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I guess I'm the typical Negro ingrate, constantly bad-mouthing Albinos - er - White people: when the fact is , White people do Sooo much just for us. I'm sure there are many other cases, but here, I just want tho thank them for all they do just for us in combating Rickets.
Race and Illness and Vitamin D By Jacob Schor, ND
Skin Color and Vit. D
We made our mistake in looking for complex socioeconomic differences as the main factors causing higher rates of many illnesses among African Americans. Of course socioeconomic factors contribute to the onset, late diagnosis and poor treatment of illnesses among many African Americans, and that is a vitally important issue, but the biggest difference between African Americans and white Americans, as much as we try to ignore it, is skin color. Races that evolved further from the equator have lost some of their ability to make melanin and as a result have become pale skinned. Paler skin allows for greater penetration of the sun's rays.
Humans get most of their Vitamin D from the sun. Darker skin decreases the amount of ultraviolet light that penetrates the skin and, in doing so, results in lower Vitamin D production. This is fine if you live close to the equator or are in the sun most of the day. If you live in farther from the equator and spend much of your days indoors, you make much less Vitamin D. The darker or blacker the skin, the bigger the problem becomes.
Vitamin D deficiency is a common problem for all Americans, but far more so for African Americans. When you look at the statistics the numbers are shocking. Black Americans are about ten times more likely to be Vitamin D deficient as whites. Black women of reproductive age are twenty times as likely to be Vitamin D deficient as white women of the same age. The average white woman has twice the amount of Vitamin D in their blood as a black woman.
LINDA S. NIELD, M.D., West Virginia University School of Medicine, Morgantown, West Virginia PRASHANT MAHAJAN, M.D., M.P.H., Wayne State University School of Medicine, Detroit, Michigan APARNA JOSHI, M.D., Children’s Hospital of Michigan, Detroit, Michigan DEEPAK KAMAT, M.D., PH.D., Wayne State University School of Medicine, Detroit, Michigan
Illustrative Case
The mother of a 26-month-old black infant expresses concern that her son is not growing properly. Born at 34 weeks of gestation at 3 lb, 5 oz (1.5 kg), he was exclusively breastfed until 11 months of age. He is a picky eater, is breastfed twice daily, and consumes minimal dairy products.
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10-Year Case Review of Nutritional Rickets in Children's Hospital of Michigan.
Judith P. Lazol, MD Pittsburgh Children's Hospital, Pittsburgh, Pennsylvania Nedim Çakan, MD Children's Hospital of Michigan, Detroit, Michigan Deepak Kamat, , MD, PhD Children's Hospital of Michigan, Detroit, Michigan, dkamat@med.wayne.edu
Abstract
Nutritional rickets has been on the rise in the United States. A chart review of patients with nutritional rickets from April 1995 to May 2005 was performed. Fifty-eight subjects were studied (62% males, 38% females, with an age range between 2 and 132 months). Of the subjects, 81% were African Americans and 14% were Arabic; 33% were Christians and 19% were Muslims. An increasing number of cases of nutritional rickets have been noted since 2000. Seventy-nine percent of patients with nutritional rickets presented at the emergency department, and in 69% of the cases, rickets was an incidental finding; 96% of patients were exclusively breast-fed, and none received multivitamin supplements. 25-OH vitamin D levels were below 5 ng/mL in 42% of the patients, all of whom were African Americans. We could document complete resolution of nutritional rickets in only 8 patients, and 3 of these patients showed sequelae of rickets.
As of the 2010 Census, the racial composition of the city was:
82.7% Black or African American; 10.6% White (7.8% non-Hispanic whites, 2.8% Hispanic whites); 3% from other races; 1.1% Asian; 2.2% from two or more races; 0.4% American Indian; 0.02% Pacific Islander.
Posts: 22721 | Registered: Oct 2005
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I went in for a physical and was attended by a young Negro nurse. The doctor (Jewish) ended the exam by giving me a supply of Vitamin D. They were 2000mg tables. I think he is trying to give me a vitamin D overdose.
Talking with the Negro nurse, she informed me that I needed to take the vitamin D because as I should know, white people can absorb vitamin D from sunlight but black people can't. I asked her where she had read that and she said the Ashkenazi doctor taught her this.
When did my people become so dumb?
Posts: 4693 | From: Saturn | Registered: Apr 2012
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Victorian scourge of rickets re-emerges THE ASSOCIATED PRESS Article published Nov 8, 2013
LONDON — Rickets, the childhood disease that once caused an epidemic of bowed legs and curved spines during the Victorian era, is making a shocking comeback in 21st-century Britain. Rickets results from a severe deficiency of vitamin D, which helps the body absorb calcium. Rickets was historically considered to be a disease of poverty among children who toiled in factories during the Industrial Revolution, and some experts have hypothesized it afflicted literary characters like Tiny Tim in Charles Dickens' ''A Christmas Carol.'' Last month, Britain's chief medical officer, Dr. Sally Davies, described the return of rickets as ''appalling.'' She proposed the country give free vitamins to all children under 5 and asked the country's independent health watchdog to study if that would be worthwhile. Most people get vitamin D from the sun, oily fish, eggs or dairy products. Rickets largely disappeared from Britain in the 1950s, when the country embarked on mass programs to give children cod liver oil. But in the last 15 years, the number of reported cases of rickets in hospitalized children has increased fourfold — from 183 cases in 1995 to 762 cases in 2011. Experts said the actual number is probably even higher since there's no official surveillance system and it's unknown whether the disease has peaked.
''It's very surprising to see this,'' said Dr. Mitch Blair, an officer for health promotion at the Royal College of Paediatrics and Child Health. ''Children come in with bendy legs, swollen wrists and sometimes swollen ribs,'' he said. ''This is not something we should be seeing because it's completely preventable.'' He said the condition was reversible once children start getting enough vitamin D, usually in tablets or injections. Blair cited a number of reasons for the jump in rickets, including changing cultural habits — like children spending more time playing indoors, the stringent use of sunscreen, and religious beliefs that mean skin is covered. Children with dark skin are particularly susceptible, since they need a higher dose of sunshine than pale-skinned children. Unlike in other countries like Canada, the U.S. and Australia, Britain does not fortify foods like milk or flour with vitamin D. In the U.S., doctors said there has also been a rise in rickets, though there are no solid national figures to confirm it.
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The Vitamin D Council How common is rickets?
The number of children that develop rickets in the US isn’t known. However, research from the UK found that about 1 in every 100 non-Caucasian children has rickets. Rickets is more common in children who have darker skin and in children who are breast fed rather than bottle fed. Rickets is a condition that only develops in children. It’s most commonly diagnosed in children between the age of 3 and 18 months.
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SO WHAT AM I FAWNING ALL OVER WHITE PEOPLE FOR?
Well as you can see, from the preceding articles, Rickets is a disease that afflicts mostly Black children - AN JUST LOOK AT THE GREAT TROUBLE THE WHITE PEOPLE WENT TO IN ORDER TO SAVE OUR CHILDREN!
Vitamin D Fortification of Foods Whether or not the DRIs for vitamin D are increased, vitamin D fortification of food remains an important public health strategy for achieving recommended intakes. Only a few foods such as oily fish (e.g., salmon, mackerel, herring) and cod liver oil are naturally rich in vitamin D. However, virtually all fluid milk in the U.S., many ready-to-eat cereals, milk substitutes and yogurts, and some cheeses, juices and spreads are fortified with vitamin D—each generally providing between 10-25% of the Daily Value.
Two forms of vitamin D are used in fortified foods and dietary supplements: vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). When a food is fortified with vitamin D or a nutritional claim is made, the type of vitamin D must be listed in the ingredient statement. While both forms raise 25-hydroxy vitamin D levels, vitamin D3 may be more than three times as effective at maintaining those levels for a longer period of time. While optional, nearly all milk sold in the U.S. is fortified with vitamin D3.
