Number 3 : SEPTEMBER 1999


The Annual Scientific Meeting is rapidly approaching. Alan Spencer and Darrell Crawford have been working hard to make it a memorable and informative meeting. Due to unavoidable delays in getting the Conference Brochure sent to members, the abstract deadline and the Early Bird Registration dates have been extended. So there is still an opportunity to send in your abstract. Once again, travel grants will be awarded at the meeting for members who present abstracts at the meeting. Please indicate if you wish to be considered for a travel grant when you submit your abstract. More information regarding travel grants is available from Alan Spencer, the Conference Secretariat, or myself.

The Annual General Meeting for AuSPEN will be held during the Conference and it would be great to see as many members as possible attend this meeting and help direct the Society to new and better things for the future. Nominations are being called for members of Council. Please put your hand up if you think you would like to become more involved in the running of the Society. I have personally found being a member of the AuSPEN Council to be very rewarding and it has been a real pleasure to be involved. I encourage anyone with any questions regarding membership of the AuSPEN Council to speak with me or another member of Council regarding the options that are available.

An important consideration for the AGM this year will be the question of the journal Nutrition. The journal has been a benefit of membership for the past 5 years. As our contract with the journal is due to expire, it is important the Council understands clearly the consensus of the membership regarding whether we should continue receiving the journal, cease the journal or associate with an alternative Nutrition journal. The questionnaire you have received will help direct the Council in understanding the opinion of the membership. This is an important decision for the Society as the cost of the journal has increased and now represents over 50% of membership annual subscription. Also the delivery of the journal has not been consistent until very recent times. I invite you to give your opinion regarding the journal either via the questionnaire, a letter, or calling either myself, Ibolya Nyulasi or a member of the AuSPEN Council.

I look forward to seeing you all on the Gold Coast in October.

Julie Bines President of AuSPEN


Dr Julie Bines, President of AuSPEN, Dept. of Gastroenterology and Clinical Nutrition, Royal Children's Hospital, MELBOURNE, Victoria 3000, Australia.
Ph +61-3-9345-5060. Fax +61-3-9345-6240

Liliana Sputore, Honorary Secretary of AuSPEN, 40 Jackson Avenue Karrinyup WA 6018.
Ph : +61-8-9445-3040, +61-8-94312769 Fax : +61-8-9446-4282
email :

Sabita Rajeshwar, Honorary Treasurer of AuSPEN , Dept of Nutrition and Dietetics, The New Children's Hospital, PO Box 3515,Parramatta, NSW 2124
Ph +61-2-9845-2225 Fax +61-2-9845-2252 email

Secretariat : 233, Rathdowne St., CARLTON. There is a combined number for contact, messages and fax : 03-9639-4677.


Alan Spencer

Dear Members,

Just a quick reminder that the 25th Annual Scientific Meeting of AuSPEN is fast approaching, October 22- 23. Hopefully all of you have by now received your registration programs, have put your registration forms in and, of course, have submitted your abstracts. The early bird and abstract deadlines have been extended as you should be aware of with the recent flier that was mailed to all members. This promises to be an excellent program with a range of high quality speakers, so I urge those of you still deciding whether or not to come to take the plunge!! It is also a good excuse for a well deserved holiday at a great time of the year. The venue is only a stones throw from the beach and a few minutes from the heart of Surfers Paradise. What more temptation do you need!!

As we have done in the past we are offering three travel awards of $400.00 each to AuSPEN members who have abstracts accepted for the conference. Submissions should be sent to Consult Fleetwood Management Services.

Alan Spencer Convenor

Growth, nutrition and the growth hormone (GH), insulin-like growth factor (IGF) axis in cirrhosis

Anthony J. Donaghy, Hepatologist
AW Morrow Gastroenterology and Liver Centre,
Royal Prince Alfred Hospital Camperdown, NSW 2050
email :

This article is based largely upon the paper presented at the Annual Scientific Meetings of the Gastroenterological Society of Australia and the Australian Society for Enteral and Parenteral Nutrition, Canberra, in October 1998.


