On HIV and AIDS by Louise Orrock



On HIV and AIDS by Louise Orrock

It seems likely that HIV is a fictitious ‘viral infection’ that was invented for political reasons and that the illnesses associated with AIDS are either themselves fictitious (eg, cancer) or the result of treatment and other circumstantial factors. If we set aside, as Descartes asks us to, the foundational facts of science that we have been told , and instead rely on observation and reasoning to decide what is most likely to be true, it seems impossible that virus cells would damage, or kill, the person. Even if one assumes that they are able to travel, despite their size, through liquids and tissues, or travel through membranes from spaces and cavities within the body, and thrive and multiply (by whatever means), and assuming that they have a motive for harming and killing the person, a virus cell that is initially imperceptible to the senses, and which remains invisible to the eye, will not possess the ability to inflict harm, whatever its number, ie, however many cells might theoretically inhabit the body at any one time (including those that may remain after their death). This is because the capacity of a large number of individual cells to inflict harm may not be substantially greater than that of the individual cell and will not be of the same magnitude as that of a larger organism of a size corresponding to that of a large number of viral cells. Even if the individual cells were able to join together to form a larger substance, as is the case, for example, with the constituent parts of a tumour or of an animal, or each produced the same toxic substance, the fact that the viral cell is invisibly small to the eye, even when a light is shone on it, implies that by whatever number it is multiplied, it will have no volume or weight and so not be capable of harm for the reason that it does not exist. When a person is sickened by, for example, the flu or the common cold, this is because the body is weak, not because it has been infected by a virus of any kind. Similarly, a person who falls ill or dies apparently of HIV infection does so because of a cumulative weakening caused by the treatment, perhaps including, but not restricted to, medication as well as other factors but not because of HIV viral infection.

First, the claim that viral cells can be viewed under a microscope needs to be treated with suspicion. Although diagnosis is by a ‘colour’ test, which it is possible now to do in the home but which needs to be sent to a laboratory for analysis, it is said to be possible to view the HIV virus cells under a microscope, either within blood samples or where the cells have been partially, or completely, isolated from bodily fluids. If, as is claimed, the virus is approximately one times ten to the minus nine metres in diameter, and if, as is claimed, a magnification of around ten thousand is needed to view the cell, the image of the cell would be one hundredth of a millimetre in diameter, ie, too small to be viewed and smaller than the image of the cell apparently seen under a microscope. In any case, it is not apparent that something as small as a virus cell would exist as a particular entity, nor that anything, whatever its size, would present a clear image with such a magnification.

A thing can be divided, arithmetically, by one times ten to the negative nine, and living things and objects (such as the image on a computer screen) may be divided into very large numbers of constituent parts mathematically (geometrically), but that does not mean that anything so small that it cannot be seen by the eye exists as a complete entity. Although particular – in the sense of whole – living things may exist at an extremely small size (even if some moving life forms appear to emerge, in some conditions, at a larger size from, for example, fruit fibres), it is likely to be possible to view them clearly only at the size at which it becomes possible to view them with the eye alone.

The eye is able to see very small things clearly at close range. For example, it is possible to see with the eye alone tiny spores of mould and also tiny insects in motion. However, the eye blurs, and also seems to magnify, objects that are at either a greater or lesser focal length (as, for example, when a page is brought too close to the eye the letters can appear larger, as can letters at the periphery of what we are reading).

A camera lens (or telescope) can allow us to see things beyond our normal range of vision relatively clearly and distinctly. Objects beyond or closer than the object we are focusing on will blur and be disproportionately magnified. Also, the object viewed becomes blurred if it is magnified, so that its image is larger than the size it would appear if viewed only by the eye at the appropriate distance. More to the point, from observation, the image of objects, such as tiny insects, will be blurred when the image viewed is larger than the size the objects appear when viewed by the eye alone.

This suggests that the nature of microscopy is such that one can only view a clear and distinct image at a size corresponding to that which could be viewed by the eye alone at the appropriate distance, so that at best a microscope may be training the eye to focus on very small objects at no, or relatively limited, magnification. The magnification needed to produce a visible image of a viral cell of one times ten to the negative nine metres would, even if it were technologically possible to achieve, be such as to make the image impossible to identify as a ‘cell’.