Vitamin D fortification of foods is regulated in the U.S. in accordance with FDA’s Code of Federal Regulations, and only select foods are authorized to fortify with vitamin D. Vitamin D (vitamin D2 or D3, in crystalline, resin or crystal form) is affirmed Generally Recognized as Safe (GRAS) at specified maximum levels of safe use for certain food categories—breakfast cereals (350 IU/100 g); grain products and pastas (90 IU/100 g); milk (42 IU/100 g); and milk products (89 IU/100 g). Vitamin D is also affirmed GRAS for use in infant formula and as an optional ingredient in margarine. GRAS regulations pertain to safety and not to the composition of standardized foods. “Standard of Identity” regulations prescribing the composition of the standardized foods come into play for some foods and specify the levels of vitamin D when fortifying. For example, the standard of identity for milk specifies that if vitamin D is added, it must be at 400 IU per quart.
Food additive petitions also have led to the authorization of vitamin D fortification for some foods. These include supplementation of calcium-fortified fruit juices and fruit juice drinks with vitamin D3, soy-based beverages and products with vitamin D2, and of cheese and cheese products (excluding cottage cheese, ricotta cheese, and hard grating cheeses, such as Parmesan and Romano) with vitamin D3. Vitamin D also may be added to olestra to compensate for any interference with absorption of fat-soluble vitamins.
Major Food Sources of Vitamin D in the U.S. Diet The Dietary Guidelines for Americans encourages consumers to get their nutrients from food and to choose nutrient-rich foods first. Although ready-to-eat cereals, juices and spreads, and select other foods are fortified with vitamin D, dairy products supply the majority of the vitamin D in the diet—nearly 70% of the daily intake in children 2 to 18 years old (see Table 2). The next major dietary sources are from the meat, poultry and fish group and the grain group, which includes vitamin D-fortified breakfast cereals
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Relationship between polymorphisms in vitamin D metabolism-related genes and the risk of rickets in Han Chinese children
Yuling Zhang1†, Shufen Yang1†, Ye Liu2 and Lihong Ren1*
Vitamin D deficiency rickets is related to limited exposure to sunlight, poor nutrition and/or decreased dietary intake of vitamin D. Although people are encouraged to obtain adequate exposure to sunlight and fortified milk with vitamin D supplements, this disease remains common and has the potential to produce an epidemic outbreak in children in developing countries, such as China. The prevalence of rickets among rural Chinese children was reported to be 26.7%.
If you live north of the line connecting San Francisco to Philadelphia and Athens to Beijing, odds are that you don’t get enough vitamin D. The same holds true if you don’t get outside for at least a 15-minute daily walk in the sun. African-Americans and others with dark skin, as well as older individuals, tend to have much lower levels of vitamin D, as do people who are overweight or obese.
Worldwide, an estimated 1 billion people have inadequate levels of vitamin D in their blood, and deficiencies can be found in all ethnicities and age groups. (1-3) Indeed, in industrialized countries, doctors are even seeing the resurgence of rickets, the bone-weakening disease that had been largely eradicated through vitamin D fortification.
Why are these widespread vitamin D deficiencies of such great concern? Because research conducted over the past decade suggests that vitamin D plays a much broader disease-fighting role than once thought. Being “D-ficient” may increase the risk of a host of chronic diseases, such as osteoporosis, heart disease, some cancers, and multiple sclerosis, as well as infectious diseases, such as tuberculosis and even the seasonal flu.
Currently, there’s scientific debate about how much vitamin D people need each day. The Institute of Medicine, in a long-awaited report released on November 30, 2010 recommends tripling the daily vitamin D intake for children and adults in the U.S. and Canada, to 600 IU per day. The report also recognized the safety of vitamin D by increasing the upper limit from 2,000 to 4,000 IU per day, and acknowledged that even at 4,000 IU per day, there was no good evidence of harm. The new guidelines, however, are overly conservative about the recommended intake, and they do not give enough weight to some of the latest science on vitamin D and health. For bone health and chronic disease prevention, many people are likely to need more vitamin D than even these new government guidelines recommend. Vitamin D is both a nutrient we eat and a hormone our bodies make. Few foods are naturally rich in vitamin D, so the biggest dietary sources of vitamin D are fortified foods and vitamin supplements. Good sources include dairy products and breakfast cereals (both of which are fortified with vitamin D), and fatty fish such as salmon and tuna.
For most people, the best way to get enough vitamin D is taking a supplement, but the level in most multivitamins (400 IU) is too low. Encouragingly, some manufacturers have begun adding 800 or 1,000 IU of vitamin D to their standard multivitamin preparations. If the multivitamin you take does not have 1,000 IU of vitamin D, you may want to consider adding a separate vitamin D supplement, especially if you don’t spend much time in the sun. Talk to your healthcare provider.
Two forms of vitamin D are used in supplements: vitamin D2 (“ergocalciferol,” or pre-vitamin D) and vitamin D3 (“cholecalciferol”). Vitamin D3 is chemically indistinguishable from the form of vitamin D produced in the body. The body also manufactures vitamin D from cholesterol, through a process triggered by the action of sunlight on skin, hence its nickname, “the sunshine vitamin.” Yet some people do not make enough vitamin D from the sun, among them, people who have a darker skin tone, who are overweight, who are older, and who cover up when they are in the sun.
Correctly applied sunscreen reduces our ability to absorb vitamin D by more than 90 percent. And not all sunlight is created equal: The sun’s ultraviolet B (UVB) rays—the so-called “tanning” rays, and the rays that trigger the skin to produce vitamin D—are stronger near the equator and weaker at higher latitudes.
So in the fall and winter, people who live at higher latitudes (in the northern U.S. and Europe, for example) can’t make much if any vitamin D from the sun.
(Hoa, wait a minute here: if the whole point of Black people from Africa turning White, was to allow them to make vitamin D in Europe: THEN WHAT THE FUCH ARE THEY TALKING ABOUT HERE????)
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I dunno, but I'm starting to get a bad feeling, these later articles are starting to sound like the Albino people started to add Vitamin D supplements to food for THEIR CHILDREN!
But how could that be???
After all, their children have White skin, which is PERFECTLY adapted to extract Sunlight to get Vitamin D.
SO WHY WOULD THEY NEED SUPPLEMENTS????
I have to look into this a little further.Posts: 22721 | Registered: Oct 2005
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Journal of Nutrition The American Society for Nutrition
Harriette Chick and the Problem of Rickets
Kenneth J. Carpenter
Harriette Chick (1875–1977) grew up in Victorian England at a time when women were assumed to be unsuited for any senior administrative position and did not even have the right to vote. For national elections, this right was finally conceded in ∼1920 in most European countries as well as in the USA after much agitation and even imprisonment of activists, but Chick “was one of those who earned the enfranchisement of women, not by militancy but by evoking sheer respect of their capacity” (to reuse a quotation originally penned in honor of someone else). By 1920, she herself was in charge of a large international research project designed to find out how best to deal with the problem of rickets that was affecting so many infants growing up in the industrial cities of Northern Europe and North America. This article recounts how her education and subsequent experience at a research institute led to her being selected for a responsibility that would normally not have been given to a woman at that time.
Rickets: The Controversial Background Rickets is a disease of young children characterized by abnormally low mineralization and thus of low mechanical strength in the developing bones. The most obvious sign of the condition is that when the child stands, its weight causes the leg bones to distort so that it becomes either “bandy-legged” or “knock-kneed.” Originally it was known as “the English disease,” but by the late 19th and early 20th century it had become an increasingly serious problem in large cities throughout both Northern Europe and North America.
One of the traditional folk treatments for rickets among fishing communities in Scandinavia and the Netherlands had long been the administration of cod liver oil (CLO). Early in the 19th century it was taken up by the medical profession in France and then elsewhere in Europe, where it had, in some places, been in use already for the treatment of rheumatism. However, by 1900 it had fallen out of favor, partly it seems because using animal organs in medicine had medieval associations: “more suited for the witches' cauldron in Macbeth than for scientific treatment,” and, in terms of the chemical analyses of the day, it was just “another fat, and a rather nauseating one” (21).
There was a general move therefore toward recommending that the infant's diet be richer in fat of any kind at the expense of carbohydrate (21). This may have been related also to the disease being less common in breast-fed infants than in those receiving “patent foods” that contained more of the cheaper carbohydrates. However, clinical studies gave conflicting findings and a more scientific way forward seemed to be the use of an animal model so that 1 factor could be varied at a time and all others kept constant.
