly destroy proteins. Examples include thermal denaturing of proteins by breaking apart their hydrogen bonds and disrupting the hydrophobic attraction between non-polar side groups.42 Very few proteins remain biologically active above 50ºC, or below about 30ºC, and most require very narrow conditions. Cooking food is a good example of using heat to denature protein, and refrigeration of using cold to slow down biological activity. As any molecular biologist knows from daily lab work, the pH also must be strictly regulated. Too much acid or base adversely affects the hydrogen bonding between polar R groups and also disrupts the ionic bonds formed by the salt bridges in protein.

Cross-reactions

Miller had to deal with the fact that the common cross-reactions of biochemical reaction products cause destruction or interfere with amino acid production. All compounds that interfere with bonding must be isolated or they will destroy the proteins. Therefore, Miller had to remove many contaminants and impurities to obtain pure compounds that are not normally found in life. Otherwise, his apparatus would have produced many destructive cross-reactions.

This is no small problem. Many organic compounds, such as ethanol and isopropyl alcohol, function as disinfectants by forming their own hydrogen bonds with a protein and, as a result, disrupt the proteins’ hydrophobic interactions.41 Alcohol swabs are used to clean wounds or to prepare skin for injections because the alcohol passes through cell walls and coagulates the proteins inside bacteria and other cells. Also, heavy metal ions such as Ag+, Pb2+ and Hg2+ must be isolated from proteins because they disrupt the protein’s disulfide bonds, causing the protein to denature. As an example, a dilute (1%) AgNO3 solution is placed in the eyes of newborn babies to destroy the bacteria that cause gonorrhea. Many heavy metal ions are very toxic if ingested because they severely disrupt protein structure, especially enzymes.

Another problem is that many of the other compounds necessary for life, such as sugar, also react strongly with amino acids and affect amino acid synthesis. For example, Miller and others had to use a sugar-free environment in their experiments.43 Miller stopped his experiment after just a few days, but if it had been allowed to go on, would the compounds he produced be destroyed or would they produce more complex amino acids? Research on Murchison meteorites found that natural conditions produce compounds much like Miller’s, and the result is stable—indicating that further time would not produce any new products.44

The Miller–Urey experiments produced many other compounds aside from amino acids, resulting in a sticky mass that was actually further from the building blocks of life than were the postulated original precursor chemicals. Toxic compounds produced include cyanides, carbon monoxide, and others—actually most of the dark matter in the solution could not be identified by the researchers in 1953.21

Undirected energy is disruptive

A critical question, ‘How much energy was necessary?’ has been much debated.45 However, all forms of energy can disrupt protein, including all of those forms postulated to be important in abiogenesis, such as UV and lightning.46

Many speculate that ultraviolet light was the source used to create life, but UV is highly toxic to life, and is, in fact, often used to destroy life (thus UV lights are used in hospitals to kill micro-organisms). The intensity of the destructive long wavelengths exceeds that of the constructive short ones, and the quantum efficiency of destruction is much higher than that for construction as well.47 This means that destruction of amino acids is four to five orders of magnitude higher than construction.

In Miller’s UV experiments, he used a select wavelength to produce amino acids and screened out other wavelengths because they destroy amino acids. Yet both chemical-building and chemical-destroying light exists in sunlight. Amino acids are actually very delicate and readily break down under natural sunlight.

The Miller–Urey experiment also had strategically designed traps to remove the products from the radiation before they could be destroyed. On a primitive earth, any amino acids formed in the atmosphere would be destroyed long before they could be removed. Even the ocean would not protect them, because UV penetrates several metres of liquid water—you can even sunburn under water. This indicates that the conditions on the early earth could never have been favourable for abiogenesis.

Even simple movement can cause major protein damage: whipping cream or beating egg whites is one way of using mechanical agitation to deliberately denature protein (the whipping stretches the polypeptide chains until the bonds break).

Miller’s research has, for the reasons discussed above, helped us to better understand why life could not have emerged naturally. In a summary of the famous Miller–Urey origin-of-life experiment, Horgan concluded that Miller’s results at first seemed to

   ‘… provide stunning evidence that life could arise from what the British chemist J.B.S. Haldane had called the “primordial soup.” Pundits speculated that scientists, like Mary Shelley’s Dr. Frankenstein, would shortly conjure up living organisms in their laboratories and thereby demonstrate in detail how genesis unfolded. It hasn’t worked out that way. In fact, almost 40 years after his original experiment, Miller told me that solving the riddle of the origin of life had turned out to be more difficult than he or anyone else had envisioned.’48

Creating life in a test tube also turned out to be far more difficult than Miller expected. Scientists now know that the complexity of life is far greater than Miller (or anyone else) imagined in 1953, prior to the DNA revolution.49 We now know that Miller’s

   ‘… much-touted experiments tell us very little about where real, functional proteins came from. Yet this inconvenient fact is rarely mentioned when headlines blare out the news that scientists have succeeded in creating the building blocks of life.’50

[Guest Alefshin]

Life is far more complex than Miller believed

About the same time as Darwin, T.H. Huxley proposed a simple, two-step method of chemical recombination that he thought could explain the origin of the first living cell. Both Haeckel and Huxley thought that just as salt could be produced spontaneously by mixing powered sodium metal and heated chlorine gas, a living cell could be produced merely by mixing the few chemicals they believed were required. Haeckel taught that the physical basis of life is a substance he called ‘plasm’ of different types such as ‘colourless’ and ‘also red, orange, and other kinds of protoplasm’ that were comparable in complexity and texture to a pot of glue or cold jelly.51

Haeckel also believed that the first single cell owed its ‘existence to spontaneous creation’ from inorganic compounds, primarily ‘carbon, hydrogen, oxygen, and nitrogen’.52 Once the brew was mixed, Huxley concluded eons of time allowed spontaneous chemical reactions to produce the simple ‘protoplasmic substance’ that scientists once assumed was the essence of life.53 As late as 1928, the cell was still thought to be relatively simple, and few scientists then questioned the belief that life commonly developed from relatively simple to relatively complex forms. They also thought evolution was ‘the formation of new structures and functions by combinations and transformations of the relatively simple structures and functions of the germ cells.’54

We now also realize, after a century of research, that the eukaryote protozoa, believed in Darwin’s day to be as simple as a bowl of gelatin, are actually enormously complex. A living eukaryotic cell contains many hundreds of thousands of different complex parts, including various motor proteins. These parts must be assembled correctly to produce a living cell, the most complex ‘machine’ in the universe—far more complex than a Cray supercomputer. Furthermore, molecular biology has demonstrated that the basic design of the cell is

   ‘… essentially the same in all living systems on earth from bacteria to mammals. … In terms of their basic biochemical design … no living system can be thought of as being primitive or ancestral with respect to any other system, nor is there the slightest empirical hint of an evolutionary sequence among all the incredibly diverse cells on earth.’55

This finding poses major difficulties for abiogenesis because life at the cellular level generally does not reveal a gradual increase in complexity as it allegedly ascends the evolutionary ladder from protozoa to humans. The reason why the molecular machinery and biochemistry of modern organisms is basically similar is that the basic biochemical requirements and constraints are the same for all life.56

The polymerization problem

The Miller–Urey experiment left many critical questions unanswered, even such basic ones as, ‘How did the chemicals combine to form the first molecules of living organisms?’34 Chemicals do not produce life; only complex structures such as DNA and enzymes produce life. Also, even if the source of the amino acids and the many other compounds needed could be explained, how these many diverse elements became aggregated in the same area and then properly assembled themselves must still be dealt with. This problem is a major stumbling block to all abiogenesis theories because

   ‘… no one has ever satisfactorily explained how the widely distributed ingredients linked up into proteins. Presumed conditions of primordial earth would have driven the amino acids toward lonely isolation. That’s one of the strongest reasons that Wächtershäuser, Morowitz, and other hydrothermal vent theorists want to move the kitchen [that cooked life] to the ocean floor. If the process starts down deep at discrete vents, they say, it can build amino acids—and link them up—right there.’33

The amino acid assembly problem is complicated by the fact that amino acids are able to bond in many locations by many kinds of chemical bonds. To form polypeptide chains requires restricting the links to only peptide bonds, and only in the correct locations. All other bonds must be prevented from being formed, no easy task. In living cells, a complex control system involving enzymes exists to ensure that inappropriate bonds do not normally occur; without this system, these inappropriate bonds would destroy the proteins produced.

To form a protein, amino acids must link together to form a peptide bond, eliminating a water molecule. But there is a far greater tendency for the reverse to happen. This would be even more of a problem in water.

Another problem is that the strong thermodynamic tendency is for the peptide bonds to break down in water, not to form.57 Without high-energy compounds such as ATP and enzymes, amino acids do not form the many polypeptides needed for life. Even dipeptides are difficult to form under natural conditions, yet the average protein is composed of around 400 amino acids.

Several recent discoveries have led some scientists to conclude that life may have arisen in submarine vents, where temperatures approach 350ºC. Unfortunately for both warm-pond and hydrothermal-vent theorists, the extreme heat has proven to be a major downfall of their theories. This is because high temperatures would accelerate the breakdown of amino acids, just as cooking meat breaks down the bonds, causing meat to become more tender.57

Another theory is that abiogenesis may have been a consequence of the ‘self-ordering properties’ of biochemicals.58 Just as electrostatic forces produce highly ordered crystals of salt from Na+ and Cl– ions, so too, some Darwinists reasoned, in the same way, life may likewise self-assemble. This approach also has failed. For example, all nucleotide base pairs have an equal affinity to the sugar phosphate backbones on each side of the DNA molecule, and consequently, their order is not a result of bonding affinity differences but is due to information-directed assembly. In other words, the information does not derive from the DNA chemistry, but is instead external to it (see next section).

Miller himself has recognized that Kauffman’s research is not viable and, consequently, he was

   ‘… unimpressed with any of the current proposals on the origin of life, referring to them as “nonsense” or “paper chemistry.” He was so contemptuous of some hypotheses that, when I asked his opinion of them, he merely shook his head, sighed deeply, and snickered—as if overcome by the folly of humanity. Stuart Kauffman’s theory of autocatalysis fell into this category. “Running equations through a computer does not constitute an experiment,” Miller sniffed. Miller acknowledged that scientists may never know precisely where and when life emerged. “We’re trying to discuss a historical event, which is very different from the usual kind of science, and so criteria and methods are very different,” he remarked.’59

Information content

Another major reason the Miller–Urey experiments failed to support abiogenesis was that, although amino acids are the building blocks of life, a critical key to life is the information code stored in DNA (or, as in the case of retroviruses, RNA), depending on the sequence of nucleotides. This in turn provides the instructions for the amino acid sequences for the proteins, the machinery of life.60,61 Michael Polanyi (1891–1976), former chairman of physical chemistry at the University of Manchester (UK) who turned to philosophy, affirmed a very important point—the information was something above the chemical properties of the building blocks:

   ‘As the arrangement of a printed page is extraneous to the chemistry of the printed page, so is the base sequence in a DNA molecule extraneous to the chemical forces at work in the DNA molecule. It is this physical indeterminacy of the sequence that produces the improbability of any particular sequence and thereby enables it to have a meaning—a meaning that has a mathematically determinate information content.’62

Paul Davies reinforced the point that obtaining the building blocks would not explain their arrangement:

   ‘… just as bricks alone don’t make a house, so it takes more than a random collection of amino acids to make life. Like house bricks, the building blocks of life have to be assembled in a very specific and exceedingly elaborate way before they have the desired function.’63

An analogy is written language. Natural objects in forms resembling the English alphabet (circles, straight lines, etc.) abound in nature, but this fact does not help to understand the origin of information (such as that in Shakespeare’s plays). The reason is that this task requires intelligence both to create the information (the play) and then to design and build the machinery required to translate that information into symbols (the written text). What must be explained is the source of the information in the text (the words and ideas), not the existence of circles and straight lines. Likewise, it is not enough to explain the origin of the amino acids, which correspond to the letters. Rather, even if they were produced readily, the source of the information that directs the assembly of the amino acids contained in the genome must be explained.34

Another huge problem is that information is useless unless it can be read. But the decoding machinery is itself encoded on the DNA. The leading philosopher of science, Karl Popper (1902–1994), expressed the huge problem:

   ‘What makes the origin of life and of the genetic code a disturbing riddle is this: the genetic code is without any biological function unless it is translated; that is, unless it leads to the synthesis of the proteins whose structure is laid down by the code. But … the machinery by which the cell (at least the non-primitive cell, which is the only one we know) translates the code consists of at least fifty macromolecular components which are themselves coded in the DNA. Thus the code can not be translated except by using certain products of its translation. This constitutes a baffling circle; a really vicious circle, it seems, for any attempt to form a model or theory of the genesis of the genetic code.

   ‘Thus we may be faced with the possibility that the origin of life (like the origin of physics) becomes an impenetrable barrier to science, and a residue to all attempts to reduce biology to chemistry and physics.’64

That is, the genetic information and the required reading machinery form an irreducibly complex system. So far, it has eluded materialistic explanations.65

The two enantiomers of a generalized amino acid, where R is any functional group (except H)

The chirality problem

What Sarfati66 calls a ‘major hurdle’ is the origin of homochirality, the fact that all amino acid biomolecules with rare exceptions (such as some used in bacterial cell walls) are all left-handed; and with rare exceptions, all sugars, including those in nucleic acids, are right-handed. Those produced in a laboratory are a half left-handed and half right-handed mixture called a racemate. Even in the laboratory, chemists use pre-existing homochirality from a biological source in order to synthesize homochiral compounds.60 Chiral molecules are dissymmetric—they exist as mirror images of each other, just as the right hand is a mirror image of the left hand (the word chiral comes from the Greek word for ‘hand’). The problem is left-handed sugars and right-handed amino acids can be toxic and prevent abiogenesis. Furthermore, most all enzymes are designed to work only with right-handed sugars and left-handed amino acids. All attempts to solve the chirality problem, including magnetochiral dichroism, have failed.67

The legacy of the Miller experiment

A major unresolved question that ‘involves psychology and history more than chemistry’ is, ‘Why has the Miller–Urey experiment had such a strong impact on the origin-of-life field?’68 Shapiro concludes a major reason is that the experiment seems to imply that we are on the verge of understanding how life was created without intelligence or design. In the public mind (and in the minds of many scientists) this experiment psychologically supports abiogenesis. But the Miller–Urey results, and the many similar experiments completed since then, actually show the opposite of what the Miller–Urey experiment purported to demonstrate. Few textbooks actually analyze the results, and most uncritically accept this experiment as proof of how the building blocks of life were produced and then imply that the only task left was to determine how they were assembled.

