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346 lines
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<p></p>
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<p>
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<strong><strong>Cataracts: water, energy, light, and aging</strong> </strong>Because of the baby boom
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population bulge, the market for cataract surgery and the little plastic intraocular lenses is growing
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wonderfully. According to the World Health Organization, there were about 20 million cataract surgeries
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performed in 2010, with 32 million expected in 2020. In the US, about 3 million cataract surgeries are
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performed annually. Revenue from sale of the intraocular lenses in the US alone was $775,000,000 in 2010,
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and is expected to reach $965,000,000 by 2017. In 2010, the Alcon company earned $1,200,000,000 from one
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type of intraocular lens. (Market Research.com) To promote the sale of the "premium'" lenses, which cost
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thousands of dollars, patients are told that the more expensive lenses will save them money in the long run,
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by making ordinary glasses unnecessary (sometimes).
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</p>
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<p>
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<span>The lens replacement surgery is now sometimes recommended when a cataract has caused only a slight
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decrease in visual acuity, or even a suspected decrease in acuity. I haven't known anyone who had the
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surgery who had been informed of the incidence of complications of the surgery, which result in
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permanent blindness for thousands of the patients every year. </span>
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<span>Some of the causes of cataracts have been known for many years, but the knowledge is usually ignored
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by the medical profession. Medical myths about the causes of disease support present practices. Myths
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about the causes of cancer, heart failure, hypertension, menopause, osteoporosis, sarcopenia,
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depression, dementia, and cataracts are designed to reinforce each other, forming an interlocking
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system, an ideology of the organism. </span>
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<span>The conventional ideology identifies pathological cells and defective proteins and bad genes as the
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causes of organ failure and disease, and "aging" is seen as a dimension in which entropy tends to
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increase those defects. </span>
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<span>This ideology discourages thoughts of "field" effects in which the function of a molecule, a cell, or
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an organ affects, and is affected by, things that aren't in direct contact with it. This is why the
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removal of a lens is treated so casually. There is some knowledge about the effects of systemic disease
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on the eye, but very little about the effects of particular parts of the eye on systemic physiology, and
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relatively few physicians are aware of the effects of one part of the eye on the other parts of the eye.
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A few of these physiological interactions within the eye are very interesting. For example, injury to
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the lens powerfully stimulates regeneration of nerves in the retina (Fischer, et al., 2000). Things
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which injure the lens enough to cause cataracts to develop might also be injuring the retina, but the
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emission of stimulating substances from the lens must be a compensating influence. </span>
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<span>Every normal tissue of the eye is emitting substances that affect other parts of the eye, and probably
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other parts of the body. Until the 1970s, the literature was dominated by the view that the lens was a
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lifeless material, like hair and toenails, and even in 2013 there is great reluctance of researchers to
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recognize its vital cellular activity.</span>
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<span>After an artificial lens has been implanted, there are great changes in the vitreous humor (which
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fills the space between the retina and the lens), with a reversal of the gradient of viscosity, and with
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changes in many proteins, including transthyretin, alpha antitrypsin, retinoic acid binding protein,
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antioxidant proteins, and the enzymes carbonic anhydrase and triosephosphate isomererase (Neal, et al.,
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2005). </span>
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<span>I haven't seen any recent studies of the effects of lens removal on the nervous system, but a 1953
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study of 21 patients reported a high percentage of behavioral disturbances following the surgery:
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"Following the operation 20 patients showed some alteration in behavior including changes in mood,
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psychomotor disturbances, paranoid and somatic delusions, hallucinations, disorientation and
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confabulations. In 3 cases the disturbance was characterized as severe." "It is concluded that disturbed
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behavior is an integral part of the reaction of almost all cataract patients because of a complex
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interaction of a number of factors" (Linn, et al., 1953). </span>
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<span>In animal studies, when the lens capsule is closed after removal of the lens, within a few weeks a
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well formed lens has regenerated (Gwon, et al., 1993); cell division is stimulated in the cells
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remaining attached to the capsule, similar to the regeneration of the adrenal cortex after its
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removal. </span>
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<span>Artificial replacement lenses are designed (with an ultrasharp edge) to block the regenerative
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migration of cells within the capsule, because the cells can quickly form a new cataract behind the
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plastic lens; those cataracts commonly form in reaction to the lens. The use of arsenic to kill these
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cells has been proposed, and probably used (Zhang, et al., 2010). </span>
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<span>The easy money in lens surgery has obviously discouraged professional interest in preventing