In Glasgow, Scotland's largest city, rickets was particularly serious. In 1908 Lionel Findlay of the university's medical school reported that puppies fed on oatmeal and whole milk would develop rickets if kept indoors, but would remain healthy if given exercise by being taken out for walks without any change in their diet (22). The workers in Glasgow linked these findings to observations that the disease was most prevalent in the crowded slum areas of the city where young children were mostly kept indoors in unhygienic conditions and found no reason to believe that the disease was linked to diet.
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Chief Medical Officer of England ‘ashamed’ as rickets makes a comeback
The Victorian-era disease rickets has returned to England, the country’s Chief Medical Officer has said, and should be fought off through a universal handout of vitamin supplements to all children under five.
In a damning report on the state of children’s health, Dame Sally Davies said that the country should be “profoundly ashamed” that child mortality rates in some of the poorest parts of England were three times higher than rich regions.
Dr Claire Lemer, a consultant in general paediatrics at the Evelina London Children’s Hospital, said that 40 per cent of children have some kind of vitamin D deficiency. However, current figures for rates of rickets are not available.
The disease was common in Victorian England, but largely disappeared from the Western world in the latter half of the 20th century thanks to vitamin D being added to everyday foods such as margarine and cereal.
Maria de Lourdes Samaniego-Vaesken, Elena Alonso-Aperte, and Gregorio Varela-Moreiras
Epidemiological evidence shows that there is a high prevalence of vitamin D deficiency especially among elderly population groups. It is a known fact that vitamin D production in the skin decreases about four times with age (55); in addition, this group is prone to avoid sun exposure and limit their outdoor activities. The SENECA study revealed that there is scarce cutaneous vitamin D production from November to May in most of European seniors. This was primarily a consequence of avoiding the sun, and surprisingly, lowest levels were observed in the Mediterranean seniors (56, 57).
How many are deficient? The SENECA study: vitamin D status in elderly population Van der Wielen et al. (56) measured 25-hydroxyvitamin D in serum (25(OH)-D), in adult population across 11 European countries during winter and found that free-living elderly, regardless of geographical location, were at high risk of inadequate vitamin D status. Thirty-six percent of men and 47% of women had 25(OH)-D concentrations below 30 nmol/L; threshold with an increased risk of osteomalacia (bone disease produced by severe vitamin D deficiency i.e. 25(OH)-D≤25 nmol/L).
Authors’ recommended dietary enrichment or supplementation with vitamin D should be seriously considered during this season. In the studied population, major food sources of vitamin D were fish (62%), eggs (20%) and dairy products (8%) and intakes (µg/day),as well as serum 25(OH)-D levels (nmol/L) were lower for women. Assessment of overall vitamin D status was regarded as marginal in 62% of seniors.
In the Optimal Fortification with Vitamin D (OPTIFORD) European project, relative contribution of both sun exposure during summer and diet to vitamin D status were analysed across five European countries, comparing adolescents versus elderly women. When dietary intake of vitamin D was assessed, authors found that elderly females consumed 3.9±5.0 µg/day, whereas adolescent girls consumed 2.8±2.7 µg/day with fish and eggs as the main food sources. However, sun exposure, measured with an adhesive skin dosimeter (J/m2), revealed that Spanish elderly women received less than half the sun exposure of their adolescent counterparts (58). This situation was not observed in the rest of the participating countries (i.e. Finland). When vitamin D exposure and status, measured as 25(OH)-D in plasma in winter versus summer, in a Spanish elderly women population were compared, both were clearly higher in the latter.
Nevertheless, vitamin D deficiency affected 28% of the women during summer time, although this percentage was doubled in winter. In addition, dietary intakes of ≥ 95% of the population sample did not reach the recommended dietary intakes for vitamin D in the summer or winter season (34.5 and 31.3%, respectively); with oily fish as the main food source
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Survey of current vitamin D food fortification practices in the United States and Canada. Calvo MS, Whiting SJ.
Abstract
Widespread poor vitamin D status in all age and gender groups in the United States (USA) and Canada increases the need for new food sources. Currently ∼60% of the intake of vitamin D from foods is from fortified foods in these countries. Those groups in greatest need are consuming significantly lower amounts of commonly fortified foods such as milk. Both countries allow voluntary vitamin D fortification of some other foods, although in Canada this practice is only done on a case-by-case basis. Novel approaches to vitamin D fortification of food in both countries now include "bio-addition" in which food staples are fortified through the addition of another vitamin D-rich food to animal feed during production, or manipulation of food post-harvest or pre-processing. These bio-addition approaches provide a wider range of foods containing vitamin D, and thus appeal to differing preferences, cultures and possibly economic status. An example is the post-harvest exposure of edible mushrooms to ultraviolet light. However, further research into safety and efficacy of bio-addition needs to be established in different target populations.
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U.S. Department of Health & Human Services National Institutes of Health
Sun exposure
Most people meet at least some of their vitamin D needs through exposure to sunlight . Ultraviolet (UV) B radiation with a wavelength of 290–320 nanometers penetrates uncovered skin and converts cutaneous 7-dehydrocholesterol to previtamin D3, which in turn becomes vitamin D3. Season, time of day, length of day, cloud cover, smog, skin melanin content, and sunscreen are among the factors that affect UV radiation exposure and vitamin D synthesis. Perhaps surprisingly, geographic latitude does not consistently predict average serum 25(OH)D levels in a population.
Ample opportunities exist to form vitamin D (and store it in the liver and fat) from exposure to sunlight during the spring, summer, and fall months even in the far north latitudes. Despite the importance of the sun for vitamin D synthesis, it is prudent to limit exposure of skin to sunlight and UV radiation from tanning beds. UV radiation is a carcinogen responsible for most of the estimated 1.5 million skin cancers and the 8,000 deaths due to metastatic melanoma that occur annually in the United States.
Lifetime cumulative UV damage to skin is also largely responsible for some age-associated dryness and other cosmetic changes. The American Academy of Dermatology advises that photoprotective measures be taken, including the use of sunscreen, whenever one is exposed to the sun.
Assessment of vitamin D requirements cannot address the level of sun exposure because of these public health concerns about skin cancer, and there are no studies to determine whether UVB-induced synthesis of vitamin D can occur without increased risk of skin cancer.
The evidence suggests that White Skin did NOT evolve "Naturally" to AID in the absorption of Sunlight.
If that were true, then White people would be PERFECTLY ADAPTED in the Northern Climes, and would not need any assistance for survival.
JUST AS BLACKS ARE AT THE EQUATOR REGIONS and all over the world. (All those Northern Blacks need do is go outside for a few minutes, with no fear of the Sun).Posts: 22721 | Registered: Oct 2005
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I went in for a physical and was attended by a young Negro nurse. The doctor (Jewish) ended the exam by giving me a supply of Vitamin D. They were 2000mg tables. I think he is trying to give me a vitamin D overdose.
Talking with the Negro nurse, she informed me that I needed to take the vitamin D because as I should know, white people can absorb vitamin D from sunlight but black people can't. I asked her where she had read that and she said the Ashkenazi doctor taught her this.
When did my people become so dumb?
What is vitamin D toxicity, and should I worry about it since I take supplements? Answers from Katherine Zeratsky, R.D., L.D.
Vitamin D toxicity, also called hypervitaminosis D, is a rare but potentially serious condition that occurs when you have excessive amounts of vitamin D in your body.
Vitamin D toxicity is usually caused by megadoses of vitamin D supplements — not by diet or sun exposure. That's because your body regulates the amount of vitamin D produced by sun exposure, and even fortified foods don't contain large amounts of vitamin D.
The main consequence of vitamin D toxicity is a buildup of calcium in your blood (hypercalcemia), which can cause symptoms such as poor appetite, nausea and vomiting. Weakness, frequent urination and kidney problems also may occur. Treatment includes the stopping of excessive vitamin D intake. Your doctor may also prescribe intravenous fluids and medications, such as corticosteroids or bisphosphonates.
