Weight Loss Camp - Weight Loss Camp Adults

A weight loss camp, weight loss resort, retreat, or holiday, is a type of residential program where people who are overweight or obese go to lose weight through exercise and lifestyle changes. In common parlance the term "fat camp" is also often used (either humorously or pejoratively) to refer to these programs. Weight loss camps typically provide nutrition classes, weekly weigh-ins, and a variety of classes and activities designed for weight loss.

The goal of the camps is to enhance the health of the campers, help them lose weight, raise their self-confidence and self-image, as well as teach them healthy life skills and choices. These camps provide weight-loss results of two to five pounds per week on average. However, the more overweight the camper, the more they generally lose in these programs. The effectiveness of these summer camps varies widely and usually depends on the quality of the individual program and biochemistry of the attending campers.

Newer programs not only focus on weight loss, but also on changing behavior through a combination of training on self-regulatory behaviors and cognitive-behavioral therapy (CBT) to ensure that weight loss persists long after campers return home. Most experts believe these are key elements of an effective program.

A number of weight loss camps are currently in operation in the United States, Canada, and throughout Europe. These camps vary greatly in terms of the methods used and outcomes (both long-term and short-term) experienced by campers. Some attendees experience long-term changes in health and physical fitness, while others gradually or immediately go back to overeating. One of the main determining factors appears to be support from other family members and friends.

In an effort to help maintain post-camp weight loss, some camps now offer more one-on-one training and/or nutritional counseling and life coaching as a way to educate and motivate long-term success.

6 Types of Weight Loss Camps for Adults



See also

  • Fitness boot camp
  • Wellspring camps
  • Heavyweights
  • Fat Camp: An MTV Docs Movie Presentation
  • Fat Camp (South Park)


References



External links

  • Parents turn to fat camps for obesity solution, ABC
  • America's Growing Waistline, WireTap Magazine
  • Getting Physical: A different kind of summer camp aims to shape winners for life Seattle Times
  • Fat camp provides you lose weight through ercercise and change your lifestyle.


Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



2 komentar :

Weight Loss Camp - How To Start A Weight Loss Program

A weight loss camp, weight loss resort, retreat, or holiday, is a type of residential program where people who are overweight or obese go to lose weight through exercise and lifestyle changes. In common parlance the term "fat camp" is also often used (either humorously or pejoratively) to refer to these programs. Weight loss camps typically provide nutrition classes, weekly weigh-ins, and a variety of classes and activities designed for weight loss.

The goal of the camps is to enhance the health of the campers, help them lose weight, raise their self-confidence and self-image, as well as teach them healthy life skills and choices. These camps provide weight-loss results of two to five pounds per week on average. However, the more overweight the camper, the more they generally lose in these programs. The effectiveness of these summer camps varies widely and usually depends on the quality of the individual program and biochemistry of the attending campers.

Newer programs not only focus on weight loss, but also on changing behavior through a combination of training on self-regulatory behaviors and cognitive-behavioral therapy (CBT) to ensure that weight loss persists long after campers return home. Most experts believe these are key elements of an effective program.

A number of weight loss camps are currently in operation in the United States, Canada, and throughout Europe. These camps vary greatly in terms of the methods used and outcomes (both long-term and short-term) experienced by campers. Some attendees experience long-term changes in health and physical fitness, while others gradually or immediately go back to overeating. One of the main determining factors appears to be support from other family members and friends.

In an effort to help maintain post-camp weight loss, some camps now offer more one-on-one training and/or nutritional counseling and life coaching as a way to educate and motivate long-term success.

11 Things To Do Before You Start a Weight Loss Program - Babble



See also

  • Fitness boot camp
  • Wellspring camps
  • Heavyweights
  • Fat Camp: An MTV Docs Movie Presentation
  • Fat Camp (South Park)


References

11 Things To Do Before You Start a Weight Loss Program - Babble


External links

  • Parents turn to fat camps for obesity solution, ABC
  • America's Growing Waistline, WireTap Magazine
  • Getting Physical: A different kind of summer camp aims to shape winners for life Seattle Times
  • Fat camp provides you lose weight through ercercise and change your lifestyle.


Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



0 komentar :

Weight Loss Camp - Weight Loss Tricks And Tips

A weight loss camp, weight loss resort, retreat, or holiday, is a type of residential program where people who are overweight or obese go to lose weight through exercise and lifestyle changes. In common parlance the term "fat camp" is also often used (either humorously or pejoratively) to refer to these programs. Weight loss camps typically provide nutrition classes, weekly weigh-ins, and a variety of classes and activities designed for weight loss.

The goal of the camps is to enhance the health of the campers, help them lose weight, raise their self-confidence and self-image, as well as teach them healthy life skills and choices. These camps provide weight-loss results of two to five pounds per week on average. However, the more overweight the camper, the more they generally lose in these programs. The effectiveness of these summer camps varies widely and usually depends on the quality of the individual program and biochemistry of the attending campers.

Newer programs not only focus on weight loss, but also on changing behavior through a combination of training on self-regulatory behaviors and cognitive-behavioral therapy (CBT) to ensure that weight loss persists long after campers return home. Most experts believe these are key elements of an effective program.

A number of weight loss camps are currently in operation in the United States, Canada, and throughout Europe. These camps vary greatly in terms of the methods used and outcomes (both long-term and short-term) experienced by campers. Some attendees experience long-term changes in health and physical fitness, while others gradually or immediately go back to overeating. One of the main determining factors appears to be support from other family members and friends.

In an effort to help maintain post-camp weight loss, some camps now offer more one-on-one training and/or nutritional counseling and life coaching as a way to educate and motivate long-term success.




See also

  • Fitness boot camp
  • Wellspring camps
  • Heavyweights
  • Fat Camp: An MTV Docs Movie Presentation
  • Fat Camp (South Park)


References

Tricks for Easy Weight Loss | Health Supplement Facts & Reviews


External links

  • Parents turn to fat camps for obesity solution, ABC
  • America's Growing Waistline, WireTap Magazine
  • Getting Physical: A different kind of summer camp aims to shape winners for life Seattle Times
  • Fat camp provides you lose weight through ercercise and change your lifestyle.


Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



0 komentar :

Metformin - Diabetes Medication For Weight Loss

Metformin (BAN, USAN and INN, pronounced /m?t'f?rm?n/, met-FAWR-min; sold as Glucophage) is an oral antidiabetic drug in the biguanide class. It is the first-line drug of choice for the treatment of type 2 diabetes, in particular, in overweight and obese people and those with normal kidney function. Its use in gestational diabetes has been limited by safety concerns. It is also used in the treatment of polycystic ovary syndrome, and has been investigated for other diseases where insulin resistance may be an important factor. Metformin works by suppressing glucose production by the liver.

Limited evidence suggests metformin may prevent the cardiovascular and possibly the cancer complications of diabetes. It helps reduce LDL cholesterol and triglyceride levels and is not associated with weight gain; in some people, it promotes weight loss. Metformin is one of only two oral antidiabetics in the World Health Organization Model List of Essential Medicines (the other being glibenclamide).

Metformin causes few adverse effects when prescribed appropriately (the most common is gastrointestinal upset) and has been associated with a low risk of having a low blood sugar. Lactic acidosis (a buildup of lactate in the blood) can be a serious concern in overdose and when it is prescribed to people with contraindications, but otherwise, no significant risk exists.

First synthesized and found to reduce blood sugar in the 1920s, metformin was forgotten for the next two decades as research shifted to insulin and other antidiabetic drugs. Interest in metformin was rekindled in the late 1940s after several reports that it could reduce blood sugar levels in people, and in 1957, French physician Jean Sterne published the first clinical trial of metformin as a treatment for diabetes. It was introduced to the United Kingdom in 1958, Canada in 1972, and the United States in 1995. Metformin is now believed to be the most widely prescribed antidiabetic drug in the world; in the United States alone, more than 48 million prescriptions were filled in 2010 for its generic formulations.

Medication, lifestyle changes slow diabetes progression in at-risk ...



Medical uses

Metformin is primarily used for type 2 diabetes, but is increasingly being used in polycystic ovary syndrome, non-alcoholic fatty liver disease (NAFLD) and premature puberty, three other diseases that feature insulin resistance; these indications are still considered experimental. The benefit of metformin in NAFLD has not been extensively studied and may be only temporary; although some randomized controlled trials have found significant improvement with its use, the evidence is still insufficient.

Type 2 diabetes

The American Diabetes Association recommends metformin as a first-line agent to treat type 2 diabetes.

Efficacy

The UK Prospective Diabetes Study, a large clinical trial performed in 1980-90s, provided evidence that metformin reduced the rate of adverse cardiovascular outcomes in overweight patients with type 2 diabetes relative to other antihyperglycemic agents. However, accumulated evidence from other and more recent trials has reduced confidence in the efficacy of metformin for cardiovascular disease prevention. Treatment guidelines for major professional associations including the European Association for the Study of Diabetes, the European Society for Cardiology, and the American Diabetes Association, now describe evidence for the cardiovascular benefits of metformin as equivocal. According to the American College of Physicians in 2012, low-quality evidence indicates metformin monotherapy is associated with lower cardiovascular mortality than sulfonylurea monotherapy and metformin monotherapy is associated with fewer cardiovascular events than metformin-sulfonylurea combination therapy. Evidence for other comparisons is described as unclear. A 2014 Cochrane review found tentative evidence that people treated with sulfonylureas have fewer non-fatal cardiovascular events than those treated with metformin (RR 0.67, 95% CI 0.48 to 0.93) but a higher risk of severe hypoglycemia (RR 5.64, 95% CI 1.22 to 26.00). There was not enough data available to determine the relative risk of mortality or of cardiovascular mortality.

