Archive for June, 2011

The Dark Side Of Genetic Engineering

THE DARK SIDE OF GENETIC ENGINEERING

Ken Fischman, Ph.D.

“Everything has both intended & unintended consequences, & the intended

consequences may or may not happen, but the unintended consequences always do.”

Dee Hock, former CEO of VISA International

In 1988, Showa Denko, a Japanese pharmaceutical company, shipped the first batch of genetically engineered L-Tryptophan to the United States. L-Tryptophan is an amino acid, normally contained in all of our cells. Naturally-derived L-Tryptophan had been sold over the counter for decades to thousands, perhaps millions, of people to relieve symptoms of insomnia or depression. There had never been reports of any ill effects.

The genetically engineered L-Tryptophan killed 37 Americans, more than 5,000 others came down with a hitherto unheard of disease called Eosinophilia Myalgia Syndrome, and many were permanently injured.

Showa Denko’s attorney admitted in federal court that it was most likely that the genetic engineering had caused the calamity. Just prior to the trial, Showa Denko destroyed the original batches of bacteria from which the L-Tryptophan had been extracted.  Showa Denko was clearly at fault, but because the bacteria were no longer available for analysis, it could never be definitively proven that it was specifically the genetic engineering that did it. The Food and Drug Administration (FDA) declared that it was not the genetic engineering that was at fault, and the deaths and injuries were probably due to some manufacturing error. Instead of banning only the genetically engineered variety, they banned all over-the-counter sales of L-Tryptophan.

When Watson and Crick unlocked the secret of DNA in 1956, they fundamentally changed our world. They enabled scientists to understand many of the basic properties of inheritance. This was followed by the introduction of techniques enabling scientists to manipulate those processes in order to alter living organisms in ways that had never before been possible. In rapid succession, scientists deciphered the code found in the sequence of molecules along the long DNA chain, and discovered that DNA produced a similar molecule called RNA, which in turn produced proteins. Some kinds of proteins make up most of our cell structures, while others function as enzymes, controlling essential bodily processes. This new field of science is called Genetic Engineering (GE) and the new forms of life produced by it are termed Genetically Modified Organisms (GMOs). They are brought to you by modern wizards called Molecular Biologists.

Molecular Biologists have been able to decipher the genetic code laid out in the linear sequence of genes and identify many of their functions.  They can snip them out of the chains of DNA and insert them in the cells of other organisms. Farmers, animal husbandmen, and scientists have been breeding animals and plants for thousands of years in order to produce new combinations of characteristics. However, up until now, these characteristics had always been ones that had preexisted in some members of the same species. Through eons of evolution, living organisms accumulated combinations and sequences of genes that for the most part work together harmoniously. However, the techniques of Molecular Biology shorten the time dimension and leapfrog the species barrier. For example, it is now possible to take the “antifreeze” gene from Flounders, a cold-water species of fish, and insert it into the genome (total array of genes in an organism) of a potato! This enables GE potatoes to survive periods of frost, and to extend their growing seasons. Thus, scientists can now combine genes that had never before been in the same organism.

The wonderful potentialities of this science have been emphasized for years by molecular biologists, the medical establishment, agribusiness, and government itself. They tell us that they will be able to cure humanity’s illnesses, produce wonder drugs grown in genetically-altered animals, grow made-to-order organs for transplantation, feed the starving millions of mankind, etc. However, none of these institutions talk about the dark side. This article explores the dark side.

In 1992 the FDA issued a ruling, stating that genetically engineered foods are “substantially” like natural foods, and therefore do not need to be regulated.  This has come to be known as the “Substantial Equivalence” rule.  The significance of this ruling was that the food industry would not have to perform safety studies and clinical tests on GMOs, such as are required before new drugs come onto the market. The ruling also removed much of the oversight that the FDA would exercise on drugs after they reached the market. The Federal Government could thus argue, and subsequently did, that because these GE foods are just like regular foods, there is of course no need to label them in order to distinguish them from other, non-GE foods.

European countries, on the contrary, have adopted a different approach  to the marketing of GMOs.  They have put the onus of proving the safety of these foods on the manufacturers, by invoking what is called the “Precautionary Principle”.  This states, in part, that “When an activity raises threats of harm to human health, or the environment, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically.  In this context, the proponent of an activity, rather than the public, should bear the burden of proof.”

Due mostly to these fundamentally different approaches, the United States and the European Union are locked in a struggle.  The Bush administration appealed to the World Trade Organization to issue substantial fines on European countries which do not allow importation and sale of GMO food from the US.

It has been repeatedly stated by both government and food industry spokesmen that there have been no documented cases of someone being harmed by GE food.

In light of these claims, an interesting incident occurred in 1996. Pioneer Hybrid, then the largest seed company in the world, wanted to make an improved soybean. Soybeans lack some of the 21 Essential Amino Acids (EAA) that human beings and most other animals need for life, but cannot produce on their own. Most of us get our EAAs from meat. Vegans, however, must carefully balance the types of plants they eat in order to make sure that they get all 21 EAAs in their diet. Pioneer extracted a gene from Brazil nuts in order to increase the soybean’s production of another amino acid, Methionine. They then gene-spliced it into their soybeans in an effort to improve their nutritional value, and hopefully the company’s profitability.

