Jo Chiti has battled weight for most of her life. “When you’re heavy as a woman, it’s depressing. It affects you emotionally,” she said.

Chiti stopped eating high fat foods, began exercising…and lost 18 kilograms. New research shows that obesity costs the United States $147 billion a year, or $1,400 a year more, for an obese person than for someone of normal weight.

Obesity costs Americans more

That’s what a study funded by the U.S. Centers for Disease Control says. What’s driving those costs are prescription drugs for obesity-related diseases such as diabetes.

Health economist Eric Finkelstein is the study’s lead author. “The only way to show real savings in health expenditures in the future is through efforts to reduce the prevalence of obesity and related health conditions,” he said.

Finkelstein says what’s alarming is not just the number of Americans who have tipped their scales, but the pace at which they’re doing it. Finkelstein says obesity affects all racial and ethnic groups, the rich and poor, and most dramatically, America’s children.

One in every five children is obese or overweight.

With food everywhere designed to tempt the tastebuds, Dr. Thomas Frieden, the director of the CDC says weight gain is hard to prevent. “If you go with the flow [fit in with others] in America today, you will end up overweight or obese,” he asserts. “This is not a result of a change in our genes. What has changed is our environment.”

Dr. Frieden says Americans consume 250 more calories per day than they did 20 years ago. He says the rising obesity rate is the single greatest contributor to a national epidemic of diabetes.

Reversing obesity requires behavior modifications

To help combat the obesity crisis, public health experts discussed the need to change people’s behavior by promoting exercise and good nutrition.
Federal stimulus money would go to local communities to encourage grocery stores to sell more fresh produce in poorer neighborhoods and to get more fruits and vegetables into school lunches.

Finkelstein says because high-calorie, low-nutrient foods cost less than fruits and vegetables, it is harder to stay on a healthy diet, and as people use more technology, they tend to be more sedentary.

As for Jo Chiti, she is excited about the changes she has made. “It feels great. I feel like a different person,” she said.

If only public health officials could bottle that enthusiasm and spoon feed it to others…

Related posts:

1. The New Obesity Scare Statistics
2. Gastric bypass surgery treats morbid obesity

SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remissions. The disease occurs nine times more often in women than in men, especially between the ages of 15 and 50, and is more common in those of non-European descent.

SLE is treatable through addressing its symptoms, mainly with corticosteroids and immunosuppressants; there is currently no cure. SLE can be fatal, although with recent medical advances, fatalities are becoming increasingly rare. Survival for people with SLE in the United States, Canada, and Europe is approximately 95% at five years, 90% at 10 years, and 78% at 20 years.

Signs and symptoms

SLE is one of several diseases known as “the great imitators” because it often mimics or is mistaken for other illnesses. SLE is a classical item in differential diagnosis, because SLE symptoms vary widely and come and go unpredictably. Diagnosis can thus be elusive, with some people suffering unexplained symptoms of untreated SLE for years.

Common initial and chronic complaints include fever, malaise, joint pains, myalgias, fatigue, and temporary loss of cognitive abilities. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms (see below), however, they are considered suggestive.

As many as 30% of sufferers have some dermatological symptoms (and 65% suffer such symptoms at some point), with 30% to 50% suffering from the classic malar rash(or butterfly rash) associated with the disease. Some may exhibit thick, red scaly patches on the skin (referred to as discoid lupus). Alopecia; mouth, nasal, and vaginal ulcers; and lesions on the skin are also possible manifestations.

Musculoskeletal manifestations

The most commonly sought medical attention is for joint pain, with the small joints of the hand and wrist usually affected, although all joints are at risk. The Lupus Foundation of America estimates that more than 90 percent will experience joint and/or muscle pain at some time during the course of their illness. Unlike rheumatoid arthritis, lupus arthritis is less disabling and usually does not cause severe destruction of the joints. Fewer than ten percent of people with lupus arthritis will develop deformities of the hands and feet. SLE patients are at particular risk of developing osteoarticular tuberculosis.

It is suggested that there might be an association between rheumatoid arthritis and SLE, and that SLE is associated with an increased risk of bone fractures in relatively young women.

Hematological manifestations

Anemia and iron deficiency may develop in up to 50% of cases. Low platelet and white blood cell counts may be due to the disease or a side-effect of pharmacological treatment. People with SLE may have an association with antiphospholipid antibody syndrome (a thrombotic disorder), wherein autoantibodies to phospholipids are present in their serum. Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged PTT (which usually occurs in hemorrhagic disorders) and a positive test for antiphospholipid antibodies; the combination of such findings have earned the term lupus anticoagulant-positive. Another autoantibody finding in SLE is the anticardiolipin antibody, which can cause a false positive test for syphilis.

Cardiac manifestations

A person with SLE may have inflammation of various parts of the heart, such as pericarditis, myocarditis, and endocarditis. The endocarditis of SLE is characteristically noninfective (Libman-Sacks endocarditis) and involves either themitral valve or the tricuspid valve. Atherosclerosis also tends to occur more often and advances more rapidly than in the general population.

Pulmonary manifestations

Lung and pleura inflammation can cause pleuritis, pleural effusion, lupus pneumonitis, chronic diffuse interstitial lung disease, pulmonary hypertension, pulmonary emboli, pulmonary hemorrhage, and shrinking lung syndrome.

Renal involvement

Painless hematuria or proteinuria may often be the only presenting renal symptom. Acute or chronic renal impairment may develop with lupus nephritis, leading to acute or end-stage renal failure. Because of early recognition and management of SLE, end-stage renal failure occurs in less than 5% of cases.

A histological hallmark of SLE is membranous glomerulonephritis with “wire loop” abnormalities. This finding is due to immune complex deposition along the glomerular basement membrane, leading to a typical granular appearance in immunofluorescence testing.

Neuropsychiatric manifestations

Neuropsychiatric syndromes can result when SLE affects the central or peripheral nervous system. The American College of Rheumatology defines 19 neuropsychiatric syndromes in systemic lupus erythematosus. The most common neuropsychiatric disorder people with SLE have is headache, although the existence of a specific lupus headache and the optimal approach to headache in SLE cases remains controversial. Other common neuropsychiatric manifestation of SLE include cognitive dysfunction, mood disorder, cerebrovascular disease, seizures, polyneuropathy, anxiety disorder, and psychosis. It can rarely present with intracranial hypertension syndrome, characterized by an elevated intracranial pressure, papilledema, and headache with occasional abducens nerve paresis, absence of a space-occupying lesion or ventricular enlargement, and normal cerebrospinal fluidchemical and hematological constituents.

More rare manifestations are acute confusional state, Guillain-Barré syndrome, aseptic meningitis, autonomic disorder, demyelinating syndrome, mononeuropathy (which might manifest as mononeuritis multiplex), movement disorder(more specifically, chorea), myasthenia gravis, myelopathy, cranial neuropathy and plexopathy.

Systemic manifestations

Fatigue in SLE is probably multifactorial and has been related not only to disease activity or complications such as anemia or hypothyroidism but also to pain, depression, poor sleep quality, poor physical fitness and perceived lack ofsocial support.

Other rarer manifestations

Lupus gastroenteritis, menstrual disturbances, lupus pancreatitis, lupus cystitis, autoimmune inner ear disease, parasympathetic dysfunction, hemophagocytic syndrome, systemic vasculitis, and like many autoimmune diseases can be complicated by myeloid malignancies.

Causes

There is no one specific cause of SLE. There are however a number of environmental triggers and a number of genetic susceptibilities.

Genetics

The first mechanism may arise genetically. Research indicates that SLE may have a genetic link. SLE does run in families, but no single, causal, gene has been identified. Instead, multiple genes appear to influence a person’s chance of developing lupus when triggered by environmental factors. The most important genes are located in the HLAregion on chromosome 6, where mutations may occur randomly (de novo) or may be inherited. HLA class I, class II, and class III are associated with SLE, but only class I and class II contribute independently to increased risk of SLE.

Environmental triggers

The second mechanism may be due to environmental factors. These factors may not only exacerbate existing SLE conditions but also trigger the initial onset. They include certain medications (such as some antidepressants and antibiotics), extreme stress, exposure to sunlight, hormones, and infections. UV radiation has been shown to trigger the photosensitive lupus rash and some evidence suggests that UV light might be capable of altering the structure of the DNA, leading to the creation of autoantibodies. Sex hormones such as estrogen play an important role in the occurrence of SLE and it is observed that during reproductive years, the frequency of SLE is 10 times greater in females than in males.

Researchers have sought to find a connection between certain infectious agents (viruses and bacteria), but no pathogen can be consistently linked to the disease. Some researchers have found that women with silicone gel-filled breast implants have produced antibodies to their own collagen, but it is not known how often these antibodies occur in the general population, and there are no data that show that these antibodies cause connective tissue diseases such as SLE. There is also a small but growing body of evidence linking SLE to lipstick usage, although lipstick manufacturers do not appear to be concerned about it.

Drug reactions

Drug-induced lupus erythematosus is a (generally) reversible condition that usually occurs in people being treated for a long-term illness. Drug-induced lupus mimics SLE. However, symptoms of drug-induced lupus generally disappear once the medication that triggered the episode is stopped. There are about 400 medications that can cause this condition, the most common of which are procainamide, hydralazine, quinidine, and phenytoin.

Non-SLE forms of lupus

Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed by biopsy of skin rash on the face, neck, or scalp.

