From the land of the Navajo, let us go southward into Mexico once again, to a coastal community of another indigenous people. Although genetically unrelated, the Navajo of the United States and the Seri of Mexico share a problem that has both a genetic and a nutritional component: adult-onset diabetes. This nutrition-related disease is one of the three top causes of death among these two Native American groups and among many other indigenous communities as well. Ironically, a half century ago, its presence as a health risk was so minor in these communities that more Indians were dying each year of accidental snake bite than of diabetes. To understand why that change occurred, and what it means for all of us, we must listen not just to epidemiologists, but to the native peoples themselves.
It was in a small, run-down health clinic on a beach of Mexico’s Sea of Cortes that an Indian elder gave me a memorable lesson about gene-food interactions. It was a lesson nested in place—the hot desert coastline studded with giant cactus; that particular Indian village, where people cooked most of their food on small campfires in the sandy spaces between shabby government-built houses; and in that clinic, with no windows and no equipment, so rarely frequented by a doctor that we had planted a garden of healing herbs around it in case there was ever a medical emergency. It was in this place that Seri Indian Alfredo Lopez Blanco challenged me—and Western-trained scientists in general—to pay protracted attention to diet change and its role in disease.
I had accompanied my wife Laurie Monti, nurse-practitioner turned medical anthropologist, who was screening Seri families for adult-onset diabetes. The disease was already running rampant through neighboring tribes, but because the Seri are the last culture in Mexico to have retained hunting, fishing, and foraging traditions instead of adopting agriculture, there was some hope that they could stave it off. Only a few of the some 650 tribal members had ever been screened for the noninsulin-dependent form of diabetes, and that smaller, earlier sample had suggested that only 8 percent of the tribe suffered from chronically high blood-sugar levels and low insulin sensitivity.
While Laurie was screening Seri families in the sole office that contained any semblance of sanitary surfaces, I was in the “waiting room”—a sort of stripped-down echo chamber full of barking dogs and crying babies—trying to interview the elders of each family about their genealogical histories. I was attempting to ascertain whether the genetic susceptibility to diabetes of individuals with 100 percent Seri ancestry might be different from those who claimed that some of their ancestors came from among the neighboring Pima and Papago (O’odham) tribes in Arizona, the ethnic populations reputed to have the highest incidence of diabetes in the world.
Alfredo Lopez Blanco returned to the waiting room after Laurie confirmed that his blood-sugar levels were unusually high. Alfredo, who had worked as a fisherman since he was a boy, had late in life become boatman and guide for marine and island biologists. In his late sixties, Alfredo often taught younger Seri about the days when their people had subsisted on seafood, wild game, and desert plants like cactus fruit and mesquite pods. He was keenly aware of the traditional diet of his own people, and of his neighbors as well. When he sat down with me, I asked him if any of his forefathers happened to be from other tribes. He answered that one of his great grandmothers was from a Papago-Pima community.
“But Hant Coaaxoj,” he called me by my Seri nickname, Horned Lizard, “I have a question for you. What does that have to do to my diabetes?”
“Well, I’m not yet sure that it does. But here’s why I’m asking. The Pima and Papago suffer from diabetes more than any other tribes. It might be in their blood,” I conjectured, groping for a way to explain the concept of genetic predisposition to a person whose native language does not contain the exact concept of “genes.” “If people have Pima blood in them, maybe they are more prone to diabetes.”
“Hant Coaaxoj,” he said dryly, “sometimes you scientists don’t know much history. If diabetes is in their blood—or for that matter, in our blood—why did their grandparents not have it? Why were the old-time Pima and Papago who I knew skinny and healthy? It is a change in the diet, not their blood. They are no longer eating the bighorn sheep, mule deer, desert tortoise, cactus fruit, and mesquite pods. Pan Bimbo bread, Coke, sandwiches, and chicharrones are the problem!”
The old man—whose sister died within a year of that conversation due to circulatory complications from her own diabetes—was pretty much right on the mark. Or at least that is what Laurie’s interpretation of her screening and my genealogical interviews later showed. Diabetes, aggravated by diet change, was clearly on the rise among the Seri, with more than 27 percent of the adults screened by Laurie showing impaired glucose tolerance. But there were also interesting differences between the village where Alfredo lived, Punta Chueca, and the more remote Seri village to the north, Desemboque, where Western foods and other signs of acculturation were much less prominent. While diabetes prevalence in Desemboque had only recently reached 20 percent of the adults in Laurie’s sample, it exceeded 40 percent in Punta Chueca.
