Humans have evolved as omnivorous hunter-gatherers over the past 250,000 years. The diet of early modern humans varied significantly depending on location and climate. The diet in the tropics tended to be based more heavily on plant foods, while the diet at higher latitudes tended more towards animal products. Analysis of postcranial and cranial remains of humans and animals from the Neolithic, along with detailed bone modification studies have shown that cannibalism was also prevalent among prehistoric humans.
The first recorded nutritional experiment is found in the Bible's Book of Daniel. Daniel and his friends were captured by the king of Babylon during an invasion of Israel. Selected as court servants, they were to share in the king's fine foods and wine. But they objected, preferring vegetables (pulses) and water in accordance with their Jewish dietary restrictions. The king's chief steward reluctantly agreed to a trial. Daniel and his friends received their diet for 10 days and were then compared to the king's men. Appearing healthier, they were allowed to continue with their diet.
c. 475 BC: Anaxagoras states that food is absorbed by the human body and therefore contained "homeomerics" (generative components), thereby deducing the existence of nutrients.
c. 400 BC: Hippocrates says, "Let food be your medicine and medicine be your food."
1500s: Scientist and artist Leonardo da Vinci compared metabolism to a burning candle.
1747: Dr. James Lind, a physician in the British navy, performed the first scientific nutrition experiment, discovering that lime juice saved sailors who had been at sea for years from scurvy, a deadly and painful bleeding disorder. The discovery was ignored for forty years, after which British sailors became known as "limeys." The essential vitamin C within lime juice would not be identified by scientists until the 1930s.
1770: Antoine Lavoisier, the "Father of Nutrition and Chemistry" discovered the details of metabolism, demonstrating that the oxidation of food is the source of body heat.
1790: George Fordyce recognized calcium as necessary for fowl survival.
Early 1800s: The elements carbon, nitrogen, hydrogen and oxygen were recognized as the primary components of food, and methods to measure their proportions were developed.
1816: François Magendie discovers that dogs fed only carbohydrates and fat lost their body protein and died in a few weeks, but dogs also fed protein survived, identifying protein as an essential dietary component.
1840: Justus Liebig discovers the chemical makeup of carbohydrates (sugars), fats (fatty acids) and proteins (amino acids.)
1860s: Claude Bernard discovers that body fat can be synthesised from carbohydrate and protein, showing that the energy in blood glucose can be stored as fat or as glycogen.
Early 1880s: Kanehiro Takaki observed that Japanese sailors developed beriberi (or endemic neuritis, a disease causing heart problems and paralysis) but British sailors did not. Adding milk and meat to Japanese diets prevented the disease.
1896: Baumann observed iodine in thyroid glands.
1897: Christiaan Eijkman worked with natives of Java, who also suffered from beriberi. Eijkman observed that chickens fed the native diet of white rice developed the symptoms of beriberi, but remained healthy when fed unprocessed brown rice with the outer bran intact. Eijkman cured the natives by feeding them brown rice, discovering that food can cure disease. Over two decades later, nutritionists learned that the outer rice bran contains vitamin B1, also known as thiamine. Antiquity through 1900
Early 1900s: Carl Von Voit and Max Rubner independently measure caloric energy expenditure in different species of animals, applying principles of physics in nutrition.
1906: Wilcock and Hopkins showed that the amino acid tryptophan was necessary for the survival of mice. Gowland Hopkins recognized "accessory food factors" other than calories, protein and minerals, as organic materials essential to health but which the body cannot synthesise.
1907: Stephen M. Babcock and Edwin B. Hart conduct the Single-grain experiment. This experiment runs through 1911.
1912: Casimir Funk coined the term vitamin, a vital factor in the diet, from the words "vital" and "amine," because these unknown substances preventing scurvy, beriberi, and pellagra, were thought then to be derived from ammonia.
1913: Elmer McCollum discovered the first vitamins, fat soluble vitamin A, and water soluble vitamin B (in 1915; now known to be a complex of several water-soluble vitamins) and names vitamin C as the then-unknown substance preventing scurvy. Lafayette Mendel and Thomas Osborne also perform pioneering work on vitamin A and B.
1919: Sir Edward Mellanby incorrectly identified rickets as a vitamin A deficiency, because he could cure it in dogs with cod liver oil.
1922: McCollum destroys the vitamin A in cod liver oil but finds it still cures rickets, naming vitamin D
1922: H.M. Evans and L.S. Bishop discover vitamin E as essential for rat pregnancy, originally calling it "food factor X" until 1925.
1925: Hart discovers trace amounts of copper are necessary for iron absorption.
1927: Adolf Otto Reinhold Windaus synthesizes vitamin D, for which he won the Nobel Prize in Chemistry in 1928.
