Naturally_Speaking_L_N_Shevyrdyaeva (1108797), страница 12

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Let's use this basic operating principle of evolution to predict, retrospectively, the direction of change in human height if evolution were the cause of the change. We know from studies conducted in industrial England that children born into lower socioeconomic classes were shorter, on average, than children born into wealthy families. We also know that poorer families had larger numbers of children. Given those initial conditions, what would evolution predict? The average population should have become shorter because the shorter individuals in the population were, from an evolutionary fitness perspective, more successful in passing on their genes. But this did not happen. Instead, all segments of the population--rich and poor, from small and large families--increased in height. Thus, natural selection, the process whereby differences in reproductive success account for changes in the traits of a population, does not explain why we are taller.

If evolution doesn't explain height increases, what does? Most geneticists believe that the improvement in childhood nutrition has been the most important factor in allowing humans to increase so dramatically in stature. The evidence for this argument is threefold:

First, the observed increase in height has not been continuous since the dawn of man; it began sometime around the middle of the nineteenth century. In fact, examinations of skeletons show no significant differences in height from the stone age through the early 1800s. Also, during World Wars I and II, when hunger was a frequent companion of the German civilian population, the heights of the children actually declined. They only recovered during the post-war years. Such data are consistent with recent research indicating that slow growth induced by temporary malnourishment can usually be reversed. Chronic underfeeding during childhood, however, permanently affects stature and other traits, including intelligence.

Second, the trend toward increasing height has largely leveled off, suggesting that there is an upper limit to height beyond which our genes are not equipped to take us, regardless of environmental improvements. Interestingly, the age of menarche, which is also influenced by nutrition, has shown a corresponding decrease over this same time period. Some scientists believe that the increase in teenage and out-of-wedlock pregnancies in the developed world may be an unanticipated consequence of improved nutrition.

Third, conditions of poor nutrition are well correlated to smaller stature. For example, the heights of all classes of people, from factory workers to the rich, increased as food quality, production and distribution became more reliable, although class differences still remain. Even more dramatic, the heights of vagrant London boys declined from 1780 to1800 and then rose three inches in just 30 years--an increase that paralleled improving conditions for the poor. Even today, height is used in some countries as an indicator of socioeconomic division, and differences can reveal discrimination within social, ethnic, economic, occupational and geographic groups.

For those hoping that humans might someday shoot basketballs through 15-foot high hoops, the fact that the increase in human height is leveling off no doubt will be disappointing. For those who understand, however, that our genes are merely a blueprint that specifies what is possible given an optimal environment, a limit on height is just one of many limitations in life, and certainly not the most constraining.

With environmental variables perhaps near their optimum, what are the prospects for evolutionary increases in height as a consequence of changes to our genetic blueprints? Apply the methods of the thought experiment above and see.

Exercise 7. Using the information from the text prove that:

1. Evolution doesn’t explain the increased height of people.

2. Improvement in childhood nutrition has been the most important factor in increasing the stature.

3. People will hardly increase their height any more.

Exercise 8. In the following text the paragraphs are mixed. Put them in the correct logical order. The first and the last paragraphs are in their right places.

African Adaptation to Digesting Milk Is "Strongest Signal of Selection Ever"

East African cattle herding communities rapidly and independently evolved ability to digest lactose

By Nikhil Swaminathan

(A) For many adults in the world, the phrase "got milk?" is quickly followed by "got a nearby toilet?" Lactose, the primary sugar in milk, is a universal favorite in infancy but into adulthood the level of lactase-phlorizin hydrolase, the enzyme that metabolizes lactose in the small intestine, decreases and digestion of dairy products becomes difficult. In some populations, however, such as those located in northern Europe, the ability to digest milk remains most likely as a result of lifestyles based around cattle domestication. In 2002 Finnish scientists localized the genetic mutation that conferred this trait in northern Europeans to two regions on chromosome 2.

(B) Tishkoff and her students tested 470 people representing over 43 ethnic fractions in the Sudan, Kenya and northern Tanzania for lactose intolerance using glucose-monitoring kits, familiar to most diabetics. The team then selected the 40 most lactose intolerant participants and the 69 most tolerant and sequenced parts of their genomes around the two markers identified in the Finnish lactase persistence study. The researchers determined there were 123 single nucleotide polymorphisms--SNPs, or changes to one base in the genetic code--associated with digestibility. Of these, three SNPs were more promising than the others and one of them was very common among Tanzanians and Kenyans, showing up in 40 to 50 percent of the sequences.

(C) Tishkoff believes that because she found so many markers associated with lactose tolerance in the sequencing of her 109 subjects, evolution clearly develops multiple solutions when there is a strong selective force. "There are some populations that can digest milk, and they don't have any of these mutations," she says. "There are more out there." Dallas Swallow, a human geneticist at University College London, agrees with that assessment. She released a study on a small Sudanese tribe in Human Genetics this past November, finding three markers, two of which Tishkoff had isolated in her study. Oddly enough, Swallow found no data on the Maryland study's primary variant. Tishkoff argues this disparity is due to geographic specificity of these mutations. Swallow, for her part, notes that Tishkoff's dramatic results may be a result of "the relative relatedness" of her sample. "If you have an ethnic group which is rather a small population in size but happens to migrate over geographic distances then they might be more related to each other than the surrounding people," she points out.

