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Dear Sir,

In the August issue of the Journal of Internal Medicine, Zimmet and Thomas [1] published an interesting article about evolutionary concepts that may help to understand the global ‘obesity epidemic’ [2] and the associated co-morbidities, especially the increasing prevalence of type 2 diabetes. However, from our point of view, some of the author's statements seem somewhat misleadingly or imprecisely.

First, the statement, ‘Humans developed as highly adapted hunter-gatherers from approximately 6 million bc’ [1] is inaccurate. The first hominid, which stood in direct relationship to the genus Australopithecus, and thus to our species Homo, was Ardipethecus ramidus (c. 4.4 million years ago) [3]. However, the ‘original group’, from which the species Homo evolved, was the genus of Australopithecines. The earliest breed of this species is Australopithecus anamensis, which dated about 4.17–4.12 million years ago [4]. Homo habilis, believed to be the first species in our line, first appeared in Africa c. 2 million years ago. Modern humans, Homo sapiens sapiens, first appeared c. 100 000 years ago in Africa, and there is no evidence for modern humans in Europe until about 40 000 years ago [5]. Taken together, the evolution of the earliest human ancestor took place 4.4 million years ago and not 6 million years ago, as reported by the authors [1].

Secondly, the dating of the ‘dawn of agriculture’ [1] is also incorrect. It is generally known that the first archaeological evidence for cultivating plants in the Near East was 15 000 years ago [6]. However, most anthropologists dated the origin of agriculture (Neolithic revolution) about 10 000 years BC [7–9].

Moreover, empiric data does not support the statement that adaptation was unnecessary for survival during the last 27 000 years. Although the genetic information of the humans of 40 000 years ago was nearly identical with that of the present human [10, 11], there were indeed some adaptations which were necessary for survival during this period. One example is the development of lactose tolerance [12, 13], another one is the reduction of pigment coating [14] in the Middle and North European population.

Neel [15, 16] developed the thrifty genotype hypothesis which was explained by Zimmet and Thomas in order to account for the immense ethnic differences in the prevalence of obesity and diabetes type 2. According to this hypothesis, ethnic groups with a very high disease rate such as the Pimas (Pima Indians) [17] and inhabitants of the Pacific Ocean Islands (Pacific Islanders like the Nauruans) [18] exhibit an especially ‘saving (thrifty)’ genotype. Neel attributed the development of this genotype to the insecure food supply in former times (feast and famine). Thus, Europeans with their comparatively low prevalence of type 2 diabetes [19] have to exhibit a less saving genotype (nonthrifty genotype). It is logical that such a suggestion is only plausible if a better food supply can be assumed for Europe than for example for the Pacific Ocean Islands in the past. In our opinion this assumption is not supported by the scientific literature. Approximately 40 000 years ago, a time period when Homo sapiens sapiens first emigrated from Africa, vigorous climates predominated in Europe. The total Scandinavian peninsula as well as large territories of Northern Germany, England and Ireland were covered by a huge ice layer. Only Southern France and Spain had a milder climate and a more rich food supply at that time [20]. In Europe, the last glacial period continued up to about 10 000 years ago. To this date the food supply in Europe had probably been rather limited. With the beginning of the agriculture era, there was no improvement of food supply – quite on the contrary. We agree with Lev-Ran [21], who pointed out that ‘the better-fed Europe relying on successful agriculture is a ‘‘myth'’’. Indeed, there are a lot of archaeological data, indicating that periodic starvation became more frequent in the early farmers than it was in the hunter-gatherers [22, 23]. This implicated a lot of severe health problems, i.e. a reduction in stature and life span and an increasing prevalence of infectious diseases [22]. The decline in the stature had been attributed to nutritional stress, especially to generalized undernourishment [24]. Taken together, there is no evidence that the food supply in Europe improved after the beginning of agriculture. In contrast, it has to be assumed, that famine was continuous in the history of Europe up to the 19th century, as shown by Lev-Ran [21]: ‘By 1789, the average caloric consumption was only 2,100 calories, i.e., the same as in the 14th century, but one-third of adult men subsisted on not more than 1,800 kcal day−1. Death from starvation was not unusual, even in London. Terrible famines regularly struck Germany, so that in Prussia in 1847 one-third of the population did not have bread. In Italy, during four centuries in the present millennium, famine struck Florence a quarter of the time (…). The impoverished past of Europe slowly came to an end only in the 19th century. So, famine in Europe was a usual and regular phenomenon in quite recent historical times’ [21]. Taken together, these historical observations clearly show that the selection for ‘thriftiness’, meaning the ability to store energy, must have been pronounced in the European population. However, there is no evidence for distinctive famines in populations like the Pacific Ocean Islands. Indeed, in the tropical–equatorial climate, without long harsh winters and the rich fauna und flora vegetation, the supply with food must have been better than it was in Europe [25]. The questions are still unanswered: why do obesity and type 2 diabetes so often occur in populations of the Pacific Islands? Why are so large ethnic differences in the degree of these ‘civilization diseases'? Whatever the answer is, the hypothesis of the thrifty genotype can hardly explain it.

Conflict of interest statement

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  2. Conflict of interest statement
  3. Editor comment
  4. References

No conflict of interest was declared.

Editor comment

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  2. Conflict of interest statement
  3. Editor comment
  4. References

The authors, Zimmet and Thomas, of the original article [1] were given the opportunity to respond to this letter, but have chosen not to.

References

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  2. Conflict of interest statement
  3. Editor comment
  4. References
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