Mark Pine

Schizophrenia has long been a diagnosis of irreversible deterioration. Eugen Bleuler, the Swiss psychiatrist, gave the condition its name in the early years of the last century, but before then it had been known as dementia praecox—early-onset dementia—implying relentless mental decline. All through the 20th century, schizophrenia was deemed incurable, although antipsychotic drugs might improve the course of the disease and reduce long-term institutionalization.

But in the last decade, psychiatrists have begun to question the inexorable nature of the disease, investigating whether the condition has a prodromal form, whether all cases of prodromal psychosis progress to frank schizophrenia, and even whether in some cases early intervention with psychotherapy and drugs might prevent the development of the full-blown disease.

An article in the Boston Globe on Sunday reported on the newly-emerging psychiatric diagnosis of “psychosis risk syndrome” and described a young man who began acting unusually and erratically shortly after beginning his first year at college. His mother, who works at a mental health crisis center, noticed her son’s behavior, and doctors who saw him at the time referred him to a program for treating first-episode and early-stage psychosis at Massachusetts General Hospital. There the young man received counseling and low-dose antipsychotic medication. He will return to college this fall.

Last year psychiatric researchers at Yale and other academic psychiatry departments and facilities in North America published research on a “Prodromal Risk Syndrome for First Psychosis.” They defined a condition characterized by a low level of symptoms and signs similar to schizophrenia, along with functional impairment of daily life due to mental and emotional abnormalities. They found that about 40% of such people go on to develop psychosis, in comparison to less than five percent of individuals who seek mental health treatment.

This year, Oxford University Press published a book titled “Psychosis Risk Syndrome” by some of the same psychiatric researchers. It considers the prospect that people in the early stages of schizophrenia, who receive “treatment, usually in the form of counseling and antipsychotic drugs, show a positive effect seen as delayed (and possibly prevented) onset of psychosis.” The scientists noted that “clinical research over the past several decades offers hints that very early application of existing treatments for schizophrenia might improve prognosis or the natural course of the disorder.”

Consideration of the possibility of ameliorating the course of psychotic illness comes at a time when genome scientists have begun to consider whether genes and their expression can change during the course of a lifetime. Both things were considered impossible until very recent years. To a certain extent, the two concepts are connected, since schizophrenia is known to have a large genetic component.

But now scientists know that genetic expression can be altered by epigenetic factors such as methylation of DNA. Might it turn out that early treatment schizophrenia can change the expression of that disease, perhaps by affecting the the genetic factors that have usually led to the progressive deterioration that so often occurs during the course of the illness?

Last month’s Scientific American Mind ran an article on research showing that young adults with a variant of the enzyme MAO-A in their brains carry, on average, up to 16% more credit-card debt than those with another form of enzyme. Although that’s not a huge effect, the story is interesting because of the enzyme implicated in the study. The investigation was performed by scientists at UCSD and the London School of Economics.

Monoamine oxidase type A (MAO-A) is a central player in brain function. It metabolizes (clears) monoamine neurotransmitters, thus lowering their levels in the brain. Three of the most important and extensively studied of these neurotransmitters are norepinephrine (aka noradrenaline), dopamine and serotonin, which are involved in mood, attention, motivation, goal-directed and instinctual behaviors.

The neurotransmitters act when one activated neuron (the presynaptic neuron) secretes one of them into the synaptic cleft to stimulate or inhibit the activity of the next neuron (the postsynaptic neuron) in the neuronal pathway. After secretion the neurotransmitter is withdrawn back into the presynaptic neuron, where it is destroyed by MAO-A.

The scientists found that young adults with less credit-card debt tended more often to carry a highly active variant of the MAO-A gene. But people with a low activity variant carried more debt:

In the new study, people with one “low” MAOA gene and one “high” MAOA gene reported having credit-card debt 7.8 percent more often than did people with two “high” versions, the researchers found, even when they controlled for factors such as education and socio­economic status. For people with two “low” versions of the gene, that number jumped to 15.9 percent.

The high-activity form of MAO-A would result in lower overall levels of the neurotransmitters in the neuronal pathways utilizing them. Conversely the low-activity form would result in higher levels of the neurotransmitters.

High levels of norepinephrine and dopamine may produce impulsive, addictive and manic behavior. These neurotransmitters are closely related in chemical structure to the drugs amphetamine and cocaine. High levels may tend to promote the same sorts of behavior that these drugs do. For example, a research study in laboratory rats found that inhibition of MAO-A increased the animals’ consumption of nicotine.

