Arizona Diet Products Helps You To Lose Weight Quickly and Safely

Dietary supplements, often containing vitamins, are used to ensure that adequate amounts of nutrients are obtained on a daily basis, if optimal amounts of the nutrients cannot be obtained through a varied diet. Scientific evidence supporting the benefits of some dietary supplements is well established for certain health conditions, but others need further study. A meta-analysis in 2006 suggested that Vitamin A and E supplements not only provide no tangible health benefits for generally healthy individuals, but may actually increase mortality, although two large studies included in the analysis involved smokers, for which it was already known that beta-carotene supplements can be harmful.

 

In the United States, advertising for dietary supplements is required to include a disclaimer that the product is not intended to treat, diagnose, mitigate, prevent, or cure disease, and that any health claims have not been evaluated by the Food and Drug Administration. In some cases, dietary supplements may have unwanted effects, especially if taken before surgery, with other dietary supplements or medicines, or if the person taking them has certain health conditions. Vitamin supplements may also contain levels of vitamins many times higher, and in different forms, than one may ingest through food.

 

Intake of excessive quantities can cause vitamin poisoning, often due to overdose of Vitamin A and Vitamin D (The most common poisoning with multinutrient supplement pills does not involve a vitamin, but is rather due to the mineral iron). Due to toxicity, most common vitamins have recommended upper daily intake amounts.

 

Since 2005, suppliers have distinguished their products as either Medical Grade or Pharmaceutical Grade products. Both of these classifications indicate products that are manufactured to be easily absorbed by the body. Normal vitamin manufacturing is not regulated in the United States to the same standards as are medicinal pharmaceuticals, although U.S. vitamins which are manufactured for food consumption by humans or animals must be manufactured to Food Chemicals Codex (FCC), grade, commonly called “food grade”.

 

 Governmental regulation of vitamin supplements

 

Most countries place dietary supplements in a special category under the general umbrella of foods, not drugs. This necessitates that the manufacturer, and not the government, be responsible for ensuring that its dietary supplement products are safe before they are marketed. Unlike drug products, that must explicitly be proven safe and effective for their intended use before marketing, there are often no provisions to “approve” dietary supplements for safety or effectiveness before they reach the consumer. Also unlike drug products, manufacturers and distributors of dietary supplements are not generally required to report any claims of injuries or illnesses that may be related to the use of their products.

 

 Names in current and previous nomenclatures

 

The reason the set of vitamins seems to skip directly from E to K is that the vitamins corresponding to “letters” F-J were either reclassified over time, discarded as false leads, or renamed because of their relationship to “vitamin B”, which became a “complex” of vitamins. The German-speaking scientists who isolated and described vitamin K (in addition to naming it as such) did so because the vitamin is intimately involved in the Koagulation of blood following wounding. At the time, most (but not all) of the letters from F through J were already designated, so the use of the letter K was considered quite reasonable.

 

The following table lists chemicals that had previously been classified as vitamins, as well as the earlier names of vitamins that later became part of the B-complex:

Previous name Chemical name             Reason for name change

Vitamin B4                       Adenine                                       DNA metabolite

Vitamin B8                 Adenylic acid                                     DNA metabolite

Vitamin F         Essential fatty acids             Needed in large quantities (does

not fit the definition of a vitamin).

Vitamin G                     Riboflavin                        Reclassified as Vitamin B2

Vitamin H                      Biotin                Reclassified as Vitamin B7

Vitamin J                Catechol, Flavin                                Protein metabolite

Vitamin L1           Anthranilic acid                       Protein metabolite

Vitamin L2          Adenylthiomethylpentose             RNA metabolite

Vitamin M                    Folic acid                          Reclassified as Vitamin B9

Vitamin O                        Carnitine                                     Protein metabolite

Vitamin P                       Flavonoids                  No longer classified as a vitamin

Vitamin PP                        Niacin                           Reclassified as Vitamin B3

Vitamin U                  S-Methylmethionine                              Protein metabolite

 

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Exercise and Health

 

Let’s talk about exercise and why it is essential for good health and weight loss. Most people who exercise regularly will tell you that it is the key, the most important single thing they do to stay healthy and fit. Many of those people won’t be reading this newsletter or going to our diet site because they don’t have any weight they need to lose. This newsletter is really intended for those of us who do have weight to lose, be it ten pounds or a hundred pounds.

 

Exercise is an essential component of any weight loss plan. Without it, you will have to diet much more strenuously to achieve your goal. Now I’m not talking about running five miles and then hitting the gym for two hours of weight lifting every day. The kind of exercise needed in a successful weight loss plan is basic and easy. Walking for one half hour daily is a very good start. Kenneth Cooper showed the world through very well done scientific studies over several years, that walking is a safe and effective way to get the benefits of exercise. Swimming is also great. Riding the stationary bike works too. The key is to start slowly and slowly progress. Many people make the mistake of overdoing their new exercise program in the beginning and after two days they are so tired and sore, they just quit. That won’t do you any good at all. That is not the way to do it.

