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Feature Essay

What if sugar is worse than just empty calories? An essay by Gary Taubes

BMJ 2018; 360 doi: (Published 04 January 2018) Cite this as: BMJ 2018;360:j5808

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Fructose Does Not Cause Diabetes.

I disagree with Gary Taubes, whom I hold in the highest regard. Let’s analyze this physiologically rather than epidemiologically. The slippery slope between “associated” and “caused” is all too familiar.


Mr. Taubes speaks of “disassociating any deleterious effect of sugar from that of the calories it contains,” but is not alarmed by fructose’s seemingly amiable companion - glucose. After all, those beta cells done in by diabetes are designed to cope with glucose, not fructose.

Conventionally, type 2 diabetes is attributed to obesity and to insulin resistance. In fact, some go so far as to say that insulin resistance is type 2 diabetes. However, while insulin resistance does cause higher blood glucose, it is not the root problem; it is dead beta cells that are the irreversible and progressive essence of type 2 diabetes. Insulin resistance is just reversible adaptations to too much blood glucose, too often; causing chronically overstuffing of muscle cells and the liver’s glucose fuel tank. Insulin resistance was branded the villain in Type 2 diabetes because it seemed disease-like, while the ubiquitous consumption of dietary carbs (glucose) seemed natural.

Obesity so often catches the eye when seeing type 2 diabetes patients that the association seems causal, but many have tried to physiologically connect obesity to type 2 diabetes, without success. One does not cause the other, but they have a common progenitor, dietary glucose, both in quantity and in transient peak effects.

Human evolution expects almost all glucose to be released little by little from the liver, just as needed. So blood glucose never rises very much or very fast and our beta cells are never overtaxed. But, when you eat carbs, blood glucose rises massively and quickly, triggering massive and quick insulin secretion; and even transient peaks, unknown during evolution, seem like massive glucose loads to beta cells which then try to respond with excess insulin production. Insulin resistance in liver and muscles further aggravates this by requiring even more insulin to force in even more glucose.

This threatens the very survival of our beta cells. The main trigger of apoptosis is failure of a cell to perform its function, but requiring beta cells to massively and quickly secrete insulin tempts them into failure and triggers apoptosis. Most type 2 diabetes beta cells have suffered apoptosis - that is diabetes.

If, eight hours after eating, the pancreas is unable to supply enough insulin to push fasting blood glucose below 90, there must be few surviving beta cells - and each of those few survivors now are asked to secrete even more insulin. Thus an avalanche effect, fewer beta cells, more asked from each cell, faster apoptosis - progressively worsening diabetes.

Treatment: Over the course of one month, reduce carbs to near zero. Rescue failing beta cells by injecting insulin during their recovery.


This indictment of glucose in type 2 diabetes does not let fructose off the hook in NAFLD and atherosclerosis. Fructose causes de novo lipogenic production of VLDL (triglycerides) which cause fatty liver, and, with the help of CETP, produces small, dense LDL particles capable of piercing the arterial endothelium and, with contributions from the immune system, atherosclerosis.

Chronically excessive glucose may have a similar effect - stay tuned.

Adapted (with too little context) from my paper in progress, “Unified Physiology of Obesity and the Metabolic Syndrome.”

Competing interests: No competing interests

05 January 2018
Charles R. Fred
Electrical Engineer
New York