RETINITIS PIGMENTOSA : A Case of Slow Loss of Vision

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Note: This article  is intended for informational purposes only, and should not be interpreted as specific medical advice. You should consult with a qualified healthcare provider before making decisions about therapies and/or health conditions.

Background

  • Retinitis pigmentosa (RP) is a group of eye diseases that affect the retina. The retina, which is located at the back of the eye, sends visual images to the brain where they are perceived. The cells in the retina that receive the visual images are called photoreceptors. There are two types of photoreceptors: rods (which are responsible for vision in low light) and cones (which are responsible for color vision and detail in high light).
  • In RP, the photoreceptors progressively lose function. Side vision, called peripheral vision, slowly worsens over time. Night vision is also affected. Central vision typically declines in the advanced stages of the disease.
  • Most cases of retinitis pigmentosa are inherited. However, some people develop the disease even if they have no family history. Others may develop the condition as part of another disorder, such as Kornzweig disease, Kearn-Sayre syndrome, Waardenburg syndrome, Alport syndrome, or Refsum disease.
  • Signs of RP can usually be detected during a routine eye exam when the patient is around 10 years old. However, symptoms usually do not develop until adolescence.
  • Worldwide, RP is thought to affect roughly one out of 5,000 people.
  • Although the disease worsens over time, most patients retain at least partial vision, and complete blindness is rare. There is currently no known cure or effective treatment for retinitis pigmentosa, but there are some possible ways to manage the condition.

Signs and Symptoms

  • Symptoms of retinitis pigmentosa (RP) vary among patients. The speed at which the disease progresses also varies.
  • The first sign of the disease is typically poor night vision or difficulty seeing in dim light. This is generally followed by limited side vision (peripheral vision) and difficulty seeing detailed images. Over time, the disorder may cause tunnel vision, which occurs when the outer edges of vision are dark, so that only objects directly in front of the eye can be seen.
  • When patients are exposed to bright light or sunlight, they often experience a glare that makes it difficult to see.
  • Central vision usually starts to deteriorate in the later stages of the disease. Symptoms of central vision loss include difficulty reading or seeing detailed images.
  • Some people with RP may eventually go blind, although most people are able to maintain some vision throughout their lives.

Diagnosis

  • Eye examination: An ophthalmologist (eye doctor) can diagnose retinitis pigmentosa (RP). Usually, the doctor uses a special instrument, called an ophthalmoscope, to view the inside of the eye, where the retina is located. If the patient is healthy, the doctor will see an area called the fundus that is orange to red in color. However, if the patient has RP, the fundus will have brown or black spots.
  • If RP is suspected, an ophthalmologist may confirm a diagnosis by performing an electroretinogram (ERG). This test measures the function of the retina. During the test, different-colored lights are flashed into the eyes as the patient looks at a large reflective globe. An electrode is placed on the eye, and a wire transmits a record of the eye’s retinal activity. People with RP have reduced electrical activity in the retina, which indicates that the photoreceptors are not functioning properly.
  • Visual tests can also be performed to determine the severity of vision loss.
  • Genetic testing: Many different genetic mutations are known to cause retinitis pigmentosa. Currently, genetic testing is available for several genetic mutations, including RLBP1, RP1, RHO, RDS, PRPF8, PRPF3, CRB1, ABCA4, and RPE65.

Complications

  • Blindness: Retinitis pigmentosa (RP) causes vision loss that worsens over time. Some people may eventually become blind, although this is rare.
  • Cataracts: Patients with RP often develop a type of cataract called subcapsular cataracts. When this occurs, the lens becomes cloudy and vision is impaired. Eyeglasses may improve symptoms when cataracts first develop. Later on, surgery may be needed to restore vision.
  • Retinal detachment: Some patients may experience retinal detachment, which occurs when the retina separates from its attachments to the back of the eyeball. Without prompt treatment, retinal detachment may lead to permanent vision loss.
  • Interference with daily activities: RP may eventually interfere with daily activities. It may become difficult to drive, especially at night. Individuals are required to pass an eye test before obtaining a new license or renewing an existing license. Some people who have poor night vision may require restrictive driver’s licenses that only permit them to drive during the day.