Insulin-like growth factor-I (IGF-I) is an essential growth factor which has been shown to play a central role in growth regulation at the whole body, tissue and cellular levels. Circulating levels are thought to be of liver origin and recent studies have shown that low IGF-I levels are associated with adverse clinical outcomes in cirrhotic patients, possibly explained by the potential role of reduced IGF-I levels in the development of cirrhotic complications such as malnutrition, insulin resistance, osteoporosis and impaired immunity. A recent study showed that IGF-I could improve hepatic synthetic function and reduce oxidative liver damage and fibrosis in experimental cirrhosis (1). This brief review will discuss the physiology of the growth hormone (GH):insulin-like growth factor (IGF) axis, the pathogenesis of the acquired GH resistance of cirrhosis, the prognostic significance of serum levels of IGF-I and its binding proteins and the effects of therapeutic manipulation of this axis in cirrhotic patients.

Physiology of the GH:IGF Axis

The somatomedin hypothesis of Salmon and Daughaday established that the majority of the growth promoting effects of GH are indirect and act via liver produced, GH dependent plasma factors known as somatomedins or insulin-like growth factors. IGF-I stimulates cellular differentiation and proliferation, is an essential cofactor for the progression through the cell cycle from phase G1 to S, is a dominant regulator of somatic growth before puberty and after epiphyseal closure plays an important role in the maintenance of body composition. The bioavailability of the IGFs is modulated by the high affinity insulin-like growth factor binding proteins (IGFBPs-1 to-6) of which the liver is a significant source. Greater than 85% of IGF-I circulates bound to IGFBP-3 or IGFBP-5 and the acid-labile subunit (ALS) in GH dependent ternary complexes which prolong IGF halflife, function as a reservoir for IGFs and limit their extravascular transit. IGFBP-2 may act as an alternative carrier for the IGFs in conditions when the capacity of the ternary complex is insufficient to carry the available IGFs. IGFBP-1 circulates at much lower levels but may provide important freely available IGF binding sites and may acutely regulate IGF bioavailability in response to changes in metabolic variables (2).

Acquired GH Resistance in Cirrhosis

The liver is the central organ of the endocrine GH/IGF axis. Under hypothalamic control, GH is secreted by the anterior pituitary gland, transported in the circulation by the high affinity growth hormone binding protein (GHBP) and acts through the hepatic GH receptor to regulate the production IGF-I, the IGFBPs and the acid labile subunit (ALS). The progression of chronic liver disease to cirrhosis results in a state of acquired GH resistance with high circulating GH levels and low levels of IGF-I (3). GH resistance is thought to be an acquired metabolic shift wherein states of stress or low substrate availability effect a change from IGF-I stimulated growth to direct fuel mobilisation. The metabolic downside of this change is tissue catabolism which is central to the development of malnutrition.

Pathophysiology of GH Resistance in Cirrhosis

Hepatocyte loss is likely to be the dominant cause of the GH resistant state in cirrhosis : GH receptors are predominantly localized to hepatocytes in normal liver and in the regenerative nodules of cirrhotic liver. Disturbance of hepatic architecture leads to shunting of nutrient rich portal blood away from the hepatic sinusoids and clinical studies have suggested that portosystemic shunting may significantly contribute to GH resistance in cirrhosis. For example, levels of IGF-I are low in hepatic schistosomiasis where there is portal hypertension but normal hepatocyte function and strong correlations can be demonstrated between high wedged hepatic venous pressure (a marker of portosystemic shunting) and high GH, low IGF-I and low IGFBP-3 levels in alcoholic cirrhotics (4). These findings suggest that portosystemic shunting has at least an effect additional to hepatocyte loss in the pathogenesis of GH resistance in cirrhosis. Nutrition is an important regulator of IGF-I gene expression and serum levels with the study of Mendenhall in alcoholic cirrhosis demonstrating that malnutrition correlated with IGF-I independently of liver dysfunction and histopathological alterations (5). This finding has suggested that IGF-I levels might be more dominantly regulated by nutritional factors than liver function.