Pathophysiology

One manifestation of SLE is abnormalities in apoptosis, a type of programmed cell death in which aging or damaged cells are neatly disposed of as a part of normal growth or functioning.

Transmission

In SLE, the body’s immune system produces antibodies against itself, particularly against proteins in the cell nucleus. SLE is triggered by environmental factors that are unknown.

“All the key components of the immune system are involved in the underlying mechanisms” of SLE, according to Rahman, and SLE is the prototypical autoimmune disease. The immune system must have a balance (homeostasis) between being sensitive enough to protect against infection, and being too sensitive and attacking the body’s own proteins (autoimmunity). From an evolutionary perspective, according to Crow, the population must have enough genetic diversity to protect itself against a wide range of possible infection; some genetic combinations result in autoimmunity. The likely environmental triggers include ultraviolet light, drugs, and viruses. These stimuli cause the destruction of cells and expose their DNA, histones, and other proteins, particularly parts of the cell nucleus. Because of genetic variations in different components of the immune system, in some people the immune system attacks these nuclear-related proteins and produces antibodies against them. In the end, these antibody complexes damage blood vessels in critical areas of the body, such as the glomeruli of the kidney; these antibody attacks are the cause of SLE. Researchers are now identifying the individual genes, the proteins they produce, and their role in the immune system. Each protein is a link on the autoimmune chain, and researchers are trying to find drugs to break each of those links.

SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement.

Abnormalities in apoptosis

• Apoptosis is increased in monocytes and keratinocytes
• Expression of Fas by B cells and T cells is increased
• There are correlations between the apoptotic rates of lymphocytes and disease activity.

Tingible body macrophages (TBMs) are large phagocytic cells in the germinal centers of secondary lymph nodes; they express CD68 protein. These cells normally engulf B cells that have undergone apoptosis after somatic hypermutation. In some people with SLE, significantly fewer TBMs can be found, and these cells rarely contain material from apoptotic B cells. Also, uningested apoptotic nuclei can be found outside of TBMs. This material may present a threat to the tolerization of B cells and T cells. Dendritic cells in the germinal center may endocytose such antigenic material and present it to T cells, activating them. Also, apoptotic chromatin and nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells that may have randomly acquired self-specificity through somatic hypermutation.

Clearance deficiency

The exact mechanisms for the development of SLE are still unclear, since the pathogenesis is a multifactorial event. Beside discussed causation’s, impaired clearance of dying cells is a potential pathway for the development of this systemic autoimmune disease. This includes deficient phagocytic activity and scant serum components in addition to increased apoptosis.

Monocytes isolated from whole blood of SLE sufferers show reduced expression of CD44 surface molecules involved in the uptake of apoptotic cells. Most of the monocytes and tingible body macrophages (TBM), which are found in the germinal centres of lymph nodes, even show a definitely different morphology; they are smaller or scarce and die earlier. Serum components likecomplement factors, CRP, and some glycoproteins are, furthermore, decisively important for an efficiently operating phagocytosis. With SLE, these components are often missing, diminished, or inefficient.

The clearance of early apoptotic cells is an important function in multicellular organisms. It leads to a progression of the apoptosis process and finally to secondary necrosis of the cells if this ability is disturbed. Necrotic cells release nuclear fragments as potential autoantigens as well as internal danger signals, inducing maturation of dendritic cells (DC), since they have lost their membranes’ integrity. Increased appearance of apoptotic cells also simulates inefficient clearance. That leads to maturation of DC and also to the presentation of intracellular antigens of late apoptotic or secondary necrotic cells, via MHC molecules. Autoimmunity possibly results by the extended exposure to nuclear and intracellular autoantigens derived from late apoptotic and secondary necrotic cells. B and T cell tolerance for apoptotic cells is abrogated, and the lymphocytes get activated by these autoantigens; inflammation and the production of autoantibodies by plasma cells is initiated. A clearance deficiency in the skin for apoptotic cells has also been observed in people with cutaneous lupus erythematosus (CLE).

Accumulation in germinal centres (GC)

In healthy conditions, apoptotic lymphocytes are removed in germinal centres by specialised phagocytes, the tingible body macrophages (TBM), which is why no free apoptotic and potential autoantigenic material can be seen. In some people with SLE, accumulation of apoptotic debris can be observed in GC because of an ineffective clearance of apoptotic cells. In close proximity to TBM, follicular dendritic cells (FDC) are localised in GC, which attach antigen material to their surface and, in contrast to bone marrow-derived DC, neither take it up nor present it via MHC molecules.

Autoreactive B cells can accidentally emerge during somatic hypermutation and migrate into the GC light zone. Autoreactive B cells, maturated coincidentally, normally do not receive survival signals by antigen planted on follicular dendritic cells, and perish by apoptosis. In the case of clearance deficiency, apoptotic nuclear debris accumulates in the light zone of GC and gets attached to FDC. This serves as a germinal centre survival signal for autoreactive B-cells. After migration into the mantle zone, autoreactive B cells require further survival signals from autoreactive helper T cells, which promote the maturation of autoantibody-producing plasma cells and B memory cells. In the presence of autoreactive T cells, a chronic autoimmune disease may be the consequence.

Anti-nRNP autoimmunity

Autoantibodies to nRNP A and nRNP C initially targeted restricted, proline-rich motifs. Antibody binding subsequently spread to other epitopes. The similarity and cross-reactivity between the initial targets of nRNP and Sm autoantibodies identifies a likely commonality in cause and a focal point for intermolecular epitope spreading.

Others

Elevated expression of HMGB1 was found in the sera of patients and mice with systemic lupus erythematosus, High Mobility Group Box 1 (HMGB1) is a nuclear proteinparticipating in chromatinarchitecture and transcriptional regulation. Recently, there is increasing evidence that HMGB1 contributes to the pathogenesis of chronicinflammatory and autoimmune diseases due to its pro-inflammatory and immunostimulatory properties.

Microphotograph of a histological section of human skin prepared for direct immunofluorescence using an anti-IgG antibody. The skin is from a person with systemic lupus erythematosus and shows IgG deposits at two different places: The first is a bandlike deposit along the epidermalbasement membrane (“lupus band test” is positive); the second is within the nuclei of the epidermal cells (antinuclear antibodies are present).

Laboratory tests

Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for SLE. Several techniques are used to detect ANAs. Clinically the most widely used method is indirect immunofluorescence. The pattern of fluorescence suggests the type of antibody present in the patient’s serum.

ANA screening yields positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal individuals. Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies (which are linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE. The anti-dsDNA antibody titers also tend to reflect disease activity, although not in all cases. Other ANA that may occur in SLE sufferers are anti-U1 RNP (which also appears in systemic sclerosis), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more common in Sjögren’s syndrome). SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus.

Other tests routinely performed in suspected SLE are complement system levels (low levels suggest consumption by the immune system), electrolytes and renal function (disturbed if the kidney is involved), liver enzymes, and complete blood count.

Previously, the lupus erythematosus (LE) cell test was not commonly used for diagnosis because those LE cells are only found in 50–75% of SLE cases, and are also found in some people with rheumatoid arthritis, scleroderma, and drug sensitivities. Because of this, the LE cell test is now performed only rarely and is mostly of historical significance.

Diagnostic criteria

Some physicians make a diagnosis on the basis of the American College of Rheumatology (ACR) classification criteria. The criteria, however, were established mainly for use in scientific research including use in randomized controlled trials which require higher confidence levels, so some people with SLE may not pass the full criteria.

The American College of Rheumatology established eleven criteria in 1982, which were revised in 1997 as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. For the purpose of identifying patients for clinical studies, a person has SLE if any 4 out of 11 symptoms are present simultaneously or serially on two separate occasions.

1. Serositis: Pleuritis (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).
2. Oral ulcers (includes oral or nasopharyngeal ulcers).
3. Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.
4. Photosensitivity (exposure to ultraviolet light causes skin rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.
5. Blood—hematologic disorder—hemolytic anemia (low red blood cell count) or leukopenia (white blood cell count<4000/µl), lymphopenia (<1500/µl) or thrombocytopenia (<100000/µl) in the absence of offending drug; sensitivity = 59%; specificity = 89%. Hypocomplementemia is also seen, due to either consumption of C3 and C4 by immune complex-induced inflammation or to congenitally complement deficiency, which may predispose to SLE.
6. Renal disorder: More than 0.5g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%.
7. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.
8. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, and/or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%. Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons).
9. Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.
10. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.
11. Discoid rash (red, scaly patches on skin that cause scarring); sensitivity = 18%; specificity = 99%.

The mnemonic to remember the 11 symptoms is ‘SOAP BRAIN MD’.

Some people, especially those with antiphospholipid syndrome, may have SLE without four criteria, and also SLE may present with features other than those listed in the criteria.

Recursive partitioning has been used to identify more parsimonious criteria. This analysis presented two diagnostic classification trees:

1. Simplest classification tree: SLE is diagnosed if a person has an immunologic disorder (anti-DNA antibody, anti-Smith antibody, false positive syphilis test, or LE cells) or malar rash.

• sensitivity = 92%
• specificity = 92%

2. Full classification tree: Uses 6 criteria.

• sensitivity = 97%
• specificity = 95%

Other alternative criteria have been suggested.

Treatment

Being a chronic disease with no known cure, the treatment of SLE is symptomatic. In essence, this involves preventing flares and reducing their severity and duration when they occur. Currently, medication is the main form of treatment.