 

Begin any new exercise program slowly. Let’s use walking as an example of how to do it right. Figure out a time that you can walk each day. Begin with just thirty minutes of moderate speed (normal) walking. After two weeks, increase the time by fifteen minutes. Now do this forty five minute walk for one month and then increase by another fifteen minutes. Now you are walking for one hour daily. Do this one hour walk for another month before any increase in duration or intensity. Now you may be ready to start jogging instead of just walking. Maybe you don’t really want to jog. No problem, you don’t have to. You can stay with your walk forever if you like; just pick up the speed a little. The formula described above works exactly the same for swimming or riding a bike.

 

Now let’s talk about why exercise is important to losing weight and keeping it off permanently. Daily aerobic exercise (walking, swimming, biking) raises your basic metabolic rate (BMR). It resets your metabolic thermostat to a higher setting. Your BMR goes up during exercise and stays at a higher level than normal throughout the day. You burn more calories and you lose weight. Simple really, but many people fail to include this essential ingredient in their weight loss plan. Exercise also increases blood flow in you brain, and makes your heart and lungs stronger and more efficient. You will think better, feel better, and even sleep better. All good things.

 

Let’s finish by talking a little about lifting weights. Weight lifting is basically an anaerobic form of exercise; not at all like the aerobic types that we talked about before. When you lift weights you stress an individual muscle or muscle group and strengthen it through a process of muscle breakdown and repair. Building lean muscle is a good idea, and it will help you stay trim, but it should only be added to your weight loss plan after you have lost approximately twenty percent of the weight you want to lose. At that point, it is a very good thing to do. Again, start slowly. You can, and should, eventually combine aerobic exercise with some weight lifting in you routine to achieve optimal health. I personally do aerobic exercise every day and lift twice a week.

 

That is all for this month. Please visit out website at arizonadietproducts.com. You will find all the products you need for losing weight and also many informative articles on health. My next newsletter in August will focus on diabetes and weight loss. As always, “the key to good dieting is good nutrition.”

 

Dr. Brad Manny

Owner/Director Arizona Diet Products

 

 

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Niacin, also known as nicotinic acid and vitamin B3, is the organic compound with the formula HO2CC5H4N. This water-soluble, colorless solid is a derivative of pyridine, featuring a carboxylic acid functional group at the 3-position. The designation vitamin B3 also includes the corresponding amide nicotinamide (”niacinamide”), wherein the CO2H group has been replaced by a CONH2 group. Niacin is converted to niacinamide in vivo, and though the two are identical in their vitamin functions, niacinamide does not have the same pharmacologic and toxic effects of niacin, which occur incidental to niacin’s conversion. Thus niacinamide does not reduce cholesterol or cause flushing, although nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults. Niacin is a precursor to NADH, NAD, NAD+, and NADP, which play essential metabolic roles in living cells. DNA repair, and the production of steroid hormones in the adrenal gland.

 

History

 

Niacin was first described by Weidel in 1873 in his studies of nicotine. The original preparation remains useful: the oxidation of nicotine using nitric acid. Niacin was extracted from livers by Conrad Elvehjem who later identified the active ingredient, then referred to as the “pellagra-preventing factor” and the “anti-blacktongue factor.” When the biological significance of nicotinic acid was realized, it was thought appropriate to choose a name to dissociate it from nicotine, in order to avoid the perception that vitamins or niacin-rich food contains nicotine. The resulting name ‘niacin’ was derived from nicotinic acid + vitamin.

 

Niacin is referred to as Vitamin B3 because it was the third of the B vitamins to be discovered. It has historically been referred to as “vitamin PP.”

 

 Dietary needs

 

Severe deficiency of niacin in the diet causes the disease pellagra, whereas mild deficiency slows the metabolism, causing decreased tolerance to cold. Dietary niacin deficiency tends to occur only in areas where people eat corn (maize), the only grain low in niacin, as a staple food, and that do not use lime during meal/flour production. Alkali lime releases the tryptophan from the corn in a process called nixtamalization so that it can be absorbed in the intestine, and converted to niacin.

 

The recommended daily allowance of niacin is 2-12 mg/day for children, 14 mg/day for women, 16 mg/day for men and 18 mg/day for pregnant or breast-feeding women.

 

Note: Niacin synthesis is deficient in carcinoid syndrome because of metabolic diversion of its precursor, tryptophan, to form serotonin.

 

 Pharmacological uses

 

Niacin, when taken in large doses, blocks the breakdown of fats in adipose tissue, thus altering blood lipid levels. Niacin is used in the treatment of hyperlipidemia because it reduces very-low-density lipoprotein (VLDL), a precursor of low-density lipoprotein (LDL) or “bad” cholesterol. Because niacin blocks breakdown of fats, it causes a decrease in free fatty acids in the blood and, as a consequence, decreased secretion of VLDL and cholesterol by the liver.

 

By lowering VLDL levels, niacin also increases the level of high-density lipoprotein (HDL) or “good” cholesterol in blood, and therefore it is sometimes prescribed for patients with low HDL, who are also at high risk of a heart attack.

 

Niacin is sometimes consumed in large quantities by people who wish to fool drug screening tests, particularly for lipid soluble drugs such as marijuana. It is believed to “promote metabolism” of the drug and cause it to be “flushed out.” Scientific studies have shown it does not affect drug screenings, but can pose a risk of overdose, causing arrhythmias, metabolic acidosis, hyperglycemia, and other serious problems.