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cataracts, or curing them, or stimulating the regeneration of new lenses. Research in the prevention of
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cataracts has encountered serious barriers to performing the clinical trials that would be necessary for
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approval. "… Clinicians have even developed the opinion that lens and cataract research is
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no longer necessary to overcome cataract blindness." (Sasaki, et al., 2000.) However, it isn't
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inconceivable that someone could find a way to make prevention, cure, or regeneration significantly
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remunerative. </span>
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<span>Although the lens has no blood supply, fluid carrying nutrients and oxygen is constantly flowing
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through it, providing the cells with glucose, amino acids, and ATP, that it uses for maintaining its
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structure. Its proteins are being renewed continually, broken down and synthesized (Ozaki, et al.,
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1985). There is clear evidence that some of the core cells retain a nucleus, and that large molecules
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can move between cells (Lieska, et al., 1992; Shestopalov and Bassnett, 2000; Stewart, 2008; Mathias and
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Rae, 2004). Despite this evidence, prominent researchers are still promoting the paradigm of inertness,
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the lens as analogous to a toenail. As in other cells, ATP maintains the proper water content in the
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cells. Besides providing energy and amino acids, the circulating fluid carries minerals and many
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hormones and regulatory substances. </span>
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<span>The absence of a blood supply to the lens has kept people from thinking of its pathology in terms of
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the inflammatory processes that are now recognized in other conditions, for example in dementia, heart
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disease, and cancer, but the same basic processes can be seen in the development of cataracts. Improved
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knowledge of lens physiology is very likely to lead to major improvements in therapies for the other
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conditions. In the lens, the state of water changes before there is any other evidence that a cataract
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is developing (Mori, 1993); detecting similar water changes in other tissues might improve diagnosis and
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treatment of other problems. Things that acutely lower the ATP content of cells increase their water
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content, and in the process, the water functions differently, becoming more randomly
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arranged. </span>
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<span>The idea that the properties of water change as cell functions change contradicts the common
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reductionist assumption that water is just the medium in which molecular interactions occur. Since
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Kelvin's 1858 demonstration that the heat capacity of water changes with its shape, and Drost-Hansen's
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demonstrations that its density decreases near surfaces, attention to the physical properties of water
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has made it possible to understand many biological mysteries, such as the decrease of volume (Abbott and
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Baskin, 1962) when a nerve or muscle cell is excited. Although the invention of the MRI grew directly
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from Damadian's understanding of water's centrality to biology's most important issues, the technology's
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most important contributions, related to changes in water structure, haven't been recognized,
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understood, or assimilated by medicine. </span>
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<span>The electrical properties of the protein framework of a cell interact with the state of the water in
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the cell, and with the things dissolved in the water, including phosphate, calcium, sodium, and
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potassium. Actin, one of the major muscle proteins, forms a meshwork in the cytoplasm of lens fiber
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cells, and myosin, the other major muscle protein, has been found in association with the actin
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(Al-Ghoul, et al., 2010). ATP (alternating with ADP+inorganic phosphate) is involved in muscle
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contraction and relaxation, and it is involved in the conversion of actin from a filament into a
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globular form. Changes in the amount of ATP and ADP are important for influencing the interactions of
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water and proteins. </span>
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<span>The actin skeleton is involved in the fiber cell's elongation as it develops from a roundish
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epithelial cell, and it's probably responsible for the ability of lens cells to contract when stimulated
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(Oppitz, et al., 2003; Andjelica, et al., 2011). These muscle-like effects of actin are believed to be
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responsible for the movement of organelles and other cell motion, such as cytoplasmic streaming. But, as
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a major part of the cell's structure, it could also be expected to act as the framework for
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electroosmotic flow of water, accounting for the circulation that maintains the cell's energy. The
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observed static electrical properties of lens cell fragments could account for a complete daily renewal
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of the fluid (Pasquale, et al., 1990), but the metabolic gradients in whole cells would probably cause
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faster flow. </span>
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<span>With oxidative energy production occurring in the surface cells, an electrical gradient will be
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created, causing water to flow away from the site of respiration. (Electroosmosis probably also accounts
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for the somewhat mysterious exit of water from the eyeball and brain, in perivascular flow.) The flow of
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water through these cells is very fast, but Ichiji Tasaki has demonstrated similarly fast movement of
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water in nerves and artificial polymers in association with electrical activity (2002; Tasaki and Iwasa,
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1981, 1982; Iwasa, et al., 1980). </span>
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<span>At least since Gullstrand's unfounded assertions in his 1911 Nobel lecture, it has been assumed that
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the lens, like a water-filled balloon, keeps the same volume when it flattens, for distant focus.