However, even if it were possible to obtain a clear image at the magnifications claimed, the difficulty would remain, even if it claimed that cells can be ‘sliced’, of obtaining a clear and accurate two dimensional image of three dimensional constituents of a three dimensional cell, in which some parts of the cell did not appear clearer than others, in which relative sizes were not distorted, and in which some parts of the cell were not hidden. A ‘powerful’ microscope, such as an electron microscope, which apparently presents clear images of the parts of cells, more plausibly, and from observation (of what one sometimes sees in the middle distance when looking, for example, at a spotlight) presents an image of the ‘fingerprint’ of the eye. This is because the amount of light from the microscope, or reflected from its mirror, is such as to obscure what is on the microscope slide (as one sees ones reflection in a window on a sunny day, rather than what is in the room behind the window) while highlighting what is behind it, the eye. The fainter image of what is being viewed may become apparent only when magnification is increased or decreased.

Second, it seems odd that HIV ‘cells’ cannot survive for long outside the human body. Why would they not, in the potentially more hospitable, and autonomous, environment (in terms of temperature, hydration, available nutrition, rest) outside the body? From observation, mould, for instance, appears to thrive in certain conditions but not noticeably within the human body, and this is true of most, if not all, living things, apart from the body’s constituent parts. What is it about virus cells that make the human body an inhospitable environment for most living organisms but the only environment hospitable to HIV virus cells? And would this not make the virus cells especially careful not to destroy their host by virtue of their number or any other means, or to alter the body significantly?

If it is because the viral cell can only live at human body temperature (although other relatively small organisms, such as fleas, can live at relatively cold temperatures, and smaller organisms seem better able to regulate their body temperature than larger ones) why would it not survive outside the body (or in other species) if the temperature approximated body temperature? And why would the temperature be correct in all climates and all physical states and throughout the body, given that body temperature can appear to vary significantly even without there necessarily being a significant change in measured temperature? And what is the body temperature of the virus?

Third, the nature of transmission seems unlikely. Why would the virus cells enter a part of the body, in the case of sexual activity, from which they might be expelled before they were able to travel, and where they would be likely to receive less in the way of nourishment perhaps (ie, where waste is about to be expelled)? If it is because they can only survive and spread by coming into contact with blood, why would this be so, given the size of the viral cell, and what would this imply about their movement within the body? If the body is able to prevent the absorption of harmful virus cells from the digestive system, despite, or because of, the small size of the virus cells, how is the virus able to leave the body of one person, enter another, survive, apparently multiply, and then travel to other parts of the body after coming into contact only with blood at, or near, the surface of the body?

For example, during sexual intercourse, the HIV cells are said to travel from the semen, blood, or vaginal discharge of one person into the blood stream of another. In the case of uncircumcised males, transmission would seem to be more likely from semen into the blood stream. How is something as small as an apparently invisible virus cell able to travel out of the semen? In the case of blood to blood transmission, how plausible is it that virus cells are able to move in blood in order, first, to leave the body of one person and, second, to multiply, remain dormant (without necessarily presenting more than ‘transient’ symptoms at the site of entry or the rest of the body), and then travel and cause harm?

From observation, a flea, larger than an apparently invisibly small ‘virus cell’, cannot move within even a fairly thin liquid once it has got into it without getting stuck or appearing to drown. How would a virus cell, or a number of virus cells, be able to swim within blood and discharges in order to enter the ‘lymph’, and from the lymph enter other parts of the body, especially as the spaces between ‘cells’ and cavities within the body are not said to constitute a hospitable environment, and cells would in any case at some stage need to leave the spaces or cavities in order to enter the body itself? On the other hand, if they could travel with ease within all bodily fluids, why can they not enter the body via mucous or saliva? Whatever the consistency, or viscosity, of different bodily fluids in different environments (eg, blood can vary in thickness, and colour), it seems implausible that an invisibly small virus cell, or its descendants, would be able to leave the area they have inhabited and travel within the body.

