Discovery of riboflavin

The British chemist Alexander W. Blyth in 1879 isolated from milk whey a water-soluble, yellow fluorescent compound he called lactochrome, appropriately named for its color and origin. ‘Lacto’ from the milk and ‘chrome’ meaning color because of the yellow pigment.

The search to identify these accessory food factors in milk, whole wheat, yeast, and liver began in the early 1900s.

McCollum and assistant Marguerite Davis produced three papers in 1915 which showed a diet containing 2% of wheat embryo or milk powder with polished rice, casein, salts, and butter fat provided enough of an ‘essential accessory’ to support growth of young rats.

The importance of lactochrome was not fully realized until later investigational studies by Elmer McCollum and Kennedy (1916), Emmett and Luros, and Smith and Hendrick that showed the preventive capabilities of water-soluble food extracts against beriberi, pellagra, and pellagra-like dermatitis.

Several years later, the physiological role of the yellow growth factor was shown by Warburg and Christian (1932) to be a component of a yeast “Zwischenferment,” which was designated the “old yellow enzyme.”

Joseph Goldberger in 1927 proposed there was an anti-pellagra factor in eggs, milk, etc., and it was the same substance as ‘water-soluble B’ identified by McCollum. Goldberger called the substance the pellagra-preventative or P-P dietary factor.

In 1935 Richard Kuhn at Heidelberg, and Paul Karrer at the University of Zurich eventually succeeded in synthesizing the vitamin, now termed riboflavin. They were awarded the Nobel Prize for this and other achievements in 1937 and 1938, respectively. Kuhn first proved that riboflavin is an essential growth factor, viz., vitamin B2.

Kuhn also developed a synthetic route to riboflavin which was licensed to the German company I. G. Farben.

Theorell in 1937 identified the isoalloxazine derivative from the old yellow enzyme as riboflavin-5′-phosphate, also called FMN (flavin mononucleotide). The structure of a second coenzymic form was established by Warburg and Christian (1938) as FAD (flavin adenine dinucleotide) and was shown to participate as the coenzyme of d-amino acid oxidase.
Discovery of riboflavin

History of carnitine

Carnitine was first isolated from meat extract by Gulewitsch and Krimberg as well as Kutscher in 1905 and was first thought to be involved with muscle function. Its structure was not established until 1927.

Gulewitsch and Krimberg identified the structure of carnitine as 3-hydroxy-4-N-trimethyl-aminobutyric-acid (C7H15NO), which was later confirmed in 1927 by Tomita and Sendju.

Then, another 20 years elapsed before Fraenkel, in 1947, while investigating the role of folic acid in the nutrition of insects found that the meal worm (Tenebrio molitor) required a growth factor present in yeast. Without carnitine, the meal worms could not use fat stores when starved.

In 1955, two observations further substantiated carnitine’s role in fat metabolism. Fritz showed that carnitine stimulated fatty acid oxidation in liver slices and liver homogenates. Fraenkel and Friedman found that carnitine could be reversibly acetylated by acetyl coenzyme A (CoA).

Fraenkel called this factor ‘Vitamin BT’; vitamin B because of its water soluble property, and the T standing for Tenebrio. Because of not being recognized as a vitamin, the name was subsequently changed to carnitine.

The word carnitine is derived from Latin word carno or carnis, which means flesh or meat.
History of carnitine

Discovery of biotin (Vitamin B7)

The discovery of biotin or vitamin B7 occurred in response to research investigating the cause of what was then called ‘egg white injury’. It goes back to the year 1927, when it was observed that rats fed egg white developed dermatitis and lost hair. This was named as egg white injury.

At that time, there was observation that the raw eggs in the diet are toxic to animals and that the skin lesions caused by the diet can be cured by treatment with a heat stable factor from yeasts or liver.

In 1924 three factors were identified as necessary for the growth of microorganisms. They were called bios II, vitamin H, and coenzyme R. It soon became clear that all three were the same water soluble, sulfur containing vitamin – biotin. Others name given to this factor were protective factor X, egg white injury protection factor, factor S, and factor W or vitamin Bw.

Using feeding studies with dried egg white, M. A. Boas first described in 1927 that mammals require the water soluble vitamin biotin.

Later in 1932 Koegl and Toennis isolate the vitamin from egg yolk. In 1936 they gave the name of biotin as the substance isolated from egg yolk. In that year it was first time recognized that egg white injury can be healed by biotin supplements.