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Zamudio, et al. (2008), have shown that "…the lens volume decreases as the lens flattens during
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unaccommodation." "The lens volume always decreases as the lens flattens." They determined that "…the
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changes in lens volume, as reflected by the speed of the equatorial diameter recovery in </span>
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<em>in vitro </em>
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<span>cow and rabbit lenses during simulated accommodation, occurred within a physiologically relevant time
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frame (200 ms), implying a rapid movement of fluid to and from the lens during accommodation." This is
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the duration of the action potential of healthy heart muscle, though it's probably not as fast as the
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very superficial changes that Tasaki saw in nerves. It's the sort of change rate that could be expected
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in an organ whose change of shape is the result of stimulation. Accommodation, with this immediate
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hydration, is produced by cholinergic stimulation, and in the healthy lens this hydration is rapidly
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reversible, as the stimulating acetylcholine disappears and the lens flattens. </span>
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<span>The failing heart muscle, unable to relax fully, becomes harder as its water content increases, and
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cancer cells, locked into a contracted excited state, become stiffer as their water content increases.
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Similarly, cataracts have been described as more rigid than normal lens tissue (Heys and Truscott, 2008;
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Hu, et al., 2000), yet their water content is higher (Racz, et al., 2000). Along with the increased
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water, the stressed cells take up very large amounts of calcium, and sodium increases while potassium
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decreases. Inorganic phosphate increases in the stressed cells, some of it entering with the circulating
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fluid, but some of it produced from the ATP which is decreasing. Serotonin, iron, lipid peroxidation
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products, nitric oxide, and prostaglandin are also increased. The increased calcium activates
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proteolytic enzymes that break down protein. </span>
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<span>In the failing heart and growing tumors, there is an increase in the quantity and the cross-linking of
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collagen in the extracellular matrix, contributing to the overall hardness, besides the contracted state
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of the cells themselves. In the cataract, cross-linking of various proteins, including collagen, also
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seems to be involved in the problem, along with the altered state of the water (Mishra, et al., 1997;
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Eldred, et al., 2011). The cross-linking enzyme transglutaminase is induced by stressors such as
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ultraviolet light which produce cataracts. </span>
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<span>When the available energy doesn't meet the cell's energy requirements, if the cell isn't quickly
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killed by the stress it will use some adaptive mechanisms, stopping some repair processes to reduce
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energy expenditure, possibly stopping specialized functions to reduce energy needs. Fibrotic changes
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occur as a result of defensive reactions in stressed cells, usually following long periods of fatigue
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and inflammation. Cortisol generally protects cells by blocking over-stimulation and providing increased
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material for energy and repair, but it can kill cells (nerve cells and thymus cells) that depend on
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glucose oxidation, leading to immunodeficiency and excitotoxic brain damage. The glucose-dependent lens
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fiber cells express the same glucose transporters, GLUT1 and GLUT3, as the brain, and the "nerve
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specific" GLUT3 is concentrated in the dense nucleus of the lens (Donaldson, et al., 2003). Exposure to
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excessive cortisol or hypoglycemia is able to quickly produce cataracts, showing the basic importance of
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glucose metabolism for lens health. </span>
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<span>Oxidative metabolism in the surface cells is probably largely responsible for the streaming of fluid
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through the fiber cells, providing some ATP and the nutrients that allow the fiber cells to maintain and
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repair their structure, but I suspect that local metabolism of glucose by the fiber cells provides most
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of the energy for keeping the protein-water system in its orderly relaxed state. </span>
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<span>The aging lens, like all normal tissues, is drier, has a lower water content, than younger tissues,