Taking 50,000 international units (IU) a day of vitamin D for several months has been shown to cause toxicity. This level is many times higher than the recommended dietary allowance (RDA) for most adults of 600 IU of vitamin D a day. Doses higher than the RDA are sometimes used to treat medical problems such as vitamin D deficiency, but these are given only under the care of a doctor and only for a short time.
Although vitamin D toxicity is uncommon even among people who take supplements, you may be at greater risk if you have health problems, such as liver or kidney conditions, or if you take thiazide-type diuretics. As always, talk to your doctor before taking vitamin and mineral supplements.
Excess vitamin D also causes brittle Bones and other serious problems!
Posts: 22721 | Registered: Oct 2005
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Mike according to your Whitey hating, wanna kill Whitey, wanna harm White children, Black racist, Black supremacist butt, White people are not perfectly suited to anywhere on earth. According to you we have no homeland, no where on earth we belong.
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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Mike if you are gonna quote me, put my full quote. What you don't like being called exactly what you are? It is you saying it Mike, due to your hatred for Whites you want us to believe that there's no place on earth that we belong, that our skin is a defect to be gotten rid, that we have no redeeming qualities & are all wicked & evil from the day we are born, have no right to exist & should just all die off already. You & your ilk (Clyde, Narmer, 42Tribes,Xyyboy, King, Mena7, Jantavanta,Bonampak,TrollPatrol,Doug,Kikuyu,Ironfaggot) look forward to the day when the last White child is born & the last White person breaths their last.
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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Mike you down Whites with every post you make. Using racist epithets towards us, making derogatory remarks towards us. Talk about lying & history stealing Mike, you are the king of lies & history stealing. You want Whites to have absolutely nothing, you want to give us credit for nothing except of course the bad. Heck you won't even give us the benefit of being indigenous to anywhere on earth, any ancestors, any history at all, no heritage, no identity, no accomplishments no nothing.
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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Roger that! I couldn’t have said it better. Are you really white?
Quote by DHDoxie == that our skin is a defect to be gotten rid, that we have no redeeming qualities & are all(no some) wicked & evil from the day we are born, .
Whites to have absolutely nothing, you want to give us credit for nothing except of course the bad. H
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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I went in for a physical and was attended by a young Negro nurse. The doctor (Jewish) ended the exam by giving me a supply of Vitamin D. They were 2000mg tables. I think he is trying to give me a vitamin D overdose.
Talking with the Negro nurse, she informed me that I needed to take the vitamin D because as I should know, white people can absorb vitamin D from sunlight but black people can't. I asked her where she had read that and she said the Ashkenazi doctor taught her this.
When did my people become so dumb?
What is vitamin D toxicity, and should I worry about it since I take supplements? Answers from Katherine Zeratsky, R.D., L.D.
Vitamin D toxicity, also called hypervitaminosis D, is a rare but potentially serious condition that occurs when you have excessive amounts of vitamin D in your body.
Vitamin D toxicity is usually caused by megadoses of vitamin D supplements — not by diet or sun exposure. That's because your body regulates the amount of vitamin D produced by sun exposure, and even fortified foods don't contain large amounts of vitamin D.
The main consequence of vitamin D toxicity is a buildup of calcium in your blood (hypercalcemia), which can cause symptoms such as poor appetite, nausea and vomiting. Weakness, frequent urination and kidney problems also may occur. Treatment includes the stopping of excessive vitamin D intake. Your doctor may also prescribe intravenous fluids and medications, such as corticosteroids or bisphosphonates.
Taking 50,000 international units (IU) a day of vitamin D for several months has been shown to cause toxicity. This level is many times higher than the recommended dietary allowance (RDA) for most adults of 600 IU of vitamin D a day. Doses higher than the RDA are sometimes used to treat medical problems such as vitamin D deficiency, but these are given only under the care of a doctor and only for a short time.
Although vitamin D toxicity is uncommon even among people who take supplements, you may be at greater risk if you have health problems, such as liver or kidney conditions, or if you take thiazide-type diuretics. As always, talk to your doctor before taking vitamin and mineral supplements.
Excess vitamin D also causes brittle Bones and other serious problems!
The Ashkenazi quack gave me a bottle of 100 Vit-D pill, each pill 2000 IU, with the advice to take 1 in morning and 1 before bed. 1 week later I received another bottle in the mail.
Considering blacks absorb their daily requirement of Vitamin D from sunlight, and almost all flour/milk products sold in America are vitamin D fortified, no black person should really need to take supplements.
Posts: 4693 | From: Saturn | Registered: Apr 2012
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As I said before Narmerthoth is correct, Europeans are primarily Albino Africans(they are NOT Dravidians) with a touch of Melanesian, don’t believe me ask Lazaridis, Duffy, Kettles, Mekova, Rees, Duffy, Norton etc. . But this is one instance I prefer NOT to use the scientific term and stick with the colloquial ie White or European
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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Xyyboy yes oh Whitey hater I am White. Ohh so you admit it. You do want Whites to think that our skin is a defect to be gotten rid of & ashamed of. You admit you want Whites to think that we belong no where on earth. You admit you want Whites to think we have no ancestors. You admit you want Whites to think we have no history. You admit you want Whites to think we have no heritage. You admit you want Whites to think we have no identity. You admit you want Whites to think we have built nothing, accomplished nothing. You admit you want Whites to think we are nothing but wicked & evil from birth capable of doing no good. You admit that you want Whites to think we have no right to exist as a people & should all just die off. You admit you don't want Whites have anything at all. The question is why?
Why do you not want Whites to know who we are?
Why do you not Whites to know where we come from?
Why don't you want Whites to think we have no ancestors (or at least no claim to them)?
Why do you want Whites to think we have no history?
Why do you want Whites to have no sense of pride?
Why do you want Whites to have no knowledge of self?
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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Woman!? you should be proud of who you are. I like some white people. There are some good ones.
I bolded the sections I agree with.. So all that nonsense you added on, I do not agree with.
-------------------- Without data you are just another person with an opinion - Deming Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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posted
You should read that paper by Romdhane et al I cited….or let someone explain it to you. Significance? Tunisians carry a lot of “founder mutations” of most genetic defects found in Modern Europeans. As I suggested, I may be wrong on the causes of the neurological and psychopathic behavior of Europeans. Some may still be due to de-pigmentation(lack of sunlight) but it is evident that 1000’s of years of inbreeding may have cause it to be so prevalent to the North. I need to investigate this further. Now I see the pressing need for the Genome Project…..at least one of them
As I said before there is quick solution to this(aside from the Genome Project)….8in. He! He! He!
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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quote:Originally posted by DHDoxies: Xyyboy yes oh Whitey hater I am White. Ohh so you admit it. You do want Whites to think that our skin is a defect to be gotten rid of & ashamed of. You admit you want Whites to think that we belong no where on earth. You admit you want Whites to think we have no ancestors. You admit you want Whites to think we have no history. You admit you want Whites to think we have no heritage. You admit you want Whites to think we have no identity. You admit you want Whites to think we have built nothing, accomplished nothing. You admit you want Whites to think we are nothing but wicked & evil from birth capable of doing no good. You admit that you want Whites to think we have no right to exist as a people & should all just die off. You admit you don't want Whites have anything at all. The question is why?
Why do you not want Whites to know who we are?
Why do you not Whites to know where we come from?
Why don't you want Whites to think we have no ancestors (or at least no claim to them)?
Why do you want Whites to think we have no history?
Why do you want Whites to have no sense of pride?
Why do you want Whites to have no knowledge of self?
Dixie-Ralph-Tricia
Think about it. All of the medical information Mike posted above clearly states that whites are lighter so they absorb more Vitamin D from sunlight than blacks.
According to The National Health Institute study, under normal situations, a few hours of sunlight per day will provide adequate Vitamin D to suffice for the whole week.
If the above NIH study is correct, then why are all European/American foodstuffs (cereal, flour, bread, milk, juices, ect.) all packed with Vitamin D supplements? To me, their being stuffed with Vitamin D indicates that the intended market lacks the facility to produce natural Vitamin D on their own; Albinos.
