Cell Proliferation Quotes

Healing is a biological process, not an art. It is as much a function of the living organism as respiration, digestion, circulation, excretion, cell proliferation, or nerve activity. It is a ceaseless process, as constant as the turning of the earth on its axis. Man can neither duplicate nor imitate nor provide a substitute for the process. All schools of healing are frauds.

When cells are no longer needed, they die with what can only be called great dignity. They take down all the struts and buttresses that hold them together and quietly devour their component parts. The process is known as apoptosis or programmed cell death. Every day billions of your cells die for your benefit and billions of others clean up the mess. Cells can also die violently- for instance, when infected- but mostly they die because they are told to. Indeed, if not told to live- if not given some kind of active instruction from another cell- cells automatically kill themselves. Cells need a lot of reassurance. When, as occasionally happens, a cell fails to expire in the prescribed manner, but rather begins to divide and proliferate wildly, we call the result cancer. Cancer cells are really just confused cells. Cells make this mistake fairly regularly, but the body has elaborate mechanisms for dealing with it. It is only very rarely that the process spirals out of control. On average, humans suffer one fatal malignancy for each 100 million billion cell divisions. Cancer is bad luck in every possible sense of the term.

Cancer, then, is quite literally trying to emulate a regenerating organ—or perhaps, more disturbingly, the regenerating organism. Its quest for immortality mirrors our own quest, a quest buried in our embryos and in the renewal of our organs. Someday, if a cancer succeeds, it will produce a far more perfect being than its host—imbued with both immortality and the drive to proliferate. One might argue that the leukemia cells growing in my laboratory derived from the woman who died three decades earlier have already achieved this form of “perfection.

Thinking has become a disease. Disease happens when things get out of balance. For example, there is nothing wrong with cells dividing and multiplying in the body, but when this process continues in disregard of the total organism, cells proliferate and we have disease. The mind is a superb instrument if used rightly. Used wrongly, however, it becomes very destructive. To put it more accurately, it is not so much that you use your mind wrongly — you usually don’t use it at all. It uses you. This is the disease. You believe that you are your mind. This is the delusion. The instrument has taken you over.

Leukemia was a malignant proliferation of white cells in the blood. It was cancer in a molten, liquid form.

Thinking has become a disease. Disease happens when things get out of balance. For example, there is nothing wrong with cells dividing and multiplying in the body, but when this process continues in disregard of the total organism, cells proliferate and we have disease.

If you extract breast cancer cells from tissue, it’s quite simple to grow them in a lab. If you add glucose, epidermal growth factor (EGF), and insulin, they multiply rapidly. If you then take away the insulin, they die. Let me repeat that: breast cancer cells proliferate with high levels of insulin and die without it. What lowers insulin levels? Fasting.

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A few hundred million years later, some of these eukaryotes developed a novel adaptation: they stayed together after cell division to form multicellular organisms in which every cell had exactly the same genes. These are the three-boat septuplets in my example. Once again, competition is suppressed (because each cell can only reproduce if the organism reproduces, via its sperm or egg cells). A group of cells becomes an individual, able to divide labor among the cells (which specialize into limbs and organs). A powerful new kind of vehicle appears, and in a short span of time the world is covered with plants, animals, and fungi.37 It’s another major transition. Major transitions are rare. The biologists John Maynard Smith and Eörs Szathmáry count just eight clear examples over the last 4 billion years (the last of which is human societies).38 But these transitions are among the most important events in biological history, and they are examples of multilevel selection at work. It’s the same story over and over again: Whenever a way is found to suppress free riding so that individual units can cooperate, work as a team, and divide labor, selection at the lower level becomes less important, selection at the higher level becomes more powerful, and that higher-level selection favors the most cohesive superorganisms.39 (A superorganism is an organism made out of smaller organisms.) As these superorganisms proliferate, they begin to compete with each other, and to evolve for greater success in that competition. This competition among superorganisms is one form of group selection.40 There is variation among the groups, and the fittest groups pass on their traits to future generations of groups. Major transitions may be rare, but when they happen, the Earth often changes.41 Just look at what happened more than 100 million years ago when some wasps developed the trick of dividing labor between a queen (who lays all the eggs) and several kinds of workers who maintain the nest and bring back food to share. This trick was discovered by the early hymenoptera (members of the order that includes wasps, which gave rise to bees and ants) and it was discovered independently several dozen other times (by the ancestors of termites, naked mole rats, and some species of shrimp, aphids, beetles, and spiders).42 In each case, the free rider problem was surmounted and selfish genes began to craft relatively selfless group members who together constituted a supremely selfish group.