The Impact of Cirrhosis on the GH:IGF Axis

GH levels are high in cirrhosis with Cuneo documenting increased 24 hour total GH production rates, increased number and amplitude of GH secretory bursts and increased GH halflife (6). Serum GHBP levels have been shown to be low in cirrhosis and an early study by Chang showed decreased GH binding to liver membranes from cirrhotic patients suggesting GH receptor (GHR) loss (7). Recent studies have further examined gene expression of the GHR in cirrhosis : Ross reported a 4.4 fold decrease in GHR mRNA levels using an RNase protection assay in a small group of adult cirrhotics and Holt described a 1.7 fold decrease in GHR mRNA levels by RT-PCR in a homogeneous group of 11 cirrhotic children with extrahepatic biliary atresia. This study also showed a decrease in IGF-I mRNA levels in cirrhotic liver.

We have demonstrated low circulating levels in cirrhosis of the three components of the circulating ternary complex : IGF-I, IGFBP-3 and the ALS, with levels correlating with disease severity as measured by the Childs Pugh score. We have also demonstrated increased fasting levels of IGFBP-1 despite high ambient serum insulin levels (3). However IGFBP-1 levels fell in response to a glucose load suggesting that impaired substrate availability during fasting in cirrhosis is a more potent regulator than insulin. High serum IGFBP-1 levels bind free IGF-I and limit both its growth producing and hypoglycaemic potential.

Alcohol and the GH:IGF Axis

Alcohol exerts specific deleterious effects on the GH:IGF axis in addition to nutritional influences and those relating to the development of cirrhosis. In an experimental model alcohol was shown to decrease GH receptor signal transduction independently of an effect on GH receptor number. A number of studies have also shown that alcohol markedly impairs IGF-I receptor signal transduction (tyrosine autophosphorylation) indicating an important deleterious effect of alcohol at the tissue receptor level.

Prognostic Significance of Serum IGF-I and IGFBP-3 Levels

An early indication of the possible prognostic relevance of serum levels of IGF-I came from the study of hospitalised alcoholic cirrhotics by Caufriez. These authors demonstrated that serum IGF-I levels correlated most strongly with aminopyrine breath test values (r=0.68 p <0.001) followed by the Childs Pugh score (r=-0.57 p <0.01) with weaker correlations observed with hepatic export proteins such as albumin (8). These findings strongly suggested that in alcoholic cirrhosis IGF-I may be a sensitive marker of functional hepatocellular capacity.

The first longitudinal data relating survival to serum IGF-I levels came from a study of 36 hospitalised alcoholic cirrhotics reported by Moller who noted that 2 year survival as plotted by Kaplan Meier curves was significantly lower in patients with serum IGF levels below 3.1 nmol/L. The same group later studied a much larger group of 352 alcoholic cirrhotics and noted that serum levels of both IGF-I and its major binding protein IGFBP-3 had significant prognostic survival value. Using a time dependent Cox regression model the authors showed that these markers provided prognostic information that was independent of other prognostic factors such as alcohol intake, coagulation factors, creatinine or serum IgM levels (9).

In a study of 64 hospitalised alcoholic patients Caregaro showed significantly diminished 2 year survival in patients with a low IGF-I z score. They did not note any significant correlation of IGF-I with anthropometric indices of nutritional status which contrasted to the findings of Mendenhall et al which has been discussed previously. The authors concluded that low levels of IGF-I in alcoholic cirrhosis may be effected by a number of factors acting synergistically : liver function impairment, portal hypertension, hyperestrogenism, abnormalities of glucose and insulin metabolism and malnutrition. The identification of factors accurately predicting survival in alcoholic liver disease has proven extremely difficult. Liver transplantation now has an established role as definitive therapy for endstage liver disease and the identification of its optimal timing is of paramount importance. Further studies of serial measurements of IGF-I and its major binding protein IGFBP-3 in patients with advanced cirrhosis are required to assess their efficacy as predictors of clinical outcome. Serum levels of these proteins are influenced by hepatocyte dysfunction, insulin resistance and nutritional factors: factors that have been shown to adversely influence survival. It is possible that IGF-I and IGFBP-3 may find a role in the indication of critical liver dysfunction and malnutrition in these patients.