In humans, inhibition of MAO-A and the resulting boost of neurotransmitter levels may often result in elevation of mood and, rarely, manic behavior. Indeed MAO inhibitors were among the first drugs approved for use as antidepressants.

I would conjecture that young adults with the genes for low-activity MAO-A and higher levels of monoamine neurotransmitters probably engage more often in impulsive and instinctually driven behavior. In pursuit of their goals, they may spend more money and use their credit cards more often, sometimes without fully considering the consequences.

VACATION: I will be on vacation next week. Mark Pine blog will resume publication of new postings on Tuesday after Labor Day.

Researchers at Boston University School of Medicine have found that amyotrophic lateral sclerosis (ALS, Lou Gehrig’s Disease) may result from repetitive trauma to the brain. The disease characteristically begins with muscle weakness and lack of coordination. People have difficulty getting out of chairs, climbing stairs, and sometimes swallowing. Slowly, inexorably, the paralysis spreads up and down from the brain through the spinal cord, affecting almost all movements, including speech and respiration.

I witnessed the horrifying progression of the disease in my uncle, who succumbed in three or four years. He lost all motion, but he remained alert and aware throughout, since only motor functions are affected. Among my last memories of him: I was 10. He sat across the dining room table from me, trying to tell me something. He had something very important to communicate, and he tried very hard, again and again, to tell me. But his speech was so inarticulate, his voice unbroken by consonants, his tone uninflected by vowels, that I could not understand. He tried, it seemed to me, for an hour, although it was probably only a few minutes. I left him, apologizing, unable to endure more. I wonder to this day what he must have experienced, imprisoned in his skin.

The cause of the disease has always been a mystery. It is primarily genetic in only a few cases; most are sporadic. But the medical scientists studied the brains and spinal cords of 12 athletes—football players, a military veteran, a boxer and others—who had suffered multiple blows to their CNS and developed neurodegenerative diseases of the brain and spinal cord. On examination, they all had abnormal deposits of two proteins, one called tau and another called TDP-43 in their brains. But three of the 12, who had been diagnosed with ALS, also had TDP-43 in their spinal cords. Those three were the only ones of the 12 to show the protein there.

TDP-43 has also been found in the CNS of persons who suffered from the sporadic form of ALS, according to the report of the research in ScienceDaily yesterday.

In my uncle’s case, I always wondered whether his illness might have been connected to his job as a milkman. The occupation no longer exists. The delivery service worked in times when milk came in the early morning, unhomogenized and sometimes even unpasteurized, direct from local farms and plants. It faded away with refrigeration and supermarkets. But I remember, for a few years early in my life, the milkbox on the front stoop and the whiteness-filled bottles deposited each morning by the man with the truck. How many heavy crates of milk did my uncle lift day after day? How far did he walk carrying bottles? It was his right arm and right leg that first showed the telltale weaknesses.

Heavy lifting is not cerebral concussion, of course. But in an article in June, the scientists noted that repetitive injury to the CNS plays a central role in many cases degenerative CNS disease characterized by abnormal accumulations of tau protein. They said

Trauma to the central nervous system is one of the most consistent candidates for initiating the molecular cascades that result in Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis.

So perhaps my uncle’s years heavy lifting and carrying, his long life of yanking on his muscles and nerves, did play a role in his disease.

Vaccination usually involves injecting someone with a dead or weakened microbe for the purpose stimulating the development of immunity. A similar thing happens when a malaria-infected mosquito bites a human. The mosquito injects a form of the malaria parasite, called a sporozoite, into the person’s blood stream. Only, the human usually doesn’t become immune but sick with malaria.

Suppose there were a way to weaken the malaria parasite after a mosquito bite, so that instead of becoming sick, a person developed immunity. Scientists in Germany, the U.K. and Kenya may have discovered how to do just that. If they are correct, it may be possible to transform mosquitoes from vectors of the disease to vectors of the vaccination.

In an article last month in Science, the medical researchers reported injecting mice with sporozoites of a malaria species that mice are susceptible to. As described yesterday in a broadcast email from ScienceDaily, the scientists then administered the antibiotics clindamycin or azithromycin to the mice for three days. Instead of becoming sick, the rodents developed strong, long-lasting immunity to the parasite.