Just before this GE soybean was scheduled to go on the market, it came to the attention of some University of Nebraska scientists. By a stroke of good luck, they just happened to have some blood sera from people who were allergic to Brazil Nuts, and they decided to test these beans on it. They got a strong allergic reaction. Quite a few people are allergic to Brazil nuts, and eating these soybeans might have killed many of them. Obviously, something else besides the gene for the amino acid had been transferred into the soybeans.

When genes are to be introduced into host cells, they do not come alone. After the donor DNA has been cut into many pieces, it is then inserted into bacterial plasmids (circular bacterial DNA), and in this form, the genes can be duplicated to any number necessary. Then, they must overcome the host cell’s defenses against invasion of foreign DNA. This is usually accomplished by attaching a “ferry,” – an infectious virus or bacterium – to that gene. The virus or bacterium can penetrate into the cell and insert the gene into the native DNA. A way also has to be found to identify and select those cells in which the new gene has been inserted and to dispose of all cells that do not contain this gene. This is usually done by attaching a so-called Antibiotic Resistance Marker (ARM) gene. This ARM confers antibiotic resistance, usually to Streptomycin. Treating the cells with Streptomycin then kills all cells which do not possess the desired inserted gene.

Genes do not function all by themselves. Most of them are active during only part of the life of the cell.  They may need the assistance of other genes, called Promoters, which “turn on” or activate them. Therefore, a promoter gene, derived from a virus,  is also attached. These genes may also bring with them uninvited guests. When genes are snipped out of their original DNA chain, the process is not exact. The chain is cut in various places by enzymes, leaving pieces of, or entire neighboring genes, attached to the gene to be inserted. The properties of these DNA Fragments may not be known and their presence may not even be detected.

From this and other evidence, a reasonable person could draw the conclusion that contrary to what the FDA and food industry say, GMOs used as foods are definitely different from regular foods, and need to be tested and labeled to safeguard the health of both ourselves and the rest of the planet.

There are several good arguments why GE foods should be labeled. For one, people should have the right to know what is in the food they feed to their families. But even more importantly, if GE foods are not labeled, and something goes wrong, and people get sick and/or die, what could be done to trace the source of the problem? Epidemiologists, those public health officials whose job it is to track down the causes of diseases and other health hazards, would have no way to trace the problem back to the GE foods.

One more important point. Agribusiness companies such as Monsanto consistently claim that their GE seeds will increase crop yields with these techniques, thus being able to feed the world’s ever-increasing human population and avoid famine and starvation. Unfortunately most of the evidence so far demonstrates that on the contrary, most of them either marginally increase or even decrease yields. One theory of why this occurs is that much of the plant’s energy has been diverted from normal growth into perpetually producing the inserted gene’s product.

A holy grail of molecular biology has been the hope that GE will one day be able to cure inherited diseases by substituting normal genes for the abnormal ones. For the first government-sanctioned attempt at Gene Therapy, children with a hitherto consistently lethal disease were selected. These so-called bubble babies have non-functioning immune systems, and need to be physically isolated from the environment  in artificial enclosures. They usually die in early childhood from infections against which they have no defense. A number of clinical trials were begun around the world, in which ostensibly normal genes were inserted into such children.  Eleven children were selected for one trial in France. Their physicians were optimistic due to the preliminary results. Most of the children showed improved immune functioning. Then one boy came down with Childhood Leukemia. They assumed that this was an unfortunate coincidence. A few months later a second child developed Childhood Leukemia.

Analysis of their DNA showed what had happened. In the first child the Promoter gene accompanying the therapeutic gene had landed square in the middle of an Oncogene called LMO-2, and turned it permanently on. An Oncogene is a gene, probably needed for normal development, which if switched on permanently, causes cancer. Analysis of the other child’s DNA provoked  much more concern. The same Promoter gene landed near the same Oncogene, but not on it. Promoter genes show a gradation of effects, depending how close they are to the gene in question. The closer, the stronger the effect.  All gene therapy trials were immediately stopped.

The results of this trial are exceptionally chilling. It showed that it matters very much where in the host genome the foreign gene is inserted. The fact is that the scientists have no idea of where the gene is going to land; where, if any, there is a “good” place to land; and no way exists at this time to direct it to such a place.  There has been much talk about “targeted gene repair” , but so far scientists have been unsuccessful in directing foreign genes to specific sites, and may never be able to do so.

Perhaps even more importantly, the question arises as to whether the insertion of the Promoter gene in the Oncogene in one case and near the Oncogene in the other, was a coincidence. Considering the vast amounts of DNA in a cell, and that a human cell is estimated to contain 10 – 30,000 genes, it is very unlikely that this was an accident. Therefore, we are left with the possibility that when foreign genes are inserted into a human cell, their destination may not be random, but directed, but not by us. In these cases, it was directed to an Oncogene, with tragic results.

There has lately been some good news in the field of gene therapy. The latest trials of this technique have met with better results.

The prospect of worldwide distribution of GMO’s is particularly troubling because they differ in several crucial respects from pollution by petrochemicals and radioactive substances.  Unlike chemicals, GMOs can replicate themselves, thus producing potentially immense amounts.  They can mutate(change) their genetic constitutions, and therefore, their properties.  Furthermore they can disperse to other environments, either on their own, or by piggybacking on other organisms by becoming integrated into their DNA.  It is quite likely that if  some of them prove to have deleterious effects, it will be impossible to correct the situation, and put them back in Pandora’s box.

