Beginning in the early 1950s a number of researchers have argued that human skin coloration is an adaptation to protect against skin cancer by blocking the harmful effects of UVA and UVB radiation (Daniels et al., 1972). A number of lines of evidence have been used to test this hypothesis. For example, Fear et al. (1976, cited in Beall and Steegman, 2000; p 199, Fig. 7.6) show that in the United States skin cancer rates and mortality are negatively correlated with latitude. In the state of Texas, skin cancer rates were approximately five times greater for light-skinned people compared with dark-skinned people. Other studies in Australia and New Zealand compared skin cancer rates of light-skinned individuals to aboriginal residents (e.g., Haynes et al., 2008; Sneyd and Cox, 2009; Olsen et al., 2012). The results were consistently the same: lighter-skinned individuals had higher skin cancer rates. To our knowledge no one disputes the association between skin color, the intensity of UV radiation, and skin cancer. Over the last 20 years there has been growing support for an alternative but not clearly contradictory hypothesis for skin coloration that we call the folate hypothesis as outlined by Jablonski and Chaplin (2000) and Jablonski (2010). The authors assemble impressive evidence that dark skin in high UV environments prevents the degradation of folic acid synthesis and ultimately folate production, thus preventing a host of problems from neural tube defects in infants to male infertility (see Elias and Williams, 2013, for a rebuttal). However, in low UV environments the problem may be allowing sufficient UV radiation in through the skin to stimulate vitamin D synthesis to prevent problems in bone formation, cognitive development, and immune function, leading to light skin as the adaptive solution. A more recent, intriguing hypothesis is that depigmentation evolved as an energy-sparing mechanism (Elias and Williams, 2013). In the process of promoting the folate hypothesis Jablonski (2010) argues that although skin cancer is reliably associated with UV radiation and skin color, the typical onset of skin cancer is at about the time when one's reproductive career is ending: therefore, dark skin would not have a selective effect in preventing skin cancer. Elias and Williams (2013) dismiss the selective potential of skin cancer using this same reasoning. For a variety of reasons stemming from a new understanding of human life history and inclusive fitness theory, detailed below, we argue that preventing skin cancer after reproduction is likely adaptive. And while a full review of this literature is beyond the scope of this article, we provide a synthesis of recent research on the dangers of skin cancer and their likely impact on fitness.
Skin cancer types Skin cancer presents as a range of disorders associated with abnormal growth of skin cells which develop into lesions classified as preskin cancer or skin cancer. Some skin cancers occur more frequently than others and are more relevant to fitness. The most common skin cancers are named for the cutaneous cells from which they arise and include the nonmelanoma skin cancers (NMSC) basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), and cutaneous malignant melanoma (CMM).
Exposure to ultraviolet radiation (UVR) increases risk of developing NMSC and CMM, though there is also a genetic predisposition (Lacour, 2002; Epstein, 2008; Nan et al., 2009; Scherer and Kumar, 2010). Rates of NMSC are estimated to have increased by 77% from 1992 to 2006 (Scherer and Kumar, 2010; Stern, 2010). This increase could be due to atmospheric changes, migration of lightly pigmented populations to lower latitudes, improvements in diagnosis, changes in sun-seeking behavior, and access to artificial UVR.
On a general scale, likelihood of metastasis in CMM is greater than in NMSC and if not treated early this cancer has high mortality. Like all skin cancers, lightly pigmented populations are at greater risk of developing CMM, although it is present in more darkly pigmented populations in lower proportions (Table 1; also see Camain et al., 1972; Soeripto et al., 1977; Bang et al., 1987; Neugut et al., 1994; Yakubu and Mabogunje, 1995; Sneyd and Cox, 2009). Accordingly, one cannot easily dismiss skin cancer as a selective pressure in the adaptation to UVR. The literature on skin cancer contains relatively few publications on risk and pathophysiology in more darkly pigmented populations (Yakubu and Mabogunje, 1995; Sneyd and Cox, 2009). Because moles present at birth can develop into CMM, some have questioned whether or not UVR has an effect on CMM (Tucker, 2008). This rejection of UVR as a driver of CMM rests largely on the heritability of this disease.
Skin cancer genetics Genes associated with skin cancer risk remain poorly understood. Some genetic markers (e.g., MC1R, ASIP, TYR, EXOC2, UBAC2, OCA2, SLC24A5, SLC24A4, MATP, IRF4, and the 1p36 and 1q42 loci) have been identified as risk factors independent of skin pigmentation, though they only explain a small amount of variation in skin cancer risk (Han et al., 2008; Scherer and Kumar, 2010). Because genome-wide associations studies (GWAS) have not identified regions that explain heritability, some have proposed that many “small-effect” genes are responsible for this variation—although others contest that current models do not include large enough regions of the genome to conclude anything about the genetic basis of skin cancer (Vazquez et al., 2012).
One possible reason that genes with strong effects on skin cancer have not been identified could be the focus on coding regions. Mutations in the promoter regions of genes can affect trait expression and are affected by UVR, providing a clear gene × environment interaction (Greenman, 2007; Ikehata et al., 2008; Singh et al., 2012; Tewari et al., 2012; Huang et al., 2013). Mutations in telomerase reverse transcriptase (TERT) gene promoter regions are more likely to produce immortal cell lines conducive to oncogenesis than are mutations to coding regions (Huang et al., 2013). Two byproducts of UVR exposure are cyclobutane pyrimidine dimers (CPDs)—mainly thymine dimers (TTs)—and 6,4-photoproducts (6,4 pyrimidine-pyrimidones) (Ikehata et al., 2008; Rünger, 2008; Tewari et al., 2012). Both CPDs and 6,4-photoproducts are associated with melanoma oncogenesis. Cyclobutane pyrimidine dimer (CPD) formation from UVB exposure has been suggested as a strong selective pressure for dark pigmentation, but UVA was not considered a source of CPD or an important factor in the evolution of skin pigmentation (Jablonski and Chaplin, 2010). Based on these results UVA may be more carcinogenic than was previously assumed. This is especially important in evolutionary contexts because UVA is more abundant than UVB, increasingly so at higher latitudes, and may have played a more significant role in the evolution of skin pigmentation than was previously thought.
