The New Raw Food Diet And How To Approach It To Reach Success

There are always new diets coming out and old ones being tried again. We have all been guilty of trying many diets to maybe have lost some weight but then proceeded to put it back on as we can not sustain it. One that many are trying, some for the first time is the Raw Food Diet. This is not only a diet but a very healthy bonus for your body.



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How Do Yacon Root Capsules Work As A Weight Loss Supplement?

Yacon root capsules are made from yacon, a vegetable that is found in the Andes Mountains in South America. The vegetable is known for its various health benefits, and the health and wellness community is now enjoying its benefits, especially in terms of weight loss. So how does it help people lose weight?



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4 Good To Know Facts About Raspberry Ketone Drops For Weight Loss

Raspberry ketone drops is just one of the many weight loss supplements available in the health and fitness market today. It can also be taken as a capsule, although there may be a bit of a difference in the effectiveness. If you are considering taking it to help you lose weight, make sure that you are well-informed about it.



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Growth Hormone for Weight Loss

Hormones are chemicals that are released by cells in the body and are detected by other cells, altering the way they function. They act as 'chemical messengers', and play a large role in how the body operates. 'Artificial' hormones may be created or synthesised and administered in the form of drugs to treat medical conditions.

Growth hormone (GH) is a hormone produced by the cells of the pituitary gland, a small gland found in the brain. GH production begins early in the womb and continues throughout life, though at a lesser rate. GH release is altered by several factors.

GH secretion is increased by:

Growth hormone releasing hormone (GHRH), a hormone released by the hypothalamus (a part of the brain);Ghrelin, a hormone produced in the gut;Fasting;High protein meals;Low blood sugar levels (hypoglycaemia). Insulin can be used to create low blood sugar levels. In normal circumstances, this would result in increased GH secretion. If this does not occur, GH deficiency may be diagnosed.The main female sex hormone oestrogen; Other hormones such as dopamine, alpha-adrenergic agonists (released during times of stress) and beta-adrenergic antagonists (beta blockers); andExercise, infection, and trauma.

GH secretion is reduced by:

Somatostatin, a hormone released by the hypothalamus;Insulin like growth factor (IGF-1): This hormone is increased by GH, is responsible for most of the effects of GH, and also reduces the amount of GH released (negative feedback);High blood sugar (hyperglycaemia);Leptin, a hormone produced by fat cells. It signals to the hypothalamus that the body has had enough to eat;Excess glucocorticoids, a type of steroid that may be administered as a drug. High levels of glucocorticoid increase the number of GH receptors on cells. These detect GH, so if there are more of them, the action of GH on cells is greater;Beta-2-adrenergic receptor activation. These are a type of receptor that are stimulated by hormones released during times of stress, and also by certain drugs such as adrenaline. If these are activated, GH action is decreased.

GH secretion is at its peak (150 µg/kg) during puberty, and declines by about 50% every seven years to about 25 µg/kg by age 55.

The main action of GH is to cause the liver to produce a hormone called IGF-1. IGF-1 plays an important role in the growth and development of children. GH acts directly and via IGF-1 to stimulate growth in the long bones of children, such as the thigh bone (femur) and arm bone (humerus).

Metabolic effects of growth hormone include:

Increased breakdown of stored fat (triglyceride), and increased use of this fat to create energy; Counteracting the actions of insulin. Insulin moves sugar from the blood into cells, so GH opposes this;Retention (holding in the body) of sodium, phosphate and water; andStimulation of protein production (a large component of muscles).

Too much GH leads to the condition known as acromegaly or gigantism. Growth hormone deficiency may occur in a range of conditions. 

Recombinant human GH (rhGH) is a form of artificially produced GH, and may be administered as a drug to manage a range of conditions, such as:

Obese individuals are known to have low levels of GH. Growth hormone reduces obesity through its actions on two enzymes which control lipolysis (breakdown of stored triglycerides into free fatty acids) and lipogenesis (fat accumulation). These hormones are lipoprotein lipase (LPL) and hormone sensitive lipase (HSL).

GH reduces the uptake of free fatty acids by adipocytes (fat storage cells). It inhibits LPL, which controls the buildup of triglycerides in fatty tissue. LPL breaks down triglycerides, releasing free fatty acids (FFAs) which may then be taken up by fat cells. GH also encourages the body to use FFAs as an energy source, and to reduce the use of sugars (glucose) and proteins for energy. The impact of GH in reducing LPL activity is greater in fat deposits within the abdomen than in subcutaneous fat. Other hormones that impact on LDL are insulin (increased activity); and catecholamines (dopamine, etc), testosterone and oestrogen (decreased activity).

The presence of circulating FFA reduces the release of GH by the pituitary. The elevation of FFA in obese individuals (due to greater fatty tissue mass) may be partially responsible for the lower levels of GH evident in obesity. There is also increased clearance of GH in obese individuals, through mechanisms that are not well understood. Also, the increased levels of IGF-1 seen in obese individuals has a negative feedback effect on GH release. Finally, the high levels of insulin seen in many obese individuals reduces the release of GH by the pituitary in response to GHRH.

GH assists the action of HSL, which breaks down stored triglycerides into FFAs and glycerol. This allows the use of FFAs as fuel sources elsewhere in the body. The glycerol portion of the triglyceride must be removed in order to enable FFAs to exit the fat cell. GH increases the number of receptors on the cell that recognise hormones that stimulate HSL activity. It also prevents the breakdown of messengers in the cell that allow the effects of HSL to occur.

GH also has a direct impact on the number and maturity of fat cells. Through IGF-1, GH stimulates production of pre-fat cells; however, GH then prevents them from maturing.

GH opposes skeletal muscle breakdown during fasting. When an individual is eating very few calories, GH encourages the use of fat for energy rather than sugar or proteins. This prevents the breakdown of muscle in order to produce proteins for energy. 

The effectiveness of GH in reducing obesity is under debate. Some research indicates that it is not effective. One 2003 review stated that "GH administered together with (low calorie) diets did not enhance fat loss or preserve lean tissue mass. No studies provided strong evidence for an independent beneficial effect of GH on visceral adiposity." Visceral adiposity is fat in and around the abdominal organs. Further, this review reported that most studies found reduced glucose tolerance (the presence of pre-diabetes) associated with the use of GH.