My review of college textbooks found that most discussed the Miller–Urey experiments, some extensively, but few texts mentioned any of the problems. Most implied that the research has conclusively shown how the building blocks of life spontaneously generated. In part, due to the common claims in textbooks and museum exhibits, many people assume that a good, if not excellent, case exists for the Miller–Urey thesis. Davies noted that when he set out to write a book on the origin of life, he ‘was convinced that science was close to wrapping up the mystery of life’s origins’, but after spending ‘a year or two researching the field’, he is

   ‘… now of the opinion that there remains a huge gulf in our understanding … . This gulf in understanding is not merely ignorance about certain technical details, it is a major conceptual lacuna.’69

The Miller–Urey experiment is now an icon of evolution, presented in most all biology, zoology and evolution textbooks as clear evidence of abiogenesis, when it actually illustrates the many difficulties of chemical evolution.22

The current status of the Miller–Urey line of research

In an interview with Stanley Miller, now considered one of ‘the most diligent and respected origin-of-life researchers’ in the world, after he completed his 1953 experiment, he ‘dedicated himself to the search for the secret of life’ but was also ‘quick to criticize what he feels is shoddy work’ in an effort to overcome the fact that the origin-of-life field has ‘a reputation as a fringe discipline, not worthy of serious pursuit’.59 Miller vowed that one day

   ‘ … scientists would discover the self-replicating molecule that had triggered the great saga of evolution … . [and] the discovery of the first genetic material [will] legitimize Millers’ field. “It would take off like a rocket,” Miller muttered through clenched teeth. Would such a discovery be immediately self-apparent? Miller nodded. “It will be in the nature of something that will make you say, ‘… How could you have overlooked this for so long?’ And everybody will be totally convinced”.’59

This hope has become less realistic as our knowledge has advanced. What we have learned, especially during the past few years, makes it less likely than ever that abiogenesis was ever possible.36,70,71 Yet the Miller–Urey experiment is now the classic, best-known origin-of-life experiment, cited in texts from high school to graduate school, in areas ranging from biology to geology and philosophy to religion.20,22 Phillip Johnson summed up the whole Miller–Urey research problem as follows:

   ‘Because post-Darwinian biology has been dominated by materialist dogma, the biologists have had to pretend that organisms are a lot simpler than they are. Life itself must be merely chemistry. Assemble the right chemicals, and life emerges. DNA must likewise be a product of chemistry alone. As an exhibit in the New Mexico Museum of Natural History puts it, “volcanic gases plus lightning equal DNA equals LIFE!” When queried about this fable, the museum spokesman acknowledged that it was simplified but said it was basically true.’72

Conclusion

It is now recognized that the Miller–Urey line of research is simply a ‘revival of the antique notion of spontaneous generation’ because it

   ‘… suggests that given the primordial soup, with the right combination of amino acids and nucleic acids, and perchance a lightning bolt or two, life might in fact have begun “spontaneously”. The major difference is that according to what biologists customarily called spontaneous generation, life supposedly began this way all of the time. According to the “soup” suggestion, by contrast, it began this way only once in the immeasurably distant past.’73

We must conclude, as Ridley did, that the early forms of life, and how natural selection could shape them, are ‘so obscure at the primordial stage that we can only guess why complexity might have increased’.

Darwin thought about the question inconclusively. He once wrote to the geologist Charles Lyell about a question ‘which is very difficult to answer, viz. how at first start of life, when there were only simplest organisms, how did any complication of organisms profit them? I can only answer that we have not facts enough to guide any speculation on the subject.’ We have more facts now, but they are still inadequate, and Darwin’s answer still holds.74

When confronted with this evidence, supporters of abiogenesis argue that science must be naturalistic, and we have no choice but to tell the best story we have, even if it is not a complete or even accurate story.4 Although widely heralded by the popular press for decades as ‘proof’ that life originated on the early earth entirely by natural conditions, the Miller–Urey experiments have actually provided compelling evidence for exactly the opposite conclusion. This set of experiments—more than almost any other carried out by modern science—has done much more to show that abiogenesis is not possible on Earth than to indicate how it could be possible.

Acknowledgments

I want to thank Tim Wallace, Bert Thompson, Wayne Frair, Clifford Lillo and John Woodmorappe for their comments on an earlier draft of this article.

References

  1. Davies, P., The Fifth Miracle: The Search for the Origin and Meaning of Life, Simon & Schuster, New York, pp. 17–18, 1999.

  2. Dickerson, R.E., Chemical evolution and the origin of life, Scientific American 239(3):62–102, 1978.

  3. Kerkut, G.A., Implications of Evolution, Pergamon, Oxford, UK, p. 157, 1960.

  4. Johnson, P., Reason in the Balance; The Case Against Naturalism in Science, Law and Education, InterVarsity Press, Downers Grove, 1995.

  5. Dover, G., Looping the evolutionary loop; review of: The Origins Of Life: From The Birth Of Life To The Origin Of Language, Nature 399:217–218, 1999.

  6. Dawkins, R., Climbing Mount Improbable, W.W. Norton, New York, 1996.

  7. de Duve, C., Vital Dust: Life as a Cosmic Imperative, Basic Books, New York, 1995.

  8. Denton, M., Nature’s Destiny; How the Laws of Biology Reveal Purpose in the Universe, The Free Press, New York, 1998.

  9. Darwin, C., Origin of Species, reprint of 6th edition, P.F. Collier, New York, p. 316, 1900. This concession to theism was absent in earlier editions.

 10. Oparin, A., The Origin of Life, New York, Dover, 1965.

 11. Poundstone, W., Carl Sagan; A Life in the Cosmos, Henry Holt, New York, 1999.

 12. Dyson, F., Origins of Life, Cambridge University Press, p. 31, 1990.

 13. <users.rcn.com/jkimball.ma.ultranet/BiologyPages/A/AbioticSynthesis.html>, 13 May 2004.

 14. Bernal, J.D., The physical basis of life, Physical Society of London Proceedings, Section A 62:537, 1947.

 15. Haldane, J.B.S., Rationalist Annual, 1928; reprinted in: Science and Human Life, Harper and Brothers, New York, 1933.

 16. Calvin, M., Reduction of carbon dioxide in aqueous solutions by ionizing radiation, Science 114:416–418, 1951.

 17. Urey, H., The Planets: Their Origin and Development, Yale University Press, New Haven, pp. 149–157, 1952.

 18. Lewis, R., Life, 3rd edition, WCB McGraw-Hill, Boston, p. 153, 1999.

 19. Colson, C. and Pearcey, N., How Now Shall We Live? Tyndale House, Wheaton, p. 69, 1999.

 20. Shapiro, R., Origins; A Skeptics Guide to the Creation of Life on earth, Summit Books, New York, p. 99, 1986.

 21. Lahav, N., Biogenesis: Theories of Life’s Origin, Oxford University, New York, 1999.

 22. Wells, J., Icons of Evolution, Regnery, Washington, 2000.

 23. Campbell, N.A., Mitchell, L.G. and Reece, J.B., Biology Concepts and Connections, 3rd edition, Addison Wesley Longman, Inc., San Francisco, 2000.

 24. Miller, S.L., A production of amino acids under possible primitive earth conditions, Science 117:528–529; p. 528, 1953.

 25. Shapiro, ref. 20, p. 100.

 26. Miller, S.L., Production of some organic compounds under possible primitive earth conditions, J. American Chemical Society 77:2351–2361, 1955.

 27. Miller, ref. 24, p. 529.

 28. Fox, S. and Dose, K., Molecular Evolution and the Origin of Life, Marcel Dekker, New York, p. 44, 1977.

 29. Sleep, N.H., Biogeochemistry; oxygenating the atmosphere, Nature 410:317–319; 2001, p. 319.

 30. Horgan, J., The End of Science: Facing the Limits of Knowledge in the Twilight of the Scientific Age, Addison-Wesley, Reading, p. 130, 1996.

 31. Jamali, F., Lovlin, R., Corrigan, B.W., Davies, N.M. and Aberg, G., Stereospecific pharmacokinetics and toxicodynamics of ketorolac after oral administration of the racemate and optically pure enantiomers to the rat, Chirality 11(3):201–205, 1999.

 32. Coppedge, J.F., Probability of left-handed molecules, CRSQ 8:163–174, 1971.

 33. Simpson, S., Life’s first scalding steps, Science News 155(2):24–26, 1999; p. 26.

 34. Flowers, C., A Science Odyssey: 100 Years of Discovery, William Morrow and Company, New York, p. 173, 1998.

 35. Scherer, S., Could life have arisen in the primitive atmosphere? J. Molecular Evolution 22(1):91–94, 1985; p. 92.

 36. Thaxton, C., Bradley, W. and Olsen, R., The Mystery of Life’s Origin; Reassessing Current Theories, ch. 5, Philosophical Library, New York, 1984.

 37. Rosing, M.T. and Frei, R., U-rich Archaean sea-floor sediments from Greenland—indications of >3700 Ma oxygenic photosynthesis, Earth and Planetary Science Letters 217: 237–244, 2004.

 38. Urey, ref. 17, p. 153.

 39. Campbell, N.A., Biology, Benjamin/Cummings, Redwood City, 1993.

 40. Campbell et al., ref. 23, p. 321.

 41. Lahav, ref. 21, p. 50.

 42. Timberlake, K., Chemistry: An Introduction to General, Organic, and Biological Chemistry, Benjamin Cummins, San Francisco, 2001.

 43. Witham, L., By Design: Science and the Search for God, Encounter Books, San Francisco, p. 106, 2003.

 44. Witham, ref. 43, p. 98.

 45. Vogel, G., RNA study suggests cool cradle of life, Science 283(5399):155–156, 1999.

 46. Williams, E.L., The evolution of complex organic compounds from simpler chemical compounds: is it thermodynamically and kinetically possible? CRSQ 4:30–35, 1967.

 47. Hulett, H.R., Limitations on Prebiological Synthesis, Journal of Theoretical Biology 24:56–72, 1969.

 48. Horgan ref. 30, p. 138.

 49. Yockey, H.P., Information Theory and Molecular Biology, Cambridge University Press, Cambridge, p. 336, 1992.

 50. Colson and Pearcey, ref. 19, p. 71.

 51. Haeckel, E., The Last Link: Our Present Knowledge of the Descent of Man, Adam and Charles Black, London, p. 120, 1898.

 52. Haeckel, ref. 51, p. 48.

 53. Meyer, S., DNA and other designs, First Things, April, pp. 30–38, 2000; p. 31.

 54. Conklin, E.G., Embryology and evolution; in: Mason, F. (Ed.), Creation by Evolution, Macmillan, New York, pp. 63–64, 1928.

 55. Denton, M., Evolution: A Theory in Crisis, Adler and Adler, Bethesda, p. 250, 1986.

 56. Cairns-Smith, A.G., The first organisms, Scientific American 252(6):90–100, 1985.

 57. Sarfati, J., Origin of life: the polymerization problem, TJ 12(3):281–284, 1998.

 58. Kauffman, S., The Origins of Order, Oxford University Press, New York, 1993; At Home in the Universe, Oxford University Press, New York, 1995.

 59. Horgan, ref. 30, p. 139.

 60. Pigliucci, M., Where do we come from? A humbling look at the biology of life’s origin, Skeptical Inquirer 23(5):21–27, 1999.

 61. Dembski, W.A., The Design Inference: Eliminating Chance Through Small Probabilities, Cambridge University Press, Cambridge, England, 1998.

 62. Polanyi, M., Life’s irreducible structure, Science 160:1308, 1968.

 63. Davies, P., Life force, New Scientist 163(2204):27–30, 1999; p. 28.

 64. Popper, K.R., Scientific reduction and the essential incompleteness of all science; in: Ayala, F. and Dobzhansky, T. (Eds.), Studies in the Philosophy of Biology, University of California Press, Berkeley, p. 270, 1974.

 65. Sarfati, J., Self-replicating Enzymes? A critique of some current evolutionary origin-of-life models, TJ 11(1):4–6, 1997.

 66. Sarfati, J., Origin of life: the chirality problem, TJ 12(3)263–266, 1998.

 67. Sarfati, J., Origin of life and the homochirality problem: is magnetochiral dichroism the solution? TJ 14(3)9–12, 2000.

 68. Shapiro, ref. 20, p. 107.

 69. Davies, ref. 1, p. 17.

 70. Levy, M. and Miller, S.L, The stability of the RNA bases: Implications for the origin of life, Proc. Nat. Acad. Sci. USA 95:7933–7938, 1998.

 71. Behe, M., Darwin’s Black Box, Basic Books, New York, 1996.

 72. Johnson, P., Weekly Wedge Update, April 30, p. 1, 2001.

 73. Serafini, A., The Epic History of Biology, Plenum, New York, p. 292, 1993.

 74. Ridley, M., The Cooperative Gene; How Mendel’s Demon Explains the Evolution of Complex Beings, The Free Press, New York, p. 84, 2001.

http://www.answersingenesis.org/tj/v18/i2/abiogenesis.asp

[Guest Alefshin]

Are wisdom teeth (third molars) vestiges of human evolution?

by Jerry Bergman

Summary

Evolutionists have taught that humans evolved from ape-like ancestors that possessed larger jaws and teeth than us. In the process of evolution the jaw has become smaller, allowing less room for the third molars and causing numerous dental problems. Our better understanding of the complex teeth-jaw relationship has revealed this explanation is far too simplistic. Research now indicates that the reasons for most third molar problems today are not due to evolutionary changes but other reasons. These reasons include a change from a coarse abrasive diet to a soft western diet, lack of proper dental care, and genetic factors possibly including mutations. Common past dental practice was a tendency to routinely remove wisdom teeth. Recent empirical research has concluded that this practice is unwise. Third molars in general should be left alone unless a problem develops and then they should be treated as any other teeth. At times removal is required, but appropriate efforts to deal with problem teeth should be implemented before resorting to their extraction.