In this new world of GE, which we are entering so rapidly, the term caveat emptor (let the buyer beware) takes on a new and ominous meaning.

The Dark Side of GE, 10/29/03

The Biology And Politics Of Breast Cancer

 

The Reader 6/9/05

 

         THE BIOLOGY AND POLITICS OF BREAST CANCER

 

                                             by Ken Fischman, Ph.D.

 

Dedicated to the memories of:

         Vicki Long

         Mary Shackelford

         Barbara Veranium

 

A Parable for Our Time

         People in a town along a river spotted a person drowning in the turbulent waters and attempted to rescue him. The next day they noticed more and more people struggling in the torrent, and redoubled their efforts to save them. They became experts in river rescue and invented more and more ways to try to retrieve and resuscitate the drowning victims.  In fact, as time went on, they became world-famous for their ever-more innovative river rescue techniques, of which they were quite proud.

         However, don’t you think it odd that in all this time, they never thought to look upstream to find out who was pushing these people in? (adapted from Living Downstream, by Sandra Steingraber,)

         In this article, I invite the reader to walk with me upstream, along the banks of that river.

        

The Biology of Cancer

         In order for the reader to better understand what cancer is and what its medical and political implications are, it is necessary first to cover a few basic biological concepts. 

         Cancer cells are cells that no longer obey the body’s controls. They revert to a primitive state, and have a tendency for perpetual growth and tumor formation.  Genes are the basic units of heredity within cells. You can think of them as a set of blueprints for building and controlling your body. There are thousands of different kinds of genes in human beings.

         DNA is the chemical stuff that the genes are made of. DNA is an extremely long molecule, made of thousands of subunits.  The genes are attached to each other in groups of hundreds, like a string of pearls. There are 46 of these strings in each human cell and we call them Chromosomes.

         A remarkable property of genes is their ability to make identical copies of themselves.  They distribute these copies, one to each of the new cells produced through a process called Cell Division.  Therefore, every cell in your body contains a duplicate set of genes.

         If every cell in your body has an identical set of genes, then why do some cells look and act differently from each other?  Muscle cells produce a protein, called myosin, that enables them to contract.   Brain cells produce neurotransmitters, which enable them to send signals to other cells.  The explanation is that all of the genes in a cell are not functioning all of the time.  There is one set of genes functioning in a brain cell and a somewhat different set in a muscle cell.

         Which groups are functioning is controlled in two different ways.  The first way is controlled by other genes; the second, is by chemical signals from outside the genes, which may even come from distant parts of the body.  Hormones are the chemical messengers involved in this kind of remote control.

         An Oncogene (“cancer gene”) is one type of controller gene that plays important roles in Breast Cancer (BRCA). It is normally involved in directing growth and cell division.  It is only when genes of this type are malfunctioning that they cause cancer.  You can think of a faulty Oncogene as if it were a stuck accelerator on an automobile.

         There are two types of cancer: (1) inherited and (2) acquired: 

         The inherited type occurs as a defect in the person’s genes and has been passed on to him/her through the egg or sperm from one, or both parents . The defective gene is therefore found in every cell of his body.  This gene can be passed on to the next generation, again through the reproductive cells. Familial BRCA is of this type. 

         Acquired cancer, on the other hand, occurs due to changes that take place in the genes in at least one of the person’s cells during his lifetime. If it does not occur in one of his reproductive cells, it cannot be passed on to the next generation. Examples are: lung cancer, Leukemias, and most BRCAs.

         A mutation is a change in a gene.  The change is passed on to the cells resulting from division of the cell that carries the mutated gene.  When these cells divide in their turn, the mutation is passed on again, and so on and so on, until there can be millions of such cells, each with the identical defect. 

         There are several ways in which these mutations can come about. One way is for a mistake to happen while the DNA is duplicating itself.  Another way is for an environmental agent, like radiation or a chemical, to come in later, and damage the DNA in some way.  A third way is for a mistake to occur later, during cell division.  The chromosomes might break or not be distributed equally between the resulting cells.  Any one of these kinds of mutations, and sometimes all three, can be involved in producing a cancer cell.

 

 

 Breast Cancer – A World-Wide Epidemic

 

         Breast Cancer is a disease that strikes one woman in seven. The incidence of BRCA has risen steadily since World War II. It increased 60% between 1950 and 1988. This increase has nothing to do with increased longevity.  For example, women born in the USA between 1947 – 1958 have three times the rate of breast cancer as their grandmothers had at same age. In 1991, 170,000 American women were diagnosed with BRCA.  The latest available figures are for 2002, with 205,000 new cases.  That is an 20 % increase in eleven years.

         This type of cancer is effecting younger women more and more. BRCA kills more women between the ages of 35-50 than any other disease.  Why has this veritable explosion in BRCA occurred?

