This paper presents evidence that UVR, which varies in intensity with solar cycles and seasons, modulates the lifespan of type-2 diabetics born before 1945. Using the death records of approximately 829,000 diabetics born before 1945, we found that ethnic minority diabetics lived significantly longer than their non-diabetic minority contemporaries. In contrast, in the last decades of the 20th century Native Americans with a high prevalence of obesity and diabetes have a shorter lifespan . However, the white diabetic females born prior to 1945 revealed what we would expect today, for example, shorter lives most probably due to vascular complications. We suspect that the difference in lifespan between whites and ethnic minorities was due to poorer nutrition and hard physical work in the latter groups; indeed, most of human history was a continuous struggle to obtain food . Many ethnic minorities had fled from famine in Europe and Asia and took laborious jobs in the United States, but despite the USA being ‘a land of plenty’, nutrition was a significant problem manifested by pellagra (niacin deficiency) at least through the 1940s .
Those with epigenetic alterations to increase metabolic efficiency and caloric storage would have a survival advantage in an adverse environment. While the hunter-gatherers of pre-historical humans generally had adequate nutrition, throughout human history there have been periodic famines in all continents with, in some cases, the loss of millions of lives [30–33]. In our study ethnic minorities, had a modest caloric intake readily metabolized by hard physical labor [34, 35]. As discussed by Lane, people for the last 6,000 years have struggled to get something to eat, and even in modern times many in the world go without adequate nutrition . Obesity was subsequently less prevalent than in the post 1950 to the present era.
There is increasing evidence that early life events have effects that modulate the adult expression of disease. We hypothesize that rapidly changing UVR is most influential at conception/early gestation, particularly at the equinoxes, and alters epigenetic expression in diabetes. Rapidly decreasing UVR at conception, for example, at the autumnal equinox, was disadvantageous to the white race (and those in other races of higher social status) possibly because of good nutrition and less physically demanding jobs where activation of ‘frugal’ epigenes only predisposes to obesity . Women in general are at a particular disadvantage probably due to a canalized tendency to retain weight for pregnancy and due to the effect of estrogens; however, rapidly increasing UVR at conception, for example, at or around the vernal equinox, may be beneficial to women due to the suppression of a calorie-conservative epigenome and may also be useful to men who are genetically predisposed to become overweight or who are underactive. A Ukrainian study has recently showed that type 2 diabetes is more common in those born in April (for example, conception in July with decreasing UVR), and is less common in those born in November and December (for example, conception in February and March with increasing UVR) .
The above observations suggest that increased skin melanin is associated with an increased sensitivity to ambient UVR as seen in Figure 1. One might have expected the reverse. However, melanin is an adaptation to increased UVR intensity, and more sensitivity to any variation in UVR may be necessary and encoded in the human genome over millennia .
One can speculate about how UVR affects an embryo in utero without direct exposure to UVR. A comprehensive review of how the skin senses the environment was recently published . With the skin sharing an ectodermal origin with the central nervous system, it is not surprising to find shared neuroregulatory compounds in both tissues, including serotonergic, melatoninergic, catacholinergic, opioidergic, and the hormone vitamin D, among several others. Circulating inflammatory cytokines, chemokines, photo-oxidation products, and nitric oxide may also play a role [39–41].
There are recent reports that hypovitaminosis D is associated with a higher incidence of diabetes [42–44]. This is especially true for those with more skin pigmentation . Those persons working in agrarian jobs would spend much more time outdoors, and by increasing their vitamin D level, could mitigate or delay the expression of diabetes. The literature supports adequate vitamin D increasing insulin sensitivity . This may be an additional reason for the greater lifespan of those with diabetes around the turn of the last century as well as greater physical activity and less obesity. Vitamin D is important in modifying a human epigenome involved with many adult disorders . However, as Figure 4 shows, in this study of our cohort of diabetics there is no difference between the summer and winter solstice in added life years and the major variation in lifespan occurs at the equinoxes. Any effect of vitamin D on lifespan would therefore extend beyond the annual seasonal cycle. Variations in food supply occurring cyclically over years, would give a survival advantage to those individuals with an increased ability to store calories and vitamin D in adipose tissue.
The heterogeneity of our sample results in some persons that benefit, and some who are harmed, by activating or suppressing the metabolically sensitive epigenome, as is evident in Figure 4. Table 5 summarizes observations from Tables 1 and 2.
We are aware that type-2 diabetes is a heterogeneous disease affecting many organ systems and contributing to death in a various ways. However, we wanted to study specifically how UVR affects lifespan, not any other clinical aspects of this disease. Separating the effects of long-term solar-cycle radiation from that of seasonal (annual) radiation was challenging. We also probably did not detect more than one-third of the diabetics in our database, but for those who were captured, diabetes must have played a significant role to be entered on a death certificate, and therefore, these cases were likely to be the most severe.
We do not have comparable death data of persons who were born and died post-1945, and another half-century will pass before that data are available. However, it is already clear that there is an epidemic of type-2 diabetes worldwide. Women are particularly adversely affected in our current environment [48, 49]. As we have shown, diabetic white women were losing lifespan even before 1945. Some of these findings are obviously due to a rising standard-of-living in highly developed countries, for example, better food supplies and an increased use of mechanical devices in lieu of manual labor.
Reports suggest that white race northern Europeans may have developed a partial resistance to diabetes over the centuries, becoming adapted to a lactose-rich diet through farming/animal husbandry, and to rapidly changing light at higher latitude through natural selection [50, 51].
Migration is probably another important factor in the increasing incidence of type-2 diabetes. People who are indigenous to a high-intensity, low-variation photonic environment, like those born near or on the Equator, who then migrate to higher latitude, may be more susceptible to the trigger of decreasing UVR at conception (especially at the autumnal equinox), and along with a nutrient-rich lifestyle, more readily acquire type-2 diabetes. This may explain, in part, the increased prevalence of type-2 diabetes in immigrants to northern Europe and to North America . Once adjusted for ethnicity and socio-demographic variables, migration alone may not be crucial to health outcomes . This opens the possibility that other factors, yet to be fully studied, like solar cycle variations of UVR and geomagnetic forces, modulate our epigenome .
One way of prospectively confirming the hypothesis in this paper would be to use ‘knockout’ mice predisposed to diabetes and see if increasing or decreasing UVR exposure in the early days of gestation (for mice, possibly as little as a 2-day exposure out of a 19-day gestation) to see if the expression of diabetes occurs earlier or later in the animal’s lifetime. Using UVR to treat humans with a genetic predisposition to diabetes must await the results of prospective animal studies along with an increased knowledge of our epigenome .