Skin cancer as a selective force in skin pigmentation Skin cancer has been dismissed or downplayed as a selective force in the evolution of skin pigmentation because it is argued to affect individuals as their reproductive careers are ending (Jablonski and Chaplin, 2000; Juzeniene et al., 2007; Elias and Williams, 2013). Jablonski and Chaplin (2012) observe that skin cancer is a disease of modernity, primarily affecting individuals living at lower latitudes than their ancestral environment and/or engaging in the tanning culture. Sun-seeking and tanning behavior does increase the risk of skin cancer and thus continues as a selective pressure on skin pigmentation. The claim that the onset of skin cancer occurs late in an individual's reproductive career, however, is not completely correct. For example, CMM is the third most common cancer in adolescents and young adults in the US and typically affects individuals throughout the reproductive period (ages 20–45), so this argument does not hold for the deadliest form of skin cancer (Diepgin and Mahler, 2002; Weir et al., 2011). The selective potential of CMM is best appreciated through an understanding of survival time following diagnosis. A meta-analysis of late stage CMM found that prior to 1985 the median time to death was 5.8 months (Lee et al., 2000; Mervic, 2012). Research conducted between 1985 and 2000 found the median time to death was 8.9 months. Although these rates are based on individuals with late stage CMM, they also assume some level of medical intervention, suggesting that during the evolution of skin pigmentation this disease would have been a strong source of selection. Further, Robins (1991) argues that selection of dark skin should not be contextualized solely in adults, as infants would also have been exposed to UVR. Although this particular argument is made in support of sunburn as a selective pressure in pigmentation, the strong relationship between lifetime UVR exposure and skin cancer risk suggests that infancy may have been relevant in the selection of skin pigmentation.
Research on evolution of skin pigmentation has focused on global variation in relation to UVR exposure as well as barrier competency. In accordance with Gloger's Rule, more darkly pigmented populations live closer to the equator, with skin pigmentation decreasing at higher latitudes. Because dark skin in humans is believed to have evolved in equatorial locations high in UVR, models describing the effects of migration to higher latitudes on darkly pigmented groups have been used to model the evolution of depigmentation in low UVR environments, perhaps in response to insufficient synthesis of vitamin D3 (Jablonski and Chaplin, 2000, 2012). This approach has been critiqued when examining lightly pigmented populations subsequent to migration to low latitudes. Rather than modeling skin cancer as a selective agent, some argue that dark skin evolved in response to UVR-induced nutrient photolysis (Branda and Eaton, 1978; Jablonski, 1999; Jablonski and Chaplin, 2000, 2012) and others posit that pigmentation evolved to increase barrier functionality as a defense against infection. The paucity of data on skin cancer incidence in darkly pigmented populations limits our understanding of these disorders as selective pressures. When considering darkly pigmented populations living in high UVR environments, it is clear that skin cancer is present at a lower incidence than in lightly pigmented groups (Bang et al., 1987; Johnson et al., 2003).
Following Blum (1961), Jablonski and Chaplin (2010), and Elias and Williams (2013) dismiss the utility of dark pigmentation as an adaptation to skin cancer because it is perceived to affect individuals beyond reproductive age. Jablonski and Chaplin (2010) write, “With early reproduction and before the extension of the average human lifespan through improvements in diet and medicine, skin cancer had no effect on reproductive success” (8966). This dismissal rests on two now dubious claims: (1) low average longevity in evolutionary relevant human societies (hunter gatherers) compared with present day societies, and (2) empirical studies of inclusive fitness behaviors of postreproductives.
The argument made by Blum which underwrites the claim of no or little effect on reproductive success was made in 1961. This dismissal has found its way into the literature (e.g., Juzeniene et al., 2009; Elias and Williams, 2013) and the human variation section of the American Anthropological Association's website (www.understandingrace.org/humvar/skin_01.html). While reasonable at the time, three major developments postdating Blum's dismissal make such claims dubious. First, there is good evidence that contemporary hunter-gatherers can live into their 60s (Kaplan and Gurven, 2007; p 236; see Table 2). This new comparative research shows that normal human lifespans are much longer than has been previously thought and suggests that longevity has a deep human history, perhaps dating to the evolution of anatomically modern humans, and is not solely a recent consequence of advanced medicine or public health measures. Second, inclusive fitness theory (Hamilton, 1964) demonstrates that indirect reproduction through kin investment (kin selection) is an avenue for fitness for postreproductive individuals. And third, the evolution of longevity and corresponding slow life history in humans suggest that investment in offspring extends beyond the period of subadulthood leading to additional avenues for inclusive fitness (Hawkes et al., 1998; Peccei, 2001). Clearly, points 2 and 3 are interconnected. We elaborate each of these points in turn.
Longevity among hunter-gatherers While it is abundantly clear that human life expectancy at birth has increased dramatically since 1900 (Finch, 2012; Burger et al., 2012) humans, prior to that time, were a long-lived species. There is good reason to believe that human longevity has not changed sufficiently in recent times such that early death in the context of evolved longevity would have no effect on fitness. Kaplan and Gurven's (2007) comparative sample of longevity among contemporary hunter-gatherers and horticulturalists (with a strong dependence on foraging) is the largest of its kind to date. They examined 19 different subsistence societies including 5 hunter-gatherer groups with little contact, 4 different forager-horticulturalists, and 9 acculturated hunter-gatherer groups. Claims about the recent extension of longevity and corresponding belief in short longevity of hunter-gatherers is often mistakenly misrepresented by life expectancy at birth estimates (e0), which range from 21 to 37 years among uncontacted hunter-gatherers (Kaplan and Gurven, 2007; p 326). However, if one examines life expectancy at age 15—the average number of additional years of life—among traditional hunter-gatherers, 64% reach age 45 (Table 2). And, on average, traditional hunter-gatherers who reach age 45 will have two decades of life left (Kaplan and Gurven, 2007; p 326). Kaplan and Gurven (2007; p 348) conclude, “Post-reproductive longevity is a robust feature of hunter-gatherers and of the life cycle of Homo sapiens. Survivorship to grandparental age is achieved by over two-thirds of people who reach sexual maturity and can last an average of 20 years” (see also Finch, 2010; p 1723). More to the point, Levitis et al. (2013) developed “Postreproductive Representation,” a measure ultimately demonstrating that postreproductive life is a derived evolutionary trait of humans and not a consequence of modern increases in human lifespan. It is defined “as that proportion of adult-years lived which are postfertile” (2013; p 68). The figures for humans range from 0.315 to 0.5 in tribal populations and up to 0.76 in modern populations. The corresponding figure for wild chimps is 0.018.