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but when a cataract begins to develop, there is a sharp increase in the water content in that area,
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something that happens in any excited or fatigued tissue. (In a stimulated nerve or muscle, for example,
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although in a closed system there would be a slight decrease in volume as its water becomes relatively
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randomized, there is normally a sudden absorption of water from the extracellular space, where the water
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has the same random organization.) With the decreasing energy charge of the cell, represented by
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decreasing ATP and increasing ADP and inorganic phosphate, the long range order of the water decreases,
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changing the activity of enzymes in a variety of ways, for example by the exchange of a high magnesium
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content for a high calcium content. While the renewal of proteins decreases because of an energy
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deficit, the activation of proteolytic enzymes by calcium degrades the cell architecture and the
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crystallin that makes up about 90% of the cell's protein, and these damaged proteins become
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progressively cross-linked, in a process analogous to the cross-linking of collagen in sun-damaged skin,
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or in cancer or a fibrotic failing heart. </span>
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<span>The diffusion of water in these congested cataract areas becomes random, more like ordinary bulk
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water, and it's likely that this randomization of the water, along with the architectural
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disorganization of proteins and changing electrical fields, impedes the longitudinal flow of nourishing
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fluid through the lens. MRI studies show relatively free diffusion of water longitudinally in the lens
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fiber cells from front to back, but not transversely (Moffat and Pope, 2002). Water that's highly
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ordered by nearby surfaces can still be very mobile parallel to the surface. </span>
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<span>The parasympathetic nerve transmitter acetylcholine is formed in the lens, as well as its receptor and
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the enzyme which destroys it, cholinesterase. Chemicals that inhibit cholinesterase, and drugs that
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mimic the action of acetylcholine on the receptor, cause cataracts. These drugs (Michon and Kinoshita,
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1968; Harkonen and Tarkkanen, 1976) cause the lens to take up water, sodium, and calcium, and to lose
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potassium, and by increasing the cells' energy expenditure, they accelerate the consumption of glucose
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while blocking other metabolism. Since these are known effects of stimulation by acetylcholine, it's
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reasonable to assume that acetylcholine is involved in the natural formation of cataracts. </span>
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<span>Besides the direct excitatory effects of acetylcholine, the increase of intracellular calcium and
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decrease of magnesium (Agarwal, et al., 2012) caused by it promote the synthesis of nitric oxide (which,
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for example, blocks the function of cytochrome oxidase, reducing the production of ATP), and the
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interference with glucose metabolism in itself is cataractogenic (Greiner, et al., 1981). </span>
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<span>Ultraviolet light powerfully stimulates the formation of nitric oxide (Chaudhry, et al., 1993), and is
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one of the known causes of cataracts. Since the cornea is more directly exposed than the lens to the
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ultraviolet rays of sunlight, the effects of injury can be seen more quickly. Exposure of the cornea to
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ultraviolet light causes swelling, reduced transparency, and the formation of nitric oxide, which enters
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the aqueous humor (Cejka, et al., 2012; Cejkova, et al., 2005). Swelling in itself, regardless of the
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cause, decreases the transparency of the cornea (Stevenson, et al., 1983); anything interfering with its
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energy metabolism causes swelling. </span>
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<span>The blue color of ordinary water is caused by its absorption of red light, possibly by its hydrogen
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bonds (Braun and Smirnov, 1993), but there haven't been many studies of the physical effects of red
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light on water itself. Since water absorbs much more strongly in the infrared wavelengths, there is a
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tendency to explain the benefits of sunlight by its infrared rays. Red and orange wavelengths penetrate
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tissue very effectively, because of their weaker absorption by water, allowing them to react with