On the other hand, many other studies have reported that GH is effective in reducing fat mass, especially visceral fat. These studies were performed on adults with GH deficiency due to pituitary disease, or low levels of GH associated with obesity in the absence of pituitary disease. One review found that "GH replacement with or without diet and exercise interventions effectively reduces visceral adipose tissue (VAT) and improves lipid abnormalities in GH deficient adults."24 This review concluded that "GH therapy decreases VAT in subjects with adult GH deficiency and in GH-replete viscerally obese adults. It is generally agreed that adults with GHD and visceral obesity should be given GH replacement therapy. The use of GH, with or without insulin sensitisers, represents a novel, albeit expensive, adjunct to diet and exercise in GH-replete obese individuals who are striving to reduce their cardiovascular risk."24

A further study showed a small but significant reduction in visceral obesity, and an increase in lean mass and body weight with the administration of GH at physiological (normal for the body) doses. GH administration at high levels was not found to be an effective treatment in viscerally obese subjects. Another study demonstrated a 1.6-fold increase in fat loss due to administration of GH compared with placebo, and concurrent increase in lean body mass.

It has been suggested that the negative results seen in some trials may be due to administration of high doses of GH leading to high levels of insulin. This leads to the formation of fat, which may offset the lipolytic effect of the growth hormone.

Side effects of growth hormone administration include:

These are reported to be reversible when treatment with GH is stopped.

There have been some concern that GH use may lead to cancer, particularly if it is given in high doses over long periods of time. A 12–35% increase in pre-cancerous polyps in the colon occurs in patients with acromegaly, and colon cancer occurs in 6.9% of cases. However, it has been suggested that individuals with acromegaly are exposed to higher levels of GH over longer periods of time than would occur with therapeutic GH administration.

Another study reported an increased incidence of leukaemia in children treated with human pituitary GH replacement therapy. Subsequent studies did not confirm this increase. A study published in the Lancet found greater risk of death from Hodgkin's disease, colorectal cancer and cancer overall in patients treated with human pituitary GH. However, in conjunction with other studies, the authors concluded that, if high-risk groups such as those with chromosomal fragility were excluded, leukaemia risk was not substantially raised.

A recent study designed to further examine this issue analysed the impact of daily GH administration to rats over two years and found no growth of cancer. One expert wrote that it is important to monitor the levels of IGF-1 and IGF-1-binding protein-3 (increased by GH) to ensure therapy resulted in age appropriate limits. IGF-1 prevents cell death, and may therefore prevent the death of cells with mutations which may become cancer cells.