Metformin has little or no effect on body weight compared with placebo in type 2 diabetes, although it causes weight loss compared with sulfonylureas, since sulfonylureas are associated with weight gain. There is some limited evidence that metformin may be associated with weight loss in obesity in the absence of diabetes. Metformin has a lower risk of hypoglycemia than the sulfonylureas, although hypoglycemia has uncommonly occurred during intense exercise, calorie deficit, or when used with other agents to lower blood glucose. Metformin modestly reduces LDL and triglyceride levels.

Prediabetes

Metformin treatment of people at risk for type 2 diabetes may decrease their chances of developing the disease, although intensive physical exercise and dieting work significantly better for this purpose. In a large U.S. study known as the Diabetes Prevention Program, participants were divided into groups and given either placebo, metformin, or lifestyle intervention, and followed for an average of three years. The intensive program of lifestyle modifications included a 16-lesson training on dieting and exercise followed by monthly individualized sessions with the goals to decrease the body weight by 7% and engage in a physical activity for at least 150 minutes per week. The incidence of diabetes was 58% lower in the lifestyle group and 31% lower in those given metformin. Among younger people with a higher body mass index, lifestyle modification was no more effective than metformin, and for older individuals with a lower body mass index, metformin was no better than placebo in preventing diabetes. After ten years, the incidence of diabetes was 34% lower in the group of participants given diet and exercise and 18% lower in those given metformin. It is unclear whether metformin slowed down the progression of prediabetes to diabetes (true preventive effect), or the decrease of diabetes in the treated population was simply due to its glucose-lowering action (treatment effect).

Polycystic ovary syndrome

Antidiabetic therapy has been proposed as a treatment for polycystic ovary syndrome (PCOS), a condition frequently associated with insulin resistance, since the late 1980s. The use of metformin in PCOS was first reported in 1994, in a small study conducted at the University of the Andes, Venezuela. The United Kingdom's National Institute for Health and Clinical Excellence recommended in 2004 that women with PCOS and a body mass index above 25 be given metformin for anovulation and infertility when other therapies have failed to produce results. However, two clinical studies completed in 2006-2007 returned mostly negative results, with metformin being no better than placebo, and a metformin-clomifene combination no better than clomifene alone. Reflecting this, subsequent reviews noted large randomized controlled trials have, in general, not shown the promise suggested by the early small studies. UK and international clinical practice guidelines do not recommend metformin as a first-line treatment or do not recommend it at all, except for women with glucose intolerance. The guidelines suggest clomiphene as the first medication option and emphasize lifestyle modification independently from the drug treatment.

In a dissenting opinion, a systematic review of four head-to-head comparative trials of metformin and clomifene found them equally effective for infertility. Four positive studies of metformin were in women not responding to clomifene, while the population in the negative studies was drug-naive or uncontrolled for the previous treatment. Metformin should be used as a second-line drug if clomifene treatment fails. Another review recommended metformin unreservedly as a first-line treatment option because it has positive effects not only on anovulation, but also on insulin resistance, hirsutism, and obesity often associated with PCOS. A Cochrane Collaboration review found metformin improves ovulation and pregnancy rates, particularly when combined with clomifene, but is not associated with any increase in the number of live births.

Gestational diabetes

Several observational studies and randomized, controlled trials have found metformin to be as effective and safe as insulin for the management of gestational diabetes, and a small case-control study has suggested the children of women given metformin instead of insulin may be healthier in the neonatal period. Nonetheless, several concerns have been raised regarding studies published thus far, and evidence on the long-term safety of metformin for both mother and child is still lacking.



Contraindications

Metformin is contraindicated in people with any condition that could increase the risk of lactic acidosis, including kidney disorders (arbitrarily defined as creatinine levels over 150 ?mol/l (1.7 mg/dl),), lung disease and liver disease. According to the prescribing information, heart failure (in particular, unstable or acute congestive heart failure) increases the risk of lactic acidosis with metformin. A 2007 systematic review of controlled trials, however, suggested metformin is the only antidiabetic drug not associated with any measurable harm in people with heart failure, and it may reduce mortality in comparison with other antidiabetic agents.

Metformin is recommended to be temporarily discontinued before any radiographic study involving iodinated contrast agents, (such as a contrast-enhanced CT scan or angiogram), as the contrast dye may temporarily impair kidney function, indirectly leading to lactic acidosis by causing retention of metformin in the body. Metformin can be resumed after two days, assuming kidney function is normal.

Diabetes medicine side effects - Oral diabetes medications chart ...


Adverse effects

The most common adverse effect of metformin is gastrointestinal irritation, including diarrhea, cramps, nausea, vomiting, and increased flatulence; metformin is more commonly associated with gastrointestinal side effects than most other antidiabetic drugs. The most serious potential side effect of metformin use is lactic acidosis; this complication is very rare, and the vast majority of these cases seem to be related to comorbid conditions, such as impaired liver or kidney function, rather than to the metformin itself.

Metformin has also been reported to decrease the blood levels of thyroid-stimulating hormone in people with hypothyroidism, The clinical significance of this is still unknown.

Gastrointestinal

In a clinical trial of 286 subjects, 53.2% of the 141 given immediate-release metformin (as opposed to placebo) reported diarrhea, versus 11.7% for placebo, and 25.5% reported nausea/vomiting, versus 8.3% for those on placebo.

Gastrointestinal upset can cause severe discomfort; it is most common when metformin is first administered, or when the dose is increased. The discomfort can often be avoided by beginning at a low dose (1.0 to 1.7 grams per day) and increasing the dose gradually.

Long-term use of metformin has been associated with increased homocysteine levels and malabsorption of vitamin B12. Higher doses and prolonged use are associated with increased incidence of vitamin B12 deficiency, and some researchers recommend screening or prevention strategies.

Lactic acidosis

The most serious potential adverse effect of biguanide use is lactic acidosis ("metformin-associated lactic acidosis" or MALA), the incidence for which is nine per 100,000 person-years. Phenformin, another biguanide, was withdrawn from the market because of an increased risk of lactic acidosis (rate of 40-64 per 100,000 patient-years). However, metformin is safer than phenformin, and the risk of developing lactic acidosis is not increased by the medication as long as it is not prescribed to known high-risk groups.

Lactate uptake by the liver is diminished with metformin administration because lactate is a substrate for hepatic gluconeogenesis, a process which metformin inhibits. In healthy individuals, this slight excess is simply cleared by other mechanisms (including uptake by the kidneys, when their function is unimpaired), and no significant elevation in blood levels of lactate occurs. When impaired renal function is present, however, clearance of metformin and lactate is reduced, leading to increased levels of both, and possibly causing a buildup of lactic acid. Because metformin decreases liver uptake of lactate, any condition that may precipitate lactic acidosis is a contraindication to its use. Common causes of increased lactic acid production include alcoholism (due to depletion of NAD+ stores), heart failure, and respiratory disease (due to inadequate oxygenation of tissues); the most common cause of impaired lactic acid excretion is kidney disease.

Metformin has also been suggested to increase production of lactate in the small intestine; this could potentially contribute to lactic acidosis in those with risk factors. However, the clinical significance of this is unknown, and the risk of metformin-associated lactic acidosis is most commonly attributed to decreased hepatic uptake rather than increased intestinal production.

Overdose

A review of intentional and accidental metformin overdoses reported to poison control centers over a five-year period found serious adverse events were rare, though the elderly appeared to be at greater risk. A similar study where cases were reported to Texas poison control centers between 2000 and 2006 found ingested doses of more than 5,000 mg were more likely to involve serious medical outcomes in adults. Survival following intentional overdoses with up to 63,000 mg (63 g) of metformin have been reported in the medical literature. Fatalities following overdose are rare, but do occur. In healthy children, unintentional doses of less than 1,700 mg are unlikely to cause any significant toxic effects.

The most common symptoms following overdose appear to include vomiting, diarrhea, abdominal pain, tachycardia, drowsiness, and, rarely, hypoglycemia or hyperglycemia. The major potentially life-threatening complication of metformin overdose is lactic acidosis, which is due to lactate accumulation. Treatment of metformin overdose is generally supportive, as no specific antidote is known. Lactic acidosis is initially treated with sodium bicarbonate, although high doses are not recommended, as this may increase intracellular acidosis. Acidosis that does not respond to administration of sodium bicarbonate may require further management with standard hemodialysis or continuous venovenous hemofiltration. These treatments are recommended in severe overdoses. In addition, due to metformin's low molecular weight and lack of plasma protein binding, these techniques also have the benefit of removing metformin from blood plasma, preventing further lactate overproduction.