         The American Cancer Society (ACS) points to ‘lifestyle’ and heredity as the prime villains.  Their brochures exhort women to: (1) exercise, (2) lower fat in their diets, (3) perform breast self-examinations, (4) examine their family history, and (5) receive regular mammograms in order to detect BRCA, etc. Yet, the great majority of BRCAs cannot be explained by either inheritance or so-called ‘lifestyle’ factors. Let’s examine a few circumstances:

         The list of chemicals and other environmental agents, known or suspected to be cancer-causing is a very long one.  Yet, in all this time, only about a dozen have been banned by U.S. government agencies.  Here are just a few of the more egregious cases.

         Twenty seven years ago evidence was presented that women working in the plastics industry and exposed to Vinyl Chloride (VC), faced an increased risk of BRCA. (J. Occup. Med., 1977). VC was acknowledged by the Environmental Protection Agency (EPA) to be a human carcinogen (cancer-causing agent). It was not banned however, and enormous quantities of it are still being produced and distributed around the world.

         Polychlorinated Biphenyls, better known as PCBs, are strongly suspected of causing BRCA.  General Electric dumped PCBs into the Hudson River in New York state until the 1970s.  There are an estimated one million pounds lying on the bottom of a 40 mile stretch of the river .

         Well known risk factors for BRCA are: (1) early 1st menstruation, (2) late menopause,  and (3) late or no childbirths. What these factors have in common is that they all increase a woman’s lifetime exposure to estrogens. 

         Estrogens are hormones, secreted by a woman’s ovaries each month. It effects only cells with Estrogen Receptors on their surface. The hormone attaches to the receptor. Then the Estrogen-Receptor complex penetrates into the nucleus and activates one particular set of genes while turning off another set. The net effect is to increase cell proliferation in: (a) the vagina, (b) the uterus, and (c) the breast. Estrogen therefore stimulates ovulation, menstruation, and breast development. 

         A full term pregnancy early in a woman’s life protects against BRCA. Why? The current theory is that breasts do not completely develop until the last few months of the first pregnancy.  Once they are developed, cell division in them slows, and because DNA in non-dividing cells is less sensitive to damage from radiation and chemicals, these women are less vulnerable to BRCA.

         Early onset of puberty is also a strong risk factor for BRCA. Consider the following  facts: The average age of female puberty in the 1940s was 13 – 14 years. At present it is 10 – 11 among whites, and even earlier among black girls. Some possible explanations are:

         Since WWII, over 70,000 Synthetic Organic Chemicals (SOCs) have been produced, some in enormous quantities, and distributed all over the world.  They have infiltrated our air, water, food, and our very bodies.

          (1) many pesticides, herbicides and other SOCs are endocrine-imitators, (i.e they have estrogenic effects).  SOCs may hasten the onset of puberty. There is strong evidence that Atrazine, the most widely used herbicide in the world, has this type of effect.  Despite this, the EPA has recently refused to ban it.

         (2) Americans eat a greater proportion of meat in their diets than any other people. Chickens and cattle are often treated with hormones in order to make them grow faster.         

         Women who have fatty diets have greater risk for BRCA.  The NCI, and many other authorities, have concluded from this that fat causes cancer, and they have told women to change their lifestyles by doing more exercise and eating less fatty foods.  Some scientists however believe that it is not the fat, but what is in the fat that causes BRCA. Many SOCs are fat-soluble, and therefore tend to concentrate in fatty tissue such as the breast and bone marrow.  The more obese you are, the more carcinogens you accumulate. (Carcinogen concentration in fatty tissues may also explain why the incidence of Multiple Myeloma, a hitherto rare cancer of the bone marrow, has increased ten-fold in the past few decades) . 

         SOCs not only lodge in fatty tissues, they become biomagnified (concentrated) there.) In addition, SOCs are not easily metabolized and excreted.  Therefore, they may linger in tissues for years. Some researchers have called fat the body’s hazardous waste site.

 

Inherited Breast cancers

 

         You have probably heard of  Breast Cancer Families, in which several generations of women develop BRCA.  Two BRCA genes have been identified: BRCA-1 & BRCA-2. Women who possess BRCA-1 also have a higher risk for Ovarian cancer, but this does not appear to be so for those who have BRCA-2. Women who inherit either mutant gene are at much greater risk earlier in their lives for subsequent steps in the carcinogenesis process (described further on in this article). This is demonstrated by the high percentage of women possessing the gene, who get BRCA in their 20s (40%), compared with the much lower percentage of women who have the gene, who get BRCA in their 80s(1%).

         A good way to distinguish between inherited and environmentally-induced diseases is to compare populations in different parts of the world. It has been observed for example, that BRCA rates in the U.S. are thirty times higher than in parts of Africa.  We can also evaluate  groups of people before and after they migrate from an area of high disease incidence to one of low incidence, or vice versa.  BRCA rates rise in Jewish women who migrate from  North Africa to Israel; rates decrease when English women migrate to Australia.  Their genes  of course remain the same. Only their environment has changed.        

         As previously mentioned, inherited Breast Cancers were the predominant form of BRCA before the 1940s.  Their incidence has not increased in the ensuing years.  They are now a tiny minority of all BRCA cases, probably no more than 5 – 10%, and effecting only about 1/3 of 1% of all women. The other 90 – 95% of BRCAs are classified by US government agencies as ‘sporadic’, meaning that the cause is unknown.