Introduction

A major conclusion of evolution is that the human jaw has shrunk from its much larger ape size to the smaller modern human size as humans evolved. In short, evolution has produced ‘an increase in brain size at the expense of jaw size.’1 In the process, the jaw has became too small for the last teeth to erupt which are normally the third molars, often called wisdom teeth. This view is usually explained as follows:

   ‘ ... our ancestors had larger jaws, so there was room in the human mouth for 32 permanent teeth, including third molars—wisdom teeth. But now our jaws are smaller. The result: There’s no longer room in most of our mouths to house 32 teeth. So the last teeth we develop—our wisdom teeth—often become impacted, or blocked from erupting.’2

In the words of Liggett, as ‘primitive man learned to ... break up his food with his hands ... the jaw and brow ridge gradually became less prominent’ due to evolution.3 The third molars are often labeled vestigial (of use in the past but not today) and used as evidence to support human evolution from a hypothetical less evolved primate ancestor.4-8 The following discussion in a once-widely used biology textbook is typical of this view:

   ‘The “wisdom teeth,” or last molars, are in man approaching a vestigial condition, since they generally do not appear until relatively late, between the ages of twenty and thirty years, and in many persons are never cut at all. In a large percentage of individuals, they are useless, and they often become impacted and have to be removed surgically.’9

The vestigial organ view was also found in the medical text books of this generation:

   ‘It is a well known fact that nature tries to eliminate that which is not used … Likewise, civilization, which has eliminated the human need for large, powerful jaws, has decreased the size of our maxillae and mandibles. As a direct result, in a surprisingly large number of adults, the lower third molar occupies an abnormal position and may be considered a vestigial organ without purpose and function. This has been termed the phylogenic theory. It implies that, because throughout the history of man the jaws decreased in size from a lack of function, some present-day adults do not have room for a full complement of teeth, and the third molar, being the last to erupt, is denied room to accommodate itself … ’10

   ‘The loss of an organ in evolution purely as a result of disuse, also called Lamarckian Evolution, has now been thoroughly disproved. The belief that wisdom teeth are vestigial organs that lack a function in the body (as was previously believed for the appendix), is less common today but still evident. It is also commonly assumed by the general public.’

The putative problem is that humans today have smaller jaws but just as many teeth as their evolutionary antecedents.11–13 The result is the common assumption that most humans do not have enough room in their mouth for wisdom teeth which lack a function and only cause us much health trouble.14 This view was evidently first widely propounded by Darwin, who concluded:

   ‘ ... the posterior molar or wisdom-teeth were tending to become rudimentary in the more civilized races of man. … They do not cut through the gums till about the seventeenth year, and I have been assured that they are much more liable to decay, and are earlier lost than the other teeth; but this is denied by some eminent dentists. They are also much more liable to vary, both in structure and in the period of their development, than the other teeth. In the Melanin races, on the other hand, the wisdom-teeth are usually furnished with three separate fangs, and are generally sound; they also differ from the other molars in size, less than in the Caucasian races. Prof. Schaaffhausen accounts for this difference between the races by “the posterior dental portion of the jaw being always ‘shortened’” ... I am informed by Mr. Brace that it is becoming quite a common practice in the United States to remove some of the molar teeth of children, as the jaw does not grow large enough for the perfect development of the normal number.’15

Although Darwin believed that soft diets may have influenced lack of jaw development in modern humans, many later evolutionists concluded the combination of the evolution of a jaw smaller than our ape-like ancestors and tooth number and size which have not correspondingly evolved was a far more critical reason for the current wisdom teeth problem.

Challenges to the evolution view

The conclusion that a smaller jaw cannot contain the large teeth we inherited from our ancestors, and consequently wisdom teeth are not needed, has recently been challenged on several fronts. Macho and Moggi-Cecchi17 concluded that compared to other primates the third molars are the smallest in Homo sapiens. Further, if the third molars are forced to develop in a more restricted space ‘they tend to be smaller than anterior’ teeth and ‘in humans this reduction often leads to agenesis [failure of an organ to develop] of the third molars.’18 Dental crowding in whites ‘seems more related to smaller alveolar space than to smaller jaws overall or to larger teeth.’19 Furthermore, in an extensive study of aberrant maxillary third molars, Taylor found a lack of evidence for a genetic trend towards elimination of the third molar from human dentition as assumed by many evolutionists.20

The problem is usually primarily with the lower third molars. A major problem with this belief is it is difficult to identify what advantage a smaller jaw would have for survival.21 Evolution of a smaller jaw would at best be a result of devolution, dysgenics caused by the accumulation of mutations. Determining tooth evolution is also extremely problematic. Although measurements of unworn unerupted fossil teeth can be measured accurately, once in occlusion, teeth ‘are subject to wear, making it virtually impossible to accurately record crown components on teeth ... ’ in the fossil record.22

It is now widely acknowledged day that these teeth are not rudimentary or vestigial: they aid in chewing our food as do all of our other 28 teeth. The outdated vestigial organ conclusion, though, has influenced the extraction of billions of teeth, the removal of many which may have been unnecessary according to current research.23

One result of this belief

Wisdom teeth extraction was for many years one of the more common surgical interventions in the Western world.24 Leff25 and others claim that a significant percent of third molars that are extracted could be saved. This observation is supported by the fact that extraction rates are influenced by local beliefs and for this reason vary considerably.26 In America some estimate 20% of all young people with otherwise healthy teeth develop impacted wisdom teeth requiring medical attention, yet in the past some estimate nine out of ten American teenagers who have dental insurance lost their wisdom teeth.27 One report concluded the cost of this operation may exceed that of most routine medical or dental procedures.28

Many dentists once routinely advised extraction of all wisdom teeth, regardless of whether they were causing problems—some even routinely removed wisdom teeth during adolescence if it only appeared that they might later become impacted29,30 McGuire even once advised, ‘in most cases’ wisdom teeth should be pulled (emphasis mine).31

Another problem cited for their removal is the possibility of cysts and tumors developing in the sac surrounding an impacted wisdom tooth. This abnormality, though, is relatively rare—usually around one percent of all impacted third molars are surrounded by cysts, although one study found the rate was 11%.32,33 Further, as cyst development is generally extremely slow, this concern can often be monitored and dealt with before it effects a significant amount of bone. Tumors are also rarely a problem and in a study reviewed by Leff involved only about ‘roughly one in a million impacted wisdom teeth.’34

One reason they were believed to cause problems was that the wisdom teeth normally erupt last, between 18 and 25 years of age. Consequently it was assumed that if not enough room existed in the jaw, teeth crowding will result. Since they erupt at about the time when the youth goes off into the world to become ‘wise’ the name ‘wisdom teeth’ was used to describe them.35 In 13–15% of patients they never develop and only from 9 to 24% of all cases do they become impacted, usually because they are pointed in the wrong direction when they break through the gum, causing them to push against the second molar.36

Reason often given in the past for removal include the belief that wisdom teeth can push the other teeth forward, causing crowding. Claims that they usually cause damaging crowding have not held up under the scrutiny of recent empirical studies.37 Although third molars have the greatest incidence of impaction of all teeth, the impaction risk is much smaller than the proponents of prophylactic odontectomy (the routine removal of asymptomatic unerupted teeth) claim.38 This conclusion is based on several large studies of impacted wisdom teeth involving thousands of cases.

Prophylactic extraction was not uncommonly based more upon assumptions about human evolution than scientific research.39,40 As Leff concludes, ‘there is virtually no evidence’ to support the claim that wisdom teeth push other teeth forward.41 In a long-term study Little et al.42 found that all teeth tend to drift forward at least into middle age whether or not the wisdom teeth have been removed (see also Cuozzo43). In an excellent study Southard concluded that ‘crowding cannot be prevented simply by extracting unerupted third molars’44 and that ‘removing these teeth for the exclusive purpose of relieving interdental force and thereby preventing incisor crowding is unwarranted.’45

Numerous other studies support this conclusion. Samsudin and Mason46 found, in their sample of 423 patients that were scheduled for wisdom teeth removal, that only 5% were assessed by the orthodontists as needing removal because of crowding. The problem of front teeth crowding evidently usually occurs for several reasons including because alveolar bone base is too small for the tooth size and shape, lack of attrition, soft tissue maturation, and mesial drift.47,48

‘Jaw and maxillary shelf size are individual genetic traits that vary according to a normal curve as do all human dimensions. Some individuals inherit very small maxillary sinus, and those toward the smaller end of the normal curve may sometimes experience wisdom teeth problems. An example is when a petite woman marries a large man and the children inherit a jaw structure that cannot completely accommodate their teeth.’49,50 These cases, though, are relatively few and are not the norm.51

Wisdom teeth problems are more common among European whites compared to Orientals and blacks.52 This conclusion is supported by research on dental problems and race that concluded that racial differences exist ‘ … in the contemporary human races with regard to occlusion, tooth size, and tooth shape … It is tempting to suppose that interbreeding would exacerbate malocclusion and increase the number of impactions.’53

This may be true partly because certain jaw shapes and sizes are associated with third molar impaction and jaw traits are an inherited trait.54 However, this is only one factor. The major factors, the size of the jaw, maxillary sinus and teeth, all vary widely in all races. A set of studies by Chung55 and Neiswander56 found significant differences in mandibles existed in the population they studied which were evidently due to a dominant gene which produced different risks of malocclusion.

In another study of race, Barrett did not find a single case of an impacted third molar in his sample of 69 adult Yeundumu aborigines.57 Yeundumu generally have large maxillary sinus but they also usually have large teeth. A problem may result when either intergroup or intragroup marriage produces a child with large teeth and a small maxillary sinus which causes crowding, or a large maxillary sinus and small teeth which results in excess tooth spacing.57 Barrett notes the diet of the Yeundumu is now less abrasive and softer, consequently wisdom teeth and other tooth problem may be more likely in the newer generations.

Curtis58 found that both predynastic Egyptians and Nubians rarely had wisdom teeth problems, but they often existed in persons living in later periods of history. He concluded that the maxillary sinus of the populations he compared were similar and attributed the impactions he found to diet and also disuse causing atrophy of the jaws which resulted in a low level of teeth attrition. Dahlberg59 in a study of American Indians found that mongoloid peoples have a higher percentage of agenesis of third molars then do other groups and few persons in primitive societies had wisdom teeth problems. As Dahlberg notes, third molars were ‘very useful in primitive societies’ to chew their coarse diet.60

Prophylactic removal concerns

For generations many dentists recommended extraction of impacted wisdom teeth because the procedure in the young was ‘much easier than in later years, when the bone becomes more dense. Also, the younger the patient the better the procedure will be tolerated.’61 This advice has now been replaced with the conclusion that ‘extracting only those third molars that remain impacted and become pathologically involved is associated with less expected costs and disability than prophylactic removal of wisdom teeth.’62

People not uncommonly have trouble with many body parts, but one can not argue that treatment which may be necessary for a minority of the population should be utilized for everyone as a prophylactic measure.63,64,65 As Daily in a summary of 145 empirical studies concluded, third molar extraction to prevent disease is no more logical then extraction of first or second molars to prevent disease.66

The research now argues that since the appearance of wisdom teeth is part of normal development, third molars that cause problems should be dealt with in the same way as any other problem teeth—namely endeavor to save them.67 This contradicts the reasoning that the human maxillary sinus is usually too small, and therefore the third molars should be removed even if they are not causing problems because they will often cause problems later.

Although a competent surgeon can reduce serious problems later in life by appropriate removal of third molars, routine prophylactic removal is now regarded by many researchers as ill advised.68 A review of 12 studies on prophylactic removal found ‘there is little justification for the removal of pathology free impacted third molars.’69 According to Samsudin and Mason70, pain was once the major reason asymptomatic wisdom teeth were removed (73.7% of all cases). Surgeons usually set a removal decision threshold based on several criteria, and if a tooth has characteristics which exceed their threshold, it is removed.71 This requires training, experience and knowledge.

Daily concluded that most prophylactic third molar extractions are medically unnecessary and the proper course is to clinically and radiographically monitor the teeth to determine pathological changes that indicates clear need for extraction.72 Routine wisdom teeth extraction is only one of many, many examples in which the implications of evolution theory has contributed to erroneous medical practices, in this case unnecessarily remove what may amount to billions of teeth. A study by Tulloch et al.,73,74,75 as part of an effort to identify ineffective or wasteful medical procedures estimated that:

   ‘Universal extraction of wisdom teeth would cost more than $278 million and would result in three million days of misery for America’s teenagers ... . Removing only problem teeth would cost an estimated $51.5 million and create 776,000 days of misery ... . If surgeons removed only those wisdom teeth that actually caused problems ... the nation would save at least $150 million a year in medical expenses with no ill effects. And tens of thousands of people, mostly teenagers, would be spared the aches, pains and complications that can result from the surgery.’76

Tulloch concludes that the universal ‘recommendation for the early extraction of mandibular molars can no longer be endorsed.’77

No doubt the hundreds of recent dental journal articles discouraging prophylactic removal have had some effect on dental practice. As a result of careful evaluation of patients with wisdom teeth complaints, a 1998 British study found of 8298 patients (a total of 25,001 third molars) that were referred to hospitals for assessment.

   ‘Over half of all patients ... had either no extractions or a single third molar extracted. Less than a quarter of all patients referred underwent removal of all four third molars. Twenty percent of all third molars assessed were not extracted. Of all lower third molars listed for extraction, 9574 (78%) were associated with symptoms or disease. Pericoronitis was the commonest indication for extraction and was cited in 39.5% of all extraction.’78

The researchers concluded that by using strict criteria to determine if removal was necessary in Britain excessive numbers of third molars were no longer being removed.

[Guest Alefshin]

Complications related to wisdom teeth removal

Removal of wisdom teeth solves certain problems such as infection that results because a partially erupted impacted tooth does not allow a bacterial tight seal around the tooth, but sometimes creates other problems, some that are very serious. The major problem resulting from removal of third molars, aside from the loss of these useful teeth, is the complications related to tooth extractions. Teeth extraction can cause postoperative pain, swelling, and tempromandibular joint dysfunction.79 The most common complications include ‘infection and dry socket, trauma to the neurovascular bundle and temporary or permanent paresthesia or anesthesia of the lip, trauma to the lingual nerve, tongue numbness (temporary or permanent) root segments left in the socket and risk of damage to adjacent teeth.’80 One Michigan study found that about ten percent of all such operations result in complications, mostly minor, but which included some serious problems such as infection, persistent bleeding, severe tooth socket inflammation, permanent numbness of the lip and tongue and occasionally catastrophic hemorrhaging which occasionally can be lethal.81,82

Extraction also has the potential of damaging gums and causing bone loss which adversely effects bone support for the second molars.83 Numerous research studies have evaluated the risk of surgery versus treating the problems sometimes encountered in wisdom teeth eruption. They have in general concluded that watchful waiting ‘would typically cause half as much discomfort and disability as extracting all impacted teeth, and only a fraction as much distress as pulling all wisdom teeth in adolescence.’84 Leff85 concludes that, if other viable options exist aside from extraction there is ‘an excellent chance they’ll never be a problem.’ This conclusion is a major reversal of the previous perception held by many dentists for decades, namely that wisdom teeth are ‘essentially useless trouble-makers—“little time bombs.”’86

Problems associated with wisdom teeth that should be attended to by a dental professional include third molars that remain incompletely erupted and only partially poke through the gum. Infection can be a problem when bacteria accumulate beneath the gum flap still covering the tooth as it erupts. Local antiseptics and trimming back the gum can often effectively deal with the concern of pericornitis (inflammation around the crown of a tooth) until the tooth erupts. This condition is estimated to occur in about seven percent of all cases of wisdom teeth problems, and can adversely influence decay or gum disease of the adjacent molar. A dentist should be consulted to aid the patient in making the best determination of how to treat this concern.

