Wednesday, February 3, 2016

Amended cancer



Cancer

Cancer, or what is said to be the proliferation of malignant or invasive ‘cells’, seems likely to be a fictitious disease that was invented for political reasons.  There is not an adequate account in the medical literature of what causes a cell to become harmful, nor a clear definition of malignancy, even if it were true that one could photograph inside the human body or view cells under a microscope, nor an adequate account of what it means for a cell or tumour to invade surrounding tissue or travel to distant organs, nor of how one cell would be able to alter another or otherwise cause harm.  

It is not clear how a cell would alter so that its behaviour became destructive to other cells or the mechanism by which it would be able to cause harm.  If the mechanism Is mutation, whether or not, or how, this occurs, it seems implausible that a cell would change, either as a result of loss of its normal control mechanisms or by design, such that it would proliferate and set out to destroy its host.   A knock or other injury, for instance, might lead to a growth of tissue around the site of injury.  But that the proliferation of cells would be caused or accompanied by an alteration in its genetic material, such that it no longer supported the body but set out to harm or kill it seems contrary to what we know about the behaviour of living things.   

First, the medical literature is not consistent as to whether cancer is diagnosed as a result of cell pathology or invasion of local tissue.   In terms of cell pathology, it is not clear how ‘cells’ can be viewed, since microscopes enlarge rather than see below to any underlying structure (where the various parts of the cell are said to lie, whether or not the cell is opaque).  Even if the magnifications claimed were possible to achieve (ie, in terms of lenses), the images one would see at such magnifications, from observation of camera lenses, would be too blurred to identify something the size of a cell.  From observation, the size of the image one sees most clearly under a microscope is the same as that of the object itself viewed at close range, such that any magnification blurs to some extent.  This is consistent with what happens when one magnifies using a camera or with the blurring of larger letters at the periphery of one’s vision that can occur when one is reading. 

The image of a cancer cell could not be seen, to use Descartes’ phrase, clearly and distinctly.    Instead, the microscope acts similarly to a kaleidoscope.    First, a microscope would not be able to view objects the size of cancer, viral or Ebola cells because the image would blur at the magnification needed, as one can see from using a camera, which can bring things closer but not magnify without losing clarity, so that what one cannot see with the eye alone is not likely to exist.   Second, when someone looks into a microscope they are not focusing on the glass slide, but on something positioned before it within the cylinder:  their focal length is shorter than the distance between their eyes and the slide.   This can be tested by removing one’s eye from the eyepiece and noticing that one has to adjust one’s vision before being able to see a similarly small object placed on, or by, the slide.   Whether the adjustment is the result of the difference in lighting or the length of the cylinder or position of the object, one is not focusing on the object on the slide.     Whether or not the object on the slide is magnified, or by how much, when one looks into the microscope one is viewing very small objects as if they were not magnified, ie, the objects may alter in size when magnified but one’s vision does not.   In other words, one is looking at magnified objects as though one were looking at larger objects with the eye alone.   Therefore, by looking into the microscope cylinder one adjusts one’s focal length so that the object on the slide would actually blur, or appear smaller, because beyond one’s normal focal point, than if one were viewing it with the eye alone, ie, without a microscope.     Third, although it might seem possible that an image of the material on the slide is projected onto a screen within the microscope, rather than viewed directly, the arrangement of the microscope makes this unlikely even if the objects one views looked like they might be projected, and some of them do not.   The arrangement of the microscope does not make projection seem all that likely: one would expect the slide to be encased,so that there is no possibility of diffusion before light also has to enter the object lenses, before magnification within the microscope takes place, and in such a way that the material to be viewed is not obstructed before it is magnified, by the glass on the microscope on the stage and on the slide slide itself.  In fact, if I remove the glass slide using my own microscope the image does not apparently change.   Also, while the more fixed objects at the lower end of the cylinder have a shadowy look that might suggest projection, this is also an effect of magnification, ie, of blurring, while the objects nearer the eye have a more translucent look.   