Therapeutic Intervention with GH and IGF-I in Cirrhosis

In severe catabolic illness, including cirrhosis, a number of studies have demonstrated that aggressive nutritional support alone does not prevent significant loss of lean body mass and much recent research has examined the role of exogenous growth factor therapy in this setting. Recombinant human GH therapy has been shown to improve protein anabolism and to impact on short term morbidity after abdominal surgery, major trauma and severe sepsis and severe burns. In growth retarded children with chronic renal failure GH effected striking improvement in height velocity and this study importantly demonstrated that GH induced improvements in short term nitrogen economy can effect significant changes in body composition with longer term therapy.

In the first reported study of GH therapy in human liver disease Moller showed significant increases in serum levels of IGF-I in a group of male alcoholic cirrhotics treated with GH for six weeks (10). Serum IGFBP-3 levels increased in both treatment and placebo groups whereas no changes in serum IGFBP-1 levels were seen. No change in biochemical liver function tests was noted and no significant side effects were seen. We studied the impact of high dose GH therapy on both the IGF:IGFBP axis and on nitrogen balance in a group of cirrhotic patients of varying aetiologies including alcohol. In the GH treated group a significant rise in IGF-I and IGFBP-3 serum levels was seen but this was markedly attenuated in comparison to that seen in a group of normal subjects we had previously treated, likely reflecting the severity of the GH resistance of cirrhosis (11). We were able to also demonstrate that improvement in serum IGF-I levels was associated with a significant improvement in cumulative nitrogen balance, likely due to improved nitrogen retention. A later study by Wallace confirmed GH induced increases in IGF-I and IGFBP-3, but also demonstrated that GH effected improvement in lean body mass as measured by total body potassium counting.

GH:IGF-I, Liver Disease and the Future

Liver transplantation is now established as definitive and life saving therapy for advanced liver disease. However the lack of graft availability has led to increasing waiting times with many centres reporting increasing mortality in patients before engraftment. The measurement of serum levels of components of the GH:IGF axis may give important information on the adequacy of nutritional intakes in cirrhotic patients and may be of important prognostic value in the timing of liver transplantation. Interventional therapy with these growth factors may impact on malnutrition and other cirrhotic complications such as impaired immunity which adversely affect survival in this patient group.


1. Castilla, C.I., Garcia, M., Muguerza, B., Quiroga, J., Perez, R., et al. 1997. Hepatoprotective effects of insulin-like growth factor I in rats with carbon tetrachloride-induced cirrhosis. Gastroenterology. 113:1682-1691.

2. Jones, I., and Clemmons, D. 1995. Insulin-like growth factors and their binding proteins: biological actions. Endocrine reviews. 16:3-34.

3. Donaghy, A., Ross, R., Gimson, A., Hughes, S.C., Holly, J., et al. 1995. Growth hormone, insulinlike growth factor-1, and insulinlike growth factor binding proteins 1 and 3 in chronic liver disease. Hepatology. 21:680-688.

4. Moller, S., Juul, A., Becker, U., Flyvbjerg, A., Skakkebaek, N.E., et al. 1995. Concentrations, release, and disposal of insulin-like growth factor (IGF)-binding proteins (IGFBP), IGF-I, and growth hormone in different vascular beds in patients with cirrhosis. J Clin Endocrinol Metab. 80:1148-1157.