Pathology also can explain some wisdom teeth problems. Many examples of local pathology exist which can affect jaw structure and consequently can cause impaction of the wisdom teeth. These include achondroplasia, Treacher-Collins syndrome and occipitomandibular syndrome. These uncommon situations, though, do not shed much light on why certain populations as a whole tend to have third molar problems.

Diet as a partial explanation for wisdom teeth problems

The two most commonly cited explanations for third molar problems, natural selection of mutations, both have been challenged by many researchers including Calcagno and Gibson.87 The fact that impacted teeth are rarely seen in animals and nontechnologic human societies indicates that some change in humans that occurred in their recent past is responsible.88,89 Many researchers have concluded that the dietary shift to soft, processed foods has caused a decrease in masticatory demands (the disuse theory) resulting changes in the teeth-jaw relationship which could lead to malocclusion and wisdom teeth.90

The earlier human diet tended to be highly abrasive ‘which caused attrition of teeth,’ according to Singh et al.91 resulting in the total arch length (the widths of all the teeth added together) to become less. Especially has ‘processed foods caused consequential reduction in masticatory functional demand’ producing a higher rate of impacted wisdom teeth.92 In other words, as is true of most body organs, lack of use causes malfunction or deterioration of wisdom teeth which is not inherited in the discredited Lamarckian theory manner.

Begg, in a study of ‘stone age men’ concluded that human teeth continually migrate in two directions throughout life, horizontally and vertically.93 Begg sampled skulls of Australian Aboriginals who had died before the westernization of Australia by the British and who had consumed a diet he judged ‘late paleolithic,’ (for this reason he used the term stone age to describe their diet). He concluded that the coarse, hard gritty, fibrous and unprocessed diet causes inter proximal and occlusal attrition which ‘permits all the lower deciduous teeth to move gradually forward relative to the uppers.’94

The result of teeth wear produces mesio drift (towards the front of the mouth) because the space required to accommodate the teeth in each jaw gradually becomes less, allowing a proper fit of the third molar teeth. This wear does not occur with the modern diet, and consequently Begg argues many westerners often don’t have enough room in their mouth for wisdom teeth, and therefore crowding of permanent canines and incisors is more likely to occur today.

Several other research studies on primitive skulls have concluded a ‘clear association’ between civilization and dental attrition, and lack of dental attrition was strongly related to teeth crowding and wisdom teeth impaction.95 In a summary of the research on diet and dental crowding, Lombardi96 concluded, ‘Dental crowding is endemic among technologically advanced populations and uncommon in primitive groups. The significant elements in the development of most dental crowding are mesial migration and the lack of inter proximal attrition. Mesial migration of the posterior teeth provides the functional replacement for the tooth surface lost to attrition because of the rigors of a primitive diet. In modern man there is little attrition of the teeth because of a soft, processed diet; this can result in dental crowding and impaction of the third molars.’

In short, this theory concludes that ‘ … inter proximal wear is highly correlated with the chewing force required by the diet. A diet consisting largely of tough foods, such as nuts, seeds, fibrous vegetables, and partially cooked meats, requires high chewing forces that cause lateral movement of the teeth relative to each other. This rubbing of adjacent teeth is the cause of inter proximal wear. The amount of particulate matter or grit in the diet is a secondary factor in inter proximal wear, although it accounts for most of the occlusal wear. Advanced populations that consume a diet composed largely of cooked meats and vegetables, as well as processed foods, do not require the large chewing forces that lead to lateral movement of the teeth and inter proximal wear. The low incidence of crowding in primitive populations seemingly results from the high degree of inter proximal attrition and not from a more harmonious concordance of tooth and jaw size.’97

Supporting this conclusion, Calcagno98 determined a significant reduction in tooth size occurred between the Mesolithic geological age and the newer Agriculturalists culture in Nubia, Africa, and a smaller tooth size reduction when the Agriculturalists were compared to the intensive Agriculturalists cultures, presumably due solely to diet changes. Another study of the Australian Aboriginals living at Yeundumu found that an estimated only 64% of the total tooth size variability of permanent teeth can be attributed to genetics, indicating that environment is of major importance.99,100

Goose101 found from measurements of jaw sizes and teeth that a decrease occurred in the palate coronal dimensions between the middle ages and the seventeenth century. He concluded that this change was unlikely to be due to racial changes or hybridization since no evidence exists of racial mixing during recent British history. Conversely, profound changes in diet has occurred since medieval times which can account for the differences found. Studies in numerous other populations also indicate that diet and other environmental factors are of major importance in tooth variation problems.’102,103,104

Sofaer et al.105 concluded that ‘genetic variation forms the lowest proportion of total size variation in the most posterior tooth of each class’ and that this fact would ‘result in a less rapid response to selection in these teeth.’ Further, the modern diet causes other teeth problems:

   ‘ ... in modern civilized man a change of diet has occurred in the last 2000 years or so and that as a result the teeth are underused and not worn down ... the discovery of cooking made chewing less necessary [and] ... in the last 250 years in Western civilization there has been a rapid development of technology, the calorific values of manufactured foods has become more concentrated, refined sugars widely available and the abrasive content of some food, particularly flour, has been markedly reduced by modern milling.

   ‘The results have been that the dentition has not been reduced in size as it should have been by attrition, and it is this that accounts for the increase in impactions. There is a rider to this second view and it is that dental attrition requires a high degree of muscle activity which in turn stimulates jaw growth. In the absence of constant chewing the jaw does not reach full size and therefore, in those who eat high-calorie cooked food, there is an increased risk of malocclusion.’106

In short, when the chewing workload is reduced, the mandible and jaw muscles atrophy, and when chewing workload is increased, the muscles strengthen and the jaw develops. Other dental problems such as malocclusion are also ‘widely believed to be a disease of civilization, and to be largely confined to recent man of European decent.’107 Clinch108 found the level of malocclusion to be three times greater in civilized peoples compared with a ‘primitive’ group of aborigines. Corruccini109 found ‘some 40–60%’ of people in the United States have malocclusions and that in ‘nontechnologic human societies’ malocclusion is rare.

Conclusions

Several factors have been found to be important in causing third molar problems and malocclusion. The most important factor is probably diet, but the influence of other factors including mutations, needs to be examined more fully to understand why wisdom teeth are more often a problem today. The once common belief that wisdom teeth problems are related to putative evolutionary modifications has now been discredited, and we can do no better to summarize this change in belief then to quote MacGregor. MacGregor concluded in an extensive study that the ‘increase of brain size at the expense of jaw size’ evolutionary view is invalid and that the:

   ‘Evidence derived from paleontology, anthropology, and experiment indicates very convincingly that a reduction in jaw size has occurred due to civilization. The main associated factor appears to be the virtual absence of inter proximal attrition, but initial tooth size may have some effect. Jaw size and dental attrition are related and they have both decreased with modern diet. Jaws were thought to be reduced in size in the course of evolution but close examination reveals that within the species Homo sapiens, this may not have occurred. What was thought to be a good example of evolution in progress has been shown to be better explained otherwise.’110

The findings noted in the many studies cited above, such as tooth and jaw sizes are generally harmonious in societies with a coarse diet, have forced many evolutionists to reevaluate their theory and postulate that reduction in jaw size ‘ … during hominid evolution has been accompanied by a general reduction of tooth size. Natural selection has presumably operated to maintain a harmonious tooth to jaw size relationship by tending to eliminate genotypes that produced teeth too large for the changing skeletal system.’111

Some evolutionists now even argue that ‘selection against excessively larger teeth would have been stronger then selection for small faces.’112 Why ‘small faces’ would have been selected for is difficult to determine.

The ‘most identifiable remains of fossil mammals consists of teeth’ because they are by far the most durable parts of the body.113 Consequently, the teeth can provide major evidence for or against a theory of morphology change. In this case the research indicates that the problems experienced with wisdom teeth in modern society are not due to mutations selected by the environment but largely to changes in diet, namely to softer, less abrasive processed foods which do not give the teeth the workout which they require to ensure proper relationship in the mouth.

References

  1. MacGregor, A.J., 1985. The Impacted Lower Wisdom Tooth, Oxford University Press, New York, p. 3.

  2. Ebbert, S. and Sangiorgio, M., 1991. Facing the dreaded third molar. Prevention, 43(7):108–110.

  3. Liggett, J., 1974. The Human Face, Stein & Day, New York.

  4. Berra, T.A., 1990. Evolution and the Myth of Creationism, Stanford University Press, Stanford, California.

  5. Kurtèn, B. (ed.), 1982. Teeth, Form, Function and Evolution, Columbia University Press, New York.

  6. Harris, J. and Weeks, K., 1973. X-Raying the Pharaohs, Charles Scribners & Sons, New York.

  7. Butler, P.M., 1963. Tooth morphology and primate evolution. In: Dental Anthropology, Brothwell (ed.), Pergamon Press, Oxford, UK.

  8. Moore, R., 1962. Evolution, Time, Inc., New York.

  9. Rogers, J.S., Hubbell, T. and Byers, C., 1942. Man and the Biological World, McGraw-Hill, New York, p. 313.

 10. Durbeck, W.E., 1943. The Impacted lower Third Molar, Dental Pub. Inc., Brooklyn, New York.

 11. Haugen, L.K., 1981. The evolutionary background for problems with wisdom teeth. Tidsskrift for Tandlaeger, 1(3).

 12. Sakai, T., 1981. Human evolution and wisdom teeth. Dental Outlook, 58(4):615–623.

 13. Zhang, Y.Z., 1982. Temporo-mandibular joint dysfunction syndrome in human evolution. Chinese Journal of Primatology, 17(3):173–176.

 14. Schissel, M.J., 1970. Dentistry and Its Victims, St. Martin’s Press, New York, pp. 50, 170.

 15. Darwin, C., 1896. The Descent of Man and Selection in Relation to Sex. D. Appleton and Company, New York, p. 20.

 16. Henschen, F., 1966. The Human Skull, Frederick A. Praeger, New York.

 17. Macho, G.A. and Moggi-Cecchi, J., 1992. Reduction of maxillary molars in Homo sapiens sapiens; a different perspective. American Journal of Physical Anthropology, 87(2):151–159.

 18. Macho and Moggi-Cecchi, Ref. 17, p. 156.

 19. Corruccini, R., 1991. Anthropological aspects of orofacial and occlusal variations and anomalies. In: Advances in Dental Anthropology, Chapter 17. Kelley, M.A. and Larson, C.S. (eds), Wiley-Liss, New York, p. 308.

 20. Taylor, M.S., 1982. Aberrant maxillary third molars; morphology and developmental relations. In: Kurtèn (ed.), Ref. 5, pp. 64–74.

 21. Bergman, J. and Howe, G., 1990. “Vestigial Organs” Are Fully Functional, Terre Haute, Creation Research Society Books, Indiana.

 22. Macho and Moggi-Cecchi, Ref. 17, p. 151.

 23. Leonard, M.S., 1992. Removing third molars: a review for the general practitioner. Journal of the American Dental Association, 123(2):77–82.

 24. Ganss, C., Hochban, W., Kielbassa, A.M. and Umstadt, H.E., 1993. Prognosis of third molar eruption. Oral Surgery, Oral Medicine, Oral Pathology, 76(6):688–693.

 25. Leff, M., 1993. Hold on to your wisdom teeth. Consumer Reports on Health, 5(8):4–85.

 26. Singh, H., Lee, K. and Ayoub, A.F., 1996. Management of asymptomatic impacted wisdom teeth: a multicentre comparison. British Journal of Oral and Maxillofacial Surgery, 34:389–393.

 27. MacGregor, A.J., Ref. 1.

 28. Tulloch, J.F., Antczak, A. and Wilkes, J., 1987. The application of decision analysis to evaluate the need for extraction of asymptomatic third molars. Journal of Oral Maxillofacial Surgery, 5:855–863.

 29. Leff, M., Ref. 25, p. 84.

 30. Singh, H., Lee, K. and Ayoub, A.F., Ref. 26.

 31. McGuire, T., 1972. The Tooth Trip, Random House, New York.

 32. Dachi, S.F. and Howell, F.V., 1961. Survey of 3874 routine full-mouth radiographs: a study of impacted teeth. Oral Surgery, Oral Medicine, Oral Pathology, 14:1165–1169.

 33. Moursheed, F. 1964. A rentgenographic study of dentigerous cysts: incidence in a population sample. Oral Surgery, Oral Medicine and Oral Pathology, 18:47–53.

 34. Leff, M., Ref. 25, p. 84.

 35. MacGregor, A.J., Ref. 1.

 36. Robinson, R.J. and Vasir, N.S., 1993. The great debate: do mandibular third molars affect incisor crowding? A review of the literature. Dental Update 20(6):242–246.

 37. Southard, T.E., 1992. Third molars and incisor crowding: when removal is unwarranted. Journal of the American Dental Association, 123(8):75–78.

 38. Singh, H., Lee, K. and Ayoub, A.F., Ref. 26.

 39. Southard, T.E., Ref. 37.

 40. Tulloch, J.F. , Eng, R.C.S. and Wilkes, J., 1987. Decision analysis in the evaluation of clinical strategies for the management of mandibular third molars. Journal of Dental Education, 51(11):652–660.

 41. Leff, M., Ref. 25, p. 85.

 42. Little, R.M., Riedel, R.A. and Artun, J., 1988. An evaluation of changes in mandibular anterior alignment 10 to 20 years post retention. American Journal of Orthodontics and Dentofacial Orthopedics, 93:423–8.

 43. Cuozzo, J., 1998. What happens to the craniofacial structure of humans who live past 100 years? Neanderthal similarities. In: Proceedings of the Fourth International Conference on Creationism, Pittsburgh, Pennsylvania, pp. 103–120.

 44. Southard, T.E., Ref. 37, p. 76.

 45. Southard, T.E., Ref. 37, p. 79.

 46. Samsudin, A.R. and Mason, A.D., 1994. Symptoms from impacted wisdom teeth. British Journal of Oral and Maxillofacial Surgery, 32(6):380–383.

 47. Robinson, R.J. and Vasir, N.S., Ref. 36.

 48. Henschen, F., Ref. 16.

 49. Mills, J.R.E., 1963. Occlusion and malocclusion of the teeth of the primates. In: Dental Anthropology, Brothwell, D.R. (ed.), Pergaman Press, Oxford, UK.

