INTRODUCTION

When the dietary recommendations were being devised initially a high intake of fat was considered to be a risk factor for certain types of cancer and in particular breast cancer in women. This conclusion was based largely on international comparisons and the results of animal studies.

RESULTS OF VARIOUS STUDIES

However the results of the Nurses’ Health Study which were published in 1999 completely undermined the conventional wisdom at the time. This major project commenced in 1976 when 88,795 female registered nurses aged 30 to 55 years free of cancer were recruited. The participants were followed up for 14 years. In 1980 they completed a food frequency questionnaire and this exercise was replicated in 1984, 1986 and 1990. A total of 2,956 women were diagnosed with breast cancer.  When the cancer incidence was related to diet there was absolutely no evidence of increased risk of breast cancer with increased intake of animal fat, polyunsaturated fat, saturated fat or even trans unsaturated fat. In fact it was found that the risk of breast cancer tended to be highest among those with the lowest fat intake. Certainly there was no suggestion that lower intake of total fat or of any particular types of fat over the 14 years of the study was associated with a decreased risk of breast cancer. So it was concluded that a reduction of total fat in mid-life was unlikely to prevent breast cancer.

This study included more cases, longer follow-ups and more person-years than any previously published prospective study on diet and breast cancer. The quality and the reliability of this work are enhanced by the fact that the diet of the participants was assessed on 4 different occasions (1).

In Korea 829,770 men and 468,615 women aged between 30 and 95 were given a medical check in the years 1992-1995. They had a follow-up examination after 10 years during which time there had been 20,566 cancer deaths in the men and 5,907 in the women. The results (Tables 1 and 2) show that the deaths from all causes and from several cancers increased progressively with the concentration of blood glucose. When the results for the first 5 years were excluded the same trends were evident which eliminates the possibility that the increase in blood glucose is actually caused by the cancer (2).

TABLE 1. RELATIVE MORTALITY RATES FOR SELECTED CANCERS AND BLOOD GLUCOSE LEVELS IN KOREAN MEN

Cause of deaths                                        Fasting Blood Glucose levels, mg/100ml
<90 90-109 110-125 126-139 >140 Diabetes
All causes 1.00 1.04 1.28 1.50 2.09 1.83
All cancers 1.00 1.04 1.17 1.28 1.29 1.27
Colorectum cancer 1.00 1.07 1.27 1.23 1.31 1.28
Pancreatic cancer 1.00 1.08 1.28 1.45 1.91 1.71

 

TABLE 2. RELATIVE MORTALITY RATES FOR SELECTED CANCERS AND BLOOD GLUCOSE LEVELS IN KOREAN WOMEN 

Cause of deaths                                   Fasting Blood Glucose levels, mg/100ml
<90 90-109 110-125 126-139 >140 Diabetes
All causes 1.00 1.01 1.24 1.42 2.35 1.99
All cancers 1.00 1.00 1.01 1.12 1.23 1.31
Colorectum cancer 1.00 0.96 1.05                  0.85 1.11
Pancreatic cancer 1.00 1.45 1.70                  2.05 1.71
Breast 1.00 1.15 0.89                  1.24 2.23

 

In an Austrian study, 63,585 men and 77,228 women whose mean age at baseline was 43 years were followed up for an average of 8.4 years. Over 5,000 cases of cancer were diagnosed. The average age of diagnosis was 64 years. Those who developed cancer in the first year were excluded.

Table 3 shows that with cancers of the liver, gallbladder and bile duct, thyroid and multiple myeloma the tendency is for the mortality rate to increase as the level of fasting blood glucose increases based on results for men and women. It should also be noted that with some of these cancers there is an increased rate at relatively low levels of blood glucose. For leukaemia, there is no consistent trend. For breast cancer in women (Table 4) a relatively high death rate is only apparent in those over 65 at the highest blood glucose level (3).

TABLE 3 FASTING BLOOD GLUCOSE CONCENTRATIONS AND THE INCIDENCE OF VARIOUS CANCERS IN MEN AND WOMEN

                                 Fasting blood glucose at enrolment, mmol/L
  2.2-4.1 4.2-5.2 5.3-6.0 6.1-6.9 >7.0
Liver cancer 1.37 1.00 1.89 2.45 3.56
Gallbladder and bile duct 0.92 1.00 1.90 3.74 3.36
Thyroid cancer 1.24 1.00 2.22 2.34
Multiple myeloma 1.54 1.00 2.26 2.42
Leukaemia 0.78 1.00 1.47 1.00

TABLE 4. FASTING BLOOD GLUCOSE AND THE INCIDENCE OF BREAST CANCER IN WOMEN AT DIFFERENT AGES

                                 Fasting blood glucose at enrolment, mmol/L
Breast cancer 2.2-4.1 4.2-5.2 5.3-6.0 6.1-6.9 >7.0
All 0.96 1.00 0.99 0.91 1.38
<50 years 0.99 1.00 0.61 0.67
50-65 years 1.05 1.00 1.08 0.80 1.12
>65 years 0.80 1.00 1.09 1.03 1.63

 

Breast cancer patients with diabetes are more likely to die prematurely from breast cancer than patients without diabetes (RR 1.76) which suggests that besides affecting the incidence rate diabetes also promotes breast cancer mortality (4).

A recent systematic review confirmed that patients with breast cancer and pre-existing diabetes suffer all-cause mortality that is increased by about 50%. This finding was consistent across different populations and was generally independent of possible confounding variables. The main implication of this study is that diabetes is associated with adverse outcomes in breast cancer throughout its full course, from initial presentation, during treatment (which influences the choice of therapy), and, ultimately, to mortality (5).