Treatment

General: Currently, there is no known effective treatment for retinitis pigmentosa (RP). However, there are some possible ways to manage the condition.

  1. Special glasses: Many patients experience glare when they are exposed to bright lights. A light amber filter can be added to general eyeglasses to help improve tolerance of bright lights.
  2. Vitamin A: Some research suggests that high doses of vitamin A (about 15,000 international units) may help slow the progression of the disease in some people. However, more research is needed to determine if this is effective. The normal recommended amount for adults is 900 micrograms for men and 700 micrograms for women. Based on recent findings, vitamin A in the palmitate form has been recommended in patients with RP.
  3. Vitamin A toxicity can occur if taken at high dosages. Excessive doses may cause nausea, vomiting, headache, blurred vision, dizziness, liver problems, and clumsiness. It may also increase a person’s risk of developing osteoporosis. Vitamin A appears safe in pregnant women if taken at recommended doses. However, excessive doses have been reported to increase the risks of some birth defects. Therefore, Vitamin A supplementation above the recommended dietary allowance (RDA) is not recommended during pregnancy. Use cautiously if breastfeeding because the benefits or dangers to nursing infants are not clearly established. Avoid if allergic to vitamin A. Use cautiously with liver disease or alcoholism. Smokers who consume alcohol and beta-carotene may be at an increased risk for lung cancer or heart disease.
  4. DHA: DHA is an omega-3 polyunsaturated fatty acid and an antioxidant. Some studies suggest that DHA may help treat RP, while others do not support this therapy. More research is needed to determine if DHA is a safe and effective treatment for this condition.
  5. Calcium channel blockers: Heart medications called calcium channel blockers, such as diltiazem (Cardizem®), have been suggested as a possible treatment for RP. According to some animal studies, calcium channel blockers may reduce the degeneration of the retina. However, not all studies have shown positive effects. Therefore, calcium channel blockers cannot be recommended until more research is performed.
  6. Gene therapy: Gene therapy is currently being studied as a possible treatment for RP. This type of experimental therapy involves replacing or deactivating mutated genes that are causing disorders. Other gene therapy techniques involve inserting a new gene to help the body fight a specific disease. A drug called ciliary neurotrophic factor (CNTF) has been shown to slow the degeneration of photoreceptor cells, although exactly how it works remains unknown. Early research shows that CNTF gene therapy may help stabilize (but not necessarily restore) vision in mice with RP. Gene therapy is experimental and is currently only available in clinical trials.

 

Source:  http://www.columbiaeye.org/content/retinitis-pigmentosa

Author Information

This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration .

A story of Struggle : Retinitis Pigmentosa Patient

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A Family Affair

Bill Carty was 28, married and had three young children when he went out to play racquetball one day. It had been years since he’d last played, “and I was surprised that, when the ball hit the wall, it would vanish from my vision,” Bill, now 55, recalls. “But I knew, right away, what it meant.”

Bill Carty It meant that he probably had retinitis pigmentosa, or RP, a sight-stealing disease that begins with the loss of peripheral vision and progressively worsens. Bill guessed as much because, on his mother’s side, five generations of the family had been affected by it. So when he received the official diagnosis, he wasn’t so much surprised as disappointed. “Even though my mother had it, my father had always told me that I wouldn’t get it – just because he didn’t want me to get it,” Bill explains.

Like so many first diagnosed, Bill went through denial, which made sense. He had a family; he was just kicking off a career with aerospace and defense-technology giant Northrop Grumman. Going blind? he thought. I don’t have time for that. “But then I started walking into things,” he says. “I’d crash into other people’s carts in the grocery store. I knew I couldn’t ignore it anymore.”

Luckily, Bill had a couple things going for him. He was referred to ophthalmologist Dr. Samuel Jacobson, a Foundation-funded researcher whose work included studying family histories to identify the genes responsible for retinal diseases. It would take a few years, but Bill’s family gene was identified. This means that they’ll quickly learn of future treatments targeting that gene.

