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Migrant Health

Migrant Australians are Healthier than the Australian-born

According to the 2001 census, just over one fifth (22%) of the Australian population is born overseas. Most foreign born immigrants come from the UK (1,036,245), followed by New Zealand (355,765); Italy (218,718); Vietnam (154,831); China (142,780); Greece (116,431) and Germany (108,220). The most common foreign ancestry reported was English (33.9%), followed by Irish (10.2%), Italian (4.3%), German (4%), Chinese (3%), Scottish (2.9%) and Greek (2%).

The Australian Institute of Health and Welfare 8th biennial report "Australian Health Inequalities" concluded that death rates for migrants were 10 to 15% lower during the 1990s than those born in Australia. However, this is against a backdrop of remarkable improvements in longevity and reduction in disability in the Australian population as a whole, as judged by the World Health Organisation (WHO) 'Disability Aadjusted Life Expectancy' (DALE). Australia is the only English speaking country in the top 10 on the DALE scale, and is second to Japan ..... more

A senior analyst at the institute (Michael de Looper) reported in the AGE (26/7/2002) that "the longer migrants live in Australia, the more their health advantages disappear and start to match Australian levels as a whole. One of the costs of acculturation is the lost health advantages ......previous research has shown that the healthiness enjoyed by first generation migrants quickly faded in their children".

Asian-born Australians are the healthiest, followed by people born in Europe. Asian-born men were 46% less likely to die from colorectal cancer and 25% less likely to die from coronary heart disease. Diet and other lifestyle factors have contributed to the better health of migrants, but the main reason appears to be due to 'selection effects'. The migration process itself tends to be highly selective for health, both explicitly by the health criteria applied by the Australian Government to people seeking to migrate to Australia and also because people who are in poor health are less likely to have the ability and economic resources to migrate.

HEC's Professor Mark Wahlqvist was also interviewed about this report and was quoted in the AGE (26/7/2002) "that migration had greatly improved the health of all Australians, especially through better diet" and that this "had helped Australia reach second place after Japan on the WHO scale of DALE.

To read more about this:

Healthy Eating Club's Professor Mark Wahlqvist and Dr Antigone Kouris-Blazos have studied the diet, health and survival of Greek Australian migrants; publications
are as follows:

Kouris-Blazos A, Wahlqvist M, Wattanapenpaiboon N. 'Morbidity mortality paradox' of Greek-born Australians: possible dietary contributors. Australian Journal Nutrition and Dietetics, 1999; 56 (2): 97-107; on-line abstract

Kouris-Blazos A, Wahlqvist ML, Trichopoulou A, Polychronopoulos E, Trichopoulos D. Health & Nutritional Status of elderly Greek migrants to Melbourne, Australia. Age Ageing 1996; 25: 177-189.
(on-line abstract)

Trichopoulou A, Kouris-Blazos A, Wahlqvist ML, Gnardellis Ch, Lagiou P, Polychronopoulos E, Vassilakou T, Lipworth L, & Trichopoulos D. Diet and overall survival in elderly people. British Medical Journal 1995; 311 (7018): 1457-1460 (on-line full text article)

Wahlqvist M, Kouris-Blazos A, Wattanapenpaiboon N. The significance of eating patterns: an elderly Greek case study. Appetite 1999; 32: 23-32; on-line full-text article

Other resources on the Australian Migrant experience:

Book written by journalist Mr Alfred Kouris on Greek migrants in Australia (primarily a social history with reference to dietary changes on migration)


High fructose processed foods linked to obesity, gout, hypertension, diabetes, cholesterol and fatty liver
There has been a "cloud" over the health benefits of fructose added to processed foods over the last few decades. Food manufacturers have been adding pure fructose to foods in the quest to lower the glycaemic index (GI) of the food because fructose does not affect insulin production therefore is considered to be a low GI sugar (this is contrast to glucose which does raise insulin levels). The food industry have also been adding fructose in the form of corn syrup (popular in the United States) or sucrose (this is half fructose) to foods, especially low fat/diet foods to improve flavour. There is emerging evidence that this may be making the obesity epidemic even worse, starting with damage to our liver cells, the hepatocytes.
The only organ in your body that can take up fructose is your liver and this is where the problem begins. In contrast, glucose can be taken up by every organ in the body, only 20% of glucose load ends up at your liver - the rest is metabolised by muscles, brain, kidneys, heart etc. .
 Fructose increases uric acid which in turn increases blood pressure and causes gout (where uric acid crystals are deposited in joints)
Fructose increases phosphate depletion of the hepatocyte which ultimately causes an increase in uric acid. Uric acid is an inhibitor of nitric oxide - nitric oxide is your naturally occurring blood pressure lowerer.
 Fructose increases fat production in the liver (also known as denovo lipogenesis) which in turn increases blood fats like cholesterol and triglycerides (glucose does not do this) and liver fat (which could result in non-alcoholic fatty liver disease). In fact fructose is being metabolised via the same pathway as alcohol and is actually damaging your liver in the the same way as alcohol. Fructose causes deposition of fat within the liver so it is actually like alcohol and alcohol is like a fat. So in contrast to glucose, it can be said that fructose behaves like a fat.
 Fructose increases inflammation which in turn increases insuln levels in the long term: fructose initiates an enzyme called Junk one in the liver which stimulates the inflammation pathway. This in turn stops the insulin receptor in your liver from working resulting in higher insulin levels in the body (pancreas responds to this situation by pumping out more insulin in the hope to get the insulin working) . Eventually insulin resistance sets in where your insulin receptors are no longer responding to the excessive amounts of insulin and thus less glucose gets into the cells and more remains in the blood (this is when diabetes is diagnosed). High insulin levels stimulate the conversion of sugar to fat which means you will be storing more fat in the liver (which could result in non-alcoholic fatty liver disease) and more fat in fat cells, especially around the abdomen and internal organs (resulting in abdominal/visceral obesity).
Fructose doesn't raise your insulin in the short term because there's no fructose receptor on your beta cell in your pancreas which produces insulin but there is a receptor for glucose (fat also does not increase insulin production). However, in the long term fructose will raise insulin due to the effects on inflammation in the liver which in turn can make you insulin resistant (mentioned above). The World Cancer Research Fund latest report recommends a reduction in sugar dense drinks and fruit juices.
 Bottom line: A low fat diet containing processed sugar dense foods is really a high fat diet because fructose (in sugar) behaves like a fat. We were not designed to eat a lot of refined sugars, we're supposed to be eating our carbohydrate, particularly our fructose, with high fibre in unprocessed foods like fruit and vegetables. If you are trying to lose weight, lower your blood pressure, blood fats or fatty liver reduce your intake of sugars/fructose in processed foods that do not contain fibre (like soft drinks, fruit juices, sweet yoghurts, cakes, biscuits, fructose sweetened protein drinks etc) even if the label says low GI.


Source: ABC Health Report - Dr Norman Swan interviews Obesity expert Dr Robert Lustig Professor of Pediatric Endocrinology, University of California http://www.abc.net.au/rn/healthreport/stories/2007/1969924.htm

Eric G. Neilson . The Fructose Nation, American Journal of Clinical Nutrition, Vol. 86, No. 4, 895-896, October 2007.

Last Updated: July 2008



Επιστήμονας Διαιτολόγος
(Clinical Dietitian)
Δρ Αντιγόνη Κουρή  PhD APD


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