Medications

Due to the variety of symptoms and organ system involvement with SLE, its severity in an individual must be assessed in order to successfully treat SLE. Mild or remittant disease can sometimes be safely left untreated. If required, nonsteroidal anti-inflammatory drugs and antimalarials may be used.

Disease-modifying antirheumatic drugs

Disease-modifying antirheumatic drugs (DMARDs) are used preventively to reduce the incidence of flares, the process of the disease, and lower the need for steroid use; when flares occur, they are treated with corticosteroids. DMARDs commonly in use are antimalarials such as plaquenil and immunosuppressants (e.g. methotrexateand azathioprine). Hydroxychloroquine is an FDA-approved antimalarial used for constitutional, cutaneous, and articular manifestations, whereas cyclophosphamide is used for severe glomerulonephritis or other organ-damaging complications. In 2005, mycophenolic acid became accepted for treatment of lupus nephritis.

Immunosuppressive drugs

In more severe cases, medications that modulate the immune system (primarily corticosteroids and immunosuppressants) are used to control the disease and prevent recurrence of symptoms (known as flares). Depending on the dosage, people that require steroids may develop Cushing’s syndrome, side-effects of which may include obesity, puffy round face, diabetes mellitus, large appetite, difficulty sleeping and osteoporosis. Those side-effects can subside if and when the large initial dosage is reduced, but long-term use of even low doses can cause elevated blood pressure and cataracts.

Analgesia

Since a large percentage of people with SLE suffer from varying amounts of chronic pain, stronger prescription analgesics (pain killers) may be used if over-the-counter drugs (mainly nonsteroidal anti-inflammatory drugs) do not provide effective relief. Moderate pain is typically treated with mild prescription opiates such as dextropropoxypheneand co-codamol. Moderate to severe chronic pain is treated with stronger opioids, such as hydrocodone or longer-acting continuous-release opioids, such as oxycodone, MS Contin, or Methadone. The Fentanyl duragesic transdermal patch is also a widely-used treatment option for the chronic pain caused by complications because of its long-acting timed release and ease of use. When opioids are used for prolonged periods, drug tolerance, chemical dependency, and addiction may occur. Opiate addiction is not typically a concern, since the condition is not likely to ever completely disappear. Thus, lifelong treatment with opioids is fairly common for chronic pain symptoms, accompanied by periodic titration that is typical of any long-term opioid regimen.

Lifestyle changes

Avoiding sunlight is the primary change to the lifestyle of SLE sufferers, as sunlight is known to exacerbate the disease. Drugs unrelated to SLE should be prescribed only when known not to exacerbate the disease. Occupational exposure to silica, pesticides and mercury can also make the disease worsen.

Fasting and massive nutrition changes, towards a low fat, mostly strict vegetarian, wholesome diet, also have been reported as a possibility to lessen the symptoms or even induce a remission.

Renal transplantation

Renal transplants are the treatment of choice for end-stage renal disease, which is one of the complications of lupus nephritis, but the recurrence of the full disease is common in up to 30% of patients.

Prevention

SLE is not understood well enough to be prevented, but, when the disease develops, quality of life can be improved through flare prevention. The warning signs of an impending flare include increased fatigue, pain, rash, fever, abdominal discomfort, headache, and dizziness. Early recognition of warning signs and good communication with a doctor can help individuals remain active, experience less pain, and reduce medical visits.

Complications during pregnancy

While most infants born to mothers who have SLE are healthy, pregnant mothers with SLE should remain under a doctor’s care until delivery. Neonatal lupus is rare, but identification of mothers at highest risk for complications allows for prompt treatment before or after birth. In addition, SLE can flare during pregnancy, and proper treatment can maintain the health of the mother longer. Women pregnant and known to have the antibodies for anti-Ro (SSA) or anti-La (SSB) should have echocardiograms during the 16th and 30th weeks of pregnancy to monitor the health of the heart and surrounding vasculature.

Even contraception was routinely advised in treating SLE patients, getting pregnant during active disease was eventually found. Lupus nephritis was the most common manifestation. Overall live-birth was 72.7%. Pregnancy lost was due to abortion and dead fetus in utero. Pregnancy outcome was worse in SLE patients who had disease flares up or emerging during pregnancy.

Prognosis

In the 1950s, most people diagnosed with SLE lived fewer than five years. Advances in diagnosis and treatment have improved survival to the point where over 90% now survive for more than ten years, and many can live relatively asymptomatically. Prognosis is normally worse for men and children than for women; however, if symptoms are present after age 60, the disease tends to run a more benign course. Early mortality, within 5 years, is due to organ failure or overwhelming infections, both of which can be modified by early diagnosis and treatment. The mortality risk is fivefold when compared to the normal population in the late stages, which can be attributed to cardiovascular diseases acquired from corticosteroid therapy. To reduce potential for cardiovascular issues, steroids should be used at the lowest dose for the shortest possible period. High serum creatinine, hypertension, nephrotic syndrome, anemia and hypoalbuminemia are poor prognostic factors. The ANA is the most sensitive screening test for evaluation, whereas anti-Sm (anti-Smith) is the most specific. The dsDNA (double-stranded DNA) antibody is also fairly specific and often fluctuates with disease activity; as such, the dsDNA titer is sometimes useful to monitor disease flares or response to treatment.

Epidemiology

The rate of SLE varies considerable between countries, ethnicity, by gender, and has changed over time. In the United States the prevalence of SLE is estimated to be about 53 per 100,000, translating to about 1 million people in the US being affected. In Northern Europe the rate is about 40 per 100,000 people. SLE occurs more frequently and with greater severity among those of non-European descent. That rate has been found to be as high as 159 per 100,000 among those of Afro-Caribbean descent.

SLE, like many autoimmune diseases, affects females more frequently than males, at a rate of almost 9 to 1.

The incidence of SLE in the United States increased from 1.0 in 1955 to 7.6 in 1974. Whether the increase is due to better diagnosis or to increasing frequency of the disease is unknown.

There are several explanations ventured for the term lupus erythematosus. Lupus is Latin for wolf, and “erythro” is derived from ερυθρός, Greek for “red.” All explanations originate with the reddish, butterfly-shaped malar rash that the disease classically exhibits across the nose and cheeks.

1. In various accounts, some doctors thought the rash resembled the pattern of fur on a wolf’s face.
2. In other accounts, doctors thought that the rash, which was often more severe in earlier centuries, created lesions that resembled wolf bites or scratches.
3. Another account claims that the term “lupus” did not come from Latin directly, but from the term for a French style of mask that women reportedly wore to conceal the rash on their faces. The mask is called a “loup,” French for “wolf.”
4. Another common explanation for the term is that the disease’s course involves repeated attacks like those of a voracious predator, leaving behind the red blotches.

History

The history of SLE can be divided into three periods: classical, neoclassical, and modern. The classical period began when the disease was first recognized in the Middle Agesand saw the description of the dermatological manifestation of the disorder. The term lupus is attributed to 12th-century physician Rogerius, who used it to describe the classic malar rash. The neoclassical period was heralded by Móric Kaposi’s recognition in 1872 of the systemic manifestations of the disease. The modern period began in 1948 with the discovery of the LE cell (the lupus erythematosus cell—a misnomer, as it occurs with other diseases as well) and is characterised by advances in our knowledge of the pathophysiology and clinical-laboratory features of the disease, as well as advances in treatment.

Medical historians have theorized that people with porphyria (a disease that shares many symptoms with SLE) generated folklore stories of vampires and werewolves, due to the photosensitivity, scarring, hair growth, and porphyrin brownish-red stained teeth in severe recessive forms of porphyria (or combinations of the disorder, known as dual, homozygous, or compound heterozygous porphyrias).

Useful medication for the disease was first found in 1894, when quinine was first reported as an effective therapy. Four years later, the use of salicylates in conjunction with quinine was noted to be of still greater benefit. This was the best available treatment until the middle of the twentieth century, when Hench discovered the efficacy of corticosteroids in the treatment of SLE.

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4. Human clinical evaluations—the surest way to show effectiveness. The best way to test effectiveness and safety of a nutritional product is to see how it works with real patients. The Functional Medicine Research Center℠ (FMRC)—the clinical research arm of Metagenics—is an on-site clinic staffed by medical professionals who recommend our nutritional approaches and monitor their success. The FMRC also conducts clinical trials that have been published in respected peer-reviewed journals.

No other company in our market segment can offer this kind of first-hand knowledge that can only be achieved a clinical setting.

5. Scientific staff and facilities—the best in our business. Not every professional nutrition company has its own staff of dedicated medical and technical professionals. We have one of the largest in-house scientific staffs—MDs, PhDs, and others—in our industry segment.

Plus we have some of the industry’s most progressive research facilities and labs, such as our MetaProteomics labs for testing the effects of nutrients on proteins and genetic expression.

It’s easy to see why so many health care professionals and their patients rely on our products.

Added Measures to Maximize Effectiveness & Value

Going above and beyond is just routine for us. Here are just a few more examples:

Appropriate ingredient form & dose—so you can be sure. Our goal is to use highly absorbable nutrient forms so the body has a greater chance of using it the way it should to promote health. This is particularly important with certain key nutrients that may be poorly absorbed, or for people who have absorption concerns. And the dosages we recommend are based on scientific research that document effectiveness and predicted safety when used as intended.

The right delivery form—to meet the demands of patients and appropriate to the ingredients. We don’t have a “one form fits all” policy. Not every ingredient should be made into a tablet or a capsule. So the ingredients often decide the delivery form for each product—tablet, chewable, liquid, capsule, softgel, soft chew, bar, or powder.