Horvitz and his colleagues discovered several genes that coded for the effectors of cell death in nematodes—the death genes. Their findings were fascinating in their own right, but by far the most unexpected and important discovery was that there were exact equivalents of the death genes in flies, mammals, and even plants. Cancer researchers had already identified some of these genes at the time, but why or how they were involved in cancer was still unknown. The link with nematodes made their function clear, while giving another demonstration of the fundamental unity of life. Not only were the human genes unambiguously related to the nematode genes, but also they could even be genetically engineered to replace the nematode genes in the worms themselves, where they worked equally well! Mutations that disabled any of the death genes prevented the nematodes from losing their 131 cells by apoptosis as usual. The implications for cancer were plain: if the same mutations had a similar effect in people, then incipient cancer cells would likewise fail to commit suicide, and would instead continue to proliferate to form a tumour.

Russell Ross reported that insulin also stimulates the proliferation of the smooth muscle cells that line the interior of arteries, a necessary step in the thickening of artery walls characteristic of both atherosclerosis and hypertension.

Terminology and classification Leukaemias are traditionally classified into four main groups: • acute lymphoblastic leukaemia (ALL) • acute myeloid leukaemia (AML) • chronic lymphocytic leukaemia (CLL) • chronic myeloid leukaemia (CML). In acute leukaemia there is proliferation of primitive stem cells leading to an accumulation of blasts, predominantly in the bone marrow, which causes bone marrow failure. In chronic leukaemia the malignant clone is able to differentiate, resulting in an accumulation of more mature cells. Lymphocytic and lymphoblastic cells are those derived from the lymphoid stem cell (B cells and T cells). Myeloid refers to the other lineages, i.e. precursors of red cells, granulocytes, monocytes and platelets (see Fig. 24.2, p. 989). The diagnosis of leukaemia is usually suspected from an abnormal blood count, often a raised white count, and is confirmed by examination of the bone marrow. This includes the morphology of the abnormal cells, analysis of cell surface markers (immunophenotyping), clone-specific chromosome abnormalities and molecular changes. These results are incorporated in the World Health Organization (WHO) classification of tumours of haematopoietic and lymphoid tissues; the subclassification of acute leukaemias is shown in Box 24.47. The features in the bone marrow not only provide an accurate diagnosis but also give valuable prognostic information, allowing therapy to be tailored to the patient’s disease.

Activation of the androgen receptor (AR) is crucial for tumor cell progression and survival of prostate cancer, and androgen deprivation therapy remains the main clinical approach in men with locally advanced tumors ■ Current therapies incompletely suppress the androgen–AR axis, but a multiple therapeutic approach, targeting androgens and their receptor, has potential to improve clinical outcomes ■ Treatment of prostate cancer cells with 5α-reductase inhibitors (5ARIs) inhibits cellular pathways regulating metabolism, cell growth and proliferation, triggering apoptosis and decreasing prostate size ■ Although 5ARI treatment reduces the risk of developing prostate cancer, patients treated with these drugs have tumors with higher Gleason scores than those who receive placebo ■ Use of 5ARIs to prevent and treat prostate cancer remains controversial, and further investigation is necessary to understand the presence of more-aggressive tumors in patients receiving these drugs

In the Tel Aviv study, a group of formerly sedentary rats of varying ages ran on a treadmill for 20 minutes daily for 13 weeks. Another pack of rats was the control group. The control group was allowed to remain sedentary—that is, those rats’ muscles were mainly not used. As you might expect from everything you’ve read so far, the exercisers increased their number of stem muscle cells, with the total increase dependent on age—but not in the way you would expect. The younger rat runners saw an increase of 20 to 35 percent in their stem repair cells. The older rats, however, experienced an even greater proliferation—a 33 to 47 percent increase. That’s right: The percentage increase in stem muscle cells was greater in the older subjects than in the younger ones. On the other hand, the nonexercising rats lost stem cells by lying around, eating and sleeping as they aged.

The generally reported lack of relationship between the severity of diabetes and the vascular complications… suggest that hyperglycemia is not the factor linking diabetes with atherosclerosis. The possibility that insulin contributes to the development of the large vessel complications of diabetes has been explored, and evidence has been presented that insulin stimulates arterial smooth muscle cell proliferation and lipid synthesis in the arterial wall.   —”Diabetes and atherosclerosis.” In J. S. Bajaj, ed. Insulin and Metabolism. Amsterdam, London, New York: Excerpta Medica 27(1979): 1-13.