For more information on obesity, health and social issues, and methods of weight loss, as well as some useful tools, see Weight Loss.Leung KC, Ho KK. Measurement of growth hormone, insulin-like growth factor I and their binding proteins: The clinical aspects. Clin Chim Acta. 2001; 313(1-2): 119-23. [Abstract]Hartman ML, Veldhuis JD, Thorner MO. Normal control of growth hormone secretion. Horm Res. 1993; 40(1-3): 37-47. [Abstract]Pong SS, Chaung LP, Dean DC, Nargund RP, Patchett AA, Smith RG. Identification of a new G-protein-linked receptor for growth hormone secretagogues. Mol Endocrinol. 1996; 10(1): 57-61. [Abstract]Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone releasing acylated peptide from stomach. Nature. 1999; 402: 656-60. [Abstract]Giustina A, Veldhuis JD. Pathophysiology of the neuroregulation of growth hormone secretion in experimental animals and the human. Endocr Rev. 1998; 19(6): 717-97. [Abstract | Full text]Van Cauter E, Leproult R, Plat L. Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men. JAMA. 2000; 284(7): 861-8. [Abstract | Full text]Salvatori R. Growth hormone and IGF-1. Rev Endocr Metab Disord. 2004; 5(1): 15-23. [Abstract]Unger RH. The hyperleptinemia of obesity-regulator of caloric surpluses. Cell. 2004; 117(2): 145-6. [Abstract | Full text]Frank SJ. Growth hormone signalling and its regulation: Preventing too much of a good thing. Growth Horm IGF Res. 2001; 11(4): 201-12. [Abstract]Gharib H,Cook DM, Saenger PH, Bengtsson BA, Feld S, Nippoldt TB, et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for growth hormone use in adults and children - 2003 update. Endocr Pract. 2003; 9(1): 64-76. [Abstract | Full text]Richelsen B. Effect of growth hormone on adipose tissue and skeletal muscle lipoprotein lipase activity in humans. J Endocrinol Invest. 1999; 22(5 Suppl): 10-5. [Abstract]Oscarsson J, Ottosson M, Edén S. Effects of growth hormone on lipoprotein lipase and hepatic lipase. J Endocrinol Invest. 1999; 22(5 Suppl): 2-9. [Abstract]Nam SY, Marcus C. Growth hormone and adipocyte function in obesity. Horm Res. 2000; 53(Suppl 1): 87-97. [Abstract]Pombo M, Pombo CM, Astorga R, Cordido F, Popovic V, Garcia-Mayor RV, et al. Regulation of growth hormone secretion by signals produced by the adipose tissue. J Endocrinol Invest. 1999; 22(5 Suppl): 22-6. [Abstract]Langendonk JG, Meinders AE, Burggraaf J, Frölich M, Roelen CA, Schoemaker RC, et al. Influence of obesity and body fat distribution on growth hormone kinetics in humans. Am J Physiol. 1999; 277(5 Pt 1): E824-9. [Abstract | Full text]Lanzi R, Luzi L, Caumo A, Andreotti AC, Manzoni MF, Malighetti ME, et al. Elevated insulin levels contribute to the reduced growth hormone (GH) response to GH-releasing hormone in obese subjects. Metabolism. 1999; 48(9): 1152-6. [Abstract]Clasey JL, Weltman A, Patrie J, Weltman JY, Pezzoli S, Bouchard C, et al. Abdominal visceral fat and fasting insulin are important predictors of 24-hour GH release independent of age, gender, and other physiological factors. J Clin Endocrinol Metab. 2001; 86(8): 3845-52. [Abstract | Full text]Iranmanesh A, Grisso B, Veldhuis JD. Low basal and persistent pulsatile growth hormone secretion are revealed in normal and hyposomatotropic men studied with a new ultrasensitive chemiluminescence assay. J Clin Endocrinol Metab. 1994; 78(3): 526-35. [Abstract]Bramnert M, Segerlantz M, Laurila E, Daugaard JR, Manhem P, Groop L. Growth hormone replacement therapy induces insulin resistance by activating the glucose-fatty acid cycle. J Clin Endocrinol Metab. 2003; 88(4): 1455-63. [Abstract | Full text]Flint DJ, Gardner MJ. Influence of growth hormone deficiency on growth and body composition in rats: Site-specific effects upon adipose tissue development. J Endocrinol. 1993; 137(2): 203-11. [Abstract]Björntorp P. Hormonal control of regional fat distribution. Hum Reprod. 1997; 12(Suppl 1): 21-5. [Abstract]Wabitsch M, Braun S, Hauner H, Heinze E, Ilondo MM, Shymko R, et al. Mitogenic and antiadipogenic properties of human growth hormone in differentiating human adipocyte precursor cells in primary culture. Pediatr Res. 1996; 40(3): 450-6. [Abstract | Full text]Nørrelund H, Nair KS, Jørgensen JO, Christiansen JS, Møller N. The protein-retaining effects of growth hormone during fasting involve inhibition of muscle-protein breakdown. Diabetes. 2001; 50(1): 96-104. [Abstract | Full text] Shadid S, Jensen. Effects of growth hormone administration in human obesity. Obes Res. 2003; 11(2): 170-5. [Abstract]Lucidi P, Parlanti N, Piccioni F, Santeusanio F, De Feo P. Short-term treatment with low doses of recombinant human GH stimulates lipolysis in visceral obese men. J Clin Endocrinol Metab. 2002; 87(7): 3105-9. [Abstract | Full text]Nam SY, Kim KR, Cha BS, Song YD, Lim SK, Lee HC, et al. Low-dose growth hormone treatment combined with diet restriction decreases insulin resistance by reducing visceral fat and increasing muscle mass in obese type 2 diabetic patients. Int J Obes Relat Metab Disord. 2001; 25(8): 1101-7. [Abstract | Full text]Bengtsson BA, Edén S, Lönn L,  Kvist H, Stokland A, Lindstedt G, et al. Treatment of adults with growth hormone (GH) deficiency with recombinant human GH. J Clin Endocrinol Metab. 1993; 76(2): 309-17. [Abstract]Verhelst J, Abs R, Vandeweghe M, Mockel J, Legros JJ, Copinschi G, et al. Two years of replacement therapy in adults with growth hormone deficiency. Clin Endocrinol (Oxf). 1997; 47(4): 485-94. [Abstract]Chrisoulidou A, Beshyah SA, Rutherford O, Spinks TJ, Mayet J, Kyd P, et al. Effects of 7 years of growth hormone replacement therapy in hypopituitary adults. J Clin Endocrinol Metab. 2000; 85(10): 3762-9. [Abstract | Full text]Gibney J, Wallace JD, Spinks T, Schnorr L, Ranicar A, Cuneo RC, et al. The effects of 10 years of recombinant human growth hormone (GH) in adult GH-deficient patients. J Clin Endocrinol Metab. 1999; 84(8): 2596-602. [Abstract | Full text]Johannsson G, Johansson J. Effects of growth hormone replacement in adults. In: Bengtsson BA, Monson JP [eds]. GH Replacement in Adults: The First 5 Years of KIMS. Oxford: PharmaGenesis; 2000, pp. 115-32.Salomon F, Cuneo RC, Hesp R, Sönksen PH. The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency. N Engl J Med. 1989; 321(26): 1797-803. [Abstract]Hoffman AR, Biller BM, Cook D, Baptista J, Silverman BL, Dao L, et al. Efficacy of a long-acting growth hormone (GH) preparation in patients with adult GH deficiency. J Clin Endocrinol Metab. 2005; 90(12): 6431-40. [Abstract | Full text]Snel YE, Brummer RM, Doerga ME, Zelissen PM, Bakker CJ, Hendriks MJ, et al. Adipose tissue assessed by magnetic resonance imaging in growth hormone-deficient adults: The effect of growth hormone replacement and a comparison with control subjects. Am J Clin Nutr. 1995; 61(6): 1290-4. [Abstract | Full text]Johannsson G, Mårin P, Lönn L, Ottosson M, Stenlöf K, Björntorp P, et al. Growth hormone treatment of abdominally obese men reduces abdominal fat mass, improves glucose and lipoprotein metabolism, and reduces diastolic blood pressure. J Clin Endocrinol Metab. 1997; 82(3): 727-34. [Abstract | Full text]Lucidi P, Parlanti N, Piccioni F, Santeusanio F, De Feo P. Short-term treatment with low doses of recombinant human GH stimulates lipolysis in visceral obese men. J Clin Endocrinol Metab. 2002; 87(7): 3105-9. [Abstract | Full text]Tomlinson JW, Crabtree N, Clark PM, Holder G, Toogood AA, Shackleton CH, et al. Low-dose growth hormone inhibits 11 beta-hydroxysteroid dehydrogenase type 1 but has no effect upon fat mass in patients with simple obesity. J Clin Endocrinol Metab. 2003; 88(5): 2113-8. [Abstract | Full text]Taaffe DR, Thompson JL, Butterfield GE, Hoffman AR, Marcus R. Recombinant human growth hormone, but not insulin-like growth factor-I, enhances central fat loss in postmenopausal women undergoing a diet and exercise program. Horm Metab Res. 2001; 33(3): 156-62. [Abstract]Attallah H, Friedlander AL, Hoffman AR. Visceral obesity, impaired glucose tolerance, metabolic syndrome, and growth hormone therapy.  Growth Hormone Igf Res. 2006; 16(Suppl A): S62-7. [Abstract]Toogood AA, Holmes SJ, Shalet SM. Monitoring growth hormone replacement therapy. In: Juul A, Jørgensen JOL [eds]. Growth Hormone in Adults: Physiological and Clinical Aspects. Cambridge: Cambridge University Press; 2000, pp. 186-98. [Book]Watanabe S, Mizuno S, Oshima LH, Tsunematsu Y, Fujimoto J, Komiyama A. Leukemia and other malignancies among GH users. J Pediatr Endocrinol. 1993; 6(1): 99-108. [Abstract]Swerdlow AJ, Higgins CD, Adlard P, Preece MA. Risk of cancer in patients treated with human pituitary growth hormone in the UK, 1959-85: A cohort study. Lancet. 2002; 360: 273-7. [Abstract]Ogilvy-Stuart AL, Gleeson H. Cancer risk following growth hormone use in childhood: Implications for current practice. Drug Saf. 2004; 27(6): 369-82. [Abstract]Farris GM, Miller GK, Wollenberg GK, Molon-Noblot S, Chan C, Prahalada S. Recombinant rat and mouse growth hormones: Risk assessment of carcinogenic potential in 2-year bioassays in rats and mice. Toxicol Sci. 2007; 97(2): 548-61. [Abstract | Full text]Sperling MA, Saenger PH, Hintz R, Wilson T, Rose SR. Special editorial: Growth hormone treatment and neoplasia - coincidence or consequence? J Clin Endocrinol Metab. 2002; 87(12): 5351-2. [Abstract | Full text]Münzer T, Harman SM, Hees P, Shapiro E, Christmas C, Bellantoni MF, et al. Effects of GH and/or sex steroid administration on abdominal subcutaneous and visceral fat in healthy aged women and men. J Clin Endocrinol Metab. 2001; 86(8): 3604-10. [Abstract | Full text]de Boer H, Blok GJ, Voerman B, Derriks P van der Veen E. Changes in subcutaneous and visceral fat mass during growth hormone replacement therapy in adult men. Int J Obes Relat Metab Disord. 1996; 20(6): 580-7. [Abstract]

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Disease Search

Welcome to the Virtual Medical Centre (VMC). The VMC team spends a lot of time researching the diseases presented here and making sure that the information we provide has come from reputable peer-reviewed sources.

