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25 November 2010

What we know about IGF-1

Could milk consumption lead to increased levels of insulin-like growth factor 1 (IGF-1), and subsequent increased risk of cancer, heart disease and diabetes? DietDoc investigates.

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Insulin-like growth factor 1 (or IGF-1, as it is also called) has been mentioned in the press and by popular nutrition writers like Patrick Holford.

Holford links milk consumption to increased levels of IGF-1 and concludes that because IGF-1 "is strongly linked with increased risk of cardiovascular disease and also breast and prostate cancer", milk is potentially harmful. Strong words indeed.

But what do the research findings actually tell us?

DietDoc did a literature survey of recently published articles describing research on IGF-1 and related compounds. In this article, she shares the most recent findings.

What is IGF-1?

Krause (2000) defines IGF-1 as "a peptide hormone that mediates the function of growth hormone; responsive to protein-energy status". In other words, IGF-1 assists growth hormone in its function and is itself influenced by protein and energy intake.

IGF-1 is produced by the human body and, according to the latest research, plays a variety of different roles in physiology. Some authors do link IGF-1 to an increased risk of heart disease, diabetes and cancer, while others have found evidence that IGF-1 plays a protective role.

Giovannucci and coworkers (2003) say, "IGF may play opposing roles in health and disease. The age-related declines in growth hormone and IGF-1 may be associated with potentially deleterious changes in body composition and functioning, but recent studies suggest that IGF-1 levels may be related to risk of prostate, colorectal, premenopausal breast and possibly other cancers."

This means that the function of IGF-1 is poorly understood and that research scientists have not reached consensus if it is potentially harmful or beneficial.

The other possibility is that IGF-1 may be beneficial at certain times of life (e.g. during childhood when growth is important), while at other times of life it may be potentially harmful (e.g. during adulthood when it may promote degenerative diseases).

Positive effects

a) Growth

Studies by Hoppe and co-authors (2004a and b) in young children, found that IGF-1 promotes growth and ensures that children grow tall.

These specific studies investigated if milk would boost IGF-1 production and showed that drinking milk increased IGF-1 and growth in young children.

During childhood, this effect is a positive one ensuring that children grow strong and tall.

b) Maturation of the digestive tract

Lonnerdal (2003) studied the nutrients and other compounds found in breast milk.

This author suggests that IGF-1, which is found in human breast milk, may assist with the development of the lining of the digestive tract and other organs in newborn babies.

Once again, this growth-promoting effect of IGF-1 plays a positive role in human growth.

c) Repair of the digestive tract

IGF-1 seems to play a protective role in boosting repair processes in gastrointestinal disorders, including radiation enteritis, chemotherapy-induced disturbances of the mucosa which lines the gut, and inflammatory bowel disease.

Novel milk and colostrum bioactive products containing IGF-1 are being developed and tested in the treatment of bowel disease (Howarth, 2003)

Negative aspects

a) Reduced or improved insulin tolerance

Two studies showed that in adults, increased levels of IGF-1 were associated with opposite results.

In one study, higher IGF-1 levels were linked to increased risk of developing reduced insulin tolerance and diabetes (Heald and coworkers, 2001).

However, Sandhu and coworkers (2002) found a "possible protective role of IGF-1 against development of glucose intolerance".

When researchers find such opposing results, it is difficult to draw conclusions. We will have to wait for additional evidence to emerge from research before we can decide if IGF-1 worsens glucose tolerance and causes diabetes, or if it plays a protective role.

b) Heart disease and cancer

Some researchers state that high IGF-1 levels will promote cell growth leading to heart disease and cancer, while others believe that low IGF-1 levels will cause age-related cell deterioration that will in turn lead to heart disease and cancer.

Researchers are also studying drugs that will inhibit IGF-1 as potential anti-cancer agents.

Once again, we are left guessing as to what role IGF-1 may actually play in these diseases. At the moment we don't know if IGF-1 causes or prevents them.

Which foods increase IGF-1 levels?

A number of researchers investigated which foods or nutrients increase levels of IGF-1 in humans. Once again, divergent findings were obtained.

The following foods/nutrients increased IGF-1 levels in humans:

  • protein derived from milk, fish and poultry, but not red meat (Giovannucci and coworkers, 2003)
  • protein derived from red meat, fish, seafood and zinc (Larsson and coworkers, 2005)
  • dietary fat, saturated fat and protein, but not carbohydrate (Heald and coworkers, 2003)
  • milk, dairy products, calcium, carbohydrate and polyunsaturated fat (Gunnell and coworkers, 2003)
  • human breast milk (Buyukkayhan and coworkers, 2003)

It is evident that many foods and nutrients raise human IGF-1 levels. What this means in terms of human health and disease is not clear yet, and a great deal of additional research needs to be done to give us definitive answers.

Should we stop drinking milk?

Given the evidence that milk consumption increases IGF-1 levels and that raised IGF-1 levels may be linked to heart disease, diabetes and certain cancers, should we take Patrick Holford's advice and stop drinking milk? The answer to this question is "no".

Too many studies show that milk is beneficial to health. Researchers like Moorman and Terry (2004), who reviewed the scientific literature relating to milk consumption and breast cancer concluded that a high consumption of dairy products as a whole or when broken down into high-fat and low-fat dairy products, milk, cheese or butter "showed no consistent pattern of increased or decreased breast cancer risk".

Norat and Riboli (2003) also reviewed the possible links between colorectal cancer and the intake of milk and/or dairy products. They came to the conclusion that "cohort studies consistently found a protective effect of total dairy products and milk intake".

If we keep in mind that milk and dairy products are the best sources of readily absorbable calcium in the human diet, which protects us against diseases such as osteoporosis, then the use of milk and dairy products, particularly fat-free versions, is more than justified.

So what can we conclude about IGF-1 and its benefits and dangers?

Only that IGF-1 seems to have both positive effects, such as promoting growth in children and repairing the digestive tract, and negative effects, such as the potential for reducing glucose tolerance and possible links with diabetes, heart disease and some cancers.

What can we conclude about foods and nutrients that raise IGF-1?

Only that we need more research to pinpoint which foods and nutrients increase levels of IGF-1 and if this constitutes a health risk or not.

What can we conclude about drinking milk and eating dairy products?

The bulk of scientific evidence indicates that these foods are healthy and can be used in a balanced diet.

- (Dr Ingrid van Heerden, DietDoc)

(References: Buyukkayhan et al (2003). Int J Vitam Nutr Res, 73:343-6; Giovannucci et al (2003). Cancer Epidemiol Biomarkers Prev, 2:84-9; Gunnel et al (2003). Br J Cancer, 88:1682-6; Heald et al (2001). Diabetologia, 44:333-9; Heald et al (2003). Public Health Nutr, 6:175-80; Hoppe et al (2004). Eur J Clin Nutr, 58: 1211-6; Hoppe et al (2004). Am J Clin Nutr, 80:447-52; Howarth (2003). J Nutr, 133:2109-12; Krause's Food, Nutrition & Diet Therapy (2000). Edited by Mahan & Escott-Stump, Chapter 17, p380; Larsson et al (2005), Am J Clin Nutr, 81:1163-7; Lonnerdal (2003). Am J Clin Nutr, 77:1537S-1543S; Moorman & Terry (2004). Am J Clin Nutr, 80:5-14; Norat & Riboli (2003). Eur J Clin Nutr, 57:1-17; Sandhu et al (2002), Lancet, 359:1740-5).

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