Another study at NIH compares Vitamin D levels of white women to black women. They concluded that although white women had higher levels of Vitamin D precursor, serum 1.25 than black women, black women birthed children with 30% higher bone density than white women. At the end, they confess that they have no idea of why this is. So, it appears the statement that Blacks have lower Vitamin D levels is based on using Albino levels as a reference. Obviously, this is ass backward, and the reference clearly should be reversed to use blacks whereas whites will than be seen to lack the ability to store excess serum 1.25 due to their lack of Eumelanin which is where the serum is stored in the liver.
Posts: 4693 | From: Saturn | Registered: Apr 2012
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Here is an old study from 2005. This is great for those who may not know what pathetic liars Albino people are.
Scientists Find A DNA Change That Accounts For White Skin
By Rick Weiss Washington Post Staff Writer Friday, December 16, 2005
Scientists said yesterday that they have discovered a tiny genetic mutation that largely explains the first appearance of white skin in humans tens of thousands of years ago, a finding that helps solve one of biology's most enduring mysteries and illuminates one of humanity's greatest sources of strife.
The work suggests that the skin-whitening mutation occurred by chance in a single individual after the first human exodus from Africa, when all people were brown-skinned. That person's offspring apparently thrived as humans moved northward into what is now Europe, helping to give rise to the lightest of the world's races.
Leaders of the study, at Penn State University, warned against interpreting the finding as a discovery of "the race gene." Race is a vaguely defined biological, social and political concept, they noted, and skin color is only part of what race is -- and is not.
In fact, several scientists said, the new work shows just how small a biological difference is reflected by skin color. The newly found mutation involves a change of just one letter of DNA code out of the 3.1 billion letters in the human genome -- the complete instructions for making a human being.
"It's a major finding in a very sensitive area," said Stephen Oppenheimer, an expert in anthropological genetics at Oxford University, who was not involved in the work. "Almost all the differences used to differentiate populations from around the world really are skin deep."
The work raises a raft of new questions -- not least of which is why white skin caught on so thoroughly in northern climes once it arose. Some scientists suggest that lighter skin offered a strong survival advantage for people who migrated out of Africa by boosting their levels of bone-strengthening vitamin D; others have posited that its novelty and showiness simply made it more attractive to those seeking mates.
The work also reveals for the first time that Asians owe their relatively light skin to different mutations. That means that light skin arose independently at least twice in human evolution, in each case affecting populations with the facial and other traits that today are commonly regarded as the hallmarks of Caucasian and Asian races.
Several sociologists and others said they feared that such revelations might wrongly overshadow the prevailing finding of genetics over the past 10 years: that the number of DNA differences between races is tiny compared with the range of genetic diversity found within any single racial group.
Even study leader Keith Cheng said he was at first uncomfortable talking about the new work, fearing that the finding of such a clear genetic difference between people of African and European ancestries might reawaken discredited assertions of other purported inborn differences between races -- the most long-standing and inflammatory of those being intelligence.
"I think human beings are extremely insecure and look to visual cues of sameness to feel better, and people will do bad things to people who look different," Cheng said.
The discovery, described in today's issue of the journal Science, was an unexpected outgrowth of studies Cheng and his colleagues were conducting on inch-long zebra fish, which are popular research tools for geneticists and developmental biologists. Having identified a gene that, when mutated, interferes with its ability to make its characteristic black stripes, the team scanned human DNA databases to see if a similar gene resides in people.
To their surprise, they found virtually identical pigment-building genes in humans, chickens, dogs, cows and many others species, an indication of its biological value.
They got a bigger surprise when they looked in a new database comparing the genomes of four of the world's major racial groups. That showed that whites with northern and western European ancestry have a mutated version of the gene.
Skin color is a reflection of the amount and distribution of the pigment melanin, which in humans protects against damaging ultraviolet rays but in other species is also used for camouflage or other purposes. The mutation that deprives zebra fish of their stripes blocks the creation of a protein whose job is to move charged atoms across cell membranes, an obscure process that is crucial to the accumulation of melanin inside cells.
Humans of European descent, Cheng's team found, bear a slightly different mutation that hobbles the same protein with similar effect. The defect does not affect melanin deposition in other parts of the body, including the hair and eyes, whose tints are under the control of other genes.
A few genes have previously been associated with human pigment disorders -- most notably those that, when mutated, lead to albinism, an extreme form of pigment loss. But the newly found glitch is the first found to play a role in the formation of "normal" white skin. The Penn State team calculates that the gene, known as slc24a5, is responsible for about one-third of the pigment loss that made black skin white. A few other as-yet-unidentified mutated genes apparently account for the rest.
Although precise dating is impossible, several scientists speculated on the basis of its spread and variation that the mutation arose between 20,000 and 50,000 years ago. That would be consistent with research showing that a wave of ancestral humans migrated northward and eastward out of Africa about 50,000 years ago. ad_icon
Unlike most mutations, this one quickly overwhelmed its ancestral version, at least in Europe, suggesting it had a real benefit. Many scientists suspect that benefit has to do with vitamin D, made in the body with the help of sunlight and critical to proper bone development.
Sun intensity is great enough in equatorial regions that the vitamin can still be made in dark-skinned people despite the ultraviolet shielding effects of melanin. In the north, where sunlight is less intense and cold weather demands that more clothing be worn, melanin's ultraviolet shielding became a liability, the thinking goes.
Today that solar requirement is largely irrelevant because many foods are supplemented with vitamin D.
Some scientists said they suspect that white skin's rapid rise to genetic dominance may also be the product of "sexual selection," a phenomenon of evolutionary biology in which almost any new and showy trait in a healthy individual can become highly prized by those seeking mates, perhaps because it provides evidence of genetic innovativeness.
Cheng and co-worker Victor A. Canfield said their discovery could have practical spinoffs. A gene so crucial to the buildup of melanin in the skin might be a good target for new drugs against melanoma, for example, a cancer of melanin cells in which slc24a5 works overtime.
But they and others agreed that, for better or worse, the finding's most immediate impact may be an escalating debate about the meaning of race.
Recent revelations that all people are more than 99.9 percent genetically identical has proved that race has almost no biological validity. Yet geneticists' claims that race is a phony construct have not rung true to many nonscientists -- and understandably so, said Vivian Ota Wang of the National Human Genome Research Institute in Bethesda.
"You may tell people that race isn't real and doesn't matter, but they can't catch a cab," Ota Wang said. "So unless we take that into account it makes us sound crazy."
posted
^Quote: Unlike most mutations, this one quickly overwhelmed its ancestral version, at least in Europe, suggesting it had a real benefit. Many scientists suspect that benefit has to do with vitamin D, made in the body with the help of sunlight and critical to proper bone development.
Oh, so THAT'S why there are no Black people in Europe - It doesn't have anything to do with Albinos killing them and shipping the rest off to the Americas:
THEY ALL TURNED WHITE!!!!
He,he,he,he,he:
Quote: Today that solar requirement is largely irrelevant because many foods are supplemented with vitamin D.
See there, White people are so smart that they don't even need the Sun anymore. Gee, I sure hope they don't turn it off.
Quote: Some scientists said they suspect that white skin's rapid rise to genetic dominance may also be the product of "sexual selection," a phenomenon of evolutionary biology in which almost any new and showy trait in a healthy individual can become highly prized by those seeking mates, perhaps because it provides evidence of genetic innovativeness.
Well, there it is, White people are officially the most beautiful people, and everyone wants to get some sexually.
Oh,oh: I wonder why then they are the MINORITY race. Hmmm, that doesn't seem to add up.
Gee, are the Albinos lying again???Posts: 22721 | Registered: Oct 2005
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First, the Penn State study is simply a branch of the "White Skin Originated recently In Europe" paper which has been addressed in many ES threads.
Second, not the state that the mutation led to "normal" white skin. Perhaps this is some what true in Asia where Asians experience very low levels of skin cancer, but it is certainly not true in Europe, and Europe is where they suggest this "normal" white skin.
Third, The study suggests that white skin originated first in Europe. We know this is untrue and that the first albinos appeared in Africa, prior to OOA. We've already studied recent studies that confirm the African origin of an intragenic deletion of the human P gene in tyrosinase positive oculocutaneous albinism. This simply means that white people (African Albinos) existed in Africa first, then migrated to Europe.