 

 Toxicity

 

People taking pharmacological doses of niacin (1.5 - 6 g per day) often experience a syndrome of side-effects that can include one or more of the following:

 

    * Dermatological complaints

          o facial flushing and itching

          o dry skin

          o skin rashes including acanthosis nigricans

    * Gastrointestinal complaints

          o dyspepsia (indigestion)

    * Liver toxicity

          o fulminant hepatic failure

    * Hyperglycemia

    * Cardiac arrhythmias

    * Birth defects

 

Facial flushing is the most commonly-reported side-effect. It lasts for about 15 to 30 minutes, and is sometimes accompanied by a prickly or itching sensation, particularly in areas covered by clothing. This effect is mediated by prostaglandin and can be blocked by taking 300 mg of aspirin half an hour before taking niacin, or by taking one tablet of ibuprofen per day. Taking the niacin with meals also helps reduce this side-effect. After 1 to 2 weeks of a stable dose, most patients no longer flush. Slow- or “sustained”-release forms of niacin have been developed to lessen these side-effects. One study showed the incidence of flushing was significantly lower with a sustained release formulation though doses above 2 g per day have been associated with liver damage, particularly with slow-release formulations.

 

High-dose niacin may also elevate blood sugar, thereby worsening diabetes mellitus. Hyperuricemia is another side-effect of taking high-dose niacin, and may exacerbate gout. Niacin at doses used in lowering cholesterol has been associated with birth defects in laboratory animals, with possible consequences for infant development in pregnant women.

 

Niacin at extremely high doses can have life-threatening acute toxic reactions. Extremely high doses of niacin can also cause niacin maculopathy, a thickening of the macula and retina which leads to blurred vision and blindness.

 

 Inositol hexanicotinate

 

One popular form of dietary supplement is inositol hexanicotinate, usually sold as “flush-free” or “no-flush” niacin (although those terms are also used for regular sustained-release.) While this form of niacin does not cause the flushing associated with the nicotinic acid form, it is not clear whether it is pharmacologically equivalent in its positive effect.

 

 

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An essential nutrient is a nutrient required for normal body functioning that cannot be synthesized by the body and must be obtained from a dietary source. Some categories of essential nutrient include vitamins, dietary minerals, essential fatty acids, and essential amino acids.

 

Different species have very different essential nutrients. Most essential nutrients are substances that are metabolically necessary but cannot be synthesized by the organism. Dietary minerals, for example, cannot be synthesized in biological systems, so (for example) a human must obtain the iron they need to build hemoglobin from their diet. Of course, this iron is recycled, but some is inevitably lost, for example during menstruation.

 

Many essential nutrients are toxic in large doses (see hypervitaminosis or the nutrient pages themselves below). Some can be taken in amounts larger than required in a typical diet, with no apparent ill effects. Linus Pauling said of vitamin B3, (either niacin or niacinamide), “What astonished me was the very low toxicity of a substance that has such very great physiological power. A little pinch, 5 mg, every day, is enough to keep a person from dying of pellagra, but it is so lacking in toxicity that ten thousand times as much can [sometimes] be taken without harm.” A similar statement can be made about vitamin C and some other vitamins.

 

List of essential nutrients

 

    * Essential substances often not considered to be nutrients:

          o Oxygen

          o Water

          o Sunlight

    * Essential fatty acids:

          o Linolenic acid (the shortest chain omega-3 fatty acid)

          o Linoleic acid (the shortest chain omega-6 fatty acid)

    * Essential amino acids necessary for all humans:

          o Histidine

          o Isoleucine

          o Lysine

          o Leucine

          o Methionine

          o Phenylalanine

          o Threonine

          o Tryptophan

          o Valine

    * Essential amino acids necessary for human children and not adults:

          o Arginine

    * Vitamins:

          o Biotin (vitamin B7, vitamin H)

          o Choline (vitamin Bp)

          o Folate (folic acid, vitamin B9, vitamin M)

          o Niacin (vitamin B3, vitamin P, vitamin PP)

          o Pantothenic acid (vitamin B5)

          o Riboflavin (vitamin B2, vitamin G)

          o Thiamine (vitamin B1)

          o Vitamin A (retinol)

          o Vitamin B6 (pyridoxine, pyridoxamine, or pyridoxal)

          o Vitamin B12 (cobalamin)

          o Vitamin C (ascorbic acid)

          o Vitamin E (tocopherol)

          o Vitamin K (naphthoquinoids)

     Dietary minerals: Biochemical studies reported in 2006 indicate that the following elements (aside from constituent elements of other essential nutrients) are required for human health:

          o Calcium (Ca)

          o Chloride (Cl-)

          o Copper (Cu)

          o Iodine (I)

          o Iron (Fe)

          o Magnesium (Mg)

          o Manganese (Mn)

          o Molybdenum (Mo)

          o Nickel (Ni)[5]

          o Phosphorus (P) (as phosphate)

          o Potassium (K)

          o Selenium (Se)

          o Sodium (Na)

          o Sulfur (S)

          o Zinc (Zn)

 

The body’s requirements vary widely. At one extreme a 70 kg human contains 1.0 kg of calcium but only 3 mg of cobalt.

 

 Elements with speculated role in human health

 

Many elements have been implicated at various times to have a role in human health. For none of these elements has a specific protein or complex been identified:

 

    * Boron (B)

    * Chromium (Cr)

    * Fluorine (F) (necessity unknown in humans)

    * Silicon (Si) (also present in rice husk).

