“High blood glucose levels caused by excessive sugar consumption are detrimental to mammalian health and life expectancy. Despite consuming vast quantities of sugar-rich floral nectar, nectar-feeding bats are long-lived, provoking the question of how they regulate blood glucose” (1). So goes the introductory sentences of the abstract of Kelm et al.’s High activity enables life on a high-sugar diet: blood glucose regulation in nectar-feeding bats (2011). The underlying assumptions of their question exemplify the lack of insight currently endemic in biomedical science.
A high blood glucose level, they claim, is a hallmark of diabetes mellitus, decreased insulin sensitivity, low life expectancy in mammals, etc. This concept presupposes both a human-centric view of mammalian biology, while at the same time one of mammalian homogeneity. It is human-centric as follows: given that many modern humans suffer from glucose metabolism disorders, a bat that lives on sugar must be chronically pathological, like a diabetic human. Yet it also makes mammals out as homogeneous with the implication that there is one ideal blood glucose level for mammals, all mammals as a class. It’s as if the authors think of these animals as falling fully formed from the sky, accidentally landing on a sugary diet instead of a more balanced one.
Nectar specialists “benefit from an energy rich food source,” but must “escape the pathological side-effects of their diet.” This way of thinking belies a near-complete misunderstanding of biological systems. It is akin to saying “wealthy people benefit from the resources they can purchase with their money, but must escape the damaging side effects of the effort required in deciding how to spend it.” If the nectar were not beneficial to the animal, it would not have evolved to consume it so voraciously. Viewing a biological system in snapshot is quasi-creationistic in its myopia. Anti-sugar hysteria has become, after all, part of the post-modern religion.
The researchers found that Glossophaga soricina bats absorbed sugars faster than average for mammals, and were able to fuel much of their flight directly from dietary sugar. This, in part, blunted the post-prandial blood sugar increase from such high consumption. Still, the bats’ blood sugar was abnormally high and persistent for mammals, reaching >25 mmol/L (450 mg/dL) at rest or >15 mmol/L (250 mg/dL) in near-constant flight. After 90 minutes, resting bats still had blood glucose >15 mmol/L, while flying bats’ levels went down to 5 mmol/L (126 mg/dL), when not re-fed.
In nature, nectarivorous bats fly from flower to flower, combining high activity with sustained sugar intake, thus likely maintaining “chronically elevated” glycemia.
Kelm et al. were surprised to find that despite this high and sustained blood glucose, hyperglycemic markers like HbA1C were “within the expected range for mammals.” They then suggest that reactive oxidative species (ROS) from an abnormally high mitochondrial proton gradient may cause aging-related damage and degeneration, but admit that recent studies question a direct cause and effect relationship between ROS and lifespan. The mole rat is a good example of this.
The paper can be summarized as follows:
1) Biomedical relevance: Human diabetes and related health problems are caused by sugar consumption (tenuous claim).
2) Purpose/premise: Therefore, a mammal that consumes a high-sugar diet should either suffer pathology similar to human diabetes, or have an evolved mechanism for “detoxifying” sugar.
3) Methods: Measure bats’ blood glucose pre and post-sugar bolus, both at rest and during activity.
4) Results: Nectarivorous bats use a great deal of ingested sugar directly as muscular fuel, blunting but not entirely preventing high and sustained post-prandial glycemia.
5) Conclusions: The bats’ glycemia is practically uncontrolled by insulin-stimulated uptake and storage, as in other mammals, and is only lowered through direct-use via energetic flight activity. Despite high glycemia and an above-average metabolic rate, G. soricina present no long-term diabetic markers and are longer lived than average for mammals of their size, respectively.
In the end, the authors suggest that a nectar diet and high activity may have co-evolved to avoid the detrimental effects of a high-sugar diet. This should have been obvious to anyone with even a cursory understanding of biology and evolution. The thing that initially blinded Kelm et al. is the designation of glucose/sugar in the category of dangerous, toxic substance. Normally, access to large amounts of nutritive substrate would not be seen as a “problem needing to be dealt with” from a biological perspective. Exposure to an environmental toxin, however, would be. An example of such exposure and evolved contingency can be seen in the cyanide-resistant bamboo lemurs (genus Hapalemur) of Madagascar.
The insane idea that sugars are toxins, like arsenic or ethanol, is blinding a whole generation of biomedical scientists to the basic tenets biological evolution. If an organism is observed consuming a specific diet, however unhealthy or gauche that diet appears to be from your enlightened nutritional perspective, chances are that the organism evolved to do so. That this is a challenging concept to so-called biologists can be lain at the paired feet of the anti-sugar hysteria crowd and the government-funded science monopoly.
- Kelm DH, Simon R, Kuhlow D, Voigt CC, Ristow M. High activity enables life on a high-sugar diet: blood glucose regulation in nectar-feeding bats. Proc R Soc B Biol Sci. 2011;278(1724):3490–6.