One could argue that contemporary hunter-gatherers are not representative of prehistoric populations because paleodemographic estimates of longevity based on human remains generally show significantly lower survivorship than those attained by Kaplan and Gurven. As noted by Kaplan and Gurven (2007; p 334) paleodemographic estimates are beset by a variety of problems such as sampling biases (e.g., Wood et al., 1992) that typically lead to lower estimates than documented in contemporary hunter-gatherers. And it is not unreasonable to argue that contemporary hunter-gathers exist in a more difficult epidemiological landscape because of STDs, tuberculosis, and other diseases that have recently entered their populations through contact with more complex societies. More to the point, there is little evidence that the subsistence landscapes in the past were significantly different than the landscapes of contemporary hunter-gatherers. The environment of current hunter-gatherers sampled by Kaplan and Gurven (Hadza, Ache, Kung, Hiwi, and Agta) ranges from desert to savannah to tropical forest locations which the first humans occupied, suggesting that their results apply to a moderately wide range of low-latitude, evolutionarily relevant environments.
Longevity and individual and kin effects The obvious question one must answer is that given that longevity is not an artifact of modern conditions what can humans do to enhance their reproductive success after direct reproduction is no longer possible or sharply diminished? The short answer to this question is the enhancement of inclusive fitness through one's positive effects on the reproductive success of kin (Hamilton, 1964). There is now considerable evidence that humans behave in ways to enhance the fitness of close kin (Cronk, 1991; Voland, 1998; Barrett et al., 2002; Gaulin and McBurney, 2003; Hames, in preparation). This is especially critical for females because of menopause, whereby they lose the ability to reproduce directly between the ages of 40 and 45 even though they will live another two decades, on average. We will first examine this issue from a female perspective and then turn to males.
As noted by Hawkes et al. (1997), the problem of female longevity in the context of menopause was first considered by G. C. Williams (1957), who argued that the riddle of human menopause could be solved through investment in children or grand offspring. A particular version of this view became known as the “grandmother hypothesis” that argues that grandmothers enhanced their inclusive fitness by either enhancing the fertility of daughters or the survivorship of grand offspring (Hawkes et al., 1997) through food transfers, child care and other acts of assistance. In a modified version of this hypothesis known as the “mother hypothesis” Peccei (2001) argues that since a woman's last child is not fully independent of parental investment for about 16 to 18 years, the survivorship of a woman's last child would be diminished if she were not to live long enough assist that child through the juvenile period. Comparative data on economic independence (when food production is equal to or greater than consumption) shows Peccei (2001) is reasonably accurate (Kaplan, 1997; Kramer 2005).
Over the last 10 years or so considerable evidence has accumulated to support the grandmother hypothesis, showing that postreproductive women are able to enhance their inclusive fitness through such means as increasing the fertility of daughters and ensuring the survivorship of grandoffspring. This research highlights the adaptive value of longevity-inclusive fitness effects even when direct reproduction ceases. Sear and Mace (2008) reviewed 45 studies investigating the presence of mostly senior kin (mothers, fathers, grandparents, older siblings) on the fertility of reproductive-aged women and the survivorship of their children. The presence of a maternal grandmother was associated with an increase in her grandchildren's probability of surviving in 69% of the cases (9 of 13), and for paternal grandmothers it was 53% (9 of 17 studies) (2008; Table 3, p 8).
It is consistently shown that since males do not go through menopause and marry polygynously or engage in serial monogamy they continue to engage in direct reproduction until near the end of their lives. For example, among the polygynous Yanomamö, male fertility peaks between ages 25 and 55 and steadily declines thereafter (Melancon, 1982; p 175, Fig. 9.2). Furthermore, polygyny is more frequently allowed by foragers than in other economic formations (Marlowe, 2003). Consequently, male reproductive careers through polygyny or serial monogamy can last decades beyond that of females (See Josephson, 2002 for a cross-cultural survey).
While there are numerous studies showing how postmenopausal women can enhance their direct fitness by continuing to survive and invest in current dependent offspring or grandoffspring there are few showing the same for men. However, recent research by Scelza (2010) shows that fathers play important social roles for their sons among Martu hunter-gatherers. Her Martu data show that men who have fathers are likely to go through ritual initiation to manhood earlier (a prerequisite for marriage) and marry earlier, and have higher fertility at age 30 compared with males who lacked living fathers who could sponsor them and therefore went through initiation later.
We have shown that human longevity is not a recent phenomenon and that postreproductive humans can enhance their inclusive fitness by increasing the survivorship and fertility of offspring and close kin. Therefore, we believe that the evidence cited above casts serious doubts on claims that skin coloration's protective value is not an adaptation for the prevention of relatively late onset skin cancer.
Modern rates of skin cancer and tests of adaptive hypotheses Jablonski and Chaplin (2010:2) acknowledge the value of dark skin in protecting against skin cancer in the following: “Skin cancers are mostly a consequence of modern human migrations and resulting mismatches between skin pigmentation and geography or lifestyle.”
We agree with their mismatch hypothesis. The key point they make is that dark skin protects against skin cancers. To understand the value of dark skin, we can think of no better natural experiment (Beall and Steegman, 2000; p 201) than to examine skin cancer rates of those whose ancestral homelands were in low UV environments but who currently grew up and live in higher UV environments. If dark skin coloration is a protective response to skin cancer then light skinned individuals should show greater skin cancer rates than their dark-skinned ancestors who continue to live in their aboriginal homelands.