Other public-health surveys of the Seri suggested why this might be the case. Punta Chueca’s residents had easier access to fast-food restaurants and minimarts than did Desemboque dwellers. Roughly 15 percent more of Punta Chueca’s residents consumed groceries purchased in nearby Mexican towns on a daily basis, rather than relying more heavily on native foods from the desert and sea. The people of Punta Chueca consumed significantly more store-bought fats (such as lard), alcohol, and cigarettes.
When data from both villages were pooled, Seri individuals with some Papago-Pima ancestry did not show up as suffering from diabetes any more than those with 100 percent Seri ancestry. And yet, comparing the villages, there was one telling difference: those with Papago-Pima ancestry who ate more acculturated, modernized diets in Punta Chueca had the highest probability of the disease. As long as the Desemboque dwellers with Papago-Pima blood remained close to their traditional diet, diabetes among them was held more in check.
This trend held even though traditional Seri individuals in Desemboque appeared to weigh somewhat more than their counterparts in Punta Chueca. This suggests that it may not be the sheer quantity of food metabolized that triggers diabetes as much as the qualities of the foods the Seri now eat—especially the kinds of fats and carbohydrates regularly consumed.
This key distinction has slipped past the U.S. National Institutes of Health Indian Diabetes Project in the Sonoran Desert, which for nearly four decades has spent hundreds of millions of dollars trying to identify the underlying cause of the diabetes epidemic among the Pima and other indigenous communities. Its scientists and educators have all but ignored qualitative differences between Native American diets, preferring to seek a quick genetic fix to everyone’s problem at the same time. Several years ago, New Yorker writer Malcolm Gladwell called it the “Pima paradox”: “All told, the collaboration between the NIH and the Pima is one of the most fruitful relationships in modern medical science—with one fateful exception. After thirty-five years, no one has had any success in helping the Pima lose weight [and control diabetes]. For all the prodding and poking, the hundreds of research papers describing their bodily processes, and the determined efforts of health workers, year after year the tribe grows fatter.”
At most, the NIH epidemiologists have quantified how the contemporary Pima and their Indian neighbors eat more fast foods than ever before, especially ones detrimentally high in animal fats and simple sugars. But what the NIH has failed to discuss with Native Americans are the countless studies, including my own collaborations with nutritionists, that demonstrate how traditional diets of desert peoples formerly protected them from diabetes and other life-threatening afflictions now known as Syndrome X. This Syndrome X is not some sinister new disease, but rather a cluster of conditions that, when expressed together, may reflect a predisposition to diabetes, hypertension, and heart disease. The term—first coined by members of a Stanford University biomedical team—describes a cluster of symptoms, including high blood pressure, high triglycerides, decreased HDL (“good” cholesterol), and obesity. These symptoms tend to appear together in some individuals, increasing their risk for both diabetes and heart disease. And of course, all of these symptoms are influenced by diet, but what kind of diet most effectively reduces their expression was something that I seemed more interested in than anyone at the NIH or at Stanford.
In the 1980s, I began to collect traditionally prepared desert foods for nutritional analysis by Chuck Weber and Jim Berry in their University of Arizona Nutrition and Food Sciences lab, and for glycemic analysis by Jennie Brand-Miller and her colleagues who had already done similar work analyzing the desert foods traditionally consumed by Australian aborigines. By glycemic analysis, I refer to a simple finger-prick test for blood-sugar and insulin levels done as soon as a particular food is eaten, and every half hour afterwards; the test determines whether the food in question causes blood-sugar levels to rapidly spike after its ingestion, thereby causing pancreatic stress and asynchronies with insulin production.
Jennie Brand-Miller, a good friend as well as colleague, determined with her students that native desert foods—desert legumes, cacti, and acorns in particular— were so slowly digested and absorbed that blood-sugar levels remained in sync with insulin production, without any adverse health effects generated. Jennie called these native edible plants “slow-release foods” to contrast them with spike-inducing fast foods such as potato chips, sponge cakes, ice cream, and fry breads. The fast foods had glycemic values two to four times higher than the native desert foods, whose slow-release qualities Weber and Berry had shown to be derived from the foods’ higher content of soluble fiber, tannins, and complex carbohydrates.