The quality of the content you see here is monitored by our editorial advisory board which consists of medical professionals. This means that you can be confident that whatever you read here is comprehensive, supported by real evidence and presented for your wellbeing.

The Virtual Medical Centre doesn?t aim to replace your doctor, its purpose is to provide supplementary information to demystify your health and help you to make educated decisions. We hope you find the information here useful and we wish you good health.

For more information about Virtual Medical Centre, see About Us.

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Heartburn

Heartburn is the common classical symptom of the disorder gastro-oesophageal reflux disease (GORD). Heartburn is experienced as a gripping, substernal (below the breastbone) discomfort that may be made worse by lying, eating or bending. In some cases heartburn may be confused with cardiac chest pain but the former is relieved by antacids whilst pain associated with ischaemic heart disease is relieved by nitrate sprays.

Heartburn is extremely common in the Australian population and is most cases can be easily managed with simple lifestyle changes and over-the-counter antacid medications. However, if the pain is persistent you may require further investigations as severe disease can progress to adenocarcinoma of the oesophagus. This is a type of cancer that develops in a very small number of patients.

Heartburn is the hallmark symptom of gastro-oesphageal reflux disease (GORD) and a common complaint amongst the general population. Heartburn is described as an intermittent retrosternal (behind the breastbone) burning discomfort that is exacerbated by eating, lying down, bending, stooping or straining. The pain is typically central but it may spread across the chest and into the neck and may be mistaken for the pain associated with ischaemic heart disease.

Virtually everyone will experience some mild heartburn at some time during their lives whilst up to 20% of the population will experience it weekly and 40% on a monthly basis. Doctors are faced with the challenge of deciding who needs further investigation for this extremely common complaint to identify those patients with gastro-oesophageal reflux that may progress to oesophagitis (erosion and destruction of the lining of the oesophagus), cellular morphological changes (called Barrett's oesophagus) and occasionally adenocarcinoma.

As forementioned, heartburn is commonly caused by gastro-oesophageal reflux disease. In this disorder the sphincter mechanism at the lower end of the oesophagus (the tube from the back of your throat to your stomach) is faulty. This means that when food enters the stomach, the gap between the oesophagus and stomach doesn't close properly and food can move backwards (reflux) into the oesophagus. This causes damage to the oesophagus and pain because the lining of the oesophagus is not designed to withstand the acidic environment of the stomach. In addition, the muscular walls are thought to spasm when food is refluxed further contributing to pain.

There are a number of conditions that can predispose to dysfunction of the lower oesophageal sphincter or make heartburn symptoms worse. These include:

Hiatus hernia- In this condition the top part of the stomach pushes up through a defect in the diaphragm (a muscular structure dividing the chest from the abdomen). This causes weakening of the sphincter and upsets the stomach's closure mechanisms. Food is more likely to propel back from the stomach to the oesophagus. Obesity. Pregnancy- Presumably predisposes to reflux due to increased abdominal pressure and loosening of ligaments and muscles (including those of the sphincter mechanism in the diaphragm) in the body in preparation for childbirth. Smoking and alcohol consumption. Medications- Certain medications used to treat blood pressure problems, depression or asthma have been associated with heartburn symptoms. If you suspect one of your medications is causing heartburn do not hesitate to consult your doctor.

In many cases the doctor can make the diagnosis of your condition from history of your symptoms alone. They will ask you detailed questions about the location of the pain and whether it spreads anywhere. The timing of the pain in relationship to meals, effects of posture and duration of the pain is also important information. Your doctor will also ask questions about your diet, smoking, alcohol and current medications. You will also be questioned about other symptoms such as blood or black material in your vomit or stools. In particular, weight loss and difficulty swallowing are important symptoms as they may suggest a serious problem.

Not all patients will have the classic symptoms of heartburn and sometimes your symptoms may seem more like a respiratory problem such as a cough or wheeze at night. Along with chest discomfort you may also have other symptoms of oesophageal dysfunction including:

Difficulty swallowing. Painful swallowing due to damage to the lining of the oesophagus. Acid regurgitation. Excessive salivation.

Unfortunately the severity of your symptoms does not correspond well with the severity of the damage to your oesophagus. This is a problem if patients have mild symptoms but there is extensive damage that may progress to more sinister conditions.

In many cases no further investigation is required, particularly if you are young with longstanding classic symptoms of heartburn. However, if you are older or you doctor is concerned they may order further tests to confirm the diagnosis of reflux and grade the severity.

These tests may include:

Upper gastrointestinal endoscopy and biopsy (tissue sampling)- This lets the doctor visualise damaged areas. Tissue samples can help exclude early precancerous changes. Barium studies- This may detect a hiatus hernia. Manometry- A tube is inserted down the nose to measure the pressures generated by the lower oesophageal sphincter. Oesophageal pH monitoring- This is done over a 24 hour period with a special device positioned in the lower oesophagus. The device can detect reflux episodes by the degree of acidity.

In most cases the main aim of treatment will be to relieve your symptoms. However in some cases the doctor may be more concerned that the oesophagus is completely healed, particularly if you have severe disease or are at risk of complications. In these cases follow-up endoscopies and biopsies may be needed. At least half of patients will respond to lifestyle changes and simple antacid medications.

Lifestyle changes

Lose weight if overweight. Raise the head of the bed- Placing blocks or bricks securely under the legs of the head of the bed can reduce the risk of stomach contents flowing back up into the oesophagus. Eat small, regular meals and avoid intake of food or beverages within three hours of bedtime. Avoid lying, bending or exercising just after eating. Avoid drugs such as NSAIDs that damage the oesophageal mucosa and drugs that impair oesophageal motility (nitrites, anticholinergics, certain antidepressants etc.). ask your doctor for advice regarding your current medications. Avoid smoking and alcohol. Avoid foods that are known to exacerbate your symptoms such as spicy foods, tomatoes, citris fruits and peppermint. Reduce stress.