         Saying that most BRCAs are ‘sporadic’ reminds me of a story about a novice boxer.  His manager sends him into the ring against a much more experienced opponent.  He is getting badly beaten.  At the end of one round he comes back to his corner with his nose bleeding, one eye almost closed, and bruises all over.  His manager tries to buck him up.  “You’re doing great kid” he says “You have him on the run. He hasn’t laid a glove on you.”  The kid turns around and looks at the manager.  “Yeh?”, he says, “Well you better keep an eye on the referee because someone out there is sure beatin the crap out of me!”                 

 

  Mechanism of Carcinogenesis

         Normal cells do not become cancer cells in one swoop. For example, Benzo(a)pyrene is the principal cancer-causing agent in tobacco smoke.  It and Croton oil are much more effective in inducing cancer when applied sequentially, rather than together. This is evidence that there is more than one step in cancer production.

         Mutations are usually chance events that could occur in any one of the cell’s thousands of genes. Routine errors could be made during DNA replication, or a gene could be damaged by a carcinogenic  agent.  The first step toward cancer is a mutation.  This is obvious because tumors continue to grow even after the carcinogen is removed.  Therefore, an event has occurred that is being passed from generation to generation of its cells.                          

        

         Another clue that cancer is a multi-step process is the long lag time, or latent period after first exposure to a carcinogen before a recognizable cancer develops.  It may take many years.  This lag time occurs because two or more rare chance events have to take place in order for a cell to become cancerous.  The probability that two rare events will both happen is the product of the chance for each of them to happen by itself. 

         A simple illustration of this is flipping a penny.  If you flip it once, the chance that it will come up heads is 1/2. If you flip it twice, the chance that it will come up heads both times is 1/2 X 1/2, or 1/4.  Imagine then that if the chances that each of these two mutations occurring in the same cell is a couple of thousand to one, the probability of both happening is a very long shot indeed. Time however, is an additional factor.  The longer the cell lives, the more likely it is that the second mutation will eventually occur.

          The stages for inducing a cancer cell are called: (1) Initiation, (2) Promotion, and (3) Progression

         1.  Initiation is usually a small subtle lesion in DNA. There are no visible changes, but it can be recognized by the body and reacted to.  The immune system may recognize changes in the cell surface and then destroy the aberrant cell. Any weakening in these defense mechanisms could lead to retention of initiated and therefore potentially cancerous cells, making it more likely that some of them will survive to reach the next stage of carcinogenesis.        

         2.  Promotion unfolds over long time period and does not involve mutations, but encourages changes in which certain genes are activated. Promotion can be stimulated by substances like Estrogens.  Here is the good news.  When the influence of these substances is removed, cells usually revert back to the previous stage.

         3. Progression – Mutations pile up at the molecular (i.e. DNA) level and chromosomes become increasingly damaged and unstable.  Some of these changed cells become cancer cells. The production of many different chromosome abnormalities in the same tumor has the effect of making it a heterogeneous group of cells with different properties.   It makes diagnosis & treatment more difficult.

          Many carcinogens have multiple roles. They can take part in more than one of these steps, and do so at: (1) different times, and (2) different concentrations. Dioxins, which are common byproducts of  incineration, suppress immunity, as well as induce mutations. This is why there is no such thing as a “safe” dose of a carcinogen. Similar exposures may pose very different threats to different people or at different times. e.g., those whose cells are already initiated, may react to trace amounts and move to the next stages.

         We are constantly exposed to more than one type of carcinogen at the same time and to many exposures of the same carcinogens over periods of time. There may be cumulative effects from multiple exposures.  DDT and another carcinogen, called AAPA, accelerate tumor formation when applied simultaneously, although neither alone is capable of doing so.  This effect is called synergism.

        

 

 A Real War on Cancer

 

         For many years, BRCA research went under-funded and the whole issue of BRCA was virtually ignored by both government and private research institutions.

         Finally, in the early nineties, women began to take note of the success of the Gay Community in turning these institutions’ attention to AIDs research.  Women quickly showed that they had learned a lesson in the politics of disease.  The Breast Cancer Fund, founded by women, emphasizes that women must stop thinking of BRCA as only a personal tragedy, and demand more emphasis on true prevention, removal of carcinogens from our environment.

         October is Breast Cancer Awareness Month.  Women are showered at that time with literature emphasizing prevention and early detection. The message is: get a mammogram, go on a low fat diet, exercise, and cut back on alcohol consumption.

         There is not one word about primary prevention though – removing chemical carcinogens from our environment.  Is this merely an oversight?

         The chief sponsor of Breast Cancer Awareness Month is AstraZenica, a giant multinational corporation, which manufactures the BRCA chemo- prevention drug, Tamoxifen.  It also produces herbicides and fungicides. In addition, AstraZenica now owns the Salick chain of cancer treatment centers.

         This seems like a cozy arrangement for AstraZenica.  It produces suspected BRCA carcinogens. It is also involved in the treatment of cancer, and it is now selling a BRCA-prevention drug.  It also gets all kinds of good publicity from Breast Cancer Prevention Month, and uses that to deflect our attention away from the environmental causes of cancer.