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A vitamin is an organic compound required as a nutrient in tiny amounts by an organism. A compound is called a vitamin when it cannot be synthesized in sufficient quantities by an organism, and must be obtained from the diet. Thus, the term is conditional both on the circumstances and the particular organism. For example, ascorbic acid functions as vitamin C for some animals but not others, and vitamins D and K are required in the human diet only in certain circumstances.

 

Vitamins are classified by their biological and chemical activity, not their structure. Thus, each “vitamin” actually refers to a number of vitamer compounds, which form a set of distinct chemical compounds that show the biological activity of a particular vitamin. Such a set of chemicals are grouped under an alphabetized vitamin “generic descriptor” title, such as “vitamin A,” which (for example) includes retinal, retinol, and many carotenoids. Vitamers are often inter-convertible in the body. The term vitamin does not include other essential nutrients such as dietary minerals, essential fatty acids, or essential amino acids, nor does it encompass the large number of other nutrients that promote health but are otherwise required less often.

 

Vitamins have diverse biochemical functions, including function as hormones (e.g. vitamin D), antioxidants (e.g. vitamin E), and mediators of cell signaling and regulators of cell and tissue growth and differentiation (e.g. vitamin A). The largest number of vitamins (e.g. B complex vitamins) function as precursors for enzyme cofactor bio-molecules (coenzymes), that help act as catalysts and substrates in metabolism. When acting as part of a catalyst, vitamins are bound to enzymes and are called prosthetic groups. For example, biotin is part of enzymes involved in making fatty acids. Vitamins also act as coenzymes to carry chemical groups between enzymes. For example, folic acid carries various forms of carbon group – methyl, formyl and methylene - in the cell. Although these roles in assisting enzyme reactions are vitamins’ best-known function, the other vitamin functions are equally important.

 

Until the 1900s, vitamins were obtained solely through food intake, and changes in diet (which, for example, could occur during a particular growing season) can alter the types and amounts of vitamins ingested. Vitamins have been produced as commodity chemicals and made widely available as inexpensive pills for several decades, allowing supplementation of the dietary intake.

 

History

The Ancient Egyptians knew that feeding a patient liver would help cure night blindness.

The Ancient Egyptians knew that feeding a patient liver would help cure night blindness.

 

The value of eating a certain food to maintain health was recognized long before vitamins were identified. The ancient Egyptians knew that feeding a patient liver would help cure night blindness, an illness now known to be caused by a vitamin A deficiency. The advancement of ocean voyage during the Renaissance resulted in prolonged periods without access to fresh fruits and vegetables, and made illnesses from vitamin deficiency common among ship’s crew.

 

In 1749, the Scottish surgeon James Lind discovered that citrus foods helped prevent scurvy, a particularly deadly disease in which collagen is not properly formed, causing poor wound healing, bleeding of the gums, severe pain, and death. In 1753, Lind published his Treatise on the Scurvy, which recommended using lemons and limes to avoid scurvy, which was adopted by the British Royal Navy. This led to the nickname Limey for sailors of that organization. Lind’s discovery, however, was not widely accepted by individuals in the Royal Navy’s Arctic expeditions in the 19th century, where it was widely believed that scurvy could be prevented by practicing good hygiene, regular exercise, and by maintaining the morale of the crew while on board, rather than by a diet of fresh food.[8] As a result, Arctic expeditions continued to be plagued by scurvy and other deficiency diseases. In the early 20th century, when Robert Falcon Scott made his two expeditions to the Antarctic, the prevailing medical theory was that scurvy was caused by “tainted” canned food.

The discovery of vitamins and their structure Year of discovery Vitamin             Source

1909    Vitamin A (Retinol)                                                                                  Cod liver oil

1912    Vitamin B1 (Thiamin)                                                                               Rice bran

1912    Vitamin C (Ascorbic acid)                                                                        Lemons

1918    Vitamin D (Calciferol)                                                                              Cod liver oil

1920    Vitamin B2 (Riboflavin)                                                                             Eggs

1922    Vitamin E (Tocopherol)                                        Wheat germ oil, Cosmetic and Liver

1926    Vitamin B12 (Cyanocobalamin)                                                                  Liver

1929    Vitamin K (Phylloquinone)                                                                          Luzern

1931    Vitamin B5 (Pantothenic acid)                                                                     Liver

1931    Vitamin B7 (Biotin)                                                                                      Liver

1934    Vitamin B6 (Pyridoxine)                                                                              Rice bran

1936    Vitamin B3 (Niacin)                                                                                     Liver

1941    Vitamin B9 (Folic acid)                                                                                Liver  

 

In 1881, Russian surgeon Nikolai Lunin studied the effects of scurvy while at the University of Tartu in present-day Estonia. He fed mice an artificial mixture of all the separate constituents of milk known at that time, namely the proteins, fats, carbohydrates, and salts. The mice that received only the individual constituents died, while the mice fed by milk itself developed normally. He made a conclusion that “a natural food such as milk must therefore contain, besides these known principal ingredients, small quantities of unknown substances essential to life.” However, his conclusions were rejected by other researchers when they were unable to reproduce his results. One difference was that he had used table sugar (sucrose), while other researchers had used milk sugar (lactose) that still contained small amounts of vitamin B.