Medications

If the above measures don't work you can try medications such as:

Antacids: For example Mylanta can neutralise stomach acid and is available at chemists and supermarkets. They can however alter bowel motions and cause fluid retention. Alginates: These are also over-the-counter drugs and work by forming a gel or 'foam raft' on top of the stomach contents to provide a physical barrier to reflux. If the above two types of drugs do not relieve symptoms within four weeks it is best to see a doctor who may arrange an endoscopy investigation (tube with a camera down the throat to have a look). Acid suppression therapy: Your doctor can prescribe two classes of drugs called H2-receptor antagonist or Proton-pump inhibitors (PPIs) which markedly reduce acid production. The latter is the best treatment for severe disease and can be used long-term to prevent recurrence. Your doctor may also try agents that speed up the stomach's emptying activity to reduce reflux.

Surgery

In a small number of patients surgery is indicated. This is only suitable if you have very severe symptoms of heartburn and the condition is confirmed by radiology or pH-monitoring. Surgery is normally done laparoscopically (key-hole surgery) and aims to fix defects in the diaphragm and sphincter mechanism. This may be considered a favourable option for young patients who would require long-term maintenance therapy.

For more information on acid reflux and heartburn and related investigations, treatments and supportive care, see Acid Reflux and Heartburn. de Caestecker J. ABC of the upper gastrointestinal tract. Oesophagus: Heartburn. BMJ. 2001;323(7315):736-9. [Abstract | Full text]Cohen S, Parkman HP. Heartburn: A serious symptom. N Engl J Med. 1999;340(11):878-9. [Abstract]Kumar P, Clark M (eds). Clinical Medicine (5th edition). Edinburgh: WB Saunders Company; 2002. [Publisher] Longmore M, Wilkinson I, Rajagopalan S. Oxford Handbook of Clinical Medicine (6th edition). Oxford: Oxford University Press; 2004. [Publisher] Longstreth GF. Heartburn [online]. Bethesday, MD: MedlinePlus; 2005. Available from: URL link Talley N, Moore M, Sprogis A, Katelaris P. Randomised controlled trial of pantoprazole versus ranitidine for the treatment of uninvestigated heartburn in primary care. Med J Aust. 2002;177(8):423-7. [Abstract | Full text] Product Information: Somac Heartburn Relief Tablets. North Ryde, NSW: Nycomed Pty Ltd; 31 July 2008.Fox M. Gastro-oesophageal reflux disease. Clinical review. BMJ. 2006; 332: 88-93. [Abstract | Full text]
Duggan AE. The management of upper gastrointestinal symptoms- is endoscopy indicated? Med J Aust. 2007; 186(4): 166-7. [Full Text]Braunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine (15th edition). New York: McGraw-Hill Publishing; 2001. [Publisher]Tierney LM, McPhee SJ, Papadakis MA (eds). Current Medical Diagnosis and Treatment (45th edition). New York: McGraw-Hill; 2006. [Publisher]DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. 2005; 100(1): 190-200. [Abstract]Murtagh J. General Practice (3rd edition). Sydney: McGraw-Hill; 2003. [Publisher]

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Diaphragm

The diaphragm, which was developed in the 19th century, is one of the oldest methods of preventing pregnancy. It is a latex dome which is inserted into a woman's vagina prior to sexual intercourse. Silicon diaphragms are also available for women who are allergic to latex.

The dome is placed so that it covers the woman's cervix, and thus creates a barrier which prevents sperm from entering the uterus. A flexible spring, found in the rim of the diaphragm, prevents the dome from moving out of place during intercourse.

The device must be fitted by a health professional, to ensure the correct size diaphragm is selected, however once a diaphragm has been fitted, a woman can easily insert and remove the diaphragm before and after sexual intercourse. Diaphragms are typically used in conjunction with spermicides to increase their effectiveness.

The diaphragm prevents pregnancy by blocking the cervical opening (the entrance to the uterus). It therefore prevents sperm from entering the uterus. If a woman is fertile, (if she has a viable egg in her uterus) sperm must enter the uterus to fertilise the egg. The egg cannot be fertilised once it has been expelled into the vagina. Thus, by preventing sperm from entering the uterus, the diaphragm also prevents sperm coming into contact with and fertilising an egg.

Most women can safely use a diaphragm. However, some women may need to delay diaphragm use, and use a different method until they can safely use a diaphragm. These women include:

Those who have experienced a second trimester miscarriage or abortion should wait for at least six weeks before having a diaphragm fitted;Those who have recently given birth should wait until at least six weeks after childbirth to have a diaphragm fitted;Those with uterine abnormalities, including uterine prolapse. These women should discuss other contraceptive methods which might be more suitable with their healthcare provider so that they can choose another method;Those with latex allergies should not use a latex diaphragm. A silicon diaphragm may be appropriate, or the woman's healthcare provider will be able to give advice about other contraceptive methods.

In addition, a diaphragm should not be used by the following women

Women with a history of toxic shock syndrome - as diaphragms increase the risk of this condition. Women who have previously experienced toxic shock syndrome should discuss other, more appropriate contraceptive methods with their healthcare provider. They should also not use a cervical cap);Women who have a high risk of HIV - as a diaphragm is typically and most effectively used in conjunction with spermicide, and commonly available spermicides increase the risk of HIV infection, diaphragm use may increase a woman's HIV risk. Women who are at risk of HIV infection, for example those who have sex with partners whose HIV status is unknown, should use condoms if possible, as these reduce the risk of HIV infection and other sexually transmitted infections. (For some women find it is difficult to use condoms, for example if their partners refuse, there are pregnancy prevention methods which they can use without their partner's knowledge including hormonal contraceptive injections or implants, or a diaphragm. However, these methods do not protect against STIs.)

The Sex in Australia survey, a national study of sexual experiences and behaviours of Australians, reported that 0.9% of Australian women used a diaphragm.

When used correctly and in conjunction with spermicide during every act of sexual intercourse, the diaphragm prevents pregnancy in 94% of cases. However, most women do not use the diaphragm correctly every time they have sex, and as typically used, its effectiveness is much lower, around 84%.

It is very important for a diaphragm user to know how to use the device correctly. The health practitioner who fits the diaphragm will explain to the woman how a diaphragm is used, when they do the fitting.

Your health practitioner may recommend that new users begin by using their diaphragm in conjunction with another method. This is not because diaphragms do not work when they are first fitted, but rather to allow the woman to get used to inserting and removing the device correctly.

Diaphragm users should also be aware that:

For effective use, a diaphragm must be used prior to every act of intercourse;When a diaphragm is correctly inserted, the woman should not be able to feel it, even during intercourse;That diaphragms are most effective when used in conjunction with spermicides;That diaphragms have some side effects, the most common of which are urinary tract infections and vaginal discharges (see below).

