Response to David Gillespie on behalf of Nut-Net


Dear David,

You have requested identification of the 'errors and dubious claims' mentioned in the Nut-Net FAQ about Sweet Poison.

By way of introduction, ‘Nut-Net’ is the abbreviation of Nutritionists Network, a professional nutrition email discussion list with more than 800 nutritionists and dietitians as subscribers. As a service to the general public, Nut-Net develops nutrition related FAQs which are made available through the Nutrition Australia website. I coordinate the writing of the Nut-Net FAQs, which represent a consensus, or if one cannot be reached, a majority viewpoint of those Nut-Net subscribers who contributed to the development of each FAQ. (I should also point out that no subscriber expressed a dissenting view on any aspect of the final wording of the FAQ on Sweet Poison.)

A similar procedure was used to develop this response, so it constitutes the Nut-Net position.

The following is not a complete list of the errors detected in Sweet Poison, but it should give you an indication of the problems Nut-Net has with the quality of information in your book and Ockham’s Razor program. The identified problems range from relatively minor mistakes (or unsubstantiated claims) to major misinterpretations of the scientific literature.

(i) On page 8 of Sweet Poison an attempt is made to draw an association between a presumed increase in sugar consumption and the onset of obesity and several chronic diseases in western nations. An association does not prove cause and effect—it can only lead to hypotheses that then need to be rigorously tested. The state of the science with respect to the effects of fructose on human health is immature, as demonstrated in later points in this response. It is at least premature, and possibly wholly inappropriate to conclude, as you do, that fructose is the sole cause of the epidemics of obesity, type 2 diabetes and heart disease.

Further, in his book In Defense of Food (p. 111) Michael Pollan1 points out that a reduction in tax on sugar in 1874 led to a massive increase in sugar consumption in England, to the extent that it comprised one-sixth of total energy intake by the end of the 19th century. This is similar to the current levels of intake in western nations, yet according to Pollan: '… rates of diseases like cancer and type 2 diabetes are considerably higher today than they were in 1900'.

We are also unaware of reports of major epidemics of obesity or heart disease in England in the late 19th/early 20thcenturies. If Pollan is correct, it appears that intakes of fructose similar to those in modern western nations do not inevitably lead to these chronic health problems. Finally, there is doubt about the strength of the association (or even if an associationexists)  between recent trends in fructose consumption and the obesity epidemic in developed nations.

For example, Alicia Sim and Alan Barclay presented a paper at the 2010 conference of the Dietitians Association of Australia in which they concluded that 'total fructose consumption is inversely associated with overweight/obesity in Australia, the UK and Japan since the 1970s'. You have previously been made aware of this paper.

(ii) On page 14 (and earlier) the claim is made that 'all food is essentially glucose' (i.e. that apart from the protein that is used for growth and repair, and also for the production of hormones and enzymes, food is converted to glucose as an energy source. This is not correct—even for the macronutrients—and it is entirely inappropriate with respect to the wide range of micronutrients and also dietary fibre. In terms of the macronutrients, fat cannot be converted to glucose (although the reverse is possible), and protein consists of two types of amino acids—the glucogenic (which can be converted to glucose) and ketogenic (those that can be converted to ketones but not to glucose).

(iii) On page 58 the following claim is made about a study conducted by Reiser et al. [Am. J. Clin. Nutr. (1985); 42 (2): 242]:

'The study had to be terminated when four of the men in the fructose group developed cardiac problems ranging from severe tachycardia (his heart rate tripled) to mild heart attacks, within the first 11 weeks.'

This is not correct—the authors of this paper point out that there was a '... lack of relationship between the onset of the abnormalities and the type of dietary carbohydrate'.