 

In the Orient where polished white rice was the common staple food of the middle class, beriberi resulting from lack of vitamin B was endemic. In 1884, Takaki Kanehiro, a British trained medical doctor of the Japanese Navy observed that beriberi was endemic among low ranking crew who often ate nothing but rice but not among crews of Western navies and officers who were entitled to a Western-style diet. Kanehiro initially believed that lack of protein was the chief cause of beriberi. With the support of Japanese navy, he experimented using crews of two battleships, one crew was fed only white rice, while the other was fed a diet of meat, fish, barley, rice, and beans. The group that ate only white rice documented 161 crew with beriberi and 25 deaths, while the latter group had only 14 cases of beriberi and no deaths. This convinced Kanehiro and the Japanese Navy that diet was the cause of beriberi. This was confirmed in 1897, when Christiaan Eijkman discovered that feeding unpolished rice instead of the polished variety to chickens helped to prevent beriberi in the chickens. The following year, Frederick Hopkins postulated that some foods contained “accessory factors”—in addition to proteins, carbohydrates, fats, et cetera—that were necessary for the functions of the human body. Hopkins was awarded the 1929 Nobel Prize for Physiology or Medicine with Christiaan Eijkman for their discovery of several vitamins.

 

In 1910, Japanese scientist Umetaro Suzuki succeeded in extracting a water-soluble complex of micronutrients from rice bran and named it aberic acid. He published this discovery in a Japanese scientific journal. When the article was translated into German, the translation failed to state that it was a newly discovered nutrient, a claim made in the original Japanese article, and hence his discovery failed to gain publicity. Polish biochemist Kazimierz Funk isolated the same complex of micronutrients and proposed the complex be named “Vitamine” (a portmanteau of “vital amine”) in 1912. The name soon became synonymous with Hopkins’ “accessory factors”, and by the time it was shown that not all vitamins were amines, the word was already ubiquitous. In 1920, Jack Cecil Drummond proposed that the final “e” be dropped to deemphasize the “amine” reference after the discovery that vitamin C had no amine component.

 

 

Throughout the early 1900s, the use of deprivation studies allowed scientists to isolate and identify a number of vitamins. Initially, lipid from fish oil was used to cure rickets in rats, and the fat-soluble nutrient was called “antirachitic A”. The irony here is that the first “vitamin” bioactivity ever isolated, which cured rickets, was initially called “vitamin A”, the bioactivity of which is now called vitamin D. What we now call “vitamin A” was identified in fish oil because it was inactivated by ultraviolet light. In 1931, Albert Szent-Györgyi and a fellow researcher Joseph Svirbely determined that “hexuronic acid” was actually vitamin C and noted its anti-scorbutic activity. In 1937, Szent-Györgyi was awarded the Nobel Prize for his discovery. In 1943 Edward Adelbert Doisy and Henrik Dam were awarded the Nobel Prize for their discovery of vitamin K and its chemical structure.

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Diabetes mellitus is currently a chronic disease, without a cure, and medical emphasis must necessarily be on managing/avoiding possible short-term as well as long-term diabetes-related problems. There is an exceptionally important role for patient education, dietetic support, sensible exercise, self glucose monitoring, with the goal of keeping both short-term blood glucose levels, and long term levels as well, within acceptable bounds. Careful control is needed to reduce the risk of long term complications. This is theoretically achievable with combinations of diet, exercise and weight loss (type 2), various oral diabetic drugs (type 2 only), and insulin use (type 1 and increasingly for type 2 not responding to oral medications). In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications should be undertaken to control blood pressure and cholesterol by exercising more, smoking cessation, consuming an appropriate diet, wearing diabetic socks, and if necessary, taking any of several drugs to reduce pressure. Many Type 1 treatments include the combination use of regular or NPH insulin, and/or synthetic insulin analogs such as Humalog, Novolog or Apidra; the combination of Lantus/Levemir and Humalog, Novolog or Apidra. Another Type 1 treatment option is the use of the insulin pump with some of the most popular pump brands being: Cozmo, Animas, Medtronic Minimed, and Omnipod.

 

In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care of a patient in a team approach. Optometrists, podiatrists/chiropodists, dietitians, physiotherapists, clinical nurse specialists (eg, Certified Diabetes Educators and DSNs (Diabetic Specialist Nurse)), or nurse practitioners may jointly provide multidisciplinary expertise. In countries where patients must provide their own health care (i.e., the United States in the developed world), the impact of out-of-pocket costs of diabetic care can be high. In addition to the medications and supplies needed, patients are often advised to receive regular consultation from a physician (e.g., at least every three to six months).

 

 Cures for different types of diabetes

 

 Cures for type 1 diabetes

 

 

There is no practical cure now for type 1 diabetes. The fact that type 1 diabetes is due to the failure of one of the cell types of a single organ with a relatively simple function (i.e. the failure of the islets of Langerhans) has led to the study of several possible schemes to cure this form of diabetes mostly by replacing the pancreas or just the beta cells. Only those type 1 diabetics who have received either a pancreas or a kidney-pancreas transplant (often when they have developed diabetic kidney disease (i.e., nephropathy) and become insulin-independent may now be considered “cured” from their diabetes. A simultaneous pancreas-kidney transplant is a promising solution, showing similar or improved survival rates over a kidney transplant alone. Still, they generally remain on long-term immunosuppressive drugs and there is a possibility that the immune system will mount a host versus graft response against the transplanted organ.