 50. Durbeck, W.E., Ref. 10. pp. 4–5.

 51. Barrett, M.J., 1957. Dental observations on Australian Aborigines: tooth eruption sequence. Australian Dental Journal, 2:217–227.

 52. Davis, W., 1998. Dean and Chair of the Department of Oral Biology, Medical College of Ohio. Interview.

 53. MacGregor, A.J., Ref. 1, p. 12.

 54. MacGregor, A.J., Ref. 1, p. 11.

 55. Chung, C.S. et al., 1970. Genetic and epidemiological studies of oral characteristics in Hawaii’s schoolchildren, II. Malocclusion. American Journal of Human Genetics, 23:471–495.

 56. Chung, C.S. and Neiswander, J. D., 1975. Genetic and epidemiological studies of oral characteristics in Hawaii’s schoolchildren, V. Sibling correlations in occlusion traits. Journal of Dental Research, 54(2):324–329.

 57. Barrett, M.J., Ref. 51, p. 227.

 58. Curtis, H.F., 1935. The relationship of attrition and the impacted mandibular third molar as found in the ancient Egyptians. Transactions of the American Dental Society of Europe, 1997.

 59. Dahlberg, A., 1963. Analysis of the American Indian dentition. In: Dental Anthropology, Brothwell, D.R. (ed.), Pergaman Press, Oxford, UK.

 60. Dahlberg, A., Ref. 59, p. 171.

 61. Wood, N., 1978. The Complete Book of Dental Care, Hart Publishing Company, New York.

 62. Singh, H., Lee, K. and Ayoub, A.F., Ref. 26, p. 389–390.

 63. Leonard, M.S., Ref. 23.

 64. Huggins, H.A., 1991. Wisdom teeth. Let’s Live, pp. 44–45.

 65. Marshall, D.A.S., Berry, C. and Brewer, A., 1993. Fatal disseminated intravascular coagulation complicating dental extraction. British Journal of Oral and Maxillofacial Surgery, 31:178–179.

 66. Daily, T., 1996. Third molar prophylactic extraction: a review and analysis of the literature. General Dentistry, 44(4):310–320.

 67. Tulloch, J.F., Antczak, A. and Ung, N., 1990. Evaluation of the costs and relative effectiveness of alternative strategies for the removal of mandibular third molars. International Journal of Technology Assessment in Health Care, 6:505–515.

 68. Robinson, R.J. and Vasir, N.S., Ref. 36.

 69. Song, F. et al., 1997. Prophylactic removal of impacted third molars: an assessment of published reviews. British Dental Journal, 182(9):339–346.

 70. Samsudin, A.R. and Mason, A.D., Ref. 46.

 71. Brickley, M.R., Prytherch, I. M., Kay, E.J. and Shepherd, J.P., 1995. A new method of assessment of clinical teaching: ROC analysis. Medical Education, 29:150–153.

 72. Daily, T., Ref. 66, p. 315.

 73. Tulloch, J.F. , Eng, R.C.S. and Wilkes, J., Ref. 40.

 74. Tulloch, J.F., Antczak, A. and Wilkes, J., Ref. 28.

 75. Tulloch, J.F., Antczak, A. and Ung, N., Ref. 67.

 76. Blakeslee, S., 1991. Study questions routine molar removal. (Alexia Antczak and Joan Tulloch report). The New York Times, June 26, p. C9, Col. 1.

 77. Tulloch, J.F., Antczak, A. and Ung, N., Ref. 67, p. 504.

 78. Worrall, S.F., Riden, K., Haskell, R. and Corrigan, A.M., 1998. UK National Third Molar Project: the initial report. British Journal of Oral & Maxillofacial Surgery, 36(1):14–18.

 79. Capuzzi, P., Montebugnoli, L. and Vaccaro, M., 1994. Extraction of third molars. Oral Surgery, Oral Medicine, Oral Pathology, 77(4):341–343.

 80. Leonard, M.S., Ref. 23, p. 82.

 81. Leff, M., Ref. 25, p. 85.

 82. Marshall, D.A.S., Berry, C. and Brewer, A., Ref. 65.

 83. MacGregor, A.J., Ref. 1.

 84. Leff, M., Ref. 25, p. 85.

 85. Leff, M., Ref. 25, p. 85.

 86. Leff, M., Ref. 25, p. 84.

 87. Calcagno, J.M. and Gibson, K.R., 1988. Human dental reduction: natural selection or the probable mutation effect. American Journal of Physical Anthropology, 77:505–517.

 88. MacGregor, A.J., Ref. 1, p. 3.

 89. Corruccini, R., Ref. 19, p. 295.

 90. Macho and Moggi-Cecchi, Ref. 17, p. 158.

 91. Singh, H., Lee, K. and Ayoub, A.F., Ref. 26, p. 391.

 92. Singh, H., Lee, K. and Ayoub, A.F., Ref. 26.

 93. Begg, P.R., 1954. Stone Age man’s dentition. American Journal of Orthodontics, 40:298–312; 373–383 and 462–475.

 94. Begg, P.R., Ref. 93, p. 302.

 95. MacGregor, A.J., Ref. 1.

 96. Lombardi, V., 1992. The adaptive valve of dental crowding. A consideration of the biological basis of malocclusion. American Journal of Orthodontics, 81:38–42.

 97. Lombardi, V., Ref. 96, p. 40.

 98. Calcagno, J.M., 1986. Dental reduction in post-Pleistocene Nubia. American Journal of Physical Anthropology, 70:349–363.

 99. Townsend, G. and Brown, T., 1978. Heritability of permanent tooth size. American Journal of Physical Anthropology, 49:497–504.

100. Townsend, G. and Brown, T., 1983. Molar size sequence in Australian Aboriginals. American Journal of Physical Anthropology, 60:69–74.

101. Goose, D.H., 1963. Dental measurement: an assessment of its value in anthropological studies. In: Dental Anthropology, D.R. Brothwell (ed.), Pergamon Press Oxford, UK, p. 179–190.

102. MacGregor, A.J., Ref. 1., p. 5.

103. Kallay, J., 1963. A radiographic study of the Neanderthal teeth from Krapina. In: Dental Anthropology, D.R. Brothwell (ed.), Pergaman Press, Oxford, UK.

104. Calcagno, J.M. and Gibson, K.R., Ref. 87.

105. Sofaer, J., Bailit, H. and MacLean, C., 1971. A developmental basis for differential tooth reduction during hominoid evolution. Evolution, 25:509–517.

106. MacGregor, A.J., Ref. 1, p. 3.

107. Mills, J.R.E., Ref. 49, p. 46.

108. Clinch, L.M., 1951. The occlusion of the Australian Aborigines. Transactions of the European Orthodontists Society, 80.

109. Corruccini, R., Ref. 19, p. 295.

110. MacGregor, A.J., Ref. 1, p. 16.

111. Sofaer, J., Bailit, H. and MacLean, C., Ref. 105, p. 509.

112. Corruccini, R., Ref. 19, p. 308.

113. Butler, P.M., Ref. 7, p. 1.

[Guest Alefshin]

The dodo bird ... an example of survival of the fittest

by Jerry Bergman

Often pictured as a magnificently overweight pigeon-like bird, the last dodo died in the late 1600s. This non-flying bird which allegedly was ‘obviously unfit’ became extinct as evolution would expect, and is often used as a prime example of natural selection and proof of how evolution works. It lived on the small island of Mauritius in the Indian Ocean, east of Madagascar, and is now known from only bony remains plus a preserved foot and head.

A careful recent examination of the dodo has revealed that many common perceptions about the bird are incorrect.1 In the words of John Maddox, of the journal Nature, ‘the dodo deserves a better press.’2 Studies on more than 400 skeletal dodo relics by Livezy, and the work of Kitchener at the Royal Museum of Scotland, have recently radically changed the common view about the bird. In the words of Kitchener, ‘Rivaling the dinosaurs as a symbol of extinction, the dodo is renown for being slow, stupid and fat. Raphus cucullatus was doomed to extinction from the day it was discovered by hungry Dutch sailors in the forest of Mauritius in 1589. Wasn’t it? Maybe not.’3

He then shows how recent thorough evaluations of the dodo reveal that a number of ideas about it are wrong. Kitchener argues that many centuries-old ideas about the dodo will soon go the way of the dodo itself.

The dodo species consisted of three flightless branches—the dodo of Mauritius, the solitaire of Reunion island, and the Rodriguez solitaire that lived on tiny Rodriguez island.

Mauritius, Reunion and Rodriquez are a group of volcanic upthrust islands located in the Indian Ocean between Madagascar and the west coast of Australia. These isolated small islands—Mauritius is only 2,095 square kilometers (809 square miles)—stand alone in a water wilderness thousands of kilometers from any neighbour island or land. In their isolated homeland, the dodoes experienced no animal predators or human hunters to bother them for many years.

The dodoes on Mauritius were discovered in 1507 by the Portuguese, and in only 174 years became extinct. Contemporary accounts claim that men brought as many as 50 large birds on board their ship a day, and often about half were dodoes.4 The slaughter was great because this very ‘remarkable bird ... existed in considerable abundance’ on these islands.5

Kitchener concludes that it was not the dodo’s physical inferiority which caused its extinction, but the ‘rats, pigs, and monkeys which arrived with the sailors and pillaged the dodo’s vulnerable ground nests.’6 One extensive study of extinctions concluded that a number of unfortunate factors are responsible for almost all extinctions.7

Actually, all animals that lay eggs near the ground surface are vulnerable, which is why so many birds have become extinct in modern times. Even birds which have a reputation dramatically opposed to the dodo’s, such as the American eagle, have been threatened with extinction for somewhat similar reasons. The passenger pigeon was the most abundant bird in America (more than 20 billion) and was obviously ‘evolutionarily successful,’ yet became extinct by the twentieth century through wanton human destruction and greed.8 The last one died on September 1, 1914 in the Cincinnati Zoo in Ohio.9

The image of the dodo, though, makes the point about evolution far more effectively than a similarly threatened bird such as the American eagle, which was saved only through the heroic and deliberate efforts of a large number of individuals.

Myth of the fat dodo

The bird’s obesity, slowness and lack of intelligence are commonly given as reasons for its alleged evolutionary inferiority. Dodoes were for years considered not just large, but grossly overweight—to the point that they not only couldn’t fly, but could hardly run from their enemies. Kitchener, though, in studying the written record, found that the earliest dodo drawings showed rather thin birds—only those drawn later show the familiar pudgy variety.10

He found that thin dodoes were drawn by those who had actually visited Mauritius—the plumper birds were drawn mostly by artists in Europe. More than a dozen original pictures (both drawings and paintings) of the dodo now exist.11

Kitchener next evaluated the hundreds of dodo bones that have been unearthed. Using methods developed by criminologists and archaeologists to reconstruct flesh on bones, he was able to determine that the skeletal pattern produced a bird ‘remarkably similar to the first drawing of the dodo.’ Namely the thinner birds.

He concluded that ‘according to four different methods, all based on the dodo’s bones, the famous flightless pigeon weighed between 10.6 and 17.5 kilograms.’12 Evaluation of the cantilever strength of leg bones produces a relationship which can be used to determine the running abilities of different sized animals. This method revealed good evidence for the conclusion that they were indeed ‘swift of foot’—a conclusion which corresponds with eyewitness accounts which stated that the dodo ‘could run very fast.’13

While this analysis is not without problems, it has produced eminently reasonable conclusions, especially since the opposite thesis has little empirical evidence in its favour. Since Kitchener’s first evaluation, original unpublished dodo drawings completed between 1601 and 1602 were rediscovered in a museum in The Hague, the Netherlands. These showed that Kitchener’s conclusions were correct—the dodo was thinner and the femur design was tilted downwards, reducing the bending forces on it and allowing it to shift its center of gravity.14

This evidence demonstrates that the dodo was an effective, fast runner. Kitchener concludes, ‘for more than 350 years the dodo has been thoroughly misrepresented as plump and immobile. The reality is, however, that in the forests of Mauritius it was lithe and active. Like other Mauritian birds it would have undergone a seasonal fat cycle to overcome shortages of food, but never to the extent that those wonderful oil paintings suggest.’15

The last survivors

Since the birds were easy to capture, Dutch colonists, along with sailors and visitors, soon consumed most of the dodo population. Animals they brought with them, especially dogs, cats, and pigs, ate the fledglings and broke the dodo eggs to consume the yolks. By 1681, the dodoes were all gone.

Rather than demonstrate the weakness of the dodo, their history effectively demonstrates the gross irresponsibility of their caretakers. According to Panati, ‘not a single naturalist had attempted to mate any of the captive dodoes; they left no descendants.’16 The last dodo in England was stuffed by English naturalist John Tradescant. When Tradescant died in 1662, his entire natural history collection was bequeathed to an acquaintance, Elias Ashmole. Because of his irresponsibility, the entire collection’s condition greatly deteriorated, and he donated the bird to Oxford University in 1683—two years after the last living dodo was seen on Mauritius. Even Oxford did not take very good care of the bird, and except for the head and foot saved by a farsighted curator, it was later burned as trash in 1755.17 Evidently ‘the museum’s board of directors took one look at the dusty, stupid-looking bird and unanimously voted to discard it.’18

The intrigue over the bird was such that by 1800 ‘professional naturalists were casting doubt on written descriptions of the bird, as well as on extant drawings ... it became scientific vogue to deny the bird’s existence and to challenge the Oxford head and foot as fakes.’19 If it was a genuine bird, the critics reasoned, certainly there would have been extensive efforts to preserve it—or at least a good skeleton.

Search for evidence

A group of zoologists searched in 1850 for evidence, to the extent of traveling to Mauritius looking for bones—and found none. Soon the dodo was denounced as a scientific fraud.20 Evidence did not surface until a resident of Mauritius, George Clark, searched the island and in time discovered numerous scattered bones. His specimens were soon shipped to major museums, and after study were pronounced authentic.

These researchers later attempted to assemble the bone fragments—many in poor condition—into complete dodo skeletons. They are now regarded as real animals, but the many other myths surrounding them have died slowly. These myths were widely believed because they seemed to support the of evolutionary naturalism.

Now that the bird has been extensively studied, we realize that the facts do not support the evolutionary myth, but do support the moral bankruptcy of humankind.