                  Sandra Steingraber, author of “Living Downstream”, a book documenting the environmental causes of cancer, states that  “By emphasizing personal habits rather than carcinogens, they frame the cause of the disease as a problem of behavior rather than as a problem of exposure to disease-causing agents…. It presumes that the ongoing contamination of our air, food, & water is an immutable fact of the human condition to which we must accommodate ourselves.”

 

How Can We Really Win The “War On Cancer”?

         The most important action we can take is to make the ‘Precautionary Principle’ the law of the land. The Principle states, in part, that "When an activity raises threats of harm to human health, or the environment, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically.  In this context,

the proponent of an activity, rather than the public, should bear the burden of

proof." The European Union has already invoked the Precautionary Principle, first against Genetically Engineered food, and now against suspected carcinogenic agents.

          Last, but not least, join an activist organization that will represent your interests. The next time that you are asked to donate to a ‘cure for cancer’, you might consider the Breast Cancer Fund when you ponder where your money will be most effective.

 

SIDE BAR

 

 

 

 

 

          

 

         

Wilderness Awareness

WILDERNESS AWARENESS WALK

by Lanie Johnson, M.A., and Ken Fischman, Ph.D.

         Now, let’s all walk to the fire circle (or meeting spot). When we get there we’ll tell you what we’re going to do next. Please just bear with us this morning – what we do now will become clear to you later on.

at Fire Circle (Meeting Spot)        

          One of the most important elements in lost proofing is awareness. . . so what we’re going to do now is a Nature Awareness Walk.  Let’s just amble down this path (start walking) What do you notice as you walk? 

first stop

(Now, let me tell you ABOUT THIS WALK. an Awareness Walk is different from a regular Nature Walk. We won’t be identifying trees or plants; instead you will be learning some new ways to be aware of things around you, things you may not usually see or hear in the woods, like birds & animals & location of water.. How? we’ll be teaching you some special skills or tools — like SUPER HEARING, EXPANDED VISION & SILENT WALKING.

Question:  First, let me ask you to name a few different professions – such as what you or your parents do (did) for a living, or, what you do or want to do.                 

         Hundreds and thousands of years ago, ANCIENT PEOPLE had no specialized professions.

                  They had to be IN TOUCH WITH NATURE to live.

                  Nature Awareness was one of their most important living skills — no one had a particular job, but each one could do just about everything they needed to do to

live in their environment, to find everything they needed in Nature (“Wildness is a state of complete awareness”  said Gary Snyder, Pulitzer Prize winning poet, and author of the book, “Turtle Island”)

Question:  How were they in touch with Nature? Through the 5 SENSES  (and maybe more)

         The Ancient Ones used their SENSES in a different way        

                  We’re here to help you learn how they did it, not by book learning, but your own EXPERIENCE — you can’t expect to become EXPERTS in a few hours but we can show you the skills and you can PRACTICE them on your own.

         Nature Awareness skills help you get CLOSER TO NATURE & also NATURE WILL GET          CLOSER TO YOU. (Whipporwill/lizard stories from Pine Barrens)

(One instructor goes over the hill with bear bells. At a signal ( howl), he/she will ring the bells; that instructor then moves to different spot and rustles leaves, breaks sticks, etc.)

SUPER HEARING

The first sense we talk about is hearing. 

         • I would like to talk about hearing in the woods. Ancient people even heard in a different fashion — Do this:  stop, listen for 1 minute (signal). What did you hear ?

(list. . . .)

         • I will teach you a simple technique in which you turn into a wild animal.                          

                  1. Stop, cup your hands behind your ears, and listen.What do you hear?                                     Now, turn your torso left and listen. What do you hear? Now, right.                                     Again?

demo                  Be like deer feeding & listening (they can turn their ears independently)

                  2. Now: listen again for 1 minute with eyes closed, using your Super Hearing

                           (signal again. other instructor does same noises in same places again)

                           What’s different? (kind of sounds, loudness, direction, wind?) What                                     else is different?

                           (Emphasize efficiency – (a) Loudness and (b) Direction)

FOX WALK

Next, we’ll learn how to walk the Ancient Ones WALKED, using your sense of TOUCH.

demo                 

Many civilized people walk heel first, weight forward, leading with the head & looking down. You can’t see Nature if you are just looking at the ground, and nature’s creatures will certainly hear you if you make that much noise!

demo                 

So, we’ll walk like this – put one foot almost directly in front of the other. Feel the ground,  first with ball of your foot, Keep your weight back and head up, so you can look around as you walk. This is called the FOX                                  WALK. 

                  The fox walk is like a slow dance, with rhythm:

demo                          

1) standing still, place alternate feet forward

                           2) Do the same, but place alternate feet forward, on the balls of the                                              foot on their outside edges and roll them inward until flat.

                           3) Continue for a few steps – STOP! Where is your weight?

                           4) Move forward, (down a gentle hill if possible)

                                    Walk close to an invisible line between your feet (not one foot                                              directly in front of the other)

                           6) Keep your eyes ahead (pick a tree, rock, etc. to look at)

                                    Feel the ground. (It is as if your feet have eyes!)

                                    If you feel a sharp rock or twig, you can change course before                                              fully committing your weight.                                                      

Another stop  (after walking to an open area)

EXPANDED VISION

How did the Ancient Ones use their eyes. How can you use your eyes in the woods? We call it EXPANDED VISION

                  let’s try an experiment:

                           1) Spread out with arms sideways, not touching your neighbor.                                             2) Look straight ahead at something small in the distance.