And a product can’t work if people won’t take it. So we also consider what people prefer. That’s why we offer many of our products in a variety of forms and flavors.

Tablets made for ultimate performance—for better results. Nobody pays more attention to tablets than we do. Our tableting technology makes sure they disintegrate within a short time, to release ingredients for optimal absorption.

And we don’t stop testing even after we create the final formula. Every product batch is tested to make sure our high tablet standards are met.

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A gastric bypass first divides the stomach into a small upper pouch and a much larger, lower “remnant” pouch and then re-arranges the small intestine to allow both pouches to stay connected to it. Surgeons have developed several different ways to reconnect the intestine, thus leading to several different GBP names. Any GBP leads to a marked reduction in the functional volume of the stomach, accompanied by an altered physiological and psychological response to food. The resulting weight loss, typically dramatic, markedly reduces comorbidities. The long-term mortality rate of gastric bypass patients has been shown to be reduced by up to 40%; however, complications are common and surgery-related death occurs within one month in 2% of patients.

Graphic of a gastric bypass using a Roux-en-Y anastomosis.

Comorbid conditions

Life-threatening health problems arise from obesity as a consequence of its mechanical or metabolic effects. These comorbidities may in turn lead to severe deterioration of health, shortened life expectancy, and lower quality of life.

Major comorbidities include:

• Atherosclerotic cardiovascular disease. Obesity is not only associated with the occurrence of hypercholesterolemia and hypertriglyceridemia, but it is also a factor in the occurrence of atherosclerosis, the deposition of fats within the walls of the blood vessels. This leads to conditions such as coronary artery disease, congestive heart failure, and “hardening of the arteries.” This group of conditions is a leading cause of death in the United States.
• Diabetes mellitus type 2 occurs mostly in middle and old age, but it is up to 40 times more likely in those who are severely overweight. It is associated with ASCVD, kidney failure, blindness, nerve damage, and amputations of the extremities, and is also a leading overall cause of death in the United States. Dysmetabolic Syndrome X, a pre-diabetic condition often associated with obesity, is accompanied by elevated levels of insulin in the blood and a high incidence of early development of coronary heart disease.
• Essential hypertension or “high blood pressure”, is much more common in obese individuals. It can lead to early development of ASCVD, as well as to kidney disease. Weight loss is considered to be an important feature of treatment.
• Obstructive sleep apnea (OSA) Persons with this condition tend to suffer from airway obstruction when asleep, as the muscles relax and the weight and bulk of tissues collapses the throat passages. An observer notices loud snoring, frequent periods when breathing ceases (apneas), and episodes of restlessness and partial awakening. The afflicted patient is often unaware of the nature of the problem, but may notice frequent awakening at night, dry mouth, a sense of having slept poorly, daytime drowsiness and fatigue, or inappropriate sleeping (such as at work, in meetings, or while driving). This condition has a significant associated mortality.
• Gastroesophageal reflux disease (GERD) is characterized by regurgitation (reflux) of acid and gastric contents into the esophagus, and sometimes into the back of the throat. Gastric acid and bile are very corrosive to the lining membrane of the esophagus, and cause it to become inflamed (esophagitis) and sometimes scarred (esophageal stricture). Reflux which occurs while sleeping can lead to sudden coughing and choking at night, a burning sensation in the throat (pyrosis), and inhalation of acid and stomach contents into the lungs, with the risk of hoarseness, bronchitis, pneumonia, lung abscess and lung scarring. GERD is often associated with development of asthma, and causation of asthmatic attacks, and may also be aggravated by OSA.
• Gallbladder disease is much more likely in obese individuals, being associated with formation of gallstones, usually composed of crystallized cholesterol, within the gallbladder. Although readily treatable by removal of the gallbladder (cholecystectomy), it may lead to life-threatening problems such as obstruction of the ducts from the liver, jaundice, and inflammation of the pancreas (gallstone pancreatitis).
• Liver disease is present in some degree in 90% of persons who undergo bariatric surgery, usually a manifestation of the metabolic effects of obesity on the liver. This may take the form of large fat globules within the liver cells (steatosis), chronic inflammation of the liver (steatohepatitis), and in a few instances, cirrhosis of the liver. The latter condition may lead to liver failure and the need for a liver transplant.
• Venous thromboembolic disease affects the legs, and causes swelling, thickening and discoloration of the skin, and ulceration of the skin. This condition begins with damage to the veins of the legs, associated with formation of blood clots (thrombophlebitis), often associated with an injury, a pregnancy (even use of birth-control pills or hormones), or a surgical operation. When a newly formed blood clot breaks loose, and floats through the veins to the heart and lungs, it is called a Pulmonary embolus, which may sometimes be fatal within minutes. More commonly, the blood clot remains in place locally, and heals by becoming a scar, which permanently damages the vein. Once damaged, the veins cannot fully function to return blood to the heart, and increased venous pressure in the legs causes swelling, impaired circulation in the skin, and sometimes skin breakdown. Obesity is a major risk factor in development of VTE, and may also aggravate the increased venous pressure in the legs.
• Degenerative disc disease is a progressive “wearing-out” of the cartilaginous disks between the vertebral bones of the spine. It occurs more often and earlier in life in obese persons, due to the markedly increased mechanical stress on the disks from the extra weight. Its most common sign is chronic low back pain, which may be disabling. This condition is also associated with sciatica, lumbar spondylosis, and spinal stenosis.
• Degenerative disease of the weight bearing joints, or osteoarthritis, affecting the hips, knees, ankles and feet, occurs earlier in life, and in greater degree, in obese individuals, due to the mechanical stresses of excess weight. Joint pain, loss of mobility, and joint replacement surgery are much more likely in obese persons.

Surgical indications

Gastric bypass is indicated for the surgical treatment of morbid obesity, a diagnosis which is made when the patient is seriously obese, has been unable to achieve satisfactory and sustained weight loss by dietary efforts, and is suffering from co-morbid conditions which are either life-threatening or a serious impairment to the quality of life.

In the past, serious obesity was interpreted to mean weighing at least 100 pounds (45 kg) more than the “ideal body weight”, an actuarially determined body weight at which one was estimated to be likely to live the longest, as determined by the life insurance industry. This criterion failed for persons of short stature.

In 1991, the National Institutes of Health sponsored a consensus panel whose recommendations have set the current standard for consideration of surgical treatment, the body mass index (BMI). The BMI is defined as the body weight (in kilograms), divided by the square of the height (in meters). The result is expressed as a number usually between 20 and 70, in units of kilograms per square meter.

The Consensus Panel of the National Institutes of Health (NIH) recommended the following criteria for consideration of bariatric surgery, including gastric bypass procedures:

1. People who have a body mass index (BMI) of 40 or higher. Or,
2. People with a BMI of 35 or higher with one or more related comorbid conditions.

The Consensus Panel also emphasized the necessity of multidisciplinary care of the bariatric surgical patient, by a team of physicians and therapists, to manage associated co-morbidities, nutrition, physical activity, behavior and psychological needs. The surgical procedure is best regarded as a tool which enables the patient to alter lifestyle and eating habits, and to achieve effective and permanent management of their obesity and eating behavior.

Since 1991, major developments in the field of bariatric surgery, particularly laparoscopy, have outdated some of the conclusions of the NIH panel. In 2004, a Consensus Conference was sponsored by the American Society for Bariatric Surgery (ASBS), which updated the evidence and the conclusions of the NIH panel. This Conference, composed of physicians and scientists of many disciplines, both surgical and non-surgical, reached several conclusions, amongst which were:

• Bariatric surgery is the most effective treatment for morbid obesity
• Gastric bypass is one of four types of operations for morbid obesity.
• Laparoscopic surgery is equally effective and as safe as open surgery.
• Patients should undergo comprehensive pre-operative evaluation, and have multi-disciplinary support, for optimum outcome.

Surgical techniques

The gastric bypass, in its various forms, accounts for a large majority of the bariatric surgical procedures performed. It is estimated that 140,000 such operations were performed in the United States in 2005. An increasing number of these operations are now performed by limited access techniques, termed ”laparoscopy”.

Laparoscopic surgery is performed using several small incisions, or ports, one of which conveys a surgical telescope connected to a video camera, and others permit access of specialized operating instruments. The surgeon actually views his operation on a video screen. The method is also called limited access surgery, reflecting both the limitation on handling and feeling tissues, and also the limited resolution and two-dimensionality of the video image. With experience, a skilled laparoscopic surgeon can perform most procedures as expeditiously as with an open incision — with the option of using an incision should the need arise.

The Laparoscopic Gastric Bypass, Roux-en-Y, first performed in 1993, is regarded as one of the most difficult procedures to perform by limited access techniques, but use of this method has greatly popularized the operation, with benefits which include shortened hospital stay, reduced discomfort, shorter recovery time, less scarring, and minimal risk of incisional hernia.

Essential features

The gastric bypass procedure consists in essence of:

• Creation of a small, (15–30 mL/1–2 tbsp) thumb-sized pouch from the upper stomach, accompanied by bypass of the remaining stomach (about 400 mL and variable). This restricts the volume of food which can be eaten. The stomach may simply be partitioned (typically by the use of surgical staples), or it may be totally divided into two parts (also with staplers). Total division is usually advocated, to reduce the possibility that the two parts of the stomach will heal back together (“fistulize”), negating the operation.
• Re-construction of the GI tract to enable drainage of both segments of the stomach. The technique of this reconstruction produces several variants of the operation, which differ in the lengths of small bowel used, the degree to which food absorption is affected, and the likelihood of adverse nutritional effects.

