Due Friday by 3:30 pm
Babies by Design
Submit a 250 word (minimum). Should we create babies by design?
Provide information on benefits and drawbacks to choosing traits for human babies and choose a side when developing your post.
Have you ever seen the movie GATTACA?
This movie depicts the life of a naturally conceived baby set against a world that designs babies to be less likely to develop disease and have genetic predispositions to disease. It is a movie about the drive and innate ability of the human spirit to fight and strive against all odds.
Watch this clip from the movie.
Gattaca Extract (Links to an external site.)
Please view the following website that will bring you through a series of pages that provides some information on whether or not you feel we should create babies by design. View the figures/pictures and captions and form an opinion and provide evidence that supports your argument.
https://www.pbslearningmedia.org/resource/tdc02.sci.life.gen.babiesbydesign/should-we-create-babies-by-design/ (Links to an external site.)
|Should We Create Babies By Design?|
“Would you like a blue-eyed or a brown-eyed baby? Is Alzheimer’s in your family? We can screen for that. And obesity? We’ll see what we can do.” In the not-too-distant future, doctors might routinely ask such questions of expectant parents. They might even alter the genes (Links to an external site.) of a developing fetus and create, in effect, custom-made babies. But should they?
Like no other species on Earth, we humans can influence what genes and traits (Links to an external site.) are passed on to future generations — and thereby impact the course of our evolution. Will our power to manipulate human heredity lead us down a dangerous path?
Explore what the future may hold, and ask yourself …
Do the benefits of new genetic tools outweigh the risks?
Genetically Modified Crops
http://www.pbs.org/wgbh/harvest/exist/arguments.html (Links to an external site.)
|ignore this table|
From cattle to corn, pumpkins to pigs, humans have been modifying the genetic makeup of organisms for thousands of years. Using the techniques of selective breeding and cross-pollination, agriculturists have effectively speeded up the process of natural selection and shaped the attributes of nearly all of the domestic species we know today. Cross-breeding two individuals that share a set of desirable traits—rapid growth and a strong immune system, for example—typically results in offspring that have a better-than-average mix of those traits. And by continuing to select individuals with those traits, the traits become increasingly standard to the breed.
Geneticists have similarly altered the physical and chemical characteristics of organisms, but even more quickly and significantly than classic breeders ever could. The technique geneticists use is called transgenic manipulation. This technique owes to the fact that all organisms—mammals, insects, plants, and bacteria—have large numbers of genes in common. And scientists now know where many of these genes are and what they do. This means that it is now possible to find the portions of an animal’s genome that are instrumental in, for instance, the production of milk, and insert genes that will change the makeup of that milk. The effect, according to proponents of transgenic manipulation, is predictable and immediate, and no other portion of the animal’s genome need be affected.
So, now we know it is possible to place genes from one type of organism into the genome of another. Scientists do so almost routinely these days. And by now, knowingly or not, most of us have been consuming genetically modified (GM) foods for years. Worldwide sales of GM foods skyrocketed from an estimated $75 million in 1995 to a staggering $2.3 billion in 1999.
The question today, obviously, is not whether we can change the genetic makeup of organisms through transgenic manipulation, but whether we should continue to do so. Industry, government, and many academic scientists tout the benefits of GM foods for agriculture, ecosystems, and human health and well-being (not the least of which is feeding a world population bursting at the seams). With equal passion, however, consumer groups, environmental activists, religious organizations, and many scientists warn of unforeseen health, environmental, and socioeconomic consequences.
For now, it’s too early to know which of the predictions for GM foods will materialize. In the meantime, transgenic technology raises difficult scientific, ethical, legal, and economic questions that need to be thoroughly debated.
ES-01-sustainability-GMOs article Are They Safe.pdf
https://www.pbslearningmedia.org/resource/oer08.sci.life.gen.obesity/the-role-of-genetics-in-obesity/ (Links to an external site.)
Obesity is a condition in which body weight and body fat are greater than what is considered healthy for a given height. Body mass index (BMI)—calculated as a person’s weight (in kilograms) divided by height squared (in square meters)—is a quick and simple way to estimate the amount of body fat, although it is not very accurate. Obesity is commonly defined as having a BMI greater than 30.
Having a high BMI can be a serious health hazard; obesity is associated with high blood pressure, osteoarthritis, diabetes, heart disease, respiratory problems, and some cancers. Unfortunately, the prevalence of obesity has risen to epidemic proportions over the past couple of decades. In the United States, the majority of adults are overweight and over 30 percent are categorized as obese. Childhood obesity has also become more common—approximately 15 percent of children and adolescents are obese—which has led to an increase in the incidence of health problems that were once rare among children.