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pigments in the cell, such as cytochrome oxidase, which is activated (or re-activated) by red light,
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increasing the production of ATP. This effect counteracts the toxic effects of ultraviolet light, but
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there are probably other mechanisms involved in the many beneficial effects of red light. </span>
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<span>Recent work by a group at the University of Ulm in Germany (Andrei Sommer, et al., 2011) has revealed
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an effect of red light (670 nm) on water that I think helps to explain some of its protective and
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restorative actions. Shining laser light onto layers of water adsorbed on a solid surface, they were
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able to show "a breathing-like volume expansion of the topmost sheets of water molecules." They explain
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this as the result of a stabilization of a more ordered state of the hydrogen bonds of the water. They
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are applying this to chemotherapy, since the expansion of water in the cell where much of the water is
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in adsorbed layers similar to their experimental set-up, alternating with its volume contraction as the
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light is pulsed, causes water to move in and out of the cell quickly, taking some of the drug with it.
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They have also proposed that degenerative changes in the connective tissues involve a loss of ordered
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water, and have experimented with light treatments to restore elasticity and flexibility. </span>
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<span>Since the water in cataracts is in a less ordered state than in the transparent lens, the re-ordering
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effect of red light could be valuable, and if the effects are the same as in their experiments with
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cancer cells, the increased volume of the re-ordered water would cause a movement of water out of the
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cataract, as it does in cancer cells in their experiment. And the known restorative effect of red light
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on oxidative production of ATP would almost certainly be helpful. </span>
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<span>Among the popular medical treatments that are likely to contribute to the development of cataract are
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glucocorticoids, and drugs that increase serotonin (Dietze and Tilgner, 1973; Korsakova and Sergeeva,
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2010), and drugs that increase nitric oxide. Free fatty acids are toxic to the lens, which contains the
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enzymes for synthesizing prostaglandins and related promoters of inflammation; the products of lipid
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peroxidation are increased in people with cataracts. Endotoxin from the intestine increases the
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formation of nitric oxide, so it's essential to minimize intestinal inflammation. </span>
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<span>High altitude very strongly protects against cataracts (Brilliant, et al., 1983). Low oxygen tension
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itself protects the lens's clarity (Akoyev, et al., 2009), possibly by the protective effect of
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increased carbon dioxide against glycation of protein amino groups. Aspirin's known anticataract effect
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apparently involves a similar protection of crystallin against glycation, but aspirin has several other
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protective effects, including prevention of protein cross-linking, and the inhibition of the synthesis
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of nitric oxide and prostaglandins and other disruptive materials (Crabbe, 1998; Beachy, et al., 1987;
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Lonchampt, et al., 1983). Progesterone's inhibition of nitric oxide production is probably protective
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for the lens, paralleling its effects in other organs. Inhibitors of nitric oxide, such as
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aminoguanidine, are protective. Anticholinergics, including atropine, inhibit over-hydration of the lens
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and prevent cataracts caused by excessive cholinergic stimulation (e.g., Kaufman, et al., 1977).
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Caffeine, in animal experiments, prevents cataracts. Uric acid, which inhibits nitric oxide formation,
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is reduced in people with cataracts. The factors that prevent or promote other degenerative diseases are
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similarly protective or harmful for the lens.</span>
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<span><h3>REFERENCES</h3></span>
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<span>Invest Ophthalmol Vis Sci. 1981 Nov;21(5):700-13. Organophosphates of the crystalline lens: a nuclear
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<span>Exp Eye Res. 2008 Apr;86(4):701-3. The stiffness of human cataract lenses is a function of both age
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</p>
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