Skin cancer incidence rates for darkly pigmented populations living at low latitudes are few. This is due in part to the lower incidence rates in these groups relative to lightly pigmented populations—since the latter have higher mortality rates from skin cancer, research is focused on combating this issue. The limited data suggest that both NMSC and CMM are present in equatorial populations (Camain et al., 1972; Soeripto et al., 1977; Yakubu and Mabogunje, 1995). Yakubu and Mabogunje (1995) tracked incidence in a Nigerian sample (n = 721) over an 11-year period, including comparative data in their analysis. The authors report 24% of subjects developed skin cancer on the head and neck with 86% of those cases being SCC—their ages ranged from 4 months to 75 years, with a median age of 39 years. While BCC normally dominates cancer of the head and neck, this does not appear to be the case for this Nigerian sample. Camain et al. (1972) report that SCC was the most frequent type of skin cancer in their sample from Senegal, though most tumors presented on the lower limbs rather than the head and neck. Soeripto et al. (1977) report skin cancer frequency in Indonesians, finding that skin cancer accounted for 17.6% of tumors in males and 9.6% in females—though the authors note that the value for females is suppressed due to high frequencies of genital tumors. Some have argued that disparate skin cancer rates between African albinos and non-albinos support skin cancer as a selective pressure for pigmentation (e.g., Robins, 1991). Albinos are known to suffer from skin cancer at a much higher rate (Lookingbill et al., 1995; Yakubu and Mabogunje, 1995) than non-albinos at any latitude, and because this trait occurs in Africa we might interpret the data as evidence of the selective potential of skin cancer. Albinism is associated with the inability to produce melanin at all, so it could also be argued that such a model is an unrealistic proxy for ancestral skin pigmentation. Even without the albinism data, this research demonstrates the presence of skin cancer in equatorial populations, though estimating change in incidence rates over time is not possible given the paucity of data (Yakubu and Mabogunje, 1995). Additionally, it is likely that skin cancer in developing nations is underreported.
In addition to skin cancer incidence rates among populations living in place, populations that have migrated from their ancestral latitude to more equatorial climates provide a natural experiment with which to judge the differential effect of UVR on lightly and darkly pigmented groups. It is widely accepted that lightly pigmented groups living at low latitudes will suffer from skin cancer at a higher rate than populations with darker pigmentation in the same region (e.g., Lomas et al., 2012). Beall and Steegman (2000) demonstrated this relationship in a sample of African-Americans and whites living in Texas, arguing that this natural experiment supported skin cancer as a selective agent in skin pigmentation. This discrepancy is also illustrated by CMM incidence in Maori and non-Maori subjects living in New Zealand. The distance that sun-sensitive populations living near the equator have traveled from their ancestral latitude is substantial and likely would not have occurred during prehistory, but contemporary skin cancer incidence demonstrates the clear adaptive benefit of dark skin pigmentation against UVR. Skin cancer has been a major health issue in these groups and the data support an increase in skin cancer incidence over time (e.g., Birch-Johansen et al., 2010). Increases in skin cancer incidence are also likely influenced by changing attitudes toward sun-seeking behavior and atmospheric depletion of ozone (Buller et al., 2011; Lemus-Deschamps and Makin, 2012).
The relationship between UVR and skin cancer may not be as clear as was once believed. CMM risk may also be influenced by the presence of skin damaged by scarring, tattoos, or burns (Camain et al., 1972; Chadwick et al., 2012). Body modification occurs in contemporary human cultures and is likely not a novel behavior in humans. For example, Sosis et al. (1997; p 242) show that tattooing and scarification occur in over half of the societies in the HRAF probability sample. Because modification of the skin—both intentional and accidental—can decrease the amount of melanin present at the site of injury (Chadwick et al., 2012), this raises the opportunity for CMM to be a selective agent associated with body modification and may help explain oncogenesis in skin not normally subjected to UVR. This may also support the claim that skin pigmentation evolved in response to infection, as more darkly pigmented skin is more resilient to this stress.
Further, Moan et al. (2008) argue that vitamin D3 has a protective effect on cancers—including skin cancers. The negative relationship between latitude and CMM is well established. The relationship between skin cancer death rate and latitude, however, is more complicated. The authors evaluated skin cancer incidence and death rate in individuals of European descent living in Australia, New Zealand, Sweden, Denmark, Norway, and the UK (Moan et al., 2008). As an additional control, the authors only included individuals that either never tan and always burn (type I skin), or those who almost always burn and occasionally tan (type II skin). Not surprisingly, subjects living in Australia and New Zealand were affected by CMM at a higher rate than were subjects living in Europe. But incidence rates relative to death rates of Australian and New Zealand subjects were actually lower than subjects living in Europe. This suggests that while CMM incidence rates are higher in Australia and New Zealand, individuals who develop CMM at higher latitudes have higher mortality. The authors owe this relationship in part to the greater availability of UVB-induced vitamin D3 synthesis. These samples share common ancestries and had lightly pigmented skin, providing some degree of control, but variation in exposure to carcinogens, diet, and healthcare cannot be ruled out as possible factors. Darkly pigmented individuals tend to present with thicker tumors and suffer from faster disease progression than lightly pigmented individuals (Johnson et al., 2003; Gloster and Neal, 2006; Haynes et al., 2008; Sneyd and Cox, 2009; Wu et al., 2011), which may be due to lower levels of vitamin D3 though delayed diagnosis and differential access to healthcare may also be at play.
Murine models support the relationship between vitamin D3 and skin cancer. BCC, SCC, and CMM all have the vitamin D (1,25-dihydroxyvitamin D3) receptor—VDR—suggesting that vitamin D3 plays some role in development and progression of skin cancer (Bikle, 2012). Mice lacking the VDR develop skin tumors after exposure to a carcinogen (Zinser et al., 2002) or UVB (Ellison et al., 2008). Other murine models have demonstrated that vitamin D3 suppresses Hedge Hog (HH) proliferation and signaling responsible for BCC, independent of the VDR (Tang et al., 2011). Additionally, topical application of vitamin D3 to cancerous lesions also slows HH proliferation and signaling. Bikle (2012) argues that in addition to controlling proliferation and differentiation of HH, the wnt/β-catenin pathways, immunoregulation, and DNA repair are also likely mediated by vitamin D3. Higher levels of D3 increase repair capacity. Complicating matters further, folate also repairs DNA damage, with capacity for DNA repair being highest with increased folate (Williams et al., 2012). High UV-induced D3 might share a negative relationship with folate, all things being equal. If D3 and folate are low, then DNA repair is seriously hindered. So disentangling the relationship between D3, folate, and skin cancer complicates matters, but does not necessitate rejecting the skin cancer hypothesis.
