Medifast Diet Products: Healthy, delicious, nutritionally complete Medifast meal replacement foods such as high protein, low carb, vitamin enriched shakes, bars, entres, drinks, and snacks. can help you loose up to 5 pounds a week!

Medifast products are loaded with vitamins to help you stay healthy. There is really no need to take extra vitamins while on Medifast. Medifast works.

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

We are so excited to see everyone at the luxurious Omni Orlando Resort this week for National Convention 2008! This will definitely be the largest National Convention ever, with over 730 attendees registered and ready to take their business to the next level. Get ready to be exposed to all of the fun, excitement, learning, and business-building opportunities National Convention has to offer!


What To Wear:

We know some of you have questions about what the different attires mean for each event found in the "Schedule of Events" area of the National Convention website. Please use the below descriptions as guidelines when packing for this week!

Casual is relaxed attire. This could be jeans, khakis, or whatever you wear to dress comfortably.

Casual/Active is your more comfortable clothing that you can move freely in. This could incorporate athletic shoes, lighter-weight clothing, etc.

Business Casual is a more formal casual dress. This could be slacks and a nice polo for men or slacks and a nice top for women.

Dinner Dress is a comfortable attire but more formal than Business Casual. This could be a nice dress shirt and slacks for men or a sundress for women.

Business or Formal is a formal dinner attire. For men, this could be a tux or nice suit. For ladies, this could be an evening dress or nice pant suit.

Swimwear is whatever you feel comfortable swimming in.


Workshops:

Get ready!Medifast National Convention has a wide variety of informative workshops that range from basic presentation skills to advanced business development. Whether you're a new Health Coach, a seasoned Business Coach, or even an experienced Business Leader, you and your business will benefit from these enlightening and highly specialized workshops presented by our top Business Leaders!

To check out a complete list of workshops before Medifast National Convention:

Go to www.tsflnationalconvention2008.com
Click on the "Workshop Schedule" link on the left panel.

For more information, please visit the Medifast National Convention web site. We can't wait to see you all in sunny Orlando later this week for what is sure to be the best Medifast National Convention to date!

Medifast has been around for a long time. About twenty years, actually. It is one of the few diets to be FDA inspected and has undergone rigorous studies. Medifast works and Medifast is safe.

The Weight-Loss Industry

Looking for a quick and easy way to lose weight? You're not alone. An estimated 50 million Americans will go on diets this year. And while some will succeed in taking the weight off, very few--perhaps 5 percent--will manage to keep all of it off in the long run.

One reason for the low success rate is that many people look for quick and easy solutions to their weight problems. They find it hard to believe in this age of scientific innovations and medical miracles that an effortless weight-loss method doesn't exist.

So they succumb to quick-fix claims like "Eat All You Want and Still Lose Weight!" or "Melt Fat Away While You Sleep!" And they invest their hopes (and their money) in all manner of pills, potions, gadgets, and programs that hold the promise of a slimmer, happier future.

The weight-loss business is a booming industry. Americans spend an estimated $30 billion a year on all types of diet programs and products, including diet foods and drinks. Trying to sort out all of the competing claims--often misleading, unproven, or just plain false--can be confusing and costly.

This brochure is designed to give you the facts behind the claims, to help you avoid the outright scams, and to encourage you to consider thoroughly the costs and consequences of the dieting decisions you make.

The Facts about Weight Loss

Being obese can have serious health consequences. These include an increased risk of heart disease, stroke, high blood pressure, diabetes, gallstones, and some forms of cancer. Losing weight can help reduce these risks. Here are some general points to keep in mind:

* Any claims that you can lose weight effortlessly are false. The only proven way to lose weight is either to reduce the number of calories you eat or to increase the number of calories you burn off through exercise. Most experts recommend a combination of both.

* Very low-calorie diets are not without risk and should be pursued only under medical supervision. Unsupervised very low-calorie diets can deprive you of important nutrients and are potentially dangerous.

* Fad diets rarely have any permanent effect. Sudden and radical changes in your eating patterns are difficult to sustain over time. In addition, so-called "crash" diets often send dieters into a cycle of quick weight loss, followed by a "rebound" weight gain once normal eating resumes, and even more difficulty reducing when the next diet is attempted.

* To lose weight safely and keep it off requires long-term changes in daily eating and exercise habits. Many experts recommend a goal of losing about a pound a week. A modest reduction of 500 calories per day will achieve this goal, since a total reduction of 3,500 calories is required to lose a pound of fat. An important way to lower your calorie intake is to learn and practice healthy eating habits.

In Search of the "Magic Bullet"

Some dieters peg their hopes on pills and capsules that promise to "burn," "block," "flush," or otherwise eliminate fat from the system. But science has yet to come up with a low-risk "magic bullet" for weight loss. Some pills may help control the appetite, but they can have serious side effects. (Amphetamines, for instance, are highly addictive and can have an adverse impact on the heart and central nervous system.) Other pills are utterly worthless.

The Federal Trade Commission (FTC) and a number of state Attorney General have successfully brought cases against marketers of pills claiming to absorb or burn fat. The Food and Drug Administration (FDA) has banned 111 ingredients once found in over-the-counter diet products. None of these substances, which include alcohol, caffeine, dextrose, and guar gum, have proved effective in weight-loss or appetite suppression.

Beware of the following products that are touted as weight-loss wonders:

* Diet patches, which are worn on the skin, have not been proven to be safe or effective. The FDA has seized millions of these products from manufacturers and promoters.

* "Fat blockers" purport to physically absorb fat and mechanically interfere with the fat a person eats.

* "Starch blockers" promise to block or impede starch digestion. Not only is the claim unproven, but users have complained of nausea, vomiting, diarrhea, and stomach pains.

* "Magnet" diet pills allegedly "flush fat out of the body." The FTC has brought legal action against several marketers of these pills.

* Glucomannan is advertised as the "Weight Loss Secret That's Been in the Orient for Over 500 Years." There is little evidence supporting this plant root's effectiveness as a weight-loss product.

* Some bulk producers or fillers, such as fiber-based products, may absorb liquid and swell in the stomach, thereby reducing hunger. Some fillers, such as guar gum, can even prove harmful, causing obstructions in the intestines, stomach, or esophagus. The FDA has taken legal action against several promoters containing guar gum.

* Spirulina, a species of blue-green algae, has not been proven effective for losing weight.