Jennie had found the same trend when comparing Western fast foods with the native desert foods that Aussies call “bush tuckers”—the mainstays of aboriginal diets up until a half century ago, before which diabetes was virtually absent in indigenous communities of Australia. As with the desert tribes of North America, once these protective foods were displaced from aboriginal diets, the incidence of diabetes skyrocketed.
Back on an autumn night in 1985, Jennie and I were sipping prickly pear punch, having spent the day comparing the qualities of Australian and American desert foods. I could see that she was brewing over some large question, and she finally teased it out.
“Gary, I’ve wondered if there might be some explanation [for why desert peoples are vulnerable to diabetes, other than what the NIH promotes], one that you as a desert plant ecologist might help me figure out. I don’t know if I’m framing this question precisely enough, but let me give it a try: is there something that helps a number of desert plants adapt to arid conditions which might help control bloodsugar and insulin levels in the humans that consume them?”
“ What?” I blurted out. “Could you say that again?” Much later, I thought of a famous comment about the heart of science: “Ask an impertinent question and you are on your way to a pertinent answer.”
Jennie laughed, aware that she was asking a question far too complex to consider in the midst of the frivolity of a dinner party. “Oh, that’s OK,” she said quietly. “I just wondered if desert plants from around the world could have evolved the same protective mechanism against drought that somehow....”
“Oh, I think I get it now, some kind of convergent evolution,” I said. “If the same drought-adapted chemical substances show up in plants from various deserts that are scattered around the world, perhaps these substances formerly protected the people who consumed them from the risk of diabetes...” Then, once diets changed, the desert peoples who once had the best dietary protection from diabetes suddenly had their genetic susceptibility expressed!
Although Jennie posed it in passing, I could not forget her impertinent question, not that night, not that week, and not for a long time. Friends like Gabriel, as well as Alfredo Lopez’s sister, Eva, had died of diabetes, but they still inhabited my memory. I mused over Jennie’s question whenever I was out studying plants in the desert, and I brought it to the attention of some physiological ecologists who had a far deeper understanding of plant adaptations to drought than I did. They reminded me that desert plants and animals adapted to drought conditions by many different anatomical, physiological, and chemical means, and that there was probably not a single protective substance found in all arid-adapted biota.
In other words, the flora and the fauna from different deserts emphasized distinctive sets of these adaptive strategies. It was simply too much for these ecologists to imagine that a cactus from American deserts and a wichitty grub from the Australian outback might all share some dietary chemical that controlled diabetes among the Pima, Papago, and Seri of American deserts as well as among the Warlpiri and Pinkjanjara of Australian deserts.
Still, Jennie’s question was rooted in a valid observation: there was an apparent correlation between the extraordinarily high susceptibility of diabetes among desert peoples and the quantity of drought-adapted plants in their diets. If some aboriginal cultures had subsisted on drought-adapted plants and associated wildlife for upwards of 40,000 years, was it not plausible that these people’s metabolisms had adapted to the prevailing substances in these foodstuffs? And if, within the last fifty years, the prevalence of these foodstuffs had declined precipitously in their diets, was it not just as plausible that they had suddenly become susceptible to nutrition-related diseases because they had lost their protection? The question to pursue, then, was what dietary chemicals—nutrients or even antinutritional factors —might be more common in drought-adapted plants than those occurring in wetter environments?
With the help of ecophysiologist Suzanne Morse, I tried to imagine how water loss from a plant’s tissue was slowed by the adaptations developed by a desert-dwelling organism to deal with scant and unpredictable rainfall. At the time, I was involved in a number of field evaluations of drought tolerance in desert legumes, cacti, and century plants. I soon learned that prickly pear cactus pads contain extracellular mucilage, that is, gooey globs of soluble fiber that holds onto water longer and stronger than the moisture held within photosynthesizing cells. If a cactus is terribly stressed by drought, it may shut down its photosynthetic apparatus, shut its stomatal pores, and shed most of its root mass, going “dormant” until rain returns. But if stress is not so severe, the cactus will instead gradually shunt the moisture in its extracellular mucilage into photosynthetically active but water-limited cells, thereby slowing the plant’s total water loss while keeping active tissues turgid.