CONCLUSIONS We have presented several lines of evidence in support of skin cancer as a selective agent in skin pigmentation. Rejected by some due to its perceived delayed age at onset, data now support CMM as a disorder affecting individuals throughout their reproductive years. It is also now clear that longevity has a deeper evolutionary history than once assumed and that kin selection can have a positive effect on fitness. Though less deadly, the late-developing NMSCs could be selective when viewed through the lens of life history theory and kin selection. The evidence for epigenetic change provides a model demonstrating the adaptive value of dark skin in high UVR environments. Epigenetic change can produce comparatively rapid changes in phenotype in response to environmental cues and is consistent with claims of skin pigmentation as a labile trait. Many issues remain, however, as future research must disentangle the relationships between UVR, skin cancer, skin damage, barrier functions, vitamin D3, and folate. Research on the evolution of skin pigmentation in groups who underwent some degree of selection for depigmentation would offer interesting perspectives on this matter—particularly in populations living at high altitudes where UVR intensity is high.
Posts: 42924 | From: , | Registered: Jan 2010
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But other researchers have rejected skin cancers as a force in the evolution of black skin partly because such growths don’t kill many people today.
Ancient, largely hairless hominids probably had skin more like that of living African apes than human albinos’, remarks biological anthropologist Nina Jablonski of the Pennsylvania State University in University Park. Apes’ pale skin, when exposed to sunlight, develops enough protective melanin pigmentation to enable tanning similar to that achieved by light-skinned people today. Apes possess a gene variant that makes tanning possible, while human albinos do not. Early Homo species carried the gene and weren’t as prone to skin cancer as Greaves assumes, Jablonski hypothesizes.
In her view, dark skin evolved in Africa around 1.2 million years ago to keep UV radiation from lowering the body’s levels of folate, a B vitamin necessary for fertility and healthy development.
Greaves responds that human albinos, despite lacking melanin, can tan with careful sun exposure. So as with African albinos today, tanning wouldn’t have deterred fatal skin cancers in pale-skinned hominids drenched in UV radiation, he argues. Albinos represent an imperfect but useful modern-day analog for ancient hairless hominids that lived in the tropics, he says.
about one in 70 people carry a recessive gene for albinism in Nigeria There are several million albinos living in Nigeria alone Despite the health problems ther must be a biological reason for it
Here is aan albino girl from Benin
So there are millions of albino babies in Nigeria with afro hair but miraculously when a Nigerian couple move to London they are able to pop out a straight haired baby I wonder how much they charge for a photgraph of that hoax ass baby
Posts: 42924 | From: , | Registered: Jan 2010
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You keep posting these White people bullsh1t studies, where they/you try to find a good and useful purpose for White skin, as if disease and defect were "Good things". At which point I immediately debunk that Albino fantasy and nonsense with facts and common sense logic. So tell me, why do you bother?
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posted
The tricky key to deriving any true and useful information from albino research paper(s) is to first understand the generic pattern of albino misinformation and general incompetence. As example, UV radiation has always been present on the planet. It is not a phenomenon that has suddenly arrived on the scene. In fact, most studies show that UV and heat levels were much higher in the past than they are today.
The misinformation that albinos existed before and evolved into black skin is as valid as the neural crest being mostly phaemelanin based and then evolved to Eumelanin.
-------------------- Selenium gives real life and true reality Posts: 4693 | From: Saturn | Registered: Apr 2012
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quote:Originally posted by Mike111: ^Lioness, why are you so stupid?
You keep posting these White people bullsh1t studies, where they/you try to find a good and useful purpose for White skin, as if disease and defect were "Good things". At which point I immediately debunk that Albino fantasy and nonsense with facts and common sense logic. So tell me, why do you bother?
Mike mother nature isn't stupid Obviously being dark skinned is unecessary in Chicago. Therefore over time body will produce less and less melanin in people setteled in Northern Hemisphere regions who dont have access to fish. Look at multi millions of Chinese and japansese for instance, many have light skin. Of course some like some Southern Europeans have relatively darker skin, you can always find exceptions if you cherry pick but the larger pattern is broad
Furthermore as you said dark skin is a protective barrier against the sun's radiatiation. But the thing that makes you stupid is you assume that the UV level in Africa is the same as it is in Canada or other places in the the Northern hemisphere. That is what makes you very stupid. You don't understand climate differences in different parts of the world
As we know of the severn layers of skin only the topmost layer is darkly pigmented in dark skinned peoples, under that top layer it's white. It looks red when blood runs in it Because dark skin is a protective barrier that means it takes longer exposure to the sun for a dark skinned person to absorb sunlight into the lowest layer of skin, the stratum basale, where vitamin D is synthesized. I've explained this to you numerous times but you are too stuck on stupid to get it. Now buzz off, liite ant
Posts: 42924 | From: , | Registered: Jan 2010
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quote:Originally posted by Mike111: ^Lioness, why are you so stupid?
You keep posting these White people bullsh1t studies, where they/you try to find a good and useful purpose for White skin, as if disease and defect were "Good things". At which point I immediately debunk that Albino fantasy and nonsense with facts and common sense logic. So tell me, why do you bother?