Phony Devices and Gadgets

Phony weight-loss devices range from those that are simply ineffective to those that are truly dangerous to your health. At minimum, they are a waste of your hard-earned money. Some of the fraudulent gadgets that have been marketed to hopeful dieters over the years include:

* Electrical muscle stimulators have legitimate use in physical therapy treatment. But the FDA has taken a number of them off the market because they were promoted for weight loss and body toning. When used incorrectly, muscle stimulators can be dangerous, causing electrical shocks and burns.

* "Appetite suppressing eyeglasses" are common eyeglasses with colored lenses that claim to project an image to the retina which dampens the desire to eat. There is no evidence these work.

* "Magic weight-loss earrings" and devices custom-fitted to the purchaser's ear that purport to stimulate acupuncture points controlling hunger have not been proven effective.

Diet Programs

Approximately 8 million Americans a year enroll in some kind of structured weight-loss program involving liquid diets, special diet regimens, or medical or other supervision. In 1991, about 8,500 commercial diet centers were in operation across the country, many of them owned by half-dozen or so well-known national companies.

Before you join such a program, you should know that according to published studies relatively few participants succeed in keeping off weight long-term. Recently, the FTC brought action against several companies challenging weight-loss and weight-maintenance claims. Unfortunately, some other companies continue to make overblown claims.

The FTC stopped one company from claiming its diet program caused rapid weight loss through the use of tablets that would "burn fat" and a protein drink mix that would adjust metabolism. The FTC also took action against three major programs using doctor-supervised, very low-calorie liquid diets, and they agreed to stop making claims unless they could back them up with hard data.

Before you sign up with a diet program, you might ask these questions:

* What are the health risks?

* What data can you show me that proves your program actually works?

* Do customers keep off the weight after they leave the diet program?

* What are the costs for membership, weekly fees, food, supplements, maintenance, and counseling? What's the payment schedule? Are any costs covered under health insurance? Do you give refunds if I drop out?

* Do you have a maintenance program? Is it part of the package or does it cost extra?

* What kind of professional supervision is provided? What are the credentials of these professionals?

* What are the program's requirements? Are there special menus or foods, counseling visits, or exercise plans?

Clues to Fraud

It is important for consumers to be wary of claims that sound too good to be true. When it comes to weight-loss schemes, consumers should be particularly skeptical of claims containing words and phrases like:

* easy
* effortless
* guaranteed
* miraculous
* magical
* breakthrough
* new discovery
* mysterious
* exotic
* secret
* exclusive
* ancient

Sensible Weight Maintenance Tips
These are also used in the Medifast plan.

Losing weight may not be effortless, but it doesn't have to be complicated. To achieve long-term results, it's best to avoid quick-fix schemes and complex regimens. Focus instead on making modest changes to your life's daily routine. A balanced, healthy diet and sensible, regular exercise are the keys to maintaining your ideal weight. Although nutrition science is constantly evolving, here are some generally-accepted guidelines for losing weight:

* Consult with your doctor, a dietician, or other qualified health professional to determine your ideal healthy body weight.

* Eat smaller portions and choose from a variety of foods.

* Load up on foods naturally high in fiber: Fruits, vegetables, legumes, and whole grains.

* Limit portions of foods high in fat: dairy products like cheese, butter, and whole milk; red meat; cakes and pastries.

* Exercise at least three times weekly.

Medifast strives to keep you abreast of changes to the Medifast field support schedule changes.
Please note that due to Medifast National Convention next week,Medifast Field Support will operate under a modified schedule, starting Monday, July 21.

Field Support will be be available to serve you next week, July 21 through July 25, from 9 a.m. to 6 p.m.

*The Medifast Client Contact Center will still operate using its usual schedule.

We appreciate your cooperation and understanding as members of Field Support join others from the Take Shape For Life Home Office and over 700 Health Coaches in sunny Orlando, FL to make National Convention 2008 the best yet!

Medifast can help you control your Adult onset diabetes. Medifast has an entire line of Diabetic products to help you.