But Bill also had ties to the Foundation itself. His parents had volunteered and contributed to what was then known as the RP Foundation, and during a Foundation conference in Orlando, Florida, in the early 1990s, he discovered the tools he’d need to function at high levels, both personally and professionally.

“I was determined to be independent,  but when I got to Orlando, it was intimidating, navigating that big crowd in the lobby,” Bill says. “But then I saw lots of people with canes and guide dogs, and they were doing a lot better than I was.” So he ordered a cane from a vendor and looked into getting a guide dog. After receiving mobility training, Bill “outed” himself, in essence – both at work, where he’s now vice president and general manager of the Defense and Government Services Division, and among friends and family.

At age 35, Bill also had to stop driving. Five years later, he took the next step and got a guide dog, which meant more training. Bill, now divorced from his first wife, recalls, “It turned out that the trainer of my dog and I became friends and, ultimately, more than friends. We got married. That’s Colleen.” Today, Colleen and Bill have a 12-year-old son.

Bill’s family history being what it is, he and his three sisters, who also have RP, have been active in Foundation chapters up and down the East Coast for the past 15 years, helping to raise, in his estimation, more than $3 million thus far. Bill, as a Foundation national trustee, is fully aware of the research it funds and has facilitated, especially recent gene therapies that show promise for the future treatment of RP.

“That’s extremely exciting,” Bill says. “And whether it makes a difference for my vision or not is irrelevant. When I speak to groups, I hold up five fingers. I’m the fifth generation in my family that we can count thus far that’s had RP. If we can stop it for the sixth and seventh generations, which are alive now, that’s what the Foundation is all about. And we will.”

story from : Foundation fighting Blindness

 

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DISCOVERING NUTRITIONAL DEFICIENCY DISEASES

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This article addresses Nutritional deficiencies. Let’s take a look back on history when people do not recognize there were subtle substances in their food. In the field of nutrition, this involves the continuing development of equipment for testing or assaying tiny amounts of chemicals. Many of the breakthroughs in medicine were made not by physicians, but by chemists and biochemists.

The topics to be addressed today include basic protein deficiency in starvation; iron deficiency anemia; scruvy; iodine-deficiency and subsequent low thyroid function; rickets from vitamin D deficiency; beriberi from Vitamin B1 deficiency; and pellagra from niacin deficiency-–and some of the stories of the discovery of their existence. It should be noted thought that new subtle nutrients are still being discovered, or research is revealing that more or less of this or that is optimal. For example, only about 17 years ago evidence accumulated that mothers need increased folic acid to reduce the incidence of certain birth defects such as spina bifida. Now it’s being added to foods!

 

Protein Deficiency

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Our first condition to be noted is that of kwashiorkor, a disease of protein deficiency. Generally, this is associated with many other types of nutritional deficiency, but the lack of protein has its own consequences. The muscles shrink, the hair develops a reddish tint, the liver swells and its fat content grows to compensate for the lack of protein, which gives the impression of a fat belly—but that is not fat, it represents a liver that is diseased and not functioning properly.

 

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One cause of kwashiorkor is of course simple famine, one of the four horsemen of the apocalypse.There are three main categories of food: carbohydrates, fats and proteins. Carbohdrates are mainly used for basic calories, for fuel for the cells to live. Fats are used also mainly for fuel, but also some of its components are important as building blocks; Proteins are broken down into amino acids that are mainly used for building blocks in growing new tissues or replacing old cells. We need all three types.

It’s possible to have a diet that is made up mainly of calories, interestingly enough. The second is used both for fuel , the fuel and the building blocks. We need both. In the picture of the baby on the right, it was probably fed on corn mush or what some might call “empty calories.” They’re not empty in the sense of providing nutrition as fuel, but it doesn’t adequately provide the variety of proteins and other nutrients to keep up health. This baby also has kwashiorkor, even though she isn’t starving. Sadly, there are babies in poor families (and even some pampered babies in rich families who get fine sweets!) who don’t get a truly balanced diet and get sick as a result!