The methodology worked because of the life cycle of the malaria parasite, Plasmodium. The microbe goes two stages: a stage of sexual reproduction in the insect, which produces the sporozoites, and a stage of asexual reproduction in a human or other mammal, which produces so-called merozoites and causes the disease.

After entering the blood through a mosquito bite, the sporozoites go to the liver, where they mature into merozoites. These forms then leave the liver to infect red blood cells in the bloodstream. About two weeks after the mosquito bite, the infected red cells burst, releasing thousands of merozoites, which in turn infect more red cells. This coincides with the chills, high fever, sweats, headache, nausea and vomiting that characterize the disease. Some of the merozoites created in this stage change back to the sexual form by becoming male and female gametes. A mosquito biting at this time and sucking a blood meal ingests the gametes and the cycle begins again.

In giving the antibiotics to the mice after injecting them with the sporozoites, the scientists interrupted the cycle at the point when the parasite exits the liver. The antibiotics prevented the parasite from invading new cells by destroying an organelle it needs to do so. The parasites were thus forced to remain in the livers of the mice but were unable to invade their blood and cause the disease. But while they remained in the liver, the white cells of the mice were exposed to many of the parasite’s antigens, and the animals developed robust immunity, much as occurs in response to an effective vaccine.

The scientists hope to test their strategy in humans by providing the antibiotics, which are relatively inexpensive, to people in regions where malaria is endemic. Dr. Steffan Borrmann, one of the researchers, said:

The periodic, prophylactic administration of antibiotics to people in malaria regions has the potential to be used as a “needle-free,” natural vaccination.

Until now, efforts to develop a malaria vaccine of the usual kind have not succeeded. On its website, the National Institute of Allergy and Infectious Disease explains, “The complexity of the Plasmodium parasite and the lack of understanding of critical processes, such as host immune protection and disease pathogenesis, have hampered vaccine development efforts.”

If “natural vaccination” for malaria proves effective, would it be possible to use similar strategies to promote immunity to other vector-born diseases by giving prophylactic antibiotics to people in endemic regions?

A new test to diagnose Alzheimer’s disease (AD) at an early stage may be at hand. Until now, the definite diagnosis of this most common form of dementia required an autopsy to demonstrate plaques of amyloid-ß protein and tangles of tau protein in the brains of deceased patients. A test that would diagnose the disease before death would permit trials of drugs on living patients who test positive, a critical requirement for development treatments. The ability to diagnose early may also be a critical requirement for developing effective treatments of AD-associated brain degeneration, ones that can be administered before irreversible brain damage has occurred.

The new test assays the levels of amyloid-ß and tau in the cerebrospinal fluid (CSF), the liquid that surrounds and bathes the brain and the spinal cord, supplies these organs with nutrients and removes their waste products. The research by scientists in Europe and America, reported this week in the Archives of Neurology, found that amyloid-ß was reduced and tau was elevated in the CSF of the AD patients.

A report by Gina Kolata in the NY Times on Monday suggested that the test “can be 100 percent accurate in identifying patients with significant memory loss who are on their way to developing Alzheimer’s disease.” But although it may turn out to be highly accurate, the reporter’s assertion of perfect accuracy may have conveyed an erroneous impression.

The researchers found that the statistical distribution of amyloid-ß levels was bimodal, i.e., there were two clearly defined peaks, indicating that CSF amyloid-ß level probably reflects a single disease process affecting the patients suffering from AD.

The scientists tested the test in three distinct populations of patients with similar encouraging results. In one carefully selected group, in whom the diagnosis of AD had been made made clinically based on signs of dementia, levels of amyloid-ß were found to indicate AD in all the patients. But in a different group of patients diagnosed after death with autopsies, which is the most accurate method, 94% of the patients with AD had levels of amyloid-ß consistent with the post-mortem findings.

It’s important to bear in mind that the results reported this week came from retrospective studies. Patient-derived data from existing databases of patients, rather than the patients themselves, were the subjects of the analyses. With the outcomes (AD present or absent) known, the scientists “looked back” to the results of previous CSF tests.

A definitive study of the accuracy of the test would have to be done prospectively. Patients whose diagnoses are not known would be followed forward in time until their diagnoses became evident. The results of prospective studies—unavoidably among less carefully selected patients—often turn out less impressive than those of retrospective ones.