References

  1. Paul Hoffman, New and Improved Dodo, Discover 12(4), p. 16, April 1991.

  2. John Maddox, Bringing the extinct dodo back to life, Nature, p. 291, 23 September 1993.

  3. Andrew C. Kitchener, Justice at last for the dodo, New Scientist, p. 24, 28 August 1993.

  4. James C. Greenway, Extinct and Vanishing Birds of the World, Dover Publications, Inc., New York, 1967.

  5. Philip Henry Gosse, The Romance of Natural History, James Nisbet and Co., London (England), p. 74, 1861.

  6. Ref. 3.

  7. David M. Raup, Extinction: Bad Genes or Bad Luck?, W.W. Norton & Company, New York, 1991.

  8. Jerry Dennis, What happened to the passenger pigeon?, Science Annual, Franklin Watts, New York, pp. 202-205, 1993; Doreen Buscemi, There will be pigeons as long as the world lasts, American History Illustrated 13(5), pp. 11-16, August 1978.

  9. Allan W. Eckert, The Silent Sky: The Incredible Extinction of the Passenger Pigeon, Landfall Press, Dayton (Ohio), 1965.

  10. Ref. 3.

  11. Willy Ley, The Lunghsh, the Dodo, and the Unicorn: An Excursion into Romantic Zoology, The Viking Press, New York, p. 230, 1948.

  12. Ref. 3, p. 26.

  13. Andrew C. Kitchener, On the external appearance of the dodo, Raphus culcullatus, (L., 1758), Archives of Natural History 20(2), p. 296, 1993.

  14. Ibid., pp. 297-299.

  15. Ref. 3, p. 27.

  16. Charles Panati; Panati’s Extraordinary Endings of Practically Everything and Everybody, Harper & Row, New York, p. 203, 1989.

  17. Ibid.

  18. David Wallechinsky and Irving Wallace, The People’s Almanac #3, Bantam Books, New York, p. 361, 1981.

  19. Ref. 16, p. 203.

  20. Ibid.

JERRY BERGMAN, Ph.D., has served on the faculty at Bowling Green State University (USA), taught at the University of Toledo, and served as associate professor at Spring Arbor College, Michigan. He has authored more than 350 articles and books.

http://www.answersingenesis.org/creation/v17/i4/dodo.asp

[Guest Alefshin]

Who invented it first?

First published:

Creation 7(2):16–17

October 1984

by Jerry Bergman

Man is proud of his ability to travel at breathtaking speeds in his machines. He can glide the space-shuttle Columbia to the earth at incredible speeds, travel around the earth in a high speed jet, but how to make the same plane fly very slowly eludes him. Owls can do it, so why can’t we?

But owls have specially curved feathers on the front edge of their wings which change the air currents as they flow past! This allows them to fly more slowly than most birds. Slow flight is quiet flight. If we could duplicate the owl wing, we could build a very fast aircraft which could also fly very slowly. The advantages would be enormous. Less noise, shorter runways, less costly airports, would be a few of the more obvious benefits.

Gaining wisdom from the owl has been one of the many fruits of bionics-the study of naturally occurring designs in order to solve scientific and engineering problems. This is nothing new. The Germans in World War II modeled their first jet plane after the streamlined shark. Early models were even painted to look like sharks. Mankind has looked to the world of nature to solve problems for centuries, and we still do so.

To cut through steel with a ray-gun has been the dream of many young men. This century that dream has been achieved. The complex maser rays and laser concentrate the incredible power of light into rays of various useful strengths: from rays so sensitive you can perform microscopic surgery with them, to brute rays that can pierce through a wall of steel. Yet radio- astronomers at Berkeley UCLA have discovered bigger and better light-energy outputs in the activities of stars such as those in the Orion nebula. Masers have been discovered in the variable giant red stars, including such types as stellar water and silicon monoxide masters. To date only molecular masers have been observed coming from space, but some scientists believe that it is inevitable that we shall find optical lasers, free electron lasers, and chemical lasers in the heavens. Some speculate it is even possible that naturally occurring gamma-ray lasers or grasers exist. When man developed a successful maser in the mid 1950s, it was hailed as a dramatic scientific breakthrough. Yet God created systems to generate such high energy-excited atoms long before man invented them.

When the first telegraph message was sent by Samuel Morse in 1844, its dots and dashes proclaiming ‘what God hath wrought’, mankind rejoiced at the ease of this new communications system. Morse code was again to be used to transmit the first radio waves across the Atlantic by Marconi in 1901. But even with the invention of radio, man was not to be first. Radio waves generated by the stars have been traveling through the universe since the time of creation. The science of radio astronomy is built on this fact.

Birds fly thousands of miles and use navigational equipment which weighs very little. Man-made planes, on the contrary, have navigational equipment which weighs a tonne or more and costs a fortune to lug around. We have copied nature, but imperfectly.

Birds and fish travel yearly from the Arctic to the Antarctic without training, arriving at the same nesting site. Bees in their navigational calculations, use the sun as a compass. At night or on very cloudy days, they rely on the patterns of polarised light for navigation. But even if it is too cloudy and the light is not available, bees have a back-up system. They can use the earth’s magnetic field to find where they are. Most people under similar conditions simply get lost.

Did you know that when the bat gives off its sound, a special muscle automatically turns down its hearing so it cannot hear its own voice, only the guiding echoes? Most people know that in flight a bat emits supersonic sound pulses (as many as 60 a second) which, if they hit something, bounce back to the bat’s ears to warn it of the object. By measuring the time it takes the echoes to return, a bat can judge the exact location of objects and then modify its flight accordingly. Somehow the modern ‘miracles’ of science in the invention of radar and sonar systems, used to guide planes safely through fog and ships through water, often pale into insignificance when compared with their created natural counterparts. [Ed. note: See also Bats: Sophistication in Miniature]

When it comes to engineering, man is not the only one who can claim success. Spiders ‘had it first’ when it comes to a system for lifting loads. They string strands of moist ‘web wire’ from a limb overhead to the object on the ground. As the web dries, it shrinks and lifts the object slightly. More wetting, more waiting, and more shrinking, results in the object eventually being hoisted right up to the spider’s nest. By this means, a spider patiently works with web cables until a selected object is high enough off the ground for the creature to build its nest. Spiders know how to spin a wall of web which can hold many times their own weight.

They have their own unique types of webs. Trade names which are marvels in geometric design and workmanship. Spiders were diving under water in air-filled diving bells long before man invented the submarine or the bathysphere. [Ed. note: See also God’s webspinners give chemists free lessons]

The first successful light bulbs marketed by Edison in the 1880s produced so much heat that they burnt out very rapidly. Even our modern light bulbs produce so much more heat than light that they are very wasteful of energy. If we could only learn from the firefly’s system, millions of dollars would be saved. They light up their lives by using a fuel called luciferin backed by a layer of reflective pigment cells covered by transparent tissue shapes to form a lens. Your car’s headlights and spotlights are patterned after that design.

A lifetime of study barely uncovers the tremendous designs which exist in the created world of nature. Beavers build large dams and spacious underground homes; wasps manufacture paper; some ants make living bridges so that their comrades can pass over water; other ants make boats from leaves to float across instead, while yet other ants practise animal husbandry, and herd aphids which they milk. Certain animals garden by planting fungi in specially prepared leaf moulds, and the famous Archer fish shoots flying insects with a stream of water, its eyes automatically correcting for optical refraction-an operation which most people cannot master however hard they try.

What can we conclude from this? Certainly not that blind chance or accident is the rule of law in nature. There are too many rules, too many laws and too much evidence of design to reach that conclusion rationally. As man learns more of the marvellous designs implanted in creation, he should be moved to appreciate evermore the wisdom of the God who made it all. The evidence of His handiwork is so obvious that not only do the heavens declare His glory, but the earth shows the evidence of His design. So much so that men are without excuse if they deny it.

http://www.answersingenesis.org/creation/v7/i2/invent.asp

[Guest Alefshin]

Understanding poisons from a creationist perspective

First published:

TJ 11(3):353–360

December 1997

by Jerry Bergman

Abstract

The problem of poisons is considered, and it is concluded that a false dichotomy exists between poisonous and non-poisonous chemicals. Nothing is toxic in small amounts, and all chemicals are toxic at high levels. Further, virtually all chemicals, even poisons and toxins, have an important function in life or human society. Because compounds can be used in a harmful way does not negate their importance when used appropriately. Fire serves us well by heating our homes, cooking our food and sterilising medical equipment, yet fire has caused the loss of an enormous number of lives. Likewise, many major poisons and toxins are shown to play critically important beneficial roles in society. It is not the compound that is the problem, but the use to which it is put. Actually, life could not exist without some compounds that are toxic to some life-forms. Conversely, our body has a complex means of protecting itself from toxins which renders virtually all toxins harmless in the amounts to which most of us are exposed.

Introduction

Toxins are poisons produced by plants, animals and bacteria or found naturally in the air, water and soil. A poison is any substance that produces injury to the body by chemical means. Some are corrosives that destroy tissue directly; others are irritants that inflame mucous membranes. The two terms ‘toxins’ and ‘poisons’ are largely synonymous and are used here interchangeably. The term poison tends to be the lay term, while toxin is the scientific term.

The subject of poisons is burdened with many misconceptions and is far more complex than assumed just a few years ago. When reading about mercury or lead poisoning, or murders in which someone used a deadly poison such as arsenic, some may ask, ‘Why would God create chemicals that cause so much harm to people?’ Atheists commonly argue that a loving God would not make deadly chemicals which have killed millions of people. Young concludes that germs and poisons are

‘perfectly understandable in terms of evolution [but] make no sense whatever in terms of design by an infinitely intelligent, wise, and compassionate Creator’.1

Actually, evolution—specifically natural selection—can ‘explain’ either situation. If no poisons existed natural selection could explain this situation by explaining that poisons ‘selected’ to extinction those animals that had less defence against them. In fact, poisons that the body cannot easily handle occur relatively rarely in nature. Levy and Primack note:

‘While there are some 7,000 plants and fungi that produce or contain toxic substances, only a few are really very dangerous. According to the Food and Drug Administration’s National Clearing House for Poison Control Centers, there were only 7,710 cases of exposure to plant poisons recorded in 1975. Of these victims, 1,990 reported symptoms, 186 were hospitalized and 3 died … most plant poisonings are relatively mild and your overt overreaction can amplify the symptoms …’ 2

A major reason for toxins in this post-Fall world is to maintain the ecological balance so necessary for life to exist on the Earth. An example is penicillin, a toxin to bacteria but harmless to humans, which has saved millions of lives. Most plants produce toxins to protect themselves from pathogens. Further, bacteria are necessary for life because they serve as recyclers of organic materials. Without them, all of the organic nutrients would eventually become locked-up in non-bioavailable forms and eventually life would become extinct on Earth. The only concern is to prevent recycling until the animal is dead. This is the function of the animal’s defence system, which includes the use of toxins.

The terms ‘poison’, ‘toxic’, ‘pesticide’ and ‘herbicide’ all imply that because some chemicals may function as toxins in some situations, they are therefore always detrimental to humans. The implied dichotomy between the words ‘toxic’ and ‘non-toxic’ is wholly artificial and impedes understanding the toxicity problem.3 Chemicals are not toxic or poisonous, only amounts are; no chemical is toxic at low levels, and all chemicals are toxic in large amounts.4 In Stevens’ words, ‘Anything in a large enough dose can prove toxic’.5

Even water is toxic if certain amounts are ingested and can cause a coma or death if ingested in high levels during a short time period.6 Such water intoxication is actually an excellent example of the fact that all substances are toxic in large amounts. Tisdale describes the result of water toxication:–

‘The volume of water both inside and outside the cells increases, but the salt does not, and brain cells swell, then shrink … . Water intoxication can occur accidentally, especially in the medical treatment of a dehydrated person. But it happens most frequently among schizophrenics … schizophrenics sometimes have a compulsive need to drink water.’7

And a Food and Drug Administration report stated they receive many reports of hospitalisations involving

‘water intoxication of young infants. Preliminary reports indicate that three infants were admitted to the hospital with seizures and hyponatremia apparently associated with relatively large intakes of free water. The other two infants were reported to have low blood sodium levels on admission that were believed to be related to water ingestion.’8

Oxygen is also necessary for life, but, as every nurse knows, excess amounts are lethal and lower excesses have been a major cause of blindness in premature babies. Oxygen toxicity develops when the p(O2) rises above 2.5 atm. (36.8 psi). The result is oxidation of certain enzymes, which damages the central nervous system and causes coma, and eventually death. A major problem in abiogenesis is how early life survived an oxygen environment, and for this reason evolutionists must postulate that a non-oxygen atmosphere existed at this time, that is, a reducing atmosphere (for the evidence against the reducing atmosphere hypothesis, see Thaxton et al.9).

Many poisons have critical uses in certain areas of life and society.10 A poison is merely an excess amount of a chemical in the wrong place at the wrong time. Low amounts of many ‘poisons’ in the right cells are actually necessary for life, and all vitamins and minerals are toxic above certain levels. Vitamins A and E are critical for life but highly toxic if taken in high dosages. The standard vitamin-mineral reference lists toxicity data for all vitamins, minerals and food supplements.11

Thalidomide: Curse or Miracle Cure?

The drug thalidomide became infamous for causing a large number of birth defects, primarily if taken at a certain time during pregnancy. Actually, only one of its enantiomers was a teratogenic agent which caused children to be born with missing or misshapen limbs.12,13 Although the image of this drug has caused researchers to avoid exploring its many potential uses, recent studies have found that it is among the most effective treatments known for leprosy and can also improve enormously the survival rate of patients who receive bone-marrow transplants.

Thalidomide has also been successfully used to treat other potentially fatal disorders, including aplastic anaemia and certain kinds of bone cancers. Aplastic anaemia is a deficiency in the quality or quantity of the erythrocytes caused by aplasia, a failure of a red blood-cell-producing organ to develop. Specifically, the bone marrow—where most blood cells are produced—fails to develop or becomes diseased. Thalidomide also reduces the graft-versus-host disease problem by moderating the voracity with which the grafted foreign tissue attempts to reject its new home. Nor is thalidomide the only toxin that is a miracle drug. In one listing of plant poisons, their use for medicine is obvious:

‘The development of blatantly poisonous compounds by plants and fungi is extraordinary in the variety of toxins that they produce. These compounds are chemically very diverse and include powerful substances that affect heart muscle and blood pressure, smooth muscle relaxants, cyanides that block cell respiration, cell poisons that inhibit protein synthesis, hormone-like compounds, hallucinogenic chemicals, irritants, blistering agents, photosensitizers and plant allergens. Some act rapidly, causing instant irritation, nausea, vomiting and diarrhoea, while others are more insidious, producing deadly delayed reactions. While the development of these potent and sophisticated chemical defenses has helped plants and fungi avoid being eaten, these poisons have also caused deaths, pain, itching and a variety of ills to people who have either eaten or come in contact with them.’14

All of these classes of poisons have become the miracles of twentieth century medicine, and more are being discovered all the time. Actually, the wonders of modern medicine are primarily due to the discovery of drugs which can cure or help persons survive what were once fatal diseases.