Fourth, the process of replication seems unclear. The virus is said to replicate within the human body, since the spaces between ‘cells’ and cavities within the body are not said to constitute a hospitable environment for reproduction (which is consistent with the stated fact that they cannot live outside the body and makes the explanation of cell alteration more coherent, if not more plausible). It is said to replicate by first binding to, and then entering, the host cell, and injecting its DNA (said to be converted into DNA from RNA by an agent within the host cell) into the nucleus of the host cell. It is not clear, first, how it would be able to enter the cell. The fusing of membranes would be more plausible if the viral cell and host cell were of a similar size, or the viral cell were larger, but a blood cell is said to be sixty times larger than the viral ‘capsid’. Nor is it clear why the injection of ‘DNA’ , which is information, would lead to the creation of new life, as the two have a different ontological status: ie, one is abstract (whether or not it is ‘embedded’) and one is concrete, in the sense of being living matter. Also, the explanation of replication suggests that the creation of the new viral cell is dependent upon interaction with the host cell, rather than simply finding the host a hospitable environment, even if it does not actually blur the distinction between reproduction of viral cells and alteration of host cells. That a decaying life form, including a viral cell, might produce a new organism seems possible from observation of nature. But there is no satisfactory explanation of why a viral cell, imperceptible to the senses, is able to reproduce with and otherwise alter the host cell, only an assertion that this is the case. Also, whether or not the literature attempts to explain this, it also seems implausible that either the initial cell or its offspring would be able to leave the host cell with ease in order to continue the process of reproduction and alteration of cells elsewhere in the body.

Fifth, it seems unlikely that cells would be able to replicate in sufficient numbers in areas such as lymph nodes in order later to cause harm throughout the body. If they have not been perceptible at the site of entry, how likely are they, according to common sense (which is based on our experience and memory of comparable events), to pose a threat to the rest of the body? On the other hand, if they need to alter cells in other parts of the body in order to do harm, and there also does not appear to be a clear distinction between replication and alteration of cells, is it likely that they would remain at the site of entry for up to several years, rather than travel earlier, also to make their possible eradication (for example, through surgery) less likely?

Sixth, a virus cell, if such a thing existed, would not be able to cause harm. If it can only survive in the human body, if this is the only environment in which it can obtain nourishment and which is not dangerous to it, how would destroying its host create a better environment? If the reason is that it does not expect to survive its host and gains an advantage in the short term, then, setting aside the question of whether this is how nature, as opposed to humanity, behaves, how would any number of virus cells be able to do damage to a living being? Although not said to be the case with HIV infection, one would think that subsequent exposure would be of relevance if harm increases with the number of cells present, and especially if the body becomes to any extent resistant to an earlier version of the virus . (And that the initial exposure would need to contain above a minimum number of viral cells such that below that number would pose no risk, either immediately or as a result of reproduction if introduced in a hypothetical AIDS vaccine).

Assuming its motive was to obtain nourishment from the host, including from feeding on it and its nutrients, how would something as small as a virus cell be able to cause harm. From observation, fruit flies may cover the skin of, for example, an apple, but cannot penetrate it in order to gain the nourishment within it. Could any number of virus cells pass through any skin, or membrane, within the body, in order to harm its tissues or organs? Small flies may enter relatively solid fruits that have had their skins removed, but they do not appear to alter the fruit’s shape substantially or cause it to decay or dry any faster than if they were not present, and, in fact, seem to feed less on the fruit itself than the mould that appears on it as it decays, so that the flies’ effect appears to be, in some way, beneficial. But if the virus’s intention was to consume a part of the body, in which case the HIV virus is essentially the flesh eating bug that was discovered some time after the discovery of the HIV virus, how could something invisibly small erode the human body? How much damage can something invisibly small do over whatever length of time and by whatever number it is multiplied? Common sense suggests that a virus cell that cannot live outside the human body would not live for a long time or multiply rapidly and in great numbers inside it. In any case, would the virus cells not seek to regulate their number so as to maintain a hospitable environment? But, however long they lived, and however rapidly and by whatever number they multiplied, something that is initially invisible will not multiply to something with mass.