My own microscope, a Prinz Opti-Craft Microscope outfit, Zoom 100x to 900x, purchased in the late 1960s, contains a slide with a butterfly scale on it contained within a glass cover slip.  With a concentrated beam of light, it can appear as though the light captures the red scale such that a red ‘wash’ appears in the cylinder, although at other times when the image on the screen is present, there is no colouration of the image.  Whether or not the mark is too small for it to be seen if the slide is removed or present, there is no significant magnification if its presence cannot be detected.  On the slide there is an opaque, cream-coloured, label, marked ‘Butterfly Scale, Japan’ (where the microscope was made).   If one turns the slide over, there is a similar, but smaller, mark, ie, apparently a second scale, or part of one (the first is rectangular, the second circular, so together they might resemble the marks of a code), in the glass of the slide behind the label.   Although I had originally thought I had detected this scale when using the microscope with sufficient light penetrating the label to illuminate the screen, thinking that the point being made might be that the light from the mirror could illuminate material in the first slide but not the cover slip (but still the cylinder), I have not seen it subsequently.  It seems much more likely that the point being made is that just as the second scale had been hidden by the semi opaque label, so any material on the slide is hidden by a semi opaque object within the microscope.  The microscope apparently has a magnification of 100 to 900 times, although only the focus is labelled 10x and 15x.    However, if there were more powerful magnification lenses within the microscope, would they reach as far as the material on the slide even if not blocked by an opaque material of some sort?  Similarly, if the microscope were internally lit, one would expect the focus of the light to be the object on the slide., but there is no beam of light with a traditional microscope.   Also, from observation, if the light, whether from behind or from the mirror, is too great, the image in the cylinder will blur, in the same way that one sometimes only sees a blur when looking into a camera in bright light.   Finally, whether or not one squints when looking into the cylinder one’s focal length is less than that needed to see clearly the objects on the slide, even if one is not apparently squinting, as can be observed if one removes one’s eye from the eyepiece.  On the other hand, if there were such a powerful zoom lens within the microscope (100 x to 900 x), ie, beyond the effect created by the cylinder itself, one would in fact expect the object to be further away, since the effect of a zoom, as with any magnification, is to extend one’s focal length.      Although the fact that and the reasons why one is not able to be able to see what is not on the slide need to be re-tested in different lights and to be better thought through, once one doubts that one is viewing what is on the slide it seems almost certain that one is viewing something contained within the microscope as well as, in some lightss, the lenses of one’s own eye projected above it. 

Instead, when someone looks into a traditional microscope, upon which the science of diagnosed disease is based, they are not viewing the material on the glass slide but an image within the cylinder.   If one illuminates the cylinder of the microscope with a mirror one sees the same image as when the microscope is lit with batteries or an electric current (which were an evolution from the original way of lighting the microscope with a mirror).   When using the mirror to light the microscope one may sees little or nothing in the way of an image on the screen of the microscope, even if there is enough light to illuminate the cylinder and screen (ie, it appears blank) but if brighter natural or artificial light (but not too much) is captured by the mirror, an image appears on the screen and before it (ie, closer to the eye).   The upper image has a more layered and translucent look and appears less fixed than the image on the screen. 

Looking into the microscope, one can see the lenses of one’s own eye  projected in the cylinder before a more fixed image on the screen.    That one is seeing the lenses of one’s eye is apparent because it is an image one sees when squinting into the light.  Looking in the microscope the effect is achieved whether or not one squints, if one closes the other eye, because of the relative darkness of the cylinder.  The more fixed image on the screen has a more shadowy look than the brighter, translucent, image of the lens of one’s eye, suggesting it might be projected from below, rather than illuminated by, the screen, or the shadowy look might be the result of greater magnification – ie, it represents a loss of clarity.  It also has a denser, more detailed, look (even though the projected image of the lens of one’s own eye becomes denser as one moves one’s, concave, eye away from the eyepiece and looks into it, such that the image appears smaller, as more compact, than if one were not looking into the glass).