Diaphragms must be fitted by a health professional. To select a diaphragm of the correct size, the health provider will conduct a pelvic examination. The health provider will first assess the woman's uterine cavity for any conditions which may make the diaphragm an unsuitable contraceptive method for the woman. The practitioner will then insert their index and middle finger into the woman's vagina to determine the required diaphragm size. A diaphragm will then be selected and inserted into the woman's vagina by the health practitioner, so that it covers the cervix. The practitioner will then check that the device fits correctly.

Women using diaphragms should be aware that a new diaphragm must be fitted after childbirth or a second trimester abortion. A new diaphragm should also be fitted if the woman experiences weight gain of >5kg. Women who do not need to have a new diaphragm refitted should replace their device every two years.

The diaphragm must be inserted prior to each act of intercourse. The health practitioner who fits the device will explain to women who are new users of the diaphragm, how to use the device. They may also give the women additional information about her genital organs, which will assist her to correctly insert the device. For example the health practitioner may show women the position of the cervix and pubic bone, using a diagram or model.

To correctly insert a diaphragm a woman should:

Begin by washing her hands;Check the diaphragm for cracks by holding it up to the light;Insert spermicide into the dome and around the rim of the diaphragm. It is important to always check the expiry date of spermicides before using them;Press the rims of the diaphragm together and insert the device deep into the vagina. The woman should choose a comfortable position for insertion, for example lying down;Insert her finger into her vagina and feel to check that the diaphragm is in the correct position, that it is covering the cervix. The cervix feels similar to the tip of the nose, and can be felt through the diaphragm;Remove and reinsert the diaphragm if she can feel it inside her vagina when she moves;If the woman has sexual intercourse several times, she should not remove and reinsert the diaphragm between sex acts. Rather the diaphragm should be left in place and additional spermicide added each time.

It is very important that the diaphragm is left in place for at least six hours following intercourse, but not for more than 24 hours. Leaving the diaphragm in place for more than 24 hours may result in unpleasant odour or vaginal discharge, and in rare cases, toxic shock syndrome. Once at least six hours has elapsed since the last sexual intercourse, a woman should remove the diaphragm according to the following procedure:

Before commencing, the woman should wash her hands;She should then insert a finger into her vagina until she feels the rim of the diaphragm;She should gently slide the finger under the rim and pull the diaphragm down and out. Care should be taken to ensure the diaphragm does not tear or break;Finally, she should wash the diaphragm using mild soap and water. The diaphragm should then be dried and stored in a cool dry place.

Benefits of the diaphragm include:

Use of a diaphragm is controlled by the woman and can be used without the knowledge or consent of her male partner;A diaphragm is effective even if it is inserted up to six hours before intercourse and thus can be inserted in advance to avoid disrupting sexual activity;Using a diaphragm may enable a woman to become more familiar with her genital organs, for example she will learn where her cervix is, and become more comfortable inserting her fingers into her vagina;The diaphragm is a relatively low cost contraceptive method, which does not require frequent visits to a medical practitioner.

Diaphragm use is commonly associated with urinary tract infections. This means that between 1-10% of users experience this side effects.

Candidiasis and bacterial vaginosis are uncommon side effects of diaphragm use, that is, they are side effects experienced by between 0.1%-1% of women who use the device. When the diaphragm is used in conjunction with a spermicide, these side effects are more likely.

Very rare cases of toxic shock syndrome have been reported in diaphragm users. Less that 0.01% of users experience this side effect.

Limitations of the diaphragm include:

The diaphragm must be inserted prior to every act of intercourse;The contraceptive protection of a diaphragm is much less effective than other methods (e.g. hormonal methods are typically >99% effective);To insert a diaphragm a woman must be comfortable with inserting her finger/s into her vagina. Women who have cultural or other objections to touching their genitals cannot use the method;Diaphragms do not provide adequate protection against sexually transmitted infections (STI). Women who have sexual partners of unknown STI status, should use male or female condoms if this is possible. Condoms offer high levels of protection against both pregnancy and STI.

For more information on different types of contraception, female anatomy and related health issues, see Contraception.

Association of Reproductive Health Professionals. Non-hormonal contraceptive methods- a quick reference guide for clinicians. 2007. [cited 2009, October 30] Available from: www.arhp.org/guide World Health Organisation. Family Planning: A global handbook for providers. 2007. [cited 2009, June 20] Available from:  www.who.int/entity/reproductivehealth/publications/family_planning/en/ Amy, J. Tripathi, V. Contraception for women: an evidence based review. BMJ. 2009. 339:563-8.Farmer, L. Everett, S. Nonhormonal contraception. Obstetric, gynaecological and reproductive medicine. 2007.18(2):33-8.Richters, J. Grulich, A.E. de Visser, R.O. et al. Sex in Australia: Contraceptive Practices in a representative sample of women. Aust NZ J Pub Health. 2003;27:210-6.

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Gastric Banding (The LAP-BAND System)

The LAP-BAND System, otherwise known as Lap Band or Lapband, is a device that can be placed around the first part of the stomach during "key-hole" (laparoscopic) surgery for weight loss. The device is actually an adjustable band made of flexible, silicone material. A thin tube connects the band to a port placed under the abdominal skin at the time of surgery. The port allows a surgeon to inflate or deflate the band around the stomach without further surgery, and hence maximise a person's weight loss following the procedure.

The LAP-BAND System (Lap Band) works by forming a small pouch before food passes into the main stomach. This pouch holds less solid food than the stomach, so it makes the person feel “full” earlier. Food in the pouch is emptied more slowly than from the stomach, so the person may also feel “full” for longer following a meal.

The effectiveness of the system does require modification of a person's diet. In particular, high-energy drinks (such as protein shakes, smoothies, meal replacements) should be avoided because they pass straight through the small pouch and do not cause the sense of fullness that leads to weight loss.

There are a number of factors to consider when deciding if this procedure is appropriate. The major indication for laparoscopic banding surgery is for morbidly obese patients to lose weight. The following are some of the main criteria are used to assess if the LAP-BAND System (Lap Band) is appropriate:

 

The LAP-BAND System has been shown to effectively cause weight loss in morbidly obese patients. The average patient will lose 87% of their excess weight after having the LAP-BAND System inserted. This should be compared to a person trying to lose weight by diet, exercise and medication therapy – where the average person will only lose 21% of their excess weight.

Large studies have shown that the average person will lose 23kg following this surgery at 2 years, and up to 43kg at 5 years post-operatively.