Variations of the gastric bypass

Gastric bypass, Roux en-Y (proximal)

This variant is the most commonly employed gastric bypass technique, and is by far the most commonly performed bariatric procedure in the United States. It is the operation which is least likely to result in nutritional difficulties. The small bowel is divided about 45 cm (18 in) below the lower stomach outlet, and is re-arranged into a Y-configuration, to enable outflow of food from the small upper stomach pouch, via a “Roux limb”. In the proximal version, the Y-intersection is formed near the upper (proximal) end of the small bowel. The Roux limb is constructed with a length of 80 to 150 cm (30 to 60 inches), preserving most of the small bowel for absorption of nutrients. The patient experiences very rapid onset of a sense of stomach-fullness, followed by a feeling of growing satiety, or “indifference” to food, shortly after the start of a meal.

Gastric bypass, Roux en-Y (distal)

The normal small bowel is 600 to 1000 cm (20 to 33 feet) in length. As the Y-connection is moved farther down the Gastrointestinal tract, the amount of bowel capable of fully absorbing nutrients is progressively reduced, in pursuit of greater effectiveness of the operation. The Y-connection is formed much closer to the lower (distal) end of the small bowel, usually 100 to 150 cm (40 to 60 inches) from the lower end of the bowel, causing reduced absorption (mal-absorption) of food, primarily of fats and starches, but also of various minerals, and the fat-soluble vitamins. The unabsorbed fats and starches pass into the large intestine, where bacterial actions may act on them to produce irritants and malodorous gases. These increasing nutritional effects are traded for a relatively modest increase in total weight loss.

Loop Gastric bypass (“Mini-gastric bypass”)

The first use of the gastric bypass, in 1967, used a loop of small bowel for re-construction, rather than a Y-construction as is prevalent today. Although simpler to create, this approach allowed bile and pancreatic enzymes from the small bowel to enter the esophagus, sometimes causing severe inflammation and ulceration of either the stomach or the lower esophagus. If a leak into the abdomen occurs, this corrosive fluid can cause severe consequences. Numerous studies show the loop reconstruction (Billroth II gastrojejunostomy) works more safely when placed low on the stomach, but can be a disaster when placed adjacent to the esophagus. Thus even today thousands of “loops” are used for general surgical procedures such as ulcer surgery, stomach cancer and injury to the stomach, but bariatric surgeons abandoned use of the construction in the 1970s, when it was recognized that its risk is not justified for weight management.

The Mini-Gastric Bypass, which uses the loop reconstruction, has been suggested as an alternative to the Roux en-Y procedure, due to the simplicity of its construction, which reduced the challenge of laparoscopic surgery.

Physiology of the gastric bypass

The gastric bypass reduces the size of the stomach by well over 90%. A normal stomach can stretch, sometimes to over 1000 ml, while the pouch of the gastric bypass may be 15 ml in size. The Gastric Bypass pouch is usually formed from the part of the stomach which is least susceptible to stretching. That, and its small original size, prevents any significant long-term change in pouch volume. What does change, over time, is the size of the connection between stomach and bowel, and the ability of the small bowel to hold a greater volume of food. Over time, the functional capacity of the pouch increases; by that time, weight loss has occurred, and the increased capacity serves to allow maintenance of a lower body weight.

When the patient ingests just a small amount of food, the first response is a stretching of the wall of the stomach pouch, stimulating nerves which tell the brain that the stomach is full. The patient feels a sensation of fullness, as if they had just eaten a large meal — but with just a thumbful of food. Most people do not stop eating simply in response to a feeling of fullness, but the patient rapidly learns that subsequent bites must be eaten very slowly and carefully, to avoid increasing discomfort, or even vomiting.

Food is first churned in the stomach before passing into the small bowel. When the lumen of the small bowel comes into contact with nutrients a number of hormones are released including cholecystikin (CCK) from the duodenum and PYY and GLP-1 from the ileum. These hormones inhibit further food intake and have thus been dubbed satiety factors. Ghrelin, is a hormone that is released in the stomach that stimulates hunger and food intake. Changes in circulating hormone levels after gastric bypass have been hypothesized to produce reductions in food intake and body weight in obese patients. However, these findings remain controversial, and the exact mechanisms by which gastric bypass surgery reduces food intake and body weight have yet to be elucidated.

To gain the maximum benefit from this physiology, it is important that the patient eat only at mealtimes, 2 to 3 small meals daily, and avoid snacks and grazing between meals, which can effectively “bypass the bypass”. This requires a change in eating behavior, and alteration of long-acquired habits for finding food. In almost every case where weight gain occurs late after surgery, capacity for a meal has not greatly increased. The cause of regaining weight is eating between meals, usually high-caloric snack foods. There is no known operation which can completely counteract the adverse effects of destructive eating behavior.

Complications

Any major surgery involves the potential for complications — adverse events which increase risk, hospital stay, and mortality. Some complications are common to all abdominal operations, while some are specific to bariatric surgery. A person who chooses to undergo bariatric surgery should know about these risks.

Mortality and complication rates

In experienced hands, the overall complication rate of this type of surgery ranges from 7% for laparoscopic procedures to 14.5% for operations through open incisions, during the 30 days following surgery. Mortality for this study was 0% in 401 laparoscopic cases, and 0.6% in 955 open procedures. Similar mortality rates – 30-day mortality of 0.11%, and 90-day mortality of 0.3% – have been recorded in the U.S. Centers of Excellence program, the results from 33,117 operations at 106 centers.

Mortality is affected by complications, which in turn are affected by pre-existing risk factors such as degree of obesity, heart disease, obstructive sleep apnea, diabetes mellitus, and history of prior pulmonary embolism. It is also affected by the experience of the operating surgeon: the “learning curve” for laparoscopic bariatric surgery is estimated to be about 100 cases. Unfortunately, the way a surgeon becomes experienced in dealing with problems is by encountering those problems over time.

Complications of abdominal surgery

Infection

Infection of the incisions or of the inside of the abdomen (peritonitis, abscess) may occur, due to release of bacteria from the bowel during the operation. Nosocomial infection, such as pneumonia, bladder or kidney infections, and sepsis (bloodborne infection) are also possible. Effective short-term use of antibiotics, diligent respiratory therapy, and encouragement of activity within a few hours after surgery, can reduce the risks of infections.

Hemorrhage

Many blood vessels must be cut in order to divide the stomach and to move the bowel. Any of these may later begin bleeding, either into the abdomen (intra-abdominal hemorrhage), or into the bowel itself (gastrointestinal hemorrhage). Transfusions may be needed, and re-operation is sometimes necessary. Use of blood thinners, to prevent venous thromboembolic disease, may actually increase the risk of hemorrhage slightly.

Hernia

A hernia is an abnormal opening, either within the abdomen, or through the abdominal wall muscles. An internal hernia may result from surgery, and re-arrangement of the bowel, and is mainly significant as a cause of bowel obstruction. An incisional hernia occurs when a surgical incision does not heal well; the muscles of the abdomen separate and allow protrusion of a sac-like membrane, which may contain bowel or other abdominal contents, and which can be painful and unsightly. The risk of abdominal wall hernia is markedly decreased in laparoscopic surgery.

Bowel obstruction

Abdominal surgery always results in some scarring of the bowel, called adhesions. A hernia, either internal or through the abdominal wall, may also result. When bowel becomes trapped by adhesions or a hernia, it may become kinked and obstructed, sometimes many years after the original procedure. Usually an operation is necessary to correct this problem.

Venous thromboembolism

Any injury, such as a surgical operation, causes the body to increase the coagulation of the blood. Simultaneously, activity may be reduced. There is an increased probability of formation of clots in the veins of the legs, or sometimes the pelvis, particularly in the morbidly obese patient. A clot which breaks free and floats to the lungs is called a pulmonary embolus, a very dangerous occurrence. Commonly, blood thinners are administered before surgery, to reduce the probability of this type of complication.

Complications of gastric bypass

Anastomotic leakage

An anastomosis is a surgical connection between the stomach and bowel, or between two parts of the bowel. The surgeon attempts to create a water-tight connection by connecting the two organs with either staples or sutures, either of which actually makes a hole in the bowel wall. The surgeon will rely on the healing power of the body, and its ability to create a seal like a self-sealing tire, to succeed with the surgery. If that seal fails to form, for any reason, fluid from within the gastrointestinal tract can leak into the sterile abdominal cavity and give rise to infection and abscess formation. Leakage of an anastomosis can occur in about 2% of gastric bypass procedures, usually at the stomach-bowel connection. Sometimes leakage can be treated with antibiotics, and sometimes it will require immediate re-operation. It is usually safer to re-operate if an infection cannot be definitely controlled immediately.

Anastomotic stricture

As the anastomosis heals, it forms scar tissue, which naturally tends to shrink (“contract”) over time, making the opening smaller. This is called a “stricture”. Usually, the passage of food through an anastomosis will keep it stretched open, but if the inflammation and healing process outpaces the stretching process, scarring may make the opening so small that even liquids can no longer pass through it. The solution is a procedure called gastroendoscopy, and stretching of the connection by inflating a balloon inside it. Sometimes this manipulation may have to be performed more than once to achieve lasting correction.