Both genetic and environmental factors play a role in the development of obesity. Individuals with varying genetic predispositions may respond differently to the same environmental conditions; for example, some people may be genetically disposed to overeat or to store body fat more easily. In other words, within a population of people who share similar environmental and behavioral conditions (such as food quality and physical activity), there will be a range of body types.
The influence of genes on obesity is strong; there is evidence that 70–80 percent of the variation among individuals in body fatness is due to genetic factors. Furthermore, specific genes have been discovered to be associated with obesity. For example, a small percentage of people (estimated to be about one in 1,000) have a genetic mutation that affects the melanocortin 4 receptor (MC4R)—a receptor in the brain that receives signals to regulate appetite via the hormone leptin. This genetic mutation changes the surface of MC4R so that it is unable to process the message to control hunger. As a result, people with an MC4R mutation are more susceptible to obesity because their brains do not receive the signal to suppress the urge to eat. With no signal to tell them that they are full, they continue to feel hungry even after their body no longer needs additional energy.
However, the genetic influence is only part of the story—lifestyle is also critically important in contributing to obesity. The recent increase in the percentage of people categorized as obese cannot be attributed to genetic changes that favor obesity (genetic changes of populations occur much more slowly); the increase in obesity is more likely a result of sedentary lifestyles and calorie-rich diets that cause an energy imbalance. Body weight is maintained by consuming as many calories as are used, and a balanced diet of healthy foods contributes to overall health. Current lifestyles often support excess calorie consumption and not enough physical activity, which result in weight gain and poorer health.
https://www.youtube.com/watch?v=flqmyzE–Fg (Links to an external site.)
The map of the human genome has provided far more than a simple list of the three billion letters that make up our genetic code. Scientists are now beginning to understand what certain groups of these letters—our genes—actually do. They estimate that about thirty thousand genes in all carry the code for every structure and function in the human body.
An important corollary to understanding proper gene function is that by doing so we gain a better understanding of gene dysfunction. Indeed, scientists have identified the genes responsible for more than two dozen diseases. So far, however, finding the genetic cause of disease has provided little more than the promise of a cure. Fixing broken genes is altogether more difficult.
A few decades ago, some scientists promised that “gene therapy” would cure a myriad of genetic diseases. Doctors would simply insert normally coded genes in place of malfunctioning ones. The normal genes would override the abnormal genes, produce whichever vital proteins were missing, and the problem would be solved. But several hurdles have stood in the way of what once appeared to be an elegant solution.
Many genetic diseases are caused by more than one gene, or are strongly influenced by environmental factors. These diseases are probably too complex to be cured through gene therapy. In an effort to cure diseases that are caused by the dysfunction of a single gene, however, many scientists are continuing to try to perfect the technique.
For gene therapy to have any long-term effect, replacement genes must be incorporated into the DNA of a huge number of a patient’s cells. If this is accomplished the genes will be replicated and passed on when cells divide. None of this can happen, though, unless the genes actually find their way into the cells’ nuclei. Herein lies the problem. DNA injected into a patient’s bloodstream has little or no chance of ending up inside the nucleus of any cell. So how do doctors get genes inside where they can be of some use? The most promising technique uses viruses as DNA delivery vehicles.
In the late 1980s, geneticists discovered that certain types of viruses, called retroviruses, could be modified to carry replacement genes into the nuclei of cells. These viruses attach whatever genetic material they carry, including the replacement genes, directly to the host’s DNA. Because viruses are human pathogens and carry inherent risks, however, progress with gene therapy has been slow.
More often than not, doctors have erred on the side of caution, stripping the viruses of their toxins and their ability to replicate, and injecting only a few thousand into the patient at a time. The effect of such cautious therapy, however, has been marginal because the number of cells receiving replacement DNA in cases like these is quite low. Leaving too much of the virus’s own DNA intact or introducing too many viruses into the patient’s system, on the other hand, can have deadly consequences.
Cystic Fibrosis II
https://www.pbslearningmedia.org/resource/cygc12.sci.life.gen.cfgene/from-the-cystic-fibrosis-gene-to-a-drug/ (Links to an external site.)
As scientists continue to study the human genome, they can better understand how the different groupings of bases that make up our genes control their function. A better understanding of proper gene function offers scientists important insights into gene malfunction, which can lead to serious diseases. Scientists have successfully identified the genes responsible for hundreds of inherited diseases. But finding the genetic causes of diseases has yet to yield a bounty of ways to treat them.
