The possibility that excessive sugar consumption is the cause of many aspects of ill-health goes back a long way.

Obesity was first observed in the wealthy who would have been the only people who could afford to buy sugar. Diabetes, hypertension and obesity were first recorded in England, France and Germany which are the countries where sugar was first introduced into the national diet.

Gary Taubes in his excellent book entitled “The Diet Delusion” provides the following examples of evidence that sugar contributes to the development of various diseases:

  • In 1924, Haven Emerson who was the director of the Institute of Public Health at Columbia University in New York concluded that:

“Rises and falls in sugar consumption are followed with fair regularity within a few months by similar rises and falls in death rates from diabetes.”

  • In 1975 Richard Doll and Bruce Armstrong commented that:

“The higher the sugar intake, the higher the incidence of any mortality from cancer of the colon, rectum, breast, ovary, prostate, kidney, nervous system and testicles.”

  • In Israel Aharon Cohen, a specialist in diabetes, found that in 5000 immigrants from the Yemen in 1949 there were only 3 cases of diabetes. By contrast, the incidence of diabetes in Yemenis who arrived about 20 years earlier was almost 50 times greater. Cohen concluded that the much greater consumption of sugar amongst those who had already settled in Israel was the critical factor which was responsible for difference in disease levels.
  • In South Africa, George Campbell who was in charge of the diabetic clinic in Durban observed that diabetes, CHD, hypertension and gall bladder disease were very common in the local white population but virtually non-existent in the Zulus living in rural areas. In 1956 he spent a year working in Philadelphia and discovered that the pattern of disease in the local black population was virtually the same as in the whites in South Africa. When he returned to Durban he noted that the Indians working in the sugar industry had a very high incidence of diabetes which he described as:

“…almost certainly the highest in the world.”

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In Great Britain between 1975 and 2000 there has been a 5-fold increase in the amount of soft drinks purchased for consumption in the home (Table 1). However this was paralleled by a precipitous drop in the consumption of liquid milk. Some of this milk would have been replaced by semi-skimmed milk for which demand expanded primarily because consumers were attempting to reduce their intakes of fat and of saturated fatty acids(SFA). The National Food Survey did not collect comprehensive information on purchases such as snacks which were consumed outside the home so the total consumption of soft drinks would have been higher than the figures indicate. The increase in soft drink consumption must have contributed to increase in the carbohydrate content of the diet and would have been predominantly sugar.

TABLE 1 CHANGING DEMAND FOR DRINKS

  SOFT DRINKS LIQUID WHOLE MILK
YEAR Gm/person/week Ml/person/week
1975 180 2708
1980 243 2364
1985 388 1888
1990 609 1232
1995 907  812
2000 976  664

 

Source: National Food Survey

Note: The National Food Survey was replaced Family Food Statistics after 2000. As a consequence it is not possible to access data which is comparable to that collected before 2000.

In the US, soft drink consumption increased by 61% between 1977 and 1997. It also more than doubled in children and adolescents over the same period. As part of the Nurses’ Health Study an investigation was conducted to determine the relationship between the intake of soft drinks and weight gain as well as the incidence of diabetes. Information was collected from over 90,000 participants between 1991 and 1999 during which time there were 741 new cases of diabetes. The incidence of diabetes increased with consumption of sugar-sweetened beverages (SSBs). Those who consumed one drink per day had double the risk of developing diabetes when compared with those who consumed one drink per month. It was also found that those who increased their consumption of these drinks and maintained the high level of intake gained, on average, 8.0 kg body weight over the 8-year period. Those who decreased consumption and maintained the low intake also gained weight but this was limited to 2.8 kg (1).

More recent information from the Nurses’ Health Study showed that the total intake of sugar is closely linked to the amount of SSBs consumed. Those who consumed 2 or more drinks per day had an intake of 179g/day while those who consumed less than one drink per month had an intake of 89g/day (Table 2). This investigation found that those consuming the high intake were about 40% more likely to suffer from coronary heart disease than those with a low intake (2).

TABLE 2 SOFT DRINK CONSUMPTION AND SUGAR INTAKE

 

Number of sugar sweetened   drinks Total sugar intake
<1/month 89
1-4/month 98
2-6/week 114
1/day 145
>2/day 179

 

In a study conducted in the USA with 810 men and women aged 25-79 who had high blood pressure it was found that, when SSBs were replaced with water, a reduction in SSB consumption one per day was associated with a weight loss of 0.49 kg after 6 months and 0.65 kg after 18 months (3).

CONCLUSION

There can be little doubt that the increase in the consumption of sugar is a critical factor which is contributing to the disastrous growth in the incidence of obesity and diabetes. This is not exactly rocket science since diabetes is caused by excessive levels of glucose in the blood. The more sugar that is consumed the more glucose is produced will enter the blood stream. In a future blog I will refer to the improvements in personal health which have been achieved by various individuals who have simply reduced their consumption of sugar and other carbohydrates.

 

REFERENCES

1.       V S Malik et al (2006) American Journal of Clinical Nutrition 84 (2) pp 274-278.

2.       T T Fung et al (2009) American Journal of Clinical Nutrition 89 (4) pp1037-1042.

3.       L Chen et al (2009) American Journal of Clinical Nutrition 89 (5) pp 1299-1306.