The citric acid cycle, also known as the Krebs cycle, is a series of enzyme-catalyzed chemical reactions of central importance in all living cells that use oxygen as part of cellular respiration. In eukaryotes, the citric acid cycle occurs in the matrix of the mitochondrion. The components and reactions of the citric acid cycle were established by seminal work from both Albert Szent-Györgyi and Hans Krebs.
In aerobic organisms, the citric acid cycle is part of a metabolic pathway involved in the chemical conversion of carbohydrates, fats and proteins into carbon dioxide and water to generate a form of usable energy. Other relevant reactions in the pathway include those in glycolysis and pyruvate oxidation before the citric acid cycle and oxidative phosphorylation after it. In addition, it provides precursors for many compounds including some amino acids and is therefore functional even in cells performing fermentation.
Overview
Two carbons are oxidized to CO2, and the energy from these reactions is transferred to other metabolic processes by GTP (or ATP), and as electrons in NADH and QH2. The NADH generated in the TCA cycle may later donate its electrons in oxidative phosphorylation to drive ATP synthesis; FADH2 is covalently attached to succinate dehydrogenase, an enzyme functioning both in the TCA cycle and the mitochondrial electron transport chain in oxidative phosphorylation. FADH2 thereby facilitates transfer of electrons to coenzyme Q, which is the final electron acceptor of the reaction catalyzed by the Succinate: ubiquinone oxidoreductase complex, also acting as an intermediate in the electron transport chain.
The citric acid cycle is continuously supplied new carbons in the form of acetyl-CoA, entering at step 1 below.
Substrates Products Enzyme Reaction type Comment
1 Oxaloacetate +
Acetyl CoA +
H2O Citrate +
CoA-SH Citrate synthase Aldol condensation rate limiting stage,
extends the 4C oxaloacetate to a 6C molecule
2 Citrate cis-Aconitate +
H2O Aconitase Dehydration reversible isomerisation
3 cis-Aconitate +
H2O Isocitrate Hydration
4 Isocitrate +
NAD+ Oxalosuccinate +
NADH + H + Isocitrate dehydrogenase Oxidation generates NADH (equivalent of 2.5 ATP)
5 Oxalosuccinate α-Ketoglutarate +
CO2 Decarboxylation irreversible stage,
generates a 5C molecule
6 α-Ketoglutarate +
NAD+ +
CoA-SH Succinyl-CoA +
NADH + H+ +
CO2 α-Ketoglutarate dehydrogenase Oxidative
decarboxylation generates NADH (equivalent of 2.5 ATP),
regenerates the 4C chain (CoA excluded)
7 Succinyl-CoA +
GDP + Pi Succinate +
CoA-SH +
GTP Succinyl-CoA synthetase substrate level phosphorylation or ADP->ATP,
generates 1 ATP or equivalent
8 Succinate +
ubiquinone (Q) Fumarate +
ubiquinol (QH2) Succinate dehydrogenase Oxidation uses FAD as a prosthetic group (FAD->FADH2 in the first step of the reaction) in the enzyme,
generates the equivalent of 1.5 ATP
9 Fumarate +
H2O L-Malate Fumarase H2O addition
(hydration)
10 L-Malate+
NAD+ Oxaloacetate +
NADH + H+ Malate dehydrogenase Oxidation generates NADH (equivalent of 2.5 ATP)
Mitochondria in animals including humans possess two succinyl-CoA synthetases, one that produces GTP from GDP, and another that produces ATP from ADP. Plants have the type that produces ATP (ADP-forming succinyl-CoA synthetase).
The GTP that is formed by GDP-forming succinyl-CoA synthetase may be utilized by nucleoside-diphosphate kinase to form ATP (the catalyzed reaction is GTP + ADP -> GDP + ATP).
A simplified view of the process
• The citric acid cycle begins with acetyl-CoA transferring its two-carbon acetyl group to the four-carbon acceptor compound (oxaloacetate) to form a six-carbon compound (citrate).
• The citrate then goes through a series of chemical transformations, losing first one, then a second carboxyl group as CO2. The carbons lost as CO2 originate from what was oxaloacetate, not directly from acetyl-CoA. The carbons donated by acetyl-CoA become part of the oxaloacetate carbon backbone after the first turn of the citric acid cycle. Loss of the acetyl-CoA-donated carbons as CO2 requires several turns of the citric acid cycle. However, because of the role of the citric acid cycle in anabolism, they may not be lost since many TCA cycle intermediates are also used as precursors for the biosynthesis of other molecules.
• Most of the energy made available by the oxidative steps of the cycle is transferred as energy-rich electrons to NAD+, forming NADH. For each acetyl group that enters the citric acid cycle, three molecules of NADH are produced.
• Electrons are also transferred to the electron acceptor Q, forming QH2.
• At the end of each cycle, the four-carbon oxaloacetate has been regenerated, and the cycle continues.
Products
Products of the first turn of the cycle are: one GTP (or ATP), three NADH, one QH2, and two CO2.
Because two acetyl-CoA molecules are produced from each glucose molecule, two cycles are required per glucose molecule. Therefore, at the end of all cycles, the products are: two GTP, six NADH, two QH2, and four CO2
Description Reactants Products
The sum of all reactions in the citric acid cycle is: Acetyl-CoA + 3 NAD+ + Q + GDP + Pi + 2 H2O → CoA-SH + 3 NADH + 3 H+ + QH2 + GTP + 2 CO2
Combining the reactions occurring during the pyruvate oxidation with those occurring during the citric acid cycle, the following overall pyruvate oxidation reaction is obtained: Pyruvic acid + 4 NAD+ + Q + GDP + Pi + 2 H2O → 4 NADH + 4 H+ + QH2 + GTP + 3 CO2
Combining the above reaction with the ones occurring in the course of glycolysis, the following overall glucose oxidation reaction (excluding reactions in the respiratory chain) is obtained: Glucose + 10 NAD+ + 2 Q + 2 ADP + 2 GDP + 4 Pi + 2 H2O → 10 NADH + 10 H+ + 2 QH2 + 2 ATP + 2 GTP + 6 CO2
(the above reactions are equilibrated if Pi represents the H2PO4- ion, ADP and GDP the ADP2- and GDP2- ions, respectively, and ATP and GTP the ATP3- and GTP3- ions, respectively).
Estimates for the total number of ATP obtained after complete oxidation of one glucose in glycolysis, citric acid cycle, and oxidative phosphorylation given in the literature range from 30-38 molecules of ATP. A recent assessment of the total ATP yield obtained in these distinct reaction cycles, taking into account updated proton-to-ATP ratios, has arrived at an estimate of 29.85 ATP per glucose molecule.
Regulation
Although pyruvate dehydrogenase is not technically a part of the citric acid cycle, its regulation is included here.
The regulation of the TCA cycle is largely determined by substrate availability and product inhibition. NADH, a product of all dehydrogenases in the TCA cycle with the exception of succinate dehydrogenase, inhibits pyruvate dehydrogenase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase, and also citrate synthase. Acetyl-CoA inhibits pyruvate dehydrogenase, while succinyl-CoA inhibits succinyl-CoA synthase and citrate synthase. When tested in vitro with TCA enzymes, ATP inhibits citrate synthase and α-ketoglutarate dehydrogenase; however, ATP levels do not change more than 10% in vivo between rest and vigorous exercise. There is no known allosteric mechanism that can account for large changes in reaction rate from an allosteric effector whose concentration changes less than 10%.
Calcium is used as a regulator. It activates pyruvate dehydrogenase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase. This increases the reaction rate of many of the steps in the cycle, and therefore increases flux throughout the pathway.
Citrate is used for feedback inhibition, as it inhibits phosphofructokinase, an enzyme involved in glycolysis that catalyses formation of fructose 1,6-bisphosphate, a precursor of pyruvate. This prevents a constant high rate of flux when there is an accumulation of citrate and a decrease in substrate for the enzyme.
Recent work has demonstrated an important link between intermediates of the citric acid cycle and the regulation of hypoxia inducible factors (HIF). HIF plays a role in the regulation of oxygen homeostasis, and is a transcription factor which targets angiogenesis, vascular remodeling, glucose unitization, iron transport and apoptosis. HIF is synthesized constitutively and hydroxylation of at least one of two critical proline residues mediates their interaction with the von Hippel Lindau E3 ubiquitin ligase complex which targets them for rapid degradation. This reaction is catalyzed by prolyl 4-hydroxylases. Fumarate and succinate have been identified as potent inhibitors of prolyl hydroxylases thus leading to the stabilization of HIF.
Major metabolic pathways converging on the TCA cycle
Several catabolic pathways converge on the TCA cycle. Reactions that form intermediates of the TCA cycle in order to replenish them (especially during the scarcity of the intermediates) are called anaplerotic reactions.
The citric acid cycle is the third step in carbohydrate catabolism (the breakdown of sugars). Glycolysis breaks glucose (a six-carbon-molecule) down into pyruvate (a three-carbon molecule). In eukaryotes, pyruvate moves into the mitochondria. It is converted into acetyl-CoA by decarboxylation and enters the citric acid cycle.
In protein catabolism, proteins are broken down by protease enzymes into their constituent amino acids. The carbon backbone of these amino acids can become a source of energy by being converted to Acetyl-CoA and entering into the citric acid cycle.
In fat catabolism, triglycerides are hydrolyzed to break them into fatty acids and glycerol. In the liver the glycerol can be converted into glucose via dihydroxyacetone phosphate and glyceraldehyde-3-phosphate by way of gluconeogenesis. In many tissues, especially heart tissue, fatty acids are broken down through a process known as beta oxidation which results in acetyl-CoA which can be used in the citric acid cycle. Beta oxidation of odd chain fatty acids can yield propionyl CoA which can result in further glucose production by gluconeogenesis in the liver.
The citric acid cycle is always followed by oxidative phosphorylation. This process extracts the energy (as electrons) from NADH and QH2, oxidizing them to NAD+ and Q, respectively, so that the cycle can continue. Whereas the citric acid cycle does not use oxygen, oxidative phosphorylation does.
The total energy gained from the complete breakdown of one molecule of glucose by glycolysis, the citric acid cycle and oxidative phosphorylation equals about 30 ATP molecules, in eukaryotes. The citric acid cycle is called an amphibolic pathway because it participates in both catabolism and anabolism.