Although there are a greater number of objects within the image on the screen than in the image of the lens of one’s eye (but nor do they take on the ‘pixel’ effect one sometimes see when, for instance, opening one’s eyes in the morning after sleep, resembling something more like a road map), the basic structure, when using my own microscope, is not that different nor the resembling objects of the structure of a different size, from the image of the projected lens of one’s own eye.  For example, when viewing the projected lens of one’s own eye, one sees translucent ‘ribbons’.  The image on the screen has ribbons of a similar length and width, albeit with a darker and more shadowy look and with ‘knots’ in them.  Although the more shadowy look suggests a greater magnification, this might be the result of projection and the greater number of objects because they are better illuminated.  Although many things in nature mimic other things, the similarity of the structure lends some support to the idea that one is viewing on the screen an object with similar characteristics to the lenses of one’s own eye and at a similar magnification, which is not significantly greater than that done by the eye itself when squinting into sunlight.  

Examination of the ‘objective lenses’ at the bottom of the microscope suggest that what one may be seeing when looking into the microscope is, in fact, the lens of a smaller eye, since, without wishing to take my own microscope apart, I can see what resembles the hard orange ‘iris’ of a bird (it particularly looks like that on a pigeon) inside the larger of the three objective lenses of the microscope, and on two when photographed and magnified.   When moving the largest of the three objective lens, the iris type object becomes more or less visible, as though the round object has been placed between two lenses, or bits of glass, but occupying a slightly smaller space. 

An image of this object may be projected directly by the light from the mirror onto the screen, although if one tilts one’s eye one can see smaller images to the left and right, suggesting some sort arrangement of mirrors, as in a kaleidoscope.  The magnification is probably comparable to that achieved by the eye and the eyepiece, since although the image is more crowded than that of one’s own eye, the width of the ‘ribbons’ is similar, suggesting that the difference between the two materials is a result in their different characteristics and better lighting  rather than a difference in magnification.  This is plausible also if one thinks that one is not seeing the whole of the visible lens of one’s own eye when squinting into the eyepiece, ie, the image of the lens of the smaller eye could fill the screen with a similar magnification if placed in the appropriate position. 

In any case, setting aside the fact that one is unlikely to be viewing biopsy cells under a microscope, if there appear to be regularities in terms of changes  (ie, if some people’s cells, but not others, appear to change in similar ways), these need not in any case indicate life-threatening changes to cells or tissue rather than the wear and tear associated with ageing.  Some terms used to denote pathology, such as ‘necrosis’,  ‘stroma’ and ‘cribriform’ and even ‘calcification’, are difficult to pin down in terms of why they are dangerous or by what mechanism.  For example, ‘necrosis’, associated with malignancy, refers to exaggerated cell death (as opposed to ‘apoptosis’, which is normal cell death) and is an indicator of uncontrolled proliferation, apparently because in an area where you have more cells, or tissue, you would be more likely to have increased cell or tissue death.  But increased cell death would suggest either a check on unnatural proliferation or would, in any case, also be associated with benign tumours or, if not, suggest that benign tumours are more likely to be invasive, in the sense of growing sufficiently to invade surrounding tissue, than malignant ones.

If cancer is not diagnosed according to particular features of the cell (nor by cell growth since this is also a feature of benign tumours) but by invasion of surrounding tissue, this would seem to imply producing changes in surrounding cells or tissue, since otherwise a benign tumour could also potentially obstruct surrounding tissue.     It is not clear by what mechanism one cell would invade another or what this would look like in cell cytology/histology.  If surrounding tissue also changes, other than because of force or obstruction, it is likely to be as a result of the same factor(s), including any viral agent, that caused the initial cell to change, rather than that the initial cell invaded the other, unless the process being described is reproduction, or replication, involving, as is said to be the case with viral cells, some sort of interaction between cancerous and non-cancerous cells. 