Mike mother nature isn't stupid Obviously being dark skinned is unecessary in Chicago. Therefore over time body will produce less and less melanin in people setteled in Northern Hemisphere regions who dont have access to fish. Look at multi millions of Chinese and japansese for instance, many have light skin. Of course some like some Southern Europeans have relatively darker skin, you can always find exceptions if you cherry pick but the larger pattern is broad
Furthermore as you said dark skin is a protective barrier against the sun's radiatiation. But the thing that makes you stupid is you assume that the UV level in Africa is the same as it is in Canada or other places in the the Northern hemisphere. That is what makes you very stupid. You don't understand climate differences in different parts of the world
As we know of the severn layers of skin only the topmost layer is darkly pigmented in dark skinned peoples, under that top layer it's white. It looks red when blood runs in it Because dark skin is a protective barrier that means it takes longer exposure to the sun for a dark skinned person to absorb sunlight into the lowest layer of skin, the stratum basale, where vitamin D is synthesized. I've explained this to you numerous times but you are too stuck on stupid to get it. Now buzz off, liite ant
Lionese
Once again, in spite of the presentation of mountains of explanatory data you continue showcase your the bottomless depth of immeasurable stupidity.
From your myopic understanding of the vital role of melanocytes and Eumelanin, you are stuck in the false belief that Eumelanin's only role is UV protection.
Since you are extremely dumb I will repost information that seems to make you believe that eumelanin is non-essential to life in Chicago.
Also, for the last time I will remind you that is limited to a very narrow band of UV in the 560nm range ONLY. Therefore, collection of solar radiation for later conversion to 1.25 serum (vitaminD) is less than 100x as efficient as Eumelanin. Therefore, your false assumption that white skin allows vitamin D to be absorbed/converted faster than black skin is totally incorrect.
quote:Originally posted by the lioness,: Because dark skin is a protective barrier that means it takes longer exposure to the sun for a dark skinned person to absorb sunlight into the lowest layer of skin, the stratum basale, where vitamin D is synthesized.
quote:Originally posted by Narmerthoth: Lionese
Once again, in spite of the presentation of mountains of explanatory data you continue showcase your the bottomless depth of immeasurable stupidity.
In this case it's not because Lioness is stupid, it's just that when all you have to say is that one lie, then you say that one lie - over and over.
Posts: 22721 | Registered: Oct 2005
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posted
this is where Narmerthoth posts scientific charts pretending that he knows what he's talking about
The simple fact is that dark skin is unecessary to survive in Chicago
If you read everything Narmerthtoth posted above none of it pertains to the difference between tropical and Northern hemisphere climates and the differences in animals of these regions
Mike and Narmerthoth thinks climate is the same anywhere in the world. They are simple that way
Posts: 42924 | From: , | Registered: Jan 2010
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posted
From reading your immediate stupid response I can see that you still fail to comprehend and put together the information I've posted.
The first graph shows that your understanding of the roles of the melanocyte are albino deep. In spite of the info neing right in front of your eyes, you still repeat the same silliness. Ask yourself, why is melatonin and seratonin manufactured in the melanocyte? Here's a hint.
A biochemical factory requires energy to process products.
Eumelanin collects and utilizes stored energy in the melanocyte chemical factory. This role of Melanocyte/Eumelanin is true in Africa or Chicago.
Notice in the above graph, the elevation of energy states shown are for Eumalanin and not Phaemelanins. Why? Simply because the only important energy collector of the two is the superconducting Copper-Selenium based Eumelanin and not the sulphur based Paemelanin.
Posts: 4693 | From: Saturn | Registered: Apr 2012
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This proves you don't need dark skin to survive in China.
Mother Narure is not stupid like like Mike and Narmertot, over time nature will figure out that the body doesn't have to keep producing the melanin of a Nigerian to survive in Norway
Not all Chinese are white skinned but multi milliions are. They are soon to have the largest economy in the world, so what Mike and Narmertot think are "defectives" are not deterred
What Mike wants is the white skin ^^^ Chinese guy to call himself an albino to help the self esteem of black people. And if this guy had a more pointy nose and wider eye shape you'd swear he was European
The Supreme leader of North Korea. Kim Jong Un
so one day guys like this are going to call themselves "defective albinos" and this will help black people to feel good?
I don't see it happening
Posts: 42924 | From: , | Registered: Jan 2010
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quote:Originally posted by Narmerthoth: From reading your immediate stupid response I can see that you still fail to comprehend and put together the information I've posted.
The first graph shows that your understanding of the roles of the melanocyte are albino deep. In spite of the info neing right in front of your eyes, you still repeat the same silliness. Ask yourself, why is melatonin and seratonin manufactured in the melanocyte? Here's a hint.
A biochemical factory requires energy to process products.
Eumelanin collects and utilizes stored energy in the melanocyte chemical factory. This role of Melanocyte/Eumelanin is true in Africa or Chicago.
Notice in the above graph, the elevation of energy states shown are for Eumalanin and not Phaemelanins. Why? Simply because the only important energy collector of the two is the superconducting Copper-Selenium based Eumelanin and not the sulphur based Paemelanin.
this is a crusty old dude trying to use old chemistry charts in place medical reference and biology
FACT #1 Dark skin is not needed to survive and thrive in Chicago
FACT #2 sunlight is not stored in the top skin for later use vitamin D synthesis That is psuedo scientific bullshit of the fake melanin Romanticists, white people have them throughly brainwashed to think skin is the more important than the brain
Obviously you can't have it both ways. Dark skin protects against skin cancer by absorbing a certain amount of sunlight in that top layer that is dark, No energy is not stored in there for later use. That is a lie. A certain amount of sunlight gets past the dark pigmented barrier and penetrates to the lowest of the 7 layers of skin where it is not stored, it is processed immediately into Vitamin D.
Don't take my word for it look up in google how vitamin D is sytheszied in the body and the role of dark pigmentation and skin cancer
-not these old crusty racist snake oil salesmen trying to hustle a "Melanin battery" and talking about factories
Look at the chart he posted "Melanin battery" Is that biology NO It's some old BS gadget
Posts: 42924 | From: , | Registered: Jan 2010
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Albinos/Whites went to the northern latitudes for a weaker Sun, no other reason than that.
No fool they went in as dark skinned. Thousands of years later in the Northern Hemisphere nature figured out this is not Ghana so people don't need to be dark
Again Mike has no understanding of how climates are different in the world
Posts: 42924 | From: , | Registered: Jan 2010
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quote:Originally posted by Mike111: ^HIS (the Koreans) "Normal" progenitor.