 

Transplants of exogenous beta cells have been performed experimentally in both mice and humans, but this measure is not yet practical in regular clinical practice partly due to the limited number of beta cell donors. Thus far, like any such transplant, it has provoked an immune reaction and long-term immunosuppressive drugs have been needed to protect the transplanted tissue. An alternative technique has been proposed to place transplanted beta cells in a semi-permeable container, isolating and protecting them from the immune system. Stem cell research has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual, thus perhaps eliminating the need for immuno-suppressants. This has been done in mice, and a 2007 trial of 15 newly diagnosed patients with type 1 diabetes treated with stem cells raised from their own bone marrow after immune suppression showed that the majority did not require any insulin treatment for prolonged periods of time.

 

Microscopic or nanotechnological approaches are under investigation as well, in one proposed case with implanted stores of insulin metered out by a rapid response valve sensitive to blood glucose levels. At least two approaches have been demonstrated in vitro. These are, in some sense, closed-loop insulin pumps.

 

 Cures for type 2 diabetes

 

Type 2 has had no cure. But, very recently, it has been shown that a type of gastric bypass surgery can normalize blood glucose levels in 80-100% of severely obese patients. The effect is not due to weight loss because it usually occurs within days of surgery, which is before significant weight loss happens. The pattern of secretion of gastrointestinal hormones is changed by the bypass and removal of the duodenum and proximal jejunum, which together form the upper (proximal) part of the small intestine. The precise causal mechanisms are being intensively researched. This approach may become a standard treatment for some people with type 2 diabetes in the near future. One hypothesis is that the proximal small intestine is dysfunctional in type 2 diabetes; its removal eliminates the source of an unknown hormone that contributes to insulin resistance. This surgery has been widely performed on morbidly obese patients and has had the additional the benefit of reducing the death rate from all causes by up to 40%. A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.

 

 Prognosis

 

Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-controlled blood sugar levels. Wider health problems accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise. According to a study, women with high blood pressure have a threefold risk of developing diabetes.

 

Anecdotal evidence suggests that some of those with type 2 diabetes who exercise regularly, lose weight, and eat healthy diets may be able to keep some of the disease or some of the effects of the disease in ‘remission.’ Certainly these tips can help prevent people predisposed to type 2 diabetes and those at pre-diabetic stages from actually developing the disorder as it helps restore insulin sensitivity. However patients should talk to their doctors about this for real expectations before undertaking it (esp. to avoid hypoglycemia or other complications); few people actually seem to go into total ‘remission,’ but some may find they need less of their insulin medications since the body tends to have lower insulin requirements during and shortly following exercise. Regardless of whether it works that way or not for an individual, there are certainly other benefits to this healthy lifestyle for both diabetics and nondiabetics.

 

The way diabetes is managed changes with age. Insulin production decreases because of age-related impairment of pancreatic beta cells. Additionally, insulin resistance increases because of the loss of lean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of type 2 diabetes and post challenge hyperglycemia in the older population. Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people.  Treatment goals for older patients with diabetes vary with the individual, and take into account health status, as well as life expectancy, level of dependence, and willingness to adhere to a treatment regimen.

 

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The diagnosis of type 1 diabetes and many cases of type 2, is usually prompted by recent-onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia), and often accompanied by weight loss. These symptoms typically worsen over days to weeks; about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.

 

Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:

 

    * Fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/l).

    * Plasma glucose at or above 200 mg/dL (11.1 mmol/l) two hours after a 75 g oral glucose load as in a glucose tolerance test.

    * Random plasma glucose at or above 200 mg/dL (11.1 mmol/l).

 

A positive result, in the absence of clinical symptoms of diabetes, should be confirmed by another of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/l) is considered diagnostic for diabetes mellitus.

 

Patients with fasting glucose levels between 110 and 125 mg/dL (6.1 and 7.0 mmol/l) are considered to have impaired fasting glycemia. Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/l two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.

 

While not used for diagnosis, an elevated level of glucose irreversibly bound to hemoglobin (termed glycosylated hemoglobin or HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is <7.0%, which is considered good glycemic control, although some guidelines are stricter (<6.5%). People with diabetes who have HbA1c levels within this range have a significantly lower incidence of complications from diabetes, including retinopathy and diabetic nephropathy.

 

 Screening

 

Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. The screening test varies according to circumstances and local policy, and may be a random blood glucose test, a fasting blood glucose test, a blood glucose test two hours after 75 g of glucose, or an even more formal glucose tolerance test. Many healthcare providers recommend universal screening for adults at age 40 or 50, and often periodically thereafter. Earlier screening is typically recommended for those with risk factors such as obesity, family history of diabetes, high-risk ethnicity (Hispanic, Native American, Afro-Caribbean, Pacific Island, and South Asian ancestry).

 

Many medical conditions are associated with diabetes and warrant screening. A partial list includes: high blood pressure, elevated cholesterol levels, coronary artery disease, past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, fatty liver, hemochromatosis, cystic fibrosis, several mitochondrial neuropathies and myopathies, myotonic dystrophy, Friedreich’s ataxia, some of the inherited forms of neonatal hyperinsulinism. The risk of diabetes is higher with chronic use of several medications, including high-dose glucocorticoids, some chemotherapy agents (especially L-asparaginase), as well as some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics).