Metformin may be quantified in blood, plasma, or serum to monitor therapy, confirm a diagnosis of poisoning, or assist in a medicolegal death investigation. Blood or plasma metformin concentrations are usually in a range of 1-4 mg/l in persons receiving the drug therapeutically, 40-120 mg/l in victims of acute overdosage, and 80-200 mg/l in fatalities. Chromatographic techniques are commonly employed.

Interactions

The H2-receptor antagonist cimetidine causes an increase in the plasma concentration of metformin, by reducing clearance of metformin by the kidneys; both metformin and cimetidine are cleared from the body by tubular secretion, and both, particularly the cationic (positively charged) form of cimetidine, may compete for the same transport mechanism. A small double-blind, randomized study found the antibiotic cephalexin to also increase metformin concentrations by a similar mechanism; theoretically, other cationic medications may produce the same effect.

The Positive Effects Of Metformin | Diabetic Connect


Mechanism of action

Metformin decreases hyperglycemia primarily by suppressing glucose production by the liver (hepatic gluconeogenesis). The "average" person with type 2 diabetes has three times the normal rate of gluconeogenesis; metformin treatment reduces this by over one-third. The molecular mechanism of metformin is incompletely understood: inhibition of the mitochondrial respiratory chain (complex I), activation of AMP-activated protein kinase (AMPK), inhibition of glucagon-induced elevation of cyclic adenosine monophosphate (cAMP), and consequent activation of protein kinase A (PKA), inhibition of mitochondrial glycerophosphate dehydrogenase, and an effect on gut microbiota have been proposed as potential mechanisms.

Activation of AMPK, an enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats, was required for metformin's inhibitory effect on the production of glucose by liver cells. Activation of AMPK was required for an increase in the expression of small heterodimer partner, which in turn inhibited the expression of the hepatic gluconeogenic genes Phosphoenolpyruvate carboxykinase and glucose 6-phosphatase. Metformin is frequently used in research along with AICA ribonucleotide as an AMPK agonist. More recent studies using mouse models in which the genes for AMPK?1 and ?2 catalytic subunits (Prkaa1/2) or LKB1, an upstream kinase of AMPK, had been knocked out in hepatocytes, have raised doubts over the obligatory role of AMPK, since the effect of metformin was not abolished by loss of AMPK function. The mechanism by which biguanides increase the activity of AMPK remains uncertain; however, metformin increases the concentration of cytosolic adenosine monophosphate (AMP) (as opposed to a change in total AMP or total AMP/adenosine triphosphate). Increased cellular AMP has also been proposed to explain the inhibition of glucagon-induced increase in cAMP and activation of PKA. Metformin and other biguanides may antagonize the action of glucagon, thus reducing fasting glucose levels. Metformin also induces a profound shift in the faecal microbial community profile in diabetic mice and this may contribute to its mode of action possibly through an effect on glucagon-like peptide-1 secretion.

In addition to suppressing hepatic glucose production, metformin increases insulin sensitivity, enhances peripheral glucose uptake (by inducing the phosphorylation of GLUT4 enhancer factor), decreases insulin-induced suppression of fatty acid oxidation, and decreases absorption of glucose from the gastrointestinal tract. Increased peripheral use of glucose may be due to improved insulin binding to insulin receptors. The increase in insulin binding after metformin treatment has also been demonstrated in patients with NIDDM [98].

AMPK probably also plays a role in increased in, as metformin administration increases AMPK activity in skeletal muscle. AMPK is known to cause GLUT4 deployment to the plasma membrane, resulting in insulin-independent glucose uptake. Some metabolic actions of metformin do appear to occur by AMPK-independent mechanisms; the metabolic actions of metformin in the heart muscle can occur independent of changes in AMPK activity and may be mediated by p38 MAPK- and PKC-dependent mechanisms.

A Diabetes Medication Primer | Diabetic Connect


Chemistry

The usual synthesis of metformin, originally described in 1922 and reproduced in multiple later patents and publications, involves the reaction of dimethylamine hydrochloride and 2-cyanoguanidine (dicyandiamide) with heating.

According to the procedure described in the 1975 Aron patent, and the Pharmaceutical Manufacturing Encyclopedia, equimolar amounts of dimethylamine and 2-cyanoguanidine are dissolved in toluene with cooling to make a concentrated solution, and an equimolar amount of hydrogen chloride is slowly added. The mixture begins to boil on its own, and after cooling, metformin hydrochloride precipitates with a 96% yield.

Array

Pharmacokinetics

Metformin has an oral bioavailability of 50-60% under fasting conditions, and is absorbed slowly. Peak plasma concentrations (Cmax) are reached within one to three hours of taking immediate-release metformin and four to eight hours with extended-release formulations. The plasma protein binding of metformin is negligible, as reflected by its very high apparent volume of distribution (300-1000 l after a single dose). Steady state is usually reached in one or two days.

Metformin has acid dissociation constant values (pKa) of 2.8 and 11.5, so exists very largely as the hydrophilic cationic species at physiological pH values. The metformin pKa values make metformin a stronger base than most other basic drugs with less than 0.01% unionized in blood. Furthermore, the lipid solubility of the unionized species is slight as shown by its low logP value [log(10) of the distribution coefficient of the unionized form between octanol and water] of -1.43. These chemical parameters indicate low lipophilicity and, consequently, rapid passive diffusion of metformin through cell membranes is unlikely. The logP of metformin is less than that of phenformin (-0.84) because two methyl substituents on metformin impart lesser lipophilicity than the larger phenylethyl side chain in phenformin. More lipophilic derivatives of metformin are presently being investigated with the aim of producing prodrugs with better oral absorption than metformin itself.

Metformin is not metabolized. It is cleared from the body by tubular secretion and excreted unchanged in the urine; metformin is undetectable in blood plasma within 24 hours of a single oral dose. The average elimination half-life in plasma is 6.2 hours. Metformin is distributed to (and appears to accumulate in) red blood cells, with a much longer elimination half-life: 17.6 hours (reported as ranging from 18.5 to 31.5 hours in a single-dose study of nondiabetic people).

Array

History

The biguanide class of antidiabetic drugs, which also includes the withdrawn agents phenformin and buformin, originates from the French lilac or goat's rue (Galega officinalis), a plant used in folk medicine for several centuries.

Metformin was first described in the scientific literature in 1922, by Emil Werner and James Bell, as a product in the synthesis of N,N-dimethylguanidine. In 1929, Slotta and Tschesche discovered its sugar-lowering action in rabbits, noting it was the most potent of the biguanide analogs they studied. This result was completely forgotten, as other guanidine analogs, such as the synthalins, took over, and were themselves soon overshadowed by insulin.

Interest in metformin, however, picked up at the end of the 1940s. In 1950, metformin, unlike some other similar compounds, was found not to decrease blood pressure and heart rate in animals. That same year, a prominent Philippine physician, Eusebio Y. Garcia, used metformin (he named it Fluamine) to treat influenza; he noted the drug "lowered the blood sugar to minimum physiological limit" and was not toxic. Garcia also believed metformin to have bacteriostatic, antiviral, antimalarial, antipyretic, and analgesic actions. In a series of articles in 1954, Polish pharmacologist Janusz Supniewski was unable to confirm most of these effects, including lowered blood sugar; he did, however, observe some antiviral effects in humans.

While training at the Hôpital de la Pitié, French diabetologist Jean Sterne studied the antihyperglycemic properties of galegine, an alkaloid isolated from Galega officinalis, which is related in structure to metformin and had seen brief use as an antidiabetic before the synthalins were developed. Later, working at Laboratoires Aron in Paris, he was prompted by Garcia's report to reinvestigate the blood sugar-lowering activity of metformin and several biguanide analogs. Sterne was the first to try metformin on humans for the treatment of diabetes; he coined the name "Glucophage" (glucose eater) for the drug and published his results in 1957.

Metformin became available in the British National Formulary in 1958. It was sold in the UK by a small Aron subsidiary called Rona.

Broad interest in metformin was not rekindled until the withdrawal of the other biguanides in the 1970s. Metformin was approved in Canada in 1972, but did not receive approval by the U.S. Food and Drug Administration (FDA) for type 2 diabetes until 1994. Produced under license by Bristol-Myers Squibb, Glucophage was the first branded formulation of metformin to be marketed in the United States, beginning on March 3, 1995. Generic formulations are now available in several countries, and metformin is believed to have become the most widely prescribed antidiabetic drug in the world.

Array

Formulations

Metformin is sold under several trade names, including Glucophage XR, Carbophage SR, Riomet, Fortamet, Glumetza, Obimet, Gluformin, Dianben, Diabex, Diaformin, Siofor, and Metfogamma.

Liquid metformin is sold under the name Riomet in India. Each 5 ml of Riomet is equivalent to the 500-mg tablet form of metformin.

Metformin IR (immediate release) is available in 500, 850, and 1000-mg tablets. All of these are now available as generic drugs in the U.S.

Metformin SR (slow release) or XR (extended release) was introduced in 2004. It is available in 500, 750, and 1000-mg strengths, mainly to counteract the most common gastrointestinal side effects, as well as to increase compliance by reducing pill burden. No difference in effectiveness exists between the two preparations.