The new test would require patients to undergo a spinal tap to obtain CSF for the assay. Some patients and even some doctors might be discouraged by the prospect of the procedure. They need not be. The spinal tap is a fairly routine test, probably done thousands of times a day. It is safe and doesn’t usually cause severe or significant side effects.

The prevalence of obesity in America has risen to 34% of the adult population, the CDC announced last week. An adult is considered obesity if his or her BMI, which is calculated from height and weight, is greater than 30. The public health agency tracks the nation’s average BMI with telephone surveys asking people to report height and weight. Since the respondents often underestimate their weight and overestimate their height, the agency corrects the raw data to compute the actual rate of obesity. Referring to its full report, the CDC said on its website:

The data show a 1.1 percentage point increase—an additional 2.4 million people—in the self-reported prevalence of obesity between 2007 and 2009 among adults aged 18 and over. The report also notes the medical costs associated with obesity are high. In 2008 dollars, medical costs associated with obesity were estimated at $147 billion. People who are obese had medical costs that were $1,429 higher than those of normal weight.

In 2005, the NIH warned that rising obesity rates could reduce Americans’ life spans by as much as 5 years, on average. The health research institute based the projection on a report in the New England Journal of Medicine that estimated a 5-20 year reduction in longevity among the severely obese portion of the U.S. population. The problem could have an especially large impact on young people. The article said,

If the prevalence of obesity continues to rise, especially at younger ages, the negative effect on health and longevity in the coming decades could be much worse. It is not possible to predict exactly when obesity among the young will have its largest negative effect on life expectancy. However, in the absence of successful interventions, it seems likely that it will be in the first half of this century, when at-risk populations reach the ages of greatest vulnerability.

Yesterday, the NY Times reported that more girls are developing breast enlargement at the age of 7 or 8, and “increased rates of obesity are thought to play a major role, because body fat can produce sex hormones.” The article was based on research by physicians at Cincinnati Children’s Hospital Medical Center, who found that overweight girls were more likely to develop breasts. At that young age, girls may be unprepared to deal with the emotional and interpersonal challenges of elevated hormones and sexual development.

There can be little doubt that the diet of Americans, who consume large amounts of high-fat, high sugar foods, is one of the main causes of the epidemic of obesity. And the U.S. food industry has contributed mightily to the problem by selling and advertising many food products with high-fat, high-sugar content, in order to boost sales.

We Americans should at the very least, as national policy, restrict the advertising of these high-calorie food products to children via TV and the internet. And parents should teach their children to eat healthfully.

In January 2008, the CDC and the FDA learned of an unusual number of fatalities among kidney dialysis patients who had received heparin. The drug, which had been manufactured in China for use in Heparin products marketed by Baxter International, proved to be contaminated with a dangerous ingredient. Following the discovery of the problem and under the supervision of the FDA, Baxter recalled the contaminated Heparin products.

This Spring, McNeil Consumer Products recalled numerous batches of its over-the-counter medicines, including pediatric and adult products marketed under the Tylenol, Motrin, Zyrtec and Benadryl brands. Consumers had complained of being nauseated by the smell and experiencing stomach pain, vomiting and diarrhea. The FDA, which regulates drug manufacturers, criticized McNeil for not acting fast enough and failing to keep the agency informed about the problem.

One of the FDA’s most important jobs is ensuring the safety of medicines. But the work has become more difficult in recent years, when the ingredients originate all over the world and the companies that manufacture and market drugs are multinational giants. But this week Sen. Michael Bennet (D-Colo) has introduced new legislation to give the FDA more power to carry out its functions.

The Drug Safety and Accountability Act of 2010, introduced by Bennet on Tuesday would give the agency new powers [pdf] to act on its own authority to order recalls of dangerous drugs. The bill would also grant the FDA new powers to require pharmaceutical companies to document all entities involved in the manufacturing supply chains of drugs and to have management plans in place for ensuring the quality of all ingredients.

Under present law, even when the FDA has reason to believe a drug is harmful, it cannot initiate recalls on its own authority. Rather, the agency must pressure pharmaceutical companies to carry them out. As a last resort, the FDA agency may go to court to have a drug product declared an imminent hazard to public health and to obtain the authority act on its own to seize it. But the FDA is usually reluctant to take such a step. Most often the pharmaceutical companies understand the possibility of an imminent hazard declaration and want to avoid the adverse publicity, and in consequence, the companies usually agree to recalls when the FDA requests them.