Only 2 per cent of our genome codes for proteins. A massive 42 per cent is composed of retrotransposons. These are very odd sequences of DNA, which probably originated from viruses in our evolutionary past. Some retrotransposons are transcribed to produce RNA and this can affect the expression of neighbouring genes. This can have serious consequences for cells. If it drives up expression of genes that cause cells to proliferate too aggressively, for example, this may nudge cells towards becoming cancerous.

Leonard Hayflick, in the 1960s, demonstrated that normal human cells have a finite limit to proliferation: the population only doubles in number about 50 times.

Cancer: the code breaks down, becomes disorganized, lets cells proliferate indiscriminately. A disease of information. AIDS: the immune system (the secret defences of the body) is suppressed. Obsessive fear of contiguity, of flows (sperm, blood, saliva), of contact. A disease of communication. What if all this reflected a brute, instinctive refusal of the flows of communic ation, of sperm, of sex, of words? If there were in all this an 'instinctive', vital resistance to the extension of flows and circuits - at the cost of a new mortal pathology, AIDS and cancer, which would ultimately be protecting us from something even more serious, or would at least be serving as an alarm signal? After all, neurosis is what man invents to protect him from madness.

Plasticity of neuroendocrine-thymus interactions during aging N.Fabris12E.Mocchegiani2M.Provinciali2 Abstract Thymic regrowth and reactivation of thymic endocrine activity may be achieved even in old animals by different endocrinological or nutritional manipulations such as, (a) intrathymic transplantation of pineal gland or treatment with melatonin, (b) implantation of a growth hormone (GH) secreting tumor cell line or treatment with exogenous GH, (c) castration or treatment with exogenous luteinizing hormone-releasing hormone (LH-RH), (d) treatment with exogenous thyroxine or triiodothyronine, and (e) nutritional interventions such as arginine or zinc supplementation. These data strongly suggest that thymic involution is a phenomenon secondary to age-related alterations in neuroendocrine-thymus interactions and that it is the disruption of such interactions in old age that is responsible for age-associated dysfunction. Melatonin or other pineal factors may act through specific receptors, but experimental evidence is still lacking. The role of zinc, whose turnover is usually reduced in old age, is diverse. The effects range from the reactivation of zinc-dependent enzymes, required for both cell proliferation and apoptosis, to the reactivation of thymulin, a zinc-dependent thymic hormone. The role of zinc may even be more crucial. According to recent preliminary data obtained both in animal and human studies, it appears that the above reported endocrinological manipulations capable of restoring thymic activity in old age, may act also by normalizing the altered zinc pool.

There is a close connection between the key concept of the genetic code and the pathology of cancer. Cancer implies an infinite proliferation of a basic cell in complete disregard of the laws governing the organism as a whole. Similarly, in cloning, all obstacles to the extension of the reign of the Same are removed; nothing inhibits the proliferation of a single matrix. Formerly sexual reproduction constituted a barrier, but now at last it has become possible to isolate the genetic matrix of identity; consequently it will be possible to eliminate all the differences that have hitherto made individuals charming in their unpredictability.

What begins as a solitary truth soon proliferates like malignant cells in the body of a dream, a body whose true outline remains unknown. Perhaps, then, we should be grateful to the whims of chemistry, the caprices of circumstance, and the enigmas of personal taste for giving us such an array of strictly local realities and desires.

Stem cells are the undifferentiated group of cells, they are unspecified and have a great potential for proliferation, differentiation and migration. Stem Cells are vital. They can rise specialized cells for body repair. Moreover, stem cell treatment has witnessed exceptional growth and development in past few years. Their consistency, self-repairing properties and profound healing response have led to the immense popularity of Stem Cell Therapy in South Africa.

breast cancer cells proliferate with high levels of insulin and die without it. What lowers insulin levels? Fasting.