5. Mendenhall, C.L., Chernhausek, S.D., Ray, M.B., Gartside, P.S., Roselle, G.A., et al. 1989. The interactions of Insulin-like Growth Factor-1(IGF-1) with protein-calorie malnutrition in patients with alcoholic liver disease : V.A. Cooperative study on Alcoholic Hepatitis V1. Alcohol and Alcoholism. 24:319-329.

6. Cuneo, R.C., Hickman, P.E., Wallace, J.D., Teh, B.T., Ward, G., et al. 1995. Altered endogenous growth hormone secretory kinetics and diurnal GH-binding protein profiles in adults with chronic liver disease. Clin Endocrinol Oxf. 43:265-275.

7. Chang, T.C., Lin, J.J., Yu, S.C., and Chang, T.J. 1990. Absence of growth-hormone receptor in hepatocellular carcinoma and cirrhotic liver [see comments]. Hepatology. 11:123-126.

8. Caufriez, A., Reding, P., Urbain, D., Golstein, J., and Copinschi, G. 1991. Insulin-like growth factor I: a good indicator of functional hepatocellular capacity in alcoholic liver cirrhosis. J Endocrinol Invest. 14:317-321.

9. Moller, S., Becker, U., Juul, A., Skakkebaek, N.E., and Christensen, E. 1996. Prognostic value of insulinlike growth factor I and its binding protein in patients with alcohol-induced liver disease. EMALD group. Hepatology. 23:1073-1078.

10. Moller, S., Becker, U., Gronbaek, M., Juul, A., Winkler, K., et al. 1994. Short-term effect of recombinant human growth hormone in patients with alcoholic cirrhosis. J Hepatol. 21:710-717.

11. Donaghy, A., Ross, R., Wicks, C., Hughes, S.C., Holly, J., et al. 1997. Growth hormone therapy in patients with cirrhosis: a pilot study of efficacy and safety. Gastroenterology. 113:1617-1622.


Both the insert advertising the BAPEN NZ course and the sponsorship of the July newsletter were generously provided by PROMEDICA, in the interest of medical education. The statement that it was provided by Alison Missen and BAPEN was misleading. The Editor apologies to all the parties concerned for these errors."


September 22nd - 25th : The Tenth Clinical Congress of the Mexican Association for Parenteral and Enteral Nutrition (AMAEE) Marriot Casa Magna Puerto Vallarta Hotel, Puerto Vallarta, Jalisco, Mexico. For registration info: email : or fax: 525-559-4793. For accommodation info: Humboldt Tours, email : or fax: 525-660-0735. Web site:

September 27th -29th : South African Society of Parenteral & Enteral Nutrition (SASPEN) : Holiday Inn - Durban South Africa For more information contact: Jane Downs Website : This is a good site and has the complete programme details.

October 1st - 3rd, 1999 40th Annual Meeting of the American College of Nutrition, Washington, DC. For more information call (212) 777-1037. Fax 212-777-1103.

October 7th - 9th, 1999 : International Symposium on in vivo Body Composition Studies, Brookhaven National Laboratory, Upton, NY. Contact S Yasumura, Bldg 490, Medical Department, PO Box 5000, Brookhaven National Laboratory, Upton, NY 11973-5000. Ph +1-516-344-3606. Fax +1-516-344-5311.

October 14th - 17th, 1999 : Seventh World Congress on Clinical Nutrition, New Delhi. Contact Prashant Saha, Secretariat, Conferences and Incentives Management, 1/33A, 3rd Floor, Nanakpura, Next to Gurudwara, New Delhi 110021. Telephone 91 11 4675262. Fax 91 11 4678030.