Toxins can also be critical for survival for other reasons. One example is the Pink Pigeon which lives on the island of Mauritius in the Indian Ocean, the island famous for being the home of the now extinct Dodo. The Pink Pigeon may be alive today only because of a mechanism called aposematism. This mechanism uses chemicals as warning signals and for protection. In this case, humans or animals who dine on the Pink Pigeon become extremely ill. Animals soon learn this and avoid the bird.

Interestingly, the source of the birds‘ toxic chemicals is evidently from a fruit—the pigeons commonly dine on this fruit and accumulate the toxin without ill effects, but it poisons those animals who eat them.15 Also, animals that defend themselves by toxins often use conspicuous colouration to easily differentiate themselves from other animals. This allows their predators to easily identify them and to avoid them.

Since high energy levels and low weight are critical for birds, obtaining the toxin from food rather than manufacturing it from scratch eliminates the need for them to use their own energy to manufacture the toxin themselves. Rarely do these toxins kill the predator; most often they make predators sick enough so that they avoid the animal which causes the problem. These mechanisms are critical to help maintain the balance of nature which is necessary for life to survive in the post-Fall world.

The Botulinum Toxin

The most poisonous substance known to mankind is botulin, a neurotoxin produced by the single-celled bacterium Clostridium botulinum.16 The bacterium that causes it is an extremely common soil and water bacteria spore. The proper conditions cause the spore to develop into the rod-shaped bacterium Clostridium botulinum. Botulin is ‘six million times more toxic than rattle-snake venom’, and a lethal dose for humans is a mere 1/10,000th of a milligram.17 Botulin poisoning usually results from eating improperly canned or contaminated food, and produces muscle paralysis.18

The toxin firmly attaches itself to nerve endings and permanently blocks neurotransmitters—chemicals which allow the nerve impulse to travel from one nerve to another at the synapse junction. Binding to nerve endings prevents the release of the neurotransmitter acetylcholine. Similar to jamming a light switch permanently so it cannot be turned on, botulin blocks the nerves, preventing the brain’s signals from reaching a muscle. If enough nerves are blocked, the muscle becomes severely weakened or paralysed. Death occurs because the chest muscles cannot perform their breathing function, producing suffocation.

Yet, this most dreaded of all toxins is a miracle drug for those suffering from dystonias and other health problems. Dystonias produce involuntary muscle spasms which cause the eyelids to blink or clamp shut, the neck to twist into painful contortions, the fingers to cramp, and vocal cords to freeze.19 The dystonias in general result from excess nerve signals to the muscles, causing them to overreact. This uncontrolled muscle spasm can result from both voluntary and involuntary production of excessive electrical brain impulses.

Botulin treatment is also highly effective in about 85 per cent of patients with the cross-eye condition named strabismus. This malady is usually outgrown by about age six months, but if it persists surgery was often the only alternative until the development of botulin treatment. Strabismus is caused by an over-active eye muscle on one side and a weak muscle on the other. The brain processes light information picked up by the retina by combining both the left and right signals. If the weak eye is too far out of alignment with the dominant one, the brain relies solely upon the stronger eye signals. If this continues for too long, the brain becomes unable to interpret images from the weaker eye, thus lets it drift—a condition called amblyopia or lazy eye. As a result, the person can use only one eye and consequently has little depth of field and experiences major difficulty in judging distances. Amblyopia also carries considerable social stigma and often results in major psychological and social adjustment problems.

The surgical treatment involves cutting away a portion of the hyperactive muscle to weaken it and allow the other eye to line up properly. The new treatment uses precisely targeted injections of botulin to inactivate the spastic or hyperactive muscle. This technique in most cases restores normal control to the patient without the need for invasive surgery. Botulin weakens the spastic or over-developed eye muscles in the same way that it weakens the muscle pull of persons suffering from botulism toxin. Unfortunately, the results are not permanent new nerve endings eventually replace those blocked by the drug. Nonetheless, it is now the most effective treatment for amblyopia and is regarded as an established medical procedure.

Botulin therapy is a major breakthrough for blepharospasm, an uncontrollable eye blinking that sometimes involves other facial, throat and neck muscles. It is also effective for both chronic writer’s and musician’s cramps—an especially severe problem for students and persons whose work involves much writing or the use of fingers such as musicians, especially violinists and pianists. Botulin also holds enormous promise for millions of Americans in helping to control spasticity and tics due to cerebral palsy or other causes.20,21,22,23

Success has also been achieved with severe stuttering by injecting the toxin into the vocal cords to provide potential relief for millions of sufferers. It is also effective for spasmodic dysphonia, a muscle spasm which affects the pharynx and results in an extremely strained voice.24 The treatment involves injection of botulin into the thyroarytenoid muscles that control the vocal cords. Additionally, one of the most useful areas for botulin is the treatment of spasmodic torticollis, an extremely painful, debilitating neck spasm which causes the head to thrust about uncontrollably.25

Other uses include treatment of laryngeal dystonia (larynx muscle spasms which cause speech difficulties), and temporomandibular dystonia (involuntary movements of the jaw, lower facial, and tongue muscles). It is even helpful for tremors such as hemifacial spasm, an involuntary twitching or contraction of the muscles on one side of the face.26 The dystonia family of diseases affects about 390 people per million population. Before the botulin treatment, few effective methods existed to help the large number of people afflicted with these problems. One study found the botulin treatment success rate was 85 per cent in a long term follow-up.27 Many persons assumed that these diseases were psychosomatic, and the discovery that they are not has both relieved sufferers and helped to reassure physicians that these patients are treatable.

Botulin is an extremely complex molecule—its molecular weight is a whopping 80 times that of insulin. Its large number of atoms must be assembled with the precision of a fine watch. Its commercial and laboratory production, primarily directed by Ed Schantz, is a complex speciality which still is more art than science. Schantz has spent almost a half century researching methods of effectively extracting the pure toxin from the bacteria. His lifetime experience was required to achieve the skill needed to isolate it effectively from the bacteria for therapy use. Because it is so toxic, a lethal dose is usually only about one-ten thousandth of a milligram.28

Ironically, the usefulness of botulin to the bacterium itself is not yet known. It is an anaerobic organism, once a major problem when home canning was common and food preservation techniques were less developed than today. Although one occasionally reads about cases, it is rare today because commercial canners must by law heat their products up to temperatures and pressures high enough to kill not just the bacterium, but also the botulism spores. Unfortunately this high heat-pressure level also destroys many of the food’s vitamins.

Arsenic—A Poison and a Vital Mineral

Probably the most famous of all poisons, arsenic, is actually a vital mineral for many animal metabolic systems. It is commonly used as an insecticide or rodenticide, and most arsenic-based pest control products contain copper acetoarsenate, or calcium or lead arsenate.29 Arsenic compounds cause death by interfering with the body’s energy-producing processes in the cell mitochondria. The specific mechanism of arsenic poisoning is usually its inhibition of pyruvate dehydrogenase, the enzyme that breaks pyruvates down in the mitochondria so they can be processed for energy production. Arsenic also decreases glucose storage and inhibits glucose production.30 It is also carcinogenic and teratogenic.

Conversely, as Lederer and Fersterheim31 note, the research data indicate that ‘arsenic is an essential element for several animal species including humans’. One vital role that arsenic plays in many animals is as an enzyme component to metabolise protein and certain amino acids, including arginine and methionine. Human adults need ‘about 12 to 25 micrograms’ per day.32 The most common methods of measuring body arsenic levels are analyses of urine, hair and fingernail samples.33 Normal persons have an average concentration of 0.005 mg of arsenic per hundred grams of hair, and excrete between 0.01 and 0.06 mg arsenic per litre of urine. Arsenic is also a vital element in the electronics industry, and is needed for preparing tissue for transmission microscopic work.

Other Toxins Now Known to be Essential Minerals

Whitney et al.34 summarise some of the evidence that indicates many other well-known toxins, including lead, mercury, barium, silver and cadmium, all play key roles in nutrition and health. Barium, a poison rated ‘5’ on a scale of 1–6 (thus extremely toxic), which even in low levels can severely irritate the eyes, nose, throat and skin, is vital for proper growth and may protect the body from ulcers. Slightly greater levels of it cause cardiac irregularities, convulsions, and death from cardiac and respiratory failure.35

Other highly toxic vital minerals include iodine (also a toxicity rating of 5) which is required for thyroid hormone synthesis. Copper is needed for normal blood-cell formation and has a major role in the production of several enzymes involved in respiration, central nervous system functioning and connective-tissue formation.36 Vanadium is required for bone development and normal reproduction; cobalt is an essential part of vitamin B12; silicon is involved in bone calcification; and nickel is critical for certain enzymes to work and evidently also for iron metabolism.37

The Miracle Element Selenium

Many other trace minerals necessary for proper health are also toxic in relatively low amounts.38 Selenium is extremely poisonous (toxic at 0.2 mg/m3) and, if inhaled in sufficient amounts, causes nervous system disorders, tooth damage and Lou Gehrig’s disease. It is also an essential element needed as a co-factor for the enzymes that function as antioxidants. These compounds reduce the amount of polyunsaturated acid oxidation, now considered by many researchers to be a major cause of arteriosclerosis.39 Selenium’s role as an antioxidant is also complementary to that of vitamin E, and neither can replace the other. The recommended intake for adults is 0.05 to 0.2 mg daily.40

Selenium also may have a protective effect against certain cancers, although its most important biological function is probably part of the enzyme glutathione peroxidase. This compound helps to minimise a cellular structure damage problem called peroxidation which, regardless of whether it occurs naturally or is chemically induced, can lead to cancer. The glutathione peroxidase enzyme destroys oxidative compounds that would otherwise oxidise chemicals in the cell, consequently destroying some organelles and eventually the cell. Selenium is also probably extremely important in bolstering the body’s immune system, and its ability to reduce the incidence of cancer may be so dramatic that some researchers recommend daily supplements for the general population.

One past outbreak of heart disease involving hundreds of thousands of children and young women in large areas of western China in the 1970s was due partly to selenium deficiency. Correction of this diet deficiency has now largely eliminated the problem called Keshan disease.41 The cause of the deficiency was the low levels of selenium in the soil in those areas, a situation that also correlates with certain kinds of cancer. Most Westerners are largely protected from severe selenium deficiencies because their food is generally obtained from a wide variety of areas around the country.42 Also, meat and animal products which are good selenium sources are a major part of the Western diet.

Chromium—Another Miracle Metal

Chromium causes cancer, corrodes skin and nasal membranes, and can damage the kidneys and the body’s immune response system (toxic at 0.1 mg/m3 or less). Conversely, it has now been proven to be an essential trace element.43 Studies of patients for whom prolonged intravenous feeding was the sole source of nutrition have vividly demonstrated the importance of chromium for normal glucose metabolism. It interacts with insulin to aid the entry of glucose into the cell at the cell membrane entry port, and consequently it controls the energy supply for cell use. When chromium is lacking, insulin effectiveness is also impaired.

Because chromium tissue concentration typically declines with advancing age, and its deficiency may be a major cause of the development of adult-onset diabetes, many nutritionists recommend regular use of chromium supplements. Studies of diets which include chromium supplements have found that the element can help control blood pressure, increase stamina and build muscle.44

Chromium also plays a critical role in carbohydrate and lipid (fat) metabolism. Chromium supplements can help to correct glucose imbalances by lowering high blood glucose concentration in diabetics, raising low blood glucose concentrations as found in hypoglycaemia patients. Because chromium deficiency can also raise serum cholesterol and LDL concentration and lower HDL concentration, chromium supplements can help to prevent coronary artery disease. Unfortunately, the more refined the food, typically the less chromium it contains. Some researchers estimate that a high proportion of the population does not ingest enough dietary chromium for this reason. Fisher concludes that up to 90 % of Westerners do not take in enough of this vital nutrient.45

Chromium is unusually high in vegetable oils, brewer’s yeast, whole grains, nuts, egg yolks, meats, and certain kinds of cheeses but is often poorly absorbed; thus supplements are often recommended. Chromium absorption levels depend upon the ion ingested, and the Cr3+ ion seems to be the form best absorbed and is most effective in living systems. The dietary supplement that is evidently most bioavailable is chromium picolinate. The body also has a natural protective mechanism to prevent over absorption by causing absorption to increase with low dietary intake and decrease with high dietary intake.

Vitamins—Too Much of a Good Thing?

Almost every school child knows that vitamins are necessary for good health. Unfortunately though, many people believe that because small amounts of all vitamins are essential, larger amounts are better and megadoses are better yet. This belief may be one reason vitamin overdose is now a major problem. Called hypervitaminosis, the most common symptoms include nausea, diarrhoea, rashes, fatigue, and eventually death. Especially of concern are the fat soluble vitamins (A, D, E and K), and the most common overdose problem is vitamin A.46 Although necessary in moderate amounts for the maintenance of skin, hair and mucous membranes, as well as vision and bone and tooth growth, high vitamin A intake can cause serious health problems and occasionally death. Many health experts recommend for this reason that supplementary vitamins should be taken only under the advice of a physician.

The Natural Versus Synthetic Debate

Much of the concern over toxicity relates to the labels synthetic versus natural, a chemical division that is artificial and often meaningless. The common assumption that compounds made by nature are good and those made by humans are bad (or at least have a far greater chance of being damaging) is erroneous. Although legal definitions have been attempted, most synthetic chemicals are nothing more than modified, and sometimes not greatly so, natural chemicals. Many are identical to the natural, but are able to be produced more simply and cheaply outside of a plant or animal. Each chemical also has to be evaluated separately for toxicity concerns regardless of its source. Because this is true for all of the ten million chemical substances listed in the 1997 Chemical Abstracts, scientists have much work ahead of them.

Many persons tend to think of natural compounds as non-poisonous and human-made ones as more likely to be harmful. This generalisation is not valid; all plants, including those used by us for food, produce their own specific natural compounds which were designed to be toxic as a means of protection against pests, including insects, fungi, and animals.47 Eating a balanced diet consisting of small amounts of a wide variety of foods is generally safe. Since all foods contain toxins, the only concern should be the level to which we are exposed of each type of compound and whether our liver can adequately detoxify the level of the compound ingested. This organ is marvellously efficient at rendering excess amounts of potentially lethal compounds harmless. Our body, if healthy and not overburdened, is actually extremely effective in rendering normally-encountered levels of most toxins inert.