1928: Albert Szent-Gyorgyi isolates ascorbic acid, and in 1932 proves that it is vitamin C by preventing scurvy. In 1935 he synthesizes it, and in 1937 he wins a Nobel Prize for his efforts. Szent-Gyorgyi concurrently elucidates much of the citric acid cycle.
1930s: William Cumming Rose identifies essential amino acids, necessary protein components which the body cannot synthesize.
1935: Underwood and Marston independently discover the necessity of cobalt.
1936: Eugene Floyd Dubois shows that work and school performance are related to caloric intake.
1938: The chemical structure of vitamin E is discovered by Erhard Fernholz, and it is synthesised by Paul Karrer.
1940 UK institutes rationing according to nutritional principles drawn up by Elsie Widdowson and others
1941: The first Recommended Dietary Allowances (RDAs) were established by the National Research Council. 1900 through 1941
1992 The U.S. Department of Agriculture Introduces Food Guide Pyramid
2002 Study shows relation between nutrition and violent behavior
2005 Obesity may be caused by adenovirus in addition to bad nutrition Recent
There are six main classes of nutrients that the body needs: carbohydrates, proteins, fats, vitamins, minerals, and water. It is important to consume these six nutrients on a daily basis to build and maintain healthy bodily function.
Poor health can be caused by an imbalance of nutrients, either an excess or deficiency, which, in turn, affects bodily functions cumulatively. Moreover, because most nutrients are involved in cell-to-cell signalling (e.g. as building blocks or as part of a hormone or signalling cascades), deficiency or excess of various nutrients affects hormonal function indirectly. Thus, because they largely regulate the expression of genes, hormones represent a link between nutrition and how our genes are expressed, i.e. our phenotype. The strength and nature of this link are continually under investigation, but recent observations have demonstrated a pivotal role for nutrition in hormonal activity and function and therefore in health.
According to the United Nations World Health Organization (WHO: 1996), more than starvation the real challenge today is malnutrition-the deficiency of micronutrients (vitamins, minerals and essential amino acids) that no longer allows the body to ensure growth and maintain its vital functions.
Recognising the inherent potential of the micro-alage Spirulina (Spirulina Platensis) to counter malnutrition and its severe negative impacts at multiple levels of the society especially in the developing and Least Developed Countries (LDC), the international community affirmed its conviction by joining hands to form the Intergovernmental Institution for the use of Micro-algae Spirulina Against Malnutrition, IIMSAM.
Nutrition and health
The body requires amino acids to produce new body protein (protein retention) and to replace damaged proteins (maintenance) that are lost in the urine. In animals amino acid requirements are classified in terms of essential (an animal cannot produce them) and non-essential (the animal can produce them from other nitrogen containing compounds) amino acids. Consuming a diet that contains adequate amounts of essential (but also non-essential) amino acids is particularly important for growing animals, who have a particularly high requirement.
Essential and non-essential amino acids
Mineral and/or vitamin deficiency or excess may yield symptoms of diminishing health such as goitre, scurvy, osteoporosis, weak immune system, disorders of cell metabolism, certain forms of cancer, symptoms of premature aging, and poor psychological health (including eating disorders), among many others.
As of 2005, twelve vitamins and about the same number of minerals are recognized as "essential nutrients", meaning that they must be consumed and absorbed - or, in the case of vitamin D, alternatively synthesized via UVB radiation - to prevent deficiency symptoms and death. Certain vitamin-like substances found in foods, such as carnitine, have also been found essential to survival and health, but these are not strictly "essential" to eat because the body can produce them from other compounds. Moreover, thousands of different phytochemicals have recently been discovered in food (particularly in fresh vegetables), which have many known and yet to be explored properties including antioxidant activity (see below). Other essential nutrients include essential amino acids, choline and the essential fatty acids.
In addition to sufficient intake, an appropriate balance of essential fatty acids - omega-3 and omega-6 fatty acids - has been discovered to be crucial for maintaining health. Both of these unique "omega" long-chain polyunsaturated fatty acids are substrates for a class of eicosanoids known as prostaglandins which function as hormones. The omega-3 eicosapentaenoic acid (EPA) (which can be made in the body from the omega-3 essential fatty acid alpha-linolenic acid (LNA), or taken in through marine food sources), serves as building block for series 3 prostaglandins (e.g. weakly-inflammation PGE3). The omega-6 dihomo-gamma-linolenic acid (DGLA) serves as building block for series 1 prostaglandins (e.g. anti-inflammatory PGE1), whereas arachidonic acid (AA) serves as building block for series 2 prostaglandins (e.g. pro-inflammatory PGE 2). Both DGLA and AA are made from the omega-6 linoleic acid (LA) in the body, or can be taken in directly through food. An appropriately balanced intake of omega-3 and omega-6 partly determines the relative production of different prostaglandins, which partly explains the importance of omega-3/omega-6 balance for cardiovascular health. In industrialised societies, people generally consume large amounts of processed vegetable oils that have reduced amounts of essential fatty acids along with an excessive amount of omega-6 relative to omega-3.