Bennet’s legislation would also give the FDA power to subpoena documents and witnesses and to assess civil penalties, and it would authorize the agency to create a database of all manufacturers of ingredients worldwide.

In the case of drug regulation, as in many other governmental functions, long-standing authorizing laws are becoming outmoded. New legislation is often required to allow agencies to carry out their missions in a globalized world. Congress should pass Bennet’s bill or similar legislation quickly. … Unfortunately, that’s probably not likely to happen in the current extremely partisan, pre-election environment.

The first clinical trial of human embryonic stem cells was given the green light by the FDA on Friday. As has been widely reported, this would be the first time that the use of human embryonic stem cells (hESC) to treat an otherwise intractable medical condition has been attempted. hESC have been the focus of much bitter controversy during the last decade related to the moral issues surrounding them. If the trial succeeds, then the promise of this long-anticipated therapy will have been realized for one actual disease, and the therapeutic claims of the proponents of the therapy will have been partially validated.

The investigation, carried out by the developer of the cells, Geron, will involve people who have sustained severe spinal cord injuries but have not suffered severing of their cords. That kind of trauma results in bleeding and inflammation at the site of the injury, and paralysis of muscles and loss of sensation in the body below the injury. The patients admitted to the study must have been injured in the thoracic (chest) region of the spine and they must be experiencing the most severe form of this type of injury with complete loss of motion and sensation in their lower bodies.

This initial trial will be small, including up to 10 patients, who will have been injured one to two weeks before receiving the stem cells. Studies in animals suggest that once several weeks or months have passed since the injury, scar formation would prevent effective treatment.

The stem cells will be administered to patients by injection through a syringe placed in a specially designed positioning device to ensure that the cells are delivered to the site of the spinal cord injury. Once they have been injected with the cells, the patients will receive an immunosuppressive drug for 46 days to minimize inflammation and stem-cell rejection.

Primarily intended as a “phase I” study of the safety of stem cell therapy, the trial protocol includes a long series of neurological examinations of the participants. Secondarily, the study will assess the return of their sensory and motor functions. The volunteers will continue to be followed for 15 years.

Geron derived the hESC from discarded embryos created as by-products of in-vitro fertilization (IVF) treatments. Using the cells, the company established immortal cell lines, which is possible because embryonic cells express a protein called telomerase that permits unlimited cell division. The company took some of the hESC and used molecular techniques to transform them into nerve tissue precursor cells called progenitor oligodendrocytes.

The study is designed so that the patients in the trial will have suffered the kind of spinal cord injury that causes loss of oligodendrocytes, a type of nerve tissue cell that supports the neurons that transmit impulses along the spinal cord. The underlying rationale of the trial is that by injecting precursor oligodendrocytes, the therapy will replace the kind of cell that was lost as a result of the injury.

Before attempting the trial in humans, Geron tested the rationale, effectiveness, and safety of the treatment in laboratory rodents with the same kind of spinal cord injury. The animal tests indicated that the therapy would likely be effective and safe in humans.

If Geron’s phase I trial shows that hESC therapy is safe and potentially effective, the study would be followed by larger phase II trials of up to 100 patients, and after that, by phase III trials of several hundred patients. The large trials would be used to definitively establish the safety and efficacy of the stem cell treatment and to learn more about how to administer it and which patients benefit from it.

If patients suffering from severe, permanent spinal cord paralysis and anesthesia recover some motion and sensation as a result of the new treatment, it would be a spectacular medical advance. Moreover, the accomplishment would encourage research into hESC therapies for other kinds of intractable injuries and diseases. For example, Geron has established stem cell lines to potentially be used for heart disease, diabetes, osteoporosis, arthritis, and liver disease, in addition to the nerve tissue cells being tested in the current trial.

As women age, their bones often lose calcium and fractures occur more frequently, a condition called osteoporosis. So it seems logical for older women (and men with osteoporosis) to take calcium supplements. Logical … but perhaps not a good idea.

The BMJ (British Medical Journal) published yesterday a meta-analysis (analysis of combined data) of five clinical trials involving 8,000 people who took calcium supplements or placebo pills. The researchers from universities in New Zealand, Scotland and the United States compared the rates of heart attacks among the participants, who were followed for an average of about four years. Those taking the calcium had a 31% higher rate of heart attacks than those taking the placebo.