Lastly, the reason for why whites are a minority on the planet is directly tied to Albinism. Sexual potency is directly connected to melanin by way of Melatonin. This is why birth rates associated with white women are estimated to be 70/10,000 compared to 200/10,000 for Africans.
Posts: 4693 | From: Saturn | Registered: Apr 2012
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Narmer & Mike cut the Albino bull ****. We Whites are NOT Albinos & we are NOT Africans.
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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-Generally the closer you are to the equator the higher the UV radiation level from sunlight is
-High UV levels can damage the skin and cause cancer
-therefore people closer to the equator have darker skin as a protective barrier Dark skin acts as a filter. It renders excess sunlight harmless by absorbing it into the top layer of skin but it lets in a certain amount of sunlight into the lowest layer of skin where Vitamin D is processed.
Posts: 42939 | From: , | Registered: Jan 2010
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Jeffrey L H O’Riordan & Olav L M Bijvoet AffiliationsCorresponding author BoneKEy Reports (2014) 3, Article number: 478 (2014)
The story of rickets leading to the discovery of vitamin D is an extraordinary tale, spread over many centuries and involving some remarkable characters with much speculation and a few mysteries, before reaching an exciting climax. It would be wrong to credit a single person as discovering rickets or being the first to describe its features, for reasons that will be set out here. Yet the emergence of the term ‘rickets’ is as important as the discovery of vitamin D itself and the possible causes of its deficiency. It permitted identification of a hitherto ill-defined disease entity, typically occurring in infants and children. It also provided a way for deciding if features of diseases that had been described earlier in the history of medicine could be seen as the symptoms and signs of related conditions.
Introduction
Abstract• Introduction• References• Acknowledgments• Author information Sorano of Ephesus is often credited as being the first to mention some of the features of rickets. Suggestions1 that there were references to this in earlier Chinese manuscripts, for example in Confucius, 200 years earlier are not convincing. Sorano worked in Alexandria and then in Rome where he practiced during 110–130 AD. One of his classic works is entitled ‘Gynecology’ in which he wrote (in Book II,48[112]), ‘When the infant attempts to sit and to stand, one should help in its movements. For if it is eager to sit up too early and for too long a period it becomes hunchbacked (the spine bending because the little body has as yet no strength). If, moreover, it is too prone to stand up and desirous of walking, the legs may become distorted in the regions of the thighs’. Temkin2 who translated the whole of the ‘Gynecology’ into English referred to this as the ‘classic allusion’ to rickets in his introduction, but he also cited the comments of Ruhrah3 who pointed out that Sorano was writing on the care of infants, not their diseases. Much later, in about 1554, Theodosius of Bologna described4 a pale child ‘that could not move or sit, indeed hardly hold it head erect and which showed in the lower dorsal region both a gibbus and a marked lateral curvature’. Whether the child actually had rickets is not clear. Later, it is said that Bartholomaeus Reusner described in 1582 ‘a disease common among the inhabitants of Holland and Switzerland, characterized by bending of bones and cachexia of infants and an insatiable hunger’. Sprengel5 who reported this, gave the reference as ‘Dissertatio de tabe infantum, Basel’. Unfortunately, no one has been able to find this article anywhere despite intensive searching over many years. A recent search of current electronic data bases were not helpful either. So it is not possible to confirm either its date or its contents or even its existence. It seems that later texts, from Holland in 1614, might be referring to rickets under the titles of ‘Ailment of Saint Willibrod’ in which children had knobs on their ribs and ‘Ailment of Saint Machutus’ in which children had deformed legs. The two ailments apparently could exist in the same child.
The word ‘rickets’ can be seen in the hand-written ‘Receipt Books’ of the Fairfax Family. The entry for 25 February 1632 has five remedies for ‘rickets in children’. The word ‘rickets’ first appeared in print in 1634 when it figured in the Annual Bill of Mortality of the City of London for that year. The Bills of Mortality were records of the numbers and causes of death in the area around the Tower of London and St Paul’s Cathedral, which is now the financial area, but which used to be a residential part, within or close to the walls of the City of London. The population covered by these bills was ~200 000. Many of the original records still exist, going back to the late sixteenth century. The annual statistics were based on the weekly records that were kept. A major change in the form of the records was introduced in 1629, although it is not clear who ordered that to be done. Previously, they had only listed the numbers dying in each of the 122 parishes in the city. In 1629, the Bills included, for the first time, an account of the causes of death, divided into ~80 conditions. Rickets was not among those listed that year, or in the subsequent 4 years. It is recorded for 1634, that of a total of 10 900 deaths, rickets was given as the cause of death in 14 of them (Figure 1). The frequency of this cause of death apparently rose progressively so that 25 years later, in 1659, there were 441 recorded entries for rickets in the year. The Bills of Mortality were compiled by the ‘searchers’ and were analyzed6 in great detail by John Graunt in 1662. Graunt may be considered along with Petty as one of the fathers of the studies of community medicine. Graunt wrote ‘the searchers who are elderly matrons, sworn to their office, repair to the place where the dead corpse lies…’. It has to be said that the accuracy of the causes of death in the lists must have been suspect. On the basis of indirect arguments, Graunt suggested that what was subsequently classified as rickets might have been misclassified in 1629, as ‘Livergrown’, although that is speculative and the features of that condition were not described. Whether that speculation is correct or not, the fact that rickets was recognized in London 11 years before the first clear clinical description of its features cannot be questioned. Moreover, its incidence seemed to be increasing, as discussed in Graunt’s analysis written in 1662. In part that increase might have been the greater awareness of the disease. A copy of the Bill of Mortality for 1634. The middle part of this, listing the number of deaths for each of the 122 parishes of the City of London, has been omitted for clarity. The causes of death are listed alphabetically and rickets is included among those on the right side. Reproduced with permission of The Guildhall Library of The City of London, London, UK.
In 1640, the apothecary and King’s herbalist, John Parkinson,7 published a massive, beautifully illustrated ‘Botanicum’, a section of which is devoted to thistles, and about one of these, a common thistle, he wrote ‘Galen saith that the roote and leaves hereof are of an healing quality and good for such persons that have their ‘bodies drawn together by some spasm or convulsion or by some other infirmity, which disease is truly to be called the rickets which happening sometimes to children doeth so bind them in their nerves, ligaments and whole structure of their body that it suffereth not to grow or prosper eyther in height, strength or alacrity’. Nothing is known about the contents of extracts of thistle that would justify its empirical use. However, it is clear from the writing of Parkinson that, in 1640, again before the condition had been fully described in the medical literature, there was concern as to how to treat rickets. Evidence for other possible references to rickets prior to 1650 is discussed by Foote.8
The first clear descriptions of rickets were published between 1645 and 1668, successively by Whistler, Boot, Glisson and Mayow (Figure 2). It can be argued that they were characterizing what was a matter of public concern and discussion at the time. The first if this quartet, Daniel Whistler, submitted a thesis for the degree of Doctor of Medicine in Leiden. The original records of the University of Leiden still exist and show that he registered for the degree in July 1645. He submitted his dissertation on 18 October 1645 and was examined on it the next day and was awarded the degree.9, 10, 11 The thesis was reprinted in 1684. Whistler went on in later years to be a founding fellow of the Royal Society and President of the College of Physicians of London. The second description, by Arnold Boot, was published in1649, possibly having been written in 1646. Boot was born in Holland but practiced in Dublin. His description12 was Chapter 12 in his book on a variety of conditions. The word ‘rickets’ is used on page 3 of the original Latin text. That work is the least well known of the quartet, perhaps because it did not contain the word rickets in the title of the book or of the chapter in which it was described. It was reprinted in 1664 and 1676. However, the longest and most detailed account of this disease by far was the book published by Glisson in 1650. He was assisted by Bate and Regemorter. Much of their text was concerned with an interpretation of the disease in the light of medical philosophy of the day, but it also attempted to explain the cause of deformity in rickets, which is a curvature of the limbs and spine. Later, in 1668, Mayow wrote about rickets and said that the only earlier publication on the subject was by Glisson; so he was not aware of the other two. He quoted extensively from Glisson but gave an alternative explanation for the cause of deformity. All four of these accounts were written in Latin. A translation11 of Whistler’s eight-page thesis into English was only published in the middle of the twentieth century. No English version of the Boot’s chapter has been published, but it has been analyzed in some detail by Van Andel.12 Glisson’s book was quickly translated into English and that version was published a year after the Latin version. The translation, published in 1927, of the work of Mayow13 is perhaps the one that is most easily understood by a modern reader.