Combinations with other drugs

When used for type 2 diabetes, metformin is often prescribed in combination with other drugs. Several are available as fixed-dose combinations, also with the purpose of reducing pill burden and making administration simpler and more convenient.

As of 2009, the most popular brand-name combination was metformin with rosiglitazone, sold as Avandamet by GlaxoSmithKline since 2002. Rosiglitazone actively makes cells more sensitive to insulin, complementing the action of the metformin. In 2005, all current stock of Avandamet was seized by the FDA and removed from the market, after inspections showed the factory where it was produced was violating good manufacturing practices. The drug pair continued to be prescribed separately in the absence of Avandamet, which was available again by the end of that year.

In the United States, metformin is also available in combination with pioglitazone (trade name Actoplus Met), the sulfonylureas glipizide (trade name Metaglip) and glibenclamide (known as glyburide in the United States, trade name Glucovance), the dipeptidyl peptidase-4 inhibitor sitagliptin (with the combination sold under the trade name Janumet), the dipeptidyl peptidase-4 inhibitor saxagliptin (with the combination sold under the trade name Kombiglyze XR), and the meglitinide repaglinide (PrandiMet). Generic formulations of metformin/glipizide and metformin/glibenclamide are available (the latter being more popular). A generic formulation of metformin/rosiglitazone from Teva has received tentative approval from the FDA, and is expected to reach the market in early 2012.

In Europe, the combination of metformin and the dipeptidyl peptidase-4 inhibitor linagliptin has approved the trade name Jentadueto.



In pregnancy

Metformin is safe in pregnancy and women with gestational diabetes treated with metformin have less weight gain during pregnancy than those treated with insulin. Babies born to women treated with metformin have been found to develop less visceral fat, making them less prone to insulin resistance in later life.



Research

Tentative evidence shows metformin may decrease the risk of cancer. A direct action of metformin on cancer cells is suspected. Metformin exhibits a strong and consistent antiproliferative action on several cancer cell lines, including breast, colon, ovarian, pancreatic, lung, and prostate cancer cells. These cellular studies were generally completed by preclinical studies showing a reliable antitumoral effect in various mouse models. In addition, the first clinical trials demonstrated a beneficial effect in breast and colon cancer.



References



External links

  • Metformin at DMOZ
  • Metformin drug information from Lexi-Comp. Includes dosage information and a comprehensive list of international brand names
  • U.S. National Library of Medicine: Drug Information Portal - Metformin




Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



0 komentar :

Body For Life - 12 Week Weight Loss Program

Body for Life (BFL) is a 12-week nutrition and exercise program, and also an annual physique transformation competition. It was created by Bill Phillips, a former competitive bodybuilder and owner of EAS, a manufacturer of nutritional supplements. It has been popularized by a bestselling book of the same name.

The first annual Body for Life competition was held in 1996. (It was then called the "EAS Grand Spokesperson Challenge".) Entrants write about their experience of the program, and send this to EAS along with their 'before' and 'after' swimsuit photos. Prizes vary each year, but in 2005 the first prize was US$1,000,000. Since, it has gone down significantly with the last payment being US$25,000 for the past few champions. Most recent champions include 2008 Grand Champions Emily Alvers and Colby Knight.

Body for Life makes use of principles that have been widely known in bodybuilding. Its differences are in the way it has been packaged and marketed so as to appeal to consumers and be understood by the public. It supports an extensive ancillary industry of gyms, nutritionists and personal trainers.

WLBC Program | Fusion Fitness | Kansas City Fitness Classes ...



Exercise

The human body adapts itself to changes in nutritional intake. If the calorie intake is reduced, the body responds by slowing down its metabolism, and by burning muscle in preference to fat. This reduces the metabolism long-term. When the diet comes to an end and normal calorie intake is restored, the individual starts to gain weight even faster than before. This is known as yo-yo dieting. Diets that focus exclusively on calorie reduction often fail in this way.

With these concerns in mind, Body for Life addresses energy expenditure (i.e. exercise) in addition to energy input. For best results, Body for Life holds that this exercise should include weight training to build skeletal muscle and increase the metabolism over the long term. This also helps to maximise the energy expenditure and fat loss from aerobic exercise.

Body for Life's exercise program is more complicated than its diet program. It suggests exercising six days a week, normally Monday to Saturday, and alternating between weight training and aerobic exercise. The seventh day, usually Sunday, is a rest day (referred to as the "free day", during which no exercise is done and unhealthy, normally fatty foods may be eaten). Weight training sessions alternate between exercises for the upper body and exercises for the lower body. This allows the exercised muscles enough time to recover fully before the next training session.

Each fortnight follows the same pattern:

Intensity index

Body for Life uses Gunnar Borg's Rating of Perceived Exertion (known as the Borg scale) for assessing the intensity of exercise based on how hard you feel you are working. It uses the variant developed by the American College of Sports Medicine, which uses a scale of 0 to 10:

  • 0 is no exertion at all.
  • 2 corresponds to very light exercise. For a healthy person, this is like walking slowly at their own pace for several minutes.
  • 5 on the scale is somewhat hard exercise, but it still feels OK to continue.
  • 8 is very strenuous. A healthy person can still go on, but they really have to push themselves. It feels very heavy, and the person is very tired.
  • 9 on the scale is an extremely strenuous exercise level. For most people this is the most strenuous exercise they have ever experienced.
  • 10 is maximal exertion: an all-out, 100% effort.

These levels accommodate differences in fitness. An unfit individual may require a level 10 effort to walk briskly uphill, whereas for a competitive athlete this may only be a level 3 effort. Over the course of the 12-week Body for Life program an individual would get noticeably fitter, so their intensity scale needs to be adjusted over time. This is considered normal.

Body for Life uses a "wave" pattern, periodically building up from level 5 to level 9 or 10 during an exercise session. This allows the muscles to warm up, and gives the body a chance to build up to a "high point" of maximal exertion. Brief but intense exercise provides maximum stimulus for the body to build strength and endurance, but without the risk of overtraining.

Weight training

Exercises for upper-body muscle groups include:

  • "Pecs" (chest), e.g., bench press, pec-deck, incline flye.
  • "Lats" (upper back), e.g., pull-down, bent-over row, dumbbell pullover.
  • Deltoids (shoulders), e.g., upright row, shoulder press, lateral raise.
  • Triceps (rear arms), e.g., push-down, triceps kickback, bench dip.
  • Biceps (front arms), e.g., biceps curl, concentration curl, hammer curl.

Exercises for lower-body muscle groups include:

  • Quadriceps (front legs), e.g., squat, leg press, leg extension.
  • Hamstrings (rear legs), e.g., leg curl, lunge, glute-ham raise.
  • Calves e.g., standing calf raise, seated calf raise.
  • "Abs" (torso), e.g., crunch, reverse crunch, leg raise.

Most of these exercise can be performed using either dumbbells, a barbell, a Smith machine, a cable machine with adjustable pulleys or a specially-designed apparatus. Two exercises should be chosen for each muscle group. Five sets of the first exercise are performed, and then one set of the second. Weights for each set should be chosen so that the specified number of repetitions can be achieved at the specified level of intensity. For example:

Weight training sessions proceed at a brisk pace, with one minute of rest between the first four sets for a muscle group, and no rest between the final two sets. The cadence for each repetition should be one second to lift the weight (while exhaling deeply), one second holding it at the top, two seconds to lower the weight (while inhaling deeply) and then one second pausing before the next repetition. Each session should be completed within about 45 minutes.


Aerobic exercise

Most forms of aerobic exercise are suitable. Common choices include walking or running (perhaps on a treadmill), cycling, swimming, or the use of a rowing machine or cross-trainer. However, exercise classes are generally not suitable, unless they are specifically designed to suit Body for Life.

Aerobic exercise sessions are limited to 20 minutes duration. They compensate for this by following the same "wave" pattern of steadily increasing intensity just like the weight training sessions. During the first 2 minutes, intensity should be at 5. Minutes 3, 4, 5, and 6 should be at intensity levels 6, 7, 8, and 9 respectively. Minute 7 goes back down to 6 intensity level and continues the wave pattern until the 19th minute where you push intensity level to 10. The last minute is a cool down to 5 intensity. You should be completely exhausted at this point so stretch afterwards.

Phillips maintains that aerobic exercise is more effective for fat loss when done first thing in the morning, because it raises the metabolism for the remainder of the day, and because the body draws more heavily on its fat stores after fasting overnight.