The structure and properties of biotin were established by US and European investigators between 1940 and 1943. The first chemical synthesis was completed by Harris and Associated of the Merck Company in 1943.
Discovery of biotin (Vitamin B7)

Discovery of vitamin K

In 1929, Henrik Dam of Denmark, a biochemist at the University of Copenhagen, discovered vitamin K. Vitamin K is a fat soluble vitamin has been implicated in both cardiovascular and bone health.

At that time Dam was studying the synthesis of cholesterol in chickens. Dam found a hemorrhagic disease in chicks that were fed a diet from which all lipids had been removed.

Dam hypothesized that an unidentified lipid factor had been removed from the chicks’ feed. It was the only substance capable of halting a hemorrhagic disease in which blood does not coagulate.

Hemorrhages were prevented when unextracted fish meal was included in the diet.

In 1930 Horvath first mentioned that an unknown factor was necessary for blood clotting in chicken.

Following further research Dam called it ‘koagulations vitamin’ or ‘vitamin K’ and the letter that he assigned it is still used today.

Dam later succeeded in isolating the agent from alfafa and identifying it, for which he received the Nobel Prize for physiology and medicine.

The structure was determined to be 2-methyl-3-phytyl-1,4-naphthoquinone (vitamin K1).

After the initial discovery of vitamin K, Edward Doisy determined that the main source of vitamin K was through the diet, particular from green vegetable and fish meal.
Discovery of vitamin K

Discovery of pantothenic acid

Pantothenic acid is a water soluble vitamin discovered as a growth factor for yeast and certain bacteria by Roger J. William in 1933. William also first to crystallize folic acid, while his brother was the co-discoverer of thiamine, vitamin B1.

He discovered that yeast requires a certain nutrient, which he called pantothenic acid. He suggested that if yeast needed this nutrient, humans might need it, too.

First isolated in 1938, Elvehjem and Jukes showed in 1939 that pantothenic acid was required for growth and prevented dermatitis in chickens.

During 1939 and 1940 William succeeded in determining the structure of the new vitamin and in preparing it synthetically.

The name pantothenic acid is derived from the Greek word pantothen, meaning ‘from every side.’ This B vitamin is widespread in the food supply, so it is well named.
Discovery of pantothenic acid

History of Vitamin D

Hippocrates, the father of medicine, used heliotherapy or exposure to sunlight to treat phthisis.

The Greek historian, Herodotus (485-426 BC), observed that Persian warriors had much softer skulls than Egyptian warriors and attributed it to the turbans worn by Persians and Hippocrates described as disease resembling rickets in 130 AD.

The first scientific description of a vitamin D-deficiency, namely rickets, was provided in the 17th century by both Dr. Daniel Whistler (1645) and Professor Francis Glisson (1650).

Cod liver oil was first described as a medicinal agent for the treatment of chronic rheumatism in 1789.

Rickets captured the imagination of many chroniclers of the eighteenth and nineteenth centuries. The cause of this was a lack of a vitamin that is not a vitamin.

Beginning in the 1820s, studies showed that administering doses of cod liver oil to afflicted children could cure rickets.

The major breakthrough in understanding the causative factors of rickets was the development in the period 1910 - 1930 of nutrition as an experimental science and the appreciation of the existence of vitamins.

It was in 1919/20 that Sir Edward Mellanby, working with dogs raised exclusively indoors (in the absence of sunlight or ultraviolet light), devised a diet that allowed him to unequivocally establish that the bone disease, rickets was caused by a deficiency of a trace component present in the diet.

In 1921 he wrote, "The action of fats in rickets is due to a vitamin or accessory food factor which they contain, probably identical with the fat-soluble vitamin."

Shortly thereafter E. V McCollum and McCallum succeeded in inducing a rickets-like disease in chickens by administering an incomplete diet. The disease could be cured with cod-liver oil. They assumed that vitamin, present in cod-liver oil, was responsible for the curative effect.

In 1923 Goldblatt and Soames clearly identified that when a precursor of vitamin D in the skin (7-dehydrocholestrol) was irradiated with sunlight or ultraviolet light, a substance equivalent to the fat-soluble vitamin was produced.

Huldschinsky, Hess and Steenbock in 1924 found that a great number of foodstuff, having no antirachitic properties, became antirachitic after irradiation with sunlight or ultraviolet light. The substance activated by sunlight was called ‘provitamin D.’

Several other independent observations in the 19th and early 20th centuries fostered further links between sunlight and cutaneous vitamin D synthesis.

The first analogue of the vitamins D were determined in the 1930s in the laboratory of Professor A. Windaus at the University of Gottingen in Germany.