In explaining this concept—called “leaf capacitance”—to me, Morse offered me a parallel to slow (sugar) release foods: slow (water) release plant tissues. The very mucilage and pectin that slow down the digestion and absorption of sugars in our guts are produced by prickly pears to slow water loss during times of drought. And prickly pear, it turns out, has been among the most effective slow-release foods in terms of helping diabetes-prone native peoples slow the rise in their blood-glucose levels after a sugar-rich meal. In fact, it was among the first foods native to the Americas demonstrated to lower the blood glucose and cholesterol of indigenous people susceptible to diabetes. As Morse and I followed up on that research, we documented that most of the twenty-two species of cacti traditionally used by the Seri have the same slow-release qualities and are available along the desert coast much of the year.
Soon, Jennie Brand-Miller, in Sydney, and Boyd Swinburn, an endocrinologist from New Zealand, gave me greater insight into how slow-release foods differ from conventional foodstuffs in they way they are digested and absorbed. As I read reports about the “low gastric motility” of slow-release foods, I began to imagine how these foods make a viscous, gooey mass in our bellies. Even when our digestive juices cleave them into simpler sugars, the sugars have a tough time moving through the goo to reach the linings of our guts, to be absorbed and then transported to where they fuel our cells.
Here then, in the prickly pear—one of the food plants in the Americas with the greatest antiquity of use—was the convergence that Jennie had been seeking: the existence of slow-water-release mucilage in cactus pads and fruit explained why desert food plants were likely to produce slow-sugar-release foods. Five years after our conversation over prickly pear punch, I found a potential answer in the very plant Jennie and I had been consuming at the time she asked her impertinent question! The trouble was, prickly pear and other cacti are not native to Australian deserts; I began to investigate if there were plants in other deserts that also contained slow-water-release mucilages.
I soon learned that cacti are not special cases that occur only in the diets of desertdwelling Native Americans; there are dozens of other plants in both American and Australian deserts that have similar slow-sugar-release/slow-water-loss qualities, albeit with different morphologies and different chemical mechanisms. Given that desert peoples have been exposed to such plants for upwards of 10,000 years—more than 40,000 years in Australia—is there any evidence that these people’s metabolisms have adapted over time to the presence of these protective foods?
With regard to the Seri, the only general genetic survey comparing them to neighboring agricultural tribes indicates that the Seri exhibit “several micropolymorphisms [that] may be important in conferring a biological advantage” in their desert coastal homeland. The study claimed that “these may emphasize the relevance of interactions between genes and environment,” for Seri hunter-gatherers express several alleles not found in more agriculture-dependent U.S. and Mexican indigenous peoples (Infante et al. 1999).
But do long-time hunter-gatherers with such polymorphisms respond to certain desert and marine foods differently than other people do? The answer can be found in research that Jennie and colleagues have done contrasting various ethnic populations’ responses to foods common to one group’s traditional diet, but not the other’s. As Jennie and her fellow researcher Anne Thorburn have explained:
the aim of [our] next series of experiments was to compare the responses of healthy Aboriginal and Caucasian subjects to two foods, one a slow release Aboriginal bush food— bush potato (Ipomoea costata)—and the other a fast release Western food—[the domesticated] potato (Solanum tuberosum). Both Aborigines and Caucasians were found to produce lower plasma insulin responses to the slow release bush food than to the fast release Western food. But the differences were more marked in Aborigines, with the areas under the glucose and insulin curves being one-third smaller after bush potato than potato (Brand-Miller and Thorburn 1987).
In other words, the Aborigines were protected from diabetic-inducing pancreatic stress by a bush food that their metabolisms had genetically adapted to over 40,000 years. Caucasians, with hardly any exposure to this or similar bush foods since colonizing Australia, did not experience such marked benefits.
When many scientists learn of these differences, they recall the theory of a thrifty gene that indigenous hunter-gatherers are presumed to maintain as an adaptation to a feast-or-famine existence, and they attribute the differences in insulin response to that gene. As originally hypothesized by James Neel in 1962, hunter-gatherers were likely to exhibit a thrifty genotype that was a vestigial survival mechanism from eras during which they suffered from irregular food availability. “During the first 99 percent or more of man’s life on earth while he existed as a hunter-gatherer,” Neel wrote, “it was often feast or famine. Periods of gorging alternated with periods of greatly reduced food intake” (Neel 1962).