Medifast can be used successfully with Adult onset or Type II diabetes. It is not recommended for Type I Juvenile onset diabetes. Medifast has an entire line of low glycemic Diabetic products to help you lose weight. The use of these Medifast products will also help you control your blood sugar.

The term diabetes, without qualification, usually refers to diabetes mellitus, which is associated with excessive sweet urine (known as "glycosuria") but there are several rarer conditions also named diabetes. The most common of these is diabetes insipidus in which the urine is not sweet (insipidus meaning "without taste" in Latin); it can be caused by either kidney (nephrogenic DI) or pituitary gland (central DI) damage.

The principal two idiopathic forms of diabetes mellitus are known as types 1 and 2. The term "type 1 diabetes" has universally replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. Various sources have defined "type 3 diabetes" as, among others, gestational diabetes, insulin-resistant type 1 diabetes (or "double diabetes"), type 2 diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of adults (or LADA or "type 1.5" diabetes. There is also maturity onset diabetes of the young (MODY) which is a group of several single gene disorders with strong family histories that present as type 2 diabetes before 30 years of age.

Type 1 diabetes mellitus


Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas, leading to a deficiency of insulin. The main cause of this beta cell loss is a T-cell mediated autoimmune attack. There is no known preventive measure which can be taken against type 1 diabetes; it is about 10% of diabetes mellitus cases in North America and Europe (though this varies by geographical location), and is a higher percentage in some other areas. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed "juvenile diabetes" because it represents a majority of the diabetes cases in children.

The principal treatment of type 1 diabetes, even from its earliest stages, is replacement of insulin combined with careful monitoring of blood glucose levels using blood testing monitors. Without insulin, diabetic ketoacidosis often develops which may result in coma or death. Treatment emphasis is now also placed on lifestyle adjustments (diet and exercise) though these cannot reverse the progress of the disease. Apart from the common subcutaneous injections, it is also possible to deliver insulin by a pump, which allows continuous infusion of insulin 24 hours a day at preset levels, and the ability to program doses (a bolus) of insulin as needed at meal times.

Type 1 treatment must be continued indefinitely in essentially all cases. Treatment need not significantly impair normal activities, if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken. However, treatment is burdensome for patients, insulin is replaced in a non-physiological manner, and this approach is therefore far from ideal. The average glucose level for the type 1 patient should be as close to normal (80–120 mg/dl, 4–6 mmol/l) as is safely possible. Some physicians suggest up to 140–150 mg/dl (7-7.5 mmol/l) for those having trouble with lower values, such as frequent hypoglycemic events. Values above 200 mg/dl (10 mmol/l) are sometimes accompanied by discomfort and frequent urination leading to dehydration. Values above 300 mg/dl (15 mmol/l) usually require medical treatment and may lead to ketoacidosis, although they are not immediately life-threatening. However, low levels of blood glucose, called hypoglycemia, may lead to seizures or episodes of unconsciousness and absolutely must be treated immediately.

Type 2 diabetes mellitus


Type 2 diabetes mellitus is characterized differently due to insulin resistance or reduced insulin sensitivity, combined with reduced insulin secretion. The defective responsiveness of body tissues to insulin almost certainly involves the insulin receptor in cell membranes. In the early stage the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary.

There are numerous theories as to the exact cause and mechanism in type 2 diabetes. Central obesity (fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat) is known to predispose individuals for insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes. Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have had it). In the last decade, type 2 diabetes has increasingly begun to affect children and adolescents, likely in connection with the increased prevalence of childhood obesity seen in recent decades in some places.

Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no ketoacidotic episodes. However, severe long-term complications can result from unnoticed type 2 diabetes, including renal failure due to diabetic nephropathy, vascular disease (including coronary artery disease), vision damage due to diabetic retinopathy, loss of sensation or pain due to diabetic neuropathy, and liver damage from non-alcoholic steatohepatitis.

Type 2 diabetes is usually first treated by increasing physical activity, decreasing carbohydrate intake, and losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. It is sometimes possible to achieve long-term, satisfactory glucose control with these measures alone. However, the underlying tendency to insulin resistance is not lost, and so attention to diet, exercise, and weight loss must continue. The usual next step, if necessary, is treatment with oral antidiabetic drugs. Insulin production is initially only moderately impaired in type 2 diabetes, so oral medication (often used in various combinations) can be used to improve insulin production (e.g., sulfonylureas), to regulate inappropriate release of glucose by the liver and attenuate insulin resistance to some extent (e.g., metformin), and to substantially attenuate insulin resistance (e.g., thiazolidinediones). According to one study, overweight patients treated with metformin compared with diet alone, had relative risk reductions of 32% for any diabetes endpoint, 42% for diabetes related death and 36% for all cause mortality and stroke. Oral medication may eventually fail due to further impairment of beta cell insulin secretion. At this point, insulin therapy is necessary to maintain normal or near normal glucose levels.

Gestational diabetes


Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental profusion due to vascular impairment. Induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.

A 2008 study completed in the U.S. found that more American women are entering pregnancy with preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future.

Other types

There are several rare causes of diabetes mellitus that do not fit into type 1, type 2, or gestational diabetes; attempts to classify them remain controversial. Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.

Wednesday Evenings:

Stay in Shape!Medifast Maintenance Call - 8:00 p.m. Eastern (5:00 p.m. Pacific). Dial 1-512-225-9427 followed by pin code: 77421#. For the fun, interactive Stay in Shape! Maintenance Call, Lori Andersen, RN, coordinates discussions with various Masters of Weight Loss who have lost 60+ lbs. and kept the weight off for at least 4 years. Each week, Lori and her guest(s) share helpful hints and tips for everyone on the Maintenance Program. Be sure to listen and participate in this exciting, informative call.