The presence (or spread) of tumours is usually detected, or confirmed in the case of those that can be felt by the hand, by x-rays or CT scans.  Again, no camera, whether or not it is said to emit ‘radiation’, can see beneath the surface of the human body, including in order to see a cell or ‘gland’ that has travelled from another part of the body.   The principle by which an MRI scan works seems more plausible, ie, that it produces images that reflect the attractions of different substances within the body to a magnet, but in practice it would not be sufficiently precise, given that the body has depth as well as area.    

If invasion is by the tumour itself, rather than by a single cell, setting aside by what process the tumour itself formed (ie, whether through invasion of one cell by another, including in order to replicate, in which case it would be difficult to distinguish between the formation of the tumour itself and invasion of adjacent tissue, or through a spontaneous proliferation of malignant cells), again, does it occupy the adjacent tissue or cause it to change?  If the tumour only moves, or displaces, adjacent tissue, this too would also be a feature of benign tumours. 

Second, the mechanism by which a cancer cell alters, harms or kills a host cell and ultimately its host seems to be asserted rather than explained, which would be consistent with the ambiguity as to whether cancer is diagnosed by malignancy or invasion of surrounding tissue.  If the mechanism is force, an obstructive tumour is as likely to be benign as malignant. If the mechanism is individual cell mutation, it is not clear why cell division would take place within the body, unless the body grows to adulthood in a way approximating cell growth, although the splitting of cells into identical ‘daughter’ cells would not in itself appear to account for either growth or differentiation within the body.  But neither is genetic mutation explained satisfactorily.

If environmental factors (or ageing) cause an alteration in RNA/DNA then it is not clear why these factors are not themselves the cause of ill health in that there appears to be no satisfactory account or description of the means by which alteration in information stored in the cells causes an alteration in bodily tissue. For instance, there is understanding of the link between inputting information into a calculator or adding computer software and the changes that appear on the screen. There is a plausible explanation of the changes to the body when a surgeon follows a particular set of instructions. In each case, there is an understanding of, first, the agency, in the sense of there being a person operating the calculator or computer or on the body, second, of the mechanical link, in the sense of what follows when one presses keys on the calculator or inserts software or makes an incision, and, third, of the force needed, either electrical or human. There is not a comparable explanation of the agency and mechanism of change within RNA/DNA. RNA/DNA, or the genetic information/instructions it contains, is said to have an independent existence and be capable of agency in the sense that it is present in the body and influences it either in the absence of environmental factors or because it alters the character of environmental consequences (since otherwise it would be unnecessary in the explanation of changes to the body). But if it does have agency, there is no adequate account of how a genetic code, an abstract entity, would have the capacity to produce changes in the body or through what mechanism (ie, what type of mechanical link). Nor can there be if, first, it is not possible to view the body clearly at the scale necessary to view changes and, second, if there is no satisfactory philosophical explanation of the link between, or ontological compatibility of, genetic information and bodily tissue.

Third, metastasis is said to be the process whereby a cancer that starts in one part of the body kills, by spreading to distant, vital organs.  A cell from the primary tumour is said[i]  to break loose when it loses its ability to stick to the initial tumour and then travels along the blood stream or via the lymph system.    In the distant organ, the cell would regain its ability to stick and then begin to proliferate.  The new mass of cells would be referred to as a secondary tumour – eg, a thyroid tumour in the lung, composed of thyroid cells rather than lung cells.  That different parts of the body begin to develop tumours spontaneously, or even that one part of the body would copy another, would seem more plausible than that there are secondary tumours consisting of cells that have travelled from the initial tumour. 

How would they travel? An apparently infinitesimally small ‘cell’ would be unlikely to be able to travel within the relatively thick blood or ‘lymph’, especially from a lower part of the body to a higher, or even if it were able to travel in any spaces between blood or lymph cells and upwards, be able then to enter distant organs, ie, penetrate, for example, the membranes of the brain or lungs.  (And why never the heart?)  From observation, larger, not smaller, animals have less difficulty surviving for any length of time in water, while smaller fish will have more difficulty with relatively viscous fluids, such as blood.    