Diet

Another key aspect of BFL is consuming a diet that is low enough in caloric intake to cause fat loss, while providing enough calories and protein to build muscle and cardiovascular endurance. In addition, BFL attempts to make choosing portion sizes and food as easy as possible to avoid overcomplication. The major aspects of the diet program include:

  • Eating 6 smaller meals per day instead of the standard 3 large meals. BFL (along with some dietary experts) maintain that eating smaller, more frequent meals throughout the day will boost the body's metabolism, causing it to burn fat faster.
  • Eating one "portion" of carbohydrates and one "portion" of protein at each meal. To keep determining portion sizes simple, BFL suggests that one "portion" of carbohydrates should equal a potato or ball of rice roughly equal to the size of the person's clenched fist. Additionally, one "portion" of protein would roughly equal a piece of meat the size of the person's palm and as thick as a deck of cards.
  • Consuming vegetables with at least two meals per day.
  • Taking a good multi-vitamin.
  • Limiting consumption of butter, cheese, mayonnaise, alcoholic beverages, and high fat salad dressings.
  • Allowance of one "free day" each week. A free day is one day a week in which the person is allowed to make dietary choices that do not correspond with the BFL eating program. Although this should not be a day to binge eat junk food, BFL encourages people to eat whatever foods or desserts they desire on this day. According to Bill Phillips, this allows the body to avoid the Starvation response and gives the dieter a chance to avoid cheating since they know they simply have to wait until their free day to have what they crave.

Body for Life also encourages people to eat mostly lean meats like chicken, fish, and turkey, as well as tofu. Carbohydrates that are multi-grain and unrefined are also encouraged. Bill Phillips encourages people to adopt this eating program as a lifestyle, and not as a temporary diet. Although the amount of protein eaten should be enough for some people to build good muscle mass, some observe that high-protein shakes and meal bars should be consumed to increase protein intake. Not surprisingly, the program suggests consuming protein products from EAS.

What It Takes!: Testimonials Regular Clients


Body for Life books and videos

  • Phillips, Bill. Body for Life: 12 Weeks to Mental and Physical Strength. HarperCollins, 1999. (ISBN 0-06-019339-5)
  • Phillips, Bill. Body for Life Success Journal. HarperCollins, 2002. (ISBN 0-06-051559-7)
  • Phillips, Bill. Eating for Life: Your Guide to Great Health, Fat Loss and Increased Energy! High Point Media, 2003 (ISBN 0-9720184-1-7)
  • Body of Work. Seventh Dream Pictures, 1998. (ASIN B0001H9T72)
Changes Health & Fitness Centre - Before and after pictures ...


External links

  • Body for Life official website
  • Bill Phillips' official website
Personal Trainer In Plymouth | Paul Hatswell


References



Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



0 komentar :

Online Weight Loss Plans - Simple Weight Loss Plans

Online weight loss plans are web-based fitness programs designed to help participants lose weight. These may include assistance in the areas necessary for weight loss such as goal setting, progress tracking, meal and workout planning and personal support from personal trainers or fitness coaches.

Diet (nutrition) - Healthy Weight Loss Plan Free | Weight Loss ...



Background

Online weight loss plans are usually interactive programs that provide the user with diet information, workout routines, meal planning, goal tracking, and feedback. Web-based programs usually attempt to incorporate all of these areas and customize them for a particular user. The user will usually fill out a questionnaire before proceeding. The questionnaire will contain information such as current eating patterns, fitness levels and goals.

A personalized meal plan and workout program are usually created for the user. One feature of these programs is the use of online tools to track improvements, and to log workout and diet information. The idea behind these tracking tools is that by tracking fitness, a person can make more progress by aiming for and meeting regular fitness goals. Programs range in price from the very basic, to highly customized programs created by celebrity fitness experts. There are also free web-based programs. While they usually provide access to online tools, they may not provide any customized plans.

Online weight loss plans usually contain some of these elements:

  • Weekly shopping lists
  • Workout routines and meal plans
  • Regular support from a fitness coach or personal trainer (some with round-the-clock support)
  • Regular tracking of progress
  • Workout videos
  • Some type of online workout calendar or journal


Impact

In a year-long study published in the Journal of the American Medical Association, participants of an online weight loss plan lost more than twice the weight of participants who took part in a more traditional program. It has been shown that people who have used online weight loss plans for 18 months were able to maintain significant weight loss. Many studies now show that Internet programs are viable tools to help people maintain weight loss over the long term. In one study, a group of 250 people lost weight over a six-month period and maintained weight loss for 12 months afterwards using an online weight loss plan. The low cost combined with the lack of need for face-to-face meetings with a nutritionist or personal trainer make Internet programs easy to maintain long-term loss. The requirement of constantly updating weight and other measurements helps to hold the user accountable as well. This could help people maintain weight loss over a long period. Many studies even show that participants that logged in to their online programs more also experienced, on average, more weight loss. There has been an upsurge of companies specifically dealing with only online weight loss. There has recently been research into the effectiveness of web-based weight loss programs in primary care settings.

WatchFit - A Simple Weight Loss Workout Plan for Beginners Part 1


References

5 Simple Steps Towards A Healthy Weight Loss Plan : Weight Loss Tips


External links

  • "Personal Counseling and Web-Based Strategies Show Modest Success for Sustaining Weight Loss, According to NHLBI Study". News Release. National Institutes of Health (NIH). March 11, 2008. 
  • Booth AO, Nowson CA, Matters H (June 2008). "Evaluation of an interactive, Internet-based weight loss program: a pilot study". Health Educ Res 23 (3): 371-81. doi:10.1093/her/cyn007. PMID 18349032. 


Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



0 komentar :

Phil McGraw - Medical Weight Loss Tulsa

Phillip Calvin "Phil" McGraw (born September 1, 1950), known as Dr. Phil, is an American television personality, author, psychologist, and the host of the television show Dr. Phil, which debuted in 2002. McGraw first gained celebrity status with appearances on The Oprah Winfrey Show in the late 1990s.

SHAPE ReClaimedâ„¢ - Tulsa - Functional Medical Institute



Early life

McGraw was born in Vinita, Oklahoma, the son of Anne Geraldine "Jerry" (née Stevens) and Joseph J. "Joe" McGraw, Jr. He grew up with two older sisters, Deana and Donna, and younger sister Brenda in the oilfields of North Texas where his father was an equipment supplier. During McGraw's childhood, his family moved so his father could pursue a lifelong goal of becoming a psychologist.

McGraw attended Shawnee Mission North High School in Overland Park, Kansas. In 1968, he was awarded a football scholarship to the University of Tulsa, where he played middle linebacker under Coach Glenn Dobbs. On November 23 of that year, McGraw's team lost to the University of Houston 100-6, which is one of the most lopsided games in college football history. Coach Dobbs retired after that season and McGraw transferred to Midwestern State University in Wichita Falls, Texas.



Education and career

McGraw graduated in 1975 from Midwestern State University with a B.A. in psychology. He went on to earn an M.A. in experimental psychology in 1976, and a Ph.D. degree in clinical psychology in 1979 at the University of North Texas, where his dissertation was titled "Rheumatoid Arthritis: A Psychological Intervention". McGraw was guided through the doctoral program by Frank Lawlis, who later became the primary contributing psychologist for the Dr. Phil television show.

After obtaining his doctorate, McGraw joined his father, Joe McGraw, in Wichita Falls, Texas, where the elder McGraw had established his private psychology practice.

In 1983, McGraw and his father joined Thelma Box, a successful Texas businesswoman, in presenting "Pathways" seminars, "experience-based training which allows individuals to achieve and create their own results." Critics claim that many of the "phrases and the terminology and the quaint sayings" used by McGraw on the Oprah and Dr. Phil shows were coined by Box and presented by McGraw in this seminar. McGraw admits that some of the material from Life Strategies, his first best-seller, is taken directly from the Pathways seminar. However, he has never mentioned Box or her contributions to his success in any of his books or TV shows. Eight years after joining Box, McGraw signed an agreement for the sale of his Pathways seminar stock for $325,000 without notifying either his father or Box of the impending sale. Box founded her own seminars entitled "Choices."

Texas State Board of Examiners of Psychologists

On October 21, 1988, the Texas State Board of Examiners of Psychologists determined that McGraw had hired a former patient for "part-time temporary employment". Specifically, the board cited "a possible failure to provide proper separation between termination of therapy and the initiation of employment," issued a letter of reprimand and imposed administrative penalties. The board also investigated claims made by the patient of inappropriate contact initiated by McGraw, but the "Findings of Fact" document issued by the board on October 21, 1988, at the end of its investigation includes no reference to any physical contact of any kind. It specifically identified "the therapeutic and business relationships" as constituting McGraw's sole issue with the board. McGraw fulfilled all terms of the board's requirements, and the board closed its complaint file in June 1990.

In 1990, McGraw joined lawyer Gary Dobbs in co-founding Courtroom Sciences, Inc. (CSI), a trial consulting firm through which McGraw later came into contact with Oprah Winfrey. Eventually, CSI became a profitable enterprise, advising Fortune 500 companies and injured plaintiffs in achieving settlements. McGraw is no longer an officer or director of the company.

After starting CSI, McGraw ceased the practice of psychology. He kept his license current and in good standing until he elected to retire it 15 years later in 2006. Appearing on the Today Show in January 2008, McGraw said that he has made it "very clear" that his current work does not involve the practice of psychology. He also said that he had "retired from psychology". According to the Today Show, the California Board of Psychology determined in 2002 that he did not require a license because his show involves "entertainment" rather than psychology. McGraw's license is currently listed by the Texas State Board of Psychology as "retired" and he holds no other active licenses to practice in any other state.