This call is now recorded live each week! To hear the recorded playback, dial 1- 512-505-6863. The recording is posted the day following the call (Thursday morning).

Medifast Doctor's Support Call - 8:30 p.m. Eastern (5:30 p.m. Pacific). Dial 1-646-519-5860 followed by the pin code: 0971#. Listen and participate in this call, where Dr. Wayne Andersen, Medical Director and Co-Founder of Take Shape For Life, or one of his colleagues discusses current topics regarding creating a healthy weight and a physically optimal life.

This call is now recorded live each week! To hear the recorded playback, dial 1-212-461-8671. The recording is posted the day following the call (Thursday morning).

Monday Evenings:

Medifast Nurse's Support Call - 8:30 p.m. Eastern (5:30 p.m. Pacific). Dial 1-646-519-5860 followed by the pin code: 0971#. Join Lori Andersen, RN, for the weekly Medifast Nurse's Support Call. Every week, Lori provides our callers with supportive information to maximize success with their weight-loss and health goals! Be sure to listen in and participate in this inspirational call. Anyone and everyone is encouraged to participate in this call.

This call is now recorded live each week. To hear the recorded playback, dial 1-212-461-8672. The recording is posted the day following the call (Tuesday morning).

Take Shape For Life Field Leadership Call - 9:00 p.m. Eastern (6:00 p.m. Pacific). Dial 1-512-305-4638 followed by the pin code: 99662#. Led by Dr. Wayne Andersen and our Field Leaders, anyone interested in building a successful business and staying current with all that is happening with Take Shape For Life needs to listen in and participate in this incredible call!

This call is now recorded live each week. To hear the recorded playback, dial 1-512-505-6854. The recording is posted the day following the call (Tuesday morning).

The Medifast diet induces a state of ketosis by limiting calories and utilizing a moderately high protein intake. Medifast allows you to lose from three to five pounds weekly using this very low calorie approach. The state of ketosis induced by the Medifast diet is mild.

Ketosis is a state in metabolism occurring when the liver excessively converts fat into fatty acids and ketone bodies which can be used by the body for energy.
Adipose tissue consists of highly specialized cells which store energy in the form of a triglyceride and release it upon hydrolysis in a process known as lipolysis, yielding three fatty acids and one glycerol molecule. These ketone bodies are a by-product of the lipid metabolic pathway after the fat is converted to energy. Ketoacidosis, by contrast, is the accumulation of excessive keto acids in the blood stream (specifically acetoacetate and beta-hydroxy butyrate).
Metabolic pathways
Most medical resources regard ketosis as a physiological state associated with chronic starvation. Glucose is regarded as the preferred energy source for all cells in the body with ketosis being regarded as a crisis reaction of the body to a lack of carbohydrates in the diet. In recent years this viewpoint, both the body's preference for glucose and the dangers associated with ketosis, has been challenged by some doctors.
Ketone bodies, from the breakdown of fatty acids to acetyl groups, are also produced during this state, and are burned throughout the body. Excess ketone bodies will slowly decarboxylate into acetone. That molecule is excreted in the breath and urine. When glycogen stores are not available in the cells (glycogen is primarily created when carbohydrates such as starch and sugar are consumed in the diet), fat (triacylglycerol) is cleaved to give 3 fatty acid chains and 1 glycerol molecule in a process called lipolysis. Most of the body is able to utilize fatty acids as an alternative source of energy in a process where fatty acid chains are cleaved to form acetyl-CoA, which can then be fed into the Krebs cycle. During this process a high concentration of glucagon is present in the serum and this inactivates hexokinase and phosphofructokinase-1 (regulators of glycolysis) indirectly, causing most cells in the body to use fatty acids as their primary energy source. At the same time, glucose is synthesized in the liver from lactic acid, glucogenic amino acids, and glycerol, in a process called gluconeogenesis. This glucose is used exclusively for energy by cells such as neurons and red blood cells.
Similar conditions
Ketosis should not be confused with ketoacidosis (diabetic ketoacidosis or the less common alcoholic ketoacidosis), which is severe ketosis causing the pH of the blood to drop below 7.2. Ketoacidosis is a medical condition usually caused by diabetes and accompanied by dehydration, hyperglycemia, ketonuria and increased levels of glucagon. The high glucagon, low insulin serum levels signals the body to produce more glucose via gluconeogenesis and glycogenolysis, and ketone bodies via ketogenesis. High levels of glucose causes the failure of tubular reabsorption in the kidneys, causing water to leak into the tubules in a process called osmotic diuresis, causing dehydration and further exacerbating the acidosis.
Diet
If the diet is changed from a highly glycemic diet to a diet that does not substantially contribute to blood glucose, the body goes through a set of stages to enter ketosis. During the initial stages of this process the adult brain does not burn ketones, however the brain makes immediate use of this important substrate for lipid synthesis in the brain. After about 48 hours of this process, the brain starts burning ketones in order to more directly utilize the energy from the fat stores that are being depended upon, and to reserve the glucose only for its absolute needs, thus avoiding the depletion of the body's protein store in the muscles.
Whether ketosis takes place can be checked by using special urine test strips such as Ketostix.
Deliberately induced ketosis through a low-carbohydrate diet has been used to treat medical conditions although most such treatments remain controversial.

Remember, Medifast works!

It's not too late to register for the Medifast National convention!
If you're serious about your Take Shape For Life business, RIGHT NOW! is the time to secure your attendance for what is guaranteed to be our most successful, unforgettable Medifast National Convention ever! You will be exposed to all of the fun, excitement, learning, and business-building opportunities Medifast National Convention has to offer.

Taking place at the luxurious Omni Orlando Resort,Medifast National Convention 2008 will feature:

Countless educational opportunities
Excellent workshops taught by elite Field Leaders
Unforgettable team building and networking with other Health Coaches
Exciting recognition activities
and so much more!
To sign up to attend or to learn more, visit the National Convention Web site or call the Client Contact Center at 1-800-572-4417!

Correction:
The dress for Wednesday's Advanced Regional Leadership Training has changed from "Ready for Executive Director Experience" to Casual. Attendees of this event will have plenty of time to return to their rooms and change into their "Dinner Dress" before the Executive Director Experience.

We encourage all attendees of this event to make a note and prepare their attire accordingly! Please visit the Schedule of Events for information (including attire) for each National Convention event!