Thus, being a little fat in cheeks and elsewhere isn’t a reliable guide. This baby may have been fed mainly on corn mush. The raw creases at the edges of the mouth is called cheilosis. Other signs include the reddish hair and empty vision. Protein deficiency, kwashiorkor, leads to mild mental retardation, because the brain lacks the nutrients to work with. Thus part of prevention is education of parents about good nutrition, and some teen parents aren’t bothering to learn what they need to about child care—their babies are thus a population at risk.

 

Iron Deficiency

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The picture shows native Indian slaves in 17th century Florida planting and hoeing. (Yes, the Spanish Conquistadores enslaved the aboriginal population! They felt entitled to do so because they were possessors of truth and goodness and the Indians were heathens who, by not being baptized, didn’t merit the privileges of full humanity—i.e., it was okay to make them into slaves.) Whereas the Indians ate a varied diet based on a hunter-gatherer cultural practice, as slaves their diet became mainly maize corn, which lacks a number of nutrients—iron being one of them.

As a result, children struggle with chronic iron deficiency. Iron is needed to build blood cells, and if there isn’t enough in the diet, the body works overtime. The bone marrow where blood cells are manufactured expands. For example, while the skull doesn’t usually have much space for marrow between the outer and inner external plates, in chronic anemia this space expands and the bone becomes strangely porous—a condition known as porotic hyperostosis (bony overgrowth).

 

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The mineral iron is quite common, and indeed is one of the main components of the planet’s core, accounting in great part for the Earth’s magnetic field. The iron atom figures in a number of biological key compounds and enzymes, especially those that derive from the “porphyrin” molecule shown on the left.The iron is the red part surrounded by the blue nitrogen atoms, and located so that depending on minute fluctuations of acidity or alkalinity, it tends to either attract a molecule of oxygen and release carbon-dioxide (as happens in the slightly less acidic environment of the lungs) or vice versa: In the slightly more acidic environment of the tissues, where new oxygen is needed and carbon dioxide is building up, there the hemoglobin molecule lets go of its loosely bound oxygen and binds instead to carbon dioxide. Thus, hemoglobin is the key messenger substance of blood, the blood corpuscle is its package, and iron is its core component. If there isn’t enough iron, the body can’t easily build up the rest of the system, the blood cells become pale—not enough red-colored molecules of hemoglobin—and the result is anemia.

In anemia, the tissues aren’t getting enough oxygen and the person feels bad, tired, and exertion quickly becomes exhausting. Not understanding that slaves and other poorly nourished people really were suffering with a handicap of low blood hemoglobin, their seeming sluggishness was interpreted as laziness, “shiftlessness,” and proof that they were unworth of respect. This reinforced the illusions of righteousness of the class of people who exploited their labor. This dynamic still goes on in many parts of the world today.

With anemia, the problem is fatigue. Since no one listened to complaints, the fatigue was interpreted as what? Right, laziness. That proves these people are unworthy, not energetic, and therefore unworthy of moral respect. It’s right that they be treated as less than full persons. No-account, lazy, worthless, blame-worthy—bad, not sick.
Treatment

Here and there in the history of medicine there were physicians who prescribed something containing iron.

The astute 17th century English physician Thomas Sydenham was wary of many traditional theories and treatments—generally tried to avoid bleeding, leeches, the use of mercury-containing drugs, and the like. He found that pale, weak people would often respond well to a tonic made by steeping iron filings into a kind of tea.

Gradually, though, mainly near the beginning of the 20th century, when a variety of biochemists were exploring all sorts of nutrients, the value of iron became more established as a remedy for anemia. This was found to be fairly common, in fact. Some girls in the 19th century were diagnosed with “chlorosis”—a condition that has not been diagnosed for over eighty years!  In retrospect, this condition may have been a mixture of psychosomatic symptoms, some anorexia, anemia due to menstruation without a compensatory diet, tight clothing, and so forth. Some of these symptoms may have been overlooked also because bleeding was still a common treatment, and being somewhat anemic was even a little fashionable.