Today, often when someone dies, we tend to look for the analogue to the fatal illness in their behavior: lung cancer results from smoking, heart disease from a lack of exercise, colon cancer from not eating enough fiber, etc. By linking death to a specific behavior, we deontologize it; we make it seem as if death is only one possibility for life, a possibility that we ourselves—or someone, someday—might manage to escape. The same thinking applies to aging as well: all the formulas for the conquest of aging (skin creme, the baldness pill, plastic surgery, low fat diets) implicitly view aging itself as just one option among many. When we view death as a “case” or an “option,” we reject its necessity as a limit. Death no longer indicates a moment of transcendence that we must encounter. According to Baudrillard, “We are dealing with an attempt to construct an entirely positive world, a perfect world, expurgated of every illusion, of every sort of evil and negativity, exempt from death itself.” In the society of enjoyment, death becomes an increasingly horrific—and at the same time, an increasingly hidden—event. Not only does death imply the cessation of one’s being, but it also indicates a failure of enjoyment. Death is above all a limit to one’s enjoyment: to accept one’s mortality means simultaneously to accept a limit on enjoyment. This is why it is not at all coincidental that with the turn from the prohibition of enjoyment to the command to enjoy we would see an increase in efforts to eliminate the necessity of death. Today, human cell researchers are working toward the day when death will exist only as an “accident,” through the modification of the way in which cells regulate their division and creating cells that can divide limitlessly. As Gregg Easterbrook points out, the introduction of such cells into the human body would not create eternal life, but it would make death something no longer necessary: “Therapeutic use of ‘immortal’ cells would not confer unending life (even people who don’t age could die in accidents, by violence and so on) but might dramatically extend the life-span.” The point isn’t that death would be entirely eliminated, but that we might eliminate its necessary status as a barrier to or a limit on enjoyment. This potential elimination of death as a necessary limit to enjoyment follows directly from the logic of the society of enjoyment. As long as death remains necessary, it stands, as Heidegger recognizes, as a fundamental barrier to the proliferation of enjoyment. If subjects know that they must die, they also know that they lack—and lack becomes intolerable in face of a command to enjoy oneself. But without the idea of a necessary death, every experience of lack loses the quality of necessity. Subjects view lack not as something to be endured for the sake of a future enjoyment, but as an intolerable burden. In the society of enjoyment, subjects refuse to tolerate lack precisely because lack, like death, has now lost its veneer of necessity.

The violence [Gewalt] of positivity that derives from overproduction, overachievement, and overcommunication is no longer “viral.” Immunology offers no way of approaching the phenomenon. Rejection occurring in response to excess positivity does not amount to immunological defense, but to digestive-neuronal abreaction and refusal. Likewise, exhaustion, fatigue, and suffocation—when too much exists—do not constitute immunological reactions. These phenomena concern neuronal power, which is not viral because it does not derive from immunological negativity. Baudrillard’s theory of power [Gewalt] is riddled with leaps of argument and vague definitions because it attempts to describe the violence of positivity—or, in other words, the violence of the Same when no Otherness is involved—in immunological terms. Thus he writes: The violence of networks and the virtual is viral: it is the violence of benign extermination, operating at the genetic and communicational level; a violence of consensus. . . . A viral violence in the sense that it does not operate head-on, but by contiguity, contagion, and chain reaction, its aim being the loss of all our immunities. And also in the sense that, contrary to the historical violence of negation, this virus operates hyperpositively, like cancerous cells, through endless proliferation, excrescence, and metastases. Between virtuality and virality, there is a kind of complicity.

Thus, the Warburg effect is how cancer cells fuel their own proliferation. But it also represents a potential vulnerability in cancer’s armor.[

We are a species that delights in story. We look out on reality, we grasp patterns, and we join them into narratives that can captivate, inform, startle, amuse, and thrill. The plural—narratives—is utterly essential. In the library of human reflection, there is no single, unified volume that conveys ultimate understanding. Instead, we have written many nested stories that probe different domains of human inquiry and experience: stories, that is, that parse the patterns of reality using different grammars and vocabularies. Protons, neutrons, electrons, and nature’s other particles are essential for telling the reductionist story, analyzing the stuff of reality, from planets to Picasso, in terms of their microphysical constituents. Metabolism, replication, mutation, and adaptation are essential for telling the story of life’s emergence and development, analyzing the biochemical workings of remarkable molecules and the cells they govern. Neurons, information, thought, and awareness are essential for the story of mind—and with that the narratives proliferate: myth to religion, literature to philosophy, art to music, telling of humankind’s struggle for survival, will to understand, urge for expression, and search for meaning. These are all ongoing stories, developed by thinkers hailing from a great range of distinct disciplines. Understandably so. A saga that ranges from quarks to consciousness is a hefty chronicle. Still, the different stories are interlaced. Don Quixote speaks to humankind’s yearning for the heroic, told through the fragile Alonso Quijano, a character created in the imagination of Miguel de Cervantes, a living, breathing, thinking, sensing, feeling collection of bone, tissue, and cells that, during his lifetime, supported organic processes of energy transformation and waste excretion, which themselves relied on atomic and molecular movements honed by billions of years of evolution on a planet forged from the detritus of supernova explosions scattered throughout a realm of space emerging from the big bang. Yet to read Don Quixote’s travails is to gain an understanding of human nature that would remain opaque if embedded in a description of the movements of the knight-errant’s molecules and atoms or conveyed through an elaboration of the neuronal processes crackling in Cervantes’s mind while writing the novel. Connected though they surely are, different stories, told with different languages and focused on different levels of reality, provide vastly different insights.