With the chemical isolation and finally synthesis of the two parent or native D vitamins, vitamin D2 (egocalciferol) and vitamin D3 (cholecalciferol), an etiology therapy for rickets and osteomalacia was established.

Vitamin D2 which could be produced by ultraviolet irradiation of ergosterol was chemically characterized in 1932. Vitamin D3 was not chemically characterized until 1936 when it was shown to result from the ultraviolet irradiation of 7-dehydrocholesterol.

In 1970, it is learned that vitamin D was not the biological active principle for healing bone disease.
History of Vitamin D

A brief history of nutritional deficiencies and chronic disease

A brief history of nutritional deficiencies and chronic disease
There is a long history of discovering relationships between nutritional deficiencies and chronic disease. One of the most well known is probably scurvy -- a disease where bones lose their rigidity due to a deficiency of vitamin C.

The historical accounts of this mostly involve sailors who, on long sailing voyages, were overcome by this nutritional disease. And it actually took hundreds of years before the right scientist came along and discovered that this was caused by a simple nutritional deficiency that could be cured by eating fruits high in vitamin C such as limes. Hence the name 'limeys' for sailors.

That's just one example of a disease caused by nutritional deficiencies. There are many other diseases such as rickets and beriberi caused by nutritional deficiencies. Asian people who historically ate polished, processed rice (white rice) frequently got beriberi, a disease caused by a deficiency in vitamin B1 (thiamin). Until the nutritional causes of beriberi were established, however, physicians of ancient Asia thought the disease was some sort of plague.

In America, the term 'redneck' actually comes from a vitamin B deficiency that caused heightened susceptibility to sunburns. Interestingly, most Americans are, today, deficient in B vitamins as well, making them technically rednecks. It also explains why many people are so easily sunburned. As explained in Staying Healthy With Nutrition by Dr. Elson Haas, M.D.:

For a long period of history, the niacin deficiency disease, pellagra, was a very serious and fatal problem. Characterized as the disease of the "three Ds," pellagra causes its victims to experience dermatitis, diarrhea, and dementia. The fourth D was death. As described previously, the classic B3 deficiency occurs mainly in cultures whose diets rely heavily on corn and where the corn is not prepared in a way that releases its niacin. One of the first signs of pellagra, or niacin deficiency, is the skin's sensitivity to light, and the skin becomes rough, thick, and dry (pellagra means "skin that is rough" in Italian). The skin then becomes darkly pigmented, especially in areas of the body prone to be hot and sweaty or those exposed to sun. The first stage of this condition is extreme redness and sensitivity of those exposed areas, and it was from this symptom that the term "redneck," describing the bright red necks of eighteenth-and nineteenth-century niacin-deficient fieldworkers, came into being.

The early colonial settlers in America, by the way, didn’t know how to properly process corn as the American Indians did. The American Indians processed corn using potash (which is highly alkaline) that makes the B vitamins in corn available for assimilation during digestion. But the American settlers, not understanding how to prepare corn, would simply grind up their corn and consume it as corn flour (corn meal). By the way, that's how most people eat corn today: as ground up cornmeal ingredients in chips and foods.

In more modern times, we know very well about what happens when you're deficient in folic acid and you are a pregnant woman: your baby may be born with serious spinal cord defects or even be stillborn. In fact, birth defects are almost always explained by nutritional deficiencies or the consumption of foods and beverages by the mother that interfere with good nutrition.

We also know that iodine is absolutely essential for human health, which is why salt is enriched with iodine. That's in an effort to prevent goiter, a disease that was quite common in the United States until iodine was finally mandated as a salt supplement (enrichment) by the FDA.

As a nation we have managed to force a handful of minerals and vitamins into the food supply that prevent only the most grotesque and physically obvious disorders and diseases caused by nutritional deficiencies. And by the way, those are the only ones that really get addressed through the food supply.

If there is an obvious and immediate link between nutrition and a particular disease such as birth defects caused by a lack of folic acid, then of course this gets recognized and addressed very quickly. But other metabolic disorders such as cancer and diabetes are more complex and so the cause/effect relationship is not so easy to see from the point of view of scientists, the FDA, and even the public. So these don't get addressed.

And that, frankly, is why the public is still not being taught the correlation between nutrition and chronic diseases like cancer, diabetes, heart disease, osteoporosis and even mental disorders like clinical depression.
A brief history of nutritional deficiencies and chronic disease
By Mike Adams.
Source: www.naturalnews.com