Neel persuasively argued that repeated cycles of feast and famine over the course of human evolution had selected for a genotype that promoted excessive weight gain during times of food abundance and gradual weight loss of those “reserves” during times of drought. Neel focused on food quantity—the evenness of calories over time—and not food quality, arguing that when former hunter-gatherers were assured regular food quantities over time, the previously adaptive genetic predisposition to weight gain became maladaptive.
However, the only early NIH attempt to characterize the diets of Pima women with traditional versus acculturated (modern) lifestyles found insignificant differences between the calorie amounts consumed by the two groups, nor was there much difference when both groups’ diets were compared to what surrounding Anglo populations ate. In other words, despite Neel’s hypothesis, food quantity alone did not account for the rise in diabetes among acculturated Pima Indian women.
Nevertheless, Neel’s argument has been cited by hundreds of scientific papers on diabetes and other diseases and has reached millions of other readers through “popular science” magazine essays written by such science-literate writers as the New Yorker’s Malcolm Gladwell, Harper’s Greg Cristner, Outside’s David Quammen, and Natural History’s Jared Diamond. What’s more, Neel’s hypothesis essentially drove the first thirty-five years of research at the NIH Indian Diabetes Project in Phoenix, Arizona, whose director and staff set their sights on becoming the first to discover the thrifty gene. Hundreds of millions of research dollars later, it is clear that their focus on a single gene and on sheer food quantity has blinded researchers to a variety of gene-food-culture interactions that may trigger or prevent diabetes.
Thirty-six years after proposing his famous hypothesis, Neel himself conceded that “the term ‘thrifty genotype’ has [already] served its purpose, overtaken by the growing complexity of modern genetic medicine,” adding that while type 2 diabetes may still be “a multifactorial or oligogenic trait, the enormous range of individual or group socioeconomic circumstances in industrialized nations badly interferes with an estimate of genetic susceptibilities” (Neel 1998).
Neel’s colleagues in biomedical research are much more direct in their assertion that there is no single thrifty gene that confers susceptibility to type 2 diabetes among all ethnic populations, or even among all hunter-gatherers. Assessing the recent identification of several genes that heighten or trigger diabetes, geneticist Alan Shuldiner of the University of Maryland School of Medicine told Science News, “I expect there would be dozens of diabetes-susceptibility genes [and that] specific combinations of these genes will identify risk” (Seppa 2002).
What these genes actually do is also different from what Neel and other pro-ponents of the thrifty genotype suspected they would do. When the NIH worked to determine whether the thrifty gene they had identified in the Pima was actually a gene for insulin resistance—which causes reduced metabolic sensitivity to sugar loads—researchers found this gene’s true function to be weight maintenance and not weight gain.
As molecular biologist Morris White of the Joslin Diabetes Center recently concluded in the pages of Science, “We used to think type 2 diabetes was an insulin receptor problem, and it’s not. We used to think it was solely a problem of insulin resistance, and it’s not. We used to think that muscle and fat were the primary tissues involved, and they are not. Nearly every feature of this disease that we thought was true 10 years ago turned out to be wrong” (White 2000).
Once again, it was my friend Jennie Brand-Miller who hammered the coffin closed on the thrifty gene hypothesis by refuting its very underpinnings—that famines were more frequent among hunter-gatherers than among agriculturists, leading to the former’s extraordinary capacity to accumulate fat reserves. In scanning the historic anthropological literature on periodic famine and starvation among various ethnic groups, Jennie and her colleagues found scant evidence that hunter-gatherers suffered from these stresses anywhere near as frequently as agriculturalists did. In fact, periodic starvation and wide-spread famines increased in frequency less than 10,000 years ago, after various ethnic groups became fully dependent on agricultural yields. In particular, Jennie noted, since Caucasians living in Europe have repeatedly suffered from famines in historic times, they ought to be predisposed to insulin resistance and diabetes if Neel’s hypothesis is correct. And yet, Caucasians are one of the few groups that do not exhibit much insulin resistance or heightened susceptibility to type 2 diabetes when they consume modern industrialized agricultural diets.