The major benefit of the LAP-BAND System is weight loss. It has been used effectively in Australia since 1994. The operation to insert the LAP-BAND System is called gastric banding surgery. This surgery is the simplest of all types of surgery performed for obesity. It is also considered the safest surgery for weight loss. In most cases, patients who have this surgery will only be in hospital for 24 hours.

Following the surgery, a number of other medical problems will be improved in conjunction with weight loss. Studies of patients who have received gastric banding surgery show improvements in the following diseases after 2 years:

Laparoscopic gastric banding surgery for the placement of the LAP-BAND System is a complex procedure. Despite this, the overall rate of complication is low. Every type of surgery carries risk. The risk of death within 30 days of this procedure is very low – less than 0.5%.

The main problems that may occur after surgery are infection (of the wound or the lungs), blood clots (in the legs or lungs) and collapse of the lungs (from the anaesthetic).

There are some specific problems that may occur following gastric banding surgery. In 5 – 10% of patients the band may slip downwards or the pouch of the stomach may dilate. In these situations, another operation is required to adjust the band position. In less than 2% of patients the band may erode into the lining of the stomach. This is a serious complication but is uncommon.

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The formula for calculating your body mass index is:
BMI = weight (kilograms) / (height (metres) * height (metres))

For example:
A man who weighs 85 kilograms and is 1.8 metres tall would have a BMI of
BMI = 85 / (1.8 * 1.8)
BMI = 85 / 3.24
BMI = 26.2

This information will be collected for educational purposes, however it will remain anonymous.

   Kral J. ABC of Obesity: Management: Part III – Surgery [5th article in series] British Medical Journal. 2006; 333; 900-3. Available online [http://www.bmj.com]Sjorstom L, Lindroos A, Peltonen M, Torgson J, Bouchard C, Carlsson B, et al Lifestyle, diabtes and cardiovascular risk factors 10 years after bariatric surgery. New England Journal of Medicine. 2004; 351(26): 2683-93.O’Brien P. (2007) The LAP-BAND Solution – A partnership for weight loss.Northern Rivers General Practice Network (cited 12th December 2007) What GPs should know about lap banding. Available online [http://www.medicineau.net.au/clinical/obesity/obesit3160.html]Allergan Australia (2007) About laparoscopic gastric banding [cited 11th December 2007] Available online [http://www.gastricbandingsurgery.com.au/about_gastric_banding.php]Wilkinson, S. (cited December 21st 2007) Obesity Surgery: Lap-Band Surgery, Am I a suitable candidate? Available online: [http://www.tasmaniaobesitysurgery.com.au/lapband.html]National Health and Medical Research Council (2003) Clinical Practice Guidelines for the management of overweight and obesity in Australia [update 19th March 2004] Commonwealth of Australia, Department of Health and Ageing [Available online: www.obesityguidelines.gov.au ]O’Brien P. Treatment of mild to moderate obesity with laparoscopic adjustable banding or an intensive medical program: a randomized trial. Annals of Internal Medicine. 2006; 144(9): 625-33.Colquitt, J. Clegg, A. Loveman, E. Royle, P. Sidhu, M. (2005) Surgery for morbid obesity. [Cochrane clinical review] Available online: [http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD003641/frame.html]Morris, P. Wood, W. (2000) [2nd edition] Oxford textbook of Surgery: Chapter 25; Surgery for Obesity [chapter author Grace, M.] Oxford University Press: Oxford.Allergan Australia (2007) About laparoscopic gastric banding [cited 11th December 2007] Available online [http://www.gastricbandingsurgery.com.au/about_gastric_banding.php]Allergan Australia (2003) LAP-BAND Data Sheet.

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Biomarkers of colorectal cancer

Tumour biomarkers are chemicals that are made by tumour cells or other cells of our body, in response to cancer or other benign conditions. Different types of cancers or tumours may be associated with different tumour biomarkers. Colorectal cancer (CRC), which includes colon cancer and rectal cancer is responsible for half a million deaths worldwide every year. There are also about one million new cases diagnosed annually, making it the third most common cancer in the world. Early detection, accurate diagnosis and intensive surveillance are important for best improving a patient's prognosis and response to therapy.

There are a number of methods that doctors use to detect CRC including sigmoidoscopy, colonoscopy and barium enema. Some newer techniques being investigated for effective detection and monitoring of CRC are CT colonography and molecular biomarkers. The use of tumour biomarkers gives doctors a non-invasive way of detecting and monitoring CRC.

Doctors can use tumour biomarkers in the detection, prognosis and management of some types of cancer, including CRC. An abnormal level of tumour biomarker is usually not enough for a complete diagnosis of cancer and is usually combined with other tests such as a biopsy. The type of biomarker detected and its levels can give an indication to what type of cancer may be present, whether or not it is malignant and what the best treatment may be.

Tumour markers are used during the treatment of cancer in order to monitor the effectiveness of a therapy and how the patient may be responding to the treatment. If levels of a tumour biomarker decrease it may mean that the cancer is responding to treatment. If levels remain the same or increase after treatment it may be an indication that the therapy is not working. Continued monitoring of tumour biomarker levels following treatment can be used to check for recurrence of the cancer.

Different tumour biomarkers are measured in different ways and from different sources. Some markers are found in blood or urine, so these would require you provide a small amount of blood or a urine sample. Other tumour biomarkers such as those involved in faecal occult blood testing (FOBT) can be isolated from faecal matter and require a stool sample. Tissue samples can also contain tumour biomarkers and may involve a tissue biopsy. This is a more invasive procedure than urine or stool sampling. After a doctor takes the sample they are sent to a laboratory for testing using various methods to determine biomarker levels. Particular foods such as red meats or fruits and vegetables can influence the assay and cause false positive results.

Two key factors for an effective tumour biomarker assay are:

The assay must be sensitive in its ability to accurately detect disease; andThe assay must be specific for the particular malignancy.

In the early detection or screening of patients for CRC, stool based markers are widely used. Tissue-based markers have been studied as possible prognostic or predictive markers of disease, while CRC biomarkers obtained from serum (blood) are primarily used for the postoperative surveillance of patients.

Tissue based markers

Tissue based markers have been investigated as possible prognostic markers and predictors of response to treatment. Thymidilate synthase (TS) is an enzyme involved in the processing of the cells genetic material and has been studied as a marker that can predict how well a patient may respond to treatment with drugs such as 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine. The transcription factor p53 has also been widely investigated as a biomarker that may predict the severity of cancer how it may respond to particular anticancer drug.