                           3) Hold your arms straight out sideways with hands a little behind                                              in front of you so that you can’t see them.

                           4) Take a deep breath & let it out slowly.

demo                          

5) Wiggle fingers; slowly bring arms forward backward while                                                       looking at that object.

                           6) When you are barely aware of your fingers on both hands, STOP.

                                    Keep looking ahead and at your fingers at the same time

                                    Notice how much more you see now – out of the corners of         

                                    eyes. You also see motion more easily – wild animals see this                                              way most of the time (If you are very still, they usually                                                       don’t see you)

         EXPANDED VISION works better without glasses, if possible (glasses inhibit                            expanded vision. They act like the frames of paintings. You learn not to                            look outside them)                                   

                  Now you can sense even more when you do the FOX WALK                                   

                  Let’s practice doing both at the same time — look at the woods like a                                     painting, which you enter like Alice going through the looking glass 

Question: What did you notice this time? (list. . . )

                                                            (walk ahead again)

Another stop

STALKING 

Now that you have become familiar with the FOX WALK, I’ll show you how to expand this so that you can get closer and observe animals (Don’t try this on a bear or lion): STALKING is difficult to do in boots – sneakers, moccasins, or barefoot are best.

story         e.g., I got 20’ from a wild deer in the open; my teacher actually touched a deer

Has anyone ever seen a dog or a cat stalking? Then you know how slowly they do it.

• Kinds of stalk:

                  cat (4-footed), heron (2-footed). people are also 2-footed

         • There are three main rules: stalk slow, stalk slow, stalk slower .

                  My teacher made us take one step/minute. I’ll ask only you to do one                             step/15 seconds.

demo        

• Steps of Heron Dance

                  1) lift knee with toes pointed downward (so as not to catch them on                                              anything as you lift)

                  2) Bring your foot down with toes up.

                  3) Touch the ground with outside edge of the ball of your foot and roll it to                                     the inside until flat.

                  4) Let your toes down and compress.

                  5) Only then, commit your weight by leaning forward. (Then your rear leg                                     comes up automatically).

                  (*Never pivot on ground. It may make noise)

         • Practice for a few minutes. Do not look down. Look at something in the                                     distance. Learn to see with your feet, as in the fox walk. 

• The 4 main elements of the Heron Dance 

                  Slow – one step/15 seconds.

                  Flow – have you ever seen Tai Chi ?

                  Compress – do not commit your weight at first.

                  Freeze (hands on chest with arms at your sides) – wait until animal resumes                                     what it was doing before you continue.

                  Animals learn that movement = danger. Unless you move, they think                                     you are a tree, a stump, etc. If you raise your hand ( = rifle); the                                              animal flees.  If the animal sees you, try imitating  a harmless grazing                                     animal, even to kneeling down and nibbling grass.(yum, yum!) 

         • TIPS: Stalk when: wind blows; animal’s head is down. Use expanded vision to pick out easiest pathway and keep your eyes on the animal at same time (It is much easier to go around a thicket          than to stalk through it.  Use a Quick Stalk when feasible (e.g. behind bushes and trees, etc.) Vary your height.  Look up, down, and in back of you.

         Let’s walk a little more

Another stop 

 STALKING GAME

         One instructor sits blindfolded with apple (or other object) five inches in front of          her/him.

         The participants stand in a semicircle (circle if it is a big group) – They stalk to          the apple.

         The seated instructor points to the noise (use super hearing at times) – The perpetrator of the noise must freeze for 1 minute (count to 60) – Another instructor is the umpire, and if he/she  points to you with stick, you freeze)

         The stalker who gets to the apple first, gets to eat it

You’ll get to try out some of your skills again when we do the Un-Nature walk

latest news

 

 

Scientists debate ‘magic number’ of wolves needed for species' survival

 

By ROB CHANEY of the Missoulian | Posted: Sunday, May 22, 2011 7:00 am 

 

Conservation groups and the federal government continue to disagree how many gray wolves are needed in the Northern Rockies to ensure the species’ survival. National Park Service photo

One of the biggest arguments left unresolved by last year's wolf lawsuit was the most obvious: How many wolves are enough?

The U.S. Fish and Wildlife Service took the gray wolf off the endangered species list in 2009, with the caveat that at least 150 wolves and 15 breeding pairs endure in each of the three states in the northern Rocky Mountain population (Montana, Idaho and Wyoming).

Recent surveys found at least 1,700 wolves in that area – more than enough to justify delisting.

But a coalition of environmental groups sued the government, claiming those numbers were wrong. To survive and thrive, they argued, the population needed at least 2,000 and preferably 5,000 wolves.

FWS biologists said they used the best available science to pick their number. Coalition members cited the well-established rules of conservation biology to justify their threshold. While the scientists dueled, U.S. District Judge Donald Molloy decided the case on a technicality and Congress reversed him with a budget rider. Wolves in the Northern Rockies are now delisted, but almost nobody's happy.

*****

Over the past decade, biologists have sought a "magic number" that would simplify endangered species debates. In 2010, an Australian team led by Lochran Traill of the University of Adelaide published a study declaring 5,000 was the population size required to prevent any species' extinction.