The researchers also presented a larger analysis involving eleven clinical trials with 12,000 people. Although these trials provided less detailed information about the participants than first five, the results were similar. Those taking calcium had a 27% higher rate of heart attacks. One important caveat: All the trials compared calcium alone to placebo. Calcium is often taken along with vitamin D, and the results may or may not be applicable to the combination.

Cardiologists from two universities in the U.K. reviewed the implications of the meta-analysis in an accompanying editorial. They noted that no increase in mortality rate accompanied the increase in the rate of heart attacks, raising the possibility of a spurious finding, since an increase in heart attacks should result in an increase in mortality. But they also pointed out that although calcium supplements improve bone mineral density, they have not been found to reduce bone fractures. In view of the possibility that they may contribute to heart disease, it would seem wiser not to take them.

The BMJ also published last January a meta-analysis of clinical trials of supplements of vitamin D with or without calcium. Pooling seven clinical trials involving 70,000 participants, Danish medical researchers found that the combination of Vitamin D and calcium reduced the overall rate of bone fractures by 8% and the rate of hip fractures by 16%. Among the patients who took at least 10 mcg of vitamin D with calcium, the rate of hip fracture fell by 26%. Taking vitamin D alone, however, had no effect on fractures.

The reduction in the rate of hip fractures from taking 10 mcg vitamin D plus calcium is substantial, particularly since hip fractures result in considerable disability and increase mortality. Still, the outcome of a benefit-risk analysis that balances the potential benefit of reducing hip fractures against the potential harm of increasing heart attacks is not clear. Although the meta-analysis published by the BMJ yesterday did not investigate heart attacks in people taking calcium along with vitamin D, the possibility that the same increase would also occur with the combination is cause for concern.

The authors of the editorial take the view that calcium supplements “seem to be unnecessary in adults with an adequate diet. Given the uncertain benefits of calcium supplements, any level of risk is unwarranted.” For the time being, the better course would seem to be eating well, including adequate amounts of food containing calcium, but not taking more of the mineral in supplements.

In Mary Shelley’s novel, Dr. Frankenstein is the creator of the monster, not the monster himself. And in the article last week in Scientific American, it is not a single scientist working alone who creates new life (actually that has already been done by Craig Venter), but a consortium of academic institutions launched earlier this year that is working together to assemble standardized parts of living organisms.

The BioFab is a “DNA factory” located within Lawrence Berkeley National Laboratory’s Joint BioEnergy Institute in Emeryville, CA. It is funded by the the laboratory, the National Science Foundation and the BioBricks Foundation. Run by scientists from UC Berkeley and Stanford, it’s website explains that BioFab will “produce broadly useful collections of standard biological parts that can be made freely available to both academic and commercial users.” The name BioFab was inspired by the Fab established by the semiconductor industry to design and manufacture custom chips. According to the BioBricks Foundation,

Using … standard biological parts, a synthetic biologist or biological engineer can already, to some extent, program living organisms in the same way a computer scientist can program a computer.

Gene promoters and ribosome binding sites are two examples of the kind of part that BioFab will design, manufacture, and stock. The former are sequences of nucleotides adjacent to a gene, where RNA polymerase attaches and initiates translation of the DNA into the corresponding messenger RNA. The latter are short sequences of nucleotides of messenger RNA that bind to ribosomes, the catalytic sites where proteins are synthesized by stringing together amino acids, according to the instructions specified in the message.

All proteins have their own sets of genes, promoters, ribosome binding sites, and other similar elements in the DNA and RNA molecules that encode them. BioFab will attempt to catalog and stock as many of these elements as it can.

In drawing a connection to the Frankenstein novel at the beginning this post, I wanted to point to the issues it raised. Just as Dr. Frankenstein failed to foresee the tragic consequences of his creative work, I find nothing on the BioFab or BioBrick websites that consider the potential negative consequences of making life parts available for order.

I do not disagree that this work should be done. But history shows that the Frankenstein-like “monsters” can and sometimes actually do arise from scientific work. Just as the monster escaped from his creator’s lab and roamed the countryside committing murders, inevitably life actually created in scientific laboratories WILL escape from those facilities and WILL in some instances inflict harm on the planet’s natural life.

If we are to do this work (and I think we should), then our government and others of the world should license and regulate the facilities in which it is done and require effective containment of the new life forms that are created.

New life forms should not be allowed to escape into the environment or to be released intentionally. Once free, life multiplies and mutates. And it is possible that some liberated creations— and their genes—would not die off but persist and spread uncontrollably.