In a Canadian investigation 512 women treated for breast cancer were followed for an average period of just over 4 years. Women with diabetes were excluded. The breast cancer recurred in 76 of the women and there were 43 deaths. The relationship with the blood insulin (Table 5) show that those with the highest levels were more likely to experience a recurrence (by a factor of 2) and to die (by a factor of 3.1) when compared with those with the lowest levels (6).

TABLE 5. BLOOD INSULIN LEVELS AND RISK OF BREAST CANCER AND DEATH

Insulin level, Pmol/L 8.1-27.0 27.0-35.3 35.3-51.9 51.9-339.8
RR, breast cancer 1.0 1.3 1.5 2.0
RR, death 1.0 1.5 2.0 3.1

 

Insulin has been shown to stimulate cell proliferation in normal breast tissue and in human breast cancer cell lines. It has also been established that the administration of insulin promotes breast tumour growth in animal models. In the Women’s Health Initiative (WHI) 93,676 post-menopausal women aged between 50 and 79 years were followed for over 6 years commencing between 1993 and 1998. Fasting insulin levels were measured and the results (Table 5) showed that the incidence of breast cancer was more than doubled at the higher levels when compared with the lowest level. It should be noted that any women with diabetes were excluded from the study and all those involved were not on hormone therapy (7).

TABLE 6 FASTING INSULIN LEVELS AND BREAST CANCER INCIDENCE

Insulin level, µIU/ml <3.9 3.9-5.6 5.6-8.8 >8.8
Hazard Ratio 1.00 1.00 1.59 2.65

 

Because of the potential role of insulin in the development of cancer there is considerable interest in studying the effect of various therapies for diabetes. An investigation in Saskatchewan with 10,309 participants (55% men) who had used anti-diabetic drugs for less than a year resulted in 245 deaths. However there were marked differences in death rates depending on the drug used. It was found (Table 7) that people exposed to sulfonylurea or exogenous insulin (agents that increase circulating insulin levels) were significantly more likely to have a cancer-related death than people exposed to

metformin (which does not increase insulin levels). When adjustment were made to the death rates to allow for other factors such as the age of the patients it was found that the risk of cancer-related mortality was even greater for insulin exposure (90% relative increase) than for sulfonylurea exposure (30% relative increase) (8).

TABLE 7. CANCER THERAPY AND MORTALITY

Therapy Cancer mortality   rate, per 1,000 person-years
Metformin 6.3
Sulphonyl urea 9.7
No insulin 6.8
Insulin 9.9

 

STUDIES WITH MICE

In an investigation with mice the development of tumours was compared for different diets. The control contained 55% carbohydrate which is roughly the same as the national diets in the UK or the USA. The experimental diets contained 8, 10 and 15% CHO. With mice that were particularly susceptible to tumour growth it was found that at 1 year old almost half of those on the 55% carbohydrate diet had developed tumours but none were detected in those on the 15% carbohydrate diet. In total 70% of the mice on the high CHO diet developed tumours and only one reached the normal life span. Less than 30% of those on the low CHO diet developed tumours while more than half reached or exceeded the normal life span. The low CHO diet reduced the plasma insulin levels which in results in a reduced glucose uptake by the tumour cells. There was a positive correlation between plasma insulin levels and tumour size which confirms that the glucose supply is related to tumour growth (9).

CONCLUSION

There is little doubt that excessive amounts of sugar and refined carbohydrates in the diet is the primary cause of Type 2 Diabetes (T2D). Confirmation is shown by the fact that T2D can be effectively cured by a diet which is low in carbohydrates and high in fat (10). It is now becoming clear that the rationale to reduce fat and especially the saturated fats (SFAs) was fundamentally flawed (11). The evidence presented here flags up the dangers of consuming excessive carbohydrate with respect to many different cancers. The fact that the risks increase as the concentration of glucose in the blood increases is particularly relevant. The case for limiting the intake of sugar and refined carbohydrates has now reached the point where it is extremely convincing. Unfortunately this is in direct conflict with the official dietary recommendations in many countries. Although there is growing awareness of the risks associated with sugar consumption, many people have difficulty in adapting their diets because they are still convinced the SFAs are dangerous. In reality, there was never any justification recommending a reduction in these fats. On the contrary they should be considered as valuable nutrients (12).

REFERENCES

  1. Michelle Holmes et al (1999) JAMA 281 (10) pp.914-920
  2. S H Jee et al (2005) Journal of the American Medical Association 293 (2) pp194-202
  3. K Rapp et al (2006) Diabetologica  49 (5) pp 945-952
  4. F Xue & K B Michels (2007) American Journal of Clinical Nutrition 86 (3) pp S823-S835
  5. K S Peairs et al (2011) Journal of Clinical Oncology 29 (1) pp 40-46
  6. P J Goodwin et al (2002) Journal of Clinical Oncology 20 (1) pp 42-51
  7. M J Gunter et al (2009) Journal of the National Cancer Institute 101 (1) pp 48-60
  8. S L Bowker et al (2006) Diabetes Care 29 (2) pp254-258
  9. V W Ho et al (2011) Cancer Research 71 (13) pp 4484-4493
  10. http://vernerwheelock.com/?p=558
  11. Nina Teicholz. (2014)“The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet” Simon & Shuster New York
  12. http://vernerwheelock.com/?p=155