 

People with a confirmed diagnosis of diabetes are screened routinely for complications. This includes yearly urine testing for microalbuminuria and examination of the retina (retinal photography) for retinopathy. In the UK, screening for diabetic retinopathy has helped reduce the incidence of legal blindness since its implementation.[citation needed]

 

 Prevention

 

Type 1 diabetes risk is known to depend upon a genetic predisposition based on HLA types (particularly types DR3 and DR4), an unknown environmental trigger (suspected to be an infection, although none has proven definitive in all cases), and an uncontrolled autoimmune response that attacks the insulin producing beta cells. Some research has suggested that breastfeeding decreased the risk in later life; various other nutritional risk factors are being studied, but no firm evidence has been found. Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes, though the causal relationship is obscure.

 

Children with antibodies to beta cell proteins (i.e., at early stages of an immune reaction to them) but no overt diabetes, and treated with vitamin B-3 (niacin), had less than half the diabetes onset incidence in a 7-year time span as did the general population, and an even lower incidence relative to those with antibodies as above, but who received no vitamin B3.

 

Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity. The American Diabetes Association (ADA) recommends maintaining a healthy weight, getting at least 2½ hours of exercise per week (several brisk sustained walks appears sufficient), having a modest fat intake, and eating a good amount of fiber and whole grains. The ADA does not recommend alcohol consumption as a preventive, but it is interesting to note that moderate alcohol intake may reduce the risk (though heavy consumption absolutely clearly increases damage to body systems significantly). There is inadequate evidence that eating foods of low glycemic index is clinically helpful despite recommendations and suggested diets in favor.

 

There are numerous studies which suggest connections with some aspect of Type II diabetes with ingestion of certain foods or with some drugs. Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin, rosiglitazone, or valsartan. In patients on hydroxychloroquine for rheumatoid arthritis, incidence of diabetes was reduced by 77% though causal mechanisms are unclear. Breastfeeding may also be associated with the prevention of type 2 of the disease in mothers.

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Diabetic Ketoacidosis (DKA) is an acute and dangerous complication that is always a medical emergency. Lack of insulin causes the liver to turn fat into ketone bodies for use as fuel. This is normal when periodic, but can become a serious problem if sustained. Elevated levels of ketone bodies in the blood decrease the blood’s pH, leading to DKA. On presentation at hospital, the patient in DKA is typically dehydrated and breathing rapidly and deeply. Abdominal pain is common and may be severe. The level of consciousness is typically normal until late in the process, when lethargy may progress to coma. Ketoacidosis can become severe enough to cause hypotension, shock, and death. Urine analysis reveals significant levels of ketone bodies (which spill over from the blood when the kidneys filter blood) well before overt symptoms. Prompt, proper treatment usually results in full recovery, though death can result from inadequate or delayed treatment, or from complications. Nevertheless, DKA is always a medical emergency and requires medical attention. Ketoacidosis is much more common in type 1 diabetes than type 2.

 

Nonketotic hyperosmolar coma

 

Hyperosmolar nonketotic state (HNS) is an acute complication sharing many symptoms with DKA, but an entirely different cause and different treatment. In a person with very high blood glucose levels (usually considered to be above 300 mg/dl (16 mmol/l)), water is drawn out of cells into the blood by osmosis and the kidneys dump glucose into the urine. This results in loss of water and an increase in blood osmolarity. If fluid is not replaced (by mouth or intravenously), the osmotic effect of high glucose levels combined with the loss of water will eventually lead to dehydration. The body’s cells become progressively dehydrated as water is taken from them and excreted. Electrolyte imbalances are also common and dangerous. As with DKA, urgent medical treatment is necessary, especially volume replacement. Lethargy may ultimately progress to a coma, which is more common in type 2 diabetes than type 1.

 

Hypoglycemia

 

Hypoglycemia, or abnormally low blood glucose, is an acute complication of several diabetes treatments. The patient may become agitated, sweaty, and have many symptoms of sympathetic activation of the autonomic nervous system resulting in feelings similar to dread and immobilized panic. Consciousness can be altered or even lost in extreme cases, leading to coma, seizures, or even brain damage and death. In patients with diabetes, this may be caused by several factors, such as too much or incorrectly timed insulin, too much or incorrectly timed exercise (exercise decreases insulin requirements) or not enough food (specifically glucose-producing carbohydrates), but this is an over-simplification.

 

It is more accurate to note that iatrogenic hypoglycemia is typically the result of the interplay of absolute (or relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine are the primary glucose counterregulatory factors that normally prevent or rapidly correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation.

 

Furthermore, reduced sympathoadrenal responses can cause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia cause both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. In many cases (but not all), short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in most affected patients, although this is easier in theory than it is in practice.

 

In most cases, hypoglycemia is treated with sugary drinks or food. In severe cases, an injection of glucagon (a hormone with the opposite effects of insulin) or an intravenous infusion of dextrose is used for treatment, but usually only if the person is unconscious. In hospitals, intravenous dextrose is often used.