Scurvy : Vit C deficiency

 

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Another condition described centuries ago and not correctly understood was the disease called scurvy. It was prevalent among a variety of groups of people who had been restricted to a narrow range of food, generally not including fresh fruits and vegetables. Prisoners, slaves, soldiers  on long campaigns, poor people or children living in asylums, orphanages, or institutions, and especially sailors—all were not uncommonly afflicted with scurvy. Their diet had little that would provide the proper nutrients, you see: It consisted of salted meats (bacon or fish), old cheese, dried beans or lentils, occasional oatmeal or other cereals, hardtack (a dense, dry biscuit), water, beer, or “grog,” which had a higher level of alcohol than beer.

Vitamin C is needed for connective tissues to form with some strength. So one sign is that the skin has little blue-red places where blood leaks out from fragile capillaries, or larger areas of subdermal (under-the-skin) bleeding that looks like a bad bruise. The gums become tender—there’s just little resistence to the prevalence of gum disease.

Really, only small amounts of vitamin C are needed, and a deficiency takes months to appear, unless one has already been marginally malnourished. For soldiers and especially sailors on many month-long or longer expeditions, biscuits can give enough calories, but those in themselves are not sufficient. Gradually, they begin to tire easier, and have other symptoms. As with iron deficiency, their upper-class commanders just thought they were lazy. After six months, the deficiencies show: The body’s capacity to resist infection plummets. Folks die from secondary infection, and sometimes from internal bleeding, because Vitamin C helps the tissues be firm. Without it, tiny blood vessels break down and people start to get small bruises spontaneously, bruise easier, and periodontal disease—gums—also bleed and get infected. As teeth have problems, other types of malnutrition also occur.

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A case study about an overly picky and obsessive child  was reviewed — a toddler, actually—who was permitted by his conflict-avoiding parents to restrict his diet. He’d tantrum if pushed to eat beyond his familiar range. As a result, this child developed a variety of symptoms for which he was medically evaluated thoroughly at some of the top hospitals in the area. They came up with a variety of rather rare diagnoses. B. A trial of larger amounts of vitamin C began to reverse his symptoms, and this was then organized into a continuing recovery program that also included psychiatric treatment for his obsessions.

Another case is that of one of these silicon valley geeks who worked late hours and relied on those cheese and cracker snacks and coffee that you can get from the machines in the break room— and he, too, came down with early symptoms of scurvy—and was misdiagnosed for a time and finally correctly diagnosed. But a few hundred years ago they didn’t know about nutritional deficiencies at all.

 

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James Lind (1716-1794)

This pioneer in the history of medicine was a ship’s surgeon in the British Royal Navy for nine years (1739-48), then shifting over to work in the Royal Naval Hospital. Lind became interested in scurvy, did some research, considered that it might have to do with the diet, and tried a variety of different diets. The ones that included fresh citrus juices clearly had the best response.

Another interesting twist: Around 1800 the potato came into much wider use in the diet of people in Ireland and Great Britain: Potatoes have only a small amount of Vitamin C, but this can be enough to sustain the body’s needs, so again, scurvy began to drop away as a condition. (One of the consequences of the great potato blight in Ireland was not only famine, but also scurvy.)

Iodine deficiency and Thyroid Function

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Another previously unappreciated mineral deficiency involves the element of iodine. This lack makes it difficult for the thyroid gland to manufacture enough thyroxin, a horomone that helps in the process of basic metabolism, the chemical processes that maintain life. Too little thyroxine and the person develops hypothyroidism or myxedema, a sluggishness

of mind and body that comes from a reduced metabolism. Iodine is a common element in seawater and fish, but in inland areas, the iodine tends to have been washed away with the millennia of rain and rivers, so areas such as Switzerland in Europe or Michigan in the United States have little iodine in the soil or the growing foods. Before iodine fortification of salt and food, people in such regions (and even today in many other areas of the world that don’t have iodine supplementation), people would get large lumps in their neck (which comes from an overgrowth of the thyroid gland—trying to make more thyroid, even in the face of the lack of a key building block—iodine, much as I described above how in iron deficiency the bone marrow also expands and distorts its surroundings). The overgrowth looks like a lump in the neck that’s called “goiter” (two examples in photos ).