Given the size of the virus cell, the mechanism of harm could not be physical force: no matter how great their number, something as small as a virus cell – even if it existed – would not be able to overpower a host. The ‘cells’ of the body are apparently invisible to the eye but, when multiplied, make up tissue and organs, whereas HIV virus cells cannot be seen by the eye (as, for example, one sees particles of dust when a light is shone on them), whatever their number. However, even if something invisible to the eye did exist, which is unlikely, something that is so small that it is invisible would not be able to harm the body, no matter how many were present. This is because the capacity of a large number of cells to inflict harm, including as they die, is not substantially greater than that of the individual cell (as, for example, a number of very small simultaneous stings will not hurt significantly more than one sting, and as the sound of several birds singing will not be significantly louder than that of the song of one bird). A very large number of very small viral cells would therefore not be able to overwhelm the body by force, including through obstruction.

But nor would it possible for the mechanism of harm to be toxicity. Usually something toxic has a taste or a smell, for example, a food that is no longer fresh or a product that contains dead organisms (eg, ammonia), especially if it contains water. But the HIV virus is said to be a living organism that has no smell or taste, for example, when isolated in numbers on a slide. A toxin that enters the body will harm it according to the nature and amount of the toxin, usually initially, and the body will generally recover. Examples of toxins include those medicines that cause unpleasant side effects and rotten food (which is likely to make the person feel unwell and which is usually expelled). From observation, it seems impossible that, since they appear to have no toxic qualities, including smell, when isolated, including after they have died, that viral cells would become so toxic within the body as to cause symptoms or kill the person.

Although the virus is said to weaken and kill cells (for example, the ‘T cells’ that normally fight infection), if the mechanism is alteration rather than cell death (which would be the case, for instance, with cancer, where the virus would presumably become an agent or catalyst, or the initial one, of cell proliferation), how would it be able to do so? How would a virus cell, or a part of it, be able to cause a harmful alteration in the tissues or organs of the human body if not by force or through some toxic quality? The process is sometimes asserted and sometimes explained in terms such that it appears to be coherent but which is either not consistent with observation of nature or seems to contradict common sense, which is an abstraction from observation . Where the process is said to be mutation of host cells, there is no adequate explanation of how this happens, of the mechanism by which the viral cell is able to alter the genetic code of host cells, in the sense either of the nature of the mechanical link between either the viral cell and host cell or the host cell and disease-causing mutation or the agent of change if it is not physical force or toxicity. But nor could there be since the link between information, contained in DNA, and living matter is not explained, in the sense of overcoming the duality between abstract and concrete, or at least of explaining how an abstract entity can act as an agent of alteration, whether or not the RNA/DNA is said to be embedded in proteins and whether or not it is itself said to be altered by environmental factors and over time (ie, ageing).

In any case, the diseases that viral cells are said to cause are themselves likely to be fictitious. For example, there is not a consistent account of what a cancerous cell looks like, i.e., of what distinguishes it from non- malignant cells or from the tissue of benign tumours (so that a diagnosis of malignancy may be made according to invasion of surrounding tissue rather than by cell pathology), but nor is it clear how a cancerous cell can invade, or otherwise affect, surrounding cells and tissue, nor how it could break away and travel to distant organs, nor how it would ultimately kill, i.e., whether it is through the alteration, destruction, denial of nutrients, or obstruction of vital organs. It seems likely that lumps in the body, including those that we know to be present near its surface, are the result of such things as knocks, and reflect injury of some sort, such as knocks, and it is possible that some might even have a protective purpose (ie, to protect against further injury). Finally, whether or not there is an attempt to explain, rather than assert, it in the literature, nor is it clear why or how, in the sense of through what mechanism or mechanisms of causation, a viral cell would be able to cause a ‘cluster’ of different illnesses.

What kills in the case of apparently fatal illnesses such as those associated with AIDS is a cumulative weakening that may be partially caused by medication (prescription or otherwise), especially when there are initial unpleasant side effects, but which may be as 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, which either weaken or else stimulate and then weaken, introduce toxins into the body, cause diarrhoea or constipation (which can cause headaches and occasionally fainting), encourage anorexia, depress or confuse and cause poor decision making, make one more susceptible to colds and respiratory illnesses (especially if one believes one ‘catches’ them from others), and as well to night sweats, rashes and spots, which are the body’s response to fatigue, cold, heat, dehydration or over hydration, and malnourishment, which, at the same time, the body may be less able to recognise and to respond to). Other factors include surgery, which weakens, at least temporarily, so increasing the risk from other depressants, because of anaesthesia or blood loss; poor diet (insufficient calories, food that is not fresh or rotten or includes ingredients derived from toxins); environmental factors, particularly inadequate heating, extreme heat, fluctuations in temperature, and gas emissions; excessive physical exercise or overwork, or too little exercise; insomnia, or too much sleep. In addition, and perhaps decisive, is the psychological stress and fatalism caused by the belief that one has a potentially fatal illness. As you do not need gravity to explain why things fall to earth, you do not need cancer and HIV/AIDS to explain why people who have received a diagnosis of either might eventually fall ill.