CT scans apparently show single cells that have travelled to another organ but it seems unlikely according to common sense (which is an abstraction from observation of comparable sensory perceptions) that a scan would really be able to distinguish a single cell even if it were possible to photograph what is inside the body.   If, instead, a large number of cells broke away, what, setting aside their motive, would propel them to a distant organ?   The hypothetical force exerted by any number of cells that remain invisible to the eye would still seem likely to be insufficient even if each contained a motor of some sort, which they are not said to do.   Whatever the stated facts of the blood stream, it also seems unlikely that this alone would be able to carry cells, particularly from a lower part of the body to a higher. 

Fourth, what is usually said to kill in the case of cancer is a recurrence, because a recurring cancer is said to be more aggressive, which one assumes means it would either grow more quickly or show greater pathology and propensity to metastasise, although in either case it seems uncertain by what mechanism a cancer cell harms and ultimately kills.   If the cells, or tissue, are malignant, and become more malignant as they ‘mutate’, it is not clear in what sense this could be true - other than that they consisted of parts of cells that were said to indicate malignancy - if they do not themselves contain agents of harm or are not able to otherwise cause alteration to cells or tissue.

If recurrence and mutation mean they are able to proliferate more quickly, aside from the fact that this need not indicate malignancy it is not clear, why and how this could be true.   If one assumes agency of some sort, then why, after surviving an attempt to eradicate it, would it seek to destroy its host (and therefore itself) or otherwise draw attention to itself?   And if recurring cancers are more dangerous than the initial cancer, and often fatally so, then why do oncologists treat the less aggressive, indolent, cancers instead of monitoring them, when surgery and anaesthesia, and, apparently, ‘radiation’, are themselves dangerous.  It also seems unlikely that drugs would be able to target parts of the body as precisely as we are told they can, or that they would not all have some impact on both the stomach and the head.

Fifth, the benign growths, or lumps of altered, tissue, caused by such things as knocks, burns, and sun exposure, might cause obstruction if they become too large, but in most cases they do not seem to grow, so that more damage is likely to be done by attempting to remove them surgically than by leaving them.   They may even have grown, after an injury, to protect a part of the body from further damage.  The most likely causes of the growth are the hardening of tissue and the accumulation of fluids after injury.    However, it seems unlikely that tumours would grow and expand to a considerable size within the body, especially as we age and weaken, unless, again, their purpose is protective.   In any case, those growths we cannot see or feel, we have no certain means of knowing whether or not they exist.  Therefore symptoms such as a persistent cough are likely to indicate weakness or irritation rather than disease. (In the same way, a cold is a sign that one is weak.  You do not catch a cold, which is the body’s way of warming up or expelling liquid).   Similarly, a shadow on an x ray is only likely to be a lighter area on a photographic negative (unless a stock image is produced). 

What kills in the case of apparently fatal illnesses such as those associated with cancer (and other diseases) is a cumulative weakening that may be partially caused by medication (prescription or otherwise), especially when there are initial unpleasant side effects, but is more likely to be caused by other factors, physical and psychological, in the environment of someone diagnosed with a viral infection (or other disease).   These include such things as alcohol, tobacco, and non-prescription medications and well as narcotics.  Other factors include surgery, which weakens, at least temporarily, so increasing the risk from other depressants, because of anaesthesia or blood loss; poor diet (bad or insufficient food); environmental factors, particularly inadequate heating, extreme heat, fluctuations in temperature, utility emissions; excessive physical exercise or overwork, or too little exercise; insomnia (eg, caused by stress or insufficient food), or too much sleep (which may cause headaches).  Perhaps decisive, for example, with respect to appetite, is the psychological stress and fatalism caused by the belief that one has a potentially fatal illness. 

It would strike most people as inconceivable that diseases such as cancer could be invented fictions, and so we have not thought about whether they are plausible according to observation, common sense or logic.   However, the term, the Final Solution (associated with the Wannsee Conference, which historians now say may have taken place in 1942, the year of the ‘Beveridge’ Report, which envisaged a health service that would deal with the five giants of disease, poverty, ignorance, squalor and idleness), might have implied the use of intravenous fluids and alcohol in order to reduce and control populations.




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