We can't wait to see you all next week at the breathtaking Omni Orlando Resort!

New Number for Recorded Playback of Medifast Nurse's Support Call



Note: The number for the Monday Medifast Nurse's Support Call Recorded Playback has been changed to 212-461-8672.

Join Lori Andersen, RN, for the recorded playback of the weekly Medifast Nurse's Support Call. Every week, Lori provides our callers with supportive information to maximize success with their weight-loss and health goals!

See the Support Call Schedule at the bottom of this email for more information on the Nurse's Support Call and other beneficial weekly calls!

Medifast helps you to obtain the essential fatty acids while losing weight! Medifast supplies all the necessary protein on a daily basis. All Medifast products are also loaded with vitamins for your health.

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
o the classic eicosanoids (affecting inflammation and many other cellular functions)
o the endocannabinoids (affecting mood, behavior and inflammation)
o the lipoxins from ω-6 EFAs and resolvins from ω-3 (in the presence of aspirin, down regulating inflammation.)
o 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:
o α-Linolenic acid or ALA (18:3)
• ω-6 fatty acids:
o Linoleic acid or LA (18:2)
These two fatty acids cannot be synthesized by humans, as humans lack the desaturase enzymes required for their production.
They form the starting point for the creation of longer and more desaturated fatty acids, which are also referred to as long-chain polyunsaturated fatty acids (LC-PUFA):
• ω-3 fatty acids:
o eicosapentaenoic acid or EPA (20:5)
o docosahexaenoic acid or DHA (22:6)
• ω-6 fatty acids:
o gamma-linolenic acid or GLA (18:3)
o dihomo-gamma-linolenic acid or DGLA (20:3)
o arachidonic acid or AA (20:4)
ω-9 fatty acids are not essential in humans, because humans generally possess all the enzymes required for their synthesis. Exceptions do occur in older people or people with a liver problem that do not completely produce a sufficient amount, and hence many supplement companies market Omega 3-6-9 blends.
Essentiality
Between 1930 and 1950, arachidonic acid and linolenic acid were termed 'essential' because each was more or less able to meet the growth requirements of rats given fat-free diets. Further research has shown that human metabolism requires both ω-3 and ω-6 fatty acids. To some extent, any ω-3 and any ω-6 can relieve the worst symptoms of fatty acid deficiency. Particular fatty acids are still needed at critical life stages (e.g. lactation) and in some disease states. In nonscientific writing, common usage is that the term essential fatty acid comprises all the ω-3 or -6 fatty acids. Authoritative sources include the whole families, without qualification. The human body can make some long-chain PUFA (arachidonic acid, EPA and DHA) from lineolate or lineolinate.
Traditionally speaking the LC-PUFA are not essential. See (Cunnane 2003) for a discussion of the current status of the term 'essential'. Because the LC-PUFA are sometimes required, they may be considered "conditionally essential", or not essential to healthy adults.
Mary G. Enig has pointed out numerous studies showing the need for omega-3 and omega-6 essential fatty acids in mammalians A 2005 study has shown evidence that gamma-linolenic acid, GLA, a product of omega-6, has been shown to inhibit the breast cancer promoting gene of Her2/neu.
Biologist Ray Peat has pointed out flaws in the studies purportedly showing the need for n-3 and n-6 fats. He notes that so-called EFA deficiencies have sometimes been reversed by adding B vitamins or a fat-free liver extract to the diet. In his view, 'the optional dietary level of the "essential fatty acids" might be close to zero, if other dietary factors were also optimized.'
Essential fatty acids should not be confused with essential oils, which are "essential" in the sense of being a concentrated essence.
Food sources
Almost all the polyunsaturated fat in the human diet is from EFA. Some of the food sources of ω-3 and ω-6 fatty acids are fish and shellfish, flaxseed (linseed), hemp oil, soy oil, canola (rapeseed) oil, chia seeds, pumpkin seeds, sunflower seeds, leafy vegetables, and walnuts.
Essential fatty acids play a part in many metabolic processes, and there is evidence to suggest that low levels of essential fatty acids, or the wrong balance of types among the essential fatty acids, may be a factor in a number of illnesses, including osteoporosis.
Plant sources of ω-3 contain neither eicosapentaenoic acid (EPA) nor docosahexaenoic acid (DHA). The human body can (and in case of a purely vegetarian diet often must, unless certain algae or supplements derived from them are consumed) convert α-linolenic acid (ALA) to EPA and subsequently DHA. This however requires more metabolic work, which is thought to be the reason that the absorption of essential fatty acids is much greater from animal rather than plant sources (see Fish and plants as a source of Omega-3 for more).
The IUPAC Lipid Handbook provides a very large and detailed listing of fat contents of animal and vegetable fats, including ω-3 and -6 oils. The National Institutes of Health's EFA Education group publishes 'Essential Fats in Food Oils.' This lists 40 common oils, more tightly focused on EFAs and sorted by n-6:3 ratio. Stuchlik and Zak, 'Vegetable Lipids as Components of Functional Food list notable vegetable sources of EFAs as well as commentary and an overview of the biosynthetic pathways involved. Users can interactively search at Nutrition Data for the richest food sources of particular EFAs or other nutrients. Careful readers will note that these sources are not in excellent agreement. EFA content of vegetable sources varies with cultivation conditions. Animal sources vary widely, both with the animal's feed and that the EFA makeup varies markedly with fats from different body parts.
Human health
Almost all the polyunsaturated fats in the human diet are EFAs. Essential fatty acids play an important role in the life and death of cardiac cells.

Remember, Medifast works!

The use of the Medifast Diabetic line in a weight loss program can help you lose weight quickly and prevent and possibly cure Adult Onset Diabetes that is caused by excess weight. These Medifast products are low glycemic and help you control your blood sugar.

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.

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.

Medifast Diabetic line helps prevent many of the complications of diabetes. The Medifast plan allows you to control your blood sugar and lose weight at the same time. Losing weight with the Medifast Diabetic line is safe and easy.

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.

Medifast offers an entire line of meal replacements specific to diabetes. All the Medifast Diabetic line is low glycemic and well tested in studies. These Medifast products have complete nutritional and vitamin content.

The classical triad of diabetes symptoms is polyuria, polydipsia and polyphagia, which are, respectively, frequent urination; increased thirst and consequent increased fluid intake; and increased appetite. Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes the symptoms develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled.

When the glucose concentration in the blood is raised beyond the renal threshold, reabsorption of glucose in the proximal renal tubule is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits the reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells, causing dehydration and increased thirst.

Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change whereas type 2 is generally more gradual, but should still be suspected.