Goiter is disfiguring, but what’s even worse is a condition that happens to the babies of mothers with not enough thyroid. They have a characteristic appearance that comes from a growth delay. If it is not corrected, they grow up stunted in height and also mentally retarded! This condition is  known as cretinism, and the children called cretins. If the children are treated early with thryroid hormone and given adequate iodine in their diets, as you may see in the picture on the left, some or much of this mental retardation can be reversed and they change their appearance!

Finally, the thyroid was one of the earlier glands to have its function recognized, though that was only in the late 19th century. Most glands we know about—tear ducts, sweat glands, and even the mucus-secreting tissues of the nose or windpipe—are “exo-crine”—meaning they secrete to the outside (exo-).

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Rickets: A Disease Arising from a Deficiency of Vitamin D

This disease was noted in the 17th century, but became more common when increasing numbers of people moved from the farm—where kids played outdoors and got more sunlight—to the city, where a child might help earn a living by working indoors. It was easy, also, to live so much in the shadows in a smoggy city that again there’s not much sunlight—and sunlight stimulates the production of Vitamin D in the skin. So for shut-ins or people in the northern climates who couldn’t get it in milk, rickets became rather common. (The adult form of vitamin D deficiency is osteomalacia, a word that hints at the main pathology: The bones “osteo” become more soft (“-malacia) and other problems arise from this!

Vitamin D is present in significant amounts in cod liver oil (also Vitamin A). When I was a kid I was given cod-liver-oil by my mom. It was a fashionable supplement in the 1920s through the 1940s, before the Vitamins were synthesized and included in many fortified foods. Though it didn’t taste good, cod liver oil was recommended for rickets treatment as early as 1789 by Thomas Percival in England, though this treatment wasn’t widely recognized. Dickens’ London was prime territory for rickets and Tiny Tim may have been suffering from it.

In the American South, an interesting problem came up: Melanin in the skin blocks ultra-violet light, so African-Americans only absorb about a third compared with caucasians. So those who work indoors or in overcasts conditions were prone to rickets, and some doctors even came to think of it as a disease of slaves! In Ethiopia, full swaddling of babies again leads to higher incidence of rickets in children there. The problem with some northern animal livers is that they are so rich in Vitamins A and D that they can make you sick—it’s called “Hyper-vitaminosis”—applicable only to the fat-soluble vitamins—and if you have a nice meal of polar bear liver it can kill you!

Beriberi: Vitamin B1 (Thiamine) Deficiency

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Thiamine is found in a variety of food, more with whole grains. With rice, the vitamin is found in the pericarp or covering of the grain, which gets rubbed off in the process of polishing. Brown rice doesn’t keep as well, it tends to get rancid, and the idea of polished white rice has always been considered a refinement, eaten by the better sorts of people. If there are enough other types of food this is not a problem, but it’s a bit like the problem described above with scurvy: Sailors, soldiers, others on otherwise somewhat restricted diets, if they don’t get the whole rice, come down with a multi-system disease called beriberi, which is found throughout Asia in a varied population. It was common in some armies and also navies, because as with Europe, common soldiers and sailors were given rather meager rations.

Beriberi was described by the Chinese around 2700 BC, but the cause was unknown. As seen on the chart to the left, it’s a multi-system disease. The fellow at the right also probably suffers from starvation—some of the prisoners of the Japanese at the end of WW2 had this condition. But other people may not be starved of protein or calories, but still become sick.

 

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Pellagra: Vitamin B3 (Niacin) Deficiency

Pellagra was not recognized in the United States until the early 20th century. This disorder, like beriberi, affects many systems in the body,though it shows most clearly in what has been called the three “D”s: dermatitis, diarrhea, and dementia.

In 1902, a Georgian farmer complaining of weight loss, great blisters on his hands and arms, and melancholy every spring for the previous 15 years was recognized to be suffering from pellagra. Four years would elapse until it was diagnosed again, this time in an Alabama insane asylum, where the classic constellation of diarrhea, dermatitis, dementia and even death appeared in multiple inmates. Over the next five years, southern clinicians would increasingly diagnose pellagra among their poor and institutionalized populations. These people subsisted largely on a diet of corn and fat pork. The situation was most acute for those living in prisons, orphanages, and asylums.  But this underestimated the problem, as only 1 in 6 people suffering from pellagra sought out a physician.