Copies of the title pages of the four publications that appeared in Latin, over a 33-year period. The first three were reproduced from originals in the British Library, London, UK. The fourth is reproduced form the original with permission of the library of The Royal College of Physicians, London, UK. (a) The thesis of Daniel Whistler, 1645, entitled ‘Inaugural Medical Disputation, on the Children’s Diseases of the English, Which the Inhabitants Idiomatically Call The Rickets’. (b) Arnold Boot’s book published in 1649 entitled ‘Medical Observations on Neglected Ailments’, in which chapter 12, entitled ‘Tabes pectoris’ described rickets and used that word in the text. (c) Francis Glisson’s book, published in 1650 with Bate and Regemorter, entitled ‘A Treatise of the Rickets: Being a Disease Common to Children. Wherein (among many other things) is shewed 1 The Essence. 2 The Causes. 3 The Signs. 4 The Remedies of the Disease’. (d) John Mayow’s tract, published in 1668, entitled ‘Concerning Rickets’.
Whistler, Boot and Glisson all used the English word rickets, and each suggested an alternative either in Latin or Greek, but those suggestions never found favor. Whistler and Glisson both discussed the origin of the word rickets without being able to say how it had been derived. Among the suggestions considered was that it was named after an apothecary called Rickets who had successfully treated the disease. The family name ‘Rickets’ was not uncommon and still exists, but there was no evidence to support that theory. Another possibility is that the word was derived from ‘rachitis’, indicating inflammation of the vertebral column. They tried, again unsuccessfully, to derive the word from Greek but they had to conclude that the origin was not known and that the colloquial term ‘rickets’ was already the accepted name at the time.
Glisson and Boot had done dissections (postmortem examinations) of patients that had died with rickets. Both Whistler and Glisson believed that rickets was a ‘new’ disease, which had only appeared ~20 years before they wrote. They both suggested that the earliest cases had been seen in southern England (in the county of Dorset) and in the West Country (in the county of Somerset). All three of these authors described the disease as occurring in London, but Boot said he had seen it in both Ireland and in Paris. The occurrence of rickets in Paris had been mentioned by Guillemeau in 1609, in a brief note.14 Thus though Whistler referred to Rickets as an ‘Engllsh Disease’, it was clearly not confined to England. Although they thought it was a new disease, they could not explain why it had appeared. Glisson thought it was related to the damp climate in England without being able to say why that should be the case. Recently, rickets has been reported15 in the skeletons of the Medici children buried in a family vault in Florence, 1547–1602.
Whistler had written ‘The disease is most frequent in the ranks of the highest citizens, next amongst the dregs of the populace, least amongst those of moderate means. The cause in the first group I take to he the intemperance of the parents and the fact that the infants are entrusted to the care of hired wet nurses’. A variety of explanations were offered for the development of rickets in children in the other two groups, who presumably were not fed by wet nurses. Later, Glisson also observed that ‘this disease doth more frequently invade the cradles of the rich than afflict poor men’s children’. Thacher et al.16 have stressed the significance of the use of wet nurses, pointing out that the concentration of calcium in breast milk falls as the duration of feeding is extended, and feeding cereal porridges in weaning, with high phytate content, might have added to the calcium deficiency.
Suggestions about treatment were along the lines of all therapies at the time for all diseases. Venesection seemed popular, especially from a particular vein on the lobe of the ear. In 1674 a letter was written concerning ‘Some observations made upon Russia Seed, shewing its admirable virtues in healing rickets’. This was written by a doctor of physic in the country, possibly a Dr Peachi or a Dr Skinner and sent to ‘Esq Boyle’, who was possibly Robert Boyle, secretary of the recently formed Royal Society. It is not possible now to say what was meant by the name ‘Russia Seed’. An interesting comment was made by Sir Thomas Browne in a letter17 written around 1664 describing birds in Norfolk. About rooks (crows) he recorded that ‘the young ones commonly eaten, sometimes sold in Norwich markets, and many killed for their livers in order to cure rickets’. Both Whistler and Glisson had included the use of rook liver, and Glisson added frog’s liver as a possible treatment. In hindsight, it is possible to wonder if that provided a source of vitamin D, although that seems unlikely. It was also suggested that patients should have their abdomen exposed to sunlight as a source of heat, and that too might have provided a source of vitamin D.
A clue as to another cause of rickets in the seventeenth century is to be found18 in Claire Tomlin’s prize winning biography, ‘Samuel Pepys, The Unequalled Self’. In that, she said ‘Londoners spat black’, referring to the periodic effect of smog, which even as recently as 1955, led to the presence of black particles in sputum and nasal droplets. She cites the diary of Robert Hooke19 On 28 September 1676, he described a cloud covering the city of London and being visible miles away to the south from Banstead Downs. Earlier, in 1661, John Evelyn had published,20 at his Majesty’s command, his ‘Fumfugium’ or ‘The Inconvenience of the Air and Smoak of London Dissipated’. In that classic work, he described the pollution and named its cause as the burning of sea coal. This coal was brought by sea from Newcastle in the north of England. He described how laundry put out to dry in the open air was soiled again by the dirty air and how gardens grew better when there was a shortage of coal in 1644, when Newcastle was blockaded in the Civil War. Evelyn said that the trouble came particularly from the ‘fournaces’ of the ‘brewers, diers, sope and salt boylers and lime burners and the like’. He suggested that a cure for the problem was to move these factories away from the center of the city and preferably downwind. There had been attempts as far back as 1272 to legislate against the use of sea coal, but none of the laws were enforced, and Evelyn’s attempts to get new laws enacted likewise came to nothing. In a little noticed recent work, Brimblecombe,21 in his book on ‘The Big Smoke, a History of Air Pollution in London Since Mediaeval Times’, pointed out the significance of the smoky atmosphere in reducing production of vitamin D by UV irradiation of the skin. In offering this explanation for rickets in London at that time, it should be remembered that cases were reported initially in the country, in Dorset and further west, and presumably there was less smoke in those parts.
It is clear that it is reasonable now to suggest that vitamin D deficiency was a major cause of the rickets described in the middle of the seventeenth century. It is not possible to say whether anything had changed that led to what seemed to be new disease in either part of the century. England at that time was a place of great inequalities, great riches setting alongside desperate poverty. Within the walled City of London it was very crowded, and there were many very narrow streets (limiting access to sunlight). With the civil wars there may have been serious food shortages, but that cannot be proved, and rickets seemed to affect both the poor and the upper class. It has been suggested22 that as a child, Charles Duke of Albany (later King Charles I of England) had rickets from 1600 to 1612. Accounts of the diet prescribed in his treatment at that time indicate that the bland diet itself may have contributed to the progress of the disease and aggravated it. His daughter, Princess Elizabeth, also died23 with rickets, so perhaps the cause in this family was different from most cases at that time. Whereas we may think of vitamin D deficiency as initially being the product of the Industrial Revolution and the resulting smoke in the atmosphere, at the end of the nineteenth and early twentieth centuries, these may, in fact, have been serious problems 300 years earlier.
Little progress was made over the next two centuries though there were reports from the Royal Infirmary in Manchester that cod liver oil could heal rickets. In 1728, Moore24 wrote on the effectiveness of shark liver ointment in the treatment of rickets. In 1724–1926 Schenk25 and Schutte26 wrote that cod liver oil by mouth for 5 weeks could cure rickets. In 1822, Sniadeki27 from Poland wrote ‘the sun, the direct action of which on our bodies must be regarded as one of which on our bodies, must be regarded as the most efficient methods for the prevention and cure of this disease’. Later Trousseau,28 in 1868 described, very elegantly, how he came to treat rickets with cod liver oil.