(iv) On page 59 it is stated that '... in 1984 the American Diabetic Association (ADA) recommended that diabetic patients be given foods that used fructose as a sweetener rather than sugarI'. Page 60 includes the claim that 'by 2002 the ADA had completely reversed its recommendation on fructose, saying that fructose should be completely avoided'. The actual wording of the ADA position statement [Diabetes Care (2008) 31:1 S61-S78] is:

'In individuals with diabetes, fructose produces a lower postprandial glucose response when it replaces sucrose or starch in the diet; however, this benefit is tempered by concern that fructose may adversely affect plasma lipids. Therefore, the use of added fructose as a sweetening agent in the diabetic diet is not recommended.'

That is, the ADA simply no longer recommends that people with diabetes use added fructose as a sweetener. This does not equate to 'fructose should be completely avoided'.

Further, the ADA2 makes crystal clear its position that sugar (which is the major source of added fructose in the Australian diet) is not the cause of type 2 diabetes:

'The myth that sugar causes diabetes is commonly accepted by many people. Research has shown that it isn't true ... The biggest dietary risk factor for developing type 2 diabetes is simply eating too much and being overweight - your body doesn’t care if the extra food comes from cookies or beef, it is gaining weight that is the culprit.'

This position statement is diametrically opposed to your claim that consumption of added fructose is the sole cause of type 2 diabetes.

(v) On page 78 the claim is made that 'every gram of fructose we eat is directly converted to fat'. This is not correct—fructose may go down the gluconeogenic pathway (leading to its conversion to glucose and subsequent storage in the liver as glycogen) or the fructolytic pathway (resulting in the production of fat). The available evidence suggests that fructose may be preferentially converted to glycogen until liver glycogen is replenished. It appears that only then will the fructolytic pathway predominate [Biochem. J. (1988) 251 (3): 795–802].

(vi) Your Ockham’s Razor program includes the claim that as a result of the previously mentioned 1985 study by Reiser et al. no further fructose feeding studies were conducted on humans. This is incorrect—fructose feeding studies involving human participants continued (and are still being conducted).

(vii) Your Ockham’s Razor program also states—without supporting evidence—that there has been an increase of 30% in food intake by Australians in the past 30 years. Dr Rosemary Stanton has provided science-based evidence against this claim (and you have been made aware of this evidence).

(viii) Your Ockham’s Razor program also includes the claim—again without supporting evidence—that fructose provides nearly 20% of energy intake in Australia, while also stating that Australian intake is about two-thirds that of the United States. The scientific literature [see for example Medscape J. Med. (2008); 10(7): 160] indicates that fructose provides ~10% of energy intake in the US. Assuming that you are correct about Australian intake of fructose being substantially less than in the United States, average intake in Australia would be somewhat less than 10% of total energy, not 'nearly 20%'.

(ix) Sweet Poison includes the claim that added fructose is a poison at any dose, and your Ockham’s Razor program calls on regulatory authorities to '… immediately ban added fructose as a food'. There is no evidence in the scientific literature to suggest that added fructose is toxic at any dose. National and international health related organisations such as the World Health Organisation, the Australian National Health and Medical Research Council and the American Heart Association all recommend maximum intakes of sugars; none of these (or any other reputable organisation) recommends complete avoidance of added fructose.

(x) You also claim that fructose is undoubtedly addictive to humans (and therefore that sucrose and high-fructose corn syrup are addictive). The evidence on this is equivocal, to say the least. For example, a recent meta-analysis [Clin. Nutr. (2010) 29(3): 288-303] concludes that 'There is no support from the human literature for the hypothesis that sucrose may be physically addictive ...'

(xi) On page 172 of Sweet Poison the claim is made that 'all processed foods contain some sugar'. This is not correct. The following is an incomplete list of processed foods that generally do not contain added sugars: Canned and dried soups; canned vegetables; frozen vegetables; dried vegetables; frozen fruit; dried fruit; most frozen ‘TV dinners’; cured meats; Vegemite; potato crisps; frozen potato chips; unflavoured corn chips; pasteurised milk; cheese; natural yogurt; unsweetened fruit-flavoured yogurt; cream; butter; margarine; cocoa powder; instant coffee; some breakfast cereals (e.g. All-Bran, Weetbix, rolled oats); and many savoury crackers/biscuits.