.
Assuming that Himba women have bone straight hair which they don't stupid
quote:Originally posted by Mike111:
YOUR (the Europeans) "Normal" progenitor.
.
Albinos/Whites went to the northern latitudes for a weaker Sun, no other reason than that.
Assuming this woman is Indian she could be the progenitor of Europeans.
As we see in Africa, albinos are not likely to form independant groups and go off on their own. The characteristic special eye problems that albinos have are another limiting factor for this
What happened was dark skinned people populated Europe. Over thousands of years nature figured out that you don't have to be as dark as a South Indian to live in France. So there is no need for the body to produce that much melanin
Even a child could understand this, it's so simple
Posts: 42924 | From: , | Registered: Jan 2010
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quote:Originally posted by Narmerthoth: From reading your immediate stupid response I can see that you still fail to comprehend and put together the information I've posted.
The first graph shows that your understanding of the roles of the melanocyte are albino deep. In spite of the info neing right in front of your eyes, you still repeat the same silliness. Ask yourself, why is melatonin and seratonin manufactured in the melanocyte? Here's a hint.
A biochemical factory requires energy to process products.
Eumelanin collects and utilizes stored energy in the melanocyte chemical factory. This role of Melanocyte/Eumelanin is true in Africa or Chicago.
Notice in the above graph, the elevation of energy states shown are for Eumalanin and not Phaemelanins. Why? Simply because the only important energy collector of the two is the superconducting Copper-Selenium based Eumelanin and not the sulphur based Paemelanin.
this is a crusty old dude trying to use old chemistry charts in place medical reference and biology
FACT #1 Dark skin is not needed to survive and thrive in Chicago
FACT #2 sunlight is not stored in the top skin for later use vitamin D synthesis That is psuedo scientific bullshit of the fake melanin Romanticists, white people have them throughly brainwashed to think skin is the more important than the brain
Obviously you can't have it both ways. Dark skin protects against skin cancer by absorbing a certain amount of sunlight in that top layer that is dark, No energy is not stored in there for later use. That is a lie. A certain amount of sunlight gets past the dark pigmented barrier and penetrates to the lowest of the 7 layers of skin where it is not stored, it is processed immediately into Vitamin D.
Don't take my word for it look up in google how vitamin D is sytheszied in the body and the role of dark pigmentation and skin cancer
-not these old crusty racist snake oil salesmen trying to hustle a "Melanin battery" and talking about factories
Look at the chart he posted "Melanin battery" Is that biology NO It's some old BS gadget
Liarness
Regarding your mislabelled factoids;
1. Albinos can "survive" in Africa/Israel, but they still have the highest skin cancer (and other internal cancers)incident rate of the world. In Chicago they capture even less UV in their melanin-less skin, so all their foods need to be fortified.
2. Melanocytes are not located "on-the-top" of skin. Only an albino who lacks them would make this mistake.
3. Of course Eumelanin STORES energy as the graph clearly shows. How else do you believe the body's chemical process can sustain itself, Magic?
LMBAO!!! You sure are a dunce.
Posts: 4693 | From: Saturn | Registered: Apr 2012
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Albinos/Whites went to the northern latitudes for a weaker Sun, no other reason than that.
No fool they went in as dark skinned. Thousands of years later in the Northern Hemisphere nature figured out this is not Ghana so people don't need to be dark
Again Mike has no understanding of how climates are different in the world
The return of rickets
by ROBIN YAPP, Daily Mail
It was virtually eradicated in Britain half a century ago as diets improved in the postwar boom.
But the childhood disease of rickets is on the rise again, nutritionists have warned.
They say it is because a generation of inactive children are not getting enough sunlight and not consuming enough milk and dairy products.
These are the main sources of vitamin D, the nutrient which protects against the bone condition - but up to 20 per cent of British children receive too little.
Experts say hundreds of children are developing the disease every year and they fear many more go undiagnosed because doctors no longer recognise the symptoms.
Rickets softens the bones and can cause deformities such as bow legs or chest and pelvis abnormalities, which may require corrective surgery.
The condition was widespread in Victorian times when it was potentially fatal. But with improved diet and the provision of vitamin D supplements it was all but wiped out in Britain during the 1950s and cases have been extremely rare ever since.
Now, the popularity of macrobiotic diets - free of dairy products, as well as meat and wheat - is being linked to the disease's re-emergence.
posted
yes Mike, because modern Britains stay indoors too much and don't live in the tropics Vitamin D deficiency is a problem. It's even more of a problem for Black and other dark skinned Britains who have skin more adapted to environments of the opposite nature-excessive sunlight, get it? All of these Britons need supplementation or eat more oily fish
And you you are not going to see those rates if rickets in southern Spain.
Similarly Blacks living in California are less at risk than those living in New York Therefore the requirements are very different depending on where you live and is more prevalent in the winter So you can't make blankets statements about America or Europe Articles can come to different conclusions based on waht regions they are looking at
People with a naturally dark skin tone have natural sun protection and require at least three to five times longer exposure to make the same amount of vitamin D as a person with a white skin tone.
Black people absorb more UVB in the melanin of their skin than do white people and, therefore, require more sun exposure to produce the same amount of vitamin D
Lancet. 1982 Jan 9;1[8263]:74-6.
Increased skin pigment reduces the capacity of skin to synthesise vitamin D3.
Clemens TL, Adams JS, Henderson SL, Holick MF. Abstract To determine the effect of increased skin pigment on the cutaneous production of vitamin D3, circulating vitamin D concentrations were determined in two lightly pigmented Caucasian and three heavily pigmented Negro volunteers after exposure to a single standard dose of ultraviolet radiation [UVR]. Exposure of Caucasian subjects to 1 minimal erythemal dose of UVR greatly increased serum vitamin-D concentrations by up to 60-fold 24-48 h after exposure, whereas this dose did not significantly change serum vitamin-D concentrations in Negro subjects. Re-exposure of one Negro subject to a dose of UVR six times larger than the standard dose increased circulating vitamin D to concentrations similar to those recorded in Caucasian subjects after exposure to the lower dose. These results indicate that increased skin pigment can greatly reduce the UVR-mediated synthesis of vitamin D.