 

 Chronic complications

 

Vascular disease

 

Chronic elevation of blood glucose level leads to damage of blood vessels (angiopathy). The endothelial cells lining the blood vessels take in more glucose than normal, since they don’t depend on insulin. They then form more surface glycoproteins than normal, and cause the basement membrane to grow thicker and weaker. In diabetes, the resulting problems are grouped under “microvascular disease” (due to damage to small blood vessels) and “macrovascular disease” (due to damage to the arteries).

 

 

The damage to small blood vessels leads to a microangiopathy, which can cause one or more of the following:

 

    * Diabetic retinopathy, growth of friable and poor-quality new blood vessels in the retina as well as macular edema (swelling of the macula), which can lead to severe vision loss or blindness. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US.

    * Diabetic neuropathy, abnormal and decreased sensation, usually in a ‘glove and stocking’ distribution starting with the feet but potentially in other nerves, later often fingers and hands. When combined with damaged blood vessels this can lead to diabetic foot (see below). Other forms of diabetic neuropathy may present as mononeuritis or autonomic neuropathy. Diabetic amyotrophy is muscle weakness due to neuropathy.

    * Diabetic nephropathy, damage to the kidney which can lead to chronic renal failure, eventually requiring dialysis. Diabetes mellitus is the most common cause of adult kidney failure worldwide in the developed world.

    * Diabetic cardiomyopathy, damage to the heart, leading to diastolic dysfunction and eventually heart failure.

 

Macrovascular disease leads to cardiovascular disease, to which accelerated atherosclerosis is a contributor:

 

    * Coronary artery disease, leading to angina or myocardial infarction (”heart attack”)

    * Stroke (mainly the ischemic type)

    * Peripheral vascular disease, which contributes to intermittent claudication (exertion-related leg and foot pain) as well as diabetic foot.

    * Diabetic myonecrosis (’muscle wasting’)

 

Diabetic foot, often due to a combination of neuropathy and arterial disease, may cause skin ulcer and infection and, in serious cases, necrosis and gangrene. It is why diabetics are prone to leg and foot infections and why it takes longer for them to heal from leg and foot wounds. It is the most common cause of adult amputation, usually of toes and or feet, in the developed world.

 

Carotid artery stenosis does not occur more often in diabetes, and there appears to be a lower prevalence of abdominal aortic aneurysm. However, diabetes does cause higher morbidity, mortality and operative risks with these conditions.

 

Diabetic encephalopathy is the increased cognitive decline and risk of dementia observed in diabetes. Various mechanisms are proposed, including alterations to the vascular supply of the brain and the interaction of insulin with the brain itself.

 

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Essential Fatty Acids, or EFAs, are fatty acids that cannot be constructed within an organism from other components (generally all references are to humans) by any known chemical pathways; and therefore must be obtained from the diet. The term refers to those involved in biological processes, and not fatty acids which may just play a role as fuel. As many of the compounds created from essential fatty acids can be taken directly in the diet, it is possible that the amounts required in the diet (if any) are overestimated. It is also possible they can be underestimated as organisms can still survive in less than ideal, malnourished conditions.

There are two families of EFAs: ω-3 (or omega-3 or n-3) and ω-6 (omega-6, n-6.) Fats from each of these families are essential, as the body can convert one omega-3 to another omega-3, for example, but cannot create an omega-3 from scratch. They were originally designated as Vitamin F when they were discovered as essential nutrients in 1923. In 1930, work by Burr, Burr and Miller showed that they are better classified with the fats than with the vitamins.

Functions

In the body, essential fatty acids serve multiple functions. In each of these, the balance between dietary ω-3 and ω-6 strongly affects function.

• They are modified to make
  • the classic eicosanoids (affecting inflammation and many other cellular functions)
  • the endocannabinoids (affecting mood, behavior and inflammation)
  • the lipoxins from ω-6 EFAs and resolvins from ω-3 (in the presence of aspirin, down regulating inflammation.)
  • the isofurans, neurofurans, isoprostanes, hepoxilins, epoxyeicosatrienoin acids (EETs) and Neuroprotectin D
• They form lipid rafts (affecting cellular signaling)
• They act on DNA (activating or inhibiting transcription factors such as NFκB, which is linked to pro-inflammatory cytokine production)

 Nomenclature and terminology

Fatty acids are straight chain hydrocarbons possessing a carboxyl (COOH) group at one end. The carbon next to the carboxylate is known as α, the next carbon β, and so forth. Since biological fatty acids can be of different lengths, the last position is labeled ω, the last letter in the Greek alphabet. Since the physiological properties of unsaturated fatty acids largely depend on the position of the first unsaturation relative to the end position and not the carboxylate, the position is signified by (ω minus n). For example, the term ω-3 signifies that the first double bond exists as the third carbon-carbon bond from the terminal CH₃ end (ω) of the carbon chain. The number of carbons and the number of double bonds is also listed. ω-3 18:4 (stearidonic acid) or 18:4 ω-3 or 18:4 n-3 indicates an 18-carbon chain with 4 double bonds, and with the first double bond in the third position from the CH₃ end. Double bonds are cis and separated by a single methylene (CH₂) group unless otherwise noted. So in free fatty acid form, the chemical structure of stearidonic acid is:

 

 The essential fatty acids start with the short chain polyunsaturated fatty acids (SC-PUFA):

• ω-3 fatty acids:
  • α-Linolenic acid or ALA (18:3)
• ω-6 fatty acids: