Re: The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes
The article by Gary Taubes (BMJ 2013 ; 346 : 16-19) focused on the current concept of 'energy balance' (or 'imbalance') and the endocrine hypotheses to account for the present epidemic of obesity. That ignored the possibility of a dietary component 'foreign' (or at high concentration, or both) as far as the mammalian kingdom is concerned, as being responsible.
This reminded me of some work carried out in the 1960s. Refined sucrose (at high concentration) is totally alien historically to Homo sapiens; although fructose has existed in the day-to-day diet since time immemorial, it is only relatively recently that that has attained anything like the high level which exists today. The fructose moiety of sucrose is metabolised in an entirely different manner to that of its glucose component1; it does not stimulate insulin release but raises blood concentrations of lactate and pyruvate whether presented to the enterocyte in its mono- or disaccharide form.2,3 It also seems possible that it influences triglyceride deposition in both liver and adipose tissue. Furthermore, there is evidence of a widespread variability in its breakdown products.4
Surely the time is ripe therefore, to learn more about the metabolic products of a highly concentrated sucrose (and hence fructose) intake, rather than attempt resuscitation of old hypotheses. It is also time to substantially reduce the dietary intake of sucrose and to monitor the effect on its deposition in adipose tissue and subsequently body-weight.
References
1 Cook G C. Absorption products of D(-) fructose in man. Clin Sci 1969 ; 37 : 675-87.
2 Cook G C. Comparison of the absorption and metabolic products of sucrose and its monosaccharides in man. Clin Sci 1970 ; 38 : 687-97.
3 Cook G C. Absorption and metabolism of D(-) fructose in man. Am J clin Nutr 1971 ; 24 : 1302-7.
4 Cook G C, Jacobson J. Individual variation in fructose metabolism in man. Br J Nutr 1971 ; 26 : 187-95.
Rapid Response:
Re: The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes
The article by Gary Taubes (BMJ 2013 ; 346 : 16-19) focused on the current concept of 'energy balance' (or 'imbalance') and the endocrine hypotheses to account for the present epidemic of obesity. That ignored the possibility of a dietary component 'foreign' (or at high concentration, or both) as far as the mammalian kingdom is concerned, as being responsible.
This reminded me of some work carried out in the 1960s. Refined sucrose (at high concentration) is totally alien historically to Homo sapiens; although fructose has existed in the day-to-day diet since time immemorial, it is only relatively recently that that has attained anything like the high level which exists today. The fructose moiety of sucrose is metabolised in an entirely different manner to that of its glucose component1; it does not stimulate insulin release but raises blood concentrations of lactate and pyruvate whether presented to the enterocyte in its mono- or disaccharide form.2,3 It also seems possible that it influences triglyceride deposition in both liver and adipose tissue. Furthermore, there is evidence of a widespread variability in its breakdown products.4
Surely the time is ripe therefore, to learn more about the metabolic products of a highly concentrated sucrose (and hence fructose) intake, rather than attempt resuscitation of old hypotheses. It is also time to substantially reduce the dietary intake of sucrose and to monitor the effect on its deposition in adipose tissue and subsequently body-weight.
References
1 Cook G C. Absorption products of D(-) fructose in man. Clin Sci 1969 ; 37 : 675-87.
2 Cook G C. Comparison of the absorption and metabolic products of sucrose and its monosaccharides in man. Clin Sci 1970 ; 38 : 687-97.
3 Cook G C. Absorption and metabolism of D(-) fructose in man. Am J clin Nutr 1971 ; 24 : 1302-7.
4 Cook G C, Jacobson J. Individual variation in fructose metabolism in man. Br J Nutr 1971 ; 26 : 187-95.
Competing interests: No competing interests