Patients (usually with type 1 diabetes) may also present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires hospital admission.

A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a vicious circle in regard to the water loss.

Genetics

Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by some (mainly viral) infections, or in a less common group, by stress or environmental exposure (such as exposure to certain chemicals or drugs). There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic "self" identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger. A small proportion of people with type 1 diabetes carry a mutated gene that causes maturity onset diabetes of the young (MODY).

There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Candidate genes include KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), which encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7–like 2), which regulates proglucagon gene expression and thus the production of glucagon-like peptide-1. Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.

Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.

Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbable glucose. The chief trigger is a rise in blood glucose levels after eating
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbable glucose. The chief trigger is a rise in blood glucose levels after eating

Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.

Much of the carbohydrate in food is converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.

Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).

If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.

Diabetes Mellitus, often referred to simply as diabetes is a syndrome characterized by disordered metabolism and abnormally high blood sugar (hyperglycemia) resulting from insufficient levels of the hormone insulin. The characteristic symptoms are excessive urine production (polyuria) due to high blood glucose levels, excessive thirst and increased fluid intake (polydipsia) attempting to compensate for increased urination, blurred vision due to high blood glucose effects on the eye's optics, unexplained weight loss, and lethargy. These symptoms are likely to be less apparent if the blood sugar is only mildly elevated.

The World Health Organization recognizes three main forms of diabetes mellitus: type 1, type 2, and gestational diabetes (occurring during pregnancy) which have different causes and population distributions. While, ultimately, all forms are due to the beta cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia, the causes are different. Type 1 diabetes is usually due to autoimmune destruction of the pancreatic beta cells. Type 2 diabetes is characterized by insulin resistance in target tissues. This causes a need for abnormally high amounts of insulin and diabetes develops when the beta cells cannot meet this demand. Gestational diabetes is similar to type 2 diabetes in that it involves insulin resistance; the hormones of pregnancy can cause insulin resistance in women genetically predisposed to developing this condition.

Gestational diabetes typically resolves with delivery of the child, however types 1 and 2 diabetes are chronic conditions. All types have been treatable since insulin became medically available in 1921. Type 1 diabetes, in which insulin is not secreted by the pancreas, is directly treatable only with injected insulin, although dietary and other lifestyle adjustments are part of management. Type 2 may be managed with a combination of dietary treatment, tablets and injections and, frequently, insulin supplementation. While insulin was originally produced from natural sources such as porcine pancreas, most insulin used today is produced through genetic engineering, either as a direct copy of human insulin, or human insulin with modified molecules that provide different onset and duration of action. Insulin can also be delivered continuously by a specialized pump which subcutaneously provides insulin through a changeable catheter.

Diabetes can cause many complications. Acute complications (hypoglycemia, ketoacidosis, or nonketotic hyperosmolar coma) may occur if the disease is not adequately controlled. Serious long-term complications include cardiovascular disease (doubled risk), chronic renal failure, retinal damage (which can lead to blindness), nerve damage (of several kinds), and microvascular damage, which may cause impotence and poor healing. Poor healing of wounds, particularly of the feet, can lead to gangrene, which may require amputation. Adequate treatment of diabetes, as well as increased emphasis on blood pressure control and lifestyle factors (such as not smoking and keeping a healthy body weight), may improve the risk profile of most aforementioned complications. In the developed world, diabetes is the most significant cause of adult blindness in the non-elderly and the leading cause of non-traumatic amputation in adults, and diabetic nephropathy is the main illness requiring renal dialysis in the United States.

Great news, the TSFL tracking study is successfully underway and we appreciate the tremendous response and support our Health Coaches have shown towards it.

We are still looking for both Health Coaches, and Medifast Clients who are looking to become Health Coaches, to participate in the study. This is a tremendous opportunity for us all to prove the value of a Take Shape For Life Health Coach in long-term weight-loss.

Earn up to $205 just by completing questionnaires!

The study involves completing a number of online questionnaires over a span of 6 ⅓ years. Health Coaches and Medifast Clients will be paid for participating in the study, and may continue with the study even if they decide to stop participating in the weight loss program.


Interested or know someone who would be? Go to http://www.success-study.com/signup/ to complete the Screening Survey. After completing the Screening Survey, eligible participants will be emailed a copy of the consent form. Participants MUST sign and mail the consent form in order to participate in the study. We can't stress this vital step enough.

We appreciate your endless support and we know that we can count on your participation in this monumental study that will further establish the value and effectiveness of Take Shape For Life!

Medifast National Convention Attire:

We know some of you have questions about what the different attires mean for each event found in the Schedule of Events area of the Medifast National Convention website. Below is an explanation and examples of each dress type so that you can start laying out your National Convention wardrobe now!

Casual is your everyday dress. This could be jeans, khakis, or whatever you wear on a normal day.

Casual/Active is your more comfortable clothing that you can move freely in. This could incorporate athletic shoes, lighter-weight clothing, etc.

Business Casual is a more formal casual dress. This could be slacks and a nice polo for men or slacks and a nice top for women.

Dinner Dress is a comfortable attire but more formal than Business Casual. This could be a nice dress shirt and slacks for men or a sundress for women.

Business or Formal is a formal dinner attire. For men, this could be a tux or nice suit. For ladies, this could be an evening dress or nice pant suit.

Swimwear is whatever you feel comfortable swimming in.

Ready for Executive Director Experience - Since you will not have time to change between the Advanced Regional Leadership Training and the Executive Director Experience, we

On Wednesday Evenings from Medifast


Stay in Shape! Maintenance Call - 8:00 p.m. Eastern (5:00 p.m. Pacific). Dial 1-512-225-9427 followed by pin code: 77421#. For the fun, interactive Medifast Stay in Shape! Maintenance Call, Lori Andersen, RN, coordinates discussions with various Masters of Weight Loss who have lost 60+ lbs. and kept the weight off for at least 4 years. Each week, Lori and her guest(s) share helpful hints and tips for everyone on the Maintenance Program. Be sure to listen and participate in this exciting, informative call.

This call is now recorded live each week! Please call 1- 512-505-6863 to listen to this call if you are unable to participate in the live call. The recording is posted the day following the call (Thursday morning).


Doctor's Support Call - 8:30 p.m. Eastern (5:30 p.m. Pacific). Dial 1-646-519-5860 followed by the pin code: 0971#. Listen and participate in this call, where Dr. Wayne Andersen, Medical Director and Co-Founder of Take Shape For Life, or one of his colleagues discusses current topics regarding creating a healthy weight and a physically optimal life.