Then a series of papers was presented by John Bland-Sutton (initially Lecturer on Comparative Anatomy and later Surgeon at the Middlesex Hospital in London) in The Proceedings of the Zoological Society ‘On the diseases of the monkeys in the Society’s gardens’. Writing of rickets, he recorded ‘this disease is extremely frequent in monkeys living in captivity in London. Nearly half the total number of monkeys introduced into the Zoological Society’s garden die rickety, provided they live a few months after reaching London. The changes in the skeleton develop so rapidly that a capuchin monkey, apparently in good health and thriving well, when introduced into the cages died horribly deformed by rickety changes in four months’. There was debate as to whether what was being described was in fact rickets, since it would appear that the picture is rather different in the monkeys from what is seen in humans and other animals, and the changes in the vertebral column and compression of the spinal cord seemed to be features seen in monkeys. In the last of these papers, Bland Sutton29 in 1889 wrote ‘that the bulk of the material has come under observation during my attendance at the prosector’s room of the Zoological Society, London during the last seven year’. That paper included observations on lion cubs and contained the remarkable statement ‘it may be mentioned that some rickety cubs, which early manifested signs of rickets, were promptly fed bone dust and cod liver oil, made a good recovery and were alive and active, presenting no signs of paralysis two years afterward’. Those observations30, 31 were, of course, made before vitamin D had been discovered and it is interesting to note that though the Monkey House was light and airy, it was enclosed by glass that would not have let through UV. Shortly after that Palm32 in 1890 looked at the geographical distribution of rickets and noted it was more common where there was less sunlight and he promoted the use of sunbaths to prevent rickets. The importance of sunshine was reinforced by the findings of Schmorl that at postmortem evidence of rickets was more common in winter/spring than in summer/autumn.
Progress in studies of the causes and treatment of rickets suddenly moved much faster, in the period 1917–1922. At the beginning of that time, Huldschinski33 advocated ultraviolet light treatment for rickets. At the same time, Hess34 showed that cod liver oil could prevent and cure rickets in Afro-American children in New York. In 1918, Mellanby showed that he could prevent experimental rickets in puppies with cod liver oil and discussed the role of an ‘accessory factor’ in the production of rickets.35 That was at the end of The First World War. At that time it was found that rickets was a major problem in Vienna but its cause was not known. A group from the British Medical Research Council led by Harriet Chick went to Vienna to study the problem. The possibility that rickets might be caused by something in the water or a feature of the diet, or something in the air, or possibly an infection, were all considered. The children with rickets at the Kinderklinic in Vienna were divided36, 37 into four groups. Two of these groups were kept in the ward and the other two groups were kept out on the balcony which must have been very cold in the Viennese winter. In the ward, one group was given the normal diet only while the other group was also given supplementary cod liver oil. The rickets in the latter group of children was healed as demonstrated radiologically, while the first group remained sick. On the veranda (Figure 3) one group was kept well covered while the other group of children, wearing remarkably little clothing, was exposed to sunlight. This second group got better. Thus it was shown that cod liver oil and exposure to sunlight both healed rickets. However, it was not clear at that time whether the effectiveness of cod liver oil was due to vitamin D or to vitamin A, both of which had been discovered by then. In 1921, Hess and Unger38 showed the importance of sunlight in curing rickets.
McCollum et al.39 gave the title ‘Vitamin D’ to Mellanby’s ‘Accessory factor’ in 1922, in a paper suggesting the existence of ‘a vitamin which promotes calcium deposition’. Then in papers published in 1924 Hess and Weinstock40 and Steenbock and Black41 described the effects of the ultraviolet irradiation of food. Thus the scene was set for the remarkable progress that followed the discovery of vitamin D. The events leading up to this have shown the sound basis on which that progress was based, and has been well described by Tausk,42 by Ebstein,43 and by Fourman and Royer44 in their historical reviews, which describe the scene leading up to the discovery of vitamin D and all that followed.
Posts: 42939 | From: , | Registered: Jan 2010
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posted
Xyyboy, according to you we Whites have nothing to be proud of. According to you we accomplished nothing, built nothing, our ancestors are not our ancestors, we have no history, we are wicked & evil from birth, we have no homeland, no place on earth. Yet you tell me be proud of who I am that's laughable. Sorry I don't read stuff written by Anti-White Black racists, other Anti-White non-White racists, or Anti-White uncle tom, turn coat, self hating Winos, or racist Anti-White Jews so I won't be reading it thanks.
BTW when are you Whitey haters gonna answer my questions I'm still waiting...
Why do you not want Whites to know who we are?
Why do you not Whites to know where we come from?
Why don't you want Whites to think we have no ancestors (or at least no claim to them)?
Why do you want Whites to think we have no history?
Why do you want Whites to have no sense of pride?
Why do you want Whites to have no knowledge of self?
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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posted
Mike. Can you take care of this? I am not sure what “she” is ranting about.
-------------------- Without data you are just another person with an opinion - Deming Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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posted
But I really want to hear your answers Xyyboy. Mike & Narmer can feel free to answer them as well. What's the matter you Black racist Whitey haters afraid to answer my questions, ya'll sceerd(LOL), Chickens, no testes hehehehehe.
BTW, NO Narmer Lioness & I are not the same. Lioness is Black as far as I know & I am White (Until proven otherwise).
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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quote:Originally posted by DD'eDeN: Black Elders have white hair on black skin Polar Bears have white hair on black skin Black Bears have black hair on white skin
White hair has no pigment, is hollow, allows light through like optic cables
Black skin due to melanin pigment transforms infrared light to warmth and blocks ultraviolet light
Posts: 7419 | From: North America | Registered: Mar 2009
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Narmer, so now you doubt I'm a White person LOL ROTFLMBO. Anyhow I have posted these very questions at the end of every dang post I've made, Ironfaggot is the only one who has answered them. Here we go again.
Why do you not want Whites to know who we are?
Why do you not Whites to know where we come from?
Why don't you want Whites to think we have no ancestors (or at least no claim to them)?
Why do you want Whites to think we have no history?
Why do you want Whites to have no sense of pride?
Why do you want Whites to have no knowledge of self?
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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posted
^ Those aren't serious questions. Actually all of them have been answered in many previous posts but you are hard-headed and as usually the case with European albinos, in denial.
I suggest you present these questions to Lionese so she can have the opportunity to publicly conduct a dialogue with herself.
-------------------- Selenium gives real life and true reality Posts: 4693 | From: Saturn | Registered: Apr 2012
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That is the great thing about the internet...you can be whomever you want to be behind the keyboard.
Right Ausar? Lioness? Evergreen. anyone else?
-------------------- Without data you are just another person with an opinion - Deming Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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quote:Originally posted by the lioness,: I'll give you the answer, revenge for slavery
That's not an answer. Surely you can maintain a more prolonged dialogue with yourself. Why not address her questions one by one as you've written them.
Posts: 4693 | From: Saturn | Registered: Apr 2012
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Narmer, cut the crap I am NOT Lioness. Ohh who am I kidding you don't believe me anyhow, as long as i know that's all that matters.
Posts: 3257 | From: Madisonville, KY USA | Registered: Nov 2011
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quote:Originally posted by DHDoxies: Narmer, so now you doubt I'm a White person LOL ROTFLMBO. Anyhow I have posted these very questions at the end of every dang post I've made, Ironfaggot is the only one who has answered them. Here we go again.
Why do you not want Whites to know who we are?
It's revenge for slavery
quote:Originally posted by DHDoxies:
Why do you not Whites to know where we come from?
It's revenge for slavery
quote:Originally posted by DHDoxies:
Why don't you want Whites to think we have no ancestors (or at least no claim to them)?
It's revenge for slavery
quote:Originally posted by DHDoxies:
Why do you want Whites to think we have no history?
It's revenge for slavery
quote:Originally posted by DHDoxies:
Why do you want Whites to have no sense of pride?
It's revenge for slavery
quote:Originally posted by DHDoxies: Why do you want Whites to have no knowledge of self?
It's revenge for slavery
I did my part I answered the question as to why these various things are wanted
Narmertot, leave me out of this I can't save you this is between you and Doxies
bringing my name up is a weak attempt to
Posts: 42939 | From: , | Registered: Jan 2010
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