We should also be very cautious, but not paranoid, about utilising chemicals which have not yet been adequately tested. Many chemicals exist which we know are extremely toxic to humans, and yet many people do not seem very concerned about them.48 An example is the finding that hundreds of the over 4,000 chemicals commonly found in cigarette smoke are extremely toxic to humans. One, radioactive polonium-210 (half-life = 138.4 days), is one of the most toxic substances known to mankind, and yet many people tend to worry more about Aspartame® which has a toxicity of something like a millionth of polonium-210.49 This information could also mean saving lives if applied to reducing toxins in one’s environment.

How Our Body Protects Us Against Excess Toxins

The average person today probably is exposed to 360 millirems of radiation annually from cosmic and terrestrial sources alone. The major cosmic source is from galactic and extragalactic locations, and the primarily terrestrial source is from radon gas and smoking.50 Researchers have discerned that a phenomenon called hormesis exists to protect us against toxins and poisons. Hormesis primarily involves the toxin stimulating the development of the body’s defences against that toxin, producing antitoxins. Thus, small amounts of many toxins including radiation may be a necessary requirement to keep the body’s immune and defence systems healthy. Arsenic, copper and selenium all play an important role in metabolism—and they also may trigger the body’s defences against excess amounts.

One research study which supported this conclusion was completed by Bernard Cohen of the University of Pittsburgh. He found that up to several hundred millirems of radiation produced no discernible negative effect on health. Beyond this though, he found a slight but significant decrease in radiation-induced carcinomas. These data were unexpected because it has been assumed, in harmony with Nuclear Regulatory Commission policy, that a zero level radiation threshold exists and that the damage rises linearly until it reaches the lethal dose level.

Cohen found that the downward trend does reverse itself, but only after it rises above a base line of about 5 rems a year, about 50 times greater than the Nuclear Regulatory Commission’s annual recommended limit. Evidently, exposure does not cause problems until about 100 rems a year is reached. This finding was supported by the research on Hiroshima and Nagasaki’s 80,000 survivors, who were divided into control and radiation-exposed groups. The control group, about half of the subjects, experienced normal background radiation. The experimental group experienced significantly higher levels. About 120 incidences of carcinoma were found in the control group, a discovery which ran 180 degrees counter to the then current conventional wisdom.51

Studies of people living in high elevations who are exposed to more cosmic sources of radiation and those who live in high radon areas, as well as people who have cardiac pacemakers which use plutonium power, also confirmed that radiation exposures up to a certain level seemed to be beneficial. A possible conclusion is that these medium levels of toxins stimulate the body’s defence system, significantly benefiting the person.

[Guest Alefshin]

Detoxifying Compounds

An estimated 10 million organic compounds are known to exist naturally or have been created by the labs of the world’s scientists. The body does not have enough genes to respond in a unique way to detoxify each one of these 10 million or more compounds that exist. The body deals with this problem in a special way described below.

Compounds that are not made by the body, including pesticides, environmental pollutants, carcinogens and drugs, as well as harmless compounds, are all called xenobiotics. The term means a chemical compound that is foreign to the body (xeno is Greek for stranger). Xenobiotics typically are dealt with by a two-pronged attack. The first step is to cause a chemical reaction which makes them more hydrophilic and water soluble to prevent their accumulation in fatty tissues. The second step involves enzymes that modify the xenobiotic structure to cause it to be even more water soluble, and consequently more likely to be excreted.52

To make xenobiotics more hydrophilic, a hydrogen atom is replaced by hydroxylation reaction which is caused by a monooxygenase enzyme complex, specifically cytochrome P-450. Cytochrome P-450 is a member of the large cytochrome family, which is famous in the electron transport system for tweaking all the energy possible out of food at the end of the Krebs cycle. The ‘P-450’ designation refers to its light-absorption level, a measure used to classify compounds. This compound absorbs light most strongly at the 450 nanometre wavelength.

The second phase of xenobiotic metabolism involves bonding through either an oxygen, nitrogen, or a sulphur atom to a more highly polar group, often the glucose derivative glucuronic acid or the amino acid derivative glutathione.

About half of all drugs are metabolised by cytochrome P-450, primarily in the liver as the drugs pass through on their way into general circulation. Consequently, drugs need to be taken in a steady dose. In this way the physician can control the amount in the body. Lowering doses rapidly lowers the blood level of the drug; conversely, increasing doses rapidly increases the blood level. If the drugs were not rapidly broken down, the body could only very slowly reduce the blood level of a drug, and one would have far less control of a drug’s level at any one time. This is critical: drugs which are harmful are rapidly broken down by the body if taken in an overdose, reducing the likelihood of long-term damage. Phenobarbital, for example, a drug commonly taken to commit suicide, is rapidly hydroxylated by cytochrome P-450; then it is dissolved in the blood and excreted. For this reason large amounts must be ingested in order to be lethal.

Although the cytochrome P-450 molecule effectively detoxifies many poisons, it can convert some compounds into carcinogens. These converted compounds may damage DNA, causing cancer or other problems. The best example is polycyclic aromatic hydrocarbons (PAHs) produced by incomplete burning and found in most smoke, especially cigarette smoke (and in some meteorites). (Complete burning, that is, with enough oxygen, does not produce polycyclic hydrocarbons.) These compounds are broken down in the body into compounds which cause serious problems. Although exposure to combustion by-products as smoke is not rare, it generally does not cause a problem because the cough reflex is triggered if the environmental smoke level is excessive. Unfortunately, this cough effect can in some cases be overcome, such as in the case of certain kinds of so-called mild tobacco smoke.

The origin of this ‘mild tobacco smoke strain’ that does not as effectively trigger the cough reflex, thus bypassing this important defence mechanism, was a mutation. Therefore, when a person is smoking tobacco, this important protection is often not triggered. Consequently, in the United States alone over half a million people die annually from tobacco smoke, and it is estimated that of those alive today, smoking will take almost a billion lives throughout the world.

Cytochrome P-450 is an inducible biomolecule, meaning that if more is needed, more is made by the body. Not unexpectedly, smokers have more cytochrome P-450 than non-smokers.53 The body’s response to carcinogens varies with genetic makeup, previous exposure, and total exposure. Even if one has a genetic weakness which allows dangerous compounds to have a greater deleterious effect, avoiding exposure will reduce this problem. Actually, the people most at risk for poisoning today in the Western world are smokers, certain industrial workers and the following persons:

‘Ever-increasing numbers of people are gathering wild plants in search of new gastronomic natural treats, bringing into jeopardy another segment of the population. Some of these wild harvests involve misidentified plants and can cause a most unhappy or even deadly experience. The number of people practicing herbal medicine (a tradition that goes back to before the time of Christ) is also on the rise. People seeking natural products (roots, leaves, and bark) to make their concoctions and potions can err and experience mild to severe poisoning. Another group … [using] wild plants, sometimes at considerable risk to themselves, are those people looking for a natural high from smoking or eating plants which contain hallucinogens, although the greatest risk here comes when such a person stumbles across a hidden marijuana plot guarded by a trigger-happy protector of his crop. There have been several deaths due to such accidental encounters.’54

In a perfect world these mechanisms would be fully adequate to prevent toxins from causing problems to humans. In the fallen world, mutations in plants and animals plus destructive behaviour on the part of humans offsets this balance, causing the problems so apparent in the world around us. Nonetheless, in spite of the fact that toxins are all around us, it is rare today for a human being to die from these causes, even though the level of toxins has dramatically increased recently due to the industrial revolution, and earlier ignorance in using such items as lead drinking cups. We are now aware of many of these dangers, and in the wealthier societies at least we have largely been able to reduce these problems by pollution control. No doubt too the fallen state since Adam has changed the world in other ways. The focus here, though, is on humans as noted in the question in the beginning of the paper.

Some Conclusions

The problems with poisons are only due to excessive amounts and how the compounds are used. Compounds which are highly toxic in some situations can be life-saving in others. The toxicity problem is solely a matter of degree, that is, all compounds are toxic in high enough levels, and no compound is toxic in low enough levels. The toxicity concern is best described as one of fit: in one situation a compound is functional, in another the same level is dysfunctional. The fact that low levels of some compounds are dysfunctional in certain situations does not support the common conclusion that some compounds are innately not dangerous and others are dangerous or toxic. The focus should be on the proper use of a compound in a given situation. A review of selected common poisons and toxins demonstrates that they serve very specific roles in health even though research on many of these elements such as arsenic and botulism toxins, has only just begun. The reason God created toxins is because they are necessary for life, especially in a post-Fall world. All compounds and elements can be either beneficial, neutral or harmful, depending upon the situation and the amount.

References

  1. Young, W., 1985. Fallacies of Creationism, Detselig Enterprises, Calgary, Alberta, p. 158. Return to text.

  2. Levy, C. K. and Primack, R. B., 1984. Poisonous Plants and Mushrooms, The Stephen Green Press, Battleboro, Vermont, pp. 1, 4. Return to text.

  3. Woods, M., 1991. Chemophobia — scientists and public clash over assessment of risk. Chemecology, 20(4):18–19. Return to text.

  4. Bergman, J., 1992. Toxicity. Chemecology, 21(1):12. Return to text.

  5. Stevens, S. D. and Klarner, A., 1990. Deadly Doses; A Writer’s Guide to Poisons, Writer’s Digest Books, Cincinnati, Ohio, p. 1. Return to text.

  6. Christian, J. L. and Greger, J. L., 1992. Nutrition for Living, Benjamin/Cummings Publishing Company, Redwood City, California. Return to text. Return to text.

  7. Tisdale, S., 1988. Lot’s Wife; Salt and the Human Condition, Henry Holt and Company, New York, p. 27. Return to text.

  8. Food and Drug Association Medical Bulletin, 1994/1995. Water Intoxication of Infants, p. 5. Return to text.

  9. Thaxton, C. B., Bradley, W. L. and Olsen, R. L., 1984. The Mystery of Life’s Origin: Reassessing Current Theories, Philosophical Library, New York. Return to text.

  10. Griffith, H. W., 1988. Complete Guide to Vitamins, Minerals and Supplements, Fisher Books, Tucson, Arizona. Return to text.

  11. Griffith, Ref. 10. Return to text.

  12. Fine, R. A., 1972. The Great Drug Deception; The Shocking Story of MER/29 and the Folks Who Gave You Thalidomide, Stein and Day Publishers, New York. Return to text.

  13. Knightley, P., Evens, H., Potter, E. and Wallace, M., 1979. Suffer the Children: The Story of Thalidomide, Viking Press, New York. Return to text.

  14. Levy and Primack, Ref. 2, p. 1. Return to text.

  15. Sunlin, M., 1995. Pigeons of a poisonous feather. Omni, 17(6):36. Return to text.

  16. Jankovic, J. and Brin, M. F., 1991. Therapeutic uses of botulinum toxin. The New England Journal of Medicine, 324(17):1186–1194. Return to text.

  17. Waters, T., 1992. The fine art of making poison. Discover, 13(8):30–33. Return to text.

  18. Lundberg, G. D., 1991. Fish botulism — Hawaii. The Journal of the American Medical Association, 266(3):324–325. Return to text.

  19. Heneson, N., 1990. Deadly toxin calms excited muscles. New Scientist, 128(1746):24–25. Return to text.

  20. Chen, I., 1991. Toxin to the rescue: tapping a deadly botulinum protein to treat neuromuscular disorders. Science News, 139(3):42–43. Return to text.

  21. Rodman, M. J., 1991. FDA approvals: new drugs, new uses. NR, 54(3):61–67. Return to text.

  22. Talan, J., 1990. Treating spasms with spoiled food. Reader’s Digest, 137(823):139–141. Return to text.

  23. Hussar, D. A., 1990. New drugs. Nursing, 20(12):41–51. Return to text.

  24. Ludlow, C. L., 1990. Treatment of speech and voice disorders with botulinum toxin. The Journal of the American Medical Association, 264(20):2671–2676. Return to text.

  25. D’Costa, D. F., 1992. Low dose botulinum toxin in spasmodic torticollis. The Journal of the American Medical Association, 267(5):646. Return to text.

  26. Jankovic and Brin, Ref. 16. Return to text.

  27. Jankovic and Brin, Ref. 16. Return to text.

  28. Waters, Ref. 17, p. 32. Return to text.

  29. Stevens and Klarner, Ref. 5. Return to text.

  30. Reichl, F.-X., Szinica, L., Kreppel, H. and Forth, W., 1989. Effects on mitochondrial metabolism in livers of guinea pigs after a single or repeated injection of As2O3 (arsenic). Archives of Toxicology, 63(4):419–422. Return to text.

  31. Lederer, W. and Fersterheim, R. J., 1983. Arsenic; Industrial, Biomedical, Environmental Perspectives, Van Nostrand Reinhold Co., New York, p. 185. Return to text.

  32. Wardlaw, G. M. and Insel, P. M., 1990. Perspectives in Nutrition, Times Mirror/Mosby College Publishing, St Louis, Missouri, p. 437. Return to text.

  33. Poskanzer, D. C., 1980. Heavy metals. In: Principles of Internal Medicine, ninth edition, McGraw-Hill Book Company, New York. Return to text.

  34. Whitney, E. and Sizer, F., 1994. Nutrition Concepts and Controversies, sixth edition, West Publishing Company, Minneapolis/St Paul, Minnesota. Return to text.

  35. Stevens and Klarner, Ref. 5. Return to text.

  36. Griffith, Ref. 10. Return to text.

  37. Wardlaw and Insel, Ref. 32. Return to text.

  38. Spallholz, J., Martin, J. and Ganther, H. E., 1981. Selenium in Biology and Medicine, AVI Publishing Company Inc., Westport, Connecticut. Return to text.

  39. Spallholz et al., Ref. 38. Return to text.

  40. Christian and Greger, Ref. 6. Return to text.

  41. Christian and Greger, Ref. 6, p. 456. Return to text.

  42. Spallholz et al., Ref. 38, p. 172. Return to text.

  43. Fisher, J. A., 1990. The Chromium Program, Harper and Row Publishers. Return to text.

  44. Fisher, Ref. 43. Return to text.

  45. Fisher, Ref. 43. Return to text.

  46. Whitney and Sizer, Ref. 34. Return to text.

  47. Woods, M., 1991. Nature makes its own toxins. Chemecology, 20(5):12–13. Return to text. Return to text.

  48. Woods, Ref. 3. Return to text.

  49. Bergman, Ref. 4. Return to text.

  50. Jueneman, F., 1996. Had your radiation MDR today? R and D Magazine, February, p. 19. Return to text.

  51. Jueneman, Ref. 50. Return to text.

  52. McMurry, J. and Castellion, M. E., 1996. Fundamentals of General, Organic, and Biological Chemistry, Prentice-Hall, New Jersey. Return to text.

  53. McMurry and Castellion, Ref. 52, p. 747. Return to text.

  54. Levy and Primack, Ref. 2, p. 2. Return to text.

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