_______________________________
J Nutr. 2008 Aug;138[8]:1482-90.
Higher prevalence of vitamin D deficiency is associated with immigrant background among children and adolescents in Germany.
Hintzpeter B1, Scheidt-Nave C, Müller MJ, Schenk L, Mensink GB. Author information Abstract In recent years, a high prevalence of vitamin D deficiency among children and adolescents has been reported in countries with moderate climates. Those with an immigrant background living under these conditions are at especially high risk. To date, representative data in Germany is lacking. We analyzed 25-hydroxyvitamin D [25[OH]D] concentrations of 10,015 children and adolescents, aged 1-17 y, who participated in the German National Health Interview and Examination Survey for Children and Adolescents. The proportion of immigrants was 25.4%, corresponding well to their percentage of the population. Among 3- to 17-y-old participants, 29% of immigrant boys and 31% of immigrant girls had 25[OH]D concentrations <25 nmol/L [severe to moderate vitamin D deficiency] compared with 18% of nonimmigrant boys and 17% of nonimmigrant girls. Furthermore, 92% of immigrant boys and 94% of immigrant girls had 25[OH]D concentrations <75 nmol/L [levels above 75 nmol/L are defined as optimal regarding various health outcomes] compared with 87% of nonimmigrants. Boys with a Turkish or Arab-Islamic background had an increased risk of having 25[OH]D concentrations <25 nmol/L compared with nonimmigrants [odds ratio [OR] 2.3; [95% CI] 1.4-3.8 and OR 7.6; [95% CI] 3.0-19.1]. The same was true for girls with a Turkish [OR 5.2; [95% CI] 2.9-9.6], Arab-Islamic [OR 5.9; [95% CI] 2.5-14.0], Asian [OR 6.7; [95% CI] 2.2-19.8], or African [OR 7.8; [95% CI] 1.5-40.8] background. Supplementation of vitamin D beyond infancy, especially in high-risk groups, or fortification of food should be considered.
Posts: 42924 | From: , | Registered: Jan 2010
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^So lioness, is it your self ascribed function to submit, and re-submit, these bogus Albino studies, which we have many times debunked, ad-infinitum?
Clearly that is indeed what you are doing, but to what end? Is it to make you, Doxie and Cass happy, or do you believe that our gallery has such short memories?
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They are not my target audience Further, the article at top is 2014 It's you and Namer re-hashing your old arguments and cute pictures of mythical Melanin batteries and Himba women dead horse psuedo science which I have to beat down again in an effort to educate
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Blacks do not suffer from any vitamin D deficient.A new study show that the 25-hydroxyvitaminD standard test does not s ascertain the bioavailability of this vitaminin the blood stream of blacks.The 25- hydroxyl form is bound to a protein,therfore bone cells ect have difficulty in accessing it.
Posts: 121 | From: Guyana | Registered: Mar 2012
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quote:Originally posted by the lioness,: They are not my target audience Further, the article at top is 2014 It's you and Namer re-hashing your old arguments and cute pictures of mythical Melanin batteries and Himba women dead horse psuedo science which I have to beat down again in an effort to educate
Fool, several real medical studies by several universities have already conclusively proven black women acquire and store vitamin D more effectively than white women.
The study shows that albinos excrete significantly higher percentages of vitamins than black women while black women retained and stored approx. 20% of daily requirement.
LOL. No doubt you'll be posting yet another bogus study on this topic tomorrow, but the National Institute of Health has already validated the conclusions of the above mentioned studies. So, you're just wasting everyone's time.
quote:Originally posted by Ponsford: Blacks do not suffer from any vitamin D deficient.A new study show that the 25-hydroxyvitaminD standard test does not s ascertain the bioavailability of this vitaminin the blood stream of blacks.The 25- hydroxyl form is bound to a protein,therfore bone cells ect have difficulty in accessing it.
As I have just explained you can't make blanket statements like that, it depends on the country or in the U.S. it depends on the state. Mike has just pointed out that rickets cases which are a result of severe Vitamin D deficiency are on the rise in Britain, And people who are deficient in Vitamin D but not to the point of have rickets are much greater in number And a higher percentage of those people are blacks and other dark skinned persons
quote:Originally posted by the lioness,: They are not my target audience Further, the article at top is 2014 It's you and Namer re-hashing your old arguments and cute pictures of mythical Melanin batteries and Himba women dead horse psuedo science which I have to beat down again in an effort to educate
Fool, several real medical studies by several universities have already conclusively proven black women acquire and store vitamin D more effectively than white women.
The study shows that albinos excrete significantly higher percentages of vitamins than black women while black women retained and stored approx. 20% of daily requirement.
LOL. No doubt you'll be posting yet another bogus study on this topic tomorrow, but the National Institute of Health has already validated the conclusions of the above mentioned studies. So, you're just wasting everyone's time.
No one should respond to a chart of which the person who posted it puposely leaves out the title of the article or link in order to try to bamboozle the readership
further, the topic is vitamin D not calcium intake
Posts: 42924 | From: , | Registered: Jan 2010
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quote:Originally posted by the lioness,: They are not my target audience Further, the article at top is 2014 It's you and Namer re-hashing your old arguments and cute pictures of mythical Melanin batteries and Himba women dead horse psuedo science which I have to beat down again in an effort to educate
Fool, several real medical studies by several universities have already conclusively proven black women acquire and store vitamin D more effectively than white women.
The study shows that albinos excrete significantly higher percentages of vitamins than black women while black women retained and stored approx. 20% of daily requirement.
LOL. No doubt you'll be posting yet another bogus study on this topic tomorrow, but the National Institute of Health has already validated the conclusions of the above mentioned studies. So, you're just wasting everyone's time.
No one should respond to a chart of which the person who posted it puposely leaves out the title of the article or link in order to try to bamboozle the readership
further, the topic is vitamin D not calcium intake
This study in it's entirety has already been posted several times on the site. In fact, both Mike and I just reposted it (for you) a couple weeks ago. LOL!
UBBFriend: Email this page to someone!
Lionese
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