Readers of this blog will be aware of many reasons why cholesterol is not a reliable marker for the risks of developing heart disease or anything else for that matter. There are very thorough studies, which demonstrate that those who comply with the cholesterol guidelines actually have the highest all-cause mortality rates (1). For women, there are strong indications that the life expectancy increases as the cholesterol content of the blood (TC) increases. Since the cholesterol strategy is a dead loss, it is relevant to ask if there is any other marker that would fulfil the role that is expected of cholesterol. In other words, is it possible to identify a way of discovering those who are high risk of life-threatening diseases so that appropriate steps can be taken to alleviate that risk? As I am highly critical of focusing on one disease, the ideal marker should be related to all those factors, which contribute to an early death.

Gamma Glutamyl Transferase (GGT)

Thanks to the work of Ivor Cummins, I have been alerted to the possibility of using GGT instead of TC (2). GGT is an enzyme that is normally used as an indication of liver disease. However when Ivor first learned that he had very high levels in his blood samples, he was keen to find out what this meant about his own personal health. It soon became very clear that those with raised concentrations of GGT in their blood had very much higher rates of all-cause mortality (ACM). A very good source of information on this topic is the Health & Iron website (3). Here are some examples of the information available:

  • In a study in Germany, the serum GGT levels were assessed among 8,043 construction workers ages 25–64 who underwent occupational health examinations in six centres between 1986 and 1988 (4). Study participants were followed for ACM until 1994. It was found that there was a strong dose–response relation between serum GGT levels and ACM. Compared with men with GGT levels below 15 U/L, relative risks were 1.46, 1.78, 2.09, and 3.44 for men with GGT levels of 15–19, 20–29, 30–49, and ?50 U/L, respectively. It was concluded that GGT is a strong risk indicator of ACM.
  • In a study in Austria, between June 1991 and September 2003, a total of 283 438 patients attending the Vienna General Hospital had blood samples taken and analysed for GGT (5). Any deaths which occurred were recorded. The mean follow-up period was 7.6 years. Here again it was found that the death rates for ACM and for various different diseases increased steadily with the GGT content of the blood (See Figure 1).


FIGURE 1. Adjusted mortality among patients according to subgroups of GGT.

The lowest category served as reference category.

  • In patients with diabetes it was found in a study with 1280 participants, aged 35–70?years, after 8.2?years of follow-up, there had been 84 deaths (6). Participants with high GGT activity had an increased mortality risk: the hazard ratio was 3.96. This association was especially noticeable in former and current smokers, younger persons and those with a higher waist–height ratio and alcohol consumption.
  • Data from the Minnesota Heart Survey revealed that for subjects below age 70 only, and compared to the lowest 1/3rd of the normal range, elevated GGT doubled mortality risk for those in the middle-normal range, more than tripled the risk in the top-normal range, and presented nearly a five-fold risk when GGT was more than the upper end of normal (7). The researchers concluded:

Our findings suggest that serum GGT within its normal range can predict CVD (cardiovascular disease) mortality in those aged less than 70 years, but may have limited usefulness for risk assessment in older adults.”

  • In the Guernsey Breast Cancer Cohort Study, GGT was measured in sera from 1803 normal women. Among these women, 251 subsequently developed cancer, of whom 96 developed breast cancer (8). Premenopausal women with serum GGT levels above the normal range had a significantly elevated HR of 4.90.

GGT and Metabolic Syndrome (MetS)

There is now overwhelming evidence that the critical factor involved in many of the common chronic diseases is insulin resistance (IR) that is caused by hyperinsulinaemia. This was discussed and explained in detail by the excellent report by Michael Joseph, which has been re-published on this blog recently (9). The fundamental cause is excessive consumption of sugar and carbohydrates. As a consequence, the pancreas is required to increase production of insulin to cope with the high levels of glucose in the blood. Most of the excess glucose (and fructose) is converted into fat. Some of this is stored which explains why a persistently high intake of sugar/carbohydrates usually leads to weight gain and obesity. In addition some of the fat is remains in the liver probably because there is nowhere else to go and is manifested as non-alcoholic fatty liver disease (NAFLD). It has been standard practice for GGT to be used as an indicator for NAFLD. In Southport Dr David Unwin has had great success with patients who have lowered their GGT by reducing the amount of sugar/carbohydrates in their diet (10). One 55-year old woman reduced her GGT from 103 U/L to 12 U/L in 3 months by altering her diet. She was suffering from a bad case of T2D as shown by the high values for the HbA1c (glycated haemoglobin). So essentially she had recovered and tests confirmed that her liver function was normal.


Without going into details here GGT appears to be a reliable measure for IR and therefore a very good indication of the risks of developing T2D, heart disease and many cancers, especially for those in middle age. On the face of it, routine checks of GGT would provide much more valuable information than can ever be obtained from cholesterol. It really would make good sense for a fraction of the huge resources spent on cholesterol tested to be used for GGT analysis.


  4. H Brenner et al (1997).
  5. L Kazemi-Shirazi et al (2008).
  6. D Sluik et al (2012).;jsessionid=9041DE233784B1DCFEA1394E8AE7B7ED.f02t03
  7. D-H Lee et al (2009).
  8. I S Fentiman & D S Allen (2010). British Journal of Cancer 103, 90-93
  9. Michael Joseph (2017).