Oprah Winfrey and the Dr. Phil show

In 1995, Oprah Winfrey hired McGraw's legal consulting firm CSI to prepare her for the Amarillo Texas beef trial. Winfrey was so impressed with McGraw that she thanked him for her victory in that case, which ended in 1998. Soon after, she invited him to appear on her show. His appearance proved so successful that he began appearing weekly as a relationship and life strategy expert on Tuesdays starting in April 1998.

The next year, McGraw published his first best-selling book, Life Strategies. In the next four years, McGraw published three additional best-selling relationship books, along with workbooks to complement them.

As of September 2002, McGraw formed Peteski Productions and launched his own syndicated daily television show, Dr. Phil, produced by Winfrey's Harpo Studios. The format is an advice show, where he tackles a different topic on each show, offering advice for his guests' troubles.

Weight loss products

In 2003, McGraw entered the weight-loss business, selling shakes, energy bars, and supplements. These products were promoted on his show with his sisters Deana and Brenda and nephew Tony among the featured testimonials on the show. These products' labels, which carried the brand name "Shape It Up, Woo, Woo!", stated: "These products contain scientifically researched levels of ingredients that can help you change your behavior to take control of your weight." This met with swift criticism from various sources, accusing McGraw (a clinical psychologist, and not a physician) of lacking the expertise to recommend weight-loss products. Facing a Federal Trade Commission investigation into Shape Up's claims, McGraw pulled his supplements off the market in March 2004, and the FTC dropped its probe. In October 2005, several people who used McGraw's products declared an intent to file a class-action lawsuit against him, claiming that although the supplements cost $120 per month they did not stimulate weight loss. McGraw settled the suit in September 2006 for $10.5 million. Some of the settlement ($6 million) may be paid to the plaintiffs in the form of Amway (Quixtar) brand Nutrilite vitamins.

The Making of Dr. Phil unauthorized biography (2003)

The Making of Dr. Phil is a biography by Sophia Dembling, a reporter from the Dallas Morning News, and Lisa Gutierrez, a reporter from The Kansas City Star. The book probes McGraw's history, with interviews of his childhood friends and former classmates. The book reports that McGraw allegedly used unethical business practices in a gym business early in his career, that he was allegedly abusive to his first wife and to his staff, while noting that he overcame adversity through setting goals and was persistent in achieving success. The book received no promotional help from McGraw or his associates.

In 2005, McGraw published another best-selling book, Family First, along with a workbook. He also signed a five-year extension of his syndication deal with his show's distributors, King World Productions, Inc. The deal will pay McGraw $15 million a year and keep the show in production through the 2013-2014 television season.

Spin-off shows

Also in 2005, McGraw's son Jay's television show Renovate My Family (a clone of ABC's Extreme Makeover: Home Edition) was canceled at the start of its second season following a renovated family's lawsuit. Jay McGraw and Phil McGraw then formed Stage 29 Productions. A week later, McGraw and son announced a new show called Moochers (a clone of ABC's Kicked Out); however, the show was canceled before any episodes aired. McGraw also released another book, Love Smart, which did not achieve the success of his previous bestsellers.

In 2006, the Dr. Phil House (a clone of CBS's Big Brother) began airing as part of the Dr. Phil television show. Following a protest by neighbors, the house in Los Angeles was shut down, and production resumed on a sound stage on a studio back lot. McGraw reached the number 22 spot on the Forbes Celebrity 100 list, with income of $45 million.

Another Stage 29 show, Decision House (a remix of the Dr. Phil House) aired from September through November 2007 but was canceled due to poor reviews and dismal ratings. Ratings for the Dr. Phil show in 2007 began to slide. In May, viewership was close to 7 million people. However, by year's end, viewership was about 5.5 million people (#10 for syndicated TV shows, and just under Everybody Loves Raymond, Family Guy and CSI: Miami). By August 2008, viewership slipped to just over 4 million people. Two weeks later, the show slipped beneath the Nielsen top 12 syndicated TV shows, and has since resurfaced. McGraw's income fell by 1/3 to $30 million, and he dropped to the number 30 spot on the Forbes Celebrity 100 list.

Late in 2007, McGraw began promoting his 2008 Dr. Phil Show extension, The Doctors. The show is hosted by television personality and ER physician Travis Stork (The Bachelor). Other experts scheduled to appear include various personalities who have appeared on the Dr. Phil show over the years, such as Lisa Masterson, an obstetrician/gynecologist; Andrew Ordon, a plastic surgeon; and Jim Sears, a pediatrician. Masterson, Ordon, and Sears appeared on the Dr. Phil show during the 2007-08 season so that McGraw could instruct them on "how to give articulate medical advice while being scrutinized by a studio audience in Los Angeles." McGraw's eldest son, Jay McGraw, is executive producer of the show. The Doctors debuted on September 8, 2008, and, as of November 10, 2008, had a 2.0 rating.

Kalpoe lawsuit (2006)

McGraw was named a co-defendant, along with CBS Television, in a 2006 lawsuit filed in relation to the disappearance of Natalee Holloway. The lawsuit was filed by Deepak Kalpoe and his brother Satish Kalpoe, who claimed that an interview they did with McGraw, aired in September 2005, was "manipulated and later broadcast as being accurate, and which portrays Deepak Kalpoe and Satish Kalpoe 'as engaging in criminal activity against Natalee Holloway and constitutes defamation.'" The Kalpoe brothers claimed invasion of privacy, fraud, deceit, defamation, emotional distress, and civil conspiracy in the suit, which was filed in the Los Angeles Superior Court.

Britney Spears "intervention" (2008)

In January 2008, McGraw visited entertainer Britney Spears in her hospital room. The visit by McGraw drew criticism from the Spears family and from mental health professionals.

The visit appeared to be part of an attempt at getting Spears and her parents to take part in an "intervention" on the Dr. Phil television show. Immediately after the visit, McGraw issued public statements about Spears' situation that Spears' family spokeswoman Lou Taylor said violated their family trust in McGraw. "This is another example of a trust being betrayed", Taylor told Today co-host Meredith Vieira. "Rather than helping the family's situation, the celebrity psychologist caused additional damage", she said. Several mental health care professionals criticized McGraw for his actions; however, fellow TV psychologist Joyce Brothers defended McGraw. It was reported that a psychologist filed a complaint with the California Board of Psychology (BOP), alleging that McGraw had practiced psychology without a license and had violated doctor-patient privilege by discussing Spears' case with the media. A copy of the complaint appeared in the media, but there is no way to verify whether or not it was actually submitted to the BOP. The BOP does not disclose that information unless an investigation is opened. Martin Greenberg, a former BOP President, said on the Today Show that this incident was not a matter that the law covers or would be concerned about.

Polk County, Florida, controversy (2008)

On April 13, 2008, a producer for the Dr. Phil show secured $30,000 bail for the ringleader of a group of eight teenage girls who viciously beat another girl and videotaped the attack. The teen had been booked at the Polk County, Florida, jail on charges that included kidnapping and assault. Producers of the Dr. Phil show had made plans to tape a one-hour show devoted to the incident and had sent a production assistant to Orlando to help book guests for the show. However, when news broke that the Dr. Phil show producer had posted bail for the teen, the outcry caused the show to cancel their plans. "In this case certain staffers went beyond our guidelines," said Theresa Corigliano, spokesperson for the Dr. Phil show. "We have decided not to go forward with the story as our guidelines have been compromised."

Riccio lawsuit (2008)

McGraw was sued by Thomas Riccio, the memorabilia collector responsible for taping the Las Vegas robbery that led to OJ Simpson's being convicted. Riccio sued McGraw in Los Angeles Superior Court for defamation, fraud, intentional infliction of emotional distress and false light for what Riccio claims to have been deceitful editing of the Dr. Phil Show on which he appeared in early October 2008.

What Italian Food Can Diabetics Eat Uk London Oklahoma Tulsa


Approach to psychology

McGraw's advice and methods have drawn criticism from some fellow psychotherapists as well as from some laymen. McGraw's critics regard advice given by him to be at best simplistic, and at worst, ineffective. McGraw said in a 2001 South Florida newspaper interview that he never liked traditional one-on-one counseling, and that "I'm not the Hush-Puppies, pipe and 'Let's talk about your mother' kind of psychologist."

For Teens, Weight Loss Sculpts New Lives | Public Radio Tulsa


Charitable foundation

McGraw announced the formation of the Dr. Phil Foundation, which raises funds to fight childhood obesity, on October 22, 2003. The Foundation also supports charitable organizations that help address the emotional, spiritual and monetary needs of many children and families.

New image weight loss clinic


Personal life

McGraw married his first wife, an ex-cheerleader and homecoming queen named Debbie Higgins McCall, in 1970, when he was 20 years old. According to her, McGraw was domineering and would not allow her to participate in the family business. She claimed that she was confined to domestic duties, which included lifting weights to improve her bustline.

During the process of annulling the marriage in 1973, McGraw began dating Robin Jo Jameson (born December 28, 1953). The couple had two children, Jay, born in 1979, and Jordan, born 1986.