To hear the recorded playback, dial 1-212-461-8671. The recording is posted the day following the call (Thursday morning).



Monday Evenings from Medifast


Medifast Nurse's Support Call - 8:30 p.m. Eastern (5:30 p.m. Pacific). Dial 1-646-519-5860 followed by the pin code: 0971#. This call is now recorded live each week! Please call 1-212-461-8672 to listen to the recorded playback. The recording is posted the day following the call (Tuesday morning).

Join Lori Andersen, RN, for the weekly Medifast Nurse's Support Call. Every week, Lori provides our callers with supportive information to maximize success with their weight-loss and health goals! Be sure to listen in and participate in this inspirational call. Anyone and everyone is encouraged to participate in this call.


Take Shape for Life Field Leadership Call - 9:00 p.m. Eastern (6:00 p.m. Pacific). Dial 1-512-305-4638 followed by the pin code: 99662#. Led by Dr. Wayne Andersen and our Field Leaders, anyone interested in building a successful business and staying current with all that is happening with Take Shape For Life needs to listen in and participate in this incredible call! This call is now recorded live each week. Please call 1-512-505-6854 to listen to the recorded playback. The recording is posted the day following the call (Tuesday morning).

An essential amino acid or indispensable amino acid is an amino acid that cannot be synthesized de novo by the organism (usually referring to humans), and therefore must be supplied in the diet. Medifast prducsts contains many essential amino acids.

Essentiality vs. conditional essentiality in humans
Nine amino acids are generally regarded as essential for humans: phenylalanine, valine, threonine, tryptophan, isoleucine, methionine, histidine, leucine, and lysine. Arginine is required by infants and growing kids. They are called essential not because they are more important to life than the others, but because the body does not synthesize them, making it essential to include them in one's diet in order to obtain them. In addition, the amino acids arginine, cysteine, glycine, glutamine and tyrosine are considered conditionally essential, meaning they are not normally required in the diet, but must be supplied exogenously to specific populations that do not synthesize it in adequate amounts. An example would be with the disease phenylketonuria (PKU). Individuals living with PKU must keep their intake of phenylalanine extremely low to prevent mental retardation and other metabolic complications. However, phenylalanine is the precursor for tyrosine synthesis. Without phenylalanine, tyrosine cannot be made and so tyrosine becomes essential in the diet of PKU patients.
Which amino acids are essential varies from species to species, as different metabolisms are able to synthesize different substances. For instance, taurine (which is not, by strict definition, an amino acid) is essential for cats, but not for dogs. Thus, dog food is not nutritionally sufficient for cats, and taurine is added to commercial cat food when the base ingredients do not meet the requirements of the cat, but not to dog food.
The distinction between essential and non-essential amino acids is somewhat unclear, as some amino acids can be produced from others. The sulfur-containing amino acids, methionine and homocysteine, can be converted into each other but neither can be synthesized de novo in humans. Likewise, cysteine can be made from homocysteine but cannot be synthesized on its own. So, for convenience, sulfur-containing amino acids are sometimes considered a single pool of nutritionally-equivalent amino acids. Likewise arginine, ornithine, and citrulline, which are interconvertible by the urea cycle, are considered a single group.
Recommended daily amounts
The following table lists the recommended daily amounts for essential amino acids in humans, together with their standard one-letter abbreviations. In some cases, humans can use either of two amino acids, so only the total matters.
Amino acid WHO-recommended daily intake for
human adults, mg per kg body weight mg per 70 kg
F Phenylalanine
+ Y Tyrosin 14 (total) 980
L Leucine 14 980
M Methionine
+ C Cysteine 13 (total) 910
K Lysine 12 840
I Isoleucine 10 700
V Valine 10 700
T Threonine 7 490
W Tryptophan 3 245
H Histidine unknown, 28 in infants (? sum with arginine) (? 1960)
R Arginine unknown, required for infants, maybe seniors (?)
Taurine may be necessary to preserve arterial and collagen pliability at 2 mg/kg/day, small but needed (142 mg/day per 70 kg human).
Use of essential amino acids
Foodstuffs that lack essential amino acids are poor sources of protein equivalents, as the body tends to deaminate the amino acids obtained, converting proteins into fats and carbohydrates. Therefore, a balance of essential amino acids is necessary for a high degree of net protein utilization, which is the mass ratio of amino acids converted to proteins to amino acids supplied.
All essential amino acids may be obtained from plant sources, and even strict vegetarian diets can provide all dietary requirements, provided they are based on a variety of whole plant foods. Some believe that careful monitoring of nutrient levels is important in strict vegetarian diets, but there are virtually no cases of protein-deficiency among populations consuming adequate calories. The only common cases of protein-deficiency occur among populations that are chronically undernourished. On the Medifast diet you can be assured that you are getting good nutrition.
Complete proteins contain a balanced set of essential amino acids for humans. Animal sources such as meat, poultry, eggs, fish, milk, and cheese provide all of the essential amino acids. Complete proteins are also found in some plant sources such as spirulina, quinoa, soy, buckwheat, hempseed, and amaranth, among others.
The net protein utilization is profoundly affected by the limiting amino acid content (the essential amino acid found in the smallest quantity in the foodstuff), and somewhat affected by salvage of essential amino acids in the body. It is therefore a good idea to mix foodstuffs that have different weaknesses in their essential amino acid distributions. This limits the loss of nitrogen through deamination and increases overall net protein utilization.
Protein source Limiting amino acid
Wheat lysine
Rice lysine
Legumes tryptophan
Maize lysine and tryptophan
Pulses methionine (or cysteine)
Beef
phenylalanine (or tyrosine)
Egg, chicken none; the reference for absorbable protein
Milk or Whey, bovine methionine (or cysteine)
Mnemonics
Using the one letter designation shown above, mnemonic devices have been developed for students wanting or needing to memorize the essential amino acids. Previous devices have utilized the first letter of the amino acids name, and in general did not include arginine which is not always essential. One mnemonic device that has been used in the past is PVT TIM HALL.
Another method uses the first letter of each essential amino acid to begin each word in a phrase, such as: "Any Help in Learning These Little Molecules Proves Truly Valuable." This method begins with the two amino acids that need some qualifications as to their requirements.
Note that these devices work by using the first letter of the actual amino acids name. Due to repetition of letters, several amino acids have one letter abbreviations that are different than their first letter (e.g. lysine is K). Thus the complete list of essential amino acids utilizing one-letter codes is MILKVWTHFR.
A mnemonic that involves only the true one-letter codes for each amino acid is: "I Have Received Much Kudos for Learning These Very Well," for IHRMKFLTVW.