(xii) On page 174 you state that 'non-caloric sweeteners ... contain the same number of calories per gram as any other carbohydrate'. This is not correct—“non-caloric” implies that no energy is provided by these artificial sweeteners.

(xiii) You provide the following definitions for units relevant to human metabolism:

a. Joule 'The metric equivalent of the calorie is a joule, and calculated using Einstein’s famous equation E=mc2 …”'(p. 203); and

b. Watt – 'Measures electrical energy consumed per hour ... a 60-watt light bulb uses 60 watts of energy every hour' (p. 137).

Both these definitions are incorrect—the joule is the basic SI unit of energy (and also of work), and is defined as the energy transformed (or work conducted) when a mass of one kilogram is accelerated at one metre-per-second-squared over a distance of one metre. The reference to ‘E=mc2’ is wholly inappropriate; we wonder if you have confused Einstein’s equation with the equation ‘W=f.d’ (work equals force times distance) which is appropriate in this context.

Similarly, the watt does not measure 'electrical energy consumed per hour'—it is a measure of power output, regardless of the form of energy, and measures the quantity of work conducted (or energy transformed) per second, not 'per hour'. One watt of power output occurs when one joule of work is done per second. (And the claim that 'a 60-watt light bulb uses 60 watts of energy every hour' is meaningless.)

In addition to containing these errors (among others), Sweet Poison selectively refers to the scientific literature and, as explained above, occasionally grossly misinterprets the literature to develop an exaggerated case that fructose is the sole cause of obesity, type 2 diabetes and heart disease.

The actual state of the science is that the hypothesis has been advanced that high (note the word high) intakes of fructose may be implicated in these chronic health problems, but there is no consensus that fructose is the sole, or even major cause. For example, Johnson et al. [Endocrine Rev. (2009); 30: 96–116] hypothesise that '... excessive fructose intake (>50 g/day) may be one of the etiologies of the metabolic syndrome and type 2 diabetes'. That is, it is plausible that high (but not low or moderate) intakes of fructose are contributing to adverse health outcomes. This hypothesis now needs to be subjected to rigorous testing. This is quite different to your conclusion that dietary fructose is unquestionably the sole cause of the major chronic health problems afflicting developed nations.

Another illustration that the debate is far from over is the exchange between the authors of a meta-analysis [Am. J. Clin, Nutr. (2008); 88: 1419-37] and the authors of an accompanying editorial [Am. J. Clin, Nutr. (2008); 88: 1189-90]. The meta-analysis concludes that fructose is safe at relatively high intakes and may even be beneficial at moderate intakes, while the editorial questions these conclusions as follows: 'Whereas some ... (adverse) effects (of fructose) have been reported only in animals, these findings raise important questions about the safety of high doses of fructose in humans'. Even if the non-peer-reviewed editorial is given greater weight than the peer-reviewed metaanalysis (and there is no reason why it should), its contents do not equate to your claim that fructose is indisputably a poison at any dose.

Another major problem is that Sweet Poison ignores (in fact denigrates) the Dietary Guidelines for Australians published by the National Health and Medical Research Council. These are science-based, and constitute the most appropriate diet-related advice currently available to Australians. Although your book includes reference to the value of dietary fibre, and mentions the problems associated with consumption of trans fats, it does not address the major health problems associated with excessive consumption of salt and alcohol. It also (inappropriately) includes the claim that physical activity is of no value for people whose aim is to lose weight, and it condones (even promotes) high fat consumption (other than trans fats).

In summary, Sweet Poison does not reflect the current state of scientific knowledge with respect to the health effects of dietary fructose. As a result, the Nut-Net FAQ will continue to recommend against this book.

Chris Forbes-Ewan
Coordinator Nut-Net FAQs
22 Oct. 10

1 Michael Pollan has written extensively on food and nutrition. His background research for In Defense of Food included consulting eminent nutritionists such as Walter Willett, Joan Gussow and Marion Nestle.



Share this page