(D) Working with this highly correlated locus, Tishkoff's team sequenced a broad region of the chromosome around this nucleotide to determine whether it arose in concert with the European mutation. "It turns out they're on completely different chromosome backgrounds," she explains. "So it had a completely different origin." Next, the team tested to see if the mutation was positively selected, conferring a reproductive advantage and spreading quickly through the population. People who had this particular SNP on both copies of chromosome 2 had identical genetic scripts for the next two million base pairs--a phenomenon that occurs when there is a strong benefit to having a particular trait." Because this section has been preserved intact without being mutated or broken up by recombination, it indicates that it is very recent and very strong. In addition, Tishkoff's team determined the date range when the mutation likely occurred: 3,000 to 7,000 years ago, which matches up well with the archaeological record that places pastoralization coming to East Africa about 5,000 years ago. The European trait dates back about 9,000 years.

(E) Now, the results of a four-year, international research project find that communities in East Africa leading traditionally similar pastoral lives evolved their ability to drink milk rapidly and independently of the northern Europeans. According to University of Maryland biologist Sarah Tishkoff, the lead author of a study appearing in today's Nature Genetics, the mutation allowing them to "get milk" arose so quickly and was so advantageous that "it is basically the strongest signal of selection ever observed in any genome, in any study, in any population in the world."

(F) Nevertheless, both researchers are pleased that their studies found at least two genetic markers in common. Swallow concedes: "It looks jolly well as though drinking milk as an adult was good for some of us at some time in our history, that's for sure." (From Scientific American Online, December 11, 2006)

Exercise 9. Make up a list of the 10 key facts about human evolution discussed in this unit. Prove and explain your choice. Then summarize all the information discussed into one report.

Unit 12. Alcohol

We drink one another’s health and spoil our own.

Jerome K. Jerome

Exercise 1. What do you know about alcohol?

1. What is its main active compound?

2. In what regions of the world is alcohol produced?

3. How does alcohol affect the human body?

4. What are the risks of alcohol overdose?

5. What causes hangover after drinking alcohol?

6. What is alcoholism? How quickly does it develop?

Exercise 2. Read the information about alcohol provided by NewScientist.com to check some of your answers in Exercise 1.

What is it? Ethanol produced by the action of yeast on sugars.

What does it do? Ethanol is a biphasic drug: low doses have a different effect to high doses. Small amounts of alcohol (one or two drinks) act as a stimulant, reducing inhibition and producing feelings of mild euphoria. Higher doses depress the central nervous system, initially producing relaxation but then leading to drunkenness - characterised by poor coordination, memory loss, cognitive impairment and blurred vision. Very high doses cause vomiting, coma and death through respiratory failure. The fatal dose varies but is somewhere around 500 milligrams of ethanol per 100 millilitres of blood.

How does it work? At low doses (5 milligrams per 100 millilitres of blood), alcohol sensitises NMDA receptors in the brain, making them more responsive to the excitatory neurotransmitter glutamate, so boosting brain activity. These effects are most pronounced in areas associated with thinking, memory and pleasure. At higher doses it desensitises the same receptors and also activates the inhibitory GABA system.

How long is its history?

4000BC - Wine and beer making in Egypt and Sumeria

3500BC - Bronze-age vessels show evidence of wine consumption in eastern Mediterranean

800BC - Distillation of spirits in India

AD625 - Mohammed orders his followers to abstain from alcohol

1850s - New York bartenders invent the cocktail

1920-33 - Prohibition in the US. Alcohol was also illegal in Finland from 1919 to 1932 and in various Canadian provinces at various times between 1900 and 1948.

Exercise 3. Now read more detailed information about the effects of alcohol on the brain provided by Anthony Dekker D.O., Director of Ambulatory Care and Community Health at Phoenix Indian Medical Center.

What are the effects of alcohol on the brain?

The product of the oldest chemical reaction studied by man, alcohol, continues to challenge researchers. Since the original work on alcohol's neurological effects in the early 20th century, new theories have regularly emerged. What we have learned is that alcohol is a sedative-hypnotic in the acute intoxication phase for most patients. But it diminishes the quality of sleep. Individuals with sleep apnea often experience longer and more severe apneic episodes and hypoxia, or oxygen deprivation, after drinking alcohol.

In other individuals, though, alcohol may act as a stimulant. Indeed, its association with violent and self-abusive behavior is well documented. At intoxicating levels, alcohol is a vasodilator (it causes blood vessels to relax and widen), but at even higher levels, it becomes a vasoconstrictor, shrinking the vessels and increasing blood pressure, exacerbating such conditions as migraine headaches and frostbite. Researchers have also thoroughly documented the effects of alcohol on the developing fetus. Approximately one third of all babies born to alcoholic mothers will develop Fetal Alcohol Syndrome or Effects (FAS or FAE), causing central nervous system dysfunctions including Attention Deficit Disorder (ADD) and impaired IQ. There are also growth and facial abnormalities associated with these infants.

In the early 1900s, H. Meyer and Charles Ernest Overton originally theorized that the effect of alcohol was achieved by altering the lipid environment of cell membranes. This theory, however, requires much higher concentrations of alcohol than are clinically observed. A recent theory, supported by several researchers, pins alcohol's effect on voltage and ligand-gated ion channels that control neuronal activity. Two distinct ligand-gated channels have been identified, inhibitory ones (GABA receptors and strychnine-sensitive glycine receptors) and excitatory ones (N-methyl-D-aspartate (NMDA) and non-NMDA glutamate-activated channels and the 5HT3 subtype of serotonin receptors).

The inhibitory aspect occurs due to a hyperpolarization of neurons, secondary to an influx of chloride ions. The neuron becomes less likely to achieve the threshold membrane potential. The excitatory receptor is dependent on the NMDA and non-NMDA glutamate receptors that control the influx of sodium and calcium, which bind to endogenous neurotransmitters (glutamate or aspartate) and depolarize the neuronal membrane. The NMDA receptor seems to have a high permiability to calcium, which acts as a catalyst to several intracellular events.

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