McGraw's son, Jay McGraw, has partially followed in his father's footsteps, publishing books aimed at teenagers based on McGraw's books and working for Stage 29. Jay McGraw became engaged to Erica Dahm, one of the famous Playboy Playmate triplets. The elder McGraw, who has been an outspoken critic of pornography, was best man at his son's wedding, which was held at his home in Beverly Hills.

McGraw is also a private pilot, with an instrument rating, flying single engine airplanes.

Weight Loss Effects Of Water - Medi Weight Loss Products | Weight ...


Bibliography

According to Suzanne Bruring, who worked for Texas Monthly editor Skip Hollandsworth as a transcriptionist from 1998 to 2003, Hollandsworth provided "verbiage as (ghost) author for a Dr. Phil book".

Array

Filmography

Array

References



External links

  • Dr. Phil (official site)
  • Official Biography
  • Phil McGraw at the Internet Movie Database
  • 2003 interview with University of North Texas alumni magazine
  • Dallas Observer article details much of Dr. Phil's life, including many critical views.
  • Scholarly article in which authors claim that the narrative arc of Dr. Phil's show is comparable to the religious conversion story
  • Texas State Board of Examiners of Psychologists, Disciplinary Sanctions against McGraw, Philip C. detailed on page 25/41


Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



0 komentar :

Anti-obesity Medication - Good Weight Loss

Anti-obesity medication or weight loss drugs are all pharmacological agents that reduce or control weight. These drugs alter one of the fundamental processes of the human body, weight regulation, by altering either appetite, or absorption of calories. The main treatment modalities for overweight and obese individuals remain dieting and physical exercise.

In the United States only one anti-obesity medication orlistat (Xenical) is currently approved by the FDA for long term use. It reduces intestinal fat absorption by inhibiting pancreatic lipase. Rimonabant (Acomplia), a second drug, works via a specific blockade of the endocannabinoid system. It has been developed from the knowledge that cannabis smokers often experience hunger, which is often referred to as "the munchies". It had been approved in Europe for the treatment of obesity but has not received approval in the United States or Canada due to safety concerns. The European Medicines Agency in October 2008 recommended the suspension of the sale of rimonabant as the risks seem to be greater than the benefits. Sibutramine (Meridia), which acts in the brain to inhibit deactivation of the neurotransmitters, thereby decreasing appetite was withdrawn from the United States and Canadian markets in October 2010 due to cardiovascular concerns.

Because of potential side effects, it is recommended that anti-obesity drugs only be prescribed for obesity where it is hoped that the benefits of the treatment outweigh its risks.

Physical Exercise - Weight Loss Workouts | Weight Loss Terms ...



Mechanisms of action

Current and potential anti-obesity drugs may operate through one or more of the following mechanisms:

  • Appetite suppression-Catecholamines and their derivatives (such as phentermine and other amphetamine-based drugs) are the main tools used for this, although other classes of drugs such as anti-depressants and mood stabilizers have been anecdotally used for appetite suppression (see: bupropion and topiramate). Drugs blocking the cannabinoid receptors may be a future strategy for appetite suppression.
  • Increase of the body's metabolism.
  • Interference with the body's ability to absorb specific nutrients in food. For example, Orlistat (also known as Xenical and Alli) blocks fat breakdown and thereby prevents fat absorption. The OTC fiber supplements glucomannan and guar gum have been used for the purpose of inhibiting digestion and lowering caloric absorption

Anorectics are primarily intended to suppress the appetite, but most of the drugs in this class also act as stimulants (e.g., dexedrine), and patients have abused drugs "off label" to suppress appetite (e.g. digoxin).



History

The first described attempts at producing weight loss are those of Soranus of Ephesus, a Greek physician, in the second century AD. He prescribed elixirs of laxatives and purgatives, as well as heat, massage, and exercise. This remained the mainstay of treatment for well over a thousand years. It was not until the 1920s and 1930s that new treatments began to appear. Based on its effectiveness for hypothyroidism, thyroid hormone became a popular treatment for obesity in euthyroid people. It had a modest effect but produced the symptoms of hyperthyroidism as a side effect, such as palpitations and difficulty sleeping. 2,4-Dinitrophenol (DNP) was introduced in 1933; this worked by uncoupling the biological process of oxidative phosphorylation in mitochondria, causing them to produce heat instead of ATP. The most significant side effect was a sensation of warmth, frequently with sweating. Overdose, although rare, lead to a rise in body temperature and, ultimately, fatal hyperthermia. By the end of 1938 DNP had fallen out of use because the FDA had become empowered to put pressure on manufacturers, who voluntarily withdrew it from the market.

Amphetamines (marketed as Benzedrine) became popular for weight loss during the late 1930s. They worked primarily by suppressing appetite, and had other beneficial effects such as increased alertness. Use of amphetamines increased over the subsequent decades, including Obetrol and culminating in the "rainbow pill" regime. This was a combination of multiple pills, all thought to help with weight loss, taken throughout the day. Typical regimens included stimulants, such as amphetamines, as well as thyroid hormone, diuretics, digitalis, laxatives, and often a barbiturate to suppress the side effects of the stimulants. In 1967/1968 a number of deaths attributed to diet pills triggered a Senate investigation and the gradual implementation of greater restrictions on the market. This culminating in 1979 with the FDA banning the use of amphetamines, then the most effective of the diet drugs, in diet pills.

Meanwhile, phentermine had been FDA approved in 1959 and fenfluramine in 1973. The two were no more popular than other drugs until in 1992 a researcher reported that when combined the two caused a 10% weight loss which was maintained for more than two years. Fen-phen was born and rapidly became the most commonly prescribed diet medication. Dexfenfluramine (Redux) was developed in the mid-1990s as an alternative to fenfluramine with less side-effects, and received regulatory approval in 1996. However, this coincided with mounting evidence that the combination could cause valvular heart disease in up to 30% of those who had taken it, leading to withdrawal of Fen-phen and dexfenfluramine from the market in September 1997.

Ephedra was removed from the US market in 2004 over concerns that it raises blood pressure and could lead to strokes and death.

Best liquid diet for weight loss - Now foods sports l-carnitine ...


Contemporary anti-obesity drugs

Some patients find that diet and exercise is not a viable option; for these patients, anti-obesity drugs can be a last resort. Some prescription weight loss drugs are stimulants, which are recommended only for short-term use, and thus are of limited usefulness for extremely obese patients, who may need to reduce weight over months or years.

Orlistat

Orlistat (Xenical) reduces intestinal fat absorption by inhibiting pancreatic lipase. Some side-effects of using Orlistat include frequent, oily bowel movements (steatorrhea). But if fat in the diet is reduced, symptoms often improve. Originally available only by prescription, it was approved by the FDA for over-the-counter sale in February 2007. On 26 May 2010, the U.S. Food and Drug Administration (FDA) has approved a revised label for Xenical to include new safety information about cases of severe liver injury that have been reported rarely with the use of this medication. Of the 40 million users of Orlistat worldwide, 13 cases of severe liver damage have been reported.

Lorcaserin

Lorcaserin (Belviq) was approved June 28, 2012 for obesity with other co-morbidities. The average weight loss by study participants was modest, but the most common side effects of the drug are considered benign.

An excerpt from the Bloom 1 Study conducted by Arena Pharmaceuticals and later submitted for FDA approval:

At the end of Year 1 of the BLOOM trial, using Intent-to-Treat with Last Observation Carried Forward analysis (ITT-LOCF), the proportion of patients achieving at least 5% body weight loss in the lorcaserin group (47.5%) was more than twice that achieved by the placebo group (20.3%). Nearly three times as many patients achieved at least 10% weight loss in the lorcaserin group (22.6%) than in the placebo group (7.7%). Lorcaserin patients who completed the first year of the trial according to the protocol lost an average of 8.2% of their baseline weight, or approximately 18 pounds, at the end of Year 1 as compared to approximately 7 pounds in the placebo group. In Year 2, patients who continued to take lorcaserin were significantly better able to maintain their Year 1 weight loss than those who were switched to placebo.

In Year 1, lorcaserin caused significant decreases in waist circumference, BMI, glycemic parameters, high-sensitivity C-reactive protein, and fibrinogen levels compared to placebo. Total cholesterol, LDL cholesterol and triglyceride levels at Year 1 were significantly lower in the lorcaserin group than in the placebo group. Lorcaserin did not increase heart rate or blood pressure; rather, heart rate, systolic blood pressure and diastolic blood pressure decreased slightly but significantly with lorcaserin treatment compared to placebo. Quality of life, measured by the Impact of Weight on Quality of Life-Lite questionnaire, improved in both treatment groups, with a greater improvement in the lorcaserin group than in the placebo group.

At the end of Year 1, 55.4% of patients in the lorcaserin group and 45.1% of patients in the placebo group remained enrolled in the study, and 7.1% and 6.7% of patients, respectively, discontinued the study due to an adverse event. Among the most frequent adverse events reported with lorcaserin were headache (18.0% vs. 11.0%, lorcaserin vs. placebo); dizziness (8.2% vs. 3.8%); and nausea (7.5% vs. 5.4%). The rates of serious adverse events were similar in both treatment groups. The rates of depression and the incidence of anxiety and suicidal thoughts were low in both treatment groups. Lorcaserin caused no significant increase compared to placebo in the incidence of new cardiac valvulopathy.