In 1985, HIV infection was reported to be the cause of a group of illnesses affecting homosexuals, heroin users, and Haitians (hhh). Although there is now a test for HIV infection that can be carried out in the home, the results still need to be obtained from a laboratory. Whether or not a vaccine would be safe and effective, apparently promising trials, for example, in Thailand ten years ago, have come to nothing. Although life expectancies for those testing ‘HIV positive’ are now said to be near normal, a diagnosis will narrow life choices and create fear. Although there is said to be a global food crisis, it seems unlikely that nature would present insurmountable problems such that humanity’s survival would depend on inventing and treating fictitious illnesses, while intended rational decisions about the targeting of individuals and populations will have been made, even on their own terms (for example, the economic and environmental consequences), in error.

* * * * THE END * * * *
Copyright Louise Orrock 2015

    • Two very obvious points I forgot, one referred to implicitly, were that not all diseases necessarily trigger an immune response, even though they now say cancer can be caused by a virus, and the things that make us feel ill are those that suppress the body’s ‘immune system’ more than a trillion invisible virus cells: heavy gassing, poor or insufficient food, cold and fluctuations in temperature, stress and sleep deprivation, etc.

      • I have obtained much larger apparent magnifications with the Apex Learner, which I was subsequently told was intended for primary school children. Although not the 800 times the lenses imply, and although the manufacturer said in correspondence I wouldn’t be able to see 800 times clearly, I was originally seeing a very clear image at apparently 400-600 times with those lenses, although it has subsequently become less clear. I say apparently because I have to, first, estimate the width of the screen that the eyepiece lens is magnifying and then estimate how many times the piece of wrappers I have been using exceed the screen, not that easy to do, first, because I have had to manipulate the wrapper by hand because the lens tube can’t get down far enough if the lens wrapper is on a slide and, recently especially when the whole screen appears not to be in focus, I have to find an object to bring from the top to the bottom of the screen and also hope I am doing it vertically.

        • I say hope I am doing it vertically because I have trouble with the back to front image especially (it’s lit from below) but this is less of a problem than I think if the object is near the centre at the top and then the bottom, which it is usually is, and the screen is less wide at the top and bottom anyway.

    • Although if a cancer causing mutation is brought on by weakened immune system, then you might say that although cancer doesn’t trigger a response a weakened immune system makes it more likely or even causes it. But I think it’s not made clear how the viral cell causes the mutation. In the account of replication it appears to mate with the host cell, relying, from the example I remember, on the enzyme from the host cell changing the RNA to DNA. It may be that I am wrong in thinking there needed to be a clearer distinction between replication and mutation if replication causes the mutation, but why would replication rely on the host except as a conducive environment rather than it being a partner. Is that sort of cross species mutation likely?

  1. Louise a couple of questions. Do you have any qualifications or specialist knowledge that leads you to this position? Just about everybody in the medical field would strongly disagree with you.

    • I was apparently given an honorary doctorate by Orison B / Taxila but otherwise, no, only O levels in biology, chemistry and physics. I have seen hints in books (including one I don’t own but have on video somewhere) that classes or nations may be discouraged from entering science, but that could sound like trying to excuse my O level results (2, 3, 3, in 1974), and also that scientists are either in government or have great influence.

  2. Not in science, although I was apparently awarded an honorary doctorate by the Taxila Institute for 5 years of online contributions. I do have a BSc Econ (International Relations) and MA in Latin American Studies from the London School of Economics and ILAS. I have in the last year looked more at microscopes and magnifying glasses (and am reading some physics) and am writing more about that.