“The challenge,” Jennie and her colleagues argue, “is to explain how Europeans came to have a low prevalence and low susceptibility to adult-onset diabetes...” (Cordain et al. 2000). Indeed, Europe harbors most of the world’s ethnic populations who have not suffered dramatic rises in this nutrition-related disease since 1950.
At an international workshop that Jennie and I hosted at Kims Toowoon Bay on the coast of New South Wales in May of 1993, we elucidated four factors that could explain why individuals of European descent appear to be less vulnerable to Syndrome X maladies—including diabetes—than do ethnic populations that have adopted agricultural and industrial economies more recently. With colleagues from four countries, including Australian Aborigines and Native Americans, we identified that the incidence of diabetes rapidly increases under the following four circumstances.
First, when an ethnic population shifts to an agricultural diet and abandons a diverse cornucopia of wild foods, its members lose many secondary plant compounds that formerly protected them from impaired glucose tolerance. This is particularly true for populations that have coevolved with a certain set of wild foods over millennia, ones that are rich in antioxidants.
Second, when the remaining beneficial compounds in traditional crops and free-ranging livestock are selected out of a people’s diet through breeding and restricted livestock management practices, their diet is further depleted of protective factors. For instance, modern bean cultivars have been bred to contain less soluble fiber, and livestock raised on cereal grains under feedlot conditions lack omega-3 fatty acids.
Third, the industrial revolution that began in Europe in the seventeenth century changed the quality of carbohydrates in staple foods by milling away most of the fiber in them. High-speed roller mills now grind grains into easily digested and rapidly absorbed cereals and flours, which results in blood-sugar and insulin responses two to three times higher than those reported from whole grains or coarse-milled products like bulgur wheat.
Fourth, the last fifty years of highly industrialized foods has introduced additives such as trans-fatty acids, fiber-depleted gelatinous starches, and sugary syrups, which ensure that most fast foods are truly fast-release foods. Jennie estimates that the typical fast-food meal raises blood-sugar and insulin levels three times higher than humans ever experienced during preagricultural periods in our evolution. Combined with the trend toward oversize servings of convenience foods and a more sedentary lifestyle, the dominance of fast foods in modern diets has made contemporary humans less fit than ever.
Although nearly all ethnic populations have come to suffer from fast foods over the last quarter century, the other changes took place in European societies over thousands of years. Whereas the genetic constituency of European peoples may have slowly shifted with these technological and agricultural changes as they emerged, the Seri and Warlpiri have had less than fifty years to accommodate these changes, and their genes are not in sync with them. Significant adaptation through evolutionary processes to new diets rarely occurs over the course of two to three generations.
And yet, most people now living in the world fall somewhere between the French and German farmers on the one hand, and the Seri and Warlpiri hunter-gatherers on the other. The majority of traditional diets have historically been more like the Pima and Papago in the Arizona deserts, where perhaps 60 percent of foods were harvested from domesticated crops in wet years while the rest came from wild and weedy plants and free-ranging game or fish. In dry years, the Papago-Pima diet shifted more toward the reliable harvests of drought-tolerant wild perennials.
While details richly vary around the world—from coastal habitats where fish were once abundant to rain forests where birds and root crops proliferated—most indigenous peoples in developing countries have maintained, until recently, a healthy mix of wild foods and diverse cultivated crops. Today, following dramatic economic shifts that have favored a few cereal grains and livestock production for export over mixed cropping, the bulk of the world’s population has been left vulnerable to diabetes. One recent reckoning suggests that upwards of 200 million people are now susceptible to diabetes and the other killers associated with Syndrome X. This is not the exception among the diverse peoples of the world; it is a pathology that has become the norm.
But while fast foods lead to rapid deterioration of healthy carbohydrate metabolism in most people—with or without the existence of a thrifty gene—a return to the traditional foods of one’s own ancestry leads to rapid recovery. This is what New Zealand endocrinologist Boyd Swinburn found when he asked me to help him reconstruct a semblance of the nineteenth-century dietary regime for the Pima and Papago. Swinburn wanted to compare the effects of a traditional versus a fast-food diet, both consisting of the same number of calories and percentages of carbohydrate and fats.