Even before the Human Genome Project produced a “rough draft” of the human genetic code in 2003, scientists were already touting gene therapy as a cure for genetic diseases. Doctors might simply insert normal genes in place of malfunctioning ones. The normal genes would take over, produce the right kinds of proteins, and any problem would be solved. But this elegant solution has yet to be realized. For one inherited disease, cystic fibrosis (CF), the biology proved much more complicated than scientists anticipated. Cystic fibrosis causes sticky mucus to block tubes and ducts in the lungs, pancreas, intestines, and other areas of the body. Because a buildup of mucus makes it easy for bacteria to grow, serious lung infections develop that, repeated over time, can severely damage the lungs. For CF patients, breathing becomes more and more difficult with time.
Cystic fibrosis was considered by many to be a prime disease candidate for gene therapy. Unlike diseases that involve multiple genes, people with CF inherit just one faulty recessive gene from each parent. However, every clinical trial failed. The modified viruses used to deliver the normal genes had trouble getting past the mucus to the cells that needed them. Even those that made it were unable to hijack the cells and replicate, as viruses normally do. So some researchers tried a different approach: they developed drug compounds to correct the function of the faulty protein made by the CF gene (CFTR). The challenge of designing a drug is daunting and involves a tremendous amount of trial and error; 600,000 compounds were tested to develop Kalydeco. Drug development timelines of 20 years or more at a cost of hundreds of millions of dollars are common in pharmaceuticals.
Decades before Michael McCarrick appeared in this video, researchers identified the most common genetic defect behind the disease—three missing letters in the CFTR gene. However, there are more than a thousand other mutations that can also produce CF, and different mutations cause different defects in the CFTR protein, resulting in milder or more severe forms of the disease. The experimental drug that McCarrick took, Kalydeco, and other so-called CFTR modulators are therapies designed to correct the function of the defective protein. While the drug was not able to save McCarrick—the damage to his lungs proved too great, and he died two months after the video was made—both adult and pediatric treatment groups in a clinical trial showed improved lung function and an increase in weight and other quality of life measures, with few safety issues. Kalydeco was approved by the FDA in January 2012, becoming just the fourth drug approved to counteract the effects of a specific gene mutation to make it
https://www.pbslearningmedia.org/resource/tdc02.sci.life.cell.mitochondria/the-powerhouse-of-the-cell/ (Links to an external site.)
Cellular respiration is the process most cells use to convert food molecules into energy. In multicellular organisms like humans and trees, cellular respiration takes place in the mitochondria. These important organelles and the high-energy molecules of ATP they produce power virtually every biochemical reaction that takes place—both in your body and in the plants and animals around you. While scientists have long understood the importance of mitochondria in energy production, it was not until the early 1990s that geneticists began to recognize that mitochondria might help explain the path of human evolution.
Efforts to understand human evolution have been fraught with controversy ever since the study of human and humanlike fossils began. One of the most enduring and heated debates to come out of the field of paleoanthropology has to do with whether Neanderthals ever interbred with early Homo sapiens. The fossil record shows that Neanderthals roamed Earth, in and around what is now modern-day Europe, until about 30,000 years ago, which means they and early Homo sapiens coexisted. But were these two groups of hominids (as scientists call all humanlike creatures) close enough culturally and, more important, genetically to have interbred?
One possible answer to this question has come from scientists studying mitochondria. These energy-producing organelles contain their own DNA distinct from the DNA found in the nuclei of most of our cells. Individual cells may have hundreds of mitochondria, which means that each cell will also have hundreds of copies of mitochondrial DNA (mtDNA). This is important given that DNA in fossils breaks down over time. After 30,000 years, fossilized Neanderthal cells have only fragments of DNA left in them—not enough to piece together the entire Neanderthal genome but sometimes enough to assemble a complete Neanderthal mtDNA genome.
As with nuclear DNA, the genetic sequence of mtDNA evolves over time. Some scientists suggest that the rate of change—the mutation rate—is fairly constant. If this is the case, then the amount of difference between the genetic sequences of two fossil individuals should be a good measure of the amount of time that has passed since the genetic lineages of the two individuals diverged.
An analysis of mtDNA taken from two Neanderthal fossils and from hundreds of contemporary humans showed a great deal of difference between the two groups. While each group showed variability among individuals within the group, there was three times as much variability between two individuals of different groups. The scientists who conducted the research say the amount of variability they observed between modern Homo sapiens and Neanderthals could not have arisen in just 30,000 years. They conclude that Homo sapiens and Neanderthals must have diverged hundreds of thousands of years ago and so could not have interbred. Critics argue that until more evidence is found, the relationship between humans and Neanderthals remains an open question.