It’s about those longevity genes AMPK and mTOR, which are important nutrient sensors. mTOR controls a number of cell functions, including cell growth and cell proliferation. For younger people who are growing or whose bodies are in reproductive mode, mTOR has many benefits. But when we get older, we don’t want to encourage cell proliferation (cancer is cell proliferation).

Garlic[43] : This amazing aromatic plant, the most powerful antioxidant known, has been used to treat and cure illnesses through the ages. Even Hippocrates recommended consuming large amounts of crushed garlic as a remedy. A study in China finds that consuming raw garlic regularly cuts the risk of lung cancer in half, and previous studies have suggested that it may also ward off other malignant tumors, such as colon cancer. It is best to let it sit for at least fifteen minutes after the pods have been crushed. This time is needed to release an enzyme (allicin) that produces antifungal and anti-cancer compounds. Alliates (garlic, onion, chives) and their cousins (leek, shallot) improve liver detoxification and therefore help protect our genes from mutations. I take it in three forms: tablet, powder and fresh. I use it in almost all my dishes and sauces, it is the anti-cancer food par excellence. Vegetables[44] : To avoid disease, nothing like a diet rich in raw and organic vegetables. The daily intake of vegetables would prevent cancers of the mouth, pharynx, esophagus, lung, stomach, breast, colon and rectum. I eat it abundantly; you could even say that it has become my staple food. I eat of course all the cabbage, garlic, onion, pepper but also asparagus, mushrooms, leek, cucumber, scallions (green onions), zucchini, celery, all salads, spinach, endives, pickles, radishes, green beans, parsley and aromatic herbs. At first, I ate cooked tomatoes but stopped because they contain too much sugar. Omega 3 :   Omega 3, in cancer, are anti-inflammatory. Omega 6 or linoleic acids (found in sunflower and peanut oils) are inflammatory. You must always have an omega 3 / omega 6 ratio favorable to omega 3. This is why I take capsules of this fatty acid in addition to eating sardines and anchovies[45]. An inflammatory environment is conducive to the formation and proliferation of cancer cells. To restore the balance, it is necessary to consume more foods rich in omega 3 such as fatty fish, rather small ones because of mercury pollution (sardines, anchovies, mackerel, herring), organic eggs or eggs from hens fed with flax, chia seeds and flax seeds, avocados, almonds, olive oil. These good fatty acids help in the prevention of several cancers including breast, prostate, mouth and skin.

The research community became fixated on an ‘accelerator’ model of cancer – one in which the normal mechanism of cell division is being actively reprogrammed by these ‘rogue’ genes, the oncogenes, to go into overdrive, thus causing the cells to proliferate wildly. This was the mindset at the time p53 was discovered in 1979.

In the bloodstream, virtually all insulin-like growth factors are attached to small proteins that ferry them around to various tissues where they might be needed. But the IGFs, when attached to these proteins, are too large and unwieldy to pass through the walls of blood vessels and get to the tissues and cells where the IGF might be used. At any one time, only a small percentage of IGF in the circulation is left unbound to stimulate the growth of cells. These binding proteins constitute yet another of the mechanisms used by the body to regulate hormonal signals and growth factors. Insulin appears to depress the concentration of IGF-binding proteins, and so high levels of insulin mean more IGF itself is available to effect cell growth—including that of malignant cells. Anything that increases insulin levels will therefore increase the availability of IGF to the cells, and so increase the strength of the IGF proliferation signals. (Insulin has been shown to affect estrogen this way, too, one way in which elevated levels of insulin may potentially cause breast cancer.) The

Every person experiences roughly one million mutations throughout the body per second,18 and in a rapidly proliferating organ like the intestinal epithelium, nearly every single letter of the genome will have been mutated at least once in at least one cell by the time an individual turns sixty.

as the University of Toronto cancer researcher Vuk Stambolic would later describe it, these breast-cancer cells seemed to be “addicted to” insulin, and when weaned off it in the laboratory they responded by dying. This kind of phenomenon was seen also in cancers of adrenal and liver cells. As one 1976 report put it, insulin “intensely stimulated cell proliferation in certain tumors”; another, by researchers at the National Cancer Institute, described one particular line of breast-cancer cells as “exquisitely sensitive to insulin.” By then, researchers had established that malignant breast tumors had receptors to insulin, which were absent in healthy breast tissue, and that the more they had, the more insulin-sensitive they were.