When twenty-two Pima Indians in his study were exposed to the fast-food diet, their insulin metabolism deteriorated enough to trigger diabetic stress without the need to conjure up any other explanation to explain it. Yet when the same individuals were placed on the traditional diet rich in soluble fiber and other secondary plant compounds, their insulin sensitivity and glucose tolerance improved. Swinburn and his coworkers concluded that “the influence of Westernization on the prevalence of diabetes may in part be due to changes in dietary composition [as opposed to food quantity]” (Swinburn et al. 1993).
I followed Swinburn’s clinical study with a demonstration project at the National Institute for Fitness outside St. George, Utah, where eight Pima, Papago, Hopi, and Southern Paiute friends suffering from diabetes came together for ten days of all-you-can-eat slow-release foods and outdoor exercise. Within ten days, their weight and their blood-sugar levels had been dramatically reduced, and everyone felt healthier. The changes began so immediately that several participants had to seek medical advice to figure out how to reduce the hypoglycemic medications they had been self-administering for years.
In yet another example, in what may be one of the most dramatic gains in health conditions ever witnessed in a short period of time, Kieran O’Dea documented the marked improvement in diabetic Australian aborigines after they reverted for a month to a nomadic foraging lifestyle in western Australia. Even though study subjects “poached” several free-ranging cows as part of their meat consumption, their diet primarily consisted of bush foods that their ancestors had long eaten. The aboriginal participants moved frequently to take advantage of hunting and plant-gathering opportunities, and they lost considerable weight while doing so.
Their consumption of calories from macronutrients was 54 percent protein, about 20 percent plant carbohydrates, and 26 percent fat. These proportions had a dramatic effect on lowering blood-sugar levels and increasing insulin sensitivity. While some critics have conjectured that their insulin sensitivity, glucose tolerance, and cholesterol levels improved merely because of the subjects’ weight loss, others have pointed out that the ratio of macronutrients they consumed certainly did not worsen their condition. While not necessarily optimal for all ethnic populations, a diet with this mixture of macronutrients clearly brought health benefits to the Australian desert dwellers that participated.
Inspired by O’Dea’s collaboration with indigenous sufferers of diabetes, I organized a similar moveable feast in the spring of 1999, engaging more than twenty Seri, Papago, and Pima individuals who also suffered from diabetes. We walked 220 miles through the Sonoran Desert during a twelve-day pilgrimage, fueled only by native slow-release foods and beverages. Although we did not measure our blood-sugar and insulin levels each day to compare our health status before and after our journey, we took note of something perhaps far more significant: the native foods we ate were considered by all the participants to be nutritious, satisfying, and filling enough to sustain our arduous pilgrimage. These foods enabled us to hike across rugged terrain for ten hours a day, followed by another hour or two of celebratory dancing.
Our collective effort made us more deeply aware that our own energy levels could be sustained for hours by slow-release foods. At the same time, we took a good hard look at the health of our neighbors and of the land itself. The pilgrimage allowed us to clearly see for the first time all the damage that had been done to our homeland and its food system, damage that was echoed in our very own bodies.
There was something else going on among my Native American companions during that walk. The Seri, Papago, and Pima pilgrims frequently expressed that their cultural pride, spiritual identity, and sense of curiosity were being renewed. And so, a return to a more traditional diet of their ancestral foods was not merely some trip to fantasy land for nostalgia’s sake; it provided them with a deep motivation for improving their own health by blending modern and traditional medical knowledge in a way that made them feel whole. They were not eating native slow-release foods merely to benefit a single gene—thrifty or not. Instead, they were communing to keep their entire bodies, their entire communities, and the entire Earth healthy.
Yes, genes matter, but diverse diets and exercise patterns matter just as much. And when the positive interaction among all three of these factors is reinforced by strong cultural traditions, our physical health improves, as does our determination to keep it that way. The Native American folks I walked with on that pilgrimage have re-doubled their commitments to keep their traditional slow-release foods accessible in their communities; they serve them at village feasts and at wakes honoring those who have succumbed to the complications of diabetes for lack of earlier access to these foods. When the persistence of traditional foods is more widely recognized as a source of both cultural pride and as an aid to physical survival and well-being, I doubt that many Native American communities will abandon what many of them feel to be a true gift from their Creator.
* Originally published 2004
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