  3. An older book on microscopes I looked at referred to the separation of medicine and physics, and literally in the sense that one doctor I spoke to in a hospital corridor told me to go and look at reception for cellular pathology (or its equivalent) but there was none at that hospital.

  4. Microscopes don’t work. Stop the diagnosis of disease.
    All enlargement makes the image less clear because it stretches the original.
    A ‘cell’ magnified 10,000 times would not be recognisable.
    Light projection will disperse the image until it is unrecognisable or before that the light will not travel far enough to produce an image.
    With lenses, despite what is said explicitly in textbooks, it seems more likely that we do not view the object directly but instead see a reflected image.
    First, when looking into the microscope we do not appear to be focusing on the glass slide, but on something positioned before it within the cylinder: our focal length is shorter than the distance between our eyes and the slide.
    This can be tested by removing our eye from the eyepiece and noticing that we have to adjust our vision before being able to see a similarly small object placed on, or by, the slide.
    Also, observation and deduction from using lenses indicates that we are more likely to be seeing a reflected object than viewing it directly.
    It is unclear by what mechanism the lens, or light leaving it, would be able to stretch the object so that we saw its image in the same position it was located.
    Non-direct viewing, whether backwards projection or reflection, matters because hypothetical enlargement is then demonstrably limited by the width and thickness of the lenses as well as by the distance between the lens and the object and the nature of light projection.
    The traditional microscope is said to contain two types of lenses: an ocular lens higher up the microscope and three objective lenses further down it, the most powerful of these said to magnify 60 times or more in a traditional microscope.
    However, observation when using any magnifying lens reveals that you soon get problems enlarging, such as upside down images, multiple images, blurring, distortion and loss of visibility.
    These indicate the limited nature of lens magnification and the fact that what is taking place is reflection rather than direct viewing of the object.
    Although both reflection and projection can explain enlargement, the sorts of distortions we get with lenses can only be explained by reflection.
    Enlargement of the image can then be explained by the object being reflected within the lens at the same angle at which light enters the lens, such that it first converges and then diverges so that the second image is larger than the first, but viewed the correct way around.
    Reduction would then take place when a larger angle produced a smaller image on the second face of the lens (as well as when we view the lens from too far away).
    An upside down image might only be explained by the edges of the object no longer being in our direct vision as we raise a convex lens but instead being above or below it so that they cannot be reflected in the same direction as the rest of the object.
    This shift is consistent with the image one sees when using a lens appearing to blur after first being the right way up and before then being the wrong way up.
    In the same way, when we look through a glass of water an image of objects to the right of our vision appear on the left inside the glass.
    Projection and reflection would also explain why a speck on a slide could not be stretched to the width of the lens: we view an image of a larger area because a larger area is illuminated, unless projection were by a speck of light behind the object, when the light would not be strong enough even if encased or the image would be too dispersed.
    Reflection also seems likely to be the cause of enlargement if we consider that a spoon held in a glass of water appears magnified, whereas a penny dropped to the bottom of a glass will look the same size.
    More simply, if we use a camera zoom we can see objects as if we were closer to them, but we get blurring, distortion and loss of visibility as we enlarge.
    We also get blurring when we try to photograph moving objects, nor could we even see an ‘electron’ moving at 2,200 km/s.
    We can see very small things, such as mould spores, with the eye alone, whereas things that are invisible to the eye – such as ‘viral cells’ – are unlikely to exist.
    While the microscope’s cylinder, illumination and tube length may improve focus, it is not constructed to achieve maximum lens magnification or projection.
    This is because the lens measurements are small and the slide placed too close to the final lens.
    In fact, the traditional microscope would not seem capable of magnifying what is on the slide more than 3.3 times (based on lengths in the Prinz 2801 microscope, using ratios to calculate angles, and assuming illumination by the mirror placed at 45 degrees).
    We may see at low magnification a wash of the stain on the slide, depending on how the microscope is lit, but not the translucent material itself, which the stain would overwhelm rather than highlight.
    However, the more complex image we see looking into the cylinder, whichever objective lens tube is viewed and, normally, whatever is on the slide, must be a hidden object within the microscope, projected and reflected at low magnification.
    This object resembles in structure and scale the lens of an eye at low magnification, and in fact with the Prinz microscope we see the lenses of our own eye in layers above the image on the cylinder screen.
    The hidden lens theory seems plausible when the microscope is turned upside down and we see objects resembling small irises just behind the objective lenses.
    Variations other than the stain when using the same microscope may only be explained by different light patterns (eg, facing the mirror towards different lights) against different materials on the slide.
    Microscopes are difficult to take apart or even break, so it is difficult to find out what they contain, but we might ask ourselves why this is so.
    Diseases were probably invented to alter the population of the world and to control behavior.
    If you doubt that science is fiction, think also about whether birds would be able to fly against a 1000 m/ph wind or travel simply by hovering above the earth’s axis.