From this perspective of cancer as a metabolic disease, insulin and IGF promote the cancer process through a series of steps. First, insulin resistance and elevated levels of insulin trigger an increased uptake of blood sugar (glucose) as fuel for precancerous cells. These cells then begin producing energy through a mechanism known as aerobic glycolysis that is similar to what bacteria do in oxygen-poor environments. (This phenomenon is known as the Warburg effect and was discovered in the 1920s by the German biochemist and later Nobel Laureate Otto Warburg, although its importance in the cancer process was not embraced until recently.) Once cancer cells make this conversion, they burn enormous amounts of glucose as fuel, providing them, apparently, with the necessary raw materials to proliferate. By metabolizing glucose at such a rapid rate, as Thompson suggests, these cancer cells generate relatively enormous amounts of compounds known technically as “reactive oxygen species” and less technically as “free radicals,” and these, in turn, have the ability to mutate the DNA in the cell nucleus. The more glucose a cell metabolizes and the faster it does so, the more free radicals are generated to damage DNA, explains Thompson. And the more DNA damage, the more mutations are generated, and the more likely it is that one of those mutations will bestow on the cells the ability to proliferate without being held in check by the cellular processes that work to prevent this pathological process in healthy cells. The result is a feed-forward acceleration of tumor growth. While this is happening, the insulin and IGF in the circulation both work to signal the cell to keep proliferating, and to inhibit the mechanism (technically known as apoptosis, or cell suicide) that would otherwise kick in to shut it down.

The study of stem cell niches in mammalian systems presents an 'arduous endeavor'; in comparison, the fly germarium is relatively easy to manipulate. In the 1990s, H. Lin, A.C. Spradling, and others used of a number of approaches to study Drosophilia GSCs and their niche, including killing specific cells in the germarium with precisely directed lasers; transplantation of cells from the ovary of one fly to another; and genetic perturbations that included the dialing up or down of Hh pathway signaling. The researchers found that following laser ablation of cells surrounding the GSCs - that is killing the niche cells - all the GSCs went on to form eggs, and the system was quickly depleted of its GSC reserve. Moreover, through genetic analyses the researchers identified specific genes required in the niche cells to maintain GSCs within the niche, as would be deduced for a gene that, when disrupted in niche cells, has the same effect as laser ablation of those cells. These studies are credited with providing the first clear experimental evidence of a stem cell niche, as well as defining what genes - what signaling pathways and other cellular activities - are important to the process. Many of the same pathways relevant in other cell types proved relevant to communication between the niche and GSCs, including the Hh pathway. The genes required for suppression of transposon mobilization by the piRNA system also have relevance to the GSC niche; disruption of the piwi gene, for example, can lead to uncontrolled proliferation of GSCs.

To understand what happens when we ingest lectin, let’s consider the example of wheat germ agglutinin (WGA), a lectin contained within wheat. Like other lectins, WGA is sticky, readily binding to other proteins it comes in contact with. After it enters our digestive tract, WGA sticks to the intestinal villi (fingerlike projections along the walls of the gut that are critical for the absorption of nutrients). The binding of WGA to the villi results in the damage and death of its cells. This destruction of the villi caused by lectins, including WGA, interferes with our ability to absorb nutrients from food. There is also evidence that lectins disrupt the gut’s natural flora. These microorganisms in our gut not only play an important role in digestion, but their disruption can result in the growth and proliferation of unhealthy microorganisms, such as E. coli, which can overrun the normal gut microbial environment and make us ill.

Duesberg reminded his colleagues that retroviruses—which have been a part of the human genome for as long as three billion years—are not “cytocidal” (cell killers). AIDS, Duesberg mused, is a disease of cell death, while leukemia is a disease of cell proliferation. By claiming initially that HIV caused leukemia, and later, AIDS, Gallo was accusing the bug of opposite reactions. Furthermore, Duesberg adds, “it would have been the first time that a retrovirus would have been pinned down as a cause of a human disease. Or even a disease in wild animals.”19