Anastomotic ulcer

Ulceration of the anastomosis occurs in 1-16% of patients. Possible causes of such ulcers are:

• Restricted blood supply to the anastomosis (compare to the blood supply available to the original stomach)
• Anastomosis tension
• Gastric acid
• Helicobacter pylori
• Smoking
• Use of Non-steroidal anti-inflammatory drugs

This condition can be treated as follows:

• Use of Proton pump inhibitors, e.g., Nexium
• Use of a Cytoprotectant and acid Buffering agent, e.g., Sucralfate
• Temporary restriction of the consumption of solid foods

Dumping syndrome

Normally, the pyloric valve at the lower end of the stomach regulates the release of food into the bowel. When the Gastric Bypass patient eats a sugary food, the sugar passes rapidly into the bowel, where it gives rise to a physiological reaction called dumping syndrome. An affected person feels his heart beating rapidly and forcefully, breaks into a cold sweat, gets a feeling of butterflies in the stomach, and has a “sky is falling” type of anxiety. He/she usually has to lie down, and is very uncomfortable for about 30 to 45 minutes. Diarrhea may then follow.

Nutritional deficiencies

• Hyperparathyroidism, due to inadequate absorption of calcium, may occur for GBP patients. Calcium is primarily absorbed in the duodenum, which is bypassed by the surgery. Most patients can achieve adequate calcium absorption by supplementation with Vitamin D and Calcium Citrate (carbonate may not be absorbed – it requires an acidic stomach, which is bypassed).
• Iron frequently is seriously deficient, particularly in menstruating females, and must be supplemented. Again, it is normally absorbed in the duodenum. Ferrous sulfate can cause considerable GI distress in normal doses; alternatives include ferrous fumarate, or a chelated form of iron. Occasionally, a female patient develops severe anemia, even with supplements, and must be treated with parenteral iron.
• Vitamin B12 requires intrinsic factor from the gastric mucosa to be absorbed. In patients with a small gastric pouch, it may not be absorbed, even if supplemented orally, and deficiencies can result in pernicious anemia and neuropathies. Sublingual B12 appears to be adequately absorbed.
• Thiamine deficiency (also known as beriberi) will, rarely, occur as the result of its absorption site in the jejunum being bypassed. This deficiency can also result from inadequate nutritional supplements being taken post operatively.
• Protein malnutrition is a real risk. Some patients suffer troublesome vomiting after surgery, until their GI tract adjusts to the changes, and cannot eat adequate amounts even with 6 meals a day. Many patients require protein supplementation during the early phases of rapid weight loss, to prevent excessive loss of muscle mass.
• Vitamin A deficiencies generally occur as a result of the deficiencies that involve the fat-soluble vitamins. This often comes after intestinal bypass procedures such as jejunoileal bypass (no longer performed) or biliopancreatic diversion/duodenal switch procedures. In these procedures, fat absorption is markedly impaired. There is also the possibility of a vitamin A deficiency with use of Xenical or Alli weight loss medications.

Nutritional effects

After surgery, patients feel fullness after ingesting only a small volume of food, followed soon thereafter by a sense of satiety and loss of appetite. Total food intake is markedly reduced. Due to the reduced size of the newly created stomach pouch, and reduced food intake, adequate nutrition demands that the patient follow the surgeon’s instructions for food consumption, including the number of meals to be taken daily, adequate protein intake, and the use of vitamin and mineral supplements.

Protein nutrition

Proteins are essential food substances, contained in foods such as meat, fish and poultry, dairy products, soy, nuts, and eggs. With reduced ability to eat a large volume of food, gastric bypass patients must focus on eating their protein requirements first, and with each meal. In some cases, surgeons may recommend use of a liquid protein supplement.

Calorie nutrition

The profound weight loss which occurs after bariatric surgery is due to taking in much less energy (calories) than the body needs to use every day. Fat tissue must be burned, to offset the deficit, and weight loss results. Eventually, as the body becomes smaller, its energy requirements are decreased, while the patient simultaneously finds it possible to eat somewhat more food. When the energy consumed is equal to the calories eaten, weight loss will stop. Proximal GBP typically results in loss of 60 to 80% of excess body weight, and very rarely leads to excessive weight loss. The risk of excessive weight loss is slightly greater with Distal GBP.

Vitamins

Vitamins are normally contained in the foods we eat, as well as any supplements we may choose to take. The amount of food which will be eaten after GBP is severely reduced, and vitamin content is correspondingly reduced. Supplements should therefore be taken, to completely cover minimum daily requirements of all vitamins and minerals. Absorption of most vitamins is not seriously affected after proximal GBP, although vitamin B12 may not be well-absorbed in some persons. Sublingual preparations of B12 will provide adequate absorption. After the distal GBP, fat-soluble vitamins A, D and E may not be well-absorbed, particularly if fat intake is large. Water-dispersed forms of these vitamins may be indicated, on specific physician recommendation.

Minerals

All versions of the GBP bypass the duodenum, which is the primary site of absorption of both iron and calcium. Iron replacement is essential in menstruating females, and supplementation of iron and calcium is preferable in all patients. Ferrous sulfate is poorly tolerated. Alternative forms of iron (fumarate, gluconate, chelates) are less irritating and probably better absorbed. Calcium carbonate preparations should also be avoided; calcium as citrate or gluconate, 1200 mg as calcium, has greater bioavailability independent of acid in the stomach, and will likely be better absorbed.

Results and health benefits of gastric bypass

Weight loss of 65 to 80% of excess body weight (the amount by which actual body weight exceeds actuarial ideal body weight) is typical of most large series of Gastric Bypass operations reported. The medically more significant effects are a dramatic reduction in co-morbid conditions:

• Hyperlipidemia is corrected in over 70% of patients.
• Essential hypertension is relieved in over 70% of patients, and medication requirements are usually reduced in the remainder.
• Obstructive sleep apnea is markedly improved with weight loss and bariatric surgery may be curative for sleep apnea. Snoring also improves in most patients. Although improved, sleep apnea may remain in some patients even after surgery.
• Diabetes mellitus type 2 is reversed in up to 90% of patients, usually leading to a normal blood sugar without medication, sometimes within days of surgery.
• Gastroesophageal reflux disease is relieved from the time of surgery in almost all patients.
• Venous thromboembolic disease signs such as leg swelling are typically much improved.
• Low back pain and joint pain are typically relieved or improved in nearly all patients.

A recent study in a large comparative series of patients showed an 89% reduction in mortality over the 5 years following surgery, compared to a non-surgically treated group of patients.

Concurrently, most patients are able to enjoy greater participation in family and social activities.

Living with gastric bypass

Gastric bypass surgery has an emotional, as well as a physiological, impact on the individual. Many who have undergone the surgery suffer from depression in the following months. This is a result of a change in the role food plays in their emotional well-being. Strict limitations on the diet can place great emotional strain on the patient. Energy levels in the period following the surgery will be low. This is due again to the restriction of food intake, but the negative change in emotional state will also have an impact here. It may take as long as three months for emotional levels to rebound. Muscular weakness in the months following surgery is common. This is caused by a number of factors, including a restriction on protein intake, a resulting loss in muscle mass and decline in energy levels. The weakness may result in balance problems, difficulty climbing stairs or lifting heavy objects, and increased fatigue following simple physical tasks. Many of these issues will pass over time as food intake gradually increases. However, the first months following the surgery can be very difficult, an issue not often mentioned by physicians suggesting the surgery. The benefits and risks of this surgery are well established; however, the psychological effects are not well understood, and potential patients should ensure a strong support system before agreeing to the procedure.

Surgeon Accredidation

The American Society for Metabolic & Bariatric Surgery lists bariatric programs and surgeons in its “Centers of Excellence” network, while the American College of Surgeons accredits providers through its Bariatric Surgery Center Network. For listings of surgeons and centers in other countries, the International Federation for the Surgery of Obesity and Metabolic Disorders lists medical associations by country.

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The name is derived from the surgeon that first described it (César Roux) and the stick-figure representation. Diagramatically, the Roux-en-Y anastomosis looks like the letter Y; typically, the two upper limbs of the Y represent a proximal segment of small bowel and the distal small bowel it joins with (which is often a blind end), and the lower part of the Y the distal small bowel (beyond the anastomosis).

Roux-en-Ys are used in several operations and collectively called Roux operations.

Schematic of gastric bypass using a Roux-en-Y anastomosis. The transverse colon is removed to clearly show the Roux-en-Y.

Schematic of gastric bypass using a Roux-en-Y anastomosis. The transverse colon is removed to clearly show the Roux-en-Y.

• Some gastric bypasses for obesity.
• Roux-en-Y reconstruction following partial or complete gastrectomy for stomach cancer.
• Roux-en-Y hepaticojejunostomy used to treat (macroscopic) bile duct obstruction which may arise due to:
  • a common bile duct tumour or hepatic duct tumour (e.g. resection of cholangiocarcinoma)
  • a bile duct injury (e.g. cholecystectomy surgical misadventure, trauma)
  • an infection/inflammation (e.g. pancreatic pseudocyst)
• Roux-en-Y choledochojejunostomy - indications same as Roux-en-Y hepaticojejunostomy.

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When the ER is the right place to go, it’s important to know what to expect once you get there. Having this information ahead of time can help make the experience a little less stressful.

Finding the Right ER at the Right Time

Talk with your doctor about what to do — and what ER to go to — before you’re in a situation where you may need to visit one. The doctor may direct you to an ER that is close to you, or one in a hospital where he or she regularly sees patients.