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Joseph Goldberger

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In 1914, the US Surgeon General sent Dr. Joseph Goldberger, a physician in the Public Health Service, south to investigate the cause of pellagra. He was impressed by the monotony of the diet eaten by the poorest Southerners, especially mill workers, tenant farmers, and institutionalized persons.Manipulating diet in experimental studies, he was able to both create and cure pellagra.

A major part of this story is that Goldberger sought for many years to promote better nutrition, a campaign that pit him against those who wanted to spend as little money as possible: Employers, of course; but also politicians whose careers to some extent depended on the contributions of their wealthier constituents.

Goldberger’s prescription of a nutritious diet was beyond the means of many Southerners, but in the 1920s, researchers found that brewer’s yeast could prevent the disease. After work in the 1930s showed nicotinic acid to be the precise defect in pellagra, flour producers began to enrich both white and corn flour with the newly identified vitamin. Such foods, coupled with rising prosperity after World War II, finally eradicated pellagra in the South. Goldberger worked tirelessly in his laboratories. here shown with his assistant and in another laboratory that was in effect more of a kitchen!

 

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Summary

It should be noted that just because it’s a vitamin doesn’t mean that it’s a panacea—another word for cure-all. The National Institute for Health (NIH) has coordinated a variety of studies into the health benefits of various vitamins. In a recent news article in the Austin-American Statesman newspaper (12/25/08, page A-13 ) a number of trials of alternative health approaches have been done by a variety of organizations. The claim by alternative health folks that the “establishment” isn’t doing anything is clearly not true—there are many groups trying to explore plausible hypotheses. But just because there are claims it doesn’t mean they are true. For example, in two long term trials involving more than 50,000 people, Vitamin C, Vitamin E, and/or selenium supplements did NOT reduce risk of cancer of the prostate, bladder, or pancreas. And in other studies, over-the-counter vitamins were of no help in preventing stroke or cardiovasc disease. As mentioned above, certain vitamins—especially the fat-soluble ones, A and D, in high doses, accumulate in fatty tissues and may in themselves be toxic and cause “hyper-vitaminosis” diseases.

 

References

Frankenburg, Frances R. (2009). Vitamin discoverieds and disasters: History, science & controversies. Santa Barbara, CA: Praeger / ABC-CLIO.

 

source : blatner.com

 

Exams Study Tips : Boosts your Memory

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Your memory plays an important part in preparing for exams. The tips and ideas in this section will help you to remember things, but people learn things in different ways so try some of them and see which ones work best for you. For example, some students like to see information written down, some prefer to listen to information and others learn better while they are walking or moving around.

Try out these different ideas. Which ones help you remember best?

  • Use pictures and visuals to help you remember things. For example, to learn vocabulary, use a picture dictionary.
  • Make diagrams and mind maps. For example, make mind maps for different topics of vocabulary or use tables to record word families.

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  • Write notes and then use highlighters and coloured pens to focus on important things. For example, use different colours to highlight pronunciation or different grammatical words.
  • Look at your diagrams, mind maps or highlighted notes again a few hours later or the next day. The more often you look at your notes, the more you will remember.
  • Write things down.

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  • Stick pieces of paper around your room with notes and look at them regularly.
  • Use your mobile phone or an online voice recorder (there are lots of free voice recorders online) to record your voice. Record yourself reading your notes and then listen to the recordings.

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  • Study with a friend. Explain things to each other and ask each other some questions. If you like listening to information, this will help you remember.
  • Read out loud (or record) just the main points you have underlined or highlighted.

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  • Listen to your notes regularly. The more you listen, the more you will remember.
  • Connect new information to things you already know. For example, when you learn a new meaning of a word, think about the meaning you already know. Is there a connection?

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  • Read your notes aloud while you are sitting or walking  around.
  • Go for a walk with a friend and test each other while you are walking.

source: British Council