"We don't have the time and resources to attend to finding thresholds for all threatened species," Traill told Science Observer Magazine. "(T)hus the need for a generalization that can be implemented across taxa (classes of animals and plants) to prevent extinction."

But another group of U.S. Forest Service researchers along with American and British professors warn that a simple tool may be a flawed tool. While they agree that an easily understood standard helps persuade judges or members of Congress of the need for action, the 5,000 figure doesn't add up. Their paper will be published in the journal Trends in Ecology and Evolution.

"It's natural for any policy maker and practitioner to look for ways of simplifying the overwhelming process of endangered species management," said Greg Hayward of the Forest Service's Alaska Region Office. "If that worked, it would be a delightful world to live in. But if you're really going to do anything positive, in terms of turning around the situation for these species, going for that simple rule of thumb isn't going to help."

Both sides use a lot of math to make their points. Traill and company looked at 1,198 species with a computer model that calculated how many of each would be needed for the plant or animal to survive in the long term. In particular, the study looked at how many are needed to ensure a species doesn't in-breed itself into extinction.

That's key because one requirement to getting off the endangered species list is a population big enough to guarantee genetic diversity. Earthjustice attorney Doug Honnold relied on that in his argument to Molloy, to show why the wolf should remain a listed species.

"If you're talking about genetics, then there are some basic genetic principles that apply across all species," Honnold said. "It's been documented with every species that's been studied."

Honnold referred to what's called the "50-500 rule" which states you need at least 50 breeding-age females of a species for short-term survival or 500 for the long term. In the case of wolves, there's usually only one breeding female in a pack of four to 10 wolves, so the total population number balloons to 2,000-5,000.

*****

The "magic number opponents" respond that genetics isn't everything. In the case of wolves, where might that 2,000-5,000 figure apply? Do we need a minimum viable population in the three states where wolves were reintroduced back in 1995? Or should the figure be spread across the six-state area now delisted by congressional fiat (adding Utah, Washington and Oregon to Montana, Idaho and Wyoming)? Does it count the Canadian wolves that have relations with American packs along the international border?

"Under the Endangered Species Act, we sort of ignore other segments of populations that are outside the United States," said Hayward's colleague, Steven Beissinger of the University of California-Berkeley. "In the case of the paper we did, one thing we found was, the particular technique people used to come up with this minimum number was very context-specific."

In other words, each animal needs its own formula. Passenger pigeons had different lifespans and breeding rates than wolves. They could fly across continents at will, while wolves may be stymied by freeways. Passenger pigeons were, in fact, the most abundant land bird in the continental United States – 3 billion to 5 billion individuals – before the population crashed between 1870 and 1890. [ note: Here I disagree with the reporter. The passenger pigeon population did not crash. It was deliberately exterminated, using the most atrocious means imaginable.]

Science rarely gets to be just science. Lots of scientific reasons justify the wolf's presence on the landscape: It reduces elk populations, which in turn improves the plant communities along streams, which brings back songbirds and beavers.

But reduced elk numbers aggravate a hunting community that's invested millions of dollars to improve elk habitat. Wolves also have proved a poster target for politicians who want to leash the Endangered Species Act.

Natural Resources Defense Council staff scientist Sylvia Fallon said the U.S. Fish and Wildlife Service knew it would face public resistance if it proposed reintroducing lots of wolves, so it picked a deliberately low 150-per-state figure to get the reintroduction in play.

"They (FWS biologists) say they came up with that number in consultation with scientists, but they never said who they were," Fallon said. "It was some guesswork factoring in social and political considerations at the time, what would be acceptable to the states and the public."

FWS attorneys rejected that claim in their court briefs, but they never got to have the argument in Molloy's courtroom. Without ever discussing what an appropriate number should be, the judge only said the federal government illegally used state boundaries to divide a natural population.

*****

Beissinger suggested a better target in the search for the elusive magic number. Instead of a unified field theory of how many of a species is needed to survive, we humans should settle on what risk factor we're willing to work with, he said.

"In my profession, we don't have a single standard that's been set for what degree of risk we're willing to accept for a species to go extinct," he said. "I could make a calculation for a species and say nine times out of 10, it would be viable there, for 50 years. Would that be good enough, or would you want a 95 percent chance, or an 80 percent chance? But it's too naive to use just measures of population size and come up with some rule of thumb whether a population is safe or not."

Reporter Rob Chaney can be reached at 523-5382 or at rchaney@missoulian.com.

Newsletters, 2011

Our Newsletters will begin in July, 2011.

With respect to our wild lands,  it will cover topics, such as Hunter Gatherers, Wilderness Survival, and Predator Prey Relationships, with emphasis on the role of wolves in healthy ecosystems. 

The environment takes in an even wider swath, so the Newsletter will also cover Cancer, Climate Change, Peak Oil, and Molecular Genetics, especially Genetically Modified Organisms (GMOs).

Anything that effects the health of the Earth is grist for our mill, and hopefully of interest to you. We will therefore upon occasion, wander farther afield if it seems relevant to your interests, to such topics as primitive skills, wilderness awareness, the evolution of man, and so on.

 

 

Please check the News category for the latest topics of interest