But in an emergency, should your child go to an ER at a children’s hospital? Because they’re dedicated to caring for kids, children’s hospitals probably have the most pediatric staff and facilities. So if it’s an emergency and a children’s hospital is conveniently located, consider going there. Otherwise, the community hospital nearest you will provide the medical care needed. If for any reason the hospital isn’t equipped to treat your child’s specific condition, the doctors there will arrange a transfer to a facility that is.

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Signs and symptoms of GERD include acid reflux and heartburn. Both are common digestive conditions that most people experience from time to time. When these signs and symptoms occur more than twice each week or interfere with your daily life, doctors term this GERD.

Most people can manage the discomfort of heartburn with lifestyle changes and over-the-counter medications. But for people with GERD, these remedies may offer only temporary relief. People with GERD may need stronger medications, even surgery, to reduce symptoms.

GERD signs and symptoms include:

• A burning sensation in your chest (heartburn), sometimes spreading to the throat, along with a sour taste in your mouth
• Chest pain
• Difficulty swallowing (dysphagia)
• Dry cough
• Hoarseness or sore throat
• Regurgitation of food or sour liquid (acid reflux)
• Sensation of a lump in the throat

How GERD Occurs

Acid reflux occurs when the sphincter muscle at the lower end of your esophagus relaxes at the wrong time, allowing stomach acid to back up into your esophagus. This can cause heartburn and other signs and symptoms. Frequent or constant reflux can lead to GERD.

When to see a doctor
Seek immediate medical attention if you experience chest pain, especially when accompanied by other signs and symptoms such as shortness of breath or jaw or arm pain. These may be signs and symptoms of a heart attack.

Make an appointment with your doctor if you experience severe or frequent GERD symptoms. If you turn to over-the-counter medications for heartburn more than twice per week, see your doctor.

GERD is caused by frequent acid reflux — the backup of stomach acid or bile into the esophagus.

When you swallow, the lower esophageal sphincter — a circular band of muscle around the bottom part of your esophagus — relaxes to allow food and liquid to flow down into your stomach. Then it closes again.

However, if this valve relaxes abnormally or weakens, stomach acid can flow back up into your esophagus, causing frequent heartburn and disrupting your daily life. This constant backwash of acid can irritate the lining of your esophagus, causing it to become inflamed (esophagitis). Over time, the inflammation can erode the esophagus, causing complications such as bleeding or breathing problems.

Conditions that can increase your risk of GERD include:

• Obesity
• Hiatal hernia
• Pregnancy
• Smoking
• Dry mouth
• Asthma
• Diabetes
• Delayed stomach emptying
• Connective tissue disorders, such as scleroderma
• Zollinger-Ellison syndrome

Over time, chronic inflammation in your esophagus can lead to complications, including:

• Narrowing of the esophagus (esophageal stricture).Damage to cells in the lower esophagus from acid exposure leads to formation of scar tissue. The scar tissue narrows the food pathway, causing difficulty swallowing.
• An open sore in the esophagus (esophageal ulcer). Stomach acid can severely erode tissues in the esophagus, causing an open sore to form. The esophageal ulcer may bleed, cause pain and make swallowing difficult.
• Precancerous changes to the esophagus (Barrett’s esophagus). In Barrett’s esophagus, the color and composition of the tissue lining the lower esophagus change. These changes are associated with an increased risk of esophageal cancer. The risk of cancer is low, but your doctor will recommend regular endoscopy exams to look for early warning signs of esophageal cancer.

If you think you have GERD, you’re likely to start by first seeing your family doctor or a general practitioner. Your doctor may recommend you see a doctor who specializes in treating digestive diseases (gastroenterologist).

Because appointments can be brief, and because there’s often a lot of ground to cover, it’s a good idea to be well prepared for your appointment. Here’s some information to help you get ready for your appointment, and what to expect from your doctor.

What you can do

• Be aware of any pre-appointment restrictions. At the time you make the appointment, be sure to ask if there’s anything you need to do in advance, such as restrict your diet.
• Write down any symptoms you’re experiencing, including any that may seem unrelated to the reason for which you scheduled the appointment.
• Write down key personal information, including any major stresses or recent life changes.
• Make a list of all medications, as well as any vitamins or supplements, that you’re taking.
• Take a family member or friend along, if possible. Sometimes it can be difficult to absorb all the information provided during an appointment. Someone who accompanies you may remember something that you missed or forgot.
• Write down questions to ask your doctor.

Your time with your doctor is limited, so preparing a list of questions will help you make the most of your time together. List your questions from most important to least important in case time runs out. For gastroesophageal reflux disease, some basic questions to ask your doctor include:

• What is likely causing my symptoms?
• What kinds of tests do I need?
• Is my GERD likely temporary or chronic?
• What is the best course of action?
• What are the alternatives to the primary approach that you’re suggesting?
• I have these other health conditions. How can I best manage them together?
• Are there any restrictions that I need to follow?
• Should I see a specialist? What will that cost, and will my insurance cover it?
• Is there a generic alternative to the medicine you’re prescribing me?
• Are there brochures or other printed material that I can take with me? What Web sites do you recommend?
• What will determine whether I should plan for a follow-up visit?

In addition to the questions that you’ve prepared to ask your doctor, don’t hesitate to ask questions during your appointment at any time that you don’t understand something.

What to expect from your doctor
Your doctor is likely to ask you a number of questions. Being ready to answer them may allow more time later to cover points you want to address. Your doctor may ask:

• When did you first begin experiencing symptoms?
• Have your symptoms been continuous or occasional?
• How severe are your symptoms?
• What, if anything, seems to improve your symptoms?
• What, if anything, appears to worsen your symptoms?
• Do you have difficulty swallowing?
• Have you gained or lost weight?
• Do you experience nausea and vomiting?

What you can do in the meantime
Try lifestyle changes to control your symptoms until you see your doctor. For instance, avoid foods that trigger your heartburn and avoid eating at least two hours before bedtime.

If you’re bothered by frequent heartburn or other signs and symptoms, your doctor may be able to diagnose GERD with that information alone. Your doctor may also suggest tests and procedures used to diagnose GERD, including:

• An X-ray of your upper digestive system. Sometimes called a barium swallow or upper GI series, this procedure involves drinking a chalky liquid that coats and fills the hollows of your digestive tract. Then X-rays are taken of your upper digestive tract. The coating allows your doctor to see a silhouette of the shape and condition of your esophagus, stomach and upper intestine (duodenum).
• Passing a flexible tube down your throat. Endoscopy is a way to examine the inside of your esophagus. During endoscopy, your doctor inserts a thin, flexible tube equipped with a light and camera (endoscope) down your throat. The endoscope allows your doctor to examine your esophagus and stomach. Your doctor may also use endoscopy to collect a sample of tissue (biopsy) for further testing.
• A test to monitor the amount of acid in your esophagus.Ambulatory acid (pH) probe tests use an acid-measuring device to identify when, and for how long, stomach acid regurgitates into your esophagus. The acid monitor can be a thin, flexible tube (catheter) that’s threaded through your nose into your esophagus. During the test, the tube stays in place and connects to a small computer that you wear around your waist or with a strap over your shoulder. Or the acid monitor can be a clip that’s placed in your esophagus during endoscopy. The probe transmits a signal to a small computer that you wear around your waist for about two days, and then the probe falls off to be passed in your stool. Your doctor may ask that you stop taking GERD medications to prepare for this test.
• A test to measure the movement of the esophagus.Esophageal impedance measures movement and pressure in the esophagus. The test involves placing a catheter through your nose and into your esophagus.

Treatment for heartburn and other signs and symptoms of GERD usually begins with over-the-counter medications that control acid. If you don’t find relief within a few weeks, your doctor may recommend other treatments, including medications and surgery.

Initial treatments to control heartburn
Over-the-counter treatments that may help control heartburn include:

• Antacids that neutralize stomach acid. Antacids, such as Maalox, Mylanta, Gelusil, Rolaids and Tums, may provide quick relief. But antacids alone won’t heal an inflamed esophagus damaged by stomach acid. Overuse of some antacids can cause side effects such as diarrhea or constipation.
• Medications to reduce acid production. Called H-2-receptor blockers, these medications include cimetidine (Tagamet HB), famotidine (Pepcid AC), nizatidine (Axid AR) or ranitidine (Zantac 75). H-2 receptor blockers don’t act as quickly as antacids, but they provide longer relief. Stronger versions of these medications are available in prescription form.
• Medications that block acid production and heal the esophagus. Proton pump inhibitors block acid production and allow time for damaged esophageal tissue to heal. Over-the-counter proton pump inhibitors include lansoprazole (Prevacid 24 HR) and omeprazole (Prilosec OTC).

Contact your doctor if these medications don’t seem to be helping after a few weeks.

Prescription-strength medications
If heartburn persists despite initial approaches, your doctor may recommend prescription-strength medications, such as:

• Prescription-strength H-2-receptor blockers. These include prescription-strength cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid) and ranitidine (Zantac).
• Prescription-strength proton pump inhibitors. Prescription-strength proton pump inhibitors include esomeprazole (Nexium), lansoprazole (Prevacid), omeprazole (Prilosec Rx), pantoprazole (Protonix) and rabeprazole (Aciphex).
• Medications to strengthen the lower esophageal sphincter.Called prokinetic agents, these medications help your stomach empty more rapidly and help tighten the valve between the stomach and the esophagus. Side effects, such as fatigue, depression, anxiety and other neurological problems, limit the usefulness of these medications.

GERD medications are sometimes combined to increase effectiveness.