October 14th - 17th 1999 : 24th Australian & New Zealand ASM on Intensive Care, Christchurch. Contact: Anne Jury, Medical Industry Association, PO Box 33 1250, Takapuna, Auckland. Phone 09 486 3000, 0800 33 55 42 Fax 09 486 3500

October 18th - 21st, 1999 : The American Dietetic Association Annual Meeting and Exhibition, Georgia World Congress Center, Atlanta. Contact The American Dietetic Association, 216 West Jackson Boulevard, Chicago, IL 60606-6995. Ph +1-800-877-1600, ext 4866. Fax +1-312-899-0008.
email: Webpage :



Programme Overview

  • Oxidative Stress and Gastrointestinal Disease
  • Nutritional Assessment
  • Nutrition and Gastrointestinal Disease
  • Mucosal Nutrition
  • Pharmaceutical Aspects of Nutritional Support
  • Diet and Nutrition in Gastrointestinal Cancer
  • Workshop on Practical Issues of Nutritional Support

International Guests

  • Dr Khursheed Jeejeebhouy MD, Professor of Medicine, Nutrition and Physiology, University of Toronto and Director of the Nutrition Support Service, St Michaels's Hospital, Toronto, who has a distinguished career in gastroenterology and nutrition.
  • Dr John McFie MD, Consultant Surgeon at Scarborough Hospital, UK. His areas of expertise are in nutrition and mucosal immunity and the role of glutamine in nutrional support.

Conference Secretariat :
Consult Fleetwood, PO Box 79, ARANA HILLS, QUEENSLAND 4054, Australia.
Ph: +61-7-3264-5970 Fax: +61-7-3264-3520
email :


November 9th - 12th, 1999 : 1999 BAPEN Course Contact Alison Missen, Dietitian, Middlemore Hospital, Private Bag 93311, Otahuhu, AUCKLAND, NEW ZEALAND. Phone : Middlemore Hospital +64-9-276-0000 or Nutrition Services Dept +64-9-276-0090
email :

November 25th - 28th, 1999 : Australian Society of Hospital Pharmacists Perth W.A. Contact Jenny Dyer, Motive Conventions, Perth, Western Australia. Phone: + 61-8-9322-2666 Fax: 61-8-9322-1417
Topics : Allergic disorders, Anaesthesia, Cardiovascular disorders, Clinical pharmacology, Endocrine disorders, Gastrointestinal disorders, General Medicine, Health care management, Infectious and parasitic diseases, Musculoskeletal and connective tissue disorders, Neurologic disorders, Nursing, Nutritional and metabolic disorders, Paediatrics, Pulmonary disorders, Radiology, Sexually related disorders, Surgery, Transplant Surgery


January 23rd -26th 2000 :  24th A.S.P.E.N. Clinical Congress , Opryland Hotel, Nashville, TN email:

March 8th - 10th, 2000 : Intensive Care: Life on the Edge NZ National ANZICS Year 2000 Conference Contact: Dr Ross Freebairn phone 06 8788109 fax 09 8781365

July 23rd - 27th, 2000 : XIIIth International Congress of Dietetics, Edinburgh International Conference Centre, Scotland, United Kingdom. Contact Vicki Grant and Wendy Adesegun, c/o Meeting Makers, 50 George Street, Glasgow, G1 1QE, Scotland, United Kingdom. 44141 553 1930. Fax 44141 552 0511.

September 17th - 20th, 2000 : Fourth International Conference on Dietary Assessment Methods, Sheraton El Conquistador Resort, Tucson, AZ. Contact Douglas Taren, Dietary Methods Conference, University of Arizona Prevention Center, PO Box 245163, Tucson, AZ 85719.

October 16th -19th 2000 : The American Dietetic Association Annual Meeting and Exhibition  Colorado Convention Center-Denver, CO. Contact: The American Dietetic Association, 216 West Jackson Boulevard, Chicago, IL 60606-6995. Tel: 312-899-0040;
or Website:
Exhibit information contact: Lisa Nicola, 800-877-1600, ext. 4755. Attendee information contact: Frances Jennings, 800-877- 1600, ext. 4866. 