    Louise Orrock © August 2016
    Google ‘Louise Orrock’ to view earlier essays on the Taxila Institute / Orison B website
    Email questions to: louiseorrock@gmail.com or to receive a petition on Change.org (100 signatures needed before it will appear there)

  5. Here is a calculation I have done for the Prinz 2801 microscope. The aperture seems to be too small for its position between the lens and the slide, so that either the focal point would be before the lens, so that if you were viewing directly you’d only see a blur or, at least, for a smaller angle, you would have crowding around the entrance to the aperture from the lens and reflection from the slide onto only part of the lens, so it would not be an optimal arrangement. Here is a calculation for 60 x objective, which you might find a mistake in:

    in theory, a convex lens – eg, one resembling a glass bead in shape – might enlarge an infinitesimally small speck to the width of the aperture or lens

    whatever the difficulties and consequent distortion and coarsening of the image, the size of the apertures are not correct, even allowing for approximation of measurement

    assuming: objective lens tube (olt) width of 8 mm, distance of lens from slide of 25 mm (or 15 mm) and distance of lens from aperture of 18 mm, 18 mm, and 13 mm respectively (8 mm, 8 mm, and 3 mm respectively)

    for 60 x enlargement (18 mm olt), we would expect an aperture of 2.2 mm to 3.67 mm (depending on where the lens is placed, the smaller figure if the final lens were in fact as far up the tube as the condenser) and it is in fact 3 mm

    8 / 60 = 0.133 mm (size of speck)
    8 – 0.133 = 7.867 (the range of aperture size)
    7/125 x 7.867 = 2.2 (the expected size of aperture at position of aperture)

  6. Until 2015, I was posting on a website called ihiqs. I posted less from 2012 for personal reasons and because I wasn’t sure who it was run by but then as I returned from a visit abroad intending to post more I found I’d been thrown off. if anyone is now posting under my name, it’s not me. I failed one attempt to be readmitted on a new test – 111 – and haven’t tried since. I do think the size of the aperture is probably the most compelling point, both because it implies convergence rather divergence if direct viewing is assumed (so you are not stretching the image) and because the angle through the lens would be such either that there is convergence to a point before the lens or that you have a smaller angle and therefore crowding at the entrance – which might result in diffusion? – but also a reflection onto only part of the lens and no possibility of a significant increase with re-reflection because of the limitation/constriction of the opaque lens tube and cylinder.

  7. The point I made on the essay itself about another scientific fictions being that there was no universe was not proved in that I think theoretically the cocoon could move in both directions, as a go kart or dodgem car, so 66,600 (I may have added an extra 6 and will check my essay) miles an hour around the sun and 1,000 miles around the earth. But you would think at least you might feel travel sick in the same way you do at the end of riding in a train for a day.

  8. The point I made on the essay itself about another scientific fictions being that there was no universe was not proved in that I think theoretically the cocoon could move in both directions, as a go kart or dodgem car, so 66,600 (I may have added an extra 6 and will check my essay) miles an hour around the sun and 1,000 miles around the earth. But you would think at least you might feel travel sick in the same way you do at the end of riding in a train for a day.

  9. The train analogy may not be valid in that it could be the motion of the wheels on the track that cause the tiredness. But you might think that the body moving in different directions at such speeds would have some effect but perhaps not – although the idea of such speeds is ‘intuitively’ a ridiculous idea.

  10. The train analogy may not be valid in that it could be the motion of the wheels on the track that cause the tiredness. But you might think that the body moving in different directions at such speeds would have some effect but perhaps not – although the idea of such speeds is ‘intuitively’ ridiculous.

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