Sibutramine

Sibutramine (Reductil or Meridia) is an anorectic or appetite suppressant, reducing the desire to eat. Sibutramine may increase blood pressure and may cause dry mouth, constipation, headache, and insomnia.

In the past, it was noted by the US that Meridia was a harmless drug for fighting obesity. The US District Court of the Northern District of Ohio rejected 113 cases complaining about the negative effects of the drug, stating that the clients lacked supporting facts and that the representatives involved were not qualified enough.

Sibutramine has been withdrawn from the market in the United States, the UK, the EU, Australia, Canada, Hong Kong and Colombia. Its risks (non-life-threatening myocardial infarction and stroke) have been shown to outweigh the benefits.

Rimonabant

Rimonabant (Acomplia) is a recently developed anti-obesity medication. It is a cannabinoid (CB1) receptor antagonist that acts centrally on the brain thus decreasing appetite. It may also act peripherally by increasing thermogenesis and therefore increasing energy expenditure.

Weight loss with Rimonabant however has not been shown to be greater than other available weight-loss medication. Due to safety concerns, primarily psychiatric in nature, the drug has not received approval in the United States or Canada, either as an anti-obesity treatment or as a smoking-cessation drug.

Sanofi-Aventis has received approval to market Rimonabant as a prescription anti-obesity drug in the European Union, subject to some restrictions. However, in October 2008, the European Medicines Agency (EMEA) recommended that Acomplia no longer be available in UK. One month later, Sanofi-Aventis decided it would no longer study rimonabant for any indication.

Metformin

In people with Diabetes mellitus type 2, the drug metformin (Glucophage) can reduce weight. Metformin limits the amount of glucose that is produced by the liver as well as increases muscle consumption of glucose.

Exenatide

Exenatide (Byetta) is a long-acting analogue of the hormone GLP-1, which the intestines secrete in response to the presence of food. Among other effects, GLP-1 delays gastric emptying and promotes a feeling of satiety. Some obese people are deficient in GLP-1, and dieting reduces GLP-1 further. Byetta is currently available as a treatment for Diabetes mellitus type 2. Some, but not all, patients find that they lose substantial weight when taking Byetta. Drawbacks of Byetta include that it must be injected subcutaneously twice daily, and that it causes severe nausea in some patients, especially when therapy is initiated. Byetta is recommended only for patients with Type 2 Diabetes. A somewhat similar drug, Symlin, is currently available for treating diabetes and is in testing for treating obesity in non-diabetics.

Pramlintide

Pramlintide (Symlin) is a synthetic analogue of the hormone Amylin, which in normal people is secreted by the pancreas in response to eating. Among other effects, Amylin delays gastric emptying and promotes a feeling of satiety. Many diabetics are deficient in Amylin. Currently, Symlin is only approved to be used along with insulin by Type 1 and Type 2 diabetics. However, Symlin is currently being tested in non-diabetics as a treatment for obesity. A drawback is that Symlin must be injected at mealtimes.

Other drugs

Other weight loss drugs have also been associated with medical complications, such as fatal pulmonary hypertension and heart valve damage due to Redux and Fen-phen, and hemorrhagic stroke due phenylpropanolamine. Many of these substances are related to amphetamine.

Unresearched nonprescription products or programs for weight loss are heavily promoted by mail and print advertising and on the internet. The US Food and Drug Administration recommends caution with use of these products, since many of the claims of safety and effectiveness are unsubstantiated. Individuals with anorexia nervosa and some athletes try to control body weight with laxatives, diet pills or diuretic drugs, although these generally have no impact on body fat. Products that work as a laxative can cause the blood's potassium level to drop, which may cause heart and/or muscle problems. Pyruvate is a popular product that may result in a small amount of weight loss. However, pyruvate, which is found in red apples, cheese, and red wine, has not been thoroughly studied and its weight loss potential has not been scientifically established.

Phentermine/topiramate

The combination of phentermine and topiramate, brand name Qsymia (formerly Qnexa) was approved by the U.S. FDA on July 17, 2012, as an obestity treatment complementary to a diet and exercise regimen.

Features of a Good Weight Loss Program | Milen's Health


Alternative medicine

Some supplements and alternative medicine have insufficient evidence to support or oppose their use.

Is Yoga Good for Weight Loss? - Meditation Techniques for Beginners


Side effects

Some anti-obesity drugs can have severe, even, lethal side effects, fen-phen being a famous example. Fen-phen was reported through the FDA to cause abnormal echocardiograms, heart valve problems, and rare valvular diseases. One of, if not the first, to sound alarms was Sir Arthur MacNalty, Chief Medical Officer (United Kingdom). As early as the 1930s, he warned against the use of dinitrophenol as an anti-obesity medication and the injudicious and/or medically unsupervised use of thyroid hormone to achieve weight reduction. The side effects are often associated with the medication's mechanism of action. In general, stimulants carry a risk of high blood pressure, faster heart rate, palpitations, closed-angle glaucoma, drug addiction, restlessness, agitation, and insomnia.

Another drug, orlistat, blocks absorption of dietary fats, and as a result may cause oily spotting bowel movements (steatorrhea), oily stools, stomach pain, and flatulence. A similar medication designed for patients with Type 2 diabetes is Acarbose; which partially blocks absorption of carbohydrates in the small intestine, and produces similar side effects including stomach pain and flatulence.

Physical Exercise - Weight Loss Workouts | Weight Loss Terms ...


Limitations of current knowledge

The limitation of drugs for obesity is that we do not fully understand the neural basis of appetite and how to modulate it. Appetite is clearly a very important instinct to promote survival. Arguably any drug that would abolish appetite may carry a high mortality risk and may be unsuitable for clinical use.

Because the human body uses various chemicals and hormones to protect its stores of fat (a reaction probably useful to our ancestors when food was scarce in the past,) there has not yet been found a 'silver bullet', or a way to completely circumvent this natural habit of protecting excess food stores. Because of this, anti-obesity drugs are not presently a practical long-term solution for people who are overweight.

In order to circumvent the number of feedback mechanisms that prevent most monotherapies from producing sustained large amounts of weight loss, it has been hypothesized that combinations of drugs may be more effective by targeting multiple pathways and possibly inhibiting feedback pathways that work to cause a plateau in weight loss. This was evidenced by the success of the combination of phentermine and fenfluramine or dexfenfluramine, popularly referred to phen-fen, in producing significant weight loss but fenfluramine and dexfenfluramine were pulled from the market due to safety fears regarding a potential link to heart valve damage. The damage was found to be a result of activity of fenfluramine and dexfenfluramine at the 5-HT2B serotonin receptor in heart valves. Newer combinations of SSRIs and phentermine, known as phenpro, have been used with equal efficiency as fenphen with no known heart valve damage due to lack of activity at this particular serotonin receptor due to SSRIs. There has been a recent resurgence in combination therapy clinical development with the development of 3 combinations: Qsymia (topiramate + phentermine), Empatic (bupropion + zonisamide) and Contrave (bupropion + naltrexone).

Array

Future developments

Other classes of drugs in development include lipase inhibitors, similar to orlistat. Another lipase inhibitor, called GT 389-255, was being developed by Peptimmune (licensed from Genzyme). This was a novel combination of an inhibitor and a polymer designed to bind the undigested triglycerides therefore allowing increased fat expulsion without side effects such as oily stools that occur with orlistat. The development stalled as Phase 1 trials were conducted in 2004 and there was no further human clinical development afterward. In 2011, Peptimmune filed for Chapter 7 Liquidation.

Another potential long-term approach to anti-obesity medication is through the development of ribonucleic acid interference (RNAi). Animal studies have illustrated that the deletion of the RIP140 gene in mice by genetic knockdown results in the lack of fat accumulation, even when mice are fed a high fat diet. Similarly, another nuclear hormone receptor co-repressor, SMRT, has demonstrated an opposing effect in genetically engineered mice. Dr. Russell Nofsinger and Dr. Ronald Evans of the Salk Institute showed that disruption of the molecular interaction between SMRT and their nuclear hormone receptor partners leads to increased adiposity and a decreased metabolic rate. These studies suggest that new drugs targeting the molecular interaction between nuclear hormone receptors and their regulatory cofactors could provide a useful new category of therapeutic targets to be developed in an effort to control obesity.

Another approach is to induce a sense of satiety by occupying space in the gastric and intestinal cavities. One clinical trial involves a hydrogel (Gelesis) made of indigestible, food-grade materials. Another pilot study uses pseudobezoars.

Other drugs in clinical trials as of October 2009 include Cetilistat and TM38837.

Array

See also

  • Weight loss effects of water


References



Further reading

Boss, Olivier; Karl G. Hofbauer (2004). Pharmacotherapy of obesity: options and alternatives. Boca Raton: CRC Press. ISBN 0-415-30321-4. 



External links

  • Prescription Medications for the Treatment of Obesity


Interesting Informations

Looking products related to this topic, find out at Amazon.com

Source of the article : here



0 komentar :

Related Posts Plugin for WordPress, Blogger...