November 12th - 16th, 2000 XII Latin American Congress of Nutrition, Buenos Aires. Contact Sociedad Latinoamericana de Nutrici, 12vo Congreso Lantinoamericano de Nutrición, Bernardo de Irigoyen 240 (1072), Buenos Aires, Argentina. (54 322) 334 15445.
Website :


There have been a couple of comments that the AuSPEN homepage is a little difficult to locate. It is actually located within the 5 megabytes of homepage space that my Internet Service Provider (ISP) - Southcom - allocates to each account holder. Like most ISPs they run a UNIX based computer to run their service from and this uses what is known as UNIX based file and directory naming conventions. When it comes to naming homepages they inevitably use the funny little character called a tilde ~ to signify that you are talking about a homepage location :

This character can be found on most keyboards on the key next to the numeral '1'. In the time that I have been maintaining the homepage we have had over 1,100 visitors so a lot of people can find it OK. However, to make it easier I shall be setting up what is called a a 'sub-domain' with Southcom. If all goes well then the AuSPEN homepage will be accessible at

This will NOT come into effect until October so don't try it out yet. I will maintain the 'old' address indefinitely - it will just automatically forward you on if you use the old address.

Some readers may have notice that the search engine Excite has a Health section :
This has useful little calculators for BMI, Ideal Weight, Caloric Need, Protein Need and Carbohydrate Need. Take a few minutes to try them out and of course select the metric option before entering any data ! The Encylopaedia is perhaps not too good if the matches I got for 'total parenteral nutrition' are anything to go by :

Matches: Abscess scan, radioactive : Food labeling : Diet for cancer : Multiple Vitamins : Hip joint replacement : Stress management : morning sickness : preventive health care : poor feeding : Knee joint replacement :

That word 'parenteral' guarantees that a lay database gets steered 'off the track' !





WE NOMINATE___________________________________(name) FOR THE POSITION OF


NOMINATING MEMBER #1'S NAME ____________________________

MEMBER'S SIGNATURE _____________________________________

NOMINATING MEMBER #2'S NAME ____________________________

MEMBER'S SIGNATURE _____________________________________

I (signature) ________________________________ ON ____________ (Date)


Please PHOTOCOPY this Form and return it completed by 27th September 1999 to Dr Julie Bines, President AuSPEN, Dept. of Gastroenterology and Clinical Nutrition, The Royal Children's Hospital, PARKVILLE, VIC 3052.


  • Probiotics, Other Nutritional Factors and Intestinal Microflora, Nestle Nutrition Workshop Series Vol 42, Edited by Lars A Hanson and Robert H Yolken, published by Raven Press, 1998, $Aus133, ISBN 0-7817-1829-5
  • Nutrition and Bone Development Nestle Nutrition Workshop Series Vol 41, Edited by Jean-Phillipe Bonjour and Reginald C Tsang, published by Raven Press, 1998 $Aus116, ISBN 0-7817-1753-1
  • Human Protein Metabolism, by S Welle, published by Springer Verlag, July 1999, $Aus139, ISBN 0-387-98750-9
  • Methods for Investigation of Amino Acid and Protein Metabolism, Edited by A E El-Khoury, published by CRC Press, March 1999, $Aus153, ISBN 0-8493-9612-3


The views and opinions expressed in this Newsletter are not necessarily the views and opinions of the Australian Society of Parenteral and Enteral Nutrition. Reports and articles on techniques, procedures and products are provided for the information of the Members of the Society and their inclusion does not imply any endorsements from the Australian Society of Parenteral and Enteral Nutrition. No liability can or will be accepted by AuSPEN or its agents for the third party use of information in this Newsletter.

Dr Tom Hartley, Editor, 10th September 1999.

Newsletter of the Australian Society for Parenteral and Enteral Nutrition
Editor : Dr Tom Hartley, 36, Pregnells Road, Sandfly, Tasmania 7150, Australia

Ph 03-6239-6475 (AH) 03-6222-8780 (BH) Fax 03-6231-3145

AuSPEN WWW Homepage :

Probably moving to by October 1999