The K-ras oncogene is often associated with cancer as abnormalities in this gene have been found in many tumours. K-ras is involved in sending signals that can regulate how much cells grow or multiply. K-ras mutations are linked to approximately half of all CRCs and have been found to be important in the early stages of the disease. Studies have identified an association between K-ras mutations and poor disease outcome in patients with CRC.

Stool based markers

Faecal occult blood testing (FOBT) is the most commonly used screening test for CRC. There are two main types of FOBT, the guaiac test and the immunochemical test. Both tests detect proteins that may be indicators of colorectal cancer.

The advantages of FOBT for CRC are that the tests are simple and affordable, non-invasive, require very little patient preparation and have the capability of examining the entire colorectal tract. They do however have relatively low specificity and sensitivity for both benign (or precancerous adenomas) and malignant CRC.

Faecal DNA tests are used in screening for CRC on the basis that abnormal DNA is excreted in cells shed from cancerous colorectal lesions. Tests usually use a panel of DNA markers in order to identify mutant genes. DNA markers can provide a more accurate test than FOBT and there are no restrictions on diet or medication. The test is however quite laborious, expensive, also lacks specificity. Examples of stool based DNA markers include K-ras, APC (adenomatous polyposis coli) and p53.

Serum based markers

Serum-based markers of colorectal cancer are mainly used for monitoring patients following the surgical removal of malignant tumours. Patients are monitored regularly following surgery in order to detect any cancer recurrences or metastases. As up to 50% of patients develop recurrent disease or metastases following surgery, this is an important part of CRC management. CEA (carcinoembyonic antigen) was the first serum marker used in patients with CRC, and although it's the oldest, it still remains the most widely used. CEA is mainly used to monitor patients following surgery for primary CRC. A number of studies have shown that intensive monitoring after cancer surgery is associated with an improved outcome if regular CEA measurements were taken. Other serum-based tumour biomarkers used for CRC include markers called CA-19-9, TPA, TPS and TIMP-1

There are three main types of the mammalian ras genes: K-, H- and N-ras. Each of the ras genes makes proteins that are involved in relaying signals between different regions of the cell. These signals play important roles in a number of important biological functions including cell division and cell growth. As mentioned above, the K-ras oncogene is one of the most frequently altered in human cancers, with approximately 50% of CRCs containing mutant K-ras.

While many early investigations suggested that K-ras abnormalities were strong signs of serious disease and poor outcome for patients, more recent studies have found that this may not be correct in all cases. This meant that K-ras might not be very suitable as a prognostic marker.

While there is little evidence that K-ras mutations can be used as an effective screening tool or indicator of prognosis for CRC patients, recent research shows that the gene as a potential marker for prediction of response to specific therapies. Studies have shown that cases of CRC that are associated with mutations in K-ras will not respond well to particular treatments. For example, it has been shown that anticancer drugs such as panitumumab and cetuxamib are not effective in patients with K-ras abnormalities. While these studies do not specifically identify which therapies should be used in the treatment of K-ras associated CRC, they are able to help in the selection of an appropriate therapy.

Tumour Markers: Questions and Answers [online]. 2006 [cited 01/05/08]. Available from: http://www.cancer.gov/cancertopics/factsheet/Detection/tumor-markersDuffy MJ, van Dalen A, Haglund C, Hansson L, Holinski-Feder E, Klapdor R, Lamerz R, Peltomaki P, Sturgeon C, Topolcan O. Tumour markers in colorectal cancer: European Group on Tumour Markers (EGTM) guidelines for clinical use. European Journal of Cancer. 2007;43:1348-1360.Duffy MJ, van Dalen A, Haglund C, Hansson L, Klapdor R, Lamerz R, Nilsson O, Sturgeon C, Topolcan O. European Journal of Cancer. Clinical utility of biochemical markers in colorectal cancer: European Group on Tumour Markers (EGTM) guidelines. 2003;39:718-727.Hassan C, Laghi A, Zullo A, Iafrate F, Morini S. Q&A on diagnosis, screening and follow-up of colorectal neoplasia. Digestive and Liver Disease. 2008;40:85-96.Ehrhardt, A., Ehrhardt, G. R. A., Guo, X., and Schrader, J. W. Ras and relatives—job sharing and networking keep an old family together. Exp. Hematol., 30: 1089 – 1106, 2002.Amado RG. Panitumumab (pmab) afficacy and patient-reported outcomes (PRO) in metastatic colorectal cancer (mCRC) patients (pts) with wild-type (WT) KRAS tumour status. Proceedings of the 2008 Gastrointestinal Cancers Symposium. 2008. ASCO.



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Cachexia

Cachexia means "poor condition" in Greek. Cachexia has been defined as a syndrome characterised by progressive loss of lean tissue and body fat. Losses are often in excess to that explained by the associated anorexia. Cachexia occurs with various diseases, especially those that are chronic and debilitating. Diseases commonly associated with cachexia are cancer, AIDS, congestive heart failure, COPD and chronic inflammatory rheumatological diseases (e.g. rheumatoid arthritis, systemic lupus erythematosus (SLE), scleroderma, polymyositis, etc).

Weight loss in cancer cachexia is different to weight loss in simple starvation , due to accelerated loss of muscle compared with fat tissue, presence of proinflammatory cytokines and prolonged acute phase protein response that contributes to increased resting energy expenditure and weight loss. Patients with cancer cachexia experience anorexia, early satiety, weakness, sarcopenia, fatigue, anaemia and severe weight loss.

There are no definitive methods for diagnosis of cancer cachexia. Clinical signs of anorexia and weight loss =5% in 6 months would be expected but clinical judgement is required.

Treatment of cachexia should be directed towards:

Treatment of underlying disease Controlling the symptoms of cachexia

Controlling the symptoms of cachexia

Several treatment options have been outlined to treat cachexia. The principle is to improve the nutrition of the patients and to suppress the inflammatory response that is eating up the body's energy. These include:

Feeding the patient with high calorie food Drugs to stimulate the appetite Drugs to stimulate the body to build up more muscle mass

It has been proposed that eicosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid, may reduce the production of proinflammatory cytokines and thus may improve energy and protein intake, performance status and quality of life in cancer patients with cachexia. This may be taken as fish oil capsules or commercial nutrition supplements. However, the results of studies into the effects of EPA have been inconsistent. Your dietitian can provide more information about the dietary management of cancer cachexia.

Article kindly reviewed by:

The DAA WA Oncology Interest Group
and
Food4Health (Helen Baker Dietitian-APD)

Kotler D. Review: Cachexia. Ann Intern Med. 2000;133:622-634.Dietitians Association of Australia. 2005. Evidence Based Practice Guidelines for Nutritional Management of Cancer Cachexia.

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