The rate of conversions of omega-6 DGLA to AA largely determines the production of the respective prostaglandins PGE1 and PGE2. Omega-3 EPA prevents AA from being released from membranes, thereby skewing prostaglandin balance away from pro-inflammatory PGE2 made from AA toward anti-inflammatory PGE1 made from DGLA. Moreover, the conversion (desaturation) of DGLA to AA is controlled by the enzyme delta-5-desaturase, which in turn is controlled by hormones such as insulin (up-regulation) and glucagon (down-regulation). Because different types and amounts of food eaten/absorbed affect insulin, glucagon and other hormones to varying degrees, not only the amount of omega-3 versus omega-6 eaten but also the general composition of the diet therefore determine health implications in relation to essential fatty acids, inflammation (e.g. immune function) and mitosis (i.e. cell division).
Several lines of evidence indicate lifestyle-induced hyperinsulinemia and reduced insulin function (i.e. insulin resistance) as a decisive factor in many disease states. For example, hyperinsulinemia and insulin resistance are strongly linked to chronic inflammation, which in turn is strongly linked to a variety of adverse developments such as arterial microinjuries and clot formation (i.e. heart disease) and exaggerated cell division (i.e. cancer). Hyperinsulinemia and insulin resistance (the so-called metabolic syndrome) are characterized by a combination of abdominal obesity, elevated blood sugar, elevated blood pressure, elevated blood triglycerides, and reduced HDL cholesterol. The negative impact of hyperinsulinemia on prostaglandin PGE1/PGE2 balance may be significant.
The state of obesity clearly contributes to insulin resistance, which in turn can cause type 2 diabetes. Virtually all obese and most type 2 diabetic individuals have marked insulin resistance. Although the association between overfatness and insulin resistance is clear, the exact (likely multifarious) causes of insulin resistance remain less clear. Importantly, it has been demonstrated that appropriate exercise, more regular food intake and reducing glycemic load (see below) all can reverse insulin resistance in overweight individuals (and thereby lower blood sugar levels in those who have type 2 diabetes).
Obesity can unfavourably alter hormonal and metabolic status via resistance to the hormone leptin, and a vicious cycle may occur in which insulin/leptin resistance and obesity aggravate one another. The vicious cycle is putatively fuelled by continuously high insulin/leptin stimulation and fat storage, as a result of high intake of strongly insulin/leptin stimulating foods and energy. Both insulin and leptin normally function as satiety signals to the hypothalamus in the brain; however, insulin/leptin resistance may reduce this signal and therefore allow continued overfeeding despite large body fat stores. In addition, reduced leptin signalling to the brain may reduce leptin's normal effect to maintain an appropriately high metabolic rate.
There is debate about how and to what extent different dietary factors -- e.g. intake of processed carbohydrates, total protein, fat, and carbohydrate intake, intake of saturated and trans fatty acids, and low intake of vitamins/minerals -- contribute to the development of insulin- and leptin resistance. In any case, analogous to the way modern man-made pollution may potentially overwhelm the environment's ability to maintain 'homeostasis', the recent explosive introduction of high Glycemic Index- and processed foods into the human diet may potentially overwhelm the body's ability to maintain homeostasis and health (as evidenced by the metabolic syndrome epidemic).
Antioxidants are another recent discovery. As cellular metabolism/energy production requires oxygen, potentially damaging (e.g. mutation causing) compounds known as radical oxygen species or free radicals form as a result. For normal cellular maintenance, growth, and division, these free radicals must be sufficiently neutralized by antioxidant compounds, some produced by the body with adequate precursors (glutathione, Vitamin C in most animals) and those that the body cannot produce may only be obtained through the diet through direct sources (Vitamin C in humans, Vitamin A, Vitamin K) or produced by the body from other compounds (Beta-carotene converted to Vitamin A by the body, Vitamin D synthesized from cholesterol by sunlight). Different antioxidants are now known to function in a cooperative network, e.g. vitamin C can reactivate free radical-containing glutathione or vitamin E by accepting the free radical itself, and so on. Some antioxidants are more effective than others at neutralizing different free radicals. Some cannot neutralize certain free radicals. Some cannot be present in certain areas of free radical development (Vitamin A is fat-soluble and protects fat areas, Vitamin C is water soluble and protects those areas). When interacting with a free radical, some antioxidants produce a different free radical compound that is less dangerous or more dangerous than the previous compound. Having a variety of antioxidants allows any byproducts to be safely dealt with by more efficient antioxidants in neutralizing a free radical's butterfly effect.
Tuesday, April 22, 2008
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