Surgery and other procedures used if medications don’t help
Most GERD can be controlled through medications. In situations where medications aren’t helpful or you wish to avoid long-term medication use, your doctor may recommend more invasive procedures, such as:

• Surgery to reinforce the lower esophageal sphincter. Called Nissen fundoplication, this surgery involves tightening the lower esophageal sphincter to prevent reflux by wrapping the very top of the stomach around the outside of the lower esophagus. Surgery can be open, meaning the surgeon makes a long incision in your abdomen. Or surgery can be laparoscopic, meaning the surgeon makes three or four small incisions in the abdomen and inserts instruments, including a flexible tube with a tiny camera, through the incisions.
• Surgery to create a barrier preventing the backup of stomach acid. This procedure, called EndoCinch endoluminal gastroplication, uses a tool that’s like a miniature sewing machine. It places pairs of stitches (sutures) in the stomach near the weakened sphincter. The suturing material is then tied together, creating barriers to prevent stomach acid from washing into your esophagus. It’s not clear who is best suited for this treatment and research is ongoing.
• A procedure to form scar tissue in the esophagus. This approach, called the Stretta system, uses electrode energy to heat esophageal tissue. The heat creates scar tissue and damages the nerves that respond to refluxed acid. The scar tissue that forms as your esophagus heals helps to strengthen the muscles. It’s not clear who is best suited for this treatment and research is ongoing.

Lifestyle changes may help reduce the frequency of heartburn. Consider trying to:

• Maintain a healthy weight. Excess pounds put pressure on your abdomen, pushing up your stomach and causing acid to back up into your esophagus. If your weight is healthy, work to maintain it. If you are overweight or obese, work to slowly lose weight — no more than 1 or 2 pounds (0.5 to 1 kilogram) a week. Ask your doctor for help devising a weight loss strategy that will work for you.
• Avoid tight-fitting clothing. Clothes that fit tightly around your waist put pressure on your abdomen and the lower esophageal sphincter.
• Avoid foods that trigger heartburn. Everyone has specific triggers. Common triggers such as fatty or fried foods, alcohol, chocolate, mint, garlic, onion and caffeine may make heartburn worse.
• Don’t lie down after a meal. Wait at least two to three hours after eating before lying down or going to bed.
• Elevate the head of your bed. An elevation of about six to nine inches puts gravity to work for you. Placing wood or cement blocks under the feet of your bed at the head end. If it’s not possible to elevate your bed, you can insert a wedge between your mattress and box spring to elevate your body from the waist up. Wedges are available at drugstores and medical supply stores.
• Don’t smoke. Smoking decreases the lower esophageal sphincter’s ability to function properly.

No alternative medicines therapies are proven to treat GERD or to reverse damage to the esophagus. Still, some complementary and alternative therapies may provide some relief, when combined with your doctor’s care.

Talk to your doctor about what alternative GERD treatments may be safe for you. Options may include:

• Herbal remedies. Herbal remedies sometimes used for GERD symptoms include licorice, slippery elm, chamomile and marshmallow. Herbal remedies can have serious side effects and they may interfere with medications. Ask your doctor about a safe dosage before beginning any herbal remedy.
• Relaxation therapies. Techniques to calm stress and anxiety may reduce signs and symptoms of GERD. Ask your doctor about relaxation techniques, such as progressive muscle relaxation or guided imagery.
• Acupuncture. Acupuncture involves inserting thin needles into specific points on your body. One small study reported that acupuncture helped people with heartburn that persisted despite medication. Ask your doctor whether acupuncture is safe for you.

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Procedure

Sleeve gastrectomy is usually performed on extremely obese patients, with a body mass index of 40 or more, where the risk of performing a gastric bypass or duodenal switchprocedure may be too large. A two-stage procedure is performed: the first is a sleeve gastrectomy, and the second is a conversion into a gastric bypass or duodenal switch. Patients usually lose a large quantity of their excess weight after the first sleeve gastrectomy procedure alone, but if weight loss ceases the second step is performed.

For patients that are obese but not extremely obese, sleeve gastrectomy alone is a suitable operation with minimum risks. Some surgeons even prefer it over gastric banding, because it eliminates the need of having to insert a foreign body. The sleeve gastrectomy currently is acceptable weight loss surgery option for obese patients as a single procedure. Most surgeons prefer to use a bougie between 32 – 40 Fr with the procedure and the approximate remaining size of the stomach after the procedure is about 2 ounces.

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Teenage obesity is a dangerous — and growing — problem. There’s no magic bullet for teen weight loss, but there’s plenty you can do to help. Start by encouraging your teen to adopt healthy habits that can last a lifetime.

Have a heart-to-heart

If your teen is overweight, he or she is probably concerned about the excess weight, too. Aside from lifelong health risks such as high blood pressure and diabetes, the social and emotional fallout of being overweight can be devastating for a teenager. It can also be frustrating to attempt weight loss and have poor results. Offer support and gentle understanding — and a willingness to help your teen take control of the problem.

You might say, “I can’t change your weight. That’s up to you. But I can help you make the right decisions.”

Dispute unrealistic images

Weight and body image can be delicate issues, especially for teenage girls. When it comes to teen weight loss, remind your teen that there’s no single ideal and no perfect body. The right weight for one person might not be the right weight for another.

Rather than talking about “fat” and “thin,” encourage your teen to focus on practicing the behaviors that promote a healthy weight. Your family doctor can help set realistic goals for body mass index and weight based on your teen’s age, height and general health.

Resist quick fixes

Help your teen understand that losing weight — and keeping it off — is a lifetime commitment. Fad diets may rob your growing teen of iron, calcium and other essential nutrients. Weight-loss pills and other quick fixes don’t address the root of the problem. And the effects are often short-lived. Without a permanent change in habits, any lost weight is likely to return — and then some.

Promote activity

Like adults, teens need about 60 minutes of physical activity a day. But that doesn’t necessarily mean 60 solid minutes at a stretch. Shorter, repeated bursts of activity during the day can help burn calories, too. In fact, any physical activity counts.

Team sports through school or community programs are great ways to get active. If your teen isn’t an athlete or is hesitant to participate in certain sports, that’s OK. Encourage him or her to walk, bike or in-line skate to school, or to walk a few laps through the halls before class. Suggest trading one hour of after-school channel surfing for shooting baskets in the driveway, jumping rope or walking the dog. Even household chores such as vacuuming and washing the car have aerobic benefits.

Suggest breakfast

If your teen fights the alarm clock the way it is, getting up even earlier to eat breakfast may be a tough sell — but it’s important. A nutritious breakfast will jump-start your teen’s metabolism and give him or her energy to face the day ahead. Even better, it may keep your teen from eating too much during the rest of the day.

If your teen resists high-fiber cereal or whole-wheat toast, suggest last night’s leftovers. Even a piece of string cheese or a small handful of nuts and a piece or two of fruit can do the job.

Encourage smart snacking

It can be tough to make healthy choices when school halls are lined with vending machines, but it’s possible. Encourage your teen to replace even one bag of chips a day with a healthier grab-and-go option from home:

• Frozen grapes
• Oranges, strawberries or other fresh fruit
• Sliced red, orange or yellow peppers
• Cherry tomatoes
• Baby carrots
• Low-fat yogurt or pudding
• Pretzels
• Graham crackers
• String cheese

Watch portion sizes

When it comes to portions, size matters. Encourage your teen to scale back and stop eating when he or she is full. It might take just one slice of pizza or half the pasta on the plate to feel full — and there’s no shame in sharing a meal, ordering a smaller portion or taking home leftovers.

Count liquid calories

The average 12-ounce can of soda has more than 100 calories and 10 teaspoons of sugar. The calories and sugar in fruit juice, specialty coffees and other drinks can add up quickly as well. Drinking water instead of soda and other sugary drinks may spare your teen hundreds of calories and a day’s worth of sugar — or even more. For variety, suggest flavored water, seltzer water or unsalted club soda.

Allow occasional treats

Late-night pizza with friends or nachos at the mall don’t need to derail your teen’s healthy-eating plan. Suggest a breadstick and marinara sauce instead of garlic bread dripping in butter and cheese, or a shared snack rather than a full-size order. Let your teen know that he or she is in control — and an occasional indulgence is OK. A trend toward healthier habits is what really matters.

Make it a family affair

Rather than singling out your teen, adopt healthier habits as a family. After all, eating healthier foods and getting more exercise is good for everybody.

• Encourage the entire family to eat more fruits, veggies and whole grains, such as whole-wheat bread, brown rice and oatmeal. Be sure to set a good example yourself.
• Leave junk food at the grocery store. Healthy foods sometimes cost more, but it’s an important investment.
• Try new recipes or healthier alternatives to family favorites.
• Banish food from the couch to curb mindless munching.
• Plan active family outings, such as evening walks or weekend visits to a local recreation center.

Be positive

Being overweight doesn’t inevitably lead to a lifetime of low self-esteem, but your acceptance is critical. Listen to your teen’s concerns. Comment on his or her efforts, skills and accomplishments. Make it clear that your love is unconditional — not dependent on weight loss. Help your teen learn healthy ways to express his or her feelings, such as writing in a journal.

If your teen is struggling with low self-esteem or isn’t able to cope with his or her weight in a healthy manner, consider a support group, formal weight-control program or professional counseling. Additional support may give your teen the tools to counter social pressure, cultivate more positive self-